10th November 2019
The Blood Brain Barrier
Here I am going backwards in time and space to try and explain, from a different angle, a fundamental problem with the LDL/cholesterol hypothesis. In doing so I hope to again make clear why I am certain the entire process of cardiovascular disease (CVD) requires a complete re-think.
In a medical school long, long ago, on a planet far, far, away, I was part of a small group teaching session on cardiology… Aberdeen 1980, actually. I have mentioned this event before, a critical moment in my life. The tutor was Dr Elspeth Smith, who was researching heart disease at the time. Research that, to my chagrin, I knew little about until several years later, when I began more detailed research into cardiovascular disease.
At one point in the tutorial, Dr Smith stated that LDL (low density lipoprotein) cannot get past, or through, the endothelium. At that time, I hadn’t much of a clue what LDL was, and very little idea about the endothelium. However, something about the intensity of her comment created an itch, one that I have spent very nearly forty years scratching.
I say this because, if LDL cannot get past the endothelium, then the widely accepted, and supposedly primary causal mechanism of heart disease, must be wrong!
Just to remind you that the central mechanism underpinning the ‘cholesterol hypothesis’ has always been that LDL leaks out of the blood past, or through, the endothelium, and into the arterial wall behind.
This then stimulates a whole series of downstream processes whereby you end up with thickenings in the artery wall narrowing the artery – known as atherosclerotic plaques. The higher the LDL level, the faster the leakage? I put a question mark there, because I don’t think I have ever seen this stated explicitly – I suppose it is implied as self-evident.
Clearly, however, if LDL cannot pass through the endothelium – the single layer of cells that lines all artery walls – then the ‘cholesterol hypothesis’ is a busted flush. Which is sort of interesting in a ‘hold the front page’ sort of fashion. ‘LDL hypothesis completely wrong – shock horror.’ Dr Elspeth Smith explains that LDL cannot get through the endothelium. Experts around the world, agree, and look for other explanations for heart disease.
This is a headline that I must have missed.
At this point you may be thinking, how do we get from LDL, and the endothelium, to the Blood Brain Barrier (BBB), which is the title of this blog. Well, are you sitting comfortably? Then I shall begin, at the end, with the blood brain barrier itself.
All doctors are taught there is a barrier between the bloodstream and the brain called the Blood Brain Barrier (BBB). Very few know what it actually consists of, other than that there is a barrier, of some kind, that prevents various things from entering the brain at will.
A barrier between the blood and the brain is critical because the brain is a highly delicate organ, which copes very badly with noxious substances, such as bacterial toxins. Which makes the BBB essential for life. However, it can become a problem if you have, for example, a brain tumour and the doctors want to give you chemotherapy. Because most anti-cancer drugs cannot get past the BBB. Some drugs can, most can’t.
However, a certain number of things must enter our brains, or we would almost instantly die. Glucose, for example. If our brain cannot get enough glucose, we go into a coma, then die. We also need amino acids (the building block of proteins), some fats and vitamins and suchlike.
Clearly, therefore, the BBB needs to be a selective barrier. It must block some things, but allow entry – and exit – of those substances that are required for brain function. Ethanol from malt whisky, for example, distilled from glucose. Well it is essential for my life anyway – in moderation obviously … obviously.
At this point you may be thinking, we are getting further and further away from LDL and heart disease, but please bear with me on this, because it does all come together at the end.
Next question, what is the BBB? The answer is that it is comprised of endothelial cells that are tightly bound to each other, and have a strong support structure underneath called the basement membrane. This membrane keeps the endothelial cells wrapped even more closely, further protecting them from any possible disruption.
This ‘tight’ binding of endothelial cells means that anything that wants to get into the brain must first pass through an endothelial cell. As you may imagine, this is an extraordinarily complicated and tightly controlled process. Substances in the blood cannot flow down a concentration gradient and straight through an endothelial cell.
LDL, for example, can only enter a cell, if there is an LDL receptor on the cell wall. The LDL links onto the receptor and then LDL and the receptor (the ‘LDL receptor complex’) is dragged inside the cell in a process known as ‘endocytosis.’
It does not matter what the concentration of LDL in the blood is – without a receptor, LDL is unable to gain entry to a cell. If it cannot get in, it cannot pass through. This is why the concentration of LDL becomes very high in Familial Hypercholesterolaemia (FH).
In this condition there is a lack of LDL receptors on all cells in the body, so LDL cannot easily enter cells, therefore the concentration in the blood rises very high.
Proof, if proof were needed, that LDL cannot ‘escape’ from the bloodstream and find refuge in the artery wall, or any other tissue. No matter what the concentration in the blood. Osmosis and/or diffusion of LDL through any cell is biologically impossible.
Therefore, getting back to the BBB, for substances to move through the BBB they first must be ‘endocytosed’ and then need to be shuttled through the cell via an active transportation system. This is known scientifically as ‘transcytosis.’ Literally, transport through the ‘cytoplasm’ where cytoplasm is the name for the jelly-like substance that fills up cells.
Once the substance has been transcytosed through the cell it must be ejected out through the cell membrane on the opposite side. Another complex process known as exocytosis.
Not everything needs a receptor to enter a cell. However, nothing gets in without the cell controlling the entry and exit. Even individual ions (charged atoms), tiny as they are, must pass through ‘gates’, or channels, to get into a cell. Calcium, sodium, potassium etc.
Their passage is carefully monitored and controlled. If this were not the case, you would instantly die. If a cell loses control of its internal environment it is either dying – or dead. See under, hyponatremic encephalopathy (for those with a scientific bent).
It has been argued that LDL molecules do not need to pass through endothelial cells, they can simply slip through the ‘cracks’ between endothelial cells. I have seen this argument used as to why ‘small dense LDL’ can cause CVD because, in this form, it is small enough to get through the cracks between the endothelial cells.
The problem with this hypothesis is that, first, small dense LDL is almost exactly the same size as normal LDL. Second, and most important, there are no cracks, or gaps, between the endothelial cells in our arteries – or the BBB. Endothelial cells in large arteries are bound together very tightly indeed. They are linked together by zips, buttons, and super-glue, then welded to create what is called a ‘tight junction’.
You can Google ‘tight junctions’ under ‘images’ to see how complex they are. There are over twenty protein bonds, sealing any gap shut. Tight junctions are so tight that they, too, can prevent the entry and exit of single ions. So, there is absolutely no way through for LDL here, either. For a quick size comparison, if a human were the size of an ion, an LDL molecule would proportionately be around the size of a super tanker.
In short, the idea that LDL can simply leak through the endothelium and into the artery wall behind requires that several key mechanisms – required for life – do not exist.
As I hope you can now see, Elspeth Smith was quite correct. LDL cannot pass through the endothelium. At least it cannot pass through a healthy endothelium, and nor can anything else either. Unless, unless the endothelium enables its passage.
Complication number one – yes, there is always a complication.
As blood vessels get smaller and smaller, like the branches on a tree, the endothelium changes dramatically. As arteries shrink down to became arterioles, then capillaries, the endothelium is no longer an impenetrable barrier.
In these very small blood vessels, the endothelium develops holes (fenestrations). Gaps also appear between individual endothelial cells, and the supporting basement membrane becomes loose. What you have is more like a sieve than a castle wall.
This ‘sieve like’ quality allows substances to move in and out of arterioles and capillaries, almost at will. Which, of course, makes perfect sense. There is little point in blood arriving at, say, the kidneys, where various waste products are removed, if it was all stuck behind an impenetrable endothelial barrier. The blood would flow into your kidneys, then flow out again, unchanged. This is not a good recipe for life.
So, yes, in the very small blood vessels, the endothelium allows the free passage of substances. But absolutely not in the larger blood vessels. If the blood simply leaked out as it passed through larger blood vessels, it would never reach the smaller blood vessels, nor get back to the heart again. It would be like having a garden hose that was full of holes along its entire length. Nothing would reach the sprinkler head.
Anyway, bringing some strands together here, the endothelium lining the large arteries has the same impenetrable structure as the endothelium lining the BBB, and therefore represents a barrier. Substances just cannot leak through this – and that includes LDL.
But can things be transcytosed through? More specifically, can LDL transcytose through it? Because, if it can, this would be a possible mechanism in support of the cholesterol hypothesis. Although, once again, you have to ask the question, why would the body have a system for actively transporting LDL through the endothelium and into the artery wall underneath. What would be the purpose of such a system? To cause atherosclerosis?
The mystery of this question is further deepened by the fact that the larger blood vessels in the body are supplied with nutrients via their own, small, blood vessels known as vasa vasorum. Literally, blood vessels of the blood vessels. These are arterioles, and capillaries, that penetrate/permeate the vessel wall.
These very small blood vessels, lying within the artery wall, have fenestrations (holes) and loose junctions that allow the free movement of LDL – in an out of artery walls. So, any LDL in the bloodstream can quite easily enter the artery – and exit the artery (and the veins) – without having to cross any barrier at all.
Which raises a further conundrum for the cholesterol hypothesis. Why would LDL that enters the artery wall, via the vasa vasorum, cause no problems. Whilst the LDL – that is claimed to enter the artery wall by forcing itself past the endothelium – creates atherosclerotic plaques. Same artery wall, same LDL.
Which then raises another question. Why do atherosclerotic plaques only form in artery walls? Why not everywhere else, within every other organ and tissue in the body. If LDL, once it leaves the bloodstream, is so destructive, acting as the focus for plaque development, why doesn’t it cause plaques within the liver, or the kidneys, or the muscles, or the gut. Only, it seems, in artery walls. [Please don’t say xanthelasma, until you have thought very carefully about it]
Strange…
But to get back on track. I wanted to see if I could answer a final question. We know that LDL cannot simply flow through endothelial cells, nor can it squeeze between non-existent gaps. But can it be actively transported through? Because, if it cannot, then this is the final nail in the cholesterol hypothesis. There is, literally, no way past. Elspeth Smith was quite correct.
[Other than via the vasa vasorum, obviously. However, veins have more vasa vasorum than arteries, so this if this is the route for LDL to enter blood vessel walls, then veins should have more atherosclerosis than arteries, which they do not. In fact, veins never develop atherosclerosis – ever.]
So, deep breath.
I wanted to know if LDL could get past the BBB. If not, then it could not get past the endothelium in the larger arteries either, end game. This is the sort of question to which you would think there should be a straightforward, yes or no answer. It took me a long time to find a definitive answer.
I did know that the brain manufactures its own cholesterol, because cholesterol is absolutely vital for brain function. Neurones are wrapped in myelin/cholesterol sheaths. New synapses have a very high proportion of cholesterol in them, and animal work has shown that – without cholesterol – new synapses cannot be made.
‘Brain cholesterol accounts for a large proportion of the body’s total cholesterol, existing in two pools: the plasma membranes of neurons and glial cells and the myelin membranes Cholesterol has been recently shown to be important for synaptic transmission, and a link between cholesterol metabolism defects and neurodegenerative disorders is now recognized.’ 1
This ‘brain’ cholesterol is synthesized in support cells, known as glial cells. These cells surround neurones and nourish neurones, and the cholesterol is transported about in its own lipoprotein called Apo E.
So, on initial analysis, it did seem unlikely that the brain would have developed its own, specific, cholesterol manufacturing capability if it could simply absorb it from the bloodstream. As it turns out, and as I eventually discovered, the brain cannot absorb LDL from the bloodstream.
‘… the blood brain barrier (BBB) prevents the uptake of lipoprotein-bound cholesterol from the circulation.’ 1
In quick summary here, the brain requires cholesterol, yet the BBB prevents it from entering the brain. Which means that an intact endothelium can completely block the passage of LDL Which means that LDL cannot get past, or through, the endothelium. Elspeth Smith was quite right.
But what did she think caused CVD, or atherosclerosis, or atherosclerotic plaques – or whatever term is currently in vogue? Well, this is one thing that she wrote about the matter:
‘After many years of neglect, the role of thrombosis in myocardial infarction is being reassessed. It is increasingly clear that all aspects of the haemostatic (blood clotting) system are involved: not only in the acute occlusive event, but also in all stages of atherosclerotic plaque development from the initiation of atherogenesis to the expansion and growth of large plaques.’ 2
She believed, as I have been trying to outline for a few years now, that to start atherosclerosis, you need to damage the endothelium, then a blood clots forms, then we are on the pathway to the final occlusive thrombosis (a blood clot that completely blocks an artery).
She believed, as I believe, that LDL has no part to play in this process. It does not, because it cannot. If you believe in the ‘thrombogenic’ hypothesis, you cannot believe in the LDL hypothesis, and vice-versa.
Which hypothesis is correct? Well, it is certainly true that the LDL hypothesis is currently in the ascendancy. But science is not, thankfully, a popularity contest like Strictly Come Dancing. Science is built on facts. Well, it is eventually. The fact is that the LDL hypothesis requires a central fact to be true but which can be proven to be wrong.
Elspeth Smith proved it to be wrong over fifty years ago, but no-one was listening. She was a hero, and I intend to do all that I can to ensure that it is her name, not that of Ancel Keys, that will echo through the history of CVD research. Because she was a true scientist. Whereas he….
Next time, why LDL also cannot damage the endothelium.
2: https://www.sciencedirect.com/sdfe/pdf/download/eid/1-s2.0-0049384894900493/first-page-pdf
Dr. Malcolm Kendrick 
Will catch up later
Thanks. Before I have even read it, but it is to keep track of the comments, which are such an important part of this community that you have created.
Thank you. This is so interesting. Makes me question again why I didn’t follow a medical career. Sue Anspach
On Sun, Nov 10, 2019, 9:53 AM Dr. Malcolm Kendrick wrote:
> Dr. Malcolm Kendrick posted: “10th November 2019 The Blood Brain Barrier > Here I am going backwards in time and space to try and explain, from a > different angle, a fundamental problem with the LDL/cholesterol hypothesis. > In doing so I hope to again make clear why I am certain the” >
Thank you for another great post.
A new post to feast on! Hurrah! And what a post. Thank you. Something to really get my teeth into.
Thank you for this great knowledge indeed – now, as always, “popularly” revealed on this blog!
Do we need to doubt the “corruption” behind the resistance from the medical establishment to endorse such obvious science?
Wow! What an interesting and well-researched article.
Quick question.
Can LDL get through the endothelium if it is damaged by early-stage scurvy. such as might be the case if the diet is deficient in vitamin C?
Also;
What is the mechanism by which haemorrhagic viruses cause bleeding through the epithelium, and can this mechanism occur in chronic disease without causing fairly immediate fatality as in Ebola/Black Death?
And;
Does the mechanism involving zonulin which the body uses to ‘flush’ the bowel of bacterial infections by loosening tight junctions there, have any relevance to the epithelial tight junctions?
Exotoxins can directly attack the endothelium and cause problems. For example, in meningococcal septicaemia, death is due to endothelial damage, widespread coagulation (disseminated intravascular coagulation) DIC. Many/most infectious agents target the endothelium.
@Malcolm , what about apoE4 genotype?
APOE variant, is known to raise levels of circulating cholesterol, particularly low-density lipoprotein (LDL) and they say it raises the risk for Alzheimer and heart disease.
How is it possibile, if Ldl can’t pass the endothelium?
I am not sure. I find the evidence in this area highly confusing and unclear.
There is no strong evidence that carriers of “ApoE”, ApoE isofrom e4/e4 and e3/e4, have higher LDL Cholesterol (LDL-c).
“among the Framingham cohort study with a large number of participants, LDL Cholesterol is the same in ApoE isoforms e4/- carriers and in the isoform e3/e3 carriers.”
“Elosua et al.(1), who investigated the association of APOE genotype with carotid atherosclerosis in men and women in the large Framingham Heart Study, concluded that “APOE4 genotype was significantly associated with a higher ICA IMT (carotid intima-media thickness) only in diabetic men” https://nneandersphysiologicalliteracy.wordpress.com/2019/05/16/debunking-rhonda-patrick-phd-on-apoe4-apoe-e4-and-ldl/
I agree with you .
But I suspect that Apoe story is used to scare people and to justify the cholesterol theory and statin madness.
Chris,
It’s understood that normal constituents of blood include LDL. Also, the cell wall of red corpuscles is largely made up of cholesterol. So, when a clot is formed at an injury site – such as arterial endothelium damaged by sickle cell disease, rampant high blood pressure, whatever – and when that clot is then covered by new endothelial cells by the endothelial progenitors always circulating with the other blood constituents, a certain amount of cholesterol will be found in that clot which is now situated within the arterial wall.
It’s not that LDL gravitates to the site, it’s just that it’s a normal blood constituent that’s there when that blood clots.
Those progenitor cells also differentiate into macrophages that begin busily cleaning up the clot detritus.
I think I have this right.
Dr Malcolm?
JD
Excellent summary of what I have learnt from all 67 Heart Disease lectures by “our” Doctor
Thanks
And thank you Doctor K
Great stuff
Why if Elspeth Smith taught this 50 years ago, is it totally neglected now?
Have their been any efforts made to demolish it as a theory?
Findings – even the most crystal-clear and indisuputable – are generally ignored if they don’t fit the prevailing paradigm.
I think of scientists and doctors, in this respect, as being like birds building their nests. They pick up various bits and pieces of vegetation (and anything else), and fit them into the nest if there is an easy way to do so. Otherwise they discard them, and have immediately forgotten them.
Cailtin Johnstone has brilliantly summed up this tendency, for instance here: https://caitlinjohnstone.com/2019/02/04/dissidents-must-understand-the-difference-between-fact-and-narrative/
Roughly speaking, I think her view is that – psychologically speaking – narrative always beats fact.
Thank you very much Dr Kendrick for this clear and evident explanation.
Vladimir Subbotin has published in 2016 an interesting article you probably know about the way cholesterol enters the artery wall: URL=https://static1.squarespace.com/static/52faa95ee4b0b0a74811f732/t/576ed362b8a79bc10875b866/1466880934734/2016+Vladimir+Subbotin+Paper+-+ATHERO+.pdf
Many thanks again, Dr Kendrick. My brain followed your wonderful article by forming lovely coloured pictures of all the components in this fascinating explanation.
As you are aware, over the years us mortals have been plagued by our blood profiles being (wrongly) interpreted by the labs, and ultimately pestered to take statins. I have mentioned that in this last year neither my endocrinologist or GP gave hinted at discussing lipid results deemed on the printouts as “outside normal limits”. Indeed my latest LDL measurement would have caused great consternation in years gone by, but not a mention this week. Interesting, eh?
Thank you
Thanks Malcolm ! I think you have sorted that issue !
Thank you Dr Kendrick
Amazing blog, you truly are the gift that keeps on giving
Kind regards
Roger A
We humans seem to have a very strong penchant for thinking in analogies—a comparison between two things, typically for the purpose of explanation or clarification. Analogies often lead to insight, however they may obscure fine details. I enjoy your adventure in the sea of details.
Still struggling with role of fatty streaks in arteries.
Fatty streaks do not become atheroscelerotic plaques.
The precursors of coronary atherosclerotic plaques in subjects up to 40 years old.
Velican C, Velican D.
Abstract
The onset of coronary atherosclerotic plaques was investigated in 400 selected cases aged 1–40 years. During childhood the atherosclerotic plaques developed on their own, in preexisting branch pads or cushions. During adolescence the atherosclerotic plaques developed on their own, in both branch pads or cushions and thickened intimas. In young and mature adults the thickened intima became the main site for plaque histogenesis, whereas the role of branch pads or cushions decreased significantly. In mature adults incorporated microthrombi were accidentally involved in plaque development. In both branch pads or cushions and thickened intimas the atherosclerotic plaques developed through several stages including: histolysis, followed by nodular proliferation of smooth muscle cells (prevalent during childhood), insudation (prevalent during adolescence), accumulation of lipid-filled and foam cells (prevalent during early adulthood) and necrosis (prevalent in mature adults). Likewise the coronary fatty streaks developed on their own, through several stages, from early to advanced lesions. We were unable to reveal the conversion of fatty streaks into atherosclerotic plaques the two types of lesions occurring as unrelated pathological processes.
Dr. Malcolm Kendrick, thank you for the reply. I was searching for info about the composition of arterial tunica intima and found this reference that answers many questions about plaque initiation.
https://academic.oup.com/cardiovascres/article/103/4/438/2931038
The complexity of cell composition of the intima of large arteries: focus on pericyte-like cells
Dr. Malcolm Kendrick, fatty streaks again
I agree with the Velicans that fatty streaks cannot be transformed into plaque. In vitro studies could prove this. This is not proof that fatty streaks are not involved in fibrous cap formation. Whatever causes fatty streaks can cause other problems.
I remember having read somewhere that “fatty” streaks have the colour of fat but contains none. De Lorgeril maybe (another contrarian, I know ).
contain, not contains , sorry.
The book I read about the fatty streaks not being fat (gobsmacking, isn’t it ?) is de Lorgeril’s “How to prevent myocardial infarction and CVA”, chapter 4 how do arteries shrink, the case of atherosclerosis.
This chapter presents the theories on atherosclerosis and plaque formation.
Unfortunately for many there is no English translation of this French book.
The googlish for the appropriate section (excerpt, I corrected the ugliest translation errors,) :
“The very early lesion, first, that some call the fat streak. What is that ? When performing autopsies, including on young people, babies, and even fetuses, we can observe fatty streaks. These are white streaks visible almost to the naked eye on the inner side of the artery. These streaks are not fat; they are infiltrates of white cells, the leucocytes. Why do we say fat when there is no fat? I do not know ! What are these leucocytes doing here? Since the leucocytes in question are repairers, we can assume that they are there to repair the artery which, during development, or because of the traumatisms of the arterial dynamic (pressures up to 200 mm of mercury), has need to be repaired continuously. Researchers have studied arteries taken at random from hundreds of rather young people who died of non-cardiac causes in Japan and the United States. They found on both sides of the Pacific exactly the same frequency, the same distribution, and the same morphological aspects of fat streaks. These fat streaks are therefore not a causal factor of infarction since the Japanese have very little heart attack and the Americans a lot! On the other hand, experimental models can reproduce these fatty streaks in arteries. French researchers have shown that by treating animals with female hormones (estrogens), fatty streaks could be removed. Estrogen – prescribed to women who are deprived of them i, are known to increase the risk of heart attack. These fatty streaks are therefore not (or little) involved in the infarction.
So dont damage your arteries… Don’t do heartbursting exercise… !!
bert
Rather, try to keep blood pressure down – stress busting meditation & plenty of rocket & beets for Nitric Oxide production
Maybe a bit simplistic but i’m trying it
Until we have better detailed advice, I would suggest:
1. Eat and drink healthily. Plain animal and vegetable foods, unprocessed and home cooked. No extra sweeteners, no vegetable fats or oils, and if possible no grains. Eat once or twice daily, and if possible fast for at least 18 hours in 24.
2. Sleep well. At least 8 hours (of actual sleep) per night on average – more is good. If you can sleep, you should. If you have had enough sleep, you cannot go to sleep.
3. Enough exercise of any kind you like, from gentle walking though games like tennis and football to running, gymnastics, or even weight lifting. Probably a minimum of 2-3 hours walking per day is ideal, but less helps. Walk 20-30 miles, and you’d be amazed how few problems you have left. (Finding something to sit down on is the most important).
4. Avoid mental and emotional stress (as far as possible).
5. Avoid pollution as far as possible. (This is easily the hardest recommendation).
In short, the best route to relative health is to get back as close as possible to the way of life for which our ancestors evolved through several million years. We have moved very far away from it.
Very nice, Tom. The only thing I would add is to create or recreate connections to family and friends and/or volunteer. That is, do something social.
