What causes heart disease – part III

In most diseases it is best to start at the beginning and work forwards. This should be the case with cardiovascular disease (CVD) too. However, for complex reasons I found myself starting at the end, and working backwards. The main reason for this is that I had to start with certainty. Yet, almost everywhere I looked there was mush. For example, the epidemiology of CVD.

Now you would think that there would be agreement about how many people actually die from CVD in different countries and at different times. Not a bit of it.

A researcher:                                    ‘The French have a low rate of CVD.’

A N Other researcher:            ‘Oh well the French, they don’t agree with the normal definitions, they don’t classify CVD properly. Who knows what the true rate may be?’

True? False? A bit true? Taking another example. I have looked at the figures from the US and, you know what. Not a single person died of Ischaemic Heart Disease before 1948. Amazing. What was protecting them? [Dying from IHD is what you would also call a heart attack, or MI]. What was protecting them was the fact that IHD did not exist in the US as a disease classification, before 1948.

This then changed. In 1948 the World Health Organisation was created, and one of the first things they did was to create an International Disease Classification system (ICD). Heart disease is 1. Cancer is 2. (example for illustrative purposes only). Of course it is a bit more complex than that. Just to look in more detail at Ischaemic Heart Disease: [See box]:


Not every country took up the ICD system. Until 1968 the French did not use the ICD codes (so I am told, which no doubt means this is not true). Therefore, in France, statistics on deaths from IHD in France, before this date, are completely unreliable.

It goes without saying that, before 1948, no-one else used the ICD system either, because it did not exist. So, what can we tell about the epidemiology of CVD before 1948? Nothing. Or at least nothing you could hang your hat on. IHD would have been mixed within a much broader ‘Heart Disease’ in the death certificate statistics. And heart disease could mean almost anything, from cardiomyopathy to pericarditis, to atrial fibrillation.

Even after the ICD system was introduced, and even after France came on board, many countries clearly did not use it in the same way. Which is why the WHO set up the MONICA study.

‘The MONICA (Multinational MONItoring of trends and determinants in CArdiovascular disease) Project was established in the early 1980s in many Centres around the world to monitor trends in cardiovascular diseases, and to relate these to risk factor changes in the population over a ten year period. It was set up to explain the diverse trends in cardiovascular disease mortality which were observed from the 1970s onwards. There were total of 32 MONICA Collaborating Centres in 21 countries. The total population age 25-64 years monitored was ten million men and women. The ten year data collection was completed in the late 1990s, and the main results were published in the following years. The data are still being used for analysis.’

It was also an attempt to see if different countries were actually looking at the same diseases, and classifying them in the same way. Even after that, the data was still not absolutely clear cut, as further studies were then set up to see if the US system ARIC, and MONICA, actually matched each other. This was 1984.

‘To foster collaboration between the World Health Organization MONICA Project and the NHLBI Study of Atherosclerosis Risk in Communities (ARIC). To ensure that valid comparisons could made between findings in MONICA and ARIC by supporting activities to standardize coding, classification, and analysis of coronary and stroke events, risk factors, and medical care according to MONICA protocol.’

In simple terms, the US has its system, ARIC, and Europe had its system MONICA. Do they actually match? In short we can see that, even as late as 1984, there was clear uncertainty about how diagnoses were being made and how data were being gathered around the world. Did it all match, or not.

Given such uncertainly on both definition and diagnosis, can we say that the US epidemic of CVD in the 1960s actually happened. Or were doctors just putting IHD on death certificates when they didn’t really know what killed the patient. Personally, I think the epidemic did occur. Actually I think it happened a bit earlier. It is my belief that it took a while for US doctors to start using the new-fangled WHO ICD system.

Anyway, the point I am trying to make is that it is incredibly difficult to find the ‘bedrock.’ By which I mean facts that are inarguable. Things you can base your thinking on that are absolutely true, or that are as close to absolutely true, as possible.

Which is why I ended up at the end, the formation of the final, often fatal, blood clot. A blood clot which, generally, forms over an existing atherosclerotic plaque. There is widespread agreement that this is the case. So we can, I think safely, start here.

[There are, undoubtedly other things going on, such as sympathetic stress, mitochondrial damage and acidosis with heart muscle. that play a hugely important role. But the clot is, usually the final event

It is also widely agreed that factors which increase blood clot formation (thrombophilc factors) increase the risk of dying from CVD, and that things that reduce blood clotting reduce the rate of death from CVD. Here are a few things that increase the risk of blood clots forming, in no particular order:

  • Dehydration
  • Waking up in the morning/getting up in the morning
  • Acute physical stress
  • Acute psychological stress
  • Having a high fibrinogen level
  • Diabetes
  • Cocaine use
  • Smoking
  • Cushing’s disease

Here are some of the things that reduce the risk of blood clots

  • Haemophilia
  • Von Willibrand Disease
  • Aspirin
  • Moderate alcohol consumption
  • Clopidogrel
  • Yoga
  • Regular exercise

I suppose I should add that all of the things that increase the risk of blood clotting also increase the risk of death from CVD, and vice versa.

This is hardly a complete surprise. If blood clots kill you, things that reduce blood clots will prevent you from dying, and vice-versa. Let us not fall to the ground in stunned amazement over this statement of the bleeding obvious.

At this point, and slightly out of sequence, I would like to introduce statins to the list of factors that reduce the risk of blood clots

Readers of this blog know that I am not keen on statins, to say the least. However, if the studies are to be believed, they do reduce the risk of CVD. Not to any great extent, but the effect certainly does exist. Many people use this fact to attack my view that raised cholesterol does not cause CVD. ‘Well, what about statins,’ they bellow in delight. ‘They lower cholesterol and reduce the risk of CVD. Case proven…next’

Well, as with all drugs, statins do many other things than lower cholesterol levels. For example:

‘Recent studies have shown that statins reduce thrombosis via multiple pathways, including inhibiting platelet activation and reducing the pathologic expression of the procoagulant protein tissue factor.’1

So, as they say, there. In fact, one could quite sensibly propose that statins work pretty much the same as aspirin. They are anti-coagulants, and lowering blood cholesterol is simply a nasty and unfortunate side-effect of statins.

In reality, statins have a far more important effect on CVD (through other actions also related to clot formation) that I will get to later. I just thought I would pop that statin fact in. I even provided a reference. I have not really done much referencing in this series up to now. I believe that it is very simple to type, for example, ‘regular exercise and reduced thrombus formation’ into Google and see what you get. Or ‘Yoga and reduced blood coagulation.’

Where was I? Oh yes. Things that increase blood clot formation are more likely to kill you from CVD, and vice versa. Nothing controversial here. But the potentially controversial bit starts right here.

Are there two processes or one?

Currently, whilst conventional thinking on CVD accepts that blood clot formation is almost always the final event in CVD. This represents a completely separate process to the development of the atherosclerotic plaque itself. In short, we have two unrelated physiological processes:

  • Plaque formation
  • Clot formation on top of plaque

I apologize for saying, essentially, the same thing in different ways. But I think it is important.

Strange then, is it not, that plaque formation and clot formation share so many risk factors? Smoking, for example. Diabetes, for example. In fact, you could say (with certain provisos) that the risk factors for plaque formation and blood clot formation, are exactly the same.

Which gives one to think. Well it certainly gave me to think. Could it be that plaque formation, and blood clot formation, are simply two different manifestations of exactly the same underlying disease process. From a pure scientific perspective, I liked the idea. I liked it because it seems clumsy to have a disease, CVD, that is made up of two, essentially unelated processes

In medicine, as in all of science, one single disease process always looks much better, much cleaner, and much more likely to be right. This is the principle of Occam’s razor:

‘The principle in philosophy and science that assumptions introduced to explain a thing must not be multiplied beyond necessity, and hence the simplest of several hypotheses is always the best in accounting for unexplained facts.

Next: The four step process of CVD

1: http://www.ncbi.nlm.nih.gov/pubmed/24422578

188 thoughts on “What causes heart disease – part III

  1. Dr. Göran Sjöberg

    Malcolm, what a great blog you now have got in my eyes!

    “Here are some of the things that reduce the risk of blood clots
    Von Willibrand Disease
    Moderate alcohol consumption
    Regular exercise ”

    I though missed garlic on your list here and as a part of my own CVD treatment and to my surprise also was favourably approved by my first cardiologist while “my last one” dismissed it as just being a part of all other nonsense I was advocating 🙂

    Funny but utterly dangerous guys those cardiologists!

    1. Christopher Palmer

      There exist grounds to wonder about modern agricultural soils and the decline of ionic strength therein. From that basis originates scope to argue that modern foods farmed on intensely farmed soils may not supply the diet with sulphur to the extent they once did.

      Sulphur is one of the elements considered essential for the healthy biochemistry of a healthy human and yet it doesn’t feature in the list of things commonly considered for candidature of deficiency. Our bodies do not use it nor need it to the same extent we need electrolytes such as sodium and potassium but it seems pretty vital nonetheless.

      Sodium and potassium are easily moved to take up oxidation states of +1 — the only states open to them, but sulphur can take up oxidation states ranging from -2 to +6, while it may need a bigger kick to get to these compared to sodium and potassium. But sulphur is highly electrodynamic and likely assists in the workings of the immune system. It’s worth hunting down what Stephanie Seneff has to say about sulphur.

      Leeks, onions and garlic are good sources of sulphur as are beets. After reading Seneff on sulphur I made it my policy to supplement. Garlic capsules and turmeric capsules can make for good supplements. I find they aid my metabolism and put a bounce in my step if a bounce was missing.

      Goran, it is worth mentioning that an atom of sulphur can sulphate a molecule called 25-hydroxycholesterol. 25-hydroxycholesterol (25-HC) has the property of being able to ramp up synthesis of cholesterol in cells. The phenomenon is researched and proven, to my knowledge, in macrophages and hepatocytes (liver cells). 25-HC is one of 49 alternate, possible, and naturally arising oxides of cholesterol that can arise within the body.

      Think of cholesterol as a parent, and that parent can give rise to 49 children. Actually cholesterol is so lablile it can spawn many more children, but the 49 is the full group of children that are oxides. The big question is how many grandchildren can the children give rise to? I have no idea. But anyway biochemistry and the nomenclature is made easier for thinking that sulphated-25-hydroxycholesterol (25-HCS) is a child of 25-HC, while also being a grandchild of cholesterol itself.

