What causes heart disease – part thirty one (XXXI)

243 Replies

What is the final event?

(The upside down*)

The final event in most heart attacks, and strokes, is the development of a large, and often fatal, blood clot. If this happens in an artery in the heart, a coronary artery, it cuts off blood supply to an area of heart muscle and can lead to a myocardial infarction (MI) [myocardium = heart muscle, infarction = death of tissue due to lack of oxygen].

There is a related, but different mechanism of action, in most, strokes. In this case a blood clot that has formed in an artery in the neck (carotid artery), breaks off and travels to the brain where it gets stuck, blocking an artery. This leads to a cerebral infarction. There are other forms of stroke, with other causes, but this is the most common.

These are generally accepted models, and for the sake of brevity, it is also the model I am using here. Although I accept that it is not that simple. For example, you can have an MI with no blood clot found. Here, from a paper entitled: ‘Acute myocardial infarction with no obstructive coronary atherosclerosis: mechanisms and management’:

‘Myocardial infarction (MI) with no obstructive coronary atherosclerosis (MINOCA) is a syndrome with different causes. Its prevalence ranges between 5 and 25% of all MIs.’1

A heart attack with no blood clot. In truth, I think this can be easily explained, within the ‘obstructive’ model, but it would take too long for this blog. I will cover it at some point.

Anyway, to get back on track. It is generally accepted that the final event in cardiovascular disease is the formation of a large blood clot. This is the thing that causes both fatal, and non-fatal, strokes and heart attacks. Which is why atherosclerosis, as a disease, is often referred to as atherothrombosis. The idea being that atherosclerotic plaques gradually build up, over decades. In the final stage, the plaque ‘ruptures’ triggering the formation of a large and deadly clot.

The suggestion here, never ever explicitly stated, is that we have two different processes in operation. Plaque formation, then the blood clot. Or maybe you could look at this as one process, in two parts. Plaque growth, then plaque rupture – causing thrombus formation.

However, it is perfectly possible for thrombi to form with no underlying plaque, so the two processes need not be associated with each other. People with Hughes’ syndrome, for example, can die of strokes and heart attacks quite suddenly, caused by blood clots, with no plaque to be seen. [Hughes syndrome causes the blood to be highly likely to clot – hypercoagulable].

Which leaves the question hanging somewhat. Do we have one process – or two? I believe that the main reason for using the term atherothrombosis, is because this allows mainstream thinking to draw everything together as different manifestations of the same underlying process. Raised cholesterol causes plaques, these rupture, then a clot develops (which would not have formed had the plaque not been there). This allows clear wiggle room, but at some point you must decide, one process or two. This is not quantum physics.

In my world, it is far simpler. There is only one process. Atherosclerotic plaque are simply blood clots, in various stages of growth and/or repair. Plaque growth represents the formation of a new blood clot, at the same point, which is not cleared away properly. The final ‘thrombotic’ event is just a big enough clot forming to do real damage.

The first time I started to think about this seriously, was when I was reading a paper called ‘A Definition of Advanced Types of Atherosclerotic Lesions and a Histological Classification of Atherosclerosis. A Report From the Committee on Vascular Lesions of the Council on Arteriosclerosis, American Heart Association.’ The things I do for fun … clearly, I am just a geek.

Anyway, this paper rambled on and on, and on. Until, whilst propping my eyelids open, my interest suddenly sharpened as I came across the section on the definition of Type V(a) atherosclerotic plaques – don’t ask. For those who enjoy a bit of scientific jargon, here it comes. If you don’t care for jargon, just look at the text I have put in bold at the end.

‘Sequential histological studies of the lesions of large populations indicate that reparative connective tissue forms in and around regions of the intima in which large accumulations of extracellular lipid (lipid cores) disarrange or obliterate the normal cell and intercellular matrix structure. Sometimes the new fibrous tissue accounts for more of the thickness of the lesion than does the underlying lipid accumulation.

The new tissue consists of substantial increases in collagen and smooth muscle cells rich in rough-surfaced endoplasmic reticulum. In cases in which this tissue is particularly thick, some or much of it may be the remnant of thrombi that were incorporated and organized. Capillaries at the margins of the lipid core may be larger and more numerous than in type IV lesions, and they may also be present in the newly formed tissue. Lymphocytes, monocyte-macrophages, and plasma cells are frequently associated with the capillaries, and microhemorrhages may be present around them.

Type Va lesions may be multilayered: several lipid cores, separated by thick layers of fibrous connective tissue, are stacked irregularly one above the other. The term multilayered fibroatheroma can be applied to this morphology. The lipid core that is deepest and closest to the media may have formed first. Mechanical forces may play a role in the modeling of such lesions.

Additional lipid cores in locations and planes different from the first could be induced as asymmetric vascular narrowing and changes in lumen configuration modify hemodynamic and tensile forces, creating a redistribution of the regions of predisposition for lesion formation.

The architecture of some multilayered fibroatheromas could also be explained by repeated disruptions of the lesion surface, hematomas, and thrombotic deposits. Organization (fibrosis) of hematomas and thrombi could be followed by renewed accumulation of macrophage foam cells and extracellular lipid between the newly formed fibrotic layer and the endothelial surface.’ 2

In layman’s terms what does it mean? It means that a number of plaques look exactly as if they were created by the repeated formation of blood clots, one on top of another. A concept further reinforced, when the paper looked again at thrombosis.

‘Thrombosis

‘It has been reported that advanced atherosclerotic lesions containing thrombi or the remnants of thrombi are frequent from the fourth decade of life on. In 1975 Chandler and Pope compiled and reviewed studies that reported the frequency and nature of lesions with incorporated thrombi.

In a recent study of a population aged 30 to 59 years, 38% of persons with advanced lesions in the aorta had thrombi on the surface of a lesion. These thrombi ranged in size from minimal (microscopic) to grossly visible deposits, and some consisted of stratified layers of different ages. Immunohistochemistry revealed wavy bandlike deposits related to fibrin within the advanced lesions of an additional 29% of persons. Because of their structure, these were thought to represent the remnants of old thrombi. Similar data were reported by other authors.

The fissures and hematomas that underlie thrombotic deposits in many cases may recur, and small thrombi may reform many times. Repeated incorporation of small recurrent hematomas and thrombi into a lesion over months or years contributes to gradual narrowing of the arterial lumen. Some thrombi continue to enlarge and occlude the lumen of a medium-sized artery within hours or days.’

Perhaps the key sentence here, from my point of view, is the following:

‘Repeated incorporation of small recurrent hematomas and thrombi into a lesion over months or years contributes to gradual narrowing of the arterial lumen.’

Here, right here, is proof of the concept that plaques definitely do grow through repeated thrombus formation at the same point on the artery. Do all plaques do this? My own belief is that they do, but in many cases the repair mechanisms and other factors disrupt a clear picture of layered plaque growth. Essentially, the core of the plaque turns into mush (known as a lipid core) which obliterates evidence of how the plaque actually grew.

What else supports the idea that plaques are, in reality, blood clots? Well, very early on in their development, rather than in the third or fourth decades of life, you can find high levels of fibrin and fibrinogen, which are key components of blood clots. Here from a paper ‘Lipids and plasma fibrinogen: early and late composition of the atherosclerotic plaque.’

‘The precursor of large fibrous plaques appears to be the gelatinous lesion, which is characterized by oedema, accumulation of large amounts of low density lipoproteins and fibrinogen in the expanded interstitial fluid space, deposition of fibrin, and smooth muscle cell proliferation. It is postulated that deposition of fibrin may be a key event, stimulating smooth muscle cell proliferation by providing a scaffold for migration, a source of fibrin degradation products which are mitogenic, and binding thrombin. Fibrin may also be a factor in lipid accumulation because it binds lipoprotein (a) with high affinity, and may also bind low density lipoprotein.’3

In short, early plaques contain a lot of fibrin (key component of a blood clot), also lipoprotein (a), which is LDL with a different protein attached. Fibrin binds to Lp(a) forming very stable, and difficult to remove, blood clots. So, it is not just in type V(a) plaques that we find evidence of blood clotting. We find it very early on as well.

Sorry, If I am getting a bit jargonified at this point – if that is indeed a word. But I am aware that some highly trained scientific people do cast their eyes over this blog, and I do not want to make this too broad brush. Also, here, I am discussing the very core of my ideas about CVD, and I want to be as accurate as I can be. Equally, I do not want to put people off by delving too deep.

So, at this point, I shall only look at one more highly scientific study, which I think is important. One of the things I always tend to do, is to look at extremes. By which I mean populations with the highest rates of CVD, or medical conditions that accelerate CVD, and suchlike.

I believe answers are to be found at the extremes. To that end I became very interested in people who received heart transplants. For they, unfortunately, develop atherosclerosis at a very high rate. It tends to be called vasculopathy, as it is not exactly the same as atherosclerosis, but that may simply be a result of how fast it develops.

‘Cardiac allograft vasculopathy (CAV) is the major cause of long-term mortality after heart transplant (HTx). Cardiac allograft vasculopathy has heterogeneous pathologic features characterized by vascular wall inflammation, fibrous intimal thickening, and atherosclerosis.’

I believe that, because it is developing quickly, it is possible to see ‘plaques’ forming and growing in a way that is very difficult in the rest of the population. Or, to put it another way, we have an accelerated model of CVD, where things are revealed that may normally be hidden.

Here is the key section from the paper: ‘Repeated episodes of thrombosis as a potential mechanism of plaque progression in cardiac allograft vasculopathy.’

‘Conclusions

In conclusion, our observations demonstrate that a finding of ML (multi-layered) appearance, which may be indicative of repeated episodes of mural thrombosis, is not infrequent in asymptomatic cardiac transplant recipients. These findings may contribute to progression of cardiac allograft vascolopathy (CAV). The current study gives new insight into the potential role of coronary thrombosis in plaque progression in CAV.’4

Once again, repeated thrombus formation and plaque growth, causing multi-layered plaque progression.

I shall finish here by quoting myself in a previous blog:

‘Interestingly, at one point Pfizer also started to promote atherothrombosis as the cause of heart disease. For sentimental reasons I have kept hold of an educational booklet produced by Pfizer in 1992. On page four it states:

‘Several features of mature plaques, such as their multi-layered pattern, suggest that the platelet aggregation and thrombus formation are key elements in the progression of atherosclerosis. Platelets are also known to provide a rich source of growth factors, which can stimulate plaque development.

Given the insidious nature of atherosclerosis, it is vital to consider the role of platelets and thrombosis in this process.’ [Well, quite]

There is little point in referencing this document, as I probably have the only copy left in existence. It is called ‘Pathologic triggers. New insights into cardiovascular risk.’ Produced by Medi Cine Inc. For Pfizer Inc Copyright 1992, All rights reserved etc. etc.

It is interesting that when Pfizer did not have a statin, they were looking away from cholesterol as a cause of cardiovascular disease. It will come as no surprise to you that this was not through some altruistic attempt to discover the truth about the true cause of heart disease. It was to help market their drug doxazosin (a BP lowering drug) which had some additional anticoagulant properties.’

Of course, I have not answered all questions here. But I wanted to give you some insight as to my core thinking on CVD. Having jumped around for years I decided to start at the end, the final blood clot, and then worked backwards.

Was it possible, I asked myself, that blood clotting was not just responsible for the final clot, but also for the entire process of atherosclerosis? I believe that the evidence is out there, and clearly supportive, if you choose to look at it this way round.

I suppose you could say that I do not believe in atherothrombosis. I believe in thromboatherosis (you’re right, I just made that word up). In thromboatherosis, plaques start, and grow, through repeated thrombus formation at the same spot in an artery. In the end, a clot gets big enough to cause a stroke or heart attack. Sometimes the clot can be big enough to kill, without any underlying plaque, but normally it will form over an already existing plaque – where plaque rupture can be the trigger.

In short, there is only one process in CVD. It is the development of atherosclerotic plaques through repeated thrombus formation, followed by the final thrombus formation. As you can see this is actually very close to mainstream thinking. The only difference is that you have to flip your thinking through one hundred and eighty degrees, to see it upside down.

 

1: https://academic.oup.com/eurheartj/article/36/8/475/496887/Acute-myocardial-infarction-with-no-obstructive

2: http://circ.ahajournals.org/content/92/5/1355

3: https://www.ncbi.nlm.nih.gov/pubmed/7634262

4: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3787274/

*for those who enjoyed Stranger Things

P.S. Pop quiz. Why do plaques never develop in the heart itself? Here the pressure is highest, damage to endothelium must be greatest and yet, and yet, no plaques – ever.

243 thoughts on “What causes heart disease – part thirty one (XXXI)”

  6. Mary Taylor

    “In short, there is only one process in CVD. It is the development of atherosclerotic plaques through repeated thrombus formation, followed by the final thrombus formation” So does this mean back to lifestyle, diet, stress less, exercise, sleep to prevent the thrombus formation? Or maybe take anticoagulants….

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    1. Antony Sanderson

      Best to deal with the “root cause”, as Ivor Cummins would say . . . so it is down to lifestyle to stops the thrombus formation in the first place. As others have pointed, when you try to intervene using drugs there are a whole host of unknown effects that come along for the ride. Aspirin is a case in point: Shown to have an anti-coagulant effect, it is ok as long as you keep an eye on the possible bleeding events in the stomach.

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  7. Jim

    Hi, I’m not sure you have ever made reference to peripheral artery/vascular disease and you may have very little interest in this subject but was hoping you could answer this. In your opinion is atherosclerosis in the artery of a limb the same process and principle as in an artery at the heart? Also, if you have a blocked artery in say one leg, would it be common to have a blockage on the other leg in the same please or would this either be a massive coincidence or even be a good clue as to the causation of the atherosclerosis? I have many, many other questions but if you could answer this it would be much appreciated. Thanks

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      1. Dr. Malcolm Kendrick Post author

        Clots form in veins via the intrinsic clotting system. This has nothing to do with endothelial damage, and the clots do not become absorbed into the vein wall. There is no contradiction here.

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    2. chris c

      The artery(ies) in one of my legs are much worse than the other. Or were, as recommended by a very clueful surgeon I started walking through the pain to revascularise myself, and have been following many of Malcolm’s and others, suggestions to see if I can’t clear some of the plaque, and have gone from barely being able to hobble from the car park into the hospital to walking regularly about a mile nonstop and anything from 2 to 5 miles in total, albeit slower than I used to.

      The main culprit was the 50+ years of undiagnosed diabetes. Or prediabetes, or not diabetes depending on the different doctors’ points of view, but the icing on the cake was when my thyroid blew up. Not sure exactly how that affected things, but when it goes high my walking ability is reduced, among other things, then after I have blasted it with an increased dose of Carbimazole for a while and it goes low, I can walk much more easily except I feel like a zombie with zero energy. I’m learning to keep it in range as much as possible. Not a factor I’ve read much about. Well hypOthyroid yes, hypERthyroid not so much.

