15th June 2018
Many years ago, whilst I was at University, a doctor called Elspeth Smith was giving a small group tutorial on cardiovascular disease. I did not know it at the time, but she was doing detailed research into the process of atherosclerosis itself. During the tutorial she made this statement ‘cholesterol cannot get past the endothelium.’
At the time I had no idea what the endothelium was, and in truth, not much idea about cholesterol. However, those six words changed my life. At least my medical life. It was as if a door had opened onto a hidden world. No-one else in the group reacted, but I knew from the way those words were spoken that this was someone who was thinking something very differently. Very differently indeed.
Here is the conclusion of one of her talks, reproduced in the book: ‘Factors in formation and regression of the atherosclerotic plaque.’ Yes, the usual jargon filled stuff, but the bit at the end is most interesting.
‘In this talk I have concentrated mainly on the factors that may be involved in the progression of the early, low-lipid gelatinous lesion into the typical fibrous plaque with lipid-rich centre that is generally accepted as the significant lesion in occlusive vascular disease and have tried to emphasize the key role that may be played by fibrin.’
Fibrin, the key component of blood clots. How strange, how completely whacky. Is this woman mad. In the tutorial, she moved on quickly, almost as if being caught in an act of disloyalty. Which, I have come to realise, she was.
I now believe that, if she had been bolder, Dr Smith would have got it. The answer as to what really causes cardiovascular disease. I have since read many of her papers, and her contributions to various books. To my mind she was right over the target, looking straight down at the answer – bomb doors open.
Unfortunately, to fit in with mainstream consensus whereby everything must rotate around cholesterol (LDL/cholesterol), she kept looping back to cholesterol, and LDL, constantly trying to crowbar them into her research. Where they did not, and do not, fit.
She also made it too complicated, falling into the trap of ultra-reductionism. A trap that becomes almost impossible to avoid if you travel down and down, further and further, into biological systems. A point will be reached whereby, as physiological systems become smaller, they also multiply endlessly in all directions, and it becomes virtually impossible to see how they link together to create disease.
If you want to see the bigger picture, you must keep moving up and down between the levels. Just as a work of art cannot be understood by an analysis of the molecular structure of the paint, human physiology cannot be understood by tracking down individual biochemical pathways looking for the tiny, essential, lever that starts it all. The single snowflake that triggers an avalanche.
Anyway, getting back to her comment ‘cholesterol cannot get past the endothelium.’ Once you come to recognise that this is true, you are forced to accept that the cholesterol hypothesis, or LDL hypothesis is wrong, because it makes no sense. This does not necessarily mean that LDL does not have any role to play, but it cannot be the necessary factor. The ‘if and only if’ factor.
Which means that, if you want to understand cardiovascular disease, you must strip everything apart and start looking at the whole thing again. If not LDL, then what? Unfortunately, the moment you do this, a number of different problems emerge. The trickiest one is trying to find absolutely agreed facts to build a hypothesis on. Which is far more difficult than you would imagine.
Some facts may seem like bedrock, but when you start to press down on them, they can begin to crack and splinter, and turn to quicksand. For example, the fact that – at a younger age – women have a lower mortality rate from cardiovascular disease than men. This ‘fact’ is quoted endlessly but is it true? Not universally. Younger Brazilian women have an almost identical rate of death from heart disease as the men. At least it was, last time I looked
So, do women really have a lower rate of cardiovascular disease due to a biological difference? Or it is all to do with environmental differences, or psychological differences, or something else?
[By the way I am not referencing much of this blog, this time. You can simply Google most of this stuff yourself. I hope by now readers of this blog will accept that when I make a statement it is not plucked from thin air].
So, do we actually know? Really and truly know? Where are the foundation facts? At one point I reached a little island of despondency where I felt that there was no fact that I could rely on. It seemed that there was nothing that could not be contradicted.
For example, heart attacks are caused by blood clots in the coronary arteries. Surely that is certain? Well, I can find you solid evidence to contradict this, and several people I communicate with will argue that the blood clot follows the heart attack/myocardial inflation (MI). Not the other way around. You think this is mad?
What is certain is that you can find people who suffer from myocardial infarctions with no evidence of any blood clot, in any coronary artery, anywhere. It even has a name. Myocardial Infarction With Nonobstructive Coronary Arteries (MINOCA). To quote from an article in Circulation:
‘Myocardial infarction with nonobstructive coronary arteries (MINOCA) is clinically defined by the presence of the universal acute myocardial infarction (AMI) criteria, absence of obstructive coronary artery disease (≥50% stenosis), and no overt cause for the clinical presentation at the time of angiography (eg, classic features for takotsubo cardiomyopathy)’
This, I should add, is not rare. Maybe 25% of all heart attacks.
Yet, and yet. If you give drugs designed to break down blood clots (clots busters) you can reduce the risk of death from a myocardial infarction (MI). So, clearly, many myocardial infarctions are caused by blood clots. Equally if you use a device to clear out an obstruction from the coronary artery and put in a stent to keep the artery open this does reduce the risk of death following an MI.
Which means that you can – on the face of it – have MIs caused by blood clots, and MIs not caused by blood clots. Apart from the missing blood clot, they are both the same thing, with damaged heart muscle, raised cardiac enzymes and suchlike. So, what the bloody hell is going on?
Equally, you can find people who die of an MI and when you examine their coronary arteries you can find that a blood clot had formed days, or weeks, before the MI occurred. So, again, what the bloody hell is going on here? The blood clot did, or did not cause the MI? Surely not if there is a gap in time, of weeks, between the clot and the MI.
At which point you find yourself asking, or at least I did, how many people have the classic MI. By which I mean a blood clot forms in a coronary artery, then the person gets immediate central crushing chest pain and a myocardial infarction. More than half, less than half? In truth I do not know, and nor does anyone else.
In fact, just to throw more confusion into the ring, it is clear that the vast majority of MIs do not actually cause any symptoms at all. Or at least not symptoms that make anyone think they were having a heart attack.
Deep coal miners in Russia die the very earliest from heart attacks, at least I am pretty sure that they do. Average age of death is less than fifty. If you examine the hearts of these coal miners they will have had, on average, six previous MIs before the final one that got them. None of which were identified at the time. So, why do some MIs cause terrific pain whilst others do not? I have no idea. Nor, as far as I can ascertain, does anyone else.
Perhaps you now have some idea of my difficulty in trying to study CVD. At times it is like trying to pick mercury up off a flat table top. Or, asking questions of someone who will only answer your questions with another question. Frustrating.
I came to realise, eventually, that I could not rely on evidence, then work backwards. Instead I had to look at the metabolism, the physiology, the anatomy and suchlike, and attempt to work out what was going on. Then create a working hypothesis and see if facts fitted into it. Alternatively, find facts that completely blow it out of the water.
So, here we go, again. My working hypothesis as to the cause of CVD is, currently, the following:
- The first step in the development of atherosclerosis is damage to the endothelium (layer of cells that lines all blood vessels). No damage to the endothelium = no atherosclerosis.
- After the endothelium has been damaged a blood clot forms over the area
- The blood clot is mainly broken down and removed – on site
- Any remaining blood clot is covered over by new endothelial cells, effectively drawing the clot into the artery wall.
- Further repair systems, such as macrophages, then break up and remove any blood clot remnants, so nothing remains….
Unless clots form more rapidly than they can be got rid of, at which point a plaque starts to develop, and grow. When it reaches a critical point, the final deadly blood clot occurs. [I will deal with the issues of MINOCA and suchlike, in the future].
Essentially, therefore, we are looking at a dynamic process whereby, if damage > repair, problems occur. However, if repair > damage, all is well. My analogy is with road repairs. [A major issue in the UK at the moment]. All roads are being damaged by car tyres, rain, ice and suchlike, all the time. If they are regularly repaired, then potholes will not form. However, if the damage outstrips repair, you end up with potholes all over the place.
In a similar sort of way if damage > repair in our arteries we develop atherosclerotic plaques. There are three things that can lead to accelerated atherosclerotic plaque development:
- Increased rate of endothelial damage
- Bigger, and more difficult to remove, blood clots forming
- Impaired healing systems
What this ‘three stage process’ hypothesis can immediately explain is why atherosclerotic plaques never develop in veins. The blood flow in veins in much slower, the blood pressure is around thirty times lower, and the biomechanical strain is much lower. Ergo, the endothelial cells in veins have a lot less ‘strain’ to deal with in their day to day lives. So, there is less endothelial damage going on.
It also explains why, if you take a vein, and use it in a coronary artery bypass (CABG) atherosclerosis very rapidly develops. It further explains why atherosclerosis never develops in the blood vessels in the lungs (pulmonary blood vessels). The blood pressure here is, again, far lower. Although, people with pulmonary hypertension (high blood pressure in the lungs) can develop plaques.
What else does it explain? Well, it explains how smoking increases the risk of CVD. Smoking has no impact on the classic risk factors such as LDL levels, or blood pressure, or diabetes. However, smoking does cause rapid and significant damage to endothelial cells.
Smoking a single cigarette causes mayhem. Endothelial cells die, as measured by a rise in endothelial microparticles in the blood, Endothelial Progenitor cells (EPCs) are released from the bone marrow to repair the damage. At the same time platelets (the key component of all blood clots) are activated. In fact, all hell breaks loose.1
When you look at the damage smoking does, it amazes me that anyone who smokes lasts longer than a week. But they do. Which just demonstrates that the repair systems in the body are extremely efficient.
Anyway, what is clear is that smoking causes CVD through endothelial damage. Precisely the same thing happens with air pollution. It is increasingly recognised that air pollution increases the risk of CV death, and that the primary mechanism is endothelial damage.
‘In healthy, non-smoking, young adults, episodic exposure to PM2.5 [fine particulate air pollution] was associated with elevated circulating endothelial microparticles, indicative of endothelial cell apoptosis [cell death] and endothelial injury’. 2
Sorry, I did reference those two. I thought they might be difficult to find.
In fact, if you look for any ‘factor’ that damages the endothelium, you will find that it increases the risk of CVD. Below is a list of some of the things that I have been looking at, in some detail. Many of which you will never have heard of, but try not to let that put you off:
- Systemic Lupus Erythematosus
- Sickle Cell Disease
- Lead (the heavy metal)
- Bacterial infections
- Kawasaki’s disease
- Avastin (and any other VEGF inhibitor (vascular endothelial growth factor)
- Rheumatoid arthritis
- Proton Pump Inhibitors (used for ulcers and suchlike e.g. omeprazole)
- Air pollution
- Chronic Kidney Disease
- Vitamin C deficiency
- Erythema Nodosum
- Cocaine use
That list is probably long enough for now. On the face of it, most of these factors may seem completely unrelated. But the simple fact is that they all cause significant endothelial damage, and they all greatly increase the risk of CVD. From 100% in the case of omeprazole, to 50,000% in the case of sickle cell disease.
You may be wondering how the hell does Sickle Cell Disease damage the endothelium. Well, sickle cells are sharp, sickle shaped red blood cells (erythrocytes) – that is where the name comes from. It should come as no great leap of the imagination to propose that having sharp sickle shaped red blood cells hammering through your arteries may be rather likely to damage them.
‘A recent study of spleens* resected from Sickle Cell Disease (SCD) patients… has shown that there was consistent vascular lesions affecting large arteries. The same finding was also shown in studies of brains from SCD patients who developed cerebrovascular accidents (strokes). These lesions were attributed to the rigidity of sickled erythrocytes causing mechanical injury to the endothelial cells. The widespread distribution of the lesions was also suspected in other studies, in which it was suggested that the sickled erythrocyte-endothelial adhesion seen in the microvasculature could be occurring in large arteries and contribute to large vessel endothelial injury, vascular intimal hyperplasia and thrombosis.’3
*spleens are often removed from those with sickle cell disease because they become enlarged and liable to rupture
And here, from the paper referenced above, is the case of a fourteen-year-old boy with sickle cell disease. Much jargon, but important jargon.
‘A 14 year-old boy was referred to our vascular unit, with gangrene of the right foot. The condition started about one year prior to this referral with ulceration of the foot which was treated conservatively. The condition of the foot deteriorated until development of gangrene of most of the foot. The boy is a known patient of SCD. His past medical history revealed right sided stroke when he was 8 years old. His parents have SCD. His brother had also SCD and died suddenly at the age of 5 years.
There were no identifiable risk factors for atherosclerosis.
On examination, there were no palpable pulses [no pulses could be felt]. He was found to have heavily calcified femoral and brachial arteries [main arteries of arms and legs]. Plain x ray of both arms showed extensive calcifications of brachial, femoral and popliteal arteries. An X ray of his right foot showed infarction and osteomyelitis of most of the bones [infection in the bones].
Plain CT [detailed x-ray] of the abdomen and pelvis showed calcification of splenic artery and calcifications of both iliacs and inferior mesenteric artery [arteries branching from the aorta, main arteries of legs and artery supplying the bowel]. Digital subtraction angiography [too complicated to explain here] showed occlusion of right external iliac artery and both superficial femoral arteries with extensive collaterals. MRI & MRA of the brain showed left parietal wedge area of infarction with total occlusion of the supraclinioid segment of left internal carotid artery [important bit of the brain] and multiple collaterals. The patient had a right below knee amputation and was discharged home on antiplatelets.’3
This fourteen-year-old boy had calcified atherosclerosis in virtually every artery in his body. With, and this should be highlighted again no identifiable risk factors for atherosclerosis.
Now, you can look at every single current hypothesis as to the cause(s) of CVD, and NONE of them can explain why this fourteen-year-old boy has widespread and overwhelming atherosclerotic plaque development. He represents the classic black swan.
On the other hand, if you believe that endothelial damage is the primary driver of CVD, this case history makes perfect sense. It also explains how the other fourteen things on my list increase the risk of CVD, whereas the current ‘LDL hypothesis’ can explain precisely NONE of them.
Which makes it – fourteen-nil to the endothelial damage hypothesis, and we have not even reached half time. Russell Ross – who first proposed the ‘response to injury’ hypothesis would be pleased with this result. As would, I hope, Elspeth Smith. Unfortunately, they are both now dead. But I hope to see that they get the posthumous recognition that they deserve.
They were telling us what truly does cause CVD, but no-one was listening. Everyone else was content to blindly follow the ‘cholesterol hypothesis’ waving flags, cheering, and raking in the money.
Very pertinent subject right now ! I know you love this guy. At least read what he has to say. >
Brilliant work, thank you!
I hope GPs wake up and stop testing their patients for cholesterol level and other non-sense.
Chance would be a fine thing, Gaetan.
My husband ( 75 ) has an HbAIc of 49…..and is being pestered to take Metformin.
His cholesterol is 4.2…..and he is being told he is at high risk due to his diabetes, and must therefore take a statin.
He is heavier than he would care to be, but careful that he eats only very nutritious foods, and supplements with all the usual things we health conscious oldies indulge in.
He has COPD, managed very well on puffers his GP prescribed for him, but which the practice nurse stopped, and the GP re-instated, then the nurse said he was to discontinue once again, as he is at risk of pneumonia.
He is active, alert, drives 20,000 miles safely every year and does all the chores I can find for him.
For crying out loud NHS…..leave us alone!
Oh I HATE when doctors, and worse nurses, treat test results rather than patients.
My mother was doing relatively well in her nineties. The hospital had her taken off her ARB and put on Amlodipine which caused her to collect fluid in her legs and stomach. GP took her off and put her back on the ARB “against the Rules” which sorted it.
She also had COPD and used one inhaler I think twice a day and another when doing things like walking uphill. The “breathing nurse” replaced these with a gadget that ground up a pill, which nearly stopped her breathing altogether, I had to call the paramedics. GP put her back on her original inhalers. Nurse took her off them AGAIN and gave her the same useless pill-grinding gadget AGAIN. Because The Rules.
ps. I’d consider the Metformin, it has numerous benefits unlike the statin. Start at a low dose and increase slowly though to avoid brown trouser events. Opinions are divided between well-controlled diabetics that choose to come off it or stay on it. Might be worth a try but it should be HIS decision.
Always a *thrill* when there is a new blog post here…. Thank you for your time and excellent work!!! Best wishes from Massachusetts! corrie
Gosh, this is masterly, Malcolm.
I just wish I could get my husband to read it.
Does ‘Disseminated Intravascular Coagulation’ fit in anywhere? A friend has just died from this.