      25-HCS is most interesting. It’s effects on cells have been researched too, and it seems it down-regulates the synthesis of cholesterol arising within cells — the polar opposite of the effects of 25-HC. In a sense sulphur is countering the effects of oxidative stress, at least in the sense of what it does to the properties of 25-HC, but the action is not only countering effect, it reverses the properties as apply to the regulation of the synthesis of cholesterol. And one might reason that if diet does not supply sulphur in adequate amounts then the prospect of foam cells proliferating in the endothelium is an increased risk.

      Acknowledgements to Steph.

      Many a cardiologist would do well to better appreciate the merits of garlic and onions . . and the contrasting properties of cholesterol and cholesterol oxides.

      1. Dr. Göran Sjöberg


        “It’s worth hunting down what Stephanie Seneff has to say about sulphur.”

        I am myself impressed by the logic about sulphur she presents as a mature scientist, relating gut flora with mental illness, but to say the least her views, far from being the established views, are being contested although they constantly seem to gain momentum with the increasing recognition of the importance of the metabolic interactions with our billions of small friends in the gut.

        Also when reading “THE CELL” sulphur constantly appears as a key element in the correct folding of the polypeptide chains in all our proteins and in the bridging with other molecules.

        So, yes, I very much agree that sulphur must be a very isignificant element in our metabolism.

        (Now as an aside i remember that it was also very important for me as youngster not to forget the small amount of sulphur mixed into my black gun powder; important as a catalytic element to enhance the performance.

      2. mikecawdery

        I agree entirely with your comment on soils. I would suggest that other essential micro-elements such as Mg and Se could be added to your list as well as sulphur

      3. annielaurie98524

        Ah, Dr. Sjoberg, please remember that Dr. Seneff is the target of discrediting (character assassination?) by the biotech industry because of her views on the toxicity of glyphosate (or adjuvants in glyphosate-containing pesticides) and the consequent problems it implies for GM foods. I believe the biotech industry tried the same tack on IARC, and are now suing the State of CA for aligning its toxicity definitions with IARC’s. So, not surprising that there are elements still attempting to discredit any opinion by Dr. Seneff.

      4. Barry

        MSM (Methyl Sulfonyl Methane) is an easy and safe way to up sulphur intake. Beware of source as there’s a lot of tainted Chinese MSM on the market. The Miracle of MSM (Stanley W. Jacob. M.D., Ronald M. Lawrence, M.D., Ph.D. and Martin Zucker) provides plenty of information.
        We should not overlook the important of iodine in maintaining health. I suspect that many are deficient in this very important element.
        Many a cardiologist would do well to better appreciate the merits of natural treatments rather than advanced plumbing work but they are not trained that way.

      5. mikecawdery


        Interesting thoughts on MSM which I understand is derived metabolically from NaPPS and is recommended for arthritis as well.

    2. Vincent Nonnenmacher

      Interesting to see how these ‘specialists’ are prompt to dismiss such long term established empirical ‘wisdom sayings’ as non sense when modern science coul try to explain that our own biochemical pathways could use garlic as a backup source of sulfur for deficiency of Cholesterol-sulfate.

      There is a very interesting article here : http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4456713/#!po=81.1475

      Where a lot of clues that our host is seeding along its 3 part wonderful threads are assembled in an intriguing explanation.

      It is exactly as a thriller, where all names are cited, even atherom formation, elevated blood pressure and trombosis are exposed not as the culprit but explanation of ways for the body to regulate flow (there is also some explanations on why such difference between arteries and veins due to electromagnetic fields differences due to water conduction and exclusion zone differences between the size and flow conditions).

      Fascinating to say the least!

  2. rnspainter

    Dear Malcolm
    Intriguing build-up … what a tease you are!
    Are we heading towards the final section of your hypothesis being that there is physical damage to the artery wall, which triggers plaque and then if the plaque is unstable it bleeds and a clot forms?
    That the artery wall is originally damaged by “bleeding” of some kind inside the wall which the body tries to repair and this ends up creating a plaque? And the cholesterol found there is just the “bystander at the scene of the accident” as someone else put it so beautifully? That the body tries to clear up the damaged cells and in so doing, induces apoptosis releasing cholesterol?
    So what is the original cause? My money is on inferior quality cellular membranes caused by wrong fat make up in diet (too much Omega 6?) and excess carbohydrates/sugars which results in cells that are compromised in some way.
    This combined with lack of exercise (which would force the artery wall to flex and open up intercellular gaps and so allow deposits inside the wall to be scoured out) which allows a build up of such damaged cells in the wall, and the plaque which then forms is unstable (due to the poor cellular adhesion and walls) and will break off eventually to block said artery wall.

    That this does not happen in veins or away from the higher pressure/flow rate areas around the heart because the pressure is lower allowing stuff to escape from the wall more easily, or the walls being more inpenetrable in the first place …

    How’s that?

    Keep it up Malcolm and I wait the final chapter with interest!



  3. Gert van der Hoek

    “There are, undoubtedly other things going on, such as sympathetic stress, mitochondrial damage and acidosis with heart muscle. that play a hugely important role. But the clot is, usually the final event”.

    In Germany some clinics claim great successes using strophantine to adress acidosis in the heart muscle. I did not see acidosis mentioned here (I may have missed it though), but there was no reason to worry, at all, you’ve got it all covered.

    Before discussing treatments it is a very good thing to look very carefully at the basics.

  4. Christopher Palmer

    Dear Dr Kendrick,

    YOUR FOLLOWING has developed considerably in the time since you launched your blog. That you receive so may comments must indicate that you receive many more in the way of ‘hits’ from readers and subscribing followers (now 3,250) who leave no comments. I recall ‘discovering’ your website and blog soon after it’s launch (and thinking, “ . . and about time too”) and noticing how an early post debunking the myths surrounding hypertension seemed to generate a significant increase in reader interest and participation – tantamount to the equivalent of a major transition event in evolution.

    Parts I, II, and III, of What Causes Heart Disease are already spawning an evident rise in interest (and sense of suspense) and so we, your followers, are eagerly awaiting the next instalment. There is every prospect it could trend to running a bit viral, and indeed there exists every reason why those who do follow you should want to encourage it to go increasingly viral around the inter-web. I think your hit rate and the number of your subscribers is set to exponentiate, and rightly so.

    AND ALTHOUGH i AM NOT A DOCTOR I have lately gained increasing insights into the factors that may affect the tendency of blood to coagulate and to clot. One is diminution of the zeta potential present in blood and as may apply with specificity to red blood cells. I have known about zeta potential for around three years now. The other pivots around Gerald Pollack’s drawing attention to the mysterious forth phase of water, which has come to my attention only very lately, and which, initially, I rejected as being a complete cartload of bulls testicles (the exorbitant price of the book at the time had a lot to do with it).

    However the Kindle edition of the book was much more affordable once it became available. Frankly The Forth Phase of Water and recognition of this fluid if structural arrangement that rests as a contrast to bulk water and that excludes solutes and colloidal particles in suspension (take breath) invites completely new outlooks from which to regard water, cells, blood, and the tendency of blood to coagulate. Such a shame the asking price discouraged me from reading it sooner.

    I THINK WE MIGHT READILY, AND WRONGLY THINK, that blood is a relatively homogeneous mix of it’s constituents. Medical science seems to have trodden this pathway for some time and never ventured off it. But actually, Earthing’s helpful and anti-coagulant effect upon the zeta potential of red blood cells coupled to Pollack’s (and others) work identifying EZ water (exclusion zone water, or water in it’s forth phase) invites in open minded, interested, and curious people the notion that at micro and nano scales blood would be far from homogeneous.

    BLOOD MUST HAVE A TOPOGRAPHY of sorts. Now where the topography of any landscape owes its features to differences in elevation the topography of blood owes its features to variations in charge and in the distribution of charge. In something that seems to us to be homogeneous, even when viewed through the lens of an optical microscope, there exists scope for variation visible only at finer scales of resolution.

    Waters’ forth phase (exclusion zone water) can be induced by contact with hydrophilic surfaces, the presence of charge, and by incident radiation. It is deprotonated to a notable and precise degree, and gives rise to exodus of protons (or protonated water as molecules of hydronium ions (H3O+)) away from the EZ region. If an EZ region forms in bulk water (or blood) the EZ region takes on negative charge while the social structure of EZ water molecules excludes the ions of any solutes and pretty much everything else.

    If EZ water pays a part in the dynamics and electrodynamics of blood (I’d bet a pound to a penny that it would) then at scales I’d loosely term ‘nano’ then blood would have variations in the distribution of charge from one tiny region to another, and variations in the concentrations of solutes and of electrolytic ions such as sodium (Na+) and potassium (K+). Plus the extent of protonation in any protonated regions has ramifications for pH balance and gradients. It will encourage some ions and discourage others potentially effecting the balance of electrolytes, I would guess.

    The topographic model for blood is just the merest hint of insight, I sense, into the highly electrodynamic aspects at work in blood chemistry, and in biochemistry. The electrodynamics of atoms is the shaker and mover driving biochemistry.

    Anyway, to draw discourse to a conclusion, amongst the list of things missing from your list of things that might increase the list of blood clotting could be the decline of zeta potential as applicable to the colloidal aspects of blood, and with particular emphasis upon the zeta potential of red blood cells. It sis easier to expound upon this through working backwards.

    Nothing restores zeta potential to red blood cells that are depleted of zeta potential so naturally, or so effectively as does ‘earthing’ or ‘grounding’. Anyone can earth. Earthing is simply the practice of removing ones shoes and walking or even resting barefoot on nice moist sand or or lush grass. Other natural surfaces will do, even soil, but sand and lush grass are notably tactile and sensual for the body.

    Under this barefoot arrangement the soles of the feet, or indeed any part of the flesh in contact, can connect with an aspect of the planet Earth’s global electrical circuit. The earth is like a battery. The upper atmosphere is highly charged positively, whilst the Earth’s surface, and its watercourses, are replete with negatively charged electrons. If the body is deficient in free electrons then a tiny (and highly healthful) current of free electrons will flow through the soles of the feet and into the network of nerves that traverse to body. The soles of the feet have the densest concentration of nerve endings than any the part of the body – nobody could ever explain quite why.

