11th October 2018
I have tended to avoid talking about blood pressure, because I am not entirely sure what I think about it as a cause of CVD. However, since more people now take blood pressure lowering medication than any other type of medication in the world, including statins, it wold be remiss of me not to at least mention it.
Another problem is that, whilst blood pressure may seem a very simple subject. Either it is high, or it is not, nothing could be further from the truth. It is immensely complicated, and fragments rapidly into thousands of different strands, looping and whirling in front of you.
For example, let us take an apparently simple question, what is a high blood pressure? Well, with almost every passing year, this changes. The experts and the guideline writers get together on a regular basis and decide that well, hey ho, we thought 140/90 was high, turns out we are wrong. It is 130/85 – or whatever. By the way, the definition of a ‘normal’ blood pressure always goes down – never up. On current trends we should hit 0/0mmHg by the year 2067. What happens after that is hard to say.
I suppose a question that may seem reasonable to ask is the following; is average normal. Not, not even slightly. In a similar fashion to blood cholesterol levels, average and normal do not even remotely match up. Last time I looked eighty-five per cent of the population in almost all Western countries had high cholesterol levels. I would suspect another eighty-five per cent have high blood pressure.
In fact, if you wish to stretch logic to its very boundaries it is possible to propose that 99.9% of the population has a high blood pressure level. How can this make any sort of sense, you may ask? Well, in a moment of ennui I opened the American College of Cardiology/American Heart Association (ACC/AHA) risk calculator. You can find it here. http://www.cvriskcalculator.com/
I put in all my risk factors, kept them all the same, apart from my blood pressure which I started moving up and down, as you do when there is nothing good on the TV. What I found was that, as I reduced my blood pressure on the calculator, my CV risk went down, and down, until I got to a systolic (upper figure) of 90mmHg. You cannot make your blood pressure go any lower than this on the calculator.
The reason why you cannot get your blood pressure below 90mmHg is that if you go below this figure, you will be diagnosed with hypotension. Hypo = low. So, we have the weird situation whereby at 90mmHg your blood pressure is perfect. Above this, your risk of CVD goes up, below this the pressure is dangerously low and should be raised.
Therefore, at exactly 90mmHg your blood pressure is ‘normal’. At any other pressure it is abnormal – in that it increases the risk of death. Which is the definition of any ‘abnormal’ clinical test. It must be said that this constitutes a pretty narrow range. A doctor should be trying to keep your systolic blood pressure between 90mmHg and 90mmHg. And good luck with that. A very delicate titration indeed.
Clearly this is nuts, and it is not based on any clinical data whatsoever. There has never been a study whereby the systolic blood pressure has been lowered to 90mmHg. Nor will there ever be one done. This, I can guarantee. The mortality rate would be catastrophic.
So, how is this figure arrived at?
It comes from a mathematical smoothing technique whereby you get all the points on a graph, then draw the ‘best fit’ line through them all. I include an example here, which is where someone (Zoe Harcombe actually) looked at the cholesterol levels and rate of death from CVD in every country in the world (these are the dots). As you can see everything is rather scattered. [Data taken from the World Health Organisation].
However, there is a trend here, and that trend can be worked out. In this case, you feed in all the data points and a formula works out the underlying association between cholesterol and CVD death. As you can see in this case, as cholesterol goes up – CVD deaths go down. If you half close your eyes (which gets rid of the outlying points) the association between the dots and the line seems clearer.
(Or maybe that is just me).
What does this prove? Well, it proves nothing very much, for certain. What it almost certainly disproves, however, is an association between raised cholesterol and CVD.
When it comes to blood pressure it cannot be denied that. as the blood pressure rises, the risk of CVD also rises. However, the association is non-linear. By this I mean that, if your blood pressure goes from 100mgHg to 110mmHg, the risk of CVD does rise (but not by a statistically significant amount]. It only rises very, very slightly.
From 110mmHg to 120mmHg another very slight rise
From 120mmHg to 130mmHg another very slight rise
It is only when you get to about 160mmHg that the risk suddenly starts to go up sharply. From then on, things become rapidly worse. So, if your systolic blood pressure is above 160mmHg you should probably do something about it. However, what is the risk for a systolic blood pressure below this? Here we must rely on mathematics.
A paper that I have mentioned a few times, because I think it is a belter is from the European Heart Journal – from the year 2000 (believe me nothing of significance has happened since then). It is entitled ‘There is non-linear relationship between mortality and blood pressure.’
It is worth quoting the first two paragraphs in full. Sorry, for those not of a scientific bent:
‘Stamler stated that the relationship of systolic blood pressure (SBP) to risk of death is continuous, graded, and strong, and there is no evidence of a threshold…’ The formulation of this ‘lower is better’ principle, in terms of the linear logistic model (often referred to simply as the linear model) is the paradigm for the relationship of all cardiovascular risks to blood pressure and form the foundation for the guidelines for hypertension [and still does].
But it is often forgotten that when a study reports a linear (or any other) relationship between two variables it is not the data itself, but the model used to interpret the data, that is yielding the relationship. Almost universally, studies that report a linear relationship of risk to blood pressure do so via the linear models, such as the Cox model, or the linear logistic model.
Formally that model can be applied to any bivariate data and, independently of the data will always show that there is a linear relationship between the two variables. Before one can have confidence that the stated linearity correctly reflects the behaviour of the data, and is not just an artefact of the model, it is necessary to carefully examine the data in relation to the proposed model. At a minimum, it must be demonstrated that the model actually ‘fits’ the data and that it does not ‘smooth away’ important features of the data.’ 1
To paraphrase, your carefully constructed mathematical model may well be bollocks. In fact, it most probably is.
The statisticians who wrote this paper went back to the Framingham study – from whence all guidelines on blood pressure have since flowed, in all countries, everywhere – and found that the data ‘statistically rejected the model.’ They made the following statement ‘the paradigm MUST be false.’
I hate to say it, but the first person to recognise that the linear model ‘in terms of the relationship of overall and coronary heart disease death to blood pressure was unjustified.,’ was Ancel Keys. I am not sure what to make of that, as Keys is my number one medical historical villain. Still, he wasn’t stupid.
Anyway, the response to the European Heart Journal paper was…. Complete silence. Nothing. No counter arguments were proposed, nothing. “First they ignore you, then they laugh at you, then they fight you, then you win.” Gandhi. In this case we never got beyond ‘first they ignore you.’ Oh well, such is life.
None of this means that blood pressure has no role to play in CVD – or vice-versa – I just wanted to make it clear that that the whole area has become such a mess that it is very difficult to see through the forest of bias. What is a fact here? Frankly, sometimes, I have no real idea.
So, where does this leave us regarding blood pressure and CVD? It leaves us with only a few certainties. First, and most important, the only blood vessels in the body that normally develop atherosclerosis are the larger arteries. These blood vessels have a high blood pressure in them. Let us say around 120/70mmHg.
[120mmHg is equivalent to a column of water about three metres high. The units used to measure blood pressure are mmHg i.e., millimetres of mercury. Mercury was used to measure blood pressure, because it is many times denser than water. To measure blood pressure using a water sphygmomanometer would need a device more than three metres tall.]
On the other hand, the larger arteries in the lungs (pulmonary arteries) have an average blood pressure of around 20/6mmHg. In normal circumstances they never develop atherosclerosis. The veins have a blood pressure of about 6mmHg. It does not go up and down, because the pressure in the veins is unaffected by the pumping of the heart. The veins never develop atherosclerosis.
This makes it clear that the blood pressure, and turbulent blood flow, needs to reach a certain level before atherosclerosis can start. I sometimes liken this to a river flowing down a mountainside, with rushing and roaring and white water foaming and raging. That would be an artery. When the river reaches the plain below, the speed of water flow drops, the river widens and meanders. That would be a vein.
I think it is pretty clear that the lining of an artery is put under far more biomechanical stress than the lining of a vein – or a pulmonary artery. Which is why atherosclerotic plaques develop in [systemic] arteries, and nowhere else.
This idea is further supported by the fact that it is perfectly possible to get atherosclerotic plaques to develop pulmonary arteries, and veins. But only if you significantly raise the blood pressure. There is a condition known as pulmonary arterial hypertension (high blood pressure in lungs). There are many causes of this, and I am not going through them all here.
Let’s just say that people who suffer from pulmonary hypertension can, and do, develop atherosclerosis in the lungs. It should be pointed out that the pressure still gets nowhere near that in the rest of the body, perhaps 50/20mmHg, or suchlike. However, the blood vessels in the lungs were never designed to cope with high(er) blood pressure, and so damage will occur at a lower level.
When it comes to veins, if you take a vein from the leg, and use it as a coronary artery bypass graft (CABG), it will very rapidly develop atherosclerosis. Both of which prove that there is nothing inherently different about arteries and veins that normally protects veins and pulmonary arteries. It is all due to pressure.
Low pressure – no atherosclerosis
High pressure – atherosclerosis
So, surely the lower you get the blood pressure the better? Maybe, maybe not. There are many, many, other issues to be taken into account here – some of which I will discuss in the next blog.
1: Port S, et al: ‘There is a non-linear relationship between mortality and blood pressure.’ Eur Heart J, Vol 21, issue 20 October 2000
I have a theory that plaque in the arteries are like calluses on the hands … it’s an aftermarket way to strengthen the tissue in that spot. It’s only when it gets overgrown that it’s an actual problem. At a reasonable level, it’s normal & healthy.
Very interesting and thought provoking – as always.
Thank you for that, This blog may well give the basis for encouraging people to stop worrying about their blood pressure, which could arguably be described as the stress that may make CVD more likely than if they didn’t worry, and didn’t take their diuretic medication, which I should imaging can be a harmful thing in ityself.
AhNotepad: Reading that paper a couple years ago made me stop worrying about my BP, or even thinking about it or measuring it. I encourage everyone to read it. It’s not terribly long.
From my parents and grandparents I got the age old (wise?) information that blood pressure for older people is 100 plus their age, all other things being well.
So being 77 and healthy I am not too concerned about my 160
James, that is what I always understood to be the case. The waste of time, money and effort in treating B/P for healthy people is disgraceful. Oh, I forgot ….you are invited to go to the GP when you are healthy, ( men / women health checks) and get advised that you need such and such medications….generally antihypertensives and statins. It is enough to make us ill. Stay out of their clutches until you feel the need for advice, my lovely Mother used to say, because they are sure to find something to treat.
Yes I remember that too. In recent years someone evolved a more complex formula along the same lines but I can no longer remember who or what it was. I wonder if the blood pressure increase is actually largely an indicator of age rather than a cause of anything.
I was going to say the same thing.
100 plus age for systolic!
That is very interesting, and I had been hoping you would turn to blood pressure one day. I note that age is not mentioned anywhere. If one’s blood pressure goes up with age, I suppose it’s because of a lower flexibility of the arteries.
Or maybe arteries harden as a response to higher blood pressure as you age.
Things, organs, don’t work as well as you get older so, in the case of kidneys, if you ‘need’ to get rid of urine, blood pressure has to rise.
Mr Chris: Age, along with gender, is the major variable discussed in the paper. Well worth down-loading and printing.
Thank you for stopping me being idle. I followed your suggestion, read the paper and even persuaded my wife to read it. It is very clear and accessible, as if Malcolm Kendrick had it!
What never fails to amaze me, is how myths about many things, such as BP rest in circulation, when overtaken by other studies. No one knows where they came from, and few bother to try to learn.
The reason I find this blog great, is not just the good doctors suggestions, but all the other information that comes out of the comments.
Having had a triple CABG 18 years ago, I follow this blog keenly and I can honestly say that it is the singularly most refreshing and reassuring material out there. Dr Malcolm’s latest contribution hits new heights by introducing 2 superb expressions- ‘belter’ and ‘bollocks’. Both of these are perfectly descriptive: I think ‘belter’ is Northern English whilst ‘bollocks’ is pretty much nationwide. Nonetheless, very fitting. Anyway, a brief semi-hypothesis….surely high pressure within a pipe is a direct result of that pipe being narrow or narrowing? Surely this doesn’t mean that high BP cause plaques? IF plaques DO form for whatever reason, then high BP is a consequence surely? I may well have twisted my own thinking on the logic here so apologies if it sounds gibberish and/or bollocks. I admittedly talk shite from time to time.
Interesting. I, as ever, am looking forward to Dr Kendrick’s comments on your hypothesis.
Stress in the arterial walls is highest where the artery is not a smooth pipe – such as changing direction, bifurcating, narrowing. Changing the direction of the blood flow adds a mechanical stress on top of the stress due to fluid pressure (blood pressure). (Like Dr. Kendricks river “rushing and roaring and white water foaming and raging”.)
A reasonable sequence might be High BP -> more stress on arterial walls -> cellular damage -> clot formation ->plaque formation (when repeatedly damaged).
And such cellular damage would occur where the stress is highest, due to blood pressure and mechanical stress where the pipes bend and change size, e.g. big arteries by/in the heart.
I’m not sure I follow your reasoning the other way, that plaques -> high BP.
I agree that this seems key to the issue. Dr Kendrick analogy to a river roaring with white water is spot on. Turbulence in blood vessels is likely to occur where the atrial walls are bifurcating, changing direction etc. We have all experienced the feel of putting our hands in the turbulence water of a river compared to the smooth feel of non turbulent water in an adjacent section. The mechanical forces are immensely different. The logic that follows is that if blood pressure rises, for whatever reason, and turbulence ensues then it must follow that the endothelium is at risk of damage.
Agreed. Though in my own case my bp was about 160/105, the lower figure seen to cause the concern however. I turned out to have 90%+ blockage at a major heart artery so requiring stenting. Bp subsequently fell.
LESSON : Significant artery blockage causes BP. No ?
All my main arteries in the heart are definitely blocked since 20 years when I refused the GABG. Still my blood pressure (at 72) is today at rest typically 110-120/60 – it was though a while since I tested and I actually have forgotten where I put the testing device.
But my “last” cardiologist I met a few years ago was able to rise the pressure he measured to about 140 /80 by actually constantly insulting me while he was “working on me” with the US-equipment and performing the BP-measurements at the same time. He could then, with a “good feeling”, prescribe the BP-medicaiton which he though knew I would never take. In his eyes I was just “almost a criminal” as he stated it.
He actually gave me a final “insulting” phone call to check if I had been at the pharmacy. I then sent him a “traditional” old fashioned letter to terminate our future contacts. I added some scientific papers to the letter which I am sure he did never read but just to “make my point” as a skeptical professor.
Well he certainly received my “contempt” for what that may have been worth.
I’m wondering about this as well. There’s this chiropractor guy who gives various lectures on you tube and he says just treating high blood pressure is off base, that the body knows what it has to do, and that if your blood pressure goes up, it is adaptive. It may be adapting to a condition that isn’t ideal, such as a blockage, but he says, it stands to reason that the body knows when it needs to perfuse an area, and that if you force the blood pressure down it means that body part gets less oxygen.
So I wonder how that relates to things like high insulin levels running your blood pressure up. That might not be adaptive.
Was your blood pressure ever high?
“Was your blood pressure ever high?”
When I had my MI and was in the emergency room it certainly was high. Otherwise it has never been a “real issue” for me for whatever reason despite my severe clogging.
There is a lot one don’t understand.
David. Doesn’t sound like shite to me. I was struck by a sentence in Dr. K’s post – “None of this means that blood pressure has no role to play in CVD – or vice-versa.” which to me suggests that everything is back to front. CVD problems cause high blood pressure as does normal ageing. I sure ain’t as bendy at 76 as I was when young and suspect that applies to my hardworking arteries too. I always decline BP medication. I don’t want to happen to me what happened to my sister in law – dizziness, hallucinations, general weakness, anxiety. She’s off the meds now and back to normal and a fit and sprightly 88.
Eeh, it meks ya think.
Long live this wonderful blog.
It’s ludicrous the way all these “experts” keep changing the goal post. Besides your cholesterol and BP examples, don’t forget bone density figures which changed to make many women “osteopenic” overnight. I’m sure there are other manipulations (supposedly done for our health and benefit) in other health areas too. This situation is one reason I’m skeptical of any of these “optimal” figures and the healthcare industry/pharmaceuticals in general.
You are right
Here’s a little story. I went in for eye exam, they check eye pressure. It’s fine. 3 months later, I had a horrible allergy attack due to being in a dust storm,and my eyes were swollen and red. I went back to doctor. I was given some drops to help. okay so they check pressure again…it’s fine. I asked why they checked pressure? They tell me, they will now check everyone’s eye pressure every time they go. I am thinking they are now trying to lower lower lower those numbers and get everyone on glaucoma medicines. Those glaucoma drops are like 110 US dollars a bottle.
Anne: Is that the little machine which gives the eyeball a puff of air while you look at the little Christmas tree?
I used to have normal blood pressure but they moved the goal posts!
You will be one of tens of millions
More than once, and they’ll move again, when sales of hypertensives drop off.
No-one wants to talk about the damage done when BP is aggressively medicated or sledge-hammered down to “Ideal” numbers.
Same thing happened to my parents and their lipid numbers… Yet they lived longer than some of their offspring who chased down more modern, lower numbers.
Just like Global Warming! People aren’t worrying enough, so this week they reduced the level where catastrophe occurs from 2 degrees to 1.5 degrees. Dutifully given full scary coverage by the BBC.
As I understand it this isn’t a new IPCC Report, that isn’t due for a few years, but a ‘reworking’ of the current report with added ‘scariness’.
In the intervening years since the last IPCC Report there has been far more data gathered on the multiple connections between the Sun and the Earth to the point where, if evaluated without prejudice or bias, the influence of AGW will be reassessed as of minor importance in total Global Warming.
This is not to suggest that there is no problem, just that the problem cannot be simply addressed by only tackling the Anthropogenic contribution. Measures to mitigate Global Warming per se are required, but they have to be as if there was no insignificant AGW involved.
Would it not be better to deal with the root causes of “high” BP, such as excess weight ? Diabetes T2 ? / Insulin Resistance ? Dietary and life-style choices that ‘dis-courage’ our natural NO production (or don’t enhance it, which includes lack of exercise & fitness)
Perhaps calibrate the doctor’s automatic meter…
Not so far-fetched, we both joke about my GPs’ machine being 4 inches in favour of Big Pharma !
Nothing is as useful as one of those vintage Mercury-column units, where the patient can also watch the bouncing stop/start. !
From a woman with a systolic BP of nearly always less than 90, very funny ha ha!
Sent from my iPhone
Don’t worry Joanne, I will come to your funeral. Short trip for me. 🙂
I sense the phrase “Follow the money” is in order. Who benefits financially from the regular reductions in the “normal” levels?
I assume it is big pharma…. A great way to sell more product to an unwitting public. The idea of health benefit is apparently irrelevant.
Alas I think it more sinister. the medicalisation of the population is power politics by stealth – on a global scale. WHO is behind it? (And who is behind WHO – and a wealth of other similar fronts?)
the comments generally recognize fear is the leverage and I hold that hidden fear is more accurate – because fear that is owned and brought our into the open transforms us – and it!
