For over thirty years I have been studying heart disease, or Cardiovascular Disease (CVD). I don’t think that I have Obsessive Compulsive Disorder…but maybe I have. I must admit that, at times there seemed to be no answers, at least no answers that did not have at least one Mount Everest sized contradiction.
At one point I simply decided that CVD was just a manifestation of ageing. It happened to everyone, at different rates. There was no cause – no causes. CVD was simply something humanity suffered from, get over it.
However, deep down, I knew that this could not actually be true. There were populations with almost zero rates of CVD, and others where the rates were extremely high. Just to give one example. Russia vs. Japan. In 2006 Russian men under the age of 65 suffered eighteen times the rate of CHD of men in Japan. I don’t think this ratio has changed this much.
I knew that Japanese men did not have any genetic protection. When they emigrated to other countries, their rate of CHD rose rapidly to match that of the surrounding population. Not always, but almost always. So it was obvious that something, or somethings, was causing massive differences in the rate. It wasn’t just fate, or genetics, it wasn’t just the ‘way it is.’ [By the way, the average cholesterol level in Russian men in 2006 was 5.1mmol/l, in Japanese men it was startlingly different at….. 5.1mmol/l]
Long, long ago I worked out that cholesterol, or LDL cholesterol has nothing much to do with CVD. Well, if two populations have exactly the same cholesterol levels and an eighteen-fold difference in the rate of CVD, cholesterol could only be causing 1/18th of the overall risk – absolute max. This figure assumes that the entire of the rate of CVD in Japan was caused by cholesterol, with no other factor playing any part. I don’t think I need bother telling what I think of that as a concept.
For a number of years, I pursued the alternative hypothesis that CVD was primarily caused by stress. There was a great deal of evidence to support this, and of course there still is. I still believe that stress (a concept which does need a bit of explanation) is the single most important cause of CVD. However, there were still many cases of death from heart disease and strokes where it was clear that stress had nothing (or nothing that I could see), to do with it.
For example, as mentioned before in this series of blogs. Systemic Lupus Erythematosus (SLE), where the increased (relative risk) rate of CVD in young women is up to 5,000% higher than the surrounding population. Now that is a proper increase in risk. In fact, it is the sort of increase that tells you that you are looking at a ‘true’ cause of CVD. Not some very wobbly and weak association.
I was also interested in Kawasaki’s disease. This is a vasculitis (inflammation of the blood vessels) that affects young children, who can then suffer heart attacks aged four, or five. Not exactly the same mechanism that causes heart attacks in adults, but very nearly. Again, this is highly significant. A condition that can kill children aged four from CVD is not just some anomaly that can be ignored. I knew I was looking at another true cause.
Later, my attention turned to Avastin. A cancer drug that was almost pulled from the market as it rapidly accelerated atherosclerotic plaque development, and death from CVD. No other risk factors needed to be present.
But how to link SLE, Kawasaki’s, and Avastin, through stress and other important risk factors such as smoking, or diabetes? When I discussed such things with ‘experts’ in cardiology, they would just end up saying that CVD was multifactorial. However, this has always seemed the ultimate cop out. ‘Yes of course, it is multifactorial.’ I would reply. ‘But how do this multiple factors actually fit together. Do they all create different diseases, or the same disease… through completely different process?’
In the end, if you are going to understand CVD you must be able to link all true causes of CVD into a single coherent process that fits all of the facts. If you cannot do this, you are really just stumbling about in the dark. Simply muttering ‘multifactorial’ whenever anyone asks you a question you cannot answer adds nothing to understanding.
Over the years, I found myself drawn back to the Scottish Heart Health study, for one very important reason. Which was that, in this study, fibrinogen emerged as the single most important risk factor for CVD. A fact that seemed to have popped out of nowhere. Never to be mentioned again. As a quick aside, in this same study it was found that the cholesterol was not a risk factor for heart disease. Another fact never to be mentioned again.
Was the Scottish ‘fibrinogen factor’ just an anomaly. A single observation, never to be replicated? I needed to find out. So I shifted my attention away from stress, to a focus on blood clotting factors. When I did so, I kept finding the same thing over and over again. Factors that increase blood clotting were always associated with a higher risk of CVD. Factors that reduced blood clotting always reduced the risk of CVD.
Just to give one specific example. High Density Lipoprotein (HDL cholesterol), so-called good cholesterol. Conventional thinking is that HDL sucks cholesterol out of atherosclerotic plaques and transports this back to the liver via the ‘reverse cholesterol transport’ system. A concept which has always seemed to me to look like a most desperate clutching at straws.
‘The antithrombotic properties of native HDL are also related to the suppression of the coagulation cascade and stimulation of clot fibrinolysis. Furthermore, HDL stimulates the endothelial production of nitric oxide and prostacyclin, which are potent inhibitors of platelet activation. Thus, HDL’s antithrombotic actions are multiple and therefore, raising HDL may be an important therapeutic strategy to reduce the risk of arterial and venous thrombosis.’1
Yes, HDL is actually a potent anticoagulant. In addition, it protects the endothelium and increases NO synthesis in endothelial cells. So, we don’t need a reverse cholesterol transport conjecture. HDL can be looked in a completely different way. I found it fascinating that the moment you decide to look at things from another direction a very different picture emerges.
Once I had my ‘clotting’ goggles on I began to ask myself: Is CVD simply the end result of dysfunctional (and I use the word dysfunctional in the broadest sense here) blood clotting?
Of course, for this to be true, atherosclerotic plaques have to be, at their core, blood clots. Well, are they? In 1856 Karl Von Rokitansky examined atherosclerotic plaques and declared them to be blood clots – in various stages of repair – or degeneration (depending on your point of view). They contained everything you find in blood clots, platelets, red blood cells, lipoproteins, fibrin and all the rest.
Karl Von Rokitansky’s problem? He could not explain how a blood clot could form within the arterial wall itself, underneath the endothelial cells. The reason why he could not explain this is that he did not know that Endothelial Progenitor Cells (EPCs), cover over clots that form in blood vessels. This, effectively, draws them into the artery wall.
Because he had never heard of EPCs, and could not counter the central criticism of his hypothesis, Rokitansky’s ideas never took off, and the cholesterol hypothesis filled the void. The rest, as they say, is history.
A few weeks ago I was presenting on CVD and I was asked, whilst waiting in the coffee line, ‘Come on then, what does cause CVD?’ The man who asked was a doctor, a pathologist, just retired, who had spent his life doing autopsies, and examining many, many, people who had died of heart attacks. I said to him. ‘Plaques are clots, and clots are plaques. It is all due to blood clotting.’
He was not in the slightest surprised. He just nodded in affirmation. ‘I thought so.’ He said. ‘I have always thought that plaques were blood clots.’ Well, what else could they be? There is little else that they could be.
For example, if you start looking at platelets and plaques, a whole new world of information opens up. Platelets are, if you remember, small blood cells that are the key ingredient of all blood clots (thrombi). They are attracted to the site of arterial damage, they clump together and then stimulate the ‘clotting cascade’ which creates clots that are tightly bound together by fibrin.
If clots are plaques, and plaques are clots, you would expect to find that platelets are intimately involved in the entire process of plaque formation. Here, I quote a long section from a book called ‘Platelets in Thrombotic and Non-Thrombotic Disorders.’ For some, this may be a big technical, but I suggest a read, and re-read.
In this section it is pointed out that clots/thrombi form at areas of endothelial damage/stress. In addition, platelet rich thrombi are incorporated into the vessel wall at sites of injury…. Yes, the whole process is outlined here. Including the fact that platelets contain a substance that causes smooth muscles to grow and proliferate (a key finding in all plaques).
Where is cholesterol in all this…nowhere. Please read and inwardly digest:
‘von Rokitanksy and Virchow were early investigators who reported that in some instances, the development of atherosclerosis involved early vessel wall injury, thrombosis, and the incorporation of thrombi into the vessel wall. In 1887, Welch gave a clear description of arterial thrombi based on the experiments of a number of investigators, showing that they began as platelet-rich thrombi and are then transformed into masses rich in fibrin. Much later, these observations were reinforced by Duguid, Morgan, More and Haust and French.
In the 1960s, we observed that platelets were deposited on, and interacted with, the walls of arteries in regions of disturbed blood flow. These are the sites where atherosclerotic lesions develop and increased vessel permeability is demonstrable.
In 1973, Moore induced ‘thromobathererosclerosis’ in rabbits by continuous damage of the endothelium of the aorta with an indwelling catheter, and in 1976, he and his group showed that prior administration of anti-platelet serum to induce thrombocytopenia (very few platelets in the blood) prevented the development of these lesions. The finding by Ross and his colleagues in 1974 that stimulated platelets release a mitogen for smooth muscle cells (platelet derived growth factor PDGF) arose from a chance observation.
They noticed that serum prepared from platelet-free plasma did not support the proliferation of smooth muscle cells in culture, but when they prepared serum by blotting platelet rich plasma, the serum supported cell growth as effectively as serum prepared from whole blood. These results gave even more credence to the theory that platelets are involved in the development of atherosclerotic plaques because they promote the proliferation of smooth muscle cells.
The progression of atherosclerotic plaques also involved platelets since platelet rich thrombi have been shown to be incorporated into the vessel wall at sites of injury. Platelet rich thrombi that form on ruptured atherosclerotic plaque may occlude the lumen of the vessel, or may embolize (break off and travel down the artery).
When the thomboemboli impact in smaller downstream vessels, organ damage occurs. These concepts about platelets and atherosclerosis have stood the test of time. The picture developed by Ross of the development of an atherosclerotic plaque is not well known, and the signalling pathways, PGDF activated are being explored. The importance of platelet interaction with the components of ruptured atherosclerotic plaque in the thromboembolic complications of atherosclerosis is now generally accepted.2’
When I read stuff like this I think. Come on guys, you know that plaques are clots and clots are plaques. It is staring you in the face. It has been staring humanity in the face for over a hundred and sixty years. Ever since Rokitansky and Virchow started to look closely.
Next: Impaired plaque repair
2: ‘Platelets in Thrombotic and Non-Thrombotic Disorders.’ Edited by Paolo Gresele. Page 5.
One of the new Imatinib-like drugs for the treatment of CML has side effects that include a very high increase in CVD. It is a tyrosine kinase inhibitor. Would you be interested in the mechanism or are things complicated enough?
Reply to Dr. Kendrick,
Numerous animal studies have shown that high SUCROSE intake increases platelet
aggregation/clotting and inducement of atherosclerotic plaques.
See Google search reference: Atherosclerosis IV: Proceedings of the Fourth International Symposium; G. Schettler, Y. Goto, Y. Hata – 2012 – Medical…”It has been reported by our group and Dalderup et al. that high sucrose … time, and a platelet aggregation test were done on the last day of the experiment”. LINK…https://www.google.com/search?q=sucrose+%2B+platelet+aggregation&ie=utf-8&oe=utf-8
It appears that sugar consumption supports your analysis, does it not?
Brilliant – so clear and I understand exactly what you are saying … I wanted to read more but you ended it leaving me with more thoughts … Don’t leave it to long before the next
It’s a leap forward to be given such a persuasive alternative hypothesis (to cholesterol, that is). This article is a timely read for me. I watched a 90 minute interview recently on youtube – Dr Mercola and Dr Stephen Sinatra talking about the benefits of grounding. Dr Sinatra said that the build-up of static in our bodies caused hyperviscosity. Our blood is ketchup instead of red wine and inflammation thrives when our blood is thick. What’s your take on this, please, Dr Kendrick?
Haven’t really looked into grounding in much detail. I am always a believer in ‘stuff we used to do’ e.g. walking around barefoot, being good for us. And ‘stuff we now do’ e.g.never being in contact with the ground, being bad for us. So, in general I am very well disposed to grounding being a good thing.
Fascinating to think that ‘the stuff we now do’ may have such profound influences on our physiology and therefore health, whether it be staying out of the sun or not being connected to the earth. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3576907/
On a similar note, I’m all in favour of old wives tales too. Some of those old wives knew a thing or two.
A very convincing narrative about the CVD-process; as always 🙂
I learn a lot!
I guess that people like me are also interested in possible external factors that may influence this process and which they can address on their own.
I sincerely hope you’re going to publish this ‘What causes heart disease’ series of blogs as a book! It’s vitally important to get this into the public domain.
Sorry, it is in the public domain already via this blog 😁
True, but more people read books than read blogs. I would definitely buy the book.
Most of this is already in Dr. Kendrick’s first book (Cholesterol Con). Maybe a 2nd edition with revisions may be a good idea.
Now things getting much, much, more intriging and interesting Dr K ! This about HDL is new from you: “…HDL is actually a potent anticoagulant. In addition, it protects the endothelium and increases NO synthesis in endothelial cells” Wow, so HDL is good after all !
I’m happy my HDL is 3.7 at the last test. Not happy that I have an artifical aortic valve with a flow disturbance across it as is usual with these things. I wonder if athersclerotic plaque forms around heart valves ? I know they can calcify due to flow disturbance. If the heart valve is mechanical then anticoagulants are prescribed, but if they are bioprosthetic (like mine) no anticoagulants are prescribed, despite the flow disturbance.
Reading your blog is the best medicine for our hearts! Thank you, Dr. Kendrick!
This paper here looks interesting. I doesn’t mention “clot” at all, but touches platelets, eNOS…
Very interesting. And very telling that a pathologist that had autopsied many CVD victims had come to the same conclusion.
So, I guess I should appreciate that I bleed profusely from minor injuries — not enough to be a problem, but quite a bit more than most folks I know. It always used to frustrate the nurses when I’d give blood — they’d have to hold the compress on my arm and keep it elevated (or get me to do it) longer than on other donors. And when I finally took the bandage off hours later, it was obvious the little puncture had continued bleeding. But I gave regularly until I was 65, then I was “too old”. And I suppose with little cuts and such, generous bleeding does flush out the wound pretty well. But I am puzzled that I also heal very quickly from those minor nicks. Wouldn’t good clotting be a must for wound repair?
Thanks again Malcolm, but what keeps intriguing me, what causes the damage in the first place? I don’t buy the argument high sheer and all that. Can’t accept that were made dysfunctional to begin with. It seems to me that we are dealing with a maintenance issue. I keep therefore going back to the hypothesis that the cause of CVD is a form of scurvy
My uneducated guess is that malnutrition causes lots of problems. I try to eat nutrient dense foods.
Interesting comment and a good point Jamesj,
Suzanne Humphries in https://www.youtube.com/watch?v=y0LLX0sgwAU her lecture on Vitamin C, refers to ‘scurvy’ in arteries near the heart, and hypothesises that the low ‘recommended’ levels of vitamin C are responsible for the initial arterial damage, and that high doses of Vitamin C are effective in curing/preventing such scurvy. (also Linus Pauling)
If this a double entry forgive my bumbling.
Thanks again Malcolm, but what keeps intriguing me, what causes the damage in the first place? I don’t buy the argument high sheer and all that. Can’t accept that were made dysfunctional to begin with. It seems to me that we are dealing with a maintenance issue. I keep therefore going back to the hypothesis that the cause of CVD is a form of scurvy
Thanks for yet another really interesting and illuminating article Dr K.
Does all of this mean that warfarin or the new anti-coagulants could be used to counter plaque formation/development, or have I got the wrong end of the stick?
So with my Low-Carb-High-Fat life style I get Lower Inflammation (to protect my endothelium), Lower triglycerides (minimising clotting factors), Higher HDL (anti-coagulant). To this I add sun bathing, getting Vit-D and NO. I guess I am doing something good for myself, if I have understood this series.
Solomon – what you’re doing sounds perfect to me – ( Of course that includes a glass of red wine, a cup of ground coffee and a little dark chocolate every day) oh and don’t forget to take your shoes and socks off and get onto grass or sand whenever possible. Life was meant to be paradise – we can find it again amongst all this modern mess!!
Yes yes we can find it again, simplicity in all things, to paraphrase the Greeks, meden agan, nothing too much.
I recon you’d be a first class physician, well grounded.- I’m off to the beach..! With a nip of red wine in me baggies:)
What is your source of NO?
That is an excellent article. It makes perfect sense. I always wonder if we’re taught to be scientific in school, why are we so unscientific in reality? For instance, why isn’t the cholesterol hypothesis still a hypothesis and why aren’t we trying to disprove the hypothesis? (And the same could be said for many other endeavors, such as a low fat diet, saturated fat cause heart disease, etc.) Why do we as humans choose a path and put all our efforts into proving that path is correct? Why don’t we instead say “At the current time, we have multiple possibilities, and we’ll perform tests to determine which one (if any) is correct”?
I was at my cardiologist’s yesterday, and he spoke fondly of PCSK9 inhibitors (not mentioning them by name but by function — probably thought I wouldn’t know what they are), and seemed to be impressed that they could lower “cholesterol” by 150 “points”. Why does no one stop to think, “Is it wise to lower cholesterol by 150 points?”
I have often asked myself the same question when I lie awake in the middle of the night.
I come up with two types of reply,
One. Doctors are very busy people, they don’t have time to question received wisdom, and medicine is a magistral profession, you learn from the prof because he knows more (not you Dr K)
Two, defence of status quo, no boat rocking, dislike of Samson style figures who brought the roof down. Look at the reaction to whistleblowers, normally they are ganged up on. I still go back to my lipids man, who say “130 LDL is too high, Ezetrol for you my lad” where I live I pay to see him, but I don’t take his advice.
Bob, saying “We don’t know” requires confidence. Senior people with lots of qualifications usually prefer to be a pedestal, all seeing and all knowing.
So true! During my nearly 70 years, I have had the greatest respect for the few in the medical profession who have had the intellectual honesty to admit that they “don’t know”.
You can pass medical school exams by demonstrating that you absorbed/can regurgitate what was taught to you. You will not pass if you cannot do that. If you can pass, but also retain your independent and inquisitive mind then you are on the path to becoming a true student of health, and a healer. Those who simply pass, no matter how well, will keep on repeating what they are told, even if it comes from a pharma rep selling pills.
Yes, I have thought this for a long time. Those people I went to school with who became doctors weren’t the brightest of the bunch, but they had good enough memories to ‘regurgitate’, as you say, the information they were given without question. Obviously there are also those like Dr Kendrick, Dr John Briffa, Dr Rongan Chatterjee etc who do question perceived wisdom and look into the ‘whys’ and ‘wherefores’ of things. Thank goodness for that!! I trained as a diagnostic radiographer many years ago and, during a physics lecture, I queried something that the hospital physicist was teaching us. He looked at his (yellowed with age) notes and agreed that it was incorrect. He also said in all his decades of teaching, nobody had ever picked up on that mistake!! So perhaps there are doctors out there who do query what they are being taught, but are either too timid to comment or are afraid of not passing their exams. And so it goes on….
I think all of your comments are true. I would just like someone to come out and say, “The evidence is conflicting. Based on that, we can’t make recommendations.” To me, if the science says it is so, then just let it be.
To me, this guy has it right:
A very interesting publication. Nutshell synopsis about research, academic bias, and finding what you look for.
Didn’t make make me more inclined to believe the cholesterol hypothesis however.
Dear Dr Kendrick,
But why only in arteries and not in veins?
And thanks for teaching me so much!
“In this section it is pointed out that clots/thrombi form at areas of endothelial damage/stress.”
Might we therefore assume correctly that damage to the endothelium from nasty foreign invaders like these would lead to the very same CVD outcomes as any other initiating factor?
Doctor, what do you think might explain the massive difference in CVD between Russia and Japan? What are those Russians doing to promote clotting?
When the wall came down, the rate of CVD exploded.
Dr. Kendrick said, “When the wall came down, the rate of CVD exploded.”
There is no more famine just feast Periods of starvation (fasting) reverses CVD. It also dramatically reduces blood viscosity. An overfed country is a country with heart disease…
I also think it was an incredibly stressful time in their history. Everything changed, nothing was the same, and for many it was not for the better. I often wonder what the correlations between CVD and social unrest/disruptions are – war, unemployment, natural disasters etc.
So things like Rutin and Isoquercetin, now being studies by Harvard Boston for their ability to stop the clot should strongly be considered? They may be the perfect antithrombotic since they work from the top of the cascade (PDI) covering both veins and arteries.
Click to access 07.pdf
Click to access 37.pdf
I’m beginning to see through a glass darkly. Write on…..
What about vitamine k2. If anticoagulants like hdl are good, high intake of vitamine k2 would be bad because it effects coagulant factors.
If my understanding is correct it’s K1 that is involved in coagulation, K2 is involved in processing calcium – ie getting it out of your arteries and into your bones.
Mine’s 3 and I’m happy with that too.
I mean that my HDL is 3 mmol/L, and I’m happy with it.
Was the difference between Japan and
Russia rates corrected for confounders such
as the possibility that Russians drank
up to 8 times the alcohol that Japanese
After reading your article I am left wondering: So what does this all mean for Joe Lunchbucket? Do you recommend foods to omit from our diets, or foods to be sure to include? How does this article help the average Joe?
re: So what does this all mean for Joe Lunchbucket?
I suspect we’ll have to wait until Dr. Kendrick’s entire explanation is laid out, at which point, absent any troubling objections, there may already exist some fully detailed dietary and lifestyle approaches that are compatible with the implications, or not.
Expect, however, that an optimized diet is going to depend on the definition of optimized (perhaps longevity vs. vitality vs. performance), genotype, phenotype, epigenetics, age, gender, present health, personal immunological history, locale, budget, lifestyle preferences and other factors to surprise us later.
Business as usual:
‘Yes of course, it is multifactorial.’
You say:” I would reply. ‘But how do this multiple factors actually fit together. Do they all create different diseases, or the same disease… through completely different process?’”
Thanks Dr Kendrick for keeping your scientific attitude along so many years. It is the only way to find a real solution for CVD. This is why so many people (myself included) appreciate your work, and the way you share your thougts with a more and more vast audience.
Yous shoud consider publishing a paper on this subject in a prestigious journal! Why not trying “Medical Hypothesis” ?
Sometimes you unexpectedly get encouraged!
I had this afternoon a surprise call from a former colleague of mine with similar CVD problems. He had for years shut his ears to my pleading to him to avoid the heart medicines and surgical interventions but had finally ended up in a real health morass not least with muscle weakness.
In the back of his head the warning bell, I had placed there, sounded and he decided to quit all medication and had evidently now returned to ‘life’. He has now finally also arrived to share my opinion that our health care system is just a part of a very criminal system orchestrated by Big Pharma. That was why he called me to give me his full recognition – heartwarming indeed!
Thanks Malcolm for your courageous fight to change the medical world!
Goran, that is heartwarming and encouraging to hear. A similar event happened with my sister in law. She was on a PPI, statins, and metformin. She was quite overweight. When she and her hubby came to visit us last summer for six weeks, she wanted to know how we had lost so much weight, and how I had “fixed” my gastric reflux. So she set herself a challenge, from day 2 of the visit she ate what we ate, stopped her PPI cold turkey. I had advised she do it gradually but no she wanted to be rid of it, luckily she didn’t experience any rebound reflux. At the end of six weeks she had lost 10lbs, no reflux and no more pains in her legs. She did carry on with the metformin until she saw her physician, and now is off that too. She is just over the moon with how she feels and looks. My B.I.L was not so eager, he also is on statins and high blood pressure pills, but she is working on him.
Do I read between the lines that you are, together with your sister in law, now living a LCHF way of life?
Well – there seems to be some family resistance. My brother and sister in law are both rather overweight and they are, to say the least, very suspicious to our way of life and to cut carbs of any sort. Diets tend to create strong feelings and there might even be addictions involved and to be denied. Decisions must come from within.
