We still get more questions about cholesterol than virtually any other topic. I have done many blogs on this topic and there have been many club threads, but let’s pull everything together in one article and present the information as clearly as possible. There will be some parts with which you feel familiar, but there is new information for everyone and some great, significant studies for you to have to hand to quote as evidence when faced with challenges from health professionals.
What is cholesterol?
The word Cholesterol comes from the Greek words “chole” meaning bile and “stereos” meaning solid followed by the standard chemical suffix (bit that goes at the end of a word) for an alcohol, which is “ol”. Cholesterol is a waxy substance – it would look a bit like candle wax from a creamy coloured candle. It is an essential structural part of the cells of all mammals. Its chemical (molecular) formula is C27H46O, which means that it is made up of Carbon, Hydrogen and Oxygen atoms.
What does cholesterol do?
The simple answer is – it keeps us alive. We would die instantly without cholesterol. Every single cell in the human body depends upon cholesterol for its structure and existence. In more detail, there are the most critical functions of cholesterol:
– Cholesterol builds and maintains the integrity of the cell walls. Every cell in our body is covered by a membrane made largely of cholesterol, fat and protein. Membranes are porous structures, not solid walls, letting nutrients and hormones in while keeping waste and toxins out. If cholesterol were removed from cell membranes they would literally explode from their internal water pressure. Human beings are simply not viable without cholesterol.
– Cholesterol plays a vital role in hormone production. Steroid hormones can be grouped into five categories by the receptors to which they bind: glucocorticoids; mineral corticoids; androgens; estrogens; and progestagens. (Vitamin D derivatives are seen as a sixth hormone system, but we will cover vitamin D separately below). Glucocorticoids help to regulate blood glucose levels and without cortisone, for example, the body could not cope with stress. Mineral corticoids regulate minerals, such as calcium, and they help to regulate blood pressure (the mineral corticoid, aldosterone, regulates sodium and water levels). The sex hormones and therefore the entire human reproductive system are totally dependent on cholesterol. Hence, not only would humans die without cholesterol, the human race would die out.
– Cholesterol is vital for digestion. The human body uses cholesterol to synthesise bile acids. Without cholesterol-rich, bile salts, the human body could not absorb essential fatty acids or the fat soluble vitamins (A, D, E and K) and serious, even life threatening, deficiencies could develop. (It is interesting, therefore, that nature puts cholesterol in virtually every food that contains fat – providing a digestion mechanism in tandem).
– Cholesterol is abundant in the tissue of the brain and nervous system and is critical for the brain and memory functions. Even though the brain is only 2% of the body’s weight, it contains approximately 25% of the body’s cholesterol[i]. Myelin is a substance that we can view as the insulation around nerves. Myelin covers nerve axons (nerve endings, for simplicity) to help conduct the electrical impulses that make movement, sensation, thinking, learning, and remembering possible. Myelin is over one fifth cholesterol by weight. One of the key reasons that we need to spend approximately one third of our lives sleeping is to give the body time to produce cholesterol, repair cells and perform other essential maintenance.
– Cholesterol is also critical for bones and for all the roles performed by vitamin D. Vitamin D is best known for its role in calcium and phosphorus metabolism, and thus bone health, but we are continually learning more about potential additional health benefits of vitamin D from mental health to immune health. Vitamin D can be ingested (and is, interestingly again, found in foods high in cholesterol) and it can be made from skin cholesterol. As we noted in our latitude observation in the Seven Countries Study, sunlight hitting cholesterol in skin cell membranes turns the cholesterol into vitamin D. Modern ‘health’ advice to avoid the sun, take cholesterol-lowering drugs, eat a low cholesterol diet – combined with there not even being a recommended dietary allowance for vitamin D – is undoubtedly contributing to avoidable modern illness.
How much cholesterol do we need?
It depends. It depends on many different things – a good place to start would be the “what does cholesterol do?” list above. We need enough cholesterol to do all of these vital functions all of the time. If we are getting plenty of exposure to sunshine, we need lots of cholesterol, as cholesterol is being turned into healthful vitamin D by the sun. A pregnant woman needs a lot more cholesterol than usual, as she needs to make an entire new human being – with all the cholesterol that it needs, as well as all the cholesterol that she needs during the strain and drain of pregnancy. Anything that harms cells – injury, illness, operation, cancer etc – requires more cholesterol than normal to repair those cells – cholesterol being fundamental to the health and integrity of every cell.
There are many things that demand cholesterol to be made and I trust my body to make the cholesterol that it needs. I would worry more if someone had an operation or injury and needed additional cholesterol and the body did not respond accordingly and make what was needed. If someone is on statins, their body cannot respond properly to the many and varied demands for cholesterol.
Where do we get cholesterol from?
We make it. Cholesterol is so life vital that it cannot be left to chance that we would get it from our diet – the body makes it constantly. The liver makes a significant part of the cholesterol that we need and almost every cell in the body can and does make cholesterol as well. We need approximately one gram (1,000mg) of cholesterol daily.
You will have heard me quote the famous Ancel Keys saying: “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.”
What Keys meant specifically in saying this was that – no matter how much cholesterol we eat, it cannot raise blood cholesterol levels. This is for two main reasons 1) because cholesterol ingested in food is so small compared to what the body produces and 2) because cholesterol levels are exquisitely regulated by the body according to what we need at any one time.
Interestingly – cholesterol in food can help the body, but it can’t harm it. If we eat more cholesterol, the body produces less; if we eat less cholesterol, the body produces more. So eating cholesterol can give the body less work to do, but trying to avoid dietary cholesterol (as many health professionals still inexplicably advise) simply means that the body will make up the deficit and produce what it needs.
Where is the evidence that cholesterol in food makes no difference to cholesterol in the blood?
Ancel Keys, the man who effectively started the whole diet/heart hypothesis (as it has become known), spent the 1950s (along with colleagues) trying to show that cholesterol in food impacted cholesterol in the blood. In The Journal of Nutrition, November 1955, Keys et al published a summary of all the studies that they had undertaken and stated: “It is concluded that in adult men the serum [blood] cholesterol level is essentially independent of the cholesterol intake over the whole range of natural human diets. It is probable that infants, children and women are similar.”[ii] Here are the conclusions from the individual studies undertaken – reported in this summary article:– “Two cross sectional surveys in Minnesota on young men and four on older men showed no relationship between dietary cholesterol and the total serum cholesterol concentration.
– “Two surveys on the Island of Sardinia failed to show any difference in the serum cholesterol concentrations of men of the same age, physical activity, relative body weight and general dietary pattern but differing markedly in cholesterol intake.
– “Careful study during 4 years of 33 men whose diets were consistently very low in cholesterol showed that their serum values did not differ from 35 men of the same age and economic status whose diets were very high in cholesterol.
– “Comparisons made of 23 men before and after they had voluntarily doubled their cholesterol intakes and of 41 men who halved theirs failed to show any response in the serum cholesterol level in 4 to 12 months while the rest of the diet was more or less constant.
– “A detailed study of the complete dietary intakes of 119 Minnesota businessmen failed to show any significant increase of serum cholesterol with increasing dietary cholesterol intake.
