(Part 2 of an occasional series about what really causes heart disease)
One of the greatest strengths of the cholesterol hypothesis is that there is no obvious alternative to replace it with. Stress? Well I believe that, in fact, stress is the number on cause of premature cardiovascular disease (although there are many provisos attached to this statement).
But if stress does cause heart disease, how does it do this? With the cholesterol hypothesis you have the massive advantage of superficial simplicity
- You eat too much cholesterol
- The level of cholesterol in your blood rises
- The excess cholesterol is deposited in the artery wall, causing narrowings/thickenings (plaques)
- Eventually these block the circulation, causing heart attacks and strokes
Dead simple?
Of course, when exposed to the harsh light of critical thought, each link in this neat and tidy causal chain crumbles to dust. But it is such a seductive hypothesis that the mind is drawn back to it again and again, like moths to candlelight. It seems so perfectly simple that it must be true.
On the other hand, as I write this, I am also studying the cover of a recent British Medical Journal (BMJ). The headline is ‘Cardiovascular Disease and Aircraft Noise.’ You may have heard about this research in the mainstream media. It seems that living near an airport raises the risk of stroke by 24%, and the risk of heart disease by 21%. It is suggested this is due to the noise pollution. Okay, nice idea, but how?
How can aircraft noise cause your arteries to thicken and narrow?
I believe that this can be explained, but only if you completely discard the cholesterol hypothesis of cardiovascular disease, and look afresh at what heart disease may actually be, and how it is caused.
Atherothrombosis
At this point I am going to introduce a relatively arcane term, ‘atherothrombosis’. No, I have not just made this word up. Nor is it recent. In fact, the basic idea has been kicking around for the last one hundred and sixty years. The concept of atherothrombosis was first proposed by Karl Von Rokitansky in 1852. He believed that thickenings in arteries, or plaques, were the end result of thrombosis (blood clots) forming on the arterial wall. Mainly because plaques looked exactly like blood clots, and seem to contain the same materials e.g. fibrin (a key ingredient of blood clots).
Virchow, another doctor and researcher, who lived during the same era, and who was significantly more influential, argued that this was nonsense. He had noted that plaques were to be found underneath the lining of the artery (endothelium). He argued that it was not possible for a clot to form within the artery wall itself. Frankly, a pretty good argument in the light of their knowledge at the time.
It was also Virchow who noted that plaques contained a lot of cholesterol, and so he hypothesised that cholesterol in the blood irritated the lining of the artery and then entered the arterial wall. Thus began the cholesterol hypothesis.
Although Virchow won the argument, the atherothrombosis hypothesis has sprung back into life at various point over the years, only to die back again. A fellow Scot called Duguid promoted the idea heavily around the second world war, and just after. Various other researchers have also supported the concept that heart disease is primarily due to blood clotting (thrombosis) – in some way.
Interestingly, at one point Pfizer also started to promote atherothrombosis as the cause of heart disease. For sentimental reasons I have kept hold of an educational booklet produced by Pfizer in 1992. On page four it states
‘Several features of mature plaques, such as their multi-layered pattern, suggest that the platelet aggregation and thrombus formation are key elements in the progression of atherosclerosis. Platelets are also known to provide a rich source of growth factors, which can stimulate plaque development.
Given the insidious nature of atherosclerosis, it is vital to consider the role of platelets and thrombosis in this process.’ [Well, quite]
There is little point in referencing this document, as I probably have the only copy left in existence. It is called ‘Pathologic triggers. New insights into cardiovascular risk.’ Produced by Medi Cine Inc. For Prizer Inc Copyright 1992, All rights reserved etc. etc.
It is interesting that when Pfizer did not have a statin, they were looking away from cholesterol as a cause of cardiovascular disease. It will come as no surprise to you that this was not through some altruistic attempt to discover the truth about the true cause of heart disease. It was to help market their drug doxazosin (a BP lowering drug) which had some additional anticoagulant properties.
Of course, as soon as atorvastatin arrived on the scene, no more was heard from Pfizer about the ridiculous concept of atherothrombosis. It was cholesterol, cholesterol, all the way, and fifty billion dollars in profit from atorvastatin.
Pity, really, because in my view, Pfizer had it right in 1992. C’est la vie.
Perhaps I am straying from the issue here. What is atherothrombosis? Or, what is the hypothesis of atherothrombosis?
It goes something like this:
- The lining of the artery (endothelium) is damaged
- A thrombus (blood clot) forms over the area of damage
- After a very short time the blood clot stops growing – and stabilises
- Blood cells called endothelial progenitor cells (EPCs) are attracted the surface of the clot
- The EPCs grow bigger, join together at the edges, and form a new endothelial layer on top of the thrombus [so the thrombus is now present inside the artery wall]
- Various repair systems go into action, to clear away the thrombus from within the artery wall
Rokitanksy did not know there were such things as EPCs, so he had no explanation as to how the thrombus could be found underneath the endothelium (single later of cells lining artery walls). The answer is, of course, that the endothelium was not there when the thrombus occurred. It reformed on top of the thrombus. Yes, simple when you know how.
Had Rokitansky known this, and won the argument, we would possibly never have heard of cholesterol ever again. Unfortunately, as he didn’t know that EPCs existed, Virchow kicked the idea of atherothrombosis into touch, and so cholesterol became the single molecule that has triggered more Nobel prize winning research than any other.
The role of endothelial Progenitor Cells
I recently asked a medical student who had the misfortune of being stuck with me for the day.
Me: ‘What happens in you scratch your skin.’
Medical student : ‘You bleed.’
Me: ‘Then what?’
Medical Student: ‘A scab forms.’
Me: ‘Then what?’
Medical student: ‘The scab falls off after your skin has healed.’
Me: ‘Good, so what happens if you scratch/damage the lining of your artery?’
Medical student: ‘A scab/thrombus forms.’
Me: ‘Then?’
Medical student: ‘Then it falls off…..’
Me: ‘Then what happens?’
Medical student: ‘It….’
Me: ‘It travels down the artery till the artery narrows, and the blood clot gets stuck somewhere?’
Medical student: ‘Ummmm….’
Me: ‘Ummmm, indeed.’
Clearly, you cannot have blood clots breaking off and travelling down arteries to get stuck further down. This would be horribly damaging. Strangely, human physiology is a bit cleverer than that. Yes, if you scratch your skin the clot/thrombus falls off after the skin has healed. This causes no harm to anything. But a damaged blood vessel has to be able to get rid of the thrombus that forms without it breaking off and travelling to the nearest organ e.g. the brain, where it blocks a blood vessel and causes a stroke.
Also, the lining of the artery wall is nothing like the skin. The most superficial layer of the skin (the epidermis) is a single layer of cells. But this layer starts life deeper down, in the dermis. Cells formed in the dermis gradually move towards the surface where they then fall off.
However, the single layered of cells lining the artery walls do not start life deeper in the artery wall, and grow outwards (or inwards). These cells come from within the bloodstream itself. These are Endothelial Progenitor Cells (EPCs). They are formed in the bone marrow and float around in the bloodstream. They are attracted to areas of endothelial damage. They stick to these areas, grow into mature endothelial cells, and form a new layer of endothelium.
A neat and perfect system for ensuring that damage to blood vessels can be covered over, and the resulting thrombus does not end up jamming up the downstream blood vessels. Ask the average doctor about EPCs and I can guarantee they have never heard of them. Never, ever. Important little things though.
As you age, the production of EPCs falls. If you are stressed, the production of EPCs falls. If you take steroids the production of EPCs falls. If you have kidney disease, the production of EPCs falls. Guess what. All of these things are associated with a vastly greater risk of cardiovascular disease. Vastly greater.
For now just to look more closely at one of these risk factors, steroids. Steroids are used in a wide range of medical conditions such as asthma, rheumatoid arthritis, and inflammatory bowel disease. Essentially, they are the most potent anti-inflammatory agents known – and in any disease where inflammation is a major problem steroids work brilliantly (for a while at least).
Steroids can be more accurately called corticosteroids, because the basic building block of all steroids is cortisol. This is one of the natural steroid hormones made within the adrenal glands. It is a stress hormone, which will be produced in much greater amounts under a situation of threat/stress.
So, what happens if cortisol levels are chronically raised? Well, there is a condition called Cushing’s disease. The underlying problem in Cushing’s disease is excess production of cortisol, which can happen for various reasons….that I do not have the time to discuss here.
People with Cushing’s disease develop a range of metabolic problems: high blood sugar levels/type II diabetes, high levels of clotting factors, raised triglycerides, low HDL, high blood pressure, central obesity etc. Production of EPCs also falls. This abnormal metabolic pattern is also seen in those who take a high dose of steroids over a long period of time, where production of EPCs also falls.
Of greatest interest is the fact that people with Cushing’s disease suffer a greatly increased rate of heart disease. Relative risk increased by around 600% – 700% (Or more). People who take steroids long-term have a ~400% increased risk of dying of CHD.