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      1. Jim

        Hi Chris, thanks for the feedback. I’m curious, have you been offered either a stent or bypass? If so, did you decline for any reason? The artery in my right leg is completely blocked & left leg is partially blocked according to my specialist. I have been suffering with my legs fatiguing quickly for some time but the final blockage happened all of the sudden one evening whilst doing a circuit training session, did you find the final blockage happened all of the sudden or was it a gradual thing? When this happened I struggled to walk from one end of the office to the other. Now however I can walk fine, as long as there are no steep hills or too many steps. I am guessing my body has cleverly created it’s own bypass, I would love to know for sure how my body has adapted and if I can do anything more to encourage it further. I am now on a LCHF diet and my latest A1c and fasting sugar levels were really good as a result, although it wouldn’t surprise me if I was pre-diabetic before the diet. Also have cut out vegetable fats as much as possible, I heard on a podcast with Dr Catherine Shanahan that eating a portion of chips cooked in vegetable fat can inhibit your endothelial function for around 24 hours, to put it in perspective, if you have a cigarette, this prevents EF for around 4 hours, this shocked me. I supplement L-arginine, B12, vitamin C, Potassium, Magnesium, pomegranate extract, krill oil among other things. I am trying to get as much sun as possible and supplement vitamin D3 just to be sure along with vitamin K2 & A to ensure the calcium absorbed from the vit D is not put where I don’t want it to. I am thinking of getting a SAD lamp for the winter months too. I am dabbling in meditation and starting yoga this week to relieve any stress. Also I have the odd glass of red wine as suggested my Dr Kendrick! What are you doing to help your situation? I would be most interested to hear from you, I’ve not found anyone with the same condition as me.

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        1. AH Notepad

          Your case looks interesting, all the more so in the possibility of self correcting circulation. Don’t agree with the krill oil though. Because of the commercialisation of every possible living thing for questionable human benefit, other earthlings have to take the hit. There is also the question of how much unwanted compounds are ingested, given the pollution of the oceans by toxic waste from industry?

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        2. Gary Ogden

          Jim: Dr. DiNicolantonio says those on a LCHF diet may need more salt. “Higher levels of ketones, greater release of glucagon, and lower levels of insulin, all of which occur on a low-carb diet, increase our excretion of sodium.” I am now adding some salt to every glass of (mineral) water I drink, especially with the hot weather and the strenuous exercise I engage in. There seems to be no downside, except in rare conditions, to increasing sodium consumption up to 6 g/day. We are salty creatures.

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      2. Gary Ogden

        chris c: A book you and everybody else, including all doctors, should read: “The Salt Fix,” by Dr. James DiNicolantonio. Turns out salt restriction is very dangerous nonsense, without a shred of scientific evidence (just the surrogate of a trivial reduction in BP). For those with diabetes, and/or hypertension, a very interesting reference: Ames, R. P. 2001. “The effect of sodium supplementation on glucose tolerance and insulin concentrations in patients with hypertension and diabetes mellitus. AM J Hypertens 14(7 Pt 1): 653-659. This article is easy to find by typing the journal name and going to the volume (14). All the articles are free. Eat your salt, folks!

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      3. chris c

        Initially my degeneration was fairly slow, until I met a dietician and was put on higher carb even lower fat than I was already dutifully eating. That made me gain 15 kg in short order and ;left me constantly hungry and semipermanently exhausted, and all my “disease markers” got rapidly worse. I was getting significant peripheral neuropathy, mainly tingling and “feet going to sleep” after meals, what they call “stocking and glove” distribution and in retrospect that was probably step 1 in the arterial damage.

        Naturally I was accused of “failing to comply” with the diet, and once again assured I was “not diabetic”.

        Fortunately around then I moved and the new GP gave me a GTT and pronounced that I had “a touch of prediabetes” since I had “only” scored 10.8, to be diabetic I would have had to reach 11.1.She gave me a written version of the previously verbal HCLF diet. That was over 12 years ago.

        As a result of reading those “cranks on the internet” I went LCHF and equally rapidly lost the weight and improved all my “health markers” though my BP remained a bit high, controlled with losartan. Gradually all my symptoms improved, and when I gave up wheat and went pretty much keto so did most everything else. I did this

        http://loraldiabetes.blogspot.co.uk/2009/04/test-test-test.html

        despite being told that “we” didn’t approve of patients testing their own blood, and soon discovered it was mostly only my 1 hour postprandials which were high, and my 3 – 4 hour postprandials went low which was why my HbA1c was still “normal” – so under current Rules I would never have been diagnosed.

        When I had my BG roughly normalised I stopped bothering to test, except occasionally, and relied on the Mk 1 nose – if I could smell ketones in my early morning pee but not during the rest of the day I surmised I was using them at about the same rate I was generating them. Which is good.

        About ten years later I suddenly degenerated, my BP went through the roof and I started collecting fluid in my ankles and the base of my stomach, and one toe became infected (ingrowing toenail didn’t help) and started turning black. The vicious bitch of a receptionist REFUSED to let me see the “minor injuries” nurse, and initially refused to let me see my GP, saying I could make an appointment for the ordinary nurse and she would decide if I needed a further appointment to see a doctor (by then the entire practice had degenerated drastically).

        I got an emergency appointment with the non-NHS podiatrist, who was a friend, and who was horrified and rang my GP. She could only offer an appointment with a different GP as she was fully booked for over a month and “the computer” wouldn’t permit it, so about a fortnight later, which time I spent largely unable to do more than hobble, and sleep in a chair for a couple of hours at a time until I had to take more paracetamol, I got to finally see a doctor. My heart rate was through the roof and he diagnosed (later confirmed by a blood test) that I was hyperthyroid (one thing that had always previously been normal) and also helpfully that I was NOT diabetic and had never been prediabetic because “the only thing that matters is HbA1c”.

        He sent me to the hospital to arrange to have my toe lopped off. Fortunately the surgeon had more than half a clue, he told me that he could stent my leg(s) but if I succeeded in walking through the pain I could revascularise myself, and gave me some heavy duty painkillers. Meanwhile the podiatrist did a sterling job of wound cleaning, and the Carbimazole got my thyroid back in line, which helped a lot.

        Eventually I got to see “my” GP who was not best pleased, to put it mildly. Around then the PCT went away as did the Practice Manager, who was replaced by a human, and the practice also became revascularised (grin) I think the receptionists and nurses were retrained to stop treating patients with contempt though it still takes about three weeks to see a doctor. Apart from that it is largely back to how it used to be before it was so comprehensively wrecked.

        I’m with you on the hills, but by walking a bit further each time and trying to slow down but not stop when my calves hurt, I gradually increased the distance and speed, while the pain and presumably the blockages improved. Thanks largely to Malcolm and a few others I have tinkered with K2, C, Co-Q10, fish or krill oil, l-Arginine, Mg etc. I suspect getting enough sun that my unsupplemented D was 95 probably increased my NO also, even in the middle of winter when the sun is out I will walk somewhere. I eat a lot of grass-fed meat, game, fish, some poultry and a wide range of coloured veggies, especially greens of various types, plus nuts, olives, herbs, spices, etc. to collect micronutrients (LIVER!!!) and lots of butter, cheese, EVOO and the dreaded coconut oil, and avoid wheat, sugar and Omega 6 oils almost entirely, and starch and “processed food” as much as possible. Oh and my fruit is limited to berries, preferably with clotted cream, ground flaxseed (and brandy!) and my drinking to a glass or two of red wine apart from all the coffee. Truly I am a dietician’s worst nightmare.

        I’m careful but not always successful in rocking my Carbimazole dose back and forth when my thyroid misbehaves, every so often it will speed up or slow down for no apparent reason. IMO thyroid along with insulin and leptin are the Master Hormones which knock on to all sorts of other stuff so I try to keep them nailed.

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        1. Mr Chris

          Chris C
          Where do you live, your description of the surgery makes it sound like the UK
          Here in Belgium, for an urgency, my decision, I can see my doctor same day, for something routine I might have to wait two or three days.
          As for the rest, why do people have to start curing themselves?,

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        2. Jan B

          What a nightmare account – but what a lifestyle and diet to come out of it. Can I come to dinner? I’d bring the clotted cream.

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      4. chris c

        I put my response on the next blog after it vanished from here.

        I suspect the key is not so much adding Omega 3 as reducing Omega 6 which in in overdose levels in a “low fat heart healthy” diet. I probably get enough from Real Fish and grass-fed meat but throw back the occasional fish oil or krill oil capsule for good measure. My vitamin D came back at 95 just from sun exposure (which hopefully also drives up the NO) and I try to get what other micronutrients I can from a varied diet, the supplementing is to see if things can be further improved.

        Gary, I haven’t read the book but follow James DiNicolantonio on Twitter where he posts some good research and links, as do Benjamin Bikman, the inimitable Ted Naiman and not a few others. I favour sea salt mostly for the flavour and also use Lo-Salt for the potassium, oh and I noticed recently iodised salt no longer seems to be available but I get some iodine from the fish and shellfish and was warned off getting too much or varying the dose much due to the likely effect on my thyroid. More J or U curves I suspect.

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        1. Gary Ogden

          chris c: Very important point. The essential fatty acids (omega’s 3 and 6) are essential in our diet, but we only need small amounts of them. I would not advocate taking fish oil, not only because of its impact on fish stocks. A bit of fish frequently enough will do the trick. As I understand it, polyunsaturates tend to be inflammatory, so reducing our consumption of of omega 6 FA’s rather than increasing the omega 3’s is the smart move.

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      5. chris c

        Indeed, we used to eat a balance of between 1:2 and 4:1 O6 – O3, now it may be as much as 20:1 or more. Elsewhere I just read another reference to the “israeli Paradox” – due to their food-combining rules they eat even 30:1 or more O6 – O3 and despite these being supposedly “heart healthy” they have very high CVD levels.

        AFAICR O6 produces more proinflammatory ecosanoids, O3 more antiinflammatory ones and we need both in the correct balance for inflammation to work properly. Also they are incorporated in cell membranes along with the saturated and mono fats (and trans fats) which makes me wonder what effect they may have on the structure of the endothelium. in excess.

        Unlike those instantly lethal saturated fats they are relatively chemically unstable especially when heated but to a degree just when eaten, and some of the products of their breakdown are none too nice, so yes too much of either is Not A Good Plan.

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  9. Gay Corran

    Getting there! What about clots caused by atrial fibrillation? What do we do about them? Or indeed about AF itself?

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  11. The Wizard

    Another well considered post Dr K. Sadly, all the evidence logically elucidated by your good self won’t stop the inexorable march of yet another cholesterol lowering “offer”. Oh how the media love to support Big Pharma, only yesterday reporting the ” exciting” news of a cholesterol “vaccine” !!! Ha ha ha….. vomit and then start to wretch uncontrollably please.

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  13. Andy S

    For mice the cause of atherosclerosis can be found in this study. (Hint- it is not the fat) What would be the effect on humans following a similar high-fat/high-cholesterol diet?

    Atherosclerosis in APOE*3-Leiden Transgenic Mice
    From Proliferative to Atheromatous Stage

    https://doi.org/10.1161/01.CIR.99.2.276
    Circulation. 1999;99:276-283

    “This study documents (1) the progression of atherosclerosis along the entire arterial tree in APOE*3-Leiden mice after 1, 4, 6, 9, and 12 months of a high-fat/high-cholesterol (HFC) diet

    At the age of 37±0.6 weeks (mean±SEM), the animals were put on a diet containing 15% cacao butter, 0.5% cholate, 1% cholesterol, 40.5% sucrose, 10% corn starch, 1% corn oil, and 4.7% cellulose (Hope Farms)
    Atherosclerotic lesions developed in the aorta and large vessels in all APOE*3-Leiden mice on an HFC diet”

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      1. Andy S

        Ellifeld, what the researchers filed to explain is how fat and cholesterol cause atherosclerosis. Sugar is assumed to be harmless, therefore blame fat. Healthcare providers believe this.
        Another way to interpret the meaning of the study is that you can eat sucrose, corn starch and corn oil you will not get atherosclerosis if you limit fat and cholesterol.

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  14. Ali

    Enzyme therapy (proteolytic, serrapeptase, nattokinase etc.) has been found to reverse and clear arterial blockages. That somehow suggests that the clots may be due to an enzyme breakdown or deficiency in the body.

    As enzymes need certain elements for their formation and pancreatic insufficiency seems rampant, there definitely seems to be a dietary factor involved somehow.

    Fresh pineapple, anyone…..?

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    2. robert lipp

      Hi Ali
      do you have any references for “enzyme therapy reversing / clearing arterial blockages”?
      I would love to read more about this?
      thanks

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    1. jgt10

      Considering the MSM focus, I doubt any network would touch it.

      Thou, it might make a smashing web series! Get some good medical animators and it could be a clotbuster … ah, blockbuster of a show!

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  17. Errett

    My guess concerning the absence of plaques in the heart—-

    We only develop atherosclerosis in the arteries. The disease doesn’t appear in arterioles, veins nor capillaries. The arteries have a much thicker development of smooth muscle tissue. The smooth muscle is in constant use in arteries and produces lactic acid like all muscles do when used.

    If the blood supply to the arteries (vasa vasorum) has sufficient oxygen and alkalinity the lactic acid is removed from the smooth muscle tissue quickly. If the lactic acid is not removed sufficently then it will damage the elastic tissue/endothelial lining of the artery. This damage initiates atherosclerosis.

    The heart isn’t exposed to this problem since it can use lactate as a fuel source.

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    1. Andy S

      Errett, I believe the blood vessels in the heart also can get gummed up, the medical term is Coronary Microvascular Disease.
      Gummed up arterial blood vessels is a systemic event and can also occur in eyes, legs, brain etc. .Leg amputations are quite popular because of restricted blood flow.

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      1. Jean Humphreys

        In my case triple CABG 20 yeas ago. One of the grafts failed and was replaced by a diverted mammary artery, only 10 months later.. After 16 years, the venous grafts are stenosed – but not too badly. The arterial graft is clean and clear.

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  18. Gary Ogden

    I’m sold. If it is more or less normal to sustain clot-forming injury to the endothelium of cardiac arteries as we age, and it mostly only becomes dangerous if the repair process can’t keep up, allowing repeated injury and clot-forming in the same spot, it behooves us to avoid the things which contribute to this disarray. Elevated insulin seems to be a major one. Stress hormones. Insufficient vitamins C and E for the repair process (and glycine for collagen formation). What else? Off topic, but of note: I’ve now doubled my K supplement, to 1.4 g/day, in divided dose. It may be the placebo, or nocebo, procebo, or anticebo effect, but I simply feel better. Also making certain to get plenty of sodium (saline poisoning the AHA would likely call it), as we’re having a heat wave of 107-109 degrees F (42-43 C), and I’ve been outside quite a bit, getting my daily heliotherapy. This sort of heat is normal here; the record is 116 (46.7).

    Reply ↓
    1. robert lipp

      Gary,
      interesting comment: “…it behooves us to avoid the things which contribute to this disarray.”