– “In 4 completely controlled experiments on men the addition to or removal from the diet of 500 to 600 mg of cholesterol daily had no effect on the serum cholesterol fall produced by a rice-fruit diet or on the rise in changing from a rice-fruit diet to an ordinary American diet.
– “In a completely controlled experiment on 5 physically healthy men the change from a rice-fruit diet containing 500 mg of cholesterol daily to the same diet devoid of cholesterol had no effect on the serum level.
– “In a similar experiment with 13 men receiving 66 gm of fat daily there was no significant effect in changing from a cholesterol intake of 374 mg/day to one of 1369 mg/day. In another 12 men the reverse change was likewise without effect on the blood serum.”
That was quite a range of studies done by Keys – who clearly initially investigated whether or not eating cholesterol raised cholesterol levels. He concluded unequivocally that it did not. He never deviated from this view.
What does the cholesterol blood test actually measure?
We need to start by saying that the blood cholesterol test is about as reliable as the England football team in penalty shootouts. The time of day, the time of year, whether or not you fasted beforehand, how much sun you’ve had recently, injuries, current stress levels, even running late for the blood test appointment – all can impact blood cholesterol levels. When people talk about their test results as if they are accurate they should be made aware of all of this.
We need to cover lipoproteins at this stage. Cholesterol is a waxy substance, remember, and fats and water don’t mix (think of dropping olive oil in a glass of water). As blood is like water, fats are not found freely floating around in the blood – they travel in things called lipoproteins. Think of lipoproteins as taxis transporting fats around the body, so that we don’t have the problem of fats not mixing in water. (This alone should tell you that fat is not clogging up your arteries – lipids are in taxis in your blood vessels – they are not directly in your blood.)
There are five lipoproteins – in order of size (largest to smallest) they are: chylomicrons; Very Low Density Lipoprotein (VLDL); Intermediate Density Lipoprotein (IDL); Low Density Lipoprotein (LDL) and High Density Lipoprotein (HDL). (Ideally chylomicrons would be called Exceptionally Low Density Lipoproteins (ELDL’s) and then the density concept would be more consistent. However…). Confusingly, VLDL is also referred to as triglyceride..
All five lipoproteins contain four main substances – cholesterol, triglyceride, phospholipids and protein. The proportions of each substance vary.
Hence LDL is not even cholesterol, let alone ‘bad’ cholesterol. It is a low density lipoprotein. LDL contains cholesterol; it is not cholesterol.
HDL is not even cholesterol, let alone ‘good’ cholesterol. It is a high density lipoprotein. HDL contains cholesterol; it is not cholesterol
The formula for blood cholesterol levels is: Total cholesterol = LDL + HDL + VLDL/5
Few people know that we can only measure total cholesterol and HDL with the standard blood test. Yes – 1 equation, 4 unknowns, 2 measurable = not very scientific.
After measuring (albeit inaccurately and inconsistently) total cholesterol and HDL, VLDL and LDL together are assumed to account for the difference. The estimation is refined with the Friedewald equation, using the estimate that VLDL is 22% cholesterol to establish that final equation:
Total cholesterol = LDL + HDL + VLDL/5
People will tell you their triglyceride levels after their blood test and are pleased when these are low. They don’t know that VLDL isn’t even measured – it is estimated.
What’s the difference between the USA and the UK measurements?
The USA uses mg/dl (milligrams per decilitre) for cholesterol measurement. Europe and Australia favour mmol/L (millimoles per litre). To convert mmol/L to mg/dl, multiply by 38.67. To convert mg/dl to mmol/L, divide by 38.67. Hence, the often quoted UK target of 5mmol/L converts to 193mg/dl in American terminology.
Why did we initially think cholesterol was a problem?
Ancel Keys reference to rabbits (and chickens) dates back to Nikolai Anitschkow’s experiment on rabbits in 1913.[iii] For some reason, Anitschkow decided to feed rabbits purified cholesterol and he managed to get their blood cholesterol levels in excess of 1,000 mg/dl. He then noticed the formation of “vascular lesions closely resembling those of human atherosclerosis” forming in the arteries of the rabbits. The obvious flaw in the experiment should have been that rabbits are strict herbivores. They do not eat animal products, which is the only source of cholesterol. Hence rabbits are in no way designed to digest cholesterol or animal fat and no one should be surprised if cholesterol or animal fat ended up stuck in any part of the poor rabbit. The only surprise is that no one thought to ask Anitschkow why he was feeding cholesterol and animal fat to herbivores. Interestingly, far less well known is that a parallel test was done on rats and dogs (omnivores) and feeding cholesterol to these species failed to produce lesions.
Why do we now think that cholesterol is a problem?
The Seven Countries study[iv] (undertaken between 1956 and 1970 and published in 1970) is the study that defined what has become known as the diet-heart hypothesis – the idea that heart disease, cholesterol in the blood stream and dietary fat are all connected. The assumption is that dietary fat – saturated fat especially – raises cholesterol in the blood and blood cholesterol levels cause heart disease. We are going to ask and answer these two key questions shortly:– Does saturated fat raise blood cholesterol levels?
– Do raised blood cholesterol levels cause heart disease?
It is interesting to note at this stage that Keys did not claim any causation when he published his study in 1970. His three claims were as follows (these are verbatim quotations from the study). In what follows CHD is Coronary Heart Disease and serum cholesterol is blood cholesterol:
– “The incidence rate of CHD tends to be directly related to the distributions of serum cholesterol values.”
– “The average serum cholesterol values of the cohorts tended to be directly related to the average proportion of calories provided by saturated fats in the diet.”
– “The CHD incidence rates of the cohorts are just as closely related to the dietary saturated fatty acids as to the serum cholesterol level.”
So Keys concluded that the incidence of heart disease, blood cholesterol levels and the proportion of calorie intake from saturated fats “tend to be related” and that was all he claimed at the time. (Just for interest, Keys also concluded that none of smoking, obesity or physical activity played any part in the explanation for Coronary Heart Disease, so his conclusions should have been challenged from the outset).
The critical errors made by the study are as follows:
1) Seven countries were handpicked when data was available for many more. Keys had presented a graph with six countries to a meeting at Mount Sinai hospital in 1953. The six countries were USA, Canada, Australia, England & Wales, Italy and Japan. The graph appeared to show an almost perfect relationship between deaths per 1,000 men and fat calories as a percentage of total calories. (You have to watch with Keys – he jumps between fat and saturated fat inconsistently). As Denise Minger shows in this great blog (http://rawfoodsos.com/2011/12/22/the-truth-about-ancel-keys-weve-all-got-it-wrong/) data was available for 22 countries and we could draw a line between six different countries to show the exact opposite relationship or no relationship at all.
The countries in The Seven Countries study were: Greece (2 cohorts i.e. regions); Italy (3 cohorts); Finland (2 cohorts); Japan (2 cohorts); The Netherlands; USA; Yugoslavia (5 cohorts). I view the selection of these seven chosen countries as conspiracy rather than error – having failed to prove that cholesterol in food raises blood cholesterol levels, Keys was still convinced that blood cholesterol levels were the enemy and was determined to prove that something ’caused’ blood cholesterol levels (other than the body making what it needs).
