16th August 2018
Having talked about the end, I shall now talk about the beginning of cardiovascular disease (CVD). Or, to be more precise, the beginning of atherosclerotic plaque development.
The problem that I always had with the LDL/cholesterol hypothesis was that it relied on a mechanism of action that sounded reasonable – if you didn’t think about it in any great depth. However, once you started looking at it closely, it become more and more unlikely. Namely, the idea that it is possible for low density lipoprotein to simply “leak” into artery walls, triggering the development of atherosclerotic plaques.
Whilst everyone, and I mean everyone (apart from about a hundred flat-earthers), confidently states that leakage of LDL in the artery wall is the first step in atherosclerotic plaque development, the pattern of atherosclerosis around the body is impossible to reconcile with this hypothesis.
Lets just start with a short list of problems. It may not look short, but it is. Just don’t get me started on ‘oxidised LDL’ and LDL particle size, and inflammation, and suchlike:
One: If LDL is leaking into artery walls, by active transport, or down a concentration gradient, or through any other mechanism you can come up with, why doesn’t it leak into all artery walls at exactly the same rate? Or, to put this another way, why are some arteries devoid of atherosclerotic plaques, when other arteries, in the same person, are highly atherosclerotic?
In the same way, how can you have a discrete area of plaque in an artery wall, when the rest of the artery wall, even the opposite side of the artery wall, is plaque free. Or, to put this another way, why does LDL leak through only in certain places, and not others?
If your answer is that LDL can only leak through in areas of arterial/endothelial damage then I would say, fine, reasonable argument. However, it means that the starting point for atherosclerosis is arterial/endothelial damage – not LDL leaking into the artery wall. And once you have damage to the arterial wall, you have moved into a completely different ball game. The ball game of endothelial damage and clot formation. Which means that you are now in my world. My rules, I win.
Two: Why does LDL never leak into vein walls? Again, if your hypothesis is that LDL can get past endothelial cells and then move straight into the artery wall, then why cannot it do this in veins? Veins and arteries have exactly the same basic structure. Arteries are somewhat thicker, with more smooth muscle and suchlike, but otherwise all is the same, and the endothelial cells lining both arteries and veins are identical in structure and function.
And no, the high blood pressure in an artery cannot force LDL into the artery wall. Whilst pressure may be involved in damaging the artery wall, pressure alone cannot be the answer. For pressure to force LDL into the artery wall, you would first have to breach the endothelial layer, at which point everything else in the bloodstream would flood into the artery wall at the same time. Then you are into the ‘damage to the blood vessels’ discussion again. My rules, I win.
Three: The arteries, at least those where atherosclerosis develops, have their own blood supply. Yes, bigger blood vessels (both arteries and veins) have their own blood vessels to provide them with the nutrients they require – the vasa vasorum, literally ‘blood vessels of the blood vessels.’
LDL molecules can freely move out of the vasa vasorum, and into the surrounding artery wall – then back again. Therefore, the concentration of LDL in the artery wall, and the bloodstream, is identical. So, for one thing, there can be no concentration gradient between the LDL in the blood flowing through the artery, and within the artery wall itself.
Equally, even if LDL did enter the artery wall by passing through the endothelial layer and then, against all the laws of physics, the concentration of LDL in the artery wall managed to rise above that in the bloodstream, it would simply be absorbed back into the vasa vasorum to be taken back into the blood circulating around the body.
To put this another way, there is nothing to stop LDL entering the artery wall, and vein walls, via the vasa vasorum. So, why does LDL entering the artery wall from the blood, that is flowing through the artery, cause damage, when the LDL entering the artery wall (and vein walls) from the vasa vasorum does no harm? Same LDL, same rules.
Four: The intact/healthy endothelial layer is impermeable to LDL, no matter what the concentration in the blood. We know this because the brain has to manufacture its own cholesterol because, in turn, LDL cannot force entry through the endothelial cells that line the blood vessels.
In the brain all endothelial cells, even in the smallest blood vessels (capillaries) remain tightly locked together, which is the ‘structure’ that creates the blood brain barrier (BBB).
‘The BBB is defined as the ‘microvasculature’ of the brain and is formed by a continuous layer of capillary endothelium joined by tight junctions that are generally impermeable (except by active transport) to most large molecules, including antibodies and other proteins.’1
In the rest of the body, when you reach the level of capillaries, these minute blood vessels are loosely bound, with gaps between the endothelial cells. There are also holes (fenestrations) in the endothelial cells themselves. Which is why LDL can move in and out of the vasa vasorum quite easily. This is not the case in the brain, or the larger blood vessels, where tight junctions are the rule.
In short, an intact endothelial layer, with the cells locked together by protein bridges – as found in the BBB and in all large arteries – cannot be penetrated by LDL. Indeed, if it were possible for LDL to simply force entry into, and then pass straight though endothelial cells, you would not need LDL receptors to get LDL into cells, and you do.
This is why, in familial hypercholesterolaemia (FH) the level of LDL rises very high. It rises very high because there are fewer LDL receptors on cells, so the LDL remains trapped in the bloodstream. Somewhat ironically, FH provides powerful proof that the LDL/cholesterol hypothesis must be wrong, because it proves that LDL cannot enter cells unless the cell has an LDL receptor. At least it disproves the idea that LDL can simply move through endothelial cells.
As for the idea that LDL can slip through the gaps between endothelial cells. This too, is impossible. Endothelial cells, in larger arteries, and in the BBB, are locked together very tightly indeed. I quote here from Wikipedia. If you don’t like Wikipedia, then go to Google and look up “IMAGES” ‘tight junctions between endothelial cells.’ You will see how impossible it is for LDL to pass between endothelial cells that line artery walls.
‘Tight Junctions prevent the passage of molecules and ions through the space between plasma membranes of adjacent cells, so materials must actually enter the cells in order to pass through the tissue.’2 Wikipedia ‘tight junction’.
Yes, there is not enough of a gap for ions (charged atoms) to pass between endothelial cells. Which means the idea that an LDL molecule, which is tens of thousands of times bigger – probably hundreds of thousands – can slip between cells is quite clearly, nonsense. It is like suggesting a super-tanker can slip through a gap that a rowing boat cannot.
Five: The only possible way that LDL could leak past or through the undamaged endothelium is if the endothelium wants it to get past. That would require active transport through endothelial cells. Now active transport exists – it is called transcytosis. A substance is absorbed into the cell on one side, it is then transported through the cell, and pops out the other side. [Transcytosis is clearly not possible with LDL, as we already know that it cannot cross the blood brain barrier BBB]
However, transcytosis only happens if the cell has a reason to transcytose a molecule. It is tightly controlled and highly complex process. It does not happen by chance, It is unaffected by any concentration gradient. It is the action of a living entity. In this case, an endothelial cell [other cells are just as clever].
The idea that an endothelial cell would be programmed to absorb LDL from the bloodstream, then actively transport it through itself, then deposit it in the artery wall behind – for no reason whatsoever – defies all laws of biology and physiology – and any other natural laws that you can think of. Especially when the artery wall can get any and all the LDL it requires from the vasa vasorum.
Now, there are more problems than this, but I am not taking it any further at present, as that is enough to be going on with. The counter argument has always been, well you do find LDL in atherosclerotic plaques, so it must have got there by passing through the endothelium.
Hmmmm. Well, as pointed out in the last blog, you can find red blood cells in atherosclerotic plaques too, and we know for an absolute certainty that red blood cells cannot penetrate the undamaged endothelium. Simply finding a substance in an atherosclerotic plaque does not mean it caused the plaque in the first place.
Having said all of this, the alterative ‘blood clotting’ hypothesis appears to immediately run into an alternative problem. When you look at early stage atherosclerotic plaques, they do not obviously look anything like a blood clot. In fact, they are often referred to as ‘fatty streaks.’ No sign of a blood clot there (at least, so it is almost universally believed).
I don’t refer to them as fatty streaks, because that immediately sets your thinking off down the fat/cholesterol LDL pathway, from where it can never again emerge. I prefer to call early stage plaques “fibrous streaks” which is far more descriptive of what they are, and what they look like.
However, that is slightly jumping ahead of myself. What I am going to do now, is to take you back in time to the 1960s and 1970s. A time when researchers were actually trying to work out exactly what was going on with CVD. Rather than now, when the LDL hypothesis is just accepted as an inarguable fact. Which means that no-one researches plaque growth any more, in any meaningful way. Or at least, they can only research it by accepting that, whatever else you see, LDL is the cause.
So, let us begin by looking at the fatty streak in more detail, as described in the book ‘Factors in Formation and Regression of the Atherosclerotic Plaque.’
‘Juvenile-type fatty streaks are the earliest lesions that can be recognized by macroscopic inspection of aortas of children. They characteristically appear as small yellow/white dots most frequently in longitudinal lines between the intercostal branches (places where arteries that travel around the chest branch out from the aorta. Intercostal means, between ribs). They stain brilliantly red with macroscopic Sudan staining, and Holman reported that they were already present in all children aged more than 3, increased rapidly in area between ages 8 – 15, and reached a maximum age 20.’
So, yes, there are such things as fatty streaks. Sorry to scare you, but they start in infancy, and every single child has them by the age of three. They reach their maximum level at age 20 (when no-one has a heart attack). However, most importantly, fatty streaks do not become atherosclerotic plaques:
‘For many years it was widely believed that they (fatty streaks) were the precursors of fibrous plaques, and it was postulated that the fat-filled cells disintegrated, releasing sclerotic organic lipid that stimulated proliferation of SMCs (smooth muscle cells) and collagen. However, there is now evidence from many different sources that suggests that fatty streaks and fibrous plaques develop by separate and independent pathways.’
‘Separate and independent pathways’. Today, if you read anything on atherosclerosis, any textbook, any research paper on atherosclerosis, it will inform you that atherosclerotic plaques start as fatty streaks which gradually grow larger and turn into atherosclerotic plaques – somehow or another. This is just an accepted fact, never challenged, constantly quoted. But it is, as with most facts in the world of CVD, wrong.
In the 1970s, a couple called the Velicans undertook a painstaking review of arteries at all ages, from those who had died of accidental causes. Children to adults. Two of their key findings are worth highlighting. The first, again, is that fatty streaks do not turn into plaques. The second is the association of microthrombi with plaque formation:
‘They, (the Velicans), record many significant morphological observations. They did not observe conversion of fatty streak into atherosclerotic plaques and concluded that the two types of lesion developed as unrelated pathological processes. ‘Advanced’ fatty streaks exhibiting cell disintegration and accumulation of extracellular lipid were first encountered in the 26 – 30 age group and increased fairly rapidly over the next decade, but again they did not observe ‘further transitional stages between advanced fatty streaks and atherosclerotic plaques.
In the third decade lipid became abundant in the plaques (the plaques, not the fatty streaks) in the form of foam cells which were particularly associated with areas of insudation. (insudation is the accumulation of a substance derived from the blood), and small pools of extracellular lipid: there was also ‘progressive involvement of microthrombi in the early steps of plaque formation.‘
What does this mean? At the risk of repeating myself to death. It means that fatty streaks exist, but these ‘lesions’ are not the things that become atherosclerotic plaques. Plaques form in a completely different way.
And, when you examine early stage plaques closely, they contain microthrombi (small blood clots) and other material derived from the blood – insudation. The Velicans did not know what caused plaques, but they observed that they began life as small fibrous streaks – not fatty streaks, with progressive involvement of microthrombi.
What is the most ‘fibrous’ material in the body? It is, of course, fibrin. Fibrin is the long string of protein the body uses to bind blood clots together. Sticky fishing line, if you will. It is formed with blood clots, as part of blood clots, and it is always found in high concentrations in and around atherosclerotic plaques.
What is important to note here is the fact that everyone believes about the growth and natural history of atherosclerotic plaques – is wrong. Fatty streaks have nothing whatsoever to do with atherosclerotic plaque development. On the other hand, fibrous streaks, fibrin and microthrombi do!
Which takes us way back in time to Karl von Rokitansky, who was studying plaques in the arteries of people who had died of accidents in the 1850s. Rokitansky noted that plaques looked very much like blood clots – in various stages of repair. He then proposed that atherosclerosis begins in the intima (the bit lying just beneath endothelial cells), with deposition of thrombus (blood clot) and its subsequent organisation by the infiltration of fibroblasts and secondary lipid deposition. ‘The Encrustation Theory.’
However, what Rokitansky could not do, the Velicans could not do, and Russell Ross and Elspeth Smith and Duguid could not do – explain the following:
How can a blood clot form under the endothelium?
The answer, as readers of this blog now know, is that the blood clot formed when the endothelium was not there. It had been damaged, and/or stripped away, at which point a blood clot formed on that area and then, once the blood clot stabilised, and most of it was broken down, apart from the fibrin and a few other bits and pieces (including Lp(a)), the endothelium simply re-grew on top of it. Like all magic tricks, it is simple once you know how it’s done.
However, the existence of endothelial progenitor cells (EPCs), that could stick to, then re-grow, on top of a blood clot, was unknown until the mid-nineteen nineties. So, prior to this time, anyone suggesting the encrustation theory, or any variant thereof, could be easily dismissed. Just as Virchow dismissed Rokitansky in 1852. ‘Do not talk nonsense Rokitansky, blood clots cannot form under the endothelium – I win.’
Because of this, with no other hypothesis to challenge it, the LDL hypothesis gained such a powerful grip, that no-one was the least interested in the Encrustation theory. The time to strike had passed, the battle had been lost. The warriors grew old and withdrew from the battlefield, and then simply died of old age. Their names forgotten, ghosts in the machine.
‘After many years of neglect, the role of thrombosis in myocardial infarction is being reassessed. It is increasingly clear that all aspects of the haemostatic system are involved: not only in the acute occlusive event, but also in all stages of atherosclerotic plaque development from the initiation of atherogenesis and growth of large plaques.