Sorry Goran, I wasn’t very clear. Yes, we (husband and I) have eaten LCHF/ketogenic way for the past two years, with great improvement in our general health and energy level. My sister in law also continued the diet, my B.I.L. is now coming around after seeing how slim and trim his wife has become, and that she has been able to go off her meds.
After the first couple of months eating this way, it was time for my annual cholesterol check. HDL were high, T.C. high, Trig low, LDL on the high side, but not too bad. I was seen by a locum at my doctors office who was very concerned, and wanted to prescribe a statin. Luckily I had done some reading, including Dr. K’s The Great Cholesterol Con, shortly before, so declined the statin, to his horror. I was then called back into the office to see my own doctor when she came back from holiday, and was pleasantly surprised (and relieved) that she was very happy with my chol. results. She asked about my diet and was very supportive of it. I’m very lucky to have such a doctor. Not so lucky with my Respirologist for IPF who wants to put me on a PPI for reflux He’s not impressed that I have “fixed” it myself with diet, thinks I shouldn’t have to deprive myself of all the good things like breads and pastries. Shaking my head here.
Hi, was she on BP meds.
Hi John, no, my sister in law wasn’t on high b.p. pills.
Realting to the PPI-issue I cannot refrain from forwarding this link to alternatives to Big Pharma as it arrived in my mailbox from Mercola this morning.
Thanks for the link Goran. I feel lucky I had done some reading about PPI’s before my Respirologist suggested them, and had started the low carb diet already. It really astounds me that he should consider such a medication with the side effects of increased incidence of pneumonia (which I need like a hole in the head having IPF already, pneumonia can be fatal), and osteoporosis which I also have. This experience just reinforces the extreme skepticism I have towards conventional medical treatments. I also no longer take Fosamax for osteoporosis. When I learned of the horrific side effects such as necrosis of the jaw, and that the half life of the drug is 10 years, well, that was the icing on the cake. The drug has not been on the market so very long, what on earth could be done about it if more effects were discovered, the drug is in the system for 10 years!
Goran, I know you wrote about your protocol before, would you mind repeating it again? What supplements, techniques are you using for CVD?
Thanks for this series, Malcolm.
I am starting to think of the plaques in blood vessel walls as being analogous to scabs forming on skin after trauma. On skin there is usually no harm caused when the scab falls off.
In blood vessels there is more potential for harm.
Looking forward to the next part.
Are there an statistics for the incidence of CVD amongst Heamophiliacs vs the general population?
Such as they do exist, they show 20% the rate of CVD of the general population. I have the reference somewhere.
I have been enjoying this series very much. I am now even more interested as my PA at the VA has just informed me that I have “a slightly enlarged distal aorta of 2.2cm. I really want to keep that from enlarging. Thank you so much for doing your best to try to educate the uniformed.
Thank you, again, for making the information readable for those of us without a higher education.
Malcolm, your second sentence helped me a lot. I am trying to recover from a tactless comment about our efforts to maintain good health. I keep reminding myself that those who criticise are not as healthy as we are.
At the suggestion of my cardiologist, I joined a drug trial called COMPASS which is titled “A Randomized Controlled Trial of Rivaroxaban for the Prevention of Major Cardiovascular Events in Patients With Coronary or Peripheral Artery Disease”. I have blocked arteries, confirmed by angiograms, but no stents. The drug trial is intended to test the efficacy of a blood thinner, rivaroxiban, in low doses to prevent clotting. It is a triple blind drug trial and is described here:
I have a high Lp(a) but LDL and HDL levels are good. I currently take 10mg Lipitor and 3,000 mg Niacin daily. Unfortunately, I had to drop out of the trail because of excessive bleeding after cuts, etc. plus I had suffered a subdural hematoma several year previously which I did not want to risk repeating. The results will be known in a few years and could add to the theory of “plaques are clots and clots are plaques”.
Eugène, K1 is the anticoagulant, not K2.
Dr Kendrick, Where does Marfan Disease fit into this excellent discussion?
Chuck – I was born with bicuspid aortic valve which people with Marfan’s syndrome sometimes have too as Marfans is a connective tissue disorder. People with Marfans and bicuspid aortic valve can often have enlarged aortas which again is due to the connective tissue disorder which can cause anyureism if not found in time. Both Marfans and bicuspid aortic valve are congenital defects which occur during the first few weeks of foetal development – there are several people with Marfan’s on the valve replacement forum I’m on. What begs the question is, do those with mechanical replacement valves who are then on warfarin for the rest of their lives have a lower risk of CHD ?
K1 is a coagulant, part of the cascade that results in clotting.
Warfarin is the classic K1 antagonist: long-time standby anticoagulant.
All the K’s contribute to coagulation:
Is the drug “Avastin” related to statins or is it a statin drug? Are you going to tell us that statins cause CVD? We’ve been told that statin drugs cause, “stable plaques” to form. What the heck are stable plaques and how are they formed by taking statins?
A good paper authored by Siri-Tarino
HDL levels – In brief: replacement of carbs with saturated fat gives the greatest benefit of all. Reduction of sugar, a noticeably good benefit. Weight loss and W3 supplementation have a modest effect. Pharmacological interventions ( drugs!) don’t seem to help at all.
I’m a GP and you might be interested in what I tell patients about eating. Basically, eat real unprocessed food. I tell them not to worry about natural fats as they are not harmful. You can see it on my website http://www.fatismyfriend.co.uk
Thanks to Malcolm’s destatinisation programme 😀 I no longer resort to statins and my alternative is to tell people about real food ways of eating. The amazing thing is that this way of eating normalises your lipids anyway, and your HBA1c so keeps your GP happy and means he/she can justify not giving you statins! It also may cause weight loss as a side effect which people sometimes like. Real food can also make you feel better as it is more nutrient dense. The sad thing is that lots of people no longer know what real food is so I have some demonstration cards.
Do you think it can sort out high blood pressure as well. would like to stop the meds.
Sometimes can sort your BP and come off all drugs if you are committed. Read “Jeff Cyr’s how a ketogenic diet saved my life” He read Volek and Phinney’s “The art and science of low carb living” for one full year before he did it. He did it for other reasons but his commitment is what made the difference and you could do that
Some people find that LCHF eating does reduce blood pressure. I have managed to reduce my BP meds twice up to now and hope to reduce still further. Suggest you have a look at Dr David Unwin’s info on the diet he is using with Type 2 patients. Fairly low carb but not too extreem. He also reports that some patients have been able to reduce BP meds. Worth a try.
Thanks. Did you reduce them on your own or with your doctor. How did you know to reduce them. thanks.
Great website, Joanne! So good to see the low-carb/high-fat approach slowly gaining ground amongst British GPs, although you are still much too few and far between! Do you see private patients?
Thanks for your positive feedback.
I’m doing a series of talks for health care professionals and also hope to do similar for the public in the future.
I don’t see private patients at present.
I’m just too busy.
Thanks for your input Joanne. Personally I can’t wait to see what the PHC can bring to the table in terms of trying to change governmental health/nutritional policy. I am so excited by your collaboration and wish you all the very best and every success.
Dr Jo, what a great website. Does it replace your previous website?
I wish my surgery was up to date on food. The last time I saw the practice nurse she showed me a picture of the NHS Eatwell Plate. I burst out laughing and then asked if she really recommended coca cola and a 65% carbohydrate to people? I asked what this diet would do to a diabetic’s blood sugar? After a lengthy and pleasant chat I agreed to lend her ‘The Big Fat Surprise’ by Nina Teicholz, which naturally she hasn’t returned.
No, I am running both websites at present. Re the Eat well plate I am reliably informed that new dietary advice is coming out of Public Health England on Monday. I am interested in encouraging people to use the real food ideas on cards like the ones Zoe Harcombe did for my patients. One of my practices has a low reading age, but in both practices the cards have proven very popular. You can see them on my Facebook page- maybe show to your practice nurse and GP?
Reply to John…
Have you already done any reading on recent research about the downside risk/benefit ratio of over-treating hypertension, particularly when it is classified as mild, moderate, or pre-hypertension? Depending on which of these categories you may fall into, you may actually be better off without any meds at all, or you may benefit from dose reduction.
“Did you reduce them on your own or with your doctor”. A bit of both. I have a great GP.
“How did you know to reduce them”. I have my own BP machine. One of the best purchases I have ever made. If you get one make sure you get a cuff machine rather than one that goes round the wrist.
Thanks. Did you do it slowly or all at once. I wish I had a great GP. I take you still take some meds.
I’m suddenly interested in finding a book regarding blood pressure medication à la Great Cholesterol Con, anyone know of one ? Just saw GP who mentions putting me on an ACE inhibitor if I can’t get my diastoic blood pressure below 80. I already eat LCHF, been eating that way for the past nine years – love it – do tons of exercise – am slightly underweight. I don’t have a problem with my BP but my GP does. He said we need to get your diastolic pressure below 80 before April. What ? Why April ? For the QOF ! I shan’t be going near the surgery for a while…….
80 sounds fine to me. Is there any specific reason he wants it even lower? There is no point you taking extra medication just to get extra Qof points. He can always exempt you if you don’t want any more tabs. There was a big metanalysis recently that came out in favour of slightly higher levels than on the guidance.
Anne, you might (or might not) benefit from intermittent fasting (IF). I also was on (and currently am on) LCHF, but IF had more impact on my blood pressure than did just LCHF. Personally, I think that “high” blood pressure really isn’t “high” at all but more like normal with age.
reply to JP Sand. Do you have any links on this. My BP if I don’t take the meds can be as high as 170 over 90 sometimes. Not sure if when you stop it takes some time to get back to normal with your heart doing all the work again.
I love to see any GP’s advocating LCHF as remedy (?) och for sustaining health. In my eyes the true Hippocratic attitude.
My own view, as an ‘anecdote’ is that it is not until you have reached the ‘end of the road’ your ears opens up for this kind of message. I realise that when the words come from a GP the impact is much stronger than when they come from a metallurgist 🙂
I would love to see your demonstration cards.
Grass fed beef?
Wild caught salmon?
Good for you! I wish we had more docs like you in the US. I think it is sad, but true, that, as you point out, most people no longer know what real food is. I never realized until about 5 years ago how different my way of eating is from that of my fellow Americans. Then, I started noticing what was in people’s grocery carts as I stood in line waiting for my turn at the checker’s. It’s shocking to see what most of my fellow citizens eat (and what they feed their kids!). That’s why they call it SAD (Standard American Diet).
Just to add to Anne’s comment.
I think too much is made of BP, not least because of the known issues of white-coat syndrome and inaccuracy compared to the Central Aortic Systolic Pressure that actually gives useful information beyond the extremes.
I have reached that age at which the Welsh NHS offers an Abdominal Aortic Aneurism examination. I had the examination yesterday and the abdominal section of my aorta shows no sign of aneurism and is thinner (diameter) than would require further monitoring. I will be going to the optician next week who will test for the pressure in my eyes – it is usually normal.
As far as I am concerned, these are far more significant indicators of a BP problem than any particular sphygmomanometer reading.
On the strength of one Sphygmomanometer reading I had been prescribed – and religiously took – an ACE Inhibitor for about 5 years until 2 years ago I was prescribed a Statin, had a reaction, read the books, found Dr Kendrick’s site, and stopped taking both. No taper, no issues.
There are real issues around high BP but they are not investigated for under QOF. If they were then NICE and the GP service would have more credibility, harsh?, maybe but that is my experience (n=1).
If my AAA test had demonstrated a problem I would have considered a pharmacological solution, having already changed my diet/exercise regime 7 years ago, but in my view the diet/exercise works. The ACE inhibitors didn’t – there was no long term reduction in my BP readings.
Stephen – I agree with you that too much is made of BP. I measure my BP at home before cardiology appointments (have aortic vallve replacement due to bicuspid aortic valve – birth defect) and my diastolic pressure (the lower one) is very much higher since surgery. I wonder why that is and I do believe there is a connection. I don’t believe taking BP meds is an answer at all because there is a reason for it being higher and it’s no coincidence. It annoys me that the GP is more interested in getting my diastolic BP down just to fulfill his QOF rather than to find out why it’s gone up ! That is seriously crazy imho.
Bob – if I fasted I would get seriously underweight ! Not joking. I eat very well on LCHF but am underweight despite eating well !
Hi Anne – I’m in the same boat as you. I eat HFLC, as much as can eat, but am now quite thin. My (admittedly useless) BMI is 18.5. I have just bought Michael Mosley’s book “The 8-week blood sugar diet” and thought to follow it to knock my 58 year old type 2 diabetes on the head but a) I think it’s been too long now and b) it’s not recommended for a BMI under 21. That’s understandable as if I did 800 calories for 8 weeks I’d slip down a drain sideways. HFLC is good because it’s so satisfying but even drinking cream makes me not gain a single pound – well, it wouldn’t, would it. I have been the same weight, 52 kilos, for some years now and am pleased to announce to the whole world that my blood sugars are pretty impressive. (applause)
Interesting comments. You are so right about white coat hypertension – I was over medicated for years because of this which is why buying my own arm cuff machine was such a step forward. They are not very expensive.
I just changed my diet and the BP came down with the help of some supplements mainly a high dose vitamin B and Magnesium. I still take some meds but have more than halved one and cut another by a third and BP still better than it was on the standard NHS recommended low fat diet.
It didn’t come down overnight but did start to improve over about 6 months (if I remember rightly).
“80 sounds fine to me. Is there any specific reason he wants it even lower? There is no point you taking extra medication just to get extra Qof points. ”
Hi Joanne – if it were 80 the GP would be fine with it, but it’s often in the upper 80’s and 90’s. I need to know why it is like that – eating LCHF for nine years now, no processed food, lots of exercise, low weight, but had aortic valve replacement due to bicuspid valve and it is ever since then that the diastolic has been “high” ! GP is just interested in the QOF ! I would love to know more about BP – been re-reading Doctoring Data but Dr K says he isn’t discussing diastolic pressure in it.
Nice website and the more supporters, particularly doctors, for a sensible diet the better. Your contribution is invaluable but rare. It worries me that so many current problems seem to stem from the days of HCLF promoted by Ancel Keys. Obesity, metabolic syndrome, Type 2 diabetes, Type 3 diabetes, Alzheimer’s (up from 1 in 50 85+ yr-olds in 1960 to 1 in 3 85+ yr-olds – not age) etc. and nobody notices. Compound this with drugs given on an algorithm based on surrogate data and with a trivial efficacy rate (high NNT) hidden behind Hazard Ratios(HR). Incidentally, I have nothing against HRs as such – useful tool but when the real efficacy is hidden as a consequence!
All very interesting, thanks. But why the low level of CHD among Japanese men? When they stay at home that is.
Mark R – maybe because Japanese society is very stable compared to ours in Europe. Their racial identity is strong. They know who they are.
Just a thought.
Dr. K – you are a star. Thank you. Every week I look forward to your truly excellent writings.
So so good, the writing skills as well as the science. giving ourselves the best in nutrition and life style is of paramount importance, but damage from past illness is something lurking there insidiously. I now look at CVD in a different light. My Ross and Wilson in nursing school so simple but for my level of intelligence OK. Thank you Dr Kendrick.
A new study may add to explain increased risk for CVD for metabolic syndrome; “The glycolytic enzyme PKM2 bridges metabolic and inflammatory dysfunction in coronary artery disease”
Abnormal glucose metabolism and enhanced oxidative stress accelerate cardiovascular disease, a chronic inflammatory condition causing high morbidity and mortality. Here, we report that in monocytes and macrophages of patients with atherosclerotic coronary artery disease (CAD), overutilization of glucose promotes excessive and prolonged production of the cytokines IL-6 and IL-1β, driving systemic and tissue inflammation. In patient-derived monocytes and macrophages, increased glucose uptake and glycolytic flux fuel the generation of mitochondrial reactive oxygen species, which in turn promote dimerization of the glycolytic enzyme pyruvate kinase M2 (PKM2) and enable its nuclear translocation. Nuclear PKM2 functions as a protein kinase that phosphorylates the transcription factor STAT3, thus boosting IL-6 and IL-1β production. Reducing glycolysis, scavenging superoxide and enforcing PKM2 tetramerization correct the proinflammatory phenotype of CAD macrophages. In essence, PKM2 serves a previously unidentified role as a molecular integrator of metabolic dysfunction, oxidative stress and tissue inflammation and represents a novel therapeutic target in cardiovascular disease.
The last line was the most interesting and easy to understand. A novel therapeutic target in cardiovascular disease… Interesting angle. I’d go for simpler things first. Sugars and starches anyone? Smoking? Sedentary life? All free & I know which I will go for rather than a new drug.
Good afternoon dr. Kendrick,
For a while I,m reading your information about cholesterol etc. Very interesting. I have a question, why is it that persons who have a heartproblem should take statins? Our doctor thinks different on this matter of cholesterol. That is very difficult when we visit him and he will prescribe statins and wanted to have the level of 2!
We find it a bit difficult to understand all you write for us as dutch people. Still we are very interesting.
Wishing you shalom from Holland.
Nanno and Coosje Op 1 mrt. 2016 11:54 schreef “Dr. Malcolm Kendrick” het volgende:
> Dr. Malcolm Kendrick posted: “For over thirty years I have been studying > heart disease, or Cardiovascular Disease (CVD). I don’t think that I have > Obsessive Compulsive Disorder…but maybe I have. I must admit that, at times > there seemed to be no answers, at least no answers that did no” >
Nanno en Coosje,
One of the books by Dr. Uffe Ravnskov is translated into Dutch: Feiten en fabels over cholesterol en cholesterolverlagende medicijnen. It is available at at least one online dutch bookstore. Dr. Ravnskov is the founder of Thincs, http://www.thincs.org/ , The international network of cholesterol skeptics. I think you may find the book a good source for arguments against statin use.
Nanno, your doctor has been trained to believe that cholesterol causes heart disease. The whole point of this site is to say that this theory is nonsense. So, if cholesterol isn’t bad for you, statins are hitting the wrong target and have damaging side effects. Here’s one fact: all the countries in Europe with the highest rates of cholesterol have the lowest rates of heart disease. In a sane world free of drug influence that would be enough.
Please read the site for numerous articles pointing out why the current cholesterol orthodoxy is wrong and leads directly to a bad (low fat) diet.
I do so agree with you. I hover around the world median level for TC. Presumably set by God, Nature or evolution, to be the sort of level I need. My doctor twenty years ago, when I first asked him, said, if we treat that level, we would have to treat half the population of Bellgium. A vey prescient remark.
Nanno and Cosje,
We are so used to assuming that our doctors – backed up by the medical research establishment – know what is best for you, that it is really difficult when that trust breaks down. However, I am convinced the the medical profession has become trapped by a set of dogmas that are just as wrong as the old idea that a vast range of problems could be solved by bleeding the patient!
Fortunately there are a lot of medical trials performed nowadays – unlike I suppose in the days of blood letting – so here are a couple of interesting links that come with references to the original research. You might want to take these to your doctor.
This tabulates a lot of evidence from different countries that those with high cholesterol live longer on average!
Regarding statins (the reason I am here is because I suffered the side effects of Simvastatin, and consider myself lucky to have escaped without permanent damage), here is a wonderful site – with references – that lists the NNT’s for a variety of treatments, including statins. NNT stands for Number Needed to Treat, and I won’t spoil your surprise when you look up statins!
Before you look the link up, as yourself what would be a reasonable number – how many people would you expect your doctor to have to treat in order to achieve some good?
Here is the page for treating people with heart disease with statins!
and here is the page that is relevant to those offered statins just as a precaution!
As you will see, every page of this site links to the places from which they obtained the data.
If your doctor argues, ask him for a better estimate of the NNT for statins!
I see a paradox here, many of those who advocate LCHF in their comments on this excellent series of blogs, cite lower TC as a result, yet the links you give take us to studies where there is an inverse correlation between TC levels and death from all causes. Moreover dr K, if I have read him correctly, does not preach for lower TC levels as end in themselves.
Thanks for the Verner link
I see a big difference between a TC that reduces of its own accord (because the body no longer needs it at the previous level) and the TC being forced down by a drug.
To me the first is a result of a healing process and the second is contributing to an underlying problem by hindering the body’s natural defences/healing.
Makes sense to me.
This is something I have wondered about too, but my impression from what I have read (I am not a medical scientist!) is that cholesterol levels are really not relevant except perhaps at the extremes. I do notice, however that Dr Kendrick seems to be invoking HDL and LDL as being anticoagulants and pro-coagulants respectively, so the entire picture seems too murky – I give up!
OTH, mortality data seems to have an importance that transcends all the detailed biochemistry – if people live slightly longer when they have plenty of cholesterol, you would need some very solid science to persuade me that lowering my level was a good idea!
Solid science seems remarkably scarce nowadays. Here is a piece about this very issue I’d quite like to read, but it is behind a paywall:
Lovely isn’t it the way the “dangerous saturated fat” data has been removed from the 2012 report. The honesty of medical science is now an issue. Ioannidis JPA (2005- Why most published research findings are false. PLoS Med 2(8): e124) said it. Prof. Peter Gotzsche said it; Dr Marcia Angell said it et al but the medical establishment is more concerned about “flogging drugs” than individual patient benefit!
You might like the following.
Data taken down from original site – WHY?
http://www.heartstats.org/documents/download.asp?nodeib=6797 This URL no longer exists?
Found it again:.
Click to access cholesterol-mortality-chart.pdf
Talk about a picture being worth a thousand words, that must be the most thought provoking set of graphs existing.
Thanks, have stored it up
Ik ben zelf Nederlander. Onze huisartsen worden op het matje geroepen als ze afwijken van de landelijke richtlijn. Deze richtlijn houd ook het voorschrijven van statines in. Blijkbaar zou gauw het cholesterol hoger dan gewenst is.
I do like the Dutch, but could I ask you to keep the discussion to English? Or provide and English translation. Thanks.
Translation: I am Dutch myself. Our gp’s are disciplined when they deviate from the nationbal directive. This directive stipulates the prescription of statins when the tc are higher than desired.
Interesting articles – what do you think Dr.K?
Many thanks for the links. I was aware of the association but the refs seal it.
Once again, Dr Kendrick, you have reduced a vast mass of information to a simple and logical conclusion. Brilliant! Now I don’t know whether in the future you will be proved right or wrong but I believe the former is far the most likely.
What I do not understand is why this early information was ignored and apparently still is. The same thing has happened with sucrose (Yudkin), blood pressure (Lancet. 2000 Jan 15;355(9199):175-80. Port S, Flawed Systolic blood pressure and mortality based on Framingham data..) cholesterol and goodness knows what else simply because of “current ideas” that have failed to look at past evidence have lead to research that has lead to drugs that affect what might be termed “incidental but mathematically associated” (surrogate data).
There is just something wrong with current medicine; the individual patient has been lost under the risk algorithms for this and that. Patients are being treated with drugs, not because they need them but because there is a remote chance that they may need them sometime in the future irrespective of whether the drug may cause serious harm (Starbridge B. JAMA, July 26, 2000—Vol 284, No. 4: US estimates of the combined effect of errors and adverse effects that occur because of iatrogenic damage)
Anne, ‘Doctoring Data’ contains quite a bit on blood pressure and it confirmed for me that I was right to avoid BP medication. My diastolic is 90. I think these number boundaries are nearly meaningless. If in doubt, don’t touch it, is my advice.
I have Doctoring Data yes, and it supports all my thinking too. My diastoic is like yours, around 90. The systolic is in so called normal range, around 110 to 130, sometimes higher – like when I got back fromt the GP and measured it ! I would not touch BP meds but I need ammo against the GP. I will re-read Doctoring Data, thanks for reminding me.