2) Even these handpicked seven countries could not establish a clear relationship. I analyse all 20 volumes of the study comprehensively in Chapter Eight of The Obesity Epidemic: What caused it? How can we stop it? and many of the countries and cohorts conclude the opposite to even Keys’ weak “tends to be related” conclusion.
3) The Seven Countries Study was not a robust dietary study in any way. I have read every word of every volume and many of the volumes on each country contain no dietary references whatsoever – Volume IV for the USA has no information at all on diet, food intake or fat. Volume VI for Finland has one passing comment “butterfat was a prominent item.” That tells me that bread and likely cake were prominent items – people don’t eat butter on its own. The Netherlands volume (VIII) has one reference to diet – simply saying that the diet is similar to that in the USA – not that the USA diet was documented.
The brief, sporadic references to diet indicate that Keys assumed cakes and ice cream to be saturated fat. He should have classified them as processed foods, predominantly carbohydrates. His fleeting references to meat and eggs confirm that he assumed those to be saturated fats. Meat and eggs have more unsaturated than saturated fat. Both meat and eggs are mainly water and then invariably there is more protein than fat. Of the (often) small percentage that is fat, there is more unsaturated than saturated fat.
So, notwithstanding that Keys did not prove a clear relationship, let alone causation, even in carefully selected countries, if he did observe any issue between diet and heart disease it would have been between what he wrongly classified as saturated fat and heart disease – cakes and ice cream in cases.
It was not until 1993, more than 15 years after America changed its diet advice and precisely 10 years after the UK did the same, that the 1993 European Journal of Epidemiology published a 25-year follow-up of the Seven Countries Study.[v]
This was the first time that Keys presented the strength of the asserted relationship between cholesterol and heart disease (still only in seven handpicked countries, remember). Keys claimed that the linear correlation coefficient between cholesterol (mg/dl) at entry to the study and coronary heart disease (CHD) death rates at 25 years was 0.72. This was presented as ‘we can predict heart disease over a 25 year period from knowing what cholesterol levels are at the start of the period.’
In The Obesity Epidemic I took Keys original data from this 1993 journal and validated his 0.72 number (to ensure that I was using the same statistical method as Keys – he used the standard (Pearson) correlation coefficient method of calculation). While repeating the correlation to test Keys’ methodology, I happened to notice that death rates worsened the further north countries were in Europe. So I then ran a correlation with an alternative ‘risk factor’. I found that, using a far more easily available ‘risk factor’, I would have been able to ‘predict’ CHD deaths with a correlation coefficient of 0.93 at cohort level and 0.96 at a country level.
That ‘risk factor’ is latitude.
Keys did not need to do any blood tests, employ numerous medics across numerous medical centres and follow up 12,770 men with invasive tests at five-year intervals. He just needed to ask the men for their postcode at the start of the study and he could have ‘predicted’ heart disease with far greater accuracy than that afforded by his own assumed predictor of cholesterol.
Does this explain any relationship that Keys may have observed between blood cholesterol levels and different cohorts? Absolutely. The further a region is away from the equator, the less sunlight that the population gets and the less cholesterol can be synthesised on the skin and turned into vitamin D. Finland is thus a country far away from the equator with little sunshine on the skin – this means that population cholesterol levels are high and vitamin D levels are low. Japan is a country close to the equator with lots of sunshine on the skin – this means that population cholesterol levels are low and vitamin D levels are high. The Finns suffer more heart disease than the Japanese – but because their vitamin D levels are low, not because their cholesterol levels are high. The ‘high’ cholesterol is merely a symptom – confirming that little cholesterol has been turned into vitamin D with sunlight.
Let’s return to those two key questions:
Does saturated fat raise blood cholesterol levels?
It has not been proven that saturated fat raises blood cholesterol levels. It has not even been proven that there is a consistent relationship between saturated fat and blood cholesterol levels. (Ask any health professional who disagrees with this to produce their evidence).
In the Seven Countries Study, the three different Italian cohorts had different saturated fat intakes (notwithstanding all the caveats above about the errors with this as a dietary study) and virtually identical cholesterol levels (that would support my research that cholesterol showed the distance from the equator more than anything else). There are many other examples even in this seminal study that undermine a relationship, let alone causation.
The Framingham Heart Study became the longest running diet, cholesterol, heart epidemiological study in the world. The director of that study, Dr. William Castelli said in 1992: “In Framingham, (Massachusetts), the more saturated fat one ate, the more cholesterol one ate, the more calories one ate, the lower the person’s serum [blood] cholesterol.”[vi](original emphasis).
The BBC Horizon programme, about The Atkins Diet (August 2004), interviewed Dr. Gary Foster who had recently led a study comparing the Atkins diet with the standard USA government low fat advice of the time.[vii] The programme wanted to see if the Atkins diet were more effective for weight loss and, in the words of the programme transcript, they wanted to test “The scientists’ biggest criticism of the diet was that the high fat would lead to high cholesterol which would clog the arteries and kill.”[viii] (Please note this example of typical media language on the subject of fat).
Foster and his team randomly assigned 43 women and 20 men to either the Atkins diet or a low-fat diet, for a one year duration.[ix] The Atkins diet started with a carbohydrate intake limited to 20g per day for two weeks and the group following this diet were given a copy of Dr. Atkins’ New Diet Revolution to follow thereafter.[x] The low-fat group followed The LEARN Program for Weight Management,[xi] which was consistent with the dietary recommendations provided by the registered dietitian for the study and with the American food pyramid. The women in the latter group were allowed 1,200-1,500 calories a day, the men 1,500-1,800. The intake was designed to be approximately 60% carbohydrate, 25% fat and 15% protein. The calorie intake in the Atkins group was not limited.
Noting that “adherence was poor and attrition was high in both groups” (although a higher proportion of the low carbohydrate group managed to stay on the diet), the conclusions were that “subjects on the low-carbohydrate diet had lost more weight than subjects on the conventional diet”. They had, in fact, lost twice as much. At three months the Atkins group had lost, on average (mean) 6.8% of their body weight vs. 2.7% for the low-fat group. At six months the comparator numbers were 7.0% vs. 3.2% of body weight.
Turning to cholesterol, the programme’s interview of Foster recorded him saying “My first reaction was could this be, this doesn’t make a lot of sense. Not only were there no bad effects of the diet in terms of cholesterol, but actually there were quite positive ones.” Triglyceride readings for the Atkins group showed an 18.7% fall at three months, compared with a 1.1% rise for the low-fat group. This was sustained with the 12 month readings showing a 17% fall vs. a 0.7% rise for the low-fat group. That means, even if the low-fat group results had fallen by 0.7%, the Atkins reduction would still have been 24 times greater.
There are also two theoretical problems with the notion that eating saturated fat raises blood cholesterol levels:
1) The starting point in the process by which the body makes cholesterol is a substance called Acetyl-CoA. Acetyl-CoA is a by product of the Krebs cycle – the process by which the body turns carbohydrates into the body’s energy currency – ATP (Adenosine Tri-Phosphate). Hence I can see how consumption of carbohydrates can facilitate the production of cholesterol, but not fat or protein. This is being increasingly recognised by the medical profession, which is now aware that sugar and processed carbohydrates can increase VLDL, also known as triglyceride – one part of the total blood cholesterol level.
