Cholesterol is innocent. How the real killers were tracked down

By Jerome Burne

A murder mystery often begins with what seems like an open and shut case – woman alone in the room, gun in hand body on the floor. She’s guilty, bang to rights. This is how the so-called ‘Cholesterol Hypothesis’ has always been presented. Cholesterol is found in the plaque that blocks arteries. So – less cholesterol, less plaque, less heart disease. QED.

However, as Dr Malcolm Kendrick pokes into the details, the apparently watertight case begins to unravel. Maybe there is a more plausible explanation. Uncovering it has led our detective hero to declare cholesterol innocent. 

This is, of course, a serious challenge to the cholesterol-lowering statin industry and all those who work in it. A U-turn would be seriously embarrassing for healthcare professionals as statins are the world’s best-selling drug, routinely recommended to everyone in the UK from 55- 60 years old for the rest of their lives. 

So what does cause heart disease?

Dr Kendrick, an independent-minded GP from Macclesfield in Cheshire, is one of the most persistent and best-informed critics of the statin story – you know, the one where lowering cholesterol saves lives. For decades, Dr Kendrick has been pointing out that the splendid cloak of evidence-based medicine worn by statins and the cholesterol hypothesis is a patched and threadbare thing, not fit for purpose. 

While Dr Kendrick has gathered an impressive following of patients and doctors who share his concerns, many would be hard pushed to summarise his response to the key question: if the villain is not raised cholesterol, what does cause heart disease? 

It’s not really surprising since, over the last few years, Dr Kendrick has been exploring this whodunnit in a series of fascinating and deeply knowledgeable on-going blog posts – which now number 65… 

Dr Kendrick’s investigation provides the basis for a biochemical detective story that starts at the crime scene – a corpse with a wodge of stuff blocking one or more arteries. How did it get there and why? What follows is my heavily condensed retelling of the story of Dr Kendrick’s painstaking investigation, as told originally in an interview with blogger and health activist Ivor Cummings, recently posted on his website.  

Causes come in two varieties

Dr Kendrick reveals that his attempt to crack the clot mystery started in medical school. ’When I was at Aberdeen University in 1982, one of my teachers remarked gnomically that “LDL cannot cross the endothelium”. I had no idea what she was talking about; I’d never heard of the endothelium, although I vaguely knew what LDL was. I felt like I’d been told a secret, which in a way I had.’ 

Just to clarify: LDL (Low-Density Lipoprotein) is the transporter made of fat that carries cholesterol around the body. Statins lower LDL cholesterol levels by reducing cholesterol production in the liver.

Dr Kendrick begins by setting out the basic principle of his investigation. There’s no soundbite answer to the question ‘what is the cause?’ because it’s clear to him that heart disease is a process, like developing rheumatism, rather than an infectious disease like tuberculosis, which really is an open and shut case. In that case, there is a single cause – the tuberculosis bacterium. No bacterium, no tuberculosis. 

But, in medical detective stories like this, finding the cause is half the battle. There are usually two criteria for causation: 1) ‘necessary’ – no condition without it; and 2) ‘sufficient’ – if you have it you will get the condition. With tuberculosis, the bacterium supplies both. You have to have the bacterium to get the disease so it’s ‘necessary’, and just having the bacterium is ‘sufficient’. 

Many of the factors described as ‘causing’ heart disease, however, are neither necessary nor sufficient, such as smoking or air pollution, although stopping either or both will reduce your risk. Raised cholesterol is also not necessary or sufficient – in fact, some big Japanese studies have found that older people with higher cholesterol actually live longer.

Damage to the arteries is where it all begins

Kendrick realised to get a fix on what was actually happening in a heart attack he would have to identify one or more conditions that were sufficient to cause it without any other risk factors being involved. In fact, he found two, albeit pretty obscure conditions.

One is sickle cell disease, in which blood cells become sickle-shaped with pointy ends, making them sharp and abrasive. ‘It’s like putting sandpaper into your blood,’ says Kendrick. The other is Kawasaki disease, which involves severe but temporary inflammation of the arteries. Although it runs its course within a few weeks, the blocked arteries sometimes swell and burst. 

