19 August 2017
Having spent many years smashing everything into pieces in an attempt to work out what is going on with cardiovascular disease, I am now going to attempt the amazing feat of bringing everything together in some sort of coherent structure. I have no idea how long this may take, so please bear with me while I first set the scene by making a couple of point that need to be made.
Point One:
‘Explanations exist; they have existed for all time; there is always a well-known solution to every human problem — neat, plausible, and wrong.’ H.L. Mencken.
Cardiovascular disease is best seen as a process. Attempts to find the key, single, cause has created the massive multifactorial monster we see before us today. Unfortunately, the trap of searching for a/the cause seems to be hard wired into our thinking. This approach has worked well for things such as infectious diseases and suchlike, but it does not work here. I have lost track of the number of times someone has come up with the new cause of CVD, then tried to crowbar all observations to fit. Or simply dismiss contradictory evidence.
- It’s caused by infections
- It’s all due to vitamin C deficiency
- It’s all due to blood sugar
- Its’ all due to inflammation etc. etc. etc. etc. etc.
It’s…….
In truth, I was as guilty of this as everyone else. I believed that ‘stress’ was the cause, and everything could be incorporated within this factor. This is not true. Stress/strain represents one factor that is capable of causing CVD – quite an important one – but it cannot explain everything.
Whilst there obviously are ‘causes’ of cardiovascular disease, they cannot be understood in isolation from process(es). What is going on, and why, and how can things that seem to cause cardiovascular disease be fitted into these processes.
It may seem intellectually unsatisfactory to move away from a simple, single, cause model. We all want the E=MC2 moment, or the untangling of the structure of DNA moment. Eureka! That was never going to happen here, or it would already have happened. If there truly were a single cause it would have been found by now – and it hasn’t.
Point Two:
The evidence base is flawed. In part because studying complex biological systems is, in itself, very difficult to do. The number of variables involved is mind-boggling, and the number possible interactions between those variables is mind boggling to the power one trillion. If you are looking for absolute certainty…. look elsewhere.
Just to give one example of how many potential factors there are. Here is part of a paper by researchers, who looked at geomagnetic disturbance and its impact on heart attacks and strokes (Russian paper):
‘It was shown statistically that during geomagnetic disturbances the frequency of myocardial infarction and brain stroke cases increased on the average by a factor of two in comparison with quiet geomagnetic conditions. These results are close to results obtained by (Stoupel, 1999), for patients suffering with acute cardiological pathology. Our recent study (with L.Parfeonova) revealed the relation between heart ventricular ectopic activity (VEA) and geomagnetic conditions in patients with CHD. On the average 1995 episodes of VEA having on one patient within 24 hours have been revealed in patients, whose records coincided with the periods of geomagnetic storms and 1440 VEA episodes for active conditions. Minimal quantity of VEA episodes was found for unsettled condition: 394. In a quiet geomagnetic condition VEA episodes appeared more often than in periods of unsettled conditions.’1
How many researchers have taken geomagnetic disturbances into account as a potential confounding factor in their research? I would suggest, none. Yet here is a factor that can (possibly) increase the risk of CVD events by 100%.
I chose this example, almost at random, to highlight the point that this stuff is complicated, and there any many, many, uncertainties involved. Can you control any study for all factors ever found to be associated (causally or otherwise) with CVD? No, you cannot.
Alternatively, you can do what many people do. Dismiss research that seems contradictory, or just daft. I can see many people automatically seeking to dismiss a Russian study about the effect of geomagnetic disturbance on CVD on the dual grounds that is a: Russian and b: bonkers. That would be unwise.
Of course, there is the other problem that much of medical research (especially in the highly lucrative area of CVD) has been funded by the pharmaceutical industry, resulting in the problem that most research findings are false:
‘There is increasing concern that most current published research findings are false. The probability that a research claim is true may depend on study power and bias, the number of other studies on the same question, and, importantly, the ratio of true to no relationships among the relationships probed in each scientific field. In this framework, a research finding is less likely to be true when the studies conducted in a field are smaller; when effect sizes are smaller; when there is a greater number and lesser preselection of tested relationships; where there is greater flexibility in designs, definitions, outcomes, and analytical modes; when there is greater financial and other interest and prejudice; and when more teams are involved in a scientific field in chase of statistical significance. Simulations show that for most study designs and settings, it is more likely for a research claim to be false than true. Moreover, for many current scientific fields, claimed research findings may often be simply accurate measures of the prevailing bias.’2
This is a famous paper, one of the most cited and read in medical research history. It was written in 2005 and things have got worse, not better, since then.
Oh, but of course, peer review keeps everything on the straight and narrow:
‘The mistake, of course, it to have thought that peer review was more than a crude means of discovering the acceptability – not the validity – of a new finding. Editors and scientists alike insist on the pivotal importance of peer review. We portray peer review to the public as a quasi-sacred process that helps to make science our most objective truth teller. But we know that the system of peer review is biased, unjust, unaccountable, incomplete, easily fixed, often insulting, usually ignorant, occasionally foolish, and frequently wrong.’ Richard Horton, editor of the Lancet.
In this morass, where does one turn?
This is a question that has no definitive answer. Shall I just choose evidence that suits my argument, and dismiss all else? To an extent, the difficulty in disentangling evidence was my spur to write the book Doctoring Data. In it, I attempted to determine what is valid and what is not. How to spot the biases and errors. How to know what it true, from the other stuff?
Answer… it cannot be done. Not for certain. Whatever evidence I choose, it can be criticised – in one way or another. Did the study I am quoting control for geomagnetic disturbance or not? As a general rule, any study – and I mean any study – can be pulled apart and dismissed, if you so wish. Which could leave most of what I do as a smoking ruin.
However, most of the research I look at has one major advantage. There is not much, if any, financial interest, behind it. Other than suppressing it, I suppose.
Yes, of course, I bring certain biases to the discussion. I am almost entirely anti-statin. I am not a great believer in blood pressure lowering – at least not at current levels. I do not believe in the cholesterol hypothesis and I think that the anti-saturated fat dogma is completely bonkers and has no evidence to support it – at all. I believe that salt is good for and, in most people, protects against CVD.
I believe that a high carbohydrate low fat diet is utterly bonkers – especially in those with diabetes. And suchlike. In short, I believe that almost everything we are told is good for you, is bad for you, and vice-versa. With the exception of smoking (bad) and exercise (good).
Having got that out of my system. Let us begin….. in the next blog.
1: http://adsabs.harvard.edu/abs/2014cosp…40E1114G
2: http://journals.plos.org/plosmedicine/article?id=10.1371/journal.pmed.0020124
Dr. Malcolm Kendrick 
@malcolm Have you read ‘ The Salt Fix’ written by James Dinicolantonio? It’s very interesting
I communicate with James on a reasonably regular basis – we share many ideas.
Loved his book! Read it twice! Added salt to water on hikes in HK last month and it was a lifesaver!
SW: Agreed! When I take my weekly hike in the high Sierra I add to 36 oz (a bit more than a liter) of mineral water: 1/4 tsp (1mL) potassium bicarbonate, 1/2 tsp (2.5mL) ascorbic acid, and 2 tsp. (10mL) Realsalt, and sip along the way. Dr. DiNicolantonio says putting salt in water is like drinking sweat, but I don’t mind drinking sweat. When I run out, which I do on a long hike, I have a spare bottle of purified water. This mineral-laden concoction, though really helps give me endurance. Even at high altitude I sweat.
DR K, is there a clue in this : https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3741888/ When Mammary artery ( IMA) is used for bypass is does not get diseased v Saph. vein…. has this been studied vis a vis CVD…. What protects IMA from atherosclerosis?
Same thing as protects veins.
Thanks for pointing to ‘The Salt Fix’. I will get a copy to read.
My copy of ‘The Salt Fix’ just arrived. This will be humbling reading, it seems well referenced. Apart from the last 5 years I was firmly in the minimal added salt camp. It’s like I bought a diesel car many years ago. We cannot avoid taking some expert opinion on trust.
“The evidence base is flawed. In part because studying [x y z] is, in itself, very difficult to do. The number of variables involved is mind-boggling, and the number possible interactions between those variables is mind boggling to the power one trillion. If you are looking for absolute certainty…. look elsewhere.”
Words I could have written myself. It is not just biological systems. You are an unusual medic. With some of my medical friends, I keep off discussion of many issues for this reason, and to stay friends.
I often struggle with, many of, my medical colleagues. They want black and white. Good and bad. Do it, or don’t do it. It is a comforting world of certainty.
sitting down, A cardiologist tried to get my husband on statins, his argument: ” I have both my parents on them…” WTF
This is going to seem way out of left field, but you might want to consider the writings of John Boyd on [un]certainty. Though he primarily focused on military affairs, his thinking is applicable to any process of information discovery & mental models of systems. The paradox he discovers is that any inward seeking system INCREASES confusion and disorder and therefore reduces certainty. In order to move forward, old mental models need to be shattered (destruction) and recreated (creation).
He only wrote one short eight page paper Destruction and Creation http://www.goalsys.com/books/documents/DESTRUCTION_AND_CREATION.pdf There are also a few video’s on youtube, particularily interesting is Conceptual Spiral (available as playlist on youtube). The accompanying slidepack is http://pogoarchives.org/m/dni/john_boyd_compendium/conceptual-spiral-20111100.pdf
Sounds interesting.
I liked this bit:
Recalling that we use concepts or mental
patterns to represent reality, it follows that the
unstructuring and restructuring just shown
reveals a way of changing our perception of
reality.Naturally, such a notion implies
that the emerging pattern of ideas and interactions
must be internally consistent and match
up with reality. To check or verify internal
consistency we try to see if we can trace
our way back to the original constituents that
were used in the creative or constructive induction.
If we cannot reverse directions, the
ideas and interactions do not go together in
this way without contradiction. Hence, they
are not internally consistent. However, this
does not necessarily mean we reject and
throw away the entire structure. Instead, we
should attempt to identify those ideas (particulars)
and interactions that seem to hold
together in a coherent pattern of activity as
distinguished from those ideas that do not
seem to fit in. In performing this task, we
check for reversibility as well as check to see
which ideas and interactions match up with
our observations of reality. Using those
ideas and interactions that pass this test, together
with any new ideas (from new destructive
deductions) or other promising ideas that
popped out of the original destructive deduction,
we again attempt to find some common
qualities, attributes, or operations to re-create
the concept—or create a new concept. Also,
once again, we perform the check for reversibility
and match-up with reality. Over and
over again, this cycle of Destruction and
Creation is repeated until we demonstrate internal
consistency and match-up with reality.
I like it, because I think that is what I am doing – albeit, I had no idea I was doing it. Smashing – recreating, smashing – recreating. Until, hopefully, something does emerge that has internal consistency, and matches up with reality. I just thought I was thinking about stuff.
Thank you for the reference to John Boyd. I did not know of him. I will follow up what you suggest.
I listened to the first YouTube on Conceptual Spiral, a very fascinating delivery on the topic. I read a book some years ago, “The Nature of Technology” by W. Brian Arthur (2009) that makes the same points. I checked the index – no mention of John Boyd; was that ignorance or wish not to reveal inspiration?
I like this drmalcolmkendrick.org, we have very good input and discussion. Might the moderator reveal what % of comment is moderated out?
About 1%. Usually adverts – very occasionally someone is being personally insulting. Anyone can make any point, hold any view, disagree vehemently – so long as they are arguing a point of view. The most common reason a comment does not appear is that I fail to spot them. I get about 500 e-mails every day, which is a little tricky at times.
“500 emails a day ” !!
I had no idea.
I wish you well dealing with the stress involved in coping with such a deluge. I am a bit amazed that you manage to write these posts.
Bill in Oz: I suspect Dr. Kendrick finds it very intellectually stimulating and satisfying. Agreed, though, that’s a huge amount of work, for which we are eternally grateful!
Here is a retired neuro-psychiatrist Dr. Miklashek with an interesting view of what causing the main health problems. Some of his idea go in line with what Dr.Kendrick has posted about stress.
“We came to realize that essential hypertension, heart attacks, and strokes; abdominal obesity and type 2 diabetes; suppressed immune function and the resultant increased vulnerability to infections; anxiety, depression, and suicide; addictive disease and other obsessive-compulsive disorders; kidney disease; thyroid disease; peptic ulcers and inflammatory gut diseases, as well as cancers, may be resulting from and, even, “biomarkers” of COASTER! Thus, a new model would be necessary to understand what was really making us anxious, depressed, so physically ill, and killing us.
This new population regulation model..
This new population regulation model is, by contrast, based on long known scientific evidence of our silent epidemic of Chronically Over Active STrEss Responses “C.O.A.S.T.E.R.”
More recent neuro-endocrine researches on animals and humans have established the gene based neuro-hormonal mechanisms of population density stress induced diseases, and even total population collapse from the triggering of “the kill-switch”. These researches strongly suggested that we rethink COASTER as a population control mechanism.”
.https://mahb.stanford.edu/wp-content/uploads/2014/08/StressRUs_2017_Miklashek.pdf
Point Of Information on the subject of moderation – I routinely find myself being blocked on a whole bunch of blogs, including some where I know the blogger personally, and on most of the others the blog owners assure me it is not them blocking me.
Since I am effectively a Nothing, I am certain this is personal, and I suspect I know who the vindictive individual is, just not how they do this – since they often have difficulty typing in a straight line she must have help from elsewhere to achieve anything remotely technological.
After a while I generally get unblocked again, until the next time.
Obviously the attempts to block high profile peeps like Tim Noakes, Gary Fettke et al. generally become public knowledge very quickly, albeit there seems to be a mainstream press embargo on such information. I ponder the mentality of people so insecure that they resort so easily to censorship to defend their dogma,
Thanks for the John Boyd reference, will peruse later. I may not be that bright intellectually, but my brain likes to find patterns.
Yes, let’s begin, again.
This sounds like the introduction to something really great.
The paper relating cardiac events to the magnetosphere is interesting, especially since it is listed under astronomy rather than physiology, and they’re looking at the effect of solar activity , but I presume that is because there are concerns about the potential effects of spending long periods in space. However, perhaps we shouldn’t be surprised as the cardiac system is electrical in nature, blood circulation is the movement of iron in a magnetic field, which could induce an electric current, and at the molecular level some molecules have an unequal distribution of charge around them. This could suggest that MRI scanners might not be as safe as they’re thought to be!
Sea creatures kept in labs miles from the coast still respond to tides. We are essentially bags of salty water, Is it apocryphal or actually true that Emergency Services report increased activity around the full moon? – aka lunacy.
Since the gravitational pull of the moon remains the same whether it is new or full, any effect must be due to changes in illumination. Maybe more people prowl about at night when the moon is bright and get themselves into trouble.
Aren’t ocean tides connected to lunar cycles? Or do I have this wrong?
chris c: They don’t do it any longer, but when my cats were growing up, they tended to go berserk at the full moon, playing chase all over the house.
According to Ayurveda it’s true. That’s why in Hinduism traditional fasting days are tied to lunar cycles
Sasha,
Good point. At new and full moon the earth, moon, and sun line up, whereas in between they are at right angles. So maybe the increased combined gravitational pull at full moon is making people (and molluscs) light-headed.
it does create bigger tides according to what I read and since we’re basically bags of salt water as was mentioned earlier, it’s not unreasonable to assume it has effects on us as well.
Sasha: Yes, as I understand it, some biological cycles, such as the menstrual cycle, are lunar. By the way, I read an article today stating that Russia is having a record wheat and corn harvest this year, with barley not far behind, bigger than any the Soviets ever produced. Wonder if the media will place the blame on Trump?
Gary: there’s some good research in acupuncture showing pulse changes connected to solar noon, for example, but it’s too long to go into here.
I also find it interesting that menstrual cycles often synchronize when women live together and, I think, Sapolsky says they synchronize according to the cycle of the dominant female.
I understand that the idea of synchronisation had been proved not to happen?
Well, having spent 3 years at an all female university run by nuns, I can tell you that synchronisation certainly appeared to happen – it was the synchronised PMT that caused the most problems!
Yes, lots of anecdotal evidence for this
I think Sapolsky talks about it in one of his lectures as a fact but I would need to go back and find where to be absolutely sure. That’s where I first heard of synchronization according to the cycle of a psychologically dominant female even though I’ve heard of synchronization for years. Anecdotally, of course
Sasha: Yes, that is very interesting.
Interesting about wheat harvests. I’m in Russia now and some people were telling me that agriculture has been destroyed in post Soviet days. Hopefully, it’s coming back.
Sasha: Yes, hopefully it’s coming back. A good grain harvest is so dependent upon the weather; it must have been good, too.
Wheat = carbs, why would you want wheat, except to feed someone else so you have a continued supply of fats?
Because wheat (and carbs) have fed people for centuries without ill effects.
At least with modern wheats and production methods that is now a contentious statement.
Yes, but it wasn’t industrial bread made with yeast accelerators, fungicides and additives, not to mention pesticide residues and glyphosate.
I agree with that. But that’s different from saying that wheat equals carbs and why would anyone eat it.
AH Notepad: If I had my druthers, there would be no agriculture, with vast fields of grains; instead, fully-integrated farms, with ruminants and laying-hens on pasture, building the fertility of the soil while sequestering vast amounts of CO2, as well as crops for supplemental feed for the animals and crops for cash flow and hedging the bets.. Farming was once much more like that. In the U.S. in the early 1970’s, the Secretary of Agriculture, Earl Butz, almost singlehandedly destroyed these family farms. I would get government entirely out of meddling with food production, except insuring safety of the products and perhaps helping insure crop insurance was easily available, because farming is very risky. It is agricultural policy, more than anything else, which has created the food disaster that is making everyone fat and sick. Grains are commodities, traded in the futures market, not food.
And because the idea that all carbs are evil is basically a religious belief…
The tides are highest/lowest when the gravity of the moon and sun are added/subtracted which corresponds to the moon’s phases (other planets have a more minor gravitational effect).
I also had friends whose kittens did that but never thought to check with the lunar cycles, I assumed it was just because they were kittens when they did the wall-of-death up the curtains and across the ceiling stuff. Interesting observation though, like the likelihood of death increasing in the early hours of the morning which I believe is genuine, also the number of disease incidences which correspond to latitude. Seasonal Affective Disorder and suicide rates too. Also I used to have depressive episodes which correlated with the sunspot cycles. A minor contributor compared to my carb intake though. Hmmm, perhaps there is something in astrology after all, just not what they think it is.
chris c, neutrino flux changes between day/night and sunspot activity could be a factor.
Not astrology, astronomy
The moon and heart disease: going to the moon is a cardiac killer.
“Last year research from the US also found that astronauts who travelled into deep space on lunar missions were five times more likely to have died from cardiovascular disease than those who went into low orbit, or never left Earth.” — http://www.telegraph.co.uk/science/2017/09/02/immune-systems-could-stop-humans-reaching-mars/amp/
That puts an end to my astronaut ambitions. Dang.
Re the synchronised cycles – pretty sure I observed this way back when I had a girlfiend who lived in an all-female college OK I left the typo in as it was pretty descriptive . . .:)
I saw the same thing happen in industry too – one morning the stores supervisor came and gave me a bollocking for over-ordering something and taking up too much of his floorspace. The same afternoon the sales manager came in and gave me a bollocking for under-ordering – in the space of a day we had shifted about a couple of weeks of stock of one particular item which a whole bunch of customers had worn out simultaneously.
The Russian wheat harvest is a bit scary, a farmer here told me the reason the wheat price had gone back up a few years back was due to increased sales to China, so if the Russians are doing increased business there they will be more inclined to support North Korea.
These kinds of patterns have always fascinated me. The astronauts thing is weird too, I’d have assumed being weightless in space would be a worse stressor than being under lunar gravity.
With astronauts I wonder if being further from the Earth’s electromagnetic field has an effect.
No I meant astrology. The concepts are completely bonkers but may conceivably be related to something which is not, maybe something as simple as daylength when you are born. Or neutrino flux when your brain starts to take in data, or . . .
In my opinion this has all become too complex and the answer lies in simplification. This will involve choosing those factors on which everyone seems to agree and build a broad preventative regime taking into account these factors. This would be aimed at preventative guidelines which are applicable to the broadest possible group and would obviously include:
Exercise
Stress reduction
Sugar use reduction / elimination
Processed food elimination
Smoking elimination
Obesity
Hypertension
Low HDL?
High triglycerides?
This is the most important part of the process and the treatment of those who already suffer from arterial diseases (disseminated or otherwise) could then by dealt with according to resources available and individual needs
If you can meet with complexity and simplicity, and treat those two impostors just the same….
Simplexity—–is an emerging theory that proposes a possible complementary relationship between complexity and simplicity. The term draws from General Systems Theory, Dialectics (philosophy) and Design.
I tend to think of it as shuttling between different levels of structure. Medicine was, and still is, predicated on thinking of the human organism as a series of ever smaller cogs and wheels, and the key to understanding is to find out how the smallest cogs and wheels work – reductionism. Once you understand all these tiny processes, you can then understand how everything fits together. It is a seductive path, in many ways. However, you cannot understand the whole simply by understanding the parts that make up the whole. Interactions at different levels of structure cannot be induced from each other. A human being lives in a complex external environment, for example, that will have all sorts of effects, at all levels within their body. Knowing everything about how a particular form of enzymatic process operates within DNA transcriptase (for example) will tell you little about the overall health of the much more complex individual, living in, say, Syria.
Alternatively, if I hand you three wooden clubs, which you can analyze in any way you want, this will not tell you anything of their central purpose – which is to be used for juggling. Again, if you give you six matches, you can analyze them for a hundred years, but it will not tell you that they can be arranged into a simplistic representation of a horse. Therein lies the massive flaw in reductionism. Understanding the parts does not, necessarily, allow you to understand anything the whole, or what those parts actually do. So, you need to look at everything from all angles, at all levels of structure, and be ready for contradictory outcomes resulting from what appears to be exactly the same input.
Or keep your head when all about you are losing theirs. Very nice article
Anton this morning I was reading New Scientist and found there a report about the effects of NO emissions from car & truck exhausts on health. ( Especially from diesel engines. ). Last year I spent 6 months in Quiapo, a bario in the heart of Manila, the Philippines : extraordinarily congested, crowded, & polluted by vehicle emissions due to almost permanent gridlock on the major roads.
Perhaps for some of us this is a factor and so worth adding to the list.
By the way, I am now home here in Oz, living on the edge of a country town with green paddocks across the road. So No emissions are no longer a major part of my daily breath.
Bill in Oz: I, too have been to Quiapo. Metro Manila has become impossibly congested. I wasn’t like that in the mid-80’s, when I first visited. The air pollution is probably the main reason longevity in the Philippines is going down.
Nor in the 1970’s when I visited it for the first time Gary. But now it is extraordinary : very over crowded with people & vehicles. I think if I had been aware of the risks then, as I am now, I would have stayed elsewhere in more up market area such as Ermita or Malate. And yes I too have wondered how the local people can survive it. Life is short there I suspect even without Duterte’s murderous drug war.
Still I met many wonderful kind Filipino people. And also met my now wife there. So from that time much good has come.
You fool! It’s all cholesterol, and eating meat. This is Settled Science and must never again be questioned.
Where’s my cheque???
(My sarcastic way of saying I agree. Looking at what has ACTUALLY changed in the external environment in parallel with the changes in the internal environment would be a good plan)
3 Cheers; the beginning of the end is in sight perhaps? Thank you. 🙂
Some Doctors experts specialists researchers etc. (over many fields of endeavour too) require certainty as a crutch; also to provide them with comfort, especially when dealing with the lives of others. Moreover, certainty is more likely to keep their “mistakes” out of the court room – where certainty is a, often illusory, pre-requisite.
But nothing is certain except death and taxes.
I liked the broken bone analogy someone posted in the comments to a previous blog: there are many ways for the bone to get broken but the healing process is the same.
Doesn’t really help those of us trying to figure out what caused their attack…or if it was indeed CVD related at all. Someone sent me a case in which her husband was thought to be having a heart attack: cpr, then defibrillated, then into intensive care, stented and so on. The medics got it wrong – no heart attack – turned out to be a potassium deficiency.
A top ten list of probable causes might be an idea for us to look into…a checklist for our investigations at home (where best to spend our time and money), some of which have been mentioned in this latest blog: e.g. stress, vit C deficiency…also homocysteine, sulphur have all met with favour through the years on this website
Oh for those Star Trek style devices where Dr McCoy would wave his hand held device over the patient and check his medical tricorder for the diagnosis.
There is one choke point in the theory of CVD we have been discussing, namely plaque formation.
Once you have plaques forming, there seems to be general agreement on the process going forward that results in a heart attack or stroke. Either the plaque gets so big it causes an obstruction, or it ruptures and the resulting clot travels downstream and causes an obstruction.
But by what mechanism do plaques form in the first place, and how is it they keep growing once they have fulfilled their leak-plugging function in the second place?
Martin
You ask an interesting question. Once plaque has formed, does it just keep growing, can it stabilise?
I am aiming at plaque reduction.
That is artery ‘healing’.
Unfortunately there is little research on this at all. And individuals who pursue a dissident ( non statinist ) path are ignored as an example of some sort of placebo or simply liars……
Bill,
Are you actively doing something(s) in pursuit of plaque reduction?
The most hopeful suggestions I’ve found are to increase all forms of vitamin K targeting the calcified aspect of plaque. Calcification is considered permanent and progressive by The Profession at large. The sparse (heretical) research papers available seem to be in contention with each other as to what form is best. So, I take it all. Plenty of K1, plenty of K2 in the form of menaquinone (long half-life, oil based) and menatetranone (short half-life, water based).
I’ve done this for more than two years since my sky-high CAC scan test results. I was refused a scrip for a follow-up CAC scan at two years to see if there was any difference because it was (naturally!) assumed that there would be none and that the test would be futile.
Frustrated by the Profession in my pursuit of knowledge! I’ll try again soon.
Alice.. This is impossible. Mad Hatter.. only if you believe it is.
Curiouser and curiouser indeed.
Ley lines and geomagnetic disturbances, of course they add to the mix.
Fantastic as usual
If ley lines and geomagnetic disturbances are being brought back into the equation, then I think grounding should also be discussed.
I think that you are right. Unfortunately, at present, there are 24 hours in each day. Yesterday I spent thirteen of them working for the NHS.
Just what I ponder about you when I read your writings! You are an inspiration.
Anyway, the next book you should write is – Effective Time Management (How to do Two Full Time Jobs Each Day).
In regards to not being sure if stress is the cause or at least one of the causes of CVD, I believe that stress is indeed the cause. Stress being defined as anything that can cause damage and that can be emotional stress or physical. Sugar/carbs, smoking, alcohol, lack of exercise, a high pressure job or lifestyle – it’s all stress. So maybe you aren’t all wrong in that notion, you just have to redefine what stress is. Keep up your good work, we all look forward to your posts and publications.
I don’t think that helps. I think the term stress should be for situations where stress hormones are elevated for an extended period from the emotional environment, otherwise the term just becomes a tautology.
Robert, you wrote “I think the term stress should be for situations where stress hormones are elevated for an extended period from the emotional environment, otherwise the term just becomes a tautology.”
Stressc an be caused by many things both emotional and physical. The body’s ‘alarm system’ responds in the same way to them all. Occasional alarms are life preserving. Chronic ‘alarms’ via cortisol, are life destructive.
I was not trying to make the definitive diagnostic classification but just noting that we have to separate the terms for causes as we come to know them. So, indeed, chronic high cortisol is a problem. To say that it is caused by stress does not get us further, so it could be heat, or chemical exposure, …, or emotional. I was suggesting keeping stress for the emotional because that is a common understanding.
Robert, the problem is that at the physiological level, the difference disappears.
If your house burns down your problem will be having lost all your possessions through a process of rapid oxidation. The problem for the forensic team will be was it a leaking gas pipe, faulty electrics, arson by others, arson by self, or what. What your insurance pays out may depend on that.
Rob, I can only respond from my own Australian perspective. And here your comment does not make sense. We are talking here about health and disease. Your comment refers to a hypothetical house fire, emergency services and insurance. These are NOT parallel situations. They are not alike.
Meanwhile : from an evolutionary perspective, I doubt that our body ‘alarm systems’ are ‘programmed’ to differentiate between a stress which is external and a stress which is internal. Stress just is. Constant stress is damaging at all levels : emotional, physical, mental, physiological, even spiritual.
Zebras don’t get ulcers by Robert Sapolsky is a great book to read. It explains stress in a fascinating manner.
I read the Zebras book year ago and gained a lot fro that. I have just bought ‘Behave: The Biology of Humans at Our Best and Worst’ by Robert M Sapolsky hoping for more insights.
Doctor, I have a pain in my chest.
Which doc would you choose?
Doctor1: Yes, you have thoracic morsus dolor. Take a paracetamol.
Doctor2: Let’s see if it is caused by angina, heartburn, esophageal cancer, a bullet lodged in there from WW2, ………………….
Thanks, for the thirty-fifth time.
I see another book in the works, Dr K. Could you at least update The Great Cholesterol Con so that we can still recommend it? Thanks. I look forward to your next blog.
I am updating it as we speak.
Terrific. I’ve purchased many as well as Doctoring Data to give to my friends – and! – my cardiologist.
Excellent news
Put me down for a copy. I’ve just read your excellent chapter in Diabeted Unpacked’, a thought provoking book. It would be nice if it provoked some thoughts in Public Health England, but they just keep digging an ever deeper hole for themselves.
Excuse my ignorance but why can’t we still recommend it anyway? Is it because of the emphasis on stress? Sorry to be stupid.
Great post. My heart becomes stronger just by reading it 🙂
A great mind is capable of change when new evidence (black swans) is presented. Looking forward to the next exploration of this multi-faceted epic.
A great read for a Saturday morning.
Point One – I’ve come to the conclusion that until I reach the point where I am totally and thoroughly confused on XXYYZZ*, then I’ve not read up enough on XXYYZZ. It was Dr Sjoberg, through one of his book recommendations in this blog, which put me onto Albert’s Molecular Biology of the Cell – this placed me into another dimension about the ‘simplicity’ of everything.
Point Two – John Ioannidis is another paper (the one from 2005) I keep glancing at from time to time, along with others. I have to bite tongue on a regular basis when listening to colleagues discussing things related to health in black and white terms (how they can love a story from the Daily Mail or Express which ‘proves’ eating / avoiding / taking WW is good / bad / makes you live longer).
I’ve had success stories in getting people off statins when not appropriate to take them (including the dreaded side effects) for which I have a mission to sow the seeds of doubt about statins in the hope that a person will go away and start looking into them for themselves.
I look forward to the next blog which, along with the subsequent comments, will led me into new avenues to research. Looking back, everything that I believed (because I accepted it was ‘fact’) at the turn of the decade is basically wrong (you couldn’t pay me to have Weetabix now – I recently found an old shopping receipt from nearly a decade ago & I’d feel sick if I had to eat some of that stuff now). [Aside, always been in good health and am more likely to stay that way now].
* Replace XXYYZZ with anything to do with health and nutrition (apart from the no brainers like no smoking). Can’t remember how many months of reading it took me to start Vitamin C supplementing daily (now onto the powered ascorbic acid – ¼ teaspoon either dissolved on in water in the morning or mixed in something like natural yogurt & the currently plentiful blackberries & elderberries that no one else seems to pick [aside – along with some cocoa power and half a teaspoon of collagen}). [Another side story: away abroad on a recent trip, I was the subject of much ridicule for my Vit C powder – I had to smile when the main cheerleader was laid low over the weekend of the trip with a stinking cold.]
