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CONDITIONS AND DISEASES PREVENTED AND HELPED BY A LOW-CARB DIET

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RESISTANCE TO AUTHORITY
RICKETS

SCHIZOPHRENIA
SICKLE CELL ANEMIA
SLOW GROWTH
STOMACH ULCERS
STROKES
SUICIDE

ULCERATIVE COLITIS ULCERS (STOMACH)




Introduction

There are many conditions in Western industrialised societies today that were unheard of, or at least very rare, just a century ago. The same conditions are still unheard of in primitive peoples who do not have the 'benefits' of our knowledge. There is a very good reason for this: They eat what Nature intended; we don't.

The diseases caused by our incorrect and unnatural diets are those featured on these pages.




Cardiovascular diseases

Dietary causes:

Carbohydrate-rich 'healthy' diet; polyunsaturated vegetable oils and margarines, processed convenience foods.

 



 

'All published efforts to help by drug or dietary reduction

 of blood cholesterol have uniformly failed.'

PROFESSOR SIR JOHN McMICHAEL



Atherosclerosis

Coronary heart disease

Congestive heart failure

Deep vein thrombosis

Peripheral artery disease and intermittent claudication

Strokes

Conclusion

 

Introduction: Atherosclerosis

Atherosclerosis is a condition whereby arteries become blocked or partially blocked. This blockage effectively reduces the interior diameter of the artery thus restricting blood flow. The body then either increases the blood pressure or oxygen transport around the body is lessened. If the coronary arteries are involved, the heart muscle is starved of the oxygen it needs. And that results the chest pain called angina, and eventually, as arteries become completely blocked either by the atherosclerosis or a blood clot, in a heart attack.

      Conventional orthodox treatment for atherosclerosis includes bypass surgery in which the blocked coronary artery is removed and a piece of vein, usually from the leg, is grafted in to replace it. Another less drastic method is a 'stent', metal lattice which is inserted into the partially blocked artery and expanded to hold the artery open. In neither case does the treatment address the cause of the disease, or do anything to help other arteries which may also be affected. Not only that, both treatments are expensive, invasive and potentially life-threatening. Around one in 20 patients dies on the operating table.

      Often these techniques do not last long and have to be repeated. The few times they have been subjected to double blind studies to assess their usefulness they failed to demonstrate any improvement in the long term survival.[1]


Coronary heart disease   

Coronary heart disease took off in the 1920s, but atherosclerosis, the 'furring up' of the coronary arteries, which the medical establishment teaches is the cause, doesn't happen overnight: it takes many years. So what factor introduced in the late nineteenth century could explain the twentieth century occurrence of coronary heart disease?

      According to Dr Kilmer McCully, Chief of Pathology and Laboratory Medicine, Boston,

 

'The major changes were in methods of food processing, especially the extraction of sugar, steel roller press milling of grains into refined flours, extraction of oils, canning, and the use of chemical additives such as bleach, bromination, etc. The effect of consuming these refined foods is to decrease the dietary consumption of the chemically sensitive B vitamins, folic acid and B6, which are largely destroyed by these methods of food processing.'

      'At a nation-wide conference at the National Institutes of Health in 1979, the traditional risk factors, such as dietary cholesterol and fats, smoking, exercise, hypertension, etc, were not found to have changed sufficiently to explain the decline in coronary heart disease mortality in the US since the 1960s. The introduction of food processing with the Industrial Revolution in the 19th century and the use of chemical additives and other processes in the 20th century is the only satisfactory explanation for the dramatic changes in incidence of vascular disease in the 20th century.' [2]

 

Studies challenge the cholesterol theory

None of the many human intervention studies into the causes of heart disease conducted over the last half century looked solely at one aspect of diet – fat. They were all 'multiple interventions' which changed several dietary constituents, and included other factors such as exercise, cigarette smoking, and so on. For this reason, ascribing any benefit to just one aspect trials is impossible.

