I have been studying heart disease for many, many, years now and I have read hundreds of different hypotheses as to what causes it. When I say heart disease, I mean the build-up of atherosclerotic plaques (narrowings) in the arteries. This can happen in the heart, the blood vessels leading to the brain, the aorta, the femoral arteries etc. etc. Usually followed by the formation of a blood clot over the plaque – leading to death.
I have read a hundred theories as to why this happens. From infective agents, to lack of micronutrients, to stress, copper deficiency and on and on. I have read theories suggesting that plaques are actually healthy adaptations, that heart attacks happen before the blood clot blocks arteries, causing the heart attack. That atherosclerosis has nothing to do with dying of heart disease – the Japanese, with a very low rate of heart disease, are just as likely to have atherosclerosis as anyone else.
In amongst this cacophony I have searched for the one factor that is consistent, and I have found nothing. Yes, mainstream medicine is still fixated on the LDL/cholesterol hypothesis. But it is perfectly simple to find population with low LDL/cholesterol levels and stratospheric rates of heart disease. Russians and Australian aboriginals spring to mind. Equally you can find populations with high LDL/cholesterol levels and very low rates of heart disease e.g. the Swiss or the French.
This leads us to the concept of necessary and/or sufficient. By this I mean a factor may be necessary for a disease to develop. Yet that factor cannot cause the disease alone. Koch demonstrated this by drinking water full of the cholera bacillus. He did not get cholera, because he was otherwise fit and healthy. He stated that a healthy person could fight off cholera, but if you were unhealthy it could kill you.
Thus, the cholera bacillus is ‘necessary’ to get cholera, but not ‘sufficient’ – on its own. The host needs to be compromised in some way.
So, are there even any ‘necessary’ if not ‘sufficient’ factors for heart disease that have been identified? The answer is quite clearly no. Many people have died of heart disease without a single identified risk factor. In short, there is no single factor that is necessary, or sufficient, to cause heart disease.
This is why heart disease is now considered ‘multifactorial.’ It has many different causes that all, sort of, act together – in some yet to be fully defined way. Whilst this must be true, to a certain extent, the concept of multifactorial allows anyone to say virtually anything, and nothing can either be proved, or disproved.
A skeptic: ‘Here is a population with a low LDL/cholesterol level and a high rate of heart disease.’
An expert: ‘Ah, that is because they have a low HDL level, they lightly cook their vegetables, they have a Mediterranean diet, they drink red wine, they [insert any one of three hundred different factors here].’
This type of discussion becomes utterly pointless after a while. You cannot, ever, get anywhere. It is like attacking the Hydra. Chop one head off and another two grow. Which is why we now have, just to look at blood lipids: good cholesterol, bad cholesterol, small and dense bad cholesterol, lightly and fluffy bad cholesterol, the good/bad cholesterol ratio, ‘dyslipidaemia’, high triglycerides, LDL particle number, and on and on. Try pinning anything down and it simply fragments in front of your eyes. Currently you cannot disprove the LDL/cholesterol hypothesis as it has become the perfect shape shifter.
Which means that I decided many years ago not to waste my time on attempting to argue against the LDL/cholesterol hypothesis too often, and pointlessly. Instead I searched for the factor that is necessary to cause heart disease. The factor that is consistent, where there are no contradictions. No need for adaptations, additions, sub-theories, sub-sub-theories.
I have to report that I never found one. Yes, it is true. There is no single factor that is either necessary, or sufficient, to cause heart disease. None. Or at least none yet identified. In truth, I do not think that such a factor ever will be found. Actually I am certain that this will be so.
The reality is that you have to move away from causal factors and start thinking about processes. Here, I believe, is where the answers lie. When you start thinking about process, you can understand why the Eskimos suffer a lot of nose bleeds, and had (when eating their traditional diets), a rate of heart disease that was….zero.
You can also understand why warfarin – an anticoagulant – protects against strokes, but does not protect against heart attacks. Whereas aspirin, which is also an anticoagulant, primarily protects against heart disease.
Yes, Eskimos, nosebleeds and heart disease. And yes, I do know that they are now called Inuit. But I still like Eskimo as it conjures up positive images in my brain.
P.S. A small prize for anyone who can correctly answer the warfarin/aspirin conundrum.
Dr. Malcolm Kendrick 
Warfarin just thins the blood. Asprin seems to have an effect in many different ways. Could the aspirin be acting as an anti inflammatory on the heart?
Good try. However other anti-inflammatories e.g. brufen, naproxen, all increase the risk of heart disease. As do steroids, which are the most powerful anti-inflammatory agents known to man. They increase the relative risk of CVD x 4.
Although aspirin is an anti-inflammatory, it can also wipes out every platelet in your body. Warfarin, apart from effectively killing rats (who can’t vomit) and rats who can (Joseph Stalin, supposedly and hopefully) interferes with the way vitamin K is used in the synthesis of molecules used in one type of clotting cascade. So, aspirin probably stops the formation of clots on a ruptured plaque whereas warfarin stops clots forming in stagnant blood, as in DVTs and in my case atrial fibrillation (just had a successful ablation BTW) where aspirin is of much less efficacy. 🙂
I am guessing Warfarin and Asprin thin the blood so the heart is under less stress to pump blood through compromised arteries?
One typo; “small and dense bed cholesterol”. Not even the modern medical establishment could hope to get away with identifying another cholesterol type to be scared of! 😉
Nope. Thanks for spotting the typo. Will change later today when I am at a computer that allows me to do it.
“Bed cholesterol” – awesome, we’ve discovered another of these nasty little blighters, these bed cholesterol molecules are only active when you’re asleep which is why so many people die of heart attacks in the middle of the night.
Therefore sleep is the leading cause of bed cholesterol and heart disease and we should strive to do it as little as possible.
Caffeine and polyphasic circadian rhythms are the answer!
Ha ha v. funny. Wish I hadn’t edited it out now.
Eskimos might get nosebleeds because the air is so dry. Saline nasal spray might help.
Hmmm, Eskimo/Inuit nosebleeds…a traditional diet containing an unusually high proportion of anti-inflammatory Omega 3 fatty acids, which also have a blood-thinning action, may lead to the nose bleeds? But do they also suffer proportionally more haemorrhagic strokes than other populations? I have no knowledge, I’m just playing around with ideas here.
You are getting warmer
Another typo methinks (or/of) “… has nothing to do with dying of heart disease”. Can’t answer the conundrum. Just wondering though, if eskimos had zero heart disease with their traditional diet, does that not suggest a consistency – that diet must be in some way responsible?
keep thinking.
Maybe we should all eat walrus. Anyway, race itself? Sunshine? Not living in over-heated houses?
Actually, I don’t see how my suggestions can explain the 20th century’s dramatic rise and then fall in heart disease. Isn’t that another key requirement of any purported explanation?
I am trying to establish process here, not causal factors. I think the two things have to be separated out. Also, of course, heart disease only has that pattern in the Western World.
Don’t stop there we need instant gratification. One more chapter. Tell us the answer now!
Tut, tut, Jerome. Such impatience. It is the curse of modern society. In the old days people took centuries to build Cathedrals, happy that they were but pages in a great book. I have spend thirty years thinking about this stuff. Finally, I believe, I have worked it all out. I kind of hope, with a few clues, everyone else can come to the same conclusions.
Will you give us the answer on Christmas Day?
Perhaps the nosebleeds depleted excess iron which some researchers believe is associated with heart disease and mortality.
Warfarin induces vitamin K deficiency.
Vitamin K inadequacy may inhibit the formation of calcium precipitates in lipoproteins, thus could contribute to calcification of bloodvessels to the heart
Warfarin induces vitamin K deficiency.
That in turn can contribute to inhibit the formation of calcium precipitates in lipoproteins, thus contributing to calcifications of bloodvessels ?
Great blog. Many thanks.
“the Japanese, with a very low rate of heart disease, are just as likely to have atherosclerosis as anyone else”.