The advantage of having a name starting with ‘A’: You always get mentioned when a book you created with others is referred to, so Alberts, Johnson, Lewis, Raff, Roberts, Walter! I keep Molecular Biology of the Cell on a table to my left. When I think I understand something I read something relevant in the book and realise I have a long way to go.
On vitamin C, about 50 years ago one my students, noting I had a cold, asked if I had read the book by Pauling. As I did not know about it, he offered to lend me a copy. I have not found it makes a big difference to the ‘cold’ (maybe dampening a bit) it does make a huge difference to soft tissue damage. Although one cannot extrapolate from the sample of one, me, I started taking a vitamin D supplement about 5 years ago, 4000 IU a day, and have not suffered a ‘bad cold’ since that time. It could be that hand washing is a major factor. After being out, shopping or on a bus, I always hand wash at home or destination before doing anything else.
Clathrate, Robert
Yes, Albert “cools you down” if you think you have a firm grip on some metabolic pathway.
That is science to me!
This is a fantastic year for blackberries and elderberries, as I’m sure you are aware. My hands are permanently stained – a badge of honour.
Frederica Huxley: Can you believe the elderberries are still blooming here? In August! The bears will have them in the fall as they fatten up for hibernation. But the blackberries and raspberries have been wonderful.
we sit atop a house of cards?
Indeed.
Have spent time reading your entire posts over the last few days. Lots to think about. I have heart disease and RA….double whammy. Refused statins. Look forward to next post.
Thought provoking as ever. This one is a gem, I think. Before my retirement I dealt with the risks of complex industrial systems that were “major hazards”. After a lifetime of trying to tussle with those and produce numerical solutions to “risk”, I got to where you are here. Never expressed it as well, though.
In a world centred around n=1 (trying to sort one’s health), it is good to accept the complexity and uncertainty, but it does not produce easy answers.
I veer away from people with “certain” solutions and total conviction of the rightness of their view. It simply isn’t that simple, and science should always be about questioning the accepted state of “knowledge”.
I look forward to the new book.
Thank heaven you write this stuff. As a heart attack survivor I know that Dr. Kendrick is a voice of reason – and there aren’t that many of them in this world where the lunatics are running the asylum.
Dear Mr. Kendrick, overall, I agree all your points. But it seems to me you complicate the matter unnecessarily.
Most of the people should switch to a low-carb diet to control their metabolic syndrome or diabetes. Also, do your best to eliminate silent inflammation factors like a chronic infection in teeth or kidneys. And you need a moderate exercise routine which includes cardio and some weight lifting. This triad obviously reduces the risk of CVD at least 70%, probably more.
The remaining сontroversial issues are interesting but minor. For example, what is the role of toxins? Specifically, lead and mercury.
By the way, have you seen this – https://www.ncbi.nlm.nih.gov/pubmed/25660917 – Dose of jogging and long-term mortality: the Copenhagen City Heart Study.
I think you may be right. The greatest difficulty, in science, and science writing, is to get the balance between ‘completely accurate/too much detail’ and ‘good enough to cover the most important stuff’.
Would you please write a post about toxins and chelation some day?
Or have you already done it?
It will arrive (I guess). I had written off chelation as nonsense. It turns out I was wrong.
sergeykushchenko: The recently departed Andrew Hall Cutler, Ph.D., P.E., developed and successfully used a chelation treatment protocol.
But maybe there is something about the impossibility of the simple stuff….?
I have type 2 diabetes and suffer the annual indignity of an inquisition from an obese nurse about my weight and exercise habits. I could easily beat her round the block.
It does seem that a low carb, low bmi, high exercise, no smoking, no drinking, no caffeine, low stress lifestyle would probably result in a low risk of cvd. Its just that it is nearly impossible for most people to do. Mentally that is.
So maybe hence the constant quest for another more complex solution? As we already have the solution but it is impossible to attain on a population basis?
(PS I suppose recommending diabetic people eat pasta every day indicates not everyone has arrived at the simple solution suggested by sergey but I think that is slowly changing).
(PPS Actually your blog is about causes and we are talking about solutions so maybe the causes are just more complex than the solutions?!)
Roblpm : what is the evidence for caffeine being a major issue for CHD ? I have read that caffeine from coffee or tea is a longevity promoter.
I read the paper résumé very quickly.
As usual the benefits turn around what is moderate etc, probably in the eye of the beholder,though many joggers I see do not look that happy, with sweat and strained faces. I used to think that these studies were too small to be relevant, but having read this blog for some time, I now think they are attempts to quantify an effect, rather than pointing to inalienable truths and magic answers.
Mr Chris: I think this paper is telling us something important, but the importance may lie in the context of all the other modern lifestyle factors which afflict us. Mark Sisson has written a great deal on what is called “chronic cardio.” On the other hand, some contradictory evidence: In northern Mexico is an indigenous group who traditionally played a ball game where they chased a ball for days and sometimes hundreds of miles. They enter and run marathons, keeping their mouths shut the whole distance, doing only mouth breathing. As far as I know, they don’t keel over from heart attacks.
I love the Horton quote. It’s coming along with me – printed out in its numbers – for my next visits with docs. Yeah, I still go to them, if only for the conversation. The conversation often revolves around the sacrosanct “peer” criterion for defining bona fide research.
http://jasonya.com/wp/the-dawn-of-peer-review/
Thank you
Dr. Kendrick, I have been following you for well over a decade, prompted by my pursuit of longevity and, originally, for my respect for the Thincs group. Alongside Gary Taubes, Uffe Ravnskov, and Weston Price, you stand as an important informer of my personal belief system.
You are an exemplar of a true expert with your passion, your focus, and honesty – a genuine maven.
I see you are now attempting to bring together the threads of your thinking. Clearly an important stage in any hypothesis development. Perhaps it is an opportunity to contribute an additional line of thinking to your arsenal?
A thought experiment respectfully submitted to you…..
You are a zookeeper. You have many species, generally mammals, in your zoo. You have decided to add some humans.
It is your job to keep your charges in good health for as long as possible. You generally seek to have them live their full life span. You know the natural life span of the other animals you keep.
You know you need to replicate/simulate their natural environment for this. If you do this well, they will not suffer degenerative disease (it is rare in the natural world). They might suffer trauma or communicable disease but they are extremely unlikely to suffer heart disease, cancer, dementia etc. etc.
You need to do the same for these humans in your charge. They are merely another species of predator mammal after all.
Questions arise. What is the “normal” life span of a human? What is their natural environment? What should I feed them?
But unlike other species, humans occupy just about every latitude and longitude with an enormous diversity of environment and diet. They have adapted really well to climate and food source variations.
There have been many evolutionary threads since the origin of the species. Yet the races are very consistent in their responses to environment and diet despite the apparent diversity. We know this by observing migrant populations. We also know this because when a healthy environment (and longevity) prevails it is healthy for all of its occupants regardless of origin.
So we do not need to decide how to keep them alive with great precision. They are after all very good at tolerating variations in living conditions. We only need to know the broad strokes of their healthy environment, the fundamentals. We can breathe a sigh of relief. It is not that hard to get it right.
For answers to the question of the fundamental health needs of the human species we might go back to a time when humans were members of “the natural world” still inhabited by wild species in our care. By this approach we discern human needs before the interference and confusion effects of civilization which is a recent change in human conditions and too recent to yet have much impact of the state of the species.
What if we replicate (as far as possible) the world of ancestral humans? It is possible the humans we are admitting to our zoo have genetic flaws as individuals leading to degenerative disease that is beyond our control. It is possible but not probable. Looks like a plan.
End of thought experiment for now.
How does this approach potentially impact CVD hypothesis development?
Perhaps it helps triage the multitude of risk factors we discern? Only factors relevant to all races and nationalities need be explored. The French (and other) paradoxes quite simply tell us what to ignore. I think you know this already so this is not new.
What about the CVD process? What cardiovascular, metabolic conditions and homeostasis factors are truly “natural”? What are the norms for a human in a “natural” state? Do we know these? Should we look at primitive human populations yet to enter civilization for answers? Personally, I am perennially confused by the question of desirable levels of the various blood and other measurements we make. Why not look at humans in their pure state?
End of pitch presentation!
Many thanks for your contribution to my excellent health Dr. Kendrick. Looking forward to Part Thirty Six.
Onward and upward.
On the ball Malcolm !!! Just one teeny thing – those crazy Russians said a 2x increase – which is a 100% increase…though I often do that meself… 😊
Oops. You are right. I shall change it shortly.
Malcolm,
That correlation with geomagnetic conditions has been noted elsewhere:
http://www.nature.com/nature/journal/v277/n5698/abs/277646a0.html?foxtrotcallback=true
I can’t get at the actual paper, but from the abstract it looks like it is something you should read (if you haven’t already!).
I heartily commend the idea of “bringing everything together in some sort of coherent structure”. There is inherent biological complexity involved, and with this . . . competing/conflicting interpretations of incomplete data. It is no easy task, but it has to be attempted.
The prospect brings to mind Camus’ interpretation of the Myth of Sisyphus. My take from his book is that life has many seemingly intractable problems (the rock) . . . but that it is important to deal with those problems in the best way we can (pushing the rock up the hill) . . . when we get to the top (success) we can enjoy the view, the revel in the success and feeling of transcendence . . . only to find on a closer look things are not quite as ‘right’ as they first appeared . . . (Thinking of a previous comments: Contradictions may have become evident, the structure may creak a little with internal consistencies). The rock rolls down the hill and like Sisyphus we have to start again – building up, refining (pushing the rock back up). . . But Camus counsels not to become downhearted at the seeming endless grind . . . keep working at it, keeping pushing the rock and look forward to the feeling of achievement when you get to the top of the hill again – wallowing in the success no matter how temporarily before the rock rolls down the hill. I was left with the impression we should do this rock pushing with optimism and enthusiasm.
I get the feeling that too many people in the medical profession have pushed their rock up to the summit once, were beguiled by the view, satisfied that that was as good as it gets, stayed there, not noticing that the rock had rolled back down and left them. They remain oblivious to the need to work on their ideas and get that rock rolling back up.
(Apologies to Albert Camus)
Thank you Dr Kendrick for your wonderful posts. We eat a nutrient dense diet. Liver and scrambled eggs for breakfast today. I am wondering how many prescription meds are bad for the heart?
Hi, Dr. Kendrick!In your last post you brought up a very interesting question!I think that behind the whole complexity of atherosclerosis decease, one obvious fact is hiding: the process of the development of atherosclerosis is quite natural and is to happen to everybody, who is lucky enough to live up to his eighties. You can’t really find any old man without atherosclerosis plaques inside his arteries, though he could have never suffered from hart attack or stroke. From this point of view atherosclerosis is an inevitable consequence of edging. This statement is backed by observation that in people with the syndrome of progeria, which causes acceleration of edging starting in their teens, the atherosclerosis starts developing along with the manifestation of edging and happens as fast, as in 1â2 years, causing the death of these poor from heart attacks or strokes. If the atherosclerosis process can be developed that fast, there is no need to explain it by stress, diabet, bad cholisterin etc. It is just a natural consequence of edging, and if we want to study the process, it is a good idea to regard the process from this point. But the atherosclerosis disease has been changed in last 100â200 years, along with the pace of our civilization that has changed our habits, forced us to eat food quite different from that our ancestors used to eat for edges and in much bigger quantities, deprives us from hard physical work on a daily basis, and adds much more stress in our life. All this civilization dependent changes in our ways of living lead to the development of atherosclerosis in younger people, who in good old times would have never developed the decease so early. This influence of our new way of living distorts the clear picture, where atherosclerosis is just a consequence of edging, and brings about all this complicate stuff about correlations of the condition with multiplicity factors. Should we regard this, as a new form of atherosclerosis, which is driven by factors, different from edging, or both conditions (normal atherosclerosis of eldery people and abnormal one of much younger guys) are developed through the same mechanism?Ann Natapova  19.08.2017, 11:05, “Dr. Malcolm Kendrick” <comment-reply@wordpress.com>:Dr. Malcolm Kendrick posted: “Having spent many years smashing everything into pieces in an attempt to work out what is going on with cardiovascular disease, I am now going to attempt the amazing feat of bringing everything together in some sort of coherent structure. I have no idea h”
As an aged, not just ageing, person I am considering having a CAC score done (inspired by Ivor Cummins). When I get the result, I will post it in this blog, hopefully to prove you essentially wrong! I do accept that I am wearing out a bit.
I thought the same thing. I “knew” I was perfectly healthy, wanted to get the statin docs off my back. Asked for and paid for the CAC test with confidence.
Well, it came back the highest reading the cardiologist had ever seen.
Overtesting can be discouraging.
I was discouraged until I read this, indicating that highly trained healthy athletes CAN have high scores – without the ongoing atherosclerosis.
http://www.cardiobrief.org/2017/07/13/coronary-artery-calcium-rises-with-intense-exercise/
Oh dear. I remember there was some program I used to listen to on the wireless in the 1940/50s where the theme song was “ignorance is bliss it is folly to be wise”. That has always stuck with me – even the tune, but I have always opted for the folly. So, you have made me more determined to know.
An aside: note how people now say ‘on the radio’ but we say wireless networking not radio networking though we are using the ‘radio spectrum’.
Robert and JD, I seem to recall that in one of Ivor Cummings videos there was talk about interpreting CAC test results. The implication was that using simple scores, (very small excepted) to predict CVD events had to be treated cautiously – Still, it is better than LDL-C. It was mentioned that another factor of CVD event risk was whether the CAC score was rising (not a good thing) or remaining the same (a good thing). Somewhere in following this topic the issue of density of calcification was raised as being a significant measure . . . high level indicated more stable plaques . . . low level indicating an unstable plaque. To use the CAC score and test results requires a certain level of skilled interpretation that I suspect most GPs might not have.
In some comment to a blog I read someone wrote that they asked the labs doing the CAC test for the CD of the images and the full figures so he could do all the calculations to workout level of CAC and the densities.
Prior to having a stent put in about 5 years ago I had an angiogram; at the same time they estimated a CAC score. I remember them them saying “The calcium level was a bit high”. A couple of months ago after coming across all this CAC stuff, I went back to the stent paperwork to see if there was a figure for Calcium . . . . Yes . . . 600 . . . oops!
But then I was on statins at the time and I have been reading recently that statins are associated with increased calcification. After walking the dietary straight and narrow for some while I am now, 5 years later, curious to know the CAC score trajectory.
There is stuff on this on the video of a panel, involving Mike Eades at the Low Carb Breckenridge 2017 conference. You can get to it from Ivor’s blog . . .
thefatemperor.com/blog/2017/3/3/dr-mike-eades-important-note-on-calcification-volume-vs-density-cac.
Thanks for the detailed post. I do understand the CAC score issues. The thing delaying me is that I would have to make a journey to a busy place for it, so I think ‘I will decide – next month’.
Antony,
I checked your link. Interesting.
All I got from my CAC report was the Agatston. No mention of density, area, or volume. Advances over the last 2 1/2 years?
BTW, my Agatston was 1,640. (One thousand six hundred forty!)
You can imagine how excited my cardiologist was – particularly after I quit atovastatin. Not dead yet.
I’ll post again this interesting, possibly confounding article:
http://www.cardiobrief.org/2017/07/13/coronary-artery-calcium-rises-with-intense-exercise/
Great piece once more Dr. K. I especially loved the quote from H.L.Mencken ( I’ll be using that one on my next G.P. visit!). I suggest that this very complex problem, that of the causes of CVD, can be broken down into just a few groupings: poor diet ( too many processed carbs and sugars), stress, sedentary lifestyles, the modern toxic industrial environment, and finally poor medical/ pharmaceutical interventions. In paraphrased words of the late, great, Eric Morecambe, these are all of the right causes, “but not necessarily in the right order”.
Thankyou, Dr Kendrick. I agree with everything in your new blog, and will follow others’ comments closely.
In the mean time I am deep into “Diabetes Unpacked”. Brilliant.
Good job we are having a Staycation these days…with so much interesting stuff to do at home. (We are playing at foodie experiments, and have a list of good stuff to read).
A question about arterial blood pressure and your skepticism about BP control. I recall reading some time ago that arterial rupture pressures are 4 – 5 times normal BP. I presume this was an animal study but it probably confirms your doubts about BP control ie that it’s a bit pointless. But what is it that makes artery walls so weak that they rupture? You could point in the direction of endothelial inflammation, or poor collagen composition or structure, but the question remains especially considering the results of this study.
https://www.ncbi.nlm.nih.gov/pubmed/23982713
If the rupture of artery walls initiates strokes or plaque formation does it suggests that, counter-intuitively, the rupture process might start outside the artery wall? If so is there a plausible mechanism?
But people develop aneurysms at the normal range of blood pressures so clearly one has to be careful on BP. Also, this is rupture, like a rip in the pipe. Arterial damage could just be due to a slight stretching that creates enough gap between some endothelial cells for the clotting mechanism to be triggered.
I’m not convinced by your answer Robert since it is clear that healthy arteries can withstand very high pressures well above normal. The medical professions focus on BP appears to be sham and arterial wall integrity ie probably poor collagen structure, is the issue and hence just another effect of malnutrition
I think you missed the meaning of my comment. The GPs have to be conservative and assume there may be problems from hypertension, they can’t just say after a CVD event – oh well, must be someone with weak connective tissue. The BP of youth must be an indicator of normal, and my own experience is that hypertension is related to high carbohydrate diet so you should should do something about high BP, though not necessarily by medication. I had put a post earlier about my own experience that Dr Kendrick seems to have missed. Here is the relevant part –
“Finally, blood pressure. About 20 years ago I was prescribed atenolol as I had a systolic pressure of at least 160. I used to run and noticed how this slowed me down. Then one day in 2000 I took two tablets by accident and spent the day lying on a bed wondering why I felt so weak. Idiopathic high BP did not suit, so I thought, I will experiment to lower it. Losing weight, which I was doing because of the change of diet proved to be what was needed, I did not need any experiment and I gently reduced the medication to zero. Now my unstressed systolic hovers around 135. I am thinking of trying a keto-style diet to see if that drops it further. But, thanks for confirming that I am probably OK now anyway.”
HI Lew NZ, my current interest is in repairing spinal discs and reversing osteoporosis in order to alleviate lower back pain (for my spouse). Supplementing C, K2, D3 and collagen has improved her bone density and increased waking distance before having to sit down. A miraculous improvement from a year ago. What has this to do with BP? Collagen also strengthens blood vessels. Results from recent visit to bone specialist: no medications required, considers vitamin K2 a fad.
“Elastin and collagen (types I and III) are the primary load-bearing elements in aortic tissue. Deficiencies and derangements in elastin and type III collagen have been associated with the development of aneurysmal disease”
“Lysine is an amino acid that your body uses to build collagen. It is an essential amino acid, which means that while your body needs it, your body cannot produce it by itself. Instead, it is provided exclusively by your diet. Red meats, cheese and nuts are all high in lysine, but they can also be high in fat.”
Fat????? Bring it on.
Hi Andy, you also have obviously implemented this and had good results. My wife has scoliosis and Rheumatoid arthritis and so far, at almost 70 we have managed to keep her out of a wheel chair ( her GP’s prediction was wheelchair by 40) by maintaining her bone density and consuming bone broth. It would seem that most heart disease is about low consumption of the right amino acids to support collagen integrity. Well done on your success.
Andy S: Spinal decompression (no equipment needed) may help, and core strengthening (such as from wall pushups progressing to floor pushups). These two things, along with sufficient A, D, and K2 from food and sun, and collagen from bone broth, have virtually eliminated my lower back pain. Can’t emphasize enough the importance of strong core muscles, and it isn’t hard to do, no equipment necessary.
Andy S
I used to have sciatica, lower back pain, alleged stenosis, etc. I found this site, http://sarahkey.com/, scrupulously did all exercises, and am now free from pain. When I had my replac mento hip operation, at the pre op the surgeon looked at my lower back and said ” fine” I queried this and was told he saw no problems. I can easily now walk 12 kms without a problem.
Mr Chris, appreciate your contribution re exercise for back pain. The confounding factor is the statin that my wife has taken for the last 9 years after CABG. She will only stop the medication if recommended by a doctor. Therefore my next step is to present a one page note to her doctor how statins use may be the cause of her back pain. Talking points:
– tendons and muscles support the spine
-cholesterol does not cause CVD, why use statins to lower “bad cholesterol”?
-coenzyme Q10 deficiency may be one mechanism for statin-induced myopathies
-Statins Deplete Vitamin K2, May Promote Coronary Calcification
-lack of vitamin K2 can result in abnormal bone and cartilage mineralization
-statin use associated with increased odds of having a back disorder, including spondylosis, intervertebral disc disorders, herniated discs, and spinal stenosis
-recent study demonstrates that treatment with statins appear to negatively affect tendon cells and extracellular matrix. The biomechanical properties were decreased and the gene expression patterns were switched to a catabolic profile.
Thanks for the pointer. I just found “Simvastatin and atorvastatin reduce the mechanical properties of tendon constructs in vitro and introduce catabolic changes in the gene expression pattern” – http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0172797
which I will study carefully. I assume this is the study you mention.
Yes Robert that is the study. Statins affect function of many different cells and tissues. Back pain may not be caused solely by ageing. Looks like statins speed up the process.
Andy S and Robert Dyson,
Thanks for turning this up.
So statins can give you tendinopapthy? As someone who suffered a lot from this problem during my seven years on Crestor at least I know now.
Bingo ! Chondroitin sulfate ( or glucosomine which is converted in the body to CS ) is collagen.
I used to get crippling sciatica. Twenty years ago I bought a kneeler chair for my computer where I spend hours a day, plus I always sit in the hardest chairs available when going out, and I walk a lot. This has done the trick I hardly get any twinges these days. I know I should exercise as well, but I usually don’t.
Another wonderful highlight in my inbox. I always look forward to your posts and as always this one doesn’t disappoint. I am so grateful to you for your selflessness in putting in all those hours working on this blog and await with happy anticipation a new book at some point in the not too distant future. Thank you, Dr. K.
Certainty is the realm of religion (one reason I’m a non-believer). Darwin (and Wallace) were, in the main right, but knew nothing of genetics. Genetics, on the other hand has proven to have limited value in understanding either evolution or the etiology of disease. Symbiosis, though not well-studied, may be one of the keys here (and epigenetics, as well). I just reread an article about metamorphosis, two entirely different genomes expressing in sequence in the same insect. How the hell did that come about? The fruit fly (Drosophila ananassae) has acquired 44 of the 45 genes of Wolbachia, a parasitic bacterium, and passes them on every generation everywhere in the world where it lives. IPAK has just published a paper on the distribution of immigrant genomes by region of origin in North America, accounting for patterns of migration, and their relationship to disease susceptibility. Food for thought (they ask for a $100 donation).
My first thought reading this post is that it has gotten worse since Dr. Ioannidis paper. Corporations effectively control most of the governments in the world (and powerfully influence academia and professional journals), and the spin machines have become very sophisticated, powerful, and overbearing. The internet cult has replaced the traditional disseminators of knowledge (which now mainly give propaganda, spin, and opinion), and it is our salvation. Plenty of nonsense on line, but what appears on line is today more likely to be true and/or useful than what appears on TV or in newspapers or magazines (or professional journals!).
Looking forward to XXXVI!
I would see epigenetics as part of genetics, and epigentics is a major factor in many diseases: over or under methylation, which can change more drastically than the genome.
Robert Dyson: I would put it a bit differently. In my understanding epigenetics refers to the environmental factors which influence genetic expression, either up- or down-regulating them. But genes, by themselves, reliably express only a relatively small number of traits in offspring. Mendel knew this. So the genome project was of great value for basic knowledge, but for understanding disease, it has limited value. I agree that epigenetics plays a big role in susceptibility to both infectious and degenerative disease. Interesting that what was once called “junk DNA” is now known to be actively involved in metabolic processes.
No, epigentics is the layer of control that determines the expression of the genes that are encoded in the double helix. Bonded to a lot of the base-pairs of the genome are other molecules, mainly a methyl group that determine which or how the gene’s codes will create a polypetide. Most of the epigenetics is determined very early in fetal development and some is environmentally modified. If you look up ‘dutch hunger winter epigenetics’ you will find a terrible and fascinating example.
Robert Dyson: Also, I think the real elephant in the room regarding health and disease is the interaction between the microbial world and multi-cellular creatures, of which we don’t yet have even a kindergarten level of understanding, and is surely more complex than cellular metabolism. I may be a bit weird, but I find learning about the microbial world utterly fascinating.
I agree. We usually see ourselves as outside the natural world that we think we can manipulate to our needs, whereas we are deeply embedded in it and we should meddle slowly to see how we go. The idea that I like is that the gut microbiome influences our brain to make us eat what suits it.
Charles Gale said above “there are many ways for the bone to get broken but the healing process is the same.”
I agree Charles.
The issue is what contributes to encouraging the healing process, what undermines the healing process, and what is irrelevant.
I think most of us here agree that ‘cholesterol’, especially LDL-C falls into the irrelevant category. ( I am uncertain about Trigylercides and HDL-C )
But with that in mind the list posted above by Anton is good.
Article on placebo surgery shows that a lot of habits will have to be rethought.
https://www.theguardian.com/science/2017/aug/20/when-surgery-is-just-a-stitch-up-placebo-effect
Robert Professor Ian Harris wrote an excellent book ” Surgery, the Ultimate Placebo” in 2016.. Published by New South Press here in Oz. The Guardian has finally caught with him & quote him, but doe not cite it at all. He is also an orthopedic surgeon in clinical practice in Sydney. He speaks of what he has himself seen happen.
Dr Kendrick, I posted a comment the other day, with a link to an interview by Dennis Mangan with Sr. Leo Zacharski. It was about high levels of ferritin iron in the blood being associated with many chronic diseases such as diabetes and CVD.
The video interview is 1.5 hours long – admittedly a long interview. But it is very informative.
However it has not appeared yet. Could it have got lost or been deleted by accident ?
Here is the link again :
http://roguehealthandfitness.com/discussion-iron-health-leo-zacharski-m-d/
I will watch this with interest as I too think ferritin levels are a neglected measurement.
Robert, this has not been an issue for me ( I took baby aspirin for a long while and developed anemia ! ) But when I discussed this with a younger brother, he said he did not know his ferritin level as his GP said they were ‘normal’. So he asked for the actual print out of his next blood test – something that should be standard I suggest. His ferritin level was over 600 which is anything but optimal for a healthy male. Subsequently he has donated blood twice and brought his ferritin levels down to 460.. It will be a while till he is at an optimal range of 60-100. But I think he is taking B3 ( niacin which chelates iron from the body )
It has been my experience that occasionally I write something here, and it never appears. I don’t think the comments that don’t appear are exceptional in any way, so human/computer error is no doubt responsible.
The entire process of managing and maintaining this blog is way beyond my abilities. And we are dealing with a very complex computer process. Blips happen & are inevitable…And now blip is sorted… So what’s to worry about 🙂
Thank you for this great input! I just fully agree!
Coherency, i.e. having a reasonable consistent map where you can place the most important parts of your life (including the Scotch Ardbeg 10 years) is essential for the mental health and also what we learn from the societal history of mankind.
The back side of this coherency idea is that you tend to believe in the religious “one-liners” of our medical system, which be definition “must” be true, since you, with most people, don’t even want to scratch on the surface not to see your world fall apart. Basically you trust your authorities even if you will die from it.
Think war!
Coherent society?
Yes, people would rather die than have their core belief systems overthrown. ‘Better dead than red…’ a slogan from the cold war, if I recall it correctly. I am not sure if this is a good thing, or a bad thing. Both, simultaneously, I suspect. ‘
Increasingly I think I dodge death from the above cause, by simply doubting every scientific ‘fact’ – but to varying degrees! Your excellent blogs have added enormously to my sense that ‘we’ know far less than we think we do. Science is based on pretty solid facts, but somehow every generation has heaped on layer after layer of less and less solid material so that in places we are now building with congealed rice pudding! Henry Bauer has written a book about the situation:
While it can be a bit stodgy in places, this book contains a lot of relevant insights.
Perhaps you should try to estimate the percentage of CVD that is caused by stress. How much CVD would be left – I mean could much of that be put down to people with bad teeth, too many years on the clock, etc.
Your examples of the way communities afflicted with stress acquired CVD seemed extremely persuasive – I’ll bet it is the major factor.
The other thing that occurs to me, is that perhaps, for the purposes of study, it would make sense to separate CVD in later years from CVD in the relatively young. I mean, things do go wrong with old bodies whatever is done, but CVD in younger people is a real tragedy.
Good
Thank you for another interesting read. There are several forms of abusing the body. Here in
France they are introducing mandatory vaccination in 2018 ( eleven in total ) No children can
go to school without them. How stupid is that for the future.
Josephine Pretty: Amazing stupidity, and in France, which has one of the highest levels of public vaccine skepticism in the world. Italy has done the same thing, after the 1 B euro GSK bribe. In Italy there have been mass public protests, ignored by the media, of course. Have there been public protests in France?
Gary, just to let you know I have posted a reply to your question about germinating seeds in water alone. It is awaiting moderation on blog 34, which will filter through, I am sure, once blog 35 settles down. All great stuff on here, I am sure we all agree, and a lot of effort on Dr K’s part.
Jenniifer: The more I think about it, I realize that seeds must have the full complement of minerals in a neat little package. The quality of the seed would matter a lot, but I’ve read enough to be certain that sprouted seeds are an excellent source of nutrition. Used to do it myself, long ago. It is interesting that the butterfat which contains the highest levels of vitamin K2 comes from cows eating rapidly-growing green grass, which is roughly the same thing as you’re getting from sprouts (and we do have the bacteria in our gut to convert K1 to K2, just like cows do). You’re probably getting higher levels of K1 from sprouts.
I’ve been thinking about metabolic rate and its possible consequences.
I’ve been remembering the frenetic life of the little shrew whose metabolic rate is so high that she/he has to eat every 2 hours. Then the great Greenland shark who can live to over 500 years with its extremely sluggish rate of metabolism.
Remembering too the centenarian survivors of World War II concentration camps – living at near starvation must have reduced their metabolic rate substantially but their longevity would not seem to have been compromised.
Many of us would probably opt for the shrew’s short life over what would perhaps seem to be a rather boring Greenland shark’s 500 years, but there must be a happy medium.
Does a higher rate of metabolism significantly increase the rate of cell turnover and so increase the risk of chromosome errors building up?
Could a more sluggish metabolic rate explain why some “overweight” people live well beyond the years expected for them – why the dire warnings can seem unnecessary?
Dr Richard Mackarness (Eat Fat and Grow Slim) wrote about Mr Constant Weight and Mr Fatten Easily. But how much is in the genes and how much do we influence our metabolic rate?
I appreciate the situation will be more complicated than I’ve suggested but metabolic rate must be worthy of consideration. And how it affects the heart?
(P.S. I’m on Jersey Channel Island among lovely Jersey cows but again having difficulty buying whole milk in any quantity. Reduced fat is certainly favoured here. So much talk. So little action. Perhaps it’s better to be the busy shrew.)
Body size, metabolic rate, generation time and the molecular clock. Martin and Palumbi http://www.ncbi.nlm.nih.gov/pmc/articles/PMC46451/?page=5
What a shame about the lovely Jersey milk. I’m in Penzance and can buy it from our local T****. And it’s not homogenised – hurrah. A case of “Oy! Shake the bottle” as in my childhood.