These are not small increases in risk. They are far greater than any of the standard accepted risk factors for cardiovascular disease. In fact, we are talking molehills next to Mount Everest here.
For now, taking the discussion back to those who live near to airports. It is known from a great deal of research that people who suffer long-term negative stress exhibit abnormal cortisol production. Although it won’t be nearly as extreme as those with Cushing’s, or those taking steroids. They also have an increased risk of dying of heart disease and stroke.
It is known that noise pollution creates long-term negative stress. It is now known that people living next to airports suffer a high level of strokes and heart disease.
Try and use the cholesterol hypothesis to explain the increased risk, and you can’t. Try and use the atherothrombosis hypothesis to explain this phenomenon and, it all fits together without any trouble at all. So, who wins this argument? Virchow, or Rokitansky?
Of course it is not nearly as simple as: stress > increased cortisol secretion > reduce EPC production > atherothrombosis…… But it is one important link in the chain.
More on this, at some point.
Dr. Malcolm Kendrick 
Dr. McKendrick,
What conditions favor EPC production? After a new layer of endothelium has covered a thrombus what conditions encourage the absorbtion of the thrombus, what conditions retart the absorbtion of the thrombus.
Thank you for your blog and blogging!
Phil
Hi, I have no data on the following idea, simply personal observations and the fact that it is a close cousin of the Airport hypothesis. I believe that if a study was done it may well show that those people who live on main roads as opposed to quite side roads/cul de sacs etc, suffer greater incidences of heart disease. If you live on a main road and sleep in a front bedroom try spending a week sleeping in a rear or quieter room and see the effect. I recently spent 3 weeks in Portugal where we slept with virtually no road noise. I have never felt better.
Thanks for the very interesting post. But what are the main causes of endothelial damage to trigger the whole process off?
A whole series of things. The most important of which is almost certainly biomechanical stress. You never get atheorsclerosis in veins, as the blood pressue is not high enough (I assume). The main areas of atherosclerotic plaque formation are areas where arteries branch (mainly). Also the coronary arteries – which are exposed to continual stretching and squeezing as the heart beats. Other things found to damage endothelium include: smoking, high blood sugar levels, acute stress, decreased Nitric Oxide production. That sort of thing
That is the direction that they should have followed. That old quote “I nearly had a heart attack” when something is frightening, suggests there has always been a known link
Jo, Correct, sort of. You can die of a ‘heart attack’ in several different ways. You can have a sudden interruption of the conduction system cusing fibrillation, or asystole (heart stops beatin). You can have a major, sudden, bloot clot form in a coronary artery. This will damage the heart enough to stop it beating. You can have a smaller blood clot that affects the conduction system – leading to fibrillation (and death). It is not necessary to have any atherosclerosis in the arteries to die in one of these three ways. The commonest form of ‘heart attack’ is for an existing atherosclerotic plaque to ‘rupture’ causing a major blood clot to form over the way. However, your general point is well made. It is interesting that after major earthquakes, the rate of death from heart attacks goes up for a few weeks. After France won the football world cup in 1998, the rate of heart attacks fell for several weeks. So, yes, the association between acute stress and ‘heart attacks’ is well known. This, however, is a differenct process to the gradual build up of a plaque.
Dr. Kendrick, it all makes so much sense now. My husband had his first heart attack at the tender age of 32. His cholesterol level was 384. This all occurred in 1989. He was on blood pressure medication and was told that was what “saved your life”. Indeed there were genetic factors there on both the maternal and paternal sides. However, now he was given cocktails of potent cholesterol drugs over the years which basically did NOTHING to halt the progression of the disease. He continued to smoke (on and off), ate what he wanted and believed all the cholesterol drugs would do the trick for him. To make a very long, sad story short, my husband died at 50 years of age. Know what he died of? Congestive heart failure. This occurred within two months of having lived through one of the worst storms in the history of the U.S., Katrina. His father, by the way, was told at 55 after his first heart attack that he had 6 months to live. He did what the doctor said. He stopped smoking, watched his diet, and kept a good weight. He lived to be 82. He never took any statins until the last few years of his life. Following the introduction of statins, he went downhill FAST. He complained of constant pain, could barely walk, was awful to live with and died shortly after he started taking them. So, all you have said about the above makes perfect sense to me.
Hi
Can plaque be decreased. I saw photo’s of before and after of an un narrowed artery, cant remember the source, probably Dean Ornish web site. The correction was claimed to have occurred after the patient went on a strict veg diet. My Cardio said that the evidence is unclear which for him probably means without a doubt. By the way had a meeting with him yesterday and asked him is opinion on the new Swedish guidelines. He had not even heard about them but he was quick to remind me for the second time that Omega3 was now discredited.
Don’t know. I think plaques can shrink over time. The problem here is that so many people have so many agendas (usually making vast sums of money), that truth flies straight out of the window. What I do know is that, when it was studied in the 1960s, the Japanese had just as much ‘atherosclerosis’ as Americans. Their CHD rate at the times was 1/20th that of the Americans. So, what does that prove.
So coronary issues are far more likely to be linked to emotions than to food!!!!??
Absolutely
The issue of losing your natural protection against arterial damage is interesting. This recent paper in Circulation – http://circ.ahajournals.org/content/107/24/3059?ijkey=7862414c73f409dc5b63762489d601a79787a82a&keytype2=tf_ipsecsha&cited-by=yes&legid=circulationaha;107/24/3059 – examines the effect of estrogen levels on EPC production in mice.
Might the estrogen levels explain why women live longer on average than men or is this too simplistic?
It would appear that the link between estrogen and EPC levels has been recognised for some time.
Women are protected against CVD at a younger age mainly to a different neurohormonal response to stressors.
Relaxin also appears to be important. In men it is produced in the prostate, so do men who have had their prostate removed have lower levels of EPCs?
http://bloodjournal.hematologylibrary.org/content/119/2/326.full
Sorry. I do not know.
You have started a very interesting thread here. You note the decrease in EPC levels with increasing age contributing to poor cardio-vascular health , and considering just some of the research on estrogen, relaxin, EPC levels, NO, and CVD (e.g. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2515412/pdf/vhrm-0403-515.pdf), the persistence of the mainstream belief in the cholesterol myth is even more remarkable.
I hope people will start looking into this area for themselves. I find it all quite fascinating. once you forget about cholesterol, the world of heart disease becomes much clearer
Do you have citations available to the literature you used for this piece? Would love to see them if you can.
I may start pulling them together. I have many.
I found the Wikipedia article on Plasmin informative (http://en.wikipedia.org/wiki/Plasmin). There’s plenty of Plasmin in the blood stream, but no tissue Plasminogen Activator (tPA) to activate it. If you have an ischemic stroke and you know when it occurred, then tPA can be administered within 3-4 hours of the stroke to break up the blood clot and reduce the impact of the stroke. This actually happened to my wife and it was fortunate that she knew about it and could remind the doctor!
From my limited experience people don’t get themselves to the ER quickly enough, not realizing what can be done for them. When I had a “mild” heart attack last May the hospital was almost effusive because I had come in promptly enough for them to treat me before serious damage was done.
Interesting, is it not, that virtually eveyone accepts that the seriuos/terminal event in heart attacks and strokes is a blood clot, blocking an artery. Yet this has no part to play in the development of atherosclerotic plaques? In my view, bonkers.
Great post Dr.K.
Re the plasmin – it is interesting that Lipoprotein (a) is probably a competitive inhibitor of plasmin action, hence is anti fibrinolytic. I think many (most?) people agree that high levels of Lp(a) do independently correlate with atherogenic heart disease (although cause has not been shown). I am sure some researchers will have looked at cortisol levels with regard to Lp (a). As an aside I live in Australia and have enjoyed the Catalyst programmes. Hopefully it will have opened up new and informed debate on the lipid hypothesis and hopefully some of the dogma will eventually be dismissed.
Re: Cardiovascular Disease and Aircraft Noise
This from 1981 – http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1568850/pdf/envhper00468-0281.pdf
Specifically refers to ‘jet aircraft noise’ increasing psychiatric hospital admissions.
I’m wondering whether this also accounts for the differences in heart disease rates between, for example, the north and south of the UK, or between Britain and the Mediterranean, or between people with darker skins living in Northern latitudes ? There are some doctors who believe there’s a connection there with people living in areas that have more sun having higher vitamin D levels and that accounting for their lower levels of heart disease. Or people with darker skins living in too northern latitudes for them to make sufficient levels of D. Of course maybe vitamin D is protective against stress and that’s how it works ?
Sunlight increases vitamin D, which increases NO synthesis in the endothelial cells. NO is the most powerful anticoagulant substance known.
I really appreciate your line of thinking on this Dr Kendrick.. as you say, once you set “cholesterol” aside, it becomes much easier to start achieving clarity… such a shame it is so profitable!