The Japanese traditionally eat a lot of natto which presumably means they also consume nattokinase, a fibrinolytic produced in the fermentation process. Streptokinase plus aspirin was apparently successful and was significantly (2p<00001) better than either agent alone in reducing vascular deaths among patients (The Lancet13 August 1988, Vol.332(8607):349–360). Just a wild thought.
“Which means that I decided many years ago not to waste my time on attempting to argue against the LDL/cholesterol hypothesis too often, and pointlessly.”
Rather like cat herding; attempting to do the impossible. And of course closed minds. As you say the truth probably lies in the interaction of many factors and processes; the simple concentration on drugs alone is a basic flaw of allopathic medicine.
May I suggest that one problem relates to the innumerable meta-analyses that abound these days. It relates to the much used term “multifactorial”. In an attempt to isolate a particular factor, other parameters are “adjusted for”. When the factor is, shall we say, age, this can tend to blur the effects of closely associated factors; possibly due to the partitioning of variance between the “adjusted parameter” and selected factor.
A small prize for anyone who can correctly answer the warfarin/aspirin conundrum.
All I know is that warfarin destroys Vit K – hence its use a a rat killer. Vitamin K is an essential vitamin and one wonders at the consequences of its disruption..
I also note from the MHRA DAPs on the two substances is that since 1965, aspirin has had fewer death reports than warfarin, despite the huge difference in product weight used in humans. I must say, I was surprised when a consultant told me that warfarin was 70% better than aspirin in AF than aspirin (relative rate) but only 4% effective in treating AF (no mention of what happens to the other 24 out of 25 that do not benefit). Effectively this means that the actual benefit over aspirin is about 1.6%; the overall extra benefit from warfarin is an unlikely event for most patients.
Nattokinase and Serrapeptase should be the subject of a future article.
Is it that asprin is a smooth muscle relaxant via its effect on prostaglandins?
Whatever happened to disprin? It seems now to be another name for aspirin but I recall it was originally a double salt of salicylic acid or some such thing. Whatever it was I had so much of it as a child that my ears are still ringing 50 years later.
Craig.
It may be related to liver disease.
Dear Dr Kendrick,
I’m a big fan and after The Great Cholestrol Con I now read everything on your blog
I’m not the person to be able to discuss anti-coagulants but it does seem to me the answer to the heart disease problem is really quite straightforward, it’s just that the answer is not one the medical profession are comfortable with so, for the most part, they simply refuse to even consider it.
The psychologist Prof Ronald Grossarth-Maticek has scientifically proven quite conclusively that psychological factors are dominant in the causation of both heart disease and cancer. They’re also quite significant in whether you contract cholera from cholera bacillus! Grossarth-Maticek gave a group of 50 year olds a specially designed therapy called “Autonomy Training” which he designed to combat stress. This was simply a talking therapy: no pills, no injections, nothing physical of any kind. A control group of the same size received the same number of hours of a therapy which was intellectually plausible but didn’t reduce stress. After approximately ten years, the follow-up revealed that the cardiovascular mortality in the control group was 4 times that in the Autonomie group and the cancer mortality 11 times. In other words Grossarth-Maticek has designed and proven in clinical trials, a talking therapy which produces an 1100% reduction in cancer rates in this important decade (from 50 to 60 years of age) and no-one in the medical profession has even heard of him. Search on the web and about the only thing you will find in English is a short introduction by a fellow enthusiast: http://www.attitudefactor.com/grossarth.htm
The mechanisms for this utterly amazing effect are also fully understood and documented but again almost universally ignored by the medical profession. Basically the hormones our body produce during stress are gravely damaging to the immune system and to our tissue repair. So people with the “wrong” attitude to life suffer chronic stress and so incur chronic failures in immunity and repair. The mechanisms are all described for the lay reader in Robert Sapolsky’s “Why Zebras Don’t Get Ulcers”.
Malcolm
As an independent woman who is very grateful for many years of Catholic schooling from elementary to graduate level training, I have to wonder if Catholics who go to confession on a regular basis have some protective effect from talk therapy or as you describe in this study of “Autonomy Training?” They go at their own free will and are given “forgiveness” such that they can unload some of their burdens of guilt and stress. A close Catholic friend and I discussed this at length recently. I gained a new perspective on this sacrament which I actually dreaded as a child. I think far too many in the field of psychiatry are too quick to write a prescription for medications that have side effects which make patients feel worse and in some cases, even cause increased rates of suicide and depression. Why are they not doing their jobs and trying at least to listen more and give solid, sound advice and therapies for those who suffer with many times fleeting episodes of depression and difficulties? Is that not just a fact of life? This whole mentality of medicating everything but a hangnail seems to be unsuccessful to say the least. The world is a place where far too much negativity prevails and creates this (at least in some individuals) self fulfilling prophecy of depression and infinite dependence on psychotropic drugs. It is sad really. Many, if not most people, do not need this but rather “talk therapy” with trained professionals who can teach the coping skills that lead to autonomy and thus, confidence in dealing with the everyday issues of stress and unhappiness. That is more effective, it seems, than medications far too dangerous than most people realize.
Thanks for your input and reference which I find very fascinating. We must come to realize and accept that we have to face and endure both minor and major violations of our trust that are a normal part of human interaction. It appears these are issues people have to face. Problems can be solved, but issues can not and have to be accepted and dealt with as they come. That is what maturity and self sufficiency really are!
Thanks again!
Warfarin can induce calciphylaxis, the presumably has something to do with its actions on K2? So extra calcification of arteries for warfarin. And Aspirin maybe doesn’t do that?
Hm, having BTDT with warfarin and blood clots, I’ve done a little homework on this so I’ll take the bait. Aspirin’s anti coagulation action is based on preventing platelets from clumping, while warfarin works by suppressing the production of Vitamin K in the liver; vitamin K is the basis of Factor V and several other factors in the blood clotting cascade. Both medications cause nosebleeds. If the Inuit (sorry, I love the sound of the word) get strokes but no heart attacks, and aspirin prevents heart attacks but not strokes, then they don’t have issues with platelet stickiness. Their strokes might be caused by a diet deficient in vitamin K, or more likely a genetic mutation such as Factor V Lieden that gives them an aggressive clotting response (a survival trait in societies where the risk of injury is high). So what causes unwanted platelet clumping? I’ll take a guess and say inflammation caused by consistently high levels of endogenous insulin. However I believe that inflammation causes strokes as well as heart attacks. Wish I didn’t have a day job; I’d go get the papers out of PubMed. You should look at Hyperlipid’s blog post on the deleterious effects of using the body as an insulin sump, based on the recent ACCORD study: http://high-fat-nutrition.blogspot.com/2014/12/accord-and-musings-on-insulin.html
Warfarin isn’t an aniticoagulant per se, it’s a vitamin K inhibitor. Asprin “is” an anticoagulent as in reduces the ability of platelets to stick together.
Further, there is overlap in effect but there are different gained effects at each end of the commonality spectrum.
“I have been studying heart disease for many, many, years now and I have read hundreds of different hypotheses as to what causes it.” It’s patently obvious to me what causes it: the factor that has the greatest earning potential.
Merrry Chrismas to one and all and a happy and healthy new year.
Indeed. But what about Tiny Tim.
Best wishes to him as well.
I must admit I’m stumped, I await the answer with baited breath.
It’s “bated breath.” 🙂
A further thought to my post above…on a traditional diet, Inuit would have only the most minimal access to starch and sugar, and thus no diabetes, and no diabetes-related heart disease?
I should have taken that thought a bit further: warfarin, being an anti-coagulant, will act on or prevent clots in the blood vessels of the brain and elsewhere, preventing the most common cause of stroke; the benefit of aspirin is chiefly anti-inflammatory and inflammatory response is the chief cause of heart attacks.
Well, I’d say the difference is that aspirin is an anti-platelet drug, whereas warfarin interferes with the coagulation process later in the cascade as clotting is consolidated. So with warfarin a dangerous clot in, say, a flaccid atrium can’t get established as easily. But the platelets can still glom onto the artery walls, and maybe even be more unstable since the consolidation of clotting is inhibited. With aspirin, the platelets are inhibited from ever starting to clot the arteries.