Infusion of recombinant tissue plasminogen activator (rt-PA) into healthy men with no evidence of thrombotic events of predisposing conditions elicited significant production of crosslinked fibrin fragment D-dimer. Thus, in apparently healthy human subjects there appears to be a significant amount of fibrin deposited within arteries, and this should give pause for thought about the possible relationship between clotting and atherosclerosis. It also provided in vivo biochemical support for the numerous morphological studies in which mural fibrin and microthrombi have been observed adherent to both apparently normal intima and atherosclerotic lesions.
In 1852 Rokitansky discussed the ‘atheromatous process’ and asked ‘in what consists the nature of the disease.’ He suggested. ‘The deposit is an endogenous product derived from the blood, and for the most part from the fibrin of arterial blood.’ One hundred years later Duguid demonstrated fibrin within, and fibrin encrustations on fibrous plaque, and small fibrin deposits on the intima of apparently normal arteries.
These observations have been amply confirmed but, regrettably the emphasis on cholesterol and lipoproteins was so overwhelming that it was another 40 years before Duguid’s observations had a significant influence on epidemiological or interventional studies of haemostatic factors in coronary heart disease.’3
Those words were written almost thirty years ago by Dr Elspeth Smith, who once taught me at Aberdeen University. I should have listened more closely, it would have saved me twenty-nine years of research. Those words too, have now been forgotten, whilst LDL and statins bestride the world.
Silence has once again descended on this area. But when you look at it through fresh eyes, and you know of the existence of EPCs, these researchers had the answer, right there, in the palm of their hands. So close they could almost smell it. They just couldn’t quite join all the dots. They couldn’t explain how massive molecules that are normally found in the bloodstream, could get inside the artery wall. So, they were defeated by the facile, impossible, ridiculous, LDL hypothesis.
A great pity, because the encrustation theory explains what the LDL hypothesis cannot. Why do plaques form where they do, why do they not form in veins? Why do they contain substances that you can only find in blood clots? Why do so many grow in layers, like tree trunks? In fact, they all grow this way, it is just that – over time – the plaque can lose structure and turn to mush.
Why does smoking and air pollution increase the risk of CVD. How does avastin increase the risk of CVD by 1,200%? How do Rheumatoid Arthritis and Systemic Lupus erythematosus vastly increase the risk of CVD? It is because they all damage the endothelium and increase the risk of blood clotting at that point of damage. I could go on listing factor after factor. Using the encrustation theory everything can be explained, simply, quickly. There is no need to distort the evidence, no need to explain away paradoxes.
Statins, for example, which are held up as inarguable proof of the LDL hypothesis. How do they actually work to reduce the risk of CVD? It is because they increase nitric oxide synthesis in endothelial cells, and nitric oxide protects the endothelium, stimulates the growth of endothelial progenitor cells, and is also the most powerful anticoagulant agent known to nature.
‘Statins have pleiotropic effects on the expression and activity of endothelial nitric oxide synthase (eNOS) and lead to improved NO bioavailability. NO plays an important role in the effects of statins on neovascularization. In this review, we focus on the effects of statins on neovascularization and highlight specific novel targets, such as endothelial progenitor cells and NO.’4
Blood clots, blood clots. All the way down. Rokitansky was right, as were Ross, Duguid and Smith (and many others). They had worked it out, and they knew what was going on. They simply failed to convince the world. My role is to resurrect these forgotten scientific heroes and place them where they should always have been. The scientists who discovered what really causes CVD.
Quite heavy going but clearly a very very strong argument. Where can this be published and publicised properly ?
Yes – are you goong to publish this in a form/context that has some chance of being taken seriously?
If only, if only, if only.
Yes, Dr. Kendrick, is it impossible for you to get articles like this in journals? I mean, you’d have to make it a lot more boring but can’t it be done?
Goldstein and Brown won the Nobel prize in 1985 for identifying the malfunctioning genes that caused familial hypercholesterolemia. Statins were then ‘invented’ to depress the amount of cholesterol produced by the liver and to encourage the production of LDL receptors. It surely proves your point: that in the normally functioning body, we don’t have to worry about the quantity of cholesterol produced as long as the regulation mechanism works. Where it goes wrong is when the mechanism has to work overtime to build plaque to cope with injuries to the endothelial lining. I hesitate to question two Nobel prize winners, but surely they (or their big Pharma friends) have wrongly extrapolated from a very unusual situation to the general populace? Why are we not focussing on the causes of endothelial injury?
“Why are we not focussing on the causes of endothelial injury?”
I’m so sorry that I can’t let this unmentioned: scurvy? (vitamin C deficiency?) 🙂
There is something about vitamin C that brings out the rabid animal in mainstream medicine. Maybe being un-patentable has a bearing. Or effectiveness, the Marik Protocol for sepsis being an example.
We primates (and guinea-pigs/fruit bats) have a mechanism to re-cycle vitamin C, but if THAT isn’t working 100% or insufficient intake, we’re in Big Trouble. – And this explains how we survive despite not manufacturing our own. 10 years ago.
Harry, you are so correct…..cut out the unhealthy carbs, thus minimising the need for excessive vitamin C, and the scurvy should be under control, and the endothelium will not be so damaged. That is my theory, for what it is worth.
What if it was just a coincidence that statins lower cholesterol? What if the way the drug really work is by lowering inflammation so then the cholesterol follows because you don’t need cholesterol to patch things if there is less inflammation. IMO that explains WHY if you don’t take enough statin,the drug does not work. So just lowering the cholesterol might not be enough of an anti inflammatory effect. What if everyone stopped measuring cholesterol and concentrated on inflammation? The blood tests would be for insulin levels, homocystein and CRP and then everyone gets the higher dose statin to reduce the inflammation. What if Familial hyper cholestermia doesn’t cause heart disease at all. What if there are families without heart disease and they have high cholesterol? What if that was all just a coincidence? What about that village in Italy, LImone, where everyone had astronomical LDL but nobody was dying of heart disease? That whole story just evaporated, along with villages of people in Japan with high cholesterol and no heart disease.
Great stuff 👍
Does it then follow that Sir Rory Collins was right in saying that statins were the ‘antidote’ to heart disease but just used the wrong argument ?
Statins are moderately effective at reducing the risk of CVD. However, the price that needs to be paid with statins – in my opinion – outweighs any benefit. Rather like aspirin, which reduces the risk of CVD by reducing the risk of blood clots forming. However, aspirin increases the risk of GI bleeding, and suchlike.
So perhaps instead of Statins, one should take powdered L-Arginine and L-Citrulline daily? Both put more NO into the blood stream. (I ask, though do so anyway – along with powered Vitamin C)
If you can increase NO, this is good. Although, if you have enough L-arginine in the diet, taking L-arginine and L-ciitrulline probably will make little difference.
“Statins are moderately effective at reducing the risk of CVD.”
This is what the clinical trials suggest (for secondary prevention in some populations). But I’m unconvinced even that is true. Secret data from industry funded studies is not science by any normal meaning of that term. Science is by definition public and subject to independent scrutiny. The absolute benefit of statins supposedly demonstrated in the clinical trials is tiny, and I’m sure easily coaxed from any of the datasets if getting a certain result is your real goal. Without public access to all the raw data we will never know. I’m very curious if Malcolm agrees with this line of thinking.
Bill: In addition, all trials have exclusion criteria, so no drug is actually tested on the general population; nevertheless, they are allowed to market them to everyone. I suspect the 1% benefit seen in statins would vanish were trials conducted without exclusion criteria.
“If you can increase NO, this is good. Although, if you have enough L-arginine in the diet, taking L-arginine and L-ciitrulline probably will make little difference.”
In the studies that I have seen citrulline and arginine are usually used in a higher dosis than one can obtain with food. Also, citrulline is more effective in raising arginine than arginine itself:
“Conclusions: Citrulline supplementation is more efficient at increasing arginine availability than is arginine supplementation itself in mice.”
Same in humans:
“L-Citrulline supplementation during endotoxemia and not L-Arginine reduced intestinal microcirculatory dysfunction and increased intracellular NO production, likely via increased intracellular citrulline and arginine availability”
I use a 750 mg capsule of citrulline three times a day and it works as well as a light blood pressure pill. Side effect: Morning wood 🙂
Also good for the cardiovascular system: taurine which I take as magnesium taurate.
That seems an eminently reasonable approach.
My favorite supplement: go outside and enjoy a sunny walk.
“Hypertension, ischaemic heart disease, stroke, the metabolic syndrome, and type 2 diabetes are major causes of morbidity and mortality, and while excessive sun exposure carries real risks, there would seem to be no real substitutes for regular small doses of sunshine onto our bodies. True, we can supplement with vitamin D3 or D2, and even supplement with the amino acids L-arginine and L-citrulline to provide endogenous sources of NO-type moieties, but are we then mimicking all that sunlight can do? Unlikely!
Cautious and regular UV exposure may well allow for major reduction in the annual burden of cardiovascular disease, and would be absolutely cost effective”.
I fully agree
Your second referenced study was another mouse study. Interesting nonetheless thanks
This is awesome.
I leave it to others to ask what we should do.
The logic is here and I agree! A lot of Popperian refutations!
I was once captured by the idea from Ravnskov an McCully that microbes were responsible for CVD through the Vasa Vasorum. There seems to be a strong connection between infections (i.e. in the teeth) and acute infarctions as in my own case. Their theory also made sense from a pressure point (arteries) of view to me.
Click to access Am-J-Med-Sci-2012.pdf
How can we discard their theory?
Infections can and do increase CV risk. They release exotoxins that damage the endothelium.
‘Every successful bacterial pathogen must at some point interact with the body’s largest organ –the endothelium. This interaction can take many forms . Bacteria can disrupt the barrier function of the endothelium to gain access to the bloodstream and then again to gain access to new organs. Many bacteria have evolved toxins which can increase vascular permeability by either killing ECs or by interfering with the cytoskeleton or cell-cell junctions.’ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5481510/
You don’t need to discard the theory that microbes can increase the risk of CVD, because they do. However bacteria only represent ‘a’ cause of CVD. They are not ‘the’ cause of CVD.
Thank you for this very interesting reference.
What strikes me , as always, is the complexity of all the processes involved. This understanding also encourage my present holistic broad brush approach to health rather than any particular one.
You’re suggesting a single cause here.
I almost thought you were finished here, but now I’m waiting now for your ‘the cause’. 🙂
Thanks for your exposé.
Sorry, if I did not make myself clear. There is no single causes, there are many. However, a cause of CVD must do one of three things: damage the endothelium, cause bigger and more difficult to clear up blood clots, or interfere with the healing process. If it does all three, then it is a powerful cause.
That’s a great post Malcolm, thank you. Was that the brief explanation! 🙂 think you should have a crack at turning your thoughts n experience n views into another book. Printed word still carries some weight.
A new book is being written.
Take your time ! – I’m still waiting on your ‘Statin’ book to arrive, let alone read it !
As a newby and complete novice, (?TIA March 2018, leaky heart valves & ApoE4, started statins 7/6/18, selp-stopped statins 4/52 later, when cholesterol halved, 3.07 & LDL 0.6 & muscles & brain **** ) firstly thank you for really informative blogs on the real causes of heart disease, is so interesting, and logical, you really are a medical detective! Thhis may not be the place, but can I ask what is probably obvious to all the knowlegeable people on your blog, but I want to ask someone who knows the answer, why am I told I need to restart statins as my cholesterol has since increased to 6.5. yet I have been able to sleep again most nights now without pins & needles, cramps and muscle pains so feel better but Im told having Apoe4 I am more at risk? From what? I seem to think its too little cholesterol? From the information I am finding, I think I need my cholesterol, especially in my brain (family hx AD both sides) . I’d be really grateful for clarification on this ?
here is a great link to a Dr Zoe Harcombe blog which will greatly help, Malcolm K features :-)http://www.zoeharcombe.com/2010/11/cholesterol-heart-disease-there-is-a-relationship-but-its-not-what-you-think/
Hi mcjocko thanks for that, reading it now, had previously read The Great Cholesterol Con but not able to keep it all in my head. Need to write me a flash card for appointments!
Deborah – go read/watch anything from @DaveKeto – Dave Feldman. I especially recommend his latest talk in Austin: https://www.youtube.com/watch?v=LEQjcQj_rwg and his Feb 2018 in Breckinridge: https://www.youtube.com/watch?v=0LuKwsz9Woc&list=PLrVWtWmYRR2Cr0_P9Ba3V27wLhCq8GCcj
Deborah, my total cholesterol is twice as high as yours. I am 71. I enjoy good health. No meds.
Thank you for your comment, I wanted to get my cholesterol levels back up when I stopped the statins, but when you’re told the opposite by Drs, until you discover the reality, its hard to think you can dispute it.
Mine too, off the charts too high to measure. I’m 74 took Lipitor and Crestor for few years, had such muscle pains then I did research into the myth of cholesterol.
Thank you Francis, and all who have reassured me. I’m not sure if Im allowed to post this here, but I have now written to my local CCG with my post statins experience feedback and a suggestion they consider running useful health promotions in the clnnics (esp cardiio one!) such as the UTube one that was suggested to me on this blog. I am hopeful but would be immensely surprised if it came to fruition, but dont ask they wont know there’s any isues or ineterst out there! I receieved a phone call back staing they will be looking into the suggestion.
quote..” ..taking statins was probably the worst thing I could have done, so I am pleased that I have now been able to increase my cholesterol again. I need my cholesterol!
