6th August 2018
One of the most difficult issues in discussing cardiovascular disease is that it is generally considered to consist of two completely different processes. The first of which is the development of atherosclerosis, or atherosclerosis plaques, which are thickenings that can grow, narrow, and block arteries over years or decades.
The second process is thrombosis (a blood clot) that forms on top of the plaque. Often thought to be due to plaque rupture – something like a boil bursting – which exposes the blood to the inner plaque material. This, in turn, triggers a sudden blood clot (thrombus) to form, which fully blocks the artery causing a heart attack. Now that, anyway, is the current mainstream view.
Or, perhaps like a volcano? The pressure from the magma builds up and up, until the ‘plug’ at the top gives way and the whole things goes off bang. I am not sure if I like that analogy, but it may capture the concept of something slowly, slowly, building up, before the sudden catastrophe occurs.
You may see nothing wrong with this model, but it creates massive and complex issues when looking for potential causes of cardiovascular disease. Because it states that we have two completely different processes here, which could have completely different causes, and how do you know which one is more important, or which one to target? Or which one to blame?
So, for instance, we know that heart attacks are more common on a Monday morning than any other time of the week1. Clearly, this is not due to the sudden growth of atherosclerotic plaques overnight on a Sunday. If it is due to anything, it is due to the early morning rise of cortisol which, in turn, makes it more likely for a blood clot to form – because cortisol is ‘pro-coagulant.’
Equally, after you have suffered a heart attack, almost all of the treatment that takes place is to do with breaking down blood clots, removing them, or prizing them apart. At its simplest, you can give an aspirin to try and dissolve the clot. Or you could give a ‘clot buster’, such as tissue plasminogen activator – (TPa).
More commonly nowadays, a catheter is inserted into the coronary artery blocked by a blood clot, to reach the clot, push through it, and open up a metal stent to hold open the blocked area. So, in one way, the acute treatment of heart attacks could simply be described as blood clot management. As could the treatment of the majority of strokes where a clot breaks off from the carotid artery (artery in the neck) before travelling into the brain and getting stuck.
So, clearly, you cannot dismiss the importance of blood clotting in causing death from cardiovascular disease. In fact, if you never had a blood clot, you would never die of a heart attack or a stroke. No matter how much atherosclerosis you had. [I am not entirely sure if this statement is correct, but it is very nearly correct].
Now, you may rather like this dual model of ‘Athero-thombosis’. However, I do not. Indeed, I hate it. For one thing I do not like having to invoke two completely essentially unrelated processes to explain a single disease. Mainly though, even if it wasn’t deliberately designed to protect the ‘LDL-hypothesis,’ that is exactly what it does.
Primarily because the idea of athero-thrombosis firmly places blood clotting, in the aetiology (causal chain) of CVD right at the end, where it can then have nothing to do with the development and growth of plaques. Which means that you can dismiss any and all associations between plaque formation and blood clotting, no matter how strong. ‘Yes well, of course, things that make the blood less likely to clot will protect against cardiovascular disease, and vice-versa. But it has nothing do with atherosclerotic plaque formation, that is all to do with LDL.’ End of discussion.
Yet, and here is a thing, not often commented on – if at all. Most atherosclerotic plaques contain cholesterol crystals. In fact, the early researchers, when they found cholesterol in plaques must have been looking at cholesterol crystals, or they would have had no idea what they were looking at.
Why is this important? Because you cannot make cholesterol crystals from the cholesterol found in LDL molecules. Why not? Because the cholesterol in LDL is primarily bound to fatty acids (call them fats), thus creating a cholesterol ‘ester’, a.k.a. ‘esterified cholesterol.’ And cholesterol esters do not, indeed cannot, turn into cholesterol crystals. The only substance in the body containing enough pure cholesterol to form cholesterol crystals, are the membranes of red blood cells (RBCs).
Next question, how do you get a red blood cell into a plaque?
The only possible way is for there to have been some form of bleeding/haemorrhage into the artery wall. Of course, once you have had a haemorrhage, you end up with a blood clot. At which point you have enough RBCs kicking about for cholesterol crystals to form. As made clear in the NEJM paper: ‘Intraplaque Hemorrhage and Progression of Coronary Atheroma.’2
‘The aim of this study was to demonstrate erythrocyte membranes within the necrotic cores of human atherosclerotic plaques, even those without recent hemorrhages, and relate them to the progression and instability of the lesions. We also examined the fate of erythrocytes in established plaques in atherosclerotic rabbits to provide a model of hemorrhage-induced progression of lesions. Establishment of a link between intraplaque hemorrhage and the expansion of the lesions would provide another potential mechanism of plaque progression and vulnerability.’
‘The finding that intramural hemorrhage in an experimental atherosclerotic lesion induces the formation of cholesterol crystals with the recruitment of macrophages supports our hypothesis that erythrocyte membranes in the necrotic core of human coronary lesions can cause an abrupt increase in the levels of free cholesterol, resulting in expansion of the necrotic core and the potential for the destabilization of plaque’
Okay, what does that all mean? Basically, red blood cells that end up in plaques cause an abrupt increase in cholesterol in the plaque, leading to destabilisation of the plaque – which is the underlying cause of heart attacks and strokes. Or, to put this another way. Repeated blood clotting occurs first, followed by intra-plaque rupture. Which is the exact opposite way round to the current athero-thrombosis model. Which means that it should really be called the ‘thrombo-atherosclerosis’ model.
The observation of blood clots going off all over the place, narrowing an artery, shortly to be followed by heart attack is outlined very clearly in this paper. ‘Unstable angina with fatal outcome: dynamic coronary thrombosis leading to infarction and/or sudden death. Autopsy evidence of recurrent mural thrombosis with peripheral embolization culminating in total vascular occlusion.’
Now, that is a lot of jargon for one title … of any paper. So, I shall translate. Unstable angina is a condition whereby the attacks of angina become more and more frequent, triggering almost all the time. It is usually the harbinger of a final, fatal Myocardial Infarction. So, yes, in one way we are looking at the end process of CVD. However, in the situation we have an opportunity to see rapid atherosclerotic development with clots forming, one on top of another which, eventually completely block the artery. That is the ‘recurrent mural thrombosis’ bit.
Here is the abstract. If you are not medically trained, you are not going to get much of this. However, what it describes is exactly what I am talking about. Repeated blood clots creating layered blood clots, one sitting on top of another, causing the artery to narrow. This is, in effect, super-accelerated thrombo-atherosclerosis.
I include this unchanged, because I want people to know that I am not interpreting what is said here to suit my argument. What the authors are describing is, exactly, what I have been banging about for years. Namely that atherosclerotic plaques are blood clots, in different stage of development and breakdown. Good luck:
‘Extensive microscopic examination of epicardial arteries and myocardium was performed in 25 cases of sudden death due to acute coronary thrombosis. Eighty-one percent of the thrombi had a layered structure with thrombus material of differing age, indicating that they were formed successively by repeated mural deposits that caused progressive luminal narrowing over an extended period of time. This episodic growth of the thrombus was accompanied by intermittent fragmentation of thrombus in 73% of the cases, with peripheral embolization causing microembolic occlusion of small intramyocardial arteries associated with microinfarcts. The period of unstable angina before the final heart attack was, in all but one of 15 patients, characterized by such an ongoing thrombotic process in a major coronary artery where recurrent mural thrombus formation seemed to have alternated with intermittent thrombus fragmentation. The culmination of this “dynamic” thrombotic process in total vascular occlusion caused the final infarction and/or sudden death.’3
Clot after clot after clot, building up a layered structure of clots one of top of another. Followed by the ‘big one’, the clot that killed them.
Another condition where you get very rapid atherosclerosis development is following a heart transplant – sad to say. The process in such patients is exactly the same as in unstable/crescendo angina, if far slower. Namely, repeated thrombus formation, leading to the rapid growth of atherosclerotic plaques. Here from the European Heart Journal: ‘Repeated episodes of thrombosis as a potential mechanism of plaque progression in cardiac allograft vasculopathy.’
[Cardiac allograft vasculopathy = degeneration of the blood vessels in transplanted heart. I don’t know why they don’t just call it atherosclerosis, but they don’t.] Now, here comes some more proper jargon from the paper If it is too dense for you, what it describes are repeated blood clots on the arterial wall (mural thrombosis), leading to the development and growth of atherosclerotic plaques.
Discussion
The current serial IVUS (intravenous ultrasound scan) study demonstrated that a substantial number of asymptomatic HTx (Heart transplant) recipients had lesions (plaques) 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(multi-layered) appearance, may mediate the progression of CAV (Coronary allograft vasculopathy).
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.12 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 pre-existing outer layers. This observation could be highly indicative of repeated episodes of mural thrombosis.’ 4
Yes, ladies and gentlemen. Thrombo-atherosclerosis. Not athero-thrombosis. Blood clotting is not simply the final event in the CVD. It is the only event, and it is how atherosclerosis starts, grows and eventually kills you. Or, to put it another way, there are not two processes in cardiovascular disease, there is only one.
You heard it here first.
1: https://www.ncbi.nlm.nih.gov/pubmed/7925507
Dr. Malcolm Kendrick 
Thank you for another well written blog post in this wonderful series.
Thank you, will. digest later
Thank you for this new great post – very close “to my heart”.
With my own experience of unstable angina a couple of years ago I understand that I am all the time at the edge of something “unexpected” to happen.
Still I today feel as if on the “safe side” treating my collateral in a friendly way..
Just now I believe in such relaxing activities as the one me and my wife were involved in today under the blue sky; working a grass turf with a scythe together with a number of friends (today around 20) and then eating the traditional Swedish herring, with potatoes and sour cream as the final “reward”. (Though, according to my “strict” LCHF regimen I should not have had so many potatoes but I love them and it was very enjoyable.)
Well, the outdoor experience happened yesterday – Sunday.
Goran I have heard that sweet potatoes are lower glycemic. If you can’t get them, perhaps you could grow them. The reason I needed distilled water was because of an alternative medicine I take that needs to be mixed in water, and unknown elements and chlorine interfere with it.
I enjoyed my visit to your fine country and am proud to add the Baltic Sea to my list of swimming experiences.
AnnaM: Yes, sweet potatoes are about the easiest thing of all to grow. We eat the leaves, steamed, as well as the root. They love heat, so only a summer crop. Predicted to be 114 today, and they look perfectly pleased. Planting in June, harvest in October here.
Goran, I had to smile about the traditional Swedish herring with potatoes. I live in the Isle of Man (a tiny island between the UK and Ireland). The traditional dish of the old Manx people is ‘Spuds ‘n Herring’ – potatoes and herring! Without the sour cream though, which sounds nice.
“…eating the traditional Swedish herring, with potatoes and sour cream…”
Wow, does that sound delicious and refreshing on a hot summer’s day!
” (…. according to my “strict” LCHF regimen I should not have had so many potatoes but I love them and it was very enjoyable.)
If you are going to sin, then do it in style !
You remember that The Kendrick has suggested Feasting on fundemental foods, in the embrace of Family & Friends (with a glass of wine…) is cardio-protective…
Reducing ‘strain’ is more useful than ‘statins’…
Dear Malcolm
Indeed a very interesting read. And a much simpler and more elegant theory than the currently accepted idea. One question you may be able to help with…The cholesterol you do find is always posited to be as a result of accumulation in macrophages within the plaque which turn into foam cells. What are your thoughts on the role and indeed relevance of these foam cells and could the be the source or an alternative source of the crystalised cholesterol seen in plaques? also, these cells take up cholesterol through scavenger receptors rather than ldl receptors. As such, could they be cleaning up the rbc membranes rather than trapped ldl particles? I cant find good proof that ldl associated proteins such as ApoE are found in plaques.
Warm Regards
Iman
Good question. This could be the process of cholesterol crystallisation. Macrophages, after all, are designed to clear all the debris up that they find. So they may well be trying to re-absorb RBC membranes. Also, remember that LDL has a twin brother called Lp(a), which is designed to become incorporated into blood clots and links tightly to areas of endothelial damage. The apolipoprotein we should really be looking for is apolipoprotein A.
Linus Pauling, at the end of his career, posted some videos describing great success with lysine supplementation (3-5 g/d) on top of the ‘usual’ oral megadose of vitamin C (12 g/d) because the lysine, and not the lipoprotein a, would bind to the lysil groups ‘sticking out’ of damaged arterial walls. Vit C would, through collagen production, prevent the walls from becoming ‘weak and leaky’, lysine would prevent the ‘cholesterol’ to stick to the wall, and his suggestion was clearly that lysine would even ‘clean up’ the walls.
I’m not going to try to lure a licensed medical doctor into a statement on this, but find the association quite telling.
Thanks for your clear and highly explanatory article
I’m going to be bold, so my apologies in advance. I recently had a painful anal haemorrhoids experience. Two clots. One of them was the size of a large grape. I called her Gertrude. When in pain, always use humour first.
Anyway.
I was on a prednisolone cream and ibuprofen. I got some relief, but not a cure. In a desperate attempt to avoid surgery, I found out about l-arginine powder. I took 6 grams (one scoop) every 8 hours. The bitterest glass of water I’ve ever drunk. This was the thursday at 2 PM. At 6 PM Gertrude was about 1/3 smaller. Pain was gone. I still have some discomfort and the haemorrhoids are now about 90% reduced in size. Next time this happens I shall not waste time with that stupid prednisolone cream.