      Do you agree with / care to comment on the following summary???
      [critical = each intervention as appropriate per individual needs and condition]
      1) lower insulin = intermittent fasting and reduced bad carbs = sugar, starch, HFCS etc.. sugar is the enemy = LCHF in one of its variants
      2) manage stress = reducing HPA axis disfunction.
      3) improve arterial repair = vits C, E, + Arginine and nitrates to get NO up
      4) reduce arterial calcification = D3, K2 (you had K only; I am assuming you mean the MK’s 4 and 7), magnesium.
      5) improve heart function Omega 3, + magnesium, potassium salts
      (all above taken naturally by real food with polyphenols phytos etc or thru supplements)
      6) hydration
      7) moderate exercise frequently (about 40 minutes), and for the older more retired blokes, not overly strenuous (= stress reduction + heart exercise).

      Comments???

      Reply ↓
      2. Gary Ogden

        robert lipp: I fully agree with all of it. I think it is possible for most people to get healthful amounts of most of those nutrients from food, with the exception of vitamin D in winter, potassium (even with a K-rich diet), vitamin C, and possibly magnesium. I don’t take a vitamin D supplement, but get lots of sun exposure and eat D-containing foods, like salmon and eggs, year round. The other three I take as supplements, and I think it a good idea. As for exercise. the best exercise for any of us is the exercise we do. There is great benefit in strenuous exercise at any age, but it only takes a few minutes a week. Dr. Mercola has some good information about this, and Mark Sisson has a wealth of good info about exercise in general. The missing thing here is salt. We’ve been told for decades that restricting salt will lower BP. It will, but only by a trivial amount, and only for a small percentage of the population. The downsides are legion. This turns out to be dangerous advice. Intersalt looked at population-wide salt consumption the world over, and found it to be remarkably consistent at 3-6 g/day. Outside of this range mortality increases, more rapidly below 3 g/day than above 6g/day. Yet the talking heads here in the U.S. recommend 2.3 g/day for the general population, and 1.5 for blacks and those over 60. There is no scientific basis for this, even less than that for statins. “The Salt Fix” explains it all in great detail. I’ve seen immediate benefits, both in my response to exercise, and in general, since I’ve added more salt to my diet (especially important for those of us in the northern hemisphere since summer is now upon us). Fear not salt!

        Reply ↓
        1. smartersig

          Eggs are an interesting item, they appear packed with good stuff and you often find people of longevity have used them but their is a studied link to prostate cancer and Choline

          Reply ↓
      4. Mr Chris

        Robert Lipp
        moderate exercise for the old. I always have a problem when I see moderate as in moderate exercise moderate drinking. Is moderate what I feel like or is there an international standard?

        Reply ↓
      5. robert lipp

        Mr Chris,
        Exercise is what it is to each individual. That is, do you have a crock knee from rugby, bad hip from a fall, medicine controlled AF heart rate, or whatever condition limiting your “moderate” level of exercise. Alternatively, you are fit active 30 yr old and run occasional marathon. Moderate for a 70+ is not the same as for a 30 year old.

        The value, to my mind, of “moderate” is the level of (physical, mental, or social) stress that the exercise produces. That hip could cause a lot of stressful pain after 10 mins of intense (HIIT) sprinting but not after 1hr walking. Too much stress reduces the exercise benefits.

        Stress is a killer, we all know this as Dr K has said so. 🙂

        If you want to learn how stress does kill see attached: http://www.news24.com/SouthAfrica/News/sabc-8-journalist-suna-venter-dead-20170629
        While the news is sad and local the medical situation makes the point stress does really kill.

        Reply ↓
  19. Maryann

    Excellent article. I loved the balance of both academic papers with a summery in layman terms. I read a article a long time ago that clots form only in arteries never in veins, If I remember correctly an analogy of rivers and streams was given. If true is this a clue?
    P.S. read your book and Loved it!

    Reply ↓
  20. TeeDee

    Thank you for making this understandable to a lay person such as myself. I found it fascinating. Of course, I have the same question as many: are there any steps that can be taken to slow down or lessen the formation of blood clots?

    Reply ↓
  21. JDPatten

    In a previous Roman Numeral I believe you suggested that any lipid that might be found in plaque was due to the substance of the cell walls of the blood cells entrapped there.
    Do I remember right?

    Reply ↓
    1. Dr. Malcolm Kendrick Post author

      Almost. I suggest that Lp(a) and LDL and VLDL do become ‘trapped’ within blood clots, which is where the triglyceride and esterified cholesterol comes from. However, cholesterol crystals are formed from (red blood cell) RBC membranes, which are high enough in cholesterol to form crystals.

      Reply ↓
  22. Sylvia Brooke

    Goodness me, I have waited a long time for someone to touch upon atrial fibrillation, and now Gay Corran has done just that. Thank you Gay.

    Over two years ago I had three stents inserted when an angiogram showed that there was a blockage in my LAD. I was prescribed beta blockers at that time.

    However, at my annual checkup twelve months ago and at a further annual check-up a few weeks ago I had an irregular heartbeat (which I was already aware of, and the surgery was aware of too). I was then diagnosed with atrial fibrillation. and then offered warfarin (which I am reluctant to take) or Apixaban (Eliquis) as an alternative, as well as the beta blockers.

    Two weeks ago, at a hospital appointment, and before making any decision to take either warfarin or apixaban, I had a heart scan and was told that my heart was pretty much the same as it was two years ago – that scan was taken before the stents were inserted.

    I know it is a big ‘ask’, and I do know that Dr Kendrick cannot give advice of any kind – and rightly so. He has far too much to lose. My question is that as I also take Levothyroxine, Elantan, Clopidogral, Bimataprost and Brinzolamide Eye drops for Glaucoma and wonder if either Warfarin or Apixaban could react badly with any of these drugs?

    Should there be a deathly hush around this question I will understand, but any snippet of information would be greatly appreciated.

    I have learned so much from this blog, and the people who visit, having stopped statins ages ago.

    Reply ↓
      1. Sylvia Brooke

        Thanks for your reply ellifeld,

        Been there, done that, none of it really helped. I suppose we are all different in our reactions to drugs. Never mind, I will just have to make up my own mind and hope that I choose the right anticoagulant in the end, or not at all!

        Thanks again.

        Reply ↓
    2. David Bailey

      Sylvia,

      Perhaps if you re-phrased your question in a way that doesn’t sound like a personal medical enquiry, it might enable Dr K to reply.

      If I had T2 diabetes, I would definitely go on an HFLC diet

      Reply ↓
      1. Sylvia Brooke

        David.
        Thanks for your reply.

        I guess my anxiety about so many things at this time got me a little carried away. However. my entry was never intended to sound like a personal medical enquiry, and I certainly never requested, or expected a reply from Dr. Kendrick.

        I do not have diabetes of any kind, but thanks for your advice.

        Reply ↓
      2. David Bailey

        Sylvia,

        I only mentioned diabetes, because you say you have glaucoma.

        After writing the above, I remembered Malcolm’s discussion of poly-pharmacy – the danger of simply taking too many different drugs. This is something I personally encountered at one stage.

        Since you obviously take quite a number of medicines, I wonder if one strategy might be to ask your doctor, “I am concerned about the dangers of poly-pharmacy, so if I were to stop taking one of these drugs, which do you think would be best?”

        Reply ↓
    3. MalcolmC

      Sylvia, Some people find that eating a ketogenic diet either brings on or stops atrial fib. If your AF comes on after carby meals you might want to switch to a lower carb diet or vice versa.

      Reply ↓
    4. HW

      I don’t know how to advise you, Sylvia, but I do share some of your concerns, namely hypothyroidism and episodes of irregular heartbeat (possible AF). Let’s hope that one of the many knowledgeable readers of this blog comes along to shed a little light on these subjects, thereby sparing Dr K the wrath of the GMC.

      Reply ↓
  23. Fergus

    Answer to pop Q
    Is there no plaque formation in the heart due to the higher pressure. A bit like high water pressure keeps the pipes from blocking?

    Anyways another study entitled “Stopping statins sits well with most patients” found
    “381 cognitively intact patients, which reported that patients randomized to stop statin therapy had better total quality of life, used fewer nonstatin drugs, and saved an average of $716 less per patient than those continuing statins, without a significant increase in cardiovascular events.”

    Strangely the authors still seemed pro statins. Sigh!

    Reply ↓
    1. smartersig

      Interesting point, could anyone confirm that veins are wider than arteries. If that is the case they would suffer from less shear stress from blood pressure. Perhaps this is why we dont get plaque in the veins

      Reply ↓
      2. sasha

        I would think that veins, like arteries, are of various width. Carotid arteries are pretty big, aren’t they?

        Reply ↓
      3. Martin Back

        The amount of blood leaving the heart must equal the amount of blood returning to the heart. Which implies that the speed of blood in the arteries times the cross-sectional area of the arteries must equal the speed of blood in the veins times the cross-sectional area of the veins.

        Since arterial blood whooshes along much faster than sluggish venous blood, the cross-sectional area of the veins must be much larger. This could be accomplished by making veins wider, or making more of them, or a combination of the two.

        Some arterial plasma returns via the lymph system, I believe, so the equation is not exact.

        Reply ↓
    2. JDPatten

      It’s my understanding that pressure increases downstream as the vessels get smaller. Central BP is generally less than brachial.

      Reply ↓
      3. JDPatten

        I got that crazy idea from reading this:

        “The idea of measuring central pressures grew from the finding that when you do a heart catheterization and you pass that wire up to the heart, you notice that, counterintuitively, the systolic blood pressure declines as you approach the heart. The mean pressure doesn’t change, nor does the diastolic pressure, but the systolic pressure declines. That fascinating phenomenon, which we can now measure noninvasively, is what is driving this field.”
        Dr Townsend, in:
        http://www.medscape.com/viewarticle/843552#vp_1

        Is it “pulse pressure” being described?

        Nope??

        (Love Henry’s mustache.)

        Reply ↓
    3. Jillm

      Thank you Dr Kendrick. Regarding the new, cholesterol lowering injection: In the Fourier trial, paid for by Amgen, there were 444 deaths in the drug group and 426 in the placebo group. Yes, more deaths in the drug group. This drug has been approved in Australia.

      Reply ↓
  24. JDPatten

    I do hope that you’ll eventually clarify the whole calcification of plaque thing.
    What are the mechanisms?
    Is it a good thing, “stabilizing” plaque?
    Is it a bad thing, making vessels “hard” and inflexible and generally getting in the way?
    Is it necessarily an aspect of healing, or some other process(es)?

    Reply ↓
    1. Andy S

      high carb and fructose > hyperglycemia > ROS + AGEs = Ossified arteries
      Love their conclusion: develop a drug to prevent vascular calcification

      J Mol Sci. 2016 Sep; 17(9): 1567.
      Published online 2016 Sep 16. doi:  10.3390/ijms17091567
      PMCID: PMC5037835
      Advanced Glycation End-Products Induce Apoptosis of Vascular Smooth Muscle Cells: A Mechanism for Vascular Calcification
      “United Kingdom Prospective Diabetes Study (UKPDS) demonstrated that intensive glycemic control started at the time of diagnosis is associated with a significantly reduced risk of microvascular disease, myocardial infarction and death from any cause in type 2 diabetes [2].

      Moreover, AGEs suppressed cellular differentiation and maturation, and induced apoptosis in many type of cells including retinal microvascular endothelium cells, retinal epithelial cells, neuronal cells, osteoblast precursor cells, and osteocytes [14,15,16,17,18].

      Conclusions
      AGEs stimulate VSMC apoptosis through excessive ROS generation. Component of NAD(P)H oxidase such as Nox4 may be a good candidate of new strategy to prevent vascular calcification”.

      Reply ↓
    1. Dr. Malcolm Kendrick Post author

      Retiring, probably. Apart from that, walking outside in the hills(golf would also be good). Build up a good sun tan. Ensure you have a good supportive social and family life. A few vitamins: B6 B12 Folate, Vitamin C and K, Magnesium, Potassium l-arginine and l-carnitine. A high fat low carb diet. A bit of meditation and breathing exercises. Smile every day, and try a few unexpected acts of kindness each week. Moderate alcohol consumption. A sense of purpose is also very good – but I don’t know where you get that from. And, as they say in Scotland, dinnae worry. Good health has three parts: Physical, Psychological and Social. They are all equally important.

      Reply ↓
      2. Dr. Göran Sjöberg

        Malcolm

        A convincing “explanation” as always to me although I must admit that I am getting more and more confused with time the more I learn from you about this CVD-issue.

        Still I am a strong believer in the “total life protocol” you are suggesting, just now sipping on my, 15 grams a day, C-vitamin drink om my night table. Retiring though, I must admit, was a seriously stressful event and with a temporally large dip in my previously rather stable CVD-curve. I presently believe that my 2400 IU/day of natural vitamin E is what is keeping my angina at bay now.

        Reply ↓
      3. Gary Ogden

        Dr. Kendrick: Thank you, thank you. This is what many have been waiting for. Best prescription for health I’ve ever read.

        Reply ↓
      5. JanB

        Such good sense. Trouble is, all those supplements gobble up a chunk of the state pension, but sunshine is free as are a social life, smiling (which tends to go hand in hand with said social life) walking and various other pleasurable activities.
        Thank you as always, Dr. K.

        Reply ↓
      6. Peggy Sue

        It seems retiring isn’t for everyone. I’ve known of at least two fellas who dropped dead of heart attacks within a year of retiring. Seemed just rotten bad luck at the time (20 or more years ago) but now I see things a little differently it makes perfect sense.

        The challenge to the system could be enormous for some individuals. Change of routine, loss of daily purpose, loss of social interaction, impact on home life (married for life but not for lunch), not to mention the change to income and security for the future.

        There are so many facets to this prevention of heart disease malarkey. Really, I think the number one essential has to be reading Dr Kendrick’s blog and all the fabulous comments that follow. I know it’s done me the world of good.

        Reply ↓
      7. Martin Back

        That reminds me of my Scottish stepfather. Every time my mother got in a tizzy, he’d say, “Dinna fash yerself, woman.” He lived to a decent age despite cirrhosis of the liver nearly killing him.

        Reply ↓
      9. Solomon

        @PeggySue, you need not break the bank, the Fermented Cabbages I eat should give me a fair percentage of the vitamins Doc. list above.

        Reply ↓
      10. chris c

        Done/doing most of that!

        However I’m starting to have second thoughts. If I fail to die prematurely from CVD that leaves me open to a far worse death from cancer, Alzheimers etc. Hmmm, decisions decisions . . .

        Reply ↓
      11. chris c

        Just not quite yet. And preferably peacefully in my own home, which everyone wants but almost none of them get. An NHS death can be truly horrific, DNR orders routinely ignored, heroic measures used to drag you back from the brink so they can tell you they are going to euthanise you by starvation AKA Liverpool Care Pathway .. . or you get warehoused until your wife/estate runs out of money to keep the nursing home in business.

        Reply ↓
        1. Andy S

          chris c: The last decades of retirement can be a nightmare as you describe. The remedy to avoid that scenario is what the good doctor has recommended. The aim is to die heathy.

          Reply ↓
  28. Martin Back

    Why do plaques never develop in the heart itself?

    I’ll take two guesses:

    1. The cardiac arteries are surrounded by heart muscle which gives them a great deal of support, therefore they don’t expand under pressure like other arteries, therefore gaps don’t open up between the endothelial cells for leakage followed by clotting to commence.

