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But it is as well to remember a warning from history: For every complicated problem there is a solution that is simple, direct, understandable and wrong. HL Mencken
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Here are the facts that I hope to convince you are true: 1: A high-fat diet, saturated or otherwise, has no impact on blood cholesterol levels. 2: Fact one is unimportant, because… 3: High cholesterol levels don’t cause heart disease anyway (the second part of the cholesterol hypothesis is wrong). 4: Statins do not protect against heart disease by lowering cholesterol levels – they work in another way. 5: The protection provided by statins is so small as to be not worth bothering about for most people (and all women). The reality is that the benefits have been hyped beyond belief. 6: Statins have many more unpleasant side effects than has been admitted. Side-effects up to, and including, death and the creation of horribly deformed babies. (You think not? Then read on.) 7: ‘Experts’ in this area should not be listened to, because they are all paid ridiculous sums of money by statin manufacturers to sing loudly from a prepared hymn sheet. Every single one of them – apart from me, obviously.
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Fact one: A post-mortem study found that a group of Japanese had the same degree of atherosclerosis in their arteries as a group of American men. Yet the rate of death from heart disease in the Japanese example was one-sixth that of America in middle-aged men and women.
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Fact two: In the majority of cases, the blood clot (thrombus) thought to have triggered the heart attack will have formed days, or even weeks, before the heart attack itself. Does this mean that acute blockage of a coronary artery does not cause a heart attack?
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Fact three: Men who dig out coal in very deep mines in Russia often die very young from heart attacks. The average age at death is 41. Yes, 41. On autopsy, most of them show signs of several previous heart attacks, yet few of them have any history of having had a heart attack, or chest pains. Does this mean that most heart attacks do not cause chest pain?
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What we do know, however, is that in people with established heart disease you can find regions of the heart where muscle is ‘hibernating’. It hasn’t converted to scar tissue, but it isn’t contracting either. It’s simply sitting and waiting. Waiting for what? For the blood supply to recover, presumably. How long can heart muscle wait like this? Quite a long time. Weeks at least, perhaps months, maybe years.
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Thus, atherosclerosis is not a case of a pipe gradually thickening with cholesterol, like a central-heating system clogging up.
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I sometimes remark to those who think my ideas on heart disease are entirely batty, ‘Why do you think that an egg yolk is full of cholesterol?’ Answer: because it takes one hell of a lot of cholesterol to build a healthy chicken. It also takes a hell of a lot of cholesterol to build, and maintain, a healthy human being. In fact, cholesterol is so vital that all cells, apart from neurones, can manufacture cholesterol, and one of the key functions of the liver is to synthesize cholesterol. We also have an entire transportation system dedicated to moving cholesterol around the body.
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Something else that I should mention at this point is that when you fire hydrogen at unsaturated fat, you create a strange type of molecule – one that is not really found in nature at all. It is a molecule with a hydrogen atom either side of the double carbon bond. This is known as a ‘trans’ bond, and is a bit difficult to explain in words. So, here is a diagram: Fig. 8 Comparison of a trans bond and a cis bond Nature tends to make all double bonds with hydrogen on the same side, which is known as a ‘cis’ bond. But mankind, with a big machine, extremely high pressure and a few heavy-metal catalysts, can manufacture ‘trans’ bonds. And fats containing trans bonds are known as ‘trans-fatty acids’. There are those – and I rank myself among them – who believe that trans-fatty acids are both, literally, ‘unnatural’ and potentially damaging to our health. How so? Because our enzyme systems are designed to deal with cis bonds, not trans bonds.
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Glycerol is actually half of a glucose or sugar molecule and when triglycerides are broken down into their component parts, glycerol travels to the liver, which combines two molecules to form glucose. The fats go to muscles to be burned up. (In short, stored fats are part sugar, providing energy.)
