When I first realised that the conventional ideas about heart disease were, to put it kindly, flawed, I decided to try and start again with a blank sheet of paper and see if it was possible to work out what was really going on. Nothing was ruled in, nothing was ruled out. At first, like almost everyone else, I began to look for alternative potential ‘causal’ factors’ e.g. potassium, or stress, or fibrinogen, or other things in the diet.
However – as I have written before – I came to realise that this was a fool’s quest. There was so much noise, so many apparent contradictions, so many possible interactions and confounding variables that you could pick and choose your evidence to support almost any factor, or set of factors, that you wanted. Gradually I began to realise that if I truly wanted to understand heart disease, I had to start looking at the underlying processes.
In order to do this, I had to try and define exactly what ‘heart disease’ might be. I already knew that that heart disease is not really a disease of the heart. It is a disease of the arteries supplying blood to the heart (the coronary arteries). It is also a disease of other arteries around the body, the arteries supplying blood to the brain (coronary arteries), the kidneys (renal arteries) etc.
What we usually call heart disease is really arterial disease, where the arterial walls are thickened with atherosclerotic plaques, which eventually narrows the lumen, or central channel of the artery, causing angina and suchlike. In the arteries around the heart these plaques can finally ‘rupture’ causing a large blood clot to form on top of the plaque leading to a heart attack or, perhaps to be more ‘accurate’, a myocardial infarction.
In the carotid arteries in the neck, blood clots can also form on top of the plaques. The clot can then break off, travels into the brain, and block an artery. This leads to a stroke or a cerebral infarction. [There are other forms of stroke, but this is the most common].
Whilst this is a relatively simplistic model, I shall use it for the purpose of this blog, because it provides a close enough description of what happens. I shall also continue to use the term heart disease to mean the development of atherosclerotic plaques and formation of clots. Using this as the definition of ‘heart disease’, what processes can explain it?
The process of arterial thickening/plaque development
Moving backwards for a moment, I believe that the main reason why the cholesterol hypothesis has proven so resilient to all contradictory evidence is that the process seemed seductively simple. You eat too much cholesterol, the cholesterol level in the blood goes up and this excess cholesterol is then deposited on the artery walls… thickening and narrowing them. I once saw an episode of The Simpsons, demonstrating this exact thing happening in Homer’s blood vessels. Once something appears on The Simpsons you know you have a meme on your hands.
Of course, this initially simple process has altered and adapted and fragmented and shape-shifted so many times that it is now almost impossible to describe what it is. It has become something like this: you eat too much ‘unhealthy food’ (which may or may not include cholesterol and/or saturated fat), this raises LDL/cholesterol levels/or particle numbers and/or size, or other things, or lowers HDL, or raises triglycerides, or all three… which causes inflammation/oxidised LDL levels to go up, leading to development of plaques/thickenings in the arterial wall…
Sorry for the vagueness of it all, but I defy you try to get anyone to give you a more accurate summary of the current bad diet/heart hypothesis. I can’t. However, despite the fact that the cholesterol hypothesis has fragmented into a more and more confused mess, people still cling to the central process of ‘eating something > blood levels of something going up > narrowing of arteries.’ Primarily, I think, because it seems so simple. A leads to B, B leads to C, C leads to D…eath.
More than twenty years ago I realised that this model was bunk. It just could not explain heart disease. But what other process, or processes, could take its place?
In order to try and answer this I decided not to begin at the very beginning. Instead, I started at the very end, with the final event in heart disease. Essentially, this is when a blood clot or thrombus forms over a plaque, fully blocking an artery in the heart. [Most strokes (ischaemic) are also caused by a blood clot blocking an artery in the brain, although the process is not the same, it is very similar.]
Clearly, therefore, blood clotting (thrombus formation) is the terminal event in almost all heart attacks, and most strokes. This is widely accepted. Indeed, almost all forms of treatment for heart attacks, and strokes, involve the use of anticoagulants of different types: clot busters, aspirin, clopidogrel… or inserting stents to prize open the blockage caused by the blood clot etc. Acute cardiology intervention could, in many ways, best be defined as thrombus management.
The importance of blood clotting in heart disease death can be further highlighted if we look at people with Hughes Syndrome. This is a condition where the blood is dangerously more likely to clot – thrombophilia. People with this syndrome are far, far more likely to have strokes and heart attacks – often at a very young age – sometimes before the age of twenty. (Mainly strokes, actually). The condition is managed with various anticoagulants.
I could continue on this theme for some time, but the role of blood clots in causing death from heart disease, and strokes, is not in the slightest controversial. What is somewhat more controversial is to suggest that the earlier process of heart disease, atherosclerotic plaque development, could also be due to abnormalities/ dysfunction, with the system of blood clotting/repair.
At present, although I have never seen it stated clearly, it seems that everyone is happy to accept that atherosclerotic plaque development is due to one set of risk factors. Then the final event, the deadly blood clot, happens…coincidentally? Due to a completely different set of risk factors? This remains unexplained.
I was never comfortable with the idea that the creation of atherosclerotic plaques has one set of ‘causes’ whilst the final event, the blood clot, has another set of, potentially, unrelated causes. This seems clumsy, and always did – two diseases welded together to make one disease? I thought it was much better to see if a blood clot/thrombosis hypothesis could explain the entire process from start to finish. This could just be me trying to make things neat and tidy, but I don’t think so.
Firstly I tried to articulate what the unified ‘clotting’ hypothesis might look like. Whilst it does not have the elegant simplicity of the cholesterol hypothesis, I hope that it is clear:
Step One: Various factors damage the artery wall (endothelial damage)
Step Two: A thrombus or clot forms on top the area of damage
Step Three: Once the thrombus has stopped growing/stabilised, endothelial cells re-grow over the top of it
Step four: As a result of step three the thrombus becomes, effectively, incorporated within the arterial wall
Step five: Various repair processes break it down and clear it up – but often not fully
Step Six: The area of ‘damage/repair’ becomes a focus for further damage/thrombus formation
Step Seven: The thrombus/plaque grows through repeated episodes of thrombus deposition/repair
Step Eight: A final thrombus forms over a large plaque that completely blocks the artery leading to a heart attack
Many parts of this are far from new. For those who have read my previous book, and blog, you will know that Karl Von Rokitansky proposed that plaques in arteries were really thrombi, over one hundred and fifty years ago. The problem that lead to his ideas being dismissed was, essentially, step three.
Whilst he recognised that arterial plaques looked very like thrombi, and contained everything you find in a thrombus, he could not explain how a thrombus could possibly come to be inside the arterial wall, covered by endothelium (the single layer of cells that line arteries). Virchow attacked his hypothesis simply by asking how this could occur – well, obviously, it cannot. Bong!
However, if Rokitansky had known what is now known, his hypothesis may well have won the battle of ideas, and the entire direction of research into heart disease would have gone off in a completely different direction.