I chuckled a bit at your interchange with the Medical Student: of course there is the usual chestnut of likening the incidence of cholesterol at the scene of atherosclerosis, to blaming firefighters as the cause of fires but I have also discussed it with others in terms of a patient complaining to their Doctor about all the unsightly scabs on their legs from scissor accidents (as a tailor perhaps)… with the Doctor suggesting that perhaps they should come up with a drug to reduce fibrin and platelet levels, so that the scabs were less likely to appear! 😛
“I believe that, in fact, stress is the number on cause of premature cardiovascular disease”. For such a short and fundamental statement of your beliefs, one might have hoped for no spelling mistakes. 😉 Sloppy proofing aside, thanks for posting this; it fills in a lot of gaps for me.
He was just testing to see if you were awake, maybe you weren’t totally, since I noticed other typos but so what! It’s the absolute sense within the article that allows us to overlook such
little foibles without comment LOL
Doug,
There is just me. Writer, editor, blogger. Full time job, children, writing a book. I kind of hope that people forgive a typo here and there. So long as the thing makes sense….I hope.
‘More on this, at some point.’ Can’t wait!
Thanks
Rather compelling, but how might this hypothesis be proved? What type of trials would ( or could….) be done? Just a thought.
Thanks.
Proof….well, that’s a tricky thing. I would be more inclined to try and disprove it. You can never prove anything, for sure, all you can do is fail to disprove it. Also, I don’t think I have outlined a complete hypothesis yet – just bits of it. In reality, I am having trouble defining the full hypothesis. Still working on it.
I don’t see a logical explanation of why the rate of production of EPCs is a factor in CVD, assuming that a thrombus forms and then is eventually covered by a new layer of endothelial cells. It’s my understanding that at the site of a thrombus one of two things can happen. 1. The plaque forms and is covered by endothelial cells. More damage occurs at the same site and a new thrombus forms and is covered, If this occurs at a rate higher than the plaque is absorbed the overall growth of the plaque progressively obstructs the artery, at which point angina occurs, but that isn’t a heart attack. 2. Sometimes a plaque ruptures and immediately blocks an artery. The plaques that rupture are the smaller ones that can’t be detected; the larger ones are more stable. I have never heard a theory to explain why a plaque should rupture.
There is also a third possibility; a clot forms somewhere else and travels through the arteries until the artery is too narrow for it to travel any further. If that happens in the brain it’s a stroke, if it’s in a coronary artery it’s a heart attack. That may have been what happened with my heart attack, because the thrombus was right at the site of a 95% blocked artery (circumflex). My wife’s stroke occurred 2 days after a lone atrial fibrillation, so that’s almost certainly where the clot came from.
Quite so and my apologies – I’d forgotten one of the basics. Still, disproving the cholesterol hypothesis doesn’t seem to have done it any harm does it? Perhaps we should start calling it the Hydra Hypothesis ?
?
Thanks
Very interesting for an interested metallurgist with severe arteriosclerosis since 14 year.
Being a lifelong researcher I believe in doing the proper homework on an subject of keen interest. With amazement, wonder and with a strong appeal to someone seriously trained in physics and chemistry I have crossed Alberts “Molecular Biology of the Cell” ftwo times. Just now I am half way through the latest edition of Guyton and Hall “Textbook of Medical Physiology” and couldn’t refrain from checking on EPC.
You are quite right – nothing there! Only religion!
And all this talk about damaged endothelium which you commented on above seems to be an ambiguous subject.
As pure biochemistry in terms of loosening up the tight junctions between the endothelia cells makes sense to me. Then high blood sugar, as you mentioned, is to me also a good rational since another sugar as mannitol is well known to loosen these bonds to make drugs pass through the very tight ones of the brain??
There is another theory (Ravnskov/Cully) which attracts me and where microorganisms which have entered the blood stream for any reason are being effectively captured by the various lipoproteins to form aggregates. These aggregates may then enter and get stuck in the minor artery blood vessels (vaso vasorum?) which transvers the larger arteries. This theory attracts me since sound physics seems here to be involved. Arteriosclerosis is mainly found, as you pointed out, where we find the highest blood pressures and here the likelihood is at the largest for these small vessels to open up and to receive these inflammatory particles. (Infected teeth and and heart disease is a well established connection which may support this theory.)
I like parts of Uffe’s theory. But, as he well knows (we have oft argued), I cannot see how it fits the epidemiology. Two populations living cheek by jowl e.g. Australian aboriginals, and Australian Europeans, have a twenty fold different in the rate of CHD. What organism only affects certain populations. What organisms affect men more than women. What organisms affect muslims rather than protestats. In Sweden, immigran muslims have five times the rate of CHD of the surrounding population.
If you have blood type O you have a lower risk of CHD (http://www.ncbi.nlm.nih.gov/pubmed/22895671) and your blood type affects the composition of your intestinal microbiota (http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3485159/). So it seems plausible that the ability of a microorganism to be consumed, survive in the intestinal tract, pass into the blood stream and cause CHD could well be influenced by blood type. Furthermore, if you accept the concept that the suitability of different foods in the human diet can be blood type dependent (as you know I do), then a food that causes intestinal inflammation in one blood type, thus possibly enabling a harmful microorganism to pass through the intestinal wall, may not be a problem in a different blood type.
It’s hard to justify the use of the examples of Australian aboriginals or immigrant muslims to counter Uffe’s theory if you accept that stress in these two cases is a major factor in CHD. Infection by microorganism may be a contributor in other cases, and blood type another factor in other cases. There are probably multiple causes of CHD just to confuse analysis. I would be willing to bet there are epigenetic factors at work too.
Richard, I am sure that there are multiple causes. But I believe that there is only one mechansism/or process
This is excellent – I love the articles and opinions I read here.
I’m hoping to enter medical school in 2015 but the problem I think I may have (assuming I’ll get the grade) is with the interview. If I say what I truly believe about the direction medicine / nutrition has taken over the past 3 or 4 decades I fear I’ll blow it. Do the interviewers want to have medical students who are likely to cause waves as their careers develop or those who’ll simply follow guidelines and the “accepted wisdom”? In other words, should someone like me lie at interview?
You are not going to be asked any of this stuff, so no need to lie. However, you outline an age old problem, for which there are no correct answers. Be utterly truthful, and get squashed. Lie, and move forward to a glorious career. In the end, it is never as black and white as this. As my father often says. ‘Life is a moral gymnasium.’ It is up to you to decide how many twists and spirals you can live with.
I find that a most interesting discussion, Dr Kendrick, and here’s why:
It is true, perhaps, that several risk factors associate with CHD, and it seems they may be concomitant.
The rise in cardiac arrests seen in the recently bereaved suggests bereavement stress can induce cardiac events. If the multi-factorial nature of risk factors is acknowledged for having some basis in fact then the prospect that they may converge upon common physiologic pathways seems worthy of consideration, exploration, and explanation.
I don’t pretend to know what causes the premature advance of cardiovascular disease but in a way I see the advance of degenerative diseases as equating to fair wear and tear of life. Degenerative diseases are evidence of the rule of entropy being enforced in biology and human physiology, if you like. BUT, a very big ‘but’, degeneration needn’t be premature, and I consider we have to concede that certain factors hasten the way in which the rule of entropy is enforced.
It is about 100 years since Nikolai Anichkov fed cholesterol to some rabbits in the lab and hastened the onset of atherosclerosis (more on that in a moment), and roughly the same age when Rutherford, Einstein, and Planck, set science on course to increasingly perceiving energy as being more fundamental or rudimentary than is matter. Additionally it is almost 70 years since just 0.6 grammes of Uranium 235 dropped on Hiroshima resulted in total devastation of the city and the death of 100,000 Japanese. Ya gotta have respect for ‘energy’. Note what less than a gramme of it can do.
In a quantum universe matter supposedly distilled out of energy to result in the stars and that which followed, I don’t know, but if energy is somehow more rudimentary an entity than is matter then everything we can witness around us is backwardly dependent upon the behaviour of energy, and it all emerged with identifiable sequentiality. God resides in the molecules, and in the sequentiality of emergence, traceable and manifest, long before the emergence of molecules themselves. God is everywhere and nowhere, baby. But I won’t make a fuss, despite it’s obvious.
In a quantum universe the similarities between mineral, vegetable, and animal, are greater than common perception suggests. The differences arise in the manifestation or treatment of energy, and not in the basic building blocks that make each possible. Species that metabolise had no future without adequate mass of species that photosynthesise. Watson and Crick advise the coding that’s so crucial as the blueprint for life boils down to an arrangement of atoms in legendary double helix.
Medicine and biology can afford to be more energy centric in the ways it views its subject.
Life owes a lot to ions, and life is only possible because water, in individual molecules of water as opposed to a body of water, is highly magnetic and attractive to ions of either persuasion. More than anything this explains how 20 or more essential elements enter the food chain making vegetable, then animal, possible. The total ion count that enters living things at the base of the food chain is high, whereas compared to our mass the total ion count within us is significant, highly functional, but nonetheless low compared to our mass.