I’d have guessed that aspirin would also work against stroke by inhibiting the platelets, which I believe it does to some extent, though not as much as warfarin. Would be interesting to see how other anti-platelet drugs affect heart attack vs. stroke, as well as other anticoagulants that counter later events in the cascade. Do they follow the same pattern as aspirin vs. warfarin?
Eskimos inhibit their platelets with fish oil, no Rx required.
Getting warmer?
Warfarin affects soluble protein clotting factors, aspirin causes platelets to aggregate less. So in a stroke, clotting factors must be more important, in a heart attack, platelets.
Eskimos have no heart disease and eat whale, seals and walrus which is high fat, high protein, low carbohydrate. Asprin also protects against heart disease. What is the aspirin doing that mimics the Eskimo diet?
Eskimos have nose bleeds that mean their blood must be thinned. What process is tying this all together? Even with the clues I don’t know.
My guess/suggestion: Warfarin is an anticoagulant, and protects against strokes because strokes happen when blood vessels (that are much thinner than ateries) are blocked, so that the viscosity of the blood has an effect. Heart disease is a product of a calcifed artery (possibly caused by magnesium deficiency – just a guess) being stressed by the high pressures and pressure changes that happen in the much wider arteries, where the viscosity of the blood makes no difference. This suggests that it is not the anticoagulant effect of the asprin that is having the positive effect on heart disease, and that it is some other property of the aspirin.
Thromboxane. Warfarin impacts calcium dependent clotting factors, but not Thromboxane. Aspirin (and to a lesser extent omega-3) reduces TXA2, increases NO, reduces endothelial damage etc, etc.
Aw….Malcolm….play fair…..I signed off for the year…..Puds to make, fairy lights to fix, etc….haven’t time for thinking straight….what’s the answer….pl…ea…se.?
I have no way of knowing if it makes sense, but have you seen this article?
http://www.lewrockwell.com/2014/12/no_author/dont-believe-the-party-line/
Aspirin stops platelet initiated clotting, warfarin acts on clotting factors..
I am guessing that it has to do with interaction with vitamin K2. Warfarin acts against K2 and thus sets up arterial calcification (insufficient carboxylation of MGP). I have not studied aspirin, but it is not apparently an AVK.
I think whatever helps and/or repairs the endothelium helps reduce the chance of a heart attack. I presume aspirin does this but not warfarin. The eskimo nose bleed thing must be something to do with the omega 3, vitamin C, apolipoprotein a connection.????
I have read that the Inuit do suffer more hemorrhagic stoke. Warfarin works on the clotting factors and aspirin works on platelet function. Omega 3 is both a weak anti-coagulant and anti-inflammatory agent. Perhaps it is able to impart the benefits of both in a biologically relevant way that works in harmony with the bodies various processes, while minimizing the side effects. Thanks for the post!
Aspirin is an antiplatelet agent, but warfarin is an anticoagulant. The former keep clots from forming by inhibiting the production of thromboxane, but anticoagulants target clotting factors by competing with vitamin K. So warfarin essentially causes the effect of a vitamin K deficiency. A deficiency of vitamin K2 could be responsible for the increase in heart disease.
Warfarin possibly truly thins the blood for smooth passage through smaller pipes in/ to the brain, whereas aspirin just prevents the platelets sticking, so not as thinned, thus thinness of blood or otherwise is not the cause of heart disease.Possibly Aspirin has special unknown constituent or is a placebo and it is all to do with how food is cooked or not as the case may be.( How do the Japanese rate on the heart failure scale?)
Warfarin is supposed to act by blocking vitamins K (K1 and K2), while aspirin does not. Vitamin K2 deficiency is a very powerful independent risk factor for cardiovascular disease (I have seen a 50% reduction of CVD after K2 supplementation, in one study), its also a risk for osteoporisis and for dental health. That is also another reason why poor dental health correlates with atherosclerotic heart disease – the common factor!
Regarding Eskimo nose bleeds – I also used to have nose bleeds and brusing on my hands, immediately after adopting a high animal fat low carb diet in 1999. There is some anti-coagulating effect exerted by one of the common fat (but I don’t know more details). Of course, Eskimos (or anybody else for that matter) on a high animal fat LC diet, also do not get heart disease either (note: it seems to protect against both arteriosclerotic and cardio-myopathic diseases, unfortunately there are almost no studies available, mostly personal professional petient’s record by some doctors who used the HF LC diets).
BTW – I enjoy your blog!
Best Regards,
Stan (Heretic)
I thought you had settled on chronic stress as being the answer. Scotland – people being forced to move into tenements away from where they grew up. Finland – displaced population after the war. Personally I’m in the not enough sunlight/vitamin-D camp.
Alan. Yes, and no. I believe that chronic negative stress is a trigger for the processes that cause CVD. However, it is linking the two things together that I find most interesting
Warfarin being anticoagulant is just that, whereas aspirin is both anticoagulant and anti-inflammatory. You need something which is both and aspirin is both whereas warfarin is just one of them.
Thrilling post as always!
With my serious – close to death experience – heart disease since 15 years I am a great medicine sceptic since then and will never touch any of the five drugs prescribed by the cardiologist who consider may resistance as almost ‘criminal’ when I met him – hopefully for the last time – last year. My by-pass refusal didn’t do anything to improve his opinion about me as a would-be steamroller of cardiologists. He was really malicious when he prescribed the statins he knew very well I would never touch. He was the ‘expert’ but couldn’t even recommend me a standard textbook of his own discipline. He had not even been able to find my medical records at the same hospital before our meeting! May God forgive his ignorant soul!
I like the scientific idea of going for the cause ore perhaps for the multiple causes.
So I have gone for your Inuit suggestion instead – though I have not been able to find seal blubber.
I bleed easily but not from the nose. The inuit way seems to work pretty well for a ‘dead man walking’ and with significant amount of E-vitamin now as a supplement the unstable angina – the reason for my last (?) encounter after which I did some R&D ‘homework’ – now seems to be history.
What are those 5 drugs?
Some quick googling reveals that warfarin works by blocking clotting factors in the blood, whereas aspirin reduces the binding action of platelets. If a heart attack blockage is caused by platelets accumulating at the site of a ruptured plaque, then something that modifies platelet action (aspirin or an omega 3 rich diet) may have a meaningful impact on reducing heart attack risk?
Dr. Kendrick, as to your question about Warfarin vs. Aspirin, it seems you have dropped a couple of hints that diet is somehow implicated, as well as some material differences in the effects of Aspirin vs. Warfarin that makes the former more effective against heart attacks than the latter.
I will therefor speculate that, since heart attack is usually caused by an unstable buildup of white blood cells (leukocytes) that can result in blockage of the artery, then perhaps it stands to reason that Aspirin, along with a certain diet, is somehow effective in discouraging (or overcoming) an excessive buildup of leukocytes. I will also venture that a diet tending to be anti-inflammatory (i.e., no grains and otherwise carbohydrate restricted) may also be helpful by adding to the positive, anti-inflammatory properties of Aspirin.
What say you Sir to my wild speculations?
//s// Wil B. from the USA, a big fan of yours every since your book, the Great Cholesterol Con, and reading your offerings on THINCS.
Cheers and Best Wishes for the holidays!
I love wild speculation. I love people having a go. Thank goodness we have not all given up.
From the rear seat of the car: “Are we nearly there yet? Are we nearly there yet? Are…”
Since you love wild speculation… now, I must preface this by stating that I’m not a medical expert, but is it something to do with the spelling of the two words? Warfarin has the W and Aspirin has the P – significant factors? and Eskimos have nosebleeds coz it’s so bloomin’ cold up there!
I think you have moved slightly beyond the barriers of wild speculation, into something else. My own belief is that you would have less nosebleeds if it was bloomin cold. But I am not sure.