I was fortunate enough to come across some very learned people having
stumbled on Dr Malcolm Kendrick’s blog researching causes of heart disease
where I was told about a video by a Dr. Peter Langsjoen
(https://ihm.life/what-causes-hardening-of-the-arteries-by-dr-peter-langsjoen/). Having watched this video, which is on a level even I can understand, my
first thought was “I wish I had seen this when I was diagnosed, when I was
offered statins, when I was sitting in waiting rooms at GP etc playing on my
phone”. At GP surgery, in some clinics, there are loop CCTV screens with often banal,
bland health promotions, that frankly are so boring and talking down to us,
that they are just ignored. This video is real, about what really happens,
why heart problems happen and tell the truth about statins. Had I known
beforehand I doubt very much that I would have taken this prescription, but I
did not have an informed choice. I was told if I had side effects, including
muscle ones, to stop taking the statins, but not why. I now realise that statins are such big money internationally that most other people advised to start statins also have no idea what these drugs are, how they work, the pathways they are blocking in the body apart from cholesterol, and the fact that reducing cholesterol is not the answer to CVD. Especially
if you are a woman….”
Thank you Dr Kendrick for your blog, it has been so enabling.
” why am I told I need to restart statins as my cholesterol has since increased to 6.5″
Because Big pharma makes a huge profit out of statins, and have arranged that individual doctors get a bonus when they prescribe them!
When I gave up statins, I knew that whatever benefit they offer theoretically, life on statins would have been a torture (possibly confined to a wheelchair, still with the statin pain). Quite apart from the misery of life like that, think of all the exercise I would have lost!
Later I also learned that statin damage does not always fully reverse – though it did in my case – so the answer can only be to just to say “NO!”
In the past, Dr. K has published links to studies that show that higher cholesterol levels correlate with lower all-cause mortality for people over 65. I didn’t get a chance to go back and look them up, but, if you’ve saved a copy of all of the heart-related blogs, you can browse them to find these.So, this being the case, why would anyone over 65 consider the use of statins for the sole purpose of lowering cholesterol?
Hi annielaurie98524 thanks for that, I’ve only recently discovered this blog after reading Dr Kendricks excellent books, which are what started me on this journey of discovery. It has enabled me to start putting the true relevant information together, heart, brain,AD, Apoe4, stress, autoimmune, osteoporosis, etc, and take control of myself, dirching the statins while my brain still works, (memory taking a break though! gluten issues as well!) takiing supplements instead and improving my diet, being outside in the sun and doing physical things! But still a lot to learn & wanted to check wehat the link was with Apoe4 before I see the Doc& confirm its no statins for me! Not now, not ever again.
Thank you. My muscle pains and tingling is gradually reducing so I am hoping like you, it goes eventually.
Ha Ha, now I know what your new book is about! 🙂
duh, just read the reply above! too late…
The endothelium dysfunction theory of heart disease is wonderful, in my opinion. After reading your sight it is what I’m following. I remember when I first read about it 20 years it just made sense. It was better than the cholesterol theory. What is disappointing to me is that I haven’t seen a proof of concept study. There are indirect studies finding the theory makes more sense. A direct study though doesn’t seem to have been done. I’m probably wrong about that, but from the little that I’ve read I don’t recall seeing it.
The first time I read about endothelium dysfunction was in a book written about Dr. John P Cooke. He mentions about treating patients at the Stanford hospital he worked at using the theory that increasing NO in the diet will decrease heart attacks. He never talked about how his patients did on his regime though.
I remember later reading Dr. Davis’s sight and work (author of Wheat Belly) about heart disease. He basically threw the kitchen sink at heart disease, trying all different kinds of theories. What was disappointing to me was the results seen in followers that took l-arginine. It didn’t help to decrease CT scans of plaque. I recall later seeing small studies that came to a similar conclusion. Figured there could be multiple reasons why that outcome happened.
With the cholesterol theory, a main argument for the theory I hear often is that ~ “since heart attacks are decreasing, something right is happening” It’s easy to argue against this thinking. I don’t believe they are decreasing, and of late there has been a slight increase if I remember correctly, reading on this sight. Many people though take a kitchen sink position on this topic I suppose.
I’m getting sick of saying it doctor but that’s one incredible piece. I’ve read nearly all but that one is very thorough and conclusive. If only Dr Malcolm Kendrick was the head of the world body on heart disease? We would see some progress on what seems to be a forever circulating carousel of codswhallop. This message somehow needs to see daylight as I’m getting tired of seeing people mainly the elderly struggling with there health after being prescribed the pill of which I don’t mention. Makes me ill. Since my close encounter and my eyes becoming open to the truth I must admit to such depressive thoughts about what evil man is capable of in the pursuit of the almighty dollar. It’s good to know people like you exist Malcolm but unfortunately this doesn’t go far enough. The powers that be have been discrediting the great minds for centuries and I’m sure you would just fall victim to the same circumstances. I guess just keep posting information and writing books and maybe one day it will gain the required traction. If people I know run into issues I just mention your name and they can take it from there. At present that’s all we can do. Again excellent article and looking forward to the next.
Eventually the truth will prevail, as truth is the daughter of time. But by then the world will have moved onto new life-suppressing stupidities and the same game will be going on.
There are exercises that promote NO “dumping” are these beneficial?
I continue to enjoy your articles and books and consider myself lucky to have access to your knowledge. Thank you!
E: Sunlight causes NO to be produced. Raising the pulse rate 10-15 beats per minute causes NO to be produced, so any moderately brisk exercise works. Important to include foods rich in nitrogen compounds in order to produce plenty of NO. I take beet kvass (fermented beet juice) every morning. Not everyone likes beets, but there are lots of nitrogen-rich foods, such as arugula. Dr. Mercola has a list of them. Do the NO dump if you wish, but it isn’t necessary.
Thank you, Gary. Does this mean sunlight exposure without sunscreen? I have used beet kvass in the past and will definitely reintroduce. Nourishing Traditions book and Dr. Mercola are good resources for me.
I am my own doctor so far and with the generous insights of Dr. Kendrick and others like yourself it increases the realm of possibility.
Have a great day.
E: Without sunscreen. I don’t buy it and never use it. I have a five-hour hike once a week at high altitude (7,000-10,000 feet), where the damaging rays of the sun are more intense, and I never get any sunburn, despite being once-blond (in childhood) and fair-skinned. Getting a light tan helps, and I think having good vitamin D status also protects from sunburn. I certainly did sunburn in youth, but not now. Read Dr. Kendrick’s post on the healthfulness of sun exposure.
Anecdotally (but as usual a LOT of anecdotes) reducing consumption of Omega 6 oils reduces the predisposition to burn rather than tan. Would be interesting to see if there’s a relationship between increased use of “heart healthy vegetable oils” and increased levels of skin cancer.
chris c: Very interesting. I didn’t know that. I did sunburn in childhood and adulthood until I altered my eating habits. Now I can spend hours in the sun with no burn. Skin cancer every few years, which the dermatologist removes, and which doesn’t concern me at all. I think I’ve had six.I do eat fatty fish once or twice a week, and nearly every breakfast includes either smoked salmon or salmon roe, so my omega 6/3 ratio is very low. I eat neither vegetable oil nor commercial foods which contain them, so my main sources of linoleic acid are nuts, which I consider health food, for the mineral content.
It might be worth adding astaxanthin – I haven’t had any issues with sunburn since I started taking it 8years ago. Astaxanthin is also beneficial throughout the body, especially the eyes.
Frederica Huxley: Yes! The salmon contains astaxanthin.
Take care, because farmed salmon has pesticides and antibiotics to counter sea ticks, and their food is not species specific! Increasing amounts of soy are fed to Atlantic salmon.
Frederica Huxley: Farmed salmon is a terrible environmental disaster. I eat only wild-caught Alaskan salmon from a source I trust.
I’ve tested this theory. I eat very low levels of omega 6 oils. Tried taking my shirt off (that skin hasn’t seen the sun in many years), had two sunny days in Connecticut, USA. Got quite red and the skin peeled.
Tried it again on one sunny day, 3+ hours, did not get red, though I also covered up after a while.
Tried it again on Cape Cod, with sunscreen, got quite red everywhere there was no sunscreen, though I did not burn.
It seems to me there is a benefit to low carb and no Omega 6 oils, but I can’t quantify it without having another one of me.
BobM: A very important step in getting healthy sun exposure is to begin by gradually getting a light tan by exposing a little bit of the pasty-white skin each day, and gradually increasing the time of exposure. This light tan is protective against sun damage. I cannot emphasize enough this first step. Some people, notably red-heads, can have a very difficult time getting this protective tan, but most of us can. This past winter for the first time I took a vitamin D supplement, and I think keeping my vitamin D status up may have played a role in my high tolerance this summer for major sun exposure. If your skin is getting red in the sun, you may be one of those who doesn’t tan easily, or you may try supplementing with vitamin D, astaxanthin, or by eating salmon or shrimp, which contain it.
I don’t know if there is any suitable animal model of CVD (and I don’t like to think about vivisection anyway), but if there is, isn’t it possible to damage the inside of an arterial wall, wait for a suitable length of time, and look for blood clots covered by an epithelial layer – wouldn’t that prove your theory beyond reasonable doubt?
Its been done.
And what was the result – I am guessing that is exactly what was discovered.
An old study, done in pigs, but all the studies of any use in this area are quite old now.
Pushing a balloon catheter inside an artery and inflating it would seem to be a very effective way of ripping the endothelium to pieces. Yet conventional medicine considers it curative. ;o)
But balloon angioplasty makes a jolly good earner for cardiologists. Possibly contributes to it so well favoured used, why ECP/EECP (which does wonders for collaterals) doesn’t get a look-in.
Wonderful, wonderful, wonderful! Now I’m interested in what endothelial damage “looks like” before the body gets the repair mechanism built. The body is so speedy at repairing damage there must be various stages of repair at the sites of damage?
Your rules, Dr K: you win. You certainly win!
Dr. K., I hope you’ll consider compiling all your heart-disease blogs into a book. I would definitely buy it, although I have never had heart-related problems (healthy and med-free at 72), just because it is fascinating science. I am still awaiting delivery of your statin book — I finally had to order from a UK vendor after getting a 2-month runaround from Amazon.
I realize your essays can’t cover everything on each outing, but I’m curious how to fit calcification into the picture. Do we think calcification has something to do with clots?
Calcification represents the ‘end-stage’ of various repair systems in the body – for some reason or another. A scar will often calcify. Areas of infection e.g. pulmonary tuberculosis will often calcify and suchlike.
Out of curiosity, is there a way to assess collaterals and their ability to take over from occluded arteries? And do stents obliterate collaterals?
In my own case I am alive today due to my collaterals developed during the preceding years to my MI 1999 by regular moderat exercise and certainly afterwards through more systematic exercise; e.g. I decided to take my bike to work (12 km) every day year around; though tough when in heavy snowfall in Sweden 🙂 .
There are no ways, as far as I understand, than indirectly, to assess the existence of your collaterals. Indirectly you can notice them by x-ray videos how the blockages of the arteries are naturally by-passed by these tiny vessels – great work by Dr. Sroka. Lately I have understood that they degrade if you don’t “keep going” or rather continue to stress your blood supply system through physical exercise.
So – “Keep going” or die is my lesson learned.
There it is. Simple. Beautiful. Elegantly explained. Endothelial damage leads to healing, thus clots and other debris, and a new layer of endothelium covers and incorporates this debris into a plaque. Repeated injury in the same spot leads to enlargement of the plaque and concomitant narrowing of the area for blood to flow, and can ultimately grow large enough to completely occlude the artery and stop blood flow if the collaterals remain undeveloped. I think I get it. Am I missing something, Dr. Kendrick, or is this a reasonable summary?
Pretty reasonable. It is what I believe to be true. It also has the advantage of fitting all the facts. Or, at least, I have yet to find any facts that are contradictory. And, believe me, I spend a lot of time looking.
Hi Dr K, I know this probably sounds rather stupid & I’m showing my ignorance, but when you know yourself and get bruises etc does that damage the blood vessel walls?
So how does one repair past damage? Or is this a totally irreversible process?
As a stop-gap, encouraging the expansion and neogenesis of ‘collaterals’ would be a Good Thing.
– So how do we kick-start their existance ?
Can strenuous exercise cause that damage? For example, something that pushes heart rate to the maximum, which would also greatly increase systolic pressure.
I have had two heart attacks and five stents, the most recent while on a statin with total cholesterol of 109….so I stopped the statin. All except one of my stents are in a small area of the LAD so I ask myself why at that one specific location? What is the mechanism that causes damage at that specific location and not throughout my system? All of us are subject to infections throughout our lives (I am 81+) so have been there many times. How can a low level of cholesterol be healthy when almost every cell of the body requires cholesterol?
My cardiologists have no answers…..so I am pursuing a dietary (ketogenic) approach to better health along with exercise!
John, have you been reading the research of Dave Feldman and his research assistant Siobhan Huggins on the immune system and LDL, you may find it very intreesting re lowering your cholesterol to the floor http://cholesterolcode.com/ and within the site: http://cholesterolcode.com/lipid-roundup-part1/
I am a youngster, only 72, but as you basically on a mild ketogenic diet since ten years now.
Talking infections. Brought up on a “standard” high carb diet I caught, every year, every nasty flue or cold that happened to pass my nose. Down in bed for a week with a very high temperature was typical. What surprised me when I adopted the LCHF diet, some years after my serious MI, was that I haven’t have a single cold or any flue. Though I was hit by pneumonia a couple of years ago which I think was due to some cheating on the diet.
Well, there are no guarantees in life but my guess is that the immune system benefits from skipping the carbs.
Goran, I’m sure you’re right. I ditched the statins and adopted a LCHF diet about 5 years ago and haven’t had a single cold since despite plenty of exposure.