    2. The heart is the hardest-working muscle in the body and mops up all the glucose in the blood feeding the heart to fuel itself, therefore glucose-mediated damage does not occur. If this is correct, then it follows that plaques will be rare in the extremities which are fed by glucose-depleted blood.

    Reply ↓
    2. gollum

      Ironically, the heart runs (preferentially / under normal conditions almost completely) on FFAs.

      This is probably one of the reasons why heart cancer is extremly rare, too.

      Reply ↓
  29. gillpurple

    My wild guesses at why plaques don’t form in the heart itself. Does the endothelium have some sort of mucus membrane? Or does the pumping of the heart itself make it impossible for plaques to attach?

    Another informative blog, thank you.

    Reply ↓
  30. Sylvia

    Ah but do take a dog on your walks, such companions as these are priceless and we are told, stroking them lowers blood pressure. It is an all round win situation, if they have you well trained, you will have excercise, social encounters and learn to stay upright in gale force winds. Better than statins any day. If I encounter you on the hills Dr Kendrick I will wish you good day and look for your mans best friend.

    Reply ↓
    1. Philip Thackray

      I would also note that the endocardium (heart equivalent of the blood vessel endothelium) is MUCH thicker in the high pressure left ventrical than in the lower pressure right ventrical.

      Reply ↓
      1. Andy S

        Phil, looks like endocardium is a tough, inert, impermeable elastic membrane unaffected by blood components. This would be similar to the elastic membrane below the artery intima layer explaining why it is possible to successfully remove an inflamed stenosed intima layer. Function of intima? Needs a separate blog.

        Reply ↓
  32. Marilyn Schroeder

    Now I’m back to wondering about “Raised cholesterol causes plaques, these rupture, then a clot develops (which would not have formed had the plaque not been there).”
    Which element of cholesterol is in play here? Is dietary modification #LCHF the ‘antidote’?

    Reply ↓
  33. xtronics

    Interesting – I’m in the ‘they got the arrow of causation backwards camp’ – I’m thinking that likely the small correlation of LDL with CAD is the result of injury rather than the cause.

    I do think the blood clot is the final bit – but what causes some people to have CAD and other not? What causes the initial damage and scarring?

    The evidence of people with high levels of insulin having CAD is out there:
    https://www.ncbi.nlm.nih.gov/pubmed/11342468
    https://www.ncbi.nlm.nih.gov/pubmed/12060058

    So if we look at insulin as a growth factor – it provides a clue – most likely more complex with cofactors and genetics involved.

    So the narrative of the initial thickening due to insulin seems incomplete to the connection with clots/foam-cells. My take is that if the arteries are damaged – the irregularities in the wall induce clotting. What causes the initial thickening (that I think happens in the inner intima of the artery wall)? Does this lead to necrosis due to lack of oxygen?

    If I accept the insulin causation narrative, then things that increase insulin levels become interesting – such as insulin resistance, which there is evidence that it can be caused by Linoleic acid consumption ( an O-6 large amounts found in seed-oil – a popular food like substance).

    BTW – we know that PCSK9 is increased during infections, and LDL(and HDL) have innate immune system functions – so during inflammation IL-6 apparently drives increases and APO(a) as well. So if we have injured arteries – leaking cytokins – one would expect a modest increase in LDL.

    What gives me joy is that finally – a decade after having CAD (and much time digging into CAD research) there are voices looking to alternative theories.

    There are other bits – we know that the macrophages that go on to become foam-cells have receptors that are triggered by oxLDL (To a macrophage oxLDL appears as a dead or dying bacteria).
    – yet I’ve never been able to find any work that would show LDL as a risk-factor if oxLDL is held constant – not exactly rocket science – the data should exist. This could be important as there are many ways to lower oxLDL.

    But I still think – the point where the arteries are injured – inf lammed – recruiting monocytes that become macrophages is after the initial damage.

    Reply ↓
      1. Joe

        Insulin resistance would be the symptom of consuming too many sugars (carbs) and not enough fat, so the actual “culprit” would indeed be sugar.

        The Two Big Lies of Type 2 Diabetes

        https://intensivedietarymanagement.com/two-big-lies-type-2-diabetes-video-lecture/

        “The disease of type 2 diabetes is excessive insulin resistance. It is this insulin resistance that leads to high blood sugars. In order to treat/ cure diabetes, you must reverse the insulin resistance. The high blood sugar is only the symptom, not the disease. Therefore, treating the symptom alone is useless.”

        Throw in some intermittent fasting, and T2D can be reversed, contrary to conventional wisdom. Treating T2D patients with insulin is like treating alcoholics with alcohol.

        Reply ↓
        1. Gay Corran

          Joe, my cardiologist just told me that obesity causes diabetes. Methinks he’s got it the wrong way round. It’s going to take a long time to tell the medical establishment about insulin. I forebore to tell him that I became pre – and then really diabetic while taking prescribed simvastatin and following (to the letter!) the recommended low fat high carb low protein, only two eggs a week, use “healthy spreads”, “if you choose to eat meat cut the fat and skin off” eat lots of veg and fruit, and 60% complex carbs at every meal as ordered by my GP and practice nutritionist. My father had atrial fibrillation and died, after several small TIAs of a massive brain bleed. He was on warfarin. Makes you question medical knowledge somewhat, with some honourable exceptions!

          Reply ↓
      2. Joe

        Gay Corran:

        Your cardiologist is tied to the diet-heart theory of heart disease, where everything is about cholesterol. That forces him to recommend a low-fat, high-carb diet, without realizing that it’s literally a recipe for obesity, type 2 diabetes, Alzheimer’s and even cancer.

        The tide is turning, though, thanks to the tireless efforts of doctors like Jason Fung and others. He’s the Malcolm Kendrick of diabetes and weight loss. And diabetes is all about insulin. Without insulin resistance, there is no weight gain, and no diabetes. Thus, your cardiologist has it precisely backwards, as do most cardiologists.

        How to Reverse Type 2 Diabetes — The Quick Start Guide

        View at Medium.com

        “It’s like packing your clothes into a suitcase. At first, the clothes go without any trouble. After a certain point, though, it is just impossible to jam in those last 2 T-shirts. You can’t close the suitcase. The luggage is now ‘resistant’ to the clothes. It’s waaayyy harder to put those last 2 T-shirts than the first 2. It’s the same overflow phenomenon. The cell is filled to bursting with glucose, so trying to force more in is difficult and requires much higher doses of insulin.

        “When the insulin levels are unable to keep up with the increasing resistance, blood sugars rise and your doctor diagnoses you with type 2 diabetes and starts you on a pill, such as metformin. But metformin does not get rid of the sugar. Instead, it simply takes the sugar from the blood and rams it back into the liver. The liver doesn’t want it either, so it ships it out to all the other organs — the kidneys, the nerves, the eyes, the heart. Much of this extra sugar will also just get turned into fat.

        “The problem, of course, has not been solved — the sugar bowl is still overflowing. You’ve only moved sugar from the blood (where you could see it) into the body (where you couldn’t see it). It’s putting a band-aid over a bullet hole. So, the very next time you eat, the exact same thing happens. Sugar comes in, spills out into the blood and you take medication to cram the sugar back into the body. This works for a while, but eventually, the body fills up with sugar, too. Now, that same dose of medication cannot force any more sugar into the body.

        “So you go to your doctor. What does he do? Instead of getting rid of the toxic sugar load, he doubles the dose of the medication. If the luggage doesn’t close, the solution is to empty it out, not use more force to . The higher dose of medication helps, but only for a time. Blood sugars go down as you force your body to gag down even more sugar. But eventually, this dose fails as well. So then your doctor gives you a second medication, then a third one and then eventually insulin injections.

        “Over a period of years, you went from pre-diabetes, to diabetes, to taking one medication, then two then three and then finally large doses of insulin. Here’s the thing. If you are taking more and more medications to keep your blood sugars at the same level, your diabetes is getting worse! Even if your blood sugars get better, your diabetes is getting worse. This is unfortunately what happens to virtually every patient. The body is already overflowing with sugar. The medications only hide the blood sugar by cramming it into the engorged body.”

        Sound familiar? Well, that’s why we currently have raging epidemics of obesity, type 2 diabetes, Alzheimer’s (which is type 3 diabetes), and even cancer (another metabolic disease). And they will continue to get worse, until we can change the paradigm. BigPharma has a lot to answer for, as do all of the major diabetes associations, which are all part of the problem, not the solution.

        Reply ↓
      3. Andy S

        Insulin resistance explained: no amount of extra insulin can force cells to absorb the excessive amount of glucose produced by consuming excessive amounts of carbohydrates over a long period of time. Once fat cells and liver are filled to maximum capacity with fat then you are diabetic. The excess blood glucose has nowhere to go. Shooting up extra insulin is why diabetes is considered progressive and incurable.

        Hyperglycemia-induced beta-cell death will lead to hypoinsulinemia, and then you are insulin dependent by needle.The sugar keeps pouring in when you follow the Diabetes Foundation recommended advice.

        Some blame diabetes on fatty liver as the cause, I blame it on the carbs. with fructose as a bonus.

        Reply ↓
      4. xtronics

        Dr Kendrick wrote:
        “I think insulin may be the culprit in diabetes, not sugar (but I don’t know how you could establish this).”

        Not sure what you mean – T1D or T2D?

        Anyway, I think BG is controlled more by insulin resistance than insulin itself.

        What is generally missing from the insulin conversation is that our biology is assumed to be engineered rather than evolved. Evolved proteins almost always have multiple purposes.

        Insulin also has MANY other effects:

        – controlling storage of fat – Decreased lipolysis
        – as a growth factor.
        – glycogen synthesis
        – Increased cellular potassium uptake
        – decreases production of glucose from noncarbohydrate substrates
        – Increased lipid synthesis
        – Increased production of trygly from fatty acids
        – decreased breakdown of proteins
        – Decreased autophagy – decreased level of degradation of damaged organelles. Postprandial levels inhibit autophagy completely.
        – forces cells to absorb circulating amino acids
        – forces arterial wall muscle to relax
        – Increase in the secretion of hydrochloric acid in the stomach
        – Decreased renal sodium excretion
        – enhances learning and memory
        – increased fertility

        I hope people figure out from above – that the narrative we have all heard about what insulin does and is for is wrong due to omission. There are also secondary effects from these primary effects – and the complexity of the whole system is beyond human understanding.

        Insulin is typical of a protein – proteins almost always act like Swiss army knives and do multiple things. This is key in understanding why what we read is almost always misleading The researchers approach the body as if it is a reverse engineering challenge – like a car – different parts have different purposes – yet biology is not a product of engineering – it is a consequence of evolution. To really understand it one would have to know all of evolutionary history – and the shear complexity is beyond human understanding. Everything interacts with everything in non intuitive ways.

        Reply ↓
      5. gollum

        This has been discussed, and discussed.. Well, any discussion of the thing is better than the standard “take insulin to equalize the scales” drivel.

        “Diabetes” is just a fancy name for when the GP thinks you have too much glucose in the blood. It can have many causes.

        It is true that the Overload scenario is the problem in many, many cases.
        And it is true that unstuffing the overload with LC is beneficial most of the time.

        However, many diabetics report elevated blood glucose even on empty stomach. And even more so in the morning with the dawn phenomenon. They are so broken their liver cannot even hold the glucose in fasting state. Or they have hyperglucagonism, Dr. Kendrick wrote a post about that, I do remember.

        The usual your-cells-need-insulin is also largely a fairytale. Your “cells” burn glucose continously and don’t have much buffering capacity. The amount of glucose in the bloodstream is in the order of 5 grams. The amount a SAD victim ingests daily is about one to two pounds. It is buffered in the liver and in sceletal muscles, in glycogen stores. … I could type and type but you can read it all in much better prose at

        http://high-fat-nutrition.blogspot.de/2009/11/liver-and-insulin-not-cooking-recipe.html

        Reply ↓
  34. Susan Pascoe

    Great suggestions. Since you mention a high fat low carb diet, what is your view of the current recommendations for a plant based diet?
    I really enjoy your writing and sense of humor. We could use more physicians as reasonable as you seem to be. Thank you.

    Reply ↓
      1. smartersig

        The people living in the Blue Zones eat little meat some not at all others only on special occasions, certainly all will be eating grass fed non battery farmed meats. Is this the most significant factor in their health, who knows but what you could do is adopt all their other lifestyle habits and eat KFC, cakes and pastries and then in 25 years get back to us and let us know if HD developed. You know it makes even more sense ?.

        Reply ↓
      2. Andy S

        Too much can be poisonous in case anyone is interested in experimenting. Smaller portions have medicinal properties. Couldn’t resist checking it out.

        Reply ↓
  36. Bill

    Why do plaques never develop in the heart itself?

    Too much turbulence in the heart chambers for clots to take hold?

    Reply ↓
  37. Andy S

    Coronary microvascular dysfunction is associated with endothelial dysfunction. Endothelium is in all blood vessels. Angina can also result from this condition. Maybe no plaque but cardiac arterioles and capillaries are compromised. Reduced blood flow > less O2 = hypoxia > lactic acid = pain

    Reply ↓
  38. Martin Back

    A plaque with a lipid core can’t be formed layer by layer. The core has to develop by some secondary process after the fibrous outer layers have been deposited by a clotting mechanism. Perhaps a more detailed look at the life cycle of a plaque is needed.

    Reply ↓
    1. Dr. Malcolm Kendrick Post author

      I disgree. I refer you back to studies on guinea pigs that I mentioned in a previous blog……

      ‘What G.C. Willis did in 1957 was to study guinea pigs. Guinea pigs are another animal that does not synthesize vitamin C. He made them scorbutic (vitamin C deficient a.k.a. scurvy). Actually, he did not make them all scorbutic. He had a control group of twelve guinea pigs that he put on a vitamin C deficient diet, then injected them with vitamin C. None of these twelve guinea pigs developed any measurable atherosclerosis.

      On the other hand, those guinea pigs on a scorbutic diet rapidly developed atherosclerosis. When I say rapidly, I mean within days. I think this point is worth repeating. If you make a guinea pig scorbutic, it will develop plaques, identical to those found in human arteries within days.

      Willis then started feeding his guinea pigs vitamin C, and he found that the lipid filled plaques quite rapidly disappeared. He describes what he saw happening to the guinea after they were fed vitamin C.

      ‘The results of this investigation indicate that early lesions of atherosclerosis are quickly resorbed. The stages of this process are first a fading of lipid staining in the region of the internal elastic membrane with later a disappearance of all extracellular fat. Active phagocytosis of lipid by macrophage occurs, and when these macrophages finally disappear no evidence of the lesion remains.’ 2

      I shall translate that passage for those with a non-science background.

      What Willis found was that if you remove vitamin C from the guinea pig diet, they develop fat filled atherosclerotic plaques within days. If you then add vitamin C to the diet again, the plaques rapidly disappear (within days). The process of removal appears to be that the fat/lipid is ingested (phagocytosed) by white blood cells – known as macrophages.

      However, if you let the plaques grow for too long, it is far more difficult to get rid of them.