Warfarin inhibits vitamin K more irreversibly and at lower concentrations than does aspirin.
Hi,
Both K2 and D3 affect Calcium transport. Taking warfarin has the side effect of speeding up calcification of arteries and probably everything else except those tissues where Calcium should be going like bones and teeth. Interestingly there are studies implication D3 supplementation in a huge reduction of heart disease too, by a similar factor than K2 (equal or over 50% but don’t remember the exact figures). One factor that inhibits D3 transport, appears to be WGA (Wheat Germ Agglutins). Probably the best way of guaranteeing a rapid progression of atherosclerotic heart disease is taking warfarine together with a liberal consumption of wheat.
My belief du jour is that yes, it is probably the four “magic” bullets: K2,D3, ketone-dominated metabolism and omega-3 fats (but that’s another topic)
Regards,
Stan (Heretic)
stan-heretic blogspot ca
i hope no one has to ever answer your examination questions! Most “heart attacks” are not caused by lack of blood flow hence blood thinners are of little use or more likely no use at all. I assume this s not the case for strokes.
“Heart disease” on the other hand is mitigated by the aspirins inhibition of Cox-1 and Cox-2 enzymes (rather than its anticoagulant effect!) and thus promoting the formation of anti-inflammatory eicosanoids from Omega 3 fatty acids. Other anti-inflammatory drugs (NSAID’S) do not act in the same way.
whoops, I should have said reducing the formation of inflammatory eicosanoids formed from linoleic acid via arachodonic acid and promoting the formation of additional anti-inflammatory eicosanoids from dihomo gamma linoleic acid
I watched a recent documentary about the Mediterranean diet. There is a lot more to it than olives and fish. I think Vitamin C deficiency might be one of the causes of heart disease. Does a high carb diet cause the body to need more Vit C?
I believe so, as many grains contain “anti-nutrients”, I think they are called phytonutrients or something. Basically they use up vitamins in the digestion process. I asked some people in a facebook group called “zeroing in on health”, who eat nothing but meat, how they get enough vitamins c, as vit c is destroyed above 70 deg C, and i was assuming he meat they is cooked. Turns out you need very little vit c if you don’t eat grains! Some of these people have been eating nothing but cooked meat for more than a decade, and are in perfect health.
We accept stress as being an important factor, so I see the question as being “how do we get from ANS to myocardial necrosis in a way modulated by aspirin?” Does CVD really involve lipids, plaques and the cardiac arteries in the way usually proposed? Why is heart rate variability such a good predictor of outcomes? Why do many studies show very little connection between blood lipids and CVD?
Thinking about this led me to read about the myogenic theory which provides an interesting point of view with some attractive features. So does that change your question to one about how aspirin affects Na + /K + ATPase activity of myocytes? I suspect it has some effect (in the right direction), but I have not had time to read deeply enough to be sure.
Ken
ps. while reading about this I saw a familiar character:
It seems to me that the question to answer, in preventing MIs is which of the causes are most directly linked to the outcome.
Stress hormones decrease clotting time, but is that their main role in MI?
Does aspirin work to improve the outcomes only through its role in increasing clotting time, or do some of the other (many?) effects of aspirin have a more significant role? One example is its effect on nitric oxide synthase – there is a link to heart disease.
Of all nutrients, glucose (in the blood, from sugars or starches or de novo) predicts CVD. Is that due more to damage to coronary arteries, microvascular damage or degradation of myocytes (reduced mitochondrial function)?
Atherosclerosis, clots and MIs are easy to see and correlated, but preventative measures that are justified according to the most obvious picture (e.g. CABG, stents, statins) are not very effective at extending life. On the other hand as Malcolm argues convincingly, stress has a strongly negative effect, and diabetics (for whichever reason) don’t do well either.
Ken
Vitamin K puts calcium where it belongs instead of letting it settle in arteries and harden them. Warfarin inhibits vitamin K. So if the arteries are hardened and then crack, they’ll bleed all the more with thinned blood. Without dairy, and with few leafy greens, the Eskimo diet shouldn’t have been overly high in calcium.
As for the nosebleeds, all I can think of is cold, dry air and a lack of zinc oxide. (Does oxidation have something to do with it?)
I read somewhere that aspirin before bedtime reduces cortisol and blood pressure, but I’ve not read that of warfarin. If stress is a factor in heart attacks, that seems relevant and would perhaps explain the difference. I can’t see where the Eskimos factor into this though. Maybe Omega3 lowers cortisol too?
“You can also understand why warfarin – an anticoagulant – protects against strokes, but does not protect against heart attacks. Whereas aspirin, which is also an anticoagulant, primarily protects against heart disease.”
Are those facts? Or were the studies rigged like so many others?
Facts, I think. Because at the time the agents studies were off patent and making little money for anyone
Maybe we need to rethink the situation with the Eskimos. In a paper publish earlier this year Canadian researchers claim that most studies have found that the Greenland Eskimos and the Canadian and Alaskan Inuit have CAD as often as the non-Eskimo populations. http://www.ncbi.nlm.nih.gov/pubmed/25064579
“You can also understand why warfarin – an anticoagulant – protects against strokes, but does not protect against heart attacks. Whereas aspirin, which is also an anticoagulant, primarily protects against heart disease.”
Dr. Kendrick. This claim surprises me a bit. In fact aspirin can reduce the risk of both stroke and heart attack. It is still the main treatment for transient ischemic attacks.
Warfarin on he other hand primarily works by reducing the risk of embolic strokes such as those resulting from atrial fibrillation.
The available evidence supports the use of aspirin for preventing another heart attack or stroke in patients who have already had a heart attack or stroke, or have other evidence of coronary artery disease, such as angina or a history of a coronary bypass operation or coronary angioplasty.
However, today the FDA does not believe there is sufficient support for the use of aspirin for primary prevention.
http://www.fda.gov/Drugs/ResourcesForYou/Consumers/ucm390574.htm
My understanding is that they do, now, but did not many years ago.
never mind aspirin….how about the news tonight that ibuprofen adds 12 years onto our life span? and a barmy commentator quipped that doubling the dose could maybe extend life by 24 years….where does this stupidity end?
I recall 30+ years ago, when aspirin was lauded as the be-all and end-all of heart protection. The medical emergencies of gastric bleeding admissions escalated as folks took it upon themselves to take “a couple” ( 2 x 300mg, bought across the counter), every day…..not the 75mg actually being prescribed.
I don’t think there is an answer to today’s conundrum……unless it turns up in my Christmas cracker, and then I will share the definitive answer with you all….promise.
Yes Malcolm. That’s been my understanding as well. But accordingly these Canadian scientists claim otherwise and present evidence that the Eskimos/Inuits never had low incidence of heart disease (I did provide the Medline reference above). So, that’s where we are now. As so often before, difficult to know what to believe 🙂
I’ve researched this matter. On their traditional diet alone they had almost no heart disease, diabetes or cancers. What they have now is entirely irrelevant and indeed misleading.
Thank you Garry. That was my understanding of the matter
Reading the abstract, I was struck by this sentence:
” Most studies found that the Greenland Eskimos and the Canadian and Alaskan Inuit have CAD as often as the non-Eskimo populations. ”
That seems to imply that the Eskimos at least did no worse than the rest of us on a diet that was saturated in saturated fat (sorry!).
Since rates of CVD vary so much from country to country, I wonder which non-Eskimo populations they used for comparison.
Some supplementary facts that might help
– aspirin does not seem to prevent heart attacks in Japan.
– in Norway, high intake of fatty fish seems (“seems” is shorthand for “is associated with but association =/= causation”) protective against IHD in people with high HbA1c but seems harmful in people with low HbA1c
– omega 6 PUFA seems to protect against IHD, but high-PUFA oils are important sources of K1 and vit E in standard diet. hydrogenated vegetable oils contain an antinutrient analogue of vitamin K. Ancel Keys thought cholesterol-lowering effect of n-6 could not account for differences in CHD in 7 countries study as range of intakes was too narrow (3-7%) to influence serum cholesterol (how we got from Ancel Keys, who for all his faults was not stupid, to “each 5% increase in substitution with PUFA” and cholesterol-lowering margarine is beyond me).