JanB, I am a few years younger than you, I have never had statins, I eat a LCHF diet, I have lots of vitamin C a day, 5 to 10g, and I get colds or similar two or three times a year. I do get over them quickly as I increase the amount of vitamin C to 50g (ish) a day, at least I think that has something to do with it. It would be nice to think a few simple changes would make significant effects on susceptability to infections, but I think it is difficult to draw conclusions.
AH – you’re probably right. Horses for courses. But after 10 years on a statin I was wreck and now I’m not. I feel that my immune system, which I feel was always pretty good before, was damaged and now it’s recovered. (A shame about my poor mangled feet though which never wholly returned to normal.)
JanB, coincidence or what? I have mangled feet too, but they were mechanically mangled. I have to pace myself as to what I can do before needing a rest, but they have improved markedly since drastically reducing carbs and taking large doses of vitamin C. Doesn’t stop me doing heavy work on railway maintenance, just reduces the amount I can do compared with unmangled people.
Feet, eh. The grief they can cause us. I particularly resent the invisible gremlin who sticks red hit pins in mine making me squeak. In spite of the fact that mine burn and tingle and simply HURT (in spite of being somewhat numb – how can that be?) and are becoming more and more misshapen, I play a lot of tennis and can walk for England.
Use ‘em or lose ‘em, I reckon.
Yes I’ve been low carb/Paleo/keto for thirteen years now and the lack of minor infections compared to the high carb low fat decades is quite spectacular.So commonplace as to be unremarkable but are there any studies?
John Alden Quick,
I have a friend who has had repeated bouts of artery closure at the same place in the right coronary artery. Her first stenting was almost twenty years ago (at 48), and she’s had four additional surgeries since. Her other arteries appear clean on angiography, and she’s a smoker yet!
I asked her to ask her doctor why she bothers with medication (statin, anti-hypertensive which was finally stopped. I understand the blood thinner, and she takes metformin for diabetes) when it doesn’t seem to prevent repeat closures of her “bad spot”, and she only had one bad spot before she ever took medication. Her doctor said statins prevent plaque from “spreading”, and her problem might be related to serious dental issues (in other words, low level infection).
Of course, single-vessel disease makes hash of the diet-heart and lipid hypotheses, but why let facts interfere with medication sales?
You might be interested in this post on single-vessel disease. It includes a link to a paper from the 1950’s pointing the finger at hemodynamics as a cause of CVD.
Standing on the shoulders of giants… that in itself takes giant thought!
Forgot to say: Nobel Prize!
More likely the igNobel prize
I’m having to restrain myself!
I would much prefer You getting a Nobel prize than the currently being pushed PCRM pawn of the name Campbell.
It was workers at Nobel’s dynamite manufacturing facilities that first discovered the importance of nitric oxide. When they were stirring the nitroglycerine their angina went away. This lead to the creating of glycerol tri-nitrate tablets (GTN) to be put under the tongue (nitro-glycerine by any other name), to treat angina attacks. Nobel himself, suffered from angina, but refused to used GTN. The nitrate in GTN stimulated NO production, thus leading to dilation of the coronary arteries – not that anyone knew this until about a hundred and fifty years later. So Alfred Nobel is – indirectly – responsible for a great deal of my thinking on CVD. Which is as close as I will ever get to a Nobel prize.
Many thanks for all of your work, Dr. Kendrick. It is a joy to see what you have accomplished and to have the pleasure of reading your passionate and elegant prose. I look forward to ordering the new book for myself and my friends.
I completely embrace this theory re: arterial damage being caused by a blood clot. BUT–what causes the damage in the first place? I will be getting the CAC scan next week. I requested it. Hoping we are getting closer to knowing how to stabilize or reduce the calcium deposits that are atherosclerosis. WHat, besides Statis, positively affect NO and thereby assist resolution of plaque formation and endothelial damage?
Sunlight on the skin. Exercise. Relaxation. L-arginine. GTN, Viagra, ACE-inhibitors, laughter, stimulation of the parasympathetic nervous system… and a few other things as well.
and for women… VIAGRA? Please do not say statin!
Where does Vitamin C fit in? Is it as important as what you have listed?
Are ace inhibitors good for you
They are not bad for you. I think that inhibition of the RAAS system can be beneficial. Probably the best way to dampen down RAAS is to eat more salt and more potassium.
Dr. Kendrick: Thanks. Both sodium and potassium. Important. I’m doing it. All in a day’s work for the kidneys.
John: ACE inhibitors do appear to have some positive value in CVD, but as Joel M. Kauffman says, “One may speculate that both classes of antihypertensive drugs [ACE inhibitors and the newer Angiotensin II-Receptor Antagonists] may provide some of their benefit by raising serum potassium ion levels.” This is the route I have chosen, ditching the ACE inhibitor (with the full support of my physician) and adding a potassium supplement (which she questioned). Dr. Kendrick’s 2013 potassium post is a good place to start learning about this vital mineral. I’m glad I ditched the drug. I never have to think about did I take it, or did I forget? Don’t have to take them traveling. I prefer to let my kidneys function the way the good Lord intended.
Is your blood pressure high. Would like to stop the meds but every time I try blood pressure shoots up
biddy99: I have no idea what it is. I’m just glad I have a blood pressure; otherwise I’d be in a pine box. I truly feel in the peak of health. For twenty five years in my doctor’s office my BP was never once taken correctly because the machine was on the wall, and the cuff wouldn’t reach anywhere suitable. So I’m not disposed to bothering having it checked any more.
Do ARBs have the same effect or is it just ACE?
Similar, but not the same. The best of the ACE-inhibitors, with regard to NO, is perindopril.
ACE-inhibitors as well as ARB’s are a plague and have caused tens of thousands of kidney injuries. According to a large study comparing several different medications diuretics seem to be the best choice for most people, having the best benefit/risk ratio. The newer medications like ACE-inhibitors, ARB’s, calcium channel blockers are used more only because they are pushed by the pharmaceutical industry, not because they are better/safer.
Speaking of blood pressure it’s ridiculous that the numbers (just as happened with cholesterol) are lowered every x years. Big pharma’s game and profit of course. While more evidence is emerging that the difference between systolic and diastolic pressure could be as important (40 used as cut off), but surprisingly in most cases the newer blood pressure medications do a worse job in lowering this number compared to diuretics.
Thank you , But shame about ARBs. Ramipril gave me chest pains but I can tolerate a tiny amount of an ARB.
As for diuretics, well Leon, indapamide put me in ICU for 3 days as it caused my sodium to plummet to a critical level. Not that unusual apparently. They really do not suit everyone.
“As for diuretics, well Leon, indapamide put me in ICU for 3 days as it caused my sodium to plummet to a critical level. Not that unusual apparently. They really do not suit everyone.”
No medication suits everyone but in general diuretics still are the best option. I tried indapamide, too and my heart rate in rest was 100 while it normally is around 64. Then I got Losartan, but as a systematic review found that ARB’s can modestly raise cancer risk (including lung cancer which my father died from) -the study even caused a dispute within the FDA- I decided to try hydrochlorothiazide. And again my heart rate went up. Taking extra potassium stopped this problem and I could tolerate hydrochlorothiazide. Maybe taking more sodium could have solved your problem. Diuretics are known to cause several deficiencies, most importantly sodium, potassium, magnesium and zinc.
Yet reliable science still demonstrates that diuretics are the best (first) choice for most people.
But no medication is perfect: hydrochlorothiazide raises kidney cancer risk.
My blood pressure is doing reasonably well with citrulline.
Check out the graph of salt intake versus life expectancy in this tweet retweeted by Dr Jason Fung. The optimum salt intake is twice the WHO recommendation, and four times the American Heart Association recommendation.
Unfortunately you have to subscribe to look at the graph.
The book “The Salt Fix” by James diNicolantonio really is an excellent read and very reassuring. It’s available on Kindle.
Thank you for your comment Leon – very interesting. The ironic thing is I’ve always had more of a taste for salty things than sweet. Not necessarily adding extra to food on the plate but certainly not avoiding it. Salty snacks have always been a weakness.
I also get plenty of potassium in my regular diet and thanks to this blog, take extra magnesium.
My bp is currently well controlled on lacidipine and a very tiny dose of candesartan – a combination that I can also tolerate without problem (so far, touch wood).
I did buy The Salt Fix and found it very good, but also rather a disappointment as it is definitely aimed at people without hypertension, encouraging them to ignore the current low salt fad.
@ Judy: Why a CAC scan on your own request? Did you consider the radiation you will get from it? According to a study I just read, radiation used in these tests varies wildly. And additional cancer risk is certain with this test. And will you be much wiser with the result? Will it change your behaviour, medication, exercise?
As for NO: I think citrulline is the easiest way to raise NO. The kidneys convert it to arginine which again leads to higher NO production. Note that citrulline supplments are better than arginine itself in raising arginine and NO production. A reasonable dose is 3 x 750 mg a day. Please note that there is no long-term safety data but I think it’s safer than most CVD medication.
Fascinating article, thank you. One question remains unanswered, what happened about 100 years ago that a very rare disease turned into a leading cause of death.
Do we know that it was rare? Remember that Virchow and Rokitansky were debating the causes of atherosclerotic plaques in 1852. Equally GTN was being used for angina over a hundred and fifty years ago. We know that Egyptian mummies were full of calcified atherosclerotic plaques. I think that there was certainly a lower incidence in the past, but I am not that it was rare – at all.
Ways it rare?
If you read Samuel Pepys’s diatribes, he mentions quite á log of causes of people keeling over and dying suddenly with symptômes similar to heart attacks.
Very rare in non-agricultural societies I believe, insofar as anyone’s been able to tell. The ancient Egyptians ate lots of cultivated grains, as did 19th century Europeans, so they are not black swans for this idea. One line of evidence supporting this is Weston Price’s work. Another is the reports of the missionary physicians who cared for populations eating their traditional diets. And of course Lindeberg.
Is it not true that ‘heart attack’ and CVD are quite modern terminology? What did people with CVD die of previously? Only thing that springs that mind is dropsy.
It’s been suggested that the high carb (grains, veggies and more grains) and low animal fats diet of the ancient Egyptians did them no favours with obesity, tooth decay and T2 diabetes .
– Evidence from their ‘non-religious’ figurines mirroring more realistic bodies of the general population, – beer-bellies, gynocomastia and the aforementioned mummies telling tales of cardiovascular disease.
Stephanie: Yes. Dr. Kendrick is talking about process here, the process of the development of atherosclerosis which can lead to heart attack. The healing process in the endothelium of the cardiac arteries gone awry, primarily. The causes of the enormous increase in this pathology in the twentieth century lie in what happened during the twentieth century. From my meager reading of history I would venture to say it was the bloodiest in human history, with enormous dislocation. Commercial foods replaced traditional farming practices. Central banks gradually took control of the world’s economies. Advancements in transportation and communication impacted all of the above, and increased stressors in entire populations.
Gary: 20th century was very bloody in the number of people killed but far from bloodiest in the percentage of the world’s population. Many anthropologists say that hunter gatherer societies, for example, have homicide rates of up to 25% of their populations while both world wars in the 20th century killed 1-2% of the total population. The good book on this is “War. What Is It Good For?” by Ian Morris. He has also written another very good book “Why the West Rules. For Now”.
Sasha: Yes, and warfare among hunter-gatherers and today are basically about the same thing: adequate supplies of and/or control of resources. I was thinking of all the factors I listed, especially dislocation of population and deprivation, working in concert to increase strain on the cardiovascular system caused by stress. Also, aerial bombing, developed by the British in the Great War to terrorize populations was invented in the twentieth century. In those days it had little affect militarily. Today, the bombs are much bigger, but nevertheless, the main value of it is in terrorizing people (with the exception of the worst military attack on civilians ever, Truman’s bombing of Hiroshima and Nagasaki). One factor I wasn’t thinking of at the time was vaccines, particularly the experimental vaccines used in the early 20th century. The “Spanish Flu” pandemic at the end of the Great War was no doubt linked, in part, to multiple experimental vaccines given to the soldiers. The Rockefellers have been developing these in their Manhattan labs since very early in the twentieth century. No doubt such research was going on in Europe, as well.
I need to read up more on the vaccine issue… I watched Vaccines Revealed and also The Truth About Vaccines. I also downloaded “Dissolving Illusions”, looks like a very well researched book.
Sasha: Yes, “Dissolving Illusions” contains a wealth of history of both infectious diseases and vaccination from the 19th and 20th Centuries for the U.S., and England and Wales, and elsewhere. Medical libraries have this information, but few know it. The threat (mortality) from infectious diseases declined to very low levels before, with the sole exception of smallpox, any vaccines were developed for them. They are nothing more than a cash cow for pharma.
Two recent articles from the Guardian.
One is quite enlightened, highlighting it makes a difference what kind of calories are eaten. Apparently, people in the 70s ate more calories than today while not expending more on exercise or manual labor:
The other tries to confirm conventional stupidity, i.e. eat between 40 and 70% of calories as carbs, if you must to high fat, avoid animal fats and meat. When will they ever learn to express that in g/kg rather than % of total input. One can easily overeat on carbs, so 70% on carbs on a 3500 cal/day diet is certainly not life extending!
My takeaway on the second article from the Guardian that you cite, on HCLF versus LCHF was the ideal is a goldilocks diet , just right. However I am sure Zoe Harcombe will do an insightful analysis of the study
I’d love to hear Dr K’s take on this study, but it was (I suppose inevitably) an observational study. So those who ate lots of carbs may well have been the ones that took more exercise, avoided tobacco etc, while those who didn’t care about their health probably ate more saturated fat. Thus even if saturated fat was good for them, they would on average die sooner! Remember that observational studies of women taking hormone replacement therapy – when a randomised trial was done, it turned out that HRT was responsible for extra deaths.