Real food campaigners and the medical profession could reach a happy agreement if only it were accepted that, all along, we have misclassified saturated fats. We could all agree that cakes, ice cream, pastries, savoury snacks, crisps, biscuits – all the things we continue to call saturated fats today – are bad for us, almost certainly a cause of heart disease, but they are not saturated fats – they are processed carbohydrates.
2) Building on this point, we actually had evidence, from Keys himself, with all his studies in the 1950s before The Seven Countries Study, that eating animal foods has no impact on blood cholesterol levels…
Remember that Keys spent the 1950s trying to show that cholesterol in food raises cholesterol in the blood. To test this he had to increase cholesterol in the diets of his human guinea pigs. The only foods that contain cholesterol are animal foods. That means meat, fish, eggs and dairy products. Hence Keys increased these foods in the diets of his participants to raise their dietary cholesterol. This had no impact on blood cholesterol levels whatsoever. This means that eating animal foods had no impact on blood cholesterol levels whatsoever.
Hence – you can happily agree with your health professional that you will avoid processed carbohydrates (what the NHS calls saturated fats), but you have no reason whatsoever to avoid any animal food because it was proved more than 50 years ago that eating animal foods has no impact on blood cholesterol levels (even if blood cholesterol levels were a cause for concern and they shouldn’t be).
If your health professional tells you to avoid any real (animal) food, they must provide you with evidence as to why. They must also explain how you will get the essential fats, complete proteins, 13 vitamins and approximately 16 minerals that are vital for your life if you avoid any real food.
Do raised blood cholesterol levels cause heart disease?
I did some original research on this – not with 7 countries, but with 192. This is the number of countries for which the World Health Organisation has data. I included all countries, made no pre assumptions about what the data would show and plotted all countries comparing deaths per 100,000 people against average cholesterol levels for that country. I did this for men and women separately and for heart deaths and total deaths. Here are the results.
This tells me that there is not even an association between high cholesterol levels and high heart disease, let alone causation. The relationship is in fact inverse – low cholesterol levels in both men and women are associated with high death rates for heart disease and all causes of death.
I had the privilege of seeing Dr Malcolm Kendrick in a debate against Professor Bruce Griffin about saturated fat and cholesterol (http://www.chemistry2011.org/participate/activities/show?id=1312). Kendrick made a brilliant comment during the debate: “Association does not prove causation, but lack of association disproves causation.”
By showing that there is an inverse association between cholesterol levels and death rates, I have not proven causation, but I have disproved the claimed relationship between low cholesterol and low death rates.
There is another very important thing to note about cholesterol and heart disease. It is assumed by those who believe the diet/cholesterol/heart hypothesis that fat and cholesterol clog up arteries – we address this absurdity in the next question. There are a number of things that can damage the lining of an artery – also known as the endothelial wall. Your health professional would probably agree that smoking, inactivity, sugar, processed food, chemical exposure, pollution, stress and so on would be on a list of things that can cause internal damage. When we suffer internal damage such as this, the body dispatches a repair kit. The substances we need to repair internal damage are cholesterol, lipids and protein – the substances carried by the LDL taxi to the scene of the damage. LDL will therefore always be found at the scene of any ‘crime’ within the body. LDL is there to repair the damage – it didn’t cause the harm any more than the police who arrive on the scene caused the crime.
Dr Natasha Campbell McBride took this analogy a stage further: “Any damaging agent we are exposed to will finish up in our bloodstream, whether it is a toxic chemical, an infectious organism, a free radical or anything else. Once such an agent is in the blood, what is it going to attack first? The endothelium, of course. The endothelium immediately sends a message to the liver. Whenever our liver receives a signal that a wound has been inflicted upon the endothelium somewhere in our vascular system, it gets into gear and sends cholesterol to the site of the damage in a shuttle, called LDL-cholesterol. Because this cholesterol travels from the liver to the wound in the form of LDL, our “science,” in its wisdom calls LDL “bad” cholesterol. When the wound heals and the cholesterol is removed, it travels back to the liver in the form of HDL cholesterol (high-density lipoprotein cholesterol). Because this cholesterol travels away from the artery back to the liver, our misguided “science” calls it “good” cholesterol. This is like calling an ambulance travelling from the hospital to the patient a “bad ambulance,” and the one travelling from the patient back to the hospital a “good ambulance.”[xii]
If your health professional tells you that raised blood cholesterol levels cause heart disease they must provide you with evidence for this assertion. They must also be able to explain and dismiss the counter evidence for all 192 countries for which the World Health Organisation has data. They must also be able to tell you what repairs damage to the endothelial wall (the lining of the artery) if not the substances carried in a low density lipoprotein (LDL).
Can fat clog up arteries?
There was an advert on UK television in 2009 made by the Food Standards Agency. The advert showed a jug of, what can only be described as, gunge being taken out of a fridge and poured down the plug hole in a kitchen sink and getting stuck in the U-Bend of the drainage system. The advert had the deep voice-over, designed to scare the life out of you, saying: “Certain foods are high in saturated fat. This is the average amount of saturated fat a person consumes in a month. If you eat too much of this, then, over time fatty deposits could build up in your arteries and this increases your risk of heart disease. If saturated fat can clog this pipe, imagine what it’s doing to yours.”[xiii] (Here’s Tom Naughton taking the Mickey out of this “public service announcement” – just 30 seconds in: http://www.youtube.com/watch?v=exi7O1li_wA)
Where do I start on how outrageous and erroneous this advert is? (I complained to the Advertising Standards Authority, but I didn’t see the advert early enough and I was ‘out of time’ for a valid complaint to be investigated). First of all, we eat food, we don’t intravenously inject it. The visual implication that we are pouring gunge directly into our arteries is ridiculous and ignorant and it is deeply troubling that the UK Food Standards Agency appears to have no understanding of the human digestive system. Secondly, saturated fat is solid at room temperature, let alone at fridge temperature, so there is no way it could be poured down a sink, as the advert manages to achieve. You would struggle to get solidified (saturated) fat down the plug hole, even scraping and pushing with a knife – as we all did in student days, before we owned our own homes. Thirdly, there is no pump or even gravity in a U-Bend. Sinks do block – plumbers make a living from such inconveniences, but not only do we not inject food into our arteries, there is a pump mechanism around the body (the heart, blood and circulatory system) to ensure regular movement of nutrients in our blood stream to all parts of the body.
Let us see what does happen when we eat pure fat. Examples of pure fat are oils – olive oil, sunflower oil, coconut oil etc – all other foods that contain fat, also have protein. Let us assume that we have just consumed some coconut oil – this has the highest saturated fat content of any food, at 92%, so this will serve as a good approximation to saturated fat. (The remainder of coconut oil is unsaturated fat – mono and poly). The oil passes from our mouth very quickly into the pharynx (the part of the throat that goes from behind the nose to the start of the oesophagus) and then into the oesophagus (the muscular tube through which food travels from the mouth to the stomach). From there it goes into the stomach (the main area for food ‘short-term’ storage and digestion of protein and carbohydrate). Fat is not digested until it passes from the stomach into the small intestine (where almost all nutrients are absorbed) and, from there, it passes into the large intestine (the main function of which is to transport waste out of the body and to absorb water from the waste before it leaves). So, our coconut oil has quite a journey through our digestive system and we haven’t yet started to describe how it can go anywhere near our arteries.