Also – in the animal model of aortic atheroma, carbohydrate restriction (10% CHO) is protective against lipid accumulation and inflammation.
http://www.ncbi.nlm.nih.gov/pubmed/19892353
and most recently here:
Cholesterol-induced inflammation and macrophage accumulation in adipose tissue is reduced by a low carbohydrate diet in guinea pigs
http://e-nrp.org/DOIx.php?id=10.4162/nrp.2014.8.6.625
(the diet was 20% SFA, 30% MUFA, 10% PUFA, 30% Pro, 10% CHO)
Don’t knock the animal studies, the lipid hypothesis began with this kind of model, it might as well end with it too.
Dr. Kendrick: It is not aspirin that protects against heart disease, but magnesium-all the trials with a positive outcome used bufferin-aspirin buffered with magnesium. See Kauffman, “Malignant Medical Myths.”
“… the Japanese, with a very low rate of heart disease, are just as likely to have atherosclerosis as anyone else.” Sorry to be pernickety, but aren’t atherosclerosis and heart disease the same thing, as suggested by “When I say heart disease, I mean the build-up of atherosclerotic plaques (narrowings) in the arteries.” Having had a heart attack two years ago, the reasons for which are still obscure – or multifactorial – you might say I am particularly interested in this topic. Great blog, btw.
I believe that the sine qua non of chd is inflammation. I think that not having inflammation protects you against other factors, but most other factors promote it. Stress, high Carb intake, high insulin etc. Common factor in most of them is hyperinsulinaemia.
We still don’t have the official answer? Until then, it seems to me that the factors that cause are the ones i said, and on the other hand I think that NO would reduce the problem, that one would get do not know how
Water: the eskimo presumably drink mainly melted snow – pretty pure stuff. So, what has been in increasing, and then decreasing, concentrations in Western water during approximately 1920 to now? I have no idea.
Different track; the decline in Western rates of heart disease is presumably due to those terrible people, GPs, overprescribing antibiotics, and thereby driving the disease-causing pathogens into retreat. Or perhaps the antibiotics in our meat are to blame – or rather praise.
Is there any correlation between those nations where heart disease rates are very different from the West’s, and those nations where cigarette smoking seems to cause much less lung cancer than in the West? I remember reading once that Southern Europeans are noticeably less vulnerable to cancer-sticks than Northern.
I know what is going on here.
The good Doctor has found the answer to life, the universe and everything (turns out not to be 42) and is stringing us along to drum up interest in his new book, which will reveal all and make him a millionaire.
How cynical. Doctoring Data has nothing in it, specifically, about heart disease.
Fergus……ooh nasty pasty during this Season of Goodwill, too!
This is a pleasant, informative site, where participants are polite, and at times, a little flipant….but no way rude.
I took it as Scottish humour. I have no problem with a bit of banter. if you can’t take it, don’t dish it out.
BTW I have filtered out a few comments from a few people who seemed determined to insult without adding anything to the conversation. Whilst I am a bit of a free speech fanatic I do not allow adverts, direct personal insults or incomprehensible gibberish to pass. It is quite amazing what some people try to post. If someone wants to insult me personally, fair enough, it will go up. My general rule is that, if you would not say it someone’s face, don’t try to post it online.
Random guess III. Warfarin doesn’t effect fibrinogen, but aspirin does effect it so alters clot formation, omega3 also effects fibrinogen?
Look to the two pathways of blood clotting.
Aspirin prevents the formation of thromboxane due to its inhibition of COX1 (which i gather other NSAIDS don’t as they act on COX2)?
I know what you’re thinking. Aspirin and presumably omega3 affect platelet aggregation and endothelial proliferation etc beneficially whereas warfarin doesn’t. Endothelium proliferates in chd
Could it be that Aspirin contain Salicylic acid, and anti-inflammatory whereas Warfarin is only an anti-coagulant?
I wasn’t being serious Doc. I actually didn’t know you had a new book out!!
Anyways I just want you to spill the beans. …… please.
Fergus
The good doctor says he took your comment as Scottish humor. So did I. The temperament persists among what we call the Scotch-Irish here in the States.
Ken. Thank God.
Dr Kendrick, I notice you haven’t mentioned my previous comment. On rereading it, I see it looks rather like spam – this may have led you to skip it. The link I posted points to an article by a doctor who has done a lot of research on heart attacks and believes they are caused by stress – specifically an imbalance between the sympathetic and parasympathetic nervous system. Here is the link again, if you should wish to give it a look:
http://www.lewrockwell.com/2014/12/no_author/dont-believe-the-party-line/
Tom, thanks I have seen it and I think it is very interesting – and not quite right
Might it be a lack of intake of linoleic acid in the traditional Inuit diet?
Because of the lack of that precursor, there is decreased synthesis of arachidonic acid (AA), thus decreased synthesis of prostaglandin H2 which results in decrease in other pro-inflammatory molecules (PGs and Thromboxanes, in particular A2).
Aspirin permanently inhibits Cyclo-oxygenase which converts AA to PGH2, which is used to produce other PGs and TXA2.
Common final pathway: without the PGs and TXs, platelets cannot release platetelet activating and pro-coagulation granules, and thus decreased fibrinogen crosslinking and no change in platelets to sticky stellate configuration, and no primary hemostasis.
This way, aspirin works for prevention of MI & (non-embolic) stroke; warfarin affects secondary hemostasis pathway (the classical Intrinsic & Extrinsic pathway).
You nearly win my non-existent prize
And then the high intake of omega-3 fatty acids in the traditional Inuit diet compete with AA in platelet cell membranes, increasing ratio of Omega-3s to AA; then Phospholipase A2 cleaves Omega-3 fats, which results in more PGI2 production (instead of PGH2). This results in vasodilatory effects and anti-platelet effects, suppressing Platelet Activating Factor, all resulting in increased bleeding time, reduction in ADP, collagen, and epinephrine reduced platelet aggregation.
I think that’s the rest…
Does aspirin prevent strokes and DVT as effectively as Warfarin? Is Warfarin even that effective?
OK – here is a wild guess.
I know Dr Kendrick believes that heart disease is often the result of stress. On that basis, warfarin probably saves people from heart attacks, but causes them in equal number because everyone knows it is rat poison, and you have to have endless checks to ensure the dose is not too high etc.
On the other hand, low dose aspirin make you feel virtuous when you remember to take it, so it helps the heart by a placebo effect.
Eskimos got no heart disease on their traditional diets because they contain no sugar, and they get nose bleeds because small blood vessels in their noses freeze and burst!
(It is probably just as well I didn’t try for medical school!)
The process is the word and the word is raw?
The Eskimo traditionally ate a great deal of the food raw. Seal heart is a delicacy eaten raw, so too the blubber. Fish is fermented in the ground and is a great way to get fat soluble vitamins A and D as well as some omega 3s (DHA and EPA).
Nose bleeds? maybe too much A? I’ll take a copy of your new book as my prize 🙂
It’s all wonderful stuff to read and to contemplate but one should take care when comparing isolated populations which are likely to have genetic differences. For instance this paper refers to a fatty acid handling mutation which is apparently widespread in coastal innuit populations and seems to have been selected for over long periods of time.
http://www.cell.com/ajhg/abstract/S0002-9297%2814%2900422-4
Craig.
I have noticed heart-failure is on the rise, hugely on the rise. I see it happening in folk who you would expect, and folk who you would not. (Not heart attack, heart failure.)
I can only suggest four converging trends which may have an impact : too much sugar, margarine/veg oils insted of tallow&butter&lard, low-fat products, benzene.
Yeah I said benzene.
Take out the lead, put “lead replacements” in petrol : watch them die.
Maybe worth an investigation?
Oh – God!
I am a dead man, still walking, to the disgust of my last (latest?) cardiologist.