The answer to the Rokitansky conundrum is, of course, very simple. If you damage the endothelium, and a thrombus forms over the area of damage (this will always occur), replacement endothelial cells do not come from within the artery wall (as happens if you scratch your skin). They come from the blood itself.
New endothelial cells develop mainly in the bone marrow, they float about in the bloodstream, and they are known in this state as Endothelial Progenitor Cells (EPCs). EPCs are attracted to areas where the endothelium is missing – where a thrombus has formed. Once there, they stick to the top of the thrombus and develop into mature endothelial cells. Hey presto, the thrombus becomes covered by a new layer of fresh endothelial cells and is now, effectively, within the arterial wall itself.
Of course, if you think about it, this has to be what happens. If a thrombus forms on your artery wall, it cannot simply fall off once the artery has ‘healed’ beneath, as would a scab on your skin. If this were to take place, the thrombus would just travel a bit further down the artery until it jammed. As you can imagine, jamming arteries with thrombi is generally pretty catastrophic. See under ischaemic stroke.
Which means that the repair system for thrombi that form on the walls of arteries has to involve covering them up – then clearing the debris away from within the artery wall itself. I would like to say that I hypothesized that EPCs must exist, before I found out that they did. But you only have my word for that.
A whole new process – and potentially causal factors
At this point, I would like you to look afresh at heart disease/plaque development as containing three interconnected processes:
- Endothelial damage
- Thrombus formation
Viewing things in this way, you can see that factors that damage the endothelium e.g. high blood sugar levels, turbulent blood flow, stress, will cause more thrombi to form; the more thrombi that form, the more that plaques will develop. Factors that make the blood more likely to clot – and also create bigger and more difficult to shift thrombi – will accelerate plaque growth, and increase the risk of the final event occurring. Factors that interfere with repair process are likely to make plaques become bigger, and more damaging.
If these are the processes, then ‘factors’ which truly are causes (rather than associations), should fit easily within this model – and indeed they do. At this point you can play a game – if you are as sad as I am! It is one that I play when sitting quietly in a train, or driving, or half watching the television. It is called, think of a risk factor and see if it has a damaging effect on any of these three processes. The other half of this game is to think of something that ‘protects’ against heart disease and see if benefits any of these three process i.e. does it protect the endothelium, reduce blood clotting, or enhance repair.
Now to let you play this game yourself. Hit Google or Pubmed, and see what you come up with. Try endothelial damage, diabetes and CVD. Or smoking, EPCs and thrombus formation. Or try, effects of insulin resistance on EPCs and thrombus formation. Try exercise, nitric oxide and endothelial function. Or yoga and endothelial health, or smoking and blood clotting, EPCs and endothelial health.
Stick in any significant risk factor for heart disease, or stick in any factor known to reduce the risk of heart disease, and you will always find that they have a major impact on one of the three key processes: Endothelial damage, thrombus formation, or repair. Usually all three… This is not a coincidence.
In the light of this, I think it is interesting to review statins. Now I am a great critic of statins, as I believe their downsides greatly outweigh their benefits. However, they do reduce the risk of death from heart disease and strokes – if not by a great amount. At present this is generally attributed to to their impact on lowering cholesterol levels.
But I thought it was interesting to ask another question. Do they also have a significant effect on any of the three processes? Why, yes they do. Firstly, to look at their effect on the key repair system of EPCs. Here is a paper called:
Increase in circulating endothelial progenitor cells by statin therapy in patients with stable coronary artery disease1.
‘Statin treatment of patients with stable CAD was associated with an approximately 1.5-fold increase in the number of circulating EPCs by 1 week after initiation of treatment; this was followed by sustained increased levels to approximately 3-fold throughout the 4-week study period.’
In short, statins increase the number of EPCs which are essential to repair areas of damage to artery walls. Well, who’d a thunk? Well, me, actually.
Now to look at another critically important effect of statins. Before doing this I have an admission to make. It is something I have known about for many, many, years. It is this. Familial Hypercholesterolemia does increase the risk of heart disease. Something that I have tended to gloss over, for obvious reasons.
In my defence I have always known that this increased risk had nothing to do with the LDL/Cholesterol hypothesis. It was something else. The something else is that that Familial Hypercholesterolaemia causes (for a number of reasons, and not in everyone) increased thrombus formation. Or, to put it another way, it makes your blood much more likely to clot.
Here is a paper from the Journal Circulation called ‘Hyperlipidemia and Coronary Disease. Correction of the Increased Thrombogenic Potential With Cholesterol Reduction2.’ It is nearly twenty years old:
‘Background: Hypercholesterolemia is a risk factor for coronary disease, and platelet reactivity is increased with hypercholesterolemia, suggesting a prethrombotic risk. The aim of this study was to measure mural platelet thrombus formation on an injured arterial wall in a model simulating vessel stenosis and plaque rupture in hypercholesterolemic coronary disease patients before and after cholesterol reduction.’
‘Conclusions: Thus, hypercholesterolemia is associated with an enhanced platelet thrombus formation on an injured artery, increasing the propensity for acute thrombosis…cholesterol lowering may therefore reduce the risk of acute coronary events in part by reducing the thrombogenic risk…’
Yes, gentle reader, statins do work to reduce the risk of heart disease, but not directly by lowering LDL/Cholesterol. Instead they work a bit like aspirin, by stopping platelets stick together over areas of damaged endothelium. They also work a bit like Clopidogrel – which does much the same thing. They also work a bit like omega-3 fatty acids (which the Eskimos eat a lot of), and causes them to have nose bleeds.
What statins do not do is to mimic the action of warfarin. Warfarin has little or no impact on platelet thrombus formation, caused by endothelial damage, it works in a very different way. Once you know this, you can, as I promised, understand the conundrum I left in the last article on this topic. Namely, why does warfarin protect against strokes, but does not protect against heart attacks. Whereas aspirin, which is also an anticoagulant, primarily protects against heart disease.
Now you know… possibly?
As always, a fascinating article. Thanks. I eagerly await the post containing your new book.
Is this conclusion as significant as it seems to my non-medical eyes? If it is, should we expect to see policy changes around statin use, primary care CHD prevention and of course welcoming cholesterol back in from the cold?
If I may, I suggest a brief article highlighting the importance of cholesterol and the consequences of reducing its levels might be a further incentive for people to think twice before taking statins.
Great post Malcolm and Happy New Year!
What this also fits nicely with is the effect of exercise where heart rates are raised – imagine the arterial wall being flexed due to increased blood flow and beating (as the heart has work harder) and one can visualise how the spaces between arterial wall cells open and close and allow foam cells in and out, EPCs in and out, repairs to be made and the “damage” largely cleared up … aided or increased by the exercise-induced artery wall flexing … do this often enough and damage might be cleared up before it becomes a problem … don’t do any exercise and allows arteries to become increasingly damaged, thickened and plaqued …
is it the coronary or carotid artery that supplies blood to the brain ?