      ‘More advanced lesions are considerably more resistant to reversal. Extensive lipid deposits clear in some parts of plaque but islands of intensely staining lipid persists in other parts. The macrophage response to such areas is only slight.’

      Thus, guinea pigs can develop lipid filled plaques within days, and this is entirely due to removing vitamin C from the diet which, causes blood clots to form. Which causes lipid filled cores to develop.

      Reply ↓
      1. Martin Back

        I imagine plaque formation as something like 3-D printing. You could print a fibrous mass, but to get a lipid core you’d have to inject the lipid into the fibrous mass afterwards.

        Reply ↓
      2. Christine Whitehead

        Martin. I imagine it more like a volcano than 3d printing. A hard shell forms in the same way a scab forms over an external wound. The core can remain soft and semi liquid for a long time. This assumes that by “core” we mean the original site of damage which takes time to heal whilst still being protected by the hard shell.

        Reply ↓
      3. Andy S

        Dr. M.K. my comments on the guinea pig experiment.
        1)- these were lab animals possibly fed a standard lab chow, low fat/high carb, corn, soybeans etc therefore needing vitamin C supplementation. Similar to existing human dietary guidelines.
        2)- guinea pigs are prone to scurvy therefore rapid response in experiment
        3)- are fatty streaks, lesions and plaques the same thing in this experiment?
        4)- Plaque with lipid core involves smooth muscle cell migration, not likely in a few days

        possible explanation:
        1)- In the intima oxLDL is formed from LDL due to lack of antioxidant vit. C
        2)- macrophages take up oxLDL to form fatty streaks called lesions or plaque in this case
        3)- restoring vit. C allows clearance of fatty streaks
        4)- no blood clots involved, everything observed are foam cells, fatty streaks
        5)- No classic plaque with lipid core protected by migrated smooth muscle cells has formed
        6)- fatty streaks were formed below the endothelium
        7)- Was there “injury” to the endothelium? ie apoptotic cells. Probably not.

        Implications: there are two types of plaque initiation
        1)- beginning as lipid core below endothelium, progressing to unstable plaque with layers of thrombi accumulation
        2)- Thrombi forming over areas of denuded endothelium.

        Reply ↓
        1. Dr. Malcolm Kendrick Post author

          You may find this paper of interest, and answers a few of your questions/issues. Role of Vitamin C in the Function of the Vascular Endothelium: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3869438/

          Key quote: With regard to the endothelium, it is worth emphasizing observations made more than 50 years ago that early scurvy generates endothelial disruption in guinea pigs, which resembles atherosclerosis and is fully and rapidly reversible with ascorbate repletion.

          Reply ↓
  39. Dr. Göran Sjöberg

    Having recovered from my retirement “chock” I have finally realized that I today own my own time and with a reasonable health (just now I feel fit!) and and an economy to survive I am free to enjoy different things of my liking. Nature conservancy is one of those things I am involved in during this time.

    Having enjoyed (?) the deep snow in northern Sweden for a month I am now enjoying my garden ponds in southern Sweden onto which I am just now looking with an Ardbeg 10 years in my hand. This seems to fit well into Malcolm’s schedule of preventing new MIs.

    Reply ↓
  40. AH Notepad

    I don’t understand that I never get notification of posts on blogs unless I post a reply, even thouigh the tag at the bottom of the page tells me I am following the blog. Something does not connect.

    Reply ↓
    1. JanB

      Hi AH – I think a reply is just part of the initial set up for any new Post, which is why we see quite a few one or two word replies, e.g. “Good.” after which you get an email to ‘confirm follow.’ It’s a bit of a faff but worth it to follow such an excellent blog.

      Reply ↓
  41. LWC

    My guess for why plaques don’t form in the chambers of the heart is turbulence. The blood entering the atria goes from a smaller volume (blood vessel) into a larger volume (chamber). The blood cells that had previously been pushed in one direction now swirl in all directions chaotically to fill the atria. From the atria they are pumped into the ventricle where there is still room to move chaotically. Then the blood is pumped into arteries to go to the lungs or the rest of the body where the diameter forces unidirectional motion.

    i would think it’s easier to effect a patch job if the flow is uniform rather than chaotic. In both conditions the pressure is high.

    Reply ↓
    1. JDPatten

      Yeah. My thinking has been along these lines – namely, that the blood zipping along in arteries creates shear forces that wouldn’t be in the heart. . . as much.
      Also, Bernoulli’s principle might well tend to lift those endothelial cells in arteries right off.

      Reply ↓
  42. Doug

    Q.
    P.S. Pop quiz. Why do plaques never develop in the heart itself? Here the pressure is highest, damage to endothelium must be greatest and yet, and yet, no plaques – ever.
    A.
    If plaques always form to repair damage then there are only 2 answers.
    1) – no damage ever happens
    2) – The damage is repaired differently. If it’s not repaired inside it must be repaired outside the damaged endothelium layer by the surrounding heart muscle.

    Is it the difference between the two scenarios? The inside of the heart is protected from rupture by the muscle itself therefor it can repair the damage differently. Whereas elsewhere it is not always the case that muscle will surround the damaged vessel?

    Reply ↓
    1. Dr. Malcolm Kendrick Post author

      Doug. I have an admission to make. I do not know the answer to my question. It is something that has vexed me for many years. I just wondered if anyone reading the blog might have a great idea.

      Reply ↓
      1. Doug

        And that’s why I keep coming back to your blog, never trust someone who says they have all the answers ….

        Have you read anything from Knut Sroka MD? http://heartattacknew.com/faq/what-causes-a-heart-attack/

        He’s focusing in on the parasympathetic nervous system (The FAQ on the left side menu gives the breakdown from classic approach to his ideas.)

        What I like is the commonality, reduce stress, build supporting relationships …. etc.

        Reply ↓
    2. Andy S

      Doug, This is a very important question. My understanding without looking too deeply from googling for answers:
      1)- Large arteries develop plaque and progress to MI, easily observable and main focus
      2)- damage to microvessels (arterioles and capillaries) progresses slowly to HEART FAILURE. A myocyte by myocyte demise. Out of sight and out of mind.
      3)- Hyperglycemia initiates both conditions (and many others i.e. destruction of pancreatic beta cells)
      4)- Repair of damage is difficult but progression can be stopped and possibly reversed by lifestyle changes (ditch the low fat recommendation)
      5)- collateral blood supply by angiogenesis to hypoxic tissues is part of the repair process
      6)- hyperglycaemia induced endothelial damage is systemic, the heart is not an exception
      7)- There could be other confounding questions and explanations

      Reply ↓
    3. Dr. Göran Sjöberg

      Dough,

      What Sroka says make sense to me!

      Though, the relation between the sympathetic and the parasympathetic nervous systems seems to be a controversial issue when relating to CVD and especially MI.

      Again – how little we know!

      Reply ↓
  43. Ray Sullivan

    First – I’ve really enjoyed this journey. Second – if I’ve understood 25% then I’m probably overstating my understanding (including the stats element – I’m a maths graduate who hated stats but now realises I need to revisit). One thing is clear – research needs to be moved from Parma, which implies government (national or, preferably international) intervention. Governments, which pay for drugs, could potentially insist all research data is released to the public domain, possibly via an escrow account which allows universities to re-analyse under strict conditions that prevents development of competing products, but allows challenges to claims. If the reanalysis fails to support claims, governments are free to but drugs from ‘better’ sources. I might be a dreamer…

    Reply ↓
  45. Errett

    Exerkines—–

    Format: AbstractSend to
    Int J Mol Sci. 2017 Jun 13;18(6). pii: E1260. doi: 10.3390/ijms18061260.
    The Therapeutic Potential of Anti-Inflammatory Exerkines in the Treatment of Atherosclerosis.
    Yu M1, Tsai SF2, Kuo YM3,4.
    Author information
    Abstract

    Although many cardiovascular (CVD) medications, such as antithrombotics, statins, and antihypertensives, have been identified to treat atherosclerosis, at most, many of these therapeutic agents only delay its progression.

    A growing body of evidence suggests physical exercise could be implemented as a non-pharmacologic treatment due to its pro-metabolic, multisystemic, and anti-inflammatory benefits. Specifically, it has been discovered that certain anti-inflammatory peptides, metabolites, and RNA species (collectively termed “exerkines”) are released in response to exercise that could facilitate these benefits and could serve as potential therapeutic targets for atherosclerosis.

    However, much of the relationship between exercise and these exerkines remains unanswered, and there are several challenges in the discovery and validation of these exerkines. This review primarily highlights major anti-inflammatory exerkines that could serve as potential therapeutic targets for atherosclerosis. To provide some context and comparison for the therapeutic potential of exerkines, the anti-inflammatory, multisystemic benefits of exercise, the basic mechanisms of atherosclerosis, and the limited efficacies of current anti-inflammatory therapeutics for atherosclerosis are briefly summarized. Finally, key challenges and future directions for exploiting these exerkines in the treatment of atherosclerosis are discussed.
    KEYWORDS:
    atherosclerosis; exerkine; physical exercise
    PMID: 28608819 DOI: 10.3390/ijms18061260

    Reply ↓
    1. xtronics

      Exerkines – yet another buzz term that lacks meaning – I suppose they are talking about cytokines or rather interleukines that are the result of exercise? (Same with bowl-flora now called microbiome. I would much rather see new science than duplication of terms. )

      Anyway – we know a bit about this from some of the exercise research. I personally reduced my fasting BG from the upper 90’s to the lower 80’s via weight lifting.

      Turns out all exercise is not the same. The fastest way to reverse T2D is via weight lifting training ( Rippetoe etc) . We know that muscle mass is somewhat correlated with mortality, but strength has a much higher correlation ( could be that only active-strong muscle mass does the trick). The changes in BG in just a few weeks is remarkable. ( All forms of exercise do some good – just that if you want the biggest return for the time involved – weight training is the deal – I also do a few sprints on my off days to keep my endurance and heart muscle in good shape).

      So once we realize that high-damaging BG is not always the result of low insulin, but rather insulin resistance things get interesting. One of the things LA(Linoleic-Acid) consumption produces is HNE – which there are papers that support a narrative that they are another cause of insulin resistance.
      https://academic.oup.com/endo/article-lookup/doi/10.1210/en.2011-1957#sthash.ZiwZ2AyH.dpuf

      At the same time – eating large amounts of concentrated seed oil (containing LA) messes with the insulin sensitivity of adipose tissue – could be the reason it lowers cholesterol – by storing evermore fat. ( I would refer you to Petro’s blog and his narrative about the proton papers )
      http://high-fat-nutrition.blogspot.com/search/label/Protons%20%2802%29%3A%20Where%27s%20the%20bias%3F

      Is it a good idea to recommend to CAD Patients to eat a PUFAs substances that didn’t go through drug studies – to lower cholesterol by making them fat? Such is modern medicine – it continues in spite of this:

      What causes heart disease part XXIII

      As a dietary element that is easily avoided LA appears to be correlated with disease and obesity. See the graphs here:
      https://xtronics.com/wiki/LA_speculation.html

      Reply ↓
  46. Terramuggus

    Jason Fung, one of my favorite medical writers and LCHF/fasting doctors has a great take on atherosclerosis, heart disease and insulin:

    “Atherosclerosis, sometimes called ‘hardening of the arteries’ is the precursor to heart attacks, strokes, and peripheral vascular disease. Since the earliest days of insulin treatment, it has been noted that it has been linked to the development of atherosclerosis. Animal studies had demonstrated as early as the 1949 that insulin treatment cause early atherosclerosis, which could be reversed by preventing the excessive insulin.

    Atherosclerosis is an inflammatory process that develops through several stages – initiation, inflammation, foam cell formation, fibrous plaque formation and then advanced lesions. Insulin facilitates atherosclerosis along every step of this pathway. Furthermore, insulin receptors are found inside human plaque and experimentally, insulin stimulates the growth of plaque, contributing to the progression of atherosclerosis.”

    https://www.dietdoctor.com/insulin-toxicity-modern-diseases

    Reply ↓
    2. Dr. Göran Sjöberg

      This reminds me and also relates to what Dr. Kraft with his 14 000 clinical measurement of blood glucose and serum insulin in parallell (upon standard glucose load testing) stated: : “Those with established CVD but who are not diagnosed as diabetics are just undiagnosed!”

      Reply ↓
      1. Dr. Malcolm Kendrick Post author

        That is one way to get rid of the need for facts – I suppose. Try telling four year old children with coronary artery aneurysms, as a result of Kawasaki’s disease, that they are simply undiagnosed diabetics. Equally, how does one explain the increased risk of CVD from smoking as being due to undiagnosed diabetes. Perhaps everyone with antiphospholipid syndrome is also an undiagnosed diabetic etc. etc. I am sorry, but anyone who attempts to squeeze all of CVD causation within the Procrustean bed of a single factor does not get my vote. In the US, the rate of obesity and type II diabetes has exploded in the last thirty years. Whilst the rate of death from CHD has stubbornly declined. Same pattern in the UK.

        Whilst I fully believe that raised blood sugar and/or insulin is an important causal factor in CVD, it is A factor. Not THE factor.

        Reply ↓
      2. Dr. Göran Sjöberg

        Malcolm,

        Great thoughts!

        But we all love those simple explanations!

        And I, myself, is a believer in the causality of the western world high carb “diets” by the simple fact that we, me and my wife, personally have experienced regaining our health by cutting the carbs. Still I believe that this only relates to people who have been caught in the metabolic syndrom – though 50 % of the western world population..

        And again – how little we know!

        Reply ↓
      3. Andy S

        Lesson learned fro Dr. Kraft: Carbohydrate restriction fixes the problem of progressing towards diabetes.

        Reply ↓
        1. Dr. Malcolm Kendrick Post author

          Yes, I am sure Dr Kraft is right about this. However, one problem we have here is that diabetes is not really a disease, it is simply a biochemical measurement. Lower the measurement and have we cured a disease? No, the underlying issues are still there, but not reflected by a high blood sugar level.

          Reply ↓
      4. Andy S

        Dr Malcolm Kendrick, had to look up “Procrustean Bed” (PB). In engineering PB principle is not used, in medicine PB approach is applicable. For example there are PB standards for cholesterol, blood pressure etc.. PB solutions are provided by pharmaceutical companies. Medical practitioners will compare your numbers to the PB Standard and if cholesterol (or other number) is out of range statins will be prescribed as the PB solution. Adverse side effects are part of the PB treatment.

        Dr, Kraft’s insulin test can identify people (with or without CVD) who are at risk of developing diabetes and can thereby modify lifestyle to avert a disaster. Smokers and Kawasaki survivors included.

        Reply ↓
  48. Mr Chris

    a most interesting paper.
    do people have a lot of fibrinogen in their blood, because there is a lot to repair, is it an indicator of poor condition of the lumen?