Mind you, when we exit this life and we are laid to rest the dismantlers and reclamation teams move in. If it were possible to trace where all the stuff we’re made of goes to when it’s reduced, then mass for mass there would be a rise in the total ion count. The earthworm is natures’ great dismantler or organic matter, and its casts are rich in ions, which explains why earthworms are so good for the soil.
Cars are an example of structure and purpose, yet the rule of entropy gets them in the end. Drive them hard and fast, fail to treat them with mechanical sympathy, or expose them to harsh environments, like lots of wind and sea-spray, and it hastens their passage through a useful life to the scrap-heap at the end. Oxidation, rust, and corrosion, enforce the rule of entropy as applies to cars.
Biology is an example of structure and purpose. Given the availability of energy sources, plentiful water in the liquid state, and a plentiful supply of mineral ions then life is a quantum eventuality. I’d go to so far as to say that under the right conditions life is a quantum certainty. Yet in this it isn’t so different from the merely matter or mineral. It is the same basic stuff but reworked in ways that exhibit more sophisticated use and manifestation of energy, leading to wilful mobility, sex, and perception.
All that said, Dr Kilmer McCully was involved,with a team of researchers In America who, in the 1970s, went to some lengths to isolate pure cholesterol and keep it pure. Then they went the extra mile and they produced batches of each of the three possible oxidised cholesterols or ‘oxy-cholesterols’. Next they added these to food fed to several species of lab animals.
Contradicting Anichkovs findings from 1913, and perhaps not, these researchers succeeded in inducing atherosclerosis in their subjects – if with a twist. Pure cholesterol was innocuous (had no effect) whilst each of the oxy-cholesterols were injurious, and one was especially striking for inducing atherosclerosis. To this day we know quite ‘why’ and largely through not knowing just ‘how’.
It seems when Keys took up with curiosity in Anichkovs work the effects of oxidised cholesterol(s) were unwittingly (and wrongly) attached to cholesterol itself. Keys hypothesis could never amount to a silk purse, it was destined to remain a sows-ear all along.
Various theorists have tried to explain atherosclerosis and cardiovascular disease. Rath and Pauling suggested it could be prevented with a plentiful supply of vitamin C, an antioxidant, indicating antioxidant deficiency could be a causal factor. Dr Kilmer McCully suggested residual homocysteine could be involved if it’s persistence was not countered by an adequate supply of B vitamins, lately Ober, Sinatra and Zucker suggest free electron deficiency contributes to lingering oxidative stress and inflammation, and we’ve heard it mooted on several occasions that oxidative stress and inflammation are causally linked to CVD.
It is nothing if not confusing.
Ober, Sinatra and Zuckers ‘Earthing’ theory made an impact on me. They say they have detected a tendency for the body to develop a detectable net positive charge. The charge they say, quite convincingly, is not healthy, and it can be redressed by taking the trouble to earth oneself by going barefoot of good ground. Slowly I began to wonder if they had properly explored the the question of how we assimilate this positive charge that was always countered until very recently, when shoes and homes, and the materials they’re now made of, resulted in growing electrical isolation from ground to the point where it almost total isolation.
After a year of wondering I had a hunch that the species that metabolise sacrifice ions as a by-product of metabolism, and the ions escape via the various pathways dedicated to waste; exhaled breath, sweat, urine, & pooh, mainly. This is not a mature area of science but did trump some results that suggest this thought could be on the right lines. In healthy subjects the pH of exhaled breath condensates (EBCs) trends to become more alkali as they exert themselves more, and anyone who has exercised hard knows that painful lactic acid can build up in the muscles. Sweat, normally strikingly acid, trends to neutral with exertion.
To my mind species that metabolise sacrifice ions to their environments through these pathways, but more anions than cations are sacrificed, and there is a residual build up of cations. Physical work involves increased sacrifice of more anions, and can lead to cationic species, like lactic acid, lingering in the body. This explains, I feel, how we develop this net positive charge. In natural situations this would never happen because we would draw a tiny current from ground to counter this cationic duress, but in our world of man-made materials we no longer do, unless we deliberately go barefoot or invest in an earthing sheet.
Airports are interesting, as is the suggested cortisol connection. Not only is there a lot of noise pollution near an airport, but there is also a lot of light pollution. Big and busy airports serve densely populated areas, and there is lot of artificial light burning when the sun is busy lighting up the other hemisphere.
In a book published in 2000 TS Wiley and Bent Formby present a thesis that the blame for heart disease, cancer, metabolic syndrome, and obesity should be placed fairly and squarely at the feet of Thomas Edison, the inventor of the light-bulb. The ubiquity of artificial light in the developed world means we’re never exposed to darkness in the ways the natural cycles of light and dark would enforce. We sleep much less too, and don’t spend enough time sleeping and dreaming. This sounds completely whacko and fanciful upon first contact, and yet they make a striking and well reasoned case.
The darkness would reset our hormones, normalising them in readiness for the next day, but sleep shortage and light pollution interferes with the process. Levels of cortisol, they say, are permitted to remain high, and they don’t get normalised by adequate sleep in adequate dark, and persistent high levels of cortisol raise levels of insulin and contribute to inflammation, perhaps via the route of oxidative stress.
Howsoever we look at it, what is known about the workings of the endocrine systems (and even the autocrine system) may work in a cascading system, where changes to one balance or level of one hormone invoke alterations to others and so on. Plus there are two sides to these important biochemicals charged with conveying regulatory messages. One side is cationic, and frequently the agonist, and the other side is anionic, and frequently antagonist. Indeed these eicosanoids and hormones are often considered to act in pairs, one initiating some physiologic process, and it’s partner terminating it. The cations are the stressors preparing us for adversity, or even resulting from it, and the anions are the soothers, perhaps, sacrificing a free electron in order to pacify a reactive cationic type.
I think your discussion of the cortisol connection is a good lead and especially so if it can be associated with increased cationic duress.
My suggestion that atherosclerosis could be likened to ‘rust’ seems a bit simplistic, but in our corner of a quantum universe it might just be evidence of the rule of entropy being enforced consistently in the worlds of mineral and animal, in that hard driving, or harsh environments add to the basal levels of wear and tear and hasten our delivery to the dismantlers. Oxidative stress, or cationic duress, might just be evidence of a quantum consistency, and it may well apply to heart disease, if only we knew ‘how’.
In the end I think we have to concede that persisting with maladaptive arrangements, either within the diet, or associating with environmental factors may add to oxidative stress, or cationic duress, and/or inflammation, with associated suppression of the immune response and degraded capacity for healing. I am in no doubt though, that the human relationship with cholesterol, lipoproteins, and saturated fat is one we can afford to brand as being essentially adaptive by nature’s standards, and not nearly so harmful as the idiots, erm I mean ‘experts’, have it.
By not reliably describing the causes of heart disease the cholesterol hypothesis may well have consigned more people to the scrap-heap than did the 0.6 grammes of matter dropped on Hiroshima. I apologise for the length of this comment, Dr Kendrick, but I do know you consider the subject important enough to warrant free and open discussion.
I might be able to sleep, now that I have got that off my chest.
Thanks, Doc, you’ve been a great help.
Have you encountered ‘Lights Out’ (Wiley and Formby)? I highly recommend it.
Chris Palmer
Blimey,
I wondered whether or not to turn this into a post on my blog. Thanks for taking so much effort
I think John Locke, David Hume, Schopenhauer and not least Karl Popper may have something to add to your reflections on entropy and causality and most probably also Parmenides and Xenophanes.
Chris, your comment is the most interesting I have read; in my next life I must endeavour to study quantum physics! Your point about energy supports the body’s requirement for fresh natural uncooked food. Often when I have eaten something fresh and uncooked there has been a noticeable increase in my energy levels so you have now convinced me to attempt to travel this road more frequently; I say attempt as I continue to love my juicy steaks, with its fat, and fried in beef dripping!
Denise Minger thought a diet of raw plant foods would be healthful – and made herself quite ill. Seek her blog. That aside raw can be used to good effect.
You’re the clever one here – you correctly diagnose your condition and prescribe the fix. The condition reads like impaired glucose tolerance and the contrast in your energy levels is advising you to ease up on the amount of white carbohydrate you eat. Continue to enjoy protein (with the native fats) but keep consumption of protein modest. Cut back on white carbs, include sufficient fat (sat & mono), and make capital use of the fibre in med and low GL plant foods (raw can add to the capital) and your body will no longer be in receipt of a more peaky supply of glucose than it was designed to cope with – which is all impaired glucose tolerance is likely to be.
Free electrons and photons impact upon health. Get enough fresh and daylight, consider blackout curtains, an earthing sheet is prudent, but a simple antistatic band worn around the ankle is as effective, and a fraction of the cost.
To this day we DON’T know quite ‘why’ and largely through not knowing precisely ‘how’.
Bless me, in that rush of blood to the head I forgot to make my main point.