Consciously accepting and implementing a course of action (including perhaps the decision to rest) is very different from being ‘reacted’ or gamed into ‘fear management’ under ‘experts’ whose pronouncements can literally kill and all the stages in between…
Many have lost or never had the deeper trust and commitment to ‘heal-thy self’ – but this doesn’t mean ‘go it alone’ or being set in defiance or opposition to potential avenues or agencies of help, so much as awakening responsibility for health and wholeness as a basis FROM which to live.
Of course we meet our fears, doubts and ‘self-negative scripts’ – but that is part of the decision to seek out and align in everything that helps while disinvesting in what hinders – and learning as we go. is that life as we know it Jim?
Medicalising and farming people is partly the market demand for unconsciousness.
But of course the pharmer sees a ‘no brainer’ in the making of false profits and so far is very successful in getting people to queue up in demanding ever more ways to degrade their consciousness – which is a significant part of my accepted definition of health.
Use it or lose it!
When the Doc wants my blood pressure low .. I feel unstable .. I can not function properly.
At 135/75 … I feel normal and can function normally. Eating a moderate amount of protein helps me keep my blood pressure to 135 / 75. I no longer stand for their pushing my BP to any lower level. I just say “NO”.
Keep saying no. Your blood pressure is perfectly healthy.
I remember when you first posted about the paper by Port et al.; I downloaded it. I think it’s worth mentioning his results – we should only be concerned about a threshold for systolic that’s age and gender dependent. Their rule of thumb is 110+(2/3) (age) for a man 45–74
and 104+(5/6) (age) for a woman 45–74. It’s only above this threshold that the risks start to increase with pressure. The threshold for serious risk is even higher, but not stated
I just looked at the paper by Port et al. in the Lancet 2000. They state you can add about 10 to the thresholds to get the level when one should be getting concerned
My BP regularly _is_ 110 so I must be a baby, as this formula applies to me because I’m older than 45… oh, wait. 🙂
I just read the paper. Fantastic! The threshold you list above is the “70% threshold” where increased risk begins. They say the “80% threshold” is where treatment is necessary, but they don’t have a formula to figure that out. Anyone have any idea what the formula would be?
Interested in comments on this !
Thanks for that Todays reading was 138/67. It usually is. Except in the cardiologist;s clinic, when the single reading was 154/76. For that, I have it in writing that I am hyperensive. That is why I don;t pay a lot of heed to the species in general, but just nod sagely until they give me what I want.
Jean, my response to you on 12th is lounging in limbo awaiting moderation. ( Dr Kendrick is doing a great job, and I am not complaining, but here it is again.)
Years ago I had an appointment with an NHS endocrinologist. Parking the car was cause for concern, then finding the department was another cause for concern. I was in good time for my appointment, so plonked myself in the waiting room, but, without time to catch my breath, I was ushered into a treatment room. I was weighed then had my B/P taken. Needless to say, when I was called to see the consultant, he commented that my B/P was raised, but that he would not take any notice of it, knowing full well the stupidity of ‘ritual’ that dominates the NHS policies and procedures in many areas.
By the way, the endocrinologist removed the meds I had been taking for years, and I now find out that I am described as a ‘non-compliant’ patient. Tut-tut.
In addition to my lost original posting, it is interesting to say that when I questioned as to whether I ought to include statins in the list of removed meds, his response was for me to ‘please myself’. I mentioned that I had already decided to discontinue them.
The drugs removed were candesartan, sitagliptin, pioglitazone, 1.5g of Metformin ( thus leaving 500mg), 40mg Simvastatin.
My sort of Doctor.
Can you clone him?
Yes there are a few good ones but so far outnumbered by the others.
Well Done Jennifer !
Tweak the good work by slanting your food intake towards LOWer carbs, moderate protein, and not fearing Healthy FATS.
This will in turn help with the T2 Diabetes…. Cutting back on the foods that “encourage” insulin resistance makes more sense than using a Pharma Big Hammer to belt down your blood glucose numbers !
Quick question for you. I’m on BP meds for hypertension. I’m 160+/110 without them. Pretty sure it’s genetic as I my mom has high BP. (And I don’t have other risk factors) BP is pretty normalish now. under 130ish/90ish. When figuring out CVD risk, would I still indicate high BP even though it’s controlled? Side note, love your bog. Best thing I’ve learned from you is understanding relative risk. (aside from everything else of course 🙂
Just wondering, do you think the diastolic or the systolic number is more important as far as being a cause or just reflection of CVD? Is there a significance to how close or far apart the two numbers are to each other?
I don’t really know. I think systolic may be more important, but it is also important to know what is driving both figures – and the distance between them
Surely the relationship is governed by the rate at which blood flows away from the arteries through the capillary system. If the capillaries don’t pass the blood through quickly enough there won’t be as significant a drop in pressure between the systolic and diastolic phases.
Should this be a result of higher blood viscosity/ lower RBC deformability then lower Serum Albumin (SA) levels may well be responsible [Your Part 56 referencing Chien term al. Biomarker Research (2017) 5:31]
You note that adverse CV events occur above a certain threshold systolic pressure, this could represent the point at which the elastic limit of arteries is closely exceeded when reflected Systolic pulse waves constructively combine, something that would be dependent on pulse wave amplitude as well as frequency. Again this could be, at least in part, attributable to low SA that results in increased vascular permeability, should that increase result in structural weakening.
Interesting thoughts. Certainly increased arterial stiffness – often due to reduced NO can create a reflective wave from the bifurcation of the aorta into the femoral arteries. If this reflected wave comes back too fast is can interfere with the aortic valve function.
RE: Is there a significance to how close or far apart the two numbers are to each other?
This is Pulse Pressure which some argue provides additional clues as to heart health.
See Wikipedia for what appears to be a reasonable and readable article.
Excess poundage (sounds better than ‘Kilogramage’) is my most reactant. Fat cells still need a blood supply, and it makes sense that the more “push” required, means higher pressures at the pump.
not for posting: errata 120 mm Hg is 1.6 ish Metres H2O
No, that’s fine. I was never that sure about my conversions.
2 of my greatest pleasures as a GP – stopping statins and blood pressure drugs in the elderly and being thanked a month later when they feel 10 years younger.
Mark Heneghan – please get yourself cloned, a.s.a.p., and into every GP surgery in the land.
This would corroborate the idea I posted elsewhere that the body knows when it needs to perfuse better and raises pressure to do so. It wouldn’t be so bad if they only worked on rather high pressures, but I see elderly people medicated into really low pressures all the time and it can’t be good for them.
Oh, that is soooo interesting. I’m sure we have all been made frightened of our blood pressure by Mr. B. Pharma. This is very reassuring. Thank you.
“your carefully constructed mathematical model may well be bollocks”: I wouldn’t myself call sticking a straight line through a fruitcake of data “mathematical modelling”. Teenage simple-mindedness, maybe, but not mathematical modelling. May I take it that the people with the teenage intellects are older than that, albeit to little purpose?
I spent a few hours at an emergency clinic, recently. First blood pressure was 171. Two hours later it was 122.
Jillm: I had a similar experience about 20 years ago. A very stressful event sent my BP through the roof (200+/120+). They took me to the ER. A nurse came in and started cracking jokes, and within an hour or so, it was back to normal, never to rise like that again. Best Nurse Ever!
This is something a lot of people don’t realize. Blood pressure is VERY dynamic! In fact, having variable blood pressure is a sign or normal functioning. I used to take my blood pressure at work (I have blood pressure issues) and it wold be a bit high, I would take a few deep breaths, wait less than a minute (trying to relax) and the second number was almost always about 20 points lower.
What do you think about the effect of transient spikes in blood pressure induced in high intensity interval exercise? I would imagine that BP goes dramatically high during intense exercise – albeit for a very brief period. Are people damaging their arteries by doing this?
“high intensity interval exercise” – this is exactly what I am trying to do as often as possible to improve my arteries or rather keep my collaterals alert as far as I now understand our physiology.
Could you explain the ‘collaterals alert’ part in that? I have no idea what you are talking about.
Harry de Boer: Pardon my butting in, but I think what he means is this: We are born with a vast network of collateral veins connecting all parts of the cardiac arteries and heart to each other. They do not develop into a fully-functioning system of conveyance of blood to the heart until stressed by need, by the significant narrowing of one or more arteries. I think he means that he wishes to keep them in tip-top shape by the normal stresses of the types of activity we have evolved to be engaged in every day of our lives, but most folks today don’t bother with, since laziness seems the commonest modern disease.
And when you tire of that, go for Super Slow weights/resistance.
(sorry, pun just presented itself !)
This always confuses me. How can blood pressure spikes during exercise be considered good whilst spikes in blood pressure throughout a normal day, bad ? (when it’s high )
If high blood pressure causes atherosclerosis which supposedly is a factor in CVD isn’t there a conflict here? Also the heart is a muscle is it not and exercising a muscle is supposed to make it stronger.
Thank you Malcolm for this on blood pressure. Logic suggests that a very high BP is not a cause but an effect of something else…So just ‘lowering’ BP via meds ? Does this lower CVD mortality ?
Bill in Oz
So, seriously overweight people (morbidly obese) who start on LCHF (or a variant) to normalise weight usually also normalise BP and benefit in other ways (I am n=1 on this). I suggest this is a practical example of BP as an effect not cause. which strongly suggests lowering BP with meds is a cop-out approach.
Current Thinking (?) appears to be on the lines of :-
“Let us surgically attack your digestive tract and that will not only fix your obesity, but cure T2 Diabetes at the same time !”
That same surgeon made sure I was gifted with the latest blood glucose monitor, despite being clearly told I had no intention of letting it dictate dosing of oral meds or even injectable insulin, and he ignored my declaration of using fasting and LCHF to accomplish both…
Even funnier, was the reason for my brief hospitliazation… to “fix” a workmanship – failure with their previous laparascopic appendectomy…
We can only assume that laparascopic – Bariatric surgery is the new “good little earner” for the hospital !!!
During my 3 days (of NOT eating their hospital food…) by BP hovered around 125-130 / 75-80, and reactive to which arm and which Nurse did the Obs.
I seem to remember in Doctoring Data that the tests for BP lowering medication and (possibly) overall death rate (or was it CVD — I’d have to check my book) weren’t great.
I recall you stating previously that BP was not a risk factor for CVD unless it is very high like 200/120. Is that still correct?
Maybe not that high. I set my figure at 160/110.
Thanks! If someone with a BP of 160/110 was not able to lower it naturally, would drugs be appropriate? Also, what do you think about the old saying of normal BP being 100 + your age/90, meaning a 100 year old person would have a “normal” BP of 200/90?
3 years ago I had shingles….the pain was unbearable. I was taken to A & E. B/P was 220/110. They thought the monitor was broken, so tested 2 others, then decided to admit me….without considering the pain of the shingles. However, I came home and rested as best I could, and was seen by a physician who prescribed appropriate meds for shingles….voila! B/P returned to my normal levels! What about Doctors looking at the big picture?
Pain causing blood pressure rise is like the ABC’s of nursing school.
Thanks so much for this info. Every decade, BP goals are lowered, so I had no trust in what they are currently advocating. This gives me a guideline to keep in mind when my blood pressure is taken. One reason I am concerned about the ever lowered blood pressure rules is that there is some variation in blood pressure readings. If you went to the doctor and your BP measurement was higher than ideal and an anti-hypertensive were prescribed, you could be at risk for passing out at some point when your blood pressure gets too low and would be at risk for a motor vehicle collision, etc.
I believe this happens a lot. Not maybe to the point of passing out but why do you think the doctor above says his patients feel better when taken off the meds?
I was on Coreg 6.25 mg twice/day. Cardiologist died. New one took me off so BP wouldn’t go too low. Put me on Metoprolol. Changed medical systems. Cardiologist wanted me on 12.5 Coreg. I refused. Taking 6.25. BP ~90/50. Nephrologist wants it up to 110/something for my kidneys. Wish they would all be on the same page, but I think nephrologist is right.
Thank you for this! Looking forward to the rest of the articles.
The following article has been around for a while, but it still makes its point as strongly as ever. Click on the information beside each figure on the main page. Click on the the blue box titled “How a disease is created.” Click on each item in the side bar to the right. There’s a lot of interesting information here:
Dr. Kendrick: Thank you very much for this. Everyone and every doctor should read this paper a few times a year. I find it interesting that the entire global warming gloom and doom scenario is also based upon a linear interpretation of data as an artifact of computer models. The IPCC prophecies of future global temperatures and sea level entirely based upon this sort of tomfoolery. The only reliable temperature data we have is for the period of the satellite era (since the early 1990’s). In that time all of the models (there are several), have run hot compared to observation. Now we have a published PhD thesis from a climate scientist at James Cook University in Australia showing that the temperature data the IPCC uses, especially that from the 19th century, and up to 1950, is garbage, “unfit for purpose.” So if the data is garbage, the IPCC reports, in their hundreds of pages, are garbage as well.
Gary do you have a link to that 19thCentury data ? I’ve been taking an interest in the Global Warming stuff recently…All the threats are based on what increasing co2 ‘will’ do to the global climate.But nobody talks about methane from agriculture especially rice. Any thoughts ?
Well a good place to start might be this graph:
The graph is made to look impressive, until you realise that the entire claimed temperature rise since 1880 is just 0.8C. The graph is cut off at 2000, probably because there has been very little warming since then!
However, rather as with statins, all sorts of statistical tricks get played.
David Bailey, that 0.8ºC rise in say 70 years is a significant increase. The sort of guestimated world temperatures from ice core data are swings of very few ºC from ice age to whatever it is called when it is hot between one ice age and the next.
Fear seems to be the way for the establishment/globalists to “rule the world” today.
Thanks David I will look through that link…And Goran that is exactly my suspicion…But when I hear ( as I did last night on the ABC RN network ) they seem so sincere…In fact as I think about it, he ( Tim Flannery in this instanse) was prosetylising – seeking converts..So once again, there is the need to be skeptical, on principle !
The same kind of blog as Dr Kendrick is writing about CVD can be written about AGW.
It’s all ‘bollocks’. 🙂
The earth isn’t a greenhouse, the climate models have been falsified by the absence of the ‘hot spot’ they predicted, the increased earth surface temperature compared to what the ‘black body theory’ would predict is totally explainable with thermodynamics: p.V=n.r.T — below in the atmosphere the pressure is higher (gravity pulling the gas molecules down) and therefore the temperature, and exactly predicted as measured. As a result if there _were_ a ‘greenhouse effect’ as proposed by Fourier, Arrhenius and whoever more, it would be another 20+ degrees (K) hotter than it is. It isn’t, so there isn’t.
There is (much) more correlation between the decreased sun spot intensities and earth’s passages through the spiral arms of the Milky Way (both leading to higher Galactic Cosmic Radiation reaching earth –> ions formed in the atmosphere –> cloud condensation nuclei formation –> low clouds formation –> higher albedo –> lower temperature). A low temperature period is neigh, rather than alarmingly high temperatures and believe me, we would prefer the higher temperature, as civilizations have collapsed in the cold past periods and flourished in the warmer periods.
And CO2, as usual during the past millions of years (ice core data!) follows temperature.
The only people that profit from the CO2 scare are (former Goldman Sachs) John Blood and Al Gore with their investment firm of carbon certificates, and of course the usual others in their social club and the governments that would share a profit through the increased taxes.
Oops, I made an error in my excitement, the sentence should have read:
There is (much) more correlation between the decreased sun spot intensities and earth’s passages through the spiral arms of the Milky Way (both leading to higher Galactic Cosmic Radiation reaching earth –> ions formed in the atmosphere –> cloud condensation nuclei formation –> low clouds formation –> higher albedo –> lower temperature) and earth’s average temperature than between CO2 and the latter.
Further, my personal theory is that the deep oceans, warming up very slowly but steadily as we are still coming out of the previous ice age, are steadily releasing CO2 through the reduced solubility of the gas as the water warms up. That’s why the atmospheric CO2 (as Murry Salby so eloquently pointed out) didn’t bulge during the crisis 20’s and it’s rate of increase also didn’t bulge when we started dumping CO2 in the atmosphere.
Bill in Oz: What I know of climate science (an incredibly complex system) I’ve learned from Dr. Judith Curry, an emeritus professor from Georgia Tech. Her blog is Climate, etc. Also worth reading is wattsupwiththat.com. Pay no attention to what Wikipedia says about Anthony Watts. The thesis advisor at James Cook was Professor Ridd, who was Wakefielded by the university for pointing out that corals have survived eons, multiple periods of glaciation and deglaciation, and they will survive still longer. I don’t know much about greenhouse gases, but it seems likely to me that CO2 has only minimal impact. Solar insolation is the overwhelming factor affecting Earth’s climate. When there is reduced sun spot activity (these are intense solar storms which slightly increase insolation), the Earth cools, as during the Maunder minimum, which caused the Little Ice Age in the 17th/18th Centuries. We are now in a period of reduced sun spot activity, which may explain the “pause” since 1998 in global warming. The IPCC does politics, not science. You can find a link to the publisher of the thesis (set up for the sole purpose of making it available) at Climate, etc. He wants U.S. $8, only right because he spent more than a decade laboring over it. It was accepted by the university. Skepticism always!
@Gary (1:59pm) The mechanism behind the sun spot activity is not the insolation (its variation is too small to have any considerable effect), but the modulation of galactic cosmic radiation which modulates cloud formation, as proposed and extensively elaborated by Svensmark et al.
Ha, ha. They say that the cattle industry raises methane because, well, apparently cows pass a lot of gas. Do you notice how anti life this idea is? CO2 is the devil and everyone contributes to the problem by breathing and farting. Death is better than life. So I love it that rice produces methane.
“David Bailey, that 0.8ºC rise in say 70 years is a significant increase. ”
No nearly 140 years – those temperatures are measured from 1880 (a convenient date seemingly chosen because the temperatures dipped slightly at that time, so the temperature rise looks greater).
You also have to ask whether how accurately thermometers were measured back then.
On top of that, many of the measurements sites have become urbanised, which raises the temperatures significantly, so a computer correction is made to the measured values! Computers are also used to estimate temperatures at sites that have gone out of use for one reason or another.
Doctors had me on 3 types of blood pressure tablets over 5 years as I experienced side effects from each one. I was dizzy, passing out, persistent cough, etc. The 4th pill the GP wanted to try said I could experience temporary blindness!! I then insisted on a halter to monitor my blood pressure for 24 hr. without the pills. The pills were lowering my blood pressure too much. I could have avoided all this stress had I done research on this condition myself. I’m 74.
an interesting and scary read is this:
Overdiagnosed: Making People Sick in the Pursuit of Health
H. Gilbert Welch, Lisa Schwartzl, Steve Woloshin
the scary part is the tales of those blacking out whilst driving, and ending up, if they survived, very much the worse for wear.
james Le fan’s book on the same subject, with an input from Malcolm is a very good read as well
Timely discussion about BP. Recent appointment with GP was about cholesterol and BP. Preparing a letter to GP stating that LDL-C measurement is irrelevant and why statins will not make me healthier. The BP of 175 and 160 a minute later was a concern for the GP. My resting BP readings at home are never this high. Explanation is the sympathetic fight/flight stress response. Taking the stairs instead of elevator might also have raised BP. I will pass on the BP medications as well. Mediterranean diet was also suggested but I will stick with LCHF.