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Ancel Keys studied the impact of cholesterol consumption on cholesterol levels in humans, and the results of his research can be neatly encapsulated in the following quote: There’s no connection whatsoever between cholesterol in food and cholesterol in blood. And we’ve known that all along. Cholesterol in the diet doesn’t matter at all unless you happen to be a chicken or a rabbit. Ancel Keys, PhD, Professor Emeritus at the University of Minnesota, 1997
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there is absolutely no way that you can turn saturated fat (or any other sort of fat) into cholesterol.
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However, let me point out the following two facts, and leave you to draw your own conclusions. Fact one The fundamental building block for cholesterol is a substance called Acetyl CoA. You need know only two things about this substance: Fig. 10 Acetyl CoA 1: It contains phosphorous, sulphur and nitrogen (none of which is found in fats, they are found in proteins). 2: It has several ring structures (none of which are found in fats).
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Fact two Synthesis of cholesterol is horribly complicated. Again, the purpose of Fig. 11 is simply to illustrate this fact (and also to highlight the complete absence of saturated fat anywhere in this process).
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The body can only store about 2,000 calories of glucose in total, and once this limit is reached there is only thing to do with it: convert it to fat, then store it in adipose (i.e. fatty) tissue. And what sort of fat does the liver choose to make in this situation? Super-healthy unsaturated fats? Ah, that would be a no. When the liver makes fats, it makes saturated fats, and saturated fats alone.
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A chylomicron is a lipoprotein, but it’s never called that. • A VLDL is a lipoprotein but it is usually called a triglyceride. • A LDL is a lipoprotein but it is called ‘bad’ cholesterol. • A high density lipoprotein (HDL), the smallest lipoprotein, is called ‘good’ cholesterol.
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The thing that raises VLDL levels is eating carbohydrates … On the other hand, a high-fat diet lowers VLDL levels. Here is one more guilty little secret of heart-disease researchers exposed.
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there is absolutely no connection whatsoever between the VLDL level and the LDL level.
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Also, that the system controlling LDL levels is unaffected by what you eat, or the amount of VLDL manufactured by the liver.
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In Framingham, Massachusetts, the more saturated fat one ate, the more cholesterol one ate, the more calories one ate, the lower people’s serum cholesterol [by which he means LDL – my note]. Dr William Castelli, Director of the Framingham Study, 1992
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‘So maybe people should be able to have their statin, perhaps if not in their drinking water, with their drinking water.’ http://news.bbc.co.uk/2/hi/health/3931157.stm
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There is increasing evidence, however, that statins may also exert effects beyond cholesterol lowering. Indeed, many of these cholesterol-independent or ‘pleiotropic’ vascular effects of statins appear to involve restoring or improving endothelial function through increasing the bioavailability of nitric oxide, promoting reendothelialization, reducing oxidative stress, and inhibiting inflammatory responses. Thus, the endothelium-dependent effects of statins are thought to contribute to many of the beneficial effects of statin therapy in cardiovascular disease. http://atvb.ahajournals.org/cgi/content/full/23/5/729
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To summarise: after 11 years, the Surgeon General’s office in the USA had found no evidence whatsoever to support the diet-heart
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If you want more information on this particular area, go and read a paper by Gary Taubes called ‘The Soft Science of Dietary Fat’, published in Science. Several versions of his paper exist on the internet.
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Teleoanalysis is a technique – and I quote directly from Law and Wald – that …provides the answer to studies that would be obtained from studies that have not been done and often, for ethical and financial reasons, could never be done.
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In fact, the French consume more saturated fat than any other nation in Europe, and they have the lowest rate of heart disease. The only other nation that comes close to their super-low rate of heart disease is Switzerland, and the Swiss have the second highest consumption of saturated fat in Europe.
