Essay on Health

Despite every effort, medicine can neither prevent nor cure heart disease. The same goes for cancer, diabetes, dementia and even arthritis. As a result, we suffer horribly as we age. Medicine pays lip service to nutrition, yet public policy allows foods depleted of essential nutrients to reach the marketplace. Examples include trans-fats, refined vegetable oils and sugar. Societies which do not eat these foods do not deteriorate as we do! Ironically, the healthy people in these societies have almost no knowledge of nutrition. While we have a great deal, we don’t use what we know because the food industry and the pharmaceutical companies with the complicity of government distort this knowledge for their own purposes.

I have insulin-dependent diabetes, a disease notorious for accelerating heart disease. When I was diagnosed at age 37, I saw the devastation wreaked by the disease in my doctor’s waiting room and was driven by sheer terror to search for a solution. For years, my wife and I experimented with diets. We learned that raw vegetables are kinder to the insulin-dependent diabetic than cooked vegetables, but I wasn’t out of the woods. In fact, I was at my wit’s end because I couldn’t keep my blood sugar in the normal range, and the harder I tried, the worse the hypoglycemic episodes I suffered. Then Dr Richard Bernstein published his low-carbohydrate approach, which is the opposite of the medical prescription. I found that the combination of my raw vegetables and his approach of avoiding starchy foods like bread and potatoes worked like a charm. I eat meat and fish with (mostly) raw vegetables and almost no refined foods, and eating this way keeps my blood sugar stable and in the normal range. I never gave a thought to heart disease, yet after fifteen years of eating this way, my wife and I both have calcium scores in the aorta of zero, which is unusual and implies a low risk of heart disease (Pletcher 2004). I’ve researched the phenomenon and I’m convinced I’ve found a reason why: people who have no heart disease eat unrefined foods. Explore the evidence with me and conclude for yourself if this is coincidence.

Kitava Islanders have no Coronary Heart Disease

Near Papua, New Guinea, there is an island called Kitava among the Trobriand Islands, which were made famous by Margaret Mead in her 1928 book about their freewheeling sexual practices, Coming of Age in Samoa. Later researchers have suggested that the islanders were pulling her leg, and that fear of sorcery is actually far more widespread than promiscuity. However, there is a truly remarkable thing about Kitava: there is today a complete absence of heart disease, and also of stroke, high blood pressure, cancer and dementia besides! Whole foods are eaten almost exclusively, and this suggests to me that a benefit of whole-food nutrition really is zero risk of CHD.

The Kitavans are by all accounts a charming people with a rich culture. They have a long history of sailing their ornate, hand-carved outrigger canoes to neighboring islands and trading necklaces and carved shells in an intricate, competitive exchange of gifts. The anthropologist Bronislaw Malinowski was exiled to the island during WWI, and published his ground-breaking cultural investigation into this so-called Kula exchange in his book, Argonauts of the Western Pacific.

In spite of an abundance of food, the Kitavan Islanders are lean and their blood pressure does not rise with age. The common causes of death are infections, accidents, complications of pregnancy and senescence. Senescence means old age: the Kitavans die of old age. You can hear the cholesterol chorus chime in with “It’s their genes!”, but a visiting emigrant islander who had lived on a Western diet for many years gave the lie to this notion. He had the typical Western health pattern of high blood pressure and abdominal obesity. And besides, the researchers noted that “compared with [Westerners] … Pacific Islanders seem more prone, not less, to develop diabetes after adopting a Western lifestyle” (Lindeberg 1999).