LCHF = yes!!! an absolute winner
Let me relativise the HF part in LCHF.
The more weight (fat) one wants to lose, the less fat one should eat in this diet. So LCLF would give a much faster weight loss than LCHF. And, with LCvHF (very High Fat) one would even gain weight as one takes in more fat than is burned.
True. Although Sumo wrestlers gain weight be eating carbs, not fat. As did Roman Gladiators. They reasoned it was better to be fat, as it meant a sword had more ‘flesh’ to get through before it hit something vital.
@Dr. Malcolm Kendrick : There is no contradition between losing weight by LC and even more by also LF vs. gaining weight through HC.
The thought that I sought to express was that while people can lose weight through LCHF, they can lose more weight if they eat less fats than HF would indicate, as the body than has to convert more fat off itself into ketones, instead of from orally ingested fats.
The reason people gain weight faster from carbohydrates than from fats is that ‘carbs’ contrary to fats raise glucose and as a result insulin, which is the ‘storage hormone’, telling our cells to open up for the glucose and the fat and turn the glucose into intramyocellular lipids (fat): a double whammy.
Oh no, I did it again:
…as the body _then_ has to convert more…
The possibility of editing posts would be appreciated.
But low-carb and low-fat is just low-calorie, with all its problems of eventual lowered metabolism and compensatory eating. Of course it leads to faster weight loss but not sustainable weight management. Yes adjust the fat part of LCHF if necessary once a person is accustomed to it, but dietary fat consumption helps the body to learn how to burn body fat and keeps us feeling full and off the biscuits — oh, and it ensures we eat and absorb the ADEK vits and have the building blocks for cell membranes, hormones, etc.
“So, where does this leave us regarding blood pressure and CVD? It leaves us with only a few certainties.”
A very good point in my eyes!
Being an “extreme” sceptic towards all CVD-medications it is though possible to “convince” even me.
I still remember reading somewhere (I have lost track on where it was) about a very convincing randomized trial carried out many years ago (50?) at a veteran hospital and on a limited number (10 – 20?) of participants with extremely high blood pressure – around 200 as far as I remember on top of my head.
Half of them were treated with medicals to reduce the pressure and all survived. The other half didn’t receive any medication and all succumbed.
Such outcomes of experiments tend to impress on almost everyone.
Ah but the treated group will have caught up by now!
Many here are saying higher blood pressure is due to aging. I know a 68 year old whose typical blood pressure is 116/76. That person exercises very regularly. I wonder how many have higher BP due to the body deteriorating due to a lack of movement. Does it matter? Of course I do not know.
Here’s my take on blood pressure, it’s rather like oxygen in a fire. If the inflammation is there (ie there is a fire) then the increase of blood pressure is adding more oxygen to the fire. In other words, the higher the blood pressure the more accelerated the progression of atherosclerosis. So if there is no inflammation then too a point it doesn’t matter a stuff.
The other issue of course is that if we accept that anything below 90 is considered too low, then anything above 91 would be considered too high especially if we happened to be a large pharmaceutical company that is selling drugs which can lower it. One would almost be tempted to sell the fear to sell more drugs.
Another thought provoking blog. Taking blood pressure from the brachial artery only measures the systolic and diastolic BP in the brachial artery, which is not a true reflection of the blood pressure in any other artery or organ. Central aortic BP is a better risk stratifier for determining ones own CVD risk. If one looks at pulse pressure amplification it can be seen that systolic pressure increases the further one measures it away from the heart. This has to be physiologically important because blood flow decreases the further away from the heart. Blood pressure will invariably increase with age due to loss of elasticity of the arteries; a similar and parallel phenomena easily demonstrated by pinching the skin and observing how quickly it returns to normal. This is a physiological response to maintain adequate perfusion to end organs like the brain, kidneys and heart as we age. Systolic BP increases with loss of elasticity of the arteries, probably due to endothelial dysfunction. An increase in systolic BP therefore causes additional strain on the artery wall and atheroma develops. But lowering systolic BP to the recommended guidelines of below 140/90 in the elderly may have disastrous outcomes by reducing perfusion of organs and thereby leading to organ dysfunction and subsequent co-morbidities. So what is the answer to slowing the progression of loosing elasticity of the arteries and developing raised blood pressure? I think it is related to maintaining a healthy endothelium for as long as possible through a healthy lifestyle and to over indulge in l-arginine, l-citrulline, proanthrocyanidins, vitamins C, K2, D3 and vitamin B complex along with resveratrol supplementation!
You forgot to mention the l-lysine. 🙂
Where can I buy that all-in-one tablet of yours?
… … and magnesium, potassium, CoQ10. ???
My current “be kind you your endothelium” regime includes but is not limited to grass-fed meat, poultry, game, fish, butter, noncommercial cheese and a wide range of vegetables, many local and seasonal. I’ve added vitamin C, vitamin K2, Co-Q10, l-citrulline, chondroitin sulphate and magnesium (malate). I get enough vitamin D and NO from sun exposure, especially this year, and I limit carbs, especially grains, and mostly avoid wheat, sugar and omega 6 seed oils. Lots of minor things like nuts, olives, red wine, 85% chocolate, herbs and spices, and I alternate between real salt and lo-salt for the potassium
Not sure if it’s working but I’m still alive . . .I am certain if I’d continued with the low fat diet I would be much fatter, on many more drugs and with fewer than the average number of limbs, and very likely already dead. But profitable.
A question about systolic increasing further away from the heart. What is the physiological mechanism for this? Since you’re further away from the “pump” and also the blood flow is decreasing further away, what accounts for the rise in systolic?
Good question. Arterial pressure varies continuously over the cardiac cycle, but in clinical practice only systolic and diastolic pressures are routinely reported. These are invariably measured in the brachial artery using cuff sphygmomanometry. However, the shape of the pressure waveform changes continuously throughout the arterial tree. Although diastolic
and mean arterial pressures are relatively constant, systolic pressure may be up to 40 mmHg higher in the brachial artery than in the aorta. This phenomenon of systolic pressure amplification arises principally because of an increase in arterial stiffness moving away from the heart. Arteries closer to the heart are more elastic compared to arteries in the periphery where they tend to be more muscular and act as a secondary “pump” to the main pump, being the heart. As the pressure wave travels from the highly elastic central arteries to the stiffer more muscular brachial artery, the upper portion of the wave becomes narrower, the systolic peak becomes more prominent, and systolic pressure increases. This occurs in all arteries. As the pressure increases the flow decreases in the more peripheral arteries as found in the foot, so pressure here will be higher. One should think of the arterial tree as being a continuous pump until it gets to the capillaries and then entering the venous side of the tree, which depends more on lower pressure, lower flow. aided by valves in the veins.
Hi Andrew, thank you very much for such a wonderful explanation, I will study this further.
I would also like to thank Dr Kendrick and everyone who contributes here. This blog is an incredible tool for learning.
Once the “tree” leaves the body’s core (including skull contents), the arteries, arterioles and capillaries are surrounded by or embedded in muscle that they also serve, where the forces and pressure responses are dynamic.
I’ve always thought that that had a great deal to do with this central/peripheral pressure differential. I suspect that central pressure and peripheral pressure are most similar during deep sleep: during the muscular paralysis of deep sleep.
It seems obvious to me that if you measure something (X) that is clearly necessary for body function – cholesterol, salt, blood pressure, heart rate, alcohol(!!),….. there will always be an optimum value. Too much of X must be fatal (even excess water is fatal), and by definition if X is necessary for body function, zero X is also fatal
Thus if you plot death rate against the level of X, the relationship must be nonlinear!
The Laffer Curve has wide applicability – generally screwing linear appearing concepts as you have so ably demonstrated.
when it comes to health then your optimum value is not necessarily my optimum value.
Surely, we simply gradually age and the circulatory system cannot be as ‘springy and rebounding’ . We can be as good as we can get and accept responsibility for our own health.
Reading about food deserts in out of the way places, far from shops with fresh food,not the Cotswolds of course, but for the disadvantaged, is depressing . Are they all undeserving poor, of course not. During nurse training, BP was 100 plus your age, thresholds of everything have been lowered. I don’t suppose I would pass any exam now regarding anatomy and physiology.
Thank you Dr Kendrick for keeping this oldie up to date.
“It is only when you get to about 160mmHg that the risk suddenly starts to go up sharply. From then on, things become rapidly worse. So, if your systolic blood pressure is above 160mmHg you should probably do something about it.”
Many of us would like to know what your recommendations are for dealing effectively with the “something”.
Deploring the venality of big pharma and the gullibility (or absence of informed, critical curiosity) of medical professionals and pointing to individuals’ experience of iatrogenesis is one thing when it’s an academic or epidemiological question. But when an individual is faced with their own abnormally high cholesterol or blood pressure readings they would appreciate a range of options to explore.
Mainstream medicine is pretty precise and clear with its recommendations. What are alternative strategies?
Exercise, weight loss, LCHF, potassium and magnesium supplementation, sun exposure, yoga/mindfulness/controlled breathing, buy a dog. Also check you don’t have Conn’s syndrome – excess production of aldosterone (the blood pressure raising hormone). Most doctors will dismiss this, but it has been demonstrated to be a significant contributor to raised BP. There is also, at times subclinical Cushing’s hanging about. If you must take a medication, go for perindopril (raises nitric oxide most of all). Then add in vitamin C/D and L-arginine. There you are, that’s thirteen.
Isn’t there an important balance to be struck between L-Lycine and L-Arginine, in order to suppress certain viral infections that are dependent on sufficient L-Arginine?
Beet/Beetroot juice supposed to lower blood pressure, a cup of juice a day, nitrate rich.
this question seems to be stuck in awaiting moderation. You had L- Arginine in your list, and I wondered why not L-Citrulline which is said to be more easily absorbed? and converts to L-Arginine in the body.
Has anyone been following the Dave Feldman (engineer, believes LDL/LDL-p and other lipids are primarily energy delivery systems created a concept called “lean mass hyper-responder”, which is an athletic person who is lean and experiences very high TC and LDL when going on a ketogenic diet) versus Dr. Peter Attia (firmly believes in the LDL hypothesis, takes a low dose statin because it’s “healthy”) discussions?
If so, what are your thoughts?
(By the way, the podcast is 3 hours!)
Life’s too short to watch podcasts but I was just reading up on Dave’s blog. I find it rather sad that intelligent people are so invested in “cholesterol” that they believe the entire complexity of the lipid mechanism exists to generate LDL to kill us. It makes as much evolutionary sense as meat suddenly causing diabetes after we ate it for millennia, or the current belief that our digestive tract evolved wrong and needs to be corrected by surgery.
Attia and Dayspring are convinced that LDL blasts its way into the artery wall through sheer force of particle numbers whereas Malcolm’s explanations are much more subtle and IMO more likely to be true, and what Dave has so far discovered is absolutely game-changing.
1. The use of mercury for blood pressure measurements suggests a long ago origin to me. If blood pressures were already measured in a distant past, when CVD wasn’t as ‘popular’ as it currently is, are there no records left of lots of people who got their blood pressure measured? Can we then not take the average of those as ‘normal’ values?
2. If it is true that arteries are in a way adapted to the pressures to which they are exposed, then maybe it isn’t very smart to use arteries that normally see low pressure as a graft in places where normally high pressures occur.
3. As explained in earlier episodes, and if I remember correctly, CVD is ‘mainly'(?) caused/initiated by damage of the glycocalyx through the presence of insulin and/or glucose in the blood. I can indeed imagine that another cause of damage to the glycocalyx is mechanical stress due to turbulence. For instance, if a plane flies over a grassy landscape low and fast enough, after passage it will look like a freshly ploughed pasture (that’s how we know the Pentagon could not possibly have been hit by a Boeing 757 flying at 500 knots: the grass was intact) and the same might pertain to the endothelium at high pressure and turbulence.
4. I don’t understand the desire to obtaining linear relationships. I think it can be easily checked whether a relationship is dominantly linear or not, by also trying to fit a higher order curve through the data and then check which least squares approximation is better, the linear or the curved one.
Of course I’m but a mere amateur who isn’t bothered by much knowledge and therefore able to spout the biggest nonsense with the utmost confidence.
Please don’t hesitate to let me know if that’s the case. 🙂
Harry de Boer: Two things: All the photographic evidence of that event has been suppressed. Even a highly skilled and experienced pilot would have found it exceedingly difficult to corkscrew down from altitude to hit the Pentagon just above ground level, meanwhile the entire security apparatus of the most richly-endowed military the Earth has ever seen failed to notice, let alone respond, to what was happening. Entirely ludicrous, the official story.
And it seems like the security cameras keep failing during these events. There were 11 security cameras around the Murrah Federal building in the 1995 blowup, but no pictures. There was a lot of discussion about the alleged perpetrator’s truck and where it was parked. Too bad those cameras all around the building couldn’t clear that up.
Two cameras captured the plane hitting the Pentagon. Just ordinary security cameras, not broadcast quality like for the planes hitting the towers, so there’s only a couple of frames which show a blurry flash. And ja question: if the hijacked plane did not hit the Pentagon, what happened to it? It’s not easy to dispose of a Boeing 757 full of passengers without a trace.
Security video of plane hitting Pentagon released, adds, S’bite from Judicial Watch
@Gary Ogden : “Entirely ludicrous, the official story.”
Yes, and the grass proves it.
You mean the same crackerjack military that was incapable of flying out its fleet of fighters from an air base in Florida prior to a hurricane? Don’t mistake incompetence for conspiracy. The military is like any large bureaucracy – incompetence lies at its very core.
Everyone likes linear because it’s easier to understand and has clear rules. Let me see if I can remember the mathematical definition of linear.
A function F is linear if F(ax) = a F(x) and if F(ax + by) = aF(x) + bF(y).
I think that’s it, anyway. (I guess you could have linearity in the log domain, too, but that would take too many of my brain cells to postulate!)
Once you get into nonlinear, it’s way more difficult. For instance, what nonlinear function actually fits the data? There are curve-fitting programs you could probably use (now — 40 years ago, probably not so much). But then how do you interpret that? And how do you translate that into something doctors and normal people understand? (An aside: a lot of natural processes seem to be a J curve, where very low = bad or very bad, higher = better until some nadir, then higher = rising risk, with maybe a flip up at some point. Salt seems to be this way — depending on who provides the study.)
The equation for most of these = set F(x) to the point where the most $ can be made for our drugs. 😉
A straight line satisfies your definition of linearity, hence the name: line-ar. 🙂
I suppose the best that can be done is to plot mortality (or whatever) against BP/ blood sodium levels or whatever, and present the plot to those trying to decide what to do, without trying to fit a neat equation to the data I don’t think any rational person would look at Zoe Harcombe’s graph (above) and conclude that cholesterol levels should be artificially lowered!
Just because it is hard to fit an equation to the data, doesn’t seem to justify fitting an obviously wrong equation!
I’d like to know if dangers from radiation or other pollutants are really proportional to the level of pollutant. This assumption means that the West is endlessly chasing minute threats on the basis that one death is one death too many. How did our ancestors survive at all with apparatus that could detect pico-gram quantities of noxious chemicals?
That was the question I also had. If blood vessels are designed for levels of blood pressure they’re exposed to, wouldn’t it follow that transplanting a vein to replace a coronary artery would predispose it to atherogenic changes?
This is exactly what happens. The same process follows angioplasty of arteries, which by removing the “plaque” damages the endothelium so its counter-productive because with a damaged endothelium, the atheromatous process starts all over again.
Thank you, Andrew. That makes sense.
Oh, and I know why Ansel Keys wasn’t interested in also bending the blood pressure data into a linear CVD risk: nobody would pay for it.
In the comments section of an earlier post Dr. Kendrick recommended Ramipril, an ACE inhibitor, as his suggested blood pressure medicine because (If I remember correctly) it increases nitric oxide. He also suggested Plavix as his preferred blood thinner. I can’t remember which post it was (comments section).
I actually recommend perindopril now, as it has the greatest benefits on increasing nitric oxide.
Thanks for the update! I’m actually on 10mg Lisinopril and it works well (127/79). I’ll ask my MD about perindopril. Is there a place to search the nitric oxide effect of various ACE inhibitors?
Aha, increasing Nitric Oxide has all sorts of health benefits (with some social benefits).
But, the problem is measurement of those health benefits – are the benefits being achieved or is it money flushed down the drain?
Arginine and citruline supposedly increases NO production – how can I test this and how do I test that it is working (achieving health results).
Suggestions are welcome
I asked my GP about perindopril. He asked me to spell it. Never heard of it. Never prescribed it. Won’t prescribe it without experience of it. (Well, how does he get that experience??)
I asked because research suggests that medicated hypertensives with “normalized” resting BP nonetheless have hypertensive elevations during exercise –– except, that is, if they’re taking perindopril:
So the ace inhibitors vary on this? I have never heard of perindopril and suspect it isn’t a US brand. I do take lisinopril.
If I asked my gp to change my bp meds to the one you have recommended would he do it
That’s really interesting to me, I had this discussion with my Cardiologist as I was concerned about the potential kidney damage from Ramipril (annual blood checks to make sure) and am a big fan of increasing ones NO due to the oodles of research coming out. I was told that perindopril was not suitable for a patient with AF and was proven to be less effective. Could you clarify this one as I do wonder if ive been fobbed off here.
A quick scan of google would appear to disagree with your cardiologist.
JD, your comment re exercise is interesting. A cardiologist I saw last year told me my BP would go down with exercise, (presumably regardless of my diagnosis) and if it didn’t, I wasn’t exercising enough.
This also ties in to another confusion I have.
Hypertension is often BP diagnosed using ambulatory monitoring where BP is measured regularly over 24 hours, regardless of what environment you are in or what you are doing – ‘sleeping’ (fat chance) sitting, standing, or walking (when you are told to stand still). I believe nighttime, daytime and overall averages are calculated to decide whether you need medication or if dose needs adjustment.
My GP knows there is no point taking my BP in her office as it’s up in the 170 region, so is happy for me to provide my home readings. However, the instruction is to sit quietly for 5 minutes, back, feet, arm supported etc etc and unsurprisingly, the averages are much lower than when I have the ambulatory monitor.
So, where do I stand? Am I under medicating? Should someone like me be exercising with caution?
You mean my comment starting “It’s ludicrous…”? (It’s still “awaiting moderation”! ??)
It’s true that BP goes up with exertion. It’s also true – generally – that that BP will come down to a bit below average for you when you’ve relaxed awhile AFTER exertion.
The idea is that if you maintain an exercise regimen (repeated exertion!), your body will accommodate and assume a lower average. That’s the idea as I understand it. True??