Great post Dr. K.
Dr. Elsbeth Smith has not yet been thrown off Wikipedia but there is no mention of her heretical views.
https://en.wikipedia.org/wiki/Elspeth_Smith
She is in the best of company: including Dr Kendrick, Craig Murray, C.J. Hopkins and many others.
See, e.g.
https://www.craigmurray.org.uk/?s=wikipedia
Fascinating, Marjorie, so I followed up.
Her Wiki entry is very slim and so probably escapes censorial review, but she gets a lot of airtime in this report which I tracked down by digging down the rabbit hole of Reference 2 on her page. Here is the link to the (nearly) 200 page report of a symposium in which she took part.
Click to access 44850.pdf
(NB you might have to copy and paste that link – doesn’t seem to work directly, but the remedy does.)
I have only skimmed it so far, but one question caught my eye which is directly relevant to this blog:
‘Oliver: Now I am sure Elspeth Smith will have a view about the infiltration of
the arterial wall.’
…. and what follows is a very long response from the lady herself.
Sadly it seems that she died in 2017, but I am sure that Malcolm will keep her memory alive.
Another step in my education. Thanks again for a great blog
Thank you Dr Kendrick
Another entertaining and informative explanation in support of your Hypothesis
I found your recent discussion with Ivor Cummins so engaging that I had to listed to it a dozen or so times, however one area of the whole Atherosclerotic process that I haven’t been able to understand or get my head around is how the plaque becomes calcified, i.e. at what point does calcium feel it has to join the party and why? If you could point me to one of your many blogs that explains this that would complete the picture for me.
Most areas of damage in the body become calcified over time. Scars turn white (due to calcuim deposition). Quite why the body ‘calcifies’ areas of damage is not clear. In the most extreme form people have myositis ossificans, a condition whereby damaged muscle turns to bone. As you can imagine, this does not end well. There is a strong relationship to a lack of vitamin K. Warfarin, which is a vitamin K antogonist, and used to prevent blood clotting, greatly increases the rate of calcification of atherosclerotic plaques. Vitamin K supplementation can reduce/reverse calcification. Whether or not calcification is a good thing, or a bad thing, is not entirely clear.
Hi Doctor
I assume for clarity that you are referring specifically to vitamin K2 (menaquinones) rather than K1 the warfarin antogonist. Correct?
Your comment above about whether or not calcification is a good thing or bad thing caught my attention. I know you can’t answer medical questions, but maybe you can point me in the right direction. I’m 72 years old and about as healthy as one could be. My resting heart rate is around 54, my BP averages 115/75, I weigh the same as I did in high school, I sleep well and eat well, there’s no history of heart problems in the family for many generations back, and so on. I still climb mountains here in Colorado and push my heart very hard for hours at a time with no ill effects. On my own, after my sister told me she had a calcium score of zero, I decided to get my calcium score. I came out with a score of 1848! Everything I’ve read thus far says I should be very concerned. It just doesn’t make sense to me. Could you point me anywhere that might ease my concern? Of course, my doctor wants me to take statins but I want no part of them. Thanks.
I understand this is a question for Dr Kendrick and I apologize for interrupting. But you may be interested in looking into Dr Ames’ Triage Theory. He proposes that living organisms will triage problems to prevent acute issues from arising. Calcification of an artery may be a defense mechanism to prevent artery bursting.
Sasha: Do you mean to prevent the plaque from bursting?
Sorry, yes, I misspoke. According to Dr Ames, it’s a mechanism to maintain the integrity of the blood vessel. And, possibly, to stabilize the plaque. But if I remember correctly, he spoke primarily of preventing bleeding.
rhHanson
I think the Doc you want to reference is Dr Gerber who also hails from Colorado (outside Denver I think)
He was, if my memory serves me correct, the doctor who says he has lowered his calcium score to zero. The key factors were vitamin D, Magnesium, and vitamin K2 (mk 4 and 7). This combo moves calcium from soft tissues (=bad) to the bones and teeth (=good).
Ivor Cummins has a number of talks (youtube); 1 of which is about calcification.
Don’t panic just yet.
Apparently, the rate of change in the score is more critical than the score itself.
rhHanson
some references to get you going:
Dr Gerber
Dr Gerber, Dr Malhotra, and Ivor Cummins
Cummins and Calcification
Please do you own research.
rhhanson,
I’m 75. I had my CAC done a few years ago, just to be sure. It was 1640.
As with you, everything else that might have indicated CVD – but for some rhythm issues – was perfectly fine.
I’ve learned to question the “solid predictability” of CAC scores and I don’t let it worry me any more.
Calcification can come on from various causes such as a past infection that might have attacked your endothelial cells systemically. There are any number of diseases that will do this. Just figure to yourself that calcification is probably the last phase of healing.
Thanks for your perspective.
Is it possible that supplementation with vitamin K2 could reduce calcification in DCIS?
It is certainly possible. I am still uncertain if it achieves anything.
@rhhanson: You might want to watch this video of a lecture (one of his last) by the late Linus Pauling:
I wasn’t able to re-watch it due to bandwidth problems where I reside, but if memore serves well he his advice to take 10-12 g vit C + 3-5 g L-lysine per day was a big help to one of his colleagues.
Harry de Boer,
Thank you for this link to this late talk of one of my true “idols”; Linus Pauling. It is a really great talk of an experienced scientist.
rhhanson
I read an article earlier this year which may be relevant to your question to Dr Kendrick regarding calcification. The article was headed:
“Prevalent CAC common in high-volume endurance activity athletes, but no long-term risk for mortality”
It went on to state:
“Men who participate in high-volume endurance activity — equivalent to running approximately 6.5 km per day or 250 to 300 minutes per week — were likely to have prevalent coronary artery calcification, but no increased risk for all-cause or CVD mortality at long-term follow-up, according to new data published in JAMA Cardiology.
“The key question addressed in the present study was whether the presence of high CAC associated with high levels of exercise training as typically practiced by masters marathon runners is associated with greater mortality. For this question, the answer is clearly no,” Laura F. DeFina, MD, president, CEO and chief science officer of The Cooper Institute in Dallas, and colleagues wrote.”
The article provided these references (sorry, I don’t know how to provide this as a link):
DeFina LF, et al. JAMA Cardiol. 2019;doi:10.1001/jamacardio.2018.4628.
Lavie CJ, et al. JAMA Cardiol. 2019;doi:10.1001/jamacardio.2018.4647.
Thanks for the info. I read those articles you referred to, at least the synopsis of the articles. I’m not sure I fall into the category of a “high volume activity doer” but I do work out just about every day and have been doing so all my life. My heart and circulatory system seem to be in great shape. I’m a little disturbed that a high CAC score is considered >100AU where my AU is greater than 1800, but there’s no sign of blockage in my coronaries. I really don’t want to go on statins so I think I’ll just keep on taking care of myself the best I can.
Enlightening! Looking forward to the sequel. Thank you for your work.
Interesting post as I have wondered for some time if there could be a link between the high level of prescription of statins and the increase in dementia / Alzheimer’s. I am not from a medical background (trained as a physicist) but I had read that the brain requires a high level of cholesterol. Could statins be interfering with how the brain manufactures cholesterol?
I was prescribed Atorvastatin with Metformin when diagnosed with type two diabetes. After a month I was sure I had dementia. I ‘lost’ all my songs, and have had to relearn them, and walked around in a daze, did all the Christmas shopping twice, lost the car in the car park – I contemplated suicide, but then threw away the tablets and have slowly recovered.
Sadly, this is a common story – to me.
It would be interesting to know the difference between people to which this happens and people who do not succumb. I assume this will be Research That Will Never Be Done.
Fascinating stuff. The complexity of the human body never ceases to astound me, and you manage to make it seem not simple, but at least comprehensible. I wish there was an endocrinologist around with your gift for teaching. Or, come to that, a cardiologist who read your blog.
As a fascinated but highly amateur and unqualified reader, I agree very strongly with your remark about the astonishing complexity of the human body.
To the extent that, some years ago, I reached the personal conclusion that it refutes any theory of intelligent design. It seems to me that the body is so complex that it could not have been designed; it could only have arisen through negative feedback, applied mercilessly over millions of years. In short, we are alive only because trillions of previous creatures lived (more or less briefly) and died, so that only the unbelievably complex systems that usually survive are left.
We are bad copies of our forefathers, but were lucky enough to find an ecological niche where we could survive and procreate.
“the body is so complex that it could not have been designed”…
I know what you mean. As a former software engineer, I was often amazed by the vast numbers of complex programs that just appeared suddenly within processors and began processing all by themselves.
>I apologize in advance<
Thank you for yet another thought provoking article. Where does LPa fit in, or is it yet another red herring?
Lp(a) is the lipoprotein that has a causal role in CVD. Because Lp(a) is an important part of the blood clotting system.
Frederica Huxley
This may interest you
re Lp(a) and vitamin C
please do your own research
Thank you!
robertL,
Thanks for the video. Reinforces what Dr K has been saying, with excellent supporting visual aids.
I was already convinced, and have been trying to ingest about 3g of C/day in divided doses, along with K2, Mg, Potassium, l-Citrulline, l-Lysine, and probably a few others.
By the way, Petro D. from Hyperlipid has a series of blog posts on Lp(a):
http://high-fat-nutrition.blogspot.com/
See “liproprotein(a)” in the list on the right.
I would be very surprised if some cardiologists didn’t read this blog.
Perhaps they keep quiet about it though!
I know that they do, and some of them contact me off-line.
If small dense LDL was able to penetrate cracks between endothelial cells, surely the artery walls would become uniformly infused with cholesterol. There is no mechanism to explain why cholesterol would congregate in plaques in some places and be absent in others.
Almost managed to read this without backtracking. (The effect of years of statin abuse slowly wearing off)
One thing did raise my curiosity, yours; “I wanted to know if LDL could get past the BBB. If not, then it could not get past the endothelium in the larger arteries either”
But the BBB is the stronger defence system is it not ?
Martin – this was intended for the learned Doctor. That’s not to say you don’t hav an answer !
I don’t think that it is. However, I can’t really prove it. I just know that if you have endothelial cells with tight junctions, supported by a sub endothelial layer, they should act the same way. I have never seen any evidence that the endothelial cells lining the BBB are different, in any way, from the endothelial cells lining the larger blood vessels.
Thank you
Somewhere recently I read or saw in a video that the weak spots where injury occurs, and thus cholesterol “patcing” sets in is at the branchings of the blood vessels. A turbulence is created in the plasma flow and this vibratory hammering weakens the tight junctions.
Another post above asks the question about low level scurvy and Vitamin C. According to the Pauling Rath thesis vitamin C is necessary for collagen to make up the web of tight junctions, and when we are low (less than 3000 mg daily C; but Pauling says animals our size would make on average 10 grams daily! so all of us are very low) . The tight junctions are weakened and that is how the barrier goes down.
I asked Dr. K. before to comment on the Pauling-Rath thesis; did I miss his answer? If Pauling is right, the solution is simple. PLEASE comment Dr. K.
I have written several blogs about the Pauling Rath hypothesis.
Good point – and there would be more of it in veins.
I think it was on Peter’s blog hyperlipid that he posted photomicrographs of an arterial wall with the cholesterol all far away from the endothelium. Obviously the pressure of all that LDL in the blood causes the cholesterol to squirt through the endothelium so fast that it ends up at the back wall and is never seen in the gap in between. Or, of course, not.
chris c, to depend on weak tight junctions for delivery of LDL to cells appears to be the wrong hypothesis
Love it.
I try to follow with personnel interest [Apoe 3/4 and high cholestrol] and understanding your posts but purely by coincindence have also just finished reading the following–https://peterattiamd.com/heart-disease-begin-tell-us-prevention/ Quite confusing but would like to hear your thoughts?
Martin Hunt: according to Peter Attia-
“To reiterate: atherosclerosis development begins with plaque accumulation in the vessel wall, which is accompanied by expansion of the outer vessel wall without a change in the size of the lumen. Only in advanced disease, and after significant plaque accumulation, does the lumen narrow.”
The confusing part is that there are at least two ways to initiate lumen narrowing with both possibly operating at the same time.
BAD CHOLESTEROL HYPOTHESIS: a slow steady progression over decades > oxLDL, foam cells, tunica intima thickening, angiogenesis via vasa-vasorum, necrotic cores, smooth muscle cell migration, rupture of capillaries leading to plaque formation
ENDOTHELIAL DAMAGE HYPOTHESIS: the quicker route to plaque formation initiated by loss of glycocalyx > apoptosis/necrosis of endothelial cells, coagulation factors, Lp(a), tunica intima thickening, angiogenesis, multiple plaque layers
CELL VIABILITY HYPOTHESIS: loss of cellular energy (ATP) > the corn oil route to plaque formation, accelerated apoptosis of endothelial cells. Many factors can upset mitochondrial ATP production.
Bottom line: no need for LDL particles to pass through the endothelium.
What a wonderful post.. really appreciate your great knowledgeable input Dr. Malcolm
https://academic.oup.com/ajh/advance-article-abstract/doi/10.1093/ajh/hpz116/5539686?redirectedFrom=fulltext
Endothelial microvesicles (EMVs) have emerged as markers of endothelial injury. However, little is known about their levels in the coronary circulation of acute coronary syndrome (ACS) and stable coronary artery disease (CAD). We hypothesized that ACS patients exhibit a more pronounced increase of EMVs both in the peripheral and coronary circulation when compared with CAD. We also investigated possible associations of EMVs with markers preclinical target organ damage.
Yes, please see
Towards a New Understanding of the Molecular Mechanisms of Cardiovascular Disease
http://www.discoverymedicine.com/Antonio-H-Reis/2019/10/new-understanding-of-the-molecular-mechanisms-of-cardiovascular-disease/
Thanks very interesting explanation—I am going to continue along this line—errett
Did you ever have a chance to discuss your theories with Elspeth Smith?
Sadly, no.
Elspeth Smith = true scientist.
And so are you, Dr. K.
If you’re ever going to find the right answers, you’ve got to ask the right questions.
I love your questions.
Plenty to think about! Thank you
Hi Dr. Malcolm,
If my counting is correct, on paragraph 32, where it reads “and the supporting basement membrane *because *loose”, it should be “and the supporting basement membrane *becomes *loose”.
Thank you very much for your enlightening posts. I’m a Portuguese citizen living in Portugal living with a couple of stents. Contrary to medical prescription, 4 years ago, after the procedure to remove the clot and place the stents, I don´t take statins (just took it in the first month after the procedure) and whenever I visit the cardiologist, like last month, she says the cholesterol levels are fine (like they always have been, prior or after the procedure to remove the clot and place the stents).
Best regards, Victor.
Dr. Malcolm Kendrick escreveu no dia domingo, 10/11/2019 à(s) 09:53:
> Dr. Malcolm Kendrick posted: “10th November 2019 The Blood Brain Barrier > Here I am going backwards in time and space to try and explain, from a > different angle, a fundamental problem with the LDL/cholesterol hypothesis. > In doing so I hope to again make clear why I am certain the” >
Thanks, will have a quick edit.
I’ve never seen anything more completely and beautifully explained! Thank you. My GP commented after my latest blood tests that my cholesterol had gone up. I said, “that’s good” and referred him to your blog.
Great blog, as always! Thank you.
Thank you for this brilliant post about how Malt Whisky is complimentary to endothelial cells, a silver lining and important note moving forward.
I read a hypothesis before that the arteries get damaged (rather than arterioles, capillaries)_because this is where blood pressure is at it highest, therefor its simply a case of mechanical stress. Also, the Q above regarding scurvy and Vitamin C, this never seems to even make it into the conversation with experts, it is a complete dead end?
Thanks for this blog, so much info and so well written that even us layfolk can understand it.
Hi Malcolm
Good article. In case you haven’t seen it, there is a nice little review in nutrition last year regarding inflammation and cvd https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5986484/
Also, teaching first year medical students I noticed that while I taught the metabolism of lipids and the transport of cholesterol throughout the body, in the exam half of them started waffling about bad cholesterol and good cholesterol. If I find out which lecturer taught them that… well a heated exchange would definitely follow. Anyway, these are descriptions or definitions I feel no right thinking scientist or medical practitioner should ever use. Cholesterol is cholesterol. It made me think that much of the problem is that people, including the educated and educators, use such bad terminology that it makes them forget how the system actually operates. They forget that it these are lipoproteins, complexes of proteins on membranes surrounding triglycerides with cholesterol in it. And they forget why ldl is different from hdl, but the reason they are different has nothing to do with the cholesterol in it. These problems are clearly huge since even medical students get it completely wrong. May I suggest that at some point you write a short blog on the transport of lipids and cholesterols again just to inform many readers of your blog what exactly we are talking about?
I agree. It is why I wrote two books. They both explain what cholesterol is, what lipoproteins are etc. I even explain what Lp(a) is, and how chylomicrons transport TGs and cholesterol directly from the GI system, via the thoracic duct, straight into the bloodstream, without passing through the liver. I did do a blog explaining how fat could not raise LDL levels, whereas carbohydrates could.
P.S. I am not an inflammation fan. I call inflammation ‘healing’ which, I realise is not quite true. But with CVD, raised CRP etc. is a sign that there is underlying damage going on, and the inflammation is the healing response in action.
Iman, I agree!
It is a sad fact to note this even among people who should know better.
As far as I remember it was, some thirty years ago, a way for the medical establishment to “get out of the trap” when it was then irrefutably shown that HDL-cholesterol was “good” relating to CVD as they minted this nonsensical terminology “good and bad cholesterol” while there is for sure only one chemical type of cholesterol molecule. As a natural science researcher I loose my respect for the “medical science” when I come across things like this in their proclaimed medical “science”.
Blood clearly gets through the brain. The barrier is clearly an inexplicable (again) medical anomaly..
OBTW the brain does need glucose to function. It does very well on fats, ask anyone on a ketogenic diet.Espicially epiliptics.
I presume you mean that the brain does NOT need glucose to function. Sorry, but that is not correct. It can use ketones for a majority of energy requirement, but not entirely. Without glucose, your brain will stop functioning and you will die. This is simply, a fact.
I am sorry to contradict you but some researchers such as Ben Bikman think that the human brain might not need glucose at all once keto-adapted. I understand that so far there has been no experimental data available proving either hypothesis.
Sorry, but I think this is not sensible. We know, beyond a shadow of doubt, that if the blood glucose level drops too low people enter a coma and die. You can be as keto-adapted as you like, but the blood glucose level will remain at a level sufficient to keep us alive – a level within ‘normal’ limits. When you break down triglcyerides for energy you will release a glycerol molecule. Glycerol is converted to glucose in the liver. So, even if you are feeding purely on fat, you will have glucose being released, sufficient to run those parts of the body that require glucose. I would suggest that no-one attempts to experiment on this area. Get a keto-adapted person, then drive their blood sugar down to zero. I suspect I know exactly what would happen. They would die. There is no experimental data available proving this hypothesis, because the proof would entail killing people. There is no experimental data proving that parachutes prevent death after jumping out of an aeroplane, for pretty much exactly the same reasons.
I understood that cells too small to contain mitochondria, such as the pointy ends of neurons, are the ones that depend on glucose. That’s why the body has several systems to increase blood glucose but only one to decrease it.
chris c: There are cells lacking mitochondria? Never heard that before.
Well red blood cells and platelets don’t contain mitochondria at all, but I think I misspoke – the mitochondria in neurons are all at the fatter end and the long thin end requires glucose to function. Of course I might be wrong, I read it on the internet but I found it a fairly convincing explanation as to why we can replace most but not all glucose with ketones.
The brain uses glucose and ketones , he does need glucose, but evebn on a zero carbohydrate ketogenic diet, the body manufactures glucose (dextrose) : neoglucogenesis. Glucose blood levels are low but sufficient.
Dear Dr Kendrick,
“There is no experimental data proving that parachutes prevent death after jumping out of an aeroplane, for pretty much exactly the same reasons.”
I beg to differ: it depends !
https://www.bmj.com/content/363/bmj.k5094
Lol – report conclusion:
‘Parachute use did not reduce death or major traumatic injury when jumping from aircraft in the first randomized evaluation of this intervention. However, the trial was only able to enroll participants on small stationary aircraft on the ground, suggesting cautious extrapolation to high altitude jumps.’
What a brilliant blog. Thank you. I love how you write, so rigorously academic and yet so light-hearted, assuredly simple despite the complexity of the topic and always with humour and a degree of the dour Scot, self-deprecation at its most charming. I love it. Thank you.
Kate
Kate Berkeley registered Nutritional Therapist and Functional Medicine Practitioner DipION, AFMCP, mBANT, CNHC Kate Berkeley Nutrition Green Farm Edwards Lane White Ladies Aston Worcestershire WR7 4QF
07971664106 http://www.kateberkeley.co.uk
>
Thank you Dr. Kendrick, I appreciate your feedback.
As brilliant as ever. Thank you.
Thanks once again, Dr. Kendrick.
Excellent. Easy for a layman to grok. Please don’t encourage use of Google. They suppress truthful health information.
Presumably arteries constantly suffer little nicks and scratches in the course of daily life. So there will always be a range of small plaques, some growing at new nicks, and some healing at older nicks which are healing successfully.
Is this picture correct, i.e., if you autopsy a healthy individual, will you find these arterial plaques that cause no problems?
Martin Back: I don’t remember where, but I have read of reasonably healthy people dying of old age, rather than CVD, with one or more cardiac arteries completely blocked. They must have had well-developed collaterals.
Citation:
“She believed, as I have been trying to outline for a few years now, that to start atherosclerosis, you need to damage the endothelium”.
Seems very conclusive, since it is impermeable for LDL.
So the really interesting question is:
what damages the endothelium in the first place?
Oxidative stress?
Glycation?
Weak cell membranes because of certain highly oxidizable PUFAs in it?
Maybe the combination of the three.
What’s your opinion?
Please my previous 66 blogs. I have outlined a number of the factors that damage the endothelium. Lead, smoking, air pollution, raised blood glucose, rheumatoid arthritis, angiotensinogen, cocaine, Kawasakis disease, VEGF-inhibitors, bacterial exotoxins, PPIs, lack of vitamin C, hyperhomcystenaemia, etc. etc. etc. etc. As for oxidative stress, if someone can tell me what this is – exactly – I will be most grateful. All animal life requires oxidative stress to function. Unsurpisingly, all animal life has worked out a millon ways of dealing with the free radicals produced by oxygen. In fact, the molecule that is most protective for the endothelium, and overall cardiovascular health, is Nitric Oxide (NO). A highly reactive ‘oxygen’ free radical. As far as humans are concerned, oxidation is perfectly healthy. The entire oxidative stress hypothesis came about because plaques contain ‘oxidised’ LDL (actually oxidised Lp(a)). The reason for the oxidation is that macrophages fire a super-oxide burst at ‘alien’ materials to both kill them (if they are a virus or bactetria) and also to allow them to endocytose the alien material. Oxidised lipoprotein remnants are a sign that the body has been trying to clear up the area of damage.
Dr. Kendrick: Thank you very much for that explanation. We have hope if our macrophages can endocytose plaques. I suppose this can happen unless they get too big or calcified.
When I wrote “Oxidative stress” I had in mind compounds as for example 4-HNE, resulting from the oxidation of PUFAs in the membrane walls, especially linoleic acid (LA). If the membrane wall (cardiolipin) contains higher amounts of LA, and LA becomes oxidized, then we get 4-HNE, which oxidises everything that comes across.
If so, the consumption of LA-containing oils could be – together with higher ROS from carbs – a possible for damages?