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seem to be consistently beneficial in protecting against heart disease. 1: Omega 3 fatty acids. This type of fat appears to have two effects that may be protective. Firstly, it has a reasonably strong anti-coagulant effect, a bit like aspirin. Secondly, it seems to protect against heart arrhythmias. (Omega 3 fatty acids, it should be added, have no effect on LDL levels.) You tend to find Omega 3-type fats in fish. So, although it rather sticks in my craw, I feel I must recommend that Omega 3 fats are probably good for you. 2: Alcohol Moderate alcohol consumption does appear to reduce the risk of dying of heart disease by about twenty per cent, on average. The type of alcohol is more or less irrelevant (although wine and beer seem better than spirits). However, extremely heavy or binge drinking seems to have the opposite effect. This may be due to the fact that after a very heavy drinking session, the blood-clotting system can ‘rebound’, making blood clots more likely to form.
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This is teleoanalysis again: • A (a raised cholesterol level) leads to B (heart disease). • B (heart disease) causes C (stroke). • A isn’t a risk factor for C in any study. • But A acting through B causes C. • Thus, A does cause C – huzzah! Faultless logic.
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In a large, screened population of men in the USA, those with the lowest serum cholesterol levels had an elevated risk of haemorrhagic stroke. http://www.fao.org/docrep/V4700E/V4700E0i.htm
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This study suggests that in Japan, where animal product intake is lower than in Western countries, a high consumption of animal fat and cholesterol was associated with a reduced risk of cerebral infarction death.
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high consumption of saturated fat reduces the stroke rate by 64 per cent. Reducing saturated fat in the diet reduces the risk of heart disease by 0 per cent.
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According to mainstream thinking, ischaemic strokes are caused by raised cholesterol levels, and ischaemic strokes represent 75 per cent of all strokes. However, over the last 50 years, cholesterol levels have risen by 20 per cent in Japan, and the rate of stroke has fallen off the edge of a cliff – dropping 600 per cent. And the rate of heart disease has also fallen dramatically.
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There is a direct association between falling cholesterol levels over the first 14 years [of the study] and mortality over the following 18 years (11% overall and 14% CVD death rate increase per 1mg/dl per year drop in cholesterol levels). Yes, you did just read that. Those people whose cholesterol levels fell, were at a greatly increased risk of dying – and at an even greater risk of dying of cardiovascular disease.
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But it is time to return the main point of this particular story, which is that a low cholesterol level, especially after the age of 50, significantly increases your risk of dying.
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However, what this study confirmed is that a low cholesterol level after the age of 50 (and under 50, if you are a man) is significantly associated with all-cause mortality: In men, across the entire age range… and in women from the age of 50 onward only, low cholesterol was significantly associated with all-cause mortality, showing significant associations with death through cancer, liver diseases, and mental diseases. You can’t get clearer than that. If you have a low cholesterol level, you are at a much greater risk of death. Perhaps you would prefer a British study? This from the BMJ in 1995: Low serum cholesterol concentrations ( 95% of the adult population.
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Glial cells, it was also known, released a substance that allowed synapses to form, and function. Without this substance your brain would be almost entirely useless. And what was this fantastic, miracle substance? Isolated neurons in the laboratory survived and grew, but showed only a few of the electrical signals generated by synapses. But when exposed to substances secreted by glial cells they produced strong signs of synaptic activity. The identity of the glial ingredient which triggered synapse formation has remained a mystery until now. But research published in the journal Science suggests that cholesterol is the magic ingredient. Yes, the magic ingredient was good old ‘deadly’ cholesterol. Without cholesterol, the chemical scourge of mankind, your brain cannot form synapses, and you can’t think properly, or remember anything. Or remember anything.
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Well, in addition to cholesterol’s critical function in synapse formation, it has now been found that a low cholesterol level leads to reduced serotonin levels in the brain. A low serotonin level is one of the key brain abnormalities involved in depression.
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quote Frank Pfrieger again: ‘A defective cholesterol metabolism in the brain may impair its development and function.’