People vary in response. I know from experience that my BP goes up on exertion and then comes down lower than my average afterwards – for a while. Has my overall average changed? Not so much, as far as I can tell. But as I’ve said, measuring pressure in your arm when you’re worried about your core tells you . . . not much. Everything is just too variable.
JDPatten: I think you’re right. The summer I did marathon training (at age 55), I recorded my BP multiple times daily, and it averaged about 105/65. Lots of running 5-6 days a week.
Sorry for late reply JD – my comment was actually more to do with BP during exercise and what should be happening (although the perindopril result is intriguing).
My BP never seems to be lower after I’ve exercised and even though I go regularly, I’ve not noticed any difference in my averages. But then I exercised regularly before diagnosis too so I guess my fitness hasn’t changed much.
I read somewhere that as I am on medication (specifically a CCB), I should exercise at a lower target heart rate to compensate but I just go with how I’m actually feeling.
BTW, the only way I would be able to get perindopril in my area would be if it was initiated by a consultant. It definitely isn’t available to my GP.
(And I’ve also lost a comment in the last couple of days – was awaiting moderation then it vanished – probably too dull).
Yeah, I used to tell myself that do-what-feels-right was best. Well, it seems I was too ambitious for my own good – pushing too hard, not resting ’cause the job needed finishing, arguing that my white coat syndrome was only in the office.
My doc was actually accommodating. For the wrong reason. He’d “lost” a patient not long before. The fellow had passed out from low (overdosed??) BP while standing in cramped quarters. Couldn’t flop to the floor which would have gotten blood back to his head. Died in the spot. So, now the doc over under-compensates.
Don’t do too much for too long. Rest often. The job, exercise, whatever, will wait for you to come back to it. Rested. Recuperated. Everything works more efficiently that way.
I now actually try to take my own (new) advice myself.
ACE inhibitors! Angiotensin Converting Enzyme inhibitors! ESCAPE!!
Inactive Angiotensin I needs to be converted to Angiotensin II in order to tense down those vessels.
Inhibitors inhibit that.
Works for a while.
But, little talked about is ACE “escape”.
Often, after a period of nicely working ACE conversion inhibition, it gradually doesn’t work anymore. The body’s compensatory systems find other means to convert that Angiotensin I into II.
Called neurohormonal escape.
Is this a real phenomenon? Hard to tell with what goes on in modern medical research.
But, to those on ACE inhibitors – keep checking your BP.
My lisinopril stopped working after a couple of years. Sneaky, but I caught it.
The same may well happen with perindopril.
Does the body know best about converting? Well, it does seem that high blood pressure is destructive of blood vessels and the organs they serve.
How high – over time – is too high?
That, and how (really!) to measure it. Those are the questions.
JDPatten: Thanks! My BP was never properly taken in the doctor’s office, but the few times it was taken since I quit lisinopril, it was as good or better than it was when I was taking it. My kidney function was assessed last December, and it was very good (94, whatever that means).
It is certainly an uphill battle to fight illness as experienced by Dr. Fettke, not least on a personal level.
‘They’ tried the same with Tim Noakes in South Africa. Despicable and totally corrupt.
Harry de Boer, Claire Hewat resigned the position of CEO at the DAA. This should not allow her to escape proscecution for negligence and derilection of duty. The same goes for all the others who were party to this perversion, with or without snouts in the trough. Resignation is should not be a “get out of jail free” card.
Well – both came out “victorious” or perhaps a better wording is that they “survived the dogmatic medical inquisition”.
Medicine/national health care is in my eyes today so devastatingly and disgustingly corrupt in the hands of Big Pharma. The discipline thus harbor just a few individuals with a true high moral to be able to withstand the pressure, like Fettke and Noakes, but at a very high personal. It is thus not surprising that the average moral standard seems to be “Just keep a low profile and abide to the rules in order to survive the system!”. Or “Don’t have any thought your own!” (Which was actually pronounced by my ‘last’ cardiologist: “I follow the rules!”.)
This reminds me of what the famous philosopher Bertrand Russell once claimed: ” Most people would rather die than THINK – and they DO!” For certain, this applies to MD’s today on various levels.
I read recently about a scary rate of suicides among MD’s – is this true and if true a mere coincidence? They should be happy with an excellent salary and still a good social status.
Sad to hear that the food in Australian hospitals is as bad as in the US. In the US, hospital patients are served soft drinks on their trays twice a day. The food is very processed, and all from boxes or frozen. In the hospital cafeteria the eggs are often powdered and watery.
Regarding JDPatten’s earlier comment about ACE inhibitors that stop working because the body figures out a way how to bypass the mechanism being interrupted and still convert Angiotensin I into Angiotensin II.
I wonder if that ties together with Dr Bruce Ames’ thoughts on Triage Theory. Because if it does, it would mean that the body perceives lowering blood pressure as a more of an immediate threat than damage to the blood vessels that would occur later.
Sasha: And if we are in reasonably good health, eat well, and stay active, it may be elevated above “normal” for an innocuous reason that doesn’t impact the progression of any disease process, and is vital for a normal life. It seems to me that, since any BP below the 70th percentile (and above dead) carries the same mortality risk, any BP within that range is physiologically necessary for the individual. Pathological would be when it creeps upward to the 80th percentile and above. I well remember when I was on an ACE inhibitor, a beta blocker, and a diuretic. When I would rise from a squatting position, I would nearly faint. Two and a half years drug free and I feel wonderful. Not dead yet!
Gary: yes, all true. I am, however, interested in this phenomenon of gradual BP rise with age. Why does it happen? Is it because aging blood vessels can not perfuse end organs and tissues as effectively as they did when they were more elastic? And the body then compensates by raising BP?
If that’s the mechanism, then it must be important enough for the body to maintain even going as far as bypassing pharmacological interventions as in the case of ACE inhibitors…
Sasha: That sounds like the most logical explanation. If the risk-reduction value of ACE inhibitors lies in increasing NO production, and there are other ways to achieve this, I’d rather skip the drugs and use other means to increase NO production.
Agreed. I would do the same thing.
Some experts believe calcified plaque is beneficial. For BP this may not be good due to carotid baroreceptors stuck in ON position calling for more blood flow. CMIT increases with age, BP will follow trend. Benefit of exercise may be to keep baroreceptors tuned up.
“Arterial baroreflex is the most important short-term regulatory mechanism of blood pressure and heart rate.1 It originates from the carotid sinus and the aortic mechanoreceptors and operates through the autonomic nervous system to buffer abrupt transients of blood pressure.2 The stretch applied to the mechanoreceptors modulates blood pressure by reciprocal changes in vagal and sympathetic nervous activity.3”
“Previously published studies suggest that in patients with significant carotid atherosclerosis, the histologic changes of the artery wall can alter the elastic properties of the carotid sinus and can cause a reduction in both the distensibility of the vessel wall and the sensitivity of the baroreceptors”
BP correlates with carotid media/intima thickness according to this study. The authors conclude that BP causes increase in cMIT, I doubt it.. Ultrasound cIMT may be best bet to keep track of plaque.
SBP was linearly and continuously associated with higher cIMT in both hypertensive and nonhypertensive participants, suggesting a detrimental effect of BP on the vascular tree prior to overt hypertension. Similarly, it suggests a detrimental effect of BP at the higher end of the normal range in treated hypertensive patients.”
Andy, why do you doubt that increased BP can lead to increased cMIT?
The study authors looked at only two things, cMIT and blood pressure. They reasoned that one of the variables caused the other. Now if one also considers “bad cholesterol” the solution is to prescribe statins and BP medications. Just kidding.
Maybe blood pressure plus something else causing cMIT progression is a more accurate interpretation. Maybe the something else is the only factor.
Saha, I posted this last week but it’s still in moderation.
When the heart pumps, the arteries will expand under pressure, storing some blood. When the heart relaxes, this stored blood will continue to feed the capillaries as the arteries contract, albeit at a lower pressure. This has the benefit of feeding the tissues with a smoother flow of blood than if arteries were rigid.
As the arteries stiffen with age, the “balloon storage” will need higher blood pressure to operate at the same volume, or will need the heart to beat faster to compensate if the arteries are too stiff to store as much blood.
A friend who was a very fit kayaker told me his heart rate was 48 bpm. I didn’t believe him and felt his pulse. BOOF… BOOF… BOOF… It was almost scary how slow and powerful his heartbeat was. To prevent his blood pressure dropping too far between beats, I assume he must have had extremely flexible arteries, or a big difference between systolic and diastolic pressures.
You just described how the heart feeds itself.
The powerful contraction of the heart musculature closes off the vessels that delve into and feed that musculature. Meantime, the various larger external upstream vessels (right, left, descending, posterior, circumflex, etc) balloon as you describe. Blood then flows to the heart musculature from that reservoir during its relaxation (diastole).
Amazing self-contained system! Closest there is to the unattainable perpetual motion machine. Good for only the better part of a century, average.
Thank you for the explanation Martin.
There’s more to it than carotid and aortic sensing.
I used to be in good shape with a resting heart rate in the high 50s. (ah, Youth! I’m talkin’ 60ish.)
Then I got an ablation that fixed my paroxysmal atrial fibrillation. Near the site of ablation there’s located nerve clusters, or ganglia. It often happens that, as a result of damage incurred there, resting heart rate increases. My resting HR went up to the low 70s instantly and has not changed in the six years since. This is a little known and little understood phenomenon.
But it’s there.
I asked my electrophysiologist about it, wondering about blood volume of each beat. I theorized that with a higher rate, each beat must be of a lower volume to maintain regular flow. He insisted that each beat had the same volume, with increased demand during exercise being taken care of by increased HR.
When I suggested that my new resting HR must therefore be supplying more flow than required, he had no answer.
Blood flow to brain is important. Agree that there are many other factors involved. Signalling molecules from heart, kidneys, hypothalmus, thyroid are also involved. A self regulating system under normal conditions. Chronic stress can upset the system.
Right. Include compromise of one or more of those regulating systems.
You’d think that the others would take up the slack to compensate, but that’s not happened in my case.
The October 4 Lancet has an article about Lp(a). Behind a paywall, of course.
“When it comes to blood pressure it cannot be denied that. as the blood pressure rises, the risk of CVD also rises.”
Or, is it that as CVD increases, blood pressure rises? A consequence of CVD narrowing the arteries is that, to maintain the same volume of blood flow, the pressure would have to rise. If CVD comes first, through damage to the endothelium as discussed earlier, higher BP has to follow.
You could assume that it’s a snowball effect: the more plaque blockage, the more pressure is needed to prevent dementia and other forms of hypo-perfusion, the more damage to the endothelium is done due to that increased pressure and its turbulence, the more plaque . . . etc, etc.
So, the choice is a curtailed life with a clear mind or a longer life compromised with dementia.
But is that scenario true??
Hypothesis: arterial glycocalyx dysfunction is the first step in the atherothrombotic process
which I assume I got from here in the first place, I had a thought: maybe if the glycocalyx is damaged the frictional losses on the flowing blood will increase, hence BP will be increased to keep it flowing
While Ancel Keys is rightly demonized for claiming that saturated fat causes heart disease, it’s less widely known that he later promoted a Mediterranean diet. As Dr. Aseem Malhotra and film maker Donal O’Neill have shown in several films (The Big Fat Fix, Run on Fat, and The Pioppi Protocol), Keys tried to publish data repudiating his fat-CVD claim but was rejected, because it didn’t fit with the prevailing wisdom. So he wasn’t a complete villain.
John H: The threshold is given in the paper: for a man 45-74, 110 + (2/3) (age); for a woman 45-74, 104 + (5/6) (age). For me at 69, the threshold of risk would be systolic 156. In recent years it has varied between 130 and 150. My diastolic has varied from 75-85 most of the time. No cause for concern, in my view.
Interesting note about BP. Line has crêpe up over the summer maybe because I did less biking. Now just back from án hour and a half spin, and after an hour my BP is wonderful. Go figure
If humans aren’t contributing to a global warming problem by much, then what possible strategies could be done to mitigate it?
Anna – what can be done to mitigate – pay vast amouns of tax, to keep the “experts” in swimming pools (heated) and first class plane tickets to go to lovely conferences.
Much more money is made by the dirty energy companies. The billioinaire Koch brothers want to make sure they keep their filthy profits by donating money to think tanks and public relations groups to convince people that global warming is a hoax. And our anti-science president does all he can to hush any talk of global warming or its causes within federal environmental departments in order to pay back the corprorate polluters who backed his election.
Partisan politics again. Provides no useful information.
AnnaM: First we must look at the actual science. Most of what we know about past temperature comes from surrogate markers, such as ice cores, sediment cores, tree ring data, and so forth. We have very few reliable temperature records prior to the mid-20th century, yet it is clear that the Earth’s climate has been warming since the end of the Little Ice Age in the early 19th century. This warming, however is slow enough to easily plan for. Nothing catastrophic about it. The alarmists are simply wrong on this point. It is a political position, and some, such as Al Gore, have profited handsomely from schemes involving carbon. Some even call CO2 a pollutant! Life on Earth is carbon-based. It is our mother’s milk. The same factors which have broken science and medicine have broken our approach to a warming climate: primarily greed, the desire for power and recognition, and the sheer stupidity of the political class.
Al Gore? And you reprimanded me about “partisan politics”? So Al made some bucks on a book and a movie? How is that compared to the big bucks made by fossil fuel companies who buy politicians and s? Yes, CO2 can be lethal if there is too much. Water can kill you if you drink enough of it. The poison is in the dose.
People have noted that drug studies are untrustworthy when they are run or paid for by the very pharmeceutical companies that peddle those drugs. I think declarations made by scientists who are paid by corporate polluters are also suspicious. You mentioned Dr. Judith Curry. She has taken money from the Koch brothers for years.
I wonder if money is what drives Koch brothers. Before the financial crisis of 2008 each one of them (the two that are politically active) was worth 17 billion dollars. By 2016 or thereabouts, with all the gains in the stock market, each one of them was worth 41 billion. (I haven’t double checked those numbers but they come from the book “Dark Money”).
As one of the brothers said: with these numbers, it’s kind of ridiculous to suggest that they do what they do for money…
Well is the Earth any less habitable than it was in 1880, when the averaged temperature was 0.8C lower? In other words, do we need to do anything – even if there was anything we could do.
David Bailey: As I see it, we can’t do anything positive to affect Earth’s climate; it is too vast and complex and thus we cannot possibly understand the whole picture. What we are doing, which will not change the climate in any way, merely warps economic activity, making everything more expensive.
Not less habitable. Greener.
I suggest hiding our heads in the sand.
Afforestation would help, as noted by the chairman of BP this week, but the areas required are huge, equivalent to another Amazon Basin. Whether this would ‘sink’ the co2 released from warming oceans is another question.
Mitigation is rather to apply best science to making changes that will happen when the Earth warms more survivable and protecting the important habitats by e.g. translocation, things we already know how to do. But above all there needs to be a concerted effort to control and then reverse the growth rate of the human population.
But Lovelock has already pointed out what to do many years since.
Stephen Rhodes, there are moves to reduce the population in place already. Amongst others, they are the pharmaceutical industry, pesticides, glyphosate, dietary associations, bill and melinda gates founation, world health organisation. The list goes on.
Stephen Rhodes: Additionally, restoring grasslands by reintroducing grazers and properly managing them would do more than reforestation to capture CO2, as soils in grasslands sequester much more of this vital molecule than forest soils.
Slightly off topic, but I posted this near the end of the last thread, so people probably missed it. I think it is important as it goes into a fairly strong religious agenda that is driving the global vegetarian and vegan dietary advice. Written by Dr. Fetke’s wife.
Dr Watson, you’re great! I’ll now try to convince my “drugs dealer” 😉
Blood pressure (bp) – arterial stiffness – brachial artery – CVD
I won’t call my following comments a n=1 experiment, but they are tests results all relating to blood pressure, arteries and CVD.
Firstly, some background/context: I’m a survivor of a near fatal CVD incident which involved cpr, then defibrillation, then intensive care then, upon regaining consciousness, concerns for brain damage due to anoxia and/or hypoxia. And a coronary artery calcium (CAC) score of 1500. Very high.
So, did I find any connection between several bp readings, one arterial stiffness test, a CVD incident and a high CAC score?
1. BP – I’ve had no known issues over the years with perhaps 8/10 readings being normal. As many commenters and home testers here know, bp readings are snapshots in time and can be influenced by time of day, locations and activities.
2. Arterial stiffness and pulse wave velocity. I had my arterial stiffness measured a few weeks ago using the cuff method, as demonstrated in this clip which clocks in at 2 mins 17 seconds:
For those interested, 3 readings were taken (left arm) to get an average reading. It cost £40.00 but the 1/2 session with a healthcare practitioner did include a lifestyle reviews (and some new age nonsense too but that’s another story!).
The gradings range from 0 to 8 with 4 being average. I was pleasantly surprised to get 5/8 – just above average, or “mild to moderate arterial stiffness” as the software manufacturers describe it.
Pleasantly surprised because of my high CAC score and concreted arteries.
But what do they mean by average? Average for a 50 something male or average across all ages?
This method may or may not be available at your doctors…I didn’t even ask.
Alternatively, sit on the floor with your back to the wall and legs out straight and try and touch your toes.
3. Noting Andrew Larwood’s comments about blood pressure being taken with the cuff on the brachial artery, I thought this method of measuring arterial stiffness might give a more accurate and complete picture. It clocks in at 4 mins and 2 seconds:
Mulling over Andrew Larwood’s comments about the brachial artery, is there any reason why the cuff is always placed on the brachial artery? Presumably it’s a good, practical location to place the cuff? Do those commenters with their bp testing machines ever place the cuff elsewhere e.g. forearm, lower leg?
So, I’m not sure what to make of these bp, arterial stiffness and CAC results (taken over a period of 2 years). In the context of a “dead man walking” CAC score, I would and was expecting both high bp and very stiff arterial reading results.
Perhaps that testing doesn’t always answer everything.
Testing! ¨¥©¨•¥†®∂ !!!
If 1,500 is dead man walking, what am I? I’ve got you beat by 140 coronary artery calcification points.
That’s not to say that either of us wins. But consider this: I passed a classic stress test last week with gliding colors. That is, no indication of CVD. Never had chest pain. Went up to the 170s in heart rate. Only 160/ 98 BP . . . controlled by losartan.
I’ve had atrial fibrillation fixed by ablation in the past – my only cardiac complaint besides modestly elevated BP.
CAC is bollox. Could mean you’re about to drop. Could mean that’s behind your CVD incident. Could mean anything for your future = could mean nothing at all. Not worth the $ to test.
JDPatten: Good for you. Way to go.
Charles, wow, a survivor well done! thanks for sharing.
Interesting questions – I hope you get answers.
Hi Charles, I believe the reason why the cuff is placed over the brachial artery is because of convenience and this method was widely adopted from 1905 and hasn’t really changed. So for new methods of measuring BP to be adopted routinely will require a massive re-education of the medical fraternity. I believe the best way of accurately measuring BP non-invasively is to use ultrasound Doppler and derive pressure from flow especially at the level of the carotid artery which would give a much more accurate value of central aortic pressure.