Carotid – the coronary arteries supply the heart muscle
You do know how to tell a tale. Thinking for yourself is always a good way to start. Your tale makes a lot of sense to me, but I would be curious to hear your thoughts on another one, a very different one—the tale of the myogenic theory of heart disease:
Does any of this make sense to you?
Indeed, of course it does. I am a great believer that acute stress can damage the myocardium – without any underlying atherosclerosis. I kept my tale, deliberately, simple. I often discuss things with Carlos Monteiro, and we think much the same things about heart disease. Where we do not fully agree is on the exact role of thrombus formation on acute myocardial damage. He believe thrombus formation is secondary to myocardial damage. I think the interplay is more complex.
Thank you. I’ll be very interested to hear your thinking about the interplay between the myogenic and thrombogenic notions of myocardial infarction. I wonder if you regard them as elements of a larger, common disease process or perhaps simply as different pathologic pathways to a common endpoint of myocardial damage.
Very interesting read as usual, Dr. Kendrick. However, do you believe that acute stress can affect other parts of the body such as the abdominal or iliac arteries enough to cause pathology? As a PAD sufferer, I think the type of pain described by those with stable or unstable angina is much like that which is experienced in those with lower extremity pathology as a result of reduced arterial flow. It is quite like a lactic acid build up feeling. Perhaps some of the pain associated with either comes from not only a lack of blood flow to the specific organ fed, but rather within the artery itself since there are numerous nerves in those walls in addition to the smooth muscle and endothelium. I still tend to believe that oxidative stress and inflammation are the culprits in either but that psychological stress and trauma can induce these attacks in those already vulnerable.
And, I agree that I am sick of seeing Kim K’s big…fake bottom, as well.
Thinking about this a little more, the myogenic theory seems to point toward primary microvascular injury (in the myocardium), with macrovascular injury (in the coronary arteries) secondary to it. The thrombogenic theory seems to point toward primary macrovascular injury in the arteries ultimately leading to infarction of the myocardium. It seems clear that diabetes and related conditions, for example, can cause both micro and macro vascular damage. So some “risk factors” would be common to both pathways to heart attack. Others wouldn’t.
I wonder if some infarcts are essentially myogenic in origin while others are thrombogenic. Or if, in your view, both processes typically occur together as small and large vessels both accumulate damage. The causal direction of pathology seems basically opposite in the two theories, so it will be interesting to hear your thoughts at some point on how this all may work. In a sense the myogenic theory seems even more radical than the (simplified) one you outlined here; not only is cholesterol thrown out the window, but so is the even more basic notion of heart attack as fundamentally a disease of the arteries. No one tell Dr. Dayspring about any of this.
It is, as you clearly realise, complex. I have kept things as simple as possible – so far.
I thought a number of studies showed that those with familial hypercholesterolemia did not necessarily die earlier? Just checked with Uve Rsvnskov’s 10 Cholesterol Myths and he appears to say high cholesterol has not been evident in significant numbers in heart attacks. He also states that women over 60 with high cholesterol (is this the same as hypercholesterolemia?) have better than average longevity. I’m not a scientist, so am unable to pull these strands of argument apart.
Lorna. You may die earlier of heart disease due to familial hypercholesterolaemia, yet be protected against other diseases – e.g. infections diseases, or cancer. Overall mortality is unaffected by heterogeneous FH, Heart disease is, moderately, increased. Other causes of death are reduced. The two concepts are not mutually exclusive.
I’ve thought that cholesterol couldn’t be the primary cause myself for quite a time because of several factors.
1. You would expect a linear correlation. There’s none.
2. Though statins work, they’re underwhelming in their success rate.
3. I knew that FH is a hyperthrombotic condition.
The other thing was that the strong correlation with inflammatory markers and with HbA1C and serum insulin suggested that inflammation has to be a very serious player in this league.
I think you’re probably spot on in your analysis.
What you’ve done, Malcolm is a Gary Taubes of a different colour. Literature is great and researchers are to be totally admired, but also deserving equal kudos are researchers of research. I know from having worked with researchers, than many of them don’t really read other research. I heard a Prof. in London say (a feted researcher himself); “I never read research. You hear it all at meetings”. You sure as hell don’t when the drug companies are controlling the agenda.
Of course you can only read a very small amount of the research, as so much is done. I do not know how you could possibly keep up with it all.
Reblogged this on raphaels7 and commented:
An outstanding example of a ‘back to basics’ line of reasoning, ever so welcome in this overhyped and unnecessarily complexified medical world
Great read. This is bringing up a lot of different ideas surrounding CVD. I’m spreading to the likes of old schoolers like Dr.Dayspring.
I can’t help but frame these 3 processes – Endothelial damage, Thrombus formation and Repair – within the context of mitochondrial health. At least, this is what makes most sense to me, currently. These 3 processes (& others) result from communities of cells carrying out their respective jobs and must ensure that individually, their priority is to retain a favorable energy state enabling them to perform their respective duties. This stems from the idea that “The standard energy of ATP hydrolysis under physiological conditions is known as delta G’ ATP and is tightly regulated in all cells between -53 & -60 kJ/mol.” Furthermore “Most cell functions are linked either directly or indirectly to the plasma membrane potential and to the NA+/K+/CA2+ gradients” (Thomas Seyfried). It seems all bets are off when cells can’t maintain energy homeostasis and hence its automatic implication in uncontrolled growth (i.e. cancer).
In the case of CVD, cells need to balance their energy all the while functioning as a unit that has 0 respite from a constantly beating heart and vascularised network. It would seem that when mitochondrial health falters, plaque accumulation and ineffective repairs is a pretty good option, all considering. The same ways hormones move up and down wildly to keep more fundamental cellular energetics from affecting the survival chances of the whole organism.
Many different offenders to mitochondrial health exist. So, the multifactorial nature of CVD lends itself to this idea: that CVD presents when the mitochondria of those cellular communities most directly related to CV processes (1, 2 & 3) are injured. Instead of say, neurological disease where a different set of cellular communities are struggling to maintain their energy homeostasis, anywhere between -53 to -60 kJ/mol according to the particular cell.
An e.g. of how some communities of cells or ‘body parts’ are more or less prone to damage, whether mitochondrial or otherwise, is given by Katy Bowman:
“There are some arteries more prone to plaque than others, which should be an indicator that diet isn’t the only place we should be looking to try and prevent plaque accumulation […] but the prevailing theory in the biomechanical community is that plaque accumulates in areas (the abdominal aorta, iliac, coronaries, femoral, popliteals, carotids, and cerebrals) where the patterns of blood flow are the most complex. […] Our point of view on arterial stiffening is inappropriate. The hardening of arteries is seen as a disease – as ‘the problem’ – but the endothelial walls’ bulk-up-with-plaque response to a mechanical strain could also be seen as an adaptation: a short-term improvement to the cellular lining. Without a thicker wall, the lumen could theoretically become porous…”
I wouldn’t presume that mitochondrial health is be-all end-all of CVD (as exemplified by the biomechanical e.g. above) but I do think it fits rather nicely with other disease presentations too (diabetes, obesity, alzheimer’s etc.).