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What are the other problems with statins? For the sake of brevity, I shall run through them at relatively high speed. Polyneuropathy Polyneuropathy, also known as peripheral neuropathy, is characterised by the following: • Facial weakness • Difficulty in walking • Difficulty using the arms, hands, or feet • Sensation changes (usually of the arms and hands or legs and feet), such as pain, burning, tingling, numbness or decreased sensation • Difficulty swallowing • Speech impairment • Loss of muscle function or feeling in the muscles • Pain in the joints • Hoarseness or changing of voice • Fatigue
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plucked the above headline from a major medical website called WebMD. So what’s actually wrong with this ‘new research’? Let’s put it this way: • People with low cholesterol levels are at a much greater risk of dying of cancer. • People with low cholesterol levels don’t get put on statins (yet). However, • People with high cholesterol levels are less likely to die of cancer. • People with high cholesterol levels do get put on statins.
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After all, we already have a few disturbing facts at our disposal: • Statins cause cancer in animals. • There is some evidence that cancer deaths are increased in the statin trials, especially in those who are ‘hyper-responders’ to statins. • A low cholesterol level is associated with a high risk of death from cancer. • It can take many, many years for cancer-causing agents to reveal themselves.
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A final thought: • Several studies have shown that a low cholesterol level is a major risk factor for people with heart failure. • Statins significantly reduce the risk of death once you have heart failure.
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Statins definitely reduce overall mortality in men with existing heart disease.
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In the ‘statins don’t work by lowering LDL levels’ corner are the following facts. This is only a small selection: • Statins protect against dying of heart failure, despite the fact that a high LDL level is associated with increased survival in this condition. • The beneficial effects of statins have been seen within weeks, days, even hours of taking a statin. And this finding does not remotely fit with the hypothesis that raised LDL creates gradual plaque build-up over years and years9. • Statins protect against strokes, but a raised cholesterol level is not a risk factor for stroke. • Statins provide the same degree of protection no matter if the LDL level is high, average, or low (HPS study). • Some studies, such as CARE, showed that the greatest degrees of LDL lowering were associated with a rise in deaths from heart disease.
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Summary At this point I shall attempt to draw all the strands on the use of statins together. First the positive data: • If you are a man with pre-existing heart disease, statins reduce your risk of dying of anything by a maximum of 0.66 per cent per year. (This figure is based on the most positive data from the most positive study – 4S. Study run by Merck, primary data analysis carried out by Merck employee.) • If you are a man without pre-existing heart disease, statins can reduce your risk of dying of cardiovascular disease – by a small amount. • If you are a woman at very high risk of heart disease, statins reduce the risk of dying of cardiovascular disease (that is, strokes and heart disease).
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Then the less positive data: • If you are a woman, no matter what your level of risk, statins will not increase your life expectancy by one day. Deaths from cardiovascular disease reduced; deaths from other causes increased. • If you are a man without heart disease, statins will not increase your life expectancy by one day.
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Then the negative data: • Statins, cholesterol tests and GP appointments and screening are costing the NHS alone billions of pounds a year. • Statins cause muscle pains and muscle weakness in up to 20 per cent of people who take them. • Statins cause rhabdomyolysis, which can be fatal. • One type of statin, simvastatin, over a period of six years, caused 416 deaths in the USA alone. • Statins cause polyneuropathy. • Statins cause memory loss, depression, confusion, irritability and dizziness. • Stains cause major birth defects.
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Finally, a couple of worrying, though unproved, possibilities: • Statins may increase cancer risk. • Statins may cause heart failure.
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The primary cause of heart disease, I finally discovered, is… stress.
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This hugely complex system consists of two basic parts: the ‘hormonal’ part and the ‘nervous system’ part. While I have provisionally called this the ‘stress system’, the term is actually horribly inaccurate.