I read that this amino acid has been used to treat atherosclerosis. I wonder if it would be a good prevention for people at risk of CVD and strokes.
That’s all.
Thank you for reading, and sorry again.
Anon,
I used to get haemorrhoids – though none as bad as you describe, but then suddenly I realised that I hadn’t had one for ages. Some time ago I started using one wet wipe as part of cleaning up with toilet paper, and I suspect the additional cleanliness means there is less irritation down there.
An old remedy for haemorrhoids is to stop using toilet paper and start washing up after bowel movements.
Anon, earlier this year I had a bleeding haemarroid…A bout May I upped the amount of Citruline maleate I take daily as part of my anti-aging program..About a teaspoon in water.. And the bleeding stopped and has never come back….
Citrulline maleate is converted in the gut unto L Arginine..and is better absorbed..It is also a god deal cheaper here in oz than Arginine as it is very popularly sold in 200 gram containers as a powder..
At the time I did not put these two tings together..So thanks for the jolt to my own awareness !
Thank you all for this off-topic discussion on something that has just hit me hard. I have ordered the Citrulline maleate powder recommended and wish you all continued good health.
Old Fogey,
Try a few packs of wet wipes as well – that won’t make for a good experiment, but it might give you a double chance of getting rid of your piles!
Sigh.
https://www.sciencedaily.com/releases/2018/07/180728084128.htm
Summary:
Pairing an online patient dashboard with ‘nudges’ to doctors tripled statin prescribing rates in a clinical trial. The study used two nudges, active choice framing to prompt physicians to make a decision on prescriptions, and peer comparison feedback which provided physicians with information on their performance relative to other physicians.
A very caring and capable country Physician – friend of mine has all but ceased statin prescribing, and that includes ‘FH’ patients. None has died, All feel better…and he lives in fear of ‘Official Questioning by Powers That Be’ for his less mainstream approach.
Then there is the deceptive (my opinion) STAREE statin trial, calling for ‘Healthy, 70+ folk to volunteer….to see what taking a statin does for (or TO, ) them.
I would have thought that reaching a HEALTHY 70+ would result in the advice of:- ‘Change nothing and keep doing – what you’re doing!’
Janet, that trial sounds positively barmy, and possibly unethical.
After years of multi tablet ingestion, I ceased said meds, and was so improved that the endocrinologist I was ‘sent to’ advised me, (and I am pleased to say agreed with me ) to continue as I was doing…in other words, discontinue the meds I had been using for 10 years. 5 years on, I am so well.
I was saddened to hear from a very healthy 75 year old man, that on being declared free of the prostate cancer he had had removed 5 years ago, he was given a prescription for a drug to take for the rest of his life, with the understanding that ‘if he misses one dose he will die’. Now, along with Dr Le Fanu, I really do not think it is appropriate for a Dr to say such a thing ( I cannot believe any such drug can be so important). The man could not tell me what the drug is, or for what, as he hangs on every word the medics tell him, and just complies without question, having been a statinister for at least 15 years.( maybe he is right to do so, as he appears so well).
Thank you
That is a chewy post! I shall have to read it several times but thank you nonetheless.
Plenty to think about again. Thank you
Monday Morning Mortality… another arrow with ‘Mental/Emotional Strain-stress’ writ large on it…
My previous cardio 101% discounted the suggestion that a year of intense M/E and financial strain as *contributory* to my cardiac catastrophe.
Which is why he’s the ‘ex’ (cardiologist).
Dismissing stress is what cardiologists do. Other than chanting ‘LDL bad, statins good’ fifty times every morning.
That heart attacks occur on Monday mornings more often than on any other day is certainly easy to understand since I am pretty confident to state that most people don’t like their jobs and many in fact certainly hate what they have to do to pay the bills. If you’ve ever been in such a situation you will know that there’s a specific feeling that starts around Sunday evening pretty much killing what should still be free time to relax. You sleep differently then from Sunday to Monday than say from Friday to Saturday. The moment you open your eyes on Monday morning with “that week again” waiting for you and I have no problems to understand why the stress level is at it’s peak then…
But what to make out of the insight then that it is blood clots from the beginning that set us on the road for doom? I mean other than thinning our blood with Whisky on a regular level 🙂
Think I’ll stick to the whisky –
Good plan.
I’d always assumed that the fact that heart attacks cluster around unpleasant events such as Monday mornings, was just that these raise your BP and dislodge a piece of loose plaque. I’d also assumed that without the unpleasant event, the heart attack would simply be delayed by a few days until the plaque came loose anyway. Was I being naive?
Not sure that naïve is the correct word.
Funny, my “good” (reasonable) cardiologist 20 years ago claimed that in my case the only thing they could come up with as a “cause” was actually my “stressed life”.
It is kinda funny how slow people are to give adequate credence to the affects of emotional states on our health an immune system. I think the easiest one to see is the flight or fight response. We have all felt the affects of that sudden rush of adrenaline and of course it is widely taught what happens: blood leaving the organs and rushing to the surface, faster heart rate and breathing, increased blood pressure, sweating and so on. And surely it only makes sense that organisms respond physically to the emotional states of the entity inside – it is what the body does really. I was quite interested when I read that this same (sympathetic) state also puts the immune system on a back burner as well as digestion. And that the parasympathetic and sympathetic are like a see-saw, and on a see-saw, isn’t balance needed for a good ride? I believe it is Thomas Cowan who promotes the idea that those who end up getting heart attacks have had their two systems out of balance for some time.
So imagine a bad day in the life of a hospital nurse (perhaps about 25% of them) when you’re on the run for 12 hours and take 5 minutes to eat and have your heart in your throat for all those hours.
LOL! The Monday-morningitis used to start Sunday lunchtime with me!
Another huge step forward in our understanding. Thank you for both the quotes and the jargon translations. And the humour and clarity with which you write.
Oh, thank you, thank you. I really appreciate, by the way, your translations of complex medico-speak in brackets for idiots like me. A stonking good read.
What about DVTs, and PEs following ? Then to add in variant angina ?
DVTs and PE are created by a completely different clotting system. Intrinsic, not extrinsic. Variant angina seems very poorly defined, and mixes up with many other things, so I cannot make much sensible comment here.
Intrinsic –
Prinzmetal’s or Prinzmetal Angina, Variant Angina and Angina Inversa …
http://www.heart.org/HEARTORG/Conditions/HeartAttack/DiagnosingaHeartAttack/Prinzmetals-or-Prinzmetal-Angina-Variant-Angina-and-Angina-Inversa_UCM_435674_Article.jsp
Causes of Variant (Prinzmetal) Angina: The pain from variant angina is caused by a spasm in the coronary arteries (which supply blood to the heart muscle).
Plus – amongst many links – Cleveland Clinic :
https://health.clevelandclinic.org/5-things-know-coronary-spasm/
First, UK : C’mas Eve 2007, fell forward from the settee with almighty pain. Second, France : C’mas Eve 2016 fell forward semi into the supermarket carte. Mammoth one that; laid me out for a week. Fortunately a chum was in the vicinity at the same time, she got me home and settled. Thereafter, from time-to-time small spasms for c.two months. Now settled, but will no doubt hit me again somewhere / sometime along the line !
DVTs, and PE – yes. ? Extrinsic / Intrinsic.
DVT = stasis – Extrinsic ?
PE = portion of clot breaking off – Intrinsic ? Lodged lower, left lung. Bits of it are still around. Breathless, chest pain. Can ignore – just so long as Variant A. stays clear of the mess !
Atherosclerosis ? Yes.
Right temple artery, found whilst checking for GCA.
Found 30% in Carotid arteries whilst intensively checking out the DVT / PE
Found left Popliteal artery, heavily calcified, occluded, whilst checking DVT
Found Right Popliteal – and leg – under 50% occluded.
Warfarin and walking it out. Stents break up, bend, lead to restenosis and the new Gore-Tigris is Nitinol, 55% base metal to which am mighty allergic – plus : “nitinol stent fractures in the SFA occur in 5% to 28% of cases and may cause complications, such as restenosis, pseudoanerism, perforation of the vessel, and embolism in the stent” … “Furthermore, nitinol stent fracture was more frequent in patients who walked more than 5,000 steps a day compared to patients who did not exercise … ” Paper : ‘Dynamic Forces in the SFA and Popliteal Artery During Knee Flexion – Consequences of stress to consider for stent durability and design’ – May 2008 / Endovascular Today /
Objective given : ‘Walk an hour a day – broken up.’
Apologies for the digression. Discussion is fascinating. Thank you Dr Kendrick.
MollyC (France)
By intrinsic, I mean the the blood clotting system intrinsic (within) the bloodstream. Which is almost all of the blood clotting factors.
By extrinsic I mean the blood clotting system/factors that lie within the artery wall. For example Tissue Factor (TF), also to a greater or lesser extend factors V and VII.
The most potent factor that drives blood clot formation is Tissue Factor (TF). It lies within artery walls, and veins walls, if they are damaged a blood clot will form, extremely, rapidly, at that point. From Wiki
Coagulation begins almost instantly after an injury to the blood vessel has damaged the endothelium lining the vessel. Exposure of blood to the subendothelial space initiates two processes: changes in platelets, and the exposure of subendothelial tissue factor to plasma Factor VII, which ultimately leads to fibrin formation. Platelets immediately form a plug at the site of injury; this is called primary hemostasis. Secondary hemostasis occurs simultaneously: Additional coagulation factors or clotting factors beyond Factor VII respond in a complex cascade to form fibrin strands, which strengthen the platelet plug.
Ah yes – Fibrin, and the test to check. Thank you Dr Kendrick. Hope you have a relaxed and pleasant evening.
Well, I had a friend who dropped dead from a clot in his leg which arose a couple of weeks after a very long flight from China. He was actually going to go to the hospital shortly…fell at the side of his car. I’d like to know more about DVT and PE if you get the chance, and how they relate to do not relate to heart attacks and strokes.
DVTs and PEs do not relate to strokes and heart attacks directly. The clot formation in a DVT is completely different to that clot formation that causes heart attacks and strokes. There is some overlap in factor V Leiden and antiphospholipid syndrome. Up to now, I have kind of steered clear of blood clotting because it is the most complicated system that exists in the human body – or at least I think it is. I may pluck up the courage to try and explain it at some point. Or at least explain how I think it works – which may not be exactly how it works.
Would most appreciate any insight you have. I have one marker of Factor V Leiden and also tested positive for Antiphospholipid syndrome. I have been on a low crb / keto diet for 18 months and take Nattokinaise. I did have a stroke 4 years ago and am trying to determine how to best support myself. Love all you do as well as Ivor and everyone else! Thank you!
Courage!?
Well, Malcolm, you certainly have that.
When you do (I am sure) explain it to us, I hope you include your estimation of the NOACs, particularly apixaban (Eliquis) in their effect – or not – as compared with anti-platelets on CVD.
As ineffective as warfarin?
Volcanoes, I like that analogy, dramatic, but an MI is very dramatic. A little alcohol may surely help! Have to be careful here, because abuse is real, a family member struggling with dependency. How to live in harmony, damned impossible. Smashing post again Dr Kendrick
Many thanks for this Dr. Kendrick, particularly when you take the time to make the whole thing much more simple for non-medical people such as myself. It will take me some time to digest this latest entry but I know that I will be a good bit wiser when I have done so. Thank you.
Reading that interesting post, together with the sections of decoded jargon that it contains, I can’t help wondering if part of the reason areas of medical theory (CVD, T2 diabetes, etc) are in such a mess, is that brain clogging jargon!
Reading dense prose, full of expressions such as ” intramural haemorrhage” must use up brain power that would otherwise be available to actually imagine what is being described. I mean “bleeding within the blood vessel wall” isn’t just simpler, it is also far more vivid, and describes a process that I’ll bet even many medics are unaware of.
Maybe, maybe not. I am familiar with the jargon and I find that it actually helps me to read this stuff at higher speed, as complex stuff can be referred to in fewer words.
Awesome
It appears that taking natto and/or nattokinase would be good advise? If so how much – maybe the dose depends on age or whether a person is doing it for prevention, because they have stents, or has had bypass. Your thoughts Dr K…Thanks
Thank you for a very lucid explanation of Thrombo-atherosclerosis. Am I to understand that this mechanism does not occur unless there has been damage to the epithelium? From your previous blogs it would appear that there are nigh constant lesions occurring due to a myriad of stresses, so it would seem that there would be a concurrent progression of thrombo-atherosclerosis.
If damage > repair (you have a problem). If repair > damage (you are OK).
So does your theory suggest a different approach to treating heart disease?
Now that we are (so you’ve explained to us) fairly sure blood clot is responsible solely for heart attack and strokes, what is the best way to get rid of blood clots before they become too dangerous?
Damage / Repair.
– Another good reason to bring vitamin C (with lysine/ proline) up to useful levels, providing the ‘raw materials for road-mending and thus bias the balance in our favour !
The alternative is ‘sub-clinical scurvy’.
Yes, I agree. Although the concept of sub-clinical scurvy is – to be pedantic – a contradiction in terms. Scurvy represents the clinical manifestations of being scrobutic (lacking in vitamin C). One may be sub-clinically scrobutic.