How far off the mark am I, Dr.Kendrick? 🙂
“I hypothesized that EPCs must exist, before I found out that they did.” In my experience, that sort of thing is quite common in research (which is effectively what you are doing here). So look upon it as encouragement that your line of thought may prove fertile. Of course it may prove wrong; at least it looks firm enough to be testable.
Mention of endothelial progenitor cells EPCs made me think of progenitor cells in general and how they they trend to become the more specialised variety of cells needed to create and replicate tissues of various types. Then in thinking about the part progenitor cells may play in healing, and how they spawn offspring whose specialist and specific nature emerges with time, I went on to think about the ‘healing current’ described rather well by Robert O Becker in the book, The Body Electric, and on to the odd things that happen when you experimentally tinker with the healing current.
Before I go on I appreciate your stepped approach to discussion of what happens, or what might happen downstream of the business of atherogenicity.
In reality, and compared to the widespread provenance to be detected in nature, western man has achieved a level of isolation from the electrical potential to be bound at the Earths surface that is almost total. Clinton Ober (who is now a buddy and associate of Stephen Sinatra who was once a member of THINCS, like you) tested his body with a voltmeter. It registered 5V+ relative to ground. Next Ober deliberately ‘earthed’ himself for a time, and after that his voltmeter registered no charge at all. It is as if when Ober earthed himself his body sucked up 3.25×10^19 free-electrons from ground. I hypothesise these free-electrons would flow to pacify 3.25×10^19 hydrogen ions (H+) that would be distributed about the body as features of a range of biochemical molecules that have become ionised through the loss of an electron or more.
Now I know what is the more natural, and I also know that which has trended to increased prevalence. Free-electron sufficiency, through walking barefoot, or through the wearing of footwear fashioned from natural skins (as is traditional amongst traditional living Inuit (Eskimos)) is more normal, but the last one hundred years amongst westerners been a trend to a level of free-electron deficiency through isolation that is now pretty close to total, absolute, and lasting. Footwear made with soles of rubber and plastic has sealed the deal, coupled to the automobile and the materials used to construct our homes
It would not be rational for a person to discount that being deficient to the tune of 3.25×10^19 free-electrons could amount to disturbance of the more correct electrical state of the body. In turn the reader of Beckers book would be aware of the odd things that happen when folks experimentally interfere with the healing current (hands can grow where feet should, by way of example), and be aware this healing current has some influence over the way progenitor cells (or their progeny) mature into type-specific cells that take on type-specific roles to produce the type of tissue that is needed at the site. Hence it would seem irrational to discount that being deficient of 3.25×10^19 might interfere with how progenitor cells develop, how fast, and well mature type-specific cells result. The level of isolation evident in the average westerner and testable with a simple voltmeter might result that healing only manages a botched repair at best, But restore those free-electrons to those electron starved hydrogen ions and you remove one of the obstacles to a proper and healthy repair.
Under suitably managed conditions in a well designed experiment Earthing has been demonstrated to restore rightful balance and cycles of certain key physiological factors such as cortisol. Free-electron deficiency has ramifications for endocrinology (or aspects of it), and endocrinology has ramifications for levels of oxidative stress, Oxidative stress has ramifications for homocysteine, and homocysteine has ramifications for the business of atherogenicity.
I could offer you a post to consider, if you like, ‘Eskimos and nose bleeds part III’
I highly recommend three books available from various vendors but give links to a familiar site merely to indicate the titles:
Funny you should post that. I read the Earthing book a few days ago, and he claims that it thins the blood amongst other things. A part of me thinks it sounds a bit woo woo, but I’m keeping an open mind. I’m thinking of Semmelweis and the reaction of his colleagues to handwashing.
Unfortunately when you start talking about it people think you’re an idiot. LOL. Especially if you are eating a low carb diet. I think my family have written me off!
Earthing/Grounding is interesting. There are plenty of people around who insist it is complete scientific garbage, but there are plenty who find it useful, me included, but perhaps more interestingly (without appealing to ‘authority’ or ‘experts’!!) a rather wide-ranging group of Drs: Briffa, Graveline, Mercola, Sinatra, … I wonder what Dr Kendrick thinks about it…
Dr Kendrick has yet to have the time to look at it in any detail.
On the above “Earthing ” theme I am currently reading “How Toxic are my Trousers?” by Shaun M Sutton. This is also available from Amazon. It’s an interesting concept which seems to be coming to the fore (or maybe taking us back to simpler days).
Madam, no true Scotsman wears trousers.
I’m on the hedge-betting side of things with woo-ish stuff like earthing/grounding/etc. There’s a ton we don’t know about energy fields and electrons/protons etc, so I’m open to the idea that they could be affected by our connection to our environment – or lack thereof.
So as part of my hedge-betting, I spend as much time outdoors barefoot as I can, and sometimes take my standing work desk to nicer locales than the office:
Good for you Ash. I, for similar reasons, hate to use anything but natural light in my office. During the winter when the days are shorter, I got ribbed a lot for it as the only light in the office would be my computer. However, my electric bills were low! I, too, love to run barefoot in my grass at home. It just feels good to me. So, if it feels that good whether from the sun on my face or the earthing/grounding or both, it surely can’t hurt!
An interesting concept, as we live today we are almost all walking talking and induction created electrolytic capacitors, the effects of which are and will remain subclinical, though there are, possible correlations, ie references to mobile phone use and brain disease.
The problem we face in the modern world, viz, if I were to ground myself to the radiator, effectively connecting myself to the earth, I would cease to be a capacitor and become a conductor! Would I be any better off.
There are a lot of people who swear by the beneficial effect of wearing permanent magnets for relief from conditions such as rheumatism and arthritis. The question of reality or placebo effect arises again. One could speculate that the beneficial effect was due to the magnets cellular straightening effect on the chaos induced by exposure to electromagmetic radiation.
In the modern world there is no escape from electromagnetic radiation, even in the remotest countryside, notwithstanding we probably arrived by car or bus, both emiters, we are constantly bombarded with radio and television induced electromagnetic waves. I reiterate, changing myself from a capacitor to a conductor, would there be any benefit or indeed may I be compunding the situation. Is it level specific or cumulative or indeed both.
Unfortunately we can no longer use innuit/eskimos as a control group, care of modern living they are as near exposed as we are.