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These are the sort of things you need when physical danger threatens, which is why this whole process is sometimes called the ‘fight or flight’ response. On the other hand the parasympathic nervous system has directly opposing actions. It slows your heart, stimulates insulin production and the release of bile. It also increases the flow of saliva, and
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an activated sympathetic nervous system – working in conjunction with raised ‘stress’ hormones – represents the ‘catabolic’ state, a state in which your body is ready to burn up its energy stores, which comes in handy in a fight, or during exercise. You have probably experienced this state after a physical activity such as tennis or squash, when you know you should be hungry but find that when you sit down to eat you have no appetite. The ‘stress’ hormones are still ruling your metabolism, and are telling you that you are not yet ready to eat. On the other hand, an activated parasympathetic nervous system, working in conjunction with a raised insulin level, represents the ‘anabolic’ state – a state in which you are ready to eat, digest and store energy – and then have a siesta.
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With food inside them, your guts would be automatically switched to ‘absorption’. But the sympathetic system would be fighting to direct blood away from the guts to the muscles.
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In short, I thought that eating under stress was likely to be pretty damned unhealthy. Equally, taking time over meals, and relaxing while doing so, was likely to be pretty damned healthy.
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Cushing’s disease, in turn, has a wide range of different effects – which are a direct result of the many actions that cortisol has around the body. For example, cortisol: • Triggers the liver to release its stores of glucose. • Stimulates the breakdown of triglyceride stores in adipose tissue, leading to an increase in free fatty acids (FFAs) in the blood. • Triglyceride breakdown also releases glycerol, which travels directly to the liver, where it is converted to glucose. • Activates breakdown of muscle protein into amino acids. • (The amino acids then travel to the liver, where they are converted into glucose.) • Acts as a direct antagonist to the actions of insulin at most sites in the body.
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Anyway, in addition to its effects on raising glucose and insulin levels, and its impact on muscle and fat distribution, a high cortisol level also causes the following abnormalities: • Raised VLDL level • Low HDL level • Raised LDL level • Raised blood pressure • Raised fibrinogen levels (clotting factor) • Raised PAI-1 level (clotting factor) • Raised Von Willibrand level (clotting factor) • Raised Lp(a) level (clotting factor)
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To round off this topic, I should probably mention that people with Cushing’s disease have accelerated atherosclerotic plaque growth, and a gigantically increased risk of heart disease.
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In situations like this, steroids are powerful and life-saving drugs. However, if you keep taking them for too long you will end up with the exact same set of abnormalities found in Cushing’s disease: high blood-sugar and insulin levels, low HDL, high VLDL/ LDL, a whole range of blood-clotting factor abnormalities, and increased visceral fat deposition. In short, the works. What’s more, people who take steroids long term are at a greatly increased risk of dying of heart disease.
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Depression first. It has long been known that people with depression are at a greatly increased risk of heart disease, but no one seems to be entirely certain why. However, when it has been studied it is clear that in depression you always find HPA-axis abnormalities.
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Smoking next. Although this may seem to be way out on a limb, it is not, because smoking actually works through exactly the same mechanisms as depression and Cushing’s disease, although the effects are more likely due to repeated short-lived HPA-axis dysfunction, rather than chronic problems.
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Cortisol and DHEA increased significantly within 20 min (P<0.05) and reached peak levels… within 60 and 30 min, respectively. Thus cigarette smoking produced nicotine dose-related effects on HPA hormones and subjective and cardiovascular measures. Mendelson JH, et al, Neuropsychopharmacology, September 2005; 30
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Finally, in this section, I wanted to mention spinal-cord injury. As with smoking, this may not initially seem to have anything to do with the HPA-axis dysfunction. However, the reality is that a spinal-cord injury impacts with massive force on the HPA-axis. This is because if you break vertebrae, and snap the spinal cord, you (usually) sever many of the sympathetic and parasympathetic nerves at the same time.