I am since long a disbeliever in medicine as well as a scientist so why not look into other hypothesis than the official statin one which doesn’t seem to keep together?
I love chemistry (just had my fresh copy of sixth edition of Alberts et al. “Molecualr Biology of THE CELL” to scrutinise) so what was then more natural for me than to look into what the Nobel laureate chemist Linus Paulin is saying about medicine although he has been denominated “the biggest quack ever” by Big Pharma.
So I am a kind of ‘openminded’ natural scientist and as such allow myself to visit obscure ‘quack’ web-sites and the latest one relates to the present topic and chocked me in its truly ‘Popperian’ refutation of what I thought was fundamental in heart attacks – blockage of arteries and in my case, all large coronal arteries, confirmed since 15 years
The following link contains a five minutes video which I consider scientific and therefore would like to recommend for viewing for everyone interested in ischemia and heart attacks.
http://articles.mercola.com/sites/articles/archive/2014/12/17/real-cause-heart-attacks.aspx?e_cid=20141217Z2_DNL_art_1&utm_source=dnl&utm_medium=email&utm_content=art1&utm_campaign=20141217Z2&et_cid=DM62427&et_rid=765396513
It seems to be all about stress if I should believe what I here read – fits with me story anyway.
Professor Sjoberg, I am fascinated watching the video…..especially having studied Radiography in the past, and taking as gospel the explanations of angiograms I learned back in the day. It seems that some of the concepts of our understanding of physiology are doing a 180degree turn-round, and I would suggest that drugs rarely solve problems. In the case of cardiac stenosis, recent statistics show how surgical intervention ( emergency or planned) seems questionable too.
Look how we have experienced a turnabout since the days of almost compulsory tonsillectomy? The detrimental over-use of antibiotics is taking ages to hit home. I am encouraged there is a growing number of eminent people questioning the toxicity if statins. And now, in the present day, we should be scrutinising the escallating incidence of bariatric surgery, as I see it as the next big No-Go area, once enough time has elapsed to observe its detrimental senarios.
I agree with Ulfric….what we consume in the name of food lies at the root of the whole problem….
I want more research done on tackling the root causes of disease and less done on counteracting the outcomes of ill health.
If the body wasn’t abused, in the first place, there would be little to fix!
But of course, that pulls the rug out from under the feet of big pharma.
Lets get back to basics….and encourage the work of those describing the damage, ( e.g. as in the video) and how to prevent the damage in the first place.
Brilliant short video….and I will endeavour to read the accompanying articles in between the festive family get-togethers.
If it turns out to be an accurate assesment of the situation statins will be replaced by a very expensive and enhanced prozac-esque therapy. They won’t be going away.
This phenomenon is my primary objection to health screening and assesments, IMHO they actually cause more problems than they address. Yes Mr Sjoberg you don’t have cancer of the earlobe but you may have had a cardiac event by being actively encouraged to worry about it.
The problem is these secondary effects are almost impossible to quantify.
I have a simple philosophy, I live as I want to live, I do what I want to do and believe me I do a lot of things that are “wrong” but at least I reduce the possibility of a fear inspired cardiac incident. I categorically refuse to have my life ruined by fear. When I’m done, I’m done, and I’m going to enjoy it. The people who want me to fearful, for their own benefit, I will have no truck with. At all.
Although I have now been living ‘happily’ with my ‘big problem’ for many years without medical interventions I have naturally been liberally interested in what has been related to the problem I must admit that I am still in a chock after my excursion to this ‘quack’ site and here being convinced (as a scientist) that the whole fundament of what is involved in MI’s is actually crumbling in front of my eyes.
What is left is the mambo-jumbo of the medical establishment where the staines are just the top of this disgusting MI-iceberg. “Doctoring Data” will probably disclose all those features.
As Flyinthesky suggests I am just now happily testing my Talisker Christmas whisky instead of the other one of my Christmas whiskies (the Arbeg) and with a large whisky in close range when enduring my first Christmas bath for a couple of hours in the large wooden barrel tub (2 meter diameter) I just installed in my garden yesterday – very relaxing – good for my heart 🙂
Sir, I am a patient with G45.0:Vertebro-basilar artery syndrome. Cholesterol 231 mg/dL LDL 133 mg/dL HDL 91 mg/dL I was prescribed Lipitor (10Mg) per day. Should I take it?
I can only say to you what I say to everyone who asks for medical advice on the Internet. I cannot give medical advice without a face to face consultation and suchlike.
I wonder if there is any way Mimi can access a list of statin-wary doctors/consultants.
David
Thank you for your prompt reply. I am now in Thailand and have no plans to visit other countries in this short period. If skype or other methods can be applied, it would be very nice. If not, I have to bet my life with my limited knowledge.
Thank you anyway for your hard effort in discovering about the Choresterol. It would be a great contribution to the world, I think so.
I recently read this article with much interest: http://www.westonaprice.org/author/tcowan/. It explains the way in which stress is a major factor in heart attacks.
Marijke, Thank you for the link, interesting stuff.
To me, a lot of where science goes wrong is having the vanity to think they can curcumnavigate natural law and design parameters.
I’ve said it before, BSE was cited as a disease, IMHO it was no such thing. We poisoned them by feeding them food they never evolved to assimilate. It also had a cherry on top, the threat of NVCJD, be afraid, very afraid, we have it in hand. Never let a good crisis go to waste.
If it comes in a fancy packet, with an appetising picture on, it odds are it’s greatest benefit is to the people that produce it.
Nothing to do with the feed. It was the organophosphate pesticides mandated by the EU (and ham fistedly implemented by the ministry of agriculture) which were applied along the cows’ spine to combat blowfly that caused that particular fiasco.
This is an interesting comment, because the BSE crisis was strange in a lot of respects. A whole new method of disease transmission – prions – was discovered/invented. Supposedly there were two variants of a gene in humans. All the nvCJD patients had one variant, but the speculation was that those with the more common variant (and who had eaten infected meat) would come down in due course.
The idea that one protein molecule could fold the ‘wrong’ way and then catalyse other molecules of the same type to do the same always seemed odd to me – after all, protein folding isn’t really analogous to crystal formation.
Do you think prions really exist and can cause disease? Back then, I just assumed the scientists knew best, but now…………….
Does this issue feature in Malcolm’s new book?
I read somewhere that presented radioactive fallout as a cause of BSE. But the idea simply states oxidative damage creates inclusion bodies, and ionising radiation accelerates oxidative damage. Inclusion bodies cause all sorts of problems. At first it seems a bit conspiracy theory crazy, but the BSE outbreak in the UK occurred 1986 not so long after rainfall from Chernobyl had contaminate grazing pasture. In the US BSE first appeared after the Hanford fire which is a nuclear site and spread nuclear particles around washington. There is a three year gap between that event and the first instance of BSE, but it’s a likely smaller amount of contamination than chernobyl. In 1946 to 1954 the US were testing atomic weapons in the pacific. They disintegrated entire islands testing the hydrogen bomb. In 1954 the first incidence of Kuru was reported in New Guinea (in an area that got a lot of rain).
http://www.markpurdey.co.uk/the_bse_theory.htm
Fascinating insight Alan, thank you for the link. It’s different paint but still creates the same picture.
“Meanwhile, with 30% of the BSE data held behind the veil of the UK’s Official Secret’s Act, it is more than likely that we will never get to hear about the true cause of BSE- well, as far as the official clique of ‘expertise’ goes.” What possible reason would there be to hide such data behind the official secrets act.
Another reinforcement of my perspective “It all works the same”
It’s rarely what “is” it’s what they want us to accept “is”.
Will we ever get an answer to the question posed? I don’t recall that it had to do with BSE, but maybe I’m on the wrong site.
Of course, in time.
Brilliant overview Dr Kendrick!