Anne, for ammunition to resist BP medication quote the analysis of the three reviews of the evidence quoted by Dr Kendrick in his online article. In short, no benefit. I believe the benefit needs to be very clear before we second guess our bodies with strong medication. So many people are on numerous drugs with no evidence on how they react with each other. This polypharmacy is a huge health problem. Very profitable, though.
A couple of days ago there was an interesting editorial in the BMJ on blood pressure targets in primary care. http://www.bmj.com/content/352/bmj.i813?etoc=
and a response at http://www.bmj.com/content/352/bmj.i813/rapid-responses
I wonder whether Dr Kendrick will respond.
I did respond and actually got some positivs responses
JD…duh, coagulant, not anti-coagulant 😦 everything I have read seems to indicate that K2 can be used with warfarin. Warfarin causes arterial calcification, so I can’t imagine that it helps to prevent CVD, however, my Aunt has been on it for years and she’s in her late eighties…
Insofar as I can ascertain warfarin is effective in about 4% of cases. It is “70% better” than aspirin which means aspirin is about 2.3% effective. Warfarin is therefore likely to give an individual a 1 in ~40 better chance of surviving. But the MHRA DAPs for both show warfarin kills more despite the fact the amount of aspirin used in humans must be vastly greater. Take your pick
A link to one of Dr. K’s other contributions here with a useful table. Perhaps the long term high seed oil intake explains the Russian and ex-Soviet experience? I haven’t found the figures for Japan to compare.
Lovely isn’t it the way the “dangerous saturated fat” data has been removed from the 2012 report. The honesty of medical science is now an issue. Ioannidis JPA (2005- Why most published research findings are false. PLoS Med 2(8): e124) said it. Prof. Peter Gotzsche said it; Dr Marcia Angell said it et al but the medical establishment is more concerned about “flogging drugs” than individual patient benefit!
Dear Dr. Kendrick what is you opinion on the next statement?HDL is good because it is a potent anticoagulant. Vitamine K2 at doses higher than 100 ug a day interfere with blood clotting. So taking Vitamine K2 is not good in preventing arteriosceloris.
You’re mixing up VK1 & VK2. Have a look at this for clarification http://lpi.oregonstate.edu/mic/vitamins/vitamin-K and this for how VK2 fits into the CVD scenario http://doctorkatend.com/
Regarding HDL, it is anti-coagulant – see this https://www.ncbi.nlm.nih.gov/pubmed/24891399 and this for a more generalized overview http://www.lifeextension.com/protocols/heart-circulatory/blood-clot/Page-01 , but, as Dr Kendrick says, not a very potent one.
If you are interested in reducing your risk of blood clots forming (without the risk of compromised clotting in the event of an injury that the std drugs such as warfarin may entail) have a look at this http://patientblog.clotconnect.org/2013/05/01/natural-supplements/ . There are plenty of natural foods that contain substances to reduce the risk of clotting but don’t expect to find extensive evidence as it is not in the interests of the pharmaceutical companies to research natural solutions that could impact drug sales. Vitamin E is often taken to reduce the risk of clotting but the interaction with VK1 needs to be taken into account see http://lpi.oregonstate.edu/mic/vitamins/vitamin-E . You may also find N-acetyl cysteine of interest see https://www.researchgate.net/publication/7173137_The_effect_of_N-acetylcysteine_on_blood_coagulation_and_platelet_function_in_patients_undergoing_open_repair_of_abdominal_aortic_aneurysm , http://gut.bmj.com/content/54/4/515.full and http://www.nature.com/scibx/journal/v4/n8/full/scibx.2011.214.html. For more general information on this useful supplement see http://www.lifeextension.com/magazine/2010/5/n-acetyl-cysteine/page-01
Thanks for your detailed response. I’ll definitely study the information.
I think your blood clot hypothesis is gonna run into problems when your fans realize saturated fat is prothrombotic. Help spread the word, doc.
Could you please supply the references to support this fact. My own view is that it would be difficult for any particular fat to be pro-thrombotic, or anti-thrombotic, as they do not tend to float about in the bloodstream. Regards.
P.S. Would you have a horse in this race, by any chance? Or a disclosure of interest to make? Just wondering, having read your comments on DISQUS.
Plenty of animal studies has shown that, I will give a reference of a recent study in humans tho
Bit in a hurry at the moment so I can’t find better references right now. Some sources indicate more of a neutral or negative effect from fermented dairy products. Otherwise positive effect from fiber, PUFAs.
Fats have multiple profound effects in our bloodstream, on endothelial function, insulin sensitivity, ldl receptor sensitivity, and so on.
Otherwise the biggest problem with this hypothesis is simply that plaque is filled with cholesterol esters, not platelet. From early fatty streaks and onward.
Suppose some would say being a vegan makes me biased. I think we all are tho, it’s just important to be aware of our biases to systematically work against them.
I am completely uninterested in animal studies on diet. Sorry, but they are just nonsense. If I were to feed my cat a vegan diet, what this prove…. exactly? That cats are obligate carnivores. Feeding mice high fat diets… just as nature intended no doubt. On another note, if you think that plaque is filled with cholesterol esters then, think again. The cholesterol found in plaques comes mainly from RBC membranes.
Yes, I would say that being vegan makes you biased. Having said that, I am more than happy to discuss evidence with you. However dropping in comments that add nothing to the discussion other than to vaguely insult readers of my blog does not add anything to any discussion. I do not have fans. What I have, I hope, is to have developed a bit of an on-line community of people who are willing to look at medicine and ideas and discuss things in an open and honest way. If you are willing to make reasoned arguments, backed up by evidence (evidence that can stand a bit of scrutiny), then fine. Finding a single reference…not fine. I can find any reference I want to support any position I wish to take.
Dr K, I admire your modesty, I really do, but you SO have fans. We all admire what you do and if they makes us fans, then so be it.
Warm wishes from a fan
Aren’t many of these animal studies as inappropriately-designed as one the early “studies” showing how “bad” cholesterol is? Rabbits (who as vegan animals would never naturally eat cholesterol) were fed large amounts of cholesterol in their diets. Not just cholesterol, but oxidized, rancid cholesterol. And then, there was a study where artificially-refined casein was fed to animals that normally would not consume this milk protein after infancy (and then only in a natural form associated with other nutrients produced by a lactating mother of the same species). One wonders sometimes what the “researchers” are thinking. Or if they ARE thinking….
Hi Johan – almost all that abstract was completely over my head but I would ask this question. Since the study involved obese adolescents did anyone consider the amount of sugar in all its varieties that they ordinarily consumed? I think it really, really matters.
I will just add this information regarding the source of cholesterol in plaques. ‘It is well known that the accumulation of cholesterol in atherosclerotic plaques can lead to plaque instability and subsequently result in acute coronary syndrome (ACS). Previous studies have suggested that cholesterol within plaques is mainly derived from apoptotic/necrotic foam cells. The cholesterol in foam cells is mostly esterified. However, the proportion of free cholesterol in atherosclerotic plaques is markedly high. Therefore, it is logical to suggest that cholesterol present in plaques might be derived from other sources. Arbustini et al. and Kolodgie et al. observed that erythrocyte membranes were present in the necrotic core of advanced atherosclerotic plaques. Further studies have shown that erythrocyte membranes contribute to a significant increase of cholesterol accumulation in atherosclerotic plaques, since these membranes contain large amounts of cholesterol. Thus, it is reasonable to postulate that erythrocytes are an important source of cholesterol in plaques.’ http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3497225/
Talking vegans I am on “the other side of the fence” as being a LCHF advocate.
What I though have noted here in Sweden, where LCHF is a very strong diet trend, is that vegans are rather militant and as far as I understand it they are today also considered ‘politically correct’ and it is very trendy to be a vegan. They are given great opportunities to fight “the meat eating” in the media. There seem to be a strong moral issue involved.
With interest I read the “Vegetarian Myth” by Lierre Keith who ruined her health by being a vegan for many years and who described the religious fervour involved among her sick fellows. According to Keith it was all about a moral stance and had nothing to do with health. After she left the vegan community she was viciously attacked when she was giving her public talks.
I just wonder why.
Isn’t the common opinion that it is the carnivores who are aggressive? My own experience is though that the mood swings runs together with the blood sugar swings and by avoiding the carbs they are much less pronounced. That might explain the vegan aggressiveness we note.
Thank you, Dr. Sjoberg, for letting us know that the “militant vegan” problem is as prevalent in Europe as it is here in the US. As an environmental scientist and organic farmer, I am appalled that they are given a “moral soapbox” they don’t deserve on any scientific basis. (disclaimer: I tried veganism many years ago, but staged back to omnivory). I have spent a lot of time trying to dispel nonscientific vegan myths on several US blogs. Some of these folks are not just militant, but vicious in their comments, wishing death and injury to omnivores (whom they characterize as “blood-mouthed carnists”). I have also wondered if some dietary deficiency underlies their vitriol. Beyond their anger, they have their own creation/evolution mythos, which is completely out of synch with anthropology/paleontology, and their own versions of chemistry and ecology. They also seem to thrive on cognitive dissonance — I always find it amusing that they refuse to use honey, because it “exploits” the labor of bees. But they have no problem eating any number of bee-pollinated veggies and fruits, produced by hauling bee colonies from field to field during pollination season, with no respite, to fertilize said crops.
I’m a fan… of reason, of honesty, of curiosity, of persistence in the quest for actual knowledge, of the willingness to share findings openly even when at risk of personal cost.
Yes. I’m with the guy who expresses this sort of stuff.
It seems I can’t reply to your last comment, I hope I will not mess up the comment order by replying to your earlier comment. Anyway.
I don’t agree animal studies are useless, they give us valuable information, but ofc the results need to be replicated in humans. This has been done many times tho. I was just short on time, like I said.
This article summarizes several in vitro, animal and human studies:
“Polyunsaturated fat has an additional antithrombotic action in the body when it is substituted for saturated fat in the diet.”
Click to access 87.full.pdf
As an example of original research:
“Twelve healthy male subjects were maintained on a saturated fat (SF) dietary regimen followed by a polyunsaturated fat (PUF) regimen. […] We conclude that a diet rich in SF, which is a feature of developed countries, may result in activation of circulating platelets. This, in part, may contribute to the initiation and development of atherosclerosis and thrombosis”
I see what you mean about how the RBC membrane cholesterol contributing to the cholesterol contents of plaque (despite giving only one reference for it). I don’t think there is support at the moment to say that it comes mainly from there, but we will have to wait for more data on it as far as I can tell. In any case, early fatty streaks are primarily cholesterol esters, and “Cholesterol concentration in erythrocyte membranes most likely reflects lipid profile over a long period of time” which is consistent with statins reducing CEM. Both facts which still harmonize with the current view of lipid targets.
Well, we should not get bogged down in that, point of my post was regarding the thrombotic effect of different aspects of diet.
Well, yes, animal studies can be hypothesis generating…to an extent. But particularly in the field of nutrition you have be very careful about feeding animals ‘alien’ diets and claiming that this will have the same effect in humans. With regard to fats and coagulation. What I know (and could provide many hundreds of references to support) is that VLDL is pro-coagulant and HDL is anti-coagulant. I know that a high carbohydrate diet (particularly in type II diabetes) raised VLDL and lowers HDL. I also know that a high fat diet lowers VLDL and raises HDL (in most people). Furthermore, I know that the country with the highest saturated fat intake in Europe is France, and I know that France has the lowest rate of CHD in Europe. The country with the lowest saturated fat intake (is/was) the Ukraine. And the rate of CHD in the Ukraine was/is the highest in Europe. I think that Omega-3 fatty acids appear to be anti-coagulant (and therefore should be good). Most importantly, I know that looking at one physiological aspect of any factor can lead you to ‘prove’ any hypothesis that you want to prove. Which is why I am very careful to say that there is no cause of CVD. We need to understand process.
But you have to look at the totality of the effect of a nutrient, not just focus on one aspect of it like HDL. An increase in HDL-C also doesn’t predict an increase in HDL functionality. Betting your heart health on a high HDL would be very risky considering the emerging evidence against that hypothesis, namely the genetic studies and the failure of HDL-raising drugs. Saturated fat is mostly coagulant, and that may very well be one of the reasons why they have higher mortality of CVD in Russia compared to fish-eating Japan. Along with higher social stress and excessive vodka consumption. On the other end of the spectrum, excessive consumption of anti-coagulant omega-3 may be part of the explanation why japanese suffer a higher incidence of hemorraghic stroke. Luckily for me as a plant eater, fruits and vegetables lower the risk of both ischemic and hemorrhagic stroke.
Talking saturated fats versus PUFA, omega-6 from vegetable oils I thought it was beyond all possible doubts that the omega-6 causes havoc in our immune system when taken in excess.
As far as I remember large quantities of vegetable oils was originally given to patients to have a kidney transplant in order to suppress their immune system so their bodies wouldn’t reject the new foreign organ. It was evidently a successful procedure but they had to stop the practice since the patients acquired cancer instead.
Very interesting paper (Zhong et al 2012). That there even is a “necrotic core” (second column, page 1) tells us how far the healing process has gone wrong, does it not?
References 5 and 6 from there make interesting reading too.
It is convenient that the glycophorins allow the origin to be tracked down so specifically.
Kolodgie et al paint a picture of a run-away process.
ps. “pultaceous” that’s a new word for me – seems to be like pulpy
Thanks for the reference (Saturated fatty acid intake can influence increase in plasminogen activator inhibitor-1 in obese adolescents.). It adds an interesting possibility to the discussion.
However, the paper itself is behind a paywall and the abstract provides no real data that one can consider. I note that the “cardiac risk” is increased in adolescents. but not information on how many actually had a heart attack. I would also point out that risk estimates are usually 90% wrong over a 10 year period. Thus in reality what does this “risk” actually mean.
They were divided into tertiles of SFA consumption, and from what I can read in the graph it’s about 6, 11 and 20 ng/ml in mean values. In a multiregression analysis, SFA was also a strong independent factor. I don’t know the clinical effect of those numbers. It’s not a prospective study, so they didn’t look at actual outcomes. Only the effect of SFA on thrombotic factors and other risk factors.
So we are left with an effect that may or may not be associated with any clinical effect than an assumption. Unfortunately assumptions like this often end up as fatal errors, like the assumption that strict bed rest was good whereas it turned out to be a killer.
The basic principles of physiology and endocrinology are relatively universal across species, and the species I have in foremost in mind, here, are those that are typically pink and fleshy.
The early species that came, with the passing of time, to populate land-masses included those that were cold-blooded. Being cold-blooded confined these species to warmer regions of our Earth, and was a barrier to ‘migration towards,’ and to colonisation of, higher latitudes further removed from equatorial regions. Warm blooded species (typically mammals, like ourselves) proliferated later, and it paved the way for pink and fleshy species with warm blood to colonise temperate and even frosty regions.
But the difficulties these pioneering warm blooded species faced as they began to take up residence in the land masses of higher latitudes is that there is far greater seasonal variation in the relative availability of food. Frankly as autumn advances and as winter approaches food becomes scarce, moreover it remains so until spring is well advanced. It has a lot to do with Earth being ’tilted’ on its axis, and to geographic and seasonal variations in the amount of incident radiation arriving on Earth from the sun. The energetics of natural food production is a variable, not a constant.
Hence species that inhabit ecologies where the energetics of food production is a variable and not a constant needed to evolve the means to cope with seasonal variations in the availability of food. Put simply, as a part of the trending emergence of warm-blooded species, and as a feature of these species moving to inhabit chiller latitudes with greater variation in the variability of food, and with particular pertinence to mammals, species began to evolve the means to put some food (or energy) aside as part of their preparations for winter. There is no one universal means to do this, but the business of energetics as applies to mammals above a certain size has it that it can be expedient for a warm-blooded creature to store energy as ‘condition’ (body-fat). So when the supply of food in winter fails to fully match the energy needs of a warm-blooded mammal in winter than the release of energy from its stores of body-fat can augment its supply of energy.
Although not true in every instance, many are the species (of mammals especially) where evolution has given rise to a physiology and endocrinology that drives hyperphagia (overfeeding) and hyperphagic habits when hypoerphagia is a real p ossibility (ie. in summer). More than one hormone is involved but prominent in the endocrinology that drives hyperphagia and the laying down of fat reserves is the hormone insulin. Unfortunately the ecology of habitats in which hyperphagia (overfeeding) has evolved to be commonplace cannot support hyperphagia all year round. Instead the decline in availability of food, due to cold or dry seasons, enforces the state of hypophagia (undefeeding). Without some form of preparation starvation would follow. Now it ought to be evident to you the extent to which hyperphagia, along with the physiology that drives it, is a viable and necessary evolutionary response to increased seasonal variation in the availability of food at higher latitudes, the very latitudes warm-blooded species can colonise that cold-blooded ones could not. Mammals of certain size can assimilate reserves of body fat because it expedient to do so, as much upon evolutionary grounds as upon the grounds of energetics that prevents starvations and keeps them alive.
Now that we have this evolutionary standpoint from which to judge the expediency of body-fats to many mammals we have a standpoint from which to concede that in the grand scheme of things an animal lays down body-fats (some saturated, some not) on the basis that that through the processes of lipolysis (release of those fats from adipose tissues) and ketosis those very same fats will be used as fuel to augment the lack of ‘fuel’ when food becomes scarce, typically in winter. In other words, amongst the reasons that animals have fat and have fat reserves is that they can be metabolised to good effect, an effect that represents the distinction between survival and extinction. The idea that animal fats are toxic to animals is childish and laughable.
The selection pressures that applied to the evolution of the human are not unique to us humans. Basic principles are common across bands of species. We have the same physiology that drives and might other whose reward hyperphagia, but those of us who live in the modern and western world do not experience the same food scarcities that might otherwise enforce hypophagia upon a seasonal basis. Hyperphagia can persist on a year round basis, and that, for physiological and endocrinological reasons, can well explain why the ease with which we can gain weight is far greater than the ease with which might lose it. For the person who has been overweight weight loss can only arise if a shift in endocrinological balance (fall in levels of the hormone insulin, and cortisol perhaps) will permit the necessary lipolysis (release of fats from adipose sites).
The notion that fats (with emphasis upon saturated fats or upon animals fats) could be angiotoxic to animals, in the face of this evolutionary standpoint, looks like it deserves scepticism, does it not?, for farts are highly expedient to survival. Like Dr Kendrick I am at a loss to perceive how fats could be prothrombiotic.
What I do know is that the evolution of the diet-heart hypothesis and the notion of saturated fats being angiotoxic owes a lot to the involvement of one prime proponent, Dr Ancel Keys. And what I believe to be the case is Dr Keys produced one or more studies that fuelled the notion of saturated fat being angiotoxic, but those studies were wanting for having a highly selective regard for available data, while the data used, in any case, was second rate for lack of standardisation in the methodologies given to collection and reporting (to WHO). Yerushamly and Hilleboe would later expose the shortcomings of Ancels Keys studies.
Furthermore, through having been obsessed by the early evolution of the diet-heart hypothesis I have trended to think that Keys was actively seeking an environmental factor (diet) that could account for hypercholesterolemia. He had come to think hypercholesterolemia could be atherogenic, it may seem, through having become aware (during the 1939-1945 conflict, possibly) of Anitchows and Chalatovs reporting of the first know instance of positive induction of atherosclerosis under experimental conditions applied to New Zealand White rabbits (their write-up was published in 1913 in German).
People are apt to be dismissive towards successful and unsuccessful attempts to induce atherosclerosis under experimental conditions but I think there remains a lot to be learned. Anitchow and Chalatov fed their rabbits upon feed doctored with added cholesterol, but they did this knowing next to nothing about cholesterol, nothing about its highly labile nature, and with absolutely no understanding of the range of oxides cholesterol can form. This lack of knowledge would represent a huge artefact (scope for confusion and misunderstanding) in their work. It almost didn’t matter, because their results did not create a stir. Only when Keys chanced upon it, perhaps three decades later did the artefact(s) make their presence known.
Research in earnest into the diversity of cholesterol oxides did not begin until the mid 1970s. Indeed progress only became more realisable after technologies such as gas chromatography emerged/ So when, circa 1950, Keys drew conclusions from the experiments that had resulted in positive induction of atherosclerosis he did so while not having the kind of regard for the lability of cholesterol we (could) have today. He knew nothing about cholesterol oxides — and he can be forgiven for that because nobody did. But having encountered the write-up of the work undertaken by the Russians, Anitschkow and Chalatov,, and having visited Russia in the post war era to meet with Russia researchers Keys seems to lean to regarding cholesterol as a concentration dependent atherogen. He then seems to lean to a view that a high fat diet positively leverages concentrations of cholesterol, going on to concoct one or more deceitful studies. The diet-heart hypothesis was born. It lacked the kind of provenance that decency can confer.
But in 1974 Hideshige Imai et al elected to further research the effects of cholesterol upon New Zealand White rabbits. They did so with a higher regard for the lability of cholesterol and the ease with which it was increasingly believed (by a few) it could autoxidise if exposed to air. Imai and his team began with some aged cholesterol and used an improved method to purify it. Hence they ended up with aged cholesterol, purified cholesterol, and a batch of cholesterol impurities extracted from the aged cholesterol sample. Then using gastric gavage as their method (chosen to offset risks of oxidation) they administered each of these to rabbits. After sacrifice of the rabbits pure cholesterol was observed to have had no effect, while the aged cholesterol and the extracted cholesterol impurities each gave rise to degeneration within arterial tissues consistent with the advance of atherosclerosis.
After Imai et al’s findings work proceeded in earnest to identify the nature of those cholesterol impurities. In all 49 alternate cholesterol oxides were identified. Up to 10 might arise in batches of cholesterol exposed to the oxidising effects of air, and amongst those are a number that give rise to effects that seem to sit neatly with those cytological changes seen in atherosclerotic tissues. A book, The Biological Effects of Cholesterol Oxides, edited by Peng and Morin, reviews the historical contexts and the advances of the work that followed Imai’s findings. Until you take the trouble to read it there will exist a great and significant gap in your knowledge.
There you have it Johan. The diet-heart hypothesis is something that rests entirely upon a highly significant artefact. For ‘artefact’ read ‘cock-up’. The nature of the artefact is that certain cholesterol oxides seem to have been responsible for the first known instance of positive induction of experimental atherosclerosis (in New Zealand White rabbits) and not cholesterol itself. Cholesterol is not nearly so injurious to cells as certain cholesterol oxides can be. Cholesterol is not a concentration dependent atherogen. Certain cholesterol oxides, perhaps under certain conditions, are demonstrably more injurious to cells and are more atherogenic than is cholesterol itself.
I suspect, Johan, you are more familiar with the myth that rose from the artefact, than you are familiar with the nature of the myth and/or how it came about. Furthermore, if you do not factor in how endocrine disturbance can contribute to oxidative stress, or how levels of oxidative stress can be countered, or how the developed world is replete with endocrine disruptors that have all but escaped notice and attention, then these gaps in your knowledge contribute to the extent to which you are satisfied by reductionism and the extent to which you are insufficiently holistic. For instance, what do you know about the electro-chemistry of thrombogenesis? I concede I know nothing. And why might it be evolutionary expedient for oxidative stress to be a link that might initiate thrombogenesis? If you cut yourself would you want to bleed forever?
There will be people who will look up to you for defending the diet-heart hypothesis, Johan, but there will also be be people who will read the thread and its exchanges who will hope that your participation here, and the replies that people have taken the trouble to cast your way will become the basis of a life-changing experience through which you become better able to distinguish myth from facts.