Here were leads he could work with. Could it be that for a heart attack to happen there has to be some sort of damage to the arterial wall? The best-known condition that does this is high blood pressure. ‘This puts biomechanical stress on arteries,’ he says, ‘especially in areas of localised turbulence such as junctions, where atherosclerosis (plaques) is more likely to develop.’ 

The next key question was: ‘What exactly happens when the walls of the artery are put under stress or damaged?’ The answer to this would form the backbone of his hypothesis – an alternative to pinning the blame on cholesterol. 

From his intensive investigations, Dr Kendrick concluded that damage to the inner lining of the artery wall, known as the endothelium, is necessary for a heart attack. 

It’s in this protective layer, which is inside every artery, where much of the action that ultimately helps or hinders heart disease takes place, he believes. But few doctors consider what’s happening in the endothelium when diagnosing heart disease – and few patients would ask.

How can the endothelium be protected?

Establishing this theory promises a new direction for heart protection where researchers investigate the factors that help to protect the endothelium and those that damage it. 

Significantly, none of the substances or events that damage the endothelium involves LDL cholesterol. Cigarettes, for instance, damage it via the microparticles they contain but the body can recover by releasing a type of cell, called the ‘endothelial progenitor cell’, which repairs the damage. Raised levels of the amino acid homocysteine – linked with both heart disease and Alzheimer’s – are also harmful. So too are the raised levels of glucose and insulin that come with diabetes. 

Age is certainly a risk factor simply because all processes like repair or renewal slow down. We can’t yet physically turn back the clock, but you can do things to reduce the harm from the disorders that come with it, such as controlling diabetes via a low carb diet. Saturated fat, however, like cholesterol, doesn’t affect the endothelium, according to Dr Kendrick.   

Having identified the importance of the endothelium, Dr Kendrick began interrogating the literature to discover more and found something vital to its protection – the glycocalyx. This is the super-slippery coating that makes it hard to hold a live fish and also coats the endothelium.

A thick endothelium has several beneficial effects including expanding blood vessels, which is good for reducing blood pressure and reducing clotting (but not too much) as well as increasing the production of the endothelial progenitor cells for repair. Interestingly, another heart-harming effect of diabetes is that it can reduce the thickness of your glycocalyx covering.

The magic of nitric oxide – a must-have for heart protection

Possibly the most important heart-protective effect of the glycocalyx is that it releases an enzyme that produces nitric oxide, which is responsible for many of these beneficial effects.

The triggers for nitric oxide release include exercise and sunlight also, interestingly, Viagra. Being unable to get an erection can be a sign you are not producing enough nitric oxide. Curious fact: statins also slightly raise nitric oxide.

Drugs that lower nitric oxide includes the widely prescribed PPI inhibitors, which have names ending ‘-sole’, such as Omeprazole. 

The EndoT theory

Kendrick’s hypothesis, which might be termed the ‘EndoT theory’, proposes a much wider range of factors that are capable of raising or lowering your risk of heart disease. It could also explain why factors such as lead and air pollution cause heart disease as both damage the endothelium. Conversely, the cholesterol hypothesis can’t explain this. 

EndoT can also explain the mystery of why a class of blood pressure pills called ACE inhibitors are more effective at cutting heart disease than other drugs with the same action.  No surprise; they increase nitric oxide production. 

Here’s the new takeaway message

By now the medical detective has constructed a new and convincing theory of heart disease that has major implications for treatment. The slow build-up of the condition starts with damage to the artery lining. A new class of attackers and defenders, some familiar others less so, have emerged. 

The challenge now facing the medical Sherlock is explaining away the familiar components of the cholesterol hypothesis. A keen supporter might argue that simply listing factors that increase the risk is all very well but it doesn’t do away with the main issue: the plaques filled with fat (lipids) and cholesterol that block arteries.