Thank you for another interesting and thought-provoking post. This one is particularly illuminating. Although, I think one only needs a decent vocabulary to understand the quoted excerpts of the paper, rather than a medical training. 🙂
“Repeated blood clotting occurs first, followed by intra-plaque rupture.”
Where does this blood come from and why is it repeated at the same location?
Hopefully my plaques have stabilized from switching to lower carb diet and adding supplements. What is the connection?
It comes from the bloodstream. It keeps repeating at the same location because, normally, there would be intact and fully functional endothelium at the point which is highly resistant to blood clots forming over it. Damaged, or dysfunctional, or missing endothelium is a focus for clotting.
Thanks for reply Dr. K, the term “intraplaque hemorrhage” is more precise where the blood comes from and the mechanism of plaque growth.
It appears that there cannot be plaque formation without intima thickening, a separate and related process.
Intima thickening also necessitates the formation of new blood vessels (capillaries). These are what are vulnerable and can rupture and expose blood to TF and form a blood clot. This could happen many times below the endothelium over many years and not cause symptoms.
Oxidized ldl and macrophages are also a part of the process that can be controlled by a low carb diet. Plaques are not self perpetuating.
Macrophages are your friend. Oxidation is also your friend. It is how macrophages get rid of detritus and infective agents that should not be there. They fire a super-oxide burst of Nitric Oxide at any ‘alien’ substances in your body. This then allows the macrophage to ingest the ‘alien’ material and get rid of it. This is how LDL is oxidised in the arterial wall. However, we see oxidised LDL and macrophages sitting together, and blame them both for causing the thing that they are trying to clear up. One might as well blame fire engines for causing fires.
And for those who blame oxidation for everything. Try holding your breath for five minutes.
Sorry, I am in a grumpy mood tonight.
Malcom
In the cause of those who have had á cardiac event, statins are said to have á positive effect. Is this so, and what Is the mechanism?
They increase NO synthesis
A bit slow here,but am I to understand that nitric oxide is the ‘ammunition’ that macrophages use to obliterate the alien material? Fascinating to learn why nitric oxide is so important to healing.
Sorry you are grumpy – not surprising given the heat!
Dr. K, the missing link for me. An explanation how the endothelium is repaired or developed over a blood clot.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2121205/
Platelets secrete stromal cell–derived factor 1α and recruit bone marrow–derived progenitor cells to arterial thrombi in vivo
Glad you got there in along your own path. In my mind it is all extremely simple, but I realise that it is not, it is just that I have all the connections and information that I have build up over thirty years, or so.
Fascinating read – thanks!
Anyone forced to live with the NHS and things like ‘QOL’ scores… is entitled to have grumpy nights!
Rx, a glass of your favourite red medicine
Clot upon clot upon clot. Makes sense. A clot-driven process. Injury followed by clotting, just like in most any other tissue. Much food for thought. Whence repeated injury to the cardiac arteries? Bravo, Dr. Kendrick. This is clearly not the end, but the criminal is on the gallows, awaiting the rope.
Malcolm thank you for this post..I am not sure I follow every link in your thinking..But I am wiling to accept the general thrust of your argument…As it supports what I already know works for me..NO Statins, Very low sugar consumption, Lots of saturated fats like butter, cheese and cream foods.. And avoid white bread like the plague..
So what should we be doing to prevent clotting – all taking Xarelto?
I had an MI in 2002 and a pulmonary embolism in 2009 and guess what, my Lp(a) value was 62+ mg/dl. No doctor with whom I have consulted in the last 20 years ever got their undies in
a wad because of that Lp(a) value. Probably because they don’t have a pill in their rapid-fire
magazine with which to obliterate it.
I believe it was Dr. William Davis who suggested that massive amounts of niacin can be
effective in reducing Lp(a) but no mainstream doctor here in Germany would ever hear of it.
But the doctor who treated my PE first prescribed coumadin and then later Xarelto.
So maybe this is what is keeping me firing on all cylinders…
Lp(a) is a difficult one. Some studies indicate it’s “bad” others seem to indicate there are benefits. This is someone who questions things:
http://cholesterolcode.com/the-big-deal-about-lipoproteina/
This is a more mainstream doctor (he talks about taking statins for Lp(a)):
https://peterattiamd.com/lpa/
I have “high” Lp(a) (say, 226 nmol/l – it varies quite a bit) but “low” hs-CRP (of 0.5 mg/L).
You could also try taking vitamin C. I started taking vitamin C to see what happens to my Lp(a), but I did not like the feeling I got when taking vitamin C, so I stopped.
“but I did not like the feeling I got when taking vitamin C”
Could you please expand on that? What kind of feeling?
Scott: I believe it was Dr. William Davis who suggested that massive amounts of niacin can be effective in reducing Lp(a)…
That was back before the current Wheat Belly / Undoctored program was more completely evolved. Niacin is no longer part of the program’s Lp(a) strategy. Evidently, with all the other program elements in place, niacin wasn’t adding any net benefit (but was adding annoyance, and bit of risk). The current strategy, in addition to core program, is an increase in suggested fish oil intake, and a strict focus on minimizing small LDL (a carb issue).
Agents that just shove the Lp(a) marker around do not necessarily enhance all-cause mortality; CETP Inhibitors, for example. The jury is still out on PCSK9 Inhibitors.
> Clot upon clot upon clot.
The image I get is tubes choked with cottage cheese.
So now what?
To quote Malcolm: “you cannot make cholesterol crystals from the cholesterol found in LDL molecules. Why not? Because the cholesterol in LDL is primarily bound to fatty acids (call them fats), thus creating a cholesterol ‘ester’, a.k.a. ‘esterified cholesterol.’ And cholesterol esters do not, indeed cannot, turn into cholesterol crystals.”
Could cholesteryl ester hydrolases convert esterified cholesterol into free cholesterol? Might this be a possible source of cholesterol crystals? https://academic.oup.com/eurheartj/article/37/25/1959/1748880
Might be, don’t think so, because then you have to explain where the iron and haemoglobin come from. You may be interested in this article. https://www.tandfonline.com/doi/pdf/10.2217/clp.10.41
‘The erythrocyte membrane is a simple plasma membrane comprised mainly of cholesterol and phospholipids . Red blood cell membranes are 1.5–2.0-times richer in cholesterol compared with any other cell in the body, and approximately 40% of their weight is composed of lipids. The volume of cholesterol in the membrane of a single erythrocyte, the majority of which is free, is estimated to be 0.378 µm3 . Thus, only 50 µl erythrocytes are needed to produce a 0.2 mm3 or more necrotic core .
Breakdown of erythrocytes in the atherosclerotic plaque can therefore result in a substantial cholesterol accumulation within the plaque. The contribution of membrane cholesterol to necrotic core volume is substantial because intraplaque hemorrhage occurs over several years. Necrotic lipid core enlargement is critical for plaque rupture. When the lipid core of an atherosclerotic plaque exceeds 40% of the plaque size, the plaque becomes unstable.
Furthermore, owing to the liquidity of lipids, stress in the plaque is transferred into the fibrous cap and thus it contributes to its rupture on a mechanical basis. The erythrocytes in the atherosclerotic plaque are degraded over days, and because the cholesterol cannot be metabolized
internally, it is available for absorption into the necrotic core. Moreover, the uptake of erythrocyte-derived cholesterol by macrophages
will, in turn, provide cholesterol to the core by apoptotic cell death.
Degradation of erythrocytes inside atheroma will result in the release of hemoglobin and iron, both of which are known to promote inflammation. Furthermore, iron and hemoglobin facilitate oxidation, production of free radicals and activation of apoptotic pathways, all of which lead to plaque instability. In addition, specific receptors localized within the erythrocyte membranes have the ability to bind to a wide array of chemokines, including IL-8 and monocyte chemotactic peptide-1. Studies from our group have demonstrated that erythrocyte membranes in patients with ACS had higher levels of IL-8 compared with patients with chronic stable CAD. All of the mechanisms mentioned previously can result in plaque growth and instability. Thus, erythrocytes appear to be key players in the progression and destabilization of the atherosclerotic plaque.’
Not to oversimplify things, but I wonder if having thin blood and low blood pressure outweigh the supposed risk of my high LDL. Whenever I bleed, it seems there’s a lot of blood which is slow to clot. I tried taking a baby aspirin years ago as people have been advised and I had to quit because when I bled it was such a mess and so prolonged. I’ve not had any doctor ever ask me about how I bleed or to take much notice of my lower blood pressure; all the doctors see is the LDL number.
Prior to the use of factor VII in haemophilia, those with haemophilia had 20% the rate of CVD death. People with von Willibrand disease (a blood clotting disorder) have less than half the risk of CVD death. Equally, those with pro-coagulant disorders e.g. antiphospholipid synrome, or factor V Leiden have a greatly increased risk of CVD death. So, no, in one way you are not oversimplifying things.
Do haemophiliacs develop arterial plaques? If not, how do the arteries deal with endothelial leaks?
Haemophiliacs are (or were) protected against CVD death. I have not seen any research on plaque formation. However, at this point things get complex as you need to look at the intrinsic and extrinsic clotting pathways. Warfarin, for example, is a great anticoagulant, but not very effective at preventing CVD – primarily because it has no (or little) impact on platelet aggregation and/or tissue factor (TF) activation of the clotting system. Haemophilia acts a bit like warfarin on the blood clotting system.
Dr. Kendrick,
On June 18, 2018 in a reply to your “part 47” post you responded to mart the heart’s request for drugs to treat MI as follows: “On that list, I would take ramipril and clopidogrel.” Is clopidogrel (Plavix) your preferred alternative to warfarin? I note that in a reply to this post (part 51) you mention that you may “pluck up the courage” to post about blood clotting at a later date.
Phil
Renfrew, PA USA
Only read it once so apologies for over simplifying but surely it would be better to offer Rivaroxaban rather than a statin ?
In my view it would be better to take almost anything than a statin.
Even with all the people taking statins (Aren’t they the leading money makers for pharmaceuticals?) they don’t seem to be reducing the risk of heart disease since it is still the leading cause of death.
Carolyn,
What you say may be true, but of course it could be that people are living longer before dying of CVD! Some measure of *quality* years lost to CVD might be a better statistic.
Statins would definitely do badly on the quality test because they make a lot of people extremely miserable!
Dear Malcolm, Very interesting article, thank you. Just trying to digest this, and found myself reflecting on an article l read elsewhere (can’t remember where) suggesting that autopsies of people who had died from heart attack sometimes/mostly (?) showed that the precise location of the problem was not areas of blogged arteries (which were often old but stable) but more recent, unstable inflammations. Just wondered what you thought about that relative to your post.
I am sorry, but when someone mentions inflammation with regard to CVD it caused my IgE levels to rise. Inflammation = healing. Inflammation = healing. Inflammation = healing.
Steroids are the most potent anti-inflammatory agents known to man. They increase the risk of CVD by at least 400%. Why, because they interfere with healing. Or, to put it another way, they block inflammation.
Whenever doctors see inflammation they call this a bad thing, and do what they can to damp it down. Outside of the known auto-immune diseases: rheumatoid arthritis, IBS, asthma etc. damping down inflammation does not work. It does not work because you are interfering with the healing mechanisms of the body, developed over millions of years. Maybe even billions of years.
Inflammation = healing
Inflammation = healing
Inflammation = healing
I would die a happy man if everyone stopped calling CVD an inflammatory disease, and started asking what causes the damage, in the first place, that leads to the body to start healing itself = inflammation.
I stand corrected on the misuse of “inflammation”. My incorrectly posed question was really about the precise location of a heart attack and whether you believed that it was likely to be at the point of more recent, unstable plaque build-up/blood clots, or the longer established clotted arteries so favoured to be stented or bypassed by surgeons.
I think it is tricky. Weather forecasters know, pretty much, the forces that create weather patterns. However, they still can’t tell you, accurately, if it going to rain on your house tomorrow.
Keep reminding us of this! Do you think anti-inflammatories, like curcumin, are harmful rather than helpful?
Does that mean I don’t have to worry about being on an anti-inflammation diet? In fact, does diet even matter and might possibly cause more stress which might be the real killer? (I mean apart from maintaining healthy weight, moderate exercise and all the other common sense stuff.)
What about high blood glucose levels/hyper insulinemia in the context of causing damage to the endothelium? Are there connections?
Could you send this to all major newspaper in London so it’s on first page of every of them?
So if you are taking anti-inflammatories for RA (as I am) is there evidence that this causes an increase in CV events?
Complicated. RA increases the risk of CVD because it is a ‘vasculitis’ i.e. damages the endothelium. Steroids can damp down this form of inflammation and will protect the endothelium from this auto-immune attack. So, it is possible/probable that there is a balancing act to be had here.
Benefit = dampens down endothelial damage/attack
Harm = dampens down the repair process at work to repair endothelial damage/attack
In todays newsletter from Dr. Mercola I read the following related to this issue.
“Vitamin D, a steroid hormone, is vital for the prevention of many chronic diseases, including but not limited to Type 2 diabetes and age-related macular degeneration (the leading cause of blindness).”