Thank you for taking the time to put together such a useful response.
What a breathtaking and awesome response!! Christopher, please may I have your permission to share your fabulous post on my FB page “I Love my Cholesterol”?
PS with or without “farts are highly expedient to survival” ? 😛
Beyond all the other faults with the research wherein “scientists” fed cholesterol-laden foods to rabbits is the obvious one, which other commenters have referenced: namely, cholesterol is an unnatural, completely foreign food for rabbits. They, being truly vegan, would never ingest cholesterol. One could as easily “prove” how harmful vegan diets are by putting, say, lions, on a vegan diet, and observing the deleterious impact on their health. Why did the cholesterol researchers not use an omnivorous animal, like rats, which are commonly used in nutritional research?
Dr K. – I absolutely love this community … It has made me a stronger person who can think further from what advise I have been given – And to be able to reasaerch what you deliver and others – thank you 😀
You mentioned that HDL is good because it is a potent coagulant. Vitamine K2 in doses of abbve 100 ug interferes with bloot clothing. So taking this amount of this vitamine in not good to fight atereriosceloris?
I think HDL is an anti-coagulant. But not a very potent one. I would think potent anti-coagulants would bring their own problems
Some deluded vegetarians and vegans do feed their dogs and cats a veggie diet. There was an article in the Sunday Times recently quoting a vet who said they were making their pets ill. Of course a well-intentioned but dumb lady dog owner commented that it was fine and her dog’s complete lack of energy was explained by his laziness. Nothing to do with her forcing her beliefs on her unfortunate and increasingly lethargic pet. These people are entitled to make themselves ill, but they have a responsibility to take better care of their pets. It’s odd that eating meat is wrong but slowly starving your pet to death is justified in a ‘good’ cause.
There is a US holistic vet, Dr. Karen Becker, who has an interesting blog on pet care. She has several times noted to her readers that, while she herself is a vegetarian (she did not say vegan), she considers it animal abuse to feed vegetarian diets to dogs and cats. Interesting that a vegan, who flaunts moral superiority in avoiding anything that causes any pain/sufferring to nonhuman animals, would cause pain and suffering to her pets by feeding them a vegetarian diet. Of course, there are many vegans who believe it is immoral for humans to have pets, since they view it as another form of animal exploitation.
Annie, The only way to understand the fanatical wing of vegetarianism and veganism is to see it as a religion. I think their behaviour then makes sense. Their self righteous assumption of superiority and the breathtaking gaps in logic. How it’s pointless to argue facts with those who believe and have stopped listening. They see meat eating as wrong, so they are the good guys and that justifies their sometimes unpleasant behaviour and easy distortion of facts. As a number of people have said, health has nothing to do with it, but it’s used and abused as a way to influence people unconvinced by the moral argument. So, fixed mouse and rat studies are trotted out to convince us that meat eating isn’t good for us. These studies never stand scrutiny but they still make headlines.
There’s a debate on YouTube between Nina Teicholz and an ill-mannered vegan. She politely quotes the science and he can’t compete, so resorts to what he just knows and believes. They are zealots who, if truth were told, would like to impose their views on others.
Stephen. I think Johan is entering the debate in a reasonable way. I think we need to accept that many vegans are reasonable, and reasoned. There are always fanatics out there, but we should not – I think – tar them all with the same brush.
Wow, apparently I offended Dr Kendrick by calling his readers “fans”, but after mentioning the “v-word” you guys just pile it on. All these things that you are speaking about, I have had exactly the same experiences speaking with meat-eaters or low-carbers. This is a human quality, nothing specific to a chosen diet. I have now provided plenty of evidence from human studies about the thrombotic effect of fatty foods, but it’s easier to just brush it off as propaganda.
Johan. You are being disingenuous, at best. Your comment was ‘I think your blood clot hypothesis is gonna run into problems when your fans realize saturated fat is prothrombotic. Help spread the word, doc.’
The moment I read that I knew that you were a vegan. I just confirmed it by looking you up on the Internet. Your comment had a particular, and clear, purpose.
I have no problem with criticism. I have absolutely no problem with vegans. I love a good argument. Where I do have a problem is when people choose to enter a discussion in a deliberately provocative way.
Whilst it was a clever ‘political’ comment. It was a extremely unhelpful scientific comment. It also carried a transparent purpose.
However, I am delighted that you have decided to enter the discussion. I will try to keep the debate as scientific as possible.
I admit I was being snarky, I’m just saying that all these comments about delusional religious militant vegan zealots could be called worse. But to quote Monty Python; “let’s not bicker and argue about who killed who”.
Heart disease is complicated, much like everything else in medicine/biology, with no one simple answer, although it depends quite a lot on the questions being asked. I too have been puzzled for many years and been in and out of more rabbit holes than I care to remember!
Malcolm pointed out that the condition Systemic Lupus Erythematosus (from which my nearest and dearest miraculously recovered many years ago) massively increases the risk of developing heart disease due to atheromatous plaques. These patients are usually young women, a group not normally at any risk. So why is that? The same is true of some other conditions in which a chronic inflammatory state exists within the body. Increasing age is also implicated – the older we get, the greater the risk of heart disease. This is exemplified in the rare genetic Progeroid syndromes (Hutchinson–Gilford Progeria Syndrome and Werner syndrome) in which patients age prematurely, and die very young, usually from heart disease. This isn’t due to inflammation directly, but to a genetic inability to repair damaged DNA (every time our cells divide and multiply they are prone to damage – that’s life!). These are big clues as to what is going on and why these atheromatous plaques develop.
The endothelium and the underlying (smooth) muscle layer of arteries are subjected to either inflammation or DNA damage, probably both. There are many causal and associated factors, for example Type 2 Diabetes as a result of Insulin Resistance, partly due to the effects of inflammatory cytokines (eg IL-6, TNF). These increase PAI-1 levels, as do VLDL/triglycerides, Leptin, ‘loads of other things’, and importantly cell senescence (old cells, not dead yet, but aged and worn out, though still some life left in them…I know how they feel!!), either directly or through inflammatory mediators.
In response to inflammation more fibrinogen is produced with the subsequent effect on the clotting system and increased risk of heart attack, as Malcolm has explained (high fibrinogen levels and high PAI-1 is not a good combination).
Cells age. We age. Unfavourable conditions (smoking, insulin resistance) can speed up this ageing process. Damaged cells either die pretty quickly or become senescent. Senescent endothelial cells and vessel-wall muscle cells, together with oxidative stress and DNA damage, leads to raised levels of pro-inflammatory cytokines resulting in further damage to the endothelium and vessel walls and progression of atherosclerosis, raised PAI-1, unstable plaque and clot formation, and even aneurysms. Damaged endothelial cells fail to secrete protective nitric oxide amongst other things. Non-laminar blood flow also leads to dysfunctional endothelium.
Ageing inevitably comes together with chronic low-grade inflammation, which leads to age-related inflammatory diseases such as atherosclerosis. How quickly depends on your genes. You can’t do much about this, but you can counter this inflammatory state by encouraging / nurturing anti-inflammatory factors. That’s another story, but in the meantime, eat your greens and oily fish, exercise, stop smoking, keep your weight down, avoid stress, eat low-carb diet, avoid processed foods, supplement with vitamin C, and get out in the sun. Like I said though, it’s more complicated than that.
If HDL is anti-coagulant, then is LDL a
How come no aspect of the diet has been touched upon yet in terms of being coagulant and anti-coagulant?
VLDL and LDL (especially oxidised LDL) and Lp(a) are pro-coagulant, and HDL is and anti-coagulant.
Dr Kendrick. I have just finished reading a Greek study of cholesterol in the membrane of erythrocytes “Total Cholesterol Content of Erythrocyte Membranes
Is Increased in Patients With Acute Coronary Syndrome” and of course, their conclusion is that statins do a marvellous job of decreasing the amount of cholesterol in RBC membranes…quelle surprise!
Your initial comment is not only insulting to this forum and to the work of Dr K. It is insulting to myself and a great number of people who seek discussion on important issues.
You are welcome to participate and add comments but you have to come up with the goods and show the full references to gold standard research. Not random studies or ideas, or dictatorial beliefs. That frankly is how we are in this mess with doctors prescribing drugs to control and limit what the body has evolved to do for the purpose of healing and survival.
Dr Kendrick is internationaly respected and whilst as you can see from his response he can fight his own corner in any debate, he may not praise himself enough for his dedicated work.
I am happy to spend time looking at all the possible views. However don’t insult me with one liners, show me the hard research and put money on your horse.
Il y a quelque chose de plus puissant que la force brutale des baïonnettes: c’est l’idée dont le temps est venu et l’heure est sonnée
has to be said though, animals are sentient beings and factory farming is abhorrent. Farm animal welfare, humane treatment, end to transport of live animals does matter. Sorry, don’t mean to add to this diversion, probably stating the obvious. My family are meat eaters. Animals should be killed near to the farm of rearing, only carcasses transported, worldwide.
Yes Sylvia, and I too apologize for going off topic but I agree that the animals should not be distressed. We used to rear a few beef cattle but had a slaughter man to do the kill on our premises. The animal was stunned whilst enjoying lovely fresh hay. Then regulations came along and made home slaughtering well-nigh impossible.
I would add that if we all went vegetarian we’d have to go to zoos and animal parks to see the animals. Can you imagine bulls, rams, stags and boars being allowed to charge around the countryside and across roads?
Sylvia, I’m a meat eater too and also support higher welfare standards and try to buy accordingly. One very keen vegetarian told me she wasn’t very interested in raising welfare standards because it undermined the don’t eat meat argument. All or nothing for her.
Maybe you didn’t read my third comment because of the time lag in comments becoming visible? I have given several references for it, otherwise just search for it yourself if you don’t believe me, it’s not hard to find.
I will add another reference just in case, here an experiment in France, comparing two regions with different saturated fat intake and different clotting time, which confirmed this relation. They also did a diet intervention which showed a reduction in SFA in the high SFA group increased clotting time (lowered thrombotic activitity) p129
Avoiding venous thrombosis is done by very mainstream advice, like eating fruits, vegetables and fish in favor of red and processed meat. Ofc, venous thrombosis is not the same as intraplaque hemorrhagic accumulation of red blood cells, which was the topic of the post, but I’m just arguing that SFA is pro-thrombotic
I doubt whether any commenters on this blog would disagree about the value of the omega 3, 6 and 9. but omega 6 if not in a 1-2 to 1 ratio with omega 3 is not good. These three PUFAS are all available in animal based diets. (Fish are part of the animal Kingdom) . On the other hand, omega 6 oils are in the heavily promoted vegetable oils.
May I suggest that you also check out Dr Michel de Lorgeril the lead investigator in the Lyon Diet Study; so far as I know this is the only lifestyle study that actually demonstrated a true cardiac benefit in humans – no animals, no surrogates
I’m not saying that fish is vegan. I’m saying that saturated fat is pro-thrombotic, while omega-3 from for example fish is anti-thrombotic. Maybe you think I won’t speak about the health benefits of fish since I’m vegan, but that’s not the case. However, skipping the fish for more plants will just do you good, as seen in the AHS-2 study where fish eaters enjoyed an intermediate protection. But everyone has to choose themselves where they want to put their risk level. The lyon heart trial was successful for these same reasons.
I think the vast amount of randomized controlled trials show little if any benefit to eating plants. For instance, in the Women’s Health Initiative trial, where 59,000 women were divided into two groups, and where the women in the test group ate more fruits and vegetable, less overall fat, less saturated fat, less red meat, and fewer calories, at the end of eight years, there was no statistically significant difference between the test and control groups, for ANYTHING — not heart disease, not cancer, nothing. Since this was such a massive RCT, there should be some benefit. Yet there was not.
And the same could be said for fiber and many other parts of plants: RCTs continuously show poor results for plants.
Moreover, if you want to eat something healthy, eat chicken liver. Chicken liver is fantastic relative to “plants” like kale:
I’ve been following a low carb diet for over two years now. I currently eat as much fat and particularly animal fat as possible every day. I’ve lost about 50 pounds, and have many other beneficial effects happen. Too many to list really. I find it difficult to believe that the diet I’ve been eating to cause me to lose so much weight and feel so great will somehow kill me simply because it has some saturated fat in it (and note that meat also has a high quantity of monounsaturated fat in it).
Further, to the extent that you use epidemiological studies to prove anything, these are worthless.
I’ve been reading Dr. Kendrick since my doctor wanted to put me on statins. I read up on them, and threw the script away. The same doctor put my sister on statins, and she takes them religiously. Now we’re in a race to see who dies first (we are both in our 60s).
But the statement “plaques are clots and clots are plaques” confuses me. One of the problems seems to be that terminology is used by medical researchers rather indiscriminately.
For instance, atheroma, plaque, and thrombus — are they all the same thing?
On Wikipedia I read “An atheroma is an accumulation of degenerative material” containing white blood cells, debris, cholesterol and fatty acids, calcium and fibrous connective tissue. Nothing about platelets. So it seems to be different from a clot (thrombus).
Atheromas do not form in veins. Dr. Kendrick says this is because they form as a result of blood velocity or turbulence, which is high in arteries but not in veins. The disturbed blood flow damages the lining of the artery (endothelium) which causes an atheroma to start. So it seems to be like a clot but why does it have a different name?
Atheromas can get hard (atherosclerosis) and break off.
As atheromas grow, the artery enlarges (forms an aneurism) to compensate for the extra wall thickness and this keeps the artery’s diameter unchanged. Up to a point. The endothelial lining over the atheroma can get damaged, and a clot can form on top of the atheroma and block the artery.
A thrombus (clot) starts when endothelial damage exposes the underlying tissue which contains TF which encourages platelets to gather and a clot to start forming. A thrombus can form in a vein as well as an artery, because veins need the capacity to heal themselves. (cf Deep Vein Thrombosis)
Causes of injury to the vessel’s wall include trauma, surgery, infection, or turbulent flow at bifurcations A thrombus which has formed at the site where an atheroma has broken off, damaging the endothelium, is called an atherothrombosis.
An embolism is formed when a broken-off atheroma or thrombus (or something else) lodges in a blood vessel (usually an artery), blocking it.
A blood vessel can also block when a clot (thrombus) grows too large, constricting it at the site of the clot. (Which begs the question: how does a clot “know” when to stop growing?)
Thrombosis = the action of forming a blood clot/the presence of clots indicating disease.
Atheromatosis = the presence of atheromas indicating disease.
Plaque = atheroma or thrombus which has got hard?
(Not sure of these.)
Platelets are present in early stage fatty streaks.
A fatty streak is the first grossly visible (visible to the naked eye) lesion in the development of atherosclerosis. It appears as an irregular yellow-white discoloration on the luminal surface of an artery. It consists of aggregates of foam cells, which are lipoprotein-loaded macrophages, located in the intima, the innermost layer of the artery, beneath the endothelial cells that layer the lumina through which blood flows. Fatty streaks may also include T cells, aggregated platelets, and smooth muscle cells. It is the precursor lesion of atheromas that may become atheromatous plaques. https://en.wikipedia.org/wiki/Fatty_streak
Wait… what? You say streaks are the FIRST “VISIBLE” sign. (How are we looking?) That must be AFTER the clot formation, after progenitor cells provide new endothelial cover, and after at least partial resolution of the “clot” which would leave red-cell-wall-stuff behind.
Did I follow that correctly?
visible to the naked eye, at least.
Interesting that it’s a “streak”. When pipes rupture because of freezing the break is longitudinal, i.e. in the form of a streak.
I’m presuming that for a streak to form, a local pressure pulse stretches but does not break the muscle wall, tearing the epithelium longitudinally, which then heals leaving a visible streak.
And in today’s med news we find:
MPT: CardioBrief: Triglycerides Cause CV Disease, Genetic Studies Say
We don’t get past the first paragraph before the corrupt consensus medical agenda rears its ugly head: “If fully validated, the new findings could lead to new drugs to prevent and treat cardiovascular disease…”
Even if we presume there’s some credence to the TG conjecture, it is TRIVIAL to lower TG with diet. What diet? Well, not the disastrous diets recommended by all consensus authorities.
By the end of the 1950-th it was clearly demonstrated that CVD patients had a disastrous ‘lipid profile’ i.e. high triglycerides, and this was due to excess carbohydrate consumption. Om top of my head I can though not remember who the famous researcher was. He was known to always carry a tube with milky blood serum along in his pocket. Anyway, with time his research was completely ignored in favour of the saturated fat dogma.
Can someone enlighten me! Triglycerides are esters of glycerol and fatty acids – i.e. fats – so how is it that eating saturated fat (or any other kind of fat) doesn’t raise blood triglycerides?
Hi David Bailey, I’m thinking back to my Biochem days and research since. I believe the serum triglyceride level is actually a measure of VLDL that is produced by the liver (which is a proxy for triglyceride levels?). When fats are consumed in the diet and absorbed they are transported via chylomicrons to the tissues…I think triglycerides are measured in the fasted state so that the dietary fats do not confound the measurement. Dietary carbs suffer a different fate. If they are not used for immediate cellular energy needs and after muscle/liver glycogen stores are topped up, the liver converts the excess to triglycerides and exports to the adipose tissue as VLDL. I think this is why people say that consuming carbs leads to an increase in triglycerides. As a slight aside, the level of fatty acids and glucose in the serum at any given time is controlled by many factors including insulin, glucagon, cortisol, adrenaline, as well as the inhibition/activation of enzymes in the key pathways (such as glycolysis, lipogenesis) by molecules such as cAMP, substrate level control, and phosphorylation. What I don’t understand is why the measurement of triglycerides (the VLDL measurement) is important (perhaps someone else can answer that).
This is a very interesting discussion. Johan Wallström argues “that that SFA is pro-thrombotic”.
Then how to explain ” The Inuit Paradox – High Protein & Fat, No Fruits/Vegetables and yet Lower Heart Disease and Cancer” (http://www.theiflife.com/the-inuit-paradox-high-fat-lower-heart-disease-and-cancer/) . This group of people eat primarily only (saturated) meat and fat, very little fruits and vegetables and are healthier than any other group of people?
The problem with conventional medicine is that offers very simple explanations for complex problems such as CVD. Cholesterol, saturated fat, etc. are too simple explanations. We must make an effort to integrate all the existing knowledge about CVD to find an explanatory framework for the resolution of the problem.
That’s what I appreciate the scientific attitude of Dr Kendrick. Plus, I admire his humility in sharing his doubts and hypotheses with this community, which is the characteristic attitude of a true scientist.
Inuits eat plenty of anti-thrombotic fish. Although I’m not saying that would be the main determinant of CVD. They also do have genetic adaptions to their high fat diet. I think the claims of their good health have also been exaggerated. Some studies have shown that they do suffer high incidence of cancer and CVD. Other people have been writing about that, I’m sure you will find opposing views if you look for it, and then you can judge if their arguments are valid. I have not read a lot on the topic myself, so I wouldn’t be able to argue for that view.
I’m totally aboard on the idea that there is multiple factors involved in CVD, although I would claim no other factor can work on it’s own without elevated cholesterol (for a reference, seek out the normal cholesterol levels of other mammals).
Or, the normal blood sugar level of a hummingbird?
Published serum cholesterol values in captive western lowland gorillas (Gorilla gorilla gorilla) are much higher than human ranges, with a national mean of 7.36 mmol/L (284 mg/dl, n = 863) http://www.ncbi.nlm.nih.gov/pubmed/17312789
Dear Dr K,
This thing is difficult enough to understand, I hope we are not going off into dietary, vegan vegitarianism. Anyone who has read your blog for any time will have been struck by the varied nature of the comments, and of the number of people who have found a solution to their problem, which proves to me, that it is multi-factorial, and that there is no one solution.
Mikecawdery’s graph showing an apparent correlation TC/life expectancy proves it to me.
Now lets here how to avoid breakin-off clots!
Johan, ” Brown bears (Ursus arctos) seem resistant to atherosclerosis despite highly elevated plasma lipids during hibernation and active state.” (http://www.ncbi.nlm.nih.gov/pubmed/22686205). Their TC levels goes as high as 600 mg/dl during hibernation. “No atherosclerosis, fatty streaks, foam cell infiltration, or inflammation were seen in any arterial samples. Brown bears tolerate elevated cholesterol levels, obesity, physical inactivity, and circulatory slow flow during hibernation without signs of -atherosclerosis. This species might serve as a reverse translational model for atherosclerosis resistance.”
I believe that you are too influenced by the dominant thought. It has never been effectively proven that cholesterol was a factor that causes heart disease, although it may have a role in this process. And in case there is an association with high cholesterol, you can not tell if high TC is the cause or the consequence of CVD. Statins lower TC but not reduce, at least in the same proportion, the rate of heart disease. Open your mind to other clues about CVD. You can be looking at the tree and not see the forest.
Great find Antonio. I think that completely sinks the argument that we should look at other animals to determine a healthy choelsterol level in humans.
Nah, generally they are much lower. Captive animals have much higher TC than wild life, this has been shown in direct comparisons in the same species. Mammals is ofc a better reference than hummingbirds.
Well well, we are going on tangents. I will leave you guys to it, have fun and thanks for the chitchat
Directed at “António Heitor Reis” post regarding brown bears:
“The transient hypercholesterolemia of major weight loss”, Stephen D. Phinney et al., Am J Clin Nutr, 1991, 53:1401-10, http://ajcn.nutrition.org/content/53/6/1404.abstract
This could be the case in hibernating bears as well, no? The lack of dietary carbs during fasting / hibernation dictates low insulin levels, so no insult coming from that side. Interestingly, bears don’t go into ketosis during fasting as humans.
“PHYSIOLOGY OF HIBERNATION IN BEARS”, ERIC C. HELLGREN et al., 1998, Ursus 10:467-477
Click to access Hellgren_Vol_10.pdf
Did we get anywhere forward by this ‘friendly visit’? From Sweden?
By the way, did he advocate the ‘cholesterol hypothesis’ or not? i couldn’t figure that out.
Oh yes I do, hyperlipedemia seems to be a necessary component to promote atherosclerosis. For example, smoking is not a strong risk factor for people with very low cholesterol. I don’t know any situation when it can occur without elevated cholesterol. But that’s not to say that many other factors can contribute too; diabetes, AGEs, ox-LDL, smoking, alchocol, some infections and so on.
Actually I just wanted to write a last comment regarding the bears. I would believe that is because of reduced blood pressure during hibernation. Shear stress is a necessary factor, as can be seen in the fact that atherosclerosis forms in arteries, but not veins. That’s one possible factor, together with ofc that they might have special adaptions to higher cholesterol during hibernation. There’s just a lot of things going on in that state so it’s probably a special case that needs to considered by itself. No need to toss out the fact that other mammals usual do have lower cholesterol. Which is true also for newborn humans, hunter/gatherers, and other low risk populations.
Click to access Hellgren_Vol_10.pdf
Johan, if cholesterol is a necessary component, why do the countries with the highest cholesterol have the lowest rates of heart disease?
Is that a coincidental correlation?
But hunter gatherers eat whatever meat and its fat that they can get and a variety of other things, but not a lot of grain type carbs or sugar.
Since CVD causes a fair percentage of total deaths, I wonder how you square your belief in the cholesterol hypothesis with this set of results:
In country after country, studies have shown that those with high blood cholesterol live slightly longer on average.
BTW, Like you, I am a programmer, so I like data like the above because it skips all the biochemistry and gets to the bottom line – how long people live!