DIC is normally secondary to sepsis. This is where a high load of exotoxins (toxins produced by bacteria in the blood) damages the endothelium, to the extent that the normal anti-coagulant mechanism breaks down. This causes blood clots to form in all organs of the body, leading to organ failure – loss of limbs – and suchlike. This is where the term Disseminated Intravascular Coagulation comes from. Death from sepsis/DIC can be reduced by up to 85% by using high doses of vitamin C. https://www.smithsonianmag.com/science-nature/could-deadly-infections-be-cured-vitamin-c-180963843/
I wrote to the Sepsis Trust following the death of a local GP from sepsis, as the family suggested donations rather than flowers. I asked the trust what their approach to treatment was. They never answered, only asked for money. I then wrote asking if they had looked at the work by Fowler et al in 2014, still only requests for money. I had the impression they were lookinh only at pharma manufactured drugs, not something reliable like vitamin C. http://europepmc.org/articles/Pmc3937164
Suzanne Humphries said she would use even larger doses.
I have that reference in my list of contacts in case I have the misfortune to need treatment, and it should give any medic the confidence they will have a sound defence if needed.
A book I read recently was a bit of an eye opener. Irwin Stone’s “The Healing Factor”, 1972, a compilation of the previous 50 years’ research on Vitamin C, along with a reasonable amount of speculation from an admitted enthusiast. As the poster says, higher doses (much higher) of Vit C would seem reasonable in sepsis treatment. Quite amazing that it took from 1972 to 2016 for someone like Marik to come along and actually try it in sepsis. That’s a hell of an indictment of allopathic medicine as it is practiced.
Can’t remember if I’ve seen it mentioned here, but the rise in sepsis cases over the last 30-odd years (fairly called an epidemic, I’d say) parallels the rise in the use (abuse?) of statins. I’m sure that’s just a coincidence.
Good! Finally starting to bring it all together.
Only thing missing (unfortunately) is where calcification comes from. Is it repair damage? Much like an old scab or scar from Endothelial cell damage?
If true, then people like myself have a hell of a lot of scars (I have a very high calcification score) – but absolutely no evidence of a battle! It’s like my body and arteries are saying, “I am fighting a battle, giving you massive calcification in your arteries… so help me!”
The problem is, I don’t know how to help my arteries! I’m healthy, have a low CRP score, eat little sugar or carbs, and have nothing on your list of possible CVD causes/risks. It’s most frustrating actually. Guess I, and others like me, are a flock of black swans…
I think some people calcify more readily than others after any ‘injury.’ Look up myositis ossificans.
There is also some pretty strong evidence that vitamin K2 may be helpful in reducing calcification. It is certainly true that if you take warfarin, which is a vitamin K antagonist, you will end up with far more rapid calcification of the arteries.
…vitamin K2 is associated with the inhibition of arterial calcification and arterial stiffening. An adequate intake of vitamin K2 has been shown to lower the risk of vascular damage because it activates matrix GLA protein (MGP), which inhibits the deposits of calcium on the walls. Vitamin K, particularly as vitamin K2, is nearly nonexistent in junk food, with little being consumed even in a healthy Western diet. Vitamin K deficiency results in inadequate activation of MGP, which greatly impairs the process of calcium removal and increases the risk of calcification of the blood vessels. An increased intake of vitamin K2 could be a means of lowering calcium-associated health risks. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4566462/
Wouldn’t K2 hinder the repairing? What about stabilized plaque? I don’t want calcium to be pulled from my stabilized carotid plaques… What about elevated Homocysteine and low CRP and ESR?
Signed: young Brazilian woman, former Warfarin user
You may have a good point. I have pondered the role of calcification. Good, or bad. I think possibly bad because once you have calcification there is nothing the body can do to repair it – I don’t think. Your three other factors opens a monstrous can of worms that would take me several weeks to reply to.
What about chelation therapies ?
“Proper” diet might reduce calcification, whereas “improper” diet might increase it…see this for instance:
This is only an n=1 study (one participant), though.
If you believe statin manufacturers, statins increase calcification…but make it more stable. Spin?
Bugger. 40, on warfarin due to dvt, constant UTIs (urostomy) and sub par kidney function.
My heart attack should be along in 5…4…3…
I’m just replying willy-billy because Word Press seems to have mislaid me – or t’other way round. Frankly, life seems bleak without the wonderful Kendrick blog.
On June 15 (to Zsazsa) as to coronary calcium, you wrote: “You may have a good point. I have pondered the role of calcification. Good, or bad. I think possibly bad because once you have calcification there is nothing the body can do to repair it …”. I have sky high calcium scores, so I’m paying attention. But what if calcification is the body’s way of dealing with a problem, which may or may not persist. Maybe the problem, with no calcification response, would be more serious than the calcification response?
Tim, re ossified arteries
Probably a good thing if not carried to extremes. Get some collaterals and stop the progression.
Yes, it would be, according to Prof Ames Triage Theory.
Have a friend with scleroderma. A consultant physician, retired young because of ill health. I was horrified she was on calcium supplements (severe osteoporosis as well) given her scleroderma and convinced her to drop them and take K2. Whatever it is they measure for scleroderma went down once she started K2, and she regrets her consultants knew nothing of K2 until she brought it to their attention, as it is too late to remedy much of her problems. Is your response to Szasza cause for alarm in this respect : do I understand correctly that taking K2 at this stage may be doing more harm than good?
Now her cardiologist is pressing her to start statins urgently because of the perilous state of her cardio system. She at first accepted unequivocally, but after I raised issues of statin calcification etc with my friend she read further. Now she is in a quandary. Do you have any comments? She writes as follows:
“..about the mystery of statins causing increasing calcification and yet reducing cardiovascular risk, it seems that spotty calcification is associated with increased cardiovascular risk, and the more of this there is present, the higher the risk. However, statins seem to lay calcium down in more dense patterns that are thought to stabilise the plaques, and help prevent rupture. Plaque rupture, as you know, is what often precipitates cardiac events, because platelet aggregation and then thrombosis occur on the uneven surface of the exposed plaque.
I still have questions, notably, how can total coronary artery calcification be in accurate predictor of risk of heart attack and cv death if statins are increasing calcification and at the same time, reducing cv risk? I have seen one paper that suggests that the predictive accuracy of coronary artery calcification for risk is only meaningful in the imaging taken before statins are started. But my question remains how come the link is still there? Because surely by this time, most of the people with high cardiovascular risk in the western world are on statins. Still, the theory that statins work by stabilising plaque with calcification remains abundant in the literature. Like you, I am sceptical about swallowing such a theory whole in the presence of contradictions. I was always the annoying person in medical school who asked ‘why?’ – I think it’s better to be the way we are, because that means that our understanding is thorough, and is based on physiological processes, rather than rote learning or parroting current thinking which may be flawed.
Nevertheless, it does seem that statins reduce cardiovascular risk. Interestingly, high dose statins reduce cardiovascular risk even more than normal dose ones. But they also increase coronary artery calcification more, and I don’t know if I am ready to take that on.
btw my friend is on massive anticoags, although no longer warfarin. Also has to take PPIs or she would choke on her reflux while sleeping, so yet more cardiac risk factors. (she has had most of her bowel removed, one leg amputated and lost several fingers.)
Vitamin K2 can help control, if not able to reduce, calcification… see this:
Oh for the days of the LDL hypothesis, easy to understand even if wrong!
Thanks for the new post. Just claiming my reply service.
Excellent Dr. K—–I wonder if the benefits of exercise, in reference to CVD, is primarily due to collateral capillary growth—-also, it seems we will need to focus on those behaviors that increase the efficiency of our natural arterial repair/protection systems. Thanks for all of your efforts—-fighting the “Good” fight.
Then this could explain the rise in heart disease in the 1950′ and 1960’s. The rise in air exhaust pollution and lead from cars, the rise in pollution from factories, from the crap they spray in the air every day ( yes, I know it is true I fly through it and see it done every day), the fashionable encouragement of smoking. Pretty much everything on the list people increased exposure to, even mercury in the vaccines.
Thank you for your perseverance and great news for Tim Noakes again.
It would also explain why the polluters, the oil companies, funded Richard Doll’s work into smoking. (Richard Doll House is the home of those who take drug company money to prove how rotten cholesterol is.)
Really good stuff, I’ll soon feel confident I know more than many GPs about CVD, simply because they don’t, or won’t, read this blog.
Another fascinating article Doc.
This is presumptuous of me, but two things give me cause to pause and wonder.
In the last post ‘Eggs are good for you who knew’ I thought you were starting to sound a bit weary. Having read a new study that showed eggs are good for you, giving yet again another reason why the current cholesterol thesis is bonkers, you said ‘Now there was a time when such an article would excite me and fill me with the urge to tell everyone…Nowadays I tend to sigh and think ‘another study for everyone to ignore’.
You’ve been fighting this corner for a long while now and yet in spite of all the shells of evidence based science that you and others have unleashed, the enemy troops still occupy the fort.
And then this new post showing the mind boggling complexity of a subject you have been grappling with for the last thirty years.
I don’t know where you find the time or the energy to deliver these fascinating, enlightening … and this isn’t stretching it, life saving articles.
There’s a wealth of research, information and informed opinion here, not just from you, but also from your contributors. Seems to me this invaluable work should be archived for public access.
But who would do it?
This blog surely must be a great area for students to complete an MA or undertake post graduate research? Apart from the knowledge base here, the worries, fears, and stories from your readers comments will make a fascinating insight into how the drug companies got away with it for so long – when that story eventually gets to be told.
Thanks for all the work, effort and humour you’ve put into this Blog – it’s great and it certainly changed my life.
Good luck with the struggle – you are winning the battle.
Should there be an asterix next to vitamin C. Is cardiovascular disease scurvy as Dr. Mathias Rath theorizes? His theory is intriguing but I’ve no idea whether it holds up. Do we need more vitamin C because the body doesn’t produce it and we are exposed to a barage of toxics in daily life such as pesticides, air pollution, PFOAs, heavy metals, fluoride, chlorine and 80,000 untested chemicals?
His theory is very good, but it is only partial explanation. I am a great believer in taking vitamin C every day. If you have enough, it does no good, but can go no harm. If you do not nave enough then it could save your life. What’s not to like? The problem with Rath is that he is an incredibly bullish and divisive character. He could start a fight in an empty room.
“Rah is incredibly bullish” etc.. Yes indeed.But if he were not in the mix fighting, change might come far slower.
I tried to take Vitamin C, to see if it would lower my “high” Lp(a)…It made me feel “strange”, so I stopped taking it. That’s not unusual for me, though. I’m trying to take Vitamin B1, as there is some evidence it reduces the number of mosquito bites you get (I’m a magnet for mosquitoes), but again, I feel strange. I have a similar problem even taking a multivitamin, so I take a pill once a week instead of daily. Maybe I’ll restart Vitamin C once a week, too.
My view is (rightly or wrongly) if you don’t feel well, you probably don’t have enough vitamin C, so have more. Maybe if you get to 200g a day and you still feel ill, perhaps you should see someone about it.
Hi what type of vc do you take and how much
Good heavens, Elspeth Smith was my father’s first cousin! I’m mortified to have to admit that I never knew that her research was on the causes of cardiovascular disease. I must find and read some of her papers.
Indeed. Be warned, they are very complex.
Any relation to Elspeth Huxley, the famous author?
Elspeth Smith was a Bruce, my father’s mother’s family: Elspeth Huxley, nee Grant, was married to Gervas Huxley, a first cousin of my father’s on the Huxley side! Just to add to the gaiety of nations, Elspeth Huxley was my mother in law, as I was married to her son Charles who is my second cousin.
I doubt the cholesterol theory will die not matter how much evidence to the contrary. It’s going to hit $1trillion dollar in sales by 2020.
Intriguing, fascinating, enlightening! Thank you Dr K. It seems that taking K2 is becoming even more important, perhaps, as it organises calcium into bones and teeth rather than arteries?
It will die – eventually.
Dr Kendrick, what will die? I don’t understand the comment given the context.
The cholesterol hypothesis, not my question on K2. I think Dr K’s it will die comment got misplaced.
I think your “it will die” comment refers to Ellifield’s comment on cholesterol, not mine on K2?
“They were telling us what truly does cause CVD, but no-one was listening.”
Had they come up with a “response to injury” blood test that spit out interesting numbers that could then be manipulated via expensive drugs, many/most would have listened.
Sad state of science… First one to develop a test to measure something, drugs that’ll manipulate the numbers on the chart, and reverse engineer a hypothesis to explain the progression of the disease “wins” the argument – which then takes on a life of it’s own and will preserve itself at all costs.
Thank you Malcolm !
1 For the excellent blog #47 on CVD..Longer than usual but all of it worthy of serious thought and digestion.
2 For moving us all on from the endless diet focused rants. 🙂
After reading the new blog and thinking for a while, it came to me that there are two aspects to healing CVD
(i) Reducing damage to the endothelium..
(ii) Improving the repair process
Could this two sided aspect also be why so many different ‘things’ seem to help ?
And now at 11.50 pm here in my part of Oz..I shall away to bed & sleep ! 🙂
Bill, Yes, the ‘Repair’ needs good quality materials to do the job ‘right’ and do it first time around. Repairing a faulty ‘repair’ usually ends up a mess.
Scurvy has been described as a disease of connective tissue – that falls apart,- caused by insufficient vitamin C.
Humans, other primates, guinea pigs and a species of fruit bat have lost the ability to synthesize it, and are prone to CVD.
Vets tell me that Guinea pigs do well with 30mg/ kg Vit, C and goats self-generate in excess of 10,000mg normally, and heroic amounts when stressed.
Apes in the jungle will ingest up to 5,000mg in their greens…
Using the other primates and guinea-pigs as guides, this implies my 100kg body needs 3,000mg per day, or half a dozen Vit C tablets of 500mg. Yet the latest (?) US Recommended Daily Intake for the average ( Slim & Trim American…) male is… 90 mg / day.
Equivalent to a morbidly obese, 3kg Guinea pig.
James I agree Vitamin C is a crucial system repair agent…I really should take more on a regular daily basis. I have over the past 40 or so years develoiped the habit of taking about 10-15 grams whenever I feel “off’…And relying on a fruit ( apples, mandarins, grapes persimins at the moment ) for vitamin C on a daily basis…But maybe that needs to change.
Another good repair supplement is chondroitin sulfate..As Dr Morrison discovered back in the 1950’s-70’s
Hmm. They (slim, trim American males) tend to resemble your morbidly obese guinea pig as well. Surely that must mean something.
All of the animals that have lost the ability to synthesise Vitamin C internally have diets that in the wild are vitamin-C rich. Perhaps all that time ago there may have been some evolutionary advantage in saving the small amount of energy that not needing the liver to make the vitamin gave them?
Brilliant Dr K! You and Sherlock: When you have eliminated the impossible, whatever remains, however improbable, must be the truth.
Please ignore – just making sure I get comments
Belated ‘comment’ …
I don’t feel so bad about my high LDL. I thought calcification could be reduced with diet. Isn’t a large part of plaque industrial seed oils (omega 6)? Is plaque and calcification the same thing?
Dr. Kendrick, I hereby award you the honorary degree of engineer. You’re one of the few doctors who lets the data tell you the theory, instead of fitting the data into a theory. Congratulations!
Yes agreed! (ex-engineer). This has been an excellent series of posts. What’s the old saying “it works in practice but it doesn’t work in theory”?
In theory, theory and practice are the same. In practice, they are not.
Naseem Nicholas Taleb
For real people, if something works in theory, but not in practice, it doesn’t work.
For academics, if something works in practice, but not in theory, it doesn’t exist.
Thanks, Malcolm. Great post and part of a fascinating blog.
It’s funny, but I don’t remember you mentioning any of this stuff when you were a medical SHO and teaching me as a final-year medical student in Aberdeen 35 years ago! It’s sobering to learn that a lot of what I’ve preached as a GP over the past 30 years was complete BS!
Two things worry me. Firstly, how do you marry your complete disregard for the CHD/cholesterol/diet hypothesis and suspicion of all things statin with your role as an NHS GP, where I imagine you are still expected to ‘tow the party line’? The second is how did you manage to get a degree from one of the finest medical schools in the world, and still not learn to count?!
Most things that can be counted don’t count, and most things that count can’t be counted? No excuse, my counting is rubbish. Nice to heart from you. I think you meant ‘toe the party line’, but hey. The party line, luckily, is not enforced as per North Korea. You can still hold a different viewpoint without releasing the dementors.
Or gain protection by being in a different party ?
Just read,with some disgust, informative article re cardio vascular surgery. Hospitals and doctors and Qs & As. As you would expect they informed us that following most interventions patients would likely be prescribed statins and low dose aspirin. When will it end?! I see PPIs are a high risk factor. What options do GERD patients have?
William Perkins: My daughter used raw apple cider vinegar, 1 tbs. (15 mL) dissolved in a glass of water, twice a day for a week or so.