Admitting my ignorance here i read here “steroid hormone” for vitamin D which is included in my “vitamin treatment” except during the summer months. Should I be scared and distrust Mercola?
https://articles.mercola.com/sites/articles/archive/2018/08/07/game-changer-of-the-year-carole-baggerly.aspx?utm_source=dnl&utm_medium=email&utm_content=art1&utm_campaign=20180807Z2&et_cid=DM226855&et_rid=386161570
Steroids is shorthand, in most cases, for corticosteroids = those artificial steroids based on cortisone/cortisol. Cortisone is manufactured in the cortex of the adrenal glands, and is converted to the active form, cortisol. This is why they are called cortico-steroids. There are many other steroid hormones: testosterone, oestrogen, aldosterone etc. Whilst they are steroids hormones (manufactured using cholesterol as the basic steroid structure) they are not corticosteroids. Vitamin D is also a steroid hormone – synthesized from cholesterol by the action of sunlight on the skin. It does not have the actions of cortisol, and carries none of the risks associated with cortisol. Mercola is generally to be trusted.
Malcolm,
Could you devote a whole post to the issue of inflammation?
When people invoke inflammation as the cause for all sorts of diseases such as Alzheimer’s, does the same issue arise?
Is this another huge medical muddle or just incorrect terminology?
Goran, you might be interested in this article on the origin of the terms steroid and sterol, which derive from a root word meaning stiff or solid.
https://blogs.bmj.com/bmj/2018/08/03/jeffrey-aronson-when-i-use-a-word-sterols-and-steroids/
Doc, what is the best measure of the underlying condition that inflammation is healing? Can we measure the fire directly rather than using the number of fire engines to estimate the extent of the fire?
HsCRP possibly. This is an inflammatory marker which appears to correlate, do a degree with CVD risk.
I take turmeric two or three times a week for ankylosing spondylitis, an auto-immune condition. In small quantities — a 1/4 teaspoonful in a mug of hot water.
A woman I know who also has AS was told of the benefits of turmeric and went crazy with the stuff, adding it to everything she ate. Her skin got blotchy and her hair started falling out. It turned out she was one of the few people who are allergic to turmeric.
So like everything, the poison is in the dose.
@Martin Back am interested in whether the tumeric is working for your AS. I have a friend who has it.
Craig, I take turmeric for symptomatic relief, specifically, restless sleep and morning stiffness. I used to take a mild anti-inflammatory for the same thing.
Whether it has any affect on the progress of AS I cannot say. At my age (70) the AS seems to have burned itself out. The only non-drug regime I can think of to combat AS is the London Diet, a strict no-starch diet, which I never tried since my AS had run its course by the time I heard about it.
Hi Martin – a fellow AS ! Interesting to meet a fellow spondy in this group.
London Diet, Ebringer. When Ebringer found that his seminal work on No Starch / Low Starch diet was efficacious with his patients back in the mid 80s, he did not proscribe red meats nor did he query industrial foods (bacon, sausages etc etc). Now, over 30 years later, we have the excellent work from the Human microbiome Research Project which highlights the damage that such food items can cause to the gut. Ebringer has handed the ‘diet’ work over to Carol Sinclair, see her book The IBS Low Starch Cook Book. Ebringer wrote the introduction to the second edition.
Have you discovered / or are you a member of KickAS (dot) org ? An international Forums group, and the best AS support group around (I have been an active member since 2004; was a by-stander member for a couple of years before that – my GP at that time (2002) recommended KA to me. Said they were ‘the best’). Their ‘Diet’ forum; ‘Recipes’ forum; ‘Success stories’ forum are well worth diving into.
I found Ebringer’s LSD diet excellent. Has held the inflammation in check, including very little red meat – found red meat to lead to inflammatory flares. In addition the cruciferous vegetables (still a problem) and nightshade vegetables (though tomatoes are now an OK item.)
I also take curcuman, including the fresh root, and also fresh ginger root – this last NOT imported from China ! (Irradiated, covered in pesticide, horrid !)
Good to meet you Martine – Take care, Go well : MollyC1i – Keeping on, Keeping on (as we all do, innit :))
My AS diagnosis was in 1975 aged 27, so I’ve had it quite a while. I found the kickas forum many years ago, but I got so depressed reading the stories that I never went back to it. As far as diet goes, nothing I tried seemed to make any difference, so I eat my idea of a healthy diet (veggies, dairy, carbs, fat, not much meat) and don’t worry about trying to control AS. Apart from the year I was diagnosed when I attended an orthopaedic hospital as an outpatient, I’ve never seen a rheumatologist. I was afraid they’d prescribe medication I don’t want to take and couldn’t afford, and tell me to stop drinking. (I eventually did stop.) The only medication I’ve taken is aspirin and OTC NSAIDS, which now I’ve stopped in favour of turmeric. I have a rigid forward-bending spine and some dodgy disks, but mostly it doesn’t trouble me, apart from a scare when my eyeball inflamed and I had to take steroid drops for some months.
Ahhh, the dreaded uveitis. That one has always scared me, but so far (t.wood) have avoided it. But, have lost central vision in R. eye, due to vascular dysregulation.
No, I don’t take any of the meds – NSAIDs for a few years, then they smacked out my gut. Horrendous repercussions, that is why I still have to dickey around with diet. Sigh. As for the biotherapies, *nope.Totally unnecessary. Turmeric does the job very nicely thank you, turmeric / curcumin, and careful with diet makes a grand job of it.
Was never asked about alcohol. Only time for that was recently, by my cardiologist. Shoot. I have a good snifter every evening, and might even have a couple -am 81 so that is fine Agree with Goran, watch the ducks on the water, watch the seasons change, go see the horses and visit friends. It is good.
Sorry about KA. We have a good few laughs over there. Not all doom and gloom ! Have made some happy on-line friendships and am happy to help out – helping out usually means checking up on information. Being a one time medical librarian has its uses !
OK. Take care Martin, go well – apologies to this group for the long side-track.
MollyC1i – Keeping on, Keeping on (as we all do, innit !)
Similarly to your fire truck analogy above, inflammation is like road repair workers. The workers can cause disruptions in traffic flow but they are needed to repair the roads. The presence of workers is not the problem. The problem is what caused the workers to be needed. Sending the workers home will leave the road unrepaired.
Has anyone ever started from the other end to look for the cause of heart attacks? By that, I mean starting with people who have zero plaque in their arteries and seeing what they have in common? I doubt that anyone has ever done such a study because conventional doctors will tell you that there are no such people. But I have zero plaque and I know others who also have none. I would guess that you have none. What is the thing we have in common? A low-carb diet that includes a lot of good, natural fats. Our epidemic of heart disease started back in the ’50s after Crisco and margarine replaced lard and butter.
It is interesting to understand the mechanisms involved in clot formation, but maybe we don’t need to in order to prevent them.
David and JBarnes,
I believe the problem with inflammation if it is chronic is that it indicates chronic stress on the body. So the inflammation is an indicator that there is a problem, but the inflammation itself is not the problem, nor the cause of Alzheimer.
As to curcumin, from all I understand of it, it is a healing substance and definitely good for us, therefore it probably reduces inflammation by healing the cause.
AnnaM,
Curcumin and other phytocannabinoids have interesting effects on health.
https://www.ncbi.nlm.nih.gov/pubmed/26945822
Cannabinoid receptors are involved in the protective effect of a novel curcumin derivative C66 against CCl4-induced liver fibrosis.
Curcumin is an adaptogen that helps with stress too.
jbarnesbaker.
I am wondering how you know you have zero plaque. I am totally ignorant of my plaque status.
In fact I have been pondering for a couple of years now about how many of the bloggers on this site know the ins and outs of much of their blood components. The healthy folks I know who visit their NHS GPs ( requested to attend well women and well men clinics), seem only to be offered tests to measure their glucose and cholesterol levels, along with height, weight and B/P measurements. As such, being healthy, there would seem to be little reason to measure much else.
Or are those who do know their personal measurements, using private facilities? I don’t wish to sound rude, but those generally classed as the “wealthy, worried well”?
Jennifer
I answered further down, but since it doesn’t show here, I’ll repeat what I said. I had a stress test that showed my beating heart and my arteries on a screen. The doctor pointed out how thin and flexible the walls of my heart were and how easily they moved. He said I had a zero risk of heat disease or stroke. I don’t see any way to argue with his assessment. (He didn’t ask how I did it, but I sent him some books and articles anyway.)
This article is very similar to XXXI https://drmalcolmkendrick.org/2017/06/21/what-causes-heart-disease-part-thirty-one-xxxi/
I find I still have the same problem I had then: an inability to visualise how a plaque starts, grows, and bursts or gets absorbed.
Plaques are described as having a layered structure. To my way of thinking, if you have a series of layers, one on top of the other, there should be an obvious age progression from older to younger, similar to layers of sedimentary rock. Yet this is never noted in descriptions of plaques. Instead, they seem to develop a fatty core, which is prone to bursting and causing problems.
I am unable to visualise how a fatty core could form within a layered structure.
Also, as the layers build up, is the new layer on the lumen side or the other side of the existing clot? I ask because you say it is contact of blood with Tissue Factor in the arterial muscle that is the cause of clot formation. If there is a clot immediately underneath the endothelium, and the endothelium leaks, does the blood pass through the existing clot layer and contact the TF in the arterial muscle on the other side, or does the old clot layer get suffused with TF so a new clot will form on the lumen side of the layer?
As an engineer I find it hard to grasp processes without diagrams. Could you refer me to a good sequence of diagrams showing the natural history of a plaque?
Peter Attia had a good website which seems to have changed recently. He is referenced above Bobm.
I’ve looked at Attia’s website, particularly https://peterattiamd.com/heart-disease-begin-tell-us-prevention/ . I’m still confused.
Martin Back, re confusion
There appears to be two ways to develop plaque:
– sub-endothelial origin as per Peter Attia reference
– successive blood clotting and repair above endothelium
My opinion now is that both theories are correct. Possible that plaque could progress by one mechanism or the other, or by both simultaneously.
Solution is to reduce carbs.
https://onlinelibrary.wiley.com/doi/full/10.1002/dmrr.613
“In conclusion, our study has demonstrated that hyperglycemia, both stable or oscillating, increases endothelial cell apoptosis through ROS overproduction at the mitochondrial electron transport chain. Endothelial cell damage plays an important role in the pathogenesis of diabetic complication. “
Hi Martin,
I’ll have a go at explaining this, the clot is caused by a tear in the endothelium, not below it, so always lumen side.
The clot should be cleared up by TPA when finished but it looks like LP(a) in the clot degrades this action in species which do not endogenously create Vitamin C (including humans),
Endothelial Progenitor Cells then come along and make new Endothelium over the clot, a bit like a pothole repair. Then if it hapens again at the same (now narrower) area you get another clot layer.
As the layers are closed off I don’t think there is any process that can clean them up so there would probably be no difference in size?
Dr. Kendrick,
To follow you thought process, it seems you are saying that some event/damage occurs to the endothelial wall that then results in a clot that covers the damage during repair. Would the cases of multi-layer clots mean that the original clot itself “failed” and additional clotting ensued? Also, why do you suppose endothelial damage originates? I know in general it is purportedly due to stress on the artery wall, but I wonder, what about intense exercise? Many people these days push limits and perform activities that bring their heart rates to near max with corresponding peak blood pressures, briefly, but repeatedly over time (days/months/years). What types of stresses typically damage the endothelial wall?
Thanks for this series – very enlightening.
I was also wondering how the endothelium got damaged. When they talk of “fatty streaks”, I have a picture of a whole strip of endothelium peeling away like a sardine can lid and needing repair.
Which makes me think: There must be a constant floating population of dead endothelial cells in the bloodstream as old cells die off and are replaced by new. They would be single cells. Are there also fragments of endothelial wall like bits of torn tissue floating around? They might have diagnostic significance if they exist.
After smoking a single cigarette microparticles (breakdown products of endothelial cells) can be measured floating about in the bloodstream. So, yes, the endothelium is under constant attack, and is constantly being repaired. I sometimes think of it like a road surface. Cars lorries battering over it ever day. Eventually potholes – unless the council comes and repairs it.
A recent episode here on UK TV saw Guy Martin (truck mechanic, motorcycle racer, sometime TV presenter) in Russia, poking around the site of the nuclear disaster in Chernobyl. It was explained that immediately following the disaster in 1986, thousands of nearby residents were forced from their homes; told to take only enough belongings to cover them for a few days, but were never allowed to return – being displaced from their roots, friends, neighbours and in some cases families.
As the years went by, and with radiation levels remaining stratospherically high, the area for many miles around Chernobyl was deemed uninhabitable. Except …… some people secretly returned to their homes and began living off the land. An amazing fact was then revealed – that those who had returned, despite being exposed to extremely high levels of radiation, survived on average for 10 years longer than those displaced who never returned.
I think this is another powerful example similar to those raised by Dr K previously, where the persistent stress and trauma of having being forced away from your homeland and social networks is far more dangerous than other forms of so called risk (saturated fat, LDL, excess salt, ……. even radiation !).
A good point was made in the posts, of Sunday nights being ruined by the anxiety of Monday morning and the foreboding of the week ahead.
Martin T
Radical geographically displacing a (conquered) people is an Ancient practice, and for good reasons.