Interesting videos on two different techniques. You will notice from both techniques that the morphology of the waveform, one with vertical lines and the two from the SphygmoCor device are different shapes which is exactly what one would expect as the waveforms are being obtained from different parts of the arterial tree. The method of recording the “morphology” of waveforms also has some effect on the shape obtained, PVR in the cuff and tonometry in SphygmoCor. In the determination of the PWV, the measurement of distance also introduces errors because the vascular tree isn’t a straight tube. Many of the commercial devices use mathematical transfer functions to calculate central aortic pressure, PWV, etc., from a number of parameters measured non-invasively such as brachial BP against an invasive Millers catheter in the aorta. Of all the commercial devices on the market I think the best one is the BP+ from Uscom. However, I still think measuring pressure from flow in the carotid artery using Doppler ultrasound is the most accurate method but clearly it isn’t a method which could be used in routine practice.
This xkcd, from September, illustrates well the problem discussed in the quote from Port’s article, about the relation between statistical models and data.
The different outputs permit the endothelium to regulate blood pressure… While endothelial cells are mainly organised with the long axis of the cell parallel with the direction of blood flow, at artery branch points the cells are less organised and the cells have multiple directions. (a weakness?) https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5381697/
ONLY 2% Because degenerative vascular changes such as aneurysm and post-stenotic dilatation develop at lower blood pressures than those necessary to rupture healthy blood vessels, mechanical stress acting on the wall cannot be the only cause for aneurysm growth and rupture. Flow impingement at arterial bifurcation apices generate only a 2% local pressure increase… https://www.researchgate.net/figure/Endothelial-cell-density-as-a-function-of-distance-from-impingement-after-48-h-exposure_fig6_51428119
From paper – “Therapeutic modulation of the nitric oxide: all ace inhibitors are not equivalent” (Comini, Bachetti, Et al – 2007):
“All ACE inhibitors increased endothelial nitric oxide synthase (eNOS) protein expression and activity in the aorta (both P < 0.0001 versus vehicle) and in cardiac myocytes (both P trandolapril ≈ quinapril ≈ ramipril ≈ enalapril (P < 0.05 perindopril versus trandolapril and ramipril and P < 0.01 perindopril versus enalapril, respectively).”
I can follow the gist of this but struggle with the statistical values e.g. P < 0.05 – can any put this in layman’s terms please ?
Apologies, my previous post appears to have lost some of the quote from the paper – it ought to have read:
“All ACE inhibitors increased endothelial nitric oxide synthase (eNOS) protein expression and activity in the aorta (both P < 0.0001 versus vehicle) and in cardiac myocytes (both P trandolapril ≈ quinapril ≈ ramipril ≈ enalapril (P < 0.05 perindopril versus trandolapril and ramipril and P < 0.01 perindopril versus enalapril, respectively).”
Still appears to be chopping some text from the quote – apologies
I have a little bit of personal information I can share on BP levels. Not entirely sure why I’m sharing but here goes nothing. Here of late I began taking a natural nitric oxide supplement. It is being advertised as being able to raise nitric oxide levels. I thought why not, I’m game to give it a try and see what happens. Expectations were low. My thoughts going into this NO raising experiment were that I would develop red urine from the beets which when seeing would have me thinking of the $30 spent seeing going down the drain. I’m pleased to say though after a couple weeks I believe of taking red beet powder raising NO levels I’m feeling quite chipper. I’m sleeping better, breathing deeper and talking better too.
I have a condition similar to Crohn’s disease. I say similar as here in America if I gave the name of my disease, Lymphatic microscopic colitis, I tend to receive stares and sometimes jokes about small microscopic things. There are few to no medications for MC. Crohns on the other hand is well known due to the constant TV adversing for Crohns medications. The people in the TV ads for Crohns look like they are in heaven. It’s a sight to see. Well anyway, with my similar to Crohns disease my BP levels can be elevated at times. I personally do not measure my BP levels. For what ever reason though the different dentists I see do measure BP levels. I don’t know why they do this. I’m afraid to ask. I’m not sure I want to hear the answer. MY BP levels are not an alarm but they are on the upper end of things. For me it is easy to understand. I’m sitting down in a dentist chair. I’m not a fan of dental drills, big needles, grumpy dentists, nor does sitting in odd shaped chairs placing more pressure on my inflamed stomach area help. MY BP levels will rise when at the dentist. The stomach often pulses. I can feel the pressure from the blood, or at least I believe that is what I’m feeling, when the colon is irritated, pulsing which is often. It can keep me up late into the night at times.
So with drinking the beet juice, high in NO, the pulsing has largely stopped. I feel calm all over. I recognize this feeling too from earlier experiments with juicing. Juicing, the blending of green vegetables, straining, and drinking them, is common for those with Crohns and similar conditions. Juicing provides a sense of calm to the stomach area. Juicing should also provide good quantities of NO I imagine.
So to wrap this novel up, I’m enjoying the NO boosting beet juice up this to this point. BP levels are likely lower. The stomach pulsing is greatly improved. I’m breathing better. The stomach pulsing can effect breathing and talking. Overall, I’ll give super beets NO raising powder a thumbs up to this point. May the good times continue. Hoping it does my heart good too.
Soul: Good for you! I take beet juice daily, too, and feel great. Have you read the literature regarding GI tract problems and the gut microbiome? This may be of help. By the way, I have a fine dentist, and he hates the chairs, too. Apparently, OSHA regulations made changes to dental chairs to make them as uncomfortable as possible. He always has to adjust it after I’ve sitten down to make room for my gluteus maximus.
Gary, a little bit and I’ve tried a number of probiotics over the years. Non helped me. I’ve seen others with Crohns like diseases though have better success with the gut bugs than I have. It seems to be a hit or miss with those. All isn’t lost for me though. Here of late I’ve been seeing some stomach improvements by avoiding beef, dairy products and pork. Fingers crossed I can stick with the diet long term. Seems people enjoy tempting me with hard to resist hamburgers.
I used to avoid getting a BP monitor, because I was afraid I might become a hypochondriac. However I gave way in the end, and I am glad I did.
Measuring my BP at home means that I can sit using the computer for a short time, which usually calms me down, and then I can take the reading from the correct position. I can also avoid stupid times to read my BP – such as while upset for some reason.
Measuring BP at home made me aware of the fact that BP varies, even after standardising the conditions. This means that in addition to the white coat effect, that you describe, having one’s BP taken in the surgery is a little like throwing a dice to select the values from what (I imagine) is a Gaussian (bell-shaped) curve. The average of more frequent measurements is going to be far more consistent.
David, For awhile I measured my BP levels at home. For me I eventually lost interest in the measurement.
David, a couple of my responses have not appeared this last few days. My points were that 5 years ago I agreed with an endocrinologist to stop many prescribed meds, including a large dose anti hypertensive…I had been prescribed all sorts of them, despite 24 hour tapes, and home measuring over years, before it was acknowledged that I have white coat hypertension.
I have now found out that I have been classed as a non-compliant patient! It reminds me of the work of Stockwell in the late 1960s, describing the concept of ‘”The Unpopular Patient” .Nurses of a previous era may recall the work.
Not taking popular meds is a blow to Big Phatma.
“Me Too” Beets helps lower my blood pressure to the point I am satisfied … 135 / 75. NO ,,, definitely for better HEALTH.
Kathryn, I’m hooked. They have me feeling better. I need my daily vitamin NO rich beets.
Soul. I like to juice beet/beetroot with apple even though labour intensive; most beet powder sold here is from China. I just started reading the Plant Paradox by Steven Gundry, MD, re lectins and the gut. He does mention curing Crohns and other autoimmune illnesses with his methods.
I like the taste of beetroot – so can anyone recommend how much I would need to eat to be effective?
Since nothing is good in excess, I wonder what effect too much NO would have – does anyone know?
David Bailey: Many other vegetables, such as arugula and celery contain nitrogen compounds. For a long time I took 1/2 cup of beet kvass in the morning and 1/2 cup in the evening, both with the 7-800mg potassium bicarbonate stirred in. Now I take only half that much. “Nourishing Traditions recommends 1 cup daily, but I’m not certain if that is based upon any scientific evidence. Dr. Mercola made a post about this two or three months ago. Check the archive under nitric oxide.
Frances, I saw that recently about China selling most of the worlds beet powders. It had me thinking if I’m poisoned it wasn’t the Russias it was the Chinese that did me in!
I’ll likely look into new NO ideas in the future. I tried juicing in the past. A problem with green vegetable juices is the cramping it would eventually give me.
It is a controversial area for many with Crohn’s and similar diseases, to use diet to treat the condition. Quite frankly some will become highly agitated about this theory. With that said, it is common for liquid diets to be used by those with Crohns and similar conditions when experiencing a flare. There are a study or two out there on liquid diets putting a person with Crohn’s into remission quicker than medication can.
A few problems I suspect with the diet route is the length of time needed to remain on it, extensive damage to the digestive system that heals poorly if at all, an idea unsupported by many in the medical field and with people in general, and probably the biggest problem food is used for social reasons. While not perfect with the side effects, sometimes poor effectiveness, and high costs it is easier for most to take the drug approach. I unfortunately have only been given one choice for my disease, the dietary route.
Much less labour intensive is to make beet kvass! Chop up local beets with a tablespoon of Himalayan salt and water to the top of a container, cover with muslin, and leave for 3-4 days, stirring daily. I make mine in a 3 litre jar. An extra added bonus is that the kvass is fermented, adding lovely probiotics!
Frederica Huxley: That’s a big jar! Do you ladle it out? I make mine in a half gallon jar (a bit under 2L), and it takes some man-handling to pour when full. I also add whey, which I make by separating raw skim milk.
I carefully pour the kvass into a sieve over a large jug sitting in the sink! I used to add milk kefir whey, but found that there is much less kahm yeast without it. Btw, I also add a few tablespoons of blackberries and elderberries when making kvass – it takes away the ‘earthy’ taste.
Frederica Huxley: Kham yeast is new to me. Is this that white stuff which forms at the top? If eliminating whey would eliminate that, I would be pleased!
I would love to hear peoples’ thoughts on this book. I keep hearing about it…
David, I guess every one is different on how much nitrate is needed. In general from what I’ve read 300 to 400mg of nitrate are needed per serving to achieve lower blood pressure from the NO that is produced. To many nitrates consumed can be a health problem. What I’ve been doing to test my NO levels is to use a saliva NO testing strip. Outside of diet too I’ve been sun bathing which also is supposed to raise NO levels.
If all the beetroot does, is supply nitrate, what is wrong with consuming a small amount of saltpeter (potassium nitrate)?
David Bailey: Isn’t that what they used to give the boys as an anti-aphrodisiac? Not that it matters much at our age.
I read the “Plant Paradox” with great interest and learnt a lot.
There is a lot of logic in that most plants have a “defense system” (lectins) of their own to avoid being eaten if they don’t want that to happen by purpose as with the ripe fruits with seeds to be spread.
I don’t remember now if green grass leaves is also an exception and invites herbivores.
BTW I think the book mentions fermentation as a way to reduce the lectins in the vegetables. I am regularly making my own sauerkraut (seen as a Hippocratic “medicine”) in a big jar. Takes a couple of days, a week, on the kitchen table (the smell and taste tell you that you have been successful) and lasts for about a month when you take your small daily toll, and when kept in the fridge. I just put a fresh load there 🙂
Goran, thank you for the information on “Plant Paradox”. I was asking because the central premise seems to go against most of our evolutionary history (unless one is an Inuit) and modern research regarding plants (Bruce Ames and his Triage Theory is one example).
I agree with you on the benefits of fermentation. It does wonders to our gut and tastes great.
Regarding cheap organs and bones – it’s amazing how best things for us healthwise are either very cheap or free: bones, fasting, time restricted eating, exercise, meditation, etc.
But I also don’t want to disregard the book without reading it…
Göran Sjöberg: I make a year’s supply, since I only grow cabbages once a year. Made 34 quart jars last winter, and have already devoured 21 of them. Love it with my eggs at breakfast (which is actually eaten at lunchtime).
I learned to ferment my sauerkrauts for at least 4 weeks, as the fermentation goes through specific stages. I recall that the maximum vitamin C develops after 3 weeks. Even though I quite often leave the kraut out for 5-6 weeks, before decanting into the fridge, my krauts are crunchy.
It doesn’t matter “at our age”??
Speak for yourself, my lad.
As for saltpetre, it was a raging rumor that they dosed us in Navy boot camp (1966. Figure my age.)
JDPatten: Still, the question remains, is it a good idea to get NO from saltpetre? The article makes it sound like instant death.
Gary – instant death is one hell of a cure for high blood pressure.
Gary, The last hot dog I ate was well before my Navy experience. I’ve kept away at least in part because of the generally accepted “wisdom” over time, that nitrates were bad for you.
How much do each of us still innocently accept as gospel that which has been spouted by all manner of experts without true examination?
Sure, less. Here and now.
But still . . .
Actually, I’ve kept away from ‘dogs mainly because they’re so overtly disgusting!
JDPatten: Disgusting, indeed. Only at the ballpark for me, which is never because I don’t follow baseball any more. Love mustard, though, but only on pork.
That yellow sauce in the US is not mustard, try English mustard, that’s mustard.
AhNotepad: I haven’t had that yellow stuff in quite a spell. Haven’t seen English mustard, but usually get either Dijon or German mustard. What is the brand name of your favorite English mustard? I’ll see if I can find it.
Colman’s is the original and best English mustard. Ready mixed is ok, but for the real thing, get the powdered, and mix it yourself.
Jean Humphreys: We do have Colmans here in the colonies. My mother always had a tin of the powdered in the spice rack in the ’50’s. I sometimes buy seed and grind it myself if a recipe calls for dry mustard.
Gary, fair do, the French and German mustards are definitely good, apart from the wheat and the rapeseed oil in some varieties. The most common English mustard is Colman’s, hot stuff, but even hotter is to buy the powder and mix up a little for the meal, (as we did when I was young). About the same effect as horseradish if you were not cautious.
I did my National Service in the army in 1965. It was rumoured they put bluestone (copper sulphate) in our coffee as an urge suppressant. Mind you, after being chased around the parade ground all day by a drill sergeant, all you want to do is sleep.
“I learned to ferment my sauerkrauts for at least 4 weeks, as the fermentation goes through specific stages.”
I didn’t know this so I think I now bring out the jar from the frige and let it stand on the kitchen table for another three weeks although it already just tastes great.
This article explains the fermentation process – this is a three week timescale, whereas the article I first read years ago when I starting making sauerkraut definitely propounded leaving it at least four weeks!
Click to access the-science-behind-sauerkraut-fermentationc2a0.pdf
Frederica Huxley: I have the book from which this is reprinted, signed by the author. Interestingly, the kimchee I make instead of sauerkraut is a two-day ferment maximum, then into the fridge.
I make both kraut and kimchee (and the sublime leekchi), but I’ve never worked out how/why kimchee ferments so much faster than kraut!
I refrigerated a batch of sauerkraut after a couple of days only. I knew it would slow the fermentation, but it stopped entirely. I took the jar out of the refrigerator after some weeks and left it at room temperature, hoping the fermentation would start up again, but it didn’t.
Lesson earned: Only refrigerate after fermentation complete.
BTW, I like my sauerkraut well-fermented, or as others call it, “rotten”.
I would imagine that you must leave your sauerkraut fermenting for a very long time to have it rotting! Kraut takes 3-4 weeks to go through the different stages of fermentation; many of us leave it fermenting on the counter for much longer than that, with no loss of crispness or taste.
Frederica, I should have put a winky emoji there. To sauerkraut-haters like my family, even a little bit fermented makes it ‘rotten cabbage’. But I do like it several weeks old, beyond the crispy stage to slightly mushy.
I have somewhat primitive equipment and often the top inch or so of kraut is actually brown and rotten from air getting to it. I just discard that layer and eat the rest.
This sounds like my own diagnosis five years ago — (microscopic) lymphocytic colitis? It’s on the same spectrum as Crohn’s, an inflammatory bowel disease (IBD). I’m fine as long as I avoid grains and legumes, as per The Whole 30 or The Primal Blueprint. Healthy fats and local grass-fed beef are my medicine 😁
greenhind, Sorry to hear you are a member of the dreaded MC club. Glad you found what works for you. I also did better with my MC when I stopped eating grains. I’ll have some rice without to much trouble.
I’ve been able to get the digestive system working completely at times when eating grass fed cheese. I never was able to fully heal though. Energy levels remained to low. I now suspect the cheese was a hinderance. Cheese has a natural tendency to constipate. So now I’m avoiding cheese, and beef along with pork. So far so good. I’ve done this diet before and lost faith after 4 months of avoidance. I believe this time I can go longer with the trial to see if I heal better, since my energy levels are improved and I’m appearing healthier.
Bone broth from the same grass-fed source is a staple in our family. The best (?) medicine for your damaged intestines according to not least Dr. Campbell Mc Bride.
I am making a new stock in my slow cooker every week.
The funny thing is that actually the best parts of the animal, the liver, the kidneys and the heart you almost get for free and certainly the bones. I had 20 kg of bones recently and they were just happy to “get rid of them”. How did we arrive at this “craziness” ?
But I guess that they will “learn” to charge you with time but just now I enjoy the “free ticket”.
I wonder if you ever take NSAIDs? Ibuprofen, naproxin, indomethacin, etc.
Ibuprofen caused my extended case of lymphocytic colitis.
A year of diarrhea before my official biopsy diagnosis.
I was guilty of assuming over-the-counter meds were innocent.
Never in my life will I take an NSAID again!
Goran, Bone broth is very popular with people with MC. At least it is popular on a chat forum dedicated to those with MC. I personally tend to take fish collagen. it seems to help a little with my condition.
Either of you ever use proton pump inhibitors – omeprazol and the like?
‘Cause there seems to be a link with microscopic colitis:
Keep away from NSAIDs.
You haven’t mentioned them, but they are well established as triggering lymphocytic colitis in the susceptible.
I haven’t had symptoms of my LC since strictly quitting all NSAIDs.
Thanks. I was aware of the link between NSAIDs and MC. I’ve never taken NSAIDs so that wouldn’t be the cause for why I developed my condition. I suspect I was born with my disease. At 15 I began to become ill, and by 19 was sick everyday. Even before the age of 15 I had health issues. Fingers crossed that dairy products, beef and or pork are what have caused my condition. An interesting for me discovery recently is that when avoiding dairy and beef my eyes change colors. They become blue. I’m hoping the new blue eyes are going to point me in the direction of becoming well.
Wow, Soul. Really interesting. What color were they before changing blue??
I’m wondering exactly how you were diagnosed. (If I may.) Intestinal biopsy? That’s the only way they can put your tissue under the eponymous “microscope”. I wonder ’cause what you describe isn’t typical. Could be something else?
I mainly have fish for dinner. No pork, certainly no grains, but I dabble in beef occasionally. Love cheese. No ill effect. The NSAIDs seem to be my culprit.