At this point, Kendrick pulls off a classic detective story twist – the demonisation of cholesterol is a case of mistaken identity. But before revealing it, let’s have a flashback to show how the mistake arose. 

The endothelium springs a leak, maybe due to blood pressure or glucose damage. The clotting mechanism swings into action. The dangerous hole in the artery wall is rapidly closed with platelets and strands of fibrinogen, along with other ingredients from the bloodstream such as bits of the LDL transporters and red blood cells.

But unlike the scab over a wound on your outside, this clot on the endothelium can’t just drop off. Instead, the endothelium absorbs it by signalling to the progenitor cells to set about providing the raw material that allows the endothelium to envelop the clot/plaque. That results in the plaque getting inside the covering of the artery wall.

The case of mistaken identity

This takes us back to the gnomic comment by one of Dr Kendrick’s teachers about LDL cholesterol not being able to be part of the artery wall. ‘Later I found she had been working on all the stuff I’ve been burrowing into’ – a theory that heart disease is about blood clotting on the artery walls due to damage there. The fact that it’s still pretty much a secret nearly 40 years later should be a major scandal.’

This is where Dr Kendrick reveals Poirot-style how the case of mistaken identity works.  He’s been to forensics where the clot has been put under the spotlight and come back with data that overturns the cholesterol hypothesis. 

The clots/plaque that cause atherosclerosis don’t contain what everybody assumed. 

For decades when researchers analysed the clots they found both cholesterol and lipoprotein; exactly what you would expect if LDL cholesterol was too high and some of it was swept into a clot as if it was forming. 

But forensics, or rather Kendrick’s relentless biochemical research, said otherwise. ‘The type of LDL cholesterol in plaques isn’t the soft waxy stuff people expect it to be,’ he explains. ‘It comes in the form of cholesterol crystals. And such crystals can’t be made from the lipid cholesterol combination that makes up LDL.’ 

The crystals of cholesterol 

These crystals aren’t something your doctor is likely to tell you about as they are fairly obscure but various bodily compounds can turn into crystals. The best known are the crystals of uric acid that cause the pain of gout. So, where do these crystals come from?

‘The only sort of cholesterol that does turn into crystals,’ explains Dr Kendrick. ‘is pure cholesterol. This is found in red blood cells because it is essential to the structure of the wall of these cells, which are found in plaque clots because they are a key part of the clotting process.’ So the cholesterol in plaque, far from being the cause of a blockage, is just part of normal clot ingredients. 

But what about the lipoprotein transporters that have also been identified in clots for many years? 

‘Wrong again!’ says our medical Poirot. ‘LDL has a twin called lipoprotein (a) – or Lp(a). It’s exactly the same as the lipoprotein in regular LDL but with the tell-tale protein (a) attached. However, if you are a researcher looking for regular lipoprotein, you’ll think you’ve found that unless you’ve also checked for the (a) protein, which is rarely done.’ 

So, where has Lp(a) come from and what’s it doing in the clot?  

Two decades ago, the late double Nobel Prize winner Professor Linus Pauling identified Lp(a) as a useful member of the endothelium protection squad. During his long research into vitamin C, Professor Pauling found that vitamin C deficiency is another cause of damage to the endothelium.  When people are seriously deficient – as in scurvy – the damage can cause them to bleed to death. )

So Lp(a) far from being a villain is something else helping to limit damage to the endothelium.

What to do now?

Since many people are sub-clinically deficient in vitamin C supplementing may be a good idea. And there are two more supplements you might consider: L-carnitine and L-arginine, which are both amino acids needed for the production of nitric oxide.

And in the future…

Hopefully, research can now start to tell us which drugs are likely to be damaging or beneficial and what lifestyle shifts might also be effective.

Jerome Burne

Jerome Burne

Jerome Burne is the editor of HealthInsightUK. He is an award-winning journalist who has been specialising in medicine and health for the last 10 years and now works mainly for the Daily Mail. His most recent book “The Hybrid Diet” was written with nutritionist Patrick Holford, published 2018. Award: 2015: Finalist for 'Blogger of the Year' Medical Journalists' Association.