Chylomicrons (the largest lipoproteins remember) are formed in the intestine, as a result of digestion, and chylomicrons are the transport mechanism for taking dietary fat (and cholesterol) from the digestive system into the blood stream and from there to the different parts of the body to do their vital work. As any young biology student will know, arteries pump blood around the body from the heart. There is no artery to take dietary fat away from the intestines.
The chain length of fatty acids determines how they are transported out of the digestive system. If a fatty acid has fewer than 12 carbon atoms, it will “probably travel through the portal vein that connects directly to the liver. If the fatty acid is a more typical long-chain variety, it must be reformed into a triglyceride and enter circulation via the lymphatic system.”[xiv]
Coconut oil has eight saturated fats, a monounsaturated fat and a polyunsaturated fat.[xv] The main saturated fats are lauric, myristic and palmitic fatty acids, with 12, 14 and 16 carbons in their respective chains. Three of the saturated fatty acids in coconut oil have fewer than 12 carbon atoms, so they go in the portal vein to the liver. (The liver is the body’s main metabolic organ and it prepares absorbed nutrients for use by the rest of the body. The liver plays a critical role as gatekeeper to the body and it gets the first chance to detoxify any harmful bodies that could threaten any other vital organs – not that anything in real food is harmful in normal circumstances). The five longer chain saturated fats and the unsaturated fats are packaged into chylomicrons, released into the lymphatic system and they glide from there into the blood stream.
So, our coconut oil has not been injected into our arteries. It has not gone into any arteries through any less invasive route. It has gone on a normal digestive process journey, probably taking a few hours for fat, still without going into an artery. Yet, the vast majority of UK citizens, thanks to the irresponsibility of the Food Standards Agency now have a vision in their heads that eating any dietary fat is going to clog up their arteries.
Here is another thought: if a juggernaut were travelling round a country’s transport system – which roads would clog up first? The minor roads – the country lanes would actually be impassable. The motorways would continue to run freely if a large vehicle were moving along one lane. So where is the logic that says fat travelling round the blood stream (and remember it is not freely travelling around the blood stream – it is in the lipoprotein ‘taxis’) will clog up the arteries and only the arteries? Veins never clog and yet surely they would clog first, not least the portal vein, if fat did block the blood stream in the way that the FSA would have us believe.
Has fat been proven to cause heart disease?
It is often conveniently forgotten by supporters of the fat/cholesterol/heart hypothesis that the causal route is supposed to be via cholesterol – as was originally claimed by Keys with his three “tends to” statements (i.e. eating fat/saturated fat raises cholesterol and this causes heart disease). Given that there is no evidence that eating fat raises cholesterol (and animal foods – whatever they may contain – have been completely exonerated) and given that the association between cholesterol and heart disease is the opposite to the one claimed, cholesterol is often ignored and a direct claim between fat intake and heart disease is claimed.
The study that might prove this has not even been done. Here are three statements confirming this from 1984, 1994 and 2009:
– “There has been no controlled clinical trial of the effect of decreasing dietary intake of saturated fatty acids on the incidence of coronary heart disease nor is it likely that such a trial will be undertaken.” (COMA, 1984).[xvi]
– “It has been accepted by experienced coronary disease researchers that the perfect controlled dietary trial for prevention of coronary heart disease has not yet been done and we are unlikely ever to see it done.” (Truswell, 1994).[xvii]
– “The ideal controlled dietary trial for prevention of heart disease has not yet been done and it is unlikely ever to be done.” (Food Standards Agency, 2009).[xviii]
Note again the casual usage of fat, saturated fat and diet – our dietary recommendations should be based on absolutely robust evidence. Whatever study they think should be done (fat vs saturated fat etc), it hasn’t been and it won’t be. I can tell you why. It is because it is completely impossible to change one thing in isolation in the human diet. The only foods that are 100% fat are oils (olive oil, sunflower oil, coconut oil etc). These are the only foods that can be changed in a dietary study without changing macronutrients (carbs, fats and protein are the three macronutrients). If we tell people to eat less cheese and more fish, for example, we vary all three macronutrients (carbs, fat and protein); we vary all three different types of fat (saturated, monounsaturated and polyunsaturated) and we vary all 13 vitamins and 16 minerals. We would then not be able to attribute any observed change in anything to one thing.
If we change just oils, we keep macronutrients the same but we vary all three different types of fat (saturated, monounsaturated and polyunsaturated) and we vary vitamins. (Oils generally have a small amount of a couple of vitamins and are devoid of minerals – they are pretty useless nutritionally). I have analysed the handful of studies that have tried to do this and found that there were more incidents of heart disease in the intervention group than in the control group. i.e. the group that switched to more unsaturated fat, assuming this to be heart healthy, actually suffered more incidents of heart disease than the group that didn’t switch to more unsaturated fat.
Dr. Malcolm Kendrick did two Seven Country Studies of his own analysing the World Health Organisation data from the MONICA study (This loosely stands for MONItoring of trends and determinants in CArdiovascular disease). Kendrick established the seven countries with the lowest consumption of saturated fat for his first seven countries. These were Georgia, Tajikistan, Azerbaijan, Moldova, Croatia, Macedonia and the Ukraine. Kendrick’s second seven countries were those with the highest consumption of saturated fat. These were Austria, Finland, Belgium, Iceland, Netherlands, Switzerland and France. Every single one of the seven countries with the lowest consumption of saturated fat had significantly higher heart disease than every single one of the countries with the highest consumption of saturated fat. This concludes the exact opposite of the Keys’ Seven Countries assertion.
In the chart below – a slide that Barry Groves and Malcolm Kendrick show frequently – we again have the situation that the opposite relationship between fat and heart disease has been shown. This again, therefore, disproves possible causation between fat and heart disease because not only has association not been shown – the opposite association has been shown.
Several recent publications have stated categorically that they can find no evidence for even a relationship between total fat or saturated fat and heart disease:
Writing in Braunwald’s book Heart Disease, Dariush Mozaffarian’s states in chapter 48: ”In the 1960’s and 1970’s, ecologic (cross-national) studies and short term feeding trials evaluating single risk factors (e.g. total cholesterol levels) suggested that higher fat consumption, as a percentage of total energy (%E), increased CHD risk. But subsequent evidence has demonstrated convincingly that the proportion of energy consumed from total fat has no appreciable effect on CHD.”[xix] This study is for total fat.
The “Women’s Health Initiative Randomized Controlled Dietary Modification Trial” was published in 2006.[xx] This was a large study of 48,835 post menopausal women, aged 50 to 79. Study enrolment occurred between 1993 and 1998 in 40 American clinical centres. The conclusion was “Over a mean of 8.1 years, a dietary intervention that reduced total fat intake and increased intakes of vegetables, fruits, and grains did not significantly reduce the risk of CHD, stroke, or CVD in postmenopausal women.” This study is for total fat.
In 2009, Mente et al published a systematic review of the evidence supporting a causal link between dietary factors and coronary heart disease.[xxi] The objective of the review was to assess the strength of evidence available, “in a wealth of literature”, supporting valid associations (my emphasis, i.e. not causation). The conclusion was “Insufficient evidence of association is present for… saturated and polyunsaturated fatty acids; total fat; linolenic acid; meat; eggs; and milk.” I.e. not even an association between any of these factors and CHD, let alone causation. This study is for total fat, saturated fat, polyunsaturated fat and linolenic acid (omega-3 fat).