      In 1988, however, an opportunity presented itself when a trial was conducted on a group of people suffering multiple food allergies who had high cholesterol levels.[3] Because of their range of allergies, their diet was restricted to cut out sugar (sucrose), milk and all cereal grains. In this diet most of their calories came not just from fat, but from beef fat. It is beef fat that, we are told, is 'unhealthy' because it raises cholesterol levels, but that was not confirmed in this study: instead of rising, the patients' total blood cholesterol levels fell by 27.5% from an average of 6.84 mmol/L (263 mg/dL) to an average of 4.9 mmol/L (189 mg/dL); their 'good' HDL cholesterol levels increased from 21% of the total to 32%; and their triglyceride levels decreased from an average of 1.13 grams per litre to a more healthy average of 0.74 grams per litre. The authors say:

 

'These findings raise an interesting question: are elevated serum cholesterol levels caused in part not by eating animal fat (an extremely "old food"), but by some factor in grains, sucrose, or milk ("new foods") that interferes with cholesterol metabolism?'

 

      Of course they are! That half-century of research wasn't wasted. It all shows that saturated fats are not the 'bad guys'; 'healthy' foods such as bread and cereals are.

      After such a study, it should be no surprise that a survey conducted in South Carolina of adults with 'bad' dietary habits – the eating of red meat, animal fats, fried foods, butter, eggs, whole milk, bacon, sausage, cheese and the use of solid fats to cook vegetables – found their blood cholesterol levels were only marginally affected by their diet.[4]

      We saw in Chapter 3 that CHD is rare in Polynesians who eat a high saturated fat diet.  In Britain a Medical Research Council survey also showed that men eating butter ran half the risk of developing heart disease compared to those using margarine.[5]

      Dr William Castelli, Director of the Framingham Study, wrote in 1992: '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. . .'

     Because cholesterol is a major component in all animals' bodies, eggs have a very high cholesterol content. That is why we are still told to eat no more than about 3 a week. Dr Uffe Ravnskov did his own test of the theory by eating a total of 59 eggs over 9 days. Did his cholesterol level shoot up? No, it fell by more than 11% from 7.23 mmol/L to 6.39 mmol/L.[6]

      Dr George V. Mann was involved with the Framingham Study and also conducted extensive studies of the Maasai, whose diet is very high in saturated fat but who do not suffer from CHD at all. His work led him to the conclusion that:

 

'The diet-heart hypothesis has been repeatedly shown to be wrong, and yet, for complicated reasons or pride, profit and prejudice, the hypothesis continues to be exploited by scientists, fund-raising enterprises, food companies and even governmental agencies. The public is being deceived by the greatest health scam of the century.'[7]

 

      And in 2005 a study conducted at Johns Hopkins Bloomberg School of Public Health of diagnosed and undiagnosed diabetics showed clearly that high blood glucose levels were strongly associated with heart disease. The authors concluded that 'Chronically elevated glucose levels may contribute to the development of atherosclerosis in people with diabetes, independent of other risk factors.'[8]

      All this points to 'healthy' carbs being the major culprits – not animal fats.

 

Plants may be a danger

Because cholesterol is found only in animal products, more and more people have been turning away from meat and towards eating foods from plants. But chole-sterol is only one of a whole family of sterols. Cholesterol is found only in meat; the other sterols are found in plants. Dr J Plat and colleagues at Maastricht University's Department of Human Biology in the Netherlands, say that these plant sterols may actually be more important in heart disease than cholesterol.

      Because plant sterols are structurally related to cholesterol, Plat and colleagues examined whether oxidized plant sterols (oxyphytosterols) could be identified in human blood and soya-based fat emulsions. They found that they could. Approximately 1.4% of the plant sterol, Sitosterol, in blood was oxidised. This may not seem very much, but actually it is 140 times as much as the 0.01% oxidatively modified cholesterol normally seen in human blood. The same was also found in two soya emulsions.[9]

      If any sterols are to blame, plant sterols are much more likely candidates because the popular idea that animal products, specifically protein, cholesterol, and saturated fatty acids, somehow factor in causing atherosclerosis, stroke, and/or heart disease is not supported by any available data, including the field of lipid biochemistry.[10] [11] [12] [13]

      On this point, it is interesting that Dr Ancel Keys, whose 1953 hypothesis began the fatty-diet-causes-heart-disease dogma did not recommend cutting down on animal fats. He recommended cutting vegetable oils.