As iI understood it:
Saturated fat, kills you
Cholesterol, in the atheromes
Plants and fish, parousia
So the answer to your question, no further forward.
A second thought about this “guy” who now seems to have disappeared.
Is it an honest ‘fight’ he is delivering which is indicated by his ‘open’, not uncommon, Swedish name. His comments were a little bit to ‘professional’ for my taste so I got a bad feeling here. His initial and final impertinent remarks added to that unpleasant feeling.
One shouldn’t be naive when considering the money which is hiding behind the cholesterol hypothesis. In Sweden we have had some unpleasant experiences with well versed “guys” popping up at our alternative sites with seemingly open identities and thus being abel to fool some visitors but when asking about their ‘open’ identity they usually evaporates which indicates with a proper salary.
But, as always, if it is an honest ‘guy’ I must apologise beforehand, although I have not yet been forced to do so on similar encounters and the follow up questions in Sweden.
I have a son who is prof of Thermodynamics in Sweden. I thought you swedes were very consensual?
About Johan W, I too searched him on Google, read his comments on other fora, and reached my own conclusions
Besides I like pseudonyms rather than faked names – then you are at least open with your “anonymity”.
“I thought you swedes were very consensual?”
Still we are few who believe in science. But I agree that we are not many today.
I haven’t “Googled” him myself.
So what did you find out?
My wife got interested and she found this morning a guy with his name belonging to a group of “Physicians for the Future” who are militant “Vegan Fighters” and this sounds more probable than a programmer though. (Evidently a sister organisation to PCRM (Physicians Committee for Responsible Medicine) ) Still you seem to be able to be become a member of this exclusive club even if you are not a physician so why not?
Evidently he carries a ‘religious’ mission to fight LCHF-adherents judging from the large number of posts people have observed in his name on our blogs (I haven’t read any of them myself – try to keep away from those scholastic fights with their religious dead ends!) and in papers and as he admits the defence of the cholesterol hypothesis seems to be an integral part of the mission. Well the vegans are in the media lime light today and get their hugs from the establishment.
We learn a lot now.
But what about sponsorships here?
There must be a lot of money around for your support if you are on the barricades in the defence of lowering the cholesterol in our blood and bodies. Mouth watering perspectives indeed!
Well – he could perhaps tell us about any support activities involved since he ‘seems’ to very ‘open’? Or is it as with the Coca-Cola sponsorships – it has to be revealed by outsiders?
I am not in favour of any naivety 🙂
There are too many dead on the medical battlefield for my comfort.
Hi there Goran
Pseudonyms: I don’t have a problem, my full name is Chris Harvey.
Johan, well I found someone with the same name on several fora, including the BMJ, with the same approach, i.e unsubstantiated assertions in a dogmatic manner. I am against internet trolls, they ruin discussion, which I think is their aim. His commenting manner on other fora led me to believe he had some form of medical background, which would fit your theory.
I am a believer in people taking a responsibility for their health, in understanding what is happening to their bodies, so a blog like Dr K’s is wonderful, I have learnt a lot from it.
Göran, would you please stop spreading unfounded rumors about me? I have already stated I do not have anything to disclose. It’s really quite offensive. Stick to the facts instead of trying to dig up dirt on me.
My own approach is to take people at face value, and believe what they have to say.
Eh, no, not professional, just another random guy with “CVD-OCD”. Work as a programmer
My diet keeps your numbers so low you don’t need pharma, so that accusation doesn’t make much sense to me. I’m following the discussion, I just don’t want to get too bogged down in tangents, since the science of diet-heart is so vast.
If your numbers don’t mean that much (e.g., people with “high” cholesterol live just as long as people with “low” cholesterol), what’s the point in keeping them low?
Glad to see you raise this point. Many commentators say they don’t take statins, and their readings are good, but judged by the the cholesterol/CVD theory. This seems to me to indicate a lingering suspicion that the doctors are right.
My own position is different, I gave up Statins, my cholesterol went back to the average for my country of residence, Belgium,, whose saturated fat consumption and CVD figures mirror those of France. Nature, evolution or God has programmed my body like that, and presumably it knows best.
Well, that would be a good question, if the premise was true. But studies on life long exposure to high cholesterol is clear.
Several lines of evidence do show that a cholesterol below 150 or ldl-c below 75 keeps you safe from atherosclerosis. I would claim this is not actually low cholesterol, but normal cholesterol. As compared to hunter/gatherers and what not.
Johan. A study in the USA demonstrated very clearly that people with LDL of 70 still have MIs. There are very few people who have MIs with very low LDLs – equally there are very few people who have an LDL below 70. So, you are not safe from atherosclerosis. You are most certainly not safe from dying prematurely. Study after study has shown that those with lower LDL levels have shorter life expectancy. Hononulu, Voralberg, etc. This is an effect seen at all ages and in both men, and women. This hunter gatherer meme is also untrue. Those who have studied the most ‘primitive’ peoples e.g. those living in the Brazilian rain forests, have total cholesterol around 4.5mmol/l. A bit lower than those in the civilized west, but certainly nowhere near your figures. (Could I ask that you used mmol/l rather than mg/dl as this keeps the figures a bit easier to understand for most readers). As may also know, or not know. In Japan fat consumption has gone up 400% in the last fifty years. Total cholesterol has risen from 3.9 to 5.2mmol/l. Rates of CHD have fallen 60% and the rate of stroke is now 1/7th that previously.
Also. Personally I am not that bothered about referencing, unless you are going to make an extreme claim. You can find any reference you like, to support any position you care to take on this subject. Most (as Ionnadis would tell you) are subject to enormous bias.
The following studies suggest that I was right (or, at the very least, not wrong). That is, “high” levels of cholesterol are correlated with longevity, and the older we get the stronger the correlation becomes, especially for women. Thus, if cholesterol is seemingly protective for older folks, why wouldn’t it be protective for all ages? That suggests to me that something besides cholesterol is at work here. Hopefully, Dr. Kendrick is zeroing in on what that might be. In the meantime, I simply can’t understand why anyone over, say, 60 years of age, would want to lower his or her cholesterol, especially artificially (i.e., statins).
Kozarevic D et al. Serum cholesterol and mortality: the Yugoslavia Cardiovascular Disease Study.Am J Epidemiol. 1981 Jul;114(1):21-8.
Rudman D et al et. Antecedents of death in the men of a Veterans Administration nursing home. J Am Geriatr Soc. 1987 Jun;35(6):496-502.
ForetteB et al. Cholesterol as risk factor for mortality in elderly women. Lancet. 1989 Apr22;1(8643):868-70.
Staessen J et al. Is a high serum cholesterol level associated with longer survival in elderly hypertensives? J Hypertens. 1990 Aug;8(8):755-61.
Harris T et al. The low cholesterol-mortality association in a national cohort. J Clin Epidemiol. 1992 Jun;45(6):595-601.
Casiglia E et al. Predictors of mortality in very old subjects aged 80 years or over. Eur JEpidemiol. 1993 Nov;9(6):577-86.
Krumholz HM et al. Lack of association between cholesterol and coronary heart disease mortality and morbidity and all-cause mortality in persons older than 70 years.JAMA. 1994 Nov 2;272(17):1335-40.
Weverling-RijnsburgerAW et al. High-densityvs low-density lipoprotein cholesterol as the risk factor for coronary artery disease and stroke in old age. Arch Intern Med.2003;163(13):1549-54.
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Räihä I et al. Effectof serum lipids, lipoproteins, and apolipoproteins on vascular and non vascular mortality in the elderly. Arterioscler Thromb VascBiol. 1997 Jul;17(7):1224-32.
Behar S et al. Low total cholesterol is associated with high total mortality in patients with coronary heart disease. The Bezafibrate Infarction Prevention(BIP) Study Group. Eur Heart J. 1997 Jan;18(1):52-9.
Fried LP et al. Riskfactors for 5-year mortality in older adults: the Cardiovascular HealthStudy. JAMA. 1998 Feb 25;279(8):585-92.
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Schatz IJ et al. Cholesterol and all-cause mortality in elderly people from the Honolulu Heart Program:a cohort study. Lancet. 2001 Aug 4;358(9279):351-5.
Weverling-RijnsburgerAW et al. High-density vs low-density lipoprotein cholesterol as the risk factor for coronary artery disease and stroke in old age. Arch Intern Med.2003;163(13):1549-54.
Onder G et al. Serum cholesterol levels and in-hospital mortality in the elderly. AmJ Med. 2003;115(4):265-71.
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Ulmer H et al. Why Eve is not Adam: prospective follow-up in 149650 women and men of cholesterol and other risk factors related to cardiovascular and all-cause mortality.J Womens Health 2004 Jan-Feb;13(1):41-53.
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Akerblom JL et al. Relation of plasma lipids to all-cause mortality in Caucasian, African-American and Hispanic elders. Age Ageing. 2008;37:207-13.
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I think you will need to separate between the two issues of cholesterol/CVD and cholesterol/mortality. For example, your first reference does say that high cholesterol meant higher risk for dying in CDV. So diet-heart is confirmed again. Now, for cholesterol/cancer connection, that’s another thing. I would say it’s reverse causation. Having cancer will make your cholesterol drop. Therefor low cholesterol becomes a marker of bad health, and will therefore be associated with higher risk. Or, you can also hypothesize that cholesterol protects against cancer. So which one is true? Well, just as in the case with CVD, the genetic studies of life long exposure gives us the correct answer for that association. They are very strong evidence, since they avoid all the normal types of confounding, and can show the effect of life-long exposures.
“Low plasma LDL cholesterol levels were robustly associated with an increased risk of cancer, but genetically decreased LDL cholesterol was not. This finding suggests that low LDL cholesterol levels per se do not cause cancer.”
But even if this was not the case, we still have to face the possibility that a high cholesterol can be damaging for the arteries and protect against cancer. Both can be true at the same time. In the case with cancer, I don’t think it is, the evidence speaks against it, and actually there is even fairly strong evidence that it is a risk factor for some specific cancers, like breast and prostate cancer. However, there might be a protective role of high cholesterol when facing a septic shock. It has been shown in rats that injection of lipoprotein protects them from the harmful effects of a subsequent injection of endotoxins (the bad stuff coming out of dead bacterias). But I don’t see a reason to go around with life long high cholesterol because of that. Maybe for sick elderly, who knows.
Johan. You are recycling arguments that have long been disproven. The Austrian study over fifteen years, in eighty thouand people, found that low cholesterol was associated with higher mortality in all groups. This was in ages from 15 – 90. The only group where this was no found was inart from younger me, where the mortality was the same at high, or low, cholesterol levels.
Causes of increased mortality in low cholesterol levels were, infections, and cancer (mainly). The Framingham study demonstrated that a falling cholesterol in the firs 14 years of the study increased overall and CV moratlity over the next 18 years of the study. A five hundred per cent increase is CVD deaths for each 1mmol/l drop in total cholesterol. This cannot be revere causation (an unproven ad-hoc hypothesis). There is no form of cancer that will lower cholesterol many years before it can even be detected – or even exists. Low cholesterol in cancer occurs in later stages. But early stage cancer does nothing.
There is also another issue here. You can only die of one thing. If deaths from cancer and infections go up, deaths from CVD will go down – and vice-versa. The only truly robust measure of importance is overall mortality a.k.a. how long you will actually live. The evidence is very clear. Those with lower cholesterol levels die younger. The difference is not huge in absolute terms, but it exists. It has been seen in study after study, and I have never seen any study contradicting this finding.
I disagree, the modern mendelian randomization studies give us the clear answer on the cancer/cholesterol connection, although I do understand your argument about that different causes will be inversely associated. This would work towards increasing the apparent association between low cholesterol and cancer, since the genetic studies did show increased risk of cvd, but not of cancer, from high LDL. I don’t think I know what austrian study you are speaking about, any chance you can link it? Plenty of other studies have shown increased risk tho, so why is that one anything more than a statistical outlier? Ofc overall mortality is the most important thing, but as far as the diet-heart idea goes we have to look at cvd mortality. If you were arguing that while LDL was a cause of atherosclerosis, a high cholesterol is still beneficial overall, that would be a complete other situation, but that’s not what you are arguing. As for infections, it might affect septic shock mortality, but then again that’s about lipoproteins rather than cholesterol. Filling your LDL particles with more cholesterol by eating SFA would not do a lot to improve that, since it’s not the cholesterol that is the active component.
This protective effect comes from lipoproteins binding to lipopolysaccarides. By the way, this effect is actually not only from LDLs though, it’s also from triglyceride rich VLDL:s. And you are saying VLDL:s should go down, right? So it’s not immediately clear what effect changing your lipid profile by eating more SFA would have on the immune system.
Here’s a new genetic study from 2015 that I didn’t see before, looking at how LDL-C predicts mortality in the elderly. This is the exact type of study we need to settle this question, since mendelian randomisation removes the confounding factors of reverse causation from comorbidity, as well as confounding from other life style factors. The result on all cause mortality is clear. People with a tendency to higher LDL die faster. This argues very strongly for my view point.
“Results of the current study indicate that a genetic predisposition to high LDL-C levels contributes to mortality throughout life, including in the oldest old, and a beneficial LDL genetic risk profile is associated with familial longevity.”
Have you read the entire study? (I have not because it behind a pay wall, and I refuse to pay lots of money to read one paper). The underlying assumption is, of course, nonsense. The set up is as follows ‘Observational studies in older subjects have shown no or inverse associations between cholesterol levels and mortality. However, in old age plasma low-density lipoprotein cholesterol (LDL-C) may not reflect the lifetime level due to reverse causality, and hence the risk may be underestimated. In the current study, we used an LDL genetic risk score (GRS) to overcome this problem.‘ This assumes that reverse causality exists. In several studies it has been proven that it does not. It is an unproven hypothesis. So, the validity of this study rests on an unproven hypothesis, which is that people with low cholesterol probably had high cholesterol at some point in their lives – because they were genetically predisposed to do so. (Which certainly takes diet out of the equation). As with all the best scientific magic tricks, the ‘trick’ takes place before the action starts. We make unproven assumption x. That reverse causality exists. Once we accept this assumption to be true (based on no evidence whatsoever), we can adjust the figures as we wish.
However, a study like this would have to explain why the Swiss, with an average cholesterol of 6.4mmol/l have the second lowest rate of CVD in Europe… Genes, diet, reverse causality… Scientifically, Mendelian studies are a symphony of sophistry. An attempt to prove that black is white. A high cholesterol level is a high cholesterol level. A low level is a low level. It matters not how it happened, diet, genes, or stress. At all ages a low cholesterol level is associated with reduced life expectancy, and if you are going to argue that, well, ‘although the cholesterol is level is low now, it was probably high when we were not looking, then you need to go and prove that this is so. Something that no-one has managed to do. Facts are facts. Unproven projections based on genetic susceptibility (which assumes we know everything there is to be known about genetic predisposition, including all the genes involved and how they interact) is pure conjecture – at best.
Gosh Dr K,
This is fantastic stuff. Thank you.
Dr Kendrick, any written resources you recommend to help with being able to read a paper and cut through all the spin? I’ve read Testing Treatments and am now reading How to Read a Paper but I’d love to learn more, if such resources are available.
You are on the right track. It is very difficult to recommend useful resources. My knowledge, such as it is, comes from knowing an area inside out. I know the names, I know the spurious arguments, I know who is going to say what, before they have said it. I can look at the title of a paper, read who wrote it, and I know – then and there – what games are being played. This, however, has been a long process. It requires me knowing who is being paid by whom, what the pharma company in question is trying to market, what their angle is etc. It is a synthesis of commercial and marketing knowledge, scientific knowledge and knowledge of all the previous games that have been played in the area. This, however, is very difficult to teach. I tend to start on the basis that I am looking for ‘that’s interesting’ rather than ‘we proved what we already knew to be true.’ Unexpected findings are the little cracks of light where the truth dares to shine through the stultifying layers of dogma. Look for these the ‘ghosts in the machine.’ Be prepared always to challenge. Look for the tortured syntax – this is where lies are hidden. Look for the incomprehensible statistics – lies are hidden here too. Trusts your instincts.
Thank you, will try to do my best… It gets frustrating how much spin is out there and at the same time makes one want to learn how to be able to see through the lies. Thank you for the work you do.
I’ve read both of your books and I recommend them to everyone I know. Do you recommend any other blogs/books like yours that focus on other areas of medicine? I treat people daily (I’m an acupuncturist) and I see side effects of drugs in peoples’ lives. If there are other writers/bloggers whom you respect, I’d love to read their work. (I have been reading books by Uffe Ravnskov and he’s excellent).
Dr. Kendrick: Thank you. So true. How often are inconvenient findings simply ignored? I downloaded and took to my physician an AHJ article analyzing Get With The Guidelines (data from136,905 hospitalizations). The tables clearly show that for patients both with and without a history of CAD, those at lowest risk for a cardiac-related admission were those in the highest quintile for both LDL and HDL, and those at the highest risk were those within the guidelines (70-99 mg/dL, second quintile)! What conclusion did the authors draw from this data? “These findings may provide further support for recent guideline revisions with even lower LDL goals and for developing effective treatments to raise HDL. Astonishing, until you read the COI info at the bottom; four of the authors disclose none, and the other four give a list of pharma ties as long as your leg. My doctor was as surprised as I was; she no longer orders cholesterol tests for me. The article is available at ahjonline.com/article/S0002-8703(08)00717-5/abstract.
Two comments on the latest studies you present
1 on the perfecthealth.com table I was worried at the lable at the top of the graph showing it had been “adapted” perfecthealth as a name is a bit “catch all”
2 the study from Leiden mentions people of 85 or 90 have genetic predispositions to low LDL. They don’t seem to have done too badly in getting to that age.
“I think you will need to separate between the two issues of cholesterol/CVD and cholesterol/mortality.”
No, I really don’t, Johan. Longevity is most important to me, and I think to most of us. And those studies (and there are more of them) clearly show that “high” cholesterol is correlated with longevity.
“Serum cholesterol was negatively related to mortality, i.e., those with a lower cholesterol experienced a higher mortality than those with a higher cholesterol. The negative relationship was significant (as assessed by logistic regression) and remained significant after adjusting for obesity, systolic blood pressure, cigarette smoking, age, history of intestinal parasitism, and socioeconomic status (as measured by years of education).”
I am unable to understand why anyone would ever want to lower their cholesterol levels (especially artificially) after reading the following studies (all 100 of them):
Also, it’s just a hunch at this point, but I think Dr. Kendrick will be able to show that something else besides cholesterol is responsible for CVD, or is just a marker for something else going on (like firemen found fighting a fire, but having nothing to do with starting it). I have my own opinion of what that might be, but let’s wait for the good doctor to give us his.
As some very wise man once said: “Live long and prosper!”
Well, Joe, that’s fine – if you want to bet your health on pure correlations from epi studies. But if you want to discuss the cause of atherosclerosis, then that’s not enough.
“if you want to bet your health on pure correlations from epi studies”
Isn’t that what we’re all doing here?
Diet-heart is supported by many lines of evidence
Johan. That is not an argument. Equally it is not true. Where, exactly, would you say that it was supported? What is the strongest single piece of evidence? Something.. anything? The entire edifice was started by Ancel Keys whose original studies were fatally biased in many ways. Since then, what? Associations here and there. Please present the strongest piece of evidence that you know of.
Dr Kendrick, I think you should read the genetic studies. Disregarding them just because the authors state that reverse causality is a possibility is not enough of a response to them. They generate objective data, data that shows no correlation between LDL and cancer. This is the most solid form of evidence that we have on causality. So far, I have not seen anyone making a substantiated case against them.
I did ask if you had read the entire study? Someone has kindly offered to send the paper to me, to read. Once I have read it I shall respond. However, several pharma insiders have written to me on this subject, supporting my stance. We shall see. Yes, perahps I disregard studies like this too quickly. But I would tend to agree with Ioannadis in this area.
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. In this essay, I discuss the implications of these problems for the conduct and interpretation of research. http://journals.plos.org/plosmedicine/article?id=10.1371/journal.pmed.0020124
That’s hard to summarize in a comment here, but I’ll try to the best of my ability as a layman. The effects of statins from 4S was the when the establishment stopped arguing about it. You may counter pleiotrophy, and to some extent that would be true, but you do have the same effect from ldl apheresis, partial ileal bypass surgery and bile acid sequestrians. It’d be hard to argue that they all have pleio effects that are just in the expected range from their ldl lowering effects.
Then there is the mendelian randomization studies that shows clear cause, that I have already talked about.
You have the animal studies that always cause atherosclerosis with a SFA/cholesterol diet. No animal model has shown atherosclerosis without hyperlidedimea, as far as I am aware.
We ofc have the basic lab experiments in vitro that show how LDL and HDL interacts with cell membranes, showing the measurable effect of reverse cholesterol transport and all the other interactions going on there, an important component in the understanding although ofc not a conclusive evidence by itself.
Many studies using EBT, US and most importantly IVUS has shown a direct linear relation between LDL-C and plaque progression. This is a very advanced way of measuring plaque volume, and with different levels of lipid lowering the progression over time can be reduced, and even reversed. Please refer to the first three videos in this series for an overview of these experiments.
Overall, I think the mendelian randomization, ivus studies and ldl-apheresis together make up an undeniable proof of relevance of cholesterol/ldl in the progression of atherosclerosis.
Mendelian randomization studies are hypothesis generation and cannot prove anything, one way or another. Statins, as you know, increase calcification. IVUS study on exetimibe showed increased IMT progression. (I pay no heed to – dietary – animal studies on CVD, they are utterly useless to discover anything about human diet/diease). The trials on HDL raising agents proved, beyond doubt, that raising HDL increased CVD risk and mortality. As you know, none of these drugs got anywhere near the market. LDL aphersis is only carried out on those with astronomical levels of LDL – at which point the impact of very high LDL on blood clotting becomes critical. I must say, though, Johan, you do know an awful lot of stuff that would notmally be considered highly specialised knowledge. What you do not do is attempt to answer the clear contradictions to the diet/heart cholesterol hypothesis. For example, how do you explain that the Japanese have far higher cholesterol levels than they did fifty years ago, a sixty per cent reduction in CHD and a 7 fold reduction in stroke? Supportive evidence for a hypothesis matters very little. What matters is finding contradictions. Contradictions to the LDL hypothesis can be found all over the place. How, for example, to you explain the complete lack of plaque development in pulmonary blood vessels, no matter what the LDL level? What is your explanation for this?
Oh and yes, I did read the genetic study on old age. I think my last answer ended up in the wrong comment thread. It was a response to the question on the best evidence of diet-heart.
Then there is the mendelian randomization studies that shows clear cause, that I have already talked about.
Johan, these studies are worse than epidemiology. Contrary to what you say, they cannot show causation. They can’t even show correlation, though the authors try hard. As Dr. Kendrick pointed out, the authors assume either reverse causality or confounding or both to account for why folk with higher LDL live longer. If any of their two criteria are wrong, their analysis is worthless (moreso than it already is).
It’s not clear from the paper (Postmus et al) when blood was drawn for cholesterol analysis, but it was done only once for each patient, it seems (and why draw non-fasting venous blood samples–this is typically done after a 10-12 hour fast). And LDL was estimated via the Friedewald equation—not measured. Meaning? The authors have no idea what these people’s LDL levels were at any other times in their lives, but they assume it must have been high in the high risk group because their SNPs say so. But that’s guesswork—never measured. They selected 51 SNPs “associated” with LDL. They can’t account, no matter how hard they try, to adjust for all the other things these SNPs affect. So, this is not an objective approach at all.