Organic cider apple vinegar does it for me on the now very very rare occasions that I get it. The main ‘cure/treatment for me though was giving up probably 90% of the carbs I ate previously. Acid reflux is now a thing of the past.
I take digestive enzymes, really as part of my cancer protocol, and I have noticed that I hardly get any heartburn any more.
Do you have experience/knowledge/opinion concerning the NOACs?
How do they differ from the anti-platelet meds with respect to vascular clot formation?
Intrinsic vs extrinsic factors and tissue factor are still confusing to me with respect to how they relate to vascular clotting, NOACs, anti-platelets, and fibrin.
As an avid follower of Dr Kendrick, and an 18 year veteran CABG receiver, I take a lot of interest in his hypotheses and his battle with the evil hordes of cholesterol mythsayers. I also came to the (amateur) conclusion that my own damage and repair process was compromised by my heavy smoking prior to my actual MI in 2000. As well as Co Enzyme Q10, curcumin, vitamin c, astaxanthin, serrapeptase, ( plus a few others), I take K2 as mentioned for calcium benefits. However, and I could be wrong, I take it in conjunction with D3, ( the ‘sunshine’ vitamin), so that the calcium doesn’t act on soft tissue and vascular system, but hits the skeletal system instead, where the benefit is best felt. Needless to say, I quit statins about 6 years ago.
It is my understanding that it is imperative to take M7 form of K2 when supplementing with D3 (or even D2,the inferior form) to ensure that calcium is returned to the bone matrix. The other supplement that is important when taken in conjunction with vitamin D is magnesium.
Thank you for another fascinating post.
I don’t see hypothyroidism in your list, despite the undiagnosed and under-treated condition being a known risk factor in heart disease. As renewal and healing processes slow down very noticeably in hypo, I assume that is where the problem lies? I can’t quite work out an explanation, but then my hypo brain also turns over more slowly than the average person’s.
I used to think my late father’s capacity to heal quite remarkable: scratches and cuts would disappear in the blink of an eye; the scar from his quadruple bypass healed and disappeared from view within weeks. It seemed to be a healthy process, but now I begin to understand one point in the damage > repair process that probably led to his premature death. As for the initial and repeated endothelial damage, he was a typically highly-stressed managing director of a company that had to battle its way through two major recessions, so his already hyperactive HPA axis no doubt raised the internal arterial stress at key junctures. My own HPA axis is disordered, and I believe one of the causes to be growing up in a home where such a stressed and frankly aggressive man dominated, causing even more stress to those around him.
“causes to have been” of course! We need an edit button.
Thanks for the article. Very informative.
Like sickle cell angularities doing physical damage, would particulates from smoke, sticky sugar bonded to blood cells (A1C as I understand the test), etc., or pharmaceuticals to treat many of the diseases you listed act as “sand paper”? I would imagine many of the people with those conditions are receiving treatment for them. Perhaps the treatments are what damages the endothelial rather than the disease in some cases?
Higher blood glucose strips away the glycocalyx – the layer of glycoprotein that protects the endothelium.
Ah, so that’s what happens! (Had been wondering.)
Malcom, fruits are sweet. Does that mean that they deliver a very high load of blood glucose to the glycocalyx ?
I hope not as fruit is my favorite source of vitamin C !
Blood is a slurry of particles, or abrasive mud, and any Fluids Engineer is able – as well as any experienced Cardiac Surgeon – to point out the Usual (suspects) sites for vascular damage, based on the turbulence alone.
Then add the corrosive chemicals such as excess glucose, cortisol / insulin etc from an unbalanced autonomic nervous system, and you really don’t need “Cholesterol” to damage the endothelium !
Is there a 15th cause of endothelial damage: serious dehydration?
Yes, there are many more.
Brilliant and as usual easy to understand. Would Vit K2 be helpful when someone has a hyperparathyroid adenoma with the resulting calcium issues including osteoporosis and artery problems.
Great post – easy to follow and well laid out.
The SCD case – a bit shocked to learn that plaque can form in any artery. I thought it was just around the heart.
I wish I could remember my CAC scan: I wasn’t paying that much attention but do they do the whole body or just the chest area?
Anyone had a scan recently?
I’m sure you could get the records.
Thanks for that very thoughtful post – I am sure that some of the general observations must a apply to a vast range of scientific studies!
Is there any possibility that part of the complication here is that some of the experimental methods in use are nothing like as clear cut as is normally claimed?
I mean at autopsy, is it unequivocally possible to distinguish blood congealed after death from an actual blood clot that was responsible for the MI?
Is it possible that essentially no MI’s are caused by blood clots, but by some sort of spasm that leaves lots of congealed blood that looks like a blood clot – either at autopsy or in the various scans used to examine the patient if he is still alive.
Could it be that clots are cleared by a mechanism that continues to operate for some time after death – thus simulating MINOCA ‘s.
I ask this because I think it is becoming increasingly obvious in so many fields of science that people get used to using fuzzy, imprecise evidence, and gradually trust it too much.
David, Interesting comment!
This issue has puzzled me since I read what Dr. Sroka wrote about this some years ago. As I see it today there are to different ways to die from a “heart attack” but there is no fundamental contradiction in my mind.
My coronary arteries have been severely clogged for many many years (heavy smoking a probable cause) but because of this I have developed substantial collaterals. My MI 1999 that “almost killed me” was certainly immediately stress related.
I don’t recall you speaking of this before. What was the stress?
There are three basic causes, triggers of MI, physical exertion, stress/anger/cortisol response, and a rapid hyperglycemic to hypoglycemic condition when the individual has COMPROMISED arteries from various antagonists which Dr. Kendrick alludes to e.g., high blood glucose. Control those parameters, and someone with severe atherosclerosis can live into old age. There are many black swans who have, to prove the point.
Thank you Dr Kendrick. Dr Joseph R Kraft’s book Diabetes Epidemic & You is interesting. Recommended.
Agree, I highly recommend Dr. Kraft’s book.
Bravo! Protect the endothelium at all costs. Gobs of vitamin C. What else? Don’t worry, be happy. Reduce carbohydrate consumption. Plenty of sleep. Sun exposure. Social connections. Move to France.
Exactly — Do what Ancel Keys did and move to the Mediterranean. Somewhere with picturesque days, cooler (but not cold) weather, lots of sun, relaxed lifestyle, and social networks. Pretty much the exact opposite of where I live. 😉
see Robb Wolf’s presentation where he mention several studies relevant to the dysfunctional mitochondria – which promotes oxidative damage:
here is the correct link to Robb Wolf’s video:
Add some grams of L-lysine to your vit. C. A dash of L-proline doesn’t go astray either.
Janet: Meat and seafood of all types are rich in lysine (the list I found even included moose, ostrich and bearded seal!). I eat plenty of these (except moose, ostrich, and bearded seal).
Wow! This is a fantastic article. Thanks Dr Kendrick. Lots to think about.
You are a beacon, long may you shine.
This appears to be a list of some of the research of Elspeth B. Smith. Very prolific.
But Wikipedia seems to think she is still alive.The entry for her, however, is described as a “stub”.
Bill in Oz: Off topic, but I’ve just become aware the Australian medical police are having a fit over a Perth billboard that asks, “Do you know what is in a vaccine?” along with a woman sitting with a pile of medical books, and at the bottom, Learntherisk.org. Have we reached such a state that knowledge is forbidden? I well know what they did to doctors who raised the alarm over Vioxx down there, and what they’ve done to Meryl Dorey. In the channel 9 news story they feature a woman who lost her infant to pertussis, yet this is a vaccine that is no longer efficacious, likely due to mutation, and they (the medical establishment) know it. For several years now there have been outbreaks around the U.S. among fully vaccinated school children. The response of the authorities to a billboard which encourages learning is frightening.
But they will blame the outbreaks of pertussis on unvaccinated children. They always do.
Yes, that billboard caused much frothing at the mouth, even the property owner of the (rented) site is running scared.
Thing is, the pro-vaccine Church refuses to answer that question, preferring to fulminate… rather than take the Golden Opportunity to “educate” the masses.
It’s not just the Diet Industry who are practised at avoiding elephants in the room… the Vaccine Dogma ignores the Inconvenient Truth that every US College outbreak of measles.whooping cough or Spon Plague, only takes down students who have been properly vaccinated. – They need to prove their status to be granted admittance.
Dogmatic human nature is alive and well !
Gary I live in South Australia.. Perth in Western Australia is roughly 3000ks from here. And I have never seen any such billboards or heard of any fuss by ‘medical police’….
Bill in Oz: Only one billboard. It was the reaction which was frightening. Such is the immense power of industry. By “medical police” I meant the AMA and public health authorities.
It seems pretty clear that any type of establishment that reacts in such a way to the idea of mere mortals getting educated has much to hide. If that’s the way the medical establishment reacts, and it is, then it’s obvious the medical establishment is not to be trusted. Period.
The emperor has no clothes. The little boy who pointed that out would have been burned at the stake in our world.
Dr. Kendrick: Granted that figuring out heart disease is like wrestling a herd of octopi, but pity the poor biologists! From the current “Natural History,” “Modern biologists have trouble with names. They can’t keep up with the 20,000 species of living things recognized each year, not to mention the millions that remain to be discovered.” 20,000 a year! Whoa!
For the better part of 47 editions I have been thinking along, sometimes making a comment, sometimes getting lost in the references. If it weren’t so serious I’d say it was a fantastic trip. Followed Rath on the side as well as Thomas Cowan. Having been trained as a psychologist, this was all new to me but it sure got my interest after I did have a coronary. I followed Cowan’s implied advice and changed my diet and never felt better.
After all the information you gave us to muse over, digest and whatever, I still can’t get it out of my head that somehow there is a Vitamin C deficiency combined with a lysine absence that seems to play a role. The repairing is done with the wrong material.
*James, Your suspicions are correct. 100mg of vitamin C / day only masks frank Scurvy, keeping it sub-clinical.
Our needs are more like 2 to 6grams per day, and an approaching level of L-lysine. ( Plus Proline too if you want the full Rath Protocol. )
Add vitamin E, and some natural Vitamin D..
I get my K2 from Brie cheese.
* Fine name that !
Which vc do you take. I was taken the powder version but it upset mt stomach
biddy99: You can get buffered vitamin C. This may help.
The best Vit C I’ve come across, from a tolerance perspective, is C-Salts. A mix of several ascorbate salts (Mg, Ca, K, and Zn) plus the acid form. You get the benefit of the added electrolytes, plus it’s easy on the stomach and intestine.
Straight ascorbic acid pills feel like they’re burning a hole in my stomach, and probably are. A gram is too much for me. I can tolerate 5 grams of C-salts without a problem, and three or four times that when I’m sick.
Socratic Dog, I dout the ascorbic acid is burning a hole in your stomach since it is considerably weaker than the hydrochloric that is already there. The sensation could be an indicator of something else, which perhaps, should be investigated. I suspect if it was investigated the treatment might be to take an aluminium based antacid, which would mean they had got you on the polypharmacy tread mill.
Offhand I think it probably is burning a hole in my stomach. Raw garlic does the same, I once ignored that feeling because I was trying to treat a Darkest Africa-acquired gut infection with said raw garlic, and ended up with an ulcer. That was not much fun, I assure you.
Was this supposed to be Part 49?
There were already Parts 47 and 48 in March.
You are right. Editing is not my forte. I have updated it, thanks.
What role does LDL cholesterol have to play?
LDL is pro-coagulant, and the LDL receptor complex has a key role in controlling blood clotting factors, such as factor VIII
A couple of papers I found recently thanks to “medical Twitter”
Is interleukin-6 the link between low
LDL cholesterol and increased noncardiovascular
mortality in the elderly?
Click to access e000789.full.pdf
Effects of Adiposity on Plasma Lipid Response to Reductions in Dietary Saturated Fatty Acids and Cholesterol
Some interesting points but a couple of howlers in that one
“Therefore, the reduction in CVD risk reported when SFA is replaced with PUFA may be due in part to inhibition of proinflammatory cytokine production.”
Er, Omega 3 yes, Omega 6 no. Frankly they have the causality reversed but interesting to see the link between chronic inflammation and LDL. If they took off their blinders and looked at LDL as an indicator not a cause they might get somewhere.
Pretty fantastic Dr Kendrick. Like deep space with the NASA telescopes.
Absolutely fascinating Dr. Kendrick. Thank you. I love the way you write, and the way you explain things. It was almost like sitting alongside you and actually hearing you speak those words on this occasion. That’s a gift Dr Kendrick, it really is.
The interesting thing for me was the fact that you mentioned Rheumatoid Arthritis as possibly having some connection with the cause of CVD (in some instances). I had Rheumatic Fever as a child – tried to get out of bed one day, only to find that I simply could not walk. When I was older I do remember my mother telling me that the doctor had warned that it could leave me with either rheumatism or a weak heart, and that I must take care of myself. However, I have been lucky enough to avoid full-blown Rheumatoid Arthritis, apart from the usual aches and pains of growing older. but you have given me food for thought about what caused me to end up with CVD and atrial fibrillation. Perhaps another little piece of my personal jigsaw is now in place, I think.
I have not looked into rheumatic fever as much as I should have done. There is a clear connection here, but I am not sure what it is.
Maybe in a few decades you might find a more personal reason to ‘look into it’ … 🙂
– Unless statin-deficiency shrtns your allotted span !
(Who needs Enemies? – with friends like us !)
What about hypothyroidism? I have read a book by dr. Broda Barnes who made a strong connection between these 2 diseases. Worth to look into it.
There is a connection, but it is complex to explain
Excellent blog as usual, Malcolm.
You can add magnesium deficiency to your list of causes, and if you believe this research, it would seem like a major contributor, although I would be very surprised if any of our local cardiologists have even read it, far less taken cognisance of it.
Here in Oz, the soil is old, tired and does little more than hold up the plants while they absorb the nitrogen, potassium and phosphorus, along with glyphosate, nicotinoids and whatever other toxins the farmers spray.
Magnesium deficiency also seems to be very difficult to diagnose, as the article states.
Plasma zinc is easily measured and frequently low here. Since zinc and magnesium are usually obtained from the same sources, I assume that if the zinc is low, then the magnesium is low as well, and recommend supplements.
I think it would almost be safe to assume that everyone in Australia is magnesium deficient, and even if they aren’t, a daily dose won’t do any harm.
Given that one of the main symptoms of magnesium deficiency is muscle cramp, I have a theory that some myocardial infarctions are caused by magnesium deficiency. A localised spasm of the muscles in the tunica media leads to closure of the artery for long enough to lead to infarction(local death of tissue), or at the very least, angina. This could also explain the sudden deaths of extremely fit runners, who will lose even more magnesium during the course of a run.
Basically all of my patients are recommended to be on magnesium and zinc, and a significant number say they feel better in some indefinable way.
With people like yourself and Aseem Malhotra in UK, Gary Fettke here in Oz, even if he has been muzzled by AHPRA, and Tim Noakes in SA, surely the mainstream of cardiology will eventually have to apply some common sense to their practice. I have noticed that some of our local heart specialists have become a lot less dogmatic about lipids and statins in the last 12 months, although there are still some who do daft things like viewing an angiography of a 65 year old woman, showing absolutely no narrowings at all, and prescribing large doses of a statin! Possibly common sense is still a long way off.
Anyway, more strength to your typing and mouse arm. You certainly give hope to us more open-minded GPs.
Thanks for that. Had I gone on with my factors I would have included homocysteine, magnesium and – of course – stress hormones. Probably included activation of the RAAS system due to a lack of salt. Angiotensin and related hormones can cause significant endothelial damage – primary due to down regulation/antagonism to NO. Yes, salt restriction is bonkers too. I shall be bloggin about this shortly
Twelve months of internalised, savage stress played a major part leading to 5x CABGs. Think deranged autonomic nervous system, cortisol, glucose+ and insulin by the bucketful.
My (ex) cardiologist dismissed himself when he insisted that aspirin-deficiency and NOT stress was the prime cause,. and garlic, fish-oils and pine-bark have NO positive effects on platelet aggregation. and vasodilation.
My new Cardio comes from a ‘Hands-On’ Therapy background, On the first consult he picked up on my ‘head’ issues…and initiated appropriate treatment.
Would not be surprised if he prescribes a glass of wine…
Many areas of Australia are deficient in Magnesium but the dry desert soils tend to have quite a lot because there is much less leaching happening..
For information about how magnesium deficiency manifests in livestock & in humnas google around for info by Pat Colby.. She was writing about this from a farm livestock perspective as far back as the 1960’s.. Her death in 2014 was a great loss here in Oz.
Same in the U.K., alas. Aged 70, I was sent home with high dose statins (along with PPIs, beta blockers and others) post MI after a clear angiogram.