    MODERN MAN HAS CEASED TO GO ABOUT HIS, or her, business barefoot. And modern man has ceased to make footwear, in the main, from natural skins and materials. Modern footwear is predominantly plastic and rubber that excludes moisture and that is not all permissive of the passage of electrical current. Modern man has achieved levels of isolation from the Earth’s global electrical circuit that is unprecedented amongst earlier humans and unprecedented amongst other species roaming free and wild. Modern man is not receiving the benefits that the ancestors did, and modern man has blood cells whose zeta potential is not being maintained at the levels nature has decreed they ought to be.

    Now I must venture into the realms of speculation.

    It is my view that modern footwear wearing modern man becomes depleted of negative ions as a normal accompaniment to metabolism. The book of Gerrald Pollack may offer some clue as to how, btw. After withdrawal from the case of being earthed a human may assimilate detectable levels of positive charge relative to ground. Up to five volts is possible and three or more volts is commonplace. My reasoning would have it that the charge would build in a time-dependent manner from the moment of isolation and does so through the accumulated loss of ions, the balance of which will contain more negative than positive ions. Exhaled breath may well be the primary pathway, and the theory of the forth phase of water may point to vesicles of water vapour having candidature for being a key carrier. The result is lingering degrees of protonation about the bodys biochemistry that would persist, disruptively so, reason may direct, until the next occasion the person takes the trouble to reconnect to ‘earth’.

    NONE OF THIS RUNS COUNTER to any of your directions on the things which raise or decrease risk of clotting, Dr Kendrick, but it represents an amalgam of two new and emergent fields of knowledge, and it is stuff they didn’t, and still don’t, teach in med-school. And while the answers to certain important questions may lack experimental and empirical backing as yet it ought to be plain which is historically the more natural state (earthed or isolated) to be in.

    Now it is not always convenient to go about business while barefoot. But one can fit ones bed with an earthing sheet – and you do not need direct contact – even beneath a regular sheet or even a regular sheet and mattress protector will do. Humidity will permit free electrons to jump the gap. Those free electrons will combat lingering protonation about the body, the zeta potential of red blood cells will be restored, the resting potential of many other of the body’s cells will be restored, and the topography of charge about the blood would be tickety-boo.

    So, WITHOUT ANY DOUBT UPON MY PART restoration of the zeta potential of red blood cells through the use of an earthing sheet fitted to one’s bed (or through other means to ‘earth’) could be added to the list of things that may maintain healthy blood viscosity and reduce risks of the coagulation and clotting blood. I am satisfied we get closer to the nub of matters through including it. A person would diminish risks of DVT too. But nobody should take me at my word without they make some attempt to satisfy themselves of the same.

    AND EARTHING is considered to redress hypertension (in the instances where other factors are not at work). http://www.earthinginstitute.net/?p=597

    1. Dr. Malcolm Kendrick Post author

      I shall look at this more closely, I hope. I do like new ideas. I have heard about this one for some time, and I like the idea of being more in touch with our ‘natural’ way of being – if that actually means anything valid. It is why I am very keen on getting out into the sun, for example, as this is what we were designed to to.

      1. Christopher Palmer


        Pollack’s book on The Forth Phase of Water is worth the trouble of reading it. Far too much to absorb in one read-through. And I can demo certain measurable effects of Earthing if desired.

        . . . I like the idea of being more in touch with our ‘natural’ way of being . . . That does mean something, and what it means is highly pertinent and valid . . .

        In the world of modernity it is the departure from our ‘natural way of being’ that is the biggest driver promoting incidence of many of the most troublesome non-communicable diseases that are not congenital in their nature – CVD being top among them. Peoples departure from a more ‘natural way of being’ puts bums on the seats of the surgery waiting rooms.

        ‘Isolation’ is disruptive to circadian cycles and balances of cortisol – with ramifications extending to other physiological factors. While Edison’s light-bulb moment means we modern humans no longer have a natural connection to natural cycles of light and dark. Again this is disruptive to cortisol and key circadian physiological a factors. It all seems to be promotional of oxidative stress, and oxidative stress (an ensemble of pathways) seems to account for kind of attrition that lies behind chronic disease. Much about modern disease is man-made.

        Naturally oriented medical practice might be considered, by it’s detractors, to represent a kind of treatment bias (cries of, ‘you’re killing patients!’, etc.), but with adequate concessions to causality in the affairs of chronic disease such bias would seem to me represent an optimal standard of care excellence. “Avoid contact with cause”, is the most decent and unbiased advice any professional could prescribe in many an instance.

      2. Anne

        Are you coming back to vitamin D ? Heart disease in northern England worse than in southern England. Heart disease worse in northern France than in southern France. The southeners get out in the sun more and therefore get more vitamin D.

    2. Sylvia

      Along with a group of other nurses we were taught Reflex zone therapy of the feet by a midwife who practised it and found it to be enormously relaxing to the recipient. But barefoot walking sounds very beneficial, can see how that actual magnetic connection to the earth takes place. No cost, just need to take care where the activity takes place. We all have become too civilised and out of touch with simple practices.

  5. Rachel R

    My buzzword bingo card from my previous comment is ready and awaiting the next installment from Dr K.
    I have added “serotonin”, “melatonin” and “sleep” to it as wildcards.
    And I have capitalised Chronic, Cortisol and Resistance. For bonus points.

    Hurry up Dr K.

  6. Tim Ozenne

    I do hope your analysis of CVD will address calcium as detected in heart scans. I have an Agatston score equal to your average 95 year old, so I’m told, so if plaque formation and clotting are pretty much the same risk, I’m a dead person soon.

    1. JDPatten

      One downmanship:
      My Agatston score is 1,640. Yes, one thousand six hundred forty.
      It was my idea to get it so that I could convince my cardiologist that my modest LDL elevation wasn’t worth a statin. I’ve always felt fine. No other standard risk factors!
      This result stunned everyone, cardiologist included. I’m on atorvastatin 20 mg and looking over my shoulder.
      If this CAC scan is such a game changer, why is it not protocol? Why is it not covered by insurance? This is Massachusetts.
      Tim, was it your call? Your wallet?

      1. Tim Ozenne

        My initial score, about 12 years ago, was about 959. My (former) MD recommended the scan, which I paid for, to motivate me to take my statins and such. Sure enough, total cholesterol and such went down to “ideal” levels, but the CAC continued to increase. I’ve had, I think, 5 scans. Three years ago–I’m 71 now–it hit 2500, so that score is in the 98+ percentile. I should have lots of block coronary arteries. I no longer see any point to this sort of test so I’ve stopped.
        Yeah, it interesting that if the scan is somehow predictive–much of the published research says it is–it’s not covered by insurance. Meanwhile, my hip bone density us -1 s.d., so my “new” MD wants me to supplement with, you got it, more calcium….

      2. Bob Niland

        re: If this CAC scan is such a game changer, why is it not protocol?

        Because consensus medicine (CM) has no treatments for it, and their favored statins actually increase the score, as Dr. Kendrick points out. CM has been resisting the use of CAC, but lately relented a bit for those with T2DM*:

        CM thinks it’s impossible to reverse calcium scores, but you need to know that Dr. William Davis has been having success in arresting the growth in most cases, and reversing it in quite a few. His Cureality site (formerly TrackYourPlaque) has quite a number of members working this issue.

        Disclosure: I contribute on Dr. Davis’ Wheat Belly Blog (on which the topic of CAC rarely arises).
        * I’m restraining myself from commenting about the CM insanity on T2D.

      3. TIM O OZENNE

        My Agatston score went from 957 in ’05 to 2307 in ’15, so according to some, I’ll be dead soon. I expect my score exceeds 4,000 now. So far as I can tell, CAC tests/scores are used only to motivate patients to take statins per their MD. I, however, think the downsides to statins outweigh any benefits for folks like me (no heart problems we know of) and some say statins raise CAC scores!
        My insurance doesn’t pay for CAC tests. Even if it did, I don’t see much reason to gather more scores given that I’m not going to use the information and the radiation risk, though small, isn’t zero. The test is about $175 around here. Not too hight if the data were somehow useful.

    2. Stipetic

      Tim, look at the previous threads on this topic and you’ll see several mentions of vitamin K2. One of its roles is to put calcium where it belongs, which is not in the arteries. It may be of benefit to you if calcium is getting deposited in the wrong places.

      1. JDPatten

        I’ve known about K2 and have been taking the menaquinone-7 form at 1 mg/day for the last ten years. Does it work? I may well have accumulated my calcification in my first six decades and none in the last. (71, like Tim.) No real way to know.
        I admit that I folded to my cardiologist’s instructions to go on a statin – thereby increasing my calcification.
        Recent opinion has it that calcified plaque is stabilized plaque, so more is good. Well, that’s counter-intuitive! I’m taking 3 mg+ of MK-7 in any case.
        Good? Bad?? I wish I knew what to believe.

  7. Mark Calderwood, MD

    Rates of atherosclerosis appears to be fairly similar in the Japanese and French as countries like the US, but their rates of CVD are lower, and they have higher rates of smoking. There must be some clotting protection for these groups. Atherosclerosis is long term whereas clots are acute events. What do you surmise is the case in these countries?

    Also,I always thought the Monday morning MI was likely a result of the increased sympathetic discharge. (Jim Fixx’s death always seemed to me an extreme example of this, though, he didn’t die on a Monday morning).

    Thanks for being the great skeptic!

  8. Lucy

    Thanks. God bless you Dr. Kendrick. something has to be done. Just from people I know, I think angioplasty, stents and bypass don’t work most of the time. I know one person that had no symptoms at all and during a routine check he had clogged arteries and a quadruple bypass. He died. I think he should have been left alone. IMO many lives could be saved if bypasses, stents were not used, or used very rarely. I took my mom in one time. She was having angina. My dad had just died. She was given stents and the doctor said: well I see three clogs here but I am only going to fix this one because I think the others are not causing the pain. I remember thinking, hmmmm how does he know that? That makes no sense. I now think she should have been left alone, and it was the stress. I know one lady and she was left alone because the doctor said she had formed collaterals. She happens to have low cholesterol. I think if she had High cholesterol, she would have had the surgery. Too late now, but I stopped letting the doctors measure my cholesterol because I think when they see high cholesterol, you are more likely to get a surgery that really doesn’t work and may kill you.

  9. Jean Humphreys

    Apologies for nothing to add in the way of a comment, but it is the only way I know to get the future comments direct to my e-mail, and thus avoid the stress of trying to keep track of what I have read.