Relocate, Enslave and Work., – Being dispirited and depressed they will invariably die earlier – at the end of their “useful” life. I’d wager ‘heart attack’ was a major COD.
– As it is today…
We thank the returned remnant of Pripyat for giving us the ‘control’ arm of that experiment.
James DownUnder,
“Radical geographically displacing a (conquered) people is an Ancient practice, and for good reasons.”
I object strongly to the description of “……..for good reasons.” No personal offence intended.
They are reasons because of the selfish and greedy nature of power grabbers (the conquerors).
Hi Malcolm,
I am confused by the last part of this statement:
Now, you may rather like this dual model of âAthero-thombosisâ. However, I do not. Indeed, I hate it. For one thing I do not like having to invoke two completely essentially unrelated processes to explain a single disease. Mainly though, even if it wasnât deliberately designed to protect the âLDL-hypothesis,â that is exactly what it does.
Good
Angina harbinger of MI as you describe it. Is gradually – or suddenly – increasing angina necessarily manifested prior to MI? No such thing as silent MI?
Also, I believe you’ve previously referred to MIs occurring without the final clot, without 100% blockage. Is that for a different post?
jD
I wonder what a MI actually is.
I have for sure have had one serious MI which damaged my heart muscle but though in a “limited” way which though made me change my “way of life” profoundly 20 years ago. Since then I have during the last ten years have had a number of “events” (unstable angina) which would have brought me to the emergency room if I had not known what I know today and taken action – but I have kept away from the ER.
Anyway, today everything seems to be OK with my heart and I don’t go for any “testing”. I let my body tell me!
Relaxing in my garden with a couple oif glass of wine (as tonight) or with a an Ardbeger whisky is for sure a “medical” treatment to my opinion.
Goran,
I wonder what angina actually is. By establishment accounts, I should be close to an MI. I’m 74 with a CAC of over 1500. (My father died at 75!)
I finished painting my large house recently. I fell twisted trees on my acres and chop for firewood. All strenuous.
No angina. No discomfort. …. No warning??
Well, JD,
All life is a wonder!
But all living creatures eventually die but what we fear I guess a gradual painful decline of health.
If one feels fine chopping wood or as myself today working with my new scythe in the garden it is with my present philosophy not a bad idea to drop “stone dead” in a healthy state at a mature age of 80, 90 or even hundred with a “tool” in your hand.
In a short while I will drop into my outdoor tub when the temperature has reached the convenient 36 C; 35 is too cold to my opinion. I will also have a nice Ardbeg at hand.
Ah, yes. Ardbeg.
Have you tried Laphroaig 10 year Goran? It’s like Ardbeg only more so.
Don’t like it. Too peaty for me.
Malcolm
There is no bad Tomatin.
You are an east side of Scotland man, support home industries!
Auchentoshan to you. My favourite is Highland Park – all the way from Orkney. Its probably Norwegian.
Auchentoshan is Glasgow and not bad. I also like Highland park, especially in the old bottles at a reduced price in French supermarkets
JD
Yes, Laphroaig 10 year is one of my long standing favorites.
But now I have fallen in the trap of Ardbeg Uigeadail (what that may mean) at the higher end of the malt whiskys but it is very strong so you have to add a little water to bring the full richness out.
By the way, isn’t whisky considered to be medicin in Scotland? The last cardiologist noted (with amusement?) in my journal that while I was refusing all their pharmaceuticals I used “alcohol” as medicine.
I also read somewhere that the long living people in southern Russia began the day with a small shot of vodka. This was also a habit in Sweden two hundred years ago but am not sure that it attributed to the general health at that time – probably overdone.
So what is the way to prevent this? Taking natural blood thinners such as fish oil, vitamin K2, vitamin E, higher intake of citrus bioflavonoids to strengthen blood vessels, all of the aforementioned or do you have no suggestions on how to avoid being a statistic of cholesterol crystals?
JD, according to my (ex) cardio, a significant portion of my heart muscle is now ‘akinetic’ thus “deaded by blockages” This last one (or more?) events occurred with NO angina or similar sensations, only eventual physical debilitation. Elective CABG x5 was the outcome. (Hindsight questions the urgency as presented !)
jbarnesbaker
“But I have zero plaque and I know others who also have none”.
You are the second person in the blog comments who has stated zero plaque – the other commenter was Jonathan Christie in Part 50’s comments: he stated he was age 72 with a CAC score of zero.
May I ask how you and the others tested for plaque?
On the one hand it seems that arterial damage/hardening/stiffness goes hand in hand with the ageing process.
On the other hand, there seems to be quite a few people who have avoided this both here and elsewhere e.g. Dr Jeff Gerber and (I think) also Fat Emperor Ivor Cummins.
So, plenty to think about in your comments about what the zero or low plaquers may have in common.
I was tested with a stress test that showed my beating heart on a screen. The doctor pointed out how “thin and flexible” the walls of my heart were. He said “your heart is beautiful.” I was 74. He said my risk for a heart attack or stroke was zero.
I’ve been on a low-carb/good fat diet
since 2000.
Glad to hear it, keep going.
Encouraging to hear for someone being on the same track as you are. Though my “last” cardiologist, I met a couple of years ago, was very dismissive – “What you are involved in is nonsense to me!” “You have just been lucky for 15 years!”
But, anyway, he reluctantly confirmed that my heart looked “just fine” in the ultrasonics bu twas happy to bring my BP up to 140 by insulting me at the same time. He didn’t comment on all the lab test values (I wonder why) except telling me when prescribing the “standard set” of pharmaceuticals (he knew that I wouldn’t take) that the statins where not for the cholesterol, which was just fine, but to “reduce inflammation”.
I think that Malcolm would have loved to meet this one.
Great guys these expert cardiologists – they must have a tremendous self confidence, alternatively cry in a corner.
Goran, I used to live in a communal house near a hospital, and many of the younger doctors and nurses came to our parties. I hated the doctors because they were always so sure they knew everything, and acted like they were superior beings.
Eventually I came to realise they had to be this way. Every day they were making decisions that were literally a matter of life and death to their patients, which we ordinary folk never have to do, and they needed that self-confidence, otherwise they would have been paralysed by doubt and unable to take action.
The attitude goes with the territory.
Another place where people have to appear self-confident is on radio and TV when they are appearing as expert commentators, whether it be on medicine, gardening, finance, or whatever. They will always act as if they know everything, even if they don’t.
Martin,
Good point you are making!
And my experience tells me that people generally see meeting a GP (or worse an “expert”) as a meeting with “a god” and that is why they go to an appointment.
Thank you for your explanation of low carb, good fats giving you a healthy heart. I certainly agree with you. However, I am wondering why you had the stress test done in the first place, especially as it showed how healthy your cardio vascular system is. Did you have some symptom to suggest you the test?
I worked on a cardiac ward in the 1980s. As a Nurse, I always wondered why those with a compromised cardiac condition were subjected to further stress, and the possible risks associated with it.
As a student radiographer in the mid 1960s, I noticed that patients were referred for multiple tests on one request card, rather than one test at a time. As such, consideration could then be given to one test before requesting another. I just wonder if tests are carried out at a whim in many cases, and Doctors have lost the art and craft of assessment and observation, totally relying on technology.
Believe me, I am not a Ludite, as I think the practice of medicine is wonderful. But we have to watch out that they are not leading to their own extinction,
I was under the impression that CAC only measures the presence of calcification in an artery/ artherosclerotic plaque ? So having a CAC score of zero is the equivalent of having no detectable clacification. However, I thought you could have non-calcified plaques that may be unstable and/or advanced with considerable narrowing – these would not be detectable by CAC measurement ? Is a CAC of zero, potentially a false sense of security ?
I may have misunderstood so am happy to be corrected.
Martin T
I think a CAC score of zero is a good thing, but as you say it cannot tell you about unstable plaque. So, be reassured, but don’t treat it as gospel.
I’ve been wondering for quite a while if vessel calcification as a result of endothelial targeted bacterial infection amounts to the same plaque configuration as classic CVD.
??
I am sure that it does. Exotoxins released by bacteria attack the endothelium first.
Martin Thomason – detectable plaques
This 2min 31 second Q and A with Dr Barry Sears may provide further info and ties in with your comments about visible/detectable and non visible/non detectable plaques. I was searching for stuff on fish oil and arteries and this sort of ties in with this post and its comments.
Dr Kendrick suggests the possible analogies of a “boil bursting” or “perhaps like a volcano”. Dr Sears has another similar one – a pimple bursting. Here’s what Dr Sears has to say:
0.11 – “2 types of plaque in your arteries. There’s the plaque you can see…the calcified plaque…and the plaque you can’t see…these are called soft vulnerable plaques…they’re like little pimples inside the artery and when they get inflamed they pop open like a pimple”
and at
1.44 – “you see less macrophages which are the cells…comin’ after inflammation…so, they’re less likely to explode and kill you.”
Here is the link:
Martin Back – plaque diagrams
You probably have done this, but I googled “arterial plaque formation” and I found this – there were plenty of diagrams/pictures to scroll through:
https://uk.images.search.yahoo.com/search/images?p=arterial+plaque+formation&fr=yfp-t&imgurl=http%3A%2F%2Fthumbs.dreamstime.com%2Fz%2Fthrombus-blood-clot-unstable-plaque-formation-artery-rupture-detailed-anatomy-illustration-illustrative-diagram-how-51840561.jpg#id=1&iurl=http%3A%2F%2Fthumbs.dreamstime.com%2Fz%2Fthrombus-blood-clot-unstable-plaque-formation-artery-rupture-detailed-anatomy-illustration-illustrative-diagram-how-51840561.jpg&action=click
Not sure if this helps – if you find any which help and you find useful, let us know.
Wow, super interesting… and I think I actually did understand a fair bit, with careful reading!!
Thanks, looking forward to the next one.
If you already have a heart condition and a stent fitted, can you overdo the regular exercise bit?
Just wondered if my daily hill climbs are too strenuous – stressful, in the light of what mmec7 said on 6 August
“Furthermore, nitinol stent fracture was more frequent in patients who walked more than 5,000 steps a day compared to patients who did not exercise … ” Paper : ‘Dynamic Forces in the SFA and Popliteal Artery During Knee Flexion – Consequences of stress to consider for stent durability and design’ – May 2008 / Endovascular Today /
Love the breezy style of the blog Doctor Kendrick, keeps everyone on their toes, always polite, (well mostly) but a hint of grumpiness if we haven’t been paying attention.
Wonderful, informative stuff – always a fascinating read, thank you for sharing all this.
James – Superficial Femoral Artery –
Biomechanical modeling of Femoropopliteal artery
Click to access campanile.pdf
ˆ FPA: a portion of the SFA and the popliteal artery is modelled as a beam (el. …. ( 1995). Arterial tortuosity in the femoropopliteal region during knee flexion: a …… evaluate and apply to the stent the dynamic external forces acting in that region.
This refers to a stent placed approximately behind the knee. Owing to the placement, the stent is liable to succumb to the actions of the knee : flexion, extension, crossing of the knees, walking, especially uphill and to climbing stairs. The reaction of the muscles – gastrocnemius / soleus – starved of oxygen and nutrients, may succumb, leading to an ischaemic event. PAD, peripheral artery disease, in its worse form, may / can lead to amputation of affected toes, foot or limb – starved of etc, and leading to : wounds that do not heal; ulcers that do not heal; infections that may / can lead to gangrene. The big scenario, we don’t need to stress, is the importance of not letting matters get this far ! Walk !
Quote “If you already have a heart condition and a stent fitted, can you overdo the regular exercise bit?”
That particular question is better answered by Dr Kendrick. But, you are referencing the ‘Femoralpopliteal artery’, PAD. peripheral artery disease. A different matter entirely. Walk.
Your heart condition is not PAD. Your stent is not running the constant bullying stress levels of a stent placed in the superficial femoropopliteal artery (the SFA / SPA). A stent in the SFA is open to breakage, crushing, dislodgement, plus stenosis, narrowing by build up of plaque, as the stent adheres to the artery walls, and eventually a re-stenosis – suggested 2 to 5 years. Which will probably in the long run, require a full bypass with implant from an artery from the fellow leg – unless it is necessary to use alternatives. Hoping in the meantime, one aint gonna run the gamut of a full blown ischaemia attack… Nasty. As a full blown ischaemia may lead to amputation. Not a happy outlook.
Stents so far are not up to the challenge of being the workhorse necessary to cope with the stresses of daily requirements. The new Gore-Tigris stent, using nitinol, which, being 55% aluminium, is malleable but is impossible for use in anyone hypersensitive to aluminium / base metals ! Cases of really nasty unwanted side effects are recorded. Initially, the Gore-Tigris, due to being malleable and not so open to the breaking, crushing and movement of the prior stents used, was much vaunted, but now one is looking at the post marketing outcomes. Not so good. As we see in the reference to : “nitinol stent fracture was more frequent in patients who walked more than 5,000 steps a day compared to patients who did not exercise …” So, back to the drawing board. The Supra (nitinol) aint the answer, it can also ‘kink’.
In the meantime, try to steer clear of such surgery by a controlled programme of exercise, walking. Building up gradually, developing and strengthening the collaterals, working around ‘calcified plaque’ so as to be able to lead a reasonably ‘normal’ life = walking in moderation, for day-to-day living. You aint gonna run no marathons nor climb mountains, but can manage daily living and stuff around the market ! Walk.