 

Oxidised LDL

Where the problem with LDL lies is when fatty acids that are transported with LDL are attacked by oxygen and oxidised.[14] Oxidised LDL is important in atherosclerosis as it causes cells called monocytes to be drawn into the artery walls. In 2004 a study was conducted with patients eating two different diets.[15] Both lowered total fat and saturated fat intakes and raised polyunsaturated fat intakes. Conventional wisdom says that these revised diets should be 'healthier'. In fact, what happened was that the levels of oxidised LDL in the bloodstream rose in both – by 27% and 19%. Another contributor to heart disease, lipoprotein (a), also rose by 7% and 9%.

      Fatty acids come in a variety of lengths. As the chain length of a fatty acid increases, it acts more and more like an oil which will not mix with water or blood. Short and medium chain fatty acids will mix in blood and exit the intestine bound to the protein, albumin, whereas long chain fatty acids with more than 12 carbon atoms do not mix and must be transported in lipoprotein carriers. LDL is used to transport these long-chain fatty acids. Saturated fatty acids do not oxidise, but unsaturated ones do. Thus, LDL is only likely to be 'bad' if you eat a large proportion of 'healthy' polyunsaturated oils.

      This is why, in a 10-year study of fats and the numbers of heart events, researchers found that only polyunsaturated fats significantly increased heart disease.[16]

      And there is another anomoly: You may not be aware of it, but cholesterol levels are always measured in blood taken from the veins, yet nowhere in the medical literature is there a single case of cholesterol having caused obstruction of a vein: atherosclerosis only affects arteries. As blood moves far slower in veins than in arteries, wouldn't that make it be more inclined to leave cholesterol deposits – if the assumption that cholesterol was the cause were true?

 

Carbohydrates and cardiovascular diseases

An indicator that carbohydrates could be a causal factor in cardiovascular diseases came from a study of coeliac patients at the University of Nottingham. Coeliacs don't eat cereal grains. Although rates of heart attack and stroke were not substantially different, adults with coeliac disease did have a lower prevalence of hypertension and high blood cholesterol compared with the general population.[17]

 

'Healthy eating' increases heart disease . . .

For over half a century we have been exhorted to eat less fat and to eat more carbohydrate-rich foods instead. A 'healthy diet' today is one low in fats and based on bread, pasta, rice and 'five portions of fruit and vegetables a day'. Here are some quotes from trials of our 'healthy diet':

 

 . . . In diabetics

'In general, study has demonstrated that multiple risk factors for coronary heart disease are worsened for diabetics who consume the low-fat, high-carbohydrate diet so often recommended to reduce these risks.'[18]

 

This is because high levels of glucose in the blood over a long period of time 'glycosylate' haemoglobin. This glycosylation was found to increase the risk of a heart attack in both diabetics and non-diabetics in a 2005 study by scientists at Johns Hopkins University.[19] In this study, non-diabetics' risk was more than doubled.

 

. . . In older women

 'Low-fat, high-carbohydrate diets [15% protein, 60% carbohydrate, 25% fat] increase the risk of heart disease in post-menopausal women.'[20]

 

. . . In the elderly

All our cells rely on a constant and sufficient supply of cholesterol. There are two aspects of the advice aimed at lowering cholesterol which may have a profound effect on both our longevity and the efficiency with which our brains work. Firstly, we have known for a very long time that blood cholesterol levels tend to increase as we get older. Indeed several studies from around the world show that the elderly with high cholesterol live longer than those with low-cholesterol. Secondly, an East German doctor, Max Bürger, demonstrated almost half a century ago that, as we age, cholesterol is lost from body tissues and neurons (brain cells).[21] (These findings were published in Leipzig during the Communist era, so it is unlikely that any Western clinician has ever seen, let alone read them.) Putting these two facts together, is it not probable that the increases of blood cholesterol seen as we age are our bodies' way of replacing cholesterol lost from tissues and nerve cells.

      This has huge implications in the context of 'healthy eating'. Advice today is aimed at lowering cholesterol levels in people of all ages, but these facts together suggest that drug or dietary regimes aimed at lowering cholesterol in people aged over seventy might well shorten their lives.