An article was published in the March 2010 American Journal of Clinical Nutrition. The article was called “Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease”, by Patty W Siri-Tarino, Qi Sun, Frank B Hu and Ronald M Krauss.[xxii] This study is for saturated fat.
The objective of the study was to summarise the evidence related to the association of dietary saturated fat with risk of coronary heart disease (CHD), stroke, and cardiovascular disease (CVD) in prospective epidemiologic studies. This article reviewed twenty-one studies covering 347,747 people with the results: “During 5-23 y of follow-up of 347,747 subjects, 11,006 developed CHD or stroke. Intake of saturated fat was not associated with an increased risk of CHD, stroke, or CVD. Consideration of age, sex, and study quality did not change the results”. The overall conclusion was “A meta-analysis of prospective epidemiologic studies showed that there is no significant evidence for concluding that dietary saturated fat is associated with an increased risk of CHD or CVD. More data are needed to elucidate whether CVD risks are likely to be influenced by the specific nutrients used to replace saturated fat.”
That last sentence is important. It brings us, rather worryingly, full circle to the ‘side note’ in the FSA letter – “SACN, which has now replaced COMA, is currently reviewing the evidence of carbohydrate on cardio-metabolic health.”
So, the current position in the latest review of all evidence available, including almost 350,000 people over a 5-23 year period, is that saturated fat is not even associated with coronary heart disease (CHD), stroke or cardio vascular disease (CVD). This review recommends more research into the nutrients that are replacing saturated fat – i.e. carbohydrates. Are we getting close to realising that our move away from real food (containing real fat as nature intends) to processed food (containing carbohydrates, processed fat and many new and unfamiliar ingredients) could have caused heart disease? Are we close to realising that not only has our move to an unprecedented level of carbohydrate and processed food led to an obesity epidemic, but, with ultimate irony, it has worsened the condition it was intended to prevent?
If your health professional tells you that dietary fat causes heart disease they must provide you with evidence for this assertion. They must also be able to explain and dismiss the counter evidence presented above.
(Pause for an important digression at this point – when researchers present many studies refuting the arguments presented in the diet/cholesterol/heart theory, they are accused of cherry picking i.e. selecting only the studies that prove their point. There are three responses to this:
1) we have repeatedly invited supporters of the hypothesis to present a case that proves causation, not merely suggests (inconsistent) association. This has not been forthcoming – hence the repeated invitations to you to ask health professionals who demonise fat and cholesterol to provide evidence.
2) Karl Popper’s “Black Swan” theory could have been written for the diet-heart hypothesis. We are told that eating fat/saturated fat (whatever) raises blood cholesterol levels and this causes heart disease. This is a hypothesis and a hypothesis can only be proven true when it holds in all cases. We can state that swans are white, but the instant we see a black swan, we can no longer say that swans are white. We may be able to say that swans in the UK are white – and then – if we see a black swan in the UK we can no longer say this. An exception to a rule disproves the rule. Every study that has shown that fat/cholesterol/heart disease are not even consistently associated, let alone have proven causation, disproves the hypothesis. There is not one such exception, but so many as to render the original hypothesis null and void.
3) the burden of proof lies with the supporters of a theory to make their case, not with the opposers of that theory to present the case for there being no case. It is for those who believe in fairies to prove the existence of fairies, not for those who don’t believe in fairies to prove that they don’t exist.)
What is the current cholesterol target?
Americans are told to have a total cholesterol level below 200 mg/dl and LDL below 100 mg/dl. These guidelines, issued by the National Cholesterol Education Programme, (http://www.nhlbi.nih.gov/guidelines/cholesterol/atglance.pdf) actually call LDL ‘cholesterol’. (How can an organisation educate us about cholesterol if they don’t even know that LDL is not cholesterol?) Appendix 1 in this document has the drug industry conflicts of interest of the committee members setting these USA targets, just in case you thought that they had been set independently, with your health interests at heart, rather than in conflict, with drug industry profits in mind.
Australians are told total blood cholesterol levels above 5.5 mmol/l “are an indication of a greatly increased risk of developing coronary heart disease“. (http://www.aihw.gov.au/high-blood-cholesterol/)
Did you know that the National Institute for Clinical Excellence (NICE) has not issued cholesterol targets for the UK? NICE is the evidence based body for the UK and this summary states (http://www.cks.nhs.uk/lipid_modification_cvd_prevention/management/detailed_answers/primary_prevention/lipid_targets) : “A target for total cholesterol or low-density lipoprotein (LDL) cholesterol is not recommended for primary prevention of cardiovascular disease.” The basis for recommendation is summarised as follows: “The National Institute for Health and Clinical Excellence (NICE) does not recommend the use of target levels of cholesterol for people taking statins for primary prevention of cardiovascular disease. This is because it found no clinical trials in primary prevention that have evaluated the relative and absolute benefits of achieving different cholesterol targets in relation to clinical events.”
This doesn’t stop the General Practice Notebook – a UK Medical Reference placing the British Hypertension Society and Joint British Societies (never heard of either of these) guidelines above the absence of NICE guidelines. The GP Notebook (http://www.gpnotebook.co.uk/simplepage.cfm?ID=382730319) says that “The BHS and JBS2 guidelines stated that the ideal cholesterol targets are: to lower total cholesterol by 25% or LDL cholesterol by 30% or to reach < 4.0 mmol/l or < 2.0 mmol/l respectively, whichever is the greater – however a total cholesterol concentration < 5.0 mmol/l or LDL cholesterol < 3.0 mmol/l or reductions of 25% or 30%, respectively (whichever is the greater), provides a minimal acceptable “audit” standard.”
So the USA advise total cholesterol below 200 mg/dl and LDL below 100 mg/dl. 200 mg/dl equates to 5.17 mmol/l and 100 mg/dl equates to 2.58 mmol/l.
Australia favours total cholesterol below 5.5 mmol/l (213 mg/dl).
UK doctors are astonishingly aiming for total cholesterol of 4 mmol/l (155 mg/dl) or LDL of 2 mmol/l (77 mg/dl) although they consider total cholesterol of 5 mmol/l (193 mg/dl) or LDL of 3 mmol/l (116 mg/dl) as a “minimal acceptable audit“. I say “astonishingly” knowing the vital role that cholesterol plays in every cell in the human body.
You may like to ask your health professional what they are trying to lower your cholesterol to and why? Check that they agree that cholesterol is utterly life vital and then ask why it suddenly turns from life vital to mass murderer at the magic number that they have just given you.
Isn’t it LDL that matters, not cholesterol?
Remember the original three statements from Keys – the incidence of heart disease, blood cholesterol levels and the proportion of calorie intake from saturated fats “tend to be related”. We have shown that it has not been proven that saturated fat raises blood cholesterol levels and it has not been proven that raised blood cholesterol levels cause heart disease (the association is inverse) and it has not been proven that total fat and/or saturated fat causes heart disease. Indeed the study has not even been done and can’t be done.