  10. Gary Ogden

    Thanks again, Dr. Kendrick. You possess good explanatory powers and a fine ear for bunk. I also find what Christopher Palmer writes about both earthing and the fourth phase of water most intriguing. I’ve mostly gone without shoes for about five years, spend a lot of time outside, and highly recommend it. It has multiple benefits, in addition to what he describes. It is much better for the health of the feet and ankles, and for balance and posture, than wearing shoes.

  11. Nigella P

    Enjoying this chaptered quest into the causes of CVD very, very much. I love that you write in such a way that non-medics can understand you. Thank you.

  12. Gay Corran

    May I echo Nigella P? Keep going, please, Dr K, though I can’t think how you have time to write so intriguingly, as well as modulating comments and running your practice…

      1. David Bailey

        So I guess you are struggling to walk on crutches, and even though you worked out what causes CVD, you have forgotten the answer – hence the endless blogs that don’t quite reach the answer!

  13. Dr. Göran Sjöberg

    Isn’t everything bewilderingly complex when i comes to health?

    For instance I just wonder why chain saws are so good for my heart. I have two of them and both are now running in my garden. If one is good two must be twice as good.

    I am now reading in Platons collected works (Republic III) about the health benefits for warriors only eating meat and also being carful when choosing doctors with the ‘correct’ attitude. From Herodotus I get the same message when he compares the meat eating Ethiopians with the bread consuming Persians as well as from Djingis kahn when comparing his riding warriors with the Chinese rice eaters. I presently tend to believe in such “meat loving” stories although it doesn’t seem to be very politically correct today.

      1. mikecawdery

        Stephen T,

        That just about sums up a whole range of chronic diseases of ageing. But I would put in a rider: It ain’t the doctor one has to avoid; it is the Bl***y DIRECTIVES written by seriously conflicted KOLs and wannabees!

    1. Mr chris

      Dr Sjoberg,
      When I was slightly younger, 70, someone advised me to get a lighter bike, and feel 20 years younger. I got two, but not sure about feeling 40 years younger.
      Is it the same with chainsaws?

      1. Dr. Göran Sjöberg

        Well if you put a nice woman on your second bike you might achieve the rejuvenating effect you are looking for.

        For me it might be the actual impression the two chain saws makes on my wife which invigorates me. I handle both my chain saws and my wife with love. Otherwise they will not work properly.

  14. tannngl

    Just a question that has plagued me since I began reading on VLC diets and CVD.

    The Masai people in Africa on study a while back have shown almost nil heart attacks as cause of death through autopsy.
    But most of them as they age do have atherosclerosis.

    Could it be that the 2 are just 2 different things and without inflammation heart attacks don’t happen?

    1. stipetic

      My guess is that the Massai don’t show microvascularistion within their plaque (or neovascularisation as someone else called it). Without these new blood vessels, there is no pathology.

    2. Binra (@onemindinmany)

      Their diet includes abundant environmental exposures of sunlight – and gut biota – so it isn’t only blood and milk. Our diet is denatured and adulterated (and medically distorted if you believe your industrial management system) and our Sun exposure demonised and in any case what we have is often when we cant access it – and we (generally) hardly touch the earth.
      In that sense they are natives and we have become aliens who cant survive without our industrial management system – which also kills us slowly…

  15. mikecawdery

    Dr Kendrick,

    Like most, if not all, your readers, I find your blogs interesting, informative and mentally stimulating (which at my age is vital). There is an old Irish blessing which goes rather like “May you get to heaven before the devil knows you are dead”. May be the modern devil is Big Pharma and its experts? Keep up the good work – new ideas like yours challenging the “consensus” are essential to progress as the history of medicine conclusively proves.

    One point that struck me immediately from the given ref: Abstract only

    Hypercholesterolemia is considered the primary risk factor for cardiovascular disease.

    Hardly a good start and then it goes on to cite NF-κΒ and many anti-thrombotic effects. But so do other drugs that are far less harmful. For example, sodium pentosan polysulphate (NaPPS – SP54). This drug used to be used in France for the prevention of post-surgical DVT but on finding a patentable low molecular weight heparinoid it was dropped by the simple expedient of claiming it was dangerous; in reality the new patented drug was far more profitable.
    The drug itself is fibrinolytic, lipolytic, (reduces triglycerides – http://www.medscape.com/viewarticle/720881_4) and has anti-thrombotic effects as well. But rarely used in human medicine. But then like aspirin it is cheap – not something favoured by Big Pharma

    1. celia

      And isn’t hypercholesterolemia a wonderful money earner. Apparently both my husband and I suffer from this supposed “disease”. My total cholesterol is now 6, his is 8. We both gave up statins and feel much fitter for it. Statins got me down to 3.1 and gave me a nasty range of adverse side effects. I’ll keep the hypercholesterolemia thank you.

      1. mikecawdery

        Wise lady. The WHO produced a graph that shows that compares cholesterol levels (BHF-HEARTSTATS). Like all unacceptable but truthful revelations the page was taken down. I wonder why?
        All cause mortality age standardized per 100,000 (source WHO Mortality ) for various conditiations. This graph showed a series of J-curves. The cholesterol levels with the lowest mortality for three conditions are as follows:
        All Cause mortality 222 mg/dl 5.75 mmol/L
        Non-communicable disease 210 mg/dl 5.49 mmol/L
        Cardiac Disease 208 mg/dl 5.44 mmol/L
        On the basis of this graph 3.1 is of well off the graph and suggests a massive increase in risk

        On the other hand David Evan’s book “Low cholesterol leads to an early death (end of Chapter 1) shows that increasing national TC levels is associated with increasing national life expectancy. You can believe the experts and KOLs or the data. Personally I prefer the data.

        Incidentally, many medical journal editors are calling for researchers to release the data on which their reports are based. http://www.icmje.org/news-and-editorials/M15-2928-PAP.pdf .

        This is to be applauded but frankly I cannot see Big Pharma responding. The results of the reassessment of Study 329 (GSK antidepressant) is too recent and devastating as it so clearly demonstrated data manipulation to get a “satisfactory” result.

  16. Diana

    NETosis – blood clots – von Willebrand factor – DNA meshwork

    But this brings us back to microbes again. Leukocytes release DNA to form NETs (neutrophil extracellular traps) to catch pathogens.

  17. Susan

    I am a retired housewife (widow), without a degree in upper education. I just wanted to say thank you for presenting the information you uncover, and so graciously share, with a style that makes it possible, for someone like me, to easily (mostly) understand. I have been a fan of yours for quite a while.

    I used to follow Peter, from Hyperlipid, when I could understand what he was writing, However, I am not able to keep up with his writing any longer, as he has gone deep into the weeds with the science.. I did learn a lot from his blog while I could keep up. I hope to follow your blog for a long time. Thanks again.

  18. Jerome Burne

    Malcolm – brilliant stuff (I think) doubts because reading it and then some of the comments has left me feeling certainly ignorant and ill-informed if not simply stupid.

    Think I followed background details on how CHD is a new (relatively) diagnosis, on how countries don’t agree on what it is, setting up of Monica to sort that out and when you start looking at what actually goes on in an attack it is much more varied and complex (inevitably ) than the standard story.

    Very impressive range of comments throwing in a range of stuff that I suspect most non-medics would get lost in but did get sense of a smorgasbord of rival theories., rather like competing far left political groups with you as the Keynes or Piketty drafting a new settlement

    I am hoping that the full “reveal” it may be possible to do a simple person’s summary and what that might mean for treatment.

    We don’t believe in cholesterol or sat fat as baddies, we don’t believe in statins as treatment but maybe blood pressure lowering is a good idea but drugs or lifestyle. Know you haven’t been that keen on diet so interested to see where that fits in.

    Best wishes


    40 Warrington Crescent

    London W9 1EL

    W9 1EL

    0207 286 9294

    07940 393 094

    Blog. HealthInsightUK.org

    Also: Body of Evidence: jeromeburne.com

    1. mikecawdery

      Jeremy Burne,

      Raising the issue of MONICA is interesting. They have reported two or three times on the national intakes of Total fat, saturated fat, protein and fruit&veg for some 40+countries in Europe. They have also included the national death rates for cardiac disease. However, they only used the word “carbohydrate” once and that was to described it as “good”. Dr Kendrick first drew my attention to this work in his book “The Great Cholesterol Con”. I have since done some more detailed statistical work on it and I found that total fat, saturated fat, and fruit&veg were all significantly but negatively correlated with cardiac death rates. Protein did not seem to vary much across countries while carbohydrate (by subtraction) was significantly and positively correlated with national cardiac death rates.

      Of course such findings were totally ignored in the reports – carbohydrates are good and that is all one should know. Just another example of research toeing the line of DIRECTIVES

  19. Milvusmilvus

    You mentioned that plaques are less likely to form in the veins. I wondered if oxygenated blood is the optimal state via movement and fresh air etc. Chronic exposure to carbon monoxide which strongly binds to haemoglobin molecules causing red cell death and increasing red blood cell turnover, might indicate why the inflammation and (cholesterol) processes are activated. Fresh alpine air more healthful than urban living perhaps?

      1. Stephen Rhodes

        Except, of course, when they are ‘cabbaged’, and apparently, especially when the ApoE4 allele is present.

      2. Jean Humphreys

        Some evidence. I had a triple bypass in 1997, followed by a re-do of one that failed, this time using the left mammary artery. In 2013 I had MI’s. Report after angiogram found the new MI’s were in a previously uninvolved artery. The two remaining venous grafts had stenosis. The diverted mammary artery was still clear, after 16 years. I believe you have said that veins used as artery replacements can clog.

  20. caldem99

    So getting back to process. Are you saying then that the beginning of atherosclerosis begins with clotting? It makes sense that clotting as part of the healing process over repeated occurrences without fully healing leads to plaque formation. Layer upon layer over time without complete resolution of injury. But what is that initial injury, and why does it occur? Super accelerated CVD as in Kawasaki’s, a necrotizing vasculitis, is hyperinflammatory, but not hypercoaguable.

    So instead of statinizing children should we anticoagulate them?

  21. stcrim

    Dr. Kendrick – you and I exchange emails about this very subject back in March. The research being done by Harvard in Boston points strongly to the anti-thrombotic properties of Rutin and Isoquercetin. They work at the top of the cascade for both arteries and veins in play. Stop the clot and you stop the event. I expect the research to end in a patented product. Rutin and Isoquercetin are safe and appear to work quite well where the final product may or may not.