 

. . . In everyone

In 2000 – Scientists from Stanford University School of Medicine, California, compared the effects of a low-fat, high-carbohydrate diet with a high-fat, low-carbohydrate diet, on blood fats and cholesterol. They found that subjects on the high-carb diet had significantly higher blood triglycerides and significantly lower HDL. These effects are not desirable. The authors conclude:

 

'Given the atherogenic potential of these changes in lipoprotein metabolism, it seems appropriate to question the wisdom of recommending that all Americans should replace dietary saturated fat with [carbohydrate].'[22]

 

Similarly, while presenting two-year results of the Glucose Abnormalities in Patients with Myocardial Infarction (GAMI) study[23] at the European Society of Cardiology Congress 2004, Dr Lars of the Rydén Karolinska University Hospital, Solna, Sweden, said that abnormal glucose metabolism is common in acute heart attack patients. 'We know', he said, 'that blood glucose increased to a level below the diagnostic target for diabetes increases the risk for mortality and cardiovascular disease.' He told delegates that patients' prognosis if they had normal glucose regulation was 'quite nice'; none in the normal group died. But amongst patients without any previously known diabetes newly detected a few days after a heart attack who had abnormal glucose tolerance 'there is a substantial increase in end points.'

      Forget cholesterol, in this study abnormal glucose metabolism was the strongest predictor of a future heart attack. And that points to 'healthy eating' as a causal factor.

 

Is atherosclerosis the most important cause of CHD?

Atherosclerosis may not be the most common cause of a heart attack. Autopsies of adults who had suffered sudden cardiac deaths found that arrhythmia was the most common cause of heart attacks.[24] As far as we know, arrhythmia is not caused by any dietary constituent, but by physical or mental stress.

 

'Healthy' diets increase heart disease risk

Here is a curious fact which you can check with any veterinary surgeon: There are three basic types of animal when it comes to diet:

·        Herbivores which eat only plants.

·        Omnivores which eat both meat and plants

·        Carnivores, which only meat

      While all three types can suffer a heart attack, atherosclerosis thought to predispose to heart attacks is only found in herbivores and omnivores. Carnivores – all species – are completely free of the condition. The only animals where atherosclerosis builds up are those which eat plants, whether they eat plants exclusively or together with meat. And this includes Man.   This suggests that, contrary to popular wisdom, it is not something in meat that is the contributory factor, but something in plants.

      In 2005, the medical Journal, Archives of Internal Medicine, published a study with showed clearly that when blood glucose levels were raised for significant lengths of time, the risk of a heart attack was greatly increased.[25]

      Long-term blood glucose levels are measured by the amount they glycosylate haemoglobin (see Chapter 21). The measurement is known as 'HbA1c'. What this study showed was that, in diabetic adults, each 1% increase in HbA1c increased the risk of a heart attack by 14%. And in non-diabetics, over a level of 4.6%, each 1% increase in HbA1c increased the risk of a heart attack by a huge 136%. Long-term high glucose levels are, of course, only caused by eating a 'healthy' carbohydrate-rich diet.

 

High-fat, low-carb diets reduce heart disease risk

By the end of the twentieth century, low-carb diets were becoming increasingly popular and the establishment kept insisting that they would increase cholesterol. In 2002, scientists at the Human Performance Laboratory, University of Connecticut, decided to test this claim with a very low-carbohydrate, high-fat diet on normal-weight men with normal cholesterol levels. The diet contained only 8% of calories from carbs and 61% of their calories were from fats.[26]

      With a diet in which nearly two-thirds of calories came from fat, you might expect – because that is what you have been led to believe – that cholesterol would rise. In fact, it did just the opposite: their cholesterol actually fell by 29% and their HDL, went up over 11%. But this wasn't all: triglycerides, which are more harmful in terms of heart disease, fell by a whopping 33%. Insulin fell by even more: 34%. The authors say that:

 

 'The results suggest that a short-term ketogenic diet does not have a deleterious effect on CVD risk profile and may improve the lipid disorders characteristic of atherogenic dyslipidemia.'