In other words it all begins with excessive cellular apoptosis overwhelming repair capacity. Cause is therefore some component in the bloodstream. Should be able to measure and compare healthy/unhealthy levels. Glucose/insulin appears to be a good indicator, LDL-C is not.
System is complex since all cells will be affected, hence many symptoms called diseases could arise from the same factor. Health of the mitochondria appears to be the regulating factor. Organism attempts to maintain homeostasis by many interrelated pathways. Eating, breathing, thinking, temperature etc, all affect the homeostatic set-point.
‘cholesterol cannot get past the endothelium.’
What about the vasa vasorum, which presumably have a fenestrated endothelium? Could the cholesterol be sneaking in via the back door?
Of course, indeed, it (LDL) must. But it also must be leaking into all other organs where it does not cause plaques to form.
Was it not your notion that cholesterol in plaques was mainly due to blood cell detritus from the protective clot at endothelial stripped sites that then get covered over with new endothelium?
I like to think it is more than a notion.
Martin Back, I think you got it. Even endothelial cells need cholesterol and therefore must have LDL receptors. Since the experts say that LDL cannot enter from the lumen side due to the glycocalyx barrier the receptors must be on the back side. Fatty streaks from macrophages and modified LDL therefore can accumulate below the endothelium. This looks like the first step in the narrowing of an artery. Necrotic pools, hypoxic areas, angiogenesis etc. can lead to narrowing of the lumen. LP(a) is require when the endothelial layer is injured. A lot of stuff can happen: glycocalyx erosion, stress rupture, endothelial cell apoptosis, vit C depletion, scurvy, etc..
Animals make their own vit C, therefore eating only eggs is not enough for humans, we have to eat the chicken as well.
Hi Bill in Oz…on Dr Rath: “but if he were not in the mix fighting, change might come far sooner”.
Indeed. Good point.
On that note it was pleasing to see that the talk Marjorie Daw provided a link for has done very well on youtube re. viewing figures:
And still with Dr Rath, and on the subject of arterial damage and repair the theme of this blog and comments so far, here is his list of nutrients (eleven of them) for optimal arterial health and repair and the reasons why;
I noted both Gary Ogden’s and BobM’s comments about endothelium protection and BobM’s final comment of “pretty much the exact opposite of where I live”.
Tell me about it – just went for a walk around my cul de sac and my nervous system received an immediate battering from the following 4 sources, simultaneously:
screaming new born baby
home alone dog barking
3 out of control kids screaming around a garden
Unpleasant stuff especially knowing that the stress hormones released during this onslaught will be damaging the arteries even more.
It was a warm sunny day here in the UK and for some of us, for the sort of reasons listed above in my list, it’s an unpleasant time of year.
I have no knowledge of any seasonal peaks and troughs in CVD events, but I bet that for many, consciously or not, there is plenty of arterial damage occurring at this time of year.
CVD deaths are more common in the winter and on a monday morning. I just wish Dr Rath were not so dogmatic. He comes across as an angry zealot, and it is difficult to see past this at times.
Charles Gale: Thanks for the link to Dr. Rath’s list. I sympathize with you about annoyances while getting a bit of fresh air. I take a weekly hike in the wilderness. This past week there was a helicopter flying seemingly non-stop. Annoying as hell. They use them for rescue, and to supply trail-maintenence crews. On the other hand, they use horse and mule trains to supply the high Sierra camps. Not annoying at all. I think mules are beautiful animals.
Charles, you misquote me. I said that if Dr Rath were not in the mix fighting the good fight, change might come far slower”.
Your misquote has exactly the opposite meaning…I think..
Malcolm, I have watched Dr Rath’s vide’s on Youtube… And I read your blogs. Both of you are quite aggressive in condemning the LDL-C hypothesis as a cause of CVD.. Both of you offer explanations which far more accurately reflect the actual scientific facts…
However you work in different media. His preferred media is the video it seems..
While yours is here on the blog..
And each media ( Video & Written ) requires it’s own different style and presentation..
I’m grateful to both of you
You may want to look up Matthias Rath with regards to AIDS in South Africa.
Malcolm I do not know very much about what actually happened in South Africa : how much Rath was accountable for those AIDS deaths and how much the South African government authorities were at fault.
But if he has anything to answer with regards to AIDS in South Africa it is the South African government which should initiate proceedings ? The relevant medical authorities seem quite good as organising such things if what has happened to Dr. Noakes is any guide.
Charles my own frustration with DR Rath’s talks and web site is that nowhere is there mentioned how much of anything he suggests is ‘effective’ or needed….It seems that can be found only out by personal consultation. Bugger !
Meanwhuile almost all of what he lists I take anyway..
Bill in Oz, I suspect Dr. Rath has applied the Procrustean principle in problem solving by claiming that vitamin C deficiency is the cause of CVD. A flock of black swans:
1- Glut-1 receptors endocytose glucose and vit C. Glucose wins the race, resulting in vit C deficiency
2- Glucose mucks up insulin receptors leading to insulin resistance
3- glucose glycates proteins, insulin, red blood cells, lipoproteins, collagen etc.
Question is: can vit C compensate for high glucose?
Cats and dogs fed a carby diet will develop human sicknesses, maybe they need more vit C.
At best it would be unwise for a clinician to give advice on doses without a consultation. We, however can suggest whatever we like as we can’t be struck off.
Three of your list of stress-inducers are part and parcel of normal reproductive family life. You should welcome those sounds, not be stressed by them. People forming families and reproducing is a good thing, not a bad thing. Repairing your house is good, not bad. A barking dog…not so much.
Offhand, I’d suggest that the problem is with you, not the perceived stressors. I mean that in a positive way.
Thank you for this interesting, informative instalment so well written and explained that we can understand it. I feel a bit of a fraud as I have no ‘skin in the game’ as I still have no issues requiring a cardiologist or even a brief heart check. However it has given me some more things to look at; when you have no formal training in this subject but have had some issues like Maureen earlier referred to with the parathyroid adenoma which was not picked up by my Doctor of 26yrs. as all of my results including cholesterol were very different that year it having gone from 2 to 6 and he was considering placing me on statins he thought, and he dismissed the raised calcium as nothing to worry about however another year later the next doctor was concerned and started me on 2000IU’s VD3 and eventually a scan and extra blood tests I was referred to a specialist at hospital he was I felt very thorough and did further scans and more blood tests and the 24hr kidney check. I had been advised to take calcium previously due to the severe fracture of my right arm after a fall but had discontinued this due to issues with my kidneys this was prior to my diagnosis and after my surgery they advised me to again take calcium however when I returned for suture removal the senior Registrar told me to never take calcium again as per instructions from the Consultant. My bone density scan indicated that my bones had been very seriously depleted of calcium and failing anyone else giving me advice I raised my VD3 to 4000IU’s I researched this and took the advice and information from Joe Mercola and added K2 which initially I had to purchase from him as the TGA had not approved it for manufacture in Australia but you can now get it here.-I added Magnesium, Vitamin C, & some of the B group. My last scan showed my bones had improved and my Vitamin D levels last tested were 103. I do not have either osteoporosis or artery problems and am very fit and healthy for a 72yr old if I did then I would research those things to assure myself that I was not causing myself more harm.
Gary I know Bill with reply to you re your vaccination points but briefly here we do not allow information that might cause concern re them to be disseminated into the community any dissent is quickly and swiftly shut down, by AMA, State Health Departments, Government Statements and the Media all children and babies must receive the mandatory number of approved shots or they cannot attend child care, kindergarten, school etc. and if their parents receive family payments these will be reduced until the proof of vaccination is provided. The parents under some circumstances may be reported to child welfare with a notation that vaccination has been refused even if as in the case of Hep B it is not mandatory. In all this no-one has been able to explain to me so that it makes any sense what herd immunity is. Sorry off topic:
Before I go I would like to thank you all for your great comments.
Topsygirl: “Herd immunity” is a concept from the natural progression of infectious disease through a population. For example, once 60-70% of a given population had contracted a disease, transmission would essentially cease, and the epidemic would die out. The term is often misused by vaccination promoters to promote very high vaccination rates, but this is incorrect. A real-life example of the loss of herd immunity is the varicella (chicken pox) vaccine. The widespread use of this has caused an increase in shingles, including shingles in children, which used to be confined to the over-50 age group. The reason is that the varicella virus, a natural “booster” to prevent shingles, is no longer circulating. Dr. Gary Goldman worked on surveillance for the CDC when this vaccine was rolled out. It is he who discovered these consequences, and the authorities did everything they could to suppress his findings, but he published them (see PubMed). What is frightening in your comment is this: “we do not allow information that might cause concern.” Do Australians put up with that? Here in the U.S. this would be considered blatant censorship, and would increase public interest in the topic. This is what happened with the pulling of “Vaxxed” from the Tribeca Film Festival. The tactic backfired, and now hundreds of thousands of people now know that the CDC tested the Wakefield hypothesis, confirmed it, and threw the data in a big garbage can (according to U.S. Rep. Bill Posey in his remarks on the floor of the House). Thanks for your comment. An interesting journey you are on. I, too, have good health, and am immensely grateful for that. What I have learned here over the past three or four years has been a big help in improving my health.
Topsygirl, you are less of a fraud than I am, I haven’t had any of the “usual” tests, nor will I given the results have no use for health purposes.
As for vaccines, if they keep going with their unbelievable stupidity, Australia will soon have a population as sick as that of the US.
excellent. this actually makes sense!
Bran oil present in Brown Rice is balance cholesterol levels .
The oil in rice bran would be a PUFA. This is known to be something to avoid.
I wonder if the Cholesterol hypothesis has even penetrated the thinking of India’s Ayuveda doctors..Hope not.. But it is a persistent invasive noxious weed in modern medical thinking.
Just a comment on vitamin C, I don’t expect many to read this but in my experience I have found freshly squeezed orange juice … from oranges, real ones, to be better than vitamin C tablets.
I’m talking loads better and very easy on the stomach too.
To save cash I buy Aldi’s proper (not from conc) with bits, and “activate” it using a couple of oranges squeezed at the time of drinking. Other brands are all less Zingy.
I assume the enzymes in the real oranges help the pre-squeezed stuff do a better job.
Just saying. Feel free to try.
My understanding of herd immunity is that it includes the fact that vaccines are not completely effective and therefore you want everyone immunized so that if there is an outbreak, it will not be able to spread very far.
Obviously, if the vaccines worked like getting the disease does, vaccination for all would not be so strongly enforced.
My understanding of herd immunity is that vaccines do nothing at all to help. If we take chicken pox as an example, it would normally be contracted in early childhood as a mild disease. This would give immunity, which would be refreshed as people came into contact with carriers, and did not develop into anything more serious. With vaccination, it may or may not work, several attempts are required to generate an adequate response, the attempts cause other problems as stabbing someone with a needle is not natures way of contracting a disease. The “immunity” (loud laughter here) is short lived, and then people risk getting shingles. That’s ok, there is a vaccine available for that too.
I think “herd immunity” is a phrase, when used by the pharma industry and the likes of Paul Offit-for-Proffit, is an attempt at an emotional trigger, which works for most people and especially politicians, unfortunately.
Could epithelial effects be the phenomenon that ties it all together, i. e., why we get what sometimes seem like random effects from dietary studies? It may be the way that researchers group dietary components, or their failure to account for the interactions of nutrients, that leads them to unsupportable conclusions. Some fats, like trans fats and refined seed oils, have a deleterious effect on epithelial tissues, while others, possibly like marine-origin Omega 3 fats, have a beneficial effect on epithelial health. Often, researchers lump all fats together, even if they have looked at only a few types (which makes about as much sense as grouping humans and chickens together because both are bipedal) and conclude that we should keep dietary fat to a minimum. AHA did something similar in their recent meta-analysis, where they lambasted coconut oil as bad, bad, bad, (because it’s a sat fat) but none of the data in the studies they evaluated involved coconut oil.
Or, a key micronutrient may be low in the diet being studied, but is key to the body’s optimal use of a macronutrient (e. g., vitamin C with protein), but “too much protein” gets the rap, rather than the deficiency of vite C preventing the proper use of protein in tissue metabolism.
Excellent article with a real wow factor. I do hope, Malcolm, that your profession pays heed to what you are telling them. I also hope you’ll be writing a book on your findings.
Bill in Oz – ooops – sorry – I did misquote you.
It always happens: you write a comment, check for errors, click on submit and then spot something wrong.
The Constant Gardener by John le Carre
Latching onto the vaccine comments, this is the theme of John le Carre’s novel the Constant Gardener. Vaccination and also Big Pharma, their tricks and corruption.
I was expecting a spy novel and was surprised by the contents. In my case, and for many regulars here, he was preaching to the choir but it was good to see it all getting some mainstream exposure.
Worth a read and also, for those people we know and who refuse to believe in any of this, perhaps slipping them a copy might be a means of enlightenment. I find I might as well talk to a brick wall sometimes when trying to get through to people.
Beware of loss of vitamin C in preparation:
Is there any drug that increases speed of repair of the endothelium? Because if there’s one maybe it have some data (could be buried inside some research) that show decrease of arteriosclerosis and less deaths from CVD.
Viagra, also ACE-inhibitors. They both reduce risk of death from CVD. These data are not hidden.
Cardiac risk factors and prevention http://heart.bmj.com/content/early/2017/03/08/heartjnl-2016-310746
Association between treatment for erectile dysfunction and death or cardiovascular outcomes after myocardial infarction
Objective Erectile dysfunction (ED) is associated with an increased risk of cardiovascular disease in healthy men. However, the association between treatment for ED and death or cardiovascular outcomes after a first myocardial infarction (MI) is unknown.
Methods In a Swedish nation-wide cohort study all men 5 dispensed prescriptions of phosphodiesterase-5 inhibitors was reduced by 34% (HR, 0.66 (95% CI, 0.38 to 1.15), 53% (HR, 0.47 (95% CI, 0.26 to 0.87), and 81% (HR, 0.19 (95% CI, 0.08 to 0.45), respectively, when compared with alprostadil treatment.
Conclusions Treatment for ED after a first MI was associated with a reduced mortality and heart failure hospitalisation. Only men treated with phosphodiesterase-5 inhibitors had a reduced risk, which appeared to be dose-dependent.
Dobroslaw, Chondroitin Sulfate is not a prescription drug here in Oz though it is in some countries.
In the 1960-70 Dr Lester Morrison did a series of long forgotten research trials on CS to see if it helped prevent heart attacks.
H Just to give you an idea of what he discovered here is the introduction to his last published research paper in 1073 along with Norbert Enrick Ph.D :
“CORONARY HEART DISEASE:REDUCTION OF DEATH RATE BY CHONDROITIN SULFATE A LESTER M. MORRISON, M.D., F.A.C.A., AND NORBERT L. ENRICK, PH.D – Institute For Arteriosclerosis Research, Loma Linda University School of Medicine; University of California Center For Health Sciences, Los Angeles and Kent State University, Kent, Ohio. Presented at the International College of Angiology Congress, Royal College of Surgeons, June 15, 1972, London, England.
Considerable evidence has now accumulated which demonstrates the anti-thrombogenic, anti-atherogenic properties of the acid mucopolysaccharide chondroitin sulfate A (CSA) in monkeys, rats, rabbits, dogs and patients with coronary heart disease (CHD).1-10
This report details the results of treatment of 60 random-selected patients with demonstrable coronary heart disease treated by orally administered chondroitin sulfate A (CSA) over a six year period of time and compared to a comparable group of 60 random-selected patients of coronary heart disease (CHD) treated only by conventional therapy over the same period of time.”
Among other things I note : 1 ) this paper predates all statins by about 20 years…2 ) It predates any acceptance of the Cholesterol hypothesis or LDL-C hypothesis. 3) Chondroitin Sulfate is a by-product of the slaughter of livestock. ( Vegens beware !! ) It cannot be patented and thus become a lucrative source of money for Big Pharma. 5) Morrison does not attempt to explain in his research paper why Chondroitin Sulfate ‘works’ and cures CVD. He is content to simply report that it ‘works’. Finally 4 ) It is also written in clear easy to read Englsh instead “Sci-glish” the modern jargon used by so many scientists which serves to conceal & confuse ordinary readers as much as it reveals.
The results were extraordinary. But I’ll leave you to read the entire paper which is available here :
TS – loss of vitamin C in preparation
Great find. I found some data which I posted in a previous blog comments section which measured the rise and fall of nutrients in food over the decades.
For the reasons supplied in your link, in addition to fresh veg (fresh? i.e. sitting on the supermarket shelf…or floor), I now buy frozen veg – “frozen for freshness” to maximise the nutrient content, whatever levels they may be with modern farming.