The Kitavans eat taro, sweet potatoes, yams, fruit, fish and coconuts, and eat very little Western food such as sugar, alcohol, grains, refined vegetable oils, and trans-fats. Almost all of them smoke (78%!), all chew the betel nut, and they exercise only at the level of a moderately active Westerner. Their cholesterol levels are said to be “unfavorable.” The reason for this is that 60-year-old males average a “bad” LDL-cholesterol level of 120, and the average 60-year-old female scores even higher at 148, while a “desirable” level is less than 100. The researchers thought this was “probably due to a high intake of saturated fat from coconut”, albeit in a diet with only a low 21% calories from fat. This seems to me to be a truly awesome failure of the imagination: whatever their cholesterol picture, it must be entirely favorable since they have no heart disease whatsoever! And this is not a fluke. Interestingly, the Tokelau Islanders (among the Cook Islands in the South Pacific) eat no less than 47% of their calories as saturated (coconut) fat, and males aged 55 to 64 have cholesterol levels averaging 245, yet they, too, enjoy robust vascular health (Prior 1981).

So far, the Kitavans have lots of supposed Western risk factors but no heart disease. This suggests that cholesterol is not actually a cause of heart disease, and that saturated fat is not, in itself, dangerous! It cannot be their low-fat diet is protecting them, because this is inconsistent with the experience of the Tokelau islanders, and with that of traditional-living Eskimos who were free of heart disease while eating the most fat of any diet ever investigated. What the diets of the Kitava Islanders, the Tokelau Islanders and the Eskimo have in common is a very small amount of refined food, unlike the Western diet.

The surviving hunter-gatherer tribes are also without heart disease:

Field studies of twentieth century hunter-gathers (HG) showed them to be generally free of the signs and symptoms of cardiovascular disease (CVD). … In this review we have analyzed the 13 known quantitative dietary studies of HG and demonstrate that animal food actually provided the dominant (65%) energy source, while gathered plant foods comprised the remainder (35%). … and a lower omega-6/omega-3 fatty acid ratio, would have served to inhibit the development of CVD. Other dietary characteristics including high intakes of antioxidants, fiber, vitamins and phytochemicals along with a low salt intake may have operated synergistically with lifestyle characteristics (more exercise, less stress and no smoking) to further deter the development of CVD. (Cordain 2002)

Polynesian horticulturalists, East African nomads, Eskimos and Cretans have also been studied and found to have negligible heart disease. All ate predominantly unrefined foods, and some (especially the Cretans) had characteristics such as smoking and “high” cholesterol which, were they Westerners, would put them in the high-risk category.

Significantly, the insulin levels of the Kitava Islanders are half those of Swedes living in Sweden (Lindeberg 1999), meaning that the Kitavans are not insulin-resistant and do not develop insulin resistance with age as Westerners do.

The Kitavans demonstrate that our conception of the cause of the diseases which kill us is mistaken.

US Healthcare: Caveat emptor!

I’m a psychotherapist. Nutrition is not my field, but I started out as an engineer so I applied my engineering skills to this new problem when I developed diabetes at 37 years of age. I knew I had to make careful study of how to avoid the complications this malady. I gained a PhD in Health Principles, and eventually published a book, Food for Vitality, on essential fatty acid disturbances in disease. The low-carbohydrate solution I found through my researches turned out to be amazingly simple and effective, yet it is diametrically opposite to the prescription of the diabetes healthcare system. The price of the diabetologists’ bad advice is complications which eventually kill most of the diabetic population. And yet the conventional diabetes diet was adopted directly from the American Heart Association diet, on the principle that since diabetics suffer accelerated heart disease, they need a heart-healthy diet. Unfortunately, the flaws in this diet accelerate both diabetic complications and heart disease.

When the measures my doctor prescribed made things worse, I researched the question and what I discovered from the scientific literature left me shocked and appalled. For example, I learned that the commonly-accepted idea that cholesterol causes heart disease must be wrong because lowering cholesterol fails to prevent heart disease. This is crystal clear. However, cholesterol is very good business for food manufacturers, drug makers, cholesterol testers, cardiologists, surgeons, hospitals and so on. I also learned that nutritional measures which do alleviate heart disease have been discovered, and rediscovered, over the years, but are simply ignored if they contradict the cholesterol idea. The healthcare system neglects nutrition, and therefore fails those who depend on it.

Most of us believe that America has the most advanced healthcare system in the world, and that we have the best care money can buy. In the narrow arena of the repair of coronary arteries and the removal of cancerous tumors, advances are nothing short of miraculous but elsewhere there is much cause for concern.