Before my eyes were greenish. What is interesting is that on a chat sight dedicated to MC discussions, most listed their eyes are being green. Curious I thought.
Yes, I was diagnosed by biopsy. The testing was done a couple times by different GI specialists. I personally have thought the diagnosis incorrect. As one GI physician told me sarcastically, it was likely a New York doctor that came up with MC, and made millions. it’s nothing more than colitis, bla bla bla. It’s been awhile since I saw him but believe that is what he said. As I have been known to joke, if I paid enough money I could have had the disease named after me – Soulism. You have Soulism.
Fascinating. Mine are brown. Always have been.
Diagnosis. Pff. Maybe.
Back when I first got a diagnosis it was for Crohn’s! Gastroenterologist sent sample to a dedicated lab on the other coast (I forget the name. Probably named after the developer – Bogus or some such.) Horrific illness. Scared the hell out of me. I dropped the NSAIDs and gradually got better. I had doubts about it. Then, a few years ago when I took only a couple of ibuprofen: relapse! The new gastro took the biopsy and pronounced the Crohn’s a false positive. Some lab guy looking through a microscope – which makes everything scientific and neat, right? – decides that he’s seeing “microscopic” colitis. Changes everything! (Nothing.)
You start crossing the street. The “answer” is on the other side. The street is a river of quicksand.
As a hypertensive (controlled) who now has an automated measuring device at home, I have now developed some doubts about what is the “correct” blood pressure of a person. Simply sitting still and breathing steadily and deeply for a minute can reduce my systolic pressure by as much as 10 mm of mercury, with a smaller corresponding decrease in the diastolic as well, while the heart rate remains the same.
I have also seen some literature suggesting that the correlation between the brachial BP and the aortic BP differs between persons, and since it is the aortic BP that would have the most influence on CVD, that is the one we should aim to measure.
I eagerly await Malcolm’s next blog.
Indeed, brachial BP is only a reflection of the pressure in the brachial artery and no where else in the arterial tree. A paper published a few years ago identified that 70% of people with what the medical establishment calls “high normal” i.e.139/90 from brachial BP measurements had abnormal central BP equivalent to patients in stage one hypertension, yet these are the patients that should be treated. I forget the exact numbers but many patients that have strokes or heart attacks are found to have had normal brachial BP.
Final try to get the extract from “Therapeutic modulation of the nitric oxide…….” to display correctly. This is only part of the abstract, the paper is behind a paywall.
“All ACE inhibitors increased endothelial nitric oxide synthase (eNOS) protein expression and activity in the aorta (both P<0.0001 versus vehicle) and in cardiac myocytes (both Ptrandolapril approximately quinapril approximately ramipril approximately enalapril (P<0.05 perindopril versus trandolapril and ramipril and P<0.01 perindopril versus enalapril, respectively). Levels of circulating nitrite/nitrate, the end-metabolites of nitric oxide, were also significantly affected by ACE inhibition, with the same order of potency. Our findings provide further evidence in favor of differential effects associated with ACE inhibitor therapy and suggest that the clinical benefits associated with these drugs may not solely reflect a class effect extending their benefit beyond blood pressure-lowering effect.”
Any help on understanding the the statistical references would be greatly appreciated.
Martin, any help in understanding the complete paragraph would be useful. It is badly written (I was going to say “poorly” but that would have been misleading). It is written by someone trying to impress readers rather than trying to give an understanding about a subject. I work from the position of “if a reader cannot understand what the author has written, the author has failed”. I accept that some things are too complicated for some people, but that paragraph is almost nonsensical.
Bah ! For some unknown reason, the middle part of the text I’m trying to post (which is shown correctly in the draft) – disappears after clicking on ‘post comment’.
I have copied the missing text only (the statistical part to which my question referred) which may or may not be shown below – if not, I shan’t try again !
“(both Ptrandolapril approximately quinapril approximately ramipril approximately enalapril (P<0.05 perindopril versus trandolapril and ramipril and P<0.01 perindopril versus enalapril, respectively)”
Nope – it won’t show the missing text. Sorry.
What happens in the body affects the mind. What happens in the mind affects the body. We are all different in both areas. Blood pressure will vary from minute to minute to maintain adequate blood flow to tissues. If one is reasonably healthy then blood pressure should not be something to be concerned about. Even the action of taking BP will affect BP.
@Gary, thanks for the suggestions about Climate Science. I like Judith Curry’s blog ..A true scientist examining hypotheses and seeing what works…
I wonder if there has been a huge mis-focus on CO2. I am a farmer. I know that growing wet rice leads to methane being released into the atmosphere. The rice uses a microrganism to access nutrients in the flood soil..The micro-organism produces methane as part of that process.
The global population dependent on rice as a staple food has increased massively in the past 120 years..Around 800 million in 1900 ti around 5 billion now…That inevitably means a lot more methane is being produced. And methane is 40 times more warming than CO2..whie in the atmosphere..And yes it does break down ( into co2 ) but as it is n increasing component of the atmophere, I suspect it is playing major role in global warming. And yes, feed lotting cattle also adds methane to the atmosphere as well.
Sorry about the total diversion away from CVD & BP, Malcolm…I will refrain from now on.
Bill in Oz: Yes, I find reading climate science fascinating, although a good chunk of it is over my head. An avid reader from boyhood, I still find acquiring knowledge a supreme pleasure. I still have the first book I ever owned, The Jungle Book, given by a librarian church lady in 1957 on my eighth birthday (she shared my birthday).
Bill in Oz: The lady from whom I buy my chocolate has painful spinal stenosis. I told her CS, along with vitamin C, might help rebuild the missing cartilage. Out of curiosity I searched CS and stenosis. One thing i found was that the cell walls of mushrooms contain Glucosamine sulfate. Any thoughts?
Gary, I cannot comment about mushroom and their CS content…I simply don’t know. But CS is readily available from Iherb etc online.. So it would not be hard foe this friend to try CS out…
Bill in Oz, fixing risk factors applies to CVD as well as climate. BP in case of CVD and CO2 as cause of weather problems. Both are complex systems.
Rapid climate change can also result from volcanic activity and altered ocean currents. Global cooling might be more detrimental for crop production.
Indeed they are complex systems Andy…And global cooling would definitely damage production of many crops….I am old enough to remember the Climate Cooling scare of the 1970’s In fact I still have a book about this on the shelf…Methan just piques my interest because rice is a crop that a substantial proportion of humanity rely on for daily food.But nobody is saying reduce rice crop production to reduce methane..It’s just sort of ignored as if it did not exist.
in much the same way as the facts of CVD were ignored for decades…
Bill, there’s a book “The End of Plenty” written by a journalist who was trained as an agronomist. I now forget the exact figures he quotes, but I think it’s something like a third of humanity is either undernourished or malnourished. A lot of them rely on rice as their main staple. Reducing rice production would probably mean either further malnourishment or death for many of them.
Sasha, I know that malnutrition is common in poor nations and that many of these people rely on rice as their major daily food.
I am just pointing to the facts. Population growth in rice crop dependent countries has been huge in the past century and is still growing..And the rice leads to increased methane in the atmosphere and global warming… But nobody is saying much about it…
An added note : Organic rice farmers here in Oz minimise their methane production by drying out their fields regularly as part of minimising methane production.But new research shows that this also increases NO release from the fields…Ummm ! Another toxic green house gas increase !
I’m an environmentalist and a physician that practices natural medicine. I used to be an engineer. I was so depressed about humans causing global warming that I become obsessed with it about 5 years ago and spent months pouring over the data. I was shocked at what I found. The science behind global warming is a joke. Politics and money appear to be the only thing keeping the story going.
Dr. John H: That’s right. Powerful forces are at work to increase the wealth of the ultra-wealthy, regardless of the effect on anyone else. Sadly, most people are sheep, or merely scraping by. Another area where policy is based upon little or no data, or suppressed data is vaccination. Read “The HPV Vaccine on Trial.” I was so angry I had trouble sleeping for two nights. The clinical trials were entirely fraudulent, designed to ignore, or entirely miss safety signals. The death rate in the trials was twice (8.5/10,000) the background rate (4.37/10,000), and 37 times the death rate of cervical cancer in the U.S (0.23/10,000). (Source: National Vital Statistics Report and National Cancer Institute)
Big Oil and Big Coal have a vested interest in denying global warming. They are terrified that countries will introduce a carbon tax, which will hurt their sales and profits. Big Ag too, because their profitable farming practices like deep ploughing that damage soil carbon might be banned. I don’t think the academics warning us about global warming are the bad guys here.
I’m not sure what part of global warming science you regard as a joke, Greenhouse gases in the earth’s atmosphere cause heat retention. That is predicted by theory and confirmed by satellite measurement. The earth is radiating away less heat than it receives, therefore it is gaining heat.
What is not certain is what is going to happen, or how soon it will happen. For instance, there was a ten-year period when temperatures didn’t rise as expected. It turned out that the excess heat was going into the ocean, which is very poorly instrumented. We simply don’t know much about what is going on on 75% of the earth’s surface.
But some consequences are already driving decisions. A patch on Earth will gain heat in the day then radiate it away at night. But because of the blanketing effect it can’t cool down as much. So night-time temperatures are creeping up. This is important for many crops. If you are a farmer planting an orchard that might last 50 years, you have to worry whether it will remain cold enough to set the fruit. And of course you have to worry whether rainfall patterns will change, as we learned here in Cape Town when we nearly ran out of water from the city dams last year.
Catastrophic consequences — giant burps of CO2 from warming oceans or methane from clathrates or carbon from permafrost; several metres of sea level rise; massive population displacements due to climate change; destruction of marine animals due to acid sea water from absorbing CO2 — who knows for sure whether or when these will happen? But they are possibilities.
My favourite theory is that when the Arctic ice cap melts permanently, increased evaporation from the Arctic ocean will drop so much snow on the surrounding tundra it will start forming massive glaciers and kick off a new ice age. But I guess I won’t be around to see if I’m right or not.
Well I suppose Dr John H might just be a plant from “Big Oil”, but before you dismiss him as such, why not explore the subject yourself a bit by reading what a climatologist has to say about this scare:
Click to access Lindzen-2018-GWPF-Lecture.pdf
Or a Nobel Prize-wining physicist:
If you replace cheap electricity with expensive electricity, there are huge profits to be made at the expense of hard working people.
I don’t know enough about climate science to comment either way but I doubt either Elon Musk or Koch brothers do what they do because of money, even though they seem to be on opposite ends of the spectrum when it comes to fossil fuels.
You are right that the oil and coal companies don’t believe the global warming theory for financial reasons. It has nothing to do with the science. At the same time, Democrats in the US want the environmental votes, which is why they believe, but again it has nothing to do with science. Sadly, the environmental movement (which I am a part of) profits greatly from the global warming scare.
This is why CO2, a necessary nutrient for all life on earth (and not a pollutant) is demonized, while real environmental issues go unheeded. We are all told GMO food is good for us, drinking fluoridated water is healthy, and the 80,000 untested chemicals in our food are just fine, and told to take toxic dangerous drugs to treat made up risk factors.
The story of CO2 is the same as the story of cholesterol- a necessary nutrient for life that has been demonized by over zealous scientists trying to make a name for themselves. Michael Mann is the Ancel Keys of climate science. Now that money and power are involved, good luck having a different opinion than the mainstream. So, academics go along with the story, or lose their jobs and their friends.
All of the points you make sound solid on the surface, however, once I dug into the science behind them they all fall apart. Of course we cannot trust politically and financially biased people as a resource. Malcolm Kendrick is one of the rare scientists that doesn’t care about being part of the group, and risks looking outside of the accepted paradigms to find the truth. It’s researchers like Malcolm that I respect in my search for the truth about climate change.
Here are some resources that helped me in my journey:
1. Former senior NASA climate scientist Dr. Roy Spencer says it simply: climate scientists “have the mistaken belief that climate sensitivity is high, when in fact the satellite evidence suggests climate sensitivity is low”. http://www.drroyspencer.com/global-warming-natural-or-manmade/
2. Jo Nova, who runs an outstanding climate blog, and is married to Dr David Evans, a Stanford PhD and former leading carbon modeler for the Australian Government. Both of them were believers until they thoroughly researched the science. http://joannenova.com.au/
3. Jim Steel, a California environmentalist who wrote a book called Landscapes & Cycles: An Environmentalist’s Journey to Climate Skepticism. http://www.landscapesandcycles.net/
4. World renowned physicists Freeman Dyson who said “I’m 100 per cent Democrat myself, and I like Obama. But he took the wrong side on this issue [climate change]” . He also says “It’s clear now the [climate] models are wrong, but it wasn’t so clear 10 years ago.” https://www.theregister.co.uk/2015/10/11/freeman_dyson_interview/
5. Read the climategate emails.
I was so shocked when I discovered the truth about global warming that I wrote a couple of short essays about it, which I would be happy to send you (if there is a way to do so).
Good luck on your journey!
Variations in the Earth’s Orbit: Pacemaker of the Ice Ages
For 500,000 years, major climatic changes have followed variations in obliquity and precession.
J. D. Hays, John Imbrie and N. J. Shackleton, December 1976
Click to access hays76sci_268464.pdf
6) It is concluded that changes in the earth’s orbital geometry are the fundamental cause of the succession of Quaternary ice ages.
7) A model of future climate based on the observed orbital-climate relationships, but ignoring anthropogenic effects, predicts that the long-term trend over the next several thousand years is towards extensive Northern Hemisphere glaciation. (my bold)
This study found correlations between the Milankovitch cycles and the record of ice ages for the last half million years as deduced from ocean floor sediment cores. While correlation is not causation, there is a fairly simple and robust mechanism linking the earth’s orbit, incoming radiation, and the earth’s response.
But even in 1976 they were concerned that the earth had been so altered by human intervention that it no longer responded in the same way to the same forcing mechanisms.
Could it be that we’ll have a brief hot period of another hundred years or so, then when all the fossil fuels have been burned and CO2 falls, the next ice age kicks in? Or will we get a runaway hothouse planet?
I don’t know. Nobody knows. There are so many possibilities. To me, we need more research, a lot more data, particularly from the oceans, and better climate models. It is far too early to pick sides and say the science is settled, let’s move on to the next problem.
Meant to add, no matter what will happen in the long run, in the short run it’s one-way traffic to a hotter planet. There are no cooling factors powerful enough to overcome the blanketing effect of greenhouse gases.
You may want to look at what solar scientists are saying. They are predicting a mini ice age soon due to low sunspot activity similar to previous mini ice ages called the Maunder Minimum and the Dalton Minimum. I have no idea if they are right, but the AGW is clearly a failed theory. There is no human caused climate catastrophe awaiting us.
These sunspot minimums are cyclical and dissipate after a few years. The Little Ice Age associated with the Maunder Minimum turned out to be a cold blip in a warming trend. I have no doubt if we have another cold spell it won’t last.
The notion that BP is a linear “continuum of risk” is used by guideline writers to justify the decreasing trend of what is defined as hypertension. Of course, the reason for their bias is largely financial.
From Thomas Dayspring, regarding lipids:
In the paper I just linked, Dayspring says:
” Any lipoprotein < 70 nm in diameter can pass thru endothelial barriers and enter the arterial wall. The largest LDL is ~26 nm in diameter. Mid- and smaller VLDLs and chylomicron remnants and IDLs are all < 70nm in diameter."
Aren't we under the impression that things such as this
cannot get by the endothelium? Also, the Subbotin article
from earlier showed that the concentration of particles
were higher farther from the lumen. Am I missing something?
Ions cannot pass the endothelial barrier
Because of the electrical charge?
Could you clarify, please? Does the LDL get past the endothelium?
His comment makes it appear that Dayspring
believes the way LDL gets into the intima is
through the endothelium. Can he really be
completely wrong on this? The Subbotin
paper makes it pretty clear that the particles
show up by other means (the vassa vasorum).
Interesting article about the endothelium. Appears that excessive intimal hyperplasia is the problem in CVD. The question is: what causes the intimal layer to gain more cells? The answer might be found in the endothelial cell tight junction disruption. Here is a hypothesis to consider:
– Altered tight junction could be a signal for creating a new cell to fill the perceived gap.
– Only the cells on the lumen side will develop a glycocalyx
– Additional endothelial cells below the first layer do not serve a useful function
– Blood pressure will definitely stress tight junctions but is only part of the problem
– Cell nutrition status has to be optimal
– Factors that disrupt tight junctions (gliadin)
– cellular ageing
– A repair process carried to extreme
“Our data demonstrated that tight junction proteins are directly damaged by gliadin as shown by means of quantitative imaging analysis.”
Andy S: The paper you linked is about the tight junctions in the intestinal lining. How does this apply to the vascular endothelium?
HI Gary, missed that.
I do most of my thinking early in the morning before the sun is up. I am an amateur scientist and posting about tight junctions was to distract from climate change.
Gut tight junctions and endothelial junctions serve different requirements and react to different stimuli.There must be similarities among all tight junctions. There is lots of information on the net about this topic.
The question to be answered is why do endothelial cells proliferate and cause problems. The tunica intima of large arteries is not a single layer of cells.
A theory about the role of Cholesterol in MI
If, as Malcolm says, Cholesterol is not only not the cause of MI but part of Nature’s repair system, what explains the presence of so much Cholesterol at the site of arterial lesions/blockages?
Malcolm has suggested that it gets ‘trapped’ somehow in the ‘scab’ that the repair system creates to repair the damage done by inflammation and this may be true but it suggests that the body’s repair mechanism simply can’t cope with the crap we’re throwing at it! It’s not designed to deal with tobacco, sugar, endless stress and all tens of thousands of synthetic chemicals we’ve created and NEVER tested on humans! And the HPA-Axis, fight/flight syndrome kinda supports the theory as it too is not designed to deal with these incessant attacks on the body and hence gets permanently switched on.
In turn, this suggest that lowering cholesterol in this antagonistic, to the body, environment, IS important! The question is how to do it without impairing the body’s defences due to the destructive power of statins?
I discovered that by exercising in the gym, every day, I could lower my Cholesterol from 7.1 to 4 but I just couldn’t keep it up (I did it for year). I still exercise every day but through walking and specific regimens that don’t have me surrounded by lycra and sweaty feet.
It didn’t work and I’m not sure if continuing with the gym would have worked either. Last week I had a 2nd attack and a 1 ½ hour procedure to stick 3 more stents in my poor, abused heart. And I’m not sure that continuing with the statin would have worked either (I gave them up 3 ½ years ago). There’s just no way of proving it except statistically, and I’m not a statistic!
So I’ll go onto the very lowest dose with the knowledge that there really is no way of knowing if will stop me having another heart attack (everything else being equal eg, diet, exercise and so on). Given where the world is most definitely heading, I don’t think it really makes much difference anymore.
Again, if there is an overall cause, it’s industrial capitalism and fetish of consumerism and the greed of the capitalist class. Removing them will make a start on repairing the damage it’s done to the planet and assuming that enough of us survive the coming collapse, MIs will be the last thing on our minds.