So, can overeating be ok (in some respects) if it makes you sluggish but not if it increases your rate of metabolism?
Thank you! Following this series for a long time and learning everytime something new! Looks like the community in here share a lot of great materials. Thank you!
That was always my hope. That a community could develop, and pursue their own ideas and learning, in a environment where everyone is trying to be positive and constructive – as far as possible.
I find comments positive and constructive. This sort of venture gives me hope that we can push back against the vested minority interests and create a better society for the majority. This sense of community is as valuable as the technical information.
Alert:
This otherwise fairly on-the-mark and thoughtful blogging cardiologist has brought up statin issues yet again. Touting the nocebo effect, fawning over Nissen, etc.
His conclusion, possibly to take to TV:
“Since statins are our most effective and best tolerated weapon in the war against our biggest killer, it behooves both patients and physicians to have a high threshold for stopping them altogether.”
I thought that some of us might relish the opportunity to comment (perhaps taking it to TV with him!)
If that’s not aggravating enough to comment on, maybe this further quote from him would be:
“Having such a high threshold means filtering out the noise from attention-seeking media and the internet-driven denials cult thus minimizing the nocebo effect”
I just left a comment.
And he commented back.
Um . . . does he not have a point?? You can’t prove the cause of a non-happening?
Dr AnthonyP missed the point ! Touching.
As I fully expected him to do.
Great comment!
I wasted about half an hour writing a detailed description of what happened to me, and it seems to have been removed. I am not amused.
?
This is the comment that was deleted – anyone is free to quote from it:
My personal experience makes me doubt the concept that muscle pain associated with statins is a nocebo effect. I was prescribed Simvastatin at age 60, simply because I had raised BP and my cholesterol was about average. I felt extremely positive about taking the statin because who doesn’t want to live longer and avoid strokes, etc. The only thing I had to be careful about, was not to eat grapefruit!
After 3 years, I suddenly got extreme cramps in one leg – which had been weakened by polio when I was a child. Because of the time lag, neither I nor my doctor thought I was suffering the ‘muscle pains’ that are mentioned on the Simvastatin patient leaflet. Not least, because what I was experiencing seemed just too severe to be described in that way, and anyway, I just assumed my problem was polio related. My walking outdoors was greatly reduced, and became very laboured, and every morning was a struggle with leg cramps. By extraordinary good fortune, I remembered that statins could cause muscle pains, and wondered if these might exacerbate whatever was really wrong with me – so I stopped my statin (my doctor also agreed that made sense). The suspicion was that I had Post Polio Syndrome, and I was sent to a consultant.
By the time I secured an appointment with the consultant, my symptoms had strangely diminished, and she seemed to feel that PPS would not come and go in that way. As I continued to improve, I thought it was time to start my statin pills again. The cramps came back in a week! In total I stopped Simvastatin on three occasions, and each time the symptoms seemed to exponentially diminish. In retrospect, I was daft not to realise sooner – the only cause of my problem was the statin! After that, it took about 9 months before I felt completely normal. I have now been free of problems (and statins!) for 4 years.
Afterwards I took to mentioning statins whenever I got talking to someone of about my age. I was staggered. I met one man who had struggled with muscle pain and severe memory loss (which nearly cost him his job) before abandoning the search for a statin that suited him. I met another (very active) man who was mentioned that he had had a bout of severe joint pains, and I started to ask about what medicine he was taking, but he said the word ‘statins’ first! Those two were not the only ones reporting problems – just the most spectacular. From my experience, I would caution:
1) Statin side effects can start after a long period of taking a statin.
2) It would seem that weakened muscles may be more vulnerable to statins, and there is therefore an obvious danger that the problems will be assigned as something else – in my case, possibly PPS, which doesn’t have a specific test.
3) The fact that I was so positive about statins, makes me really doubt that I suffered a nocebo effect! If I didn’t have a nocebo effect, I am very doubtful that this is the true explanation for this side effect.
4) There may be patients who are suffering statin side-effects, but are innocently still taking the drug – this is a really horrible thought.
I don’t take a statin now, and I agreed with my doctor that I didn’t want my cholesterol measured. I am also much more wary of the medical profession – if it aint broke, don’t fix it!
I think you have a very important issue here – time lapse. We got used to this with smoking and cancer, now maybe with too much carbohydrate and metabolic syndrome, but generally too many clinical trials are not long enough.
Aside: I am reading the “Diabetes Unpackaged” and note our dear doctor is even more cynical than me – he notes that “metabolic syndrome” seems to have gone out of use as I had noted myself. He suggests that the reason is that it does not suit those who sell drugs because we know how to cure “metabolic syndrome” in most cases by change of diet.
Malcolm,
Just to clarify – if your ‘?’ was directed to me!
I tried to add a comment at this site, describing in detail why I don’t believe my statin side effects were a nocebo response:
My post was simply removed from the site. I don’t know why, but it obviously makes me angry because I think the idea that statin side effects are just nocebo responses is just an excuse not to investigate them properly.
It was, because I wasn’t sure what site you were talking about e.g. this one.
I read the paper in the Lancet and it seeemed to me that people had already been selected as not having a problem taking statins, and the trials were old and not testing for side effects.
A Cochrane Review of January 2016 was very specific that statins had zero effect on the treatment of Alzheimer’s.
Robert
The Cochrane 2016 review of statins in 2016 was not their most glorious episode in my opinion. As I understand the Cochrane reviewer was up against Rory Collins, and I was not convinced by the outcome. Perhaps I am a member of the Internet denial cult?
Then the reviewer may not have pleased Prof Sir Rory, as the suggestion had been that statins might help with Alzheimer’s and the review was a most definite rebutal of that idea. I too have doubts about meta-analyses, but they exist, and we can make something of them especially when they have a zero outcome.
As I said last week, a very slightly more ‘open minded’ statinist…No need to expect anything else. He is not sceptical about statins..he is a convert.
I left a comment and some questions on the skeptical cardio’s blog
Dr Kendrick, I’ve looked through the sceptical surgeon blog. There is no indication that he can see past pharmaceutical statinism even though he claims that this blog is ‘interesting’.
So what’s the point of comments here generating interest there I wonder ? My own hunch is that this USA not very skeptical surgeon may be just seeking to drive or redirect readers towards his website.
Im sure causes are multifactoral but CVD like cancer exploded in the 20th century. Surely this is enough to point to the fact it is a modern lifestyle issue. After that, who knows….my own hypothesis I am currently developing is following the obesity curve. I was interested to discover its parabola neatly follows the sale of microwave ovens!
And that coincides with the appearance of ready meals and sundry junk foodstuffs.
mediapenguin: Looking at the graph (U.S. data), I see that CVD deaths began to take off post-WWI, and didn’t level off until the 1960’s, beginning to drop by the end of the decade.
If you want an interesting correlation look at coffee consumption and CVD in the USA. These two links go to graphs that show both the rise and fall in CVD and Coffee consumption over the last 100 years.
US Coffee consumption, Annual Gallons per Capita 1910-2011
http://knowyourgrinder.com/coffee-consumption-trends-worldwide-2016/
Death Rates for Cardiovascular Diseases US 1900-2006 ( about 1/3 down the web page)
https://www.nhlbi.nih.gov/about/documents/factbook/2008/chapter4
Correlation Causation but holy crap these two graphs are pretty similar, if you consider a coffee drinker starting in their mid 20’s and having their first CVD event 20 to 30 years later the extended peak in the CVD disease graph matches perfectly.
I know coffee is supposed to protect against CVD but of course this one scientific ‘fact’ couldn’t be wrong now, could it?
Could this also predict the rise in female CVD? Coffee being a workplace indulgence and women only recently matching men in the workplace could this predict the recent rise in female CVD?
Doug
I would recommend extending your data analysis to include other countries.
Ah. Try coffee my way. Just add water (but not too much).
Jean Humphries: Or my way: Raw cream from cows on pasture, the more the better!
But people don’t just have coffee in their coffee, or just have coffee by itself. An increase in coffee comsumption means an increase in comsumption of a lot of other things – for example sugar, and maybe milk substitues made from those healthy polyunsaturates.
Doug,
Here is a site that will dampen your enthusiasm for correlations!
http://www.tylervigen.com/spurious-correlations
David Bailey: Hilarious!!
If you want to analyze the impact of environmental factors on CVD, age-specific or age-adjusted rates are more informative than death counts (e.g. MMWR, for US trends 1900–1996).
Karl: This appears to show the peak year as 1952 (the year my father died of an MI). Yet, I have the vital statistic records which show the peak at 1968, after a leveling off at 1960.
Yes, the trends for total CVD and coronary heart disease are different. Coronary disease may have peaked around 1968 (but it is not included for years before 1950s in the char, probably because older statistics is seen as too unreliable at that level of detail). Total CVD peaked earlier, because other heart diseases and stroke started to decline before coronary disease.
In the US CHD did not exist before 1948, because they did not use the diagnosis. It was only in 1948 that the WHO International Classification of Disease (ICD) was taken on-board in the US. ICD(4), at which point CHD became a diagnosis. I believe that the rise seen from 1948 until about 1960 was an artifact – created as doctors got used to using the new diagnosis. My contention is the CHD peaked in the US shortly after WWII.
Could this also be a reflection of simply ‘conservatism’ in the US medical profession ? As in a reluctance to adapt to the new WHO disease classification of 1948 ?
If so the CHD statistics would rise numbers in the USA for a period as newly trained doctors graduating after 1948, gradually replaced older doctors not trained to diagnose the ‘new’ disease.
And looking at the chart, that seems to be what happened.
Dr. Kendrick: Very interesting! The document I have been using is “Leading Causes of Death, 1900-1998,” and it gives the top 10 for each year. “Diseases of the heart” appears to be the only category regarding heart disease for each and all of those years up to 1949 when arteriosclerosis appears, so it appears the peak from 1960-68 would include all cardiac-related deaths minus those from atherosclerosis. Confusing in any case. The top 10 for 1900: 1. Pneumonia (all forms) and influenza. 2. Tuberculosis (all forms). 3. Diarrhea, enteritis, and ulceration of the intestines. 4. Diseases of the heart. 5. Intracranial lesions of vascular origin. 6. Nephritis (all forms). 7. All accidents. 8. Cancer and other malignant tumors. 9. Senility. 10. Diphtheria.
By 1910 “Diseases of the heart” moved into first place.
Top ten in 1998: 1. Diseases of the heart. 2. Malignant neoplasms, including neoplasms of lymphatic and hematopoietic tissue. 3. Cerebrovascular diseases. 4. Chronic obstructive pulmonary diseases and allied conditions. 5. Accidents and adverse effects.* 6. Pneumonia and influenza. 7. Diabetes mellitus. 8. Suicide. 9. Nephritis, nephrotic syndrome, and nephrosis. 10. Chronic liver disease and cirrhosis.
*adverse effects was added in 1979.
From 1953-1961 “Congenital malformations” was #9.
In 1949 “General arteriosclerosis” was added to the list, and in 1968 it was changed to plain old “Arteriosclerosis,” then to “Atherosclerosis” in 1979.
By 1979 “Homicide and legal intervention entered the fray, at #14. By 1998 it had moved up to #10 for males.
Changing diagnostic criteria seem to have made a hash of understanding long-term trends in heart disease.
This is how polio was made to appear to begin to disappear shortly after the release of the Salk vaccine, by changing the diagnostic criteria and giving paralysis other names, such as Transverse myelitis, Guillain-Barre syndrome, and as caused by enteroviruses such as Coxsackie and ECHO.
Indeed. Data are not simple to analyse. I have long suspected that the early Japanese figures are very dodgy. Their rate of stroke was astronomical. It is now seven fold less than fifty years ago. I understand that stroke was a ‘good’ diagnosis. Dying of a stroke meant you were highly intelligent. Also, cancer was a diagnosis that people did not want, at all. To have cancer brought shame upon all. It is all far less certain than we would wish.
Gary, “adverse effects” in the leading cause of death category needs defining to be useful to a patient. A quick google (with cut and paste) turned up the following:
-situations in which an inappropriate decision was made when, at the time, an appropriate alternative could have been chosen.
-An adverse event is defined as an injury caused by medical management rather than by the underlying disease or condition of the patient.
-Numerous studies have assessed the incidence of adverse drug events (ADEs), defined as an injury resulting from medical intervention related to a drug.
-Not surprisingly, the potential for medication-related error increases as the average number of drugs administered increases.
-Current estimates of the incidence of medication errors are undoubtedly low because many errors go undocumented and unreported.
-Some errors are also difficult to detect in the absence of computerized surveillance systems.
TYPES of ERRORS
Diagnostic
Error or delay in diagnosis
Failure to employ indicated tests
Use of outmoded tests or therapy
Failure to act on results of monitoring or testing
Treatment
Error in the performance of an operation, procedure, or test
Error in administering the treatment
Error in the dose or method of using a drug
Avoidable delay in treatment or in responding to an abnormal test
Inappropriate (not indicated) care
Medication Use Processes
Prescribing
• Assessing the need for and selecting the correct drug
• Individualizing the therapeutic regimen
• Designating the desired therapeutic response
Dispensing
• Reviewing the order
• Processing the order
• Compounding and preparing the drug
• Dispensing the drug in a timely manner
Administering
• Administering the right medication to the right patient
• Administering medication when indicated
• Informing the patient about the medication
• Including the patient in administration
Monitoring
• Monitoring and documenting patient’s response
• Identifying and reporting adverse drug events
• Reevaluating drug selection, regimen, frequency and duration
Patient safety is also hindered through the liability system and the threat of malpractice, which discourages the disclosure of errors. The discoverability of data under legal proceedings encourages silence about errors committed or observed. Most errors and safety issues go undetected and unreported, both externally and within health care organizations.
Iatrogenesis (from the Greek for “brought forth by the healer”) refers to any effect on a person, resulting from any activity of one or more persons acting as healthcare professionals or promoting products or services as beneficial to health, that does not support a goal of the person affected
Causes of iatrogenesis include:
• side effects of possible drug interactions
• complications arising from a procedure or treatment
• medical error
• negligence
• anxiety or annoyance in the physician or treatment provider in relation to medical procedures or treatments
• unnecessary treatment for profit
Yes, and when physicians become more apt to report CHD, this would contribute to the reported decline in other heart diseases (and maybe even stroke). But you can actually find the headings “diseases of coronary arteries” and “angina pectoris” in mortality statistics from the U.S. already from the 1930s, but they are probably not reliable for comparisons with later rates, because unspecific cardiac causes such as “chronic myocarditis” are more common (e.g. Vital statistics 1900–40, p. 238, 80 MB scanned PDF).
Gary, the U.S. was apparently the world capital of smoking in the 1950s, but Ancel Keys didn’t conside it when deciding that saturated fat was responsible for heart disease. He’d made his mind up and we’re still dealing with the consequences.
Japanese men have always smoked like chimneys, and most still do. I have always found this a rather difficult to understand fact. Considering rates of CHD has always been very low in Japan.
Do they smoke kiln dried or air dried tobacco?
AH Notepad: What is the difference between kiln-dried and air-dried tobacco? One bad, the other worse?
Gary, my understanding from decades ago was kiln dried tobacco had a higher sugar content than air dried. I understood that cigars are made from air dried tobacco, and at the time (1960s) French cigarette smoke smelled like cigar smoke.
AH Notepad: I recall reading somewhere that, in regard to lung cancer, there is a high correlation with cigarettes, a low correlation with cigars, and no correlation with pipe smoking.
Maybe their cigarettes are not full of sugar. French smoke quite a lot, too. But are they saved by the french paradox?
Another black swan.
Gary Paola
The French also quite go at it with bread, quite a lot of wheat bellies around.
Mr Chris: I recently met a young couple from Paris while hiking in the redwood forest. She said they buy bread every day. They were quite fit, with no bellies showing.
As are plenty of Italians who eat bread daily if not a couple of times a day.
Gary Sasha
There are many comments that true salvation liés in LCHF, my comment was intended to say that France’s outlier position in respect of CVD deaths, does not appear to be only diet dependent.
The black swan?
AH,
I started smoking Gauloises when travelling through France in 1973. I don’t know what the smoke smelled like, but when you tore a new packet open, the tobacco smelled like a horse’s stable.
Did it explode? Or was it the labelling that made it seem like an explosion? Or did it seem like an explosion as the population grew? Or was it so many people smoking an artificially dried tobacco which increased the sugars content, and the increase in acrylomides when it was pyrolised?
There were so many changes happening at roughly the same time, it could have been many things. Weston Price provided what I see as strong evidence that refined carbohydrates had immediate and significant effects, but could one of those been to increase the rate of CVD?
You may well be right, but there’s no way of being definite as we can’t rewind the clock.
But did the rate increase due to better diagnostics? Or did it really go up? Or did it go up when people started eating veg-oils about the same time? Correlative bits are useless if not followed with some kind of experimental science. Even the arrow of causation is usually nothing more than a narrative.
Insulinresistance is the problem, it,s driven by high bloodsugar, bad sleep, stress etc.
Vitamin C, Magnesium, Kalium, and Sodium etc. needed to maintain a healthy bloodpressure.
Stress and CVD
F.A.O. David Bailey
I refer to your comment about trying to “estimate the % of CVD that’s caused by stress”.
Based on my experience last year it would have to be an estimate. I nearly died from something and having no conventional risk factors such as being e.g. a heavy drinker or smoker and knowing my stress levels, that was my default cause. Tried like anything to get tests done for corstisol production but the months went by and I gave up on the idea figuring that it was too late to get the snapshot of the levels at the near fatal point in time. Even paid to see an endocrinologist but she wasn’t interested and she stuck to the mainstream diet/heart hypothesis. And I signed up as a volunteer for trials – never heard from anybody.
As someone remarked to me, having no conventional risk factors, you’d think someone would be interested in what happened.
Nope.
I’m not sure how you’d get any data about stress/CVD. I think as Dr K has commented upon, stress/anxiety/depression is probably the one ailment where patients can self diagnose and GPs seem more than happy to prescribe medication, despite there being 3 standards tests for cortisol. What data are there wouldn’t seem to be support by tests/science.
Well in his book about heart disease, Malcolm reported a lot of details about how CVD was more prevalent in populations under stress. That would seem to be a good way to approach the question. Obviously anyone who has just had a CVD event, will be under rather a lot of stress – so I doubt if it makes much sense to sample stress hormones at that time.
for one, a gp is not really ”formed” to detect depression, anxiety and high level of stress. Unless the patient mention being under heavy stress, being depressed or anxious. Then the gp will refer this person to a psychologist perhaps, or prescribe anti-depressors.
Anti-depressors have never been proven to work more than a placebo and they are full of ill side effects, including suicide. Yes, you read that right suicide…
Now, the relationship between stress and CVD/CVH is not simple to detect because, most people would not make the link at all. For example, a young entrepreneur running a business in his infancy while having financial problems, a wife and young children to feed. Who makes the connection between this and heart attack? besides me, not many.
Data? almost impossible to find, because Stress can be attributed to any diseases and is rather vague. Other than the work of a few doctors, which are open minded and can see how bad stress can deplete our ability to maintain a healthy body ( hpa axis/ parasympatic/sympathic sytem/adrenals) The vast majority of doctors are simply unaware of the work done in this field and its huge importance imho.
There is a need of a new paradigm shift in medicine where the body is not seen as car parts, lubricants and oil changes, to see human beings in their wholeness. For example, the well being of an individual and the relation between the physical, emotional and spiritual dimension of that person, which needs to be in harmony i strongly believe.
Charles,
Stress is certainly well recognized by the present establishment as a “cause” and in my own severe MI case twenty years ago considered as the only “cause” they could come up with. As far as I understand stress “reduction” through the “effective” beta-blockers is what is behind these pernicious pills.To me, though, this is pharmacological “playing around” with our most fundamental autonomous nervous system (the vagus nerve connecting brain and body, including the heart) without “understanding”. Wasn’t there about 100 000 cardiac deaths at hospital heart surgeries attributed to this “ignorance” and a professor who got defamed?
I dropped the beta-blockers after a couple of months and then returned from a zombie existence back to life as a human being and when looking into my back mirror I am very happy about my decision those years ago. As I understand, when you have got used to them they seem to be very hard to get rid of as with most psychopharmacological drugs.
Digging deep into this vagus connection, the heart performance I found in Dr. Srokas take on this matter was very revealing when he analyzed the complete loss of the heart rate variability prior to an MI, relating this to the improper balance between the sympathetic and the parasympathetic nervous system (vagus connection!), especially in the early morning hours when the brain gets “connected” to reality and our “engines” start up through the sympathetic action – rather though “unsympathetic” in my opinion 🙂 .
I can confirm this “bad” timing through personal angina attacks experienced now and then during my “CVD-carrier”, though, today those attacks are basically kept a bay through my heavy natural vitamin E supplements (1200 IU/day).
What is “CVD-carrier”? I enjoy reading your posts, but this but I do not understand.
Robert,
Sorry about my Swedish language bias. As an American friend told me. After a while we think you Swedes mean what you are saying when I commented seeing him approaching : “Eric you look like an executive!” – but with the wrong pronunciation making him think he looked like someone who was to be executed.
Should have been “CVD-career” if you could talk about such a thing. Anyway it has had it’s up and downs during almost twenty years now – today it is up 🙂
Goran,
Propranolol has been used for decades to ease performance anxiety. Imagine standing in front of a vast audience with your violin, not really ready to perform the solo concerto. You’re shaking all over with fear. If you had taken the pill a couple of hours before, you would not be shaking. Your anxiety (Stress!) would still be there – reduced somewhat only because of your confidence that you wouldn’t be shaking. Beta blockers have a direct physical effect, not an emotional one. My violinist daughter can tell you.
My own brief encounter with metoprolol for arrhythmias rendered me rocking chair bound till I quit. Quality of life is not something that doctors tend to favor over longevity.
(BTW, did you mean “CVD-career”, above?)
This is the secret drug addiction of many orchestral players. It is a very bad situation in reports I have read.
Robert, I think niacin or niacinamide would be better than pharma concoctions. Alternatively people shouldn’t do things they’re not built for, or they have to accept the consequences of pushing the envelope.
wish there was an auto-follow-this-blog function. I’ve got lots of catching up to do.
add the free chrome add on Feeder. It will notify you of new posts, comments etc when you subscribe to a page. You would need to subscribe to each new blog post to be notified of comments with links to the comments.
I do that already, it’s the new blogs I need the auto-follow for, so I get everything ever posted on Dr. K’s site. . I can’t do a Chrome autofeeder thingy as I use an iPad.
Ah notepad
I too use an iPad. When we get á new episode from Dr K, you have to comment, at the end of your comment you need to tick for follow and alert by email to both categories. When I do so WordPress sends me a confirmation, I confirm, and then voila as they say in Lille
Mr Chris, that’s what I do too, but my dream is to just have everything sent without the preamble.
Excellent! It’s so refreshing to see actual scientific thinking at work in the field of medical sciences! Keep up the good work! And keep up the fight against everything that isn’t scientific and open minded. Love your work!
Thank you. I try to be scientific, but still fall into all sorts of traps.
Regarding your last comments, dear Doc,
“I am not a great believer in blood pressure lowering – at least not at current levels.” Etc
Out of interest, what levels would you consider appropriate for an Rx intervention????
160/110
160/110 at any age or before the age of 80?
I would pretty much recommend stopping all forms of ‘preventative’ treatment by the age of 80.
That’s a good thought, unlike Bill in Oz, I would rather not live forever!
However, reading this blog is such a cheering and delightful exercise that my life will certainly be prolonged.
Taken after sitting quietly for ten minutes?
Mr Chris: I have a first-rate GP, but what drives me nuts is that there is no way to properly take BP in the examination rooms. The machine hangs on one wall, barely reaching the examination table. The table is too high for the feet to reach the ground. There is nowhere to rest the arm at the height of the heart. I am a very chatty person (teaching smallish children for quite a few years demolished any residual shyness I possessed), right up to the time she starts pumping up the cuff. So I pay no attention to what it says, and don’t bother to take it at home, since it is well below Dr. Kendrick’s numbers (I think he is correct, based upon all the research I have done, with the caveat that age matters, too). Over the past 2 years or so it has been 131-148/78-88, and it hasn’t gone up since I stopped the ACE inhibitor. I suspect that, properly taken, it would be better than that. I think I also have some level of white-coat syndrome, though my Doc doesn’t wear one (thank goodness!).
Higher than I guessed.
That’s reassuring. Thank you. (and I’m not being sarky, by the way.)
Gary,
My GP is happy for me to read my own BP at home. The machine only costs about £20, and is fully automated, so provided you sit in the correct position, you should get a good reading. Even so, you will find that the readings vary more than you might think – it shows how silly it is to rely on one spot reading at the surgery.
This process has removed almost all the concern I used to have about BP readings, so I think that even if I did have a reading at the surgery it would be in line with my own.
My BP has actually fallen a little (with no change in my medication) and I attribute that to the reduction of stress after retiring from full time employment.
Part of me would like to drop the BP medication too, but since it doesn’t give me side effects, I keep taking it as a good luck talisman!
David Bailey: Thanks for your input. We actually have three or four of those contraptions (my wife invariably buys multiples of everything, as if she’s forgotten we already a few of them). I just don’t care anymore. It is what it is. Just because we can measure something doesn’t mean we should. The most powerful psychiatrist in the U.S. (he oversaw the revision of the DSM IV to the DSM V) recently spoke at a conference. His two pieces of advice for a long life? 1. Avoid falls. 2. Stay away from doctors. I eat well, sleep well, and feel good every day. I have an interesting, very active life, with almost no stress. I worry about nothing. The small things don’t matter, and the big things I can’t do anything about, anyway. I haven’t watched the boob tube in decades (except for the Simpson’s), and I stopped reading the newspaper a few years ago. I care about what is going on in the world, of course, but what can I do about it? Other than educate people, not much.
Appears to be a recent shift by my GP recommending home BP monitoring since readings always high at the office . Suspect GP would like to treat my BP since I am on zero medications. Standard of care requires treatment for BP and “bad cholesterol”.
Strokes from elevated BP could be a concern if plaques are unstable, ie damage exceeds repair capacity. That is why we are here to learn how and why the endothelium gets damaged.
Here’s entertaining: my BP was “acceptable” for a long while, and I was actually able to reduce to a minimum dose of losartan after low carbing for a while.
Then it jumped up on the nurse’s machine.
I was sent to the doctor, presumably for a medication increase, but it was what it always was on *her* machine. Just as it was on my cheapo wrist meter.
I was loaned a 24 hour monitor (damn annoying contraption) which showed it jumped around a lot but clustered in what they considered to be the “safe zone” around 120/80.
Next time the nurse’s machine agreed. My verdict: her meter had gone out of calibration and was readjusted. The engineer in me ponders how common this is, and how often (and how) they are checked.
Dr Kendrick, so you would treat at 160/110 but what ‘maintenance’ level would you then be happy with for your patients taking their BPs at home? Are you saying the current level of 140/90 is also unnecessarily low, particularly in the absence of other risk factors?
Peggy, I was 150 over something when I had a lengthy talk to the nurse about nutrition when my blood was closing to boiling point. It was the usual guff from the overweight nurse about eating low fat foods and getting 50% of my calories from carbs. In short, do what’s got us into the current mess on diabetes and obesity.
This is what the NNT website said about the value of blood pressure medication:
For mild/medium hypertension 140 – 159 (systolic) or 90 – 99 (diastolic) the NNT is nil. No benefit. A red (NO) verdict in Dr Newman’s NNT system. But the NNH is 12, so one patient in 12 was harmed by side effects and stopped taking the drug.
I was happy to refuse BP medication. The benefits of a medication should be clear and this wasn’t anywhere near for me.
I would be happy to treat above 160/110. However, I would first advise such things as increasing salt and potassium intake, going on a lower carb diet, taking more exercise, using breathing exercises etc. Drugs as a very last resort. Of course, I would always do a work up of some sort to see if there were any underlying ‘treatable’ causes e.g. Conn’s, or sublinical Cushing’s, or suchlike.
@malcolm Think about that. I work as a sport physician in Italy. Here if you want to compete in any sport you have to do the annual check which includes an cardiovascular stress test. If your Bp at rest is higher than 140/90 you can’t compete at all. You can’t even go to the gym….
On the basis of what?
Source: Diao D, Wright JM, Cundiff DK, Gueyffier F. Pharmacotherapy for mild hypertension. Cochrane Database of Systematic Reviews 2012, Issue 8. Art. No.: CD006742
Efficacy Endpoints: Mortality, stroke, coronary artery disease, cardiovascular events
Harm Endpoints: Stopping medication due to adverse events
Narrative: Hypertension affects almost 29% of adults in the United States, most of whom are taking medication to lower their blood pressure1. Blood pressure control has been shown to reduce the chances of developing cardiovascular problems and stroke (Mancia et al, 2009), however these reductions are derived from studies of patients with moderate or severe hypertension, and those with a history of prior cardiovascular events such as heart attack or stroke. However, evidence has been unclear on whether pharmacological treatment for previously healthy patients with ‘mild’ hypertension is beneficial.
This review included four randomized-controlled trials enrolling 8,912 subjects with mild elevations in blood pressure (systolic blood pressure 140-159 or diastolic blood pressure 90-99) without preexisting cardiovascular disease. Patient data for individuals satisfying the inclusion criteria were obtained from three studies; pooled data was used from the fourth study since it met the a priori inclusion criteria of having less than 20% of its total subjects with moderately elevated blood pressure.
At a period of four to five years follow up, no differences were seen in mortality, cardiovascular events, CAD, or stroke. Approximately 9% more patients in the treatment arms withdrew due to medication side effects.
Caveats: Studies included in this analysis were of variable quality, some with questionable randomization, incomplete blinding, or partial follow up. Additionally, antihypertensive agents were often older, or used in higher doses than in current practice. Subjects often received non-thiazide diuretics and beta blockers, rather than low-dose thiazides, ACE inhibitors, and calcium-channel blockers, drugs which appear to confer a slight advantage in outcomes2.
Included trials were often powered to detect composite endpoints and underpowered to evaluate individual outcome measures. For low-risk patients with mild hypertension, a study powered to detect differences in mortality or cardiovascular outcomes would require more subjects followed for more time. To account for this some authors have called for trials utilizing intermediate/surrogate endpoints such as left ventricular hypertrophy or microalbuminuria3. We disagree, because of the misleading results that such surrogate markers can often generate.
While data for higher risk patients do suggest a benefit from treatment of hypertension, and the lack of statistically significant benefits in low risk patients may be due to inadequate power, there are important notes of caution here. The high rate of drug discontinuation is concerning. Moreover, it is well known that occasional serious, potentially life threatening adverse events occur with antihypertensives (angioedema with ACE inhibitors, toxicity and bradycardia with beta blockers and calcium channel blockers, electrolyte disturbances with diuretics). These risks are reasonable when there is a proven benefit. In the absence of proof of benefit, the risk of inficting serious harm with the drugs becomes ethically dubious. In one study that represents nearly 80% of the data included, for instance, women experienced higher mortality in the treatment group than in the placebo group4, thus understanding impact on subgroups may be critical. In the final analysis this low-risk population may be a perfect example of a group in whom, despite documented relative risk reductions, extremely small absolute reductions (in rare outcome events) are trumped by increases in harm.