Let us look at what we spend, and what we actually get. Mirabile dictu – incredible to relate – America spent 1.5 trillion dollars on healthcare in 2001. That’s $4,887 on each man, woman and child in America, which adds up to 14% of the Gross National Product. To put this figure in perspective, consider that it=s by far the highest in the 10 industrialized nations, yet our life expectancy is near the bottom, our infant mortality is the worst, and we have the fewest Aquality-adjusted life-years.@ This means that while the life expectancy of a 65-year-old increased by about 3% in the decade, the expected years of life with "core activity restriction" increased by 34% for women, and by 51% for men. We’re getting sicker younger with each passing generation, in spite of spending more on healthcare than anyone else on Earth.

The popular perception that we=re living a great deal longer than we did a century ago is quite wrong, a figment of statistics. It is true to say, statistically speaking, that life expectancy at birth was 47 years in 1900 and 75 years in the year 2000, but the telling statistic is that the life expectancy of a 65 year old male in 1900 was 12 years (i.e. he’d live to 77), and the life expectancy of a 65 year old male in 2000 was 16 years, an increase of but four years. The key to the puzzle is that infant mortality was 216 per 1,000 births in 1900, and only 6.3 in 2000:

Infant mortality has fallen. (Click on images for large view)

Running water, indoor plumbing and refrigeration controlled the infectious diseases and permitted more babies to survive, but medical advances have improved our circumstances towards the ends of our lives hardly at all. We used to die of infectious diseases, and now we die of heart disease and cancer, so it’s really only the manner of our passing that has changed:

Deaths from infections disease have fallen dramatically. Interestingly, the introduction of antibiotics and vaccines did not steepen the fall: in other words, measures such as the chlorination of water, refrigeration and improved sanitation did far more than medicine.

As deaths from infectious diseases fell, deaths from heart disease and cancer have risen. Mortality from heart disease is deceptively low because the figures are age-adjusted to the 1940 population, in which there were far fewer older people. There were 1.7 times the number of people aged 65-84 years in 2000 than there were in 1940, which means that the heart-death rate in 2000 was 1.7 times what the graph shows (because most heart deaths take place in this age group.) The 1940 point is accurate at about 300,000 deaths, and the 2000 point would be about 1,400,000 were the graph not age-adjusted. That there has actually been an increase in the incidence of angina corroborates this: angina almost doubled between 1978 and 1995 in a sample of British men aged 55-59 (Lampe 2005).

We know that heart disease is not caused by a cholesterol-lowering drug deficiency, and that cancer is not caused by neglecting to take chemotherapeutic agents. But the truth is that we don’t really know what causes heart disease or cancer, and today’s ideas don’t suggest preventive strategies or effective treatments. Healthcare is virtually helpless to prevent these epidemics.

Medical care itself is estimated to have caused 783,936 deaths in 2001. Among other things, there were adverse reactions to drugs (106,000), medical errors (98,000), infections acquired in hospitals (88,000), botched surgeries (32,000), unnecessary procedures (37,136), even malnutrition (108,800) and, amazingly, bedsores (115,000), making the healthcare industry itself the third leading cause of death in America.

To add insult to injury, according to a Harvard University study of 2001 data, half of all personal bankruptcies in the U.S. were caused at least in part by medical bills, and most of these people had health insurance!

Yet in more Aprimitive@ cultures eating their traditional diets, people who survive childhood infections and accidents die of old age with their faculties intact at pretty much the same age we do. The health surveys are unequivocal, the facts inarguable. Perhaps their immunity from our degenerative diseases is because of the higher nutrient content of their traditional, unrefined diets. This seems to me to be self-evident, but are we using this information to improve our health? We don’t use this information to improve our health because we mostly don=t know about it, and, what=s worse, we don=t know we don=t know!

There are known knowns ... but there are also unknown unknowns.

The ones we don=t know we don=t know.