Apologies – spinning off into a side subject.
mmec7
Thank you for your very comprehensive and thoughtful reply to my question.
Sorry I got the wrong end of the stick entirely!
One of the problems with having limited knowledge of the necessary medical jargon.
Although I must say mostly very complex ideas are often brilliantly simplified in this excellent blog. So much so that I feel confident enough to stand my ground with my own doctor and I hope the next cardiologist I run in to.
Also as you have so ably demonstrated any mis-understandings are soon put right by the knowledgeable and dedicated band who follow Dr Kendrick.
Thanks again for your reply and good luck with your own journey, in comparison my problems are a very paltry affair All best James
Thrombo-atherosclerosis (unstable plaques)
There has been plenty to think about in this post on thrombo-atherosclerosis and as a regular it’s also been a case of revisiting and remembering Dr Kendrick’s previous posts and comments on the subject.
I’d forgotten there were 2 types of arterial plaque:
1 – the unstable plaque described in this post: plaque plus clot(s) = either (1) rupture or (2) eventual arterial blockage and
2 – stable, calcified plaque. Or, as described by Dr Barry Sears in the link I provided in a previous comment where he describes the 2 types of plaque: “calcified plaque…it’s surrounded by concrete which isn’t gonna hurt you.” I should point out I don’t know much about Dr Sears or if he’s ever been name checked in readers’ comments.
Which has generated the following questions:
– At what point does the body’s repair/healing mechanism dispatch calcium to these unstable plaques to stabilise the area? It seems to be a very precarious and perilous state…especially as you can’t detect them, according to Barry Sears (again): “you can’t see them by any type of radiology…it’s impossible”. Perhaps there is a lot of merit in checking for arterial stiffness through things like pulse wave velocity or HRV (heart rate variability) and so on. However, I’m not sure if arterial stiffness through ageing = plaque.
and
– Should we be consuming vitamin K2 to keep calcium in the bones and teeth and away from the arteries? It seems to me that a calcified plaque is better than one ready to burst.
Readers may like to visit Dr Kendrick’s 2016 post on calcification and here’s the link:
Extracts include:
“Not all plaques calcify. Some do, some don’t” and
“calcification is not an accident…it seems to be an organised and regulated process” and
“if calcification is a physiologic defense mechanism…why would you want to reverse it”
These 2 posts seem to be a natural pairing and you’ll find a bit more on vulnerable plaques in this post on calcification.
Random thoughts generated from all this include:
If you do have calcified arteries/plaques, does that mean any new areas of thrombosis will also calcify?
Or is calcification a reflection of your health at any given time e.g. if you are low on vit K2 when the process starts, then the calcium will transfer more readily to your thrombosis?
If only it was as simple as cholesterol and/or we were docile, passive people who bit into the cholesterol hypothesis!
GreenMedInfo is reporting today that statins increase the risk of getting cataracts.
A book called How Statin Drugs Really Work: And Kill You One Cell at a Time (by Yoseph) says statins kill the cells that make cholesterol in the liver and in the brain. That might explain why we have such high rates of Alzheimer’s and dementia. The ads for some statins claim they keep your body from making cholesterol so it makes sense. What do you think?
Statins do not kill the cells, at least not directly, they block an enzyme critical to the synthesis of cholesterol. HMG CoA reductase.
Cholesterol is, in turn, essential for breath health and function. It is the main chemical used to make synapses, it forms a critical part of the support structure of neurons and the myelin sheath. So, if you block cholesterol production in the brain, it is almost inevitable that this will cause significant problems. Statins, for example, as associated with a fifty fold increase in the risk of developing Amyotrophic Lateral Sclerosis – as I blogged about a few months ago. They also increase the risk of polyneuropathy and Parkinson’s.
Interesting couple of fact-ettes for the statinistas. Note: This was before I realised that total cholesterol score is pretty meaningless. Prescribed three different statins over 2-3 years; brought total score down from about 7.2 to 5.2. Then radically changed lifestyle and diet etc and within four weeks cholesterol reading 3.2. Told sceptical GP I wanted off statins. “Let’s have another chat when it goes back up”, he quipped. Three months later, ex statins, cholesterol range between 3.8-4.2. In fact, I can almost predict the score dependent on what I eat. Then I stopped beta blocker and aspirin. Never felt better.
That,s how the Yoseph’s explain it. It’s an excellent book that also goes into the fascinating checkered history of Statin Drugs and the phony FDA hearings that brought Lovastatin the first Statin to market.
So, if they made a drug that increased the production of cholesterol in MS and ALS patients, would that help them regenerate their myelin?
I don’t know, but it is something that could well be worth trying.
This might interest Dr Kendrick –
https://www.medscape.com/viewarticle/893921
High Cholesterol Tied to Lower Cognitive Decline Risk in Oldest Old
Batya Swift Yasgur, MA, LSW – March 14, 2018
Elevated cholesterol levels in individuals older than 85 years has been linked to a reduced risk for marked cognitive decline, compared with persons 10 years younger whose cholesterol levels were similarly elevated, new research shows.
Investigators found that cognitively intact people between the ages of 85 and 94 whose total cholesterol had increased from midlife had a 32% reduced risk for marked cognitive decline during the next decade, compared with individuals aged 75 to 84, who had a 50% increased risk.
“These findings do not imply that the cholesterol itself had a protective effect or that increasing cholesterol consumption will confer a benefit on people of this age,” lead author Jeremy Silverman, PhD, professor of psychiatry, Icahn School of Medicine at Mount Sinai, New York City, told Medscape Medical News.
Instead, “cholesterol may be a marker for some other protective factor present in these people who are making it to age 85 and maintaining their good cognition at that age,” he said.
The study was published online March 5 in Alzheimer’s and Dementia.
(more…)
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Dr Kendrick. After years following your blog, and enjoying all the aspects under discussion, I like it when the topic returns to the original subject….cholesterol. I just cannot understand why members of the medical profession continue to prescribe statins and promote a low fat diet.
It is a modern day crime mystery of incredible proportion. Just when will medical practice cotton on?
Changing established dogma takes decades.
@jbarnesbaker I have book you referred to. Was recently trying to find it to re-read but couldn’t.
It is still on Amazon.
Thanks for providing the video link Charles – very much appreciated.
Your points give plenty of food for thought. What now puzzles me is: if calcification of a plaque is a good thing (providing stability and reinforcement against ‘bursting’), then why is a high CAC score (high levels of detectable calcified plaque) such a high risk and predictor of imminent demise ?
My earlier point was that a CAC score of zero is seen to be a marker of very low risk of a cardiac event within the next XX number of years – but that zero CAC score could be achieved despite having a large, soft, unstable plaque on the verge of rupture.
It would seem we need to treat a low or zero CAC score with a degree of caution as it may mask the true state of one’s endothelium.
Martin T
If you have lots of calcified plaque, you will have – most likely – lots of vlunerable palques as well. Hopefully all turning into calcified plaques, rather than bursting.
First, thanks again for writing another part of this series…
Just wondering, what is your thought on the other 50% without occlusion, from the statement/article below: “The conclusion is that while thrombosis associated with MI is a real phenomenon, it does not occur in more than 50 percent of cases—which leads to the question: why do the other 50 percent, those without an occlusion in the coronary arteries, even have an heart attack?”
https://articles.mercola.com/sites/articles/archive/2014/12/17/real-cause-heart-attacks.aspx
My view is that when they come to look for the thrombus, it is gone.
If the thrombus is already gone (cleared by self-healing) and a subsequent heart attack occurs, then the damage > repair… the body or heart in particular was not able to cope with the damage though there’s the attempt to heal it up to the last second…
You should look up hibernating myocardium. There is a clear temporal gap between thrombus formation, and the MI – in most cases.
Solomon
high-sensitivity c-reactive protein (hs-crp)
You may find this info useful – it’s a good basic guide:
https://labtestsonline.org.uk/tests/hs-crp
For example, it explains the difference between crp (general inflammation) and hs-crp (inflammation from atherosclerosis)
Just come in – have not checked it out –
Association of Statin Exposure With Histologically Confirmed Idiopathic Inflammatory Myositis
JAMA Intern Med; Aug 07, 2018
https://jamanetwork.com/journals/jamainternalmedicine/article-abstract/2687990
Inflammatory myositis? should this be called myositisitis.
What does “potentially rare” mean? Are statins potentially harmful or harmful? Maybe that is why you need a blood test to check CK level to see how the treatment is progressing.
Have only just now opened the link : 18.23 Paris time, 09/08/2018. Have been out all day at a hospital appointment. An no, the problem discussed in this link has no bearing on me nor my own health problems. I saw the ‘statin’ title together with ‘Inflammatory Myositis’ and though members might be interested. No, I have nothing to do with headliners,nor with Editorial comment…!
Right. So what does this link have to disclose –
New Online
Views 1,223 Citations 0
116
Comments 1
Original Investigation
July 30, 2018
Association of Statin Exposure With Histologically Confirmed Idiopathic Inflammatory Myositis in an Australian Population
Gillian E. Caughey, PhD1,2,3; Genevieve M. Gabb, MBBS, MPH4,5,6; Saffron Ronson, BPharm (Hons)3; et al Michael Ward, PhD3; Timothy Beukelman, MD, MSCE7; Catherine L. Hill, MBBS5,8,9,10; Vidya Limaye, MBBS, PhD5,10
Author Affiliations
JAMA Intern Med. Published online July 30, 2018. doi:10.1001/jamainternmed.2018.2859
editorial comment icon Editorial
Comment
Editor’s Note
Statin-Associated Myopathy—An Elusive Clinical Problem
Gregory Curfman, MD
Full
Text
Key Points
Question What is the association between current exposure to statin medications and histologically confirmed idiopathic inflammatory myositis?
Findings In this population-based case-control study of 221 patients with idiopathic inflammatory myositis and 662 age- and sex-matched controls, there was a statistically significant 79% increased likelihood of statin exposure in patients with idiopathic inflammatory myositis compared with controls.
Meaning Given the increased use of statin medications worldwide and the severe adverse effects of idiopathic inflammatory myositis, increased awareness and recognition of this potentially rare adverse effect with statin exposure is needed.
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Full text is available. For anyone wishing to pursue, then good, it’s open.
mmec7: A worrisome finding, seemingly worse among women. Another nail in the statin coffin.
O notice that this study looks at an Australian population. Ummmm We Aussies are not that different to the rest of the world..So take heed.out there..It would be nice to know that Australian medical doctors have read ths study..But I fear most will e too busy or too allergic to do so..
Yes, I had to smile at the Aussie bit – like, errrrmmmmm looking around trying to discover what the differences may be ? Musn’t rock that ole P&O liner though 🙂
This study was done in South Australia where I live. And it ‘fingers’ statins ! I tried to look at the whole article but it is paywalled..
And to my knowledge no one here in SA media has commented on it.
No surprise to hear it first from you Malcolm. You are the only one who simplifies technical mumbo jumbo so the common man can interpret. Can’t tell you how many fears you’ve alleviated for my family and I. Truly a free thinker. Just a couple of little gems for your perusal. Have been unable to get decent meat from the butchers so have approached cattle farms where they are raised correctly. On their blog post to the health benefits of said cattle the following. Lower in saturated fat so great for heart health and lower in cholesterol to maintain healthy blood and heart health (f*** off you plonkers). The one industry you’d think would benefit from the whole cholesterol b.s would be them. Secondly from the doctors practice of Australia to you. My mother after reading your book proceeded to go on a low carb higher fat diet and hey presto all her health markers were better. When the doctor asked what she had done she said she’d embarked on a semi keto diet. Great said the doctor but just remember to cut the fat off your meat? As you can see fighting an uphill battle.
CardioBrief has a post today on the new Lancet paper concerning the hazards of sodium restriction. Worth a read. The salt restrictors can’t get their heads around it, and are sticking to their guns! Madness.
This morning I received a newsletter from Dr. Mercola that made me confused.
“The Nitric Oxide Dump workout stimulates your body’s release of nitric oxide (NO), improving your mitochondrial health, slowing down age-related muscle decline and boosting heart health”
What is this?
Nonsense?
My CVD-self certainly believe in strenuous activities of short duration but I don’t understand the beneficial “process”.
Mercola has the American failing of trying to turn everything into controlled powerful process where everything is precisely measured. In the UK we have a ‘little snooze’. In the US they have a ‘power nap’. You cannot relax in the US, even when you are asleep you are ‘powering yourself’ to success. Short bursts of high intensity exercise certainly seem beneficial, but you don’t need some specific HIT ‘nitric oxide dump’ regimen. Hacuna Matata.
I think your comment is “on the spot”.
Having lived for year in the “Great country” I have noticed this annoying attitude everywhere – “Don’t worry – be happy”.
Ironically, the first time I saw research reflecting the cardiac benefits of HIIT was from the UK (Manchester? Nottingham?).
And again, with even more irony, here I find myself in Lincoln this morning, dragged to my very first Crossfit class, taught by a Scot.
Dr K….Somewhere in the comments (too many to go back through), someone mentioned Mercola and you gave the impression that he was OK (can’t remember your exact words). So how does this gell with the fact that his website has been elevated to #3 in the Top 10 Worst Anti-Science Websites (up from #6)? Most opinions I read say he’s a quack.