33 Comments

  • Excellent article – the Statin Lobby is so powerful that unfortunately the General Public are unable to reverse their long held belief that Statins prevent heart disease. GP’s are committing a ‘crime against humanity’ if they prescribe Statins to any patient – regardless of their age. Stains interfere with the normal functioning of the liver, we call this process “meddling with the primal forces of Nature”. Yes, Statins are the number one selling drug world-wide, but sadly that will remain so for decades to come. Big Pharma controls Government thinking and that’s a fact.

    • Editorial

      Thanks. The hostility and threats directed at those challenging the cholesterol hypothesis do suggest that Evidence Based Medicine (EBM) has failed as a rational way of deciding what works. At one time non-drug treatments were routinely dismissed as signs of the coming “endarkenment”. Ironically the EBM supporters now seem to be hurrying towards “endarkenment” very fast, describing disagreementabout the benefits of any officially approved medicines in ways that seem indistinguishable from heresy.

      • Like climate change………..policy based evidence making in action.

      • EBM fails all sufferers from hypothyroidism and all those ‘new’ diseases like CFS, ME and fibromyalgia.
        The idea that the only evidence that an be considered is the randomised, double-blind control trial is ridiculous and definitely not science!
        Absence of evidence is not evidence of absence!

    • Can I also add though when many GPs are approached with any questions re Statins they refuse to accept any hypothesis but their own. I’ve stopped stains but my GPs still query every time I see them. I did have side effects but didn’t realise they were due to the statins until I stopped (after possible 8 years taking.) Fortunately my main GP is happy(ish) but even she mutters we will reconsider in a few years. I did have a probable TIA so I do get their concern. As my blood pressure is low they “allow” me not to have statins but pressure will come. I think you’ll find many members of the public are more savvy than thought but GPs have all the power and scare tactics.

  • In the era prior to about 600 million years ago it is unlikely that cholesterol even existed. However other members from the family of sterols would have been in existence by that time but these would have been confined to examples of phytosterols (ones synthesised by plants) and mycosterols (ones synthesised by fungi).

    Synthesis of the first ever molecule of cholesterol probably arose because of genetic mutation of the sort that has driven evolution in general. It would have quite normal for a particular organism (likely a member of the family of fungi) to synthesise one or of the sterols from the group termed mycosterols but a mutation of a key gene(s) resulted in change to an particular enzyme. This mutation will have had consequence for synthesis and instead of producing the mycosterol (such as ergosterol, perhaps) the mutation resulted in synthesis of cholesterol in its place.

    Cholesterol altered the trajectory of evolution; it opened up an entire new bough along which the tree of life could develop. By paving the way for a radical new type of membrane for cells cholesterol paved the way for the further evolution of cells. Cells could begin trending to the assortment of cell types we can observe in animals today. Put simply, without cholesterol’s entry into the chemistry set of life approaching the order of 600 billion years ago then animals simply would not be possible.

    It is worth sparing a thought for the Cambrian explosion that began around 540 million years ago. The period is one where the fossil record shows unprecedented growth in the numbers and diversity of phylogeny (mew species), a high proportion of which were creatures the like of which had not existed before. Was it the radical new cell membranes that resulted from a structural alliance of cholesterol and phospholipids that spawned the Cambrian explosion?

  • I’m a great fan of Kendrick. But does his tale satisfy what seems to me to be an absolute requirement: is it consistent with the sudden rise and sudden fall of heart attacks in middle-aged people? The peak was in the 60s and 70s. The decline set in before diet propaganda could have had had any effect, and before the widespread decline in smoking.

    Heart attacks are now mainly one of the bumpers-off of old folk. But not so long ago they mowed down (mainly) men during their working lives, leaving behind, often enough, a widow with schoolchildren still at home.

    If his proposition can explain this pattern, fine. If not, then More Work Required.