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• Spinal-cord injury leads to severe HPA-axis dysfunction and raised cortisol levels. • Patients with spinal-cord injury have low HDL levels (and other lipid abnormalities, e.g. raised VLDL levels). • Patients with spinal-cord injury have sharply raised blood-clotting factors, including fibrinogen, Lp(a), and plasminogen activator inhibitor-1 (PAI-1). • Spinal-cord injury leads to insulin resistance, up to and including frank diabetes. • Spinal-cord injury patients develop visceral obesity. • Spinal-cord injury patients are at a greatly increased risk of dying of heart disease.
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Finally, I would like to point out that the three factors in the INTERHEART study that protected against heart disease were: • A high intake of fruit and vegetables • Exercise • Alcohol consumption Two of these factors – exercise and alcohol consumption – have beneficial effects on the HPA-axis.
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In the ‘response to injury’ hypothesis, the first step in plaque formation is that a patch of endothelium (the thin, fragile, single-celled layer lining the arterial wall) becomes dysfunctional, damaged, or – more likely – is just plain stripped off. When this happens, a section of the underlying arterial wall is exposed. This, in turn, acts as a very powerful stimulus to the clotting system to form a blood clot (or thrombus) to plug the gap. Once the thrombus has covered over the area of damage, the clotting process is brought to a halt. This is the basic ‘response to injury’.
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Blood escapes for a bit, then a clot/thrombus forms, which turns into a scab. After a while, the skin re-grows to seal up the scratch under the scab, and the scab falls off. If the same process were to happen in your arteries, then any blood clot that formed on a damaged bit of endothelium would eventually fall off, travel a bit further down the artery, and then jam solid once the artery narrowed. This would cause catastrophic problems – including, for example, strokes. Clearly, this is not a good thing. Therefore, blood clots forming on arteries cannot be allowed to fall off when the endothelial healing process is complete – unlike scabs on your skin.
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In order to stop blood clots breaking off artery walls, and causing downstream havoc, they have to be drawn into the artery wall and then disposed of. How does this happen? Answer: your bone marrow creates millions upon millions (upon billions, probably) of ‘pre-endothelial’ cells (also known as bonemarrow-derived vascular progenitor cells [VPCs]) that travel about in your bloodstream. When they see a breach in the endothelium, it’s their job to cover it up.
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Scientists at Duke University Medical Center have discovered that a major problem with aging is an unexpected failure of the bone marrow to produce progenitor cells that are needed to repair and rejuvenate arteries exposed to such environmental risks as smoking or caloric abuse. The researchers demonstrated that an age-related loss of particular stem cells that continually repair blood vessel damage is critical to determining the onset and progression of atherosclerosis, which causes arteries to clog and become less elastic. http://dukemednews.org/news/article.php?id=6765&index=2
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Namely (if you are still clinging to the cholesterol hypothesis), how can plaques form behind an intact endothelium, when LDL cannot penetrate intact endothelium? The answer is, of course, that plaques (which contain Lp(a) – a form of LDL – and LDL itself) start life as thrombi on top of damaged endothelium. When new endothelial cells re-grow over the top of a thrombus they effectively draw it into the artery wall, along with Lp(a) and LDL.
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plaques do not gradually grow by absorbing substances from the bloodstream, molecule by molecule, in some agonisingly slow diffusion-type process. They grow through repeated acute episodes of endothelial damage, followed by thrombus formation, all taking place on top of an existing plaque. In short, plaques grow in sudden, discrete episodes.
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As this passage makes clear, repeated thrombus formation over plaques is what makes them get bigger. How else could you find fibrin, a key component of blood clots – and one that absolutely cannot pass through the endothelium – in distinct layers within plaques? How else could you find blood clots of different ages within plaques? You’re right, you couldn’t.
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supporting the conjecture that thrombus formation is central to heart disease is the knowledge that the final event in heart disease is plaque rupture, with the formation of a very big blood clot on top of the plaque – big enough to completely block a coronary artery.