 

      That last study covered only 6 weeks. In the same year, doctors at the Division of General Internal Medicine, Duke University, Durham, North Carolina, conducted a similar study over 6 months.[27] Patients could eat as much meat, cheese, eggs, fish, butter and fat as they wanted, but their carb intake was restricted to no more than 25 grams a day. Over the period of the diet, the participants lost an average of 21.3 pounds, and showed a 6.1% drop in cholesterol, and almost a 40% drop in the level of triglycerides in their blood. In addition, their HDL levels increased by about 7%. This is all good stuff. In an interview for Reuters Health, the study's main author, Dr Eric Westman said 'We were somewhat surprised to find that patients' blood lipid profiles improved, even though there was much more fat in the diet,' he said. 'We had thought the fat in the diet would increase the cholesterol.'

 

Summary

Ever since 'healthy eating' was introduced a couple of decades ago, the establishment has tried to show that a diet high in animal-fat is harmful. Yet not a single trial has ever managed to do this. Not that this should come as a surprise as it was shown as long ago as 1968 that 'hyperlipidaemia can be controlled by a diet which is low in unsaturated fat . . .'[28] (emphasis added). You see, the only fats that have ever been implicated in heart disease are the 'healthy' polyunsaturated vegetable oils. Yet, perversely, it is those fats that we are told to eat more of!

 

Early testing doesn't help

Doctors reckon that, to reduce heart disease, it is necessary to screen for the disease regularly so that it can be caught in its earliest stages and treated before it gets too bad. Unfortunately, the figures don't support the theory. Doctors in Canada and the USA ordered more cardiac tests and procedures between 1993 and 2001 than ever before – yet there was no reduction in heart attacks over the period. This is extremely worrying, they say, as all this testing is pushing the Canadian health insurance system to breaking point and heart care costs have doubled in the last decade. [29]

      But, early testing isn't going to work if the follow-up therapy in based on a flawed premise. The evidence shows is that it is carbs and polyunsaturated fatty acids that increase the heart attack risk. Yet those are exactly the foods that people thought to be at risk of a heart attack are told to eat. It's lunacy – and expensive lunacy, at that.

 

Congestive heart failure

It seems that high blood glucose levels may also be an important cause of another heart disease: Congestive heart failure (CHF). United States researchers had found evidence to suggest that raised fasting blood glucose levels were a risk factor for CHF among elderly individuals, particularly those who had diabetes. CHF and diabetes are age-related disorders that frequently coexist. Despite this, there was uncertainty as to whether raised glucose levels act as a risk factor for CHF, as studies produced conflicting results.

      To investigate this further, Dr Joshua Barzilay and colleagues at Emory University School of Medicine, Atlanta, Georgia, studied patients, aged 65 years and above, for up to 8 years.[30] They discovered that each one 'standard deviation' increase in fasting blood glucose increased the risk of CHF by 41% in participants.

      Dr Barzilay and team suggest that raised glucose levels may affect CHF risk in several ways: it might reflect poor compliance to medications or poor medical care; the glucose might compromise artery linings and affect blood flow to the heart, or cause fibrosis and stiffness of the heart muscle itself.

 

Deep vein thrombosis (DVT)

DVT is a potentially fatal condition. It is euphemistically called 'economy class syndrome' because it was first reported in people who sat for long periods in the economy section of aircraft on long-haul flights. More recently it has also been reported in people who sit for long periods at their office desks. DVT is a condition where clots (thromboses) form in the deep veins of the legs, which may then travel to other parts of the body. If the clot goes to and blocks a major blood vessel – in the lungs or heart, for example – it can have fatal consequences.

      When my wife and I flew out to Singapore in 1962, we had never heard of DVT. There we were, sat on an aircraft for twenty-four hours with not the slightest knowledge of such things. But, in those days, neither had anyone else. Planes were slower; they were also smaller, with less room to move around; and we sat for much longer. So why didn't we get DVT in those days? Why is it that DVT only reared its ugly head in the last decade or so?