    • Editorial

      The rise of heart disease in the fifties and subsequent decline is a long running puzzle – journalist medic Dr James Le Fanu sugested that the pattern matched an infection. Certainly the pattern is not explained by a rise in fat consumption and the decline began long before the arrival of statins. So I think it bit hard to dismiss it out of hand when it provides an explanation for a number of other puzzling causes, such as lead and PPIs and suggests factors that increase benefit – deliberately raising nitric oxide.
      However this blog is only a surface skim and Kendrick does suggest one possible explanation – smog. It was very heavy in the 50′s (I’ve no idea if it was worse than in previous decades) and he does identify particles that create smog as damaging to the endothelium, and then clean air act blew the smog away. The full version may have more on that.

    • I too am a fan of Dr Kendrick and I’ve read all his books since you recommended him to me when I was bemoaning the continued delay of Ben Goldacre’s Do Statins Work book. Thank you for that.
      I think this article is a fair summary of Dr Kendrick’s published work. For a more in depth understanding I would recommend his last book, A Statin Nation.
      I agree though that more open minded research is required to fully understand the causes of CVD. However, I am satisfied that cholesterol is not a significant factor.

    • As a long time reader of Dr. Kendrick’s posts and books, I believe he may have attributed the spike of heart attacks in the ’60s and ’70s to the stress/strain caused by WWII, 20-30 years preceding. The “heart attack” is the last step in a decades long progressive assault on the endothelium.

      I believe Dr. Kendrick has also noted that “heart attacks” spike in the decades following forced migrations, which cause a tremendous stress/strain on these unfortunate peoples, regardless of their cholesterol levels.

    • Some of Malcoms blogs covered “stress” on national levels across Europe through the latter half of the 20th Century. National stress included – recession, regime change/national instability etc.
      There he found more consistency with rates of CVD levels than with diets and other risk factors.
      Perhaps that is a crucial piece of the puzzle – I cant remember the details (i.e. what blog number etc)

      • Editorial

        Absolutely – Malcolm has long pointed out links between stress and heart disease -I didn’t include it becasue i didn’t have space. Hoping a fuller version of his HDH (heart disease hypothesis) will soon be available

    • There is always More Work Required. This is just the nature of complex systems. Understanding them takes time. Lots of time.

      Dr Kendrick’s thesis is that anything which damages your arterial endothelium is a risk factor for heart disease and / or stroke. And if the damage exceeds the repair process, you will at some point suffer an “event”, whether major or minor.

      One of the many, many things which can damage the endothelium is infection, whether from viruses or bacteria. There is also the immune response to the infection to be considered. There is a line of thinking which suggests the CVD epidemic which peaked in the late 1960′s, was triggered by the 1918 Spanish flu epidemic.

      https://www.ncbi.nlm.nih.gov/pmc/articles/PMC387427/

      To my mind, this is a plausible hypothesis. People who were middle-aged when the heart disease epidemic peaked were people who were quite young during the 1918 epidemic. As more people are born following the epidemic, there is a drop-off in CVD mortality following the peak.

      One problem with the paper is that it uses CVD mortality instead of incidence, which I think woud be a better guage. But, I find the concept compelling and consistent with Dr Kendrick’s hypothesis.

  • Great summary of the issue. Now the big challenge is to have it grasped and understood by the masses of medical professionals.

  • My travel insurers are asking if I have ever refused Statins. Well I had tried them and they didn’t suit me so I have refused them ever since. Do I deserve to be penalised? I was told my colesterol was slightly raised.

    • My GP wanted me to take statins even though my cholesterol readings were low and had been for quarter of a century. When I protested he said “they can never be too low”. Blithering idiot!

      • That made me chuckle. It reminded me of the quote from Jack Bogle,”It’s amazing how difficult it is for a man to understand something if he’s paid a small fortune not to understand it.” I understand that GP’s have financial targets to enlist patients on Statin treatment.

        • In one of his most recent posts Dr Kendrick indicated that lead, the metal, damages the endothelium. The mid 1900s There was a tremendous amount of lead in the environment from the use of leaded gasoline. That has been reduced dramatically in recent years. Maybe that’s why the “peak” was in the 60′s and 70′s.