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shall now tie a few things together: • Plaques start life as small areas of damage to the endothelium, which are normally healed by the body’s natural repair mechanisms – thrombus formation and endothelial re-growth. • Plaques grow through repeated episodes of endothelial damage and blood-clot formation in the same spot. • Plaques kill you when they ‘rupture’, creating a major blood clot that then blocks an important artery somewhere in the body.
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So what factors have been found to cause ‘endothelial dysfunction’? They include: • High blood-sugar levels, especially ‘spikes’ of blood sugar following a meal • High insulin levels • Acute mental stress • Smoking • Cocaine use • Cortisol • High levels of adrenaline
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Next, I think it is important to look at the factors that make the blood more ready to clot, and more ready to form big and difficult-to-shift blood clots. These are, somewhat unsurprisingly, blood-clotting factors, such as: • Fibrinogen (Fibrinogen is a small strand of protein. When you stick hundreds of bits of fibrinogen together, it turns into a long, thin, very strong strand of fibrin. This binds blood clots together.) • Lp(a) • Plasminogen-activator-inhibitor-1 (PAI-1) • Von-Willibrand factor • VLDL (VLDL stimulates blood clots to form.)
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The importance of blood clots in heart disease is also supported by the fact that virtually every drug that reduces the risk of dying of heart disease is, essentially, an anti-coagulant. For example: • Aspirin – stops platelets becoming ‘activated’ and sticking together (activated platelets are critical to thrombus formation). • Warfarin – reduces various clotting factors in the blood. • Alcohol – stops platelets sticking together. • Tissue plasminogen activator – breaks clots apart. • Statins – have strong, dose-dependent, anti-coagulant activity. • Streptokinase – a clot-buster. • Clopidogrel – stops platelets sticking together (see aspirin). • ACE-inhibitors (used to lower blood pressure) – ACE-inhibitors stimulate nitric oxide synthesis in endothelial cells. Nitric oxide is the most powerful anti-coagulant in the body.
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In effect, the HPA-axis ‘burns out’ and just pumps out the same amount of cortisol night and day, with no alteration in response. It becomes inflexible and non-variable. Which means that if you decide to measure the cortisol level at 8 a.m., or 9 a.m. (which are the standard times for such tests to be done), it can often be low in people with HPA-axis dysfunction – although not always, it depends on the degree of HPA-axis dysfunction.
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Per Bjorntorp. Some years ago, he recognised that you need to do more than a solitary cortisol measurement to diagnose HPA-axis dysfunction. He knew that the human body is a flexible and dynamic organism. Health, and healthy systems, are constantly adapting and reacting. When you lose flexibility and responsiveness, you die.
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Perhaps the most spectacular example of this is heart-rate variability, i.e. the amount by which the heart rate alters from beat to beat. This is, possibly, the single most sensitive indicator of a healthy heart, and a loss of beat-to-beat variability is one of the most powerful single indicators of the risk of dying of heart disease.
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Bjorntorp wasn’t just looking for high, or low, levels of cortisol at 8 a.m. He was more interested in seeking a loss of HPA-axis flexibility, and ‘burn-out’ of the axis.
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Such measurements clearly show that normally regulated cortisol secretion is associated with excellent health in anthropometric, metabolic and hemodynamic variables. Upon perceived stress cortisol secretion is increased and followed by the Metabolic Syndrome X [insulin resistance, abdominal obesity, elevated lipids and blood pressure]. In a minor part of the population a defect, ‘burned-out’ cortisol secretion occurs, with decreased sex steroid and growth hormones secretions and strong, consistent, associations with the Metabolic Syndrome X. Psychosocial and socioeconomic handicaps with tendencies to abuse and depressive-anxious mood changes are consistently associated… [with HPA-axis dysfunction]. We suggest that the Metabolic Syndrome X is due to a discretely elevated cortisol secretion, discoverable during reactions to perceived stress in everyday life. Bjorntorp, Ann MY Acad Sci, November 1999
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In my view he should have got a Nobel prize, for he proved beyond doubt that exposure to various stressors causes HPA-axis dysfunction, abnormal cortisol levels and then heart disease – precisely in that order.