‘My role is to resurrect these forgotten scientific heroes and place them where they should always have been. The scientists who discovered what really causes CVD.’
Great Mission Statement Doc.
Our role, is once you’ve got these heroes on their plinths, will be to make sure there is an extra plinth for the man who put them there!
In the meantime we can all spread the word, tell others about this blog, buy the books… from the publisher!
And await the next publication!
Eye opening stuff.
And with judicious editing, there’s enough useful matter in these Reader Replies to fuel yet another one.
A Book of The Blog. Now there’s a novel idea…
No blog has ever brought tears to my eyes… this one did. Superb work. Simply superb.
I guess there really is no 100% way to avoid endothelial damage. The best we can do is our best, armed with the knowledge to be as preventative as is possible. Meanwhile, if the focus shifts away from LDL science can work toward a therapy for those with Lupus and other diseases that damage the endo …. fine work Dr K
So if damage is caused by lots of ‘things’ in the blood, and their concentrations are the same in the arteries and veins then I assume it’s the force/pressure difference that causes the “things’ in the blood to cause the endothelial damage in the arteries and not in veins? This may have been covered in one of the earlier parts of the series.
Most likely “things in the blood” are not the same in arteries vs veins
That’s great – as ever. Thank you so much for all your time and energy taken to educate us all. How you find the time I’ll never know.
It took me a while But I have now read all this post and ploughed quickly through the commetns.I have one comment. You use the term “Encrustation’ to describe process of plaque formation. As I read this I pondered on how we form a ‘scab’ on the skin if there is a wound to heal. Is there calcium in the crust which make scabs also ?
Scabs of course peel off after a while as new skin forms underneath. If a plaque peeled off it would block the artery. But why isn’t there a parellel process in the coronary arteries ?
BTW : I would rather call the “Encrstation theory” the “Scab theory”. Seems more descriptive and easier to understand !
Bill, one of Dr K’s earlier blog posts covered this aspect “scabs on skin” and “scabs on endo” and the processes involved – I can’t remember which blog.
Yes that’s true Robert…I dimly remember reading about that.. I think the differnec is that a scab can peel off and be disposed of with out any further problem.However a scab on the surface of an artery would immediately cause a blood clot if it peeled away… Thus the body deals with the scab by growing a new endothelium on top of the scab..Which of course is the start of a block in the artery…
So can the body dissolve a scab that has been covered over with an endothelium layer in the artery ?
I think the answer is yes..But just now I cannot think of any regular process which would do this..
Can you help here Malcolm ?
Thanks for that jog to the memory Malcolm ! Macrophages are the body’s own method of getting rid of such debris even though under the endothelium layer of the coronary artery..
I went looking for further information about this process and came up with this article :
“Cardiac macrophages and their role in ischaemic heart disease” at :
But after reading it I was none the wiser…
At the back of my mind lies the thought : Macrophages when they have broken down and absorbed the scab debris in the artery wall, become enlarged foam cells. But can these ‘foam cells’ safely make their way out of the intima or are they trapped there – leading to further problems ?
They are trapped
Ummmmmm! I had a hunch you might say that.! Foam cells was the word in the back of my head…But surely that is not the complete end of the story..The body does have a healing response surely. The formation of collaterals arteries is one such the response
A thrombus converting to a “scab” is a biological process involving formation of new EC’s, smooth muscle cell migration, new blood vessels to supply a thicker intima layer, smooth muscle cell calcification, macrophages etc.. Skin scabs involve an entirely different process.
Thanks for the correction..I was aware thta there are differences..But I was keen to establish the similarities..Which help illuminate what is going on for us who are less technically trained…
For me the exchange above about this is worth every second .. And far more illuminating than trying to follow the diet argument which is raging still between a few folks here..Bow that really is a complete waste of time & energy…
For those various diet dictators, I have this message : Look diet is not that important..just stay away from the bloody sugary crap and industrial, chemically created seed oils !!
now let’s go back to what this Post is about ; 1 ) what causes CVD ? and 2) If one has CVD what are the most effective ways of healing from this disease ?
We KNOW : 1) Cholesterol does not cause CVD 2) Saturated fats doe not cause CVD; 3 ) CVD is basically a bio-mechanical problem in the arteries : The coronary arteries are damaged either by the actual pressure of blood being pumped or by toxins in the blood 4) Smoking because of the toxins in the smoke causes CVD; 5) Stress causes CVD. 6 ) The body has a capacity to heal these liesons in the coronary arteries; 7 ) Vitamin C is needed for this healing process to happen; 8) In the absence of Vitamin C the body instead attempts to heal the liesons with ‘scab’ like plaques. 9 ) Plaques bulge into the artery reducing blood flow and or increasing the pressure of the heart to pump harder.10) Uncalified plaques are more liable to rupture and lead to a heart atatck. 11) Plaque stabised by a process of calcification are less liable to rupture and lead to heart attacks..12) Calcified plaques still partially block the artery. 13:)The development of collateral arteries is the body’s way of handling this problem. 14) Vitamin C is needed for the growth of collateral arteries..The more the better but not so much as to cause loos bowels !
Hi Bill, I like that: diet does not matter as long as it is healthy. How does a bad diet cause CVD? Maybe we need a better term than “diet”.
A clear, logical, and persuasive explanation of how plaques may form.
One thing that bothers me. If endothelium damage is so deleterious, how is it that prolonged bed rest is so harmful to the heart? It seems to me that bed rest should result in lower blood pressure and slower flow, ideal circumstances for the endolthelium to heal.
Martin the body is programed by evolution “Use it or lose it”. The body responds to prolonged bed rest by reducing the amount of normal rebuilding which is constantly happening. This includes the endothelium of the coronary arteries.
The avarice of the pharmaceutical and food companies in peddling their poisonous products at the expense of our health, and in buying the support of the medical profession and politicians with some of their surplus ‘spoils’ to ensure their dominance remains unchallenged, fits perfectly the adage “it has been said that for evil men to accomplish their purpose, it is only necessary that good men should do nothing”.
Thankfully we have in Dr K a good man who isn’t prepared to sit back and do nothing – and neither are we.
Write to your MP, challenge your doctor, refuse to buy the rubbish being pushed out, tell your friends and family – anyone who will listen !
Surely the weight of evidence is now reaching critical mass and will sooner or later bring down the Cholesterol house of cards ?
Keep up the stirling work Dr K – your posts have been a fantastic therapy and comfort for me (both mentally and physically) since my heart attack 3 years ago at the age of 45.
Fibrin serum levels for unstable plaque testing?
Dr Kendrick writes in this post “early stage plaques…that they began life as small fibrous streaks…what is the most “fibrous” material…fibrin”.
The previous post covered the development of blood clots on the unstable plaques and we learnt that these unstable, ready to burst, pre calcified plaques could not be detected (apart from surgical means).
As opposed to calcified plaques and a CT scan. I think the comments confirmed that if you had a high calcium score then you also had these unstable plaques. But for those with a score of zero or those for whom the cost of a CT scan is too much…
…Dr Kendrick has discussed fibrin and fabrinogen many times before, so much so that it prompted me to get my fabrinogen serum level tested in 2017.
Revisiting my test result, I was curious that the lab range was from 1.9 to 4.3 g/L.
No zero. Strange, maybe.
Not strange. My notes from the time state that fibrinogen determines the stickiness of the blood and that we need adequate levels to stop bleeding when injured. And if too high = e.g. too much blood clotting”.
Having confirmed the presence of fibrin in the early stages of plaque development, surely a readily available serum test for fibrinogen (with a result above the adequate levels for blood clotting i.e. outside a normal range) indicates the presence of these unstable plaques?
Thanks Charles..That makes sense to me.But I wonder if any of our mainstream statin dispensing doctors are aware of the existence & role of fibrinogen ?
Thank you. It makes you wonder in how many other areas there is research that has become ‘unfashionable’ but is still worth looking at. I am thinking of cancer and the Warburg effect particularly.
Since cancer cells can only thrive on glucose it seems to be a very good idea to reduce the blood glucose levels which can be done on a strict ketogenic diet. (It is amazing that cancer patients are given sweet drinks as supplements – I read more than 40 % sugar in such drinks if I remember right.)
Professor Thomas Seyfried has made great research in this field and with amazing results. He has also written a great book “Cancer as a Metabolic Disease”.
‘Cancer as a Metabolic Disease’ is a very interesting book. I was amazed at one of my colonoscopy ppointments, following a PET scan, to find out that the consultant did not appear to know how the PET scan showed up the cancer only that it did. I ended up delivering a lecture on the Warburg effect to the consultant and a student while lying on my side with a camera up my rear end!!
Actually, apparently they really need iron as well.
“Since cancer cells can only thrive on glucose it seems to be a very good idea to reduce the blood glucose levels which can be done on a strict ketogenic diet.”
I have the impression you are either not well informed or you tend to believe pseudoscience, half-truths or plain nonsense. It’s not a big secret that cancer cells can thrive on nutrients other than glucose:
I predict that the ketogenic diet might prove to be a good tool in some specific health problems but will turn out to be a disaster for the general public using it for no sound reason. The study was already discussed here: 4 years off your life in general, if you follow a ketogenic diet.
That Lancet study is statistically incomprehensible – I have asked a couple of statisticians to comb through it – it takes time to tease out all the techniques use. However, if you believe that an observational study, where the populations were seriously mismatched at the start (the high fat group had twice as many people with diabetes- for example) can determine causality, when the OR was 1.2, then you are also believing in pseudoscience – I am afraid. As you know, I do not believe that diet has a major influence on many/any health outcomes. What I do not believe is that, suddenly, we find a high fat/protein diet can take four years off your lifespan. That is a greater effect than smoking – and no-one noticed an effect of this size before?
But I think he’s correct in saying that glucose isn’t the only thing malignant cells use for fuel
You are correct that cancer cells do not only thrive on glucose. But a lot of cancer cells do, and they are happy with anaerobic respiration. I had a diagnosis of cancer I would most certainly go onto a Keto diet.
Log in problem! “Thrive” is perhaps a “funny” word to use and I should with my use of this word also have chosen the word “preferably” instead of “only”. Another way to put i is that glucose accelerates tumor growth. If one, as I have done, has read Seyfried’s book twice (tough reading though!) one gets a pretty good picture of the complexity (as always) involved in the cancer metabolism in their damaged mitochondria. Seyfried understands, in honor of Warburg, the wrecked metabolic mechanisms of the cancer cells probably better than anyone today. Nobel class research indeed in my eyes. I suggest Leon to get better informed by spending some times with his excellent book himself.
And for sure glucose molecule stands out in the cancer metabolism which is the very reason for it to be used as the carrier for the active component in the PET-scan which struck me when I first saw the scan in Albert’s et al. “Molecular Biology of the CELL” a couple of years ago. This is also a very good reading to get informed and thus be another good book (especially the sixth edition) for Leon if he is not already familiar with this basic text.
Cancer’s other main fuel source is glutamine. @Leon I have read Seyfried’s book and wouldn’t refer to it as Pseudoscience. His central argument that cancer cells resort to fermentation due to impaired mitochondrial respiration is well supported. More so than the genetic mutation theory where cells in the same tumor can have vastly different mutations. We have made very little headway into a cancer cure despite pouring massive amounts of money into it.
“if you believe that an observational study, where the populations were seriously mismatched at the start (the high fat group had twice as many people with diabetes- for example) can determine causality, when the OR was 1.2, then you are also believing in pseudoscience – I am afraid.”
My pseudoscience remark I made because of the oversimplification of the link between glucose and cancer. I often come across such oversimplifications in health topics while reality is a thousand times more complex – often these oversimplifications are made by health gurus and the like. Unfortunately many people take these oversimplifications for “the truth”, sometimes with disastrous consequences.
I (hope I) believe very little, even (or especially?) in science.
I now remember our discussions about vegetarianism and eating meat, and it seems to me that both of us might be quite biased as to the outcomes of the study: More plant based food increases the human lifespan, more meat decreases our lifespan. Not amazing that we are “opponents” regarding this study: After all it underlines my case for vegetarianism 🙂 But you know my stance: It’s simply an ethical issue and I’m not going to debate the quality of the study. Even if in reality vegetarianism would take 4 years of our lifes, think of all these millions of animals not suffering – it would be worth it! And no, I’m not a hardcore vegetarian, just thinking logically but not always living up to it.
I also simply don’t have the competence to judge the quality of this particular study, nor do I have statisticians available like you but I read this:
“Additionally, to minimise the likelihood of reverse causation, we did a sensitivity analysis whereby individuals with cardiovascular disease, diabetes, or cancer at baseline were
excluded from the analyses. These post-hoc analyses also yielded similar results.”
That statement seems to invalidate your objection with regard to the “diabetes mismatch”.
Also, in the ARIC study the percentages of diabetics seem to be quite evenly spread in the different quartiles – unless I am missing something and you have acces to more data than I have.
“As you know, I do not believe that diet has a major influence on many/any health outcomes.”
Huh? You yourself said you would follow the ketogenic diet if you had a diagnosis of cancer. Deficiencies in vitamins and minerals and their -sometimes severe- consequences are well known. It’s no secret that many foods contain cancer-protecting or carcinogenic substances – often the same substance being able to protect against or cause (contribute to) cancer, depending on the dose.
The link between diet and health is extremely complex and we still know extremely little about it but I think it is rather strange to believe diet has no major influence on health outcomes.
In my family there was a person who ate only sugar and sweets and she died age 80 and of course we all know examples of smokers who never go cancer and lived well in their nineties, but those are people with good genes, lucky people who can do whatever they want, but for people with “ordinary” genes I am afraid there is a lot of interaction between environment (including diet) and genes.
“What I do not believe is that, suddenly, we find a high fat/protein diet can take four years off your lifespan. That is a greater effect than smoking – and no-one noticed an effect of this size before?”