Jürgen Wildhardt,
https://www.karger.com/Article/Fulltext/446704
Medicines and Vegetable Oils as Hidden Causes of Cardiovascular Disease and Diabetes
“In this review, we present evidence that statins and warfarin, as well as certain types of vegetable oil, cause both CVD and DM in part through a common mechanism involving the inhibition of vitamin K2-dependent processes. This provides the rationale behind the ob- served positive association between CVD and DM, that is, these substances cause both CVD and DM, resulting in the apparently positive association between the 2 diseases”
“Thus, the data imply that the increase in DM is associated with an increase in car- bohydrate intake, particularly fructose, which is several- fold more reactive than glucose with hemoglobin”
If the “leaking endothelials” hypothesis were correct then HDL particles must all leak out in the first few centimeters of blood vessels. The graph I’m viewing shows the biggest HDL is less than half the diameter of the the smallest LDL (100 A vs. >200 A). On the other hand, if even the smallest HDLs don’t leak out (60 A) it seems there’s no way for giant LDLs to “leak”.
Dr. Kendrick: arteries, veins and LDL hypothesis
https://link.springer.com/article/10.1186/s12938-019-0669-7
Hydraulic conductivity and low-density lipoprotein transport of the venous graft wall in an arterial bypass
“Autogenous vein (e.g., the greater saphenous vein) segments are widely used in vascular bypass surgery to relieve arterial occlusion. Nevertheless, when implanted into the arterial system as grafts, veins will develop a rapidly progressive and structurally diffusive form of atherosclerotic lesions which has been termed as “accelerated atherosclerosis” [1, 2, 3, 4], and this has become the major cause of venous graft late failure [5, 6].”
Vein tight junctions are not very tight compared to arteries. Appears that high blood pressure canl force LDL particles into sub-endothelial space. Oxidized LDL then becomes driving factor for plaque initiation.
Sorry, but high blood pressure forces LDL particles into the sub-endothelial space? How does high blood pressure do this? [When I say that veins never develop atherosclerosis, perhaps I should have added, unless they are forced to act as replacement arteries]. As for vein ‘tight junctions’ not being very tight compared to arteries – do you have any support for this statement?
Dr. K. vein grafts are the exception.
Looks like LDL particles can exit capillaries and end up in lymph. LDL particles are mobile and could accumulate in any tissue (except brain).
https://www.sciencedirect.com/science/article/pii/S000527360700346X
“Large artery endothelial cells, which are exposed to high flow rates, display a well-developed system of TJ. Within the microvasculature, TJ are less complex in capillaries than in arterioles, and even less in venules. As previously mentioned, post-capillary venules are the primary site of leukocyte extravasation, and accordingly, they display a high content of permeability mediator receptors, such as those for histamine, serotonin and bradykinin. At the opposite, the blood–brain barrier (BBB) and the blood retinal barrier (BRB) are particularly rich in TJ and endothelial TJs have been mostly studied in these locations”
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4274060/
LDL and HDL transfer rates across peripheral microvascular endothelium agree with those predicted for passive ultrafiltration in humans
https://www.sciencedirect.com/science/article/pii/S030100821730062X
Lymphatic drainage system of the brain: A novel target for intervention of neurological diseases
Thanks for providing these references. I have been looking at tight and gap junctions for some years. The complexity is amazing. It is also amazing that leukocytes can open up junctions and pass through. I like to think of endothelial cells as modified white blood cells, because I think that is what they are. Their close relationship to white blood cells seems as though it must be key to so many things, but I cannot quite grasp why this would be.
Right, Dr K. As you yourself pointed out, endothelial progenitor cells can differentiate into Big Eaters (macrophages) as needed. Can those endothelial cells become a large white blood cell if they’re not essentially blood cells themselves/
Now, if there is indeed a problem with the tightness of veins as arteries in CABG, how differently does the use of the mammary artery work out in CABG?
Slighty better, I believe. Probably because it developed into an artery in the first place, so will be more able to withstand the higher arterial pressure than a vein.
How does the LIMA perform? I can only say how mine has done. Three cabg’s initially.. 1 failed within a couple of months (overwhelmed by scar tissue) 15 years on, one cabg blocked, and was stented. The other is somewhat occluded. The Lima is still running clear. Coming up to 22 years.
The blood brain barrier is obviously what keeps reality out and thoughts in. See Twitter for details.
Seriously though this is a particularly awesome post.
chris c: Indeed so, an awesome post. I would add that our politicians, in both the U.S. and UK, have a BBB made of thick lead, allowing nothing at all in.
Hear! Hear!
We.re coming up on an election here in the UK: the choice is between Boris the idiot and Jeremy the vegan. I’ve known several people who could do a much better job, but they didn’t want to.
Forgive me fellow bloggers, but I can’t resist! Yes, the General Election is in full swing here in the UK. Jeremy the vegan, as you call him, may not be the perfect solution, but having struggled as a Registered Nurse during the Tory administrations up to 1997, believe me, from May 1997 under Labour, things could only get better, and they did! 13 years of improvement.
Electors need to open their eyes and ears, and take heed from what us oldies witnessed in the NHS back in the day. From 2010, things have deteriorated at a pace of knots to the dreadful state of affairs in our NHS that we experience today.
Thinking, educated electors, should know who not to trust with our Health Service.
Jennifer: Interesting. Here in the U.S. we have something of the opposite situation. We have the Democrats, equivalent to Labour, who have become the corporate party, and very dangerous, indeed, leading the way to censorship of social media not only about vaccine risks, but about all alternative health treatments. The Republicans, equivalent to the Tories, who have always been the corporate party, sound like they have retained their sanity by contrast. Despite what you have heard about Trump, he is no worse than any of his predecessors. He is hated by the political class because he is an outsider who sometimes says out loud uncomfortable truths. What is frightening to me is the level of corporate control being exerted everywhere. The elimination of informed consent for medical treatment is advancing in the U.S., state by state. Many millions died stopping the madness of, among other things, medical experimentation on humans. Thus the Nuremberg Code. This is no longer in effect in five U.S. states, and industry is working hard to make it so in all fifty.
Thanks Gary. History is so important, and we must pay attention to its lessons . It concerns me that the UK political and health systems are heading down the paths of the US systems. I note a blogger today does not like political views being discussed on this blog, but I learn much from your points when discussing health care across the pond. Of course, it is easier to bury our heads in the sand, but Dr K. kindly allows us to voice our opinions in a polite manner.
Jennifer: Yes. History is an essential teacher. A partisan political diatribe I would find offensive here (but wouldn’t censor), but a clear-eyed look at what is going on in our world is always a good adjunct to all the other things we do for our health. The truth is that politics, always a dirty business, has been entirely captured by wealth. Few politicians today actually represent voters, except in local government. Very worrisome are organizations like the EU, WHO, and powerful governments like that of the UK and U.S. This also includes the political parties. This is directly on subject, since the way Medicine is taught and delivered is today completely captured by the pharmaceutical industry, as are governments. Statins have given them immense wealth while doing untold damage and no good at all, and vaccines are expected to reach U.S. $60 billion in profits by 2020, while doing untold damage as well, damage denied by media and government alike, and rarely compensated for.
Jeniffer, I agree with your sentiments that Dr. K. Would probably block posts if they were inappropriate. From time to time objections appear on the CVD blog because “diet” is mentioned. Objections appear because vaccines are mentioned, You name it, someone can probably find a reason to object to it. As for politics, in general we would not be in the situation we are if it were not for politics, and the controllers (lobbyists). So objecting is a bit of an ostrich reaction. Additionally trying to silence someone because they talk about a prohibited subject is symptomatic of the current leftist dogma.
Off topic, but very good for the health: My daughter and I have been laughing hysterically about an event which happened yesterday here in the colonies. A congressman by the name of Eric Swalwell was being interviewed on national TV and appeared to have let what Buzzfeed calls an “absolutely enormous fart.” He denies it, but you can see the facial muscles tense slightly as he leans slightly to the side as the sound erupts.
Jennifer Is any Health Service coping with increasing demands and expectations? I recall on these blogs I think of the words of a cardiologist who reckoned his job was to keep people alive for long enough to die of cancer. Each succes in the health service might b said to b a case of kicking the can down the road and creating more problems that might not needed addressing if nature had been allowed to do it’s bloody business. The aging population will b increadingly demanding of each health service.
Yes I suspect the Tories whatever they say are aiming to sell even more of the NHS to American insurance companies/HMOs who are lining up to buy in.
It’s a vicious circle, wrong dietary policy and things like avoiding the sunshine are giving rise to more disease and more sales of profitable medications.
Either we are forced to accept American low quality food or to give up meat, neither of which will help. What will? I don’t know short of returning to the past before there were “epidemics” of noncommunicable disease.
I like the concept of kicking the can down the road. Of course the reduction in CVD means more people are living to die of other things, and currently to devolve into a half life via Alzheimers which is immensely profitable for the care home industry. And to end up on polypharmacy, again massively profitable. Maybe if the NHS hadn’t spent so much on statins they would have more resources to deal with other things.
Chris C. I agree whole heartedly, you put it so well. As such, I intend to keep my heart as healthy as possible, so off to make my rye/spelt sourdough and annual supply of red cabbage sauerkraut ( thanks to Goren), thus taking a break from politics. Happy everyone?
🙂
chris c: I had no idea they were selling the NHS to U.S. insurance companies. Bad idea. These parasites suck up about 30% of all the money spent here on “health care.”
Read today that BUPA, and other private health insurers, are now emulating their US colleagues by overriding consultants by not allowing certain procedures and medicines to be covered by insurance.
“We have the Democrats, equivalent to Labour”
Gary, this is a common mistake where people equate the Democrats with UK Labour and the Republicans with the Conservative Party. A lot of people here in Australia likewise think Australian Labor equals Democrats and Liberal equals Republicans, or their UK counterparts. Nothing could be further from the truth. Although here in Oz I’m perceived as somewhat to the right of Genghis Khan, in the US my views on most issues would fit comfortably within the Democratic Party. On any particular issue the Democrats would be slightly to the right of the Australian Liberals, our “conservative” party. In any other country than the US the Democrats would be seen as a moderate centre-right party but this is obscured by the overblown rhetoric coming from the Republicans, which IMO is precisely why they do it. For example, Harry Truman was denounced by the Republicans of his day as a Communist. So the man who opposed Soviet aggression in Korea and the Berlin Airlift, initiated the Marshall Plan and founded NATO and the CIA was a Communist. Really?
In reality the Democrats and Republicans resemble the 18th and 19th century UK Tory and Whig parties. The Tories were the representatives of the landed gentry (ie inherited wealth) and the Whigs represented the merchants – the middle class of their day. In the 19th C they morphed into the Conservatives and Liberal parties, with the late 19th C Liberals being supported by the trade unions in much the same way as US unions support the Democrats. (The Labour Party didn’t become significant until working class men in the UK could vote from 1918 on, whereon the unions switched their support) Similarly today the Republicans serve the interests of the plutocrats (particularly since the billionaire-funded Tea Party stooges have largely purged any moderate Republican candidates) while the Democrats attempt to act in the interest of the majority of citizens. I say “attempt” because it requires so much money to run for office in the US, from town council to Congress or the Presidency, that all candidates of either party have to court the rich.
“…a particularly awesome post.”
It really is.
If LDL is unable to cross the BBB and all that vital cholesterol has got to be synthesised in the brain itself then surely interfering with that synthesis with a statin is going to be bad for your brain cells. I have to wonder whether the epidemic of Alzheimer’s we are facing today and a whole host of demyelinating diseases like multiple sclerosis and ALS is a direct result of the widespread dosing of the population with statins. Plus the way statins block the production of a whole host of downstream hormones including estrogen, testosterone, Vitamin D and CoQ10, leading to muscle & bone loss and probably heart failure among other effects.
IMO the medical profession and pharmaceutical industry have been recklessly carrying out a massive uncontrolled experiment on the population at large and we are now seeing the long-term consequences of that.
I fully believe that statins can cause neurological damage.
Dear Dr Kendrick,
I am glad to hear that you believe that statins cause neurological damage. I beg to go one better than you – I KNOW that they do from personal experience. I am still living with a certain amount of hangover. But what do I know? I am merely an uneducated person who has not been trained to respond like Pavlov’s dogs. When they train more curious and thoughtful people to be doctors, and desist from squashing their questions, we shall all be better served.
Yes, I fear they have damaged me. I’m full of regret (and pain)
Likewise statins have damaged me, and I have never taken any. However, if I tell people who are taking them, and who are complaining of aches and pains and brain fog that it might be a good idea to look into it, they pile on the ridicule and say they prefer to trust their doctor. More vitamin C……………..
And if I can go another step, was speaking to a professional type who insisted on quitting statins some years ago, he fully believed that they contributed to depression. Alcohol certainly not a factor, active & sporting.
I assume the statins were prescribed as a precaution.
ahNotepad,
I know your frustration, however, when I am talking to someone about statins, I just tell them my experience – trying not to sound as if I am playing doctor. Quite often what I tell them rings a bell, and then the conversation becomes more fruitful.
I also point out that statins aren’t meant as a short term medicine, so there would be no harm in taking a 3 week statin holiday to see if they feel any different.
Janetgrovesart,
The medical profession has left us on our own when it comes to residual pain after stopping their statins – so it seems appropriate to share potential solutions.
After I stopped that statins, I got a sharp reduction in pain, but I decided to exercise my legs by walking regularly – pushing back until I could do the hills I used to do – using pain killers to reduce the residual pain. I found that doing that, the pain seemed to decrease exponentially over a period of about 9 months. At that point I needed no further pain killers, and I have barely taken one ever since for anything.
Somehow I had the feeling that muscles like being exercised and without it, they might still have been painful.
David – I could walk for England, such a walking enthusiast I am. I clock up 15000 rapid steps most days and fully believe in its overall beneficial effects. It’s the contracted tendons in feet and ankles in the night that get me down. Dreadful when I was taking statins (for at least 10 years) and an abrupt cessation along with the excruciating muscle cramps day and night when I stopped six years but gradually it’s creeping back and the pain is sickening. Just something to live with, I guess. I never realised just how painful old age is. (I’m 77.) Thankfully, it’s only at night so I can walk, walk, walk and play lots of lovely tennis.
Thank you for your post.
JanB
janetgrovesart,
Regarding what you wrote, 15000 sounds a most impressive number of steps per day. Last year, I visited an acupuncturist for sciatica and more recently for osteoarthritis. The story they tell is quite interesting.
First of all, they (or at least the man I visited) knew very well about the problems statins cause – I think they provide the alternate therapists with a lot of business!
More importantly, he claims that most of the cases of these two problems are actually caused by muscles over contracting. Since his treatments work rather well, I am inclined to believe him. The nerve trapping of sciatica is the result of over tight muscles in the back, and likewise, overly tight muscles pull the bones of the knee joint together too much and inflame them as a result.
I found 3 -4 visits seemed to fix my sciatica, and I am hoping this latest treatment will also work well – it has certainly helped already.
My point is, I suggest you visit one of these guys and see what they say. It would also be nice if you could report back on what you find – because I think there are all too many people living with residual statin pains.
I’ve treated statin induced neuralgias with acupuncture and had good results.
@Jerome Salvage
Statins reduce mortality from heart attacks but don’t reduce total all-cause mortality because the deaths from cancer, accidents and suicide increase. Why more accidents and suicides in statin users? A lot of accidents, particularly single vehicle motor accidents, are actually suicides that get misclassified for various reasons and since depression is a major factor in suicide ………
Fortunately I got nowhere near that point, but I can imagine some people may get worn down by the shifting, nagging pain in the muscles and joints – their suicide may not be due to depression as such.
Why more accidents? Let me tell you a story.
My mom was driving with my dad when she asked him ‘what’s that?’ She was pointing to a yield sign like she had never seen one before in her life. She had been on statins for around a year.
It wasn’t long after that I convinced her to ditch them, luckily she recovered her mind and is still sharp going into her 79th year. Thanks to Dr. M.
All my love Dr. M. You saved my mom. Unfortunately my father in-law trusts the doctors more than me…. and yes he has started to lose his mind. It’s weird, he confuses tomorrow with yesterday among other things. What an evil drug statins are.
Hi Doug, I don’t disagree that the brain fog arising from statins could cause accidents. Also “naturally low or therapeutically reduced cholesterol levels may be associated with adverse psychological health symptoms, including depression, aggression, and hostility”
https://www.ncbi.nlm.nih.gov/pubmed/23725920
I’d expect that aggression would manifest itself as reckless driving and a tendency to get into fights, behaviours that can easily prove fatal. All in all, it makes you wonder why the medical profession still pushes statins given all the downsides.
Good to hear about your mom. That generation have been indoctrinated that “the doctor is always right” and it’s often impossible to convince them otherwise. I had that problem with my father and obviously your FiL is the same way.
Doug
I can only describe statin induced brain fog as failure to develop thoughts meaningfully, to develop thoughts in context, thought processes become isolated with the processor finding himself (in this case me) high & dry and stranded. “Now where was I ?”
Extremely annoying and for anyone with ambition, problematic. Listening to Donald Trump’s garble confirms he is stattinised !
I have some money that says you are all wrong. Signed, R Collins
Both my elderly parents have dementia but neither has ever been on statins so it is more complicated than blaming statins for everything
mikezeem, from the work Chris Exley has done, it is more likely aluminium is significant in the occurrence of dementure. To throw fuel on the fire, it may have an association with fluoride in water, though that is a bit of a long shot since fluoride toothpaste is another source of ingestion. Fluoride is a neurotoxic poison. References for this are Stephen Peckham, and Paul Connet.
mikeezeem Over the top comment if U don’t mind me saying. Nobody is blaming statins for everything. Just because u don’t take statins does not give any guarantee that anyone will b free from neurological problems. But the point is that statin users have tendencies towards cognitive issues. Too many users attest to similar symptoms which lessen significantly after “de-statinising”. Too many others attest to muscle pain. Correct me if I’m wrong, but dementia is seen to feature strongly with the elderly, regardless of any medication .
mikeezeem: Indeed, it is more than statins. Professor Chris Exley had published some good work on the role of aluminum in regard to this.
Also glucose and insulin
http://www.tuitnutrition.com/p/alzheimers_13.html
I’m officially confused about LDL.
This blog post from Peter Attia, MD suggests that those of us with high LDL-C are doomed to an early death: https://peterattiamd.com/191110/ (Interestingly, it ties together LDL-C and blood pressure.) I know from other posts and articles that Dr. Attia views high LDL-P as the primary contributor to cardiovascular disease (as I understand his writings; I have no science background).
If anyone with a research or science background can comment on the Attia article, I would greatly appreciate it.
Hi menlo, looks like Peter Attia proved that there is bad cholesterol and it should be reduced. Not a scientist but I like my cholesterol high.
It is well-known that diabetes causes damage to the artery walls as well as damage to the kidneys. Mike Eades writes about a RCT in Pakistan where they treated patients with diabetic nephropathy (kidney failure) with thiamine:
https://proteinpower.com/blog/thiamin-and-diabetic-nephropathy/#more-2869
One of the characteristics of kidney failure is high levels of protein in the urine. Diabetics are known to be low in thiamine. The researchers treated 20 patients with 300 mg/day of thiamine for 3 months, followed by a 2 month wash-out period. The results were spectacular – 7 of the patients had their urinary protein return to normal levels and ALL of the other 13 in the treatment group saw their levels improve, whereas only a few of the control group improved. Clearly the thiamine was enabling healing of the endothelial lining of the kidney tubules.
Given that the endothelial lining in the kidneys is an extension of that of the blood vessels, might thiamine supplementation also help heal the lining of the veins and arteries?
Response to Chris C and Gary Ogden.
My ancient A & P book (last published in 1987) states that erythrocytes do not contain mitochondria.
Jennifer: Thanks. Had to look it up. Red blood cells.
As a nutritionist I like very much to read your posts and comment with my patients. Thank you for your hard work.
Further to my earlier question on zonulin, I have had a trawl of the wonder-web and find that it is a precursor to haptoglobin 2 which is a permutation of haptoglobin 1.
Haptoglobin 1 is thought to have evolved about 800 million years ago and haptoglobin 2 arose in humans about 2 million years ago and is not present in any of our close relatives..
Haptoglobin 1 is involved in recovering haemoglobin released into the bloodstream from damaged RBCs, thereby reducing inflammation otherwise caused to the epithelium by the haemoglobin. Haptoglobin 2 is less efficient than haptoglobin 1, depending on the exact form of haptoglobin 2 it can be up to 5 times less effective than the most efficient form of haptoglobin 1.
Zonulin itself is implicated in celiac disease, causing weakening of Tight Junctions and allowing (e.g.) gluten to penetrate the intestinal mucosa.
It is thought that many immune diseases result from the loosening of tight junctions by zonulin aka haptoglobin 2 precursor, and there is speculation that this loosening of epithelial tight junctions also occurs at the blood brain barrier as people suffering brain cancers have higher expression on haptoglobin 2 and zonulin. Our close primate relatives, without haptoglobin 2 precursor, suffer hardly any immune diseases while we, with zonulin, have racked up over 70.
Zonulin was first identified in 2000 by Dr Fasano at the University of Maryland Medical School.
It shows a high amount of sensitivity to let the intensity at which a teacher makes one little remark decide the direction in which a man’s research will be directed many years later. Hat off!
The ‘obvious’ preference for single malt whisky of the writer is shared.
Typo: …”and the supporting basement membrane because loose…”
That surely must have been ‘becomes loose’?
And: “…so this if this is the route for LDL to enter blood vessel walls…” doesn’t sound completely right also.
I think a complete copy of reference [2] can be found over at sci-hub. Of course the good doctor can’t be caught publishing a link to a ‘pirated’ paper so I’ll do it for him:
https://sci-hub.tw/10.1016/0049-3848(94)90049-3
Hi Harry, thanks for the reference. Was surprised how many times vascular smooth muscle cells were mentioned.
I’m reading an interesting book, one that reminds me of the disagreement with the cholesterol theory. The book is written by Dr. Joel Wallach. The book covers a lot of ground but the part I’ve read up to reminds me of the disagreement with the cholesterol theory concerns a theory on the cause of cystic fibrosis.
Dr. Wallach then a vet physician, came across a deceased primate rhesus money that appeared to have cystic fibrosis. This was thought to not be possible. Only humans were believed to have the condition.
Dr. Wallach then went about showing slides of the pancreas of the deceased monkey to experts in the cystic fibrosis field, not indicating that the samples came from a monkey. All the experts agreed, and signed off on, some ever wrote letters stating the slides showed clear cystic fibrosis.
Then Dr. Wallach went about showing that he had come to believe cystic fibrosis wasn’t a genetic disease. Instead it was a nutritional deficiency disease.
That was going to far. Dr. Wallach’s boss called him into his office and fired him. The boss said, everyone knows cystic fibrosis is a genetic disease. To say otherwise is to cause to many problems for others with careers in the field.
To obtain new employment Dr. Wallach sent his resume out. He quickly landed a new job. The job didn’t last long as a few weeks later he was fired again. This time he was told the NIH told the new company he worked with that if he wasn’t fired the NIH would not provide anymore funds to the company for research. As he was told, due to his disagreement he could never be a vet researcher again.
The similarities between questioning the cholesterol theory and questioning the cystic fibrosis theory had me thinking how religious like the medical field can be. Medical doctors seem similar to the preachers of old that would throw out disbelievers or even burn at the stake those questioning religious doctrine.
I don’t know if Dr. Wallach’s theory is right or wrong about cystic fibrosis. It shouldn’t be a medical crime thought to question and research for new answers. Doing so will step on others toes, but to make progress that needs to occur.