    Reply ↓
    1. Dr. Malcolm Kendrick Post author

      People with more fibrinogen in their blood are far more likely to die from CVD. Here from the Scottish Heart Health study:

      Fibrinogen was found to be an important risk factor for coronary heart disease in men and women, with and without pre-existing coronary heart disease. There appears to be a threshold effect, with those in the highest fifth of the distribution having a much increased risk. Estimated age-adjusted hazard ratios by sex and pre-existing coronary heart disease group for the highest to lowest fifth of fibrinogen range between 1.93 and 4.86. Fibrinogen is also important as a risk factor for coronary death and all-causes mortality, with a similar threshold effect. Comparing the two extreme fifths, the hazard ratios for coronary death are 3.01 and 3.42, and for all-cause mortality are 2.59 and 2.20, for men and women respectively. Adjustment for cotinine reduces the hazard ratios, but further adjustment for the other 11 risk factors has little effect for coronary heart disease events. After full adjustment there is a remaining significant (P < 0.05) hazard ratio for coronary death and death from any cause and for a coronary heart disease event for those free of coronary heart disease at baseline, amongst men, comparing the highest to the lowest fifth.

      CONCLUSION:
      Fibrinogen is a strong predictor of coronary heart disease, fatal or non-fatal, new or recurrent, and of death from an unspecified cause, for both men and women. Its effect is only partially attributable to other coronary risk factors, the most important of which is smoking. https://www.ncbi.nlm.nih.gov/pubmed/9503176

      Reply ↓
      2. chris c

        “Estimated age-adjusted hazard ratios by sex and pre-existing coronary heart disease group for the highest to lowest fifth of fibrinogen range between 1.93 and 4.86.”

        Good grief! That’s huge compared to “cholesterol”, or bacon. And we knew this in 1998. Why did we forget? No drug to market to reduce it?

        Reply ↓
  49. Charles Gale

    I tend to agree that insulin is not THE factor (and in my case not even A factor).

    I’m a long term HCLF and have just bought a blood sugar test kit from Boots – the type you dip some litmus paper into your urine and see if it changes colour.

    So far: all negative – no sugar in the blood.

    Over the last year, I haven’t really changed my mind about Dr Kendrick’s stress hypothesis being responsible for my encounter with the Grim Reaper.

    Reply ↓
    1. JanB

      Charles Gale – unless you have a low renal threshold (unlikely) then a urine glucose test isn’t going to tell you with any accuracy whether you have increased blood glucose as the BG has to go fairly high before it registers in your pee. If you really want to know you’ll have to get a blood glucose monitor.
      Cheers

      Reply ↓
      2. chris c

        JanB I posted this on the previous blog in reply to your query about diabetes but it never got through.

        (I have been blocked here and on several other blogs AGAIN and to my knowledge NOT by the blog owners. Usually this happens on Google blogs, this time they are all on WordPress. I’m pretty sure I know WHO is doing this, just not HOW. Inquiries are ongoing)

        You may find some interesting stuff if you dig around here

        http://www.diabetesgenes.org/

        There are actually a whole bunch of different conditions grouped under the title of “Type 2” diabetes. What I have is shared by a small but significant number of others all over the world. It is characterised by symptoms of diabetes beginning in early childhood and including symptoms of reactive hypoglycemia, followed by a slow progression and normal or even low body weight. Only about half the people I know have gone on to be DIAGNOSED diabetic – which is supposedly set where at least 50% of the beta cells are deceased. The others, like me, remain “prediabetic”. It’s similar to one of the MODYs but not monogenic, the familial distribution is wrong.

        In my family it predominantly affects males, someone else has it mostly in females and in others it is more equally divided between the sexes, or I should say among the genders. One believed as a child that old people shed limbs in the same way that trees lose their leaves in autumn, that’s how common it was in her family.

        The mechanism appears to be a failure to produce, or store, or release, Phase 1 insulin, but Phase 2 insulin remains intact for a long time. Or if you believe Roger Unger the insulin fails to shut down postprandial glucagon. Either way, glucose spikes after eating too many carbs – where too many is a fraction of what dieticians claim is essential – then the insulin turns up late to the party and stays after all the glucose has gone home, driving BG low and causing a panic reaction where the alpha cells dump a load of glucagon and the rest of the endocrine system joins in, producing cortisol, epinephrine, norepinephrine, neuropeptide Y etc. to get the BG back up, and induce carb cravings. Rinse and repeat.

        Unlike “genuine” MODY insulin resistance is also a major factor. Sound familiar? The usually suggested treatment is to eat carbs every couple of hours, The treatment that actually works is to reduce carbs until the BG no longer spikes, then the insulin no longer spikes, then the IR comes down, and let your body run predominantly on fats and ketones.

        Does any of this sound familiar at all?

        If not, don’t worry, there are a whole bunch of other variants, none of them fitting the usual explanation that diabetes is caused by being fat and lazy and being fat is caused by eating fat and meat.

        Reply ↓
        1. Jan B

          chris c – thank you for your long and considered reply. It’s much appreciated. It’s so hard to get any detailed information about diabetes. No one seems to know much, and just trots out the same old same old – insulin resistance, even though I have not a single symptom of it. My newest GP looked at me and said “But you’re not fat.” I’m considering if I ought to clear out my bank account by having a genetic test, maybe, but most definitely an insulin assay. I’m in the dark and need proper knowledge. LCHF though really works well for me so I shall keep to that even though it makes my DN almost pass out at the thought of me eating (good) fats.
          Thank you again.
          Jan B

          Reply ↓
      3. Antony Sanderson

        Jan have a look at diabetes.co.uk . . . there a lot of fellow diabetes sufferers of many different types who discuss diabetes issues.

        Reply ↓
      4. Antony Sanderson

        Jan there is diabetes site based in the uk . . diabetes . co . uk – On the site there are diabetics of different sorts who discuss their issues. They might provide some clarification.

        Reply ↓
  50. Randall

    Dr. Kendrick you wrote that a blockage in an artery is caused by clotting. I watched many videos of surgeons removing plaque from arteries. Although I could include many videos, I will concentrate on one. The surgeon removing the plaque describes the plaque as a combination of cholesterol and calcium. Please watch one minute of this video at the 20 minute point – Warning – graphic. https://www.youtube.com/watch?v=wQ1yIT8dt3Y

    Reply ↓
    1. Dr. Malcolm Kendrick Post author

      Over time thrombi convert to (what we call) plaque and plaque converts to calcium. Unless the surgeon thinks high serum calcium levels are the cause of plaque. Equally if he is pulling out plaque he is looking at red blood cells, fibrin, bits of platelets, white blood cells, triglycerides etc. Fro a little more detail about what is actually in a plaque you may wish to read this paper. (I include the abstract)

      Characterization of Signal Properties in Atherosclerotic
      Plaque Components by Intravascular MRI
      Walter J. Rogers, Jeffrey W. Prichard, Yong-Lin Hu, Peter R. Olson, Daniel H. Benckart,
      Christopher M. Kramer, Diane A. Vido, Nathaniel Reichek

      Abstract—Magnetic resonance imaging (MRI) is capable of distinguishing between atherosclerotic plaque components
      solely on the basis of biochemical differences. However, to date, the majority of plaque characterization has been
      performed by using high-field strength units or special coils, which are not clinically applicable. Thus, the purpose of
      the present study was to evaluate MRI properties in histologically verified plaque components in excised human carotid
      endarterectomy specimens with the use of a 5F catheter– based imaging coil, standard acquisition software, and a clinical
      scanner operating at 0.5 T. Human carotid endarterectomy specimens from 17 patients were imaged at 37°C by use of
      an opposed solenoid intravascular radiofrequency coil integrated into a 5F double-lumen catheter interfaced to a 0.5-T
      General Electric interventional scanner. Cross-sectional intravascular MRI (1563250 mm in-plane resolution) that used
      different imaging parameters permitted the calculation of absolute T1and T2, the magnetization transfer contrast ratio,
      the magnitude of regional signal loss associated with an inversion recovery sequence (inversion ratio), and regional
      signal loss in gradient echo (gradient echo–to–spin echo ratio) in plaque components. Histological staining included
      hematoxylin and eosin, Masson’s trichrome, Kossa, oil red O, and Gomori’s iron stain. X-ray micrographs were also
      used to identify regions of calcium. Seven plaque components were evaluated: fibrous cap, smooth muscle cells,
      organizing thrombus, fresh thrombus, lipid, edema, and calcium. The magnetization transfer contrast ratio was
      significantly less in the fibrous cap (0.62613) than in all other components (P,0.05) The inversion ratio was greater
      in lipid (0.9160.09) than all other components (P,0.05). Calcium was best distinguished by using the gradient
      echo–to–spin echo ratio, which was lower in calcium (0.3660.2) than in all plaque components, except for the
      organizing thrombus (P,0.04). Absolute T1 (range 3006140 ms for lipid to 6306321 ms for calcium) and T2 (range
      40612 ms for fresh thrombus to 59621 ms for smooth muscle cells) were not significantly different between groups.
      In vitro intravascular MRI with catheter-based coils and standard software permits sufficient spatial resolution to
      visualize major plaque components. Pulse sequences that take advantage of differences in biochemical structure of
      individual plaque components show quantitative differences in signal properties between fibrous cap, lipid, and calcium.
      Therefore, catheter-based imaging coils may have the potential to identify and characterize those intraplaque
      components associated with plaque stability by use of existing whole-body scanners. (Arterioscler Thromb Vasc Biol.
      2000;20:1824-1830.)

      This paper on plaque morphology is also worth a read.

      A Definition of Advanced Types of Atherosclerotic Lesions and a Histological Classification of Atherosclerosis
      A Report From the Committee on Vascular Lesions of the Council on Arteriosclerosis, American Heart Association

      Herbert C. Stary, A. Bleakley Chandler, Robert E. Dinsmore, Valentin Fuster, Seymour Glagov, William Insull, Michael E. Rosenfeld, Colin J. Schwartz, William D. Wagner, Robert W. Wissler

      http://circ.ahajournals.org/content/92/5/1355

      Abstract

      Abstract This report is the continuation of two earlier reports that defined human arterial intima and precursors of advanced atherosclerotic lesions in humans. This report describes the characteristic components and pathogenic mechanisms of the various advanced atherosclerotic lesions. These, with the earlier definitions of precursor lesions, led to the histological classification of human atherosclerotic lesions found in the second part of this report. The Committee on Vascular Lesions also attempted to correlate the appearance of lesions noted in clinical imaging studies with histological lesion types and corresponding clinical syndromes. In the histological classification, lesions are designated by Roman numerals, which indicate the usual sequence of lesion progression. The initial (type I) lesion contains enough atherogenic lipoprotein to elicit an increase in macrophages and formation of scattered macrophage foam cells. As in subsequent lesion types, the changes are more marked in locations of arteries with adaptive intimal thickening. (Adaptive thickenings, which are present at constant locations in everyone from birth, do not obstruct the lumen and represent adaptations to local mechanical forces). Type II lesions consist primarily of layers of macrophage foam cells and lipid-laden smooth muscle cells and include lesions grossly designated as fatty streaks. Type III is the intermediate stage between type II and type IV (atheroma, a lesion that is potentially symptom-producing). In addition to the lipid-laden cells of type II, type III lesions contain scattered collections of extracellular lipid droplets and particles that disrupt the coherence of some intimal smooth muscle cells. This extracellular lipid is the immediate precursor of the larger, confluent, and more disruptive core of extracellular lipid that characterizes type IV lesions. Beginning around the fourth decade of life, lesions that usually have a lipid core may also contain thick layers of fibrous connective tissue (type V lesion) and/or fissure, hematoma, and thrombus (type VI lesion). Some type V lesions are largely calcified (type Vb), and some consist mainly of fibrous connective tissue and little or no accumulated lipid or calcium (type Vc).

      This makes it clear that there is rather more complexity to an atherosclerotic plaque than simply calcium and cholesterol.

      Cheers

      Reply ↓
      1. smartersig

        Dr Kendrick, I would be most grateful if you could outline what are you own personal habits to hopefully ward off heart disease. If you could please include anything eg diet, supp’s, lifestyle practices that you use. I of course will take anything you write as not a recommendation to others but simply your own personal choices.

        Reply ↓
      2. JDPatten

        What is left behind after an endarterectomy is performed?
        According to what you’ve described to us, a loss of endothelial cells results in a clot on the missing spot and then new endothelial cells form in place over that.
        If this process continues at the same spot without time to heal and clear the “clot”, layers build up — but the area will always have the new protective endothelial cover, yes?
        If the whole thing is pulled out, that leaves the whole area bare and needing a new clot and endothelial cover, no?
        It all just starts again!?

        Reply ↓
    1. Gary Ogden

      Dr. Göran: Thanks for the link. They are worse than I thought. A plague on human health. Also, my ascorbic acid powder has finally arrived! I’ve come to find out that most supplement ingredients are now sourced from China. The one I ordered is made in Scotland, so it must be good! How many grams do you mix with how much water? Thanks!

      Reply ↓
      1. AH Notepad

        Gary, as I understand it, vitamin C dosing is dynamic. In general I have 1/2 tsp (2.5g) in a mug with around 2g potassium citrate and one of the efervescent vitamin C tablets. This makes it palatable for me, though others find it too bitter. Robert Cathcart’s videos on youtube explain that if you are using 10g to 15g vit C a day in normal health, then colds, hayfever, stress and other factors may increase the requirement to 200g+. You also have to take enough. Not enough may make you feel better but if you reduce the dose to normal you may feel worse, whereas if you have enough for a few days you will feel ok when you reduce the dose. It’s all indicated by bowel tolerance.

        Reply ↓
        1. Gary Ogden

          AH Notepad: Interesting. I stir 1/2 tsp of the ascorbic acid powder into the mineral water I drink, and find the acidity refreshingly delicious, like lemon-lime soda pop. I sometimes do this twice a day, for 2-4g. I don’t get sick, and don’t have any diseases that I know of, so I’m going to stick with that amount, due to the expense ($ 0.15g). I also put a bit of salt in it. Potassium citrate sounds acidic. The potassium bicarbonate I take is alkaline. I stir it into my beet kvass (1/4 tsp into 4 oz. twice a day for 1.4g total), and it seems to be neutralized by the lactic acid. I makes an agreeable flavor. Interesting to note that, since I increased my salt intake (and pay better attention to hydration), I no longer get those common minor injuries from my workouts (usually hip and/or knee). The potassium may have something to do with this, too.

          Reply ↓
          1. AH Notepad

            I’m not sure what you mean by ($ 0.15g) My ascorbic acid is £46 per 5kg, or just under 1p per gram. If my understanding is correct that’s about one tenth of your costs. I have just done a pH test on the potassium citrate and with 2g in about 25ml water it is 7 to 8. Ascorbic acid for the same conditions is around pH2. After a days significant exercise I often get prone to cramps the next day which appears to be eased by some potassium, but I know that’s not very scientific, just a lot more comfortable.

          2. Gary Ogden

            AH Notepad: Yes, you’re getting it much cheaper, about 1/3 the price I’m paying. I believe a penny here is the same as a penny there, i.e. one hundredth, so $0.15 is fifteen hundredths of a dollar. I think the exchange rate is $1.26 US to the British pound, and I’m aware you have guineas and shillings and farthings, and so forth, but do you not use the decimal system with your currency? I would beware, though. Your ascorbic acid may come from China, as most of it does. The other interesting thing I’ve noticed since I’ve increased my salt intake is: No more cramps! This may have something to do with the potassium, or better hydration, or all three. I used to get painful foot or calf cramps, usually when lying down, but no longer.