Being involved in this for 20 years now I wonder what a heart attack actually is. A MI is something very specific and which you find out afterwards by measuring some proteins released from the injured muscle cells in your heart. (In my own case these measurements were extremely high).
Angina is a completely (?) different matter but when it hits it is very easily mixed up with a heart attack or a MI. Everything seems though to be covered by the expression a “heart event” and registered as such as far as I understand when you arrive at the ER. (Big Pharma favors this terminology since it is diffuse contrary to “end points”.)
Some years ago I had “unstable angina” which appeared a number of times and it was sometimes very painful experiences. They were though different compared to my original MI 15 years earlier which was not that painful but of a more comprehensive “unwell” feeling with a long duration, hours. I have learnt that the angina attacks passes within less than half an hour.
If I had not been the “well read” sceptic I am today I would have certainly had called an ambulance a number of times (as they advised me to do after my first(?) MI). But I have endured my many angina attacks which today are though very mild and few which i ascribe to my daily high doses of natural vitamin E. When the attacks were very severe, those years back, I actually medicated myself with a large shot of whisky which brought immediate relief. (My last cardiologist confirmed the effect and promptly noted my “alcohol abuse” in the hospital journal.)
To your last interesting point about our stressful capitalistic society I am just now reading a very interesting “classic” on this subject “WHEN CORPORATIONS RULE THE WORLD” by David C. Korten and a book which I certainly can recommend to anyone interested in this subject.
About large shots of whisky, I note that since we joined á whisky Academy two years ago, our whisky consomption, single malt, has probably tripled with no obviously side effects.
Verb sat sapienti.
I’m reading “How statin drugs really lower your cholesterol and kill you one cell at a time” by the Yosephs. I think I have understood how statins work, blocking the mevalonate pathway, with mycotoxins. What I still don’t understand is how they stimulate NO production?
Whilst trying to understand that I came across a paper “PLEIOTROPIC EFFECTS OF STATINS
James K. Liao and Ulrich Laufs” which states that too much cholesterol “Hypercholesterolemia impairs endothelial function, and endothelial dysfunction is one of the earliest manifestations of atherosclerosis, occurring even in the absence of angiographic evidence of disease (42, 43).” same citation.
so statins kill your cells yet boost NO production. If that is positive, are there not safer methods of doing so , such as L-Citrulline, or even the humble beetroot.
The relevance of this blood pressure is more NO= lower blood pressure?
Thank you for another brilliant post. Very reassuring. I prefer the natural NO raising supplements rather than the Pharma ones…
Testing and also CoQ10
JD Patten – snap! I agree with you. I’ve had quite a few tests done over the last 2 years – nothing amiss – apart from the high CAC score. My joke was that most people measured their life expectancy in years and my life expectancy was any second now.
Changing the subject, for those interested in the CoQ10 side of things, here’s a blog emailed to me from the News in Nutrition website:
As ageing arteries seem to need a rise in blood pressure to fulfil the body’s needs (and yes, this may contribute to strokes) so drugs which prevent this rise must be contributing to a sluggish supply to the brain and hence to dementia?
No evidence of any CVD with BP under 160/100, but my own study of myself found that over 11 years, every medical provider except one, measured my resting BP incorrectly as per definition. You have to be sitting in a chair at rest for at least 3-5 minutes, NO talking, elbow at level of heart prior to taking the BP…
It is not normal to have a constant BP, it goes up and down with your activity, Major concern for Iatrogenic outcomes esp in older people when their BP is medically depressed causing blackouts and falls.
Interesting study I read years ago and now cannot find again: Competitive weight lifters (n=7) had cardio caths performed prior to competition =normal, then they lifted huge weights whilst having their BP monitored in competition , big jump in BP ( see red in the face), then had a post competition cath done . The post cath showed areas in the coronary arteries with ( micro tears) and signs of inflammation….aka endothelial damage …….
Yet another reason to exercise moderately ….and to keep your vascular system elastic…and be aware of how your BP is affected …….
BTW…the variance for resting BP is over 5% under best controlled circumstance so +/- 6 points systolic is clinically the same number. Also all the studies ( and life insurance table) show a bimodal distribution peak at 120/80 and 140/90 with a longer tail going over 140/90 until you reach 160+…so where do the lower is better recommendation come from? NOT science….
I have been plagued most of my life by doctors who look but do not see (with a few honourable exceptions).
My BP was first noted to be high decades ago and I was put on losartan. At the same time he noted my “weird lipids” – low HDL, high LDL, sky high trigs – without relating them to the BP or the fact that most of my symptoms were of diabetes, or conditions “common in diabetics”.
No it had to be that I was eating “too much fat” so I was sent to a dietician, who was determined to remove even more fat from my diet and replace it with even more carbs.
As a result my BP started going up, plus I started to gain weight. Here was a massive signal which was dismissed as “failing to comply with the diet”
Finally after moving I met Dr Half-Clueful who diagnosed the diabetes – and of course gave me a high carb low fat diet leaflet, exactly what I’d already been eating. Now I knew what I was dealing with I ate the exact opposite and my BP fell from about 150/95 back to 120-ish/80-ish. I think this happened before I lost the weight the dietician made me gain.
I read a recent and rather disappointing paper that suggested sodium-sensitive BP led to insulin resistance. Well I think they got that exactly arse about face, it’s the hyperinsulinemia from IR plus a high carb diet that wrecks the kidneys’ ability to deal with the sodium. Get the insulin down and sodium is no longer problematic.
I suspect this is what is behind most hypertension. Not all, obviously, I have a friend with Conn’s. IMO it’s a symptom of something else and fixing the something else fixes the BP and probably the medical conditions it “causes”.But where’s the profit in that?
I also suspect in my late mother’s case her hypertension was mostly related to being over 90. She was quite stable on candesartan until she was hospitalised and the hospital replaced that with amlodipine, after which her BP became very changeable and she would collect fluid alternating between her stomach and her ankles. GP changed her back to candesartan and this problem went away, I hadn’t previously realised how different the effects of different classes of drugs can be. I’m also on amlopdipine now, I guess it must be extra cheap or something – but I’m still only on a low dose and my BP is usually around 140/80. At my age that’ll do.
“Root causes”, said in an Ivor Cummins accent
I forgot to mention that I’ve been taking concentrated beetroot twice a day for over three years as well as D3/K2 every other day and B12, blah, blah but obviously they didn’t work. I think the issue is so complex that there is no single solution that fits all and there never will be.
Consider the following: When I was in hospital after my massive 1 1/2 hour procedure, I had a convo with a cardiac doc and he hauled out the ‘taking statins reduces MIs by 25%’ nonsense (I’ve heard it before). I pointed out to him that aside from the suspect nature of the data being used to arrive at that figure, there is a much deeper issue involved here, namely, that with so many variables being involved in heart disease it’s impossible to make ‘like-for-like’ comparisons.
So, if you take 100 people and you give half of them statins and the other half nothing, the variations between individuals is so wide, with so many factors involved, making meaningful comparisons is impossible.
Take my case: I live in London (now), it’s one of the most polluted cities in Europe, diesel particulates kill an additional, is it 8000 people a year here? So how do I know to what degree air pollution, NOT the absense of a statin has contributed to my heart attack? And that’s just one factor! Diet, environment, stress, I don’t know, 2nd hand smoke, ganja, genetics, the 50,000 synthetic chemicals we’ve added to the environment, NONE of which have been tested on humans. How do you separate it all out? You can’t! It’s impossible and we are the living proof! We don’t need statistics. For example, some people smoke 50 a day for their entire lives and don’t get heart disease. Duh!
That’s the problem with statistics, and I’m NOT a statistic! I read recently that the more big pharma spends on research, the fewer solutions they create. We’ve turned numbers into a fetish and in the process we’ve turned people into numbers.
I guess my own arteries are certainly “aged” with all the blockages. Still my BP is “amazingly” low within this context and this might be seen as a “Popperian” refutation to what you suggest. Though, as they say, “We are all different!” but what that may implicate is beyond my present understanding in this case
My concern is only for blood pressure kept lower than the body wants and needs it to be, by drugs.
Here is a reference to a supportive study (although, of course, the drug companies have studies to claim the opposite):
Late onset hypertension may lower dementia risk
To quote from it,
“One reason for the association could be that in order to obtain normal cognition, the brain needs a certain blood flow level, which may change with age. According to this explanation, those who develop hypertension later in life may have developed a compensatory method to keep the necessary blood flow level. The authors reference other studies showing that individuals with lower blood flow may have higher rates of cognitive decline.”
Common sense, I feel. Obvious – or am I missing something?
Personally, I’d rather risk a vascular incident than have long drawn out cognitive issues.
Our BP is obviously a weird subject but I am myself believing in our homeostasis and much less in any pharmacological interference.
Although a high BP has never been a real issue for me I actually noted a while ago when an extended period with a very stressful family event occurred that the BP left my comfortable 110/60 level and at worst tended towards 140.
To proactively adress the “causes” for a high BP is what I myself, together with most of us presumably, prefer. If you cannot adress the “life situation” cause you suspect you may still take proactive actions as e.g. take long walks and if possible in a natural surrounding as in a park or in nature. I also believe that reducing the carbs and especially all sweets is a good move. (Could that explain my own ‘successful’ BP control?)
BTW, I have a friend who had a very high BP (above 200) some years ago and then I encouraged him to immediately get properly medicated. He told me that he could easily raise his BP to those levels by just thinking of something unpleasant.
If blood pressure rises as you get older, does it fall as you get younger? Yes, according to this pediatric reference chart. https://www.pedscases.com/sites/default/files/VitalSignsChart3.pdf
I guess the smaller you are, the shorter the length of blood vessels, thus the lower the pressure needed to overcome friction.
What was interesting to me was, the smaller you are, the faster the heartbeat. Not sure whether this is because the heart is proportionately smaller and/or weaker, or it has to pump blood faster because kids burn up energy faster.
Hope this chart displays correctly using <pre>…</pre> tags:
Mark Sanders: My comment was not meant in a partisan political way. I’m concerned with what science tells us, and that mainly is that there is great uncertainty about climate. I voted for Al Gore in 2000, and, while I now don’t think very highly of neither him nor most politicians, he probably wouldn’t have been as bad as what we got. He also likely won in Florida. The votes were never properly counted, and he didn’t mount a challenge, as was his right. He made a great deal of money through carbon-trading schemes. Nothing intrinsically wrong with making a pile of money, but I don’t consider financial schemes a particularly honorable way to do so. In this, he joins many others who have done so, and doesn’t deserve to be singled out for it. His great sin from a scientific perspective, in my view, is in promoting the hockey-stick graph, which is not science, and his alarmist statements. We simply don’t know the impact industrialization has made on our warming climate; thus, anything we attempt to do about it is putting the cart before the horse, and costly for the great mass of humans who are energy poor.
The ACC/AHA risk calculator is a load of bollocks.
If I set my age as 67, BP as 120/80, total cholesterol as 130 and HDL as 100, male, non-smoker, not diabetic, and not African-American then my 10 year risk of heart disease or stroke is 7.1%
If I get a year older, my rate is 7.9% and I should be on a “moderate to high intensity” statin
At age 70 (all other markers remaining the same) my 10 year risk is 9.7%
At age 75 it’s 15.7%
Waitaminnit…. I think I’ve cracked it: The #1 risk indicator for heart disease or stroke is AGE. So all I have to do is stop having birthdays…
Or Stop the body’s programmed aging !
And that is being done.
Google Josh Mitteldorf for some suggestions.
Bill in Oz: Thanks. Lots of good information there. I think I must be doing a few things right. The graying of my hair and beard stopped progressing ten years ago or more, and I noticed yesterday on my hike that I could do perfectly well with nose breathing only, even on relatively steep stretches, once I was warmed up. I always have some cheese, nuts, and raisins on the drive to the trailhead, then my body always tells me when it wants more fuel, usually after 2-3 hours of hiking. Then I have renewed energy.
Yes Gary ! Good info all round…
The real insight that Josh presents is that we are “Programmed” to grow old and die. It’s in our genes and the way that our ‘epigenetics; operate. However there are ways of short circuiting the aging program… Regular exercise, fasting, working, & many of the supplements mentioned here on this blog.
Sometimes I get upset, as today when I found a “letter” from “Diabetes Wellness” in my mailbox asking for support in order to “stop” the world wide diabetic epidemic through “adequate research” to find a “pill” that will cure.
A big “scam” in line with the “pink ribbon” and cancer research.
It is to me beyond any doubt that by simply avoiding what actually makes your blood sugar rise, the carbs, you can get out of your nightmare. (In fact in a few days according to our own experience.) And according to Dr. Jason Fung also intermittent fasting can actually reverse T2D.
I don’t see any flaws here – only scientific logic!
I’m a 16/8 faster of many years and I find my blood sugar higher at the end of the fast over 5 usually more than its steady 3 over the day. I also have a diabetic friend whose also goes up. I’m of the thinking that a long fast starts to stress the body a bit and is wandering where it’s energy is coming from so realeases cortisol to raise blood sugar. I have seen plenty of T2D studies o 800 calories per day that seem to control BS again. That I feel is more to do with the weight loss I’m sure
Me and my wife are today also basically 16/8 fasters since this does not involve any stress when we are on a mild ketogenic regimen. Basically we are not hungry in the morning and have thus no urge for “breakfast”. (We tried prolonged 1 – 2 days fasts but considered them rather stressful so we abandoned them.)
In essence this means that we have our first (no restriction) main meal at lunchtime/early afternoon. My T2D wife is today also avoiding the vegetables which give great taste together with a lot of spices to the meat stews I cook (I have created quite a reputation for my dish and everyone seems to love it, bone broth being the base) not to irritate her bowel. I take care of the solid vegetables while she stays with the grassfed meat and the broth. In the early evening we may later enjoy some cheese with one or two glasses of “natural” wine which contains an absolute minimum of artificial additions so abundant in “ordinary” wine – there are shockingly around 200 allowed.
Our life principle today is as far as possible to avoid the ubiquitous “slow poisoning” from everywhere today – not least from Big Pharma but also from Big Agro. It is for sure an uphill fight but well worth the fight to our experience.
I have measured my lowest blood sugars (and highest ketones) after 4.5 day fasts. My blood sugar was near 60 in US units (3.33 in European units). Normally, it’s above 100 in the morning when not fasting that long.
I don’t understand the numbers you are using. What is the 5 and the 3?
What I find interesting about fasting is that since going low carb my body essentially does it for me, I usually have a thickly buttered oatcake with smoked salmon and a cup or two of coffee soon after I get up, largely to let my liver and pancreas know that my throat hasn’t been cut and they don’t need to dump a load of glucose.
I routinely go 6 – 8 hours and sometimes up to 14 hours before I get hungry and need to eat again, during which time I am presumably metabolising the food from my previous day’s meal(s). Sometimes I will have one meal, any time between late afternoon and late evening, and another snack many hours later, other times I may eat two smaller meals.
On occasion, mainly when eating out with friends or relatives, I will eat too many “calories”. What happens next is that it takes longer before I get hungry again. If too many of those “calories” are carbs, all bets are off, just like when I “based every meal on starchy carbohydrates” especially Holy Health Grains, and even (THE HORROR!) did a taste test on every brand of margarine I could find, I would be ravenous a couple of hours after eating or my blood glucose would plummet.
I suspect it’s what we evolved to do, eat until we are full and then not eat again until we are empty.
Are oats ok with LCHF regimen?
Sasha – oats send my blood glucose soaring, even raw rolled oats, which I love, or rather, used to love. HOWEVER, oatcakes and particularly the cheesy oatcakes I eat contain, after subtracting the fibre content, a mere 3.1 grams of carb which is neither here nor there if you only have the one, which I do, and it only affects my BG very slightly.
I have one at breakfast and one at lunchtime, both of which I look forward to fervently.
Thank you, Jan. Very interesting.
I also use oatcakes – to hold up the grass-fed butter, cheese, smoked salmon, turkey etc. – and something I just remembered I haven’t had for a long time – smoked cod’s roe which I prefer to caviar.
Mine are only 5 – 6g carbs, I generally aim at around 50g/day, mostly in the evening when I am most insulin sensitive. As I overreact to wheat, which spikes my BG and makes me blow off like a carthorse and suffer GERD and other digestive grumblings I avoid the ones which contain wheat (they stuff the damn wheat into everything along with sugar/HFCS, soy, seed oils etc. if you don’t watch out).
I also sometimes eat SMALL quantities of rice or quinoa to soak up the fatty juices from a curry or stir-fry, I get through a kilo or less a year. In my body these are doable.
My glucometer – the one I was expressly told not to use – shows a lot of helpful information. Alternative viewpoint – it reinforces my orthorexia.
I thought insulin sensitivity goes down in the evening, that’s why people crave carbs at night.
Or does it vary from person to person?
Most of the Type 2s I know, like me, have higher IR in the morning. Originally I was limited to 15g carbs at breakfast and 30g by evening without spiking my BG. Now nearly fifteen years later it’s more like 10g at breakfast and 50 – 80g, sometimes 100g, in the evening (not that I do that quantity regularly, but I can on occasion).
More Type 1s are prone to being more insulin sensitive in the morning, but again it varies a lot between individuals. Nondiabetics – who knows, are there many left?
I wonder if the “eat your carbs at breakfast” research is funded by Kelloggs or the SDA.
A recent study by Michael Snyder using CGMs on “nondiabetics” showed massive glucose spikes from a morning bowl of breakfast cereal. Of course some dieticians are using that to prove that “nondiabetics” also have glucose spikes. I have news for them . . .
How is higher IR in the morning determined?
I found the easiest way to lower my blood pressure while taking a reading is to hold my arm straight out resting on a chair. I tell my MD there is less pinching this way. This over comes white coat syndrome.
It doesn’t help that many nurses (and doctors too) have lousy technique when it comes to taking BP. The set up in many consulting rooms is such that there’s nowhere for the patient to rest their arm, which can raise BP in that arm. I’ve experimented with this at home — If I rest my arm on my desk, so that it’s completely relaxed my BP is a good 20 points lower than if I hold it out at the same level.
I have small veins (for an IV to stay in more than an hour or two, or for the vampires to get blood to test, they have to use a pedi set). I’m guessing my arteries are also on the narrow side. Basic fluid dynamics would require more pressure to move the same volume of blood through the narrower tubes.
Against the predictions of the linear logistic model, neither all-cause nor cardiovascular deaths depended on systolic blood pressure in a strictly increasing manner. The linear logistic model was rejected by the Framingham data. Clearly, the new model shows that the current cut-off value of 140 mm Hg for systolic hypertension for all adults is unjustified
http://math.ucla.edu/~scp/publications/mortality.PDF and https://www.ncbi.nlm.nih.gov/pubmed/10675116
Randall, Fantastic study! Thank you for posting. The rule of thumb for drug treatment show that the cut-off value for hypertension should be 120+(2/3)(age) for men and 114 (5/6)(age) for women. Unfortunately, the data only goes up to age 74. Does anyone know what the limits are for 74+ years old?