      We talked about HbA1c above. This glycosylation tends to make the blood stickier. It makes it clot more readily. The reason we didn't get DVT was probably because of the way we ate in the 1960s. The answer to DVT is not necessarily to move about more, do special exercises and wear anti-DVT stockings. These all may reduce the risk, but they don't address the cause: a 'healthy' diet. All one needs to do to prevent DVT is eat less carbohydrate-rich foods.

 

Peripheral artery disease and intermittent claudication

Peripheral arterial disease (PAD) whether symptomatic or not, refers to a disease which blocks or partially blocks the arteries of the legs and feet. It affectsbetween 10 and 25% of people over the age of 50. PAD is most commonly caused by blood clots and clogged arteries and, but may reflect another disease, such as arteritis, aneurysm, and embolism. In recent years, it has become evident that PAD is an important predictor of substantial coronary and stroke risk. A 10-year study conducted at the University of Minnesota found several factors that increased the risk of PAD. These were raised levels of glucose and insulin in the blood and to the effects of those raised blood glucose and insulin levels.[31] Blood cholesterol was not implicated.

      Intermittent claudication is a cramping pain most often seen in the calf and leg muscles, which is induced by exercise and relieved by rest. It is the result of partial or complete blockages of the leg arteries caused by an inadequate supply of blood to the affected area. Leg pulses are often absent and feet are often cold. A complication of diabetes, claudication is the most common reason for leg amputation.

      Getting blood glucose levels down has been found to be very effective in alleviating this condition.[32] And the best way to do that is with a low-carb diet.

 

Strokes

The risk of recurrent strokes is increased in people with impaired glucose tolerance according to Dr Sarah Vermeer of Erasmus Medical Center, Rotterdam) and co-workers.[33] Compared with patients who had normal glucose levels (5.8-7.7 mmol/l), stroke risk was nearly doubled in those with impaired glucose tolerance (7.8-11.0 mmol/l) and nearly tripled in patients with diabetes (>11.0 mmol/l).

      High blood glucose levels and consequent high blood insulin levels produce two effects that are responsible for inducing strokes.[34] [35] [36] These effects are:

·        increased thickening of the blood and increased stickiness which tends to clot and block the blood vessels and,

·        the increased permeability of the capillary walls leading to the smaller blood vessels and capillaries leaking and rupturing.

      Many studies have demonstrated that a breakdown of the endothelium, the inner lining of arteries and veins, occurs early in the insulin-resistant state and can predict future cardiovascular events. Similarly, insulin resistance has been associated with the metabolic syndrome, which also increases the risk of adverse cardiovascular outcomes. In July 2004, Willa A. Hsueh, MD, and colleagues at the Division of Endocrinology, Diabetes, and Hypertension, University of California, Los Angeles, reviewed the evidence that improving the function of the endothelium with a variety of drugs could prevent both cardiovascular disease and diabetes.[37] However, as raised glucose levels are an independent risk factor for stroke in people both with and without diabetes,[38] by reducing the levels of insulin in the blood, a low-carb, high-fat/protein diet does the same job naturally, making unnatural drugs redundant.

      Obesity has also been shown to be a marker for stroke. And considering the strong link between obesity and hypertension, it's easy to understand why there has been such a steep rise in hypertension among Americans in recent years. Obesity has reached epidemic proportions in the United States, and the enormously high levels of hypertension among the population appear to follow this trend closely.

      Roughly 25% of the adult US population suffers from high blood pressure and the problem is even more widespread among the elderly, of whom 50% are sufferers. Simply put, the heavier we become, the more prone we are to hypertension. This adds to the weight of evidence against our so-called 'healthy' diet.

 

Conclusion

By the time the establishment began its crusade aimed at preventing premature heart disease deaths in 1983, the number of such deaths in Britain had already fallen by 30% from their peak in the mid 1960s. What 'healthy' advice to increase fruit and starches in the diet, and eat less fat has done is the exact opposite of what was expected, as the numbers of cases of cardiovascular diseases have risen alarmingly since we took that advice on board.

      However, many members of the medical profession and academicians have such a lot invested in the 'fat-causes-heart-disease' paradigm that it would now be professional and academic suicide for them to admit the truth.