  52. John U

    Jan B and others – I have recently come across a FB page devoted to TD2 hosted by Jeff Cyr. If you know how to navigate on FB, you can find him. His writings are very detailed and relatively easy to follow if you take your time reading. The content is very dense. I can’t vouch for the accuracy, but I was quite impressed. Jeff is another person who developed severe T2D at mid age and spent a lot of time educating himself. Worthwhile to join FB and read the stuff he has written. I learned a lot.

    Reply ↓
    1. Jan B

      Thanks for that,John U. There’s a lot to take in – as you say, it’s very dense but I shall do my best to take it all in. From a fairly perfunctory read of the first post all my signs, ratios etc. seem spot on yet my BG remains almost always outside the normal range, even with medication and a really low carb intake. Of course it goes much too high if I eat like a normal person – how I long for a slice of my homemade bread, toasted and well buttered – sigh. I suppose it’s the same problem for everyone. We are all different in our responses to health problems….but how I wish I could find the info I need for MY problem. The DN says insulin insensitivity and yet I don’t have a single symptom of it. Yes, I’m thin especially by today’s standard though not by the standards of 40 or 50 years ago when every woman’s goal was a 24 inch waist.
      Excuse the rant. I feel much better with that off my chest. I shall go and do the ironing which also counts, I think, as ‘moderate exercise.’
      What a wonderful site this is. My thanks to the good doctor.

      Reply ↓
      1. Gary Ogden

        Jan B: In “The Salt Fix,” Dr. DiNicolantonio writes about people who are thin and diabetic, I think in the chapter called “We are Starving Inside.” He mentions that “Cutting carbs causes you to become a ‘salt waster,’ excreting more salt than you would on a more balanced diet. . . . Thus, if you are going to cut your carbohydrate intake, you want to increase your salt intake to match the additional salt loss by the kidneys and to help prevent the subsequent rise in insulin levels to compensate for this loss.”

        Reply ↓
        1. Jan B

          Yes, interesting. I found that when I finally and properly committed to a HFLC diet I became ‘hungry’ for salt and adapted my intake to how much I could taste it. That is to say, if I added a small amount of salt to, say, my breakfast eggs and couldn’t taste it I would add more but if I could taste the small amount I wouldn’t add more, because I assumed rightly or wrongly that my body was telling me how much I needed. That may sound potty, now I come to think of it. However, I will definitely buy The Salt Fix.

          Reply ↓
      2. chris c

        I started on usenet, moved to various forums and blogs and have specialised in looking for other thin Type 2s, who are legion. Theoretically from 5% – 20% of “type 2s” are non – overweight, while 80% of fat people are nondiabetic. Count Pareto would have had something to say about that.

        The actual % will remain completely unknown as long as so many doctors believe the fat+diabetes theory and simply will not look for it in skinny people, unless they are obviously Type 1.

        I used to know Jenny, who has amassed a load of research

        http://www.bloodsugar101.com/

        and have actually met Alan

        http://www.loraldiabetes.blogspot.com/

        who has a lot of more practical advice.

        Currently there is a good-natured battle on Twitter between David Unwin, Ted Naiman and several other doctors both sides of the Atlantic where patients show absolutely remarkable improvements in A1c, lipids, BP and anything else they choose to measure. The true tragedy is that I saw this again and again on the ADA’s own forum, back well over a decade ago, yet they took absolutely no notice.

        Reply ↓
  53. AH Notepad

    I had better get a copy of “The Salt Fix”. Loss od sodium is seriously bad for the system, so could a remedy be to use sodium ascorbate instead of ascorbic acid? That mixed with one of the effervescent tablets which contain sodium bicarbonate could help. Then again does it show that trying to look for advantages will always have a disadvantage, with the biggest advantages being gained by keeping away from the big pharma toxic offerings.

    Reply ↓
    1. Gary Ogden

      AH Notepad: I think you may be right, and this may be why Dr. Suzanne Humphries recommends either ascorbic acid or sodium ascorbate. We do need chloride, but our physiological need for sodium is much greater, and it exists in a high concentration in the blood. With healthy kidneys we pee out any excess sodium we ingest, while the kidneys reabsorb most of the sodium in the vast volume of blood they process each day. Dr. DiNicolantonio suggests that restricting sodium may cause or exacerbate problems in kidney function (My doctor says these are common; methinks perhaps as a result of bad medical advice!).

      Reply ↓
  54. John Collis

    I have just watched a film called “What the health”, unfortunately it is a Netflix original and therefore is only available to Netflix subscribers or through their website http://www.whatthehealthfilm.com/ but it basically propses that a lot of chronic disease in humans is down to eating animal products and that by eating a solely plant based diet it is possible to reverse some of these conditions within two weeks. They criticise the involvement of the various animal product companies in the sponsoring of the different medical organisations in the states, like the AHA, the American Diabetes Association and a breast cancer awareness organisation and also their involvement in the FDA. If anyone else has watched this film then I’d be interested to see what other people think.

    Reply ↓
      2. smartersig

        I get the impression that Rob Wolff does not allow any pro Veggie comments on his blog. Certainly mine have been rejected it would seem.

        Reply ↓
    2. smartersig

      Yes I have watched it, inspiring stuff. A whole food plant based diet is the only diet proven to reverse heart disease but sadly the meat and diary propaganda machine is very powerful. You can catch it on Youtube by the way.

      Reply ↓
      2. Charlie

        The Ornish trial even with all the confounders wasn’t that successful;
        “The absolute change in the arterial widening that Ornish found was only 3 percentage points. Moreover, arterial widening itself has been found not to predict heart attack risk with any accuracy. Rather than the build-up of plaque, it is a certain type of unstable, break-away plaque that is now thought to clog arteries and cause heart attacks.

        Also, one should note that although there were fewer cardiac events in the diet-and-exercise group, the ultimate endpoint, death, did not favor the Ornish group: two people died in his diet-and-exercise group (out of 22 total) vs. only one of the controls.” https://ninateicholz.com/critique-of-dean-ornish-op-ed/

        Plus it also had poorer markers for insulin resistance;
        “Moreover, although not acknowledged by the AHA, we know that the ratio of triglycerides to HDL is a very strong predictor of heart disease; among the best [8]. A triglyceride-to-HDL level of less than 2 is considered ideal. Over 4 is considered risky. Over 6 is considered very high risk. The intervention group’s average triglycerides-to-HDL ratio leapt from 5.4 to 6.8! It went from bad to worse. Thus, the third problem with the study is that it actually showed a worsening of heart disease by other important measures.
        The bottom line is that Ornish’s study never showed what it claimed to show.”
        http://www.ketotic.org/2015/05/ornish-diet-worsens-heart-disease-risk.html

        And the vegetarian myth just doesn’t hold up not even in epidemiology;

        A new study from Australia finds yet again that vegetarians don’t live longer than meat eaters.
        https://rosemarycottageclinic.wordpress.com/2017/06/25/even-in-the-land-of-barbies-and-beer-vegetarians-dont-live-longer/

        Reply ↓
        1. smartersig

          Which is why I eat fish, even the study you cite shows that fish eaters live longer than meat or veggie only eaters. People on a plant only based diet need to beware the B12 problem and perhaps Carnosne deficiency

          Reply ↓
        2. smartersig

          I am a member of the Veggie society in my home town and I observed that their diet is pretty much as bad as a meat eaters diet in terms of sugar and white flour products. Most of them are veggie for ethical reasons and you would be surprised how many are ignorant of the health angles. So the point I am making is equating Ornish or Esseltyn with overall veggie stats is not really like for like. As I said before the Aussie study shows quite clearly that Pescetarians live longer not meat eaters

          Reply ↓
        3. Mr Chris

          Charlie
          about the ratio Triglycerides/HDL should optimally be under 2, I have seen this many times but have never seen an explanation.
          Any ideas?

          Reply ↓
          1. Andy S

            Mr Chris, TG:HDL ratio correlates with sdLDL level. Lots of sdLDL is considered bad, therefore keep ratio low. Carbs raise TG (bad), saturated fat raises HDl (good).

          2. smartersig

            Taken from the Oxford Epic study

            “Within the study, the incidence of all cancers combined was lower among vegetarians than among meat eaters, but the incidence of colorectal cancer was higher in vegetarians than in meat eaters.”

          3. smartersig

            And just to confuse us a little more

            “For the study, researchers at Loma Linda University in California analyzed the dietary habits of more than 70,000 people. Those who ate a vegetarian diet had a 22% lower risk of colorectal cancer than those who weren’t vegetarians. Among those who ate a vegetarian diet that included fish, the reduction in risk was even greater — 43%. A vegetarian diet that includes fish and other seafood is called a pescovegetarian diet.

            Keep in mind that the study didn’t show that a vegetarian diet caused this lower risk, just that diet and risk were associated. The results were published online in JAMA Internal Medicine.”

        4. Gary Ogden

          Charlie: Thanks! This should put to rest the vegetarian/meat eating silliness in regard to disease. Eat what you wish, just make sure it’s high quality, Stay away from flour and sugar and vegetable oils as much as possible, but certainly don’t worry about having cake or soda pop once in a while. In fact, don’t worry about anything; won’t do you a bit of good. Follow Dr. Kendrick’s list of healthful behaviors. Be sure to get plenty of salt, especially in hot weather, and stay well-hydrated. Be wary of conventional medical advice and anything published in the media. Enjoy this fascinating planet we live on.

          Reply ↓
    3. chris c

      Vegan propaganda. There’s a LOT of it about, mostly uncritically accepted by the mainstream media.

      Two immediate thoughts – if meat was actually toxic waste as these people and too many dieticians and many researchers claim, we would have become extinct millennia ago. Instead the “epidemics” of modern diseases started when we began believing actual toxic waste was “heart healthy”.

      Peter Cleave, 1973

      “I don’t hold the cholesterol view for a moment…For a modern disease to be related to an old-fashioned food is one of the most ludicrous things I have ever heard in my life…If anybody tells me that eating fat was the cause of coronary disease, I should look at them in amazement. But when it comes to the dreadful sweet things that are served up… that is a very different proposition.”

      Remember back to what our grandparents ate.

      Now go look at the ACTUAL sponsors of the ADA. AHA, AND, the UK equivalents and the same in all other countries. Mostly you will see drug companies, carbohydrate processors and margarine manufacturers.

      To vegans these are all good because they are plant-based, even if it means an industrial plant.

      HTH 😉

      Reply ↓
      1. smartersig

        A vegan whole food pant based diet is the only diet that has been shown to reverse heart disease, why that is may be debatable but while you are debating your HD may be getting worse.

        Reply ↓
          1. smartersig

            The Ornish trial may not have been randomised nor perhaps the large number of Esseltyn patients who have benfited from a WFPD. The difference however to your statement and mine is that you are taking a purely scientific viewpoint based on trial evidence. I am taking a more pragmatic viewpoint which is that many people are sick or getting sick from HD and they need to place their bets NOW. So what should they do given the best available evidence, well Orhish and Esselltyn patients appear to do well on a WFPD and the Blue Zone pop’s also a high pant based diet. Are you suggesting therefore that we should all carry on with the trad western diet until that double blind placebo controlled trial comes along ?.

          2. Dr. Malcolm Kendrick Post author

            A double blind placebo controlled trial is not possible. A randomised controlled trial is. Science does have a specific terminology. Also, a scientific viewpoint means ensuring that, as far as possible, bias is removed from the gathering of evidence. I would not believe any clinical trial set up to prove that a certain way of doing things is definitely good, carried out by people with a clear financial stake in the outcome, and with no control, and no external validation. I am flattered that you think I am taking a purely scientific viewpoint. It is the only viewpoint that has any validity. It is a hard discipline to follow, seeking objective truth.

          3. smartersig

            Are you saying that when Esseltyn states that he improves and in cases reverses heart disease with a WFPD you are not willing to take his word because he has a financial interest in saying so ?. I fail to see how he could benefit long term as there would be a concensus amongst patients that his methods are quackery and I have not seen or heard any such opinions from his patients in fact quite the opposite.

          4. Dr. Malcolm Kendrick Post author

            When someone else, someone objective, repeats findings, then I take them seriously. Bias in research is very difficult to eradicate. But when someone does research to prove that the thing they are promoting, works – well, good for them. But independent verification is when research becomes serious.

          5. smartersig

            So you want a doctor to do a plant based research project who would not want to adopt it as a treatment should it work. Why would your own personal curiosity not be spiked sufficiently to try this on some of your own patients ?.

          6. Dr. Malcolm Kendrick Post author

            That is a pure straw man argument. ‘A straw man is a common form of argument and is an informal fallacy based on giving the impression of refuting an opponent’s argument, while refuting an argument that was not advanced by that opponent. One who engages in this fallacy is said to be “attacking a straw man”.’

            What I want is scientific research to be objective. When someone carries out research to prove that they are right, I expect them to be successful. What is needed is someone who expects to prove something wrong, who then finds the same thing as the first person found. Then you are looking at something that might be interesting. The primary purpose of scientific experimentation is to prove something wrong i.e. ‘disprove the null hypothesis.’ Unfortunately, the vast bulk of medical research is specifically designed to prove things right.

          7. smartersig

            I have problems with the idea that they stand to gain by making WFPD claims. This is how the scenario would run. Doctor makes claims that his WFPD approach halts heart disease. Loads of patients flock to his practice. He makes a few dollars in the short term but in the medium to long term shed loads of patients are complaining that he did nothing for them. In a connected internet based world this would not be difficult. I am only hearing satisfied customers. Doctors are quickly discredited. Who is benefiting then, the all powerful Brocolli lobbying industry ?.

      2. Andy S

        HI smartersig, RE Ornish Study: Intensive lifestyle changes reduce plaque
        – 10% fat
        – vegetarian diet
        – exercise
        – stop smoking
        – reduce stress
        – group support

        This study does not convince me that soy tofu is healthier than eggs and meat, or that fat causes CVD. Apparently vegetarians/vegans get more cancer.

        JAMA. 1998 Dec 16;280(23):2001-7.
        Intensive lifestyle changes for reversal of coronary heart disease.

        Ornish D1, Scherwitz LW, Billings JH, Brown SE, Gould KL, Merritt TA, Sparler S, Armstrong WT, Ports TA, Kirkeeide RL, Hogeboom C, Brand RJ.