At this point, a true scientist would question the original hypothesis. However, when dietary guidelines for the entire Western world had already been changed and cholesterol lowering industries had emerged, generating billions of dollars every year, there was rather more at stake than scientific integrity.
Instead of being rejected, therefore, the hypothesis has mutated. Cholesterol became good cholesterol (HDL) and bad cholesterol (LDL) – despite the fact that the formula for cholesterol is C27H46O – there is no good or bad version. We know that HDL and LDL are lipoproteins, not cholesterol, and that they carry cholesterol – along with other vital substances for repairing cells. (Please correct the health professionals who continue to use this erroneous and misleading terminology.)
LDL is actually the residue of the lipoprotein IDL, which is the residue of the lipoprotein VLDL, so the liver does not make LDL. LDL is formed after a number of complex chemical interactions in the body transforming VLDL to IDL to LDL. If someone tells you that the liver makes bad cholesterol you can tell them – there is no such thing as bad cholesterol and the liver doesn’t make low density lipoproteins either. If someone tells you that eating saturated fat can raise LDL, demand to know how. You can quote Dr Kendrick from The Great Cholesterol Con (p35): “How can eating saturated fat raise LDL levels? It is not merely biologically implausible, it is biologically impossible.”
When cholesterol per se did not stand up to scrutiny, LDL and HDL became the focus (despite the fact that the blood cholesterol test can only measure HDL). LDL and HDL also don’t stand up to scrutiny, so we have had claims that it is the ratio of LDL to HDL that matters. We have had small dense LDL vs large fluffy LDL. we have had all sorts of claims. As Dr Malcolm Kendrick says – “Oh for God’s sake, can you not just give up and admit you are wrong?”[xxiii]
Here’s the evidence exonerating LDL:
A small study was published in 2001. (http://chestjournal.chestpubs.org/content/120/6/1953.full.pdf) It was clever in its simplicity of approach. The idea behind the study was to test the LDL levels of young adults who arrived at an American hospital having a heart attack. Put in scientific terms, the objective of the study was as follows:
“To define the clinical profile of young adults with optimal low-density lipoprotein (LDL) cholesterol levels who present with acute myocardial infarctions (MIs); to compare and contrast differences in the clinical profiles of young adults admitted to the hospital with MIs who have LDL cholesterol levels < 100 mg/dL and those with LDL cholesterol values > 160 mg/dL.”
The conclusion of the study was:
“Young adults experiencing acute MIs typically have acceptable cholesterol levels (i.e.< 130 mg/dL) or optimal values (i.e. < 100 mg/dL)”. (Kwame O. et al, Chest 2001;120;1953-1958) i.e. young people having heart attacks have normal or below normal levels of LDL.
The initial study was quite small, but the goal was clearly important to understand in more detail. Hence the net was cast more widely to gather far more data on cholesterol levels of people admitted to hospital with heart attacks. Data was subsequently gathered from 231,986 hospital admissions, across 541 hospitals. The lipid levels were documented in 136,905 cases.[xiv]
Dr Malcolm Kendrick presented this in a slide at the 2011 Western Price Conference in London:
This graph, and the detail from the American Heart Journal, shows that the average (mean) LDL levels for Americans aged 20 and above, in 2006, entering a hospital because they were having a heart attack were 104.9mg/dl (2.6mmol/l). For those of you familiar with different averages, the mode (most common) is the highest bar in the graph – showing LDL levels of approximately 90mg/dl (2.3mmol/l). The average (mean) LDL level for all Americans was 123mg/dl (3.1mmol/l).
70% of the people admitted to hospital having a heart attack had an LDL level below the average (mean) for the whole population. Half of the people arriving at hospital with a Myocardial infarction (heart attack) had an LDL level below 100mg/dl (2.6mmol/l). Hence, people with so called ‘optimal/ideal’ LDL levels were arguably at higher risk of a heart attack as people with higher LDL.
You would think that, with such a magnitude of data and overwhelming evidence, the conclusion would be – one’s LDL appears to have nothing to do with one’s chance of having a heart attack, Except, perhaps, that low cholesterol may be riskier than high cholesterol. The conclusion from this study, incredibly, was that LDL goals should be set even lower!
As Dr Kendrick says – we can lower LDL to the extreme (zero) and we’ll all be dead.
What do statins do?
Statins block something called the mevalonate pathway in the human body. Think of mevalonate as cell food, just as glucose is brain food. Mevalonate is utterly vital for the life of every cell in the human body.
Here is a quotation from a book, How statin drugs really lower cholesterol and kill you one cell at a time, (Yoseph & Yoseph), which every doctor should be compelled to read before prescribing statins: “Mevalonate is the essence of cell renewal. In all cells, mevalonate travels down the mevalonate pathway to make cholesterol and isoprenoids (five-carbon molecules). Both stimulate the cell to grow, replicate its DNA and divide into two cells. This is the ‘cell cycle’. This is life.”[xxv]
Cell renewal is continuous throughout the body – cells lining the gut are turned over every 10 hours to 5 days; skin cells are recycled every two weeks; liver cells are replaced every 300-500 days and bone cells last a decade.
Without the cholesterol and isoprenoids made by the mevalonate pathway, none of this cell rejuvenation happens. Isoprenoids make our cells replicate and renew. Without mevalonate and without isoprenoids, cells age and die. They cannot be replaced.
CoQ10 is an isoprenoid. CoQ10 is vital for cell energy. Heme-A is an isoprenoid. Heme-A is vital for cell energy and drug metabolism. Isopentenyl adenine is an isoprenoid. Don’t worry about the names of any of these – just understand that Isopentenyl adenine is vital for DNA replication. DNA is the blueprint of every cell. Before a cell divides, it replicates its DNA and the new cell can be formed from the same blueprint. There are other vital isoprenoids – all are stopped from functioning by the destruction of the mevalonate pathway.
As we can see from the flow chart, statins are called HMG-CoA Reductase inhibitors. Statins disable reductase. Without reductase, the mevalonate pathway cannot function. Without the mevalonate pathway, cells cannot rejuvenate. It follows that the life of every cell in the human body is catastrophically impaired by statins.
How long does it take cells to be affected? That depends on the life cycle of the cell – 300-500 days for liver cells and up to 5 days for the cells lining the gut.
In chapter four of the Yosephs’ book there is one of the most incredible explanations about what statins actually do, which I have not seen elsewhere. The Yosephs describe the fact that statins are not just HMG-CoA reductase inhibitors, they are also reductase stimulators…
Life preserving responses are hard wired at the cell level – our body will do whatever it takes to keep us alive; every cell will do its bit to keep us alive. Because reductase is the ‘food’ for cell reproduction, taking something that impairs this process (statins) triggers the body to try to overcome the damage that is being done. Reductase production increases to try to reopen the mevalonate pathway. It’s a terrific attempt by the body to fight back. However, the Yosephs sadly note: “So far, they have not figured out how to save statin-fed dying cells except by adding back mevalonate.”
There are two ways in which every cell of the body can get the cholesterol it so vitally needs: 1) it can make cholesterol and 2) it can take cholesterol from the blood stream.