So, back to “the process”: –
Eskimos have zero heart disease
Eskimos have nosebleeds, ergo their blood is low in clotting power
The Eskimo diet is high in omega 3s which give rise to eicosanoids which lower clotting power
Westerners have high rates of heart disease
Western diets are very low in omega 3s and very high in omega 6s
Omega 6 fatty acids give rise to eicosanoids which almost all increase clotting power
Aspirin inhibits the COX enzymes and lowers “clotting” eicosanoids, and help in heart disease
Warfarin inhibits clot formation in slow-flowing blood by preventing vitamin K1 recycling which lowers calcium-dependent clotting factors – not helpful in heart disease because blood flow is not slow-flowing in the coronary arteries.
So is “the process” that of blood clotting?
If so, then prevention is indeed multifactorial since inhibitors include omega 3s, magnesium, vitamin C, niacin, vitamin K etc. – many of which are miserably under-represented in the Western diet – and promoters include omega 6s which are monstrously over-represented in the Western diet
Forgive me if I’ve repeated in part the comments of others, it’s taken some time for the concepts to coagulate in my brain, so to speak
Other multifactorial promoters would then include the usual suspects: smoking, being sedentary, metabolic syndrome etc to the extent they promote clotting
Interestingly, I had thought I wasn’t at risk since my coronary artery calcium score is zero, rare in a 30-year insulin-dependent diabetic – my doc said “We think that’s genetic!” which is meaningless but at least he stopped with the statins. However, if it’s about clottability the Sword of Damocles is back …
Have I slept through the answer? Can’t find the solution to your conundrum, or who, if anyone, won the small prize.
Your not alone …all would dearly love a proven supported answer to these health medication problems.
Surfeit of mince pies? Vat of Glenlivet?
From another post: “it is not necessary to have any atherosclerosis in the arteries to die in one of these three” types of heart attack.
Hmm, I got the wrong end of the stick. You were specific, you’re talking about “the process” behind atherosclerotic plaque in heart disease, which I don’t have, but which is very common in diabetics such as I.
So what’s different about me?
I had Chronic fatigue syndrome, cured myself with Dr Cathcat’s vitamin C regimen, 140 grams per day for the first weeks without so much as a rumble from the guts. Fast forward 10 years, Linus Pauling patents a cure for atherosclerotic heart disease, basically vitamin C and lysine. I unknowingly self-administered Pauling’s therapy before he invented it – I have a zero calcium score which suggests it worked – no chance of a placebo effect if!
How’s it supposed to work? By strengthening the ground substance of the arterial wall, rendering it impervious to damage from turbulence and so forth so that the endothelium isn’t damaged so clotting doesn’t take place so Endothelial Progenitor Cells aren’t called upon to cover over the clot and form an atherosclerotic plaque.
So Pauling’s take on “the process” is sub clinical vitamin C deficiency renders the arterial wall vulnerable to damage and the repair process of new endothelial cells covering over the clot cause atherosclerotic plaque when it’s repeated many times
Aspirin lessens clotting by inhibiting the COX enzymes, lessening the necessity for repair and therefore slowing the development of atherosclerotic plaque. Warfarin lessens clotting and/or helps dissolve clots in slow-flowing blood so has less relevance to atherosclerotic plaque formation. Eskimos have nosebleeds because they have such huge amounts of omega 3 fatty acids in their diets that they have trouble forming clots.
If you’re interested in a correlation, heart disease mortality decreased in western countries as ascorbic acid was added to junk food, fruit juice, and supplement use increased. Hard to avoid it now.
I like that! Pauling researched the amount made by critters, reckoned humans would make about 1000mg if we still had the gulonolactone oxidase enzyme – digestive efficiency being about 50%, he figured the optimum intake to be 2000mg or better. I’ve taken at least 1000mg per day for the last few decades for fear of relapse since CFS was so egregiously ghastly. He reckoned 250mg would be a good RDA, pointed out that due to induced enzyme formation we can use more if we take more. So I don’t think his suggested intake is available from foods and if my experience is any guide, atherosclerosis might not be as prevalent if he’d carried the day
I always like Rath and Pauling’s vitamin C Lp(a) hypothesis. Vitamin C certainly can do no harm, and may do a lot of good – with regard to CVD that it
I think he estimated 18g daily for humans compared to animals, with 2g being a minimum RDA for reasonable health.
Pauling ate a high-fat diet, scoffed at fibre, and lived to be 93.
Cameron and Pauling’s case-control study describes in Cancer and Vitamin C is convincing and was never replicated, so was never refuted. Studies that claimed to refute it used fraudulent variants of the original methods that could not possibly have produced similar results.
Today, vitamin C and cancer research is going strong. It looks as if it certainly does have an effect at the doses Cameron and Pauling used.
Ascorbic acid acts as a pro oxidant in vivo so concerns about it protecting tumours are unfounded.
I thought Pauling’s work had been discredited as his studies were all badly designed. The feeling was that he went out of his area of expertise and wouldn’t countenance any evidence that vit C wasn’t the cure all he thought (even though that evidence was about). Confirmation bias at work even in someone obviously brilliant. Also there is some evidence that vit C in high doses can interfere with chemotherapy and in some studies can increase tumour size in mice.
Discredited simply means successfully attacked by the mainstream. Wegener was ‘discredited’ by Einstein for his tectonic plate hypothesis. Warren and Groves were ‘discredited’ by the mainstream medical establishment – for many years. Semmelweiss was ‘discredited’ by the medical establishment and ended up in a mental asylum. John Snow was discredited, Mendel simply ignored, etc. etc. The history of medicine is littered with those who were discredited – becoming credited – often long after they died. Uffe Ravnskov has been discredited for years for suggesting that saturated fat has nothing to do with heart disease. Now, his views are becoming virtually mainstream. I have been discredited for criticizing the cholesterol hypothesis, etc. etc. To me, discredited usually means… attacked for being right. You only get attacked if you are a threat, and you are only a threat if your ideas are a powerful alternative to existing ideas. As a wise man once said to me. ‘You know you are over the target when the flack is at its greatest.’ There is no point in expending energy trying to discredit people whose ideas are clearly nonsense. I see someone at the center of a storm as someone who should be listened to.
Pauling never got a chance to prove, or disprove, his hypothesis. I think he overstated the case [the hypothesis was never, actually his, it started with Matthias Rath]. However, the studies done on vitamin C were flawed and, one could make the case, deliberately, poorly designed. Animal models, for example, are meaningless – as animal synthesize their own vitamin C and can never be deficient in it. [one or two species excepted].
I am sorry, but I also become highly irritated when scientists claim an area of expertise for themselves. There is nothing better in science than someone moving across to study different area, as they are not burdened by pre-existing dogma. There is nothing easier, if you want to discredit someone, than claiming they are not an ‘expert’ in the area they are now studying. As if anyone has any idea what may define an expert in the first place.
The Rath Pauling hypothesis has a great deal to commend it. And yes, Rath, has been ruthlessly attacked for other reasons. However, he at least explains the possible function of Lp(a) in heart disease – and no-one else has even bothered to explain the function of this particular lipoprotein at all. Rath, by the way, was the man who advised the South African Govt that AIDS was primarily due to poor diet, and suggested that AZT was more likely to kill people than cure them, so he is always dismissed at a raving loony. However, his earlier work was very interesting and, once again, mainstream bean-counters are unlikely to progress medical research. It is the fringe lunatics who are more likely to do this. If you have the time, look up Rath and heart disease and Lp(a) on Google. You may find it eye-opening.
Sorry, I have ranted enough. But you managed in one short comment to hit my three area of maximum senstivity in one go. I shall go and lie down.
When I was in college, Lynn Margulis was “discredited” by my professors, who said she was nuts. (They also laughed at tectonic plate theory.) Her theory that mitochondria evolved from bacteria is now mainstream, but in her later years she still had trouble getting grants because her ideas weren’t mainstream. This is one problem with “peer review” in my opinion. The “peers” are usually mainstream thinkers who question anything outside current dogma.
Jeremiad, you say? Well, Jeremiah was discredited too.