    Click to access 07.pdf


    Click to access 37.pdf


    1. Stephen T

      Bob, I give up too. It always did look like a determined attempt to keep the cholesterol hypothesis limping along when overall cholesterol was shown not to be harmful. There’s always triglycerides. Maybe they’ve finally hit something that does matter!

  22. Sasha

    A question: since atheromas form only in arteries (except pulmonary arteries) and since oxidation is now thought to be a factor in plaque formation and its effects on CVD, could we say that oxygenated blood is itself a risk factor in the whole mechanism?

    Regarding electromagnetic fields, Dr Becker’s books go in depth on this issue…

        1. Dr. Malcolm Kendrick Post author

          At the risk of sounding a bit pompous. Until you know exactly what the process of plaque development is, you cannot (in my opinion) possibly work out possible causes. I think that people jumping to a million different causes has been the greatest problem in this area. Vitamin D, C, E, K2, folic acid, B6. I think you can make a case that they have some effect. But by looking for a cause, then trying to wrap the process around it…. that way lies madness. I would also tend to shy away from the word cause. There is no cause, there are things that can accelerate, or decelerate, the process.

      1. Dr. Göran Sjöberg


        That is exactly my own view. Everyone seems to love ‘oneliners’ – too simple explanations.

        My own attitude is to work in a broad manner. Whatever oneliner is involved it doesn’t hurt to include what is suggested has no adverse effects.

        E.g., “It is the sugar which is the culprit!” – well then take i away. “Staturated fat is good for your heart” then go for it. “Omega 6 vegetable oils ruins your immune system!” – take it away. “Garlic reduce blot clotting!” – add that to your food. Etc. Etc.

      2. TS

        So is there a clue here? Pulmonary arteries are under much less pressure than other arteries. Have a thinner structure too; less elastic tissue, thin distensible wall.

        1. Dr. Malcolm Kendrick Post author

          Of course there is a clue here. If plaques never develop in veins or pulmonary vessels (unless there is pulmonary hypertension), and these blood vessels are subject to exactly the same level of everything in the bloodstream as the arteries, then this is more than a clue. It is a six hundred pound gorilla jumping up and down shouting ‘Over here! Look over here. Biggest clue possible right here, right in front of your eyes. Look, look, what do you see’

          Add this to the fact that if you take a vein, and stick it where an artery should be i.e. use it a a bypass graft in the heart (CABG), then atherosclerotic plaques develop at super-high speed.

          So, a vein, with no atherosclerosis now acts as an artery. Where it very rapidly develops atherosclerosis. This will occur in exactly the same human being where, at the same time, the veins will continue – never – to develop atherosclerosis. What changed? What single thing changed? Vitamin levels, homo cysteine, LDL, diabetes, oxidative stress…. No, the only thing that changed was bio-mechanical stress.

      3. TS

        The thinner wall of the pulmonary artery must be irrelevant, since it and veins themselves have the capacity to become atheromatous under the right – or should that be – the wrong circumstances.

      4. Diana

        Pulmonary artery hypertension and iron “deficiency”? Hepcidin up, again.

        Iron deficiency and raised hepcidin in idiopathic pulmonary arterial hypertension: clinical prevalence, outcomes, and mechanistic insights. (Rhodes, 2011)

      5. johnnyv

        Because they do not contain vasa vasorum, especially vasa vasorum in the tunica media.
        Vladimir M Subbotin has a paper fingering enlarged tunica intima having hypoxia induced growth of vasa vasorum into the tunica intima.
        If that is the case what causes thickening of the tunica intima beyond what can be supplied via diffusion?

      6. mikecawdery

        Dr Kendrick,

        May I suggest that Vitamin D, C, E, K2, folic acid, B6. and other factors are all related to good health. It would only be in conditions of deficiency (not necessarly a “medical” deficiency) that they would have an effect. I believe that it is this is how the “anti” studies have “proved” that there is “no benefit” from supplementing. An example of this is the second treatment of an “anti-oxidant cocktail” in the HPS where CoQ10 was excluded despite the fact that Merck acquired a patent for combining CoQ10 with simvastatin only a few years earlier.

      7. Binra (@onemindinmany)

        You go on a little below to say:
        “So, a vein, with no atherosclerosis now acts as an artery. Where it very rapidly develops atherosclerosis. This will occur in exactly the same human being where, at the same time, the veins will continue – never – to develop atherosclerosis. What changed? What single thing changed? Vitamin levels, homo cysteine, LDL, diabetes, oxidative stress…. No, the only thing that changed was bio-mechanical stress”.

        If Seneff et all are on the right track – the framing of all this changes – for the suspect (atherosclerosis) becomes an less efficient rerouted means of delivery of cholesterol sulphate – to the heart. The electrical significance viz Pollack (EZ) and others also connects to plasma physics – vortex physics. I will come back with a link to that if I don’t meet references to it in your own or other’s comments. The choice of the term ‘plasma’ for blood fluid AND for the various modes of charged matter is a striking moment of pause to wonder in my opinion.

  23. michael goroncy

    My experience and ‘take’ living with CHD.
    Had the pleasure of experiencing 2 x MI’s at age 38, 29 years ago. CABG within a year.

    Still ‘smoke and drink like a witch’….understand the negatives….go figure!

    Journey with this ‘spooky’ disease:

    (1) Consuming a ‘hat-full’ of medications (and supplements). Don’t take anything, I don’t understand. Have been on max dose ‘statins’, not because of cholesterol, but because of at least 9 inflammatory effects. Also ‘aspirin’ for multiple reasons, and Clopidigrel. At this stage, and at least the last 15 years, have seen the positives and pathways of these drugs.

    (2) Currently all coronary arteries occluded and running on collaterals. If our host ‘Malcolm’ is heading towards the ‘Endothelium’ and ‘Nitric Oxide’, I will introduce you to ‘Lois Ignnaro’, a ‘Nobel laureate’ for his work regarding NO. and his protocol.
    (3) With cholesterol, I only look at LPa, APO B, and Trigs.
    (4) With regard to ‘Earthing/Grounding’, by retired cardiologist, Sinatra. I looked into this about 7 years ago…looked like my sort of caper (no effort). Fortunately live on the coast with temperate climate and very doable. Anecdotally, my observations were impressive. Within 2 weeks, I noticed 4 things were taking place at the same time. (a) Walking along the beach in ankle deep water for 20-30 min was very refreshing and energising. And the effects lasted for the rest of the day. (b) There is something about ‘cleansing the feet’ that to me that is unknown…..won’t get all biblical here. © A calming, spiritual effect by the sound of the waves, observing the vista, sky/clouds,slow deep breathing, diagrammatically with 3 in and 6 out….perhaps! A lazy mans yoga. (d) Sulphated D3 from the sun and light. You only need 10-15 min of sun on body to produce 10,000 iu. No sunglasses, let the light into the retina to allow ‘Circadian rhythm’ to work it’s magic. This may be a problem for people with macular problems that cannot tolerate sunlight.
    (5) Have tried many unconventional ‘ add ons’ in the past…..perhaps another day.

  24. anonymous

    I have two questions.
    1) Does ECT (electroconvulsive therapy, a.k.a. electroshock) increase the risk for clots?
    2) Where are clots more likely to form, in big arteries like the aorta or in small arteries arteries, like those found in the brain?


  25. anonymous

    I have two questions.
    1) Does ECT (electroconvulsive therapy, a.k.a. electroshock) increase the risk for clots?
    2) Where are clots more likely to form, in big arteries like the aorta or in small arteries arteries, like those found in the brain?

    Just 11 months left to wish everyone were better, including me.


  26. stipetic

    Maybe you’ll help me through my delusions. I no longer think the process of laying down cholesterol plaque is from the lumen side into the (tunica) intima as is traditionally thought, but the cholesterol comes from red blood cell membranes from the adventia side via neovascularisation (this is where VEGF comes in). Then I can see a process driven by unliganded iron that could account for both abnormal plaque and clot formation.

  27. B

    Love this site …. It’s really making me think for myself … Taking control, making my own decisions and being hugely positive … Please hurry up and post ….. The four step process of CVD… 😀

  28. caldem99

    So chronic hypertension regardless of cause is the active process leading to atherosclerosis? The greater the degree the greater the “biomechanical stress”?

      1. caldem99

        Didn’t think so. Antihypertensive therapy probably would have had a more dramatic impact on CVD. Got to be endothelium turnover and abnormal clotting. Von Willebrands in pig model markedly reduces atherosclerosis formation.

        Thanks for your erudition! Your books have been tremendously helpful and I recommend them frequently.

  29. TS

    This looks as though it could be helpful but I haven’t read the review because you have to pay for it. Does anyone know of something similar and free?

    The role of red blood cells in the progression and instability of atherosclerotic plaque.

    Tziakas DN1, Chalikias GK, Stakos D, Boudoulas H.

    This review attempts to present a focused summary of selected areas of the rapidly growing knowledge regarding the red blood cells role in atherosclerotic plaque progression and instability. A summary of the characteristics of the erythrocyte membranes is provided, followed by a brief review of the in vitro and in vivo work that has helped clarify their role in atherosclerosis. Mechanisms by which erythrocytes enter the atherosclerotic plaque and contribute to its progression and instability are presented. Finally, some elements that may be clinically important regarding erythrocytes in coronary artery disease are discussed.

    Copyright 2009 Elsevier Ireland Ltd. All rights reserved.

      1. TS

        Thank you for this link. Rather a pity that the authors seize the opportunity to promote statins – their assumption that lots of cholesterol in the red cell membranes must be a bad thing.
        It made me wonder why the red blood cell membranes need so much cholesterol and this is what I’ve read:

        Quite apart from being a precursor of all steroid hormones and vitamin D, cholesterol
        1. Prevents cell membranes from being too fluid or not fluid enough. Helps to prevent extremes in the consistency of cell membranes.
        2.By stabilizing certain proteins together in lipid rafts, cholesterol is important in helping these proteins maintain their function. This can include forming blood clots or thinning blood and pretty well anything else that is necessary.
        3. Helps cells communicate with nearby cells
        4. Helps cells respond to hormones in far away cells

        I love cholesterol!