I wanted to make a suggestion. Have the effects of stress, or things that arise under the effests of elevated cortisol, been investigated for their effects upon ion sacrifice? Might increased stress raise the level of anions scarificed in EBCs or the other pathways, just as increased exertion appears to do? Have you attempted to look for whats been established and reported?
I have no idea, btw, but I wonder if I can sense the prospect in my water.
Chris
Thank you, that’s kind, .. .. but as you well know from experience reverse engineering the crap outa the cholesterol hypothesis is no easy task, and I learned everything I know from a handful of individuals who slaved hard and long, burning midnight candles, assimilating the facts in the face of all the nonsense. I’m lucky, my oocupation demands attention, but while giving it the attention it needs there is plenty of time to think. I just resequence the things I pick up along the way. ‘Biochemistry for Dummies’ was a big help.
What role does chronic neuropathic pain have on arterial and heart muscle health? I have taken statins for more than a decade and have both proximal muscular pain and atrophy in the legs.
Karen. I would speak to your GP. Those are both, possible, statin related side effects (but may not be). Perhaps ask for some tests. Sorry, but I cannot provide anything more than general advice on the Internet – for obvious reasons.
Thank you for your reply. The problem is that GPs do not have the expertise when looking at the long-term implications- I have gone back time and again with the issue- what I really should do is ask for specific tests,but lack the knowledge of what to ask for. Tricky- when the last thing I want to do is burden my GP with requests for tests when presenting with what could be (serious?) side-effects.
Not being a medical doctor I may comment on your concern.
I would never dream of taking any statins myself although the doctors prescribe them to me all the time since I have a serious CHD. And nerves for sure need their cholesterol to stay healthy so no wonder in my eyes that your nerves have suffered from a drug that lowers your cholesterol.
Chronic neuropathic pain is also a late diabetic implication which made my wife suffer severely without the health care system being able to figure out that she was severely diabetic. When we realised that, dramatically, by ourselves 1999 and we made then a logical decision to cut “all” carbs out of our diet since the carbs are exactly what makes diabetics ill.
In half a year the neuropathic pain was gone and also her vision in darkness returned so she could drive the car again when it was dark.
Neither of us take any medication and it works fine as long as we stay away from the carbs.
Thanks Professor- I do have diabetes but the neuropathic pain is from chronic Complex Regional Pain Syndrome. I have had nerve conduction studies and EEG that indicate little or no diabetic neuropathy.
When you mentioned that stress was a likely cause of heart disease, I’d just assumed it caused high BP, which either caused the original arterial damage, or ripped the plaques off the arterial walls. Was this just way too simple, or is this likely to happen too?
David
A bit too simple, I think
Is it possible to measure EPC numbers easily, and is there a way to boost their numbers if necessary? That might form a great therapy!
You cannot measure EPC numbers easily. It is a pretty specialised test. Boosting EPCS numbers is not eary
The link with stress, David, links to the hormone cortisol (and other of the glucocorticoids perhaps) and elevates the amounts of homocysteine that may be circulating in the body.
Homocysteine is an interim breakdown product associated with the normal metabolism of methionine. Methionine is an essential amino acid generally more abundant in meat.
Homocysteine belongs to the class of reactive oxygen species or ‘free-radicals, it is fat soluble, and so its’ presence in lipoproteins (such as LDL) is a distinct possibility. In healthy people on a healthy balanced diet homocysteine would be rapidly reduced by the action of fat-soluble B vitamins (antioxidants) that can sacrifice an electron to pacify the radical (damaging and reactive) aspects of homocysteine. Left unattended to homocystein may be throught to oxidative stress and it may convert healthy cholesterol to an oxycholesterol (there are three known oxycholesterols). Cholestane triol is reckoned to be the most potent of the oxycholesterols and when it is present in LDL it may induce changes in the behaviour of the cells in the endothelial layer of the arterial walls resulting in the proliferation of foam cells and the development of the plaques that cause the problems.
Homocysteine looks to be the pathophysiological common denominator that marks the point of convergence between the several generally well accepted risk factors for heart disease.
Kilmer McCully is the grand-daddy of homocysteine theory of arteriosclerosis but in his discussion of several risk factors he didn’t give much time to the issue of stress. Research that succeeded Dr McCullys greatest advances has since associated rising levels of cortisol with rising levels of homocysteine. Hence homocysteine theory can now embrace stress and anxiety for the risk-factors they have long be considered to be.
The question has been asked of Dr Kendrick, ‘can arteriosclerosis be reversed?’ I wouldn’t know, but in monkeys experiments indicated addressing levels of homocysteine may permit natural processes to de-construct the plaques and, if you like, ‘reverse’ the progress of arteriosclerosis.
Personally I think homocysteine theory, annexed with the cortisol connection, that links with the plaque inducing properties of cholestane triol, looks to be the great unifying theory that can accept and embrace a lot of water that has passed under the bridge, including the ascorbate (vitamin C) theory of Rath & Pauling.
The rise in BP links with other changes that accompany a rise in cortisol. A rise in blood sugar, a rise in levels of the hormone insulin, and a rise in gluconeogenesis. It has a lot to do with fight or flight preparations the body makes on our behalf and that we don’t have much conscious control over.
That’s a reasonable charcoal sketch is not, Dr Kendrick?
I like it a lot. The main thing we have to do is to mave away from the endless search for a ’cause’ and accept that we need to understand the process first.
Thank you Dr Kendrick, that means a lot to me after a tortuous five years of figuring, and the short delay preceding your affirmation suggests to me you have subjected the sketch to a cursory checking.
In the rush of blood to the head a mistake did creep in, I think, in that I may have misdirected that B vitamins are fat-soluble. Mind you some progress does warrant a bump or two along the way.
The environmental factors, in addition to the commonly referenced ones, that may bear upon cortisol do get quite interesting. More on this in the New Year perhaps.
Merry Christmas!
If not cholesterol causing CHD, and indeed your theory of “atherotrombosis”, would not aspirin and Plavix working to stop platelets from sticking by beneficial? I have had CVD since 1988 and am on both of those therapy’s – I have had very high doses of a statin and believe I’m now having side effects. Cardiology is trying to get me to take a statin again saying that even if they don’t work through lowering cholesterol, there is perhaps an anti-inflammatory benefit from them citing many trials (in aggregate, not specifically) that show they really work. I’m not convinced. I do find your explanation of CHD development very plausible. As you say: once you take the cholesterol hypothesis out….
Twice during the past 10 years my very nice GP informed me that my cholesterol reading was a tad high and that he was about to give me statins after which he could not see my heels for the dust as I made a quick, a very quick, exit! My neighbour who has been taking statins for around the same period appears to be unconnected with the real world. Another associate on statins severely assaulted his wife but does not accept that this could be caused by the medication and of course, he could be right, who knows? He also likes his ‘tipple’ so could there be a contraindication; so many questions seeking answers.
Hi
Not sure that this belongs in this thread but here go’s as I wanted to pass this on to see if anyone has had similar experiences. I share many peoples views on here that cholesterol is probably not the culprit but I do suspect that if its elevated then it may well be a sign of problems. Since coming off statins some 7 months ago I was happy that my LDL level had remained below 3.0, creeping back up to around 2.9 after binning the statins and adopting a med diet. After 3 weeks on holiday and whilst sticking to my diet I returned to find that my cholesterol had spiked to 3.4 LDL and a total 5.3. This was 4 weeks ago and I hoped this was just a blip. Just after Xmas I had a follow up test and hoped that my LDL had returned to 2.9 but was stunned to find it at 2.18 with my total at 3.8. It had not been this low since taking the statins and I have been scratching my head to pinpoint what may have caused it. The only significant change to my regime in the last 4 weeks is that I have started taking Krill oil, one tab a day. Now before any one jumps on me I have no vested interest in promoting any drug or supplement but I have read claims that Krill oil can reduce cholesterol by 30%. Yes I know its not this that is of interest but the anti oxidant effect of the krill but I was wondering if anyone else has found such results from using it.
Those cholesterol numbers do not mean much, smartersig, because it is well established, but not especially well known that cholesterol is not atherogenic, not in the least. Cholesterol becomes atherogenic if it is oxidised to one of three possible oxycholesterols, and the leading oxidising agent may well be homocysteine. A book on the subject, one aimed at the professionals, is due out in mid January.
What seems promising to matter more than the amount of cholesterol present is the amount of oxidised cholesterol that’s present. The assessment is a bit like MOT time where the mechanic gleefully informs there are rusty brake pipes that need replacement. one difficulty is we do not have an easy reliable test for oxycholesterols, but the tests for homocysteine and cortisol are pertinent, limited in the true diagnostic setting, assistive, possible, and affordable. They are catching on, but not yet so common as the truly infantile and next to useless ‘lipid profile test’ which is the common test for ‘cholesterol’ – that isn’t really a r test for cholesterol at all.