Most opinions I read say that I am a quack. The anti-science movement is, unfortunately, primarily a ‘support the current dogma’ movement. No thought required. All you have to do is question something like ‘sunshine is bad for you’ or say that ‘salt is perfectly healthy, put as much on your food as you want,’ and the attacks begin.
I tend to think of those who have decided to able to decree what is, and what is not, science as those who would have unthinkingly supported the ‘strict bed rest after an MI’ advice. Something that killed tens of millions, but when Bernard Lown suggested that patients should be allowed to sit up on a chair after a few days, he was greeted with Nazi salutes by his fellow doctors. See https://bernardlown.wordpress.com/2011/02/03/a-chair-to-the-rescue/
What a fine man and physician, Dr. Lown (and a very good, articulate writer). I did not know about the Nazi salutes, an extreme act of cruelty toward the top student in his high school class who nevertheless had great difficulty getting into medical school because of the Jewish quotas in the Ivy League universities. Or Dr. Semmelweis, who had the audacity to suggest doctors wash their hands. Or Dr. Wakefield, who, along with his twelve co-authors, found (and they weren’t the first to do so) bowel disease to be commonly co-morbid in autism, a finding considered today to be among the commonest conditions, but had the temerity to suggest investigating a connection with the triple jab MMR because of evidence-parent reports, since their children were too young to articulate it. Our CDC did do such research, on Atlanta schoolchildren, and confirmed the hypothesis. They then changed the protocol, eliminated 40% of the data to eliminate the signal, and threw all the original work in a trash can. Except the statistician on the study team, Dr. William S. Thompson, who knew what they were doing was unethical and illegal, who kept copies of all the original work, and who hired a whistle-blower attorney. He is still awaiting subpoena by Congress, who for four years have shown themselves too cowardly to take on the ruthless evil, in the form of the pharmaceutical industry. Or Dr. Bob Sears, a prominent pediatrician and author here in California, who had the temerity to write a medical exemption to California’s new, draconian vaccine mandate for a child who had a previous, serious adverse reaction to a vaccine. In truth, quackery is more likely to come from the mainstream than from outside it.
Speaking of salt, I’d like more info sometime on that. I’m a little doubtful.
AnnaM: Read “The Salt Fix, Why the Experts Got It All Wrong-and How Eating More Might Save Your Life,” by Dr. James DiNicolantonio. Everything you need to know about salt, and the danger of salt restriction. I personally take an additional teaspoon of salt on my strenuous workout days in warm weather, dissolved in mineral water, and 1/2 teaspoon in cool weather. The kidneys are admirably suited to take care of any excess sodium.
Gary
Have read the book, it is very good.
I.m a saltophile, people always nag me about it, I now ask if they have read the book,
I once mentioned your name to my Dr, and his comment was that you were rather left field! We live within cycling distance of Macclesfield, so he may even have met you.I didn’t pursue the matter!
Left field is OK. I consider that a compliment
I happened to mention the Kendrick blog to my GP and he said “Kendrick? Malcom Kendrick? We trained together. A good bloke.”
I agreed.
The biggest quack ever in the medical field was claimed to be Linus Pauling and he is certainly one of my favorits in order to regain my health; e.g. 15 g of vitamin C/day.
Pauling who was able to decipher the nature of of the chemical bond and for this received his first Noble prize and the second for his pease work is for me as much a “scientist” you can get. To call him a quack tells more about the people who did it.
https://en.wikipedia.org/wiki/Linus_Pauling
With this profound scientific attitude he approached the medical field and realized the lack of science in this field an founded an alternative – Orthomolecular medicine – 50 years ago.
https://www.isom.ca
foodnstuff: Beware of what you read about quackery on line, especially those blogs who have the words “quack” or “skeptical” in the title. The industry has a vast PR operation, and some of might sound legitimate and independent, but it is not. Dr. Mercola is sometimes over the top (for example the NO dump), but it is all based upon good science. I get the newsletter every day, but read little of it any more because my knowledge base has expanded greatly. There are occasional gems, though, particularly interviews, such as that with Dr. DiNicolantonio. Also be aware that the term “anti-science” is political in nature, and is used to belittle those who question the official narrative (such as global warming).
Anti-science is an ad hominem. It is also very unlikely. I have never met an anti-science person in my life. Even if a person believes God created the world in 6 days they are still perfectly pro-science in most other ways. They just happen to believe different data is reasonable in this case.
Who is doing the rating?
When I am told that someone is a quack, my first reaction is to investigate who is making this allegation and why! In the case of Dr Mercola, he has consistently gone up against accepted medical dogma, and In so doing has brought down the wrath of its proponents. His interviews are illuminating and his articles are often thought provoking. I certainly do not accept his word without further investigation, but, like Dr Kendrick, he makes one think out of the box.
Intuition suggests to me that the kind of people who make a thing of compiling lists such as the Top 10 Worst Anti-Science Websites are probably a little too quick to dismiss the kinds of newly arrived hypotheses that Mercola is prepared to explore.
No, I’m not sure about Mercola either, but I admire him for not dismissing a hypothesis just because it seem counter intuitive. One has to be able to swim a while with wacky seeming ideas to become placed to decide if they are a floater or a sinker.
If every matter were simple, obvious, and intuitive we would have no need of science. On occasions science and the scientists do well to be provocative. Science has actually progressed by odd seeming people running with ideas that nobody else dares to tread.
There exists far too much click bait out to foil you into thinking it is educating you.
foodnstuff,
Have you ever stopped to think what exactly the term “Anti-science” actually means? It clearly doesn’t mean people who hate science for one reason or another – say because it produced nuclear weapons – because in such a case the person isn’t disagreeing with the science used to produce the bomb, but it asserting that it should not have been done.
What possible sense does it make to label someone anti-science because they use scientific arguments to attempt to refute some scientific dogma. Surely it would make more sense to point out the error in their reasoning?
It is just another version of the ad-hominem attack. ‘You’re not a scientist, so we don’t have to listen to anything you say, and nor should anyone else.’
I think it is also a reverse of Appeal to Authority, another common logical fallacy.
Unfortunately those called anti-science often are (or were) senior scientists! Think of Henry Bauer.
I think Mercola is hurting not his bottom line but his credibility by aggressively marketing his products, and by at times appearing to promote a blanket anti-vaxx stance.
To give him credit, he promotes a broad range of unorthodox ideas and promoted some ideas early on that turned out to be real gems, but one needs to apply critical thinking when browsing his website.
Funny, it bothers me not that Dr Mercola sells the products that he feels will help people, and I have never thought that he is aggressive in doing so. Why does his selling products have anything to do with his credibility? btw, in all the years I have been following Dr Mercola, I have bought maybe one or two of his products.
Agreed. Mercola is pretty reliable, has a good research team. Don’t agree with everything, but, can ignore. As for ‘selling’ products – and he has to make a living. He is careful in his researches and sure takes the hassle out of scratching around searching for reliable and substantive information ! He ‘holds the curtain back’…! Have only bought a few items, postage is expensive.
Again, here’s something tangentially related:
it is about ticks leaking alpha-gal into their victims’ bloodstream, triggering meat allergy.
Half way down:
“A recent study by scientists at the National Institutes of Health, which included Commins and Platts-Mills as co-authors, linked allergic sensitization to alpha-gal with a greater risk of arterial plaques, a hallmark of heart disease. It’s unclear whether having alpha-gal antibodies specifically increases your risk of developing plaques or whether some other factor increases a person’s risk of heart disease and sensitization to alpha-gal. But if it turns out that meat allergy pushes people toward cardiac arrest, it would imply that encounters with the lone-star tick contribute to the leading cause of death in the United States.”
The rest of the article muses why ticks around the world seem to have gained the ability to induce meat allergy in the last 30 years. This might be the microbiological trigger for heart disease we have been looking for, exept it came when CVD was waning already.
More likely a pharmaceutical company has found a drug that reduces alpha-gal antibodies and is looking to create a market.
Ever the cynicist, aren’t you? I wouldn’t put it beyond any one company to support papers that create a market, but why wait several years after publication without making an announcement? All this time, a potential patent is ticking away even before clinical trials have been started.
Actually, the musings kind of make sense. Old world apes have lost the gene to make alpha gal to be better able to fight the malaria parasite. Our gut bacteria keep leaking alpha gal into the blood stream, but this triggers antimicrobial antibodies rather than allergic ones. People (and mice) with higher alpha gal and antibody concentration are harder to infect with malaria. Bacteria in the ticks make the alpha gal that trickles into the bite wound.
Now, gut biomes may have been changing due to use of antibiotics and our diets. Tick biomes may have changed to changes in habitat and use of pesticides.
Now why would the antibodies promote plaque formation?
I think you probably do not know how pharmaceutical companies work. They think long-term, they find some ‘new’ thing that may increase the cause of – say – CVD, they start looking for products that may have an effect on that thing. Then, as they are developing a drug to affect that thing (ten years from the lab to the market) they start to seed ideas into the ‘market’ so that by the time their drug is ready to launch, the world is clamouring for the drug. I am not a cynic, I just know how this all works.
If the drug fails during development, you will no longer hear of alpha gal, ever again.
You may recall that raising HDL was all the rage, and the benefits of high HDL made headlines all over the place. Until the HDL raising agents all failed miserably. You don’t hear so much about HDL any more. Pharma companies desperately want to move on from simply lowering LDL, to expand the market, but at present, nothing else is looking profitable for them.
Point taken. I was wondering how much of the popuation was subject to those tick bites and whether that would constitute enough of a market. But all it takes is some indication creep later on to include those folks who have the right gut bacteria…
It is always worth remembering how many scientific studies are ultimately retracted or turn out to be wrong!
What is your experience/opinion of the drug advocated by Thomas Cowan, “strophanthus”? Some research indicates has a long history of it preventing MI.
Q10 also reduced the concentration of the coagulation factor fibrinogen in the blood. A healthy fibrinogen level fluctuates between 1.5 and 2.8 grams per liter. When the trial started, both groups had unhealthy high fibrinogen levels, but after 12 weeks, the concentration in the Q10 group was in the healthy range. http://www.ergo-log.com/after-heart-attack-q10-makes-blood-vessels-healthier.html
This is all really interesting. I’m a long time ‘sufferer’ of high cholesterol and triglycerides. The triglycerides having been ignored totally by my doctor until only recently. He is now extremely worried about them (as am I – my figures are in the extremes).
What would the current thinking for extremely high triglycerides be? They seem to be a good indicator of how your body is dealing (or not) with carbohydrates so should I be concerned?
Are they more indicative of a problem than cholesterol? I have had occasional bouts of abdominal pain which may or may not be related to pancreatitis. I have found the ‘Wheat Belly’ book by William Davis interesting but it does smell of ‘money machine’ and I find myself approaching it with care. I’m thinking that LCHF is worth looking into but would welcome any advice.
Also check your thyroid function
Will look into that too!
Dr Kendrick has explained on a number of occasions that he can’t give anything that might be construed as a consultation over the internet, so paradoxically it is left to those of us who aren’t doctors to comment!
I’d certainly be inclined to eat a LCHF diet rather than the official recommendations of the medical profession. Just reintroducing hard cheese, butter, and a bit more fatty meat might help. You could then discover whether this made you feel better, and also if it improved your blood test results.
I share your caution about money machines, but of course the biggest money machine is big pharma!
You don’t say how old you are, but I’m 68, and I have come round to the point of view that we all die sooner or later, and the stress of being tested for this and that (and particularly waiting for the results) is just not worth it – just relax!
I understand Dr Kendrick’s stance. General advice from the community is what I was after so thank you. I’m 41 but am increasingly approaching your ‘just relax’ world view.
David Bailey: Well said! I shun all tests, including BP, most supplements, except vitamin C and potassium, and just live well. Joy in living is the best antidote to the vagaries of existence.
I forgot to add, don’t take statins – just look up some of Dr Kendrick’s blogs about statins if you need more information!
David,
“but I’m 68, and I have come round to the point of view that we all die sooner or later, and the stress of being tested for this and that (and particularly waiting for the results) is just not worth it – just relax!”
Exactly!
That is what I have arrived at myself, not least by having read the book “Overdiagnosed” some years ago.
To view the grown up mallards now and then arriving in my pond outside my bedroom window eating the “carbs” (oat grains I have put out) is one of my ways to relax.
Paul Mather: My advice would be to not do anything suddenly, but reduce carbohydrate consumption gradually (over a period of weeks) to low levels. The only metabolically healthy way to compensate for the missing calories is to increase fat intake. I gave up all grains cold turkey, and was fine, but everyone is different. In three weeks I lost all belly fat (I didn’t have a lot, but as a long-time long-distance runner, I shouldn’t have had any). This will certainly lower your triglycerides. The fats I increased are: animal fats from pastured meats, raw butter from pastured cows, fatty fish, coconut oil, red palm oil, and occasionally olive oil, though it is not my favorite. Purchase the highest quality of all of these you can find, as glyphosate is now ubiquitous in the air, water, food, and vaccines, even in places where it is banned, though its days, we hope, may be numbered, thanks to what likely will turn out to be the first of many victories in a recent California case. Good idea also to eat your greens, as these help increase bile production to digest all that fat. My favorite greens (steamed, with butter, salt, and pepper) are sweet potato, red Malabar spinach, dandelion greens, beet greens, turnip greens, and spinach, all from the garden, in season.