Donald Rumsfeld

The dissemination of this knowledge is hindered at every turn by vested interests, media bias and medical prejudice, and this is made possible by our trusting naïveté.

The doctor of the future will give no medicine, he will interest his patients in the care of the human frame, in diet and the cause and prevention of disease

Thomas Edison

But this promised tomorrow has not come to be, and I see that this is because the forces of misinformation are ascendant. The price is poor health and premature death for millions, a staggering and unimaginable toll of human misery, with chronic pain and minds lost to dementia instead of the productive old age in strong extended families seen in traditional societies.

So the Conventional Wisdom fails

John Kenneth Galbraith coined the term in his 1958 book The Affluent Society. According to him, conventional wisdoms are beliefs which “serve the ego”, meaning they make us feel good by giving us a sense of belonging to the conservative orthodoxy, confirming we are correctly oriented with regard to the issues of the day. These beliefs are articulated at all levels of sophistication from blue-collar to university professor. With cholesterol, clever men put forward an idea which everybody now clings to as if to a life-belt.

For what a man had rather were true he more readily believes

Francis Bacon

Galbraith wrote that minor disagreements with the conventional wisdom are “much cherished” and “the very vigor of minor debate makes it possible to exclude as irrelevant, and without seeming to be unscientific or parochial, any challenge to the framework itself”, and “… the conventional wisdom often makes vigorous advocacy of originality a substitute for originality itself.” But when a serious challenge emerges, “… men react, not infrequently with something akin to religious passion, to the defense of what they have so laboriously learned.” In other words, the conventional wisdom is comforting and saves us the effort of thinking for ourselves, but is not necessarily true. “The enemy of the conventional wisdom is not ideas but the march of events … the fatal blow to the conventional wisdom comes when the conventional ideas fail signally to deal with some contingency.”

In this case, we see that the Kitavan experience disproves the cholesterol-causes-heart disease idea: they have lousy cholesterol levels and no heart disease whatsoever. The “march of events” in this case is that more than half of us die of heart disease in spite of changing our diets in accordance with the cholesterol idea. One of the attractive features of the cholesterol theory is that everybody thinks they understand it – that LDL-cholesterol is “bad” is self-explanatory. However:

A stupid man's report of what a clever man says can never be accurate, because he unconsciously

translates what he hears into something he can understand.

Bertrand Russell

If the cholesterol idea is not true, then understanding it is indeed unfortunate for people of any intellectual level. And if the clever men who came up with the cholesterol idea were not entirely pure of motive, then what we may actually be seeing is the greatest marketing coup in the history of Western civilization.

My healthcare misfortunes

When I got back trouble, my doctor prescribed traction in hospital. He wouldn’t discuss the chiropractic alternative, and I was surprised at how angry he seemed at the very idea. I’d never seen him angry. In fact, a chiropractor quickly solved my problem, and some time later the American Medical Association was found guilty of violating the Sherman Antitrust Laws by conspiring to destroy the chiropractic profession. In the Permanent Injunction, Judge Getzendanner made it clear that the American Medical Association knew of a study showing chiropractic to be twice as effective at half the cost of medical treatment, and that she felt it necessary to order the Injunction sent to every member of the Association because she had no confidence that the AMA would change its ways unless forced to do so. My doctor, a good, kind man, was deceived by his own Medical Association in its attempt to eliminate competition.

(The American Medical Association is) … just another mean trust

Harry S Truman

Later, I got chronic fatigue syndrome. I’d had it before (I was diagnosed with infectious mononucleosis) when I was studying Mechanical Engineering at London University. I spent six weeks in Coppett’s Wood Isolation Hospital (to protect me from further infection) because there was (and still is) no known medical treatment. I was exhausted beyond belief for six months and almost lost my place at the University. But by now, I=d read Irwin Stone=s The Healing Factor: Vitamin C Against Disease, so I asked my doctor about Dr Robert Cathcart=s regimen of massive vitamin C intake for infectious diseases. Again, he seemed disappointed, as though the diagnosis had unhinged me and I’d fallen into quackery. I got the sense that dealing with this kind of question was, for him, the most disagreeable part of practicing medicine.