When someone takes statins, the cells are impaired from making cholesterol so they try to take the cholesterol from the blood stream. The LDL receptors on each cell go into overdrive and try to ‘receive’ more LDL from the blood stream to compensate for the fact that the cell can’t currently make as much itself. This lowers the cholesterol in the blood stream and doctors are happy. They know not what they have done.
That’s how statins lower cholesterol and that’s how statins kill us one cell at a time.
There have been many queries about how to resist pressure from doctors who want to put people on statins. The recommended question is “What are the consequences of blocking my mevalonate pathway?” If a doctor can reassure you that blocking a vital pathway in the human body is nothing to worry about, I’d be interested to know how.
Can cholesterol ever be too high?
Familial hypercholesterolemia is a genetic condition caused by a gene defect on chromosome 19. The defect makes the body unable to remove LDL from the bloodstream, resulting in consistently high levels of LDL in the blood. One in 500 people (a non UK specific estimate) have familial hypercholesterolemia – in some cases of FH the LDL receptors work to an extent (just not very well); in other cases the LDL receptors work barely at all. (As a comparator number against the one in 500 with FH, one in fourteen people in the UK are taking statins).[xxvi]
My logical consideration of FH suggests to me that the problem is that the LDL receptors don’t work properly and therefore the LDL (lipoproteins) cannot get into the body’s cells in the way that they are supposed to. This means that cells don’t get the vital LDL, carrying the vital protein, lipids and cholesterol needed for the cell’s health. LDL in the blood stream is high because the LDL has stayed in the bloodstream and has not been able to get into the cells – where it is supposed to go. Hence high LDL blood levels are the sign that someone has FH. The high LDL levels are, however, a symptom and not a cause or a problem per se. The problem is that the health of every cell is compromised by LDL not getting to the cell. This includes heart, brain and muscle cells – all cells. An FH sufferer can therefore have heart problems – because of too little LDL reaching the heart cells – not because of too much LDL. How differently things can be seen when one is not blinded by thinking that cholesterol or lipoproteins are bad.
Ironically, the most serious form of Familial Hypercholesterolemia would receive no benefit from statins anyway. As the extreme form of FH is characterised by LDL receptors working barely at all, even the body going into crisis mode, and trying to take LDL from the blood stream with increased LDL receptor activity, will not work if the LDL receptors are not working well enough in the first place. Hence the LDL will stay in the blood stream with an extreme sufferer of FH and yet the statin has reduced what little chance the FH sufferer’s body had of making cholesterol within the cell. The FH sufferer should ideally be given medication (if anything existed) to stimulate cholesterol production within the cell, so that the cell would at least get the vital cholesterol it needs, even when it couldn’t get it from the blood stream.
Cholesterol is utterly life vital. It is so vital that your body makes it. You would die instantly without it.
The original study that started the whole diet/cholesterol/heart hypothesis did not even claim causation. It did not establish consistent association. It nonetheless led to dietary advice being changed by the governments of the Western world. Epidemics of obesity and ill health have occurred since.
It has not been proven that saturated fat raises blood cholesterol levels. It has not been proven that high blood cholesterol levels cause heart disease – the relationship between blood cholesterol and heart deaths is actually inverse, as it is for blood cholesterol and all deaths. It has not been proven that fat consumption causes heart disease – the study has not and cannot be done.
The hypothesis can be mutated as much as its supporters like but it still does not stand up to scrutiny – the large study of hospital admissions of adults having heart attacks shows that 70% of these had LDL levels below average. Knowing the protective properties of LDL, this makes complete sense.
Statins block a critical pathway in the human body. They impair the body from doing what it was designed to do. They impair the process by which cells rejuvenate. If statins worked fully and stopped the body’s production of cholesterol completely, people taking statins would drop dead.
The doctors’ fundamental oath is “First do no harm.” Prescribing statins breaks this oath.
How can this have happened? One statin alone, Lipitor, has been worth $125 billion to Pfizer since 1997.[xxvii] This statin is the most lucrative drug in the world. It is not the only statin. I truly believe that the cholesterol lowering industry (drugs and fake foods) will go down in history as one of the greatest crimes committed against our fellow humans. If your health professional believes otherwise – they need to present you with evidence.
[ii]Ancel Keys, J. T. Anderson, Olaf Mickelsen, Sadye F. Adelson and Flaminio Fidanza, “Diet and Serum Cholesterol in Man: Lack of Effect of Dietary Cholesterol”, The Journal of Nutrition, (1955).
[iii] Anitschkow N., “Ueber die Veranderungen der Kaninchenaorta bei experimenteller Cholesterinsteatose”, Beitr Pathol Anat, 56:379-404. (1913).
[iv] Keys et al, “The Seven Countries Study: Volumes I-XX”, Circulation, (April 1970).
[v]Keys et al, “Inter-cohort differences in coronary heart disease mortality in the 25-year follow-up of the Seven Countries Study”, (Tables 1 and 4), European Journal of Epidemiology, (1993).
[vi] William Castelli, Archives of Internal Medicine, (July 1992), 152:7:1371-1372.
[vii] Gary Foster et al, “A randomised trial of a low-carbohydrate diet for obesity”, New England Journal of Medicine, (May 2003).
[ix] The Horizon programme transcript says that 120 people were involved in the study, half on Atkins, half on low fat. This was not accurate. There were 63 participants in the Foster study. The programme also mentioned and interviewed Dr. Eric Westman, who had done a study with 51 subjects placed on a American Journal of Medicine, (July 2002).
[x] Atkins RC. Dr. Atkins’ new diet revolution, revised edition, Avon Books, (1998).
[xi] Brownell KD, The LEARN program for weight management 2000, Dallas: American Health Publishing, (2000).
[xiv] Gordon Wardlaw, Anne Smith, Contemporary Nutrition, seventh edition, McGraw Hill (2009).
[xvi] Committee on Medical Aspects of Food Policy, “Diet and Cardiovascular Disease: Report of the Panel on Diet in Relation to Cardiovascular Disease”, (1984).
[xvii] A Stewart Truswell, “Review of dietary intervention studies: effect on coronary events and on total mortality”, Australian New Zealand Journal of Medicine, (1994).
[xviii] Letter from the FSA to Zoë Harcombe, (25 September 2009).
[xix] Eugine Braunwald, Braunwald’s Heart Disease: A Textbook of Cardiovascular Medicine, 9th edition (2009).
[xx] Barbara Howard et al, “Low-Fat Dietary Pattern and Risk of Cardiovascular Disease, The Women’s Health Initiative Randomized Controlled Dietary Modification Trial”, Journal of the American Medical Association”, (February 2006).
[xxi] Andrew Mente, Lawrence de Koning, Harry S. Shannon, Sonia S. Anand, “A Systematic Review of the Evidence Supporting a Causal Link Between Dietary Factors and Coronary Heart Disease” Archives of Internal Medicine, (2009).
[xxii] Patty W Siri-Tarino, Qi Sun, Frank B Hu and Ronald M Krauss, “Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease”, American Journal of Clinical Nutrition, (March 2010).
[xxiii]Dr. Malcolm Kendrick, The Great Cholesterol Con, published by John Blake, (2007).
[xxiv]American Heart Journal 2009;157:111-7.e2
[xxv] Yoseph & Yoseph, How statin drugs really lower cholesterol and kill you one cell at a time