        OBJECTIVES:
        To determine the feasibility of patients to sustain intensive lifestyle changes for a total of 5 years and the effects of these lifestyle changes (without lipid-lowering drugs) on coronary heart disease.
        DESIGN:
        Randomized controlled trial conducted from 1986 to 1992 using a randomized invitational design.
        PATIENTS:
        Forty-eight patients with moderate to severe coronary heart disease were randomized to an intensive lifestyle change group or to a usual-care control group, and 35 completed the 5-year follow-up quantitative coronary arteriography.
        SETTING:
        Two tertiary care university medical centers.
        INTERVENTION:
        Intensive Lifestyle Changes (10% Fat Whole Foods Vegetarian Diet, Aerobic Exercise, Stress Management Training, Smoking Cessation, Group Psychosocial Support) For 5 Years.
        MAIN OUTCOME MEASURES:
        Adherence to intensive lifestyle changes, changes in coronary artery percent diameter stenosis, and cardiac events.
        RESULTS:
        Experimental group patients (20 [71%] of 28 patients completed 5-year follow-up) made and maintained comprehensive lifestyle changes for 5 years, whereas control group patients (15 [75%] of 20 patients completed 5-year follow-up) made more moderate changes. In the experimental group, the average percent diameter stenosis at baseline decreased 1.75 absolute percentage points after 1 year (a 4.5% relative improvement) and by 3.1 absolute percentage points after 5 years (a 7.9% relative improvement). In contrast, the average percent diameter stenosis in the control group increased by 2.3 percentage points after 1 year (a 5.4% relative worsening) and by 11.8 percentage points after 5 years (a 27.7% relative worsening) (P=.001 between groups. Twenty-five cardiac events occurred in 28 experimental group patients vs 45 events in 20 control group patients during the 5-year follow-up (risk ratio for any event for the control group, 2.47 [95% confidence interval, 1.48-4.20]).
        CONCLUSIONS:
        More regression of coronary atherosclerosis occurred after 5 years than after 1 year in the experimental group. In contrast, in the control group, coronary atherosclerosis continued to progress and more than twice as many cardiac events occurred.

        Reply ↓
      3. chris c

        Look, like a LOT of other people I already ate an Ornish-style high carb low fat grain-based vegan diet, back over 40 years ago. That was when I passed my first gallstone and had my first attack of gout, both misdiagnosed, and all my symptoms which I now know were glucose/insulin problems got worse. NOT doing that again!

        Most of my life I dutifully ate HCLF and slowly but inexorably got worse. Like a lot of people I have a record of my “health markers” going south. When a dietician had me replace even more fat with even more carbs I got rapidly worse. I was accused of “failing to comply” with the diet – but when I actually DID stop complying all my markers and my symptoms improved hugely and stayed improved for well over a decade now. I consider this to be Gold Standard – pre- and post-intervention results from the same subject. Lots of other subjects show similar responses. Some don’t of course.

        Of course I’m going to die prematurely, just not for the reason you believe. Oh and I do still eat a vegan diet – with my meat. Hint – it was the Holy Health Grains that were doing for me, aided and abetted by the “vegetable” oils. Losing them made the biggest measurable change.

        Reply ↓
        1. smartersig

          I agree with you on this, personally I am not convinced that Ornish’s inclusion of say pasta is a good idea which if we are both right heightens the notion that other parts of his protocol are really kicking ass

          Reply ↓
      4. Charlie

        Mr Chris ;
        The ratio is correlated to insulin resistance and metabolic syndrome. Which is associated with a higher risk of CVD. So the worst the ratio the greater the possibility of having health problems. That why is recommended a ratio of two or lower. Carbohydrates and low fat in most people makes the ratio worst.

        Reply ↓
  55. Clathrate

    Hello John, I know what my opinion of the film is (I don’t want to give my opinion away – I’ve tried to post 3 times previously and if they are awaiting moderation than I might have given it away already). Take a look at Robb Wolf’s blog at:
    robbwolf.com/2017/07/03/what-the-health-a-wolfs-eye-review/

    (If you do have a read of the blog, please give us an update on your views or if you have any further questions, thanks.)

    Reply ↓
    1. smartersig

      Robbwolf states that heart disease is decreasing ( due to reduced smoking) but meat consumption has increased, therefore he feels its crazy to assume meat causes HD. I do not follow this reasoning. Smoking is probably a greater contributore to HD than meat and therefore it is quite possible for reduction in smoking but increase in meat to have a net effect of lowering HD. In other words we might have seen even lower rates of HD if both meat and smoking had gone down.

      Reply ↓
      1. sasha

        As he mentions numerous times, the only way to prove causation is to do a proper study. At this point you saying that giving up meat might decrease HD even further is pure speculation.

        But if you look at epidemiological evidence, it refutes your ideas about meat. There are plenty of traditional societies eating meat without ill effects. That evidence also refutes a lot of LCHF assertions…

        Reply ↓
          1. AH Notepad

            There are (or were) societies that eat hardly any plants and they didn’t suffer much from heart disease either. Heart disease seems to have some connection with modern refined carbohydrates and of course smoking. To give the impression that WFPD will cure most of peoples’ ills is at best misleading. WFD may be supportable, but claiming only plants can do it is exaggeration.

          2. smartersig

            Yes but in the context of a modern western civilisation WFPB has reversed or halted heart disease. If you want try one of the alternatives, maybe eat mainly whale blubber then by all means go for it.

          3. AH Notepad

            I would dispute WFPD has any effect on reducing or reversing herd disease. Plants cannot provide all the nutrients required by humans. It is obvious in some cultures that people who cannot afford meat are poorly nourished, and may suffer “diseases” which prove fatal in some cases. So maybe you would say they didn’t die of heart disease, but in the end they are just as dead. What it boils down to is, but you will not accept this, your hypothesis is flawed.

          4. smartersig

            Other than a potential B12 deficiency a plant based diet can be sufficient although personally I prefer to include fish.

          5. Andy S

            AH Notepad: ORNISH/WFPD/VEGAN discussion is important

            American Heart Association recommendation,low fat, low cholesterol diet (protein, 15%; carbohydrates, 65%; fat, <20% of energy; cholesterol, 1). This diet actually causes CVD.

            The Lifestyle Heart Trial (ORNISH) Intensive lifestyle changes
            – 10% calories from fat,
            – avoid saturated fat
            – Avoid meat, dairy, and eggs
            – avoid simple sugars
            – emphasize the intake of complex carbohydrates and other whole foods. Consuming plant-based foods in forms as close to their natural state as possible (“whole” foods). Eating a variety of – vegetables, fruits, raw nuts and seeds, beans and legumes, and whole grains.
            – aerobic exercise on a regular basis
            – stress management training
            – smoking cessation,
            – group psycho- social support

            COMMENTS: fine tuning the ORNISH protocol to reverse CVD
            – 10% fat, 15% protein means 75% carbs: current trend is towards low carb/high fat
            – Saturated fat, meat, dairy, eggs have been proven to be innocent of all charges
            – whole grains could be problematic ie leaky gut/brain
            – go easy on sugary fruits
            – limit starchy vegetables, leafy greens good
            – micronutrients ie d3, k2, Mg etc are important
            – periodic fasting and limited eating window has benefits
            – etc.

          6. smartersig

            In my book low carb does not mean all carbs it means simple carbs. Sadly when anyone mentions low carb eating everyone (not saying you) assume we are talking Atkins, I certainly am not. Some people find it hard to give up meat and to them I suggest eating only meat that is almost certainly free range grass fed eg rheindeer, buffalo, bison maybe even Goat etc. As one contributor pointed out via the Aussie study, Pescetarians live the longest so personalyy I will stick to that line of nutrition

          7. Andy S

            HI smartersig, people tend to develop phobias from advice espoused by Dr. OZ, and dietary guidelines, health care providers, WHO, ADA, etc.. To list a few: cholesterol phobia, saturated fat phobia, red meat phobia, sun exposure phobia. At the moment my personal phobias are: elevated blood glucose levels caused by excess carbs/protein, wheat, linoleic acid/seed oils, herbicides/pesticides. In the past I have thrown out a few egg yolks, eaten cholesterol free cookies and followed the dietary guidelines. We are all different in some respects and what works for the average person in a study might not be applicable due to confounding variables. Self experiment, keep an open mind, and keep learning is my advice.

            Is eating plants healthy? Plants have evolved defence mechanisms to combat predators. Some predators have evolved to be immune from plant toxins. More studies are needed before I adopt a 100% plant based diet.I do eat a lot of leafy greens from my garden, the rabbits like them too.

          8. smartersig

            If ever that definitive study comes along we will all be long gone. In the meantime a number of studies show Pescitarians live the longest and fish based populations have evidence of health and longevity. Roll roll up and place your bets

          9. AH Notepad

            Sorry Andy S, but the style of your post is ambiguous to me. Are you saying the ORNISH system is good or are you saying it’s bad?

          10. Andy S

            AH Notepad, the ORNISH system has many components in addition to food choices. Former president Clinton was on ORNISH, not sure if still on it or how it affected him. I have no personal experience with the ORNISH food choices. LCHF works for me and is the opposite of ORNISH. Any diet can show improvements in short term even a “no food diet”.

      2. Andy S

        This Ornish study does not prove that eating meat causes HD or reverses HD by eliminating meat. Other studies show that vegetarians/vegans get more cancer. I am not convinced that eating tofu (vegetable protein) is healthier than eating eggs and meat (animal protein).

        JAMA. 1998 Dec 16;280(23):2001-7.
        Intensive lifestyle changes for reversal of coronary heart disease.

        Ornish D1, Scherwitz LW, Billings JH, Brown SE, Gould KL, Merritt TA, Sparler S, Armstrong WT, Ports TA, Kirkeeide RL, Hogeboom C, Brand RJ.
        Author information
        Erratum in
        JAMA 1999 Apr 21;281(15):1380.
        Abstract
        CONTEXT:
        The Lifestyle Heart Trial demonstrated that intensive lifestyle changes may lead to regression of coronary atherosclerosis after 1 year.
        OBJECTIVES:
        To determine the feasibility of patients to sustain intensive lifestyle changes for a total of 5 years and the effects of these lifestyle changes (without lipid-lowering drugs) on coronary heart disease.
        DESIGN:
        Randomized controlled trial conducted from 1986 to 1992 using a randomized invitational design.
        PATIENTS:
        Forty-eight patients with moderate to severe coronary heart disease were randomized to an intensive lifestyle change group or to a usual-care control group, and 35 completed the 5-year follow-up quantitative coronary arteriography.
        SETTING:
        Two tertiary care university medical centers.
        INTERVENTION:
        Intensive lifestyle changes (10% fat whole foods vegetarian diet, aerobic exercise, stress management training, smoking cessation, group psychosocial support) for 5 years.
        MAIN OUTCOME MEASURES:
        Adherence to intensive lifestyle changes, changes in coronary artery percent diameter stenosis, and cardiac events.
        RESULTS:
        Experimental group patients (20 [71%] of 28 patients completed 5-year follow-up) made and maintained comprehensive lifestyle changes for 5 years, whereas control group patients (15 [75%] of 20 patients completed 5-year follow-up) made more moderate changes. In the experimental group, the average percent diameter stenosis at baseline decreased 1.75 absolute percentage points after 1 year (a 4.5% relative improvement) and by 3.1 absolute percentage points after 5 years (a 7.9% relative improvement). In contrast, the average percent diameter stenosis in the control group increased by 2.3 percentage points after 1 year (a 5.4% relative worsening) and by 11.8 percentage points after 5 years (a 27.7% relative worsening) (P=.001 between groups. Twenty-five cardiac events occurred in 28 experimental group patients vs 45 events in 20 control group patients during the 5-year follow-up (risk ratio for any event for the control group, 2.47 [95% confidence interval, 1.48-4.20]).
        CONCLUSIONS:
        More regression of coronary atherosclerosis occurred after 5 years than after 1 year in the experimental group. In contrast, in the control group, coronary atherosclerosis continued to progress and more than twice as many cardiac events occurred.

        Reply ↓
        1. smartersig

          Who cares whether Ornish proves or not that meat causes HD if his method works ?. You know I hope this is not the case but I sometimes feel like people are more desperate to keep meat in their diet than they are about halting their heart disease

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          1. Dr. Malcolm Kendrick Post author

            No, some people are just desperate to ensure that ill thought through ideas are not presented as truth, on the basis of one persons research into his own ideas, to prove himself right.

          2. smartersig

            It is not one person, Ornish, Esseltyn, Pritkin, the guy who documented zero heart disease in rural african communities during the first part of the previous century (name escapes me) Macdougal …….. and so on

          5. Jan B

            Correct me if I’m wrong ( and I probably am) but don’t other non-human animals who follow a plant based diet just eat and eat and eat ALL DAY presumably just to get sufficient nourishment from a not very nutrient rich diet. Not a lot of time left for thinking, writing, reading and all the other rather wonderful things we humans do.

      3. chris c

        IMO it’s looking more and more likely that the “epidemic” of CVD came and partly went completely without reference to ANY dietary factors.

        OTOH the “epidemics” of obesity, diabetes and a whole bunch of other metabolic diseases came as a direct result of following the diet that was supposed to reduce CVD. Ongoing are the massive increases of cancer and Alzheimer’s which have a longer lead time.

        There are feedback loops, HCLF and Omega 6 oils both drive insulin resistance. Hyperinsulinemia and IR drive or are factors in most of these increases, and are also one factor in CVD. A recent study showed an RR of over 12 between IR and cancer, which as Ted Naiman pointed out is up there with the correlation between smoking and lung cancer.

        Do you feel lucky?

        Incidentally interesting, some studies including one I think performed and funded by the ADA showed correlations between HbA1c and microvascular damage, and peak BG readings with macrovascular damage.

        My metabolism is only partly wrecked and reverting to a diet similar to my Gran seems to have fixed it (without the pastry and jam though, I’m not in the WI), Far fewer carbs though, I could probably never handle more than about 50g/day.

        For people whose metabolism has suffered worse damage it may be necessary to go further back in time to more purely “paleo” diets.

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  57. Bill In Oz

    Any thought Doctor Kendrick on Chondroitin sulfate ? I ask this be because of recently discovering the research done back in the 1970’s by Dr Lester Morrison. He had remarkable results using CS in a two armed research trial with 60 patients in each arm, followed for 6 years. Ten grams a day for 90 days and then 1.5 grams a day indefinitely. The 2 groups were treated the same apart from the treatment group having CS.

    There were 4 fatal incidents in the CS group plus 2 non fatal heart incidents. By contrast the non CS group of 60 had a total of 42 heart incidents including 14 fatal heart attacks. The difference was huge, In fact I wonder if continuing with such a trial would be permitted now on ethical grounds. It was so obvious that CS was working.

    Morrison details his research in this paper :
    https://www.dropbox.com/s/17vsix1d1qbctft/morrison1973.pdf?dl=0

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  58. John Collis

    I didn’t realise what a can of worms I’d open by what appeared to be a simple question. With regards to herbiverous animals, they cannot be true herbivores as they don’t wash their food to get rid of those nasty insects. Also they don’t spend all their time eating, cows have to eat their food twice by chewing the cud and rabbits/cavies eat their own faeces to extract even more from their diet.
    With regards to that film, I thought, perhaps naively, that there was going to be balanced discussion presented (I had never come across either the narrator or the production company before and I wasn’t aware of Joaquin Phoenix’s views and attitudes towards veganism either). Overall, I think that the film is based on poor science, a view shared by https://sciencebasedmedicine.org/what-the-health-a-movie-with-an-agenda, also it is akin to Ancell Keys experiments feeding meat to herbivores to justify the diet/cardiav event link.
    As a registered nurse, there was one assertion that really concerned me, and that was when one particular lady was told that she was likely to have an MI in the next 30 days because her C-reactive protein (CRP) was raised significantly. I know that CRP is a marker for inflammation, but as a specific predictor for MI?

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