Sure, I prefer to get my nutrients from food but surely it must be getting harder and harder to ignore the use/necessity of supplementation nowadays?
Yes Charles, and I favour Birds Eye frozen peas – they taste as though they have some goodness left in them (if you don’t boil them!)
What about this on honey? I’m drawn towards kind things said about honey – quite a naughty bias I suppose. I buy lots of quality honey and give it to people as presents so I hope my trust in it is well-founded.
TS: Thanks! Perhaps we should all start eating honey. After all, what’s good for a rat, with the exception of cats, is good for a human.
Reminds me of a poem I learned in school by that polymath, Anonymous:
I eat my peas with honey,
I’ve done it all my life.
It makes the peas taste funny,
But it keeps them on the knife.
Frozen peas, one of the few “processed” foods that are better than the real thing. The farmers are given instruction when to sow to achieve a rolling wave of ripe peas throughout the season to keep the freezer plant fully loaded. The peas are regularly tested for peak ripeness and the harvesters may stand down for half a day until the other half of the field is ripe, or adjourn to a different field and return a day or two later. They are only grown within a radius of something like two hours by truck to the factory.
Science and technology may occasionally improve on the quality of food. But then there’s this
Click to access NBU-43-189.pdf
you probably don’t want to be eating
“Phytosterol-based edible oleogels: A novel
way of replacing saturated fat in food”
chris c, a disturbing read ,of a novel way to replace saturated fats in food to achieve a pointless physiological effect. I wonder who funded this report. Answers on a postcard please.
Indeed, and to finish my thought I wonder what will be the effect of incorporating such faux fats into cell membranes – including of course the endothelium. Like interesterified fats they may just turn out to be trans fat lite. But that’s all good, because animals.
“Copper – supports stability of the artery wall via the improved cross-linking of collagen molecules”.
Oh dear – I fear another supplement may be added to my list.
However, I don’t think it has featured much on Dr Kendrick’s website or the comments. At least it doesn’t ring a bell…either here or anywhere else. Maybe not that essential?
Does anyone here take copper for arterial/CVD reasons? A handy-dandy buyer’s guide would be great!
I have got a bottle of copper supplements in my cabinet but I only take it haphazardly.
Though I wonder about collagen as a “supplement”. It is well known by “health gurus” that bone broth is full of collagen, and if I havn’t misunderstood something, is considered to be the best way to heal the damage endothelium of the intestines; a condition called “leaky guts”.
Perhaps a copper supplement could boost the healing by the bone broth?
Charles Gale: What I know about copper (admittedly not much): We only need tiny amounts, and too much is not good. Easy to get from food, such as (in mg/100g) beef liver 14.57; cooked oyster 4.29; chocolate 3.23; nuts 1-2.1; also some crustaceans and mushrooms. I do notice the high-quality multi my wife and daughter take has no copper, but in addition to all the usual vitamins it has calcium, iron, magnesium, zinc, selenium, manganese, and chromium.
We in (Western end) Oz have copper water pipes in our houses… so I reckon I get enough from drinking/cooking water, plus osmotically from long showers…
Thank you for taking an interest in my ‘CVD-journey’ but I think I must have mentioned the stress “cause” though perhaps not specifically.
In essence there was stress (or perhaps “strain” to use Malcolm’s terminology) on many different levels the preceding year and especially a few month before the MI. To start with I had one of those nasty flues with a week in bed with very high temperatures. At work there was certainly high stress levels and finally privately my mother who was on a visit during Christmas time was in a bad health state.
The idea of stress as a “general” cause is well in line with what Malcom claims.
When it comes to Dr. Sroka he has dwelled on the “nervous” state, i.e. the unbalance in the autonomous nervous system, well known as an indicator of stress, where the down-regulation of the parasympathetic “take it easy part” and measured as the loss of the heart rate variability is the critical factor preceding an acute MI.
My health idea, as you probably know, is to work with a really broad brush and where “food as medicine” is an important part of this work concept. The central part which is also in line with what Malcom stresses is to avoid toxins of different kinds that may hurt the endothelium and here we can make a long list. And at the same time i believe it is important to support our ability to take care of the toxins by taking vitamin supplements where vitamin C today is at 15 g/day.
Maybe this would help in understanding why some may have MI without actually knowing it – as mentioned by Dr. K, where the repair > damage:
Thanks for this, it is a really good graphic demonstration of the power of collateral circulation, and how it develops. It does not actually explain how MIs can be painless – I do not think – but it does explain why non-acute stenting is a waste of time. I would recommend all readers of this blog to have a look at this article
Fascinating article! As to pain during a MI, I would note that throughout my episode I never experienced ‘pain’. My only indication was an odd,painless tightening mid sternum – a sensation so mild that I ignored it, continuing on my daily 4 mike walk, until I realized late afternoon that something was seriously amiss!
Thank you for this reference! This is a much better illustration of the collaterals than the one I found with Dr. Sroka. But the essence is the same – the “futility” of CABG since nature has already fixed the bypass on its own and in a much more convincing (clever?) way then the artificial surgical one. The corporate medical industry could never have much liking of nature – could it?
So I am still happy that I “refused” the comprehensive CABG all those now almost twenty years ago and instead decided to work on the improvement of my collateral status not least by regular exercise. (E.g. by taking my bike the 12 km to work each day, the year around – tough when there was a dm of snow to ride through or at minus 8 degree C (my limit for taking the car).)
At the same time you need, to my opinion, with all means, and at your best, try to stop the deterioration process that led to the critical situation. To totally quit my monstrous addiction to cookies was a great step forward I believe. Though when I had logged 1000 km on my bike computer I offered a great “birthday” cake to my group at work to celebrate my “survival” or rather revival.
I guess that my attitude confirms what my favorite Schopenhauer tells me in his teaching “The World as Will and Representation”. E.g, I here read that the “will to live” is a heathen practice contrary to what all great religions teach us about the futility of “life”.
Amazing pictures! There are so many fine collaterals, the heart looks like a tangled tumbleweed.
It’s my pleasure Dr. K. Also, it’s great to hear stories such as the likes of Mr. Goran’s and many others…
Now I saw that your reference was actually to Dr. Sroka but certainly a more elaborate version than the one I came across earlier. But I guess Dr. Sroka can not be the only one “out there” to realize the evident contradiction between the official “money making” view on heart attacks (MI) and the physiological reality.
Here is another story about natural bypass:
Mr. Goran, I’ve been following Dr. K’s blog since I’ve read about the idea of “Human Heart, Cosmic Heart” from Tom Cowan after coming across an article about the adrenal-heart connection (links below) which is based on traditional Chinese medicine that “The kidneys nourish the heart.”
As I understand it, it is well recognized that MI among women, contrary to that among men, often pass with weak symptoms. I have never seen a good explanation to this fact.
In my own case there was certainly pain involved but not acute to any extreme levels. As in your case mine was rather a profound state of “un-wellness”, a complete lack of energy during a half day or so, that made me ask my wife to bring me to the emergency room at the hospital where I though had to wait for quite a while before they realized my bad shape but only when my wife had pushed them to act in emergency.
When the cardiologist later confirmed the seriousness of my MI he said: “The next time be sure to be brought in by an ambulance to avoid the waiting.”
As Dr. Sroka tells in the reference supplied by alcura a blod clot blockage in a main artery without built up collaterals is likely to be a fatal event. Interestingly he claims that when a stent is inserted at a stenosis the collaterals do rapidly regress and a future blockage here will thus be of this fatal kind.
Really interesting reading!
In my eyes, today, an MI, contrary to a blockage without backup collaterals, is (with Dr. Sroka) a rather diffuse phenomena invoked by disturbances of the nerve impulses which make a part of the heart stop working as a muscle and which will make that part of the heart “die” and later turn into a scar tissue.
In my case they were surprised to find very little of that scar tissue by the ultrasonic examination, but for sure it is there and which makes me a very slow bike rider – everyone pass me but “I don’t care” as I use to say. Though I am very strong snd can sustain short bursts of tough exercise (heavy lifting, wood chopping working with my chain saws) . Again, I should be happy about my collaterals and keep them “going” by such tough exercises.
This feels like a “unified theory” to me.
I was told the same by my cardiologist, when he heard that I had waited an hour in A&E to be triaged! As I was totally unaware of the danger I was in, it never occurred to me,or my husband, to push to the front of the queue.
Mr. Goran, it’s proven, including your case, that HIIT (instead of the well-known “cardio” exercise) or anaerobic activities, help develop the natural bypass. So instead of jogging for instance, sprinting with resting pace as well as tabata-style exercise are far better that aerobic exercise.
Alcura, as a correction to what you wrote, in traditional Chinese medicine kidneys do not nourish the heart but there’s a kidney heart axis of mutual control. It has to do with five phase theory in TCM. A similar relationship exists between liver and pancreas, for example.
My cardiovascular surgeon suggested I develop collaterals to my leg arteries rather than stenting them. This worked spectacularly which I suspect he knew would happen. It seems a minority of doctors and surgeons understand this but IMNSHO it should be more widely known and understood.
So, does the prevalence of these occult (?) MIs, especially in women where there may be only a vague, indigestion-type pain, mean that most of us “ladies of a certain age” have had an MI and have no idea we had one? Wouldn’t there be something else? Worsening of the pain with time if one doesn’t go to the ER and get it addressed? Reduction of physical capacity too fast to be due to normal aging? Chronic fatigue that comes on suddenly? Anything? I’d always thought that an MI was a life-threatening event, but some commenters seem to be saying you might have one, and never have any idea until maybe your doc sees something during a routine physical? Doc: “Oh, I see you had a heart attack”. Patient: “Huh? When?” Doc: “Sometime in the past.” Well, duh!
At 78 I can appreciate your questions about MI. Here is my limited, brief understanding of what is happening:
1- heart tissue requires oxygen for proper function
2- mitochondria produce energy (ATP) using glucose or fat
3- when oxygen is low mitochondria revert to forming lactose as a fuel to produce ATP
4- if oxygen supply falls too low a heart cell will die (necrosis) and release troponin
5- many cells can die and not cause symptoms, but troponin level can still be detected
6- chest pain could be due to lactic acid, similar condition to leg cramps when muscle overexerted
7- a gradual decrease in oxygen supply (hypoxia) will stimulate angiogenesis (collaterals)
8- hypoxia can result from clogged arteries or exercise
9- therefore hypoxia can be good if properly applied through exercise, good at any age, no hypoxia: no collaterals
10- ageing process decreases ATP production, less Q10 etc.. Diet becomes more important.
11- All is not lost if artery narrowing is halted.
Andy S: Thank you very much. Well thought out and explained. Yesterday I had my most arduous hike since my twenties-10 miles (16k), with about 3,000′ (915m) of climbing. One stretch, at 9,440′ (2,865m) it was so steep I had to stop every 5-10′, but with no level spot to stand. Pulse was very high, but with no symptoms of anything, and I soldiered on. Hopefully no hypoxia, necrosis, or any other nasty things. I had planned to make it to the next lake next week, which would be twelve pretty rugged miles, but I now think ten miles is my limit!
@Sasha, if you read the links I’ve provided about kidneys, they are actually referring to our adrenal glands which sit above the kidneys that produce cardiotonics out of cholesterol!
Sorry, just found your comment, my mail has been putting comments into junk folder for some reason. What was it that I said, which made you refer to adrenals?
I just found your original comment. Yes, adrenals would be a part of “Kidney” system in Chinese medicine but kidneys don’t “nourish the heart”. Liver does. Kidneys control the heart in TCM (traditional Chinese medicine). Look up five phase theory if you are interested in knowing more.
Not specifically on topic, but consistent with concerns raised by Dr. Kendrick –
FTL: The extensive government trial was intended to settle an age-old question about alcohol and diet: Does a daily cocktail or beer really protect against heart attacks and stroke?
To find out, the National Institutes of Health gave scientists $100 million to fund a global study comparing people who drink with those who don’t. Its conclusions could have enshrined alcohol as part of a healthy diet.
As it turned out, much of the money for the study came from the alcohol industry. Earlier this year, The New York Times reported that officials at the National Institute on Alcohol Abuse and Alcoholism, part of the N.I.H., had solicited that funding from alcohol manufacturers, a violation of federal policy.
Copper info – many thanks guys.
Collateral info – fascinating data especially a comment in Alcura’s link which states that it seems “the natural development of the collateral system generally keeps pace with the development of the coronary stenoses”.
Plenty to think about should pressure be applied by the doctors for any (or further) stenting or CABG.
But it leaves me baffled, especially when you are told the reason (1) you ended up in intensive care and (2) you were stented was due to arterial blockage. Don’t the collaterals take care of this – that’s why they develop?
And what about heart strength and ejection fractions? A low ejection fraction makes sense if there is arterial blockage, then how come the network of collaterals aren’t keeping things flowing to and from the heart? The heart shouldn’t be struggling to pump with a good network/blood flow. Unless, I suppose, the heart is damaged and not pumping.
Time for a cuppa and some further reading.
The extent of the collateral network would have been seen on your coronary angiogram.
If you had a complete blockage, and it caused myocardial damage, then you didn’t have an alternative collateral circulation to that area. Period, I’m pretty sure. Good collaterals mean a complete blockage of a major coronary artery can be a non-event.
I don’t believe anyone is ready to suggest alternative treatments to emergency stenting (or bypass surgery, if it comes to it) in the case of an acute myocardial infarction with 100% occlusion, or close to it, of the culprit coronary artery. Encouraging collateral development seems a reasonable alternative to stenting of non-completely occluded coronary arteries, which has been shown to achieve nothing anyway.
I see a lot of “ischemic cardiomyopathy” nowadays, enlarged heart with much reduced contractility, reputedly caused by “ischemia”. I don’t recall seeing it twenty years ago. That presumably ties in here somewhere. Statins?
Statins are a mitochondria poison.
Lower cardiomyocyte ATP= lower heart pumping = ischemia
“New research suggests that muscle weakness and related side effects that can arise from statin use is likely due to the drug’s effect on the energy production centers, or mitochondria, of muscle cells.”
“For example, heart attacks are caused by blood clots in the coronary arteries. Surely that is certain? Well, I can find you solid evidence to contract this,”
Shouldn’t that be ‘contradict this’ ?
You are right, thanks.
Great write up dr kendrick, if hypothetically speaking you had an MI and were given the aspirin,clopidogrell,eplerenone,beta blocker,statin,ramipril drug combo what ones would you keep and what ones would you ditch and what would you replace them with, im sure alot of people would be interested in this answer.
On that list, I would take ramipril and clopidogrel.
Wouldn’t many MIs pass as indigestion which is ignored or forgotten about because it’s not unusual for the person? (Especially as people expect heart attacks to have a distinctive pain.)
And why can’t a clot / narrowing be dispersed / repaired after it has done some muscle damage, during the time collaterals were taking over?
What about the muscle lying dormant while extra routes are being established? What does dormant muscle look like? Could it be mistakenly interpreted as dead?
The word used in cardiology is not dormant, it is hibernating. It looks like heart muscle that is not contracting.
Biddy99 – vit C – “powder version but it upset my stomach”.
I alternate between 2 powder versions of vit C (the brand name recommended by Dr Suzanne Humphries):
1.sodium ascorbate and
2. ascorbic acid
The ascorbic acid powder – wow! It has that familiar, sharp taste associated with citrus fruit or unripe berries. I find it hard to drink in large quantities and you may get rumbling inside/upset stomach.
For those reasons there is sodium ascorbate powder, which is buffered i.e. it is gentler on your stomach and recommended for those who either get upset stomach and/or need to take high dosages and may get rumbling/upset stomach at high consumption levels.
There is also calcium ascorbate for those that may want to limit sodium intake. I don’t find the buffered forms as immediately effective for me personally as the unbuffered, but they seem to work well for cats and dogs — yes, I give the sick rescue animals extra C — if human capacity for making various nutrients declines with age/illness, it makes sense that this is likely true of other mammals that might make sufficient amounts under normal circumstances.
I don’t know that there is a problemfor most people with sodium intake, ut suzanne cautions against calcium salts as that apparently does have undesirable effects.
A little off-topic again on Prof. Noakes. I hope by this time , everyone knows he was completely exonerated. Her’e his message expressing appreciation for all that signed the petition in his behalf. https://www.change.org/p/12991092/u/22903105?utm_medium=email&utm_source=petition_update&utm_campaign=359158&sfmc_tk=4wItZyjwN5T%2fps1%2bClFoPoNCcH7yCkbkD3v44zSFXOkiFEph0nYaXKDzYCPG4hVJ&j=359158&sfmc_sub=8587341&l=32_HTML&u=64084108&mid=7259882&jb=3
alcura, your reference to Weston Price above is also good reading.