Cortisol matters because variation in levels of cortisol induces variation in levels of homocysteine, and if homocysteine cannot be reconverted to methionine because levels are high and insufficient B vitamins are available then homocysteine is now thought, at the real cutting edge of cognitive advance, to potentate conversion of cholesterol to oxycholesterols including the highly atherogenic cholestane triol.
It gets truly intriguing to become fully informed as to what factors can bear upon cortisol and thence bear upon any proliferation of oxycholesterols. I await the book excitedly.
Your lipid profiles reported by the lipid profile (‘cholesterol’) test are likely to be dynamic and not consistent, so you cannot place much store by any fluctuation anyway, irrespective of their lack of true pertinence to atherosclerosis and heart disease. But what they reflect is shifing balances inherent to metabolism. You may get contrasts in lipid profiles as a result of switching metabolic balance between fat sequestration and fat-burning.
Fat sequestration is ‘summer mode’ where creatures, mammals like ourselves, gain weight in readiness for winter, and fat sequestration is made possible if two co-factors, insulin and glucose, are plentiful. Fat burning is ‘winter mode’ when reserves of body fat are burned to evolutionary advantage, and the gates for the shift in metabolic balance are opened when levels of insulin and glucose fall.
Some sources say that seemingly beneficial alterations reported by the numbers of the otherwise meaningless lipid profile test may well report the contrasts between ‘summer mode’ (lots of glucse and insulin present) and ‘winter mode’ where the inputs pressed towards our metabolism permits ‘winter mode’ (fat burning) to take effect, making good use of lipolysis and ketosis.
Taking krill oil in therapeutic doses sis still an intervention, just as is taking statin medications, and there is every prospect that the vendors may overstate the benefits while understating any possible risks.
For clarity though any intervention needs to have an understanding of cause to be elegant and needs to intervene as close to the cause(s) as is possible. Krill oil may be beneficial, but there may be better and more elegant ways to disrupt the relationship of cause and effect and closer to cause. So science may establish krill oil is helpful but without knowing quite why. I think the target should be cortisol and homocysteine, and their may be ways we can adress these is more restorative, as opposed to interventionist ways. The distinction is subtle, while reaming quite pertinent to human needs.
On taking krill oil you are crossing the chasm between allopathic medicine, where the principal objective is profit, to natural medicines which cannot be patented and so the public is not held to ransom. Regrettably, today, allopathic medicine has the monopoly and seeks successfully to suppress its competition. There are a number of natural substances which thin the blood and others which clear plaque from arteries and without adverse side effects but those are not licensed by NICE so your GP is not about to prescribe them. In the arena of natural medicine the individual is on his/her own at navigating through the minefield of information and disinformation but the benefits from doing so can be considerable and not only for one’s self and family but also for family pets.
Thanks Robert, if you have any specific advice then please feel free
smartersig, Apart than registered medics others are prohibited from giving specific advice on health matters, which is understandable, but, what I would suggest is not to pay too much attention to your cholesterol level and focus more on maintaining a robust immune system; while this may not be the panacea to all that ails you, it sure will prove to be a stout and loyal friend. All vegetable oils are known to have an adverse effect on the immune system so look closely to your diet. At least, if you die, you will have died healthily!
One of the things I have noticed since coming off statins a month ago is that 1) I have lost 2cms of central obesity and 2) my b/g readings are appreciably lower. The study by Koh et al supports the link between raised glycoselated haemoglobin, central obesity and the use of statins. I wonder too if this can also be linked with chronic stress or the EPC dilemma?
Karen M’s remark is interesting.
Coming at the puzzle from the business of digestion, chyme (mashed up food in the gut) is broken down into constituent macro-nutrients. Carbs are digested to glucose and glucose is passed over the gastrointestinal divide into the bloodstream. Digested fats are assembled into triglycerides (a polymer molecule comprised of one molecule of glycerol with three dangly fatty acid chains attached), phospholipids, amongts things, and the whole she-bang gets form a chylomicron around (essentially) a nucleus that is a bundled mass of cholesterol.
Why?
Nobody can really say quite why, however the business seems to constructive constructive to the entirety of the fleshy side to the tree of life. As its passed over the gastrointestinal divide chylomicrons begin the distributive journey via the lymphatic network and not venous blood per sé.
From a perspective of systems analysis this has me curious. If chylomicrons are relatively inert until called for or until chancing into a functional reception then, to me, they look like they can be a good temporary store of energy in those fats.
Eating low-fat looks like a sure fire way to cause problems, because it will invariably mean more carbs in the mix, and more carbs means more glucose, and more glucose challenges the bodies finite capacity for the short term management of excess glucose, and so surplus glucose gets converted to body-fats, and largely under the direction of elevated levels of the hormone insulin.
If the reported link between raised glycoselated haemoglobin, central obesity and the use of statins is a valid observation then it begs questions as to what is bringing about the results.
If statins impair the biosynthesis of cholesterol (from mevalonic acid), which is precisely what they do, then there is a reduced supply of cholesterol from which to fashion lipoproteins, and there is conceivably reduced capacity for the legitimate transport of fats, and reduced capacity for the release, transport, and rightful metabolism of sequestered energy present in body-fats. Put the business of fat metabolism under duress and that places added demands upon the trafficking of glucose. And there’s more.
The reduction of cholesterol biosynthesis achieved by girding the production of mevalonic acid under the action of statin therapy dictates less cholesterol available for re-formulation into bile acids, and the supply of bile acids to the gut is part of the loop that supplies the necessary cholesterol to the guts that then in turn is returned in the body of the chylomicron. In other words its possible and not implausible that statins in inhibit the legitimate formation of chylomicrons in the gut. In English that means less fats will be passed over the GI divide and more will pass with stools, and that places more demands upon the supply and management of glucose adding more to the persistence and stress of hyperinsulinaemia along with the expanding waistline that very visually indicates that state.
A link with chronic stress?
Hyperinsulinaemia is a conduit of physiologic stress, but I think Karen means anxiety related stress.
Emotional stress and anxiety, sleep disturbance certainly, will lead to raised levels of the stress hormone cortisol. Cortisol commands a hormonal cascade that will influence the balance of other hormones, and very adjacent (to cortisol) in this cascade is insulin. Insulin levels will rise if cortisol levels rise and stay elevated, and insulin works like a stop-go board where the direction of fat-metabolism is concerned.
Chronic hyperinsulinaemia has your body basking in relentless summer, stashing energy (as body-fat) in preparation for winter. Physiologically speaking if insulin remains high then winter never comes and all that energy sequestered in extra inches of added abdominal fats will not be utilised.
The pattern of demand (for energy) is essentially flat-line at the level of collective mitochondrial demand, and while it varies slightly between resting and active it’s around 1 calorie every forty seconds.
The pattern of supply (of energy) seen at the mouth is typically ‘peaky’ and dictated by the frequency of and intervals between mealtimes; perhaps 700 calories ingested at one sitting.
The contrasting patterns point to a significant need for attenuation, ‘smoothing’, or buffering of energy. It’s reasonably well known, despite widespread acceptance is some way off, that the capacity to buffer glucose as glycogen is finite, and beyond that surplus supply of glucose must be converted to fats and laid down as body-fat. But the biggest con of medicine (cholesterol and saturated fat cause heart disease – when they don’t) is compounding the problem of hyperinsullinaemia and obesity, arguably. And few people have really given enough thought to the legitimate transport of legitimate metabolites and the alternate pathways they follow. In English, not enough thought has been given over to this need for buffering or ‘smoothing between point of supply (mouth) and point of consumption (mitochondria). It simply hasn’t entered heads that chylomicrons and cholesterol, lipoproteins and cholesterol (chylomicrons conforms to the design of a lipoprotein and is the largest member of the family), may have a legitimate rôle to play in the legitimate transport, distribution, (and if you like ‘warehousing’ of legitimate metabolites we love to hate – fats!
Now suppose a person is placed before a multi-fuel stove, a stockpile of wood and a stockpile of coal. Tell them you’d like to reduce the stockpile of coal, but then go on to say the best way they can do this is to feed the stove from the stockpile of wood. Their response is predictable and consistent with cognitive dissonance.
Tam Fry (he heads the National Obesity Forum) insists on directing people with large waistlines and significant stockpiles of energy residing in body-fats should continue to feed their metabolism with plenty of carbohydrates, and thus by promoting perpetual hyperinsulinaemia he is contributing to the problem and not the solution. It sounds an odd proposition, but if you want the balance of multi-fuel metabolism to switch to fat burning, it helpful to include sufficient fats in the diet, and plain inexpedient to persist with the over-supply of carbohydrates that accompanies the low-fat dietary model.
I cannot commit to this comment what I think of the Tam Frys and Peter Weissbergs of this world. But I am going to write to them and point them to this thread, and I am going to supply them with a print of ‘Heart of the Matter’, an actuarial review of the cholesterol hypothesis written up by Garth Lane. The PDF is to be found on the web, and it is worth a read.
Let’s get on the offensive, I say. God (nature) is on our side.
A very interesting read Chris, thank you. By chronic stress I mean not only emotional but also hormonal stress- due to the neediness of abnormally functioning organs for valuable energy perhaps.