This all makes absolute sense so thank you. I think I will be on a bit of a journey over the next few months to see what works for me. Saying that, it is difficult to know which markers to rely on and which to ignore though in order to see if I am making progress. A whole foods diet restricting processed carbohydrates (and other carbohydrates moving from the base to further up the ‘food pyramid’) is sound advice in any case so I will give that a really good go.
Paul Mather: The only marker in the usual cholesterol panel that I can think of which has predictive value (I think this is well established) is the TG/HDL ratio. It should be below 5 (mine is 0.5). Dietary self-experimentation, reasonably done, is an excellent way to improve health. Dr. Kendrick’s blog is a great place to help you navigate the terrain, especially considering the constant rubbish about food the mainstream has shoved down our throats over the past 30-40 years.
Paul,
When I abandoned statins (I more or less had to) the doctor asked me if I wanted to be tested for cholesterol any more, because there wasn’t much point if I wasn’t going to take a statin, and I agreed not to be tested in future. Even if you are tested, you might want to consider this series of studies:
http://vernerwheelock.com/179-cholesterol-and-all-cause-mortality/
In summary people with more cholesterol in their blood live slightly longer than those with less!
David Bailey, the current situation in the UK appears to be you will possibly get an increased p payment from a pension annuity if you have high cholesterol (‘cos as we all know you are more likely to suffer from CVD). So it might be good to find out that you have high cholesterol.
What an excellent nail in the statin coffin – have sent the link to a couple of friends who have been ‘terrified’ to come off them – and this in spite of keeping them up-to date with continued links Dr Kendrick’s blog. Also sent to friends who have chucked the statins. They will feel right chuffed.
Good one David.
Paul,
I read in the great book “Good Calories & Bad Calories ” by Gary Taubes that already 60 years ago it was shown (by Ahren?) that for people who were hyperlipidemics (like you?) that it was the carbs in the food that were responsible when they turned into fat.
Hence, I think it is well recognized the that skipping the carbs will bring the triglycerides in the blood down for people like us. Anyway it works fine for me on LCHF.
And, b.t.w. if you want to lose weight LCHF is an excellent procedure. I have lost 20 kg and my wife 16 and we are “normal” weight since ten years now. A friend visited me the other day and told me he got tired of his 116 kg and in a few month he shed 20 kg of those but is now complained that he is now stuck on 96 – he wants to shed 10 more. He was envious of my “performance”.
If it is healthy to lose weight is though arguable as I understand Malcolm. Weight loss seems to be more about our vanity and our social culture.
Paul,
BTW I am myself 72 but friend is “only” 37.
Thank you for your advice on this Göran, I really appreciate you taking the time to respond. My biggest concern with a LCHF is energy levels. I am an avid cyclist so am used to carbo loading before a big event. Indeed, I have been brainwashed into thinking it is a necessity! And then during long rides of 50 miles or more I am used to stopping for beans on toast, cakes etc. I’m presuming that I would need to eat carbs during longer events but how do people generally cope with endurance type exercise and low carb? Is there a ‘carbo loading’ LCHF equivalent?
Paul Mather: Yes, there is an alternative to carb-loading for athletic performance. I have not looked closely at it since my days as an endurance athlete are over, but Mark’s Daily Apple has made several good posts about it, and is a reliable source of information about all things athlete.
To Paul Mather:
You’ve heard of Chris Froome, right? He’s won four Tour de France races, and attributes his success to eating a LCHF diet. It made him a fat burner, instead of a sugar burner, which means he’s never out of fuel (energy). He carries it around with him, in his remaining body fat.
If you eat too many carbs, you’re unable to burn body fat. So you can’t access it for energy.
Thanks Gary. Mark’s Daily Apple looks really interesting but ever so slightly scary! I will take a look though – it may be that there is some good stuff under that health guru sheen! Are there any other websites/blogs that people have found useful for a LCHF lifestyle change?
Paul Mather: I was thinking in terms of athletic performance because you said you are a cyclist. From a medical perspective, both Dr. Tim Noakes and Dr. Jason Fung are good in regard to the positive physiological and practical effects of carb restriction. Dr. Mercola has a very large archive of good information about health and fitness. There are more, but I can’t think of any at the moment.
Joe: I have heard of Chris Froome! Being a Brit myself – and a cyclist – he is a total legend in my eyes! And I had absolutely no idea that he followed a LCHF diet! I shall read up him this evening. What a great inspiration 😀!
Göran, Gary and Joe: Thank you so much for your responses. I have a good deal to research but feel like there is a real opportunity to sort out my health going forward without relying on medication and poor advice. I feel much more positive about my position now which is great 😀.
Unstable plaques (of this blog) vs calcified plaques
I’m still mulling over all this and the possible benefits (I hope!) of calcification of these unstable plaques ready to burst, as commenter Martin Thomason nicely put it in a query:”if calcification of a plaque is a good thing providing stability and reinforcement against “bursting”. Is there another possible benefit arising from calcification.
As follows…
…we know there are areas where plaques do not form e.g.
– veins (unless grafted by a surgeon into a high pressure system) and
– to quote Dr Peter Langsjoen from his June 2018 presentation (I’m cherry picking here): “as you get further out into the arterial tree you don’t see blockages of arteries…you don’t get them in your fingers…you don’t get them in your feet…we also have pulmonary arteries the arteries that go to your lungs. They don’t get this atherosclerosis either cos it’s a low pressure system”.
(I’m not sure if blockages excludes plaque formation)
If there are areas where you do get damage/repair e.g. coronary arteries, once damaged/repaired is that it? Are there no further places for new plaques to develop?
Do the coronary artery calcium (CAC) scores ever max out, implying/meaning there is nowhere left for new unstable plaques to develop? Based on scores posted over time by commenters on this website they do seem to keep nudging up, often into the thousands.
Essentially, kinda hoping that when you get to a certain high CAC score the damage is done and no further worry about new plaques, because they don’t appear in certain areas.
My CAC result only contained the score with no details on arterial coverage e.g. your CAC is XX and covers 60% of left artery might be better info. I’m sure that info has to be known cos they’ve scanned the area.
Anyone care to share what info they got from their CAC testing, beyond the score?
Thanks.
Malcolm, a query buzzing in my head..I think I read that the CAC score is fundamentally a measure of calcium in the plaque of arteries..But the calcium is also part of the stabilising process in plaque formation..which are therefore inherently less likely to cause a heart attack..So are the CAC scores measuring something beneficial rather than harmful..??? Or have I got this wrongways about ?
If you have a high CAC score you have lots of calcified plaque – which is safer than having lots of unstable plaque. However, the pathway is from unstable to calcified, so if you have lots of calcified plaque you will also have lots of unstable plaque on the way to becoming calcified.
Thanks for that explanation..So is there a method of measuring the level of unstabilised plaque ? And I am also remembering that plaque is part of the body’s own natural healing process for leisons in the cardiac arteries…No plaque formation at all means we die – quickly.
Well. Hopefully no reason for plaque to form in the first place. The development of plaque means that damage > repair. What we want is for repair > damage.
Malcolm I am 71 and I was given a CAC of just over 1000 in November 2016, Most of it in one artery, the left ( ? ) circumflex artery. The cardiologist prescribed an 5 fold increase in the statin dose each day…
Ummmmm ?
After researching and thinking, I declined his medicine. And he then more or less told me to go away & die..
More researching and thinking lead me here. I am still here 18 months later.. …
And yes it is better to avoid the need for the body to heal itself with plaque in the coronary arteries.And if at all possible remove those causes from ones life.
But if it has already happened understanding the role that calcified plaque play is
in preventing a heart future attack is also crucial…
I’m sure you agree with all this. So to end this comment :
Thanks you for this blog, your posts, and for bringing together all the people who are part of this community. I appreciate your energy, time, dedication, thinking and knowledge. It helps us all in our lives…
Thank you
From Jama – Effect of Statin Treatment vs. Usual Care on Primary Cardiovascular Prevention Among Older AdultsThe ALLHAT-LLT Randomized Clinical Trial (More people die when taking statins) No benefit was found when pravastatin was given for primary prevention to older adults with moderate hyperlipidemia and hypertension, and a nonsignificant direction toward increased all-cause mortality with pravastatin was observed among adults 75 years and older. https://jamanetwork.com/journals/jamainternalmedicine/article-abstract/2628971#164877033
Surely on ethical grounds they must have stopped the trial ?.Or at least taken the partients off the statins ?
Randall: There are also EXCEL, which showed an increased AR of 0.3%, and AFCAPS, which showed an increased AR of 0.09. Both of these were lovastatin trials, which appear to show it to be the worst of the bunch.
Out of the box: Another one is Jack Kruse. A fascinating read from time to timme.
I read one of Dr. Nortin Hadler’s books, I think it was the last well patient. He said, there was something fundamentally wrong with “doing violence to the offending plaques” in heart disease. He thought, and showed from statistics, that fooling with the plaque doesn’t do much of anything. This would explain why. I think there are a few doctors over the years that thought CABG and angioplasty should be sent to the dustbin of bad ideas because they mostly don’t work.
https://www.sciencedaily.com/releases/2018/08/180813113309.htm
A research team at the Broad Institute of MIT and Harvard, Massachusetts General Hospital (MGH), and Harvard Medical School reports a new kind of genome analysis that could identify large fractions of the population who have a much higher risk of developing serious common diseases, including coronary artery disease, breast cancer, or type 2 diabetes…………
Here’s how the score worked for coronary artery disease: The algorithm pored over more than 6.6 million locations in the genome to estimate a person’s risk of developing the deadly disease, which is the most common type of heart disease and a leading cause of death for adults in the United States. Of the individuals in the UK Biobank dataset, 8 percent were more than three times as likely to develop the disease compared to everyone else, based on their genetic variation. In absolute terms, only 0.8 percent of individuals with the very lowest polygenic risk scores had coronary artery disease, as compared to 11 percent for the people with the top scores.
Errett,
Thanks for the link. Interesting article. I read it as they’re trying to “model” disease risk based on genetics. Seems like a good concept, but who knows if they’re accounting correctly for the right genes. After all, not all of the high-risk people got CVD (at least at the time of the study) and not all of the low-risk people avoided it.
The article includes this gem:
“Importantly, according to Khera, the people with high polygenic risk scores for coronary artery disease did not necessarily exhibit other warning signs of disease risk (such as hypertension or high cholesterol).”
It amazes me that seven decades after CVD was “officially” defined, there is still no reliable way to predict who will get it and who will not. I largely blame Keys for focusing too much attention on diet and lipids. It’s as though he yelled, “Squirrel!”, and most people still stare at the squirrel.
Thank goodness there a few folks like Dr K who are not so distracted!
No comments since 8/10. Just testing to see if this reflects a blog issue.
Goran: Completely off topic, but since it is related to your field, I thought you’d be interested to know that University of Michigan researchers have developed an alloy which can capture near infrared light, and can be used in photovoltaics.
Well, Gary, I am retired since a couple of years now so I have basically left all materials research. Materials is though an extremely broad field and I was myself very far from the topic you brought up.
Currently in Edinburgh touring with my brood. Picked up a book, Spook Street, by Mick Herron. It’s a spy novel (excellently written) in which the plot revolves around an old spy who loses his memory (and thus becomes a danger). A character asks if he’s taking any medications, and his grandson replies, “Only statins.” I think word is getting out and seeping into the common culture.
I know someone who had exactly that experience. He wasn’t a spy, bu ran a specialist shoe and boot repair shop. He was put on statins and almost lost his business because people would come in and place an order, and he would write down the details and completely forget about it!
I always used to have the impression that when drugs had nasty side effects, the medical profession would gradually realise and the drug would be withdrawn. Now it seems as if that mechanism doesn’t work any more.
Martin Back – “sequence of diagrams showing the natural history of a plaque”
This may be of use in response from a previous comment by you…from a good source too: Fat Emperor Ivor Cummins:
http://www.thefatemperor.com/blog/
The diagram appears at 1min 24 seconds and includes both the rupture and thrombus stage.
I haven’t watched the rest of the film yet but do question Ivor’s written comment about CAC scans being “cheap”. The best I could find for mine was £400.00 and they went a lot higher.
Paul Mather – “extremely high triglycerides”
You may want to read this 2008 post by Dr Mike Eades on the subject:
https://proteinpower.com/drmike/2008/02/04/elevated-triglycerides-are-driven-by-carbohydrate-consumption/
and also this on cholesterol results from Mark Sissons’ Daily Apple website dated 2011:
https://www.marksdailyapple.com/how-to-interpret-cholesterol-test-results/
Bill
Your cardiologist more or less told you to “go away and die”.
You’re not alone – I had similar with them putting the fear of god into me if (1) I didn’t have a coronary device implanted (you bet I signed the consent form lying there at my weakest and most vulnerable) and (2) I’d die if I stopped taking meds – both of which was keeping me alive they said.
I am not medically trained so forgive my ignorance, what causes the clots in the first place? Is it damage to arterial walls caused by free radicals?