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The most deadly long-term stressor that can affect entire populations is something that I define as ‘social dislocation’ – something that as a concept, needs some further explanation. The most straightforward example of social dislocation would be something like ethnic cleansing, whereby a population is forced from their homes at the point of a gun then herded elsewhere. During this process, social and family networks are severely disrupted; family members lose touch – or are killed. Many people find themselves in a different country where they may not speak the language.
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SOCIAL DISLOCATION AND HEART DISEASE – AN INTERNATIONAL COMPARISON Finland – highest rate of heart disease in the 1960s/early 1970s In the 1960s and early 1970s, Finland had the highest rate of heart disease in the world.
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1948, a large part of Finland was handed over to Russia, and the Finns living in this area were forced to relocate back into Finland. Some 400,000 of them. This has been described as the greatest proportional ‘forced’ relocation of any people in the history of Europe.
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Scotland – highest rate of heart disease in the 1970s/early 1980s There was a time in the 1970s when Scotland had the highest rate of heart disease in the world. The rate was far worse in the west of Scotland than the east. Everyone points to the predilection of Glaswegians for fried Mars bars and the like, as the reason for their very high rate of heart disease. What no one points to is the fact that Glasgow is the only major city in Britain to have dramatically shrunk.
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Which goes to show that migration is not necessarily deadly. What kills you is the break-up of the surrounding community.
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CHD did not exist until 1948, it is likely that the rate of heart disease rose rapidly during the 1920s and 1930s, peaked some time in the late 1940s and has fallen ever since. I do not think it is any coincidence that this followed a period during which the USA took in more immigrants than any other country in the history of the world. From 1905 to 1914, one million immigrants per year arrived in the USA. Then, in the 1920s, 1930s and 1940s, the rate of heart disease shot up. Since then it has gradually fallen. This is a pattern that is exactly repeated in other countries that took in huge waves of immigrants.
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the International Journal of Epidemiology: ‘Considerable increases in total serum cholesterol levels do not offer an explanation of the recent decline in mortality from coronary heart disease in Japan.’ So much, then, for the fast-food conjecture.
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SOCIAL DISLOCATION AND THE PHYSICAL MARKERS OF HPA-AXIS DYSFUNCTION While social dislocation cannot be measured, it can be demonstrated that in populations that I would consider to be ‘dislocated’ there are a whole series of measurable metabolic abnormalities to be found. All of which point, in big bright neon lights, straight towards HPA-axis dysfunction.
Location 3971:
Male Russian life expectancy is now 20 years less than that in most of western Europe. And this pattern can be seen across eastern Europe: Latvia, Lithuania, Poland, the Ukraine. You name an eastern European country – after the Wall came down they were all plunged into a health crisis. In truth, Poland seems to be emerging from the other side, and heart-disease rates have been falling for more than ten years. Hopefully, the other countries will soon be following suit.
Location 3993:
A low peak cortisol response was significantly related to high baseline cortisol, current smoking, and vital exhaustion. The findings suggest a physiological mechanism of chronic psychosocial stress, which may contribute to increased risk for cardiovascular death.
Location 4070:
Apart from having better social networks, women also seem to deal with stress in a different way.
Location 4088:
However, it is not just better social networks and superior coping mechanisms that make the difference. It is clear that men, when exposed to the same type of psychological stressor, have a much more violent HPA-axis reaction.
Location 4112:
During the first hour after using cocaine, the user’s risk of heart attack increases nearly 24 times, according to the first large study of the long-suspected relationship between cocaine and heart disease. The research is reported in today’s Circulation: Journal of the American Heart Association.
Location 4134:
So the number four doesn’t wipe out us westerners, but Mondays do. In Japan, though – if you are a woman – Saturdays are deadly. I wonder why? Isn’t marriage a wonderful thing…
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