And if you look carefully at Table 2, the association they claim is not consistent across the studies they chose (and that’s not discussing the subjects they decided to exclude from the analysis for various reasons). The Leiden study shows a benefit of high LDL on mortality, the Rotterdam shows no difference, and the LLS study entirely drives the results they claim. However, I still haven’t figured out how they can claim a 13% increase in mortality in the high risk LDL group for the combined studies (Table 2 again), when the incidence rate (deaths) for the high LDL group is lower (169.11 deaths/1000) than the incidence rate in the low LDL groups, which is 173.31. Something seems off with the confidence intervals given the raw data–there may have been some adjustment (ie. torturing) of the data post-hoc. Regardless, assuming their data is accurate, and given this analysis is not based on serial measurements of LDL, a 13% increase is miniscule—noise, in essence. Not casual, definitely.
Thank you for this analysis. Most helpful
Sasha wrote: “…being able to read a paper and cut through all the spin?”
Follow retractionwatch.com for while to get a sense of the perfidy and incompetence afoot.
On the specific topic of nutrition papers, I had some remarks further down in a comment on another blog: http://www.wheatbellyblog.com/2015/10/go-ahead-eat-your-meat/comment-page-1/#comment-62697
Perhaps non-coincidentally, the topic on that thread was yet-another bent anti-meat paper.
Thank you, Bob!
It doesn’t matter if they make incorrect assumptions about reverse causality since there is no possibility for reverse causality in this study. That’s why they are doing it, to test those hypotheses. The correlation between SNP:s and LDL has already been established, they are not guessing. The measurement of LDL:s is just a double check, so it doesn’t matter if the LDL-C is just calculated.
Regarding the criticism of the statistical data, I don’t have the knowledge to respond to that. They do explain the lack of statistical significance by the smaller sampling sizes of the first two studies. If it seems bogus, send them an email and ask? They also do suggest a bigger follow up study, so I guess we just have to wait and see. Meanwhile, for us who didn’t reach 90 years yet, we can make sure to keep a low cholesterol since the other bigger studies are quite clear with a big change in effect.
“In a meta-analysis combining nonoverlapping data from 312,321 participants, naturally random allocation to long-term exposure to lower LDL-C was associated with a 54.5% (95% confidence interval: 48.8% to 59.5%) reduction in the risk of CHD for each mmol/l (38.7 mg/dl) lower LDL-C”
Johan, you said: It doesn’t matter if they make incorrect assumptions about reverse causality since there is no possibility for reverse causality in this study.
Reverse causality is what they are testing for and what they are claiming, so I’m unsure why you don’t think it matters. Anyway, if they truly wanted to test their hypothesis, it can be done directly instead of this inferential stuff. They could actually measure peoples’ LDL over time and see if there is reverse causality. Straight forward; no tricks, no smoke, no mirrors. And I believed it’s been shown that reverse casuality is not the case (no reference at the tip of my fingers to support this).
I’ve looked at the data, and the statistical shenanigans section again, and it does appear as if they did post-hoc adjustment (don’t have the protocol available to see if any of this was pre-specified)—they adjusted for age, sex, cohort and, where necessary (!!!!), familial relations. Adjustments should always be looked at with suspicion as they allow a enormous source of bias to potentially enter the data—the researchers get to pick which criteria they want to adjust for, sometimes ensuring the results they want. The reason I say this is that adjustments are done arbitrarily since the adjustment factors are approximations based on the finding in other epidemiological studies (approximations of approximations in a non-homogenous population (ie. inter-subject)). By the time the variability in each of these approximations are added up, they often surpass the actual difference researchers see in their conclusions (the 13% increase risk for high LDL seen in this study). This is why you hear the term GIGA thrown around a lot with studies dependent on adjustments to twist the results in line with the researchers’ theory (GIGA = garbage in, garbage out). Personally, I’d stick to the raw data, which shows for the combined data that there is no reverse causality. People with high LDL live longer no matter what their “risk” factor is.
Of course, Daniel Steinberg and Scott Grundy, pharmaceutical industries top salesmen, are big fans of the Ference meta-analysis you linked to. But meta-analyses are, well, meta-analyses. They are epidemiology squared. Highly susceptible to GIGA. However, it doesn’t appear like Schooling et al were fooled by the Ference study ( http://www.ncbi.nlm.nih.gov/pubmed/23500241 ). This is what they had to say:
More generally, this study illustrates the difficulty with interpreting such as Mendelian randomization estimates. Mendelian randomization studies are most suitable for refuting causality rather than establishing the exact size of a causal effect. First, such a Mendelian randomization estimate will only indicate the true size of a causal effect if the level of over- or under-estimation of the genetic associations with the exposure and outcome are similar (and nondifferential). If the observed genetic association with the exposure is more understated than that with the outcome, then the estimate may be too large. Conversely, if the observed genetic association with the exposure is less understated than that with the outcome, then the estimate may be too small. Second, an exposure could appear to be causal in a Mendelian randomization study if it were a marker of an intermediate factor between genetic variants and exposure that also caused the exposure and outcome. As such, Mendelian randomization estimates should be interpreted as hypothesis testing, that is, able to disprove a postulated causal effect, rather than indicating the size or existence of a postulated causal effect.(Bolding mine)
Ference et al responded to Schooling (http://www.ncbi.nlm.nih.gov/pubmed/23500263 ). I doubt Schooling et al was impressed.
I think you should have higher standards in the studies you pick. How about something non-epidemiological and non-meta-analysis?
Thank you Stipetic for your work in this area.
I missed to respond to one of your comments, Dr Kendrick.
I disagree with you about mendelian randomization being purely hypothesis generating. But I don’t think I can give any more factual support for that other than just that most scientists would agree with me on the high value of them as strong evidence of causation.
You state that IVUS studies showed increase IMT progression for ezetimibe, but you disregard the fact that overall those studies show clearly the value of LDL-lowering. Yes, specific drugs will have off target effects, both beneficial and deleterious. However, overall this is very solid evidence.
Regarding Japan, they have had great reductions in smoking and salt intake, and subsequent improved hypertension. Ofc also better healthcare lowers risk of incidence by screening and risk of mortality by emergency care. This is also despite an increase in diabetes. I am sure we agree diabetes is a risk factor for heart disease, right? So obviously an increase in some risk factors can be overridden by a reduction in other risk factors.
I don’t completely agree with your mindset on contradictions. LDL is a well established risk factor already, just like hypertension, diabets, smoking and so on. When we see something that seemingly contradicts it, we should try to learn more about this specific case, not only throw out everything we already know. Science progresses one small step at a time, otherwise we would be stuck endlessly trying to formulate the perfect hypothesis that doesn’t have a single superficial contradiction. And there is no way that you will be able to construct a hypothesis on atherosclerosis that will not have some obvious contradictions. Sugar the culprit? Well, CVD in the US is down, while sugar up. Infections? Well, CVD up in the 1900-1950 while sanitary conditions improved. With that being said, ofc we always need to be able to rethink old ideas too.
As for pulmonary blood vessels I would guess it’s because of lower blood pressure? Just like in veins. Some shear stress seems neccessary. It seems to be possible though:
(just the first hit on google, I have not read anything about it so I can’t defend any position here)
You can make a statement such as ‘LDL is a well established risk factor’ all you like. That does not mean it is true. The IMPROVE-IT study with ezetemibe was THE single most manipulated study I have ever, ever, come across. And that is saying something. End point were not being met, so they changded the study protocol half way through, altered the end-points, doubled the number of subjects, and still claimed it was a valid study. Ho, ho. The only purpose of the study was the pave the way for the PCSK9 inhibitors as even the FDA were beginning to notice that the effect on LDL lowering by statins could not be related to clinical effect. Even Steven Nissen was quoted as saying that LDL levels were unimportant.
In general though you have – as yet – said nothing that I have not heard – or read- a hundred times before. It is a bit like listening to a well played record. These views are the views of the mainstream. Endlessly repeated. I provide a contradiction e.g. Japan (where 58% of men still smoke) and you just throw chaff into the air. Oh well, diabetes, or what. Improvements in hypertension. I don’t think so. The Japanese have higher blood pressure than the Russians (which takes salt and hypertension out of the equation), they smoke the same (which takes smoking out of the equation), they have exactly the same cholesterol level, and 18 times less heart disease – age matched men under the age of 65. Which takes male sex and age out of the equation. So where do the Russians get 18 times the rate of heart disease from. Not cholesterol, not smoking, not blood pressure, not age…. what? (not diabetes either, although the figures here are less certain). There is a awful big gap here that has nothing to do with standard accepted risk factors.
Dear Dr K,
I try not to intervene where I have nothing t add, but I do not think that Johan discusses any of the points you raise, but is always off on another tack. Not a good sign.
No, but this is a typical response. Rule one, so I am told. If you are winning an argument, tighten it. If you are losing, widen it. If you try to attack the diet-heart LDL hypothesis against a true believer they simply flip about at high speed. You know you are engaging when you get debate on a single point. Most people never stand still long enough. Usually you end up with the ‘Oh, it’s multifactorial.’ Which is where Johann left us. It is not an answer. It is just a way of avoiding the subject.
Umm…it’s colder there? 🙂
For the Russians, the high linoleic acid intake from sunflower oil is likely one of the culprits.
I don’t know if I agree with that statement. Russian sunflower oil is very different from what’s available in the West, besides Russians often use unrefined sunflower oil which, from what I understand, retains a lot of its good qualities. My mother used it for everything from salads to frying. When she died at 57, (not CVD) related, I spoke to the pathologist. She said that my Mom had arteries of a 20 year old, completely free of any signs of atherosclerosis. I know it’s n=1 but still…
Sasha: You may be entirely correct; what I suggested is speculation, and is complicated by the fact that different types of sunflowers possess different FA compositions, from the high-oleic (19% LA), to the non-hybrid (68% LA). What is clear from abundant research is that a high LA/DHA-EPA ratio in the diet (in the SAD as much as 30-50 to 1) has negative consequences for human health. The high CAD rate in Russians may very well have more to do with insufficient fish in the diet, or to a whole host of other factors in combination. What should give anyone pause, though, about putting industrial seed oils in their body is the appalling production process, and the likelihood of rancidity in storage.
Gary: Yes, I am also speculating… But I would also like to add that none of my relatives especially on my mom’s side suffered from CVD and they all lived into their mid 80’s or early 90’s, except two who died from cancer. Even though, from what I remember, sunflower oil was what we used for everything – cooking, salads etc because it was the only oil available. None of my relatives ever took statins or much of any polypharmacy with which modern Westerners are bombarded.
Also, sunflower oil in Russia tastes very different from what I’ve seen in the States, in fact, my mom would only buy it from Russian stores in the US claiming better taste. So, it could be due to different strains of sunflowers and different production techniques. If I had to guess, I would say it has to do with better processing techniques that are used in the old world. My German patients, for example, claim that they can eat all the foods (cheese, bread, etc) in Germany but react to them in the US. I think it has to do with all the preservatives and additives that are being used in the States. It’s also quite possible that these techniques have direct effects on plaque formation and endothelial inflammation.
Sasha: Very interesting comment! It may be that sunflower oil is a red herring in CVD, since it is mainly the processing (hexane extraction and high heat) that render PUFA dangerous. Interestingly, I saw a woman carrying a bottle of sunflower oil out of the Trader Joe’s yesterday as I entered, so I looked at the label once inside. It’s from Ukraine! And it is high-oleic (low in PUFA). I don’t buy or consume very many industrial products, so I don’t look at labels much, but this is the first Ukrainian product I’ve ever seen, and I wonder how it was produced. Wonder if politics played a role in its availability (I feel bad for those people, with their history, and the East/West tug-of-war over their lives and fate). I can’t blame the Germans for finding American bread and cheese distasteful. It can hardly be called food, and does have additives, such as folic acid and iron not used in continental Europe. I no longer eat grains, but for decades I made my own sourdough bread. High quality cheeses from real farms are becoming more widely available, although you won’t find them in the grocery store, except for places like TJ’s and Whole Foods. Our department of Agriculture is attempting to put a stop to such heresy as real food, but people are voting with their dollars. As for cooking fat, I use what is available, and since I buy meat by the whole or half animal, I end up with as much animal fat as I can use, which I render. Wish those fabulous eastern European sausages were more widely available here. Probably import rules make them difficult to find.
Gary: I also have no idea why the difference but I do remember my mother only buying Eastern European brands and only unrefined sunflower oil. She bought them in “Russian” stores that proliferate in any major metropolitan area: NY, LA, Philadelphia, etc. In my opinion, these oils taste different from commercially available sunflower oil in the mainstream US stores. Maybe has to do with how they are produced.
I also agree with cheese and bread comment, I know a German lady who says that whenever she goes back to Germany to visit her elderly parents, she can eat all the cheese and bread she wants without an allergic reaction but not so in the States. She says German government subsidizes producers who stick to old methods of food making. In the US we seem to subsidize Big Ag.
I know another lady who is a microbiologist and recently became interested in all the additives in US commercial food supply. She read up on them and started testing them in her lab for their effects on some of the bacteria present in our gut. She was so horrified by what she found that she know bakes her own bread.
yes, I have read Schoolings comment on them. I will leave that discussion to the professionals. However, I would certainly not say they are epi by any means.
We were speaking about the changes in Japan. No need to to bring in Russia to confuse the picture even more. I believe my arguments stands. Just saying it is a broken record is not much of an answer. It’s fully possible that other improvements have been more important. No one has ever stated that cholesterol is the only risk factor.
Japan vs Russia is another story, drinking, less fish consumption, and so on. Like I’ve stated, the anti-thombotic effects of fish might have played a big role there. Maybe even DNA? I can’t give you the exact answer to those questions but I don’t see any reason to believe that LDL-C should be removed as a risk factor just because it doesn’t win over all the other risk factors in every case.
Imagine that you have cholesterol of countries on the X axis and CVD death on Y axis. Yes it might not be lienar. Now imagine you put smoking, diabetes, alcohol, BMI, CRP, Lp(a), HDL, clotting time, or any other CVD-related marker on the X-axis. Would you have a linear relation? Of course not. Disproving a risk factor because of a lack of association between countries which vary by so many factors doesn’t make sense. We would have zero risk factors left. Swiss low in CVD despite high cholesterol? Well, between swiss people, high cholesterol is still a risk factor. There is nothing magical happening here. Just confounding factors like improved healthcare and such.
Well doc, it’s been nice talking to you but I believe we have reached the end of the road for this time. Like you said, you have heard all my arguments already and I have heard basically all yours already. Hibernating bears was a first tho! =D And also RBC membrane content, very interesting. Adieu
Johan. I suppose my only comment would be that these have not been your arguments.
After a good night sleep my new borne thoughts go to the medieval times and especially towards the renaissance when established dogmas were challenged by the emerging intellectual hypothesis which were in better concord with real world phenomena. Official representatives earned in those days, as today, their salaries by advocating or rather defending their out of touch dogmas and they could be exquisitely elaborate in their power wielding position.
E.g. – these intelligent and well trained scholastic people could go into details about how many angels that could be gathered on the tip o a needle without pushing one-another off the tip. By getting into such intellectual minutes and apparently immune to any ridicule they were hoping to avoid the obvious challenge to the existence of the actual phenomena. They made the agenda as we say today. And there was at the same time no lack of Platonic arrogance on their part since they were obviously the guardians who had seen the light from the sun and because of this they later on could stand the expected ridicule from the ‘ignorant’ and still ‘chained’ prisoners in the darkness.
And there was always a stake to be used – just in case.
(This reminds me about the the Swedish cardiologist who recently bitterly complained in his medical chronicle about how many hours he had spend to convince 95 % of his ignorant patients to accept the sacramental Statin pills he was prescribed. If he didn’t reach 95 % percent he was himself to get in trouble as he explained.)
“But The Times They Are A-changing!”
I am enjoying Dr Kendrick’s running ‘Hypothesis’. Which is informative and may prove to create beneficial protocols in the future.
However, what has become ‘painfully obvious’ is the overwhelming biases by the the comments.
For example: when a ‘Vegan’ aka Johan Wallström enters the den, he is snubbed.
Although he has made some good points and been respectful.
At the other end of the spectrum there is ‘Goran Sjoberg’, a prolific commenter here. Who is encouraging people to not take ‘medication or surgery’ for Cardiac problems.
This is extremely deleterious advice. And I find it odd that Dr K does not comment (or anyone else)
and that in itself indicates heavy ‘Earth Mother’ inclinations with a deceptive bias of ‘anti statin, anti-big pharma’.
(1) Had 2 x Infarcts and CABG at age 38…now 66
(2) Smoke and drink ‘like a witch’…..insanity I know
(3) Carnivore and fat lover
(4) Don’t think I haven’t taken a supplement that exists
(5) Self administered EDTA x12 many years ago, IV Vit C 22,000 iu, B12 shots. And a extreme H2o2 IV x 8…..’lab rat mentality’.
(6) Have been aggressively critical of ‘Big Pharma’ for decades. They lie, cheat and are in the business of profit, and are not obligated to disclose all they know. Although! Drugs do save lives and extend lifespan. This is the area where you have to educate and evaluate your own circumstances. We are all different in detail.
(7) Anti indiscriminate use of statins in ‘Primary Care’ and Pro in ‘Secondary’.
(8) With ‘Lipids’ only take note of Trigs, HDL, LPa, APOB….other ‘Pathology’ is blood sugars and liver enzymes.
Put that in your pipe and smoke it.
Mike. Johan has not been snubbed, he has been invited to contribute – and has done so. As for the rest of your information. Interesting, though I have no idea idea what to make of it. Or think of it? Personally, however, I know that the evidence for CABG and angioplasty (in the non-acute setting), is that neither provide any significant benefits. And this is widely known and accepted by many international cardiologists. As for statins. In primary prevention, they provide no benefit on overall mortality, and in secondary prevention increase life expectancy by around four days, after five years of taking them. So, now I have commented. If I thought someone was providing dangerous advice I would also comment.
Nice one, Dr Kendrick 🙂
Mike, to the best of my knowledge Dr. Goran has never advised or encouraged others not to “take medicine or surgery for cardiac problems”. He does describe his own health journey and how he has been successful in improving it, in opposition to his doctors advice. That takes courage and I find his posts informative and thought provoking. Others on this blog have also been badly burned with conventional medical treatment, and have taken similar courageous steps to solve their problems. I don’t think your “heavy Earth Mother…deceptive anti statin anti-big pharma Big Pharma” comment is either fair or logical as you describe yourself as having been ‘aggressively critical of Big Pharma for decades’ But actually, re reading your post, I honestly don’t know where you are really coming from, some of your beliefs seem to be similar to other contributors to this forum, and some are a bit off the wall, frankly.
Johan did not get “snubbed”. He entered the discussion with a snarky, unhelpful comment; he was reluctant to provide any references to back up his hypothesis until pushed by several people. When a few (myself included) commented on the tendency for vegans to take a nonscientific approach, he began whining that people were “bashing vegans”. That was not so. If someone cannot defend his position, he has no legitimacy in a discussion of scientific issues. When Johan finally gave a few references that proved to be equivocal, to put it kindly, and was pressed for more definitive information, he “self-deported”. As a scientist, I find your characterization of Dr. Sjoberg as a “new-age guru” type entirely baseless. He has not encouraged people to stop taking treatments, but rather, to use their own intelligence and abilities to become better informed and make better choices. People are beginning to realize that a lot of the new-drug hoopla, which is, of course, funded by the self-serving pharmaceutical industry, is neither science-based, nor in their best interests. The pharmaceutical industry, BTW, has been slapped with the largest fines and has been the subject of more lawsuits for lying about results, endangering people’s health, and, yes, causing thousands of deaths from their faulty products, than any other industry. I am encouraged to see so many lay people making the effort to research the facts so that they can take control of their own lives and health.
Annie, read my comments again and you will see that I was in a hurry while writing the second post, that’s why I only gave one reference for it. I’m certainly not reluctant to give references for any of my claims. When I came back from dance practice I added more sources. But hey, you can always search for it yourself too, you know. A good way to go about it is to try to search for support for your opponent’s viewpoint, that can help to keep our personal confirmation biases at bay. That’s my usual approach if someone makes a claim I have not encountered before. If you are not convinced by the references I gave you, on what basis do you refute them?
I didn’t “self-deport”, I explained like two times that I don’t want to go into all the tangents. There is just so many angles to look at this subject, and I would certainly be happy to give my thoughts regarding several of the questions asked to me, but I just don’t have the time to answer everything. The problem is, according to my experience, that whenever I answer one question there will just be another new apparent anomaly being brought up to the table, and it just turns into an endless stream of superficial arguments, without ever nothing being learned. That’s why I do prefer to stick to one subject at a time, at least to some extent.
Yes. This is why I didn’t want to get bogged down with diet/cholesterol in this series – and present a differetnt hypothesis that will (I believe) stand on its own. And can be attacked/criticised on its own.
Johan, your comment is not relevant to my comment. I was replying to a person that claimed some commenters “drove you from the site”. My purpose in commenting was to point out that this was not the case, as Dr. Kendrick (and others) invited you to continue your discussion. You, yourself, made a comment that many other commenters, not I alone, interpreted to mean you were withdrawing from the site. And, certainly, I know I could easily research your contention that “saturated fat increases blood clotting tendencies”, IF I were interested in pursuing an allegation that flies in the face of current findings, does not show any quantifiable EFFECT on longevity and health (but is a mere “marker”), and references sources that hide behind a paywall or fail to discuss confounding factors. It sounds as if you have your priorities straight in not allowing a likely pointless Internet argument to distract you from more enjoyable, relevant, worthwhile pursuits. Please be realistic enough to understand that you are not unique in this regard — there are many that read this blog with great interest, but that also share your devotion to pursuits that are more relevant to their lives.
Ofc it’s relevant, you were accusing me for being reluctant to give references for my claims. Thrombosis is a well known risk factor for heart disease, so it already shows clear effect, and saturated fat does influence that. That’s not to say it’s a big contributor for the process of atherosclerosis itself, but for actual events it is a clear risk factor. Therefor the pro- and anti-thrombotic effects are very important for disease rates.
Thank you for ‘community’ support since is always a sad thing thing to be exposed to impertinent accusations.
To add to my “anecdote” we had a heavy wet snowfall this night and I just returned inside after a fight with that snow. This is typically a ‘red flag’ for patients with severe CVD. Amazingly this time I didn’t even experience any effort angina as I did a couple a years ago. I wonder just why. This amelioration could not possibly be due to any Big Pharma heart drug or any by pass surgery.
And now I am to devour my sunday wild boar steak which is just steaming from the pot.
A sad thing i though that my bottle of Lagavulin, 16 years, which I have now tried for the first time, is empty. I could have enjoyed another ‘shot for my heart’ of this excellent whisky in front of my fireplace after the snow fight and the great wild boar steak. I will now not know if it goes together with the boar since this animal might be more Irish than Scottish according to J.P. Mallory.
A new review of endothelial dysfunction in CAD. Apart from oxLDL not much mention of cholesterol in all this causality.
Another paper, this one about linoleic acid and ED amongst other things. Very high consumption of LA rich seed oils is most likely what keeps the Russians falling over.
‘Of all the fatty acids, LA appears to be the one with the most profound and deleterious effects on endothelial barrier function’
If you are going to try the vegan experiment then you might want to avoid the seed oils completely, get plenty of good palm oil, cocoa butter, or olive if you must. Then you ought to avoid wheat too, and beans, and refined carbs. Doesn’t leave much does it?
Is this the same as CLA, which we are always told is the new elixir?