Dr. Kendrick, it appears that what happens in the tunica intima contributes to plaque initiation.
https://www.ahajournals.org/doi/10.1161/ATVBAHA.119.312434
“Smooth muscle cells (SMCs) are the most abundant cells in human atherosclerotic lesions and are suggested to contribute at least 50% of atheroma foam cells.”
“At the onset of atherosclerosis lipoproteins that diffuse into the artery wall are trapped through a charge-charge interaction with SMC-secreted proteoglycans, primarily in the deep intima.7 These trapped lipoproteins are modified and aggregated, becoming a substrate for uptake by the surrounding SMCs. At this stage, monocyte/macrophages are located primarily in the subendothelial region away from the deposited lipids.9 Over time both SMCs and macrophages take up modified lipoproteins to become foam cells independently and interactively.”
Looks like the foam cells would cause thickening of the intima layer and cause formation of new vasa vasorum blood vessels. Smooth muscle cell migration into the intima is also interesting.
Explanation why VSMC migrate and proliferate:
Click to access jbc.RA118.005398.full.pdf
Hyperglycemia induces vascular smooth muscle cell dedifferentiation by suppressing insulin receptor substrate-1-mediated p53/KLF4 complex stabilization
“In summary, glucose-induced downregulation of IRS-1 results in loss of P53/KLF4 association thereby decreasing p53/KLF4 complex induction of myocardin and p21. Reduced myocardin and p21 leads to enhanced VSMC dedifferentiation and proliferation in diabetic mouse aorta. The results have important implications for understanding the mechanism by which hyperglycemia facilitates atherosclerotic lesion formation.”
Andy, this is just ‘stuff’. More and more and more ‘stuff.’ You can keep going down the reductionist route to find answers, but you won’t find answers there. To understand physiological systems you need to look at them from a number of different levels of scale. What does this paper mean, why is it important. Does it add anything of real value to the discussion? What hypothesis does this paper support – and how?
Dr. Kendrick, appreciate your feedback. Unfortunately I am obsessed about causes of CVD and what can be done on a personal level. Insulin resistance appears to be a big factor and hyperglycaemia could be causal. Whenever someone says that X is involved, my reaction is to find out what effect hyperglycaemia has on X. Reducing blood glucose spikes would be a good prophylactic strategy. I am not concerned about high cholesterol as long as the TG/HDL ratio is low. Fatty streaks are a fact of life. Tunica intima appears to be where problems start. Smooth muscle cells can migrate, proliferate, take up modified LDL particles, turn into bone cells and enable repair.
Structural damage to the endothelium is a separate additional problem. How much happens on the lumen side or intima side of endothelium is debatable.
“What does this paper mean, why is it important. Does it add anything of real value to the discussion? What hypothesis does this paper support – and how?”
– epigenetic factors (high glucose in this case) alter function of VSMC, important because VSMCs helps to stabilize plaque
– discussion is about plaque formation, foam cells are there from the beginning
– hypothesis supported: reduced lumen area could be detrimental to survival
– does not support the bad cholesterol hypothesis
– new discoveries are made every day, this one helps to explain vascular calcification
– important to question everything and keep searching
Malcolm,
I think it is a very important response you are giving andy.
As a now seasoned “researcher” in the natural sciences I have followed the “reductionist” path in medicine for 20 years to the “bitter end”, not least by ‘deep studies’ of the molecular biology of the cell (Alberts et al.), and have realized that finite answers are not to be found there (though ‘much understanding’). The staggering complexity of ‘life’ is mounting as you march along to find the “truth” at the bottom 🙂
As you state I believe that you have to approach any medical issue through a multilevel analysis to gain a reasonable “world view” of the issue.
On the importance of nutrition on health we may slightly differ in opinon. Here I am siding with Weston Price who I think had the right attitude.
Göran Sjöberg
I am not a reductionist, just curious. When I read this: “Hyperglycemia induces vascular smooth muscle cell dedifferentiation by suppressing insulin receptor substrate-1-mediated p53/KLF4 complex stabilization” I focus only on “Hyperglycemia induces vascular smooth muscle cell dedifferentiation”, the rest I do not understand and is ignored. Helps to understand where foam cell come from, that is enough. Maybe not, what is a dedifferented smooth muscle cell and why is this important?
Andy,
You wrote:
“Unfortunately I am obsessed about causes of CVD and what can be done on a personal level.”
I don’t know if you have specific reasons to worry about CVD (e.g. if it runs in your family), or indeed how old you are, but when I gave up statins – with all the ”benefits’ they are supposed to confer – I realised that we only have a finite lifetime, and it is all too easy to waste some of it worrying as to how we will die – because, of course, we certainly will.
Nearly 15 years ago, John Ionnidis wrote a paper that shows on statistical grounds that ‘most’ published (biological) research findings are false:
https://journals.plos.org/plosmedicine/article?id=10.1371/journal.pmed.0020124
This is worth skimming even if you omit the detailed derivations (it is still my intention to plough through these 🙂 ). I haven’t seen a refutation of his argument.Thus, almost certainly many of the papers you cite, will actually be simply wrong! This is part of a problem, with so much dross, people wanting to prove something can cheery pick from this vast collection!
I think it is also important to realise just how easily medical science (not to mention other sciences) can veer off the truth. There is always a rich trail of red herrings and some financial inducements, to lure researchers off course.
If you feel a need to reduce your risk of CVD, I suggest you follow some version of the High Fat, Low Carb diet, or at least severely restrict your sugar intake, take a reasonable amount of exercise, and relax.
David Bailey, “obsessive hobby” might be more accurate diagnosis. Not worrying about dying, but would prefer to die healthy. So far at 80 no health issues but aware of the ageing process. Never followed the popular diet recommendations from the AHA or equivalent.
I also try to learn from other peoples (family, friends neighbours) mistakes. Not too many male friends left.
In a recent study published in the journal Nature, researchers from the University of Texas (UT) Southwestern Medical Center and New York University School of Medicine discovered how LDL circulating in the blood makes its way to arterial walls. They found that an endothelial cell membrane receptor protein called scavenger receptor class B type 1 (SR-B1) is responsible for bringing LDL to the arteries – promoting its accumulation, which eventually results in atherosclerosis.
Hi Phil, found the transcytosis ref
https://www.researchgate.net/publication/332627560_SR-B1_drives_endothelial_cell_LDL_transcytosis_via_DOCK4_to_promote_atherosclerosis
Study shows that blocking SR-B1 eliminates atherosclerosis. Assume that this applies to capillaries as well as large arteries. Confounding factor is amount of modified LDL in circulation that will end up in foam cells.
Hi, andy,
There’s a more reader-friendly (at least for this reader) description of and commentary on the paper here:
biotarget.amegroups.com/article/view/5112/html
One thing I haven’t gotten from the Huang et al study is that it shows “…blocking SR-B1 eliminates atherosclerosis.” Significantly reduces it perhaps, but “eliminates” sounds a bit strong.
The commentary also notes that the SR-B1 expression is greatest at points where arterial blood flow pressure is also greatest. That suggests to me the SR-B1, which also binds HDL, may be there for a reason.
It’s certainly a fascinating finding, and it challenges the notion of “passive penetration” of LDL through the endothelium. I’m not sure it supports the lipid hypothesis, but folks smarter than I am can decide that.
Hi LA Bob, an easier read and introduced an additional point, “HDL competes with LDL for binding to SR-B1.” The importance of TG:HDL ratio can now be explained. High ratio means that there are a lot of small dense LDL particles outcompeting fewer HDL particles for transcytosis. LDL particles could enter the sub-endothelial space either by (a) via vasa vasorum or (b) luminal side endothelium. Read somewhere that in case (a) dedifferentiated VSMCs form foam cells, and in case (b) macrophage foam cells predominate.
Hi, andy,
“The importance of TG:HDL ratio can now be explained.”
I’m very reluctant to go that far. Why?
1) I’m a layman.
2) I have questions about the SR-B1 transcytosis finding.
(I have questions about a lot of things, but I’m not going to live forever, and holding my breath for answers won’t help).
For example, why do we have a binding entity that handles two distinct families of lipoprotein?
Does SR-B1 trancytose all variants of HDL?
What else does SR-B1 bind in the arterial endothelium?
Why is SR-B1 preferentially expressed in athero-prone regions of the artery? Is it because such regions are more damage-prone?
Are there “variants” of SR-B1 that transcytose LDL and “variants” that don’t?
Why is physiology arranged this way, especially as not everyone gets atherosclerosis?
I “get” that HDL and LDL may “compete” for the SR-B1 binding. But it needn’t be limited to small-dense LDL. If you follow the Dayspring / Attia view of LDL, it’s the particle count that matters, not the particle size.
Here’s a 2015 paper that covers a lot of the same territory as Huang et al, but I don’t see any indication Huang refereces or acknowledges the 2015 paper.
https://academic.oup.com › cardiovascres › article-pdf › cvv218
You might also look at this post at the Hyperlipid blog.
http://high-fat-nutrition.blogspot.com/2019/06/on-belief-structures-in-lipidology.html
There are images of arteries with various stages of atherosclerosis in autopsied folks who died of other things, and the earliest ones don’t show immediate sub-endothelial intrusion. But there is intrusion lower down at the junction of the intima and the media.
So, what’s it all mean? Beats me, but a 2004 article about HDL and SR-B1 includes a thoughtful line.
“…interpretation and extrapolation at this point should be done with caution.”
https://www.jci.org/articles/view/21072
Hi LA Bob, good to question everything
Somehow I missed Peter’s article about endothelial transcytosis, but was aware that fat droplets accumulate closer to the media side of intima. It is easier to study transcytosis in large arteries. What if this is the preferred method of cells adjacent to capillary endothelium to have access to LDL. In that case the vasa vasorum of large arteries could be the source of LDL particles into the intima. Apparently cells do best if they are not more than 4 cells away from a capillary. Dependance on loose tight junctions is another possibility. In any case fatty streaks are a fact.
Question about importance of LDL particle number. Suspect this is important only when consuming low fat /high carb and liver is source of LDL.
If LDL enter the tunica intima, there should be a way for LDL to exit by same mechanism. Tunica intima is more than one cell thick and needs access to LDL.
Glucose competes with vit C for absorption, sounds similar for LDL and HDL.
andy,
My link
https://academic.oup.com › cardiovascres › article-pdf › cvv218
doesn’t seem to work.
This one might be better.
https://www.google.com/url?sa=t&rct=j&q=&esrc=s&source=web&cd=10&cad=rja&uact=8&ved=2ahUKEwin3Nbw2u_lAhXkmOAKHXWQAaoQFjAJegQIBRAB&url=https%3A%2F%2Facademic.oup.com%2Fcardiovascres%2Farticle-pdf%2F108%2F2%2F268%2F17195052%2Fcvv218.pdf&usg=AOvVaw36AXBgnzPoh7hRqAh56t4e
Or if you google SR-B1 hdl arterial endothelium and click on “A novel assay uncovers an unexpected role for SR-BI in LDL …” you should get there.
tl:dr We evolved a receptor purely to kill ourselves. SHUT IT DOWN NOW!!! Little thought as to what else it may have evolved to transport
Elspeth Smith
Brasil / São Paulo/ interior
Just fyi, I can’t sign up to follow your blog. Is that a new issue? “Your subscription did not succeed, please try again with a valid email address.” Is the message. I can’t figure out why it would think it’s not valid. I use that email all the time.
Not sure how I became “not following” in the first place. I just noticed your posts weren’t reaching me anymore.
OK that’s weird. Just after I posted that, I got the green “Following” image on the lower right. Gremlins.
I think Google are after me.
Hello Malcolm,
I would like your opinion on an article piece that I presume is published, that I received via email. The title is “Plaque and heart health: what is SR-B1 and how does it cause “bad” cholesterol to enter into artery walls”. It is an article published in Science.News 11/11/2010. It basically says that these are a type of receptor that draws LDL into the arteries and they are now looking for some drug development to block this process. Seems like they just want to keep the cholesterol theory going by hook or by crook. But if you could find the article I would appreciate your take on it.
Thank you
Re. Thrombogenic Hypothesis, don’t blame the fibrinogen
Fibrinogen and other clotting factors are good unless they are exposed to high glucose.
https://journals.sagepub.com/doi/full/10.1177/1076029618792304
Glucose Concentration Affects Fibrin Clot Structure and Morphology as Evidenced by Fluorescence Imaging and Molecular Simulations
I’ve tracked down comment on a paper of Dr Smith’s, referenced in US Senate hearings on nutrition in the late 70’s. I can’t attach a photo of the page, but hope that you can access the url.
https://books.google.co.uk/books?id=ktk1AAAAIAAJ&pg=RA2-PA25&lpg=RA2-PA25&dq=Dr+elspeth+smith&source=bl&ots=rPuw_RJXiX&sig=ACfU3U3VZndDWsy9_jHauiUu_A2N1BdttA&hl=en&sa=X&ved=2ahUKEwivvcy8nurlAhXJRBUIHXT-AYQ4FBDoATABegQIChAB#v=onepage&q=Dr%20elspeth%20smith&f=false
Frederica, great reading indeed from 1977!
Thank you for the reference!
It basically confirms most of what I “believe” in regarding the cholesterol and CVD-issue.
Nonsense/deception!
Frederica, an interesting history lesson
In 1911 not much heart disease, people not obese, CRISCO introduced to replace butter
In 1977 heart disease epidemic, introduce dietary low fat low cholesterol guidelines
In 2019 obesity and diabetes rampant, heart disease and cancer biggest killers
Maybe the modern donut fried in CRISCO or equivalent is the problem. The donut hypothesis.
Even worse, the transfat Crisco (which I grew up with, alas) was intended to replace lard in baking.
IMO not far from the truth! Peter at Hyperlipid and Tucker Goodrich among others have unearthed a great deal about how polyunsaturated fats affect everything down to the functioning of the mitochondria. Then of course there was the Rose Corn Oil Trial way back when. Omega 6 oils are one thing that has increased markedly in the diet, along with carbs, and the two together are synergistic.
I think it is clear that PUFAs are not terribly good for human biochemistry and physiology – at least not in the quantities that are now consumed.
What causes heart disease?
Whatever causes chronic damage to the endothelium – Dr. Malcolm Kendrick.
What causes cancer?
Whatever causes chronic damage to cell metabolism – Prof Thomas Seyfried on The Canteen Podcast minute 44:45.
madMax, was aware of the professor but good to hear the message again. Perhaps most diseases have a metabolic component. Diet and glucose were mentioned frequently, here is a reference to make this comment relevant to current discussion:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6696313/
Endothelial Dysfunction: Is There a Hyperglycemia-Induced Imbalance of NOX and NOS?
“The aim of the current review is to describe the normal, healthy physiological mechanisms involved in endothelial function, and highlight the central role of NOX in mediating endothelial dysfunction when glucose homeostasis is impaired.”
I had some further thoughts. Saturated fat molecules stack neatly, which is why they are solid at room temperature, though not at the equator where plants make use of them. Monounsaturated fats are not too dissimilar. Polyunsaturates have structural kinks at the double bonds which keep them liquid at room temperature, quite apart from their chemical reactivity.
When incorporated into cell membranes, such as when eaten to excess as most people are encouraged to do, their inability to stack neatly causes said cell membranes to become porous.
I speculate that maybe the incorporation of a lot of omega 6 into endothelial cells may affect their structural integrity and make them more susceptible to damage from the numerous damaging factors.
Frederica,
I am now reading that report with great interest, though I was quite aware about the nutritional fights of those days and the Mc. Govern hearing specifically. But it is interesting for me to note that it seemed to be the consensus of that time forty years ago, as still today, that animal fat is bad for your health although researchers as Dr. Ahrens , being part of the hearing, stated that there was certainly no sincere science behind such a consensus.
And today the defamation of saturated fats seems to have evaporated all together – funny!
So, what’s left? To me there is the conflict between true physiological nutritional research and what is considered to be politically correct. All this is up my throat!
Yes, it is certainly an interesting report from 1977 when it seems we got awry regarding the health and nutrition.
There is a saying that when you repeat a lie often enough it becomes a truth (consensus?) and at that time that had happened with the fat/cholesterol/CVD-myth about twenty/thirty years after its “inauguration” by Ancel Keys (?).
Behind all this I find strong agriculture industry interests and especially about the benefits from corn. And when the Japanese invention of turning corn into cheap syrup was acquired by us-industry it may be considered as a revenge for Hiroshima considering the effect on the US population.
Yes, there is a lot of interesting reading in this 1977 report!
E.g., I wonder, 🙂 , if it was actually Malcolm himself as ‘a young student’ (although Dr. Alan P. Thal is here stated as the author) who stated:
“Even more importantly, it appears that the fat deposition in blood vessels may, in fact, be secondary and that the process is begun by a poorly understood form of arterial injury. This, in turn, is followed by a layering of blood clot on the inner surface of the artery. The cholesterol scar tissue and calcium which come to form the ultimate features of the narrowed artery, appear to be the result rather than the cause of this initial injurious process.”
For certain there were people who understood all those years back what it was all about.
A word of warning now!
The amended material to this Mc. Govern report is “immense” although much is very interesting. And it is beyond my ability to digest all that without “unlimited” time. I wonder if anyone did read all that.
Still the fundamental impression remains: “No dietary guidelines based on true science could be given.” Still that was exactly what happened and this did not prevent the obesity and T2D epidemics we are facing today.
I’m persevering through the supplemental material slowly, there’s 400 pages of it. Some has turned into an eye test and is illegible or barely legible, plus it is entertaining to see the rubber gloved thumb appear on the scans between pages.
There’s some good stuff there, and some very wordy stuff too. Hard to believe from today’s viewpoint that so many people used to question the cholesterol hypothesis/diet heart hypothesis which have since become irrefutable dogma.
Thank you! What an excellent read. I’d seen quotes from the likes of Taubes. Teicholz and probably Adele Hite but never before read the whole thing.
Sir John McMichael’s statement starting from page 13 and his written statement from page 23 makes me think he was the Malcolm Kendrick of his day, stating facts in the face of The Narrative. At least he wasn’t accused of killing people. he was just ignored.
Lots of good stuff among the Supplemental Material starting from page 65. I’m only part way through. Some of it is highly relevant in the face of ongoing vegan propaganda – Cambridge University has banned beef and lamb from its canteens, Norwich University has banned beef and there’s an upcoming anti-meat BBC documentary being heavily trailed, plus yet another “vegan documentary” The Game Changers. Apparently your p*nis will shrink and drop off if you eat meat. It must be true, we all went extinct millennia ago. Oh, wait . . .
Yes we do require *some* Omega 6, just not this much, and in better balance with the Omega 3
Re. Brain problems for us elderly folk
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6604433/
High triglyceride/HDL cholesterol ratio is associated with silent brain infarcts in a healthy population
“SBI was defined as an asymptomatic, well-defined lesion of ≥3 mm with the same signal characteristics as cerebrospinal fluid on T1- or T2-weighted images [1]. The burden of SBI lesions was classified as absent, single, or multiple. Intracranial atherosclerosis (ICAS) was defined as an occlusion or stenosis greater than 50% of an intracranial vessel on MRA”
What could one do today to stop progression? multiple choice question, explain why
1- Take a statin
2- start low carb diet
3- follow AHA dietary recommendations
4- take an aspirin
5- take vitamin C and other supplements
6- ask GP to explain cause and treatment
Angelica,
I have been having problems too with Dr. Kendrick’s blog, everything just went haywire after trying to log on yesterday, and when I gave up completely and tried to shut down I got the message ‘Configuring windows do not turn off your computer’ which went on so long that I had to give up altogether. This evening, when I finally turned back on, the same message was still there and it has been a real problem to gain entry once again.
Funnily enough, I have almost had the feeling that someone is looking over my shoulder when I am on the computer sometimes. Several times over the last couple of weeks I have had silent ‘phone calls, from all over the world, which have always happened shortly after I have been on line. One was even from the Russian Federation would you believe. All of them now on my BT blacklist. I registered with the TPS years ago, but nobody appears to take the slightest bit of notice of that either.
Sylvia – two or three years ago, after enduring up to 10 ‘nuisance’ calls a day, we bought ourselves a BT phone on which you can block any unwanted call at the press of a button. Bliss. In my experience the TP Service rarely works because most seriously nuisance callers ignore it.
Those silent calls are very unnerving. I believe most of these unsolicited calls are computer generated and sometimes their system hiccoughs hence the sinister silence.
Janet, thanks for your reply re the silent calls. They don’t spook me or anything like that, it is just so darned annoying when it happens. It seems to go in spates, with two or three calls a day sometimes, and it definitely happens shortly after ‘closing down’ after being on the laptop.The ‘Who Called Me’ site gives the geographical area from which they come and it is literally from all over the world. How on earth they may have my landline number on file is a mystery. The telephone you have sounds a good idea, I might get in touch with BT and see what is on offer.
Best wishes, Sylvia. PS I hope your new venture is working well for you.
My answer to silent phone calls. Reply, using the most disgusting language you can produce on the spur of the moment. This has worked well for me for over 50 years.
Shirley,
I think along with Jan’s advice re. a new phone, and your suggestion of a bit of disgusting language I will crack the problem in no time at all. I well remember telling a scammer, some time ago, to go away and examine his conscience and stop trying to fleece people, when he was trying to take me for a fool. His reply was “Madam, you are obviously a mother, would you allow me to ring you back and explain just why I am doing this”. I was tempted to hear just how he would explain himself, but thought better of it.
I must say I can only agree with Dr. Kendrick’s comment, a little lower down in this blog that “Society is entering a very dangerous place indeed (he is actually talking about anyone who dares to be a critic of vaccination here) but I consider it also relates to so many aspects of life today and sadly, in my opinion, is so very true.
Have a good day Shirley. Roast beef for Sunday dinner eh?
I would advise against returning a silent call, thats exactly what the scammers want and will try to keep you on the line as long as possible while they’re clocking up charges on your phone bill. See info here
https://www.donotcall.gov.au/consumer-alerts/missed-overseas-calls/
In other cases it may be telemarketers. I’ve been told that when an operator in these call centres finishes one call, the software will automatically dial 3 numbers from their database and as soon as one answers the other 2 get disconnected. My advice is ignore all numbers you don’t recognise and let them go through to voicemail. If it’s important they’ll leave a message, if not you don’t want to talk to them anyway.
I believe the TPS removes you from their list after a while, then of course your number can be sold on to everyone else. Even if you then go back on the list your number is still out there. Someone I knew (a Policewoman) was getting nuisance calls and requested a non-directory number. The first call was to tell her the new number was now live. The second call was marketing, and they had her name. I only use my landline for internet. I turned the ringer off.
The Windows thing sounds like a stuck update. My Windows 10 box sometimes takes ages with a number of reboots, every month. I dread the day when this computer which is still on XP dies.
Chris c & Andy.
Thanks for your replies re. silent calls, it was good to learn that the Windows 10 configuration thing was probably just a hiccup on my computer. All of your comments were very helpful, and somewhat enlightening too, and all very much appreciated.
Sylvia.
For those who prefer to read about the Vitamin C study, Dr. Rath foundation. Latest study:
https://www.dr-rath-foundation.org/2019/03/dont-skip-the-vitamin-c-only-regular-supplementation-can-ensure-cardiovascular-protection/
In summary, therefore, this study provides further proof that Dr Rath’s explanation of the underlying cause of heart disease, namely, that it primarily results from vitamin C deficiency, is correct. In a previous study published in 2015, the Dr. Rath Research Institute confirmed this explanation by showing that structural impairment of the vascular wall induced by vitamin C deficiency is sufficient to trigger the deposition of Lp(a) and progression of vascular plaques. This latest study now adds another important aspect to the picture by demonstrating that only a consistent daily intake of vitamin C can ensure cardiovascular health.