        • My doctor prescribed a statin and I just let his so he would feel better. After I left I just threw the prescription away.

    • Sounds like the pharma crowd has been talking to the insurers. Just another nasty little trick to pressure us with their lies.

  • Excellent summary of a complex subject. I believe the statin protagonists have been blinded by their insistence of putting two and two together but making five. Yes – statins reduce cardiac risk, though not a lot. Yes, statins lower cholesterol. But that does not necessarily mean that statins work by lowering cholesterol. A results in c, B results in C, but B need not result in C.

    Many years ago I was puzzled by an oxymoron. Rheumatoid arthritis resulted in an increased risk of coronary artery disease. Successfully treat it, and the cardiac risk returns to normal. But cholesterol goes up. More recently drugs such as evolucumab have been found to lower cholesterol substantially, but without any change in cardiac risk. These two taken together make it impossible for cholesterol to be related to cardiac risk. How can risk reduce in the former case, yet cholesterol rises? How can you cause a dramatic lowering of cholesterol but not get a similarly dramatic fall in cardiac risk? The answer is simple – something else is involved. And given that rheumatoid arthritis (and other connective tissue disorders such as lupus and vasculitis) have a high risk it becomes likely that it’s blood vessel inflammation that is the prime problem, and as Malcolm Kendrick suggests the deposition of cholesterol in arterial plaques represents a secondary phenomenon. So, the statin apologists ask, how is it that statins reduce cardiac risk? Because they are anti-inflammatory! Not a lot, of course – which is why they don’t, in fact, work very well if you examine absolute rather than relative risk reduction – something the apologists won’t do for efficacy (because it ruins their “wonderful” results) but do for side-effects, because it makes the figures look much better.

    Statins are a con. Researchers need to redirect their efforts, and understand that incontrovertible facts which don’t fit with the cholesterol hypothesis mean that the hypothesis must be wrong.

  • Many thanks for this very interesting article. One small point, you mention early in the piece that “LDL is a transporter made of fat…”. I understand that the transportation molecule is a lipoprotein, which transports, among other things, cholesterol and fat.

  • Thank you for the article. The knowledge base of the responses here is beyond any contribution I can make to this debate, but I am just so pleased to have found Dr Kendrick’s Blogg and now this one Health Inight.
    When my cadioligist doubled my statin dose after I managed to reduce my cholesterol from 5.8 to 2.9, I asked her if cholesterol could go to low? She echoed a comment here, “No, it can’t be low enough”.
    This started a long journey of doubt and confusion.
    I didn’t realise how much we were being manipulated into accepting suspect medical treatment. Thank you for shining a light into dark corners.

    • I have read research that has linked very low cholesterol levels with an increased risk of suicide. Any truth in this?

      • Editorial

        Can’t give a defintive response, but it wouldn’t be surprising. Drastically lowering levels of any of the many vital compounds in our system could be expected to have knock-on effects; there is lots of cholesterol in the brain.
        The suicide risk surfaced at least a couple of decades ago.
        More recently, the new, even-more-effective, son-of-statin drugs known as PCSK9 (eg Repatha (evolocumab) rammed cholesterol even further down. However despite lots of studies, the companies could never find one that showeed longer survival. Question would be did they keep data on enough patients to detect changes in suicide rates?

  • Thank you for this excellent summary. I have read Dr Kendrick’s excellent work. I believe he does also factor in stress though of course this in itself is tricky. Everyone reacts differently to stress. Cholesterol and the obsession with high carb low fat medical advice have much in common. Someone decides something and it becomes “fact”. The untold damage from that advice is only now being seriously recognised. Anyone who queries the current “accepted” truth is demonised.

  • I read this following Dr Kendrick’s recommendation in his blog. I appreciated this summary of Dr K’s ongoing thesis on what causes heart disease, which I am following. Very clear and understandable to those of us with only a little knowledge. Thank you.