Mr Chris, fat biochemistry is very complex and very specific. Stearic acid is the 18 carbon saturated fat which doesn’t seem all that different from LA, an 18 carbon polyunsaturated fat, but it is handled very differently and has benign effects. CLA is different again, actually seems to be a hell-brew of complex 18 carbon fats of various shapes. Goodness knows where they end up!
It was not my intention to belittle Goran Sjoberg.
My critique was factual and his comment cannot be erased.
I am certain if Goran feels maligned, he will not hesitate to correct. Which I can’t see happening any-time soon.
Malcolm’s comment regarding ‘non-acute setting’ is a point worth considering regarding ‘Medication and invasive medical procedure’
(1) I know I am ‘preaching to the choir’ and not telling anyone here something they don’t already know. Just in case somebody is not savvy with how reality works. This is my take….and I don’t wish to ‘Labour’ the point and distract from Dr Kendricks theme.
(2) Medications are usually over-prescribed and not intelligently ‘tailor made’ to individuals. This is generally a messy scene. Throw in the ‘Dietary advice’ of ‘Heart Foundations’ and ‘Diabetes grant whores’ who have killed more people than ‘Pol pot’ and you have a rough idea of what to not pay any attention to.
(3) GP’s/PCP’s are not to blame. They are trapped in a web of ‘Politics/Guidelines/Pharmaceutical propaganda’. For example: If your cholesterol reaches a certain threshold, they are obligated to prescribe a statin. Otherwise they can be subject to litigation. There are sub standard GP’s (I actually met one who hadn’t heard of ‘Homocysteine’), also another idiot that told me I don’t need a statin script because my cholesterol was good…That after being on statins for many years. Your medical care is in your own hands, and you need to make an effort to seek a DR with whom you have a good repoire and bedside manner.
(4) Surgical intervention….’The good, bad, ugly’ of medicine. Which is a scene of ‘Greed/business and ill advice’. A bit clouded due to ‘Private health insurers’ and ‘Mercenary Cardiologists/surgeons). It is without doubt that ‘Stents’ and ‘CABG’ are often unnecessary. Although in my case it was of benefit…after an MI, I couldn’t walk 20 meters without breathlessness/angina.
(5) Again, apologies for straying from the topic.
Really, I certainly don’t feel ‘maligned’ but, and evidently I don’t seem to be the only one, I don’t see your point. It is in my eyes a little bit blurry.
You know but perhaps don’t understand, that I am just an ‘anecdote’ who according to my last (?) cardiologist, during 16 years that had passed since my ‘close to death experience’ 1999, have been practicing what he explicitly considered to be an almost criminal act when having not only refused the comprehensive by-pass surgery offered but on top also the great heart medication offered. He wasn’t the least impressed by seeing me sitting rather fit in front of him – it was just a question of pure luck when I asked him if he was ‘surprised’. He was also very explicit in telling me that he was not at all interested in what I had been up to during those years – he didn’t want to hear.
“You can talk anyone over (I was a professor at that time and he knew that) but not ME!”
When he, ‘following the guidelines’ (he was very explicit again), prescribed five drugs it didn’t bother him at all to know that I would never touch them.
“Anecdotes” of an academical type are for sure difficult patients for medical experts who KNOW.
Well he couldn’t even recommend me a good textbook in cardiology when I asked him specifically about it before leaving him behind me. He was, though, probably not interested in his own occupation – wouldn’t surprise me the least. Leaving him a sad but solid feeling was that he had never thought very deeply about what he was involved in and would not read the scientific papers I couldn’t refrain from sending him afterwards.
As an experienced researcher in the hard core natural sciences (superalloy metallurgy) I had though done my proper ‘homework’ before my ultimate refusal, those years ago, and when also I basically arrived at what Dr. Kendrick stated above – little to be gained but a lot to lose for BigPharma.
I took me about a month to arrive at that conclusion.
Dr. Kendrick, this series of posts on cause of CVD is excellent and I think you have it figured out.
I have always been most interested in your step 1 — ED. Are you aware of the ongoinng work and hypothesis of M. Brownlee and colleagues on this? Your S. African reference (part IV) seems to be in agreement with their thesis which goes back to the 1990s.
The basis of the Brownlee hypothesis is summaries toward the end of his 2004 Banting Award lecture, and is a substantial variant of (but related to) his broadly accepted thesis on causes of diabetes complications.
If ED is so important (which I do believe), why is the commercial ED test EndoPat so little used (my question is only partly rhetorical)?
Because of a high calciumscore found during a CT scan, my doctor ordered a angiography. Any tips for me?
I refused myself the last time, two years ago, wouldn’t add anything which I didn’t know already. Angiography is not without risks anyway and the knifes are still waiting for me since 16 years.
Instead I went for a daily dose of 1600 IU of natural E-vitamins to solve my unstable angina problem. It seems to work pretty well for an anecdote like me.
It was another downpour of massive wet snow last night and I have today a new heavy fight since the plower didn’t make it much easier.
And no Whisky if something unexpected should happen 🙂
Ask your doctor what is the purpose? If you have a high calcium score then you need to do something about the calcium and not have a doctor/technician stuffing probes into you which can, and do, cause serious problems. Dr. Kendrick covers this to a degree in his book Doctoring Data (Chapter 8) and you can find plenty of information on the internet. Please have a look at this (link originally supplied by Mike Cawdrey) http://myheartsisters.org/2012/06/28/avoiding-avoidable-cardiac-care/ .
What is likely to happen is that your doctor will recommend that you have a CABG, which at best is only partially effective (it too will become blocked over time for the same reasons that you developed the problem in the first place and quite likely more quickly because a vein tissue is weaker than arterial tissue) and worse is a total waste of time because your heart may have developed a bypass system of its own which won’t necessarily show up on scans.
There are a number of people commenting on this blog that have overcome their issues by lifestyle changes. My recommendation is that you do the same – but that is a decision for you to make. Regarding calcium please see http://doctorkatend.com/ (second reference today!). Does it work – I don’t know but Dr Kate provides references to cases where calcium related issues have been resolved following the protocol she recommends.
Whatever you decide – good luck!
Eugène, having had three (five stents) I would never agree to another. Read up on Vitamin K2 research and draw your own conclusions from there. Stents are not a viable solution and two of mine were put in to fix the first one because after a year it had already blocked up again. Andrew.
Triglcyerides are also called VLDL (Very Low Denstity Lipoproteins). They are not triglycerides, but contain triglycerides (as do all lipoproteins). Fat intake mainly increased chylomicrons. Large lipoproteins. The nomenclature in this area is nuts.
Andrew, any good suggestions on reading up on K2? Thank you.
Hi Sasha, lef.org; Weston Price Foundation; and Kate’s book, which has been mentioned, and k-vitamins.com (which is an excellent site by a man who cured his CVD with supplements). I hope that this helps.
Thank you Andrew.
I agree with Barry. If you get an angiography, the chances are high that you’ll get one or more stents, probably none of them needed. Or even a CABG. If you don’t do something about the calcification (what’s causing it), you’ll just have to deal with more blockages again. Dr. Kate’s book is a good one, and can tell you how to go about that, using vitamins K, D, and A. And no need for stents or CABG. It’ll help direct that calcium in your blood to your bones and teeth, where it belongs.
Also, depending on your lifestyle, moderate exercise can help you build up your collateral artery system, which can actually “bypass” those blockages. Here’s a link that explains how that’s done. A “blocked” artery doesn’t necessarily mean that your heart isn’t getting more than enough blood, as you can plainly see in those images. Which is why the vast majority of stents are unnecessary.
Essentially, your heart can perform its own “bypass” operation, no surgery needed.
But whatever you decide to do, good luck!
Eugene, my advice would be to take the high calcium score very seriously. You will have had CVD developing for years or decades — it is mature now. For reversing the CVD adopt a serious low-carb diet and reduce number of meals to one or two per day. And adopt some form of resistance and heart-rate training, but only as appropriate to your current health.
Meanwhile, to ward off some of the risk of ischemic events some drugs (and supplements such as the hormone precursor vit. D) might make sense in the short and medium term. That is a judgement call. Angiography might only be useful to detect something for short-term intervention, and carries some risks — it is a judgement call but certainly not useful for long-term resolution.
P.S. Eugene, I am no MD but read a lot. Certainly I would defer to Dr. Kendrick, but any MD would be reluctant to advise a would-be patient via a blog.
ED is irrelevant to your case — you have mature CVD unfortunately. That puts you at serious risk for an ischemic event. I would say that avoiding such should be first priority, and slowly reversing the damage to the arteries, etc. should be a long-term effort. It CAN be done, but it takes a lot of persistence as well as a correct approach.
The implication of the theory of CVD aetiology (M. Brownlee et al) that I believe correct is to minimize insulin resistance in the endothelial tissues most specifically, so as to reduce excessive cellular energy production by beta oxidation in those same tissues to normal evolutionary levels. The diet and the exercise will both be critical to this.
But take care of the ischemic-event risk first and foremost.
Above is link to Brownlee’s 2004 Banting Lecture transcript. In it a brief aside is entitled: “How does the unifying mechanism explain diabetic macrovascular disease?” His group has continued to study and publish on this thesis since.
The idea that a tissue unusually guaranteed of constant supply of glucose as fuel (endothelium) during all of evolution can be damaged via excessive ROS and reliance upon FFAs as fuel because of non-evolutionary conditions (derived from modern diet, mainly) appeals to me. There has also been unusually strong epidemiological supporting evidence, and continues to be.
Arteries vs. veins – I have read various blogs where it is mentioned that the turbulent flow, specifically at arterial bifurcations may be a causative factor in endothelial damage. Being an engineer by education and having worked many years in the area fluid flow and fluid conductors, I find this hypothesis very weak. I don’t find blood to be a remarkably abrasive fluid, and turbulence by itself is not a particularly damage causing action (not to be confused with cavitation). And blood flow velocity is pulsar, and even peak velocity is not very high. Granted, the endothelial layer is extremely thin, but I still find it hard to believe that it takes 50 years or so to damage it irreparably so that it now requires clots to form to heal. Why so long if the blood flow is the same for 50 years? What has changed?
I am much more apt to believe that some other mechanism has been in effect causing progressive damage to the arteries (similar to corrosion in pipes) which now becomes apparent at arterial bifurcations where the stress would be the highest and the area which would exhibit weakness first. Hence, I believe that the damage seen at bifurcations is probably just another event whose real cause is not related to the flow velocity of the blood. The artery has already been damaged.
Does anyone have any information on this subject?
I tend to agree with you on this. However, if you take a vein and subject it to the biomechanical stress of an artery (as a CABG) it will rapidly develop plaques. Also, the only time you will get plaques in the pulmoary arteries/veins is if there is pulmonary hypertension (high BP in the lungs).
Yes, I can understand stress leading to micro fractures in arteries, and the stress (pressure) is the highest in the area near the heart (pump). Downstream, the pressure should diminish, and therefore stress damage should be less likely. Fractures should also be more likely to occur when the atrerial material (membranes) become less elastic over time due to whatever bio-mechanism might cause such transformation.
Look at it another way. What happens if you subject a pipe made of material that is inadequate for the task i.e. pressure fluctuations result in fatigue cracks forming which damage the surface? Eventually it will fail. Arteries are under significantly higher stress than veins so if the structure of the arterial wall is weak and becomes damaged then the process of damage repair/limitation detailed by Dr. Kendrick occurs.
The next question is why is the arterial wall incapable of dealing with the stress imposed after millions of years of evolution and why particularly so in Western cultures – or those that have adopted our diet – and not in many other cultures? The simple answer is that the Western diet in deficient in substances that maintain the integrity of the body and high in substances that damage it.
The disease process can start very early in life and progress steadily over the years or you may start out without a problem and by poor lifestyle decisions develop problems later. If you take genetics out of the equation then progression of disease will be fundamentally dependant the balance of good versus bad factors in diet. I realize that there are many other factors influencing health but good diet is the prime requirement for health. If you don’t provide the substances that the body needs then it can never perform in an optimum manner.
Barry, thank you for the earlier links. In one article I picked up the news about Dr David Newman (of the NNT website) being arrested for a non-intimate sexual assault on a patient. I have no idea what to make of this. His Ted talk is excellent and his work seems to be driven by strong principles. Such an assault would be utter madness. There’s part of me that hopes it’s all nonsense, but of course the complainant has her version of events.
Stephen, yes, Dr Newman’s TED talk is excellent as is his book Hippocrates’ Shadow and his work on NNT. and as far as sexual assault charges – let’s assume innocence till proven guilty and even if he’s not, it doesn’t invalidate his epidemiological work
Yes I totally agree with you. I just wanted to clarify that probably blood flow and turbulence were not likely to be the CAUSE of aterial damage, as proposed on some other sites.
I too have reservation about this, but there is a possible reason why turbulence might become an issue. G. Pollack has been raising the profile of the effects of electrical charge in processes where it has previously been ignored. It may be the case that blood flow, even when highly turbulent, cannot impact the endothelium if all components are similarly charged (-ve). But should the charges be ‘stripped’ by oxidation (as some pharmaceuticals do) then charge-less or +ve charged components of the blood will impact the endothelium and those impacts will preferentially occur where velocities are greatest – and that will be in zones of turbulent flow.
If that would be true, the cause would most probably have to electo-chemical in nature rather than mechanical. I don’t believe that the mechanical forces due to blood flow would be significant enough to break normal tissue bonds, even in the endothelium. Just my opinion – can’t provide any references.
You may find this interesting https://people.csail.mit.edu/seneff/2015/WAPF_heart.pdf . It’s also available as a Powerpoint presentation on Stephanie Seneff’s site https://people.csail.mit.edu/seneff/ – look under Weston Price Foundation Wise Traditions Articles and Presentations, third bullet point down item 2.
While awaiting Malcolm’s next instalment on this interesting topic.
Allow me to introduce some ‘Trivia’ regarding ‘Whisky/Whiskey.
It has always been my understanding, that the difference in spelling is attributed to ‘The country of origin’.
If the name of the ‘Country’ contains the letter E…it is spelt ‘Whiskey’.
So! If distilled in Canada or Scotland, that would be ‘Whisky’..and so on and so-forth.
I haven’t drunk Whisky since my 20’s, although I would like to.
Don’t trust myself to drink hard liquor and have only drunk wine for the last 30 years…1-2 litres everyday.
Nice story is when I had my CABG in 1988, was fortunate enough to have ‘private health cover’. Excellent hospital with great menu’s and wine list. My first meal after ICU, I ordered a carafe of red wine…..Now! That’s what I call civilised.
Life is a very interesting experiment 🙂
Hospitals here in France don’t usually have a great wine list, but it is drinkable and some establishments provide it free of charge (others make a small charge). Another great advantage, at least in the 3 that I have frequented, is that if the house wine is not up to scratch and you have your own brought in … there is no corkage!
I absolutely love this series and can’t wait for the next installment.
I do have one question which you may address in future installments. But I thought I would ask it anyway, as I am 59 and just been diagnosed with CAD in mid-February. So, with that egotistical excuse, here goes:
In reading up on CVD and CAD I kept coming across the terms ‘plaque’ and ‘calcium’ used almost synonymously. But even a cursory investigation of the properties of the buildup in the coronary arteries, is, at least originally, has no calcium component. So when, how and why does it calcify? I have found no study so far that gives any more explanation than this one: http://bit.ly/1LKKGT0 And it only concludes that “These and other recent findings indicate that calcification is an active process and not simply a passive precipitation of calcium phosphate crystals, as once thought.”
Is this really the most current hypothesis on why–over time–we have a combination of lipids/bloodclot/plaques turn into calcium? That it may not be an accident?
I have spent the last two weeks or so deciphering studies and everything else I can find that might help me understand what I am facing. I have a degree in physics and just retired in 2013 as a Senior Software Engineer, so I am not unfamiliar with analysis. My initial impulse was to start at the beginning. You are the one who gave me a clear understanding of why I was floundering.
No one that I have found has started with a basic hypothesis (a general theory, if you will) from which all else can follow. But to me, that general theory needs to include the calcification. There has got to be a reason that an essential bone process is part of an evolutionary effort to repair damage to the arterial endothelium.
So, sorry for the long preamble, my question is: Why does the plaque become calcified? How does the calcification work? What are the components involved? Does it stop at some point? Does something reverse it?
Any viable hypothesis should account for it.
Thank you for what you are doing. So far, it is the best general theory I have encountered .
Yes, the calcification process is quite difficult to pin down. My own feelign is that, long term damage leads, eventually, to calcification. A low grade version of Fibrodysplasia ossificans progressiva – where muscle turns to bone after injury. So, repeated damage/repair damage/repair leaves calcification. However, there are those who believe in nanobacteria being responsible – and many other theories. I have to say that I am not sure about this area.
re: …those who believe in nanobacteria being responsible…
Well, there is that persistent correlation between oral infections and CVD, with some dissident dentists pointing the finger at oral spirochetes in particular. It could as easily be that these microbes, or their toxic byproducts, are just taking advantage of a person who is CVD-enabled for unrelated reasons.
Might we learn something from long-distance runners and their orthopedists? There are plenty of “heel spurs” out there.
Recommend you look at this http://doctorkatend.com/ and get the book. Explains the relationship between calcium in diet coupled with deficient vitamin status (vitamin A and vitamin K2) that results in the depositing of calcium where in shouldn’t be (including arteries). Dr Kate refers to case studies where vitamin K2 (together with co-factors) have reduced calcification. Also take a look at the role of magnesium http://www.mgwater.com/index.shtml .
Mycoplasma & calcification:
Talking mycoplasma I read now in my “The Cell” (Alberts et al.) that this about the simplest of all living organisms with about 500 genes compare to the usual numbers of 10 000 or so. Still, according to the same book, we don’t even understand how this most simple organism works in general but though in the details.
Such a fact should encourage humility not only among the people working with altering our genes but also among doctors.
As I understand it, the body deposits calcium in lots of different places where damage, inflammation and repair occurs – e.g. commonly in joints and tendons, such as in the shoulder, and in breast and brain tissue. Can well understand why you are searching for the reason and no doubt you are also attending to the triggers for the endothelial damage – all the things being addressed in this blog.
Interesting NEW article about vitamin C and health authorities workings:
Interesting article. I wonder why this blog did not accept comments. Another concern I have about taking antioxidants in large quantities is the possibility of interference with our own body’s use of ROS in the mechanisms of apoptosis. There is reason to believe that ROS are used by the body to do a number of useful things. Then may not be just “bad” chemicals to be eliminated. So, does a high dose of Vit C interfere with such processes? Judging by all the reports cited in the blog, it would appear to not be the case, but I would still be cautious.
“Another concern I have about taking antioxidants in large quantities is the possibility of interference with our own body’s use of ROS in the mechanisms of apoptosis”. What is the basis of your concern? Is there a reference you can share that would provide further information on this possibility? Based on various estimates of the amount of Vitamin C in the diet of early man (I’ve seen estimates of 2000-5000 mg/day), and the theory that humans lost the ability to synthesize it due to its abundance in the diet, it would seem that those supplementing with even mega-doses are just replacing what they once consumed.
Thank you for the link!
When I am now sipping on my daily glass of water with 6 grams ascorbic acid it now doesn’t feels like a waste of money although not prohibitive – about 2 Swedish krona a day for those 6 grams.
Add to that the cost for my other daily anti-oxidant, 1600 IU natural vitamin E, the cost increases with another 5 krona and with my other supplements (e.g. fish oil, K2 and D3) I probably spend about a British Pound in total every day on things considered utterly useless by Big Pharma. (Expensive visits at the restroom as someone noted.) I just wonder what the cost is for those five heart drugs am now missing. In Sweden we have though a public coverage for most of the cost associated with such drugs although I have to pay for out of my own pocket for the vitamins.
But a healthy life style must be worth a pound sterling a day I guess and with a glass of red wine (Cyclist, Biologique, Côtes Du Rhône Villages, at this very moment in front of my fireplace) there is another pound added and of course there is no coverage for that either.
Come on Dr.K – I need another fix of your wonderful factual blog – however whilst we all wait I did stumble across this interesting article …
In a previous post Johann said that cholesterol was a necessary component of heart disease. I asked him to explain the fact that all the countries in Europe with the highest rates of saturated fat consumption, and blood cholesterol, were also the countries with the lowest rates of heart disease. I didn’t get an answer. David Bailey asked the same question in a slightly different way and he didn’t get an answer either.
We probably all know on here that association isn’t proof of causation. But the absolute absence of association between cholesterol levels and heart disease is a compelling fact.
When you get the opposite result to that predicted by your theory, the theory’s wrong. An engineer would recognise this immediately. Somehow most of those clever minds in medicine just keep tweaking the theory and looking for ever more convoluted ways to explain those awkward facts.
“When you get the opposite result to that predicted by your theory, the theory’s wrong.”
Well, it depends on how tight your theory was in the first place. Of course, if your theory is difficult to falsify, then it was never much of a theory to start with. Which is where I would place the cholesterol hypothesis.
I understand you have read your Popper 🙂
A lot of scientists seem to sidestep this golden rule when it’s inconvenient, but they leave no legacy except a fat wallet and damaged people.
To Dr. Kendrick:
Yes, unfortunately, politics and money can sometimes trump science, as in the case of the cholesterol theory of heart disease. 😦
Wait until you see what they do with ZikaV. They’re not even investigating toxic chemicals, just that mostly harmless little virus, that’s never caused much of anything before.
Ah, yes, but it’s easier for one to whip people into a frenzy of fear about such rarities as zika and ebola, and then use their clouded judgment to more readily accomplish items on one’s agenda, than to bite the corporate hand that feeds one, even when said hand is wrecking the planet.
But, perhaps, the Galileos and Tychos are gaining on the Ptolemaists. I got this link tonight to an article, with several source references, from a site that was my lifeline to decent seafood when I lived in the midwest US. More evidence from science research to exonerate fat, and indict sugar, as the real “heart-attacker”: http://www.vitalchoice.com/shop/pc/articlesView.asp?id=2328&cohcid=0bbf03e8000000000000000000000796b971&utm_source=bronto&utm_medium=email&utm_term=It+Ain%27t+Fat+or+Cholesterol+…+What%27s+the+Real+Heart-Attacker?&utm_content=03/07/2016&utm_campaign=VC-news-3-7-2016&_bta_tid=3.Z2Q.B5a5cQ.DTgY.Af8BMQ..Ar6gJw.s..l.ARev0w.n…I_j70A&_bta_c=ek376fmnv54frwt5j5berqdp212w3
About a million years ago, when I was getting my BS in physics, Feynman was my idol. Not some rock star, but the consummate scientist.
Well, don’t look for them to change anytime soon. For how many hundreds of years did “establishment” astronomers keep tweaking Ptolemy’s epicycles to maintain the dogma of the geocentric solar system?
I get the impression that a broad swathe of science is infected with the same problem. For example, galaxies don’t rotate in the way that the laws of gravity would predict, so they invented dark matter! That is so much easier than suspecting that the existing law of gravity might not work over huge distances!
Annie-Laurie, there was a documentary about Feynman on BBC TV last year. It was on late at night and I was just about to go to bed, but I found him a spellbinding character and I had to watch the programme to the end. As you know, he ends up investigating the Space shuttle disaster and finding the problem with the frozen ‘O’ rings.
I can see why he was your idol. We need people like that and we need them to speak out. Fortunately, some do.
Thank you for the link, but I get a message that the content is “blocked it in my country on copyright grounds”, D*mn!!! I am irritated, annoyed, and p*ssed! Not at you, dear friend, but at our government censors. Maybe I can find a way around this. I expect this sort of thing in China, but, not in the US.