Ultimately, while we require more and higher-quality research to answer this question definitively in a contemporary milieu, these data strike us as being of adequate power and quality to label this intervention as ‘Red’, indicating no benefit. The reversible nature of the harms and the weakness of the data, however, suggest to us that a rating of ‘Black’ (harmful) would convey more certainty than is justified. Although we are aware of clinical guidelines that have come to a different conclusion5, 6, 7, 8
Author: Gary Green, MD
Published/Updated: February 2, 2013
On the basis that 140/90 is hypertension. We know that they choose the evidence they like. Real evidence says that statins are bad for 99 per cent of people.But they want the entire world to take them. The same is for BP. I often feel very embarassed, all above with healthy athletes older than 60 . I ask them to measure BP at home hoping that it is lower than 140/90. I think that this is ridiculous! Italy is the only country in the World wich has these draconian rules.
Paola: How long has this rule been effect? In our national senior athletic competition this year in the U.S. a lady of 103 set a new 100+ age-group record for the 100m (I think 40 seconds+). She said she took up running in her 90’s because she was always out in the garden, and the phone would ring, and she’d have to run in to answer it! Most likely her BP is over 140/90! All of the running competitions I participated in were in the masters division, and as near as I can recall, the only requirement was to not show up completely naked. NB: For non-athletes, masters is 40-59, senior 60+.
In Italy since 1982 (!) there is a Law which obligates every person who wants to do competitive sport (no matter the age) to undergo a medical exam and get a certification.This includes : urine test, spirometry, rest ecg and cardiac stress test and blood pressure measurement. They base the results on current guidelines, which state that 140/90 is hypertension. If your blood pressure is not under this values, you can’t have the certification to compete. That is to say no maratons, no tennis tournaments and so on.
Paola: This is awful. We didn’t evolve requiring a medical test to have fun (or for any other reason, for that matter). This is about state control. I weep for Italy, especially now with the forced-vaccination law.
Gary/Paola
Read “Age is just a number ” by Eugster who took up competitive running at 90 and held the world record at age 97. I noted however he died aged 98.
Still way to go.
Malcolm
If thats the law in Italy, thats what it is.
I was equally interested in this sentence in the study;
Approximately 9% more patients in the treatment arms withdrew due to medication side effects.
When I ask my friends who talk about blood pressure medicines why they don’t try beetroot juice insteadthey look at me in horror, what disregard what the doctor said etc etc.
Changing attitudes is a long row to hoe
Dr. Kendrick: Thank you very much for posting this paper.
Competitive sport has to be taken out of this discussion as clearly body systems go to extremes. Can you do competitive sport on blood pressure lowering medications? I don’t know but think it would be a hinderance to performance.
Yes you can. But you can’t use diureticse or beta blockers .
Robert Dyson: I competed on BP drugs. Only the beta blocker had an effect. When I quit it, I set new personal records. This matters. There was wonderful camaraderie among the club I trained with. It was a community with a mutual-support system. We weren’t competing with each other, but with ourselves. It may not have have improved our longevity, in fact may have shortened it, but it was great fun, and I think that’s the most important thing in life, to have fun every chance we get.
I am glad to see that you suggest salt, potassium, exercise, no smoking and a lower carb diet, before going to drugs. But I am intrigued by your statement ” I would always do a work up of some sort to see if there were any underlying ‘treatable’ causes e.g. Conn’s, or sublinical Cushing’s, or suchlike.”
Can you explain a bit more on this ?
Doc,
I find, looking back on it, that I breath most days of the week. 🙂
So, how does one turn this into a rigorous intentional exercise?
I very nearly died as a result of taking a blood pressure medication but unfortunately, I do need to take something. I guess I’m resigned to that but obviously, I would like to take the minimum dose possible.
At the moment I’m told my bp at home must average less than135/85 but that goes along with the usual low fat, low salt, low cholesterol advice so I am suspicious.
I’m an otherwise perfectly healthy woman – ideal weight, great diet, lots of age-appropriate exercise etc – so I want to know what I can really be content with when I take it at home (because the doctors nearly killed me my bp is understandably raised enormously when I’m sat in front of one of them).
Thanks to Dr Kendrick and this blog in general I am quite content with the cholesterol and salt side of things. However, I cannot seem to get a balanced view of where I am/should be with my bp.
PS Dr Kendrick, could you point me in the direction of the breathing exercises you refer to please? Many thanks.
I have used Resperate in the past http://www.resperate.com/ I have no connections with this company in any way shape or form. It is a simple little device and works well – if used. I tend to close my eyes and do it all by myself nowadays. 6 breaths a minute whilst visualising happy times, and happy people, and things for me to look forward to…. Like finishing my next damn book, and Scotland winning the world cup. Rugby or football, I am not bothered which.
Dr Kendrick, you are absolutely wonderful!
Me and hubby will certainly try the breathing exercises you do, along with lovely thoughts….Golden Wedding this week, so there are plenty of nice things to occupy our minds.
Thanks for all your encouragement to us to keep well or improve our health.
( both a couple of stones heavier than 50 years ago, but we were probably a bit underweight then, along with other students in the 1960s)
Why do you need to take something, if I may ask?
Peggy Sue: Read Port, et al., Lancet 2000; 355: 175-80. I don’t know what your age is, but this shows that for women 44-54, there is no increased mortality risk for systolic BP below 142; for women 55-64, no increased risk below 160; for women 65-74 no increased risk below about 168. They also have a chart showing 100-150 as “normal,” 150-158 as “high normal,” and above 158 as hypertension. This would essentially agree with Dr. Kendrick’s numbers.
I have wondered about blood pressure for a long time with intention to research it, but there is always so else much to do. Thank you for the start. What I want to look into first is simple mechanical effects, what is the elastic strain produced in various vessels from that change from diastolic to systolic, is there hysteresis when the range is extreme, then do endothelial cells simply flatten a bit?
Robert Dyson: I have no idea about any of this. It is a good thing you have an interest in the biology of BP, and can share it with us. All that Sidney Port and colleagues showed was that, on the population level, the mortality risk of elevated BP does not begin to rise until 10-20 mmHg above what the guidelines call for (in the 45-74 age group), and then it rises gradually. So Dr. Kendrick is correct in his target for treatment.
Peggy Sue . . . the white coat syndrome is not unusual. My wife was miraculously cured of her persistent high BP in her second pregnancy . . . The doctor suspecting medical centre stress lent her a BP measuring unit. Disappeared by the time she got home that afternoon, and it remained disappeared for the rest of the week.
My BP is a steady 110/65 . . . a couple of years ago during a two part visit to the doctors . . . first a check up by the diabetes nurse, measuring amongst other things the blood pressure, (came out as a130/80 – I was rather surprised) . . . then my GP . . . who was also surprised at the figure . . . retook the BP . . . => 120/70. He was happy, I less so. I got home and took my BP myself . . . it was down ~112/68. Then I realised what had happened . . . . The diabetes nurse had been surprise at the low HbA1c (38 mmol/mol) and asked what I was doing . . . (She may have wished she had not asked) . . . I got into an excited enthusiastic polemic about my LCHF diet. It was like a dam bursting. Not exactly white coat syndrome . . more self inflicted.
It might be an interesting experiment to see what the BP does during an England vs Scotland rugby match – rather depends on how well Scotland are playing I suppose. 😉
Antony Sanderson: This may be why my BP is usually elevated when the doctor takes it. I always talk like a magpie when I’m there about things I’ve learned here or elsewhere.
RESPeRATE! Thanks.
I love the sound of the Resperate but I fear it is rather outside my budget! However, further googling brought up other online/self help options which warrant further investigation. I definitely think this kind of thing would be of benefit in my case.
Paola, I need to take something for my BP because if left untreated it does tend to be 160+. It was so high in a clinic once (over 200) that they actually did a renal MRI of some kind to ensure there were no problems in that department (which there weren’t).
Look into Vipassana meditation. It’s free to learn))
Peggy Sue,
What BP med was it, may I ask, that nearly did for you?
JD, it was mainly indapamide but in combination with an ARB. I’d been fine (or so I thought) for ages then a serious infection came along and my sodium plummeted to a near fatal level. Not uncommon apparently!
Gary, I lose track of where your comment was but thank you for reminding me of the paper re BP risk in women. I think it was referenced in a previous blog but I had forgotten. All helps me keep a perspective on the whole thing.
I’m just about stable on a CCB now so hopefully I’ll be able to avoid doctors for a good while. Will no doubt do me no end of good.
I heartily agree with Richard Horton, editor of the Lancet.My wife has just had two papers rejected by ignorant peer reviewers.
By 2030, direct medical costs of CVD in the USA will approach 1 trillion dollars—-
Manag Care. 2017 Mar;26(3):48-49.
The seesaw of CVD: Deaths down, costs up.
[No authors listed]
Abstract
Coronary heart disease deaths will decline (USA) by 30% between 2010 and 2020 because of improvement in “cardiovascular health metrics” (avoidance of smoking, more physical activity, and so on) all metrics listed at link below. But this less-deadly era of CVD is going to be a more costly one, with direct medical costs of CVD more than doubling by 2030 to $918 billion from $396 billion in 2012.
PMID: 28510527
Click to access ucm_319831.pdf
Errett: Rapaciousness, not a particularly American sin, but developed to high art here. A trillion, though, is little more than a spit in the ocean compared to what the costs will be to provide services for the, by then, well over 2 million adults with autism, along with those for the children (most of the 1.1-1.6 million with a diagnosis are under 30, the tipping point being birth year 1988-1989). The elephant in the room, truly. Educational services for autistic children are already breaking the bank in Connecticut, our richest state, and in Scotland and Ireland.
The annual US Budget is $3.8 trillion—-as of 2015—-so an annual expense for CVD approaching 1 trillion (2030) seemed excessive to me. Our GDP is 18.57 trillion. I didn’t realize the extent and costs involved with autism—Thanks for the perspective—I’m starting to wonder if our species’ genetic future will follow a classic parabolic path—–All The Best
Yes JD, I was found to have a high Calcium score last November ( 1060 ) with a significantly blocked circumflex artery.
Since then I have researched online and by books etc to develop my own program. Life Extension Super K is part of that daily supplement ‘program’, along with Vitamin D3, Magnesium, ( as suggested by Dr Dennis Goodman in New York ), Chondroitin sulfate, ( as used by Dr Lester Morrison in the 1970’s ) , Ubiquinol, Gotu Kola, ( as suggested by Life Extension ), 6 grams of Fish oil , Niacin ( B3 ), 3-4 grams of vitamin C, and more recently Potassium bicarbonate as suggested by Dr Kendrick.
I also take some other supplements as part of my anti-aging program : DHEA, Pregnenolone, alpha lipoic acid, berberine, acetyl carnitine, and arginine.
In addition to supplements, I try to get to the gym 2-4 times a week for 90 minutes each time, try to eat a lower carb diet, & try to maintain a low ferritin iron level – around 40-80.
Also I fast for a day once a week, as part of my own program of maintaining a stable lower weight. that Iwas last year – 8 kg lost since 1/1/2017 !
It is a lengthy list all up. And it would be nice to know how effective it is. But frankly I do not know. In fact I suggest that the ‘quacks’ ( our old Aussie slang term for medical doctors ) would be hard put to know either. One way would be via a second angiogram/calcium score test. But this is seen as a ‘waste’ of Medicare ‘resources’ and not usual allowed.
I think you are going to live forever mate.
Dr K and cobber Bill
I too think you will live for ever, if you have time too!
As my very lovely wife is a good deal younger than me, I do live in hope ! :-))
PS : the one item missing’ from the program is viagra.as recommended by your good self. I raised this with the GP a couple of weeks ago. He declined to prescribe and offered simavastatin instead as the more modern drug which in turn I declined…
But perhaps the new GP I have lined up to see will have a more flexible in attitude.
I was encouraged when i read in coroner’s news report, that he ‘constantly thought’ about a local young patient who had died because of his mistake in diagnosing a throat infection. NB : This patient was also seen by 5 other medical staff in the week before her death. None of the other 5 picked it up either. But none of them admitted to having made any mistake.It takes courage and humility to admit to such a mistake. So I will see him and see what transpires.
The real Wizard of Oz.
So interesting, as always, and also all the discussion. Wow, what a group!
Thank you!
CAC test
I refer to Robert Dyson’s comment “I am considering having a CAC score done” and JD Patten “asked for and paid for the CAC test”.
I went down this route last year. My GP refused to let me have one (we know you are clogged up and I guess they think it’s irreversible) and thus went down the private route and got a variety of quotes. Annoyingly, the cheapest/most affordable one wanted a GP referral. I haven’t been back to ask him for a letter yet.
JP Patten – Are you in England and if so where did you go?
Regards
Charles, do you have a choice of GP there in the UK with NHS ? From the tenor of many comments I suspect that you do not. And from my perspective not a very clever situation. One has no choice in medical care.
By way of explaining : here where we live in my home town of 14,500 people, there are 5 different medical surgeries with 3-7 GP’s in each. And each practice is owned by the founding doctor or by a group of doctors practising there. So it does offer some opportunity to choose a GP and to change GP if necessary.
You can choose to use a different GP surgery if you wish, in the UK. You can choose to see a certain GP within the surgery, if you wish. That, at least, is the theory.
Thanks for that quick reply. There is some choice under NHS. But I see that theory may not equal practice at times in some locations. I would guess that in the bigger cities & towns there is more choice. And much less in rural areas and smaller towns & ‘villages’. ( A term hardly ever used here in Oz )
Charles . .
Good to hear your experience.
I am considering asking my GP about having a CAC test. I was anticipating him saying that in our cash strapped National Health Service (UK) that unless I had symptoms of heart problems a CAC scan was not on offer. The next bit of the conversation would be “Do you know where I could get one done at my own expense?” . . . If he says “no” . . . I can now ask, thanks to your comment Charles . . . “If I found a suitable test clinic would you write a referral letter” . . . saving another journey, another GP interview.
Sorry. I went to a suburban Boston hospital here in Massachusetts. It did require a scrip, and it did cost me $98.00 with no insurance coverage.
which hospital did you go to?
With all my arteries severely clogged since 20 years a least I today always measure BP 110/60 at rest at home.
I wrote that in a letter to the cardiologist with whom I had an appointment two years ago. Evidently he didn’t like like my letter and we was “at war” from the very first minute and when he measured my PB it was when he was working on me with the ultrasonic device and at the same time he deliberately worked on making me upset with his comments. I wonder if he not was very disappointed to find my heart in an “excellent” condition but perhaps happy to have successfully raised my BP to 140 and then with no problem to prescribe PB-medication.
No ethics?
I think you mean BP?
Yes – of course!
All was insulting from the beginning to the end. He knew that I would never touch any “heart medicine” but still he prescribed five different including the statins although my cholesterol was “perfect”. As an extra insult he called me to check if I had been to the pharmacy.
From what planet does this kind of arrogant cardiologists come I wonder.
Is there BTW a PB-medication?
Dr. Göran Sjöberg: Yes but it is highly toxic. Pb comes from plumbum, which may be why the Roman Empire fell to pieces.
Goran,
Um . . . which PB were you referring to??
https://www.allacronyms.com/_medical/PB
🙂
There is an Aussie expression to describe such a person, It is crude but fitting : “arrogant fuck wit “. I am sure that Swedish has a crude phrase that is just as apt.
Dr. Göran Sjöberg: Not a real doctor. Real doctors listen to the patient. I had a great conversation with the dermatological surgeon who was remodeling my cheek (Mohs surgery) yesterday. She emphatically agreed that the patient must be in charge, that the doctor is there to help. She also uses multiple grams of vitamin C each day (liposomal).
CAC testing
Yep, I did try changing GPs within my local practice/surgery but ran into the same brickwall/mentality with my new GP – no straying from NHS/NICE guidelines. But I do have the option to change practice.
$98!!!. The best price I could find within reasonable travelling distance in Hampshire England was about £400 and the worst £800. I think other followers of Dr K have suggested going abroad where it can be affordable despite flights etc.
Tempted to go back and try and get a letter from the GP.
But I don’t want to use up all my favours/luck/requests with him but it shouldn’t be like that. Managed to find NHS/NICE guidelines stating I was eligible for DNA testing for Familial Hypercholesterolemia – he resisted, double checked and has agreed to enquire further. No such luck with CT – CAC testing.
To those interested in CAC testing,
CAC aritcle here: http://www.acc.org/latest-in-cardiology/articles/2016/06/14/09/17/when-is-measuring-a-coronary-artery-calcium-score-cost-effective .
Written by main stream cardiologist but interesting none the less. There is some evidence that a low dose statin (say 5 mg Atorvastain per day) has pleiotropic effects not related to cholesterol lowing. Google pleiotropic effects of stains. At such low doses there seem to be benefits without the problems of high dose statins. I personally break a 10 mg Atorvastain pill in half and take everyday.
Phil
Philip Thackray
Renfrew, PA USA
There is some evidence that statins prolong life by reducing cholesterol and lowering the rish of heart attacks. Is the calcium related evidence of the same soundness?
The CAC evidence is very sound in a way that statin evidence is not. Check out on http://www.thefatemperor.com/blog/2017/8/8/calcification-and-cac-with-the-expert-professor-matthew-j-budoff-md-faac
Statins certainly lower cholesterol production by the liver. The evidence that lower cholesterol prolongs life is selective spin. There are those pleiotropic effects of statins that for a subset of people may lower heart attack risk. The recent book “Fat & Cholesterol Don’t Cause Heart Attacks” with an article by our dear doctor is a good reference on this. Some examples of statin research read like comedy, to precis – we find no effect from this statin which just shows that people must keep taking it and we have to double down on research to resolve this anomaly.
Phillip, the author of that article ignores or is ignorant of the very real side effects of statins.
Also he bases the medical decision whether to have an angiogram and get a CAC score on the financial factors operating in the USA which I think is solipsistic.
Dr Kendrick’s blog embraces individuals from all over the planet. The financial aspects differ from country to country across the globe.
Moving on, let’s go back to discussing the causes & cures of CHD,………
A blast from the past (don’t know the date, but likely before the Age of Obama) clipping from our local propaganda rag:
By Gardiner Harris
New York Times
Federal health officials added new safety alerts to the prescribing information of statins, cholesterol-reducing medications that are the most widely-prescribed drugs in the world, citing rare risks of memory loss, diabetes [sic] and muscle pain.
It is the first time that the Food and Drug Administration has officially linked statin use with cognitive problems like forgetfulness and confusion, although some patients have reported such problems for years. Among the drugs affected are such huge sellers as Lipitor, Zocor, Crestor [sic] and Vytorin.
But federal officials and some medical experts said the new alerts should not scare people away from statins.
“The value of statins in preventing heart disease has been clearly established,” said Dr. Amy G. Egan, deputy director for safety fin the FDA’s division of metabolism and endocrinology products. “Their benefit is indisputable, but they need to be taken with care and knowledge of their side effects.”
Reports about memory loss, forgetfulness [sic] and confusion span all statin drugs and all age groups of patients, the FDA said. There have been dozens of well-controlled trials of statins, but they have offered few hints that the drugs cause any kind of cognitive impairment, Egan said. Still, the FDA has received many reports that some patients felt unfocused in their thinking.
Statins seem to increase blood sugar levels in some patients by small amounts, and when millions are treated, that change leads more to be diagnosed with diabetes. The FDA had already placed an alert about diabetes risks on the label of Crestor, a big-selling statin made by Astra-Zeneca, because a Crestor trial showed an increased risk. The agency decided to extend that alert to all drugs in the class with the exception of Pravachol, an older medicine manufactured by Bristol-Myers Squibb.
That statins can cause muscle pain in patients, particularly at high doses, has long been known, but in its new alert the FDA reminded doctors that some other medications increase the likelihood that statins linger in the body longer than normal and increase the risk of muscle pain.
Notice the weasel words of Dr. Egan.
“Side effect” as a cause of death or disability does not sound too bad, better than being victim of “adverse effect”. No need to scare patients.
I also found this in the pile of evidence on my desk:
“Statins and All-Cause Mortality in High-Risk Primary Prevention”
“Conclusions: This literature-based meta-analysis did not find evidence for the benefit of statin therapy on all-cause mortality in a high-risk, primary prevention set-up.”
ARCH INTERN MED/VOL 170(No. 12), June 28, 2010
http://archinte.jamanetwork.com/
Philip, a quote from CORONA study “It is interesting to note that outcome in the observational studies was independent of cholesterol level, and other observational studies have reported that low cholesterol levels are associated with a poor prognosis in heart failure patients and in the elderly”. Should one stop taking statins after 75?
Mevalonate pathway disruption by statins affects function of many types of cells and how the overall system functions. Statins are a mitochrondrial poison, not good. There must be a better way to prevent CVD.
Gary, Crestor is what the arrogant cardiologist prescribed for me last year. It was fortunately a low strength dose.(10 mg ? ) . But once i had checked it out for it’s side effects, I stopped taking it. It was just for a short couple of months at low dose. So I did not notice any side effects directly. But the cardiologist in the meantime had upped the dose to 30 mg. I binned that prescription. And am still glad of it.
Might be worth asking other patients – and pharmacists – for their recommendations. Or any consultants – some hospital consultants were so unimpressed by the errors made by the GPs in the “health centre” one place I lived, that they encouraged a couple of young GPs to start an alternative practice, and one recommended me to get in there before their lists were closed, which didn’t take long. The difference was like chalk and cheese (full fat of course). Whether that would be allowed in the days of PCTs I don’t know – or in today’s world of CCGs.
I’ve actually heard of people travelling to Thailand for medical tests/procedures. Their hospitals seem to be well regarded, plus you get a holiday (and other benefits if required) all for much less than the cost of private treatment in the UK. Main downside is airline food and airport security.
Statistical correlation only, but very high HDL level is associated with increase in mortality rate:
For men with extremely high levels, the mortality rate was 106 per cent higher than for the normal group. For women with extremely high levels, the mortality rate was 68 per cent higher.
https://www.sciencedaily.com/releases/2017/08/170823094124.htm
It has been accepted wisdom for many years that the more good cholesterol people have in their blood, the better. But the good cholesterol, also known as HDL, might not be as good as we think.
Errett, this stdy says that too low a level of HDL-C and too high a level of HDL-C was correlated with higher mortality. This suggests a U shaped curve – where ‘just right’ is best.
But there is no suggestion of definition of what ‘ very high’ or’ ‘very low’ might be.
PS : this link ( paywalled unfortunately )
http://www.sciencedirect.com/science/article/pii/S095528630200284X
states that people who take Niacin ( B3 ) have a 30% reduced risk of heart attack if taking Niacin but not taking statins. The abstract states :
“Abstract
Niacin has been widely used as a pharmacologic agent to regulate abnormalities in plasma lipid and lipoprotein metabolism and in the treatment of atherosclerotic cardiovascular disease. Although the use of niacin in the treatment of dyslipidemia has been reported as early as 1955, only recent studies have yielded an understanding about the cellular and molecular mechanism of action of niacin on lipid and lipoprotein metabolism. In brief, the beneficial effect of niacin to reduce triglycerides and apolipoprotein-B containing lipoproteins (e.g., VLDL and LDL) are mainly through: a) decreasing fatty acid mobilization from adipose tissue triglyceride stores, and b) inhibiting hepatocyte diacylglycerol acyltransferase and triglyceride synthesis leading to increased intracellular apo B degradation and subsequent decreased secretion of VLDL and LDL particles. The mechanism of action of niacin to raise HDL is by decreasing the fractional catabolic rate of HDL-apo AI without affecting the synthetic rates. Additionally, niacin selectively increases the plasma levels of Lp-AI (HDL subfraction without apo AII), a cardioprotective subfraction of HDL in patients with low HDL. Using human hepatocytes (Hep G2 cells) as an in vitro model system, recent studies indicate that niacin selectively inhibits the uptake/removal of HDL-apo AI (but not HDL-cholesterol ester) by hepatocytes, thereby increasing the capacity of retained HDL-apo AI to augment cholesterol efflux through reverse cholesterol transport pathway. The studies discussed in this review provide evidence to extend the role of niacin as a lipid-lowering drug beyond its role as a vitamin.”
This is the reason why I take 1000mg. each day.
NB : I do not take it to prevent birth defects or a miscarriage as found by the Victor Chang institute in Sydney 2 weeks ago. And that is world class medical research. But I notice the ‘experts’ poo poohed it and told pregnant women or women contemplating having child, to ignore it. Good grief they might have fewer patients !
Bill in Oz: If you click on the link to the study in the article you can find the figures. As I recall the sweet spot for men was 73 mg/dL, and the danger zone was above 115. Mine has varied between 74 and 92; I’m not concerned, for lots of reasons.
Thanks Gary, I see that “The concentration of HDL cholesterol associated with the lowest all-cause mortality was 1.9 mmol/L (73 mg/dL (54–77)) in men and 2.4 mmol/L (93 mg/dL ) in women.”
With these figures in mind I just checked back on my own HDL-C in the past year. On the 20/9/16 my HDL-C was 1.0 mnol which is low.
I then started taking low dose Crestor as prescribed by the statinist cardiologist. And it FELL to 0.9 mnol on 24/2/2017 meaning an increased risk of heart attack !
I gave the statins the flick and started taking B3 ( Niacin ) and HDL-C was back up to 1.3 mnol on 1/5/17.
Now that means that the Crestor ( the statin ) increased the risk of me having a heart incident. And it was prescribed by the doctor cardiologist and recommended by the GP. This is utter bloody medical stupidity.
I’ll aim at the HDL_C sweet spot of 1.9 mnol and no statins.
Bill in Oz: Good. My attitude is: no drugs; nutrients only, and find joy in living. I must find a good source of niacin; you’ve convinced me. The health food store is a few minutes by bicycle, and I’m sure they have it. I’m not fond of taking pills, though.
Gary, Good luck with finding it.
I am in Australia. I had to look around a fair bit to get just B3 ( Niacin ). All the local health food shops and pharmacies only offered it mixed with other unwanted stuff. Finally I rang a local supplements manufacturer and discovered they made it and they could supply it via a pharmacy. Done deal !
But maybe in the USA, Iherb have it in their range.
Bill In Oz, The Victor Chang study was a beat up. ABC Media Watch did a nice story on it last week.
http://www.abc.net.au/mediawatch/transcripts/s4721720.htm
Just who I wonder are you without any name mate ? And I wonder why you are promoting the ever so politically correct media watch program on the ABC ?
The journalist who hosts media watch is no science journalist. He’s a hack political journalist Which explains his loud ‘gotcha’ style of reporting. And the ABC also reported this research. But the ABC & SBS journalists got a ‘get out of jail card’. Only the other commercial media get slammed.
By the way there is a substantial ideologically driven effort here in Oz by medicos to try and regulate, control the availability of cheap supplements to the population. They want us all only to take their pharmaceutical industry drugs instead. This ‘media watch’ dead panning of Niacin simply reflects that ideological position.
Turning to specifically to Niacin ( B3 ) : it is a relatively cheap over the counter supplement. It also has very few side affects. I use it as part of my own heart health program. And now it has been found to reduce miscarriage & birth defects in the Victor Chang research. If I was a women wanting a child and with a history of miscarriages, I would take Niacin. After all the quacks have nothing better to offer.
But that spoils their heroic efforts to market pharmaceutical drugs via doctor’s prescription.
Yes, and possibly the cholesterol is raised to help with an ailment – an ailment which results in death.
Would you care to expand on that? Your meaning is rather obscure.
Bill In Oz, I think you may misunderstand where I am coming from. I am come here to exchange information about health improvement, not politics. I like Dr Kendrick’s site, and entirely dogma free environment and general scientific skepticism. I’ve been a scientist in the past with a background in the biochemistry / anti-cancer area. I have moved to a completely different industry for the last 25 years. I dislike the corporate side of science as a justification for profit at the expense of people’s health. That is my agenda
Personally I detest political correctness, I dislike most of the ABC agenda. Believe it or not, I actually quite like your posts, agree with a substantial amount of your information.
The reason I posted that link to that particular story is it revealed the most flimsy of evidence for greatly exaggerated claims about vitamins extrapolating from a very small mouse study to a small sub set of humans with a very specific genetic mutation affecting a metabolic pathway. The story seemed to call out the scientism bullsh*t that I abhor.
As for being unnamed, -.- does it matter? Judge my posts on the strength of the information I provide, rather than some arbitrary label. Dr Kendrick has sufficient information about me as site admin & owner.
Please all feel free to disagree over the science and the interpretation of the science. Too many people, in research, are playing golf, when they should really be playing tennis. (or words to that effect). We are never going to fully agree on all scientific research output, but that is healthy.
I am not a scientist. I am a retired organic farmer with a life long interest in science. I respect the work that the Victor Chang institute does. Given that Niacin is an over the counter supplement, no pharmaceutical company is ever going to fund research into it’s uses. So whether further research takes place depends on government or philanthropic funding. And both of them are in limited supply in Oz .
But let’s put that aspect of Niacin aside for a while. There is a very interesting article by PD Mangan from 2015 at
http://roguehealthandfitness.com/niacin-as-a-life-extension-drug/
Mangan points out that Niacin promotes autophagy. – the bodies process of getting rid of senescent or defective cells. He’s interested in that because autophagy is age enhancing or age reversing. Autophagy also happens when we ‘intermittently fast’. Mangan suggest that it taking Niacin when fasting could boost autophagy.
Excessive Ethanol?
Just out of interest, why is it that you disbelieve pretty much all of the health hype and “studies” and “research” which has been pumped out over the last 20 years or so on pretty much every substance and/or activity under the sun, but nonetheless still wholeheartedly support those the two pillars of the Health and Fitness industry – smoking-bad/exercise-good? Are the researchers/companies/people involved in studies in those two areas somehow magically immune from the corrupting influence of potential financial gain and/or increased popularity/votes/support etc? Just wondering.
I’d suggest you try reading both of Dr Kendrick’s books (the Kindle versions are very cheap and fully referenced). What you will discover is that the outcome of various studies often bear remarkably little resemblance to the medical advice given out to the public. Consider for example, this long list of studies into the relationship between blood cholesterol and longevity:
http://vernerwheelock.com/179-cholesterol-and-all-cause-mortality/
Those with high cholesterol live slightly longer than those with less. Some of the studies also looked at LDL specifically, and the same trend was observed.
Has anyone read this article looking at Subbotin’s work: http://breaknutrition.com/heart-disease-and-cholesterol/ off topic a bit from causes but mechanism is best of a bad lot!
SW, just read it. Can’t talk about causes if the mechanism is not clearly understood. Subbotin’s explanation of how CVD starts makes sense. There is no endothelial damage to cells in contact with lumen in early stages. Other factors in later stages besides oxLDL are most likely involved, such as destruction of glycocalyx of endothelium cells by high glucose to initiate inflammatory response.
An article in Edgemedianetwork, I was surprised to read that since the mid 80’s more women than men have died from heart disease and that more men survive an MI than women.
This is in America. Dr Jacqueline Eubany, hope I remembered her name correctly, has written a book, Women and heart disease. It also says that the gap is widening between survival of the sexes. Had not heard this and though I remembered Dr Kendrick covering women and CVD can’t remember exactly what. Have I missed something.
Males have greater age-specific heart disease mortality rates than females, especially at younger ages. But the absolute number of deaths, or proportion of all deaths, from heart disease has not differed much between the sexes during the 1900s. When mortality is pushed up in older age groups, heart disease may become more common as a cause of death among females. However, according to the latest statistics, it is again somewhat more common among males than among females in the US (NVSR for 2014, p. 9; cf chart of time trends I generated, with a slightly wider definition of heart disease). I suspect this is because of a greater propensity in recent times to report Alzheimer’s and other dementias, instead of chronic heart disease, as a cause of death in the old, especially in old females.