Hi Frances, re vitamin C
“In summary, therefore, this study provides further proof that Dr Rath’s explanation of the underlying cause of heart disease, namely, that it primarily results from vitamin C deficiency, is correct.”
By preventing scurvy does not guarantee freedom of risk from heart disease.
No, it does not. But if you become deficient in vitamin C, you are are far greater risk of CVD. Especially if you have a high Lp(a) level.
Dr. Malcolm Kendrick
Appears that most of oxLDL is bound to LP(a). Vitamin C is an antioxidant and therefore would help to stop oxidation of LDL particles thereby reducing LP(a) levels. Other oxLDL would be scavenged by macrophages or VSMCs. On the prevention side some LDL particles are more prone to oxidation depending on diet.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4956483/
Lipoprotein(a) and Oxidized Phospholipids in Calcific Aortic Valve Stenosis
Andy, check out Bruce Ames’ Triage Theory which posits that when there is a deficiency of any of the approx 40 essential vitamin and mineral nutrients the body will prioritise those processes essential for short-term survival over those involved in long-term survival. Bruce then went on to prove this in regard to Vitamin K and selenium, apparently chosen because they are used in relatively few processes rather than hundreds. However if it’s true for K and Se it’s almost certainly true for the other nutrients too. This makes eminent evolutionary sense since if the organism doesn’t survive in the short run it won’t get the opportunity to reproduce and pass on its genes.
Using Triage Theory it becomes clear that what medicine calls scurvy is only the end-stage of severe vitamin C deficiency, when the lack of vitamin C is so severe that there isn’t even enough to maintain those vital short-term survival functions. Conversely, the absence of the symptoms of scurvy is no guarantee that you are not deficient – a state that the vitamin C advocates describe as subclinical scurvy. In regard to atherosclerosis I’ve seen it stated (maybe by Malcolm) that there is a continuous process of damage and repair to the artery wall, and heart disease is when the repair processes can’t keep up with the damage. Since C is essential to the formation of collagen it’s clear that a deficiency is going to hamper the repair process. Vitamin C deficiency may not be the only cause of atherosclerosis but it is surely a major one.
BTW the RDAs for the vitamins and minerals were set to be enough to prevent only the most obvious manifestations of deficiency – eg scurvy, pellagra, tickets etc. Using Triage Theory the RDAs are almost certainly too low.
Hi Stuart, re Triage Theory of allocating vitamins and minerals
I suspect that hyperglycemia might upset the triage response.
https://cardiab.biomedcentral.com/articles/10.1186/1475-2840-1-1#Tab2
How hyperglycemia promotes atherosclerosis: molecular mechanisms
Andy, I don’t see that glycation alters the triage mechanism – rather the other way around, that if antioxidant vitamins are in short supply they are going to be restricted to vital functions such as the immune cells, leaving less available to protect LDL and other proteins. IIRC the immune cells have much higher C levels than ordinary cells and if you get an infection the requirement for C skyrockets. It’s noticeable that animals that make their own C don’t get atherosclerosis whereas guinea pigs (which like humans can’t make C) do get atherosclerosis when deprived of C.
Stuart, perhaps epigenetics trumps triage
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1312295/
“Atherosclerosis affects only herbivores. Dogs, cats, tigers, and lions can be saturated with fat and cholesterol, and atherosclerotic plaques do not develop (1, 2). The only way to produce atherosclerosis in a carnivore is to take out the thyroid gland; then, for some reason, saturated fat and cholesterol have the same effect as in herbivores.”
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3992312/
“A 2-year-old neutered male golden retriever dog presented for lameness secondary to ulcerations of multiple digital paw pads was diagnosed with vasculitis and hypercholesterolemia. Despite treatment, ischemic necrosis progressed to include all distal extremities and the dog eventually expired due to myocardial infarction secondary to severe atherosclerosis. The rapid demise and the dermatologic lesions may have been secondary to cholesterol embolism syndrome which has never before been reported in a dog.”
Question: would vitamin C have made a difference?
Dr., not the topic of this post, nevertheless, please, careful with vaccination thing. In addition to not helping with your “quack” rating on the one site, the more important point would be that just as the medical community can make many hypertensives via lowering 140 to 130, so too a change in diagnostic criteria can increase the claimed number with autism. There is otherwise risk with everything, say, the risk from the ionizing radiation from the CT scan. Did you read the comments? Mercury in the vaccine. Yeah. Like the mercury in my dental amalgam. Any word on some lowering of cancer, etc., owing to less amalgam and more composite? You otherwise said it yourself, as we now have the spectrum, and so as you wrote, if things keep up, maybe 1% will be defined as healthy. And, please, remind them that just because mom and dad did it doesn’t make it good (you know, those chicken pox parties)(with the downside possibly being some painful shingles later in life). Lastly, remind them that he now somewhat decreased life expectancy increased primarily because of lower infant mortality and early childhood death. Liked your one example of the garden hose (have used that with my physicians re my BP, i.e., like the garden hose, there should be a range of pressures causing no harm, then an upward slop, and then all goes to hell rather quickly. As I’ve said, I tend to think that evolution would have favored the garden hose and the increased with every extra 1 mm
There is no way of being careful with the vaccination thing. If you dare make the slightest comment criticising vaccination – in any way – you become an anti-vaxxer and get a target painted on your chest. This is the exact opposite of science. When trying to discover facts becomes, virtually, a crime, our society is entering a very dangerous place indeed. A place I want nothing to do with.
Ugh, I know, say anything critical about vaccinations and you are likely to have Bill Gates cyber stalking you for months at a time. Don’t do it! It’s annoying as can be.
I’ve often wondered how many vaccinations one is required to have before shaking Gates’s hand. I’m guessing at least a dozen.
I wouldn’t have believed it was possible to make a garden hose that didn’t work, until I bought one. What looked like wire braid embedded in the plastic was actually different coloured plastic, and it twisted shut on every opportunity. Eventually it twisted shut when I was watering the front garden and then split, drowning the sunroom before I could get back to the tap and turn it off. There may be an analogy in there somewhere.
chris c, garden hose and CVD similarities
1- analogical reasoning can lead one astray, wires will make a hoses stronger, calcification strengthens arteries
2- Two dimensional analysis used when problems only occur in 3 or more dimensions
3- Tests were done ” in vitro” and expected to apply “in vivo”
4- marketing
Sorry, let me fix some typos, well, one anyway, that last line there, so, I tend to think that evolution would have favored the garden hose and not the increased risk with every extra 1 mmHG.
Oh, and here’s the site, by the way:
https://rationalwiki.org/wiki/Malcolm_Kendrick
Denialist. You and the other holocaust deniers (that’s the impression some are trying to create).
And for more, the L-Arginine that might help with new smaller vessels but run the risk of some latent virus being not so latent. Been there and had that happen. So right out the film, Little Big Man, life contains a particle of risk. And, licked? I’m not licked, just tarred and feathered, that’s all.
Now well and truly lastly, recall that last great tsunami. Some at the one locale avoided any great harm owing to their history saying that when the earth shakes and then the water recedes like that, run for the hills, which they did. You posted a link to some human with a website address of wellness.com. Run for the hills.
Nice theory but wrong.
There are vascular endothelial receptors capable of “ingesting” LDL.
For example, LOX-1, present in the coronary vasculature, has a role in the cellular Ingestion of oxidised LDL.
Dr. Smith was sadly incorrect.
To assume that the BBB functions the same as the coronary vasculature Endothelium is a massive simplification. Endothelial structures are adapted to their site. Glomerulus Endothelium is also significantly different to gut Endothelium.
I think I made it entirely clear that LDL could get into endothelial cells. However, there was no mechanism for trancytosis, or exocytosis. In what way, therefore, was Dr Smith incorrect? I think I also made it quite clear that endothelial cells in different organs are completely different. In addition gut endothelium does not line blood vessels. So, your comparison makes no sense to me?
Wow, someone disputed an actual fact with you! I’m stunned and actually pleased to see the debate. As a lightweight, I’d just like to add the observation that I’ve yet to see the person who has CVD and a perfectly healthy gut flora, at the same time. The “process” could be a more general disease process that has multiple manifestations across the many types of endothelial tissues. That would explain things like why Vitamin C deficiency affects so many things including endothelial damage in arteries, the skin on one’s legs, immune function… etc. The CVD disease process could simply be a general breakdown in the body’s ability to protect itself from ordinary/routine pathogens. If so, then the atrophy of the thymus which is generally considered “normal” would coincide with a rise in CVD under certain conditions like lack of Zinc or Vitamin C. Maybe the process is so broad and full of “normal” happenings, that it’s hiding in plain sight.
Please don’t post political stuff.
This is a cvd/heaith blog.
There are a million sites out there to vent about politics
mikeezeem.
Everything in life is politics, with health matters at the core of every aspect of living.
You awake in the morning,
You open your eyes, take your first conscious breath for the day ahead….all based on politics.
1) awake in a comfortable home, or a DOORWAY? That is the result of a political decision.
2) open your eyes to see your surroundings, or not if BLINDNESS occurred through untreated illness/ accident.? That is the result of a political decision.
3) Breathe easily, or breathe air contaminated by unregulated EMISSIONS ,or UNTREATED CVD. These are the results of political decisions.
Yes, this is a CVD. /Healh blog….now tell me politics does not enter the equation.
Jennifer,
Sure. But wait. Monetary considerations pervade everything as well. How about egos? Everything. Everything pervades everything else.
That ends in its tracks any concise discussion of ideas in any particular field .
Consider further:
Wake.
Have b’fast & coffee.
Watch/listen to the morning news. Of course it’s all about the violent flux of current politics.
Experience indigestion – the immediate outward symptom of the kind of stress that contributes to the strain that is CVD.
Your post immediately increases that stress a tiny increment. Sorry. It does.
Let’s continue our particular discussion about CVD and simply concede that trying to make sense of the politics we live in is a CVD contributory factor just as was the collapse of the Soviet Union . . . and leave it at that.
JDPatten: Good point. I stopped trying to make sense of it some time ago. There is no sense to be made of it. The simple fact is that we humans are imperfect. Accepting this reality has been a real boon to my health, and I no longer have a home in any political faction. I’m reading an excellent book called, “No Good Men Among the Living,” which is taken from a Pashtun proverb which ends, “and no bad men among the dead.” Multiple layers of meaning there.
JDPatten, I listen to the news nowadays very little since there is much spin and little fact. However, I would not stop someone from voicing their thoughts about politics, even on this blog. If the moderator sees it as infringing the guidelines, it will no doubt be blocked. In all other respects objections to posts comes nearer to shutting down discussion. Something I suspect most posters here would take a dim view of.
AhNotepad,
I have no objection to the discussion of political trends, policies, or decisions that might directly effect CVD prevention, treatment, research, or correction vs. exacerbation of misguided concepts.
But arguing about the machinations among heads of state and the contentions among political parties and hangers-on would not be missed here, I think.
Heck, there’s contention enough strictly within “What Causes Heart Disease”, don’t you think?
Jennifer
I read this site because i am interested in health issues .
Call me naive or call me uneducated, but there are no political reasons for my interest in CVD
There are thousands of sites online to talk about politics if that interests you, but this site is about health matters
mikezeem, you may not have a political interest in CVD, but how can you be sure that it is not political decisions that that has an effect of the occurrence of CVD? If you are to believe the information on this site, one of the major causes seem to be social upheaval, or social disruption. Either of those are likely to have roots in political decisions. Similarly, decisions by governments to promote things like saturated fats clogging arteries, and breakfast cereals being healthy, when Tim Noakes, Gary Fettke, Joanne McCormack, David Unwin, Zoe Harcombe, Robert Lustig, Aseem Malhotra, Ivor Cummings, and many others have information to show research shows otherwise. This indicates how prevalent, and possibly misguided, political influence is, and yet it has such a large adverse effect.
Thank you Dr. Kendrick for permitting such discussion, and allow the unsettling of the “scientific” dogma.
Global warming? Anybody? 🤭
I have just spent an hour reading some links generously provided by fellow bloggers on this site. Such investment in my time adds to my overall knowledge.
You and I will never agree, but, forgive me for saying, but I despair at your apparent naivety and tunnel vision.
Here, here.
No politics!
Not for any number of reasons, not the least of which is that one risks exposing one’s imbecility thus coloring all of one’s subsequent commentary.
Its tricky really. I suppose is depends on how wide you draw the boundaries of politics.
Dear Malcolm, can I introduce something which is related to one of your books, which I enjoyed, which I believe may need the wording changing minutely to get the sense correct: note that I am using this platform as it is the only way I know of contacting you (I don’t use other forms of social media).
The last paragraph of the chapter on salt in ‘A Statin Nation’ reads:
“Despite the evidence, the current recommendation is that everyone should eat less than 6g of salt a day. Guidelines which, were they be followed, would increase rather than decrease life expectancy. Yet again the official advice is wrong”.
The penultimate sentence in this quote suggests (to me) that following the guidelines would increase life expectancy. Surely you meant the last sentence to have the form:
“Guidelines [ie having less than 6g of salt a day] which, were they to be ignored, would increase rather than decrease life expectancy.”
I hope you can forgive me if you feel I am being either pedantic, I do think this could cause confusion for readers.
Finally a note of thanks for ‘The Great Cholesterol Con’, ‘Doctoring Data’, ‘A Statin Nation’ which I have enjoyed and continue to enjoy immensely.
Someone showed me this magnificent video – I am not sure it has been posted here before:
David, Thank you for this link!
Well worth watching!
I was not aware of this interview between two of my “favorite house scientists” but their message is quite convincing not least for me (or rather confirming) what I as a CVD-‘victim’ and my T2D wife have been up to for the last ten years.
Had issues with commenting.Just a test.
Important to note that the BBB does in fact have LDL receptors. Brain requires LDLs for omega fats. Look at
https://www.ncbi.nlm.nih.gov/m/pubmed/28108572/
Researchers are exploiting the receptor using synthetic peptides to deliver drugs to CNS.
One more proof that LDL cannot randomly pass.
Hi Maksim, couldn’t resist looking into this.
https://www.karger.com/Article/Fulltext/446704
A new function for the LDL receptor: transcytosis of LDL across the blood-brain barrier.
“Lipoprotein transport across the blood-brain barrier (BBB) is of critical importance for the delivery of essential lipids to the brain cells. The occurrence of a low density lipoprotein (LDL) receptor on the BBB has recently been demonstrated. To examine further the function of this receptor, we have shown using an in vitro model of the BBB, that in contrast to acetylated LDL, which does not cross the BBB, LDL is specifically transcytosed across the monolayer.”
Suppose there is a similar situation in other blood vessels whereby cells requiring LDL send signal to endothelium to endocytose LDL particles. High LDL in lumen would not affect how much is transported in this scenario. Possible explanation why FH is not a problem, or why attempting to lower LDL is ineffective.
That last post should have read to Stuart and Chris c.
Thanks again, along with my apologies, Sylvia.
In case it was’t posted already, a study was released over the weekend that was critical of practice of stents for heart attack prevention along with bypass surgery for prevention.
“Stents, bypass surgery show no benefit in heart disease mortality rates among stable patients”
http://med.stanford.edu/news/all-news/2019/11/invasive-heart-treatments-not-always-needed.html
excerpt:
A large, international study led by Stanford and New York University found that invasive procedures are no better than medications and lifestyle advice at treating heart disease that’s severe but stable.
Yeah I saw that, it basically points people to statin use instead. Why would someone undergo heart surgery if it’s just as good as statins? Personally I have a “I will accept a stent, but not a bypass” speech all buffed and prepared against the possible day… but I”m really already convinced that statins are not my path. These decisions are very individual though. I wouldn’t claim that everyone should do what I do.
I try to maintain a perspective that includes the insight of cultural forces that have created happiness around dangerous and unhealthy foods. Like doughnuts and cookies as symbols of reward. Undoing that kind of health damage is very hard. It’s more akin to becoming a monk of some type.
To protect people from it we should start to find healthier rewards. Like immature coconut meat. Or, recently someone mentioned matcha pudding on a paleo forum. Or long-process sourdough gluten free and sprouted flour breads which are becoming a bit of a rage right now. Such rewards shouldn’t be alternatives, but should stand alone with equal satisfaction quality and cultural acceptance so they can truly give people the emotional effect of a reward.
To remake health, and especially lifestyle change, it’s necessary to make some social changes. “I baked cookies!” should have equal billing with “I made coconut pudding with cinnamon-chocolate sauce!” and “I spent two weeks baking this optimal loaf of bread, and every 5 days I bake another one!” If we accomplish that we’ll go farther than shaking fingers at no-no behaviors. We need some more can-do and a bit less dour doubt. Keep the cookies, but make other equal delights too.
No taste bud left underwhelmed.
Since I went low carb/paleo/keto fifteen years ago my food has never been so rewarding – so much so that after I’ve finished I don’t need to eat again for ages.
Tonight’s meal – lamb’s liver and a giant mushroom lightly fried in EVOO, lightly boiled purple sprouting tips and three slices of grilled bacon, two thickly buttered oatcakes and a glass of Cab Sauv.
I might get hungry again before bedtime, in which case I have a herring.
Apart from the taste and the health benefits most of what I eat takes little time to prepare or cook, a far cry from my lentil and bean casseroles with brown rice (man)
Soul, re stents and bypasses
Hopefully soon there will be an announcement that angiograms and stress tests can be replaced with a CAC test.
Soul, yes, yes!
For those interested it is also “easy” to find the truth that there are no benefits from stents and by-pass for CVD-victims other than in emergency settings.
This I realized myself 20 years ago a few month after my serious MI which also made me refuse the “offers” and later also all CVD-medciations.
When I saw the article I thought, hurrah! – another windmill charger! One has to put up the good fight.
it is surprising how much information and for how long it has been said, that bypass and stents are not beneficial outside of emergency situations. I was recently reading an older book printed in 1980 about “how to avoid bypass surgery”. As can be imagined it was loaded with information on how unhelpful studies have found the procedure to be.
Sadly, doubt much will change here in the US till the financial windfall from the procedures becomes less lucrative.
Clinical Implications For Cardiovascular Disease
https://www.dovepress.com/variable-effects-of-ldl-subclasses-of-cholesterol-on-endothelial-nitri-peer-reviewed-article-IJN
Authors Hua J, Malinski T
Received 13 August 2019
Nanomedical Research Laboratory, Ohio University, Athens, OH, USA
Nanomedical Research Laboratory, Biochemistry Research Facility, Ohio University, 350 West State Street, Athens, OH 45701, USA
Tel/fax +1 740 597 1247
Email malinski@ohio.edu
Background: Elevated levels of low density lipoprotein (LDL), “bad cholesterol”, is not an accurate indicator of coronary disease. About 75% of patients with heart attacks have cholesterol levels that do not indicate a high risk for a cardiovascular event. LDL is comprised of three subclasses, with particles of different size and density. We used nanomedical systems to elucidate the noxious effects of LDL subclasses on endothelium.
Experimental: Nanosensors were employed to measure the concentrations of nitric oxide (NO) and peroxynitrite (ONOO−) stimulated by LDL subclasses in HUVECs. N-LDL and ox-LDL (subclass A: 1.016–1.019 g/mL, subclass I: 1.024–1.029 g/mL, and subclass B: 1.034–1.053 g/mL) stimulated NO and ONOO− release. The concentrations ratio of (NO)/(ONOO−) was used to evaluate the noxious effects of the subclasses on endothelium.
HUVEC= human umbilical vein endothelial cells
Results: In HUVECs, the (NO)/(ONOO−) ratio for normal endothelium is about 5, but shifts to 2.7±0.4, 0.5±0.1, and 0.9±0.1 for subclasses A, B, and I, respectively. Ratios below 1.0 indicate an imbalance between NO and ONOO−, affecting endothelial function. LDL of 50% B and 50% I produced the most severe imbalance (0.45±0.04), whereas LDL of 60% A, 20% B, and 20% I had the most favorable balance of 5.66±0.69. Subclass B significantly elevated the adhesion of molecules and monocytes. The noxious effect was significantly higher for ox-LDL than n-LDL.
Conclusion: Subclass B of “bad cholesterol” is the most damaging to endothelial function and can contribute to the development of atherosclerosis.
Contrary to the current national guidelines, this study suggests that it’s not the total LDL, rather it is the concentration of subclass B in relation to subclasses A and/or I, that should be used for diagnosis of atherosclerosis and the risk of heart attack. By utilizing specific pharmacological therapy to address the concentration of subclass B, there is a potential to significantly reduce the risk of heart attack and atherosclerosis.
Keywords: low density lipoprotein, nitric oxide, endothelium, peroxynitrite, cell adhesion
And curiously there is a simple way to revert pattern B to pattern A LDL – a low carb diet. I suspect we are looking here at an indicator of other processes rather than a cause.
chris c, I wonder how long it would be before a drug is developed to prevent formation of small dense LDL. Reductionists have figured out something that can be implemented today “let diet be your medicine”.
Some of the diabetes drugs have been described as “low carb in a pill”, specifically the ones that make you piss out the glucose. Better idea – don’t eat it in the first place then you don’t need the pill. Oh hang on, how s that profitable???
Peroxynitrite/Nitric oxide
continue—-The discovery that mammalian cells have the ability to synthesize the free radical nitric oxide (NO) has stimulated an extraordinary impetus for scientific research in all the fields of biology and medicine. Since its early description as an endothelial-derived relaxing factor, NO has emerged as a fundamental signaling device regulating virtually every critical cellular function, as well as a potent mediator of cellular damage in a wide range of conditions. Recent evidence indicates that most of the cytotoxicity attributed to NO is rather due to peroxynitrite, produced from the diffusion-controlled reaction between NO and another free radical, the superoxide anion. Peroxynitrite interacts with lipids, DNA, and proteins via direct oxidative reactions or via indirect, radical-mediated mechanisms. These reactions trigger cellular responses ranging from subtle modulations of cell signaling to overwhelming oxidative injury, committing cells to necrosis or apoptosis. In vivo, peroxynitrite generation represents a crucial pathogenic mechanism in conditions such as stroke, myocardial infarction, chronic heart failure, diabetes, circulatory shock, chronic inflammatory diseases, cancer, and neurodegenerative disorders. Hence, novel pharmacological strategies aimed at removing peroxynitrite might represent powerful therapeutic tools in the future. Evidence supporting these novel roles of NO and peroxynitrite is presented in detail in this review.
errett, hyperglycemia affects everything
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2225483/
“Although hyperglycemia has been proven to cause peripheral nerve dysfunction in patients with diabetes, the biochemical mechanisms for this effect are poorly understood [94]. Recent studies in experimental animals have indicated that hyperglycemia stimulates the production of nitric oxide, which reacts with superoxide anion to form peroxynitrite, which is damaging the endothelium and perineurium”
Hi Dr. Kendrick. I had an idea, maybe you’ve already thought of it.
My grandson was born a year ago with hemophilia. His body makes no factor eight. I remember thinking, “On the bright side, according to Dr. Kendrick, he’s unlikely to suffer a heart attack.” Is there any way to cross reference heart attack sufferers with hemophilia and cholesterol levels?
A good thought, and something I looked into a while ago. It is true that, prior to the isolation of blood clotting factors, people with haemophilia had a much lower rate of CVD death. Around 1/5th. Although the figures are complex, due to death from other causes, and somewhat difficult to interpret data. Nowadays, however, with factor VIII replacement, there is little different in death rates from CVD.