Frequency Htz/Ghtz, intensity, duration, background exposure. All near impoosible to quantify and any conclusion we come to has possible negative connotations, liability, litigation et al, so it’s not happening. The only thing we do know about is resonant frequencies, at a cellular level, the effects are measurable, atomic bombs, radiothereapy et al. What we don’t know about, sound familiar? is the effect of non resonant frequencies. One could describe these as sympathetic frequencies but nobody is looking.
Further, one also has to consider the modulation effect by the combination of frequency, there are a lot of different frequencies abounding. Modulating a frequency in one band can create a resonance in another.
Excellent, rigorous reasoning and a very good read. As always. If there was any justice you would be booking your flight to Stockholm shortly! But we both know there isn’t any so you can maybe wait a while yet……. 🙂 One question: if statins do have the effect you describe, why do they not work better in primary prevention of CVD? A priori, one might expect them to ?
Reducing risk of 1:10 to 1:11 = significant. Reducing risk of 1:20 to 1:21 = non significant. [figures are for illustrative purposes only]
End of para 3. Is it a typo?
blood to brain = carotid.
I notice the odd query about that in a couple of responses.
I wonder if you have any thoughts on the relationship between thrombus and arterial calcification
Your next step should be to work with The Simpsons editors to create an episode where Homer’s EPC cells are seen struggling to reach a thrombus in his coronary artery before it breaks off – getting there just in time!
Plucky EPCs to the rescue…hmmm… It could work, on another planet populated mainly by people who are more interested in science than Kim Kardashian’s bottom. [If that is how you spell her name].
What an amazingly fast reply! Can I ask a serious question? How long do these processes take approximately – how long to create the damage, how long to form the thrombus, how long to cover it with EPC cells, and how long to drag it to safety behind the blood vessel wall?
Are we talking hours, days, or months – I have no idea!
I believe there is a constant process of damage/repair going on. If you tip that balance one way, heart diseases progresses. Tip is the other, heart disease regresses. The speed of which is depending on how far you tip the balance.
So if you’re right (and I’m quite certain you are) the $64k question becomes: how are we to reverse this dreadful process which kills half of us?
The answer is to do many different things. One thing is not enough.
Yes of course, that is a corollary of your thesis!
Personally, I avoid cigarettes, sugar, vegetable oils, and hydrogenates – which all increased mightily in the early decades of the 20th century and probably account in large part for the ascent of heart disease
I embrace exercise and a lowcarb diet based on fish, broth, eggs, butter, vegetables, meats and alcohol.
Despite being insulin-dependent for 30 years, my coronary artery calcium score is zero, HbA1c 5%, BMI about 24 etc.
In short, I’m a 69-year-old demonstration of the consequences of applying your ideas – which is why I find your blog so fascinating
What I’d really like to know is:- what do you do?
I try to do all the things I recommend (but fail quite a lot). I exercise, I try to do breathing exercises for ten mins a day, I drink alcohol (too much probably), I try not to let things stress me. I try to be kind to people – sometimes I fail. I try to keep up with friends and family. I am not too bothered about diet, but will eat high fat stuff given the choice. I rely on good genes. No early CVD anywhere in my gene pool, nor cancer. I try to be positive and happy as much as possible. I try not to get too angry about bias and corruption in medical research.
‘I try not to get too angry about bias and corruption in medical research.’ – Better not read Peter Gotzsche’s book ‘Deadly Medicines and Organized Crime’ then – it’s a superb book, but guaranteed to raise anger & stress levels.
It sits on my bookshelf…. read twice
Oh dear! Here I am thinking we are going to get the definitive answer, and lo and behold, we still have to work out for ourselves how to distinguish which of the different things available suit our individual make-up and lifestyle to obtain optimum health outcomes.
I reckon Jonathan is about right regarding diet, and Dr K is on the right tracks regarding deep breathing, moderate exercise, and avoidance of stress.
I am now going to put all of my technical books into deep storage, get on with my chores of making quality meals for hubby and me, putting the house ship-shape after the festivities (better than visiting the gym),
then enjoying life to the best of my abilities.
I have resolved to read Dr K’s book when it arrives shortly….but thereafter….leave the rest to Pot Luck…..sorry if that sounds defeatest.
As we started last month considering the clotting conundrum, I think I have come to the conclusion that life itself is a conundrum, so I will just smell the coffee ( with double cream, naturally) and get on with it.
And how’s that working for you? Are you guided by the risk factors we can believe in – do you track your calcium score etc?
“I drink alcohol (too much probably)” – but how else can we get our recommended ‘6 ounces equivalents’ of grain foods? It’s our civic duty …
What a sensible and interesting approach. Does it mean, however, that heart disease and stroke are caused by different mechanisms? How do the three factors related to strokes? I read somewhere that acute stress causes the blood to thicken (I’m sure there’s a more scientific term!) making MI more likely – or have I imagined this?
Doc, how is your proposed mechanism compatible with the mysterious rise and fall of heart attacks over the last century or so? Could it be, for example, that in “Step One: Various factors damage the artery wall (endothelial damage)”, the factors include damage by a pathogen? Then the rise and fall might naturally look like the rise and fall of an infectious disease.
I was trying to make it clear that heart disease has no single cause…
I have looked at infectious disease (many people like this hypothesis). But the epidemiology clearly contradicts this as a possibility. Why do men get more CHD at a young age than women. How could CHD be rapidly rising in Lithuania in the 1990s, whilst falling rapidly in Poland (countries that share a border). How can different ethnic groups living in one country e.g. Australian Aboriginals x 30 the rate of CHD in young women compared to ‘European Australians’, have such very different rates of heart disease – living in the same countries. Whilst CHD is falling in many countries, it is still going up in many other countries…. Please find me an infection that could explain this. [And I can lob in several other major contradictions here as well]. I think infections clearly play a role in heart disease, but they cannot explain what we see.
I imagine different levels of stress could explain a lot of that – for example, Lithuania was maybe more at risk of some for of trouble with the USSR, whereas Poland possible felt well free of that danger. The trouble is, I imagine it would be easy to invent a stress explanation for almost any pattern of disease.
Political instability must be very stressful – I remember how awful we all felt in the Cuban Missile Crisis (probably a bit before your time).
That crisis was extremely short – so I wonder if it shows up as a spike in the CHD records – possibly with a short delay.
In “Great Cholesterol Con” one argument that I found personally very persuasive was that atherosclerosis couldn’t be caused by cholesterol because atherosclerosis occurs in arteries only and not veins and there are equal amounts of cholesterol present in both artery and vein. Bear in mind I’m an engineer not a doctor but it seems to me your suggested mechanism of damage/clot/EPCrepair is no better at explaining the artery/vein anomaly – or am I missing something? I can see BP (hence damage) is always greater in the artery than the vein but isn’t it true that people can get atherosclerosis at relatively modest BPs such as 140mmHg, in which case why don’t people with massive BPs such as 200 also see atherosclerosis spilling over into their veins?