I used to follow the ‘third-of-the-plate-should-be-carbohydrate’ mantra but fell off the wagon many years ago. I was falling asleep the whole time and, yes, I had hyperglycaemia and hyperinsulinaemia despite eating ‘more healthily’ than the dietitian imagined.
Since reading Dr Kendrick’s and others works I have been more wary. I’ve gone back to butter as, in some way, it is like a superfood- small amounts, valuable nutritional benefits. Same with eggs. I ave found protein is more sustaining than carbohydrate weight for weight.
Pingback: New Cholesterol Guidelines. Guess what? Basically EVERYONE is supposed to take them! | The Tin Foil Hat Society
Thanks Karen, the issue of protein on the balance of the mix remains a big question in my mind. I don’t think need is great, and habitual excess has been linked with complications. Few ‘tribes’ in the wild ever exceed 40% by calories, I read, and many fare well on much less. I can feel a rush after after protein, and I am at a loss to explain why.
I have a theory that supply of bile may be regulated, and that may couple with sufficient fats in a meal to attenuate (slow) digestion. Oleoethanolamide could be involved in a feedback signal but I just don’t know.
I agree about the quantity of protein- small is beautiful. The rush is fine in the morning but useless in the evening. Brings to mind the old saying- breakfast like a king, lunch like a working man, dine like a pauper.
Right here is the right webpage for anyone who wishes to find out about this topic.
You understand so much its almost tough to argue with you (not that I actually would
want to…HaHa). You definitely put a fresh spin on a subject
that’s been written about for ages. Great stuff, just great!
Hallo Dr McKendrick,
Thanks for your very interesting discussion above. I have another suggestion. People who live near airports do not like to go out into their gardens or go for walks because it is so noisy and so they stay inside. As a result their vitamin D level is very low because sunshine is our major source of the vitamin – even in here in the UK. Some 95% of an optimum D level comes from sun exposure – generally about 5% from food. Lack of sun exposure in people living near airports also means that their cholesterol levels are high because vitamin D is made in the skin from 7-dehydrocholesterol. Cholesterol and its metabolites presumably accumulate in the absence of sun. VItamin D has a beneficial effect in reducing risk of heart disease (refs supplied on request). Therefore in the absence of regular sun exposure, which may be caused by a noisy environment, low vitamin D, high cholesterol and heart disease may all be associated.
Hi
Not sure that this belongs in this thread but here go’s as I wanted to pass this on to see if anyone has had similar experiences. I share many peoples views on here that cholesterol is probably not the culprit but I do suspect that if its elevated then it may well be a sign of problems. Since coming off statins some 7 months ago I was happy that my LDL level had remained below 3.0, creeping back up to around 2.9 after binning the statins and adopting a med diet. After 3 weeks on holiday and whilst sticking to my diet I returned to find that my cholesterol had spiked to 3.4 LDL and a total 5.3. This was 4 weeks ago and I hoped this was just a blip. Just after Xmas I had a follow up test and hoped that my LDL had returned to 2.9 but was stunned to find it at 2.18 with my total at 3.8. It had not been this low since taking the statins and I have been scratching my head to pinpoint what may have caused it. The only significant change to my regime in the last 4 weeks is that I have started taking Krill oil, one tab a day. Now before any one jumps on me I have no vested interest in promoting any drug or supplement but I have read claims that Krill oil can reduce cholesterol by 30%. Yes I know its not this that is of interest but the anti oxidant effect of the krill but I was wondering if anyone else has found such results from using it.
Hi
Just an update on my previous message. As I said I am in the cholesterol being the canary in a mineshaft camp and as I said previously I had found that my LDL had crashed in 4 weeks from 3.4 to 2.15 and then when I double checked to 1.65. I put this down to taking Krill oil. Today I went for another test (same source 2 weeks later) and although I have felt a bit run down and under the weather the last few days, I expected my LDL to be stil under 2.5 at the most. My reading came out at 3.8!! (double checked). Thats the highest its ever been in the last 12 months. Has anyone got possible explanations for these see saw readings.
Not so many years ago the science on vitamin D indicated that it was harmful at high dosages and recommended that it be kept low in the diet and many followed this advice. If vitamin D, at higher than dietary levels, was essential to the human diet surely nature would have compensated for this in those who live in the northern or southern hemispheres where the sun, for around five months of the year, is a welcomed stranger? From personal experience, whenever I take higher then dietary levels of this vitamin (which apparently is recognised as a hormone) I suffer from headaches; it may therefore be appreciated that I am suspicious of the hyperbole this vitamin is currently receiving.
The adaptive evolutionary response to residing at more temperate latitudes is fair skin, Robert, and fair skin helps peoples who dispersed to temperate latitudes synthesise sufficient vitamin D, (providing they didn’t work shifts and didn’t spend 8 or more hours a day labouring under cover).
In fair skinned people skin colour is naturally and seasonally dynamic. From autumn onwards the natural arrangement for fair skinned people is that skin pigmentation will fade whereas from spring onwards the synthesis of melanin adds to the deepening pigmentation of the skin. Fair skinned ‘tan’, to provide a natural sunblock affording protection from overexposure to the UV components.
People who have thought their status of calciferol (vitamin D) to be low, and that have made the effort to redress sometimes report the benefit that they no longer burn so easily and tan more readily. This has the look of an adaptive arrangement, whereby synthesis of melanin is discouraged if levels of vitamin D are low. Then dark skinned peoples who are modern migrants to temperate ‘western’ latitudes, or people who expose little skin to the sum on religious and dogmatic, or cultural, grounds have to be aware of the risks of vitamin D deficiency. When I changed jobs to works as a landscape and maintenance gardener I noticed I tended to tan, and not to burn, and I noted I seemed to tan more readily and earlier in the season. It is as if spending much more time outdoors resulted in my becoming more ‘seasoned’ or ‘habituated’ to the sun, and so raised (restored) vitamin D levels could be a plausible explanation for this.
The availability of certain fats and oils within potential food sources varies with latitude, incidentally, and in plants saturated fats are more abundant in tropical species. In contrast certain PUFAs are more abundant in species more at home in temperate zones. Omega-3 fish oils are abundant in cold-water fish. Contrasting melt points have a lot to do with this, and in plants and cold-blooded creatures important lipids must remain fluid at the temperatures they are exposed to and must live under. This makes for an intriguing line of reason and curiosity. Might the supply of marine omega-3 offer some compensation for declining opportunity to synthesise vitamin D? So does Eskimo Joe’s catch of Arctic char compensate for the fact he gets few opportunities to sunbathe? This would make an interesting line of study.
I think vitamin D deficiency is a very real prospect at temperate latitudes for people who live in western developed nations and whose occupation or economic standing dictates they don’t really spend so much time out of doors. I don’t think the hyperbole should arouse too much suspicion, but cautious scepticism is always prudent.
A female Muslim, living in Scotland, and observing the dress code prominent in the culture, has little opportunity to synthesise vitamin D. She has even less, perhaps, if she’s taking statins under the direction of her GP.
‘Bullshit baffles brains’ (as many an army recruit must learn to accept as (s)he progresses through his/her training); a matter that afflicts peoples of alternate backgrounds and occupations without concessions.
I recall as a youngster at school that one would get a small bottle of unpasteurised milk daily to prevent rickets due principally to malnutrition and the lack of vitamin D, and interestingly, the milk proved to be an effective prophylactic. Regrettably, today, most milk, and in Scotland all milk, is pasteurised and that the human body cannot survive on it, while, alternatively, the body can survive on raw milk. Homogenisation is said to cause milk to alter the structure of its protein which allows it to pass through the stomach and into the blood stream undigested apparently resulting in autoimmune diseases.
Some years ago when Kellog’s corn flakes were analysed it was found that there was more nutrition in its cardboard boxes so what did Kellog do; it added synthetic vitamins which can apparently be problematic. When other food producers also add synthetic vitamins how then can we know that we are not taking an overdose?
Consider too that when some children are given corn flakes with fat free or fat reduced milk that is pasteurised for breakfast is there any wonder that some may suffer from similar symptoms to ADHD when at school?
Eskimos! Recall that the traditional Inuits had a diet high in marine oils and predominantly of PUFAs and cardiac problems were almost unknown among them. Indeed, it is known that they suffered from few of the problems of those on a Western diet and it was only when they veered towards the Western diet have they suffered in the same way. There were, however, three problems with the Inuits diet; one, it made the blood too thin which could result in bleeding to death when injured and, two, it also had an adverse effect on the walls of the arteries which caused them to balloon and, three, it ramped-down the immune system.