I am just in the beginning of a best seller book “The Dorito Effect” by Mark Schatzker from 2015 an which I find very interesting. It is an overwhelming account of how our eating habits are manipulated into the junk food business by Big Food and Pharma by luring our flavor senses in the back of our nose.
Goran, if you have not already read them, you might be interested in Dr. Lustig’s books on the manipulation of our minds by the junk-food industry.
I have acquired an aversion to that phrase ” junk food”. What I dislike, I suppose, is that it seems to sneer at the poor, who tend to eat such food, and yet the concept is rather poorly defined.
I mean, go back a few years and people knew what they meant by ‘junk food’ – it was food that was packed with saturated fat and salt to make it taste good. This was considered to be really evil because it was well known that salt and saturated fat also give you heart attacks! Well, at least in this corner of the internet, saturated fat and salt are not seen as problematic, and yet that same sneering phrase is applied.
Here is a breakdown of the contents of Doritos:
This guy seems mainly concerned that Doritos contain ‘pork enzymes’ – um so exactly what – Cheese is made using rennet which is obtained from the stomachs of calves.
I wonder which ingredients you object to, or whether it is just that such crisps are a bit moreish. Bear in mind that few people would eat a large amount of such food by weight.
I’m not against the idea that we should eat more natural food, but maybe it is worth remembering that even the poor like the odd party and they can’t always afford nibbles that would not attract the description of ‘junk food’!
I was told at one point. It its food it’s not junk: if it’s junk it’s not food. I think the main problem has come with excess carb consumption. Excess is different for different people, and varies according to other factors such as age and exercise taken. Humans also seem to have a problem in that carbs do not seem to create satiation in a way that, say, butter would do. You can go on eating crisps and popcorn until you go pop. Some of the popcorn containers you see at the cinema would house a family of four.
indeed ! But the extent that carbohydrate ‘foods’ are processed could be a significant part of the problem. A lot of what was there to start with has been removed.
White bread from ‘pure’ refined white white flour for example.. Wholemeal bread which is simply white bread with colouring added…Ditto pasta,pizza bases etc..And the increasing reliance on these processed carb foods… Spaghetti which is 95% white flour mixed with some water, then with 5% sauce added at the end…
I tend to eat dark rye bread ( organic if available() which is processed far less. With lots of butter and other ingredients like meat, cheeses, onion, tomatoes capsicums etc to make a great sandwich, I definitely know when I’ve had enough..
Bill in Oz: Yum, yum! You can make me a sandwich any day of the week.
My favorite size, and with a family member on each side devouring it, it didn’t last long, but made me terribly thirsty. Never liked soda pop, so snuck in a water bottle. Don’t do that any more, and am amazed I survived all that chemical “butter.”
There is some interesting research about different food satiety: http://nutritiondata.self.com/topics/fullness-factor
There is also data coming from MyFitnessPal: https://www.researchgate.net/publication/305709786_Online_Food_Diary_Dataset
And really interesting analysis of this data:
I wonder about the restaurant at IKEA – junk food?
I don’t think so.
They are today here i Sweden offering a brunch at an incredibly low price for IKEA Family members. All you can eat at 49 sw. krona, i.e. about 5 USD. Something for “poor people”?
So this morning we over-indulged on heaps of bacon, meatballs, scrambled eggs, small sausages, chicken nuggets and topping the heap off with some cubes of butter (organic) and a few slices of cucumber(looks nice) and wash all down with a couple of cups of coffee.
We though carefully avoid all bread, pastries and sweets offered at the brunch.
And we stay satiated and anecdotally lean as ever, actually now getting leaner, which seems like a contradiction when we look around to see what the more heavy guys have on their plates.
Funny world we are living in.
Well, no-one is perfect and tempting food traps are all around.
Attending a meeting tonight at a local antiquarian association sandwiches on white bread was served at the coffee break and we just couldn’t resist. At home we now read blood glucose values of 8.6.
This is interesting
looks at the effect of the combination of carbs AND fat which is seldom found in nature but common to most “processed food”. I suspect especially worse when the carbs are wheat and sugar and the fats are Omega 6.
I’m leery about “food reward” when they assume brain circuits override the endocrine system which is IMO illogical when you consider evolution, More likely the brain fine-tunes the endocrines.
The problem with the Optimizing Nutrition website is the data analysis uses data from people. Those people are the “crazies” who actually record what they eat. (I was one of them, when I was on low fat and proud of myself for eating less than 10% of fat by calories per day.) It’s a very select group of people and not generalizable to the common population. (And that assumes all the data is correct.)
Also, everything he does is “on paper”. In other words, you could measure that you ate X grams of say blueberries or spinach or whatever. He would then use whatever the calorie program told him was correct for calories and nutrition info. But if you’ve ever looked at your effluent (i.e., poop) after eating some of these things, you might notice that not everything got absorbed. That’s an error not accounted for. And this doesn’t include anti-nutrients and the like.
Then, there are the errors that the calories and other info on the labels are wrong:
See also: https://www.precisionnutrition.com/problem-with-calorie-counting-calories-in
So, for Optimizing Nutrition, it’s interesting data, but most likely wrong at best and completely flawed at worst.
BTW my blood glucose reading is just now 5.9 mmole/L which doesn’t seem to indicate T2D or (?) CVD; according to Dr. Kraft two inseparable diseases.
And 5.6 for my severely T2D diabetic wife.
Where I come from in the North East of England, the percentage of obesity is frightening. As a people watcher, I have observed the so called “poor” shopping and generally living their lives. Sadly they do not have the monopoly on consuming “junk food” (seen plenty “suits” stuffing their faces in the street!) Simply, an alarming number of people(poor, working class, middle class, or so called upper) have something in common. They do not know, or care to know how to prepare or cook meals from scratch! Some of them think potatoes come from the freezer cabinet in Asda, not the ground!(True) They simply wouldn’t know how to “put a meal together”. Why should they? After all, you can pick up a full meal from the freezer/chiller cabinet, stick it in the microwave, and grab a seat in front of the tele? We, the lucky few, know the answer to that, sadly they don’t. They never will, until someone tells them the truth. You can produce excellent nutritional meals cheaply and quite easily, it’s not rocket science! I usually tell them “if you can read, you can cook”. It’s that easy. We are being lied to in the name of profits, simple as that. All the talking in the world won’t stop people stuffing their faces with crisps, sweets, pastry, McDonald’s burgers, cheap curries from supermarkets, because they DON’T KNOW how to do anything different. The art of cooking is almost lost, and they don’t know what they are missing, it’s a joy! Wel, I love it! 😉
Yet strangely when I lived there back in the seventies, obesity was, well about as rare as it was everywhere else. No doubt the change came about immediately following the adoption of “low fat” diets. To a degree the snacking follows the diet as well as the other way round, if you get carb cravings every couple of hours you have to eat carbs every couple of hours (ask me how I know!)
The beauty of my adoption of low carb/paleo/keto is that my cooking (mostly from fresh ingredients) never takes long, and I can live off my stored energy for most of the day. If I overreat (it has been known) it just takes longer before I get hungry again. Knowledge once known and then lost.
I’ve been told by plenty of women over the years that they refuse to cook for “ideological reasons”. I suppose that means that cooking healthy food means you’re by the white patriarchy.
Personally, I thought they were just lazy. And stupid.
Then there’s the corollary, men who cook are pansies. Yet strangely most of the “best chefs” are male. My mother did most of the cooking but father was more than capable when required. Yet he took sole responsibility for baking bread. When I was married we pretty much shared the cooking, shopping and washing up. As do a significant number of people I know who are much younger. I suppose this attitude goes back to when women were expected to stop work when they married, but that’s getting to be a long time ago now.
I was reading this article: ISA 2018 report: ODYSSEY Outcomes analysis shows that lipoprotein(a) is a marker of cardiovascular risk. It said that lp(a) was an independent predictor of MACE, that is, independent of LDL.
One criticism that came in, “According to Professor Kausik Ray (Imperial College, London, UK), the current analysis fails to take account of the cumulative benefit from LDL cholesterol lowering…”
I get the feeling most researchers can’t tie their shoes without considering LDL.
Andy S, (I hate WordPress — it shows a “reply” link quite randomly – some posts have it, some don’t).
Thanks for the info on the how of “hidden” heart attacks, but it does not answer my questions Are such MIs really so common? And if they show no symptoms or effects, how is one to know if one has had such an occurrence? There is much disagreement among “expert” sources, with AHA saying they are more common in women, and Harvard Health saying they are more common in men; some saying there are 4 signs you are having one, some saying 7; some saying you’ll experience after-effects and some saying maybe not. Many imply that you need a special, high-tech imaging technique to find out if you’ve had one (sounds like a plug for recovering costs of expensive equipment). And does such testing really help? Knowing the role of stress in CVD, you may get stressed out over testing and the cost thereof, the statistics, etc., and afterward, due to all the stress and commotion, have a silent heart attack. But, then, you won’t know you did until a year has passed and you go in for your next physical.
Hi annielaurie, re silent MI prevalance
“In 2000, He at al21 reported that the severity of coronary artery calcification by electron-beam CT can predict silent myocardial ischemia on stress photon emission CT. When the calcium score was between 11 to 100, 2.6% had silent ischemia compared with 11.3% with scores between 101 to 399, and 46% with scores above 400. Nearly 4000 subjects were studied.”
In other words: the more that arteries are gummed up with plaque the more chance of silent MI (and the more chance of regular MI)
Solution to avoiding MI is to stabilize plaque by reducing risk factors.
Maybe yet another question is whether anyone should care! This sort of research sounds like yet another way to scare the hell out of people and sell more drugs and other procedures! (I am becoming incredibly cynical as I get older).
It seems that beta blockers, clopidigrel, and aspirin are typical post MI. Hard to comprehend why or how slowing the heart helps the healing process. And apparently aspirin is not a proven option. Statins were on the list as well, but I refused. Interestingly I had a heated discussion with the Cardiologist’s assistant, re my refusal ,who declared he was taking statins. That really impressed me. Definitely a strong argument!
Beta blockers caused me frightful neck and shoulder aching, and even now, two months after stopping the medication, I am still not healed. As for refusing to take statins, the cardio team simply refused to even listen, let alone discuss the matter! They really did not appreciate being gainsaid, and implied that statins were crucial to healing from an MI.
Ah, David, I guess I’ve been incredibly cynical about the medical establishment since my skeptical youth. And I get more so as I get older (72 in a few days). So some of my comments on hidden MIs were a bit of playing devil’s advocate to see if others shared my opinion, which you expressed so well.
I do a monthly art-class-learn-and-share for a nonprofit group I belong to. Yesterday, I was so sad through the whole thing, listening to the folks talk about their latest problems with their insurance companies, their docs, etc., their issues dealing with what most Americans think of as “normal aging conditions” — arthritis, sciatica, T2D, bad lipid profiles, etc., and all the side effects from their many prescribed drugs. I wanted so much to say, “Stop! There’s a better way! You can take control of your health!”. But, I know from past experience, they’ll think I am some kind of mumbo-jumbo medicine nut. These guys were actually, here in 2018, when Harvard and Yale Med Schools (and others) offer a specialty in it, talking in amazement about the effectiveness of acupuncture (which they characterized nonetheless as some kind of voodoo).
“Statistics show” that the average American over 65 takes an average of 5 prescription meds. Not taking any at all, I guess I was a bit skeptical about said statistics. But now I know a few folks that are using my “allotment”!
I don’t think you should be too impressed that your cardiologist takes statins – remember some people don’t get side effects, and some such as myself get them after some time – 3 years in my case. It was because my problems didn’t start soon after starting statins that my GP and I both thought it was something else. I only realised Simvastatin was definitely causing my problem through good luck – you can read all the details here, if you want.
A little GOOGLing will reveal there are cardiologists on both sides of this debate.
In my case at least, any extra life extension from taking statins would not be worth the reduction in mobility and pain that they caused me, not to mention that exercise is very difficult with these side effects. ALSO, some people report that they suffer damage that doesn’t fully disappear after stopping the drug. Fortunately my side effects faded completely after about 9 months.
Just say NO!
Malcolm, is the MINOCA scenario compatible with the ’response to injury” hypothesis?
Emotional stress (injury) constricts arteries, reducing blood flow and possible MINOCA.
“There are differences in MINOCA patient’s clinical profile compared to those with obstructive lesions. It is remarkable the association with emotional disorders and its impact on prognosis.”
OT: Two years ago a valued commenter on this blog, retired veterinary researcher Mike Cawdery, was murdered, along with his wife. Their killer is now being sentenced.
I don’t have a link, but there is a Daily Mail article today about a study showing caffeine aids in endothelial repair.
“there is extensive previous research demonstrating the health effects of caffeine at a “physiologically relevant amount” — namely, four cups. “It’s known that four cups or more of coffee lowers the risk for heart attack, stroke,, and diabetes,” says Altschmied. Now, they know the reason why this happens: Caffeine can “push” a protein called p27 into the mitochondria, or energy powerhouses, of heart cells. This, in turn, can help those heart cells function more efficiently.” — https://www.inverse.com/article/46253-coffee-heart-health-caffeine
Much as I am happy to read this, being a coffee lover myself, I have learned on this blog to be cynical about any research touting the benefits of any particular substance. There is so much money riding on the promotion of said substance that positive research can be bought. And coffee is the most valuable traded commodity in the world, after oil, allegedly. — https://www.rogersfamilyco.com/index.php/know-top-ten-traded-commodities/
I am not sure how they define “traded commodity”, because coffee is only No 22 on the list of agricultural products by value, down there with apples, bananas, mangoes, palm oil and onions, way below wheat, soybeans, tomatoes, and sugarcane. Rice is the most valuable commodity, followed by — avert your eyes, vegans! — cow’s milk, and cattle, pig, and chicken meat. — https://en.wikipedia.org/wiki/List_of_most_valuable_crops_and_livestock_products
Is it possible the Daily Mail article was a follow-up or update on this 2011 study: https://www.ncbi.nlm.nih.gov/pubmed/21349479 ? Even extremist vegan advocate Dr. Greger recognizes caffeine’s benefit to epithelial tissue. Maybe caffeine’s effects are the reason that more studies, as time goes on, show that coffee and tea consumption is linked to lower all-cause mortality and lower morbidity.
That makes me wonder, again, if epithelial health is the key to avoiding, not only CVD, but all the major nasties. So many autoimmune and other “modern” conditions seem to start with damage to the epithelial tissue in the digestive system, and Dr. K makes a strongly convincing case that “CVD-spectrum” conditions start with damage to epithelial tissue in the circulatory system. Well, time to go make a cuppa joe or a spot of tea….
annielaurie98524: Thanks for that link! They make it sound like coffee is the best CVD preventive ever. I drink it because I like it, and usually have about 4 cups spread out over 8 hours or so.
Thanks for another great blog, Malcolm. I started reading all I could about heart attacks and cholesterol because of a family history of early fatal heart attacks. Your blog was a starting point for me after an enlightened GP lent me a copy of your book “off the record” and told me that the pressure to prescribe statins made him want to retire from being a doctor.
Since then I have discovered I have very low free T3 (with a normal TSH which meant it never got picked up by my local doctors surgery). Reading all I could about hypothyroidism led me to recently read Dr Barnes’ book from 1976, ‘Hypothyroidism, the Unsuspected Illness,’ and I am also half way through another he wrote, ‘Solved, the Riddle of Heart Attacks’ (it’s available to read free via this link http://jeffreydachmd.com/wp-content/uploads/2013/09/Broda_Barnes_Solved_Riddle_Heart_Attacks.pdf).
He said that when smallpox was eradicated, tuberculosis became the next big ‘killer’. When antibiotics were introduced, the people who previously were dying young from infection (which low thyroid function predisposes you to), were surviving into adulthood, and it’s this section of the population that are predisposed to heart attacks from atherosclerosis secondary to poor thyroid function. So this accounts for the steep rise in heart attacks.
He said that probably 40% of the population have low thyroid function. The 5% figure that is quoted now is for those who get picked up by the modern TSH blood test, which fails to pick up the other 35% who have low thyroid function. Other current doctors agree with this figure, some thinking it even higher than 40%. Another book I’m reading by Mark Starr MD, ‘Hypothyroidism Type 2; the Epidemic’ agrees with Barnes’ findings, and talks about the people outside the 5% having a problem whereby thyroid hormone isn’t able to access the body’s cells, as it’s meant to do.