BP does not ‘spill over’ into veins. the BP in the veins tends to be about 0 – 10mmHg (max). BP can be higher in the veins/arteries in the lungs, and in pulmonary hypertension (raised BP in the lungs), atherosclerosis can develop in the ‘veins.’ Also, if you use a vein as a bypass in the heart (as in bypass surgery), it very rapidly develops atherosclerosis.
I can confirm that one from personal experience!
I had two by-pass ops in 1997 – two venous grafts, and one mammary artery re-route to replace the third venous which failed. Following a contretemps in 2013, the angiogram showed that the two venous grafts had “significant athersclerosis” and the arterial graft was clear and running freely. The 2013 MIs were in an artery that hadn’t done such a thing before.
It can develop atherosclerosis or simply fail because veins by nature are low pressure high volume vessels and arteries are high pressure low volume vessels. So, if you use a vein to bypass an artery, you’re asking it to do a job for which it was not intended. Hence they can and often do fail. To use an analogy I have used before: it is like sending a boy out to do a man’s job. Arteries and veins are structurally different for that reason. Recently I have talked to those with arterial disease needing grafts say their physicians do “vein mapping” to ensure they are using the most healthy veins for by-pass. However, it is still tenuous for the reasons stated above, I should think. The best hope we can have for avoiding the knife is, of course, through good nutrition and exercise. In fact, I do believe there is hope that some forms of atherosclerotic plaque can be reversed. Let us not overlook the many people who have significant atherosclerotic plaque, but efficient collateral blood supply such that they do not have any heart tissue death as a result. The body is an amazing machine and is constantly confounding us.
And I don’t believe women are more prone to heart disease after menopause either. The only reason they MAY be is that women are aging and menopause is just one aspect of aging. As women or men age, they are more prone to many illnesses. That is just a fact of life. The menopause increases the chances of heart disease is just another scare tactic used to sell more drugs, in my lay person’s most humble opinion, that is.
For those of us who live with persistently high levels of LDL cholesterol but refuse to take statins how do we increase circulating EPCs? Should we take Asprin, Clopidogrel, or omega 3 supplements?
Exercise is best, as far as I know
Might your theory also explain why women are protected from CVD before menopause, and then gain the same degree of risk as men after menopause? Does any such difference exist within the eskimo population, or is the risk the same for men and women regardless of age? Perhaps women have different clotting tendencies before and after menopause.
I recently read the Peter Gotzsche book mentioned above and in it he says that in fact the increase in CVD after menopause is a myth. When you chart the incidence of CVD it mirrors men’s but with a time delay. There is no spike or increase after menopause. I hope I am remembering correctly. Perhaps someone who has read it can confirm this.
I think that might have been me.
Sheesh… My already very healthy scepticism is blind sided once again. I thought the “woman suffer more heart disease after menopause theory” was universally accepted. Dr. kendrick, do you have a post about this?
No, but there is absolutely no evidence that the menopause has any impact on CVD. Yes, women do suffer more heart disease after the menopause. Men suffer more heart disease as the get older too.
Jo, I am also a great admirer of Dr. Peter Gotzsche. The number of people who are taking anti-depressants in the last 30 or more years is staggering. Yet, as he states, there are more people completely disabled by “mental illness” who take these psychotropic medications such they can’t work. So if the overwhelming wide-spread use of anti-depressants was so effective, more people would be able to live normal healthy lives. Depression, even major depression, can happen to anyone. But, generally, people benefit from talk therapy, sometimes behavior mod therapy and such like. Above all, given time and a good ear, they can and will recover on their own. This mentality has only increased people’s dependence on some “crutch” which actually creates a condition that does not have to exist for life. It is not their fault either. We have all been duped into believing a pill can solve everything. Dr. Gotzsche tells it like it is and I am inclined to agree with his no nonsense approach to medicine, particularly Psychiatry.
Its about blood iron levels. I think I have read that.
People make up a new hypothesis almost every day, it is a little game. Let me see, what do women do before the menopause? They menstruate and thus lose iron. Ah, iron must cause heart disease then. Bong!
I have read many reports on how pollution(heavy metals and chemicals) can affect our arteries, brains, and our bodies in general. I did not realize, nanoparticles are becoming so invasive.
Well, I am not up to Eskimos and nosebleeds III. Dr. Kendrick, I have been having nose bleeds since December 18th after reading Eskimos and Nose Bleeds I. Just when I thought I was healing…Eskimos and Nosebleeds part two emerges. Please someone get the conundrum (Warfarin vs. Aspirin or Statins or whatever) because I am afraid I am going to hemorrhage through the tear ducks here. Really, think it might be psychosomatic? I have never had nosebleeds and it is not like I live in a cool, dry place. This is the tropics. Just kidding, Dr. K.
Dr. Kendrick, there appears to be many ways in which the body has a proliferation or decrease in EPC’s. The study below suggests that more natural means of increasing EPC’s lies in something virtually all of us can do to avoid atherosclerosis or at the very least, stabilize this disease. So, if statins act to increase EPC’s, then would not a good exercise routine do as much? One would think so. And, I do believe on the face of it, this theory and the associated studies are of great value particularly in light of the date of this study, which is 2003. There are many out there who have avoided the knife by increasing their exercise levels and stabilized vascular disease. I think I may be one of those people. It seems a small price to pay for not having the nasty side effects of statin therapy.
Fascinating blog, Dr. Kendrick and much appreciated for another lesson well learned and another chance at hope.
Physical training increases endothelial progenitor cells
My hasn’t it gone quiet here! In my case it is that family disease NIB (nose in book). I daresay there are plenty of others in the same situation.
I want to say sincere thanks to the Good Doctor, who has handed me confidence between paper covers. Nobody can give me a healthy heart. I has gone too far for that. At least now, I can weigh for myself the odds of nasty drugs having a helpful effect. It will make my way easier to find, in the business of enjoying the years I have left.
We also got the NIB in our family and today “Doctoring Data” arrived in my mail box.
With the noose in the introductory pages I read that I should rather enjoy life than measure my blood pressure but with the usual evening reading of 110/60 tonight I still feel that I could enjoy life for still a while.
Jean, you may not be able to get that “healthy heart”, I don’t know. I am not a doctor. However, surely there are those you love like family and friends who would benefit from your teaching. I have made many mistakes myself with my health. I smoked for years. I never did anything like take drugs or become extremely overweight. I do love my sweets, however. But, the mistakes I made, I have used as a lesson to others like my own children and many friends and business associates. If you can teach and help others…your life can and will make a huge difference. I admire you for constantly educating yourself through reading, and thinking, and really wanting to know the why. I drove my parents crazy from the time I could talk. I always wanted to know…why; about everything. I have not changed much. Make the world better by never getting tired of wanting to know…why.