In a comment, Dr Kendrick said…
Thanks Karl and Martin and indeed Dr Kendrick. My cerebral cortex no longer keeps hold of information, should have remembered or gone back over this wonderful blog.
The hippocampus probably, no wonder I had a TGA.transient global amnesia.
I am currently reading a new book, “Diabetes Unpacked”, where various authors, including Malcolm Kendrick, are responsible for each of the 14 different chapters. Dr. Zoë Harcombe is the main editor for this book published through “The Noakes Foundation”. Although I am, as a stern LCHF-adherent, familiar with most of the issues brought up, it is good to have the “belief system” confirmed through solid scientific facts exposed from different angles.
I am now at chapter 13 by professor Noakes where he is strongly advocating the LCHF way of life as a true remedy for our modern ailments as most of us who have suffered severe CVD and/or diabetes tend to do after having restored our health with this “new” lifestyle.
It is a “great book” which summarizes what it is “all about” – buy it and support our fighters for change!
Get convinced that Hippocrates has been right all the time when claiming your food to be your medicine!
Goran. I agree; and the DVD is compelling, especially part 2.
I remain thinking of the HPA (hypothalamic-pituitary-adrenal) axis as a pivot point. Everything affects it – stress, glucose overload and therefore diet, and no doubt the light spectrum, etc.
Come on !
T’is the LDL that cause heart disease !
Low-density lipoprotein: the culprit. From evidence to counselling, drugs, and vaccination
https://academic.oup.com/eurheartj/article-abstract/38/32/2447/4085603/Low-density-lipoprotein-the-culprit-From-evidence?redirectedFrom=fulltext
Here is da proof !
Low-density lipoproteins cause atherosclerotic cardiovascular disease. 1. Evidence from
genetic, epidemiologic, and clinical studies. A consensus statement fromthe European Atherosclerosis Society Consensus Panel
https://www.eas-society.org/page/LDLcausesASCVD
Tough read it seems. I’ll need some time . Then see whether I change my statinophobic mind.
I fail to undestand the reasoning behind your comment except for mischief making. Perhaps you could come back with the funding sources for EAS.
Pedrin, The consensus article you provide via open access link, has 63 lines in the “Conflicts of Interest” section at the end.
All ( except two) of the researchers who signed on to this statement are beneficiaries of the pharmaceutical industry, either in grants, salaries, honoraria etc..
It is very difficult for such people to see the truth clearly when their income & livelihood depend on them not seeing. ( Not my words, someone else’s. I forget who. But accuarte none the less. )
Bill in Oz: That quote comes from Upton Sinclair.
“It is difficult to get a man to understand something, when his salary depends upon his not understanding it!”
–Upton Sinclair
https://en.wikiquote.org/wiki/Upton_Sinclair
I am not getting paid to not understand some comments in this blog, I don’t understand them for free. Perhaps they are obtuse, perhaps they are fatuous.
It’s pay walled Pedrin. I wonder did you pay EUR €33.00, GBP £26.00 or USD $42.00, for a three page article in this journal ?
Effectively whatever ‘proof’ you are talking about is hidden and effectively not subject to review by the general public or commentators here either. That makes it a bald unsupported assertion. And that is not a joke.
pedrinhadeazucar: I almost had to laugh! The Edward Jenner mythology has been repeated to the point that it is now “factual.” Even the University of Edinburgh, from whom he purchased his “medical” degree, claims that he “invented” vaccination. Something quite similar was used in the Ottoman Empire, and likely elsewhere, before he was born. Lady Mary Wortley Montagu brought the practice to England in 1717, but it “. . .fell into general disrepute in Europe after 1728” because the mortality rate was 2-3% among the inoculated, and it “. . .spread the disease more widely by multiplying the foci of infection.” (Frederick F. Cartwright, “Disease and History,” Rupert-Hart-Davis, London, 1972, p. 124). It was revived in 1743, and “. . .became a lucrative branch of surgical practice. . .especially among the well-to-do.” (Victor C. Vaughan, MD, “Epidemiology and Public Health,” C.V. Mosby Company, St. Louis, 1922, p. 189).
Bill In Oz and AH Notepad:
Of course there is a tongue in cheek mischievious intention but not only that.
I’m sorry but the papers are not in the public domain I could get them, though. ANd Am yet to read them but first glance is : this is going to be tough.
For the moment all that is accessible is here as an insufficient abstract:
https://www.ncbi.nlm.nih.gov/pubmed/28444290
I expect Malcolm Kendrick will get them .
I don’t need to look up the authors’ conflicts of interest, I would be surprised if they wouldn’t.
Nevertheless they present data and arguments that we contrarians should examine.
Don’t we also have a conflict of interest . Of course we do, we have an intellectual one. It is very difficult to accept being wrog and examine the possibility we could. We have this conflict of interest but we could be right. I hope so by the way when I see my cholesterolemia (had to test it for in insurance company, with PSA and HIV );
Just as much as we have a conflict of interest but yet could e right , the multiconflicted authors that support LDL as the cause of atherosclerosis could be right .
I don’t think a paper can be discarded just based on CIOIs .
No one’s fault but we meet here the concept of bullshit asymetry:
“The amount of energy necessary to refute bullshit is an order of magnitude bigger than to produce it.”
http://ordrespontane.blogspot.fr/2014/07/brandolinis-law.html?m=1
More in deth on scientific publishing hier:
The Unbearable Asymmetry of Bullshit
http://quillette.com/2016/02/15/the-unbearable-asymmetry-of-bullshit/
I did manage to read the full report proving that LDL-C causes heart disease. Unfortunately there was no explanation how it does it.
Pedrin, I gain no financial benefit from being a ‘contrarian’ and an ‘anti-statinologist’. In fact the opposite. If I was content to just accept the various statinist prescriptions I was handed out and just take them, financially I would be better off. The scripts are available via Medicare here in Oz and so extremely cheap.
However none of the supplements I take having examined the research and read here on Dr Kendrick’s blog, or on Mangan’s Rogue Health blog, are subsidised by Medicare. In terms of direct outlay they are far far more expensive. And I have adopted some & dropped others as I find out more.
Turning again to the links you provided, there is a very old saying here in Australia :
“Bullshit baffles brains”.
Believe me, it is said with complete & utter disdain and disrespect whenever scientists put forward stuff that no one beyond the select few can understand what is meant.
And frankly, this mystification is unfortunately a a common characteristic in science journals and research papers.
I am extremely glad it, it has no place here.
If I’m wrong, I am not being paid for it, and am not deliberately lying with intent to deceive and get loadsamunny.
Someday, your immune system may be pressed into service to fight heart disease. Researchers have discovered that a simple sugar can stimulate immune system “clean up” cells to reduce disease-causing plaque in arteries. https://www.voanews.com/a/heart-disease-immunity-sugar-molecule/3892180.html
Randall: Interesting, but deserving of a proper amount of skepticism (as a potential intervention). That university is doing ground-breaking research in the human microbiome, so, to me, they have a lot of credibility. I wonder what VOA stands for? At one time it meant Voice of America, a U.S. government-run cold-war propaganda operation aimed at the USSR and eastern Europe.
Randall, stimulating the immune system to produce more macrophages thereby reducing plaque is the opposite of why statins are considered beneficial. The effect of statins is to reduce inflammation by decreasing macrophage activity. CVD is considered to be an inflammatory disease, too many macrophages weaken plaque and cause plaque rupture. So how can more inflammation be beneficial? The answer might be found by looking at what can be done to reduce the need for excessive macrophages like reducing excessive oxLDL formation.
Re. to quote Bill in Oz about getting back to discussing “causes and cures of CVD” reminds me of my favourite instalment of Dr Kendrick’s – part 24 on vitamin C. Well written, pitched perfectly (i.e. the technical data were understandable to the layperson), handy dandy lists/bullet points and so on.
It would be high on my wish list that future instalments would tackle the causes in a similar way e.g. one on stress, one on homocysteine, one on fibrinogen and so on. And thus get a thorough dissection.
These 3 for example have occurred many times on this website as causing endothelial damage and triggering the damage/repair process. And there are plenty more suspects to be assessed or re-assessed.
Charles, thank you for the referal back to What Causes heart Disease Part 24. I read it months ago and have just reread it again. As you say, it is stunning in it’s clarity and simplicity. And for that a hearty thanks to Dr Kendrick !
As it happens I am very interested in the discussion of Vitamin C. I have taken Vitamin C since my 20’s whenever I came down with a flu or illness. I was an early adopter of Linus Pauling’s ideas on Vitamin C. I still have his book from 1973 on Vitamin C.
Turning to carnitine, Dr Kendrick in another comment today, I mentioned that there are significant differences in the science. There are indeed.
I have taken carnitine for the past ( about 1 gram a day ) for the past 4 years on the recommendation of an anti-aging medico at the time.. When I first read the Part xxiv, I was pleased and immediately increased the daily dose of carnitine.
A few days later there was an article & discussion about heart disease here in Oz, on a popular blog. In the discussion I mentioned the links in your blog. I got a quick reply from a very prominent nutrition expert here named Rosemary Stanton. She suggested that I immediately read 2 articles from 2013 that proved that carnitine increased heart attack incidents. I will not give the links here as I think the research was faulty. I think that it had a vegan promoting agenda.
But such is the research out there now : a huge amount, written in incomprehensible English, funded by we know not whom for agendas that are not public.
That is why I am here each day – seeking accurate information written clearly without a hidden agenda. And a community of others equally interested in the same things. So my thanks to all here as well.
Bill in Oz: Some in the vegan and vegetarian community do have an agenda, and it is like religion. There is a powerful vegetarian group in Washington, D.C. called CSPI (Center for Science in the Public Interest) who singlehandedly got healthy animal fats removed from fast-food fryers, to be replaced by trans-fat. When the political winds shifted some years later (the science was unequivocal of their hazards long before this), they used their bully power to have them replaced by vegetable seed oils, which may be nearly as bad. They appear to be associated with increased lung cancer rates in Asian women.
Yes, I think you are right Gary about this. Vegetarianism & veganism has become powerful in many areas of life. In fact I suspect that shops selling fried food are obliged to use industrial oils, instead of saturated fats, here in Oz as well.
I do not eat deep fried food at all now but I have a visceral memory from my youth of fried food cooked in tallow. It even tasted different.
On a slightly different tack, I was at the gym the other day and there was a stall there. It was manned by 2 overweight people who never train at the gym. And they were selling vegan supplements & prepared foods. I wonder if the gym management would allow a butcher’s shop to set up a stand cooking & selling samples of cooked meats for us omnivores ? Somehow I doubt it. though I’d be pleased.
So here in Lincolnshire the chippys mostly use pure beef dripping – I have seen it delivered, and you can tell by the way it hardens on the wrapping paper. When you think about it, we are animals and our own fat is animal fat – so our bodies should understand what they are deaing with – a natural food instead of an industrially processed thing.
Jean, that seems to be be the way humans have evolved. As for industrial oils, they are maybe fit for putting in an engine. Bur eating it ? Surely not.
Jean – that makes such TOTAL sense. By the way, I envy you your fish and chip shops and their use of beef dripping. On the odd occasions when I used to make chips I always used dripping and the flavour…….fabulous. A completely different experience.
For a real fried food horror story:
Thieves fry Kenya’s power grid for fast food
The culprit is an unusual one: A vandal who is selling the toxic oil, drawn from the transformer, to chefs who use it for frying food in roadside stalls. Five litres of the viscous, PCB-laden liquid sells for $60. It looks like cooking oil, but lasts much longer, users say.
Kenyans’ appetite for fried food and cheap frying oil is stalling the country’s urgent efforts to build a modern electrical grid, even as it sows the seeds of a public health crisis, experts say.
And with utility companies reporting similar vandalism across East Africa and as far away as South Africa and Nigeria, the crime spree is becoming another thorn in ambitious plans to electrify Africa.
Note that the CSPI only turned against trans fats after the Foodlike Substance Manufacturing Industry developed interesterified fats as a replacement. It remains to be seen how much harm they do. But they are Not Animals so that is OK.
To quote the inimitable J Stanton (gnolls.org) on “vegetable” oils
“If you can put it in a truck and the truck starts, it is NOT FOOD”
also
“birdseed and diesel fuel are NOT food groups”
Chris I used to know a bloke who went round all the fish & chip shops in the far Eastern suburbs of Melbourne collecting their drums of used industrial oil. He had system for cleaning it up and then poured it in his diesel 4WD. Cheap fuel !
There is debate in some health circles about ‘industrial oils’ by which I refer to canola, sunflower, safflower, palm oil, etc. Some folks say that some of them are healthy. I stay way from all of them !
The reason I stay away from them & call them industrial oils, is that process of making the seeds of all these plants ‘fit” for consumption is as roughly as follows :
Collect all the seed at a factory
Crush the seed to a mass
Heat it up to around 80-90 degrees centigrade
Press out the oil
Clean off all the particulate matter in the oil by filtering it
Purify the grey coloured oil by mixing it with caustic soda
Oil & left over caustic soda are separated.
At this point the oil is a vaguely colourless liquid
To make margarine it is hydrogenated by bubbling hydrogen gas through it and colouring added to make it yellow and attractive to us.
No thanks. Butter for me !
Bill in Oz: And they are rancid before they even reach the supermarket shelves, bottled in clear plastic, so any light they receive while sitting there increases the rancidity. Plus they have a very high omega 6/omega 3 ratio, which is inflammatory.
One of our local farmers produces “cold pressed” rapeseed oil. I tried it and it tastes like crap, though less so than the commercial varieties, and cold pressed fails to note that the screw press actually heats the seeds/oil just by the compression process alone. It is a nice golden colour though.
Much though I like to support local industry and local farms I think I’ll leave this one and stick with the EVOO, butter and coconut oil. They could market it as organic diesel but we’re supposed to stop using diesel cars though it’ll take a while to replace diesels in trucks, agricultural machinery and ships.
Seen this about the background to veg(etari)anism?
http://letthemeatmeat.com/tagged/Seventhday_Adventists
It is good to support local food growers. But canola oil is not fit human food. It is a very close relative of rape seed which is proved poison for humans but grown as fodder for cattle in cold climate areas.
A a former organic farmer I suggest he grow something that really is good for people to eat without the health hazards of industrial oil.. I’m sure there are alternatives and some even more valuable per kg.
The problem comes when you have a million or two invested in all the kit to grow and harvest grains and seeds. Actually over the years a lot of “alternative” crops have been trialled and several are still grown regionally, linseed and borage for example. Oilseed rape itself used to be just one such “alternative” crop once, unknown when I was young, the nearest equivalent would have been mustard.
Not a few of the Big Farms on the lighter land have gone into onions, salads, even lawn turf, but then you need to invest in different harvesters, irrigation kit, etc.
Some of the small farms appear to be financially successful with the likes of grass-fed beef, sheep and free range pigs – incomes are less but so are expenditures. The last dairy farm in the area switched to beef many years ago, and interestingly a new dairy farm opened recently – but they had the capital to invest in local production of butter, ice cream etc. and local milk delivery to shops and businesses – just selling milk to the likes of supermarkets was a cause of massive losses. Ironically said supermarkets are now facing butter shortages and starting to pay more for the milk, while complaining that so many farms went out of business. Duh!
Ummmmm. Yes farming involves a huge investment in equipment, labor, skills, developing markets etc. Changing direction is hard thing to do. and constrained also by climate, weather, finances, age and family support. But if the crop is not fir for purpose like Canola, then change is inevitable as the customers dry up.
Here is Oz, merino sheep for wool used to number about 150 million. That market disappeared as woolen clothing was replaced by artificial fibre. Now there are but 55 million sheep here and most of them are meat types as the world market for lamb & mutton has gone gang busters.
Such is farming the world over whether conventional or organic, whether cropping or livestock or horticulture.
Oh yes, here we are surrounded by “wool churches”, but a few centuries later and it costs more to shear the sheep than the wool is actually worth.
OTOH lamb prices have rocketed, I think due to sales to the Middle East, I’ve paid more for lamb than venison on occasion. Mutton became trendy again a few years back but not sufficiently so that many farmers thought it worthwhile to attempt to keep their sheep alive for that long.
Goat milk and cheese has taken off, but sadly goat meat less so.
There used to be a hemp works in town. That’s another crop that was revived recently as breeders developed a non-psychoactive variety. A new factory opened but closed again soon after as demand fell off again – the fibre was being used in various industries, not sure what replaced it. I joked with one farmer that when times were hard he could clip and dry some leaves into little baggies and sell them around the London pubs. He couldn’t get done for actually selling drugs, but might fall foul of the Sales Description Act.
Meanwhile Bayer are donating a percentage of soy seed sales to the American Heart association, which explains a lot.
Chris I was in the UK back in 2008 for a few weeks. I spent soem days travelling South from Manchester to Monmouth & Bristol and then West to Totness in Devon. I made contact & visited 5-6 organic farmers along the way.
All seemed to be doing well. Organic dairy, meats & vegetables. And 2-3 were supplying a huge organic box delivery company based just outside Totness. With 60 million people in the UK in such a small area, there is significantly more demand than in Australia where 24 million live in a space 50 times the UK in area but 2/3’s low desertish rainfall.
Of course the value of land in the UK is higher than here which is a real problem as many farmers in the UK are actually ‘tenant farmers’ with less of a stake in caring for land as well as being productive. Tenant faring is very very rare here..
6 Times When Inflammation Is Actually Good For You https://www.prevention.com/health/when-inflammation-healthy Seriously, macrophages try to fix damaged arteries by cleaning up cellular waste, including misshapen proteins, excess fat and dysfunction cellular structures called organelles.
LDL particles that are not oxidized are not atherogenic. How is that for a statement? Dr. Tom Dayspring’s name is there. Much more at http://eatingacademy.com/cholesterol-2/heart-disease-begin-tell-us-prevention
Randal, there was a period when I was a fan of Dr Attia. I read almost all his posts, 2-3 times ! And followed the discussions as well. The article you cite is also quite good.
However, there is a certain problem with his blog: all the comments are usually directed to him as the ‘expert’ doctor of medicine. And as he is busy medical doctor with a busy practice and a young family, he has recently taken to replying to comments with quite brief and sometimes cryptic remarks.
A further thought : the blog on the process of arteriosclerosis provides little by way of solutions to cure CVD. In fact even the LCHF diet which he endorsed over the past 7-8 years as his own preferred diet, gets the nod as a way of healing CVD. I remember his comment that CVD increases with age – seemingly inevitably. Still I look forward to his promised book.
Bill in Oz: I, too, have lost interest in reading Dr. Attia’s posts. Can’t quite put my finger on why. Don’t seem to finish reading them any further enlightened than I already am, perhaps.
Gary, I suspect that is slightly unfair. He did a huge amount of work detailing exactly why LDC-L is irrelevant to CHD.. There are his 8-9 big posts on this still available to read as well as his ones on diet and arthereosclerosis.
I am grateful for all his work in these areas.
I think he has just become much more busy as an MD in the past 2 years ever since leaving NUSI. With patients in San Diego & New York, he is travelling a whole lot more in recent years. And he is a whole lot younger that I suspect most of us here – in his thirties. He is married with 2 young kids. And naturally his wife and family should have & deserve his primary attention.
Bill, went thru the Attia post in detail . . . mainly because I wanted to get it quite clear in my mind the hypothesis that LDL particles are the driver for atherosclerosis – yet again.
He is quick to dismiss the idea that the cholesterol load of the LDL particles, LDL-C, is an issue in predicting the development of atherosclerosis . . . and supports the idea that it is the LDL-P, the number of LDL particles, that is the driver of atherosclerosis. (“driver of” or “associated with”??)
Basically, the greater the concentration of LDL particles the more likely “to penetrate” the intimal layer.
Problem 1: How do the LDLs do the penetrating? And in particular, can the rate of this process be shown to be dependent on the LDL-P concentration – simple diffusion model? – not really.
The next step is for the some of the surface phospholipids of the LDL particles trapped in the intimal layer to become oxidised . . . because of exposure to “reactive oxygen species”.
Problem 2: Where are these reactive oxygen species coming from? They could come from the immune system . . . but according to model they have not come onto the scene yet . . it is stated the already oxidised LDL causes signals to be sent to recruit the monocytes => macrophages to invade the intima and deal with the oxLDLs.
There are other issues, one, for instance with the idea of the thickness of the intimal layer being a surrogate for CVD . . . This notion supports his suggestion that CVD starts from birth . . . the intimal layer does indeed seem to increase in thickness with age. But the idea that CVD is so structurally programmed into us from birth is a bit difficult to come to terms with.
Having said this . . . I love his writing style.
There is no paper that I’ve found (and I have really looked) that shows LDL correlated with CAD if oxLDL is held constant. The weak correlation of LDL with CAD has a causation problem – there are several drugs that lower LDL – yet all-cause-mortality won’t budge. Only statins seem to make a tiny difference – NNT of 84 for 5 years of treatment of known heart disease is nothing to brag about. (could be that statins work via NO or calcifying unstable plaque ). Causation is tough to prove – easy to claim.
The macrophage has a receptor that recognizes oxLDL (likely looks like a dead or dying bacteria) inducing it to swallow it up. These macrophages can become foam-cells – block off arteries. But non of this is about the initial cause of CAD.
If we prevent a clot from forming – it won’t prevent the cut. If we remove the smoke – it does not extinguish the fire.
That being said – reducing weight will reduce the intima thickness – and apparently foam-cells as well. LDL actually goes up if one is losing weight – the body apparently uses LDL to transport fat from adipose tissue.. ( wonders – it has a purpose – I’m very doubtful that we evolved LDL to cause heart disease.)
Lowering oxLDL is rather simple – reduce the intake of PUFA – ( you can hear the medical community tip-toeing away from the PUFA=healthy narrative ). Some polyphenols also lower oxLDL – but may also mess with the insulin system. There have not been definitive studies to find an optimal dose of polyphenols and there are 100’s with differing effects. .
But we are only talking about managing the response to the injury. I’m interested in the causation – likely the thickening of the inner intima long before foam-cells and clots. This might well be caused by high insulin levels or stress – but likely is not ‘knowing’.
Burns to the skin – another bit of epithelial tissue similar to what lines arteries – CAUSE HDL to go down – changes to LDL as well – so which is cause and which is effect?
Hard to avoid AGE’s, there will always be glucose in blood. High glucose will just speed things up like in postprandial glucose spikes. Looks like ageing has a lot to do with glycation, unavoidable.
Rate of ageing could be controlled by LCHF, K2, C, D3, Mg, etc.. in addition to low PUFA
J Vasc Res. 2009;46(6):572-80. doi: 10.1159/000226225. Epub 2009 Jun 30.
Advanced glycation end products induce calcification of vascular smooth muscle cells through RAGE/p38 MAPK.
Tanikawa T1, Okada Y, Tanikawa R, Tanaka Y.
Abstract
BACKGROUND:
Monckeberg’s calcification in diabetes, known as medial artery calcification, is an independent predictor of cardiovascular mortality. However, the mechanism underlying this phenomenon remains to be elucidated. We demonstrate that advanced glycation end products (AGEs) induce calcification of vascular smooth muscle cells through the receptor for AGE (RAGE)/p38 mitogen-activated protein kinase (MAPK) signaling pathway.
METHODS:
We detected vascular calcification by von Kossa staining. Alkaline phosphatase (ALP) activity was determined by measuring p-nitrophenol. Osteocalcin concentrations were measured using ELISA. Western blotting for protein phosphorylation and real-time RT-PCR for expression of mRNA were used.
RESULTS:
AGEs induced calcification of vascular smooth muscle cells. AGEs also induced the expression of Runx2 mRNA. In addition, AGEs increased ALP activity and osteocalcin secretion. Furthermore, AGEs induced phosphorylation of p38 MAPK, and this phosphorylation was inhibited by the anti-RAGE blocking antibody. Increased ALP activity was inhibited by the p38 MAPK inhibitor or anti-RAGE blocking antibody. Furthermore, the p38 MAPK inhibitor and anti-RAGE blocking antibody both inhibited AGE-induced calcification of vascular smooth muscle cells. Diabetic serum induced calcification of smooth muscle cells and the calcification was inhibited by RAGE blocking.
CONCLUSION:
Our findings indicate that AGEs induce calcification of vascular smooth muscle cells by osteoblast-like differentiation of smooth muscle cells through RAGE/p38 MAPK.
Re statin benefits, also reduces inflammation by reducing level of macrophages. Only question is what happens when repair process is altered, does oxLDL accumulate and cause other problems?
xtronics: Thank you for this thoughtful piece. Well done.
Yes!
Tom Dayspring has just a few Conflicts Of Interest.
OTOH some less conflicted people have dug up some more interesting and more likely (IMO) to be causal factors and my current supposition is that things that damage the LDL may also be things that damage the arteries, and other metabolic players
Lipoprotein Heterogeneity and Apolipoprotein B Metabolism
http://atvb.ahajournals.org/content/17/12/3542.long
from 20 years ago
Study of the Use of Lipid Panels as a Marker of Insulin Resistance
to Determine Cardiovascular Risk
Click to access permj19_4p0004.pdf
Insulin resistance is associated with increased cholesterol synthesis and decreased cholesterol absorption in normoglycemic men
http://www.jlr.org/content/45/3/507.long
Increasing Lipolysis and Reducing Atherosclerosis
http://www.nejm.org.sci-hub.bz/doi/full/10.1056/NEJMe1706907?query=TOC
(or you could just eat fewer carbs)
High Glucose Concentration Increases Macrophage Cholesterol Biosynthesis in Diabetes Through Activation of the Sterol Regulatory Element Binding Protein 1 (SREBP1): Inhibitory Effect of Insulin
http://journals.lww.com/cardiovascularpharm/Fulltext/2008/10000/High_Glucose_Concentration_Increases_Macrophage.5.aspx
Insulin and glucose play a role in foam cell formation and function
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1550220/
Interrelationships of Hyperinsulinism and Hypertriglyceridemia in Young Patients with Coronary Heart Disease (from 1968!)
http://circ.ahajournals.org/content/38/6/1156.short
Associations of fats and carbohydrate intake with cardiovascular disease and mortality in 18 countries from five continents (PURE): a prospective cohort study
http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(17)32252-3/fulltext
(only just out and can only get to the abstract)
Are the PCSK9 inhibitors the panacea of atherosclerosis treatment?
http://www.tandfonline.com/doi/full/10.1080/14779072.2017.1348231
don’t really need to go beyond the COI for this one
TA Turner’s institution has received research support from Amgen and Sanofi for clinical trials and central laboratory analysis. EA Stein has received consulting fees from Amgen, Regeneron, Sanofi, Genentech, Roche, The Medicines Co, ISIS, Catabasis, AstraZeneca, CymaBay, CVS/Caremark and BMS related to PCSK9 inhibitors and other lipid lowering drugs. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.
Big thanks to George Henderson and others on Twitter for these . . . and if I got any of them from Malcolm’s blog originally, well the statins must have rotted my brain . . .
P.S.
Further to my previous comment about my personal wish about how the causes and cures of CVD/events might unfold on this website, another benefit would also be to hear from people who could conclusively identify the cause (e.g. vit C deficiency, excess insulin) of their incident.
I’ve followed Dr Kendrick (and his website too) for over a year, and spent a lot of my recovery time catching up on his blogging, and that is one element which is missing. It seems to me,if memory serves, it’s generally all 3rd party reporting from research or from the authors of their CVD hypothesis.
On the other hand, as a rare minority (like all of you following Dr Kendrick) knee jerking against mainstream thinking and trying to find out what happened, it’s a nightmare…especially as the months/years go by and that moment in time is lost. It would be helpful to find out from people how they ascertained the cause of their CVD incident…or even if they are bothering.
I know people are and so am I. I’m hoping to get some follow up blood testing on my vit C supplementation/lp(a) situation. Then I’m moving onto fibrinogen testing (but not quite clear if it’s a cause or part of the response to endothelial damage.
Can’t wait – bring on the next blog!
It’s like trying to stamp out a fire, wherever you stamp it pops up somewhere else.
https://www.theguardian.com/science/2017/aug/27/anti-inflammatory-drugs-may-lower-heart-attack-risk-study-finds
1) Why not start with an anti-infamatory diet?
2) That old chestnut is here, “Statins are the mainstay drugs for heart attack prevention and work primarily by lowering cholesterol levels.”
3) It then goes on, “But a quarter of people who have one heart attack will suffer another within five years despite taking statins regularly. It is believed this is because of unchecked inflammation within the heart’s arteries.”
4) Has this got something to do with it? “The cost of 1 dose of canakinumab 150 mg is £9927.80 (NICE)”.
I’m getting as cynical on this as our Dr M K.
Robert
And how about this from the same article,
The researchers reported an increase in the chances of dying from a severe infection of about one for every 1,000 people treated,
And the little click bait half way down leading to an article on the so-called nocebo effect
Oh good grief! Add these to your statin and PCSK9 inhibitor. Or spend a fraction of the money on grass-fed meat, fish and fresh vegetables, butter, cheese, EVOO and coconut oil to name but a few. I suspect I know which would have more effect, and taste better too. The NHS could prescribe Rolls Royces and still have change left over.
Here we go again.
“A New Drug Lowers Risk of Heart Attack and Cancer”
http://time.com/4916414/drug-inflammation-heart-attack-cancer/
Low dose statin
I left a reply above (Aug 22, 2017 @7:10) where I mentioned low dose statin (for example 5mg per day atorvastatin). Here is a link to a discussion from 2003 on the Thincs.org site: http://www.thincs.org/discuss.lowdose.htm#Douane1 . No randomised controlled trials have been done on the effect of low dose statins so nothing defensible can be said about low dose statin use + or -. But I think it is an interesting discussion for those who follow Dr. Kendrick’s blog especially as Dr. Kendrick himself is participating.
Phil
Philip Thackray
Renfrew, PA 16053 USA
I wonder if anyone else saw this from cardio brief ?
“we are now entering “an era with a plethora of treatment options for the secondary prevention of atherosclerotic cardiovascular disease. Human genetics has highlighted that atherosclerotic cardiovascular disease is multi-factorial, with several underlying causal pathways. We now have a treatment for several of these pathways.”
CANTOS Validates Role Of Inflammation In Heart Disease
by Larry Husten
I wonder if the statinists are looking at this . 🙂
Bill, “Novartis tested canakinumab (plus standard of care) against standard of care alone..”
Statins in both treated and control group, standard of care includes statins. Canakinumab alone does not reduce “bad cholesterol”, satins are here to stay.
Bill in Oz: Sometimes CardioBrief is worth reading, sometimes not. Today was a good post about PURE.
I agree completely Gary. But it’s worth it for the pearls.
Low dose statin,
The discussion I linked above actually starts here: http://www.thincs.org/discuss.lowdose.htm .
Phil
Philip Thackray
Renfrew, PA 16053 USA
You may have seen article in the guardian today.
Anti inflammatory drug may lower heart attack risk.
Us scientists find heart attack survivors given canakinumab injections have fewer heart attacks and also lower risk of cancer.( hope my spelling is correct) .
Any thoughts! Have to give them full marks for trying.
Sylvia, this is applied logic. CVD is an inflammatory disease, the cure is to sell a drug to inhibit inflammation. Statin’s days are numbered.
“In my lifetime, I’ve gotten to see three broad eras of preventative cardiology,” he said. “In the first, we recognised the importance of diet, …” And then they recommended a low fat high carbohydrate diet (plus polyunsaturated fats) that causes inflammation.