I’ve tried to summarise it in a couple of paragraphs (no mean feat with my brain fog!) and there’s obviously more to it than that, but his books are clearly written, and supported by research (he personally reviewed 70.000 autopsy protocols at Graz. Austria, carried out between the years 1930-1970).
What would you make of this?
I’m reading Dr. Barnes’s book ATM. It’s very interesting. Coincidentally, the thyroid gets a mention in Richard Lehman’s column this week.
The overdiagnosis community regards “subclinical” as a warning: do enough tests, and we can all be subclinically something; eventually we realize that we are all subclinically dead… Judging from this review, nobody actually knows what do about “subclinical hyperthyroidism”. — https://blogs.bmj.com/bmj/2018/06/25/richard-lehmans-journal-review-25-june-2018/
Unfortunately, the review he references is behind a paywall.
Sci-hub to the rescue (no more paywalls for science): http://sci-hub.tw/https://www.nejm.org/doi/full/10.1056/NEJMcp1709318
I had an interesting & possibly hopeful experience at my local GP’s practice the other day. I was to see their nurse about setting up a “Care Plan” so I could get my chiropractors consultations paid for by Medicare here in Australia. Yes my back does go out occasionally and this needs treatment by a local chiropractor.
Anyway it was a complicated process that required seeing the GP practise nurse for an extended interview with me providing details of my diet, health weight etc…(Typical bureaucratic process ! ! )
The practice nurse asked me about the statins that their cardilogist had prescibed me a year ago.I told her I had refused them and that he had then refused any other treatment options or even see me. She was shocked. at his actions. And immediately admitted that Statins have side effects. She nodded when I said that a lot of those side effects are not attributed to the statins as they are ‘common’ in older folk and so SEEN as inevitable anyway by medical folks..
When we talked about diet she was completely current with the healthy choice of a low crab/high saturated fat diet and the ill health effects of a high carb processed food diet.
At this point I was a bit shocked as here was a medical person almost completely aware of the issues we have been discussing for so long. The only point where we disagreed was on the role of LDL-C on CVD. On this she seemed to still accept the ‘official; ideology. So I told her about this blog Malcolm. And I think I may drop off your book there for her to look at.
The wheel is slowly moving !
That must have been a heart warming (sorry!) moment for you!
I have noticed that some doctors on the internet get parts of the story that Dr K tells, but don’t put it all together. For example, without naming names, they may not get the fact that cholesterol has almost certainly been wrongly blamed for heart disease (so they may talk about reducing cholesterol by changes in diet), or they will talk about the need to reduce salt, or extol the value of a ‘healthy’ diet without defining what they mean by that. etc. Alternatively they may get obsessed with supplements.
I think like you, this blog is the best place to send medical people who are starting to open their minds. It also contains a host of links to other relevant places.
totally off topic, about an Australian ob gyn who kept making egregious mistakes and was covered for by other local doctors and lawyers:
Great blog entry Dr Kendrick.
Personally I have been making adjustments to my breakfast routine having read ‘Breakfast the most dangerous meal of the day’. It seems we are most insulin resistant in the morning perhaps due to the cortisol surge on getting awakened. With this in mind I did some personal blood sugar testing and was surprised to find that porridge shot me from fasting 80 to 116 when made with water and no additions. I have now switched to beans and the occasional eggs. If endothelial damage is the key then insulin must be playing a part as diabetics suffer from rampant artery damage.
Can’t blame insulin resistance on insulin. Glucose glycates insulin receptors and insulin thereby requiring more insulin ie insulin resistance. If insulin is creating problems blame glucose.
If we are back on diet, here is a book to scare you all to death:
Grass-Fed Nation: Getting Back the Food We Deserve
Essentially he is telling us that modern farming, above all its concentration on wheat is killing the soil, and therefore our means of feeding ourselves. By the way, he reckons that it is at the origin of modern diseases.
Mr Chris, I would like to believe Graham Harvey, but is he right any more than any other author? I think wheat, particularly the modern high yield, short straw varieties, cause many problems, but am I right? The major problem we have is too high a population to support, and many people looking for ways of “saving” lives, and looking for ways of living longer. If his book can scare people death, it should be mandatory reading. I would survive the challenge.
Is he right? Well, having changed my little bit of an allotment to the type of cultivation which he admires, I note an increase in visible microbe Life.
As to the more general aspect of your question, I feel each of us should take his own health in hand And decide for himself on the balance of his understanding what seems more likely. If I wait for more studies etc, I could be easily be part of the praire écosystème by then!
smartersig: Also keep in mind endothelial repair. Just as important as minimizing damage. We know vitamin C plays an important role, as do certain amino acids. What else?
That’s odd. I’ve read that we are most insulin sensitive upon waking. I think I pulled that from Jason Fung’s blog. It stuck with me because he and I both skip breakfast, despite acknowledging that it was actually a great time to eat.
Observationally most Type 2 diabetics and prediabetics are more insulin resistant in the morning and more insulin sensitive by evening. I am mostly limited to 10g carbs at breakfast but can do 50 – 80g and sometimes more by evening. Not that I usually do but I can. I know others with an even more marked slope.
Conversely the opposite pattern is more common with Type 1. Not sure what happens with “nondiabetics” if there are actually any left. Best way to find out is 1 hour postprandial glucose tests, or a CGM. Actually testing insulin/c-peptide would be gold standard but unavailable.
Possibly why some people crave carbs and sweets in the evenings.
Sorry this is slightly off topic, but some of you may remember that I wrote about how my partner’s physical stamina when cycling improved sharply after she had taken a Q10 supplement for a short time. She still takes Q10 and the improvement has been maintained!
Recently she went for a checkup regarding her asthma, and was told that her asthma had improved. She asked the consultant about Q10, and he said he knew nothing about it. This prompted me to GOOGLE Q10 and asthma, which produced this:
Given that Q10 is part of the chain of reactions used by every cell in the body to release energy, I suppose it isn’t surprising that taking this supplement helps in a variety of ways.
Far Infrared Radiation therapy is being investigated for its role in endothelial repair.
And, add vaping to the list of things that damage endothelial tissue: https://articles.mercola.com/sites/articles/archive/2018/06/27/e-cig-flavoring-harms-blood-vessels.aspx?utm_source=dnl&utm_medium=email&utm_content=art3&utm_campaign=20180627Z1_UCM&et_cid=DM217218&et_rid=348256020
From the article mentioned above:
“Effects of FIR on CVD
Evidence has indicated that FIR rays exert protective effects on CVD. Several weeks of sauna therapy markedly enhanced flow-mediated endothelium-dependent dilation of the brachial artery (P < 0.001),16–18 which was associated with an increase in cardiopulmonary exercise tolerance.17,18 Because endothelial dysfunction is typically observed in patients with hypertension,19 hypercholesterolemia,20 diabetes mellitus (DM),21 and obesity and patients who smoke,22 sauna treatments probably play a therapeutic role for patients with coronary risk factors, suggesting that sauna treatments improve vascular endothelial function.
Compelling evidence has indicated that vascular endothelial function is closely associated with endothelial nitric oxide synthase (eNOS), which catalyzes the amino acid L-arginine into L-citrulline and nitric oxide (NO) in the endothelium. NO is a crucial vasodilator substance, which prevents the progression of atherosclerosis by dilating blood vessels and inhibiting some arterial disorders such as platelet aggregation and the migration and proliferation of smooth muscle cells.23 Ikeda et al. reported that one month of FIR sauna therapy significantly upregulated eNOS mRNA and protein expression …..”
Regarding your post above (it didn’t have a reply button) on statins and mitochondria, if that is so that statins attack mitochondria, then there should be a fairly strong relationship between statin use and cancer. But your post also seemed to imply that it is the mitochondria in muscle cells that are affected by statins. If that is the case then perhaps the relationship would not be that strong after all, as I don’t think there is much tendency to get cancer in muscles.
AnnaM: every cell in every tissue is affected by statins, from guts to brain. Statins are mitochondria poisons.
“An alarming increase in breast cancer incidence, some of which were recurrences, was seen in women randomized to pravastatin in the care trial11 Thereafter, cancer was an exclusion criterion in randomized statin trials. In clinical practice, however, it is not infrequent to find an association between recurrence of breast cancer and concurrent statin therapy15.”
“Breast cancer occurred in 1 patient in the placebo group and 12 in the pravastatin group (P = 0.002). “
Thanks for that extraordinary (and disturbing) link.
“An alarming increase in breast cancer incidence, some of which were recurrences, was seen in women randomized to pravastatin in the care trial11 Thereafter, cancer was an exclusion criterion in randomized statin trials. ”
So they recognised the cancer problem in the trials, but still permit women to be prescribed statins (presumably including pravastatin) to women!
Wow that’s scary! Not entirely unexpected though for drugs that shut down an entire pathway, which must have evolved for a reason other than to kill us, just to change one number. And worse, changing that number in women appears to have even less effect than in men.
This raises an amazing part of the statin scandal. One side can’t admit that statins really cause seriously unpleasant side effects. To dodge that obvious conclusion, there is the absurd claim that statins cause no more side effects than do placebo pills! This means that no decent research seems to have been done on why statins cause muscle problems, and why some people are more susceptible than others.
If statins cause these effects because they reduce cholesterol levels too low (together with Q10), then I guess PCSK9 inhibitors will do an even ‘better’ job, and we will know quite soon, but since some statins, such as Simvastatin (the one that attacked me), are reputed to do cause more problems than others, I suppose the mechanism might be something else.
I had a rather encouraging conversation with a woman I met at the ice rink today. She was just learning to skate, and was not in the first flush of youth. She said she was recovering from a stroke, so I warned her about statins and their side effects. It turned out she was also a doctor, and freely acknowledged that statins had serious problems.
It looks like statins have a few modes of damaging action. Possibly low cholesterol, low coQ10, and the mitochondria problem.
Given the importance of stress and clotting in Dr. Kendrick’s theory, I was interested to read the following in Dr Barnes’s book http://jeffreydachmd.com/wp-content/uploads/2013/09/Broda_Barnes_Solved_Riddle_Heart_Attacks.pdf
“At one time I was studying the cholesterol content of deer’s blood . After catching the animal, the drawn blood would often clot before I could remove it from the syringe The adrenaline of excitement had accelerated the clotting – one of Mother Nature’s methods of reducing hemorrhage in case an accident causes a laceration.
Any type of excitement will call forth a burst of adrenaline from the adrenal medulla, but if the emergency lasts, for more than a few minutes, the cortex of the adrenal (the exterior portion of the gland) begins to secrete more of its hormones. The latter are not so rapid in action, but their effect lasts much longer.”
Dr. Barnes regards thyroid deficiency as the main cause of heart disease, and notes that the adrenal gland produces cortisone which inhibits the thyroid. He noticed that the patients he was treating for thyroid deficiency got heart attacks at a rate of only 2 per 1,000 patients whereas in the Framingham study the rate was 150 per 1,000, both over a period of 20 years.
He states that animals which have their thyroids removed become more susceptible to infection and atherosclerosis. Similarly, the 40% of the population with thyroid deficiency are susceptible to infection and atherosclerosis. Thus the pattern as described by Lazyredhead above: Before antibiotics, low-thyroid people died of infection; after antibiotics, they survived the infection and died years later of atherosclerosis. Which fits the pattern of rapidly rising heart attack deaths he observed in the 1970s at the time the book was written.
It strikes me (as always today) how little we know about the pathogenic parts and paths of our physiology. Just think about the 20 000 proteins interacting in poorly understood ways.
One problem with the thyroid deficiency theory is that after the 1970s, heart attack deaths started falling again and are now far lower than their peak. How could thyroid function be the cause of this fall?
Perhaps it is iodine supplementation of salt, which started in 1924 according to Wikipedia. A healthy thyroid needs iodine, and children who were started on iodine-enriched salt in the 1920s would be hitting the heart attack age in the 1970s with normally functioning thyroids and thus not getting the heart attacks their non-supplemented forebears used to get.
I’m not sure how widespread the uptake of iodized salt was. I remember in the early 1960s in South Africa, one day when I was fourteen my mother gave me some money and said, “Run down to the store and get me some cooking salt.” So I nipped down to the store and asked for salt. The shopkeeper said he only had iodized salt. I had never heard of iodized salt, but he assured me it tasted just the same as ordinary salt, so I bought it and brought it home and gave it to my mother. She told me to take it back, she wasn’t using any iodized salt in her cooking. “But ma, the man says it tastes just like ordinary salt.” No dice. I had to return the salt and get my money back.
So maybe the uptake in iodized salt was gradual, accounting for the gradual decline in heart attack rates. For myself, I have always used iodized salt, and my thyroid seems to be fine.
Hypothyroidism is very common even with iodine supplementation. Synthroid is prescribed more than any other drug, at least in the US. Also, there are seems to be many undiagnosed cases of hypothyroidism.
Surprisingly we are all very tempted to find and cling to one single cause for any illness instead of looking for an holistic approach and one which I, with advancing age, more and more embrace.
Nearly there? According to the AHA, lots of people are now very nearly there. The trigger level for blood pressure treatment has been lowered.
Updated blood pressure guidelines from the American Heart Association (AHA) mean that many more Americans, notably older people, are now diagnosed with high blood pressure, or hypertension. This may sound like bad news, but the new guidelines highlight some important lessons we cardiologists and heart health researchers have learned from the latest blood pressure studies. Specifically, we have learned that damage from high blood pressure starts at much lower blood pressures than previously thought and that it is more important than ever to start paying attention to your blood pressure before it starts causing problems.
High blood pressure accounts for more heart disease and stroke deaths than all other preventable causes, except smoking.
As president of the AHA and a cardiologist, I completely support the latest guidelines. I know they will save lives, especially when blood pressure is accurately checked and when people make therapeutic lifestyle choices to lower their blood pressure.
We’re all gonna die.
Of course, we’re all gonna die. The name of the game is to put it off as long as possible.
I think that needs a qualification. As long as possible while maintaining sufficient faculties, and comfort so you can enjoy it. People with severe, chronic conditions possibly think “as long as possible” is too long.
Yes, but you miss the whole point of ratcheting down the standards. The more you lower the threshold, the more “patients” you create, the more prescriptions for such-and-such condition can be sold, and, thus, the higher profits for the pharmaceutical companies. It’s not just blood pressure that they fiddle with. Check out what’s happened with the “ideal weight” charts the last few years.
PS. As I understand it, blood pressure doesn’t cause problems. It is the problems which cause high blood pressure.
There is a degree of overlap.
What is high BP?
If I run upstairs, make the coffee my BP goes to 15/16 , and I am 78. Should I read the paper for ten minutes before taking it, does anyone have á link for age related norms
As I recall Andrew Marr flew back from the States, did some HIIT and had a heart attack. Lifestyle, concatenation?
I think I would check your BP machine? Those figures do not make any sense to me. Andrew Marr ruptured an artery in his neck, I believe. I think that exercise is good, but some people take it far too far – then it is bad.
Please accept my apologies, I should have cited the figures as 8.5/15.
Was Andrew Marr’s problem from exercise or something else
Do you have a cure for seniors who are too elliptic in what they write??
I still do not understand your figures. They bear no relationship to anything I know to be a blood pressure. Normally measured in millimetres of mercury. A standard figure would be, say, 120/70mmHg.
Here they are 155 /80
Please excuse me
Aha, that makes sense. Thanks.
Mr Chris: Too early in the morning to figure out a clickable link, but see Sidney Port, et al., “Systolic blood pressure and mortality,” from The Lancet, Vol 355, January 15, 2000, pp. 175-180. An analysis of the Framingham data. “Findings: Against the predictions of the linear logistic model, neither all-cause nor cardiovascular deaths depended on systolic blood pressure in a strictly increasing manner.”
thanks for that, it is behind a paywall, but I am hoping my son can get it for me.
If my systolic is 155 after running upstairs and usually around 13 (with a little help from L Arginine), I hope I can go on reading this excellent blog with its comments some years more!
Mr Chris: The mortality risk shown in the data depends on age and sex, and refers to resting BP. 155 after running up stairs sounds perfectly normal to me. Figure 3 in the paper shows no increased risk for men 45-54 below 142 SBP, for men 55-64 below 150 SBP, for men 65-74 below 160. Again this is resting blood pressure. As far as I know, it is normal for BP to rise for lots of reasons, including physical activity, talking, laughing, stress, and so forth. When I found and printed the Port paper it wasn’t behind a paywall.
When I looked for the Port paper on the Lancet web site, I could read the abstract for free, but the full text was 30$. As I said, I found a relative in a University who got the full text for me.
What often strikes me is how slow the dissemination of knowledge like this is, many in the medical profession seem light years behind.
Thank you for bringing it to my notice.
Mr Chris: Maybe it costs money in the UK, but not in the U.S?