      But you don't have to put up with it; you can do something about this mess, yourself. The evidence has demonstrated that it is glucose and insulin which increase the risk of a heart attack. And glucose and insulin are raised only when we eat a so-called 'healthy' carbohydrate-based diet. So, to protect against cardiovascular diseases, you should reduce your intake of fruits, bread, pasta, and breakfast cereals and replace them with foods such as fatty meat, eggs, fish, butter and cream.

     

References


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[2]. Kilmer S. McCully, M.D. Personal communication, 27 March 2002.

[3]. Newbold HL. Reducing the serum cholesterol level with a diet high in animal fat. South Med J 1988; 81: 61-3

[4]. Lackland DT, Wheeler FC. The need for accurate nutrition survey methodology: The South Carolina experience. J Nutr 1990; 120: 11S: 1433-1436.

[5]. Nutr Week 22 Mar 1991; 21:12: 2-3.

[6]. Ravnskov U. The Cholesterol Myths. New Trends Publishing Inc, Washington DC, 2000. p 109.

[7]. Coronary Heart Disease: The Dietary Sense and Nonsense. George V. Mann, ed. Veritas Society; London, 1993.

[8]. Selvin E, et al. Glycemic control, atherosclerosis, and risk factors for cardiovascular disease in individuals with diabetes: the atherosclerosis risk in communities study. Diabetes Care. 2005; 28: 1965-73.

[9]. Plat J, et al. Oxidized plant sterols in human serum and lipid infusions as measured by combined gas-liquid chromatography-mass spectrometry. J Lipid Res 2001; 42: 2030-2038.

[10]. Ravnskov U. Op cit.

[11]. Enig M. Know Your Fats: The Complete Primer on Fats and Cholesterol. Bethesda Press; Maryland, 2000, 76-81.

[12]. Smith R, Pinckney E. Diet, Blood Cholesterol, and Coronary Heart Disease: A Critical Review of the Literature. Vector Enterprises, California, 1991

[13]. George V. Mann, ed. Coronary Heart Disease: The Dietary Sense and Nonsense. Veritas Society; London, 1993.

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[15]. Silaste M-L, et al. Changes in Dietary Fat Intake Alter Plasma Levels of Oxidized Low-Density Lipoprotein and Lipoprotein(a). Arterioscler Thromb Vasc Biol. 2004; 24: 498-503.

[16]. McGee DL, et al. Ten year incidence of coronary heart disease in Honolulu Heart Programme – Relationship to nutrient intake. Am J Epidemiol 1984; 119: 667-676.

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[18]. Chen YD, et al. Why do low-fat, high-carbohydrate diets accentuate postprandial lipemia in patients with NIDDM? Diabetes Care 1995; 18: 10-16

[19]. Selvin E, et al. Glycemic control and coronary heart disease risk in persons with and without diabetes: the atherosclerosis risk in communities study. Arch Intern Med. 2005; 165: 1910-6.

[20]. Jeppeson J, et al. Effects of low-fat, high-carbohydrate diets on risk factors for ischemic heart disease in postmenopausal women. Am J Clin Nutr 1997; 65: 1027-33

[21]. Max Bürger. Altern und Krankheit als Problem der Biomorphose. 3rd Ed,  Georg Thieme, Leipzig, 1957.

[22]. Abbasi F, et al. High carbohydrate diets, triglyceride-rich lipoproteins and coronary heart disease risk. Am J Cardiol 2000; 85: 45-48

[23]. Norhammar A, et al. Glucose metabolism in patients with acute myocardial infarction and no previous diagnosis of diabetes mellitus: a prospective study. Lancet 2002; 359: 2140-4.

[24]. Michalodimitrakis M, et al Lessons learnt from the autopsies of 445 cases of sudden cardiac death in adults. Coron Art Dis 2005; 16(6):385-389.

[25]. Selvin E, et al. op cit.  

[26]. Sharman MJ, et al. A ketogenic diet favorably affects serum biomarkers for cardiovascular disease in normal-weight men. J Nutr 2002; 132: 1879-85.

[27]. Westman EC, et al. Effect of 6-month adherence to a very low carbohydrate diet program. Am J Med 2002; 113: 30-6

[28]. Editorial. Prevention of coronary heart disease. BMJ 1968; 2: 689-90.

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