I try never to miss a chance at doing a little education – I had a brief conversation with the Cardiologist’s Junior last time I was in hospital- apparently he had never heard that statins can cause brain rot – I hope he believed me! I bend people’s ears at the slightest provocation, and have convinced a few.
Sadly, I can never get back to having a “whole” heart – too much scar tissue. I have to make the best of what I still have. Hence the shunning of pills.
The latest episode of Inside Health on Radio 4 discussed the PLAC blood test for inflammation (as another bit of evidence to help patients decide to go on statins.) Nice to hear that Dr Mark Porter is resisting getting a prescription.
Good to hear that Dr Mark Porter is a little more thoughtful than his predecessor in the Times Medical column. You could rely on a weekly nag to take your statins from Dr Thomas Stuttaford. I believe he was a signed up member of the “Put them in the Water” association.
Not finding any other place to comment properly at this blog I may as well do it here – some might read my comment – you never know!
I have now read “Doctoring Data” in one sweep and must confess that it is about the best book I ever have read about what I myself have become increasingly aware of during the years since my own serious heart attack 1999 – the complete corruption of the ‘discipline’ of medicine, though a discipline which I once in my ignorance believed to belong to the same natural sciences as much as my own field of metallurgy. Since I refused the ‘cabbage’ (CABG – bypass) and all the ‘pills’ proposed I especially enjoyed the part of the book dealing with the ‘futility’ of this ‘praxis’.
Now I just wonder about the traditions of hanging Scots in opposition to ‘key values’ within the UK. What about the survival time when they have spotted one serious case?
Anyway I took the liberty of immediately writing a chronicle about my reading of the book before even having read more than one third of it.
Interested readers may improve their Swedish or try some Google translation – please enjoy proper praise!
Thanks for your review….Google translation was fun….but fortunately my book arrived at 11:30am….and I got stuck in, first with the DVD, then polishing off the first 2 chapters by tea time. My husband and I were then sidetracked into the Peter Duesberg/Bruce Charlton conflict as highlighted by Dr K….and we are beginning to loose faith in any forms of freedom of discussion, ( i.e. beyond the confines of our household). Such goings-on are hindering the progress of medical science, and is a cause for real concern.
I was delighted to see the quote by Thomas Jefferson, as I eagerly opened my book….it sort of sums up much of the debate we are all enjoying on this blog……encompassing politics, medical science, education, and particularly ethics.
Page 57..bullet point 3…. typo…..’morality’… seems to explain the whole shebang even better than ‘mortality’ me thinks!!
Professor, firstly, I am a tad bit envious you have gotten your copy of the book, but, then again, I do live in the U.S. I am oh so curious. Do you have any angina or anything since 1999? Usually when one has a “heart attack”, it seems the next best step is to cut that person from stem to stern and bypass or give them pills. Of course, my own father in law did the same as you and lived to be 83. He refused any operations, pills, etc. He loved his brandy, a cigar on occasion and just kept fairly active. His son, my darling late husband with all the modern medical miracles, did not make it to 51.
Perhaps you have blogged here about it, but I don’t recall. Please tell me.
My father had the most lovely and intriguing library filled to the ceiling with scores of books about history mostly. He and I would spend hours sometimes talking about his genealogical studies of those in our “clan”. He traced the family tree back to 1066 and was proud to say there wasn’t a scoundrel among them (I don’t believe that!) He did most of it well before the convenience of computers. He told me of the many hardships the Scots endured both before and after they arrived in America. George Washington himself preferred the Scots Irish to fight the American Revolution because of their physical and mental prowess. I hung on my father’s every word. He often said “That is the blood that courses through your body and it is that heritage that will carry you through many a hardship”. He knew the Scots to be a hard, hardheaded, and industrious lot both physically and mentally. I loved those stories and have all his books. I think of it often. Sometimes I feel I love to read these posts of you Europeans, because it brings him back to me. When I saw your comment on the Scots…I just had to jump in there. Sorry to be rather off subject.
So Professor…what is your and your lovely wife’s secret?
Thank you for enjoying my comment about Malcolm’s book!
I am sure that you will devour his book as I did in one ‘gulp’ – scary reading for sure!
“So Professor…what is your and your lovely wife’s secret?”
How do I answer your question?
The simplest way would be to advice you to do what your father taught you and the lesson learnt from your ‘second’ father – keep away from the ‘docs’!
Get informed to take control of your health which means that you should not be bullied around by official dogmas which is exactly what the ‘Doctoring Data’ is telling you. But that piece of good advice goes for all parts of life to my experience. Throw out your TV-set is a good starting point and spend all that, all of a sudden, available time on reading ‘heavy books’ instead and complemented by searching specific information of interest through our marvellous internet.
So the ultimate aim should to my opinion ‘stay in control’ and enjoy life.
Of secrets – my wife and myself have been reading the ‘heavy books’ together now for many years, one by one, and basically everyday, taking our turns i reading and talking and often with more talking than reading. It is most probably a good way to preserve your critical thinking and in common – might be a glue in a marriage; now about 40 years.
Congratulations, Professor. I will take that advice and follow it. I shall read those heavy books as I have quite a few to examine. Many of them date back to the 1800’s and before, some heavy and most a little dusty, too. I also have a plethora of lovely letters from our family genealogy searches that warm your heart.
Thanks again, Professor. You are living well. God Bless!
“The simplest way would be to advice you to do what your father taught you and the lesson learnt from your ‘second’ father – keep away from the ‘docs’!”
This reminds me of the early days of the space program. The technicians were amazed how long various satellites lasted, and this turned out to be because they never got ‘serviced’ once they were in space!
Dr. Kendrick, Warfarin would be contraindicated for treatment of acute myocardial infarction due to its variability in how each patient would react and due to the fact that traditionally it takes many days to begin working. It would take extreme and special blood monitoring for the heart and would make the possibility of bleeding out in the heart much higher. The newer LMWH (lower molecular weight heparin) is safer. Further, my research shows Warfarin is an anticoagulant drug and aspirin an anti-platelet drug. Blood platelets are inactive until damage to a blood vessel or coagulation causes them to explode into sticky irregular cells that form a thrombus. Aspirin and other anti-platelet drugs are safer for both heart attacks and strokes. Am I close? I have not read the other responses in a while. I may be close, but I am not thinking I will get a cigar.
Again, I can’t wait to get your book. I ordered Goldacre’s book but don’t want to read it until I finish “Doctoring Data”. The cover is fabulous, Dr. Kendrick!!
My copy of Doctoring Data arrived last week too. I am in Canada. I have raced through it and am about savour it slowly over the next week or so. I am so impressed with the wealth of information and detail and common sense perspective in this book. It reinforces my courage to follow my own health path, and to keep questioning and researching to be as informed as I can be. Dr. Kendrick I thank you.