After thinking on it some more, I came to that same conclusion since his blood will clot normally with factor VIII replacement. But at least you have me thinking, which is never a bad thing!
Stuart: I simply meant that as a rough equivalence, in the sense that, in the U.S. the Democrats have traditionally, up until the ’90’s, represented working-class interests, and the Republicans the interests of business and wealth. But much has changed over the last three decades or so. There isn’t much working class left, but Trump, a Republican, received a large percentage of their votes. The southern states were solidly Democrat, until President Nixon hoovered them up into the Republican Party with a racially-charged campaign. Today they are solidly Republican. The truth of the matter is, on economic issues there are only relatively minor differences between the two parties on core principles, and the differences on social issues exist only at the extremes within the parties. Politicians in both parties are so thoroughly dependent upon campaign funds to win elections that they represent the interests of their funders rather than their electors. The great irony and tragedy here is that all that campaign spending makes little difference in how people vote. Most of the public votes party rather than issues, which makes me want to pull my hair out, what little I have left!
Gary. After nearly 10 years on statins my hair was so thin, but I didn’t link the two. After 6 years without them I now have a huge mop of grey curls. Is there a link? No political party will get me to pull them put…so hang onto what hair you have left.
Jennifer: Is there an anti-statin? A drug which would grow one’s hair back? The good news is that, although I’m shiny on top, the hair I still have is mostly brown, and while most of my life my beard looked pretty crappy, it is now quite full and mostly brown, except at the temples where there is a bit of grey. Maybe ignoring the media and political spin is good for the health!
Gary: what have you changed to make your beard grow back?
Sasha: Good question. About 2001 I started eating raw dairy-milk, cream, butter, and cheese-from pastured cows. 2005 I stopped eating all prepared foods, and began cooking all my own meals. Around 2010 I switched to a Weston A. Price Foundation type of diet. 2015 or so I stopped eating grains, and the same year I stopped shaving. In the last couple of years I have reduced my carbohydrate intake and increased fat consumption. I suspect that these changes have not only improved my health, but my hair, too, although the baldness hasn’t changed (I don’t care one bit about this; my beauty contest days are over). Adding vitamin C, potassium, and citrulline have all made a positive difference.
Gary: thank you for answering and congratulations on better hair!
Jennifer. I’ve never taken statins. My GP has got the message that I’m taking enough pills already, thank you. But I did once lose all my hair following a bad attack of measles, aged 13.
As a young woman, I was a week-end only hippy, wearing it long and loose when not at work. In my early 40 s I went grey. Dyeing my hair gradually damaged it so I stopped that, but its length then made me look older rather than younger. So, despite my husband’s entreaties, I eventually had it cut off to chin length, and have worn a similar style ever since. I have promised him I will never, ever, get a blue rinse.
As a 70 year old woman, my hair is thinning visibly at the crown. Topical steroid lotion does encourage some regrowth when it gets particularly sparse, but I can’t be on it all the time. I have investigated wigs, but it’s not bad enough yet to justify the expense, and I don’t really fancy wearing anything not firmly attached to my head! I’m not hypothyroid.
There are many, far worse, problems associated with old age, so for now I will count my blessings.
Have you all seen this?
https://articles.mercola.com/sites/articles/archive/2019/11/19/center-for-disease-control-and-prevention-funding.aspx?utm_source=dnl&utm_medium=email&utm_content=art1HL&utm_campaign=20191119Z1&et_cid=DM393417&et_rid=753030075
Thanks Anna. We have seen it now and thank you for sharing. What a disgrace he documents. I like Mercola’s site, but don’t always agree with him, but he makes me think.
Of course, for those choosing to ignore the article, it won’t impact on them, or so they think. ( I am getting argumentative today)
Yes, I have now seen this interesting report – truly scary reading.
Thanks Anna!
I am myself a fan of Dr. Mercola although sometimes there seems to be too much of “scare mongering” involved. But as always it doesn’t hurt to be aware of the dangers around which threaten our health, especially when the rates of cancer, T2D, CVD and high blood pressure are so epidemic today and when the medical community “has no clue” what it is all about.
My own attitude today (but not 20 years ago) is therefor that of caution and thus to stay away from all possible suspect culprits in our surroundings, from PUFA’s to excessive dentistry X-rays, when reasonably possible. For that reason I also spent a lot of money to remove all my old “silver fillings” in order to get rid of the internal exposure to the mercury vapor manifestly being constantly emitted from them. It was notable to see the almost excessive care by which the involved dentists proceeded in contrast with the carelessness these fillings were once introduced.
Mercury amalgam fillings are regarded as completely healthy while you are alive.
When you are dead they are an environmental hazard and have to be removed.
I’ve heard that the mercury exposure was a reason for high levels of “mental” illness among dentists. Current ceramics are still hazardous to the dentists but not so much for the patients.
Here’s a report on a six-year Australian study which finds taking statins has no negative effect on cognition in the elderly and might even have positive effects.
https://www.usnews.com/news/health-news/articles/2019-11-18/statins-wont-harm-aging-brains-and-may-even-help
The article ends with hilarious irony.
“In the meantime, he doesn’t advise taking statins for the sole purpose of maintaining your mental abilities, since these drugs can have side effects.”
Statins -Wonder Drugs!!! Is there anything they can’t do? (sarcasm alert)
Gary Ogden
You seemed like a nice guy, but how can you be if you’re an apologist for Trump.
Don’t tell me how awful his political opponents are, just tell me how you can have any time for a nasty, bullying, mysogynistic creep
I have not stopped political e mails. But I like everyone to be civil.
I enjoy the latitude you give your commenters. But politics has become so charged. I support Trump, not afraid to say so, and now I will be excoriated.
Back on CVD, I had another thought. My daughter has been found to be a carrier of hemophilia and has been diagnosed with mild hemophilia herself. She has always had problems with bleeding excessively during childbirth. Would this group have lower rates of CVD, apart from the fact that they (carriers) are all women?
Don: Thanks. Applause here. The dog and pony show in Congress makes me feel even more protective of him.
I should add, she does not need to take any medication for her hemophilia as her body makes about 40% of the normal levels of factor VIII.
Malcolm,
I wasn’t sure if you meant e-mails, or posts on this blog – but if you did, a fair few still get through.
I am a UK Trump supporter. I am always amazed by the vague (but vehement) criticism of President Trump. We have been pulled into far too many US military campaigns in the past, and I approve of his desire to avoid conflict rather than promote it. The poor people who vote for him, obviously gain from not having their kids, or their friends’ kids sent abroad to fight. That must lower stress levels – and therefore lower their incidence of CVD. I also feel less stress with him in power – at least as compared with Hillary Clinton, who was ready to start more war ‘when’ she became president.
I also feel, that if any world leader might decide to take on Big Pharma, it could be him.
David, out of curiosity: why do you think Trump (or any other world leader, for that matter) would be inclined to take on big pharma?
mikeezeem: I’m not an apologist for anyone. I recognize the flaws of every political candidate, and hold my nose as I vote. Like the other 12% of Bernie voters, I switched to Trump, as the lesser of two evils. That the political class hates him so much I consider to be something in his favor.
Gary Ogden, president Trump and CVD relevance ?
Trump popularized the term “Fake News”. More use of that term should be used in medicine. Need a blog on how to spot fake news.
andy: No relevance, except that he has shaken things up a bit in the swamp, as have real scientists like Dr. Kendrick in the world of CVD. It’s just kind of amusing to see TDS (Trump Derangement Syndrome) burst forth into full flower, complete with name calling. But I’m finished commenting about politics. Government policy certainly has relevance to CVD, but not political figures.
andy,
No such blog necessary. If you’re reading something medical in the main-stream media (or even in the not-so-main-stream media), it is probably “fake news!”
Come to think of it, Dr Kendrick’s blog helps us identify fake news elsewhere.
If Obama had withheld money to a foreign nation in order to get that foreign nation to state on television that Obama’s political opponent was under investigation, would you think that was OK?
I am a registered Independent. I think, for instance, that some government regulation is good and too much is bad. Some taxes are good, too much is bad. I could easily vote for a McCain-type Republican (if there was one).
But coercing a foreign government to “investigate” your political opponent by withholding funds that government needed to combat Russian invasion is wrong. It’s simply wrong. And if Clinton can be impeached for lying about having sex with an intern, what Trump has done definitely rises to an impeachable offense.
And the Republicans are losing people like me. Permanently, when they do things like this and like lying about Supreme Court justices and the like. I can’t in good conscience vote for a Republican at this time, and maybe never.
BobM: The purpose of foreign aid is to advance the strategic interests of the U.S. government. This is always the case. Occasionally aid is given by rich nations for humanitarian reasons, but this is usually done under the auspices of the UN. Other than this, aid always has strings attached. In his last year in office, Obama signed the largest-ever weapons-sales contract with Saudi Arabia, while assisting them with logistics, intelligence, and refueling in their destructive bombing attacks on dirt-poor Yemen. This has been an untold tragedy, especially for civilians, and it has strengthened Al Qaeda in Yemen. This has been done to advance Israeli strategic interests, and it is ongoing. So aid is always contingent on adherence to the wishes of policymakers, even if unspoken. I find it refreshing that Trump spoke directly with the new president of Ukraine about tackling the serious problem of corruption, which was part of the platform he ran on. The president has the Constitutional duty and sole authority to make foreign policy; it is the role of bureaucrats to carry it out, not to undermine his decisions. And indeed, just a few days ago, Ukraine announced the indictment of Burisma’s founder. A Ukrainian parliamentarian stated that the money paid to Hunter Biden was laundered money, stolen from the people of Ukraine, not from company profits. As for Joe Biden, read Andrew Cockburn’s “No Joe! Biden’s Disastrous Legislative Legacy” in the March, 2019, Harper’s. A leftist writer in a leftist (though mainly literary rather than political) magazine. Enough to make anyone puke.
There has been a campaign by Democrat partisans in the permanent government (mainly DOJ, FBI, the intelligence agencies, and the State Department) since before Trump took office, even before the election, beginning with a counter-intelligence operation against his campaign, which morphed into the Russiagate hoax. All counter-intelligence operations are conducted with the full knowledge and approval of the sitting president, in this case Obama. My own congressman, Devin Nunes, partly unravelled this, when he was chair of the Intelligence Committee, but the agencies from which he subpoenaed relevant documents stonewalled him all the way. Now Russiagate has morphed into Ukrainegate, while the actual business of oversight and governance in Congress has come to a halt. Like Oakland, there is nothing there, there. Soon, DoJ IG Horowitz and AG Barr and U.S. Attorney John Durham will be opening this can of worms (I hope).
There are plenty of Republicans I’m appalled by, and would never vote for, mainly the neocons, such as Bolton and Pompeo, and the Christian Zionists, such as Pence, but in my home state of California, the Democrats have become a menace, a wholly-owned subsidiary of the pharmaceutical industry. No physician in California, save those who treat the rich and powerful, will ever feel safe writing a vaccine medical exemption for a patient. A medical dictatorship. Doctors are fully intimidated. So I have no choice except to vote for Republicans, and thankfully, all of my representatives, all of them Republicans, have sensible views on the issues I care about. I have nothing but contempt for the two political parties, and the swamp that is Washington, D.C. What Congress is doing now is nothing but political theater.
Not so keen on non CVD matters on this blog but you make a good case. Personally, I think it’s worth noting that Trump is not a warmonger, is he in a position to resist the big arms manufacturers, also the pharma giants? – financial independence making him less vulnerable ?
Jerome Savage: Yes, financial independence gives him a bit more flexibility. Pharmaceuticals is the most powerful industry of all, fully capturing all the levers of government, so Trump will only be able to put a bit of a dent in it. We see from the recent dog and pony show in Congress that the swamp is biting back (in this case, the careerists in the State Department, who think they are the ones who formulate foreign policy, when it is clearly and exclusively, under our Constitution-Article II, Section 2-up to the President to do so, and their only role is to implement it). Such is the state of civic education in our nation that few, even in Congress, understand this. I’ve been reading the Edward Snowden book, “Permanent Record,” and I’m inclined to think we’re totally screwed, our Fourth Amendment tossed to the wolves, our lives monetized by the oligarchs. On the other hand, knowledge empowers us. It is a beautiful world and life is good. It is Thanksgiving here, our best holiday. We are eternally grateful here in California for buckets of rain, rain in the forecast for the next eight days! We made the pumpkin pie last night, and it smells fabulous; ham is in the oven; garden vegetables, mashed, and cranberries awaiting their turn. So today the hell with the idiots in charge. We are blessed to be alive!
Gary Finishing upbeat is good. Here we are constructing a public hospital that’s gonna work out as the most expensive hospital in the world per bed, could be half a billion over budget. But the public & public representatives seem to hav no appetite for taking anyone to task. When the public accounts committee took exception to the extravagance of a major public funded charity, the chief beneficiary in the charity sued the PAC & won her case. Double slap in the teeth to the taxpayer. But, hell look on the bright side ! Hmmm. But where ? Need to search hard. Ah well there’s always Van Morrison !!
Jerome Savage: Right you are. I find great joy in being alive, despite knowing we are governed by the denizens of a fetid swamp. Just finished Edward Snowden’s book, “Permanent Record.” We’re totally screwed, so might just as well eat, drink, and be merry!
Jerome, got links to information on those cases? Alternatively the names of the hospital and charity so I can google them myself. TIA
Mike, I never said that statins are the sole cause of dementia. You can have vascular dementia from a series of mini strokes. With Alzheimer’s, Dale Bredesen has identified 36 separate causes and many people have more than one cause. For an intro see
https://www.beingpatient.com/dale-bredesen-end-of-alzheimers/
As Dale says, patching one hole in the roof isn’t much use if the rain is pouring in through the other 35 holes. You have to address as many causes as possible. I would add statins as a 37th cause, an entirely avoidable one.
Probably THE major cause of AD is insulin resistance of the brain, and many researchers refer to AD as “Type 3 Diabetes”. Due to the IR brain cells are starved of glucose and eventually die. See this video of a talk by Dr Mary Newport
Another major factor seems to be high homocysteine levels. A 2010 RCT showed that in elderly people who had high homocysteine and were showing signs of Mild Cognitive Impairment (early signs of AD), treatment with high dose B vitamins (folate, B6 & B12) reduced brain shrinkage significantly compared to the placebo group.
http://healthinsightuk.org/2015/08/06/policy-on-alzheimers-sure-we-want-a-cure-just-so-long-as-its-not-cheap/
A reanalysis of their data found that the reduction in brain shrinkage was confined to those with higher levels of DHA/EPA omega-3s
https://www.ncbi.nlm.nih.gov/pubmed/25877495
Incidentally, Bredesen would consider that the level of homocysteine defined as low in that study – <11 – is still way too high, which suggests to me that they might have got even better results if they'd been more aggressive. Regardless of homocysteine level, sustained B12 deficiency on its own can also cause irreversible brain damage. But good luck finding a doctor that tests B12 or homocysteine as a matter of course.
Oops, that linkto the Mary Newport video is not the one I thought it was. Here’s the link to the one I meant
@#$&*!!!!
I don’t know what is going on here. I definitely posted the correct link to the Mary Newport video I meant. After I posted I clicked on the link and it took me to the correct video, but now it has been directed to this other one again.
The video I mean is of the talk Mary gave at an Epigenix Foundation conference. Go to the Epigenix YouTube channel and it’s the one titled “Mary Newport, MD — Hyperketonemia for Alzheimer’s Disease: A Case Report”. Particularly instructive is where Mary shows the brain scans of 3 AD-diagnosed patients and 3 supposedly non-AD people. One of the non-AD patients has more beta-amyloid plaque than one of the AD patients and another shows a significant amount! This demonstrates that AD is progressing for a long time before a doctor will diagnose it and by the time they do you’ve lost a significant proportion of brain cells. The message to me is take action now.
Hi Stuart, re Alzheimer’s
What action are you contemplating?
Stuart, interesting novel treatment for AD include intranasal insulin spray. Treating brain insulin resistance with more insulin appears logical, works for T2DM according to experts.
Dr. Mary Newport discovered that ketones can be used as fuel for brain instead of glucose. Insulin resistance affects glucose availability. An indicator of insulin resistance is TG:HDL-C ratio. Takes a long time to enough brain cells to be diagnosed with AD.
Wonder what would be long term effect of supplementing with ketones and not addressing insulin resistance?
“Treating brain insulin resistance with more insulin appears logical, works for T2DM according to experts.”
These would be the same “experts” who have had such success in curing T2DM? Sorry for the sarcasm, it’s not directed at you Andy but at those bozos the endocrinologists who try to put out the fire of T2DM by dowsing it with fuel (insulin). Since IR is caused by exposure to excessive insulin via the excessive carbs in the SAD an insulin spray will probably show short-term improvement but only lead to further IR in the future. As usual, mainstream medicine only treats symptoms, not root causes.
I see exogenous ketones as a stopgap measure to keep your brain cells alive while you reduce your IR by fasting and ketogenic diet and address Bredesen’s other 35 “holes in the roof”. But IR is definitely the major cause of AD in most people. Also there seems to be a lot of evidence that high insulin is a major factor in all the diabetic complications regardless of blood sugar levels, plus promotes cancer. Continuing to have IR implies you’re still eating a high-carb diet which to my mind is counterproductive. Better to go keto and supplement with MCT and coconut oil to kick-start the process.
Hi Stuart, re “experts”
I was referring to “medical experts” whose only focus is to treat diseases. To find cures one has to look for “scientific experts”. The money is in treatment not in curing. Most scientific medically related studies end with hope of discovering novel therapeutic patentable drugs by altering some biological pathway, especially if funded by pharmaceutical interests. Patient has to investigate if dietary modifications can achieve the same result.
Novel way to reduce TG:HDL ratio. Combine TG lowering therapy with HDL raising therapy.
https://www.abstractsonline.com/pp8/#!/7891/presentation/35087
Session LBS.06 – Late Breaking Science VI: New Frontiers in Lipid Therapy
– RNA Interference Targeting Hepatic Angiopoietin-Like Protein 3 Results in Prolonged Reductions in Plasma Triglycerides and LDL-C in Human Subjects
Goran
“I also spent a lot of money to remove my old silver fillings”
There is quite a bit of concern about mercury and nickel in fillings – for example, the vitamin C guy Dr Thomas E Levy has written and talked about this.
Also, I think there are (possibly) links to CVD.
Can I ask for more details about the removal of your old fillings, for example:
– Have the mercury fillings been replaced and with what?
– How much of a struggle was it with your dentist to get the fillings removed? Most of us here will be familiar with struggles with mainstream healthcare practitioners with anything unorthodox.
Thanks!
Charles,
Here (America) I had all of my mercury fillings replaced at least 25 years ago. After the mercury is removed a pocket is formed in the tooth and a material (some kind of porcelain) is shaped to fit the pocket and properly form the surface of the tooth. My dentist told me that over time the inserted piece bonds to the tooth itself. That seems surprising but in all this time I’ve never had one come loose.
Phil
I haven’t had my amalgam fillings removed, just replaced as they start to leak (I had some real cowboy dentists in the past).
One of my excellent dentists determined to continue doing NHS work when most of his colleagues gave up, and at first he got so much extra work that he took on a new partner. Eventually he gave up when they started paying him less, and late, and he was basically restricted to doing amalgam fillings and extractions.
Since then I had had ceramic replacements and as you say I haven’t had one leak or work loose. Amalgam may be cheap but only in the short term. Long term the modern stuff is far more cost effective quite apart from being less toxic.Incidentally since going low carb my teeth and gums are in much better shape and seldom even need cleaning with that horrid ultrasonic scraper.
chris c: Yes, mine, too-teeth and gums ridiculously healthy. I think the vitamin C helps, too.
Probably also D and K2 as well for the calcium metabolism. Sunshine and cheese, what could possibly go wrong?
I read somewhere that increased tooth decay was seen as an inevitable consequence of high carb low fat diets, but was considered a trivial problem which could be solved by employing more dentists..
Chris, when you refer to porcelain fillings do you mean that white resin that they fill the cavity with and then harden with UV light?
Charles Gale: Here in the U.S. there is a protocol for removing mercury fillings from teeth. It involves a vacuum device for removing the debris and fumes, as well as a separate air supply for both the patient and dentist. Those who do it here are called “biological dentists.” I had only one properly removed (the only one left; the others having been removed haphazardly over the decades of routine dentistry, such as extraction). The Chinese government has just announced a new five-year plan (2020-24) which will entail a large expansion in the number of coal-burning generating plants. Greta’s going to have a fit. Coal burning I believe is the major environmental source of mercury, particularly in fish.
Charles, thank you for your concern.
Since “silver fillings” are not officially recognized as hazardous in Sweden you have to do it on “your own” and pay out of your own pocket for the replacement with composite material – I guess a ceramic powder mixed some polymer which hardens upon UV-radiation. These replacements have worked fine for me.
The funny thing here was that my dentist who was a high level ‘performer’ said that it was not necessary to remove them but at the same time told me that he had been a part of the process in which “silver fillings” were finally ruled out in Sweden. He turned a little embarrassed when I asked him why that was done if it was not necessary.
I guess it is all about economy. If the hazardous aspect of mercury in your mouth is recognized there are innumerable people like me with a number of old fillings to be replaced at health care expense.
From my personal point of view it is all about precaution and reducing “stress” from all different ‘minor’ poisons you are constantly exposed to and the idea of being exposed to mercury vapor, which is chemically is very reactive, and generated from foreign objects inside you own body finally made me, as the old metallurgist researcher I am, to take personal action/responsibility for my own health as I did with my CVD issue.
As I said it was amazing to see how the team (it was actually a part of an educational performance) so meticulously proceeded with plastic covers all over and especially in my mouth where the only part exposed was the actual tooth the were working on. I was kind of incredulous to combine this procedure with an affirmation that these “silver fillings” are innocent regarding your health.
I think that Dr. Mercola has a lot to say about this issue.
Garden hose and CVD similarities thread continued…
…I have pronounced vascularity (i.e. prominent veins) on the back of my hands and forearms.
And a high CAC score (i.e. confirmed arterial blockage).
Rightly or wrongly…vivid imagination?…but I often visualise someone standing on a garden hose to produce this vascularity: one side of the foot ready to burst, the other side of the foot the hose is flat.
But I can’t remember if the vascularity occured after my CVD incident, or was always there.
Charles Gale, one has to consider effect of nozzle and flexibility of hose. Try to visualize a small diameter thick walled hose transitioning into a larger diameter thin walled hose with a throttle at the exit. I have one of those self retracting hoses that could be used in an experiment.
Charles, I’m in my late 50’s and I’ve had prominent veins on the back of my hands (and elsewhere) for many years. I started taking K2 a few months ago, and my veins look like they did 25 years ago, I’d say 70% decrease. Nothing else i’ve tried has had this effect, including high dose vitamin C. I am currently experimenting with 3 different K2 supplements: Innovix Labs mk-4/mk-7 mix gel caps, Thorne mk-4 liquid and Thorne mk-4/vit. D liquid. My wife and I are trying them. We use our experience plus also muscle testing to decide which one we like the best. (Haven’t decided yet).
I like that the Innovix one has both mk-4 and mk-7, and I like that the Thorne ones are liquid (in organic olive oil). I read a nice write up a bit ago by Chris Masterjohn about K2 and the benefits of the different forms and I picked his top recommendations to try along with calling the manufacturers to be sure their products met my high standards.