Andy S: CardioBrief had a post about this. This wonder drug is about squeezing fabulous sums out of the “health care” budget, and nothing more.
At ten thousand quid a dose, you run the risk of getting a heart attack just by looking at the price tag of canakinumab.
Regarding ” E=mc2.” That is a brand name, not Einstein’s real equation. His real equation ( for objects at rest) is E0=mc2 and all it means is that ther REST- energy ( the ONLY energy) is being put equivalent to mass. Mass and energy are NOT the same like everyone believes. Mass is a poincare scalar and is always the SAME in different reference systems. While, energy, is the fourth (time) component of a four-vector and is different in different systems. Energy and mass are NOT things , nor stuff at all, they are totally abstract properties- numbers.
Matter is something entirely different from mass. It is a MYTH that matter is converted into energy in nuclear reactions. NO! NO!!!!! It is only STUFF- PARTCILES that are ever transformed into one another.
You cannot do damage to cells with “energy.” You need actual STUFF for that Photons are NOT energy- they are partciles, objects, stuff.
And to take down Colpo, McDonald, CarbSane publicly:
The first alw of thermodynamcis is being ABUSED by Internet salesmen like them. The TO physcists in the wordl repsonally told me. Thermodynamics si NEVER ANY kind fo EXPLANATION for any phenomena. Weinbger himself stressed that. The fiorst alw of themrodynamics does NOT AT ALL ADDRESS IS:
*Lipids are stuffed inot fat cells
*Processed to extract chemcial fuel
*Or simply eliminates as waste and excreted.
ANYBODY invoklin the first law of themrodynamcis in an obesity discussion is MISUSING these principles and taking them ourt of context, say TOP physcists to me. Thermnodynamcis DOES NOT AT ALL EXPLAIN- EXPLAIN obesity.
Actually Weinberg notes themrodynamics is more a mode of reasoning than a law or principle.
There are no “laws’- there are only fallible human models Sceintsits HATE the term” law “- they are not mandates, as David Gross notes. They are our best guesses that went through the sieve as hoes got smaller- they are TENTATIVE and WILL BE MODIFIOED OR even ABANDONED in the furture- this is very expected.
Sean Carroll has a GREAT ARTICLE about how energy is NOT conserved in General Relativioty and this number, energy, is NOT conserved in the rapidly expanding universe either. Only locally when time translational invariance conditions are present .
Physics is TAIHT wrong- these principles are NOT FIAT. THE PLAYING FIELD determines the rules. And there is no reason to think the universe will be the same in the far future- it very likley will not. Dr Krauss notes this. The laws of physics may evolve. Even speed of light is called into question by recent physcists at Perimeter Institute. We need to find out right away which laws are WRONG as FEYNMAN stressed.
Well you’ve lost me there.
I don’t think everyone believes that mass and energy are the same. But there is conversion. For example, U235 has a rest mass. When U235 undergoes fission the resulting atoms also have rest mass, and the sum of the rest masses of the products are less than the mass of U235. We have gamma rays and the product atoms shoot off with a lot of kinetic energy. This is what we mean by conversion of mass to energy. The mass change results in the energy/momentum 4-vector.
I am not sure what you mean by thermodynamics is not an explanation for anything, for instance it allowed Carnot to explain the efficiency limit of a heat engine. Entropy has very deep implications for the way our bodies work.
There is no “conversion of mass to energy.” I have that directly from top nuclerar physcists from Caltech. Nucleaer reactions involve changes in BINDING energies- no mass to energy conversion. It is taught this way because explaining bibnding energies is extremely complex. But technically, there is NO conversion of mass inmot energy. Lev Okun addressed this.Also, Steven Weinberg HIMSELF said therodynamics is NEVER any kind of explanation. Explanation being the key word. Frtehr, I have Nobel physcists ttoally agreeing with me that peoepl like Lyle McDoanld are totqally abusing the first alw of themrodynacis- it does NOT explain obesity at all. And the physics that governs biology may me very different than the physics that governs the universe as Dr. Krauss has suggested- there are observations over thelast decade that suggest this.
That is another misconcpetion that there is. There is no conversion of matter ( something totally different from mass) into energy either.
I am not entirely sure where you are going with this?
The Internet has a lot of misinformation. Thankfully, Professor Matt Strassler has a blog to correct Internet gurus and their misinformation. Matter and energy are not at all related- at all. Nor did Einstein ever say that they were- there are bogus Einstein quotes all over the Internet.
Now, mass ( only a property, not stuff and very different from matter) is *somewhat* related to energy.
In both nuclear and chemical reactions, what is occurring, is the transformation of rest-energy into kinetic energy. According to the theory of relativity, the mass of a particle is the measure of the REST-ENERGY. Einstein, when not sloppy or careless, debnoted it properly Eo=mc2.For objects in motion, energy is always GREATER than mc2.
My sources are tops- I have communicated with Lev Okun years ago ( a world class top expert in Einstein’s special and general theories of relativity and the man who named hadron particles-he was also the former head of the Institute for Theoretical and Experimental Physics ,in Moscow, Russia. I have also communicated with Alan Guth, Steven Weinberg and many more. I know what I am saying here and it debunks the Internet gurus.
Strassler respected Okun a lot. There is no physcist alive who knows the ORIGIN of the universe- and that is directly from Weinberg.
So many myths are out there and it’s the Neil Tyson types spread msinformation- I despise the science popularizers- the public is being MISLED
What about the increase in mass as particles approach relativistic speeds. Surely some of the energy used to accelerate the particle has been converted to mass, otherwise where could the extra mass have come from?
Tom Murphy is an associate professor of physics at the University of California, San Diego. He has a cure for obesity that does not involve the first law of thermodynamics, only what you call “stuff”,
“Now understanding that the body will continuously shed mass even if the food supply is shut off” – this is not a good diet plan, you may starve even while losing little weight. Hormones decide what energy goes where, we are not simple furnaces. My own experience when I tried that in the days that I accepted the low fat high carb recommendations was that every now and then something would flip in my conscious thought and I would eat a dried fruit or biscuit before I caught up with what was happening. I still remember it, wondering – why did I eat that?
Robert,
Considering the body purely as a black box, we are simple furnaces; furnaces which start burning themselves if you stop feeding them fuel.
What you are saying is the quality of the food affects the control mechanism, which is a different matter, I submit, than considering pure weight gain and loss, which is a simple matter of the accumulation and shedding of molecules.
Another health warning –
http://www.independent.co.uk/news/science/high-salt-diet-heart-failure-double-risk-study-food-drink-lifestyle-a7912771.html
‘High salt intake is one of the major causes of high blood pressure and an independent risk factor for coronary heart disease and stroke’
I added a comment pointing to “The Salt Fix” that I am reading now, also pointing out that I dropped my BP by 10s of mmHg by going low carb.
These food and health debates have really caught my interest now.
Robert, I wonder if they attempted to differentiate by the amount of processed food that the survey participants studied.
Maybe the high salt consumers were also the high processed food consumers. In which event the effects of each are confounded.
It’s curious : I do not eat much processed food at all. But I would really struggle to eat 12-13 grams of salt a day even though I love anchovies !
I agree. In all trials related to food of whatever type my first question is, what are the details of what is being eaten, which carbs, which lipids, which proteins, which vitamins etc & how was stuff prepared, cooked at what temperature etc. We don’t really know in any case unless it is a diet in a controlled environment as self reporting is flawed. I too eat near zero pre-prepared food.
Bill in Oz: I eat hardly any processed food so I have to work hard to get sufficient salt. It sure makes food taste so much better! From “The Salt Fix,” “By the sixteenth century Europeans were estimated to consume around 40 grams of salt per day; in the eighteenth century, their intake was up to 70 grams, mainly from salted cod and herring, an amount four to seven times the current intake of of salt in the Western world.” Wonder if they were dropping dead.
Robert
I too am reading “the Salt Fix” pretty interesting stuff.
By the way about diet, I am back on my daily beetroot juice laced with apple juice to mitigate the earthy taste. Pity is, not many in the wider public will try it, if the medical community don’t push it, it can’t be true!
I like beetroots as the are, though I do a salad with olive oil & vinegar as the flavour modifier.
Mr Chris. I wrote to Dinicolantonio asking about this study. I hope he could help us. But I think that the low salt and low fat dogmas are so powerful that today is very simple to produce studies which strengthen them.
https://www.ncbi.nlm.nih.gov/pubmed/26551354
Do you know this Jama study? A lot of medical procedures are not evidence based, but they are still used and abused, always repeating that they are effective.
The AHA in June said that saturated fats are deadly for the heart. They lower ed them to 5 per cent. And they show ed a study which proves they are right. This study is the famous one conducted many years ago, where a lot of data were lacking. The full data show that polynsat fats cause a higher mortality.Just the opposite they claim.
Paola: See my comment regarding the Finnish study and Dr. DiNicolantonio’s figures. There is no disagreement! They are essentially the same. The lowest risk group in the Finnish study consumed roughly the same amount of sodium (2.66-3.46 g/day) as what “The Salt Fix” calls the “Sodium Set Point” for most people, which is 3-4 g/day. Less than 2.66 g/day, according to the Finnish study confers a slightly higher risk for heart failure (1.0 vs. 0.83).
Are we talking about sodium or salt? 1 gr salt = 0,4 gr sodium. So 4 gr of sodium= 10 gr of salt. WHO recommends no more that 5 gr of salt= 2 gr of sodium.
Paola: Yes, very important to understand this. In the Finnish study the quintiles were based upon NaCl. The quintile with the lowest risk (HR 0.83) consumed about the same amount of Na (2.66-3.46 g/day) as what “The Salt Fix” describes as the “Sodium Set Point” for most people (3-4 g/day Na). So there is no disagreement between them on this point. What the Finnish study doesn’t mention is that consumption below that level confers a higher risk. This is one of the main points of “The Salt Fix,” that low sodium intake is dangerous.
The Guardian headline today is “New heart treatment is biggest breakthrough since statins”, so unless it is killing people that must be true.
*splutter*
A curious feature of that report (which I hope some of the experts here will comment on), is that it refers repeatedly to “Heart Failure”, but mixes in CVD in places. As I understand it, heart failure is a quite distinct disease – deteriorating heart muscle.
It seems clear from the description that this was an observational study, and the phrase “When the results were adjusted for age, sex, study year and area” might hide a lot of sins!
Terminology in medicine is horribly imprecise, it is a constant challenge.
Robert, there appears to be a connection between insulin and salt retention therefore low carb=less insulin=less salt retention=less BP.
Salt is bad if you eat low fat/high carb as per dietary recommendations.
https://www.ncbi.nlm.nih.gov/pubmed/1988777
High salt diets have never proven bad . There is no serious evidence at all.
Paola
Bit of a problem there’ all these guys in Finland beavering away for years, presumably they based it on something?
Based on what? Lies….Do you still believe in this science? In The salt fix everything is well explained. No evidence on saturated fats, no evidence on salt.
A sad, but valid, commentary on the current state of medical research.
Paola/Dr K
my comment was about the salt study in Finland was perhaps too elliptic. When you say that it based on lies, this means for twelve years many people sat about falsifying data, which seems unlikely. Now the study was based on urine sampling for excreted sodium, and the participants were mainly from Karelia, which had a checkered history as an area to say the least. So what elements in this study do you think were badly conducted or imagined? Since it is a major study, its results are going to bounce around for years.
I think I have lost track of this discussion thread. Remind me again about the salt study in Finland?
Mr Chris…have you read the entire study?
Paola
no, I have only ready the synopsis on the ECS site. Do you have a link for the full paper?
Tku
Paola/ Dr Kendrick
http://www.medscape.com/viewarticle/884824#vp_1
this is the most complete citation I found. As I asked, did all the people correlating and collecting this data make it up? How does it square with “The salt fix”? how does one decide one source is better than the other?
As is often the case, “journalism” garbles science. There is no disagreement between these findings and Dr. DiNicolantonio’s fine book, at least is regard to heart failure, the only endpoint in the study (I think). Look at the fine print: HR for 13.73 g/day NaCl (5.4 g Na) HR = 2.1. These numbers are not overwhelmingly strong, in terms of risk, except the last one, especially considering the small numbers of people in the study.
In “The Salt Fix,” on p. 121, he talks about the “Salt Set Point,” which is determined by bodily needs. He says for most people this is around 3-4 g sodium/day, about the same as the lowest risk group consumed in the Finnish study! What the Finnish study shows is that low sodium intake (<2.66 g/day) is associated with a higher risk for heart failure! Also telling is this: "To those ends, he called for legislation and education to help tackle the issue, alongside collaboration with the food industry." The wonders of the mommy state, and those zealous guardians of our health, the food industry!
Mr. Chris: As is often the case, “journalism” garbles science. There is no disagreement between these findings and Dr. DiNicolantonio’s fine book, at least in regard to heart failure, the only endpoint in the study (I think). Look at the fine print: HR for 13.73 NaCl (5.4 g Na) HR= 2.10. These numbers are not overwhelmingly strong, in terms of risk, except the last one, especially considering the small number of people in the study.
In “The Salt Fix,” he talks about the “Salt Set Point,” which is determined by physiological needs. He says that for most people this is around 3-4 g/day Na, roughly the same amount the lowest-risk group in the Finnish study consumed. What the Finnish study shows, but which remains unmentioned, is that low sodium intake (<2.66 g/day) gives a higher risk for heart failure! Also telling is this: To those ends, he called for legislation and education to help tackle the issue, alongside collaboration with the food industry.” The wonders of the mommy state, colluding with those zealous guardians of our health, the food industry!
Andy S: If I understand the abstract correctly, “. . .potassium infusion largely prevented the decrease in plasma potassium, as well as the decrease in urinary sodium and potassium excretions,” this paper is validating potassium supplementation to counteract the sodium-retaining effects of insulin. Seems to me that this (K supplementation) is probably a good strategy for the insulin-sensitive as well as the insulin-resistant. And we now know that salt is a health food.
Thoughts? http://www.dailymail.co.uk/news/article-4827700/Wonderdrug-prevent-thousands-heart-attacks.html
‘Every company wants its clinical trials to succeed. Right? Well, usually.
On June 22 2017, with little fanfare, Novartis announced the topline results of CANTOS, a large-scale trial of its interleukin 1-beta antagonist, canakinumab (Ilaris). The drug is used to treat rare inflammatory disorders.
The CANTOS trial tested the efficacy of Ilaris in patients with high C-reactive protein levels following an acute myocardial infarction. It was hoped that the drug might reduce the combined risk of cardiovascular death, nonfatal myocardial infarction and nonfatal stroke.
The trial was big (>10,000 patients) and really expensive. If I made that investment, I would want the trial to succeed.
The investigators wanted success. They hoped to demonstrate that inflammation was important in the genesis of new coronary events. The CANTOS trial was poised to provide that evidence.
But CANTOS started >6 years ago, and kept going and going. The trial was not stopped early because of superior efficacy. After 6 years of no news, most observers thought the trial would be neutral.
Then on June 22, a surprise. Novartis announced that CANTOS had met its primary endpoint. Wow! Trials that continue unstopped for 6 years are rarely successful. This was really unexpected.
I am certain that the investigators were delighted. If the announced topline results are confirmed, they will have demonstrated that inflammation leads to new coronary events. Amazing!
But was Novartis happy?
I forgot to mention one thing about Ilaris. It is expensive. Not a little expensive. Think outrageously expensive.
Remember PCSK9 inhibitors? These drugs markedly lower serum cholesterol. In the FOURIER trial, evolocumab (Repatha) reduced the risk of cardiovascular death, nonfatal myocardial infarction and nonfatal stroke by 15%. Did the sponsor of the trial celebrate? Not after the payers pushed back on the price. Repatha costs about $14,000 per year for one patient. According to the payers, the magnitude of benefit on the primary endpoint was disappointing, and the drug did not reduce cardiovascular death by itself. Their conclusion: it may not be worth $14,000 per year.
Now it seems that both Ilaris and Repatha reduce the risk of major cardiovascular events. Repatha was not warmly welcomed because it cost $14,000 a year.
But Ilaris does not cost $14,000 a year. It costs $16,000 per injection! And for its current indications, the injections are commonly given monthly, so the annual cost is about $200,000. In CANTOS, the drug was given quarterly, and thus, it could cost $64,000 per year.
If Novartis charges $64,000 annually for Ilaris, payers might expect it to reduce cardiovascular events in a major way and to decrease the risk of cardiovascular death. But if the drug did any of these things, the CANTOS trial would probably have been stopped early — and it wasn’t.
My prediction: Ilaris may cost $64,000 for a 15-20% reduction in the risk of a major cardiovascular event, without decreasing cardiovascular death by itself.’ https://www.medpagetoday.com/blogs/revolutionandrevelation/66319
Thanks for the comment & information about the Cantos trial. It will never be a mass market heart disease drug at that extraordinary price.
I got the figure in my earlier post at just under £10,000 per shot of canakinumab from NICE, I think for arthritis. Your observation about the trial length must be pertinent. Oh dear!
Two years ago I thought that the PCSK9 inhibitors were going to replace statins as the new wonder drug. There must be a deperate search for off-label possibilities now for both.
Your earlier comment about the lack of precision in medical terminology has worried me for a long time. I have seen it in information leaflets I have checked for my local hospital. We don’t have to go overboard to educate people a bit. And, ‘cholesterol’ is the most abused term, which I think must be deliberate.
I’d rather they just give me $64K/year, which would certainly reduce my stress by allowing me to pay my bills, eat grass-fed beef and take vacations to Tahiti. I’m not sure my insurance would pay for that though… perhaps I can be included in an experiment?
Before I clicked it today, I had noticed this and was going to post –
http://www.telegraph.co.uk/science/2017/08/27/new-wonder-drug-hailed-biggest-breakthrough-fight-against-heart/
FTL: “Dr Ridker, from the Brigham and Women’s Hospital in Boston, said: “These findings represent the end game of more than two decades of research, stemming from a critical observation: Half of heart attacks occur in people who do not have high cholesterol.”
“For the first time, we’ve been able to definitively show that lowering inflammation independent of cholesterol reduces cardiovascular risk,” he said.
He said the findings had “far-reaching implications,” opening up a new generation of treatment. “In my lifetime, I’ve gotten to see three broad eras of preventative cardiology,” the heart expert said.
“In the first, we recognized the importance of diet, exercise and smoking cessation. In the second, we saw the tremendous value of lipid-lowering drugs such as statins. Now, we’re cracking the door open on the third era.”
So… half of those who have heart attacks have “normal” lipids, which casts doubt on the entire basis for statins, yet they had “tremendous value.” Now that their patents are expired, we’ve luckily stumbled upon a really expensive drug that targets inflammation. It’s interesting to read through the skeptical comments below the article.
Another blogging doc’s analysis – down to the calculation of absolute risk reduction and NNT. Significantly, he leaves out the pricing.
JDPatten: Good analysis. This was a very ill, select group. The visceral fat alone may have been responsible for a large part of elevated inflammatory markers. LCHF diet and an exercise program may well give a higher than 1.8 AR reduction. Investors won’t fork over the doubloons for that, though.
If you give one set of patients a powerful anti-inflammatory, and compare with a placebo, isn’t it possible that those on the drug feel more mobile (no arthritis, and maybe it reduces statin pain) and they therefore exercise more, and thus get less CVD?
David Bailey: Very reasonable conjecture.
The last paper had PCSK9 reducing MI but increasing other ‘heart deaths’. All cause mortality actually increased (non significantly) .. Another drug that lowers LDL but not mortality…
I think a Daily Mail headline of that style, and any associated article is worth very little.
The Daily Mail (other ‘news’ sources are available) was only one of several newspapers to headline the story this morning, the BBC site caught up a few hours ago. They also say that this treatment is an adjunct to statin treatment not a replacement.
Of course it would be an adjunct and not a replacement for statins, they are worth $30bn a year, couldn’t possibly stop using them. I think other recent posts here confirm my scepticism though.
There was an item on BBC Radio 4’s World at One this afternoon about this drug (Ilaris). I was expecting the usual pro-statin type approach but instead they interviewed Dr Aseem Malhotra, a cardiologist in the UK, who presented similar views to Dr Kendrick. He said that Ilaris didn’t prolong the lives of patients, so it was of little benefit and advocated exercise and a better diet, which would be much more effective and help prevent over-medicalisation and nasty adverse effects. Looking him up I see he’s written a book ‘The Pioppi Diet’.
He is a good man Dr Aseem Malhotra. We communicate regularly.
Pioppi is where Ancel Keys had a home that probably helped him change his mind on fats, though he could not get his paper on this published – the ultimate example of publication bias. I think one of the key ingredients of the meals of people of Pioppi is that they are leisurely and communal with lots of gossip – you can’t fix lack of that with a pill.
Robert Dyson: And they do hard physical work. It is their entire way of life which promotes longevity, not one particular facet, such as food. They live meaningful lives. From the Italians I have known, I would say they know how to live well, how to enjoy life.
Gary I am reading a book called “The Island of the Ancients: the secrets of Sardinia’s Centenarians” by Ben Hills.
Sardinia is one of the Blue Zones with many people living to be 100 of more. In this book the theme of hard physical work and strong family ties and community ties emerges strongly. Diet is mentioned but as one centenarian said when asked ” we ate whatever”, meaning whatever they could get from the land as they were mostly so poor that bought food was hardly available at all. It appeals to my organic gardener/farmer soul.
Mind you just aging to 100 is not quite what i am after. Much better to live fit and healthily for a good long time. by short circuiting the programmed aging we have all inherited courtesy of evolution.
PS : red wine seems to help in Sardinia though. 🙂
Bill in Oz: Yes. I think that food plays a relatively minor role in health and longevity, providing what is eaten is of good quality, with adequate protein. I can’t even buy organic produce because what comes from my garden is so much fresher, and I know the health status of the soil in every part of it. What I’ve discovered in recent years is that volunteers choose the most nutrient-rich spots to grow. I no longer have to plant parsley, arugula, Japanese red mustard, even carrots are coming up volunteer! But the smartest ones are the wild ones, the three or four species of dandelions I eat with relish. They know, and grow in, the very best spots. Sometimes I have to rip them up in October because they’ve invaded the garlic-planting spot, which gets the best, sunniest location.
Yes Gary, good home grown food is part of the secret. And I have the same experience in my gardens. Giant Red mustard, Red Russian Kale, Parsley Aragula and chard ( = silverbeet but with red or pink or yellow stems) all come up self seeded if I allow them to. I let them flower and set seed through Summer and then pull up the mature plants and put the plants where I want them to grow in Autumn.
They are all Winter garden crops for me germinating in Autumn & doing well here through Winter as we have no ground freeze. No dandelions though. Most farmers treat them as a weed here and they get sprayed. 😦
In Spring I always have tomatoes & pumpkins germinating in the compost heap. Usually they are the earliest fruiters.
Reading with interest on Dr Kendrick´s writing about absolute risk vs relative risk, I would like to point out a brand new publication of a new drug by Novartis:
https://novartis.gcs-web.com/novartis-cantos-study-demonstrates-ACZ885-reduces-cardiovascular-risk
You will find many references to this (canakinumab) in earlier posts.
For me I need the overall map where I can fit most of the fragmented pieces of information in order to create un intelligible whole.
I love reading books (rather than specific papers of doubtful “refutations”) and the thicker the better ( 🙂 ) and which bring the overall picture.
Diabetes unpacked is one late in the row of my reading to “understand”. Another book which I am now digesting for the third time is the ” Vegetarian Myth: Food, Justice, and Sustainability ” by Lierre Keith. She refers to Malcolm Kendrick several times – a good sign. So if you are looking at health issues from a nutritional point of view an in a broad perspective I think that this book is a “must” to read and perhaps get shaken.
Thank you Dr Goran. I, too, am re-reading some of my old faithfuls, along with the recent publications we are all enjoying this month. I am honing in on the authors I feel I can trust to ensure I am doing my darndest to take me and hubby into good health for our later years.
Having said that, we are fortunate to have the means and,(dare I say it, without sounding conceited, the intellect) to decipher the good publications from the bad.
I am sad to report today that we have made a 120 mile leisurely trip on public transport, (usually rush to places by car), and feel heartbroken by the levels of deprivation we have encountered on the streets of our towns and villages. The 8 years of austerity are showing their effect, and I feel ashamed at the destitution we have witnessed in England.
All the lovely research about food and medicine, which we learn on this blog and the publications we have access to, is of little use to the folks we saw today……poorly shod, emaciated and seemingly without hope.
There I go again…..Politics is at the root of it all, but this is not the blog to enter such discussions….just thought I would share my inner thoughts.
Although this seems peripheral to the topic I suspect this shows there may be more genetic factors than we know for how we interact with food and the outcome for CVD:
https://blogs.scientificamerican.com/observations/the-genetics-of-eating-disorders/
Robert, this looks like a promo for Eating Recovery Center. I wonder if they consider LCHF a fad diet or an eating disorder. Blaming genes takes the responsibility away from the patient.
This morning a very interesting report : 27% of people who had heart attacks in Australia had no risk factors : no smoking, good diet, fit from exercise, etc.
http://www.abc.net.au/news/2017-08-29/heart-attack-study-more-than-quarter-of-patients-no-risk-factors/8849008
From your link, “You’ve watched your cholesterol” There’s the rub for in that phrase what diet dangers were hidden? I suspect there was a HCLF statin risk factor.
A perfect example of a reporter/journalist writing the story on automatic pilot ! However there are other aspects to that report which were interesting. An hour or so afterwards there was a second story about the death from a heart attack, of an Australian Iron man local hero here.
He was 47 and had retired from Iron man competition, but still living a fit strong life. In fact he died on the way home from being in the surf at the Gold Coast. A family trajedy as he left a wife and 4 young children. But the key issue is that he was not old or unfit or diabetic or even high LDL-C.
The need to look beyond Cholesterol is thus obvious.
Could this be likened to a turbo-charged engine? The old long stroke, low stress engines went on for decades. The high power, small capacity short stroke engines die much earlier, but they look impressive while they’re working.
I doubt it AH Notepad. he looks very fit and strong in all the photos published. Nothing ‘short stroke’ about him.
http://www.abc.net.au/news/2017-08-28/former-ironman-dean-mercer-killed-after-crashing-his-car/8848380
But as Dr Kendrick has pointed out heart attacks can occur because for many different reasons or causes.
Bill,
I sometimes wonder with those macho types whether they conceal any symptoms they experience, thinking they’ll just “run it off”, or they don’t want to look weak or worry their families, or they simply don’t believe they could have a heart problem, given their fitness regime.
Bill, a high level of sdLDL particles is considered a risk factor but not included in a lipid panel. The ratio TG/HDL is a good indication of sdLDL level. Ratio below 2 in American units is considered good. Carbs raise TG, saturated fat raises HDL, therefore LFHC means less sdLDL
What is definition of a healthy person?.
Study says four cups of coffee per day can lower risk of death
The findings — as concluded by the Hospital de Navarra in Pamplona, Spain — suggest that those who drink at least four cups of coffee per day had a 64% lower risk of death than those who did not consume, or hardly consumed, coffee, USA Today writes.
— And you always thought the risk of death was 100%
Always is, always will be.
Pretty sure you’re right on this, Dr. K. It’s going to get us in the end so relax, people, stop worrying and enjoy life.
Agreed that we are all finite: I would rather take steps to keep as healthy and sane as possible until my allotted time is up! Having said that, I must definitely enjoy life.
What shocks me when we discuss about low dose statin, low dose aspirin, etc. is the fact that illness is not a lack of health anymore, but it became a lack of drugs. This reminds me Henry Gadsden, the CEO of pharmaceutical giant Merck, who gave an interview to Fortune magazine in which he said that he regretted that he couldn’t sell drugs to healthy people. He said his dream was to be able to peddle his company’s wares to everybody, like chewing gum giant Wrigley’s.
Mr. Gadsden’s dream soon began to come true. A
Paola, sitting at the back of the entire issue of CVD & diabetes, is the fact that it becomes far more common as we age. ( Yes some young folk die as well, but mostly the older. )
Elsewhere I have read that the body is ‘programmed to die’. In fact a scientist named Josh Mitteldorf last year wrote a book on exactly this: “Cracking the Aging Code, the new Science of Growing old and what it means for staying young”.
Mittelforf suggests that diseases like CVD & diabetes, are a result of programmed disfunctioning in the body. Thus the search is now on to find the supplements & drugs etc which short circuit that programming.
Bill, programmed ageing as cause of diseases such as CVD and diabetes does not make sense. Sounds too hopeless. Proper maintenance and repair is needed to maintain quality of life.
Andy, I have been following this deabte about aging being ‘accidental’ or programmed for about 6 years… There are scientists still holding that is cannot be. But frankly the evidence is now too strong. Some of the discussion in Mitteldorf’s book is presented here online
Bill, I have not read Mitteldorf’s book but had a look at his blog, interesting reading. Biology is all programmed and sickness is due to interference with some part of the program. My goal is to be as healthy as possible until the end. The best advice that I have seen so far is to reduce mTOR activation by limiting glucose and protein. Autophagy as in cellular repair plays a big role.
I think these changes have as much to do with epigenetics as with anything else. Otherwise, why would younger and younger people develop T2D, for example?
Yes Sasha, epigenetics is involved and probably telomere length as well. From what I have read the body has multiple clocks to signal when things like programmed aging should happen.
You could look at what is occurring as ageing faster. HCLF based on wheat, sugar/HFCS and industrially produced Omega 6 seed oils makes you old younger so you need the drugs as antidotes to put the ageing process back on track.
Kerching! all round.
Off topic(ish) – one of the girls in the supermarket is pregnant again, Last time this happened she looked like a basketball on a pogo stick, while most of her non-pregnant colleagues resemble zeppelins. I should ask what she eats, I suspect like most of the fit healthy old folks her reply would be “none of that low fat rubbish for a start!”
It did say “over the course of about 10 years”.
Martin Back: The fountain of youth, coffee! Eternal youth. Who knew?
In fairness, if you are drinking coffee, you are not likely dead.
As Dr. Jeffrey Friedman noted, those with certain gene defects will becoem very obese irrespective of how much they eat.
The body regulates fatness and composition largely involuntarily. The body has defensive mechanisms whcih can exert control. Voluntary efforts are very limited, especially in certain people. Genetics- that the most major player in how we all look. Only Internet gruus sell their books etc and promote blame etc. Genetics are a monstrously big player – Friedman corrects misconceptions. . We havbe no solutions currently
Dr Kendrickl- where I am going with the other comment if pointing out to you that E=mc2, written THAT way, is NOT even true , NOR represents Einstein’s REAL work. His real work for objects at rest was E SUBZERO=mc2. Lev Okun STRESSED that. E=mc2 is a POP CULTURE BRAND NAME
Einsteins TRUE discovery was the REST-energy, as the late GREAT Lev Borisovitch Okun routinely stated..
I am suitable enlightened. I thought I was just using a shorthand metaphor for the, often futile, search for simplicity.
The conclusion to draw from this is that many people have had their genes changed from what they were up to the 1970s. Before that most people were relatively slim. Nowadays they are relatively large. I don’t believe the gene theory, it is more likely to be the modern high (supposedly healthy) carbohydrate diet. Simples.
IMO different genes may direct the same environmental insult into different directions, and different environmental insults into the same direction. In a different environment, such as we evolved with and lived in until recently, they just sit there unactivated. Well they evolved to deal with specific and time limited problems like gaining weight to see us though winter/famines or see off infections, etc. Now they are switched on and locked on and we are fattening for a winter that never comes and riddled with inflammation to attack nonexistent infections.