Whale meat again, don’t know where, don’t know when …
Robert,
The Inuit who depart from their traditional subsistence way of life and venture into the western grocery stores do indeed exemplify the changes in health prospects that reveal increased risks of developing chronic disease. Type-2 diabetes seems to be one of the chronic conditions at the leading edge of these increased risks, and both Inuit and Australian Aboriginals can share susceptibility to alcohol abuse once displaced from traditional culture and exposed to western ‘culture’. Back in 2009 I delighted in chancing upon a well-written and insightful blog that had a post or two on the topic and led me to other online features discussing the subject from a close and empathetic standpoint. http://tundramedicinedreams.blogspot.co.uk/
Aidan Goggins has recently made a contribution to the blog of HealthInsightUK discussing the merits of fish oil supplements as compared to statins as preventative measures. His is an interesting essay, strong in several ways, but weak in cross-referencing alternative treatments with the causal factors for heart disease. http://healthinsightuk.org/2013/12/16/a-guided-tour-round-the-statin-wonderland/
Humans emerged out of Africa, and dispersal to geographical (global) ubiquity is a question requiring an answer. By what routes did the ancestors migrate and what resources sustained them along the way? The fossil record is scant. One theory has it that major. if you like, continental advances were possible when sea-levels were lower in generally highly glaciated periods, when the land-bridges would be their most extensive, but this still invites the question what routes led dispersing humans and/or proto-humans to land-bridges? Alice Roberts wrote about this and the BBC devoted a series to it. The experts have more than one theory, and struggle to establish an evidential basis that would remove the elements of conjecture. If coastal routes were involved their would have been major esturial challenges to cross, but the shorelines can be productive and sustaining places to forage. Perhaps the scant nature of the evidence provided by the fossil record could be explained by the fact that early man migrated his way to global ubiquity via shorelines and exploiting coastal resources when sea levels were lower than today. Any possible supporting archaeology would lie far out to sea and have likely been destroyed. Perhaps less well known is the prospect that one of the major and lasting phases of the human diet could have involved a great deal of coastal foraging with plentiful seafood. That could have left an impression upon the evolution of human physiology or genetic adaptation .. and go on to infer the modern diet could be deficient in seafood. Yet some traditional peoples fare well on diets containing no seafood at all and little in the way of plant matter. Then against this one must remember that heart disease is a mutli-factorial affair and no single risk factor seems to have leading command over outcome. Besides, the pathways that link seemingly disparate risk factors with a common physiological process, atherogenesis, need to be reliably explained.
The traditional Inuit eat very little in the way of plant matter, and the same is true of Evenks. Do you happen to know if the diet of the Inuit or Evenks supplies similar levels of vitamin C as does the westerner that conscientiously consumes his five-a-day?
Dr Alice Roberts, a vegetarian, considered the Evenki diet, one high in animal fats and one that is not especially diverse in content, to represent another to add to the list of paradoxes.
What evidence leads you to suggest that traditional Inuit suffered from suppressed immune systems and what process backs that up? Did they suffer from a lot of colds, or were they exposed to rhino-virus, influenza, and other communicable strains only after contact with westerners? After they make the change to habitually visit the westerners grocery store does Inuit susceptibility to western, ‘non-communicable’ disease constitute an indication of physiology and immune function operating under duress? What do they buy, and what do they forsake?
Yes, Christopher, we ‘meat’ again!
In defence of my knowledge, one of my problems is that I can read English in sentences and as a general reader and amateur enthusiast in natural medicines, naturally I am not prompted to take note of all that I read but I do also learn from experience and observation. Ignorance is not only bliss but it does make life much simpler.
From my recollection there exists research which shows that when plaque was analysed it was found to consist of a massive 70% made from PUFAs, 23% from saturated fats, and 7% from other sources. Saturated fat would appear to consist in its structure of both mono and poly unsaturated fats so it could reasonably be deduced that saturation per se is not problematic.
From personal experience of having had a quadruple by-pass after being a vegetarian for eighteen years I can confirm that both mono and poly unsaturated fats caused me to have angina and withdrawing from those dispersed the symptoms. Now twenty-three years later and having abandoned the post-operative medication that made me unwell and taking very little vegetables and fruit in my diet, and aged 83, I am in remarkably good health and still retain a libido!
Arctic explorers apparently could survive on pemmican which consisted of both meat with its saturated fat and Captain Scott in his endeavour to reach the South Pole took the best dietary advice available and was advised to take pemmican without its fat content which was one of the catalogue of minor incidents that led to the expedition’s disastrous end. Had he, instead, followed the traditions and practices of earlier explorers his team may have survived.
When research was carried out to find the best substance to suppress the immune system after organ transplantation it appears that PUFAs proved the most effective but, with its use thereafter, there was found a dramatic increase in cases of cancer and probably other ill-health problems judiciously unreported.
On learning how heart-healthy traditional Inuits were on the diets they followed, it made me wonder what made them appear so prematurely old and what caused their deaths? What I discovered, through reading, that it was principally aneurysms, caused by weakened blood vessels that were caused by the high incident of PUFAs in their diet. Another cause of death was, when injured, bleeding to death owing to blood that was too thin caused by PUFAs.
Do I need to continue?
Here are other considerations about plaque and cholesterol.
Stress and anxiety are understood to suppress one’s immunity and particularly when long-term.
Prior to the days of crude oil, paint was made from vegetable oil and what happens to paint when it is exposed to heat and oxygen; it hardens; and when vegetable oil is consumed then apparently a not dissimilar effect occurs at the cellular level of the body.
While the traditional Inuits had arteries clear of plaque it might be found that it is only in the presence of carbohydrates that causes fat to turn to plaque. What interests me is the similarity between this process and that of glycation. Probably hence the reason why the Inuits suffered in a similar manner on veering to the Western diet and probably why low carbs diets can be beneficial.
Just to add a little confusion to logic, it is interesting that Dr Robert Lustig (Sugar; the bitter truth) says that the Japanese find the same results from a high carbohydrate diet that others find when on the low-carbohydrate diet.
From personal experience, while my intake of fruits and vegetables is low I do love almost all that is produced from grains such as cakes, biscuits, breads, pastries (and etcetera). As a guess, I would contribute my current good health in advanced age to having a diet that is high on saturated fat. I am reasonably certain that lashings of saturated fat are a buffer against ill-health; all that is required to justify this view is for scientific research is catch-up!
In the event of any confusion to what has been said above then to keep my arteries clear of plaque I take serrapeptase (generic name) at 80,000iu on an empty stomach which is necessary to work its magic; a substance recommended by the late Dr Hans A Nieper. The cartel of pharmaceutical companies do not want the public to know this.
Robert you might these links:
Click to access methylmagic.pdf
http://www.drbriffa.com/2014/06/11/clowns-to-the-left-of-me-jokers-to-the-right-why-wont-those-calling-for-statin-papers-to-be-retracted-use-some-science/
Low sulphate?
FYI, Stephanie Seneff interviewed by Dr Mercola –
The comment I wanted to draw to everyone’s attention is 12:30 minutes in
John, Thank you for this. I communicate regularly with Stephanie, and I like many of her ideas.
I became aware of heart attacks being a cholesterol deficiency problem (although would not be describing this in those terms) a number of years ago when I had to have a quadruple by-pass (1990) after being a vegetarian for 18 years. Subsequently I read and experimented with various substances and diet before this feature became obvious. At the time (around 2000 AD) I was not aware of any science to backup this viewpoint and often came under attack from others whenever I commented. Today, I am convinced that lashings of saturated fats in the diet is a buffer against ill-health but again, cannot prove it. The video was interesting and I will view the others that follow shortly.
Hi
I had conversation with a veg cafe owner the other day as I complained that so much of her menu choices were carb’ led. She said that it was difficult to avoid carbs in preparing a veg menu. Could this be the big flaw with vegitairianism. ?.
smartersig, This is certainly my experience but avoid telling it to a vegetarian or anyone who gets the butcher to trim the fat from their meat order unless you want a lengthy debate. More apropos, my first wife (of 45 years of togetherness) shared in a diet that was high in carbohydrates (but little meat) from the beginning of our marriage and interestingly she experienced difficulty at carrying pregnancies. Later in life she had a penchant for soft and fruit drinks when she suffered from breast cancer and a fatty liver to which she succumbed.
My present wife, whom I have been with for 15 years, was a very ill woman when we first met and also (may it be added) a vegetarian! She was the product of a traumatic background and was being mistreated for depression. I cajoled her to abandon her diet which, reluctantly, she did (this is all about love) when her condition improved. I tried her on some natural products when one morning on arising she said, “For the first time in my life I feel normal!” What I had difficulty at grasping was, if this was the first occasion she had felt normal, how then would she know what normality was?
Today, she is almost 70 (just a chick) but looking young, healthy, and very energetic. Our diet is principally meat with lashings of fat (great for tasty gravies) but, interestingly we continue to have carbohydrates and I am fairly convinced that it is the high fat intake that protects us but, I stand to be corrected.
Great Post Robert, Thanks
Aw, this was an exceptionally good post. Finding the time and actual effort to
generate a good article… but what can I say… I put things off a lot and never seem to get
anything done.
This is my first time visit at here and i am actually
impressed to read everthing at one place.