Malcolm, maybe you can answer this?
Dr. John H: I suspect there was insufficient data to extend the age-group beyond 74, but logic would indicate that the risk is similar above that, although age is the number one factor in the risk of death.
If we apply the formula to a 100 year old male, the hypertension cut-off point at which intervention is advisable would be 187. Does that sound reasonable?
I wouldn’t intervene in anything with a 100 year old man. What would I be trying to do, prevent from dying prematurely from CVD?
Dr. John H: Sounds reasonable to me. I think anyone who makes it to 100 can have any damn blood pressure they please. Are you 100?
Dr. John H, If the carotid arteries of a 100 year old person are severely stenosed then the baroreceptors would sense low blood pressure and the heart would pump harder to maintain adequate blood flow to the brain. In this case the brain might compute from the formula that 187 BP is required but 155 might be sufficient.
After an ‘interesting ‘ phone call to my local surgery last week re the continual non availability of my prescribed medication I checked my BP and found it to be 197/97 with pulse of 97
Suspect that during the final minute of the call that my SBP would have been over 200
Five minutes later it had subsided to 170/90 and then slowly returned to a normal 115/70 with 55 pulse with no ill effects but not something that I, as a 74 yr old, care to experience again.
I have often thought of trying a similar experience, but I also try to avoid getting angry as far as I can, because clearly that experiment shows the cost!
Dr John H said:
“This is why CO2, a necessary nutrient for all life on earth (and not a pollutant) is demonized, while real environmental issues go unheeded. ”
I agree 100%, and I would like to bring this back to CVD – I mean, I think part of the reason for the CO2 scam (at least as I see it), is that it is convenient as a distraction. In the same way, doctors probably feel more comfortable with patients if they can fuss with cholesterol levels and drugs, than if they had to say, “Look, there isn’t a lot we can do about your risk of getting CVD!”
The problem of politicised science is clearly common to both these subjects, and I am glad Malcolm permits some discussion of Global Warming (if not taken to excess) because it shows that distorted science is a general problem – not unique to medical science. Discovering fake science in any area coupled to billions of profits, is something to be expected.
I believe the whole climate denial industry is funded by corporate polluters with the aim to use politics as a tool to prevent us from doing anything to correct a bad situation.
Blood pressure (BP)/pulse wave velocity (PWV) and also saltpetre
Andrew Larwood – many thanks for your comments on BP and PWV – it’s turning out to be a far more complex and interesting post by Dr K on BP than I anticipated. A lot going on and to think about, such as Big Pharma’s interventions and so on.
Gary Ogden/David Bailey – saltpetre? I thought it was bromide. As a schoolboy (doing army cadets) we had to spend a week at an army camp during summer holidays where we heard that bromide was put in the tea to act as a sexual suppressant. Apparently, it had the added bonus (?) of causing constipation – very handy when out on the moors doing manouevres!
Never mind saltpetre for the troops. It is the other chemical that is used to cure pork to make bacon the proper British way. It is impossible to buy over the counter now – only available as a curing mix with sodium chloride (salt), since it can be used to make a variety of home-made explosive.
Yes, that sounds like kahm yeast. Best to skim it off, as it can cause off tastes. Alas, it still sometime happens in kvass made without whey!
Frederica Huxley: Thanks. I’ll try my next batch without whey, to see what happens.
Increase in falls among the elderly:
Which is no surprise when….
“Antihypertensive medications were associated with an increased risk of serious fall injuries, particularly among those with previous fall injuries.”
But no worries because we have the ever-popular falls clinics because, you see, it’s the old folk doing something wrong.
There is a link between increased CVD death rates and higher heating/ electricity costs. This link is for 2017 and discusses the deaths that occurred due to moderate cold with poorer people not heating their homes due to expensive heating bills. Moderate cold in Winter increases the infection rate and puts added stresses on the heart and increases BP….
Bill, I so agree with this analysis. Energy costs are astronomical, neoliberalism. I cannot rant about Thatcher and Reagan. And I do not think people should expect to be kept by the state, only the truly vulnerable. Apologies Dr Kendrick. But the bigger picture matters in my view. This country has sold the family silver for sure. Though I have been retired from district nursing for 12 years, the lovely families I met in a very poor area stay with me. I hope I don’t sound patronising, I am a council house girl. You can take the girl out of a council estate, but you cannot take the council estate out of the girl. Sorry again for my social discourse.
This is undoubtedly true, but it is also true that this group come from the wartime generation. My elderly relative has plenty of money but insists on watching TV in the dark and wearing every jumper they possess to avoid putting the heating on!
Unfortunately, they can become very vulnerable very quickly if they do become ill and the stress on their elderly systems can be considerable.
I would argue megadoses (using the ridiculously small RDA as the reference) of vitamin C would mitigate against falling victim to illnesses.
AH Notepad, Yes, the RDA for vitamin C is indeed suitable for morbidly obese Guinea-Pigs with a smoking habit. (30 mg/kg baseline + 30mg for the 2nd kg of FAT, and another 30mg for the Evil Weed !)
Based on what other primates consume in their constant foraging, I estimate we hairless apes need around 3,000mg per day.
90 mg / day, or less than ONE mg/kg, and our Red Blood Cells’ unique ability to effectively re-cycle oxidised Vit.-C merely keeps us out of frank scurvy. But we must have (adequate) vitamin C to start with.
Bill in Oz: Thanks for the link. Jo Nova is very good.
@Gary, I have been following up on your suggestions about ‘climate science’ blogs.. And found this one based in Oz which starts off with the premise of being ‘sceptical’ as a requirement for any budding science person.
It even has posts about medicine. And I read again the post which documented the lower survival rate of CVD patients admissions in hospitals where the cardiac surgeon were at conferences (70% ) versus the survival rate when they were present at the ET admissions, (20%)
Bah, I got my logic confused above : It should read “improved” survival rate for CVD patient admissions when cardiac surgeons were at conferences…Apologies to all.
Statins did not lower Lp(a) (are sticky and high risk) Initiation of statin therapy reduced LDL cholesterol (mean change −39% [95% CI −43 to −35]) without a significant change in lipoprotein(a). https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(18)31652-0/fulltext
CRF= Cardiorepiratory Fitness
Increased CRF was associated with reduced long-term mortality with no observed upper limit of benefit.
The adjusted mortality risk of reduced CRF was greater than or equal to traditional clinical risk factors, such as cardiovascular disease, diabetes, and smoking.
Extreme aerobic fitness (CRF ≥2 SDs above the mean for age and sex) was associated with the greatest survival and was notably beneficial in older patients and those with hypertension. Cardiorespiratory fitness is a modifiable indicator of long-term mortality, and health care professionals should encourage patients to achieve and maintain high levels of fitness.
Dr Kendrick has written a number of posts on blood pressure over the last few years. One thing I’ve not seen mentioned is the work of Dr James Lynch. Lynch discovered that blood pressure rises when a person speaks (or reads aloud or signs or otherwise communicates verbally). Typically, the rise is small, and blood pressure quickly falls when the person stops speaking.
In “hypertensives”, the blood pressure rises much higher and stays elevated longer. Blood pressure medicines have no effect on this condition.
It was years ago I read one of Lynch’s books, The Language of the Heart, which described the phenomenon in detail and how he learned of it.
Here’s an interview with Lynch which summarizes his views:
Here’s a book online with a section on “white coat hypertension” which mentions Lynch’s work:
Good News About High Blood Pressure
Seems like a way to connect stress / strain with heart disease.
Almost 2 thousand years ago an old Chinese medical text said: “too much talking injures the Heart”. I am always amazed how they figured this stuff out thousands of years ago.
Sasha: If this is true, shouldn’t women be dying in droves?
Thank you for the links. Very interesting reading.
If you measure your own BP, it soon becomes clear that BP varies quite a bit – and that is when you are seated in the right position, a suitable period of time after eating, and basically relaxing. Obviously it must go a lot higher if you are cycling up hill (say), yet exercise is good for you!
My question is, if high BP actually causes harm (as opposed to being correlated to something else which is harmful – cortisol levels, maybe) what would a doctor measure in an ideal world – lowest BP, average BP, maximum BP, or what. I mean someone who takes exercise is likely to get a higher maximum BP than another person who doesn’t – so it isn’t really obvious. If he does a lot of exercise, that may even raise his average BP
My question exactly!
And you put it so succinctly.
. . . Doc Kendrick??
One part of the answer I think is to look at variability. As you say, BP is not a static number and the less static it is, the more variation and flexibility, the better. So if you just took an average of a person who did some extreme exercise it could indeed make the average higher. I think what you would want to look at more is how does the individual’s blood pressure show flexibility?
My take on blood pressure. 120mmhg converted to psi is 2.32psi 170mmhg is 3.28psi. Here’s an experiment most people can conduct: get 2 bicycle tires and fill one to 2.3 psi and fill the other one 3.3 psi then get someone to release the 2 valves at the same time while you’re holding a finger in front of the valves the same time. If anyone can feel a difference in air pressure I will be very surprised. Actually the difference is miniscule. But the medical profession says if your blood pressure increases by 1.0 psi that will damage the arteries. Another example is 140mmhg to 160mmhg, difference of .4 psi. By the way normal pressure in the eye is between 10 and 21 mmHg. Estimate of 10-Year Risk for Coronary Heart Disease Framingham Point Scores https://www.nhlbi.nih.gov/health-pro/guidelines/current/cholesterol-guidelines/quick-desk-reference-html/10-year-risk-framingham-table You will note BP does not have a big score compared to other risks.
The paper cited by Dr. Kendrick There is a non-linear relationship between mortality and blood pressure is only four pages long and well worth reading.
It is based on another paper which is behind a paywall, but I gather the current BP guidelines are based on an analysis of the Framingham study which is faulty because A) they didn’t control for the fact that BP increases with age; B) they didn’t control for the fact that BP is higher in women than in men; and C) they didn’t control for the fact that in the latter part of the Framingham study many people were on BP-lowering drugs which skewed the result.
The paper concluded that if you are at or below the 70th percentile BP for your age and sex, there is no benefit to lowering your BP further. The rule of thumb is that it is at 110 + (2/3) (age) for a man 45-74, and 104 + (5/6) (age) for a woman 45-74.
For the mathematically-challenged, here is a table:
Above this pressure the risk starts increasing, but you need to be above the 80th percentile before medication is considered necessary. (They don’t give a formula for the 80th percentile pressure.)
Incidentally, they note that the observed benefits of BP lowering medications may not be due to lower BP, but rather due to some other factor. For instance, different drugs which lower BP an identical amount have different impacts on CVD risk. Rather like statins which might work because they stimulate NO production rather than lowering cholesterol.
IMO, blood pressure is being treated like the cholesterol hype. “Only when SBP exceeds the 185 mark does the number of deaths start to increase steeply.” https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4195935/
Randall: Thanks for the link. Good paper.
New study from Sweden – Cold weather brings heart attacks
Not all of this makes sense. Air temp, I can understand. Cloudy weather, low atmospheric pressure, wind in winter means higher temps and cleaner air in my book.
Really great and in depth look at wall shear stress WSS in the coronary arteries: https://twitter.com/CoronaryDoc/status/1055063529454256130 “In the first clinical outcome study, using #FAME II database, we showed that high WSS in proximal segments of lesions predict MI in patients with obstructive CAD
WSS had incremental prognostic value over #FFR
WSS was calculated using bi-plane angiograms”
That’s a very interesting set of tweets. A Tweetorial! First time I’ve heard of that.
If I’m reading correctly (and I’m probably not considering the level of the material), it appears blood viscosity is a significant factor contributing to wall shear stress. Does that tie in platelet aggregation with the disease process?
Interesting that low shear stress is associated with plaque progression. Am I reading that right? I wonder how that works.
The other thing I notice is that the presence of plaque seems to affect the wall shear stress. Am I reading that right? I’m not sure how it explains how plaque got there in the first place.
Thanks for the contribution.
Your ACE inhibitors might be killing you with CANCER even as they boost your nitric oxide and improve your endothelial function.
Or maybe not. Are confounding factors making it look that way?
Do you have reason to feel confident until the dependable RCTs come in? (will they even be done?)
Is perindopril a really good or a really bad idea??
JDPatten: I’m in the “10 years or longer” group. My lungs have been feeling kind of funny lately. On the other hand, this was in UK patients, and I live on the other side of the pond. But, 31%. Yikes.
The butter deniers are back!
‘ Butter and cheese may be fine in modest amounts in a balanced diet, but the saturated fat that they contain is potentially risky. Too much of it causes the liver to overproduce “bad” LDL cholesterol, which is implicated in heart disease. ‘
That “balanced diet” again. At least the ‘bad’ is printed as “bad”: is there a hint of a problem there? Also, note “potentially risky”, how much is that too much, how many grams?
Yeah, was goin to post that link. From Moscow with love…
A truly awful piece of hack journalism, something that will have former editors spinning in their graves.
Has the Guardian no shame?
Rhetorical question actually, it no longer does.
As evidence, if any were needed, fewer and fewer of such articles that scream out for open comment to correct glaring lies are ever opened for public comment.
I usually have the highest respect for the Guardian. It is probably among the top five newspapers worldwide. But its medical reporting is a mixed bag, and its nutritional reporting is consistently poor.
I wonder what their motivation is. Just because the Daily Fail occasionally runs a pro low carb story is hardly a good reason to go firmly in the opposite direction. One should think the story of big pharma corrupting the medical system, causing needless cost and suffering in folks from all walks of life should be right up their alley.
Or is it personal, like Jane Brody at NYT who has probably invested so much personally in terms of lifestyle and nutrition changes that she just cannot admit she has been betting on the wrong horse?
The noticeable feature of that article, was the lack of numerical facts. Why not have told us the percentage gain to be had by taking statins – or even the suggestion to GOOGLE “statins NNT”! Even if the protective effect of statins is real, it is so pitifully small!
Thanks for the link. The diet heart hypothesis people are really pulling out all the stops aren’t they !
There were some great quotes in the article. My favourites:
“This is more than bad science, according to leading scientists and medical authorities. It will cost lives.”
“Mainstream scientists usually keep their disquiet to themselves. But last week, some broke cover over what they see as one medical journal’s support for advocates of a high-fat diet. More than 170 academics signed a letter accusing the British Journal of Sports Medicine of bias….”
“He (Malhotra) was accused by Prof Rory Collins at Oxford University of endangering lives. Collins said scare stories about statins could do as much harm as Andrew Wakefield did when he claimed that vaccines caused autism.”
“That is flat-earthism, says Collins. “The claims that blood LDL cholesterol levels are not causally related to cardiovascular disease (which is really in the same realm as claiming that smoking does not cause cancer) are factually false,” he maintains. He believes there is an argument for refusing to give cholesterol-deniers a platform, just as some will no longer debate with climate change sceptics.”
Why is it that mainstream science cannot stand debate ? Their reaction to dissenting opinion is to muzzle it and scare the population into taking their advice.
This article eloquently demonstrates who the true seekers of truth are in this debate.
In the reporting of this, I was much taken by a quote from Dr Malhotra which they attributed to a steal from GBS “I learned long ago to avoid wrestling with a pig – you get dirty: besides, the pig likes it” No more need be said.
What a dangerous load of codswallop! It is obvious that Collins and Co are feeling somewhat vulnerable.
Or: “never argue with an idiot; they will bring you down to their level and beat you with experience”.
Dear Malcolm, you are a religious fundamentalist!
“My belief about the cholesterol sceptics is that they are a bit like religious fundamentalists,” said Neely. “They are not open to argument. Whatever argument you present, they will find another argument because this basically defines who they are.”
This is classic:
“But there is also evidence that some people get muscle pain because they expect to after everything they have heard. It is called the nocebo effect.”
I had hernia surgery recently and expected to have some awful pain for days, I was even given co-codamol (that I didn’t use) just in case it was really unbearable, but I had the anti-nocebo effect, the discomfort was minimal. My own guess is that most people who have been prescribed statins don’t know about any side effects – until they turn up.
My story (that I have told several times on this site) demonstrates that statins cause nasty muscle problems even when you expect the reverse!
My muscle problems started after 3 years on the drug, so neither I nor my doctor thought statins were to blame.
By incredible good luck, I suggested that I stop the statins until I was better, just to simplify diagnosis of what was really wrong.
After a while without statins in my system, the symptoms vastly diminished, so I resumed taking statins because I still thought of them as really valuable. Then the side effects returned, so I stopped again! This cycle repeated several times, before the penny dropped! Thus by a pure fluke, I demonstrated that (at least in me) muscle pains were really a result of taking statins.
The irony is that the whole “cholesterol hypothesis” and “diet-heart hypothesis” and all current dietary “thinking” IS based on religious fundamentalism. There was a great link posted above: here are two more about the influence of the Seventh Day Adventists
“The majority of people in the UK and the US are now overweight or obese, with all the heart and vascular problems that brings, and the trend is ever upwards.”
Such irony! This only happened since low fat diets – where the only acceptable fat is industrially produced omega 6 seed oil – were invented. The Guardian is pushing veganism even more than the rest of the mainstream media. I predict that meat is going to be taxed soon, and probably banned altogether once the “vegan meat” factories are onstream, and this will NOT have the effects either on human health or the environment that the likes of George Monbiot claim. This will continue to be denied for years, if not decades, by which time it will be impossible to go back.
Meanwhile sales of statins and the other profitable antidotes to the inappropriate diet will continue to increase. Which is what is really important.
When this blog went dark for a week I hoped it was just Malcolm taking a well deserved break. Then I became paranoid that “they” had got him. After all he banned a vegan which must not be allowed, Meanwhile the dieticians want Aseem’s head on a spike because he “inappropriately reversed” Tom Watson’s diabetes and caused him to lose scads of weight. If the dieticians actually knew what they were doing they should have been able to achieve this, but they didn’t and never do, with a few honourable exceptions.
Conventional Wisdom is currently fighting back hard, and dirty.
Here are two recent videos discussing the glycocalyx
and the endothelium:
Dr. Robert Cywes, see starting at 34:27
Ivor Cummins starting at 17.46:
Both say that particles do go through and around
the endothelial cells. I still say that Subbotin disputes
this pretty well:
Particles cannot go through and round endothelial cells. End of.
Cool, and I agree with you. It is interesting that
there are so many presenters lately who have
been saying that LDL particle count is important
for the (illogical) reason that more particles will
cause more particles to go through or around
the endothelial cells. What info could disabuse
them from this notion?
Nothing. If past experience has anything to go by.
Could I ask a question that is slightly off-topic? A while ago we were discussing that fact that omeprazole and the other PPI drugs were associated with more CVD. This makes me wonder if useful drugs like diclofenac are associated with more CVD, only because they tend to cause excess acid in the stomach, that results in a prescription for omeprazole!
Is there any reason why that extra acidity could not be countered with over the counter Ranitidine?
As I understand it, it is often the lack of sufficient acid in the stomach that causes the problems then addressed by PPIs!