  30. Gay Corran

    “Nope”. I’m glad to hear that. And from Dr K’s books and earlier blogs, it would seem that even chronic high BP doesn’t actually kill people, and lowering BP with drugs doesn’t seem to affect the mortality rate in people with high BP. I’ve always thought that BP needs to be whatever it is to keep the blood pumping away, and lowering it to the level of a 25 year-old is a false deduction. Yes, 25 year-olds are less likely to die than 70 year-olds who have high BP, but why blame only the high BP? American beef-eaters are found to have a higher mortality rate than non-beef-eaters, but is it the beef, or the huge white bun, fries, and sweetened milk shakes that go with it? Love the clues, and the learned posts, and the whodunnit style mystery. Will any of the posters get it right before Dr K lets us in on his conclusions? Keep going, Dr K!

    1. Sasha

      And yet, pulmonary hypertension causes atheromas to form in pulmonary arteries, a place where you normally don’t see them. So, it seems, increased pressure within a blood vessel will increase physical stress on it, initiating stress-damage-inflammation-repair (atheroma) chain…

    2. mikecawdery

      Just one point. In the case of aneurisms in the aorta would not high BP increase the risk of rupture to a greater or lesser extent? It is the only situation where there would be a possible association between high BP and a fatal rupture.

      1. Susan

        Mike, This is of interest to me as I recently had an ultrasound to check out my gallbladder. No gallbladder disease was detected from that scan, but my PA’s nurse let me know that I have a “slightly enlarged distal aorta”. That’s it. Nothing else said about it except to expect another ultrasound in two years to check on it. I am not entirely sure in which direction to go with this information. I am 62, not overweight, have low triglycerides, good vitamin D, high HDL and have good blood pressure, I do, however, have high LDL. When it is not miserable out, I walk about 3 miles a day for the sheer pleasure of it. I cannot wait to read the next installment from Dr. Kendrick.

  31. B

    STRESS …so if we can’t turn the stress response off and an imbalance happened between the pro-inflammatory cytokines and anti-inflammatory ….this can cause inflammation? ….allostatic load? So could diet be fuelling the fire of inflammation?

  32. Milvusmilvus

    Now I am wondering if the arteries become less flexible with the aging process because the SNS is failing the body in a similar way the elderly are less able to regulate their temperature and their physical reactions are slower etc. SNS derived damage leading to stiffened and inflexible arteries that succumb to damage by the debris flowing past.
    I like to think of it being like a fast flowing river wearing away the riverbanks in places where there is less resistance and silting up where the flow subsides.

  33. JDPatten

    Hm?? But above, Dr Kendrick, you said “Nope.” to chronic hypertension. Meaning… it matters what the cause of the hypertension is?

  34. JDPatten

    How about the arterial pressure differential – the so-called pulse pressure?
    Old guys (Like me!) tend to present with a greater pulse pressure along with basic hypertension, atherosclerosis, etc, etc… (sigh).
    More wear & tear when there’s a greater jump from diastolic to systolic?

    1. mikecawdery

      Yes I have asked this question – it apparently should(??) be 40 mmHg but is often more. Does it really matter.

      1. Steven Morrissey

        Regarding pulse pressure (PP), its value seems to depend on the arterial stiffness as well as the underlying blood pressure.
        It has been found that the ratio of systolic blood pressure (SBP) to diastolic blood pressure (DBP) is more or less the same as the golden ratio (1.618…). A higher ratio is linked to increased mortality.


        Click to access ulmer2009a.pdf

        If the SBP/DBP ratio is higher than 1.62 I think it suggests that the arteries are stiffer.
        I believe that if the aorta is not stiff than the SBP / DBP ratio would be approximately 1.62
        As a corollary DBP/ PP ratio would also be approximately 1.62 (because of the definition of the golden ratio)

        The pulse pressure is a measure of stiffness but it needs to be looked at in terms of the systolic and diastolic BP values. For instance these two readings below would give the same PP however the interpretation would be different:

        162/100 is high but the arteries do not appear to be stiff since the ratio is ratio 1.62
        142/80 doesn’t look too bad but it would suggest that the arteries are stiff since the ratio is 1.77

        Personally I would regard the first situation as less of a problem since medications can bring the BP values down, but I don’t think anything is officially recognized as being able to alter arterial stiffness at present. Maybe K2 can reduce arterial stiffness but we have to wait for the further trials to complete.

        I hope this helps.

      2. mikecawdery

        Steven Morrissey

        Sorry for the delay in responding. Just picked up your comment while reviewing and reminding myself of all that is going on. Thanks very much. It was indeed most helpful and useful; my poor old aorta must be solid

  35. Elph

    I am a first time commenter but have been reading this site for a while. I am really impressed at the quality of both the information presented and the knowledge of those that comment. There is also a level of respect accorded to commenters that I have not seen on other sites. There is a genuine interest in helping others to learn and understand. I’m not at all surprised at how complicated this is given the following list of ‘factors’ influencing CVD that seem to be floating around: Lp(a), small dense LDL, CRP, Vitamins C, D, K2, cholesterol sulphate, ferritin levels, AGEs, Calcium, Cortisol, thyroid, refined carbs, PUFAs, collagen…just off the top of my head. I agree with a previous poster…my head hurts!!

  36. Craig E

    I have been reading this blog for some time but am a first time poster. I must say that I am impressed by both the quality of the information presented here and the depth of knowledge revealed by the commenters. There is also a level of respect accorded to posters that is absent from other sites. It seems everyone is interested in helping to increase the level of understanding on each topic. With respect to CVD – I am surprised that anyone can sift through the following list of factors that I have read about: Lp (a), small sense LDL, CRP, high blood pressure, vitimans C,D,K2, collagen, calcium, AGEs, cholesterol sulphate, cortisol, thyroid, red blood cells, ferritin, refined carbs and PUFAs…just off the top of my head. Who would have thought that my original journey looking into cholesterol/statins would take me down so many other garden paths. Hats off to all of you for helping me in my quest for the (non Pharma/authority/$$$ based) truth

  37. mikecawdery

    Dr Kendrick,

    Came across the following today:



    I think that it is those like you Dr Kendrick that are effectively forcing the issue of data transparency by challenging the comfortable “consensus”. Please keep it up

  38. Margo Bonner

    Katy Bowman is a biomechanist whose book Move Your DNA talks about how modern lifestyles make us ill. We sit too much — in chairs and on the sofa rather than on the ground or the floor, our heads jutting towards an electronic device and our hands and arms forward on a keyboard. When we do move, it’s as gym-type “exercise” that only shifts large muscle groups in repetitious movements. She says that we evolved to walk (a lot!) and on textured and uneven surfaces, to squat, to carry heavy things in our arms, to climb, to swing, to reach in all directions, and not doing these human activities anymore shortens or lengthens our muscles into rigid patterns that affect blood flow and turbulence. She attributes development of atherosclerotic plaque to this lack of movement. I have her book Move Your DNA on Kindle and I keep rereading to keep me motivated to get moving.

    1. David Bailey

      I like to take a reasonable amount of varied exercise (never in a gym), but I suppose I tend to baulk at the incredibly prescriptive rules that you find in books such as you describe. People will tell you exactly what to eat, in what quantities, and from where it should be sourced! Others tell you exactly what exercise to take, and effectively tell you to avoid occupations that make heavy use of the computer, etc etc. One thing is pretty certain – when we were swinging about in trees, barely anyone would have reached 50+, so who knows how healthy they would have been if they had!

      1. Margo

        Not prescriptive, and I’m so sorry that my description yielded the impression. And obviously, from your reply it’s not for everyone. I happen to love and enjoy natural movement but chacun a son gout, definitely. Wishing you the best.

    2. Dr. Göran Sjöberg


      I guess this issue is complex as everything involved in our physiology.

      But still something must be involved that tells you that moderate exercise is good for your heart.

      And the famous change that took place about 60 years when treating CVD infarction patients ago is for sure telling.

      Before this change these patients were tied to their beds and forbidden to move. 50 % of them died. Then a daring head of a heart clinic suggested that his patients instead should be allowed to move about in a moderate way and to the horror of his staff turned into practice. I don’t remember the figures on top of my head but there was an undeniable staggering reduction of the death rate.

      If I would have had my very serious MI before that change of practice took place I would most probably not have survived.

      I still remember that I was taken by surprise when I was forced out of bed when treated under intensive care 1999 so the idea that MI-patients should not move was then still ingrained in the general opinion.

      Sometimes I think about this when I am working with my two chain saws and chopping my firew wood today in an almost excellent physical condition irrespective of my severely clogged coronary arteries.

      1. Margo

        Dr, Sjoberg, thanks so much for posting that historical information. I had no idea about movement restrictions to treat heart conditions! Fascinating. But I remembered when I read your post that my father, when diagnosed with high blood pressure, stopped moving out of fear–would drive the car two hundred yards to the mailbox to pick up the mail!–until his doctor told him move or die. The statins and coumadin ruined his quality of life, though he made it to ninety, when he died of the operation to remove the calcifications from his carotid artery. Like you, I love how I feel when I move, walk miles every day, and now in my mid-seventies cherish and protect my mobility. But not everyone feels that way and people should do what makes them feel whole I think.

      2. Dr. Göran Sjöberg


        That’s right!
        Fight the drugs!

        But with innocent vitamins supplements you may, as I do but to the disgust of Big Pharma, liberally experiment. And, as you say, it is your body which tells you when you are doing well. It is a pretty sophisticated living measuring instrument to say the least.

        Our adored neighbour recently passed away at 94. She was in an excellent health condition and with a brilliant intellect without any drugs until she got into the “health care system” about a year ago. I did pay her a number of visits during that year and it was very heartbreaking to see the breakdown effects on her intellect by the drugs she was exposed to.

    1. Dr. Göran Sjöberg


      Naturally, I take garlic instead.

      Aspirin is undeniably a powerful poison for living organisms which should make you suspicious. I wonder if it is to keep the animals away that the Salix type of bushes incorporate aspirin in their bark.

      1. Diana

        Dr. Göran Sjöberg

        Neither Salix bushes nor any other plant incorporate aspirin in their bark. You probably mean salicylic acid. Aspirin is not equal to salicylic acid. SA is not a poison, but a potent signalling compound across kingdoms (microbes, plants, animals).

      2. Charlie

        Dr. Goran; Maybe of interest to you:
        “The supplement Aged Garlic Extract can reverse the buildup of deadly plaque in arteries and help prevent the progression of heart disease, according to a new study scheduled for publication in the Journal of Nutrition.

        The research, conducted at LA BioMed, found a reduction in the amount of low-attenuation plaque, or “soft plaque,” in the arteries of patients with metabolic syndrome who took Aged Garlic Extract. Metabolic syndrome is characterized by obesity, hypertension and other cardiac risk factors.”