It doesn’t seem to be the amount of fat/protein that matters but its source. Taking it from animals seems to deliver bad karma 🙂 An effect of this size has been seen before:
Pramil N. Singh, Joan Sabaté, and Gary E Fraser, “Does Low Meat Consumption Increase Life Expectancy in Humans?,” American Journal of Clinical Nutrition, 2003
(2 of the studies in which a low meat intake significantly decreased mortality risk also indicated that a longer duration (>/= 2 decades) of adherence to this diet contributed to a significant decrease in mortality risk and a significant 3.6-y (95% CI: 1.4, 5.8 y) increase in life expectancy)
So not really a new discovery.
And as for the comparison with smoking: If most meat-eaters would get lung cancer or COPD of course the size of the effect would be easily seen but now that all cause mortality is influenced and also the majority of the population eats meat, the longer life span of vegetarians (a small minority group) is easy to miss.
Still trying to convince you to give up eating cadavers 😉
As for “I had a diagnosis of cancer I would most certainly go onto a Keto diet.” I think it would be wiser to first consider the exact type of cancer and then decide. What -for example- if your cancer feeds on arginine and you increase arginine by lowering carbohydrates and eating more proteins/amino acids?
I would suggest you read this, short blog on the Lancet study. I think it covers most of what needs to be said. about the study https://evidencebasedmedicineunboxed.blogspot.com/2018/08/low-carb-and-mortality-unnecessary.html
Interesting discussion/debate that now took off here on Malcoms blog!
The merit of opposing blog interactions over the internet?
Yesterday evening I was actually attending a “harvest party” organized by vegetarians in a nearby community. Really good food was served – no problem with that. We also were offered a glass of wine 🙂
Being a “meat eater” I didn’t have though any conflicts with the participants. On the contrary we were agreeing that we need to stop the destruction of our societal base – the soil since they as myself were active permaculturalists trying to restore the fertility of our base.
I am now organizing a visit to a permacultural farm (Ridgedale http://www.ridgedalepermaculture.com ) in middle Sweden where they have pasturing animals as an integral part of their endeavor and operations – in the spirit of Alan Savory.
It all seems to be a question about “moral” (and not mistreating animal – read here Lierre Keith “The Vegetarian Myth) and here I see myself as a LCHF advocate a means of shaking hands with vegetarians but perhaps not with vegans since they seem in my eyes to be rather hostile towards any meat consumption.
if you are interested in permaculture and soil health, I recommend this book:
Grass-Fed Nation: Getting Back the Food We Deserve, by Graham Harvey.
some time ago you posted a link to a video of a meeting you had been to about someone who set up a farm in Varmland, and his simple farming methods. If you still have it I would be grateful
Göran: Another book you would enjoy: “Cows Save the Planet and Other Improbable Ways of Restoring Soil to Heal the Earth,” by Judith D. Schwartz.
For those inclined towards philosophy I should add that with the basic idea I now learn from the book “Postmodern Ethics” by Zygmunt Bauman i just now read. Moral is a “face to face” activity while ethics in our modern society makes such moral more or less impossible on a larger scale and where we just find corruption on a systematic level under the guise of ethics – read e.g. statins.
“I would suggest you read this, short blog on the Lancet study. I think it covers most of what needs to be said. about the study https://evidencebasedmedicineunboxed.blogspot.com/2018/08/low-carb-and-mortality-unnecessary.html”
Talking about “evidence based medicine”: You did not address the “diabetes mismatch” that exists in the Lancet study according to you.
In law, the general rule is that a person who alleges something must prove it. I suppose it is the same in “evidence based medicine”.
All I can read at the link you gave are some general, gratuitous remarks not going into details about the study itself. If that’s the state of “evidence based medicine”… Lord save us from it.
Anyway, “evidence based medicine” is just another hype and exaggeration. People got the electric chair based on “evidence” – do you really think “evidence based medicine” will do any better?
Of course it is good that “evidence” is more stressed in medicine and the therapies it applies but “evidence” can be very volatile and then there is the problem who is to be the judge. And I can think of many other problems with this “evidence based” approach. I am sure your NHS and our own Dutch health service loves this approach as it can be used (and is used) to strike a lot of medical interventions that might or might not work.
Unfortunately both patients and doctors more and more tend to forget that medicine is not only a science but also an art and especially “evidence based medicine” denies the latter. This doesn’t mean I am advocating for quackery, but as my amazing Belgian GP always says: In medicine nothing is black and white, there is a lot of gray.
And last but not least: I wonder what the evidence based fellows would say or are saying about your own explanation of CVD (which I think is excellent, as you know).
To finish, yes, observational studies have their problems but diet-wise they are often the only studies we have and one cannot simply discard them just for that reason. That’s where evidence based medicine also fails: It tends to affirm what is already quite certain and discards everything that is uncertain. And it is especially in these uncertain gray areas that the “evidence” needs to be weighted, not just simply excluded.
My starting point for evidence based medicine is to look at who did the study in the first place. Walter Willet and his team have been relentlessly pushing the high carb message for maybe forty years. They have also relentlessly attacked the HFLC movement in any and all ways. Now, amazingly, they do a study which finds that high fat diets are bad for you. If this study had been done by a group with no axe to grind, no horse in the race and suchlike, I would start with a very different perspective. You may say that is being judgemental, but when you know that someone has based their entire scientific career on promoting a thing, it comes as very little surprise that their findings always support that very thing.
When someone comes up with a controlled clinical study demonstrating that a high fat low carb diet is dangerous to health – or vice-versa – I shall pay attention to it. Until then, I will not expend much effort on it. It is a distraction.
Anything by Walter Willet is based on epidemiological evidence, It has a snowball’s chance in Hell of being correct.
“My starting point for evidence based medicine is to look at who did the study in the first place.”
Haha, I can relate to that. I followed the male circumcision debate for almost two decades now and it was very amusing when a small collection of European doctors/scientists came with the accusation that American Pediatrics are culturally biased towards circumcision ( http://pediatrics.aappublications.org/content/early/2013/03/12/peds.2012-2896 ). Of course for many Europeans it is the other way round and they are similarly biased *against* circumcision.
Moreover, many of these doctors/scientists who accused the American pediatrics are notorious anti-circumcision activists producing bad “study” after bad study while being blind to studies that don’t fit their world views.
“Walter Willet and his team have been relentlessly pushing the high carb message for maybe forty years. They have also relentlessly attacked the HFLC movement in any and all ways. Now, amazingly, they do a study which finds that high fat diets are bad for you. If this study had been done by a group with no axe to grind, no horse in the race and suchlike, I would start with a very different perspective. You may say that is being judgemental, but when you know that someone has based their entire scientific career on promoting a thing, it comes as very little surprise that their findings always support that very thing.”
Same as with the anti-circumcision activists above. Thanks for this insight.
Yet, while this study may be questionable, if you search pubmed you can find other studies showing that a high percentage of fat in the diet has its drawbacks.
I think that for healthy people, it’s time to go back to normal: Moderate amounts of fats, unrefined carbs and proteins. I don’t believe in extremes. HFLC undoubtedly is extreme.
“When someone comes up with a controlled clinical study demonstrating that a high fat low carb diet is dangerous to health – or vice-versa – I shall pay attention to it.”
I’m afraid we will never see meaningfull controlled clinical studies in humans of this kind. They cost too much and will take too much time to see effect. Though of course that doesn’t mean the effect isn’t there. So the only thing we can do is making as much meaning of observational studies as we can.
I think in all honesty we can say that high intakes of red and processed meat (which probably happens in HFLC) are associated with increased mortality. And it doesn’t matter that much whether it’s just an association or a cause. Even if it is “merely” an association, the higher death rate in meat-eaters probably still is tied to the diet. Most probably because meat-eaters consume less plant-based food and have a lesser intake of protecting substances in plant-based food.
The ketogenic diet for example is often deficient:
” Past studies have also reported some deficiencies in trace minerals like selenium, copper, and zinc in the serum levels of patients on ketogenic diets, suggesting that appropriate supplementation of trace minerals is needed while on the diet”
Leon Roijen, you can find almost anything you want on Pubmed, it doesn’t mean it is undisputed fact, or even remotely like fact at all. Any claim the information is “peer reviewed” is bordering on meaningless as the reviews could have been by people who believed the information and had no wish to question it.
for your consideration:
Right! I spotted that too.
This deserves being picked apart.
Grassroots are evidently working against the medical dogma since LCHF works to regain health but the guys behind this “study” don’t like this idea for whatever reason. You may guess! (E.g 500 millions of diabetics off medicine is a big Pharma “killer”.)
What struck me was that the “low-carb” covered in the study ment 40 % carbs.
My thinking today is, in order to be “therapeutic”, you need to reduce carbs to less than say 10 % when you may go into mild ketosis. There was a hint about this in the text when they attacked the LCHF.
Well – don’t make life too complicated.
Just skip all the carbs you can possibly do away with and see what happens to your health. And if that move gives you a striking and immediate improvement you might be convinced that LCHF could work for you as it has for me and my wife and evidently for millions(?) of people worldwide.
AnnaM: Another “sounds like science” article based on dietary questionnaires. Rubbish bin is where it belongs. A ward-feeding study would have scientific value, but where would they find thousands of people who’d spend 25 years eating in a hospital and nowhere else?
Haha, I felt delighted reading about that study, it made my day. Of course the low carb diet is crazy and I have always suspected so but here we have proof. Almost all dietary exaggerations cause more harm than good. The poor diabetic people are made to believe it can cure their (pre)diabetes, but of course it doesn’t. As soon as these people go back to a normal carb diet, their diabetes will reappear or get worse again – maybe even worse than before because such rigorous diets can greatly alter one’s metabolism. Such a diet is like statins: maybe good for one or two particular diseases, but long-term it will cause a bunch of other problems.
“As soon as these people go back to a normal carb diet, their diabetes will reappear or get worse again”
Of course it will. That’s how they got T2 diabetes in the first place. “Normal carb” diets usually mean high carb diets. Tnanks to their effect on our HORMONES, especially insulin and leptin.
“because such rigorous diets can greatly alter one’s metabolism.”
Except that they don’t. What alters one’s metabolism is the familiar calorie counting diet, and sometimes it never recovers, even after going back to a LCHF diet.
“The poor diabetic people are made to believe it can cure their (pre)diabetes, but of course it doesn’t.”
Except that it does. T2 diabetes is a DIETARY disease (too much sugar, starches, and refined foods), and only a change in diet can prevent or reverse it. LCHF plus a little intermittent fasting.
You can read about it here:
The Diabetes Code: Prevent and Reverse Type 2 Diabetes Naturally, by Dr. Jason Fung
“Of course it will. That’s how they got T2 diabetes in the first place. “Normal carb” diets usually mean high carb diets. Tnanks to their effect on our HORMONES, especially insulin and leptin.”
A diet high in sugar, like ice-creams, sugary drinks, sweets and so on is not a normal carb diet.
A diet that delivers a reasonable amount of (unrefined) carbohydrates doesn’t cause diabetes. I never saw any proof for your assertion.
That’s the problem with hypes: before it was the fat, now it’s the carbohydrates.
“Except that they don’t. What alters one’s metabolism is the familiar calorie counting diet, and sometimes it never recovers”
Well, I have seen the same with the low carb high fat diet. A guy on a forum who started low carb high fat and now has very serious hypoglycemia after returning to his former diet, even months later. Of course it’s anecdotal but plausible.
“Except that it does. T2 diabetes is a DIETARY disease (too much sugar, starches, and refined foods), and only a change in diet can prevent or reverse it. LCHF plus a little intermittent fasting.”
Nope. Wrong. It’s true that beginning type 2 diabetes can sometimes/often be reversed by more exercise and improving diet, but no low carb high fat diet is needed for this effect. It’s the refined sugars that are the biggest problem and a very high carbohydrate content in general. But there really is no need to go “low carb”.
Low carb high fat is a big experiment and everybody using this diet basically is a laboratory rabbit.
High carb low fat was also a dietary experiment.
“A diet high in sugar, like ice-creams, sugary drinks, sweets and so on is not a normal carb diet.
A diet that delivers a reasonable amount of (unrefined) carbohydrates doesn’t cause diabetes. I never saw any proof for your assertion.
That’s the problem with hypes: before it was the fat, now it’s the carbohydrates.”
A diet that contains a lot of sugar, starches, and refined foods and drinks, is all it takes to cause hyperinsulinemia and insulin resistance, which inevitably leads to obesity and T2 diabetes (not necessarily in that order). Fat can’t do that, because it has virtually no effect on insulin or insulin resistance. The low-fat diet was never scientific, it was purely POLITICAL.
“Well, I have seen the same with the low carb high fat diet. A guy on a forum who started low carb high fat and now has very serious hypoglycemia after returning to his former diet, even months later. Of course it’s anecdotal but plausible.”
“now has very serious hypoglycemia after returning to his former diet”? Then you’re basically admitting that LCHF is the way to go! One can only imagine what his former diet was.
On the other hand, you really shouldn’t take your medical advice from a “guy on a forum,” not even this one. You should read Dr. Fung’s book. It will not only change your opinion, it will change your life.
“Nope. Wrong. It’s true that beginning type 2 diabetes can sometimes/often be reversed by more exercise and improving diet, but no low carb high fat diet is needed for this effect. It’s the refined sugars that are the biggest problem and a very high carbohydrate content in general. But there really is no need to go ‘low carb’.”
Dr. Fung reverses T2 diabetes for a living. So do a growing number of doctors, like Dr. Sarah Hallberg, for example. You should watch this video:
Reversing Type 2 diabetes starts with ignoring the guidelines, with Dr. Sarah Hallberg
I hope you will watch it. And exercise is NOT required. Just a change in DIET.