NEW STUDY: Huge Diet Study Shows Carbs, Not Fats Are the Problem Carbohydrates and Fats: Unexpected Findings (not to us) https://www.medpagetoday.com/meetingcoverage/esc/67566
Yes, been reading it.
I didn’t take away from what I read that there anything that was THE problem. Certainly saturated fats have been wrongly demonised, (I had some superb fatty bacon and free range eggs for lunch) , what I did take away was your remark that that diets is not THE cause or answer. Am I paraphrasing you correctly ?
Inflammation is the cause…
Reducing inflammation without lowering cholesterol cuts risk of cardiovascular events
Posted: 28 Aug 2017 07:54 AM PDT
Investigators have announced results of a clinical trial culminating from 25 years of cardiovascular research work. The team reports a significant reduction in risk of recurrent heart attacks, strokes and cardiovascular death among participants who received a targeted anti-inflammatory drug that lowered inflammation but had no effects on cholesterol.
The most powerful anti-inflammatory agents yet discovered are corticosteroids, and they vastly increase the risk of CVD. So, I hardly think the case is proven for, or against, inflammation by this one study – that had no impact on overall, or CVD, mortality.
Was “the team” funded by an inflammation manufacturer or associate?
There exists what I understand a powerful anti-inflammatory enzyme (dietary supplement) called Serrapeptase (serrapeptidase) http://www.webmd.com/vitamins-supplements/ingredientmono-1115-serrapeptase.aspx?activeingredientid=1115
Eating 55% carbs is ‘moderate’? That’s the position held by Public Health England. The road to diabetes, as recommended by those paid to improve public health.
That’s not true. There are plenty of people who get as much in their calories from carbs without developing diabetes. The question is – what kind of carbs and in what form.
I would love to read it but it demanded I log in or register. When I attempted to register, nothing ( zip, rien, nada, ) happened. In other words a ‘private’ exclusive source. That’s very frustrating.
Re reducing inflamation.. For years I have seen references to tumeric ( the spice used in Indian food) being an anti-inflamatory. So I often add to my own cooking.
“I would love to read it but it demanded I log in or register. When I attempted to register, nothing ( zip, rien, nada, ) happened. In other words a ‘private’ exclusive source. That’s very frustrating.”
If you meant the WebMD article, click the X top right of the signup! popup to get rid of it.
If you meant the PURE studies they are on Sci-Hub
http://dx.doi.org.sci-hub.bz/10.1016/S0140-6736(17)32252-3
http://dx.doi.org.sci-hub.bz/10.1016/S2213-8587(17)30283-8
http://dx.doi.org.sci-hub.bz/10.1016/S0140-6736(17)32253-5
Results rather underwhelming, but trends in the right direction – or the wrong direction if you are a dietician or other dogmatist. This one is going to run and run in the mainstream media as the Usual Talking Heads get their paychecks to decry it.
“The best diets will include a balance of carbohydrates and fats – approximately 50-55% carbohydrates and around 35% total fat, including both saturated and unsaturated fats. ”
”Our data doesn’t support low carb but certainly it supports a moderate carb intake of 55%,” said Mente.”
This is very far from what some bloggers here advocate, like 5% carbohydrate.
Gaetan, 55% of calories sounds way too high to me to be called ‘moderate’, although I doubt that many people need to get as low as 5%. I’d describe myself as a low carb junk avoider, but I don’t count carbs or calories.
Low carb has definitely done me good. The virtual disappearance of hunger might be the key. I lost weight easily and effortlessly and feel much better, both physically and mentally. Nina Teicholz has made the point that carb intake in 1970s America was 30% when obesity was a mere 10%. I think avoiding junk and sugar is the best and least controversial advice.
Most people who avoided junk and ate 20-30% carbs would probably be fine.
Gaetan: “Our data doesn’t support low carb but certainly it supports a moderate carb intake of 55%. . ..” is a statement almost completely devoid of useful meaning. It neither validates nor invalidates low carb eating. Have they data for diets with 5% carbs? The usefulness of PURE seems to me to be in its refutation of the absurd Dietary Guidelines for the United States, which spread like a cancer elsewhere, and which were developed and promoted by politicians and commercial interests, not scientists. Refutation is what science, at its best, mostly does.
I, for one, think it is perfectly ridiculous to look at dietary healthfulness through the lens of macronutrient ratios. The exceptionally healthy people Dr. Price encountered in his travels had diets with a wide variety of different macronutrient ratios, and some, like the Gaelic of the Outer Hebrides (oats), and the Swiss of the Loetschental Valley (rye), relied heavily on grains.
It is clear from a wealth of anecdote that many have improved their metabolic health through carbohydrate restriction, so this is an undeniably useful tool of healing for some. But population data concerning diet says nothing at all about how we as individuals can sustain our health through food choices. It can help us learn what to avoid, though.
I was quoting some parts of the study Randall posted.
One problem i see with nutrition, as well as medicine in general, is that we don’t know who to believe anymore. It seems science has become more beliefs than facts. It is also hard to claim facts when we do not completely understand how the human body works. Statins, anti-depression pills, anti-acid, aspirin, Tylenol the list goes on, the mechanism of action for most of the drugs prescribed is unknown. Unknown!! And yet we claim it’s science. We don’t know the mechanism of knocking someone unconscious with a powerful anesthetic, yet we use it because it works.
Concerning nutrition, carbohydrate, proteins, fats, who knows which ratio which should eat to have optimum health? nobody!! as far as i know. We would need a much deeper understanding of human biology and how a molecule of food may affect every organ in the body after digestion. A tremendous task at hand.
Again reading vegans, those who eat meat are idiots, unconscious people with no respect for animals…cancer causing food…
Reading those on paleo, they advocate eating animals etc.
atkins, keto, veggie, a real party mix!
Seriously, what do to out of this mess with everyone pulling the rope on their side?
I think it’s useful to start with letting go of the belief in linear causality at least in most chronic illnesses.
Depends if your metabolism has already been broken or not.
Gran used to eat pastry and jam along with her bread and potatoes. She got a bit portly towards the end but still lived to be 90.
I suspect the key is what she – and other “primitive” peoples – DIDN’T eat, such as for example massive quantities of Omega 6 seed oils, and CIAB made from stuff that isn’t actually food, plus equally massive quantities of sugar/HFCS and modern wheat.
Once exposed to that kind of thing for long enough your insulin/glucose axis is permanently fritzed and then the 55% carbs becomes a death sentence.
Link to above comment – https://www.sciencedaily.com/releases/2017/08/170828105413.htm
One dose of Canakinumab will buy me 6,700 cups of coffee at a good coffee house. I think I’ll stick with the Spanish research and have an extra cup of coffee each day rather than the anti-inflammatory. It’s better for my pocket, and probably for my heart too.
Anthony check out this about Chondroitin sulfate
http://blog.newsinnutrition.com/2017/06/heart-disease-is-a-sulfate-deficiency-problem/
This is the explanation that links Lp(a) and CVD and CS
It fits nicely with Peter Attia’s explanation of how Lp(a) particles damage the endothelium of coronary arteries.
Bill, I downloaded copy of “Coronary Heart Disease: Reduction Of Death Rate By Chondroitin Sulfate ” 1972 – which I think you highlighted in the blog. A small but compelling study. (CS seems to do as good a job on CVD mortality reduction, if not better, than any statin).
I have been taking chondroitin/glucosamine supplementation for years as a means of keeping my fingernails from continually cracking/breaking as I fingerpicked the guitar. . . And thanks to the above study I will continue to take the CS supplements with renewed enthusiasm.
I looked to see if there were any proposed mechanisms for the action of CS. Came across “Treatment with chondroitin sulfate to modulate inflammation and atherogenesis in obesity” Atherosclerosis 2016.
They put the effectiveness down to CS interacting with “the main local cells involved in the
atherosclerotic process, that is, endothelial cells and monocytes. CS interaction with TNF-a-inflamed coronary endothelial cells or monocytes reduces the secretion of IL-6, IL-8, C-reactive protein and chemokines by endothelial cells and the secretion of IL1-b and TNF-a by monocytes and macrophages.” and “CS also interferes with the TNF-a-induced secretion of IL-6
and IL-8 in monocytes and macrophages” . . . Oh dear! We are talking inflammation suppression again . . . Oh double dear! . . taking CS, am I leaving myself more susceptible to infections by (over?) dampening the immune response?
Up until I found this paper I assumed the chondroitin, a glycosaminoglycans, simply bolstered the protective glycocalyx covering of the epithelium, increasing protection, along with all the other things that improve endothelial health . . . beetroot, rocket, exercise, low serum GL.
Concerning the proposals by Dr Stephanie Seneff mentioned in the newsInNutrition blog, describing the putative function of cholesterol sulphate and sulphated glycosaminoglycans in providing an environment to assist the passage of red blood cells through narrow capillaries. This is described in the paper . . .
“A novel hypothesis for atherosclerosis as a cholesterol sulfate deficiency syndrome” 2016
I have a lot of time for Dr Seneff – her’s was the first work that I read that described why I was suffering statin induced myopathy and had developed T2D . . . she was at the start of the journey of my questioning all aspects of human health and diet; her words giving me an encouraging impetus in many directions. However, on the ‘structured water’ issue, central to the ideas of electromagnetic fields assisting the passage of blood, I need more convincing . . . and certainly have not shut the door . . .
Thanks Anthony for this comment and the suggested sources. I will look them up and see what is said there. It helps my own thinking evolve more. But inflamation seems to be the key.
I remember reading somewhere ( here maybe ) that a ruptured plaque in an arteray was like a burst pimple with puss oozing out. When a pimple bursts the puss can be washed away without consequences. But if it happens inside the artery, a blood clot forms quickly. And that is big trouble.
So yes maybe CS lessons inflammation.
By the way, do you have a link to the work by Seneff in which which described how statins lead to T2D ? I’m assuming it was not th study about atorvastin which causes 10% of takers to develop T2D.
Coffee contains sulphur. Could this be the reason for the CVD benefit the Spanish researchers found?
“the vast majority of sulfur atoms in green and slightly roasted coffee beans are part of the protein matrix (acceptable quality of fit), whereas in the course of the roasting process thermal degradation of proteins and reactions of proteins (protein fragments) with other coffee compounds (esp. carbohydrates) (and perhaps with “air” during the grinding process) produce considerable amounts of additional sulfur compounds ” — Characterization of Sulfur Compounds in Coffee Beans by
Sulfur K-XANES Spectroscopy
Martin Back: Thank you for this, and for the interpretation, as it is hard to read on the screen. I wouldn’t be at all surprised if sulfur was found to be part of the reason coffee is protective. I prefer a very dark roast (but my beef rare, as in bloody).
I always puzzle when people talk about “sulphate” defficiency, whether they really mean the SO4- 2- ion (as in sodium sulphate) or whether this is yet another piece of weird medical terminology. For example, I was also puzzled by the term “triglycerides” – which clearly means fat (three fatty acid residues attached to one glycerine molecule) – however Dr K explained that actually medics use this terms (possibly only in part) to talk about VLDL!
It is amazing how medical research can do so well with such muddled terminology (sarcasm intended).
That may tie up with work by Stephanie Seneff.
AhNotepad, this is my understanding why chondroitin sulphate helps to prevents CVD:
– damage to glycocalyx initiates inflammatory reaction
– glycocalyx damage is endothelial injury
– Chondroitin sulphate required to repair glycocalyx
– hyperglycemia damages glycocalyx
Andy, thanks for your concise dot point precis. Great work !
But after reading your last point “hyperglycemia damages glycocalyx”, I thought what about
“Hypertension damages glycocalix.”
I then did a Google and found this English language abstract from a Spanish language research journal. My Spanish is nowhere near good enough now to even hazzard a translation of the whole academic article. But the abstract seems very interesting. It only discusses the impact of hypertension on the veins. But I suggest the same process takes place in the arteries.
Abstract
“Frati-Munari AC
Glicosaminoglicanos en las enfermedades vasculares
Rev Mex Angiol 2012; 40 (3)
Language: Español
References: 100
Page: 89-99
PDF: 255.91 Kb.
[Full text – PDF]
ABSTRACT
Glycosaminoglycans (GAGs) are formed by long chains of dimers of an amino-sugar and an uronic acid, mostly sulfated and bound to proteins in proteoglycans. GAGs are located in the extracellular matrix of every organ and they perform several functions. In vessels they form the endothelial glycocalyx and are found in the extracellular matrix of endothelium and subendothelium. Glycocalyx is the first barrier between endothelial cells and the bloodstream with its shear stress, adhesion molecules, circulating cells and coagulation components. GAGs in extracellular matrix (mainly heparan sulfate) regulate activity of chemokines, cytokines, growth factors, cell migration and molecule filtration through endothelium. Chronic venous hypertension damages glycocalyx allowing adhesion molecules activity and inflammation causing endothelium and deeper venous wall impairment, deforming venous valves and favoring filtration of liquids, proteins and cells into the pericapillary and perivenular space, leading to skin inflammation and ulceration. Impaired glycocalyx and endothelial dysfunction are also important initial steps in the atherosclerotic process and in diabetic microangiopathy. GAGs are involved in these pathogenetic ways. Therapeutic GAGs in vascular diseases includes heparin for prevention and treatment of thrombosis, and sulodexide. The latter has been particularly useful in the treatment of advanced stage chronic venous disease with skin ulceration. Also, has been successfully used in peripheral obstructive arteriopathy and in diabetic microangiopathy.”
Andy, taking up your statement “Hyperglycemia damages the glycocalyx” I did a google and found this big open access pdf article from the journal, “Cell & Tissue Research” from 2008.
https://link.springer.com/article/10.1007/s00441-008-0685-6
And yes, hyperglycemia causes glycocalix damage leading to endothelium damage.
And this is very relevant for all type 2 diabetes sufferers.
Well done !
But there are also folk who do not have diabetes. I am one of them. But I do have hypertension. Hence my interest in “hypertension causing clycocalix damage”.
And the only useful research source of information on this is the spanish journal I cited before with the English abstract.
Thanks again for these lines of thought !
Bill in Oz, I am in the same situation. I believe we all get damaged in the same way diabetics or not. Blood pressure is a concern to my GP and am presently monitoring to give him a report. New monitors can download results to doctor. Question is what can be done to bring down high BP. Loosing weight, plaque reversal protocol, reduced eating window, adequate micronutrients, increase NO, stress reduction. etc. could be used to bring BP down or at least stop progression.
Andy, I googled this and Bill Davis’ Wheat Belly site turned up. He put up 2 video’s in June and came out with the following list of suggestions :
1Take magnesium ( citrate form )
2 Take Fish oil
3 Vitamin D
4 Take pre-biotics ( potato soaked for days in apple cider vinegar is one of the recommended prebiotics )
5 Intermittent fasting
6 Melatonin
7 Eliminate grains
8 Meditation
I still eat some carbohydrates ( organic breads, sweet potato, vegetables) have not taken pre-biotics and do not meditate very often. The other 5 I already do.Plus i get to the gym 3 times a week. With very no reduction on blood pressure. Bugger !
So at my consult with the new GP last Tuesday we discussed blood pressure medication. An Angiotensin Blocker named Irbesarten. So now I’m trying it but have had to stop taking potassium. And that I regret.
PS : The new GP listens a good deal more than the old one. A significant improvement. And he did not rush things either. He mentioned that statins are the ‘standard of care’ for folks with CVD. But he listened to my response that they had significant side effects associated with the reduced LDL-C. He also listened when I pointed out that the Crestor I took for three months spiked my triglyceride blood levels and reduced HDL-C, as well as reducing LDL-C. None of which is at all clever.
Bill in Oz, recently my BP in morning before breakfast is 140-145, i evening is around 130. Could be cortisol in am. At doctors BP can hit 171.
Bill Davis recommendations are good. Not sure about probiotics surviving stomach acid. Listening to youtube health discussions is my form of meditation.
As we age arteries get calcified and accumulate glycated collagen leading to stiff arteries and increased BP. Reversing these conditions if possible could be a slow process requiring much dedication.
Not sure what effect medications would have on maintaining adequate blood flow to critical tissues. Reduced blood flow to brain by lowering BP might not be a good idea. Heart can produce new blood vessels to avoid hypoxia, not sure if this happens to brain tissues. Does this have something to do with dementia?
Andy, your thoughts sound good to me. My BP is currently much higher consistently. So it is making me work my through my diet. One conclusion so far : I love fruit, especially in the past few months, apples. 4-5 a day is common and they each have quite a bit of fructose sugar in them. ( ~ 12 grams each ) So I will cut back to one a day for week and see what happens..
Bill in Oz: I got niacinamide, 0.5 g from the health food store. Couldn’t get CS by itself, so I got the glucosamine sulfate, 1.5 g/ CS, 1.2 g combination. It also has vitamin C ,60 mg, and manganese gluconate, 1 mg.
Gary, that was my experience here in Oz at the local health food stores and pharmacies. That’s why I went to Iherb. I suppose there are other online companies that stock such things but I have not dealt with them.
Great stuff you guys!
Phase 1 insulin may be shafted decades before “diabetes” is diagnosable, leading to postprandial glucose spikes. Phase 2 insulin may be hugely raised by chronic insulin resistance. Insulin is a major player in hypertension and among many other things causes the kidneys to retain sodium. It’s also inflammatory and may be independently related to arterial damage. Basically the glucose and insulin get out of phase so you are hit with alternating spikes. May tie in with EPIC-Norfolk (Kay-Tee Khaw) and the huge New Zealand studies (Elley et al, and another I can’t recall just now) showing a correlation between HbA1c and CVD starting from “normal” A1c levels and rising linearly.
I think the focus on blood glucose has been a barrier to understanding.
Chris, I understood this section : “…insulin may be hugely raised by chronic insulin resistance. Insulin is a major player in hypertension and among many other things causes the kidneys to retain sodium. It’s also inflammatory and may be independently related to arterial damage.”
However the rest was a trifle technical and even after reading it 2-3 times I am none the wiser. Can you restate it in a simpler way ?
Bill, first a big thank you for the paper you listed above which is magnificent. I already knew quite a lot of it, though I seem to have forgotten some of it. It also introduced a whole lot of information I didn’t know previously, so a major learning experience, Which Is Good, and will need further re-reading until my brain has suitably absorbed it all.
I was attempting to de-simplify current dogma about “diabetes”. Type 1 is relatively straightforward, usually an autoimmune attack destroys the pancreatic beta cells leading to a catastrophic loss of insulin production.
Type 2 is more complex. When it isn’t busy, the pancreas manufactures insulin on spec and stores it in granules within the beta cells, then when you eat carbs it can release a major quantity all at once – Phase 1 response – incretins are one factor governing its release. Phase 2 insulin is generated as required, at a lower rate but for longer.
In many – but not all – forms of “Type 2” the Phase 1 insulin response is broken first, sometimes even decades before the Phase 2 is affected, so glucose will spike rapidly after eating carbs, then the Phase 2 cuts in and the spike drops. Sometimes the Phase 2 fails to shut down properly so the blood glucose drops below normal following the spike and insulin continues to be high for too long. Insulin resistance further complicates the picture, requiring even higher insulin levels to overcome. IR or some other miscommunication between the beta and alpha cells – which generate glucagon to release glucose from store as glycogen – may also be a player.
The result is that instead of insulin, glucose and glucagon being finely balanced – in genuine nondiabetics BG seldom goes out of a very tightly controlled range of 4.5 – 5.5 in UK numbers, and insulin output is generally in the region of 20 – 30 units – everything gets out of sequence so first there is a glucose spike, then an excessive insulin spike, then an excessive glucose drop then a spike in counterregulatory hormones like glucagon, cortisol, adrenaline, noradrenaline, peptide Y (or do I mean YY?) before everything returns to normal. By which time you have developed carb cravings and set the whole cycle off again.
IMO each step of the process causes systematic damage, probably also including arterial/endothelial damage. Eventually the beta cells expire from overuse and insulin goes into permanent deficit. It’s only in a relatively late stage in the process that “diabetes” is finally diagnosed, by which time the body may have been facing metabolic hell for years.
Bill in Oz: Thanks for the link. Dr. Seneff is a very bright lady who does meticulous research. I’ve heard her speak five times, once about her early research concerning the importance of dietary sulfur, and how cholesterol in or near skin surface is sulfated under sun exposure, and that Vitamin D sulfate is produced from ChS, both of which are rendered hydrophilic in the process, for transport in the blood. The paper is fascinating. I only got partway through because of time constraints and because I’m already familiar with the hypothesis. My favorite sentence: “The consumption of garlic is inversely correlated with the progression of atherosclerosis.” Music to the ears of a garlicoholic!
” “The consumption of garlic is inversely correlated with the progression of atherosclerosis.””
Unfortunately Gary,as a commercial organic garlic grower who also still grows his own each year, and frequently eats garlic, this has not been my experience. I wish it was that protective.
Dr. Stephanie Seneff describes the complex effects of statins on sulphate production in episode 8 of the series published by http://www.gmosrevealed.com/. This also covers the link to glyphosate. I think I will have to buy a book, a video is too fast to assimilate all the information. Video available until midnight UK time.
The earlier interview in this episode covers fluoride.
Yes,
Dr. Seneff I find a very interesting researcher since she has been digging for so long into the connection between our intestinal microbiome and our mental health where sulphur seems to be the essential element in this connection. Her main theme seems to be that the pesticides and the glyphosate in particular today is ruining our microbiome and through this venue is causing havoc in our metabolism.
Seems plausible to me.
Goran, I have been trying to find the sources which describe Senef’s hypothesis. about the role of sulfate in the blood & arteries. Here are three of them :
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4456713/
https://holisticprimarycare.net/topics/topics-h-n/nutrition-a-lifestyle/1882-sulfate-the-most-common-nutritional-deficiency-you-ve-never-heard-of.html
http://blog.newsinnutrition.com/?s=Chondroitin+sulfate
I am ignoring her work on Glyphosate as it does not have much relevance here in a blog about heart disease. And I recognise that there are ‘credibility’ issues as well because Senef’s area of expertise originally was in computers & electronics.
But despite this I think there is something in the hypothesis that sulfate is essential in our bodies and blood circulation system. It makes sense to me to think that evolution has developed ways of minimising the mechanical stresses on artery walls created by the pumping of blood by the heart.
Sulfate anions are maybe one way, serving to minimise blood turbulence.
Ascorbate ( vitamin C ) acting as a first line of repair mechanism for the arteries when damage occurs.
And when ascorbate is lacking ( as happens with humans as we cannot make our own and have to get it via our diet ), the secondary, less effective, repair system starts happening. But this results in the creation of plaque.
In this hypothesis Lp(a) could be a causal factor when Lp(a) levels are high in the blood by causing damage to the endothelium of the arteries. Alternatively it may not a ‘causal’ factor as such. Rather Lp(a) could be a a particle lipid in the blood which gets caught up in the whole process.
As you can see I am just trying to think through this stuff as I write.
But I have in the back of my mind Dr Lester Morrison’s research from 1973. He did a 6 year trial of 2 groups of 60 patients. All 120 persons in the trials had had heart attacks, diagnosed CVD or diagnosed hypertension. Both groups got the same standard medical drugs available in the 1967-72.
The treatment group got 10 grams a day of Chondroitin Sulfate for three months and then 1 gram a day for the rest of the trial. Morrison documents 42 CHD ‘incidents’ in the control group in the six years. But there were just 6 in the Chondroitin Sulfate group in six years. And that is such a difference that it is amazing. Here is his own published paper
https://www.dropbox.com/s/17vsix1d1qbctft/morrison1973.pdf?dl=0
My apologies for going on so long (obsessively !! ) about this. But it seems important to me. Maybe I am wrong in this thinking or have got something confused. If so I would love it if someone here could suggest how.
I am ignoring her work on Glyphosate as it does not have much relevance here in a blog about heart disease. And I recognise that there are ‘credibility’ issues as well because Senef’s area of expertise originally was in computers & electronics.
Linus Pauling was not trained in medicine, he did however win two Nobel prizes, one of which was on vitamin C. Ansel Keys was not medically trained, and far too many people listened to him. As far as I know Professor Sir Rory Collins was medically trained and what a load of rubbish he talks.
I would believe Stephanie Seneff since just because she trained in one subject doesn’t mean she can’t learn something else. There are MANY people trained in medicine who are pedalling substances worse than snake oil and telling us what we should do, and I suggest MOST of them are misinformed fools who just want to keep their salary coming in.
A H, in an earlier blog about Vitamin C and heart disease Dr Kendrick discussed the fact that one of the people popularly associated with this hypothesis was discredited for touting miraculous cures for HIV in South Africa. Net result nobody has done any further research on Vitamin C & heart disease, despite it being very plausible.
There are some similarities here. Seneff I think is on the money with her explanation of Chondroitin sulfate and heart disease. But some of her writings in other areas make her a target of powerful actors seeking to discredit her.
I’d prefer not to have this baby thrown out with the bath water.
I try to speak in plain English as ambiguous or unclear statements lead to confusion. I am unsure what you meant by the reference to babies and bathwater. In respect of Stephanie Seneff, somebody who publicises inconvenient truths is always likely to be a target for the greedy or ignorant trolls.
Bill, why would the body make a bad lipoprotein (Lp(a)) that damages endothelium? Peter at Hyperlipid has this explanation:
“What does Lp(a) actually do?
It preferentially accumulates oxidised lipids and binds them in a form where they cannot be immediately excreted from the plasma. It also puts a great big sticky label on them that allows them to firmly bind to damaged tissue.”
Since we can do something to reduce lipid oxidation I am no longer concerned with Lp(a).
Lp(a) has a clear function, and is only made by animals that cannot synthesize vitamin C. The Apolipoprotein A molecule is identical to plasminogen (other than a single amino acid), so it blocks the fibrinolytic enzyme tissue plasminogen activator Tp(a). Thus any blood clots formed cannot easily be broken down. THus Lp(a) acts as ‘glue’ to hold together cracks in blood vessel wall. It does not damage the endothelium. It protects it.
Dr Kendrick, I hope that you will be able to explain this further to us soon. It would be welcome at least by me.
What you say is very different to what I have read elsewhere. in these writings Lp(a) is blamed as a causal factor in CVD. Or at least directly associated with raised risk of CVD. So I feel slightly confused about it’s purpose and significance.
Back in 2015 Dr Peter Attia in the USA at his eating Academy blog site provided hat I thought was a good explanation of the process of CVD..But apart from promising to also write a separate post about Lp(a) it was not mentioned. And the separate post has never appeared.
Andy S
You wrote
Since we can do something to reduce lipid oxidation I am no longer concerned with Lp(a).
Could you enlarge on that please, since I have high Lp(a) ?
Thanks
Mr Chris, here is a reference to LCHF and LP(a)
https://doi.org/10.1186/1743-7075-3-19
Elevated plasma Lp(a) is a risk factor for cardiovascular disease because of both atherogenic and thrombotic properties [4]. The 12% decrease in plasma Lp(a) is a novel finding considering that plasma Lp(a) levels are reported to have a strong genetic influence [29, 30] and that diet usually has little positive influence on Lp(a) levels [5, 31]. Important to note is that most diet interventions that have examined Lp(a) response emphasized fat restriction with moderate to high carbohydrate intake, which sharply contrasts the macronutrient contribution in the current intervention. Reducing total and saturated fat intake has been shown to increase Lp(a) during weight maintenance [32] and have no effect on Lp(a) during weight loss [33]. The significant decrease in Lp(a) in this study suggests that carbohydrate restriction, as opposed to fat restriction, may play a greater role in modulating Lp(a) levels during weight loss. Diets relatively high in trans fatty acids in comparison to saturated or unsaturated fatty acids can significantly increase plasma Lp(a) [34]. Thus, the 38% reduction in trans fatty acid consumption could also have also influenced this parameter.
Andy S
Thanks for that, I understand that L-Carnitine also reduces Lp(a)?
Bill in Oz: Keep it up. You always add something to the discussion. By the way, I think we should all be concerned about glyphosate. The “inert ingredients” in the commercial products containing it make it far more toxic.
Gary, re Glyphosphate.. Yes it is a toxin. It kills most micro-biota in the soil when it is applied. However the extra ingredients ( surfuctants etc ) in the Roundup herbicide mean that it is poisonous to people directly.
So in all my 25 years of organic farming and gardening I have only ever used it 3-4 times with lots of precautions. And no cropping of the area for three years afterwards.
My remark was not meant as a criticism of Senef. Just an attempt to stay focused on the blog’s topic of what causes heart disease.
Bill,
Thank you for these references.
I was not familiar with this “electric” approach to CVD by Dr. Seneff but which seems to be well founded in the physical chemistry I am familiar with. Once I though came across some research work (by prof. Karl E. Arfors) pointing to the importance of electric charging when relating to the blood flow in capillaries in the same vein as in your first reference .
How much we don’t know – as usual! How much more to learn before we die! If knowledge is at all possible – the eternal philosophical question.
Goran, this ‘electric’ approach was new to me also. But as the heart itself beats to an electric clock, it is very probable that evolution has also provided an electric system of minimising blood turbulence and thus stress on arterial walls.
Dr. Göran Sjöberg: Yes, the new learning is the fascination for me, integrating it into what I already know and understand. I do not suffer from cognitive dissonance when I learn something that turns upside down what I thought I knew. This is part of the adventure. I think intellectual humility, along with a good dose of the Stoics, is the useful stance which aging teaches us.
The wind has changed !
http://www.independent.co.uk/life-style/health-and-families/low-fat-diets-kill-you-study-food-drink-eat-health-barcelona-cardiology-canada-a7918666.html
Great stuff, but my prediction is that the ‘experts’ will stay quiet for a while, and then ‘forget’ that study and carry recommending low fat on as before.
Hopefully as we visit the causes and cures of CVD, sulphur will be covered (it has cropped up previously).
Until then, does anybody know how to test for sulphur? I see in some of the comments above the mention of lp(a).
High lp(a) ties in with Pauling/Rath and low vit C.
If you do have high lp(a), are we now saying that it could be either (1) low vit c or (2) low sulphur generating the presence of the lp(a)?
Hi Charles, I replied to your comment. But I got confused and wrote it as a reply to Goran. See above.
A slightly off topic comment : there would be little point in solving the CVD issue if we are all afflicted with dementia !
Dr Kendrick, there is a Health program here on ABC radio national managed by a ( former ) Scott named Norman Swan. This week he broadcast a report on low dose Lithium in the water supply seems to alleviate or prevent dementia.
http://radio.abc.net.au/programitem/pgx6XXW8D6?play=true
I have a negative emotional response to the name Norman Swan, as he was the lead hound in the attacks on Maryanne Demasi who ‘dared’ to produce and present two programmes on ABC (catalyst) criticising the diet-heart hypothesis and the overuse of statins. He basically set out to trash her, and he managed to destroy her career. So, I hope you will excuse me if I fail to respond positively to anything Normal Swan has to say about anything. Yes, that is not the response of a true scientist, who should be oblivious to the source of any data – but there you go. I suppose I feel guilty because I warned her what would happen before the programmes came out. Clearly I did not give her sufficient warning. She was brave, but bravery counts for little when the pack turns on you. As they say in Australia ‘the bastards.’
Dr Kendrick, I do not have a high opinion of Norman Swan either. He is extremely arrogant. I also have been in contact with Marianne Demasi and know the role he played in destroying her career at the ABC. It is not something I admire.
However the Health Report does occasionally have interesting items on it. This one about low dose lithium in water supply is one such.