Since I don’t feel like biking around with BP monitor, I always wear a HR monitor when biking and ease myself in when the fine weather comes. My max HR. Is about 160, so on hills when I get into the 140, I ease off until my HR drops back to 120. I know I am using HR as a surrogate measure of BP but I don’t see what else I can do.
Mr Chris: Good idea to monitor HR. I have no idea how it would function as a BP surrogate. I vaguely remember from training for running that getting it to 90% at times was useful. That would 144 for you. I don’t recall exactly how to determine one’s maximum, some number over 200 minus your age. I know during my hikes when I hit a 20% or greater incline I have to stop periodically for 20-30 seconds to let it come down a bit, but I don’t monitor it. I know when I’m lying down in bed it is always 60, since it tracks perfectly with the ticking of the clock.
thanks for your reply. As you say, there are many formulae for assessing maximum heart rate, there is the classic 220 minus your age, which does not work for seniors, and I am told is only reliable for 50% of the normal population. I found a formula which gave me a maximum of 170, and I tested it by jogging round the running track twice, and then went fairly full out for 100 metres, and I got 160.
On the subject of overexercising, there was a mention some time ago on here of a book called
” The Haywire heart : how too much exercise can kill you and what to do about it.” by Christopher Case and Dr J Mandrola etc. I was inspired to look it out by Dr K’s remarks about over-exercising. The authors claim that over-exercising can lead to Atrial fibrillation etc due to upsetting the electrics of the heart. An interesting read.
Mr Chris; Gary.
Resting heart rate does not tell you enough. Your BP fluctuates throughout the day and night accommodating the activity you’re engaged in. I’ve mentioned before that weight lifters can reach 300 mm of mercury systolic pressure during a lift. You must look at more than the tail of the elephant to know the whole story. 24 Hr ambulatory monitoring is probably the best view we can get as of now – provided the results are interpreted intelligently.
This article suggests that even if your BP is beautifully controlled by medication, your BP might well be too high during exercise. (Pay-wall. Sorry.)
JDPatten, scientists are probably working on developing medications to control exercise induced high BP. White coat BP syndrome is another risk factor to explore.
OTOH exercise induced high blood pressure could be the last straw for someone out of shape, with vulnerable plaque, weak arteries, clogged arteries, heart failure, excess medications, etc..
Good hypotheses . . . except if you haven’t read the article.
From the article:
We recruited 59 participants: 16 normotensives, 16 treated–uncontrolled, 16 treated–controlled, and 11 untreated hypertensives, matched for age, body mass index, and cardiovascular fitness (as measured by a volume of oxygen inspired [Vo2] peak test). This study was approved by Southwest- Exeter National Health Service Research Ethics Service (16/SW/0004) and local Research and Development. All participants provided their writ- ten informed consent before participation. Participant demographics are shown in the Table. Twenty-nine of the participants (49%) were women and 27 (93%) of these were postmenopausal. Participants attended the Clinical Research and Imaging Center–Bristol at the same time of day, and the laboratory conditions were at a set temperature (22°C). All par- ticipants were asked to abstain from intense exercise 24 hours before the study. All experimental protocols conformed to the Declaration of Helsinki. See the online-only Data Supplement for inclusion and exclusion criteria.”
JDPatten: only read the abstract
According to my GP I would be classified as “uncontrolled hypertensive” that has also refused statin treatments and flu shots.
The study suggests that we should be concerned about exercise induced rise in BP. What are we going to do about it and who is at risk? Perhaps a heathy lifestyle would be protective.
So if endothelial damage is the start, and if blood vessels subjected to higher pressures (arteries) are susceptible, how does exercise fit into this? Especially HIIT, where heart rate and BP can be pushed quite high. Would this form of exercise be considered damaging to the endothelium?
It is all balance between damage and repair. Whilst HIIT probably does cause some damage, it also – to a far greater degree – stimulates repair.
Link to the article in question : https://news.heart.org/medicine-fails-to-control-blood-pressure-during-exercise/
Swedish researchers reported that having tonsils or the appendix removed before age 20 is associated with increased risk for heart attacks by 44 percent for the tonsils and 33 percent for the appendix https://europepmc.org/abstract/med/21632600
Dr K, when is 50th post coming out! I have a feeling your 50th will be something special! 🙂
Will it be really special – an elixir or eternal youth perhaps?
It will be an ‘L’ of a post, as the Romans say. ;o)
Smoking tobacco is a major cause of CVD. Laws enforcing plain packaging here in Oz have reduced the numbers of smokers. On behalf of tobacco companies some countries appealed this to the WTO. Which has just landed. down a ruling allowing this type of health law.
Doc, Apologies if this is a stupid idea, I’m not a scientist but I had and idea for a laboratory test for your hypothesis (if it hasn’t been done or is possible): Undamaged arteries from cadavers, connected to circulatory pump mimicking human blood pressure (I know they have these for bypass surgeries), clean blood recirculating loop through undamaged arteries–blood, pump, arteries, blood (I could draw a picture of it but hopefully that makes sense). Then, add independent exogenous particulates to blood, i.e. smoke, sugar, fat, etc… Maybe pump for 4 weeks varying pressures and examine endothelium. Damaged or not? Just a thought
I would imagine dead tissue would probably not give you the answers you are looking for.
Dr. K., lipoproteins have to cross the endothelium to supply interstitial cells, this happens at the capillaries. Large artery endothelium is thicker ie, more than a single cell and have tighter junctions to cope with pressure therefore need for vasavasorum. Explanation how foam cells happen to form below endothelium.
LDL and HDL transfer rates across peripheral microvascular endothelium agree with those predicted for passive ultrafiltration in human.
Microvascular endothelium is fenestrated and has loose basement membrane. Try looking, instead, at the blood brain barrier. Here, there is a single layer of endothelium in capillaries, and LDL and HDL cannot get through.
Dr. K. different tissues and different function of ECs.. Lymph system returns LDL to circulation.
A new function for the LDL receptor: transcytosis of LDL across the blood-brain barrier.
“in contrast to ECs in many other organs, the brain capillary ECs contain no direct transendothelial passageways such as fenestrations or channels.”
Don’t worry, I have been studying the research on endothelial transcytosis for thirty years. It does not exist. The brain synthesizes its own cholesterol, because it cannot get it from the bloodstream. Glial cells manufacture cholesterol and transports it to neurons via ApoE lipoproteins. Glial cell manufactured cholesterol is essential for the formation of new synapses.
I do not believe that anyone can show LDL receptors are used to transcytose LDL through the BBB in vivo – in humans. Isotope studies done in animals demonstrate that no cholesterol synthesized in the liver appears in the brain. Yes, you have to kill the animal and chop the brain up – not something that you would get ethical approval for in humansI suspect. I believe this to be definitive proof that cholesterol cannot cross the BBB via transcytosis, or any other mechanism.
Cholesterol not being able to enter the brain from an ample supply in the blood resonates well with the much increased risk of ALS in statin users. Scary.
Dr. K.: returning to the coronaries
Appears that there are several ways that the EC’s can be damaged. EC replacement seems straightforward and should not form plaque. As discussed in previous posts there are stages in the initiation, development and rupture of plaque. The process involves macrophages, oxLDL, foam cells, angiogenesis, calcification, pressure gradients, rupture and repair, smooth muscle cell migration, etc. as per the current popular theory.
I have a hard time understanding how and why a new endothelial layer should form over a blood clot. Help!
“Fatty streaks are the first signs of atherosclerosis that are visible without magnification. They consist of lipid-containing foam cells in the arterial wall just beneath the endothelium.”
This paper is now very old, but it explains what is seen if you deliberately damage the endothelium of a pig aorta. First step blood clot forms, second step blood clot is mainly got rid of. Third step is that a new layer of endothelium forms on top of the remnant blood clot. This is due to endothelial progenitor cells (EPCs) sticking to the surface of the clot and forming a new layer of endothelium – on top of the clot. These researchers did not know that there were such things as EPCS, but they describe them, and the process of re-endothelialisation perfectly. Also, fatty streaks do not become atherosclerotic plaques. Fibrous streaks do. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2093824/?page=10
Dr. K. re. clots and holes in endothelium
Thanks for the info, a hole in the endothelium has to be repaired, The EC’s apparently know how to do the repair, a bit of leftover clot is not an obstacle. Anyone with multiple artery repair levels is heading for disaster.
The guinea pig with low vit. C would fit the clot/repair model of plaque formation very well. No need to bring LDL into the picture. A scurvy type of plaque formation.
In humans, where did the blood to form the clots come from? My understanding is that it came from neo-vascular blood vessels at periphery of fibrous cap. A bit of erosion of EC’s will expose the blood. A lot of stuff seems to happen below the original endothelium before there is leakage of blood into the lumen. Need to find the missing link.
Um. The blood comes from the bloodstream that is flowing past the endothelium all day, every day.
Dr. K. right, it’s not the blood that caused blood clots.
Actually this paper ‘Repeated episodes of thrombosis as a potential mechanism of plaque progression in cardiac allograft vasculopathy’ may be better, it demonstrates that in patients with heart transplants, atherosclerosis develops rapidly through repeated episodes of blood clotting – causing progression of the plaque. This is a good model because atherosclerosis develops very rapidly in this population – you can see the progression clearly. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3787274/
Here is a part of the discussion.
IVUS = Intravenous ultrasound (looking closely at the coronary artery wall).
HTx = heart transplant.
ML = multilayered.
CAV = cardiac allograft vasculopathy (disease of the arteries in heart transplant patients)
mural thrombi = blood clots stuck to the side of the artery
The current serial IVUS study demonstrated that a substantial number of asymptomatic HTx recipients had lesions with complex lesion morphology, such as multiple layers, intraluminal thrombi, and plaque ruptures. Furthermore, this study implies that recurrent episodes of coronary thrombosis, presenting as ML appearance, may mediate the progression of CAV.
Multiple layers are often indicative of repetitive, periodically occurring asymptomatic thrombus formation. Post-mortem studies for native atherosclerosis demonstrated healed plaque ruptures and erosions with multiple layers of distinct tissue components. ML appearance identified by cross-sectional IVUS imaging has been interpreted as mural thrombus. To our knowledge, this is the first longitudinal IVUS study, demonstrating multiple layers not only at a single time point (ML appearance) but also longitudinally (ML formation). The present serial IVUS study demonstrated that lesions with ML formation exhibited new inner layers with distinct echogenicity overlaying preexisting outer layers. This observation could be highly indicative of repeated episodes of mural thrombosis.
A previous autopsy study in 64 allograft hearts showed that 19 arteries had recent or organized luminal thrombi. Another postmortem study demonstrated coronary thrombi in 81% of transplanted hearts with CAV, and notably, most of the thrombi (78%) were non-occlusive mural thrombi, consistent with our observations. The current study extends these previous in vitro observations and confirmed these findings in vivo, and suggests that coronary thrombosis might occur more frequently in CAV than previously suspected….
In conclusion, our observations demonstrate that a finding of ML 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 CAV. The current study gives new insight into the potential role of coronary thrombosis in plaque progression in CAV.
“Yes, you have to kill the animal and chop the brain up – not something that you would get ethical approval for in humansI suspect. I believe this to be definitive proof that cholesterol cannot cross the BBB via transcytosis, or any other mechanism.”
Just to clarify this, are you saying that statins can cross the BBB, but not cholesterol, and is it the case that the same biochemical pathway operates in the brain as does in the liver – the pathway that is blocked by statins?
If so, that would seem to mean there is a real danger that the brain will end up starved of cholesterol on a diet of statins!
Indeed, indeed. I remember so very well all the brain-rot troubles I had during that two years of taking the poisonous stuff. That is to say: I remember it now, but could not then. So many “Do I come here often?” moments.
Again just to clarify, is it the case that people who have a heart transplant, suffer a lot more CVD?
No, but they have a lot more atherosclerosis in their coronary arteries. CVD = cardiovascular disease, which means atherosclerosis in various arteries throughout the body. Thus. the term CVD incorporates strokes, bowel infarction and suchlike.
“Yes, you have to kill the animal and chop the brain up – not something that you would get ethical approval for in humans I suspect.”
I can think of some I would put forward for this procedure.
More seriously David Bailey has paralleled my thought, what do statins do to glial cells? Alzheimers also crosses my mind at this point.
Parkinson’s, Alzheimer’s. and all other degenerative brain conditions.
I see ‘cardiovascular’ means ‘heart and blood vessels’. I always thought it meant ‘blood vessels of the heart only’.
You learn something new each day.
Here’s a 10 minute Mercola video about a 3 minute, high-intensity workout that he calls the Nitric Oxide Dump. You have to scroll down a ways to find it.
I receive newsletter from Mercola but when I try to open the links to his home page an error message now always appears.
I just wonder why – it has never been any problems before.
I started getting that too when I was trying to access it from Russia.
I am strongly in favor of high-intensity workouts of short duration, e.g. through my garden work, since I believe it helps me to stay alive by maintaining the “healthy” collaterals. I recently learnt that these collaterals will degenerate if you are not constantly “provoking” the heart muscle.
I have also, for many years now, used my bike to “provoke” the system but am today very annoyed by not being able to sustain uphill riding of longer durations without getting exhausted. Now i wonder if I did a mistake yesterday when I finally acquired an electric bike that gives uphill assistance when needed. Whatever, the bike rides are now much more enjoyable since my wife does not need to wait for me at the top of the hill. It is actually the other way around now. We’ll see if she also gets an electric one.
The exercises in the video are not High Intensity, but are designed to give you the benefits of High Intensity exercise without the stress and exertion.
I have started doing them at odd moments in the day, for instance in the morning while waiting for my coffee to brew. I think they are pretty good for getting the circulation going, but they won’t get you ripped and ready for your Men’s Health cover shoot. ;o)
Chiyo Miyako of Japan is the world’s oldest verified living person at 117 years, as of June 29, 2018. By age 105, the death risk actually levels off — suggesting there’s no known upper limit for human lifespan. http://www.kurzweilai.net/theres-no-known-upper-limit-to-human-longevity-study-suggests
“The inventor Ray Kurzweil, famous for bold predictions that occasionally come true, estimated in 2005 that, within 20 years, advances in medical technology would enable humans to extend their lifespans indefinitely.”
It’s not happening. The age of the world’s oldest person doesn’t trend upwards. They are normally about 114 years old when becoming the world’s oldest living person, and when they die a few years later the next person to be the world’s oldest living person is also about 114 years old.
I’m not sure what they mean by “death risk” in the article. The older you get, the more likely you are to die. For reasons that aren’t entirely clear, [gerontologist Robert] Young says, the odds of a person dying in any given year between the ages of 110 and 113 appear to be about one in two. But by age 114, the chances jump to more like two in three. both quotes from http://www.slate.com/articles/technology/future_tense/2011/07/the_worlds_deadliest_distinction.single.html
Another “must read” post Dr. K. Could you tell me the guestimated risk of CVD when suffering from migraines? Mine have virtually disappeared since following a LCHF diet, but do occasionally still raise their ugly head! Thanks for your enlightening work ( and respect to your regular contributors in the comments).
The risk can be calculated (if you believe it to be accurate) from the Qrisk3 calculator, which includes migraine. https://qrisk.org/three/
Endothelial damage via il6, insulin stimulated epigenetic changes. Didn’t know if you saw this one
Joe: Thanks. Interesting is the term, “sterile inflammation.”
This seems to be the actual research article that Joe refers to:
This article seems to be up your alley.
Will have to read all the parts in my next commute. Thanks doc!
A recent Peter Attia pod cast (Oct 16 2018) with Dr Tom Dayspring reminded me of this comment from above.
“Anyway, getting back to her comment ‘cholesterol cannot get past the endothelium.” Dr Dayspring says that Apo B and if I understood him correctly also other LDL particles. This is one of the papers he references:
Am I missing something?
Great series BTW
Why do cells require LDL receptors if LDL can simply force its way into, then through, endothelial cells? Why do endothelial cells have tight junctions between then, that can prevent the passage of ions, only to allow LDL (and only LDL) into the arterial wall behind?
Why have vasa vasorum?
RonC: He begins by saying: “Atherosclerosis is initiated by the subendothelial accumulation of ApoB-lipoproteins, which initiates a sterile inflammatory response. . . .” From all that we have learned from Dr. Kendrick about the process of atherosclerosis, this seems to be putting the cart before the horse, As I now understand it, injury is the initiator of the inflammatory event, and all the other debris which accumulates is part of the response by immune cells to heal the injury, with the growth of new endothelium responsible for the fact that the plaque then resides within the endothelium. Why would lipoproteins first accumulate under the endothelium, as if they’re lonely and need to snuggle?