“Low carb high fat is a big experiment and everybody using this diet basically is a laboratory rabbit.”
But it wasn’t based on SCIENCE. It was based on POLITICS. The science has always supported a LCHF diet, going all the way back to William Banting, and his “Letter on Corpulence,” in 1863.
I do hope, however, that you will put your biases aside long enough to read Dr. Fung’s book and watch Dr. Hallberg’s video. You’ll learn exactly what has taken place, and why we now find ourselves engulfed by obesity and T2 diabetes epidemics. It might even save your life.
Leon Roijen, unfortunately it wasn’t a study, it was a meta-study, or so it appears. I wouldn’t be surprised if the benefits were quoted as relative and not absolute.
“High carb low fat was also a dietary experiment.”
Exactly and we now know the disaster it caused. Aren’t we to learn from the past?
“A diet that contains a lot of sugar, starches, and refined foods and drinks, is all it takes to cause hyperinsulinemia and insulin resistance, which inevitably leads to obesity and T2 diabetes (not necessarily in that order). Fat can’t do that, because it has virtually no effect on insulin or insulin resistance.”
If you had read my comment well, you would have seen that I never denied this. My statement was that I haven’t seen proof that a normal, moderate carb diet with unrefined carbs is The Big Cause of Diabetes. That’s all I said.
“now has very serious hypoglycemia after returning to his former diet”? Then you’re basically admitting that LCHF is the way to go! One can only imagine what his former diet was.”
I don’t know his exact diet before low carb but I do know that he didn’t suffer from hypoglycemia with his usual diet before he tried low carb. Only when he went back from low carb to his usualu diet he developped hypoglycemia. That certainly doesn’t make the case for low carb: it shows going low carb and then going back to your previous diet can seriously derail your metabolism. Also he wasn’t the only one, in forums I saw a few more people with that or similar problems.
“On the other hand, you really shouldn’t take your medical advice from a “guy on a forum,” not even this one. You should read Dr. Fung’s book. It will not only change your opinion, it will change your life.”
Excuse me, but please learn to read: I didn’t say I took medical advice from this “guy on a forum”, I just told you about his experience with low carb high fat.
And about books….because something is written in books, it doesn’t mean it is true either 🙂
“But it wasn’t based on SCIENCE. It was based on POLITICS. The science has always supported a LCHF diet, going all the way back to William Banting, and his “Letter on Corpulence,” in 1863.”
I think science much more supports a varied diet than either extremes, be it low carb/high fat or high carb/low fat.
“You’ll learn exactly what has taken place, and why we now find ourselves engulfed by obesity and T2 diabetes epidemics.”
I am already well aware of it. As I started saying, I never denied the problem with refined carbs.
To: Leon Roijen:
“a normal, moderate carb diet with unrefined carbs”
Please define what normal and moderate mean to you, because it means different things to different people. For example, I drink a moderate amount of alcohol. But the Russians would probably consider me a teetotaler. 🙂
Also, because HORMONES (insulin, leptin, ghrelin, etc.) control our appetites (no matter how much will power we have), eating too many starchy carbs can easily lead a person to downing two double chocolate cakes per week, washed down by a case or two of beer. Sugar *addiction (is real, Leon. Both psychologically, and physiologically.
“Only when he went back from low carb to his usualu diet he developped hypoglycemia.”
Hypoglycemia can have lots of causes. Medications, too much alcohol, liver disease, excess insulin production, hormone deficiencies, just to name a few. I’d wager that your friend had/has T2 diabetes.
“I didn’t say I took medical advice from this “guy on a forum”, I just told you about his experience with low carb high fat.”
With all due respect, you’re using his experience to support your claim, when you don’t even know what caused the hypoglycemia, what his previous diet was, etc. Why would you do that?
“And about books….because something is written in books, it doesn’t mean it is true either”
What would you say has more credibility. widely respected M.D.s who actually treat obesity and diabetes, or a guy in a forum?
“I think science much more supports a varied diet than either extremes, be it low carb/high fat or high carb/low fat.”
A “varied diet” means nothing. A LCHF diet consists of all the macronutrients, fat, carbs, and protein. Ditto for HCLF diets. It’s HOW MUCH of each macronutrient that matters.
The reason we currently have obesity and T2 diabetes epidemics is because the actual science was over-ruled by BigGov, BigPharma, and BigFood. The Standard American Diet has never been backed by science. Due to an irrational fear of cholesterol and fat, and our farmers wanting to sell more CHEAP food, we are currently in deep doo-doo, healthwise. It re-elects more politicians, sells more drugs, and keeps the farmers happy. Unfortunately, it makes the rest of us sick.
“I am already well aware of it. As I started saying, I never denied the problem with refined carbs.”
Apparently not, given your comments in this thread.
But since I have a hard time beating dead horses, I’ll just end here by wishing you well.
“Please define what normal and moderate mean to you”
Let’s say around 150 grams carbs daily, depending on one’s amount of exercise.
“Sugar *addiction is real, Leon. Both psychologically, and physiologically.”
I have no doubt about that, Joe.
“Hypoglycemia can have lots of causes. Medications, too much alcohol, liver disease, excess insulin production, hormone deficiencies, just to name a few.”
Sure, ok, might be a coincidence but this guy tried the low carb high fat diet for a few months, then went back to the diet he had before and *then* developped hypoglycemia. Sounds to me like his metabolism was disturbed. And as I said, I heard of several other persons with similar problems.
“A “varied diet” means nothing. A LCHF diet consists of all the macronutrients, fat, carbs, and protein. Ditto for HCLF diets. It’s HOW MUCH of each macronutrient that matters.”
I think I made myself clear already: Neither the LCHF nor the HCLF diets I consider healthy.
Moreover a LCHF diet often lacks important micronutrients.
“”I am already well aware of it. As I started saying, I never denied the problem with refined carbs.””
“Apparently not, given your comments in this thread.”
Well, I think we can agree on a lot of things. High carb diets and too much refined carbs are bad. I agree. I just don’t follow the low carb hype (under 100 grams).
Neither do I, primarily due to a lack of willpower and a liking for beer.
I like Instapundit’s terse description of the news: ” It’s an observational study based on self-reporting, though, which means it’s probably junk.”
Also, this article has a few interesting comments about the study:
David Bailey – “animal model of CVD”
I didn’t expect pigs – I was expecting guinea pigs, perhaps because I recalled Dr Kendrick’s post
on vitamin C:
In this post, Dr Kendrick recalls how GC Willis initiated plaque formation in guinea pigs by removing vitamin C from their diet.
I’ve quickly read the link Dr Kendrick provided about the pigs and note to initiate mural thrombi involved “traumatising the intimal surface directly”.
How did they do that?
And, re-assuringly, calcification within 10 days.
Not sure if comparing pigs with humans is a like for like comparison, but also I recall an episode of River Monsters in which Jeremy Wade mentioned that cannibals compared human flesh to pork in taste and thus Jeremy Wade used a leg of pork to demonstrate how stingrays attacked.
Ouch! Even longer than the last blog 😁
More on mummies…
Adding to the thread on mummies and CVD/atherosclerosis in the past, here’s a bit more on mummies from Dr Mike Eades’ website:
This is a review of a book called Napoleon’s Glands by Arno Karlen and a chapter called “mummy powder, mummy blood”, about autopsies on Egyptian mummies.
Dr Mike Eades writes in his review that “in reading through the roll call of these disorders, the following sentence leapt out at me:
“blood-vessel disease was common, contrary to assumptions that it rises from urban stress and a modern high fat diet”
and this sent Dr Eades on quite a quest…hence the title of his post.
And here’s another focusing on the Egyptians diet and health:
You ask if you “get bruises etc does that damage the blood vessel walls?”
I note from a few other comments you’ve posted in this instalment by Dr Kendrick that you are new, so welcome.
It probably means that you may have missed a link I posted in a previous instalment. It’s a talk by cardiologist Dr Langsjoen. It’s a brief 15 min presentation on arteries which he gave in June 2018 and here’s the link:
It’s worthwhile checking out the whole talk during which he discusses arterial trauma. From approx 5.25 to 7.17 he provides 2 examples which may answer your question but the examples are extreme and unusual as he makes clear.
Thanks for posting, watched it twice! I liked his answer re Stents and Bypass as well as Statins. Once again, prevention by observing cultures ( historically mainly now) that live long and healthy lives, it’s not rocket science! It is what you DON”T put into your mouth more than what you do. After living in France during Uni and on and off even now, I learned not to snack as well!
Thank you so much for directing me to that video, it’s a real eye opener, I’m learning so much now. I think that video should be on one of those ‘informative’ loop CCTV TV health promotions they have in GP and clinic waiting rooms. I think I’ll suggest it to our local CCG!! Let you know their reply….
Thank you for the link, watched the whole video, excellent. Written to local CCG suggesting they play it on the cctv screen in local GP & hospital clinic waiting rooms. Also commented on my 4 week experience of statins & side effects with some suggestions about informed consent when statins are being newly prescribed, why they are bring prescribed, what to expect & that the CCG should be auditing their effectiveness, cost and medicel. Like the audit committee used to try to do with paeds diabetes before it was an official requirement for continued funding.
Nitric Oxide (NO) production – beets, beet kvass and beetroot
I was getting a bit confused if what we call beetroot here in UK was also beets. The answer is yes.
Yesterday, by strange coincidence, BBC radio had a report on research being done on beetroot and NO production. Here’s the link:
Charles Gale: Yes, in the U.S. we call them beets; perhaps our mania for efficiency turns a two-syllable word into a one-. Thanks for the clip. They seem to imply that taking it in the form of juice makes the good stuff more bioavailable. I put my potassium supplement (700-800 mg K) into my beet kvass, which has plenty of salt, so I’m getting three supplements in one.
One can also eat beet stems. Similar in taste to chard and very good for you
I didn’t expect to find so much rubbish in a single article
Cholesterol found in plaque is crystalline in nature. This is what’s left as a result of the breakdown of red corpuscle cell walls as found in the blood clot resulting from endothelial damage. (Do I have that right?)
There is also cholesterol as found in LDL – not crystalline. But there is no more of this LDL than would be found in the subject’s whole blood or blood clot. (Do I have that right?)
You have cited anti-platelets as beneficial. I presume that is because the bulk of clotting is minimized at sites of endothelial damage, minimizing the job macrophages need to do. (Do I have that right?)
There must be an optimum degree of clotting, because too little would not provide a good base for subsequent endothelialization. Or… is the clot actually not necessary for progenitor cells to lay down new endothelium? Surely hemophiliacs experience endothelial damage like the rest of us. Is it that they simply don’t have the burden of clearing out the clot garbage?
(Do I have that right?)
if cigarette smoking and pollution damage the endothelium, why is this damage mostly to the coronary and carotid arteries? Why no infarction of the spleen, pancreas or gallbladder?
You can get infarction in other organs and in the guts and the pancreas etc. The coronary and carotid arteries are where the arteries are exposed to the greatest biomechanical stress.
I suppose that didn’t quite answer Gilles’ point – are you saying perhaps the damage from smoking ‘needs’ biomechanical stress in order to end up causing plaques? E.g. that smoking causes tiny areas of damage, that then spread in areas of biochemical stress? I mean one of your key points is that plaques only normally form in the arteries feeding the heart and the brain, and yet when a vein is used to bypass an artery, it does get plaques!.
No and NOS Good article and questions L-Arganine and Citrulline but lists NO NOS enhancement strategies. Your comment would be welcome Dr K:
Strategies to restore or enhance NO
‘There are finite ways to safely and effectively enhance or restore NO availability in the human body. These are highlighted in Figure 1. Part of these strategies target NOS enzymes as a means to enhance NO production and other strategies provide NO as an exogenous NOS-independent source of NO. Since most chronic diseases are characterized, or at least associated with dysfunctional NOS, NOS-dependent strategies utilizing L-arginine and/or L-citrulline have proven largely ineffective [3,4]. This article will focus primarily on NOS-independent strategies.” Next follows a chart. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5137939/
@SW That’s an old article: Citrulline is very promising: http://www.mdpi.com/2072-6643/10/7/921
I think it is still too early to know how effective citrulline really is, but I do know that it can lower blood pressure (studies show so and I experienced it myself) and relieve erection problems in men (NO +).
How much did you take and where did you get. How much did it lower your bp by. Thanks
Thanks for the article on l Citrulline. I take l arginine , sine it was in the pill Dr K put together some years ago, Prokardia?, but I now see why L Citrulline is a better choice. If it lowers you BP, and has those other effects, what’s not to like? What dosage do you take?
Hello Mr chris,
I take 750 mg of citrulline (not citrulline malate) 3 times a day. (total=2250) I am still not sure if it is better to take it away from food (amino acid competition) or if it can be taken with food.
I didn’t yet experiment with it to see if taking it with or without food influences blood pressure.
What’s not to like? Well, there are no long term safety studies and theoretically citrulline that is turned into arginine could stimulate dormant herpes viruses. So if you have a herpes outbreak it would be wise to at least temporarily stop the citrulline. Also from research we know that some cancers can be starved by witholding arginine from the body – so theoretically again, putting a rather great amount of arginine in the body could stimulate the growth of these cancers.
Personally I think/hope these risks are only theoretical but one can never be sure. But if you look at -for example- the risks of blood lowering medications, they are less theoretical, proven and very real. So as long as citrulline lowers my blood pressure enough, I prefer it to medication.
I take 750 mg, 3 times a day. My blood pressure was often around 150/10 in the evening and now it usually is arounf 130/90. I can’t remember very well but I think the effect kicked in after a week or so.
The funniest thing is that at the doctor’s office (white coat effect) it always used to be 180, while now with the citrulline it is around 150 when my family physician measures my blood pressure.