I was diagnosed with Ideopathic Pulmonary Fibrosis (IPF) four years ago. Any site I’ve googled about this disease is just chockablock with the most dismal, hopeless, and in one occasion just horrible statements. “This devastating disease carries 100% mortality within 3 years of diagnosis” “uniformly fatal” “akin to being slowly strangled”. (that’s the horrible one). What? Here I am four years later, leading a normal life with very bearable limitations and I don’t feel like I’m being slowly strangled. I’d like to get ahold of whoever said that and give him an idea, as he for sure hasn’t experienced it, and has no bloody right to say it.
So, where do they get those numbers from I asked myself. After all, 100% is kind of final sounding isn’t it. (but really, that goes for us all doesn’t it, IPF or not). Is everyones’ name put on a list when diagnosed, then crossed off when they croak? I kind of thought not, but called or emailed several sites to ask: do these numbers come from death certificates? If a person with IPF dies of a heart attack, or complications of diabetes, or gets hit by a bus, does IPF go on the certificate? Why yes, it does. Has there been any effort to find out many people were already in poor health when diagnosed, How many smoked? Are obese? Had other health risks? And so on. And I was told that there has really been no thorough research into it, that the numbers come from doctors offices without further analyses and individuals aren’t followed. I wonder what those stats really mean then, how many people go on different stats having died several times from different diseases?
Like many who follow this blog, I chart my own route even though it feels sometimes like I’m jumping off a cliff. I ignore the traditional dietary advice, refuse medications that I think are inappropriate and harmful, such as the PPI my doctor wanted to prescribe for gastric reflux (common with IPF), and which cleared up all by itself on a high fat low carb diet. One of the problems with PPIs can be severe rebound reflux if you try to stop them, and a higher incidence of pneumonia, which I don’t need thank you very much.
So, here I am four years after diagnosis, no worse than I was then. This afternoon, being a lovely sunny rather cold afternoon, my husband and I have been walking out on a frozen lake near our house. Such a wonderful thing to be able to do that, and if nothing else, this diagnosis has woken me up to the true and simple joys of life.
Maureen, your account is an inspiration. I have been following your ways of disregarding medical and dietary advice for just short of 2 years, and I am feeling fit and well.
However, I have said in the past….non-compliance can be a lonely path, paved with doubts about one’s (non)actions.
I am a slowish reader….hanging onto each word and re-reading paragraphs until the penny drops…but as I approach chapter 6, this book has unleashed a wonderful feeling of empowerment; permitting me to follow my instincts, without having to justify myself any more. In examples specified as far as I have read, I actually did question a number of ‘givens’ both during my NHS careers, and as a recipient of such care…..(oh, if only I had pushed harder)….but like most people, I needed an income, and felt obliged to endure (and indeed, suffer) the very treatments and lifestyles I was expected to promote.
I had no way of checking my hunches, and am so grateful for this book…..I can feel many long discussions arising in our (retired, non-salary-dependent) household, spanning ‘expertise’ in medicine, law, management, politics and education.
This is a great way of keeping the old grey matter exercised.
The other worry is the issue of self fulfilling prophecy. I had a boss who was diagnosed with something that sounds very similar to what you have. I can’t remember exactly what it was, as it was a while ago. When I googled it, the prognosis was dire. I would have left my job to spend more time with my family before the inevitable end. She, however, continued in her demanding job and is still alive today. I don’t know how her health is, but I admire the fact that she didn’t give in, and carried on with life. I feel inspired by her strength and courage, as I am yours.
Naturally you have convinced yourself that you have solved a great riddle. I don’t pretend to understand fully the processes here you talk about, but I do understand something about the psychology of science.
Once you start believing in your theory, you become attached to the theory and objectivity is difficult. To really prove your theory, you now need to now disown it and try to destroy it. Find any evidence that contradicts the expectations, design and imagine experiments that will disprove it. Be totally determined to find the flaws and want your theory to be wrong!
Then, when you have exhausted yourself, disappointed that you cannot bring your theory down, admit defeat and conclude you were right in the first place!
Only then Jedi you be, oops I mean scientist!
Thank you for your kind instruction on science
Gordon, I think what you fail to realise, is that this isn’t really a struggle between two scientific ideas. It is a struggle in which one side – those that make the guidelines for doctors – just keep on saying that the guidelines haven’t changed! As in several areas of corrupted science, there is no attempt by those in power to engage in scientific debate about these matters, just a variety of attempts to shut people up.
Those same people in power, also decide which studies get funded – which further skews the scientific process.
The real tragedy is that in a whole variety of areas modern science has given up all pretence of even-handed weighing of the evidence.
Dr. Kendrick – I read the question – “protect the endothelium, reduce blood clotting, or enhance repair”. The answer is very simple (Rutin and/or Isoquercetin). They both start at the top of the cascade thus preventing both vein and arterial clots. My original interest in Rutin was due to a DVT with bilateral, multiple pulmonary embolisms. If even partly true this covers both bases for me and is very exciting. Any thoughts? I’m email this to you also. -Steve
Click to access 07.pdf
Click to access 37.pdf
Good DOc Kendrick, I just read a fascinating idea by Chris Masterjohn…..just to sum up what I think he asserts, if that stats are correct, people with FH lived longer with it in the 1800s-. But then it became more problematic (when sanitation improved- less infection) the next century, 20th.- Then it might be that the immune system was well aided by ‘high cholesterol’ earlier (19th century) when warding off infection. But then when infections became less trouble, other factors began affecting the’ FH’, like ‘heart disease’ .
I’ve heard about this in 2 other instances. The heterozygous with sickle cell are protected against malaria, while the homozygous are in trouble….And in a book by Charles Mann, ‘1491’, he asserted that the indigenous people in America had immune systems more tuned to parasitic defense. When the Europeans brought over novel viruses and bacteria, those cut down the natives….until they could adapt. The immune system only has so much energy and resources to combat invaders…..and it focuses on the ones that are known to it…..
This is my favorite post of yours….It is genius and very helpful.. I agree that inflammation, damage, thrombi, repair issues are IT. .I know a few people with FH, and it is a conundrum for them……..But, they are the smartest folks I know!!!!!!!!!!!
I realise this is an older posting by Malcolm, but I’m looking for studies confirming whether hyperinsulinaemia as found with insulin resistance results in higher fibrinogen levels – fibrinogen of course being a huge risk factor for heart attacks. I’ve found a few older references and a relatively small study which appears to show the relationship between insulin and the regulation of fibrinogen levels. Could anyone enlighten me to save me from hours of internet searching? Thanks.
so what causes the damage to the artery walls? My dad has 6 stints and since this may be hereditary I would like to protect myself. or at least be aware how to lessen the chances of a fatal clot.