Thanks for spotting this, because I think that anybody who makes a substantial comment like his, would surely keep a look out for any responses. The fact that he didn’t respond further makes me feel that he wasn’t really interested in the truth of the matter – but in banging the establishment drum!
Could it be that this blog isn’t very popular in certain medical science circles 🙂
I should bloody well hope so.
David, Johan’s silence is deafening. The question of why the countries with the highest levels of cholesterol have the lowest rates of heart disease is one I’ve never heard addressed. Mike has pointed out that they no longer make this information easily available. I wonder why? Feynman said it more eloquently, but when the results are the opposite of the theory, the theory’s wrong. Clearly the countries with sky high rates of heart disease and low cholesterol haven’t listened properly.
Where for art thou, Johan?
Well, sorry I don’t have time to respond to so many questions. Everyone have their own favorite anomaly and I do not think that I have an obligation to respond to every objection made against the diet-heart idea just because I made a statement regarding thrombotic effects of different aspects of the diet.
It’s also hard to refute a claim that you don’t give references for, but I guess you are thinking about graphs like this?
I believe what you are looking at is high cholesterol as a marker for higher animal fat consumption, which correlates with increased prosperity, which would correlate with increased health care quality. You can see how countries on the bottom are poor countries with increased mortality from infectious disease and low health care availability. However you mentioned also CVD as outcome, not all cause mortality. But here too, a good health care system will screen people for high risk factors and treat them accordingly. There might also be other factors at play, I am sure other people will have more to say on that issue.
Here is a link to the abstract of the voralberg study. Sorry it was on 150,000 people over fifteen years. I have the full paper somewhere
Why Eve is not Adam: prospective follow-up in 149650 women and men of cholesterol and other risk factors related to cardiovascular and all-cause mortality.
Ulmer H1, Kelleher C, Diem G, Concin H.
To assess the impact of sex-specific patterns in cholesterol levels on all-cause and cardiovascular mortality in the Vorarlberg Health Monitoring and Promotion Programme (VHM&PP).
In this study, 67413 men and 82237 women (aged 20-95 years) underwent 454448 standardized examinations, which included measures of blood pressure, height, weight, and fasting samples for cholesterol, triglycerides, gamma-glutamyl transferase (GGT), and glucose in the 15-year period 1985-1999. Relations between these variables and risk of death were analyzed using two approaches of multivariate analyses (Cox proportional hazard and GEE models).
Patterns of cholesterol levels showed marked differences between men and women in relation to age and cause of death. The role of high cholesterol in predicting death from coronary heart disease could be confirmed in men of all ages and in women under the age of 50. In men, across the entire age range, although of borderline significance under the age of 50, and in women from the age of 50 onward only, low cholesterol was significantly associated with all-cause mortality, showing significant associations with death through cancer, liver diseases, and mental diseases. Triglycerides > 200 mg/dl had an effect in women 65 years and older but not in men.
This large-scale population-based study clearly demonstrates the contrasting patterns of cholesterol level in relation to risk, particularly among those less well studied previously, that is, women of all ages and younger people of both sexes. For the first time, we demonstrate that the low cholesterol effect occurs even among younger respondents, contradicting the previous assessments among cohorts of older people that this is a proxy or marker for frailty occurring with age.
Nice try, except that early on in this discussion, another commenter provided a reference showing the longevity-higher cholesterol correlation for several wealthy European countries. I’ll take a cue from you and not go back through all the comments and find it for you, but leave this as “an exercise for the reader”. BTW, the caliber of this blog is orders of magnitude above the news-service types, where people lob their inflammatory comments, move on, and feel no responsibility to defend same. This blog is a science-based community, so, yes, if you make a statement about a physiological correlation, the other commenters DO expect that you will respond to their challenges/questions. Why else would you participate? And isn’t it the mark of a scientist, or at least a science-oriented layman, to investigate evidence that might lead him to examine a long-standing belief, and perhaps be open to modifying his stance if the evidence would warrant such?
No Annie, I don’t have the responsibility to answer each unrelated question. I tried to back off when we got off topic from my comment, remember? As far as my comment goes, I tried to answer. Why would you think that I know every detail about differences in cholesterol levels per countries and how hibernating bears work, just because I added that saturated fat is thrombotic? I’m not the establishment, I’m just a guy.
Thanks for the link Dr Kendrick, that’s an interesting study, I will read it.
Johan. Yes, thank you for not backing off. I think it important, and necessary, to have someone here who is willing to ‘fight the other side.’ We are always too happy to surround ourselves with those with whom we agree. It is more comfortable that way. However, we can refine our thinking far better if we have a capable opponent.
Johan, as someone (I believe it was Dr. K himself) pointed out, you can be disingenuous in your replies. I’d charitably call it a tendency toward “inaccuracy”. I did NOT say you have a “responsibility” to answer questions or comments. I said, “if you make a statement …, the other commenters DO expect that you will respond to their challenges/questions. Why else would you participate? “. Perhaps purposely misstating what other commenters have written helps you to justify your allegation that people are “attacking” you. If you participate in a science-based blog, and use various excuses not to respond to what appear to be legitimate, sincere challenges to your statements, don’t be hurt/surprised/offended when other commenters take you to task for your proclivity to lob a bomb and then retreat. As “Give-‘Em-Hell” Harry Truman said, “If you can’t stand the heat, get out of the kitchen”. I am not suggesting that you don’t participate, merely that you refrain from making controversial statements that you are unwilling to defend or substantiate. And saying, “Numerous studies have shown that x” is neither a defense nor a a proof.
That study shows the deleterious effect of high cholesterol on heart disease. Now again, this post was about the cause of heart disease, so looking at all cause mortality (while ofc important) is a distraction from that question. Saying that high cholesterol is protective against cancer is a complete other argument than saying that atherosclerosis is not caused by high cholesterol.
It is a very strong drug to have lost your faith in the medical enterprise and realise that pure greed is behind it all but worse is when you as me has lost all confidence in the health care system.
I had a long talk about heart ailments with a man walking his dogs when I was working (and resting) on the heavy snow. He was my age and evidently surrounded by people with different kind of ailments that comes with age. Other walker by’s were joining our talk and everyone agreed that the medical companies were greedy and not the least interested in anyones health.
What was striking me was though that they not at all did see the whole health care system as corrupt and in the hands of Big Pharma. Contrary to me they still trusted their doctors when they prescribed their drugs.
I think it is funny to read the same thing about the doctor-patient relationship in the “Collected works of Platon” written 2500 years ago. That we should trust the doctors was beyond questioning even in those early days but I think this is something that goes well back to all shamanistic predecessors, 50 000 years ago as you may read from the cave wall paintings in Southern France.
Well – we trust Malcolm 🙂
Initially I assumed that my bad reaction to Simvastatin was due to my being a special case polio leg, it was only after a number of conversations similar to yours, that I realised the scandalous truth! Now I am something of a statin bore, and if someone roughly my age mentions pain or weakness in their limbs, I ask them if they are taking statins! I think I may have helped a few people who were caught in the statin trap of diminishing health and endless trips to the doctors to solve a problem created by the greed of big pharma.
Wow, I do the same, i.e ask if they are taking statins. A very large percentage of queries are answered in the affirmative, however very, very few seem interested in reconsidering their practice, defering to the judgment of their medical practitioner instead.
In similar conversations, I explain why I took myself off Statins and point them to this blog, the books by Dr K, but I never try to convine them, this is a matter for individual decision.
I hugely recommend this brilliant and understandable book to everyone:
“How to build a Universe. From the big bang to the end of the universe” by Ben Gilliland. My desert island book. (but its hard copy version, not electronic). Off topic but a favour to all!
It is in fact available as a Kindle book – but I was wondering how it relates to my comment about dark matter.
Dark matter (along with everything else) is discussed, and with plenty of humour. The text is revisited by the use of lots of drawings and diagrams which do not translate well in the Kindle form (so I am told). Anyway, it’s a book that is lovely to have to refer back to again and again. (Feeling very guilty that I am so off topic!)
All the best discussions ramble about a bit. I will pull things back a bit if they wander too far away from the subject we started with.
I understand this book is humorous, but is it also sceptical? I mean the Newtonian theory of gravity (or its General Relativistic equivalent) has only been tested properly on the scale of the solar system, but when it seems to fail at galactic dimensions, the main response has been to protect the theory by introducing a totally hypothetical concept of dark matter.
This situation beautifully parallels the cholesterol theory of CVD, where even after studies have shown that people live slightly longer if they have more cholesterol in the blood, researchers prefer to explain this by claiming that low cholesterol is a marker for some other disease(s), so that the theory that high blood cholesterol is intrinsically bad for you survives at the expense of assuming a whole new (and untested) hypothesis.
“All the best discussions ramble about a bit. I will pull things back a bit if they wander too far away from the subject we started with.”
Just so, and I added a thumbs-up to this. . . . .
The reason our bodies are warm to the touch when alive and become cold after life expires owes more to the quantum effects of the electron and to effects that the theory of quantum electrodynamics (QED) attempts to explain. It is a life and death distinction, but warmth that radiates from us when were alive has a lot to do with electrons radiating photons of infra-red radiation when they fall from a higher quantised energy station in orbitals around molecules to a lower one.
I imagine, Malcolm, that you were taught chemistry from an atom-centric perspective. I know I was, and I think this is still the case today. Explanations for the various properties and interactions that can be witnessed in chemistry were attached to the names of elements and molecules, whilst in turn the attaches to the nature and distinctions of the atom, or to the configuration of atoms in compound molecules. But when atoms interact in chemical reactions can you recall what happens to the nuclei therein?
Answer: zip, nowt, diddly-squat. Huh?! How so?
Well, if the individual nuclei undergo changes that is trending to a nuclear reaction. In chemical reactions the nuclei in atoms are generally not affected, and all the reactions arise in the domain of electrons. I gather from having picked up a glossy, magazine-like, modern chemistry book that some chemists are beginning to link arms with aspects of physicists and chemistry is beginning to make concessions to an otherwise and hitherto overlooked actuality that electrons better account for chemical phenomenon than atoms do. The reason being that its the shifting and shuffling of electrons in their quantum domains that is the domain of contrasts and atomic nuclei are largely unaffected. Electrons account for chemical effects better than can the nuclei of atoms.
The difference between health and well-being and the trend away from health and well-being that then accounts for ill-health begins to look a lot like ‘music’.
If life and biochemistry is a quantum phenomenon then our understanding of it could make concessions to the fact that the elemental components are drawn from a specific region of the periodic table. These various elements bring electrons with quantised energies that rest in the goldilocks zone. Beyond that range elements have electrons that are too numerous and whose higher shells and orbitals contain energies that rest outside the goldilocks zone for life.
Life, as my mind is trending to perceive things, requires electrons to performing their quantum electrodynamic tricks in way that sits in the correct part (range) of the scale and makes for a kind of harmony and melody. When electrons start misbehaving, dancing to ‘music’ whose ‘notes’ come from outside of that ‘chosen’ scale, and whose quantum electrodynamic dealings introduce discord, then the living thing ‘trends from melody to malody.’
Reading Richard Feynman now, I find, it seems he had a lot to say that seems pertinent to the distinctions between good-health and ill-health, without having giving much thought to it. Of course endocrinology, endocrine disruptors, and oxidative stress still figure in the etiologies of chronic diseases, but ‘cancer’, it seems to me, is an outcome in which quantum violations have played their part.
‘Inflammation’ is evidence of additional quantum electrodynamic activity arising in the region where inflammation is detected. Dealings of oxidation and reduction there are more intense, there is more protonation and deprotonation arising than elsewhere. Often this is part of the healing process or part of the immune defence responding, but if it persists out of context it results in lasting harm that assimilates with the passing of time.
It’s when I am trying to be most creative and progressive in the written expression of my thoughts that my typos proliferate the most and my proofing lets me down the most. The above references to Feynman, to QED, to the quantum aspects of biology, and to ‘inflammation’ could have been expressed a whole lot better, but in the ‘moment’ the above was how they came out, warts and all. And in reality the ‘moment’ they were written in was actually a fair chunk of an otherwise busy day. The lack of refinement, poor proofing, and lingering typos rendered the comments more difficult to follow than should have been the case.
The thread was beginning to make concessions to stark reality that the affairs of nature are underpinned by an underlying and extensive interconnectedness that the sciences and discussion do not always reflect. I was attempting to lend support to the emergent awareness, here and elsewhere, that the interconnectedness of affairs ought not to be lost upon us if we wish to properly understand those very same affairs, and that is something we could all think about to good effect.
Thanks for the ‘thumbs down’; it deserves many more. But thanks too for the ‘thumbs up’, and to those that gave them. You must have seen the sense my mistakes did their best to obscure.
Perhaps we should be less picky about one another’s typos, as we all make them, often enabled by that sometimes obnoxious and sometimes helpful auto-spell-check function. And often those typos can provide a little unintended humor, and research does seem to support the benefits of humor on heart health. I did get a chuckle out of paragraph 8 of your longer comment of today. Yes, f*rts are highly expedient to survival, and fats are as well.
Dr. Goran: Yes we do.
Here’s a link to the BBC documentary about the remarkable Richard Feynman, described as the most captivating communicator in science.
Thank you for this ‘rambling’ diversion. To be frank I didn’t know anything about Feynman and I really enjoyed what I now learned about this fascinating physicist.
“When you get the opposite result to that predicted by your theory, the theory’s wrong.”
is for sure a great statement but still I think Malcom’s “Popperian” satement above is much more appropriate in terms of “what is science”.
E.g., the theory “Ghosts exist!” is impossible to refute and for that very reason it is in my eyes a theory not worth considering. And if it was not for the money involved the same thing should be obvious with the cholesterol hypothesis.
To my present understanding there are very few medical theories that can be refuted and not least the one about the statins. Just replace “Ghosts exist!” with “Statins works!” and there you are.
We trust in Malcolm 🙂
Goran, I agree. The money to be made from statins and the cholesterol theory of heart disease keeps the thing going, along with a deep reluctance to admit they’ve been absolutely wrong for fifty years. But cracks appear daily in the low-fat world. Yesterday featured a paramedic on BBC Radio 4 who was concerned about developing diabetes and put aside her fear of fat and adopted a low carb diet. She lost two stone and felt much healthier. A few years ago the interviewer would have scoffed, but it was accepted without question. When something works, we tend to tell other people.
As for the remarkable Richard Feynman, I was equally ignorant about him until last year. What a range of talents! And he stayed human and funny.
I suppose “work” can be interpreted by the medical establishment to cover even the smallest degree of effectiveness, but the many analyses showing only minimal benefits (i. e., extended life of a few days to a few weeks, and then only for those that have had a previous heart attack and have taken the drug for 5 or more years) convince me that statins don’t work, in any practical sense of the term “work”.
How sad that this great mind left us long before his time. I so hope that the enlightenment on protecting one’s health that comes from this blog, and from the sharing of experiences by commenters, will enable other like minds to better protect the bodies that house them, and linger with us for a long, long time!
Well, Johan has finally answered the question in his own way (see above, responded to by Dr K). He says the fact that the countries with the highest rates of cholesterol have the lowest rates of heart disease is, wait for it, “An anomaly.” A huge, great elephant in the room, I’d say. “There’s none so blind as those who don’t want to see.”
This guy seems to be smarter than most I have met so far. Usually we se them draw to fast and then limp on but here we just note a certain arrogance and elegant dribbling – I am impressed. I don’t see any benefit in getting involved in any scholastic arguing here. The guys who defended the Ptolemy view of the heaven were not stupid – on the contrary.
Evidently this guy has got a mission since he seems to be fully occupied defending the “politically correct” everywhere where there is to find resistance, as far as I have understood.
So what is his actual agenda I am asking myself and as long as we don’t know he walks quite steadily on.
If I would have been a part of the establishment I wouldn’t hesitate for a minute to give him a great salary – he earns it.
Joahn certainly knows all the arguments, all of which I have heard many times. What is more surprising is his knowledge of the latest Mendellian randomization stuff. This, of course, is the PCSK9 argument. Which is being used by Amgen et al to support their new, hyper-expensive, agents. Not many. outside a pretty restricted group of medical researchers, would have any idea about this research (if one may call it that). It is surprising to find a computer programmer, with a purely amateur interest in CVD, up to such speed here. It is incomprehensible to most. And deliberately so. As Montaigne once said ‘Difficulty is a coin the learned make use of like jugglers, to conceal the inanity of their art.’
Thank you for this illumination 🙂
What I have learnt from similar events is a common feature of the ‘innocent’ underdog approach, which after a while exposes itself by self evidence, and a disguise you here so well looked through.
Another feature I have seen in similar cases is on the other hand the top dog arrogance which I assume comes along with the cynicism which probably is another absolutely necessary feature if you have a paid mission. In the worst cases I have seen they tend to turn into mocking and this case we have already seen small signs of this attitude.
When the payment is finally revealed together with their true affiliations they usually try to disappear into the shadows again. The great thing with the open internet is that there are numerous eyes watching.
Naivety doesn’t belong the survival kit on internet or in real life.
We will probably see.
As before, life is an interesting experiment and as you pointed out Montaigne had a deep insight into of the nature of the human mind. Even Platon in the name of Socrates had interesting things to tell about the evil nature of the “ruling classes” 2000 years earlier and basically saying that you have to be smarter than those you are robbing if you should be able to stay on top. Montaigne, in his tower, had for sure read his Platon.
We shouldn’t underestimate the evilness of Big Pharma. I read recently that a surprisingly large number of competitors, in the form of alternative practitioners, unexpectedly had committed ‘suicide’ in Florida within a short period of time. One had two holes in his head which might have been a professional mistake.
No, Ben Gilliland is not sceptical about dark matter in his book ‘How to Build a Universe’ but he is honest about what is known and not known. He is a brilliant communicator just trying to enlighten the average Joe Bloggs. He admits that we don’t know what dark matter is although it outweighs normal matter by about six to one. It’s called dark matter because we can’t see it. It is, as he says, immune to the charms of the electromagnetic force, which is why we can’t detect it with our eyes and telescopes since they rely on the electromagnetic spectrum. We do know it exists because we can detect its gravitational effect on the normal matter that we can see.
Its existence was first suspected in 1933 by Fritz Zwicky. The galaxies should have been flying apart because of insufficient gravity (not enough mass) and he concluded that there must be something invisible and undetectable making up all the missing mass and keeping a galaxy gravitationally bound together. And, “All the extra gravitational mass we get from dark matter is just what we need to get all that gas collapsing into nice star-making clouds before the expanding universe can tear it apart.”
Quantum mechanics challenges us immensely. Richard Feynman’s thoughts on virtual particles are explained. The world he, Einstein and many others uncovered led Erwin Schrodinger to declare, “I do not like it, and I’m sorry I ever had anything to do with it.”
Einstein offered his cosmological constant without knowing what it was – but he seems to have been right in the end.
You can be reassured that these scientists are merely saying that a something has to exist although they don’t know what it is. They are the real scientists – not the fools promoting the cholesterol myth.
All very grounding – it’s difficult to take yourself too seriously afterwards.
How’s this for a passage:
“Simplified greatly, in the world of quantum mechanics, matter exists in a state of constant flux – particles are transformed from neat, tangible spheres into diffuse clouds of probability in which they exist (and don’t exist) in all positions (and none at all) and in all states (both as particles and waves) at the same time. It is a world where electrons can travel back in time; where matter can “borrow” energy from the universe and appear from nowhere; and where we can force particles to ‘decide’ what they will be (or whether they exist at all) just by trying to look at them. And yes, that’s the simple version.”
I think a vital point here is that if the galaxies were each orbiting its centre of gravity under the inverse square law of gravity, then the typical structure of a galaxy – such as spiral arms – would rapidly (in an astronomical sense) blur out because the inner stars would rotate much faster – just as the earth orbits the sun in far less time than Pluto.
Dark matter is used to explain this anomaly (in addition to the galaxies flying apart at speed). However, the conceptually much simpler alternative, known as Modified Newtonian Gravity (MOND) is disliked because it would invalidate so much modern cosmology. This sounds remarkably similar to the cholesterol theory of CVD – save the theory by inventing new hypotheses!
That is fascinating David – more to read up on!
Although sober, allow me to stagger in with a few ‘random’ bits and observations.
(1) To elaborate on Malcolm’s point regarding ‘medical papers/studies’. Make it a habit to ‘start at the end’ and establish who funded the research/ the panel/ vested interests. Don’t even bother reading the study if you are sort of sure, it is likely to be biased and of not worth reading.
(2) I think I am in the minority of people here. My journey with CHD is not consumed with theories, but reality living with 3 decades of diagnostics, drug consumption, supplements and extreme measures of trialling ‘black magic’ in the form of IV use of unproven substances…by the time any could be researched and approved, I will be long gone. My life, my well-being, my decision/choice.
(3) There appear to be 3 groups of people who are involved in the topic of ‘Heart Health’. A: Those that have a vested interest. B: Those that live with the burden of this disease. C: People that are ‘spooked’ if the ‘pump’ malfunctions…it’s game over. The topic is a long one with no short answers.
(4) Most people have a ‘fear of death’…must plead guilty here. Then there is a minority that are convinced we ‘go to a better place’..where do I join?
(5) Don’t have ‘a horse in this race’ with the ‘cholesterol/heart’ circus. Apart from a select group of lipids that appear to have relevance.
(6) I lied about the ‘sober’ bit.
(7) Of the numerous ‘add-ons’ I have adapted. I have found over the past 5 years that ‘Grounding/earthing’ has had a profound effect upon my well-being. Being barefoot and walking along a beach for 20-30 minutes a day, gives me a increased vitality/freshness and better sleep. Although the proponents stress their point with a ‘party trick’…’Darkfield microscopy’.
CVD – Göran
Some GREAT NEWS (didn’t know where to put it, I think it deserves a post of it’s own). David Unwin, Southport GP who introduced High Carb Low Fat diet to his diabetic and overweight patients, achieving great results, has been awarded the NHS Achiever of the Year for Innovations!
Maybe there is hope, maybe there is cause for optimism that somebody is aware of what is going on in the wider world than NICE guideline / protocol writers!
There’s hope for you yet, Dr K!
Wouldn’t surprise me the least 🙂
I you don’t eat more calories than you use of whatever when trapped in the metabolic syndrome you certainly improve. Fasting seems to be embraced by everybody today – even me and my wife.
The fundamental logic, though, tells you that carbs increases blood sugar and insulin levels if you are T2.
So why not – go fasting!
Maureen, from googling Dr. Unwin, I believe you mean HIGH FAT low carb.
Maureen, that’s great news. Well done, Dr Unwin! I tried to get my practice nurse interested in his work on my last visit. I described NHS treatment of type 2 diabetics as ‘medieval’. “You can’t deal with carbohydrate? Well, eat lots of carbohydrate, take drugs and go steadily down hill.” We did better a century ago.
AnnieL – my comments regarding antioxidant intake were not based on any important studies, so I can’t supply any references to support my concerns. I have read in numerous sources that substantial amounts of ROS are produced in the mitochondria during the process of energy production. Our body also synthesises antioxidants, probably one of the most important is superoxide dismutase. It was also mentioned in the articles that the ROS were actively employed by the body to help in apoptosis of rogue cells. I don’t know if any of this information is valid, but I found it to be credible and food for thought.
Oops, sorry, I did indeed mean High Fat Low Carb! Sorry, in my excitement I actually attributed the standard failing diabetic diet to him! Well done again, Dr Unwin!
Good job everyone is so observant on this blog Maureen but don’t worry we all knew what you meant.