Dr. John H: re veins, an interesting observation that needs an explanation
This is what might be happening: Veins are thin and flexible but with inadequate D3, A and K2 there will be calcification in the soft tissues making the veins more rigid and pressure will increase making the veins bulge in some places. Awesome that condition can be reversed so quickly.
https://www.ahajournals.org/doi/10.1161/HYPERTENSIONAHA.116.08869
The combination of low vitamin D and K status was associated with increased blood pressure and a trend for greater hypertension risk.
Dr, John H, calcification everywhere, thanks for bringing up this topic
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6804219/
Pathological Mineralization: The Potential of Mineralomics
“Here, we discuss and bring attention to a biological mineralization process sometimes overlooked, but with a huge impact on human health: pathological mineralization.”
Don’t forget cheese! . . . be right back . . .I’ve also been supplementing with K2 (belt and braces) but it doesn’t seem to have affected my veins. But then I have had damage from fifty years of undiagnosed diabetes, and recently my thyroid was playing up. Last test it was still high but no longer considered treatably so. And now my doctor has left, I have yet to discover if she took early retirement or moved elsewhere. Now I have to train a new one.
Politics, can’t get away from it. Robert Lustig’s characteristically long video explaining to Google staff about sugar and metabolic syndrome.
A really great talk – thank you!
AhNotepad, important lesson
Robert mentioned “logic” once. Possible that bad logic causes CVD.
Proof that saturated fat causes CVD using fuzzy logic:
Premisses
1- Fat people have more CVD
2- Fat people have more T2DM
3- T2DM associated with CVD
4- Substituting PUFA for sat, fat lowers LDL
5- LDL is bad cholesterol and causes CVD
6- Eating fat makes one fat
Conclusion: Saturated fat causes CVD
andy.
AhNotepad, important lesson
Robert mentioned “logic” once. Possible that bad logic causes CVD.
Proof that saturated fat causes CVD using fuzzy logic:
Premisses
1- Fat people have more CVD
2- Fat people have more T2DM
3- T2DM associated with CVD
4- Substituting PUFA for sat, fat lowers LDL
5- LDL is bad cholesterol and causes CVD
6- Eating fat makes one fat
Conclusion: Saturated fat causes CVD
This seems false logic rather than “fuzzy” logic. It reminds me of the three tailed cat.
1. No cat has two tails.
2. One cat has one more tail than no cat.
3. Conclusion: One cat has three tails.
I don’t think Lustig was saying anything like “sat fat causes CVD”. I think you will find he was saying sugar (particularly refined sugar, and even more particularly high fructose corn syrup HFCS) is metabolised in the liver to cause both NAFLD, and deposits fat elsewhere. This metabolic syndrome is the problem, via complex chemistry in the liver.
“LDL is bad cholesterol and causes CVD”. Why did I not see this? I saw LDL was a marker for CVD, not that it was the cause.
“Eating fat makes one fat”. In which case why does Lustig say exactly the opposite, and stresses “All calories are not the same”? This being the mantra of the sugared beverage manufacturers.
AhNotepad, My comment had nothing to do with Lustig except the word “logic”. Came across the term “fuzzy logic”. In medicine there is also the possibility that something can be interpreted not only as true or false, but also as existing somewhere in between. There appears to be a lot of fuzziness in study interpretations. Too many variables perhaps, such as unknown unknowns, known unknowns, or just guesses. Don’t take a study at face value, dig deeper.
Andy, my comment was merely to post a link to Lustig’s presentation. He seems to have dug far deeper than most. I don’t see where fuzzy logic came in. Fuzzy logic was a trem coined for use in engineering where hard logic could not cope with machines coping with the “real” world, so some flexibility was needed.
AhNotepad, I was expanding on “logic” at 29:43. The “fuzzy” part was added by me, nothing to do with the video. There appears to be a lot of fuzziness in medical science. Perhaps not, according to orthodox fundamentalist medicine practitioners.
You missed out “because it comes from animals”
That video is interesting because it shifts almost all the ‘blame’ onto fructose – which, of course, is half of sucrose – ordinary sugar. That makes me wonder whether the other carbohydrate foods, which generally consist of glucose polymers, are half as dangerous as is often claimed.
Interesting. What in your opinion is to blame?
ahNotepad,
The only thing I would say, is that sugar (50% fructose) seems a good deal worse for you than the same amount of pasta, say. I mean, there are people who eat a lot of pasta, and seem to manage OK, so I begin to think that the crucial damage must be mainly due to fructose.
Like half of Italy, for example…
A very good explanation of how glucose causes obesity. Other consequences of excess glucose/fructose:
https://microbiomejournal.biomedcentral.com/articles/10.1186/s40168-019-0713-7
“Conclusions
We have clearly shown that a high-fructose diet-induced aberrant structure of the gut microbiota and reduced fecal SCFAs levels, demonstrating a contribution of gut dysbiosis to hippocampal neuroinflammation in C57BL/6N mice. “
https://link.springer.com/article/10.1007/s00125-017-4541-7
“To the best of our knowledge, this is the first prospective study of the association between diabetes (assessed using HbA1c levels) and cognitive decline that analyses data from more than three cognitive assessments over time.”
https://www.psychologytoday.com/ca/blog/diagnosis-diet/201609/avoiding-alzheimer-s-disease-could-be-easier-you-think
Dr. Malcolm Kendrick,
What is this statement based on:
“Why would LDL that enters the artery wall, via the vasa vasorum, cause no problems.”
Reply to myself:
Premisses that LDL is harmless when entering via VV
>LDL can enter VV via capillaries
>veins have VV
>arteries have VV
> veins do not get plaque
Conclusion: LDL does not cause plaque when entering via VV
False Analogy (comparing apples with oranges):
>Arteries high pressure, veins low pressure
>Arteriey walls thick, vein walls thin and flexible
>Arteries have thick tunica intima/media, veins have thin tunica intima/media
>LDL retention time longer in arteries, lower in veins
>Prandial state glucose levels 20-25% higher in arteries than in veins
>High glucose in arteries damages artery glycocalyx, more inflammation
>High glucose in arteries results in more ROS, oxidation of LDL
>Proliferation/migration of VSMC in arteries due to high glucose
TG cross BBB: (Now I have to check what is effect of low insulin on brain)
https://www.nature.com/articles/ijo2017231
Triglycerides cross the blood–brain barrier and induce central leptin and insulin receptor resistance
“In conclusion, we showed that triglycerides cross the BBB and induce central receptor resistance to leptin and insulin, with resulting effects on feeding and cognition. These results suggest that targeting triglyceride levels in blood could be a strategy for treating obesity and the cognitive problems associated with CNS resistance to leptin and insulin.”
Researchers find vitamin B1 deficiency key to vascular problems for diabetic patients
https://warwick.ac.uk/newsandevents/pressreleases/researchers_find_vitamin/
Researchers at Warwick Medical School, University of Warwick, have discovered that deficiency of thiamine – Vitamin B1 – may be key to a range of vascular problems for people with diabetes. They have also solved the mystery as to why thiamine deficiency in diabetes had remained hidden until now.
Diabetes is increasing in incidence in the UK and elsewhere and one of the most significant health problems associated with the condition are vascular complications: microvascular complications, such as damage to the kidney, retina and nerves in arms and legs; and macrovascular complications, such as heart disease and stroke.
The University of Warwick researchers, led by Professor Paul Thornalley, have shown conclusively that diabetic patients are thiamine deficient in blood plasma. They were also able to solve the mystery of what was happening to thiamine in diabetic patients and connect it more closely to vascular complications in diabetic patients.
In a paper entitled “High prevalence of low plasma thiamine concentration in diabetes linked to a marker of vascular disease”, published in Diabetologia on 4th August, the team found that thiamine concentration in blood plasma was decreased 76% in type 1 diabetic patients and 75% in type 2 diabetic patients. This significant decrease had been previously masked as the conventional way of assessing levels of thiamine status was to measure the activity of an enzyme called transketolase in red blood cells. Past studies had seen normal activity of this enzyme and assumed normal levels of thiamine when in fact the normal enzyme activity was due to increased amounts of two proteins THTR-1 and RFC-1 that help transport thiamine into red blood cells. The increased levels of these proteins were a direct response to there being a deficiency of thiamine in the body.
The researchers found that the decreased availability of thiamine in vascular cells in diabetes was linked to a marker of microvascular and macrovascular complications. It likely reflects problems in endothelial cells (endothelial cells line the body’s entire circulatory system) and increased risk of atherosclerosis (chronic inflammatuion in the artery walls).
The researchers found that the decreased plasma thiamine concentration in clinical diabetes was not due to a deficiency of dietary input of thiamine. Rather it was due to a profound increased rate of removal of thiamine from the blood into the urine.
The researchers feel that important areas for future study are: confirmation of low plasma thiamine concentrations in diabetic populations of other countries independent of local diet; the evaluation of thiamine and thiamine derivatives to correct low plasma thiamine concentration in diabetes, reverse vascular dysfunction and prevent vascular complications; and investigation of the mechanism of increased removal of thiamine from the blood into the urine in diabetes.
Note for Editors: This study was funded by a project grant from Diabetes UK
Paper online at: http://www.springerlink.com/content/r4723142882735l5/?p=de1637f799b94f9eaf1affc684404efb&pi=1
Charlie, re low B1 and diabetics
A quick search revealed that B1 is required for carbohydrate (glucose) metabolism. Small wonder that B1 levels would be low if one is hyperglycaemic.
I recall benfotiamine (a water soluble derivative I believe) being used with some success, along with alpha lipoic acid and vitamin C.
My neuropathy was at the level of “feet going to sleep” and tingling hands after eating carbs. When I stopped the carbs it slowly reversed.
I’ve known a couple of nondiabetics with peripheral neuropathy which turned out to be B12 deficiency too.
chris
“My neuropathy was at the level of “feet going to sleep” and tingling hands after eating carbs. When I stopped the carbs it slowly reversed.”
Exactly that happened to my T2D although her neuropathy was very severe. When she cut all carbs her improvement was dramatic and within one year her symptoms were almost all gone. Although upon cheating with the carbs they could severely return.
chris c/Goran, re neuropathy
Appears that the CNS is also involved in insulin and glucose regulation. Imagine what can happen as we age and have lost some critical neurons in the brain. One can go low carb to improve symptoms, but the sensitivity to high carbs remains.
https://bioelecmed.biomedcentral.com/articles/10.1186/s42234-018-0009-4
Review of the role of the nervous system in glucose homoeostasis and future perspectives towards the management of diabetes
Amazing isn’t it? I have also known not a few diabetics who similarly reversed retinal damage. Opticians/opthalmologists see this occur but other doctors, not so much – though with an increasing number of exceptions.
Hi Chris, natural forms of thiamine are water-soluble and have to be taken in divided doses during the day to avoid getting excreted in the urine. The advantage of benfotiamine is that it is fat-soluble so it can be stored by the body thus can be taken once a day. Benfotiamine was developed in Japan to treat peripheral neuropathy in alcoholics and like diabetics alcoholics are thiamine deficient, so it is reasonable to think that it may treat diabetic PN as well.
Paul Thornalley seems to be the same PJ Thornalley who wrote a paper hypothesising that many of the complications of diabetes are due to thiamine deficiency. He was subsequently involved in a study in Pakistan where 7 out of 20 diabetic nephropathy patients (35%!) treated with thiamine reverted to normal kidney function and the other 13 all improved. Analysis here
https://proteinpower.com/blog/thiamin-and-diabetic-nephropathy/#more-2869
You have to wonder whether the results would have been even better if combined with a low carb diet.
Thiamine help protect 3 of the pathways of diabetes damage. Leaving a need for an aldose reductase inhibitor. There are naturals inhibitors that can help.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4575143/
Even if you think you have your blood glucose under control. There can be damage at different levels and A1c is not a good indicator of blood glucose swings. Genetics play a role on levels that can cause damage, some people can suffer damage in the pre-diabetic range while others not.
This study explains cause of AD. Good to know if you have avoided CVD. Explains the mechanism, unfortunately the researchers put the blame on their version of a high fat diet (high in saturated fat, meat and fructose)
https://www.frontiersin.org/articles/10.3389/fnagi.2019.00236/full
The Involvement of Peripheral and Brain Insulin Resistance in Late Onset Alzheimer’s Dementia
“Thus, it is not surprising that HFD has been associated with a large number of metabolic diseases, such as obesity, systemic insulin resistance, metabolic syndrome and T2DM”
IMO “high fat diets” are only a problem when they are also high carb.
Totally off topic, and I apolize, but sad yet very interesting story. Her late husband was a GP in Macclesfield:
https://www.spiegel.de/international/zeitgeist/joy-milne-can-smell-parkinson-s-before-it-is-diagnosed-a-1295601.html
Article is in English, by the way. Just in case someone was discouraged to click…
Google this – cataracts are a known side effect of statins
I wonder how much heart disease is caused by poor scientific methodology? (A failure to apply the scientific method properly — eg gather facts, form hypothesis, test hypothesis, draw conclusion — so often it falls down in the hypothesis testing part, where the wrong experiment yields poor conclusions that become wired into dogma is one example. Another is forming a hypothesis in the absence of facts, and then seeking — and possibly pubishing — only the facts that support the hypothesis.)
Naturally, bad methodology does not cause heart disease — hence the tongue-in-cheek statement, but it sure can associate with it. And that’s part of the problem. Association/correlation is not necessarily causation.
Prominent veins usually mean that you have low levels of subcutaneous fat, which is why bodybuilders aspire to them. When I was in my teens and 20s I had very low body fat levels – shivering at temperatures when others were comfortable and my belly button showed the actual button rather than the hole that most people have. With a 38″ chest and 30″ waist I had to get my suits made-to-measure since my waist was 6″ less than the standard size for a 38REG. Sadly I no longer have that problem. My once prominent veins are now submerged in subcutaneous fat, alas.:(
In a skinny person the veins are prominent because they are more visible. I would think that prominent veins in a non-skinny person would be caused by excessive fluid or blood not being returned to the heart fast enough due to lack of movement.
Stuart: Thanks for that explanation. I have very little subcutaneous fat (and very little visceral fat since converting to low carb). This explains the prominent veins on hands, forearms and feet. On the other hand, I’ve recently discovered I need to increase my caloric intake, as I kept losing weight-down to 133. I’m now back up to 145, and won’t be happy until 150. I don’t eat a moderate-protein form of low carb, as I do muscle building exercise three times a week, and need extra protein.
Vascularity thread continued
Following my hand vascularity/CVD hosepipe comment, I had a few further thoughts:
(1) I’ve never seen a well fed (PC euphemism) person with vascularity
(2) Many years ago at school I did cross country running – I recall another slim (we all were) runner stating it was a sign of fitness – who knows?
(3) Vascularity is more prominent in warmer temperatures
(4) Being undecided if vascularity was a good or bad thing – I did some googling and found many tips/guides on how to achieve vascularity – it’s much desired among body builders, for example.
Dr. John H:
(1) Can I conclude (with your 70% decrease) that you consider vascularity a bad thing?
(2) Why did you latch onto vit K2 for this? For many of us here, vit K2 will be associated with arterial calcium and useful in shifting the calcium away from the arteries.
Chris Masterjohn’s vit K2 resource is excellent and I’ve often checked his buyer’s guide.
Charles Gale: I’ve been thinking about this issue, too. Blood vessels sticking up. Didn’t know is is called vascularity! I’ve had this for a long time, mainly in the hands and forearms, and sometimes in the lower legs. But, wonder of wonders, it doesn’t happen all the time. In warm weather and during exercise they stick up. In cold weather they don’t. In any case, it seems to me that both ways are normal, for me anyway.
Charles, I wasn’t thinking about my veins when I got interested in trying a K2 supplement (after reading Chris Masterjohn’s guide). I was though very surprised at the effect it had on my veins!
Mercury fillings – interesting comments folks. I recall during 6 monthly check ups being asked about getting the mercury fillings taken out.
If a new filling is required, my dentist did give me the option of mercury (cheaper) or ceramic (I think but more expensive).
Certainly my (private) dentist only uses composite, white fillings now. She did say that she would not bother to replace my two amalgam fillings as they were in good condition and showing no signs of breaking up or leaching.
The great advantage of the composite fillings is that the resin is adhesive to the tooth dentine, so the dentist does not have excavate a ‘bell-pit’ to take the amalgam, making the filled tooth much stronger than one using the old technique would be.
For the past month i’ve been trying an experiment with the salt I use to cook with. I switched out the refined salt I’ve used for an unrefined sea salt. The difference between the two being that unrefined sea salt has other minerals in it besides just sodium. I consider it a more natural salt, something our ancestors would be more familiar with. From what I’ve read we began to refine salt, removing other minerals, and making it close to being entirely sodium about 100 years ago.
To my surprise I’ve found the unrefined salt to taste better, and it makes me feel better also. Of course when it comes to feeling better, it hard to say with certainty. The mind can play tricks. But it does seem since I made the switch in salts I have more energy of late.
The taste with the unrefined salt is more pleasant. I find I can consume more of it in a food dish. With the refined typical salt, if I use to much of it the food dish can taste poorly to me.
With salt being historically an item of concern with blood pressure and heart health thought to mention.
Soul: Yes, unrefined salt is better in every way. My concern with sea salt is contamination, so I’ve switched to salt mined from ancient deposits. We have a fine salt here, mined in Utah, called Redmond. In the past I’ve also used various Himalayan salts.
Soul, it is good to remove refined salt, which I think is highly contaminated. However, modern sea salt is apparently contaminated with minute plastic particles. Better to use ancient rock salt, such as Himalayan, but go steady on how much you use.
Thanks Jennifer and Gary. Come to think of it, one of the authors mentioned that concern about micro plastic bits found in sea salt. The author didn’t believe it a big issue as the amount of plastic was tiny, but he pointed out similar as you, there are other natural mineral rich salt options such as mined salt if one was concerned. I’ll give mined salt a try once I’m done with the bag of sea salt I have now. It would be more in line with family tradition. A grandfather was a miner out in the west.
It was interesting reading the couple of books I bought on the potential health benefits of natural salt minerals. One of the authors was making a case that athletes that sweat a great deal do not live long lives. He thought that could be due to the loss of minerals from sweating. He hardly provided proof but it did have me thinking that it might explain why the southern US states, where it is hot and sweaty half the year, reports lower life spans.
Than again one of the authors based his book on the idea that doctors live shorter life spans than others. As far as I know most doctors are not sweaty messes most the time. Would be bad for business if true I would imagine.
Hamalayan has considerable iron. Stay away from if male or post-menopause unless you are for some other reason iron deficient.
Soul wrote: “one of the authors based his book on the idea that doctors live shorter life spans than others”
Would that be the veterinarian Joel Wallach’s book “Dead Doctors Don’t Lie”? I found it quite entertaining when he talked about his experiences as a vet working with wild animals in Africa and US zoos and I agree with him that mineral deficiencies are an important issue that mainstream medicine ignores. However I was less impressed with his enthusiasm for pyramid selling of his mineral salts.
On a related note, I think that human medicine could learn a lot from veterinary science. At least vets don’t condescendingly dismiss their patients’ real complaints as psychosomatic or due to a placebo effect. As Wallach says, farmers can’t afford large vet bills for their livestock so have to make sure they stay healthy in the first place. If only that approach was applied to humans.
Can someone please clarify for me which is correct:
A) Insulin resistance is when the cells need more glucose but their insulin response is below par for some reason, so more insulin is needed to nourish them with adequate quantities of glucose which has meantime built up in the blood through not being absorbed.
B) Insulin resistance is when the cells have adequate glucose and don’t want any more, so more insulin is needed to force them to absorb the glucose which has built up in the blood through over-consumption of sugar and carbs.
No doubt there will be more informed replies than this, but as I understand it:
1) It is not that fat cells ‘need’ more glucose, their function is to stock it in times of excess and release it when needed.
2) Insulin tells these cells to perform their function and soak up glucose from the blood.
3) Insulin resistance happens when something (the insulin receptors) become less responsive to insulin – presumably another feedback loop of some sort.
Like you, I would like an unambiguous explanation of the expression ‘insulin resistance’ – including the mechanism that causes it – if known.
I don’t know if this is Jason Fung’s best explanation of insulin resistance, but I generally find his explanations useful:
https://idmprogram.com/insulin-resistance-hormonal-obesity-viii/?source=post_page—————————
FTL: Not only do high carbohydrate intake lead to high insulin levels, high insulin resistance also leads to high insulin levels. As we shall soon see, it is this insulin resistance that leads to the time-dependent effects of obesity.
However, there is one important question unanswered. What causes the insulin resistance in the first place? Is the problem with the key (insulin) or the lock (insulin receptor). It is quite easy to measure the insulin and it become clear very quickly that insulin is the same hormone whether it is from a non obese or an obese person. There is no difference in amino acid sequence or any other measurable quality.
Therefore, we would have to conclude that the problem is not with the key (insulin). The problem lies in the lock (receptor). The insulin receptor does not respond quite the same way that it used to. This is insulin resistance.”
I think the key is glucagon. But I have never quite worked out how it all fits together. The answer continues to elude me. Try looking at the Robert Luft symposium on youtube by Professor Unger. You will never look at insulin in the same light.
Dr Kendrick. Regarding glucagon. Having watched videos by eminent doctors, as recommended by fellow bloggers interested in diabetes, I understand that there are unanswerable complexities of the subject. I used to ask why we could not have a test to monitor our insulin production and its non-effectiveness. ( seemed pretty logical to me). My question hit a blank face. So to ask the same question regarding glucagon would be a waste of breath I think. And yet knowledgeable researchers often conclude that glucagon is implicated even more than insulin, in managing glucose metabolism.
Seems an area needing much more investigation, and I feel that the over-use of toxic elements in our foodstuffs and lifestyles will ultimately be implicated.
Martin Back: Short answer, A and B are both correct. A applies to brain, B for peripheral tissues. In brain looks like leptin can modulate insulin levels.
Martin, I look forward to answers, if anyone can supply.
Last year I had a catastrophic raise in blood glucose , over several days. Alarm bells sounded all round, and my GP said at my age it was almost certainly due to severe insulin resistance (as you state in A). The treatment available would have to be insulin, which we agreed seemed like cognitive dissonance. All settled down very quickly, and I am using a small maintenance dose, which I am afraid to stop, despite glucose levels being perfect. I am now advised that my deteriorating eyesight is due to major changes in insulin usage, despite HBA1c varying between 44-51, described as “too tight” for an insulin user.
What am I to do?
As to your comment B), I would think that reducing CHO intake ( as I have done for many years) ought to remove any need for extra insulin, which we don’t need, other than to clear dangerous glucose out of the circulation. Where it is cleared to is a real problem.
I have tried all means available to irradicate a raised glucose ‘dawn phenomenon’, and told I must not use evening insulin to combat it, at risk of having a hypo in my sleep. Yet, my decent HbA1c appears to be unaffected by the high morning levels. I have been told that it is short-lived glucose spikes that cause the diabetic-related complications….and these are easily missed between readings from self testing glucose with finger pricks.
Again, what am I to do?
Did you have an infection at the time? – that can greatly increase the requirement for insulin, some Type 1s may have to double the dose to remain euglycemic with a cold, then go back to normal as the infection subsides.
If I remember correctly HbA1c relates to macrovascular complications, glucose spikes relate to microvascular complications, or it may be the other way round, oh dear, anywaty neither are good.
Some people find that a late night snack, eg. of nuts, may help the dawn phenomenon – the liver wakes up in the early hours, decides you are not starving so doesn’t need to release glucose. May take some experimenting to find the right snack though.
Hi Jennifer, your high blood sugar may not only be due to carbs consumed but also to production of glucose in your liver from excess protein, especially if you’ve replaced the carbs with protein rather than fat. The low carb diet is low in carbs, high in fat and moderate in protein – a point that often gets overlooked.