There is no point avoiding CVD if we wind up with dementia, sitting all day in old age home watching TV on drugs to sedate us. As that happened to my own elderly mother for some years, it is important in my thinking. By the way PD Mangan at Rogue Health also has an article re low dose Lithium preventing /delaying dementia.
By the way the interview is with an Australian who has lived in Denmark and was peripherially part of the team of researchers who made this correllation : old folks in areas where Lithium was present in the water supply in very small amounts, had lower rates of dementia than people living in areas where the water supply had no Lithium in the water..And we are not talking about the doses prescribed for people with Bi-Polar disorder; the quantity involved is around 1% of that level.
Malcolm,
What a good input!
It strikes me that brave people always are “at risk” of being broken down facing the tremendous resources of our “enemies”, Big Agro and Big Pharma. But the rare brave ones, like Maryanne Demasi (and yourself to my opinion), advocating the true science in health matters are still “popping up” for the benefit of mankind.
I feel grateful to all of you, committed daring brave “guys”, who have not least helped myself to restore my health and to believe in the possibility for a “change” in a corrupt world.
Dr Kendrick, what did happen to Maryanne Demasi after those excellent documentaries were broadcast? I keep hearing a hint or two, but I’m unclear what Norman Swan and others did to this talented lady.
I did a blog about it.
Stephen, All ABC programs after being broadcast are available for viewing for free on it;s IView website. The 2 Catalyst programs were made unavailable by ABC management after the hue & cry by Norman Swan.
Also the program itself went off air at the end of that series and did not resume the following year. Marianne Demasi was ‘let go’ – sacked. In a recent email she said she was glad to be away from all the BS. I think she is working as a freelance science journalist.
The ABC TV program ‘Catalyst’ was put back on air 2-3 weeks ago at a new time ( Tuesdays at 8.30 pm ) and format wit different staff. I have watched the start of 2 programs but frankly wound up bored and switched off. The Catalyst staffers are all playing it safe. That’s what I expect from commercial TV. But not on the ABC.
You can see the the Heart of the matter Part 1 Dietary villains, part 2 cholesterol drug war on YouTube . . . Great viewing.
I noted that Maryanne Demasi, joined with Robert Lustig and Aseem Malhotra in authoring a great paper “The cholesterol and calorie hypotheses are both dead — it is time to focus on the real culprit: insulin resistance” Jul 2017
http://www.pharmaceutical-journal.com/opinion/insight/the-cholesterol-and-calorie-hypotheses-are-both-dead-it-is-time-to-focus-on-the-real-culprit-insulin-resistance/20203046.article
Very succinct.
Anthony, re “insulin resistance” as a cause of cvd. The authors conclusion:
“In summary, for many patients at high risk of CVD, one of the safest and most effective ways to reduce the risk of heart attack and stroke is to consume a high fat and low glycaemic load Mediterranean diet and engage in regular exercise”
Using the term “hyperglycaemia” instead of “insulin resistance” would cause less confusion as to where to put the blame for CVD. “Carbohydrate intolerance” could be another term.
If high insulin causes problems blame the glucose as the primary cause.
Hi, Andy . . re; “real culprit: insulin resistance” . . . I have been struggling with the idea of insulin resistance as being the “root cause” of CVD as well as it being involved in a whole lot of other ills. Up until about the start of this year I had assumed that one of the main contributors to CVD was sustained high glucose levels (damaging the epithelium . . . now I would say the glycocalyx/epithelium) . . . I would have said that the insulin levels were raised to deal with the high levels of damaging glucose . . . and that after a time this process of insulin mediated glucose removal became more inefficient . . . resistance to the effect of insulin in adipose tissue, skeletal muscle and liver set in . . . and the level of insulin had to be raised to effect the required removal of glucose. In this perspective the rise in serum glucose matches insulin resistance . . . so I would have said that insulin resistance seemed to be a sort of surrogate measurement for high serum glucose. (Like you, my focus was on glucose being the primary cause for CVD)
If things were as straight forward as I have described then you could talk of hyperglycaemia as being a convincing predictor of CVD. However, when we talk of hyperglycaemia we are talking of diabetes . . . high fasting GL levels, high HbA1c. We know these correlate with CVD event because T2D is a risk factor for MI, but what about GL levels below that range?
What people like Maryanne Demasi, Robert Lustig, Aseem Malhotraseem, Jason Fung, Jeffry Gerber and Ivor Cummins, Tim Noakes, as well as the late Dr Joseph Kraft, seem to be saying is that the high levels of insulin – hyperinsulinemia – seems to be one of the most significant contributors to CVD. They seem to be saying that physiological damage, including the vascular system, is occurring long before elevated glucose levels (fasting GL/HbA1c) identify diabetes. (This makes using hyperglycaemia as a predictor of CVD problematic)
During the early stages excessive glucose is kept in check by high insulin levels . . . however, as insulin resistance increases more insulin is needed for it to be effective (mechanism?). . . insulin levels go up. They would say that during this time physiological damage that could lead to a heart attack is being done, and they would propose a better correlation of IR with CVD (with IR as a surrogate indicator of insulin levels) – than a correlation of CVD and fasting GL / HbA1c.
(Please, all the above mentioned, forgive me if I have errors through oversimplification)
Questions
In those early stages of raised insulin levels when fasting GL does not identify a metabolic problem . . . is it the transient postprandial spikes in glucose levels that cause all the damage . . . damage occurring before the insulin steps to remove the glucose?
We know elevated glucose levels can damage (glycate) proteins in of the glycocalyx/epithelium, but if these GL levels are low because insulin levels are high . . . does the high level of insulin in the blood alone have means to damage the vascular system?
I know insulin signalling in cells has many other functions other than enabling GLUT4 transporters to the cell surface allowing glucose removal from the blood. For instance it is a growth promoter . . . it seems to work through various cascade pathways that activate the mTOR complex. If so, it would suggest that IR should correlate with increased cancer rates. But do some of these extra functions influence the progress of atherosclerosis?
I have been wanting to get to grips with the idea of insulin resistance for quite a while, but you see from the above I have not go very far. From a comfortable position where I thought I was able to explain my T2D (erstwhile T2D) I now find turmoil – brain buzzing – Like the 5-Alive robot . . . I need more input.
So what upset my apple cart ? . . .
KRAFT – Father of the Insulin Assay: https://www.youtube.com/watch?v=w0nV-_ddXoc
Fat Emperor in LC USA Keto Getaway Florida: https://www.youtube.com/watch?v=xiUNNJrTDRQ
And if you want to get really nerdy . . .
Ivor Cummins – ‘The Pathways of Insulin Resistance: Exposure and Implications’ https://www.youtube.com/watch?v=U_Gcq8bEUq8
God! Ivor you have a lot to answer for.
Hi Anthony, I look at the CVD problem from a consumer point of view, what dietary recommendations to follow for best results. Metabolic syndrome was easy to understand and apply, keep TG/HDL ratio low. What can we do about insulin resistance? Is this metabolic syndrome with a different name or a different way of looking at the problem?
Andy, A couple of doctors on video said that metabolic syndrome was caused by insulin resistance. They did not go into the detail I would have liked . . . but I guess if you are fixing metabolic syndrome (for the majority of us it would be keeping a check on the carbs, getting the weight down, doing sensible exercise) then your insulin demands will be reduced and so your insulin resistance will decrease . . . if this was not the case then reversal of T2D could not happen.
Like you I see TG/HDL as the important markers. If that is low, like you say, metabolic syndrome/insulin resistance is being controlled.
As far as I can see the only significance for the ordinary punter (like you and me) in all this is that diagnostic needs would be better met if insulin resistance or Kraft glucose tolerance were measured early on – identifying possible metabolic issues in the making – rather than leaving things festering for 10-20 years only to be picked up rather late in the day when diabetes is diagnosed.
Metabolic syndrome has been called. Reaven’s syndrome, syndrome X, insulin resistance syndrome, and pre-diabetes – to name but four. Everyone describing much the same thing.
Interaction Between Vitamin D and Lipoprotein (a) on the Presence and Extent of Coronary Heart Disease.
Li K1, Yang X1, Wang L1, Chen M1, Xu L1, Yang X2.
BACKGROUND:
Given both lipoprotein (Lp)(a) and vitamin D have been found to be associated with coronary heart disease (CHD) risk and a biochemical link between vitamin D and cholesterol on atherosclerosis has been proposed, we hypothesised there could exist an interaction between Lp(a) and vitamin D on the severity of CHD.
METHODS:
Lp(a) and 25-OH vitamin D were measured in the plasma of 348 consecutive patients (mean age 62.4±10.5 years; 56.3% male) undergoing coronary angiography at our Heart Center. A multivariate logistic regression model was used to estimate the odds ratios (ORs) of CHD.
RESULTS:
Of these patients, CHD was identified in 212 (60.9%). A multivariable logistic regression model showed multivariable-adjusted ORs (95% CI) of CHD for patients with Lp(a)≧30mg/dl and vitamin D <10 ng/ml, Lp(a) <30mg/dl and vitamin D <10 ng/ml, and Lp(a)≧30mg/dl and vitamin D ≧10 ng/ml were 4.62 (2.04-10.46), 1.79 (1.00-3.17), and 1.70 (0.88-3.31), respectively, compared with those with Lp(a) <30mg/dl and vitamin D ≧10 ng/ml; the multivariable-adjusted ORs of a higher Gensini Score for the above three corresponding groups were 3.48 (1.84-6.60), 1.59 (0.96-2.65), and 1.55 (0.86-2.79), respectively. The interaction term between Lp(a) and vitamin D in each of the above two models was significant (p=0.004 and p=0.005, respectively).
CONCLUSIONS:
Among patients undergoing coronary angiography, there existed an interaction between Lp(a) and vitamin D on the severity of CHD. Future cohort studies are warranted to confirm this finding.
https://www.ncbi.nlm.nih.gov/pubmed/28238617
Had a look at the “Interaction Between Vitamin D and Lipoprotein (a) on the Presence and Extent of Coronary Heart Disease” paper . . .
Wasn’t sure what type of interaction there was between Lp(a) and Vit D . . .
Wasn’t clear as to what the effect of Vit D levels on CVD was . . . (always thought low was bad)
I can never compute/take in the meaning of the figures in the Results section of papers . . . so I have to edit it . . .
The following are a copy of the brief notes I took . . .
———————-
“Both elevated Lp(a) and vitamin D deficiency appear to increase CHD risk even more in the presence of other risk factors.”
However, if you have both of the above you are in a really bad way.
Method and results
Lp(a) and 25-OH vitamin D were measured in the plasma of 348 consecutive patients
(mean age 62.4_10.5 years; 56.3% male) undergoing coronary angiography at our Heart Center.
Of these patients, CHD was identified in 211 (60.6%).
A multivariable logistic regression model showed multivariable-adjusted
ORs (95% CI) of CHD for patients with . . . .
Lp(a) 330 mg/dl and Vit D <10 ng/ml . . . . . . . . . . .4.62 (2.04–10.46)
Lp(a) <30 mg/dl and Vit D <10 ng/ml . . . . . . 1.79 (1.00–3.17)
Lp(a)330 mg/dl and Vit D 310 ng/ml . . . . . . .1.70 (0.88–3.31)
. . . compared with those with Lp(a) <30 mg/dl and vitamin D 310 ng/ml;
The multivariable-adjusted ORs of a higher Gensini Score (shows degree of CVD) for the above three corresponding groups were 3.48 (1.84–6.60), 1.59 (0.96–2.65), and 1.55 (0.86–2.79), respectively.
The interaction term between Lp(a) and vitamin D in each of the above two models was significant (p=0.004 and p=0.005, respectively). ??????
The interaction
Patients with severe hypovitaminosis D and abnormal (high) Lp(a) had the highest OR of CHD, which exceeded the sum of the two individual ORs, i.e. patients with severe hypovitaminosis D and those with abnormal Lp(a).
(Can you just add Odds ratios in that way?)
TedL I like to be able to say, “Ahhhhh this is interesting and valuable, thank you ! ” But frankly I do NOT understand what this abstract is saying.
Are they saying that higher vitamin D3 leads to more Lp(a) and more CVD ? Maybe, maybe not.
Are they saying that low Vitamin D leads to more Lp(a) and higher CVD rates ? I do not know.
The abstract is poorly written and confusing. And the original article is not available.
I suspect this is another example of “Bullshit baffles brains”
Here is the web address for the article about Lithium by PD Mangan. He believes that it also helps prevent/slow aging. Interesting.
http://roguehealthandfitness.com/lithium-extends-lifespan/
Bill, I too found the abstract baffling which is why I had to go download the paper. Give 6/10 (generous?) for the usefulness of the research. Was hoping there might be speculation explaining the apparently synergistic effect of the Vit D and Lp(a) . . . no such luck.
Atorvastatin causes diabetes in nearly 10% of users?
Am J Cardiol. 2014 May 15;113(10):1593-8. doi: 10.1016/j.amjcard.2014.02.011. Epub 2014 Mar 1.
Effect of change in body weight on incident diabetes mellitus in patients with stable coronary artery disease treated with atorvastatin (from the treating to new targets study).
Ong KL1, Waters DD2, Messig M3, DeMicco DA3, Rye KA1, Barter PJ1.
Abstract
Features of the metabolic syndrome are independent risk factors for new-onset diabetes mellitus (NODM) related to statin therapy. Obesity is the predominant underlying risk factor for the metabolic syndrome and diabetes mellitus. This study investigated whether change in body weight may predict NODM in statin-treated patients. A total of 7,595 patients without prevalent diabetes mellitus at baseline from the Treating to New Targets (TNT) study were included in this analysis. They were randomized to atorvastatin 10 or 80 mg/day and monitored for a median of 4.9 years. NODM developed in 659 patients (8.1% in the 10-mg group and 9.2% in the 80-mg group). There was a significant increase in body weight (0.9 kg, p <0.01 in both men and women) over 1 year after randomization. The increase in body weight was greater in patients with NODM than those without NODM (1.6 vs 0.9 kg, p <0.001). The association of change in body weight with NODM risk remained significant after adjusting for confounding factors (hazard ratios 1.33, 1.42, and 1.88 for quartiles 2, 3, and 4 compared with quartile 1, respectively). Similar results were obtained in patients with normal fasting glucose level. In conclusion, 1-year change in body weight is predictive of NODM in patients who underwent statin therapy from the TNT trial. Our study highlights the importance of weight control as a lifestyle measure to prevent statin-related NODM.
—-
Could the experts who comment on this blog tell me if the rate of NODM over 5 years is high or to be expected. It seems high to me.
“Our study highlights the importance of weight control as a lifestyle measure to prevent statin-related NODM”. In other words, if you get diabetes while taking our statin it’s your own fault for being a fat lazy slob! But why are we fat? Because of the insulin/pre diabetes, of course. And statins are known to disrupt the body’s glucose control system. But it’s still al our fault for being fat… Head, wall, bang bang bang…
Disclaimer: I am not an expert.
I read these abstracts and I ask myself, what have they actually proved? Note that there is no control group of people not taking statins, because to diagnose someone with stable coronary artery disease and not put them on statins is the medical equivalent of murder.
— If you put on weight, you run an increased risk of getting diabetes. Well, duh.
— If you give people a dose of statins eight times larger, they near-as-dammit run identical risks of getting diabetes.
This latter is to me the interesting result. I conclude that statins per se have little influence on getting diabetes. Then why would diabetes be associated with statin use? I suspect the reason lies in the consulting rooms.
Doctor says: “Mr Smith, you have a heart condition. Here is a prescription for statins, and try to take things a little easier.”
Doctor thinks: I’ve prescribed statins so Mr Smith can’t sue me for malpractice. If he would just stop stressing so much about things he would be a lot better off.
Mr Smith hears: “You are about to drop dead from a heart attack. The only thing standing between you and an early grave and ruin for your family is these pills. Under no circumstances must you cause your heart the least bit of exertion, it is so fragile.”
Mr Smith thereupon takes as little exercise as possible, and in consequence fails to burn up free-floating glucose in his blood and develops diabetes.
:
Martin, You are right to be cynical about such research; however, I cannot agree with your view that statins do not in themselves increase the likelihood of becoming diabetic. There is plenty of better evidence available from elsewhere.
You mention “If you give people a dose of statins eight times larger, they near-as-dammit run identical risks of getting diabetes.” . . . and conclude “This latter is to me the interesting result. I conclude that statins per se have little influence on getting diabetes. ”
What is says to me is that the pathological dose for harm probably follows a curve that rises sharply then flattens off between 10mg and 80mg atorvastatin. It hints at how little of the statin is needed for harm.
As someone who was losing weight, exercising, feeling good, and wanted to do everything right I went for a check up. Everything fine except the cholesterol TC. Took the statins I was given feeling I was making a great move. Then over the years the HbA1c steadily increased . . . but the weight was still going down, I was still exercising. The HbA1c should be going down. After 3 years I drifted into the T2D zone.
Where I agree with you is that statins do enervate, weaken, or as my wife said “They are making you into an old man”. This happened to me after a further 2 years . . . by this time my 1hr walk around the village was now 1hr 20 mins. Breathlessness was a problem. Once you get to this state exercise becomes and issue.
Martin your hypothesis is plausible. But I wonder whether there is any evidence and how reliable the evidence is – or would be. All medical consultations are private & confidential between the patient & the doctor. So it’s sort of a complete black box.
But the study meanwhile got the result 10% of people prescribed Atorvastin develop type 2 diabetes. Now that is a major problem medically, socially, financially, And as it happens one close to me as my younger brother has been on statins for years and also recently developed Type 2 Diabetes.
Prima facie, statins seem part of this disease development process. And so I suggest statins need to be researched with this issue to the fore. I wonder if the pharmaceutical companies would fund such research.
Bill,
For a definitive test of whether statins give you diabetes you need to run a double-blind trial where some participants are given statins and others a placebo. But this is not possible under current ethical guidelines AFAIK because statins are required to be prescribed to coronary artery disease patients.
Then consider that patients with CAD have very likely been living an unhealthy lifestyle which would predispose them to diabetes anyway, and the statin dose-response curve which is almost flat, and I find it hard to put the blame entirely on statins for the diabetes.
Martin ,you wrote ” patients with CAD have very likely been living an unhealthy lifestyle which would predispose them to diabetes anyway” Yes that may be true. But these patients have probably been following the standard American Diet with lots of carbs, sugar and industrial oils, and not much saturated fat…. As promoted by major corporate ‘food’ companies and indeed by government mandated food guidelines.
And then statins are prescribed as the cure all…But in fact are not fit for purpose…
It is probably only dissenters like us here who have escaped this process.
Like Gay Corran, I could not believe the conclusion the study came to. It noted that between 8-9% of the people taking atorvastatin were getting new on set diabetes mellitus in their study. They found an *association* between level of weight gain and the likelihood of NODM (not significant in everyday sense, but for all its small size, significant in a statistical sense – ie reasonably confident of its modest value) . . . and they went on to morph the *association* in the second from last sentence into a *predictive feature* . . . then in the last sentence they further morphed it into a contributory *causal influence*; . . . that is: curbing the weight gain would “prevent” NODM.
(it might – it might not – act of faith?)
Forget all the weight control waffle . . . I now can say to those that want to hear that I have a recent pro-statin study that shows that ‘about’ 1 in 10 people who take atorvastatin for 5 years will end up with type 2 diabetes.
This is to go with the “14% of postmenopausal women end up with NODM” study
The transatlantic undersea cable is garbling my comments. The important point I was trying to make is that the lowest risk for those in the Finnish study was for those consuming about the same amount of salt as Dr. DiNicolantonio describes as the “Salt Set Point” for most people, which is around 3-4 g/day of sodium. In the Finnish study the lowest risk group (HR 0.83) consumed 6.77-8.80 NaCl (2.46-3.46 g sodium). Those consuming less than that had a slightly higher risk for heart failure.
Hmmm (he wrote pensively) – part 35 (in which Dr Kendrick has proposed a year zero approach to CVD and to start again) has generated over 400 replies, and we’re covering plenty of causes and cures already.
LP(a) which I believe has simplistically been described as a mobile repair molecule now appears to be linked to, and generated by:
Low Vit C
Low vit D and
chondroitin sulfate (CS)
I guess if you have low lp(a) in your blood test result you can eliminate these 3 as causes of your CVD. If you have high lp(a), perhaps a bit more difficult to ascertain which of the 3 to suspect. I think there are blood tests for vit C and definitely for vit D. I wish the people who put forth their hypotheses provided this sort of help. Now and again I try and make contact but they don’t all reply. Also, I’m not quite sure where they are in the intensive care units to do all this hypothesis testing/research. Especially when you are in that 27% where the conventional risk factors don’t apply. I volunteered for research but still haven’t heard back. As someone remarked to me last year, you’d think they’d be interested if you are in that 27%.
Re people from other disciplines taking part in research – I welcome it e.g. Stephanie Seneff and the Fat Emperor to name 2 who cut through the rubbish.
Anthony Sanderson – subject to moderation by Dr K, can you let me know which CS supplement you have had success with?
Charles, I am taking Chondroitin sulfate ( currently 10 grams a day of ‘Now’ brand via IHerb because none of the pharmacies here in my home town have it in stock.
Anthony I think takes Glucosomine which is converted in the body ( microbiome process ) to CS.
So my simple ( simplistic ? ) logic says why not take the CS form that is used by the body.
.
Charles,
As Bill points out I have been using a dual supplement glucosamine HCl (500mg) chondroitin sulphate (400mg) for the past 20 years. Initially because I had joint pains in the ankles. (A work colleague insisted it should be the dual supplement – it was the one that worked for her on her lower back issues). For me the ankle pain went . . . placebo? chance? change of circumstance? . . . Kept on taking it because, as I have mentioned in a previous comment, it seems to help protect my nails. I will be trying chondroitin on its own to see if it is effective in this regard..
Having read about the anti-inflammatory effect of chondroitin sulphate on the vascular system I suspect that, of the two in the supplement, chondroitin might be the principle agent for joint inflammation.
Not sure about Bill’s glucosamine => chondroitin sulphate in the gut.
But it did spur me to do a quick, cursory look at glucosamine as a metabolite and found that . . . “Faecalibacterium prausnitzii, the only cultured representative of Faecalibacterium, is able to metabolize both diet-derived polysaccharides and host-derived substrates such as *N-acetyl glucosamine* from intestinal mucus [50]. It is also a major butyrate producer and exhibits anti-inflammatory effects in a colitis setting.” This fits with the notion that the microbiome seems predisposed to produce short chain fatty acids . . . such as beneficial butyric acid and acetic acid. Wonder if this is the basis for any physiologic action of glucosamine, and bearing in mind the idiosyncrasies of individual guts, why some swear to the efficacy of of it while others seem unconvinced.
. Was hoping there might be speculation explaining the apparently synergistic effect of the Vit D and Lp(a) .
Hi Bill in Oz
Thanks for the CS recommendation.
If you don’t mind me asking, do you take CS supplement as a precaution/preventive or because of some diagnosis? e.g. Antony Sanderson mentions his nails in a comment.
Charles I am taking CS because I had angina last year & was diagnosed with. CAC score of 1060 last November with a circumflex artery almost blocked. So my reason is ‘preventive’.I will take 10 gram a day till mid September – a total of 90 days at 10 grams a day & then 1 gram a day going forward, as per the Morrison protocol from 1973.
Dr. Morrison provided compelling evidence in the 1960s that heart and blood vessel disease could be reversed and prevented with natural molecules, particularly chondroitin sulfate. https://www.lewrockwell.com/2010/01/bill-sardi/the-man-who-cured-heart-disease-naturally/
That’s an interesting article Randal with lots of sources for Morrison’s research work. I had seen it before but forgotten it. So good catch !
For creamy summer desserts:
Stirring a little lemon juice. Into double cream thickens it – no need to whisk.
@malcolm look at this:
http://www.medscape.com/viewarticle/884921?nlid=117592_1982&src=WNL_mdplsnews_170901_mscpedit_fmed&uac=208106MV&spon=34&impID=1423769&faf=1
Another sad example of corrupted science.
Important find – From the Department of Medicine, University of California, San Diego
It now appears that oxidation of LDL plays a significant role in atherogenesis
Oxidized LDL is cytotoxic for endothelial cells in culture
LDL particles rich in polyunsaturated fatty acids are more readily oxidized than are LDL particles enriched in saturated fatty acids or monounsaturated fatty acids
The content of vitamin E and other naturally occurring indigenous antioxidants will influence the susceptibility of LDL preparations to oxidation
modification of LDL by endothelial cells in vitro can be completely prevented by the addition of antioxidants such as vitamin E
The polyunsaturated fatty acids in cholesterol esters, phospholipids, and triglycerides are subject to free radical-initiated oxidation and can participate in chain reactions that amplify the extent of damage.
The lipoprotein fraction gently extracted from atherosclerotic lesions (both rabbit and human) contains oxidized LDL
Vitamin E, on the other hand, is very effective in protecting circulating LDL against oxidation ex vivo
My take: do not eat vegetable oil in any form, saturated fat cases no harm, oxidized LDL damages the inner most artery wall and then arteries plug up but antioxidants like Vit E completely prevented damage in their study http://www.jbc.org/content/272/34/20963.full
Randall, there was not any mention of small dense LDL. Apparently sdLDL is more easily oxidized than large fluffy LDL even in absence of PUFA. PUFA + sdLDL = very bad.
sdLDL is result of carb metabolism and level can be measured. Also TG/HDL-C ratio indicates level of sdLDL particles. Rather than statins go low carb and low PUFA. Something to discuss with my doctor who is recommending statins.
Andy,
Isn’t opening a “discussion” with the average GP (but though more likely with a cardiologist) just like starting a fight with a windmill?
One answer – LDL particles that are not oxidized are not atherogenic. Dr. Tom Dayspring’s name is there. http://eatingacademy.com/cholesterol-2/heart-disease-begin-tell-us-prevention
That depends on where you believe oxidation takes place.
Casually looking through the website of an Australian science journal I discovered a reference to some research reported last year. Following up I found this.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5112585/
It reports on experiments to encourage the development of senescent intimal foam cells within the arterial walls of mice. This established that arterioclerosis had been ‘created’ and that such foam cells are ‘deleterious’ at all stages. The researchers then went on to eliminate the senescent cells from plaques, using “p16-3MR (3MR) mice (14), a transgenic model that expresses the herpes simplex virus thymidine kinase under the control of the p16Ink4a gene promoter”. The senescent cells were then eliminated ( killed ) upon administration of ganciclovir (GCV) a fairly potent antiviral drug with many side effects..
I am not keen on being a guinea pig by trying the process reported from this research. But
this report jogs my memory of an article I read of PD Mangan recently about autophagy.
http://roguehealthandfitness.com/intermittent-fasting-decreases-heart-disease-risk/
Autophagy is the process whereby the body gets rid of, kills, senescent cells. Autophagy is boosted by intermittent fasting. Mangan also discussed how a traditional chinese herb Berberine promotes improved autophagy when fasting.
http://roguehealthandfitness.com/berberine-promotes-fat-loss-and-activates-autophagy/
In my younger days when i studied yoga & meditation I was told of the benefits of fasting and even on one occasion fasted for 5 days. I felt great at the end of that fast. However the Indian teacher turned out to be a sexual predator of younger female followers. He was also into money in a big way. So I gave the flick to him and his teachings.
But it seems that the fasting ‘teaching’ may have been accurate.
I would not recommend listening to anyone who says this Chinese herb does this or that. That’s not how traditional Chinese medicine works. It treats patterns, not conditions. Each herb has its particular energetics and can be good for one pattern but detrimental in another.
Bill, thank you for the information and links. You might be interested in the attached link.
http://foodmed.net/2017/08/29/intermittent-fasting-key-beat-diabetes-cancer/
Dr Kendrick, at number xxxv. on the 19th of August, you decided to start again. Now it is the 3rd of September and there are 557 comments.
Bugger ! Just taking in all this discussion is a mammoth task. And we seem now to have reached an ‘exhaustion’ point with comments dropping off the past couple of days.. What do you think is worthwhile ? What do you think is truly useful and applicable ?
I am struggling with part XXXIV. It is a complex argument.
Stephen,
Thank you for the reference!
It must be evident for “all those who are interested” that the features of the Hippocratic world map are today becoming more scientifically distinct and that the whole map also becomes more convincing.
“Stay away from the carbs!”
“Go for the the animal fats!”
And that fasting may “reset” you endocrine system.
And you may for ever wonder why there is such a ingrained resistance to these obvious facts in the present medical system.
Dr. Goran, standard of care equation:
symptom > diagnosis = prescription
Nutrition, metabolism, cause of disease are too complex and few can agree what causes what. A retired person with plenty of spare time and motivation (like being sick) might find better solutions for their symptom. Google has liberated us.
Goran
Short, sharp and to the point !
But what of protein ?
Do you really mean xxxiv ? Or xxxvi, the next in the series ?
Back to the future.
Ahhhhhh !!! Can we bear the uncertainty ?
Removing atherosclerotic plaque using ultrasound. Lots of info https://www.google.ca/search?q=Removing+atherosclerotic+plaque+using+ultrasound++&ie=utf-8&oe=utf-8&gws_rd=cr&dcr=0&ei=wYitWbnpM8PdjwSwj4fQAQ
Randal
I read through this quickly. Towards the end is this statement ” This type of technology looks promising for the removal of atherosclerotic plaque in humans, provided that the dissolved material from the plaque is collected. The collected material must not flow through the blood stream to other arteries, thus causing blockage of arteries. ”
Now there is the issue. One of the major immediate causes of MI is unstable plaque blocking the artery ‘downstream’. I wonder if they attempted to actually do it.
The other issue left un-discussed is how the plaque grows in rabbits. When fed a diet that was 2% cholesterol, the rabbits then got blocked arteries. How & why ? No discussion & no answers. Humans are not grass eating rabbits. and rabbits are not adapted to eating such feed.
I suspect that these folks need to develop their research some more with animals closer to us humans; chimps maybe ? But then they is probably not allowed by research ethics committees nowadays.
I wonder about how to “present” fact and am therefor trying to keep away from the main stream media since most is distorted by vested interests in a “popular” form.
Still, sometimes you come across (through all open eyes on internet) programs that are telling you something.
Here is one program which well profoundly summaries nutrition and health through the eyes of an engineer like myself.
However, the “American flamboyant media format” of presentation is still hard for me to swallow although I lived for a while in the US and got used to it.
This is a version of Elvis lives!
https://www.theguardian.com/science/2017/sep/05/could-a-drug-that-mimics-a-zero-carb-diet-help-us-live-longer-healthier-lives
Interesting, but why are they not mentioning the keto diets that have been around for years.
But the things that never dies is:
” To make up the calories, the mouse diet contained 90% fat, which could be dangerous for humans to adopt. Stephen O’Rahilly, director of the Metabolic Research Laboratories at Cambridge University, said high-fat diets drive up LDL or “bad” cholesterol in humans, and so raise the risk of heart disease.”
and
“But for it to be useful in humans we would have to somehow dissociate these effects from the adverse effects on circulating LDL cholesterol,” O’Rahilly added.”
So, big pharma will make a zero-carb pill, but it will have to be taken with canakinumab injections. You will live longer to buy these for longer.
Real food anyone?
Following the announcement on 5th September 2017 that Jeremy Corbin was reprocessing himself as a vegan, the BBC ran a news interview with a recently claimed convert, who just had animal products now and then, who said she had never felt better and that her cholesterol had dropped by 4 points. If only she knew………….