This waving around of “expertise”, “qualifications” etc by people has a logical flaw in it, as I love to point out to people like David Katz.
The flaw in the logic is this. “I say this, I have all this experience so my opinion is correct.” What this lacks in logic is that usually there are many other people of similar experience who hold a different view and that ultimately no experience matters if someone else with none, turns out to be right. And, it wasn’t a rant. Whenever someone makes a statement of opinion now, it has to be considered to be a rant. You shouldn’t apologise for it!
25ml of distilled malt lquor twice daily, if symptoms persist increase dosage.
Big Pharma disinfo. Vitamin C is very unlikely to be harmful in any amount which doesn’t cause loose stools.
…and I’m going to look up Rath and heart disease and Lp(a) on Google.
The University of Google can be great – sometimes.
I based my assumptions of Pauling on his overblown claims for vit C and cancer cures. I haven’t changed my mind on that.
However the stuff on Rath and heart disease and Lp(a) is fascinating and seems to make sense. Definitely needs more research.
He recommends 6g Vit C a day. That is a lot. One orange is 45mg so 6g is 133 oranges! I would be worried about side effects at those levels. I guess I’m biased against mega doses of anything.
The Pauling Lp(a) theory is very interesting but it’s hard for me to accept that our requirements for vit C would be such that we need to supplement mega doses well above what can be obtained from diet. Especially since the healthy hunter gatherers still in existence today do not require supplementation to be healthy.
It’s more likely that vit C mega dosing is required to compensate for a poor diet. And according to the Jaminets in their excellent book The Perfect Heath diet, and Taubes, Good Calories, bad Calories, a lower carb diet requires less vit C. Vitamin C and Glucose share the same receptor for uptake into the cell. Here is a quick excerpt from wikipedia:
“GLUT1 is also a major receptor for uptake of Vitamin C as well as glucose, especially in non vitamin C producing mammals as part of an adaptation to compensate by participating in a Vitamin C recycling process.”
So Pauling is very possibly right, but mega dosing may not be required as long as one is eating a proper nutrient dense, lower carbohydrate diet.
http://highsteaks.com/forum/health-nutrition-and-science/vitamin-c-ascorbic-acid-and-keto-carnivore-diets-542.0.html
The above (below?) link is for those who want to get up to speed on Vit C and meat and carbs and such.
Eg:
“The inhibitory effect by glucose of the actions of ascorbic acid could well explain the lack of beneficial effect of ascorbic administration in many studies reported in the literature because few, if any, such studies controlled for dietary carbohydrates.
In light of the current dietary sugar excesses and concomitant obesity epidemic, clinicians should be reminded of the great importance of the long recognized but largely unappreciated inhibitory action of glucose against ascorbic acid.
In summary, ascorbic acid is essential for effective immune system function and, further, it can be a potent immune system stimulator when high glycemic dietary carbohydrates are restricted.”
Just another of the millions of reasons to dodge the carbs.
http://www.paulingtherapy.com/science.htm addresses Lp(a)
If you read Pauling himself on C, you enter a universe undreamt of by Wiki and the conventional wisdom. Studies cited to refute the notion that vitamin C reduces the duration of the common cold actually demonstrated that it’s effective. The Mayo studies cited to refute vitamin C’s effectiveness against cancer used 10g orally vs. Pauling and Cameron’s 10g IV, stopped C as soon as there was tumor growth and gave chemo – Pauling called them fraudulent. Interestingly, no one died while taking the C but they went down like flies on the chemo – Levine of NIH showed that C IV reaches concentrations which have a pro oxidant effect toxic to cancer cells, but oral vitamin C does not so the Mayo studies were either naive or something much worse. Pauling’s book How to Live Longer and Feel Better is an eye opener even after all these years
http://www.3news.co.nz/Living-Proof-Vitamin-C—Miracle-Cure/tabid/371/articleID/171328/default.aspx
This is the story of a NZ farmer who was condemned to death by doctors but saved by family insisting on Vit C therapy
http://www.odt.co.nz/print/126632
headed and ignored by medics is interesting.
Doctor does not always know best
But did any one learn? NO! It is easier to switch off life support!
The therapy consisted of massive, IV doses of Vit C.
Dr Klenner in the middle of the 20th century used high doses of Vit C with success in several conditions with success orally (treat to tolerance) and parenterally (IV).
Should have mentioned: “Survival times greater than 1 yr after the date of untreatability were observed for 22% of the ascorbate-treated patients and for 0.4% of the controls”
http://www.ncbi.nlm.nih.gov/pubmed/279931
I wonder how many cancer patients have been screwed out of a year of life by Dr Moertel, the Mayo investigator. We might add Dr Moertel to that number since he died of cancer aged 66
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.
And that is just what all the epidemiologists did! But they selected their own little factors, put the into a program and got the “positive????” answer they wanted. Result: many different and often contradictory answers with the loudest shouter coming out on top. Example: Keys and Yudkin; Keys shouted loudest but Yudkin was right. And then the obesity/diabetes/CHF/Alzheimer/et al /epidemics followed.
The Lancet
13 August 1988, Vol.332(8607):349–360, doi:10.1016/S0140-6736(88)92833-4
Originally published as Volume 2, Issue 8607
RANDOMISED TRIAL OF INTRAVENOUS STREPTOKINASE, ORAL ASPIRIN, BOTH, OR NEITHER AMONG 17 187 CASES OF SUSPECTED ACUTE MYOCARDIAL INFARCTION: ISIS-2 ISIS-2 (SECOND INTERNATIONAL STUDY OF INFARCT SURVIVAL) COLLABORATIVE GROUP
Those allocated the combination of streptokinase and aspirin had significantly fewer deaths (80% vs 132%) than those allocated neither. The differences in vascular and in all-cause mortality produced by streptokinase and by aspirin remain highly significant (2p<0001 for each) after the median of 15 months of follow-up thus far available.
Has aspirin plus streptokinase ever been tested against statins. I suspect not; ALLHAT demonstrated that a cheap, more effective drug loses out in the market to Big Pharma promoted, more expensive, less effective drugs.
a bit late to the ball as usual….
I seem to remember this question at the October TUK conference (then again I blame my 54 year old RAM – & it’s not a sheep). Probably read it in your CC book too.
Very informative reading thank you all.
… from tectonic plate movement > relatively quick Darwinian adaptation e.g.fishing – (neanderthals couldn’t fish apparently-but bears & John West can) & the ‘ginger gene’ for Sunshine? – I made that latter bit up sorry, makes sense to me anyway… >
stressors -not just in head but a response to environment change & hormones ensure reproduction > F/F response ignored + cortisol production >
autoimmune response to regulate, however diabetes & al ensue.. (hibernation/thyroid) >
calcification ‘medussa effect’ without benefit of K2/brie & calcitonin disabled – I made that bit up again, oops >
to heart disease – why just the arteries around the heart tho’? Brachial plexus too? (impingement from spareribs Hox gene malarky with HypotT dx + after years).
Also reading ‘The Calcium Lie’.
Dr K your’e too canny to give away the meaning of life!
I don’t want the prize, highlander (?) – I just want to be able to walk up the Orme.
By George I think he’s got it… 🙂
Surprised to get a smiley response – the wrong fred for a booby prize?
Can’t help thinking I’m just being humoured ‘tho… (I remain melancholic & a tad alcoholic). Perhaps the ‘ginger gene’ & ‘medussa effect’ hypotheses need (c)? (my ‘fab 5’ vitalmins were nicked). No matter, I’ll keep questioning everything… 😀
Re aspirin, my brither in law has Kawasaki, and he was told he could take aspirin or cod liver oil. He opted for the latter. Not sure why they are equivalent for that condition.
I am sorry, but the Eskimos never had “a rate of heart disease that was….zero.”
That has been proven false in quite a few studies.
I also noticed this error in your book “the great cholesterol con”
All the studies in question are referenced here:
https://nutritionfacts.org/video/omega-3s-and-the-eskimo-fish-tale/#sources
All 7 citations are under “sources cited”