      3. Jo Beaumont

        I know I was taught willow leaves ( salix ) was where aspirin came from. Our sheep love them and come to no harm. We often comment they probably have a headache…especially when the ram is in with them!!

      4. Dr. Göran Sjöberg

        I must admit that I have not done much deep research on this subject. On top of my head I though remember that long time administration of acetylsalicylic acid, which I understand is the working substance in Aspirin, to CVD patients has been severely disputed. My own drug scepticism made me stopped taking the drug one year after my MI and after having done my proper home work on the subject and then I replaced it with liberal use of garlic in my food to the approval of my fist cardiologist but to the frowning of my last (?) one.The best effect is achieved when you put the garlic fresh on your plate.

        My wife told me that when she was studying biology they had to do a lot of practical experiments on small living creatures of different kinds in test tubes. To finish the experiments, to the disgust of many of the students, they just had to add a little aspirin which killed everything off nice and fine in the test tubes. But the most important effect of the aspirin was evidently the strong effect on the proliferation of the cells. After these kind of experiences she and her fellow student were very reluctant to take ‘aspirin pills’ against headaches.

  39. TS

    1. There is an inciting injury and an inflammatory response.
    2. Under acute stress, pressure increases so that the cholesterol rich red blood cells are pushed against and into the injury and are degraded as
    3. the clot and repair forms over them.
    4. When the process is repeated the plaque builds up and eventually becomes unstable as the cholesterol content from the red blood cells increases. The fibrous cap of the clot ruptures under the mechanical stresses.

  40. TS

    and the blood clots get incorporated in the plaque and add to its size.

    Yet to quote Tziakas et al (Significance of the cholesterol content of erythrocyte membranes in atherosclerosis):
    “Haemorrhages within the plaque arising from rupture of intraplaque microvessels and erosions of the atherosclerotic plaque have been proposed as major mechanisms by which red blood cells can reach the plaque.”

      1. Craig

        Malcolm, thanks for initiating and sustaining a very interesting discussion.

        So, a plaque is a type of scar which is inside out compared to the type of scar which forms on regular skin. A quick browse of wikipedia re: keloid scars etc, discusses various types of collagen involved in scar formation and transformation, perhaps there are other types involved in the strange inside-out scars which form within arteries. There must be some mechanism away from the inner surface or outside of the arteries which is responsible for removing the fibrous clot material, the rbc’s, fibrin etc, and forming a stable scar ie plaque. That process will go wrong under certain circumstances. Maybe it is inhibited by disease or lack of enzymes or nutrients or by physical/chemical trauma. With this in mind it’s hard to understand how transplanting sections of veins and arteries wouldn’t result in the destruction of these support structures necessary to repair further scarring, no wonder that there are problems with bypasses. Might as well use teflon tubing. The role of collagens in scar formation supports (part of) the Pauling hypothesis since vitamin C is an important co-factor in collagen formation.

        The mention of pulse pressure triggered a few thoughts. I understand there are various ways of analyzing the signals in pulse waveforms — where a pulse travel through a waveguide eg an artery there will be transmissions and reflections at every discontinuity. Think of this like pulse echoes. If there is a blocked tube somewhere it should show in the waveform but even under healthy operating conditions where pulse energy recombines with pulse echoes you will get both higher and lower local pulse pressures. If the basic pulse pressure is already high it is possible that the peaks of these pulse standing waves will be very high in some places. That’s on top of the hydraulic turbulence which you would get at the discontinuities themselves and not necessarily in the same places.

        It should also be possible to introduce small acoustic pulses and evaluate the resulting signals at various locations in the circulatory system, if someone isn’t already doing that. This is pulse reflectometry, useful in musical acoustics and other areas.


      2. Craig

        PS: when veins are grafted in to replace blocked arteries, what happens at the junctions? Are there new scars at each end of the section, instantly forming new plaques?


      3. David Bailey

        I am guessing that RBC’s are going to figure in your theory. I seem to remember reading that those who give blood are less likely to get CVD. If that is true, perhaps there is a link in that they will have slightly fewer RBC’s on average (I guess) as a result of their donations.

        Of course it might just be that those who take drugs for high BP aren’t supposed to give blood, so the comparison gets skewed.

  41. Ken

    Dr. Kendrick,

    Okay, after your comments to me in part 1 of this series, I decided to cheat and bought (and read) your book. So, I will refrain from commenting until you present your hypothesis.

    Great book. Your conclusion was elegant for its simplicity, and the funny thing is, it was taught to us by our parents/grandparents when we were young, before it became common for doctors to order annual blood work and treat to those numbers.

    By the way, it is not just Russian coal miners who see an increase in CVD. Appalachian coal miners also see an elevated risk. Researchers seem to blame the increased risk on pollution, since in the U.S non-Appalachian coal miners have a lower risk, but they completely overlook the fact that Appalachian coal miners work in tunnels in the ground versus the others who strip mine on the surface.

    I happened to notice that when I was testing your hypothesis on the CVD deaths in my family. I’ve always been told that my genetics put me at risk, but your explanation fits the facts much better.


    1. Rtd RGN

      Although this really does sound simplistic. On a sunny day “go out and play” – thereby topping up the vitamin D and reducing stress. As far as the blood work goes, I reckon measuring for C-reactive protein would be a much better indicator of athero- sclerotic risk than the current cholesterol obsession.

  42. mikecawdery

    Not entirely on Topic but interesting nonetheless and what patients are up against

    From [Side Effects of Lipitor, Lovastatin and other Statin Drugs]
    Melanie Mace
    Some startling facts: FROM Rxisk.org

    • Prescription drug spending in the US reached a whopping $329.2 billion in 2013.
    • In 2011, 4.02 billion prescriptions were written in the US, with more than half of Americans on two prescription drugs.
    • Drug side effects are a leading cause of death in hospitals and may be the leading cause of death outside hospitals.
    • 100% of patients suffer unintended effects from their prescriptions.
    • The annual cost of drug side effects is estimated to be considerably more than $100 billion, yet comprehensive, relevant data necessary to manage a solution is not collected.
    • More than 95% of drug side effects go unreported, and there are serious gaps and delays in getting relevant feedback on effects of pharmaceuticals once they are released to the market.
    • Regulators do not have reporting systems geared to capturing the data needed for effective post-market monitoring.
    • And every day there are new reports of prescription-happy doctors, slack regulators, Big Pharma venality, and horrific human suffering.

    1. Barry

      And here is the end result of our wonderful sickness industry http://pharmadeathclock.com/ (sources at the bottom). When it comes to trauma modern medicine has a lot going for it but when it comes to management of illness – be it genuine or a newly discovered condition for which a drug company just happens to have a treatment for – then we see things rapidly going downhill. So sad that the potential for so much good results in so much harm.

      1. mikecawdery


        Thanks for the link. And I thought Starbridge’s report (JAMA, July 26, 2000—Vol 284, No. 4) and Null and Dean’s report (Journal of Orthomolecular Medicine Vol. 20, No. 1, 2005) were pretty disastrous. As you say in surgery there is tremendous benefits but modern pharmaceuticals are a very different kettle of fish. When efficacy rates of 4% and less are considered “great” something is seriously wrong.

  43. mikecawdery

    Lower blood pressure targets: to whom do they apply?
    Mattias Brunström , Bo Carlbergemail
    Published Online: 07 November 2015
    Article has an altmetric score of 10
    DOI: http://dx.doi.org/10.1016/S0140-6736(15)00816-8

    For many decades, the optimum blood pressure treatment target to prevent cardiovascular disease has been debated. Until 2013, most guidelines suggested that the general population with hypertension should be treated to achieve a blood pressure goal of lower than 140/90 mm Hg, but that the goal for some high-risk groups, such as patients with diabetes and chronic kidney disease, should be a blood pressure of lower than 130/80 mm Hg. In 2013, most guidelines relaxed the recommendations for high-risk patients, based on a lack of evidence, which was brought to attention after the disappointing results of the Action to Control Cardiovascular Risk in Diabetes (ACCORD) trial.
    To read this article in full you will need to make a payment $31.50 for a comment????

    Even when there is a lack of evidence the only response is relaxation of the recommendations for high risk patients WOW!

    1. Craig

      “Even when there is a lack of evidence the only response is relaxation of the recommendations for high risk patients”

      Especially when you consider this:

      ” Heightened pulse pressure is also a risk factor for the development of atrial fibrillation. The authors of the meta-analysis suggest that this helps to explain the apparent increase in risk sometimes associated with low diastolic pressure, and warn that some medications for high blood pressure may actually increase the pulse pressure and the risk of heart disease.”


      Makes you wonder – if one of these clowns came up with a drug which raised your blood pressure you might be better off.


      1. mikecawdery

        Thanks for that link.
        You probably have spotted the following:
        Every single time we take blood pressure, we can get the patient’s pulse pressure, and while it’s not a perfect index of how stiff the arteries are

        At least gives some idea of what pulse pressure (PP) may indicate (PP = SBP-DBP)

        Your comment re “clowns” is absolutely correct. It is my belief that letting docs anywhere near associative statistics programs has been a disaster.

        Another example of astroturfing and agnotological reporting is in the Lancet
        Supported by AstraZenaca !!!!

        Not a sign of a p value less than 0.3 but still waffle suggesting an effect and a whole lot of missing data, Is “clowns” not highly insulting to real clowns who at least make some people laugh?

        I really and truly despair of what emanates from the medical establishment

      1. Gay Corran

        I certainly did enjoy! Thank you for posting it, Brian Wadsworth. I have a feeling Dr K has also put it before us, either in one of his books, or in a blog. Most interesting. Turns the usual GP advice on its head and gives me a properly researched reason for my refusal to take debilitating BP lowering drugs!

      2. Pat

        Brian Wadsworth
        Thank you very much indeed for this very interesting article which suggests the current medical mantra of putting most of the world and almost all of the elderly on BP lowering drugs should be consigned to the WPB (waste paper basket) just like statins.

        Not sure if (as Dr K suggested earlier) BP was measured in a different more appropriate way whether it would apply. In the meantime this is very useful backup to my skeptical stance. Good for lowering my systolic BP which at almost 130 was deemed to be too high for a 70 year old diabetic!

  44. Pete M

    Could it be the combination of pulse pressure and oxygen saturation? Veins only have to cope with 70% saturation, arteries get 98% or so – except the pulmonary artery where the blood flow is on its way to become saturated…

  45. goransjoberg2015

    Well – everything seems to be at sleep her just now but I guess Malcolm is working hard in the background to soon surprise again.