  • Despite it is a reasonably concise and clear summary of some matters there exists one significant error in what you have reported.

    The glycocalyx is not super-slippery. EZ water, however, can be very slippery.

    EZ water is strong in two dimensions but virtually friction-less in the third dimension. One of the functions of the glycocalyx is to promote the formation of EZ water in the zone immediately proximate to it.

    A net curtain analogy can convey a basic principle. Imagine you just laundered a houseful of net curtains. Now that they’re dry you fold one, and then another, and so on. As you go you stack them in what you hope will be a neat pile. But net curtains are not towels. Folded and stacked towels resist rule of entropy Folded and and stacked net curtains simply do not want to remain neatly stacked. The curtains are strong in the X and Y dimensions but offer no resistance to shear between the layers (the Z dimension).

    Everybody will have had an encounter with EZ water but next to nobody will know that they have.

    When lessor forms of life colonise a timber deck they render the deck exceedingly simply — but crucially only when wet. Clean the deck and the deck can be wetted againb but isn’t so slippery when wet. The explanation? the blanket of algae that has coloniosed the surface of the timber deck has tiny molecules called glycoproteins sprouting from each of the cells of the algae, many of them, and togther these reult in something that can be lkikened to a glycocalyx.

    When you step on an aged dry deck you are really stepping on the low-lifes and not the timbers. When you step on a wet deck you are really stepping on a thin blanket of EZ water that sits just above the blanket of algae that grows upon the deck. When you step on a clean but wet deck you actually step on a thin film of regular water.

    When all is tickety-boo the membarnes of the cells of the endothelial have healthy ‘colonies’ of glycoporteins stemming from them and these promote a healthy blanket of EZ water. The EZ water protects from shear stress.

    Thus Dr Kendrcks thrombogenic hypothesis hasn’t quite yet evolved into something that is complete. It needs an adjunct. It needs to address how the EZ zone can be eroded and under what conditions.

    Parties including Steff Seneff had looked into erosion of the glycocalyx and waht they say is interesting and correct, to a point, perhaps. But I think cognitive steps can be taken in additional directions because to coin one of their terms, the process of EZ demise could be pluricausal.

    • Editorial

      Fascinating comment. Sent to Malcolm who was very interested. Can put you in touch – all very much above my pay grade. Is place on the site where you can message me

      • “. . . all very much above my pay grade.”

        I think you will find that my “pay grade” is beneath you own, Jerome, and though I am in receipt of of a wage it has nothing to do with my health and biology related inquiries.

        In the comment are terms would bear fruit if inserted into search engines. There exists no reason at all why the propositions should remain above your pay grade.

        Malcolm Kendrick has spent many hours pondering aspects of CVD. He considers raised blood pressure one of the more reliable risk factors. I am sure he has indicated his trust in raised pressure, flow, and increased shear stress resulting in damage to the endothelium. With a healthy glycocalyx and a healthy blanket of EZ, so an unassuming (and super-slippery) footbridge once informed me, there would be next to no shear stresses bearing upon endothelial cells — however that is a very early hypothesis whose propositions require more work to bolster them.

        Diminish the EZ or undermine the fortitude of the glycocalyx and shear stress (friction) would rise just as with a lumber deck when you jet away the algae.

        • Editorial

          Christopher hi – not clear why you apparently object to my use of a pretty standard metaphorical phrase, which means not knowing enough to answer or comment usefully on something. It has nothing to do with actual pay. More specifically it means that i am not an academic researcher, I am a journalist who is able to summarise research and present it in an accessible way to other non-specialists – the people my blog is aimed at. You had supplied a very well informed and useful comment which i passed on since i was in no position to make a response.

          Also find puzzling your suggestion that i could use google to find out more. I obviously know this but i don’t need to know more. I’m the messenger here. It is above my metaphorical pay grade to plunge into this meaphorical rabbit hole. That’s the place for you and Malcolm bounce around ideas. If you come up with a new formulation that would be relevant to interested non-speicalists, I’d be happy to report on it too.

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