I don’t know if it is allowed to mention brands here. I use the citrulline from Now Foods.
Before citrulline I tried Q10 and magnesium but these substances did not lower my blood pressure. Maybe/probably also citrulline won’t work for everybody, but I think the evidence for citrulline is better than for Q10 and magnesium.
Useful analysis of Citrulline may be found here: https://examine.com/supplements/citrulline/ I find this website very helpful for analysis of all supplements. I don’t have any kind of affiliation to it, just have found it exceptionally helpful when trying to find scientific research on the use of supplements.
It is odd how many really great scientists there were 100 years ago. Some made great strides in cancer research too, and appear to have been right. I think Warburg is being rehabilitated now.
The moderns are lost in a morass of details that are off the mark.
On the other hand, Lyell and Darwin had their reasons, emotionally, for preferring a uniformitarian view of planetary history and yet I’ve got quotes that show they were well aware that the geological record shows catastrophism.
One reason they didn’t like catastrophism is that it sort of puts up a barrier in the game of incrementally figuring out deep history. If no great changes have happened, it makes the planet more transparent to analysis. But if there were extinction level events that altered things greatly, it seems there was less for them to do and less ability to analyse it.
I have today a bias towards digging deep into reading philosophy and as retired I have now got the “free” time necessary.
Just now I have been caught by a great book by Zygmunt Bauman; “Postmodern Ethics”. With interest I here read what he has to say about how the idea about “risk” is a great way to increase the profits for Big Pharma. To create fear is an extremely good marketing strategy and here “risk calculation” is the marvelous tool to go ahead.
Cholesterol mongering would be a prime example of this successful business strategy.
I guess “good philosophy” is to explain “the obvious”.
More on animal models for CVD…
…pigs and guinea pigs have been covered and I remembered Dr Matthias Rath’s 2018 Cyprus presentation in which they also did this. I’ve posted the link before but here it is:
At 31.20 he presents a slide called “an animal model simulating human arteriosclerotic metabolism”. To help prove his and Pauling’s vitamin C hypothesis they couldn’t do it in humans so they had to use animals. Rath states they:
“created an animal that mimicked the metabolism of humans…we knocked out the abilities of these animals to produce vitamin C…what will happen to their arteries? Will they develop the cracks and lesions…”.
He doesn’t state what animals were used but the picture on the slide is a rat.
Animal model for CVD is covered from 31.20 to 36.22.
Thank you for this wonderful blog. I always look forward to reading the next instalment. Thank you from the bottom of my heart.
There must be an optimum degree of clotting, because too little would not provide a good base for subsequent endothelialization.
Or… is the clot actually not necessary for progenitor cells to lay down new endothelium?
Surely hemophiliacs experience endothelial damage like the rest of us.
Is it that they simply don’t have the burden of clearing out the clot garbage?
great post. Thank you for continuing to ask vital questions and seek truth.
When I think of “scientist”, I think of men like you. Your kind seems few and far between these days 😦
Science is in a sad state, but even so, it doesn’t change the truth.. There is sits, waiting to be revealed. I think this series is getting us closer to understanding the cause and progression of CVD than perhaps we’ve ever been.
Well I’m not sure that this may be your best post yet.
Pity it’s all rubbish though. Look
“While the Machiavellian machinations of this controversy lie beyond the scope of this article, we would encourage those who remain unconvinced of Keys’ pioneering contribution to human nutrition science to read a White paper on Keys and the Seven Countries Study, commissioned by the True Health Initiative (Pett et al. 2017). This paper examines the primary source material and provides explanations for many of the common methodological criticisms aimed at the Seven Countries Study. It vindicates a man who has done so much to establish the dietary guideline on SFA and in doing so, prevent an immeasurable number of premature deaths from CHD.”
Taken from here
it must be true cos they have “science” in their title.
OK the sarcasm switch is off now. I threw up a little in my mouth reading that and had to rush to the toilet when I saw it came from the True Health Initiative, home of militant vegans like David Katz and Michael Greger. They are just about the only group still pushing the Diet Heart Hypothesis and the Cholesterol Hypothesis as if all the work before and since Keys didn’t exist – such as the likes of what you have been writing about. Not to mention all those rogue doctors like Aseem Malhotra and David Unwin and Gary Fettke inappropriately reversing diabetes, and all those probably now hundreds of researchers actually doing Science, not to mention the now millions of people improving their own health (look at the size of Rita Venter’s “Banting” group in South Africa and an even larger one in Nigeria).
Then there’s the “low carb will kill you” study listed above. The fightback continues and it currently looks like the dogma is winning. I wonder how long before your new book is burned.
There is a lot at stake if mainstream loses its grip on the food chain! Same with Pharma and AG chemical companies…..
Wow, this lady does a bang up job of deconstructing that WHO report which said processed meat causes cancer and red meat probably does. Very shoddy and dishonest. To me, this is another confirmation of my impression that there is a big agenda by (?) to promote vegetarianism and veganism world wide.
I can feel relaxed on my LCHF animal based diet!
Ana, how did you upload You Tube Video? I can only get the link to work, thanks so much!
SW, I think you have to use the full URL i.e. https://www.youtube.com/… that you get at the top of the YouTube page. You probably did “right click > Copy video URL” on the video and got the short version https://youtu.be/…
The short version works just as well. I “Right click > Open link in new tab” to play it.
She starts with saying that she was able to reverse every health problem she ever had by switching to a meat-based, ketogenic diet – like such a diet would be a cure-all.
Well, sorry, but such a silly remark immediately disqualifies her talk.
Mark’s Daily Apple had a good dismemberment of the latest Willet garbage, excuse me, “study,” in the Lancet in today’s post.
GreenMedInfo has an interesting post today on a paper which shows that vitamin C prevents the degradation of the sex hormones (in vitro).
I have followed Dr Eades for years, you may also want to have a look at a Sydney Doc who puts fiber in perspective as well, DR Mason https://youtu.be/xqUO4P9ADI0
( I am not sure how to upload you tube, I hope this works) S
Thank you for your such a great blog and great post!
Now, deep down in the “Postmodern Ethics” by Zygmunt Bauman, in this early morning (the best time or deep thoughts), i realize the sad but evident fact that moral is defined by the “victorious” (Read BigPharma) and not by the “Losers” who are the victims, e.g. for their statins.
“We (Big Pharma) are saving the lives of millions of people!.”
“We (Big Food) are saving millions of lives by the “heart healthy” vegetable oils and margarine. That is why we put a heart health symbol on our products!”
You want to cry with me?
I’m glad Malcolm that you have ended this long discussion mostly about diet and CVD. Frankly I find it a distraction.
Now getting back to what this Post is about :
1 ) what causes CVD ? and
2 ) If one has CVD what are the most effective ways of healing ourselves ?
We KNOW :
1) Cholesterol does not cause CVD
2) Saturated fats do not cause CVD.
3 ) CVD is basically a bio-mechanical problem in the arteries : The coronary arteries and especially the glycocalyx of the arteries are damaged either by the actual pressure of blood being pumped or by toxins in the blood
4) Smoking because of the toxins in the smoke causes CVD;
5) Stress causes CVD.
6 ) The body has a capacity to heal this damage in the coronary arteries
7 ) Vitamin C is needed for this healing process to happen
8) In the absence of Vitamin C the body instead attempts to heal the damage with ‘scab’ like plaques.
9 ) Plaques however bulge into the artery reducing blood flow and/or increasing the pressure the heart needs to pump.
10) Uncalified plaques are more liable to rupture and cause a heart atatck.
11) Plaque stabised by the process of calcification are less liable to rupture and lead to heart attacks..
12) Calcified plaques still partially block the artery.
13 )The development of collateral arteries is the body’s way of handling this problem.
14) Vitamin C is needed for the growth of collateral arteries..The more the better but not so much as to cause loose bowels !
15 : Chondroitin sulfate ( as discovered by Dr Lester Morrison in the 1960-70’s) is very helpful in rebuilding the glycolcalix of damaged coronary arteries.
No I can progress on to the Diabetes post & discussion which you have just started.
Malcolm once replied when Inwearily asked why every discussion about CVD dégénéra tend into diet issues, ” one of Ancel Keys achèvements was to make people think CVD and diet are related.
This is á paraphrase, but probably accurate.
“14) Vitamin C is needed for the growth of collateral arteries..The more the better but not so much as to cause loose bowels !”
The more the better is not true. I have seen some research showing problems with higher doses. 400 mg divided over the day is enough.
You could add citrulline and taurine as agents that are promising in CVD.
The researh “you have seen” does not agree with the research of Pauling, Klenner, Humphries, Stone, Szent-Gyorgyi, Cathcart, to name but six. What was your “research” that carries such authority? I think we should be told.
That’s true. 400 mg a day seems to be too low according to what I read and also my personal experience.
“Linus Pauling Institute Recommendation
Based on the combined evidence from metabolic, pharmacokinetic, and observational studies and from randomized controlled trials, it has been argued that sufficient scientific evidence exists to support an optimum, daily vitamin C intake of at least 200 mg/day, which is substantially higher than the current RDA (11). Studies conducted at the National Institutes of Health showed that plasma and circulating cells in healthy, young subjects attained near-maximal concentrations of vitamin C at a dose of 400 mg/day (11). Because of the very high benefit-to-risk ratio of vitamin C supplementation, and to ensure tissue and body saturation of vitamin C in almost all healthy people, the Linus Pauling Institute recommends a vitamin C intake of at least 400 mg daily for adult men and women.”
I have delved into this a long time ago, there are several problems with too much vitamin C. I don’t recall all I saw in studies, but one is the debate whether vitamin C can also be a pro-oxidant in the body. I think that’s quite possible. And if it is just an anti-oxidant and protects the cells of your body, it could also protect cancers cells.
Also see this article:
Fat In Stomach Can Turn Vitamin C Into A Cancer Trigger
More vitamin C could also mean a higher iron uptake which also isn’t necessarily a good thing.
And I’m sure more issues can be found. I wouldn’t overdo it. Certainly not long-term.
Leon: I don’t know enough about Vitamin C to say either way but maybe others who read Linus Pauling’s work could comment.
The Linius Pauling Institute seems to have a view significantly different from the view of Linus Pauling.
“Although Pauling’s megavitamin claims lacked the evidence needed for acceptance by the scientific community, they have been accepted by large numbers of people who lack the scientific expertise to evaluate them. Thanks largely to Pauling’s prestige, annual vitamin C sales in the United States have been in the hundreds of millions of dollars for many years. Pauling also played a role in the health food industry’s successful campaign to weaken FDA consumer protections laws. ”
Quackwatch is the worst source. I will take Pauling’s word over theirs.
The name quack watch says it all, don’t play the argument play the man. I have seen Dr Kendrick on one of that type of site.
By the way I spent some time on the Linus Pauling site this morning, but didn’t find Leon’s citation, I was probably looking in the wrong place.
Sasha: Me, too.
“By the way I spent some time on the Linus Pauling site this morning, but didn’t find Leon’s citation, I was probably looking in the wrong place.”
It’s almost at the end of the page: https://lpi.oregonstate.edu/mic/vitamins/vitamin-C
About Linus Pauling also see: https://sciencebasedmedicine.org/high-dose-vitamin-c-and-cancer-has-linus-pauling-been-vindicated/
Thanks for that, I checked it out, there is the mention of 400 Mg for the over 50s. As regards the other article I am in two minds often in medical research you find what you want to find.
This is the problem with non BP cures, who do you believe , overhyped articles or mainstream? For the record I am Goldilocks carbs and meat.
On another topic, I think it was you who posted some Time ago á link to the Dutch health service concerning blood pressure norms for the over 70s?
As for Heinz spaghetti sauce, well one mans meat is another mans poison.
Hi Bill in Oz
Excellent – well laid out 15 bullet points – clear, concise and understandable and easy on the eye to read.
Glycocalyx hasn’t appeared on my radar yet and Stephanie Seneff’s thoughts on chondroitin sulfate have been hard to understand but from your comments I think I need to do some further research.
P.S. Bill in Oz
Having posted my comment on your excellent summary, I turned my attention to part 53 on diabetes and there is glycocalyx being brought into the discussion on CVD.
Your hypothesis on the start of atherosclerosis makes more sense (w.r.t the observations) than any other hypothesis I have ever read. However, once the clot has formed and macrophages have started the work on the repair of the clot, can high serum levels of oxidized-LDL be problematic? (People claim that oxidized LDL particles are not recognized by the LDL receptors but they are recognized by macrophages, so they tend to accumulate in the macrophages and foam cells in plaques.) As a person with heart disease and very high levels of oxidized LDL, any answer to this question would be very helpful to me.
Two interesting side- lights here –
1) HDL can go through endotheilal cells, it’s a smaller particle than LDL and transits them to do it job of collecting cholesterol from macrophages.
2) fibrin synthesis in liver is stimulated by the products of polyunsaturated fatty acid peroxidation with the following etiology – this concise explanation is from a Hep C paper but you will see the same thing in NAFLD and T2D when these precede athero, also in alcoholic liver disease.
There is still a lot that we do not know about hepatic steatosis and hepatitis C. These studies have suggested that the presence of fat in patients with hepatitis C is associated with markers of progressive liver disease in that fat was associated with increased stellate cell activation, but the mechanism by which this takes place is uncertain. It is possible that this occurs secondary to saturation of beta oxidation pathways within mitochondria which then leads to free fatty acids becoming more available to intracellular microsomes where they undergo lipid peroxidation. There are three main products of microsomal lipid peroxidation: malondialdehyde, 4-hydroxynonenal, and hydrogen peroxide. Malondialdehyde has been shown to activate stellate cells to produce fibrin, and may be responsible at least in part for liver fibrosis in patients with non-alcoholic steatohepatitis.
Very nice article! Thank you for sharing!