Also take a look at the talk by Professor Roy Taylor of Newcastle University (UK) titled
“Reversing the Irreversible: Type 2 Diabetes and You”
https://campus.recap.ncl.ac.uk/Panopto/Pages/Embed.aspx?id=c3bef819-e5f4-4a55-876f-0a23436988ed
He put patients on an 800 calorie/day diet for 8 weeks and imaged their liver and pancreas at intervals. The patients progressively metabolised the fat in their livers and once the liver fat was almost gone started to metabolise fat in the pancreas. As the pancreas fat reduced their beta cells started to increase their insulin production. Most of them saw their blood glucose levels after 8 weeks were back to normal. I would expect that their IR was reduced somewhat, but 8 weeks might not be enough to fully normalise it.
Rather than follow Taylor’s 800 calorie diet, why not just do a water-only fast? No calorie counting, no expensive supplements. Jason Fung says that his patients generally lose their diabetes symptoms after 3 weeks of a water-only fast. However something he doesn’t stress enough IMO is that he puts the patients on a LCHFMP diet after they come off the fast.
Obviously if you do either the 800 calorie diet or the fast you’ll need to stop the insulin or risk hypoglycemia. Your glucose meter is your friend.
Most concise & first explanation on search;
“Insulin resistance is when cells in your muscles, body fat and liver start resisting or ignoring the signal that the hormone insulin is trying to send out—which is to grab glucose out of the bloodstream and put it into our cells. Glucose, also known as blood sugar, is the body’s main source of fuel”
OK Jerome, but which part has gone wrong, and why?
Is it the insulin receptors, and if so, what has changed?
Clearly insulin is insulin, so at first glance it cannot change, but I suppose it could get glycated or something.
Excellent question. But no one seems to know. Can we assume the problem is not within the cells per second?
Hi Jerome Savage: re cause of insulin resistance, looks like it begins in gut
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3707834/
Microbial Reprogramming Inhibits Western Diet-Associated Obesity
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6191495/
Inflammation and Gut-Brain Axis During Type 2 Diabetes: Focus on the Crosstalk Between Intestinal Immune Cells and Enteric Nervous System
“The gut-brain axis is now considered as a major actor in the control of glycemia. Recent discoveries show that the enteric nervous system (ENS) informs the hypothalamus of the nutritional state in order to control glucose entry in tissues.”
Insulin resistance: The diminished ability of cells to respond to the action of insulin in transporting glucose (sugar) from the bloodstream into muscle and other tissues. Insulin resistance typically develops with obesity and heralds the onset of type 2 diabetes. It is as if insulin is “knocking” on the door of muscle. The muscle hears the knock, opens up, and lets glucose in. But with insulin resistance, the muscle cannot hear the knocking of the insulin (the muscle is “resistant”). The pancreas makes more insulin, which increases insulin levels in the blood and causes a louder “knock.” Eventually, the pancreas produces far more insulin than normal and the muscles continue to be resistant to the knock. As long as one can produce enough insulin to overcome this resistance, blood glucose levels remain normal. Once the pancreas is no longer able to keep up, blood glucose starts to rise, initially after meals, eventually even in the fasting state.
My take on insulin resistance – it evolved as a mechanism for nutrient partitioning, where it takes on different values at different tissues. Thus when glucose is scarce it can be reserved for the tissues that need it while fats and ketones feed everything else.
Whole body insulin resistance is a means for rapid storage of a glut of food, such as in autumn when there are lots of fruit (fructose) and Omega 6 fats (nuts and seeds). The jacked up insulin level blockades fat metabolism so all fat and excess food is stored as body fat to see us through winter. Strange how the body produces palmitate, that instantly lethal saturated fat. eh?
In the modern world winter never comes and we keep on storing food in perpetuity – the body fat cannot be accessed while insulin levels remain high, so a once adaptive mechanism has become maladaptive.
Some of this works at the level of the mitochondria. Some might be in the brain – triglycerides getting through the blood-brain barrier block leptin which like insulin is a “master hormone”. Roger Unger makes a good point about IR between the pancreatic alpha and beta cells preventing the insulin from stopping the output of glucagon. IMO the ability to adjust insulin sensitivity is crucial, but commonly broken.
Developing new diabetes drugs has been hampered by the fact that findings from many mouse models of diabetes have not translated to humans. So Kevin Corbit, a senior scientist at Thousand Oaks, California–based drug company Amgen, decided to start looking at obesity and metabolic disease in other animals. “When I was thinking about things that are quite fat, one of the first things I thought of was bears, and what they do to prepare to go into hibernation,” he says. “But of course you don’t see bears running around with diabetes and heart disease.”
Corbit and scientists at the Washington State University Bear Center in Pullman measured blood sugar levels, insulin levels, body weight, and other markers of the metabolism in six captive grizzly bears before, during, and after hibernation—in October, January, and May. Surprisingly, even as each bear gained more than a hundred pounds in the fall, their cells remained sensitive to insulin, and their insulin and blood sugar levels stayed constant. In people, such an immense weight gain would likely cause insulin resistance. It wasn’t until well after they’d begun hibernating that bears experienced a temporary, seasonal episode of insulin resistance, but even that was completely reversed come springtime. “This type of physiology had never been described before and was completely opposite what’s seen in humans,” Corbit says. [my bold] — https://www.sciencemag.org/news/2014/08/how-fat-grizzly-bears-stay-diabetes-free
So maybe when you develop insulin resistance it means, “Stop eating! We need to burn up accumulated fat.”
We all love “simple” explanations but the issue of our most important blood sugar regulation, as I today understand it, is rather complex where actually the glucagon plays a major role in turning on and off the gluconeogenesis in the liver.
A lecture by prof. Roger Unger opened up my eyes a couple of years ago for this intricate relationship where insulin resistance/insensitivity is of crucial importance especially in the alfacells producing the glucagon. The insulin spike produced, upon a carb rich meal, by the beta cells in juxtaposition to the alfacells should immediately turn off the glucagon production in the alfacells and thus stop the production of the glucose in the liver. But due to the insulin resistance of the alfacells this does not happen so the blood sugar shoots up although there is already enough circulating in the blood from the meal.
The essence of T2D?
I love this lecture for its “deep understanding” of the issue and I can’t contradict him although he keeps clear from the “minefield” of what we should eat (my favorit subject 🙂 ).
Given the publicity for the Lancet study this week where 400,000 participants were monitored for Cholesterol, which is then declared a predictor of later atherosclerotic disease, I’d appreciate your insight into this research, Dr Kendrick.
Who financed it?
Its relentless, never stops – BBC today;
“Prof Stefan Blankenberg, from the University Heart Center, Hamburg, said: “The risk scores currently used in the clinic to decide whether a person should have lipid-lowering treatment only assess the risk of cardiovascular disease over 10 years and so may underestimate lifetime risk, particularly in young people.”
Up to eight million people in the UK take statins, which lower levels of bad cholesterol in the blood.
It is estimated one in every 50 people who takes the medication for five years will avoid a heart attack or stroke as a result”
Lip service then to healthy lifestyle
“An active lifestyle and a healthy diet can also reduce cholesterol.”
And to support the hypothesis that the body doesn’t know what it is doing – evolutionary malfunction.!!
“British Heart Foundation medical director Prof Sir Nilesh Samani said: “This large study again emphasises the importance of cholesterol as a major risk factor for heart attacks and stroke”
Link wont copy but it’s not hard to find. Piece by Fergus Walsh study re over 25’s.
Depressingly familiar slant.
Would love to see this dissected.
Jerome Savage, re cholesterol study
Rather than focusing solely on cholesterol as a risk factor the authors should rehash the study using TG:HDL ratio.
https://jim.bmj.com/content/62/2/345
“A TG/HDL-C ratio of 3.5 or greater was reported by McLaughlin et al.6to be highly correlated with insulin resistance and atherogenic dyslipidemia in men; this threshold was also associated with metabolic syndrome. They proposed that the TG/HDL-C ratio provides a simple way to identify insulin-resistant, dyslipidemic patients who are likely to be at increased risk for CVD. “
A bit off topic but I am mentioning it because the documentary “The Game Changers” has been talked about on here before. On Joe Rogan Experience there’s a debate between Chris Kresser and one of the film’s authors. It’s an interesting watch.
Andy
Thanks for that. For the MSM, if anything is any more than a slogan, the public dont want to know. Very difficult to get past “cholesterol is bad” syndrome.
About getting past “cholesterol is bad” syndrome… why not ask the person where they heard that. Chances are it was a routine checkup at a doctor’s office. Ask if it was the doctor who said it. I just went to an ordinary everyday Cardiologist part of the Duke University health system, and she shocked me by being supportive of the keto diet and being anti-statins!!! The nurses though, they were still in the same rut.
Angelica @ nixgluten
Green shoots – but as the MSM reports on the recent Lancet article shows old notions die hard – especially where big money is at stake.
Went to the sawbones yesterday. BP was 132/76. Woohoo!
Gary
Just had a hip replacement. When I went in, my BP was 185; 100, when I ca.e out of the theatre it had fallen to 110:70 and now is back to 135 85.
Mr Chris: Good! Just goes to show our BP varies depending upon the circumstances. I would prefer it never be taken again. As long as I have blood pressure I’m alive. That’s good enough for me.
Gary
Slightly forgetful before my op I did not note the paper you cite about blood pressure, by I think Porter. This time I will print it out
Mr Chris: Sidney Port is the first author. An essential paper to alleviate concern about elevated BP. I photocopied it as an early Christmas present for my new doctor.
Gary
Thanks for that, it is now printed and filed away where I know where to find ut!
I’m not entirely sure it’s a useless statistic, it’s just way overused. I have migraines and it really helps to know my bp. It took me a long time to get off of beta blockers, but if I eat too much salt, I will trigger a migraine that’s triggered by the slightly higher bp. It only has to go to 150/90 and I am in pain. Then again, I can exercise and that doesn’t trigger it, just long term elevation. A bp monitor is really important to me now that I’m not relying on a bp med for migraines.
Also, if the migraine is triggered by bp, then using something like a decongestant will make it way worse. I don’t know why but it does. If I take my bp and it’s not elevated, then it’s probably a gut thing triggering my headache and decongestants will help. I can’t really tell you why. But I think this is the reason why they don’t give you ergotamine in the ER for migraine. It can backfire. The best ER med I’ve ever had was toradol via IV, for migraine. I don’t know why it isn’t standard.
But the point is, bp is important, just overused. It’s only one datum, medicine keeps trying to reduce human health to a few numbers. It will never work.
https://www.bbc.co.uk/news/health-50648325
Regards today’s BBC article, Zoe Harcombe metely states,
“Surely no health reporter can be this ignorant?https://bbc.co.uk/news/health-50648325
Cholesterol is C27H46O. There is no good/bad version!”
Meanwhile Dr Aseem Malhotra
“Colin Baigent’s comments truly and utterly sickening”
One extreme comment “@BBC and @BBCFergusWalsh
should be charged and tried with attempted mass murder and genocide”
One commentator in favour of the report was advised by Daniel Perot “Declaration of interests – FJB and CW report grants from the ASPIRE Cardiovascular grant award, Pfizer, during the conduct of the study……… Have a nice day ;)”
Jerome, I am interested in the BBC report and Zoe Harcombe’s comments. Would you clarify the point you are trying to make, as the statacco relation of the comments by Harcombe and Malhotra don’t convey much, have no references, and they don’t appear on the BBC report page. Thanks.
AHN Its a tweet from Dec 4th. and I see Dr Aseem has since entered the debate with “Non HDL cholesterol is a surrogate for TC/HDL ratio which is a marker of insulin resistance. Headline should be ‘measure insulin resistance from age 25’ but instead evidence based medicine has been hijacked by #BadPharma and their industry funded cronies https://bjsm.bmj.com/content/51/15/1111”
Dr Zoe Harcombe, PhD on Twitter: “Surely no health reporter can be this ignorant?https://t.co/rKpyBIzXLX “There are two types: (HDL) cholesterol is “good” because it helps the body stay healthy (LDL) is “bad” because it can clog the arteries.” Cholesterol is C27H46O. There is no good/bad version! @BBCFergusWalsh” / Twitter
Quite
The bad news is that you have CVD, the good news is that you have Alzheimer’s.
Skimmed through the following references to connect some dots:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6685093/
Brain Insulin Resistance and Hippocampal Plasticity: Mechanisms and Biomarkers of Cognitive Decline
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5369608/
Fructose consumption reduces hippocampal synaptic plasticity underlying cognitive performance
https://www.sciencedirect.com/science/article/abs/pii/S0197458096002138
Frequency of hippocampal formation atrophy in normal aging and Alzheimer’s disease
https://www.theatlantic.com/health/archive/2018/01/the-startling-link-between-sugar-and-alzheimers/551528/
Dr, Kendrick, a question for you. In a normal cholesterol blood test LDL is estimated. Could the reason for not measuring LDL is because it is not really a cholesterol but a cholesteryl ester?
No, the main reason is that accurate LDL measurement is tricky. It is usually only estimated. Which carries all sorts of errors.
https://www.sciencedaily.com/releases/2019/12/191205183417.htm
The study, published in the journal The Lancet Diabetes & Endocrinology on Dec. 5, provides the first evidence that the measurements of BPA (Bisphenol A) relied upon by regulatory agencies, including the U.S. Food and Drug Administration, are flawed, underestimating exposure levels by as much as 44 times.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4143868/
Experimental studies suggest that both acute and chronic BPA exposure at environmentally-relevant “low-dose” could affect the physiological functioning of CV system and promote abnormal CV activities such as arrhythmias, cardiac remodeling, atherosclerosis, and altered blood pressure.
https://wellnessmama.com/54748/hidden-sources-of-bpa/
My apologies if this has been posted previously, but I figure (if not), this should be of interest to readers:
https://www.thepermanentejournal.org/issues/2019/fall/7225-statins.html
FTL: “Because cardiac relaxation in diastole is highly dependent on adenosine triphosphate, a reduction in myocardial energy production can cause diastolic dysfunction.3 The impairment of mitochondrial energy production by low levels of myocardial coenzyme Q10 (CoQ10)4 and statin-induced depletion of CoQ10 have been described.5 A clinical trial of 14 patients with hypercholesterolemia treated with 20 mg of atorvastatin for 6 months documented the development of diastolic dysfunction in 10 of the 14 patients that was reversed with CoQ10 supplementation at 300 mg/d.6
Our hypothesis is that statin-induced CoQ10 depletion may cause impairment in diastolic function and that the widespread use of statin therapy, particularly in elderly individuals, may be a contributor to the increasing incidence of HF. We postulate the existence of a clinical entity designated statin-associated cardiomyopathy (SACM), which can be defined as an impairment in heart muscle function secondary to statin drug therapy of a severity sufficient to cause HF. Furthermore, we hypothesized that SACM as a drug-induced condition should be at least partially reversible by cessation of statin therapy and administration of CoQ10.”
I know this is off-topic, but I have reached the age when we are offered free Shingles jabs (Shingrix). I’d be interested if anyone here has any relevant information, or simply wants to share their own decisions on this matter.
We know one or two people who have had this disease, and it does sound unpleasant, so I am somewhat tempted to go and have it!
David, like you I am at the age to be offered a shingles jab. One of the side effects of shingles that I read about is neuropathy. Having had chemotherapy two years ago I already have my share of neuropathy in hands and feet – not enough to stop me doing anything but annoying – so I decided to go for the jab. No problems with it but I had to endure a long, unpleasant lecture from the practice nurse about my vaccination record (a blank page) and how I am putting the rest of the world at risk by not buying in to ‘herd immunity’. She tried to persuade me to have a flu jab at the same time but I resisted and won’t go again! Jean
David Bailey: I know little about this issue, but Age of Autism posted an article called “Doctor Describes Serious Reaction to Shingrix.” Worth a read.
BBB and FH and xanthelasma (Dr Kendrick writes “please don’t say xanthelasma, until you have thought very carefully about it”)
Dr Kendrick mentions very high LDL in FH and states “proof…that LDL cannot ‘escape’ from the bloodstream and find refuge in the artery wall, or any other tissue”.
Which got me thinking about my FH testing a few years back and the physical signs of FH (according to the British Heart Foundation handbook and quick guide to FH, and I quote their definitions):
– Tendon xanthomata: these are swellings made from cholesterol on your knuckles, knees or your Achilles tendon
– Xanthelasmas: these are small, usually yellow coloured lumps of cholesterol near the corner of your eye.
Plus high LDL and high total cholesterol (the Simon Broome criteria for diagnosis of FH states total cholesterol “above 6.7 mmol/L”).
I had/have both a cholesterol deposit on one knuckle and high cholesterol and was thus a eligible for a genetic test for FH. And got tested.
I didn’t have FH.
So, my cell receptors are OK and as someone remarked about my knuckle, the excess cholesterol has to go somewhere.
It’s clearly not finding it’s way into my arterial wall because it’s currently either:
– in my bloodstream and
– ending up in places like my knuckle.
A high calcium score indicates chronic arterial damage and thus there will be some cholesterol in the plaque too.
But what’s the mechanism for xanthomata and xanthelasmas? And why those places? Hasn’t it escaped to find refuge in these other tissues/places?
Conclusion?
That xanthomata and xanthelasmus are further evidence that LDL can’t get through/into the arterial wall. If the arterial wall could absorb cholesterol, then it wouldn’t remain in the bloodstream at such high levels and wouldn’t be visible to the eye.
Hi Charles Gale: xanthomas are accumulations of foam cells, different tissues/different names. Foam cells accumulate oxLDL, triglycerides and lipid droplets.
Foam cells are also visible to naked eye in intima layer of arteries. How do LDL particles get there? Does every cell (apart from neurons) in body need access to LDL?
https://www.sciencedirect.com/topics/medicine-and-dentistry/xanthoma
“XANTHOMA— Localized collection of lipid-laden histiocytes
Histiocytes are cells which are fully differentiated from the monocyte/macrophage lineage and Langerhans/dendritic cells.”
“Plus high LDL and high total cholesterol (the Simon Broome criteria for diagnosis of FH states total cholesterol “above 6.7 mmol/L”).”
Charles Gale, that’s a very interesting cutoff. 6.7 mmol/L works out to just under 260 mg/L. For total cholesterol that would be high but not outrageously so.
Seven plus years ago (last time I had blood work), my total cholesterol was 350 mg/L (just over 9 mmol/L) and my calculated LDL-C was 255 mg/L (about 6.6 mmol/L).
I guess coming in 1/10 of a mmol/L under the Simon Broome criteria is why I’ve never had any obvious xanthomata. Whew!
Randall – LDL testing
Your comment about LDL testing reminded me of this article by Dr Mike Eades on the topic. It’s from a few years ago and here’s the link:
https://proteinpower.com/blog/low-carbohydrate-diets-increase-ldl-debunking-the-myth/
Basically:
– LDL can be measured directly from the blood but it’s difficult and expensive
– Thus, most labs calculate LDL using the Friedewald equation
– But, triglycerides (high or low) “upset” the Friedewald equation i.e. not accurate
– the Iranian equation can be used for low triglycerides
Going through my files in response to your comment, I see that I was running my cholesterol results through an online LDL calculator (because my triglycerides were low – less than 100 mg/dl). Here’s the one I used:
https://www.thecalculator.co/health/LDL-Calculator-683.html
Selecting one batch of results, my LDL changed as follows:
LDL cholesterol by Friedewald (1972) formula was 7.32 mmol/L
LDL cholesterol by Iranian study (2008) formula was 6.31 mmol/L
Charles Gale – thx for reply. The NMR blood test is a direct measurement of LDL particle number and size of LDL particles, and also direct measurement of HDL and VLDL subclasses. Best of all it measures oxLDL which I believe is the big trouble maker.
An Establishment cardiologist’s blog, in which he name-calls and denigrates those who hold to ideas different from the Establishment.
An opportunity affirm your own stance publicly, to comment with pointed questions; even counterarguments?
A waste of time, IMO
JD P
I would of the belief that statins cause neurological disorders including cognitive matters. Not so much memory loss but definite weaknesses in placing matters in context & moving between subjects. Loss of mental agility you might say. I was given to understand that this might have been as a result of the loss of Cholesterol – essential for the brain. But this hypothesis is called in to question by the fact that the brain creates it’s own cholesterol. My understanding was that statins diminished cholesterol in the blood, derived from the liver. Dr Kendricks post on the BBB got me thinking (it would take a lot) and gets me in to contortions of thought on the subject.
Is a little knowledge a dangerous thing ?
Jerome,
My intent was that folks who congregate here go a bit farther afield and actually engage misconceptions in the all-too-real Establishment.
Unlike Sasha, I don’t think any effort in that direction is a waste of time. Chip away at them. I do. At the least, you learn something about yourself.
I have some trouble calling up ordinary words and must often fudge in a real-time conversation. I had complied and took a statin for three months several years ago.
Aha?
No. The word thing started before that. Who knows why?? It’s important to keep track of meds and their effects. What the statin DID do was to create aching muscles, fever and other flu-like symptoms – WITHOUT the actual fever or flu. There’s talk going around now about this nebulous concept of nocebo, the mirror of placebo – if you’re told of negative side-effects, you’ll experience them. How embarrassing is that? Well, in my innocence at the time, I didn’t know anything about side effects. No nocebo. As a matter of fact, my GP and I went through various “flu” hypotheses before I looked back and realized that the start of the statin and the “flu” coincided in time.
I quit. “Flu” went away. Briefly rechallenged with that statin. “Flu” came back.
AHA! Quit for good.
We’re all different and can expect completely individual responses to meds – negative and/or positive. It can be really difficult to nail down culpability/beneficence when there’s only the one “study” participant.
JDP
An indication of the validity of the cholesterol – CVD hypothesis is served up by the reaction of the conservative & pro-establishment daily mail readers when the CH & CVD link is trumpeded. Even this mass of soft thinkers gets completely riled (almost exclusively) by old pro statin narrative. To me this is unexpected but indicates perhaps bitter experience, often shared with fellow sufferers. It is also in distinct contrast to the same readership’s reactions when the subject of vaccination comes up. In the latter case ther is a noticeable level of aggression aimed at anyone who questions the benefits of vaccination.
The establishment’s line i& the Mail’s conservative reputation holds & the old order is restored. Interesting, very interesting.
Simon Broome criteria for FH
Sorry folks (and LA Bob), I quoted the total cholesterol of 6.7 mmol/L for a child by mistake (child defined as
under age 16).
For an adult:
“total cholesterol above 7.5 mmol/L or LDL cholesterol above 4.9 mmol/L in an adult”.
More details on the criteria for (definite and possible) FH can be found in the British Heart Foundation’s “Life with familial hypercholesterolaemia”…and other places too, I guess.
Reading Andy’s comments on xanthomas, it’s a lot more complex than I imagined i.e just an accumulation of excess cholesterol, perhaps like limescale deposits in hard water areas.
Stuart
Hospital cost overrun – more than half a billion
https://www.google.com/amp/s/www.belfasttelegraph.co.uk/news/republic-of-ireland/harris-defends-multimillion-euro-childrens-hospital-cost-overrun-37761973.html
The charity CE given reason to claim for compensation – tables turned.
https://www.google.com/amp/s/www.irishtimes.com/news/crime-and-law/courts/supreme-court/supreme-court-says-pac-treated-angela-kerins-in-unlawful-manner-1.3908048%3fmode=amp
Nice article, nice info for who is suffering from anxiety and depression.
https://www.hupcfl.com