    Malcolm’s blog one of the best in my world but I have another one, Dr. Mercolas, which is very informative, for me at least, with his numerous interviews with knowledgeable people although I must keep in mind his *vested’ interest in supplement business.

    Now his latest one is two leading researchers on the presumably long time disastrous effects on our energy metabolism where the injuries on our mitochondria seems to be the key component in the understanding.

    Here is how Mercola introduce the interview.

    “Jeffrey Smith interviews Dr. Alex Vasquez, M.D., Ph.D., author of about 100 papers and 15 scientific books, and Stephanie Seneff, Ph.D., a Senior Research Scientist at MIT and author of about 200 papers, about the impact of glyphosate — the active ingredient in Roundup — on your mitochondria.”

    With my current interest in the molecular biology I will most probably acquire the “textbook” on mitochondria by Dr. Alex Vasquez, sounds solid as mentioned in the introduction of the interview. Reminds me of my reading of Thomas Seyfried’s book about cancer, which I also was alerted into by Mercola, but now hopefully Dr. Vasquez’s book doesn’t carry the same price tag.

    We’ll see 🙂

  46. Dr. Göran Sjöberg

    Well – having now watched the full 50 min video I found it to be a real treat by researchers who apparently know what they are talking about. i can for sure recommend it to all who might be interested in the connection between their health and what they put in their mouth.

    Myself, I tend nowadays to go almost 100 % organic and being now even more convinced than before that this could be worth the extra cost involved.

    There are though no guarantees in life for eternal health but always room for improvement.

      1. Dr. Göran Sjöberg

        As previously mentioned I am a little weak for Dr Mercola’s blog and often impressed by his interviews with people offering alternatives to the official medical views where I have lost most of my earlier confidence. Now I got interested in Dr Alex Vasquez and the books he has written.

        Then as you tend to do nowadays i ‘Googled’ on him and what did I find?

        Evidently Dr Alex Vasquez is all on his own with an institute of some kind where there seems to be no other but him. He might be right in what he claims about the importance of the mitochondria and especially about any dysfunction of these important organelles but still I remember how I was led astray by another seemingly serious researcher talking about the dangers with fish oil and with a similar emphasis on the mitochondria.

        Perhaps I am overcautious today 🙂

        But professor Thomas Seyfried and his emphasis on the mitochondria still feels very solid in his alternative view on cancer.

  47. mikecawdery

    Just found the following paper by Dr de Lorgeriil
    Journal of Controversies in Biomedical Research 2015; 1(1):67-92.
    Doi: http://dx.doi.org/10.15586/jcbmr.2015.11
    Review Article
    Beyond Confusion and Controversy,
    Lorgeril – Can We Evaluate the Real Efficacy and Safety of Cholesterol-Lowering with Statins?
    Michel de Lorgeril,1 Mikael Rabaeus2

    In conclusion, this review strongly suggests that statins are not effective for cardiovascular prevention. The studies published before 2005/2006 were probably flawed, and this concerned in particular the safety issue. A complete reassessment is mandatory. Until then, physicians should be aware that the present claims about the efficacy and safety of statins are not evidence based.
    Question: What drugs are based on evidence?

  48. Diana

    Erythrocytes. What a strange phenomenon.

    Budding and direct division of adult human erythrocytes in serum-free cultures (NIIMI, 2009)

    “Adult human erythrocytes have a long lifespan (120 days) despite the absence of a nucleus. Their expansion is generally known to involve enucleation of erythroblasts 1) . However, pioneering works by Emmel (1912, 1914, 1924) 2−4) and Cohen (1982) 5) have suggested a hypothesis based on observations of blood samples from pig embryo and the California salamander, Batrachoseps attenuatus , according to which non-nucleated erythrocytes undergo budding or constriction and direct division. A biography of Emmel was written by Kampmeier (1929) 6) , however, there has been no further research on human erythrocyte budding and direct division to date. In this paper, we confirm and provide evidence lending support to this hypothesis by showing budding of adult human erythro – cytes and direct division following delayed addition of erythropoietin in serum-free cultures. “

  49. John F Graham

    FYI Regards John

    Why January is the month you’re most likely to die: Factors like the chronic chill and genetics cause the year’s highest death tolls, Daily Mail, 19 January 2016


    “Figures from the British Heart Foundation prove that there are significantly more deaths from coronary heart disease during January. Furthermore, a 2012 study by Harvard university shows that levels of bad cholesterol and triglycerides (fats in the blood linked to heart disease) peak in January, and are lowest in summer.

    The reason for this is not yet clear. “

    1. mikecawdery

      Vitamin D levels in blood follow the same pattern – low in winter, high in summer! Another association???

      Epidemiology Vitamin D Deficiency and Risk of Cardiovascular Disease

      Thomas J. Wang, Michael J. Pencina, Sarah L. Booth, Paul F. Jacques, Erik Ingelsson, Katherine Lanier, Emelia J. Benjamin, Ralph B. D’Agostino, Myles Wolf, and Ramachandran S. Vasan

      Circulation. 2008;117:503-511 published online before print January 7 2008, doi:10.1161/CIRCULATIONAHA.107.706127

      Conclusions— Vitamin D deficiency is associated with incident cardiovascular disease. Further clinical and experimental studies may be warranted to determine whether correction of vitamin D deficiency could contribute to the prevention of cardiovascular disease.

      Take your pick. Daily Mail or the AHA journal Circulation.

    2. mikecawdery

      The WHO produced a graph that shows that compares cholesterol levels (BHF-HEARTSTATS) with WHO All cause mortality age standardized per 100,000 (source WHO Mortality ) for various conditiations. This graph showed a series of J-curves. The cholesterol levels with the lowest mortality for three conditions are as follows:
      All Cause mortality 222 mg/dl 5.75 mmol/L
      Non-communicable disease 210 mg/dl 5.49 mmol/L
      Cardiac Disease 208 mg/dl 5.44 mmol/L
      These levels a way higher than the current medically approved target levels

      http://www.heartstats.org/documents/download.asp?nodeib=6797 This URL no longer exists?

      Just another fact that was removed because it did not fit the “gospel”

      Hurray found it again on:

      Click to access cholesterol-mortality-chart.pdf

    3. Craig

      Xmas sugar-starch burden obviously so t.a.g shoot through the roof. If it’s the same here in the Southern hemisphere then you have supporting evidence.


      1. mikecawdery

        Unfortunately the OZ medical establishment seems to be more concerned about lowering cholesterol and flogging sunscreens

  50. Jennifer

    Oh my goodness! For some reason I have not received parts I and II of this most fascinating discussion….I must have dropped off the mailing list for some reason. Anyway…..I will attempt to catch up on all the informative responses, which are great.
    As an aside, I am glad to say that I am now almost 3 years into having given up statins, anti-hypertensives and 3 hypoglycaemic meds, and still doing well.
    This is just in case any of you regulars out there thought I had shuffled off this mortal coil, (having failed to respond as I normally do.)
    Mind you……I have been to the docs over the last few months (over things that needed sorting) ….and strange that no matter what the problem…..the discussion has ALWAYS worked its way round to diabetic control and B/P management, and blood tests, no doubt for cholesterol levels…….Oh and the incessant reminders that I am due a ‘flu jab.
    I fail to see the connections, but maybe I am just academically thick, ( but otherwise physically OK)

    1. John

      Hi, how did you manage to give up the bp meds. Did you wean yourself off them slowly. Did you have any problems when you stopped. I stopped but started to have a racing heart and blood pressure went really high.

  51. leigh

    Astounding and miraculous benefits of statins have now come to light. It has just been discovered that statins can cure the most common form of blindness, as well as reduce cholesterol levels! I suppose Big Pharma will soon espouse and exploit its usefullness of allowing mere mortals to walk on water. A Jesus drug, if you will. Bet it can’t get Liverpool FC to start scoring goals though……

      1. Dr. Göran Sjöberg

        This coincides with my present belief that the sympathetic/parasympathetic balance, or rather out of balance, is here very important and where the parasympathetic activity seems to be very close to zero, as measured by the heart rate variability, often at four o’clock in the morning, and minutes before an acute heart attack.

        I have in vain tried to understand how this external autonomous balance actually connect with the internal heart nerve system and was anticipating a meeting and a talk with a heart surgeon who had produced a doctoral theses “Atrial Fibrillation in Cardiac Surgery” with the hope of some clarification. To my utter amazement he did not have the faintest idea of what I was talking about and when I brought out a scientific paper about the subject to discuss and have his comments on he seemed to look the other way.

        Then I dropped the subject since it was a common friend who had brought us together. The heart surgeon had probably been misled by my friend and thought that I was trying to get a speedy connection to a by-pass after having refused for 15 years.

  52. jaxthefirst

    “Waking/getting up in the morning.”

    Are you serious about that, Dr K? Honestly? How can something that pretty much everyone – with the exception of some night workers, some of the very rich and some of the very poor – do, be considered a “risk” factor? It’s pretty unpleasant, true, but virtually everyone has to do it, so surely there aren’t enough people who don’t to form a sufficient number to make a meaningful comparison to the people who do? Has there ever been a study into it, and if so, why didn’t it make headlines? Thousands of people would have given up working in an instant, with the excuse that “it’s better for my health”!! Isn’t it a bit like saying “sleeping at night” or “eating bread” or “watching any television at all” is also a risk factor?

  53. Rachel R

    Since Malcolm is keeping us hanging, I have little to do but keep adding to my buzzword bingo card. Had some blood tests recently to investigate B12 deficiency, and as an incidental finding I discovered yesterday that I have a transferrin saturation of 58%, apparently that’s not terribly normal. Or good.
    So I’m adding in “iron-mediated oxidation” because, well, no reason. For fun.
    Don’t keep us waiting too long Malcolm, my card is getting full, and my suggestions more ridiculous.

    1. David Bailey

      I got B12 deficiency because statin pain resulted in my taking diclofenac, which also raises stomach acid, so I was given omeprazole, which lowers the acidity so much that B12 can’t be absorbed! It is called poly-pharmacy! The whole thing came to light after I’d dropped the statins for some months, and no longer needed the diclofenac, and hence didn’t need the omeprazole. I read about low stomach acid and B12 absorption, so I asked for a re-test. Otherwise I would have been on B12 injections for life!

      I just wonder if any of that relates to your situation.


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