I went ahead anyway because I knew the risk was negligible, and anything that might help the aching, grinding exhaustion (seemingly worsened by sleep) was worth trying. I took “mixed mineral ascorbates” because they’re easier on the stomach, but I eventually learned that the minerals themselves were important and contributed to my improvement. After three weeks of very high doses of vitamin C – up to 140 grams per day – I was on the road to recovery. I felt it was a miracle. Since then, I’ve encouraged three other chronic fatigue sufferers to treat themselves, and two of them recovered as I did. (The third person had a normal bowel tolerance for vitamin C of about 10 grams, so her chronic fatigue hadn’t been caused by a bug).

But how can it be that my doctor didn’t know about this effective, natural anti-viral treatment? After all, Dr Fred Klenner published his findings that intravenous vitamin C cured polio when sufficiently large doses are used as long ago as 1949! (Klenner FR, The Treatment of Poliomylitis and Other Virus Diseases with Vitamin C, Southern Medicine and Surgery, 1949; 111(7):209-14). Instead, when two-time Nobel Prize winner Dr Linus Pauling published studies indicating that intravenous vitamin C is an effective anti-cancer agent, Dr Charles G Moertel of the Mayo Clinic refuted his claim with two of the most bizarre studies in the medical literature, which have been interpreted as bunk designed to protect the incredible profits from the so-called chemotherapy concession: “oncologists purchase prescription chemotherapy drugs from their manufacturers and wholesalers, administer the drugs to patients … Government audits have found that profit margins for doctors of 80 to 90 percent are not uncommon in these transactions.”

The vast majority of research published since then has supported Pauling’s approach, most recently demonstrating the likely mechanism by which intravenous vitamin C is effective against cancer cells (Chen 2005), and providing reports of three cases (Padayatty 1006). It may be no coincidence that Dr Moertel died of cancer aged 66 years, while Dr Pauling took 18 grams of vitamin C per day and died (also of cancer) at 93 years of age.

There are striking examples of facts that have been ignored because the cultural climate

was not ready to incorporate them into a consistent theme.

Ilya Prigonine

And then there are facts which are commercially inconvenient. It seems that pharmaceutical companies advance their interests by using advertising dollars to encourage (or the withdrawal of advertising dollars to coerce) medical journals such as the Journal of the American Medical Association to de-emphasize research on real results and natural remedies like vitamin C:

Medical journals are no more than an extension of the marketing arm of the

pharmaceutical companies.

Dr Richard Smith, editor, British Medical Journal

There seems to be no study too fragmented, no hypothesis too trivial, no literature citation too biased or too egotistical, no [trial] design too warped, no methodology too bungled, no presentation of results too self-serving, no argument too circular, no conclusions too trifling or too unjustified … for a paper to end up in print.

Dr Durmond Rennie, editor, Journal of the American Medical Association

Medical schools are renowned for the paucity of their nutrition courses, and renowned also for their massive dependence on drug company money – let alone the billion dollars a year that the drug companies invest in the continuing education of doctors. As a consequence, my doctor is ignorant and distrustful of natural remedies and unknowingly acts against the interests of his patients. He is deceived, once again for commercial reasons, but this time by the pharmaceutical industry.

Then I got insulin-dependent diabetes. This was a big shock, and the more I learned about diabetic complications the more scared I became. The long-time diabetics I met in my new, specialist doctor’s waiting room had a smorgasbord of rampant heart disease (in spite of the supposedly heart-healthy diet), kidney failure, fading eyesight and even “salami amputations” made necessary by galloping atherosclerosis in their legs. A study of insulin-dependent diabetics in Pittsburgh found their risk of dying in any particular year was 2%, more than 20 times the risk of a non-diabetic (Dorman 1984).

Neither a man, nor a crowd, nor a nation can be trusted to act humanely

or to think sanely under the influence of a great fear.

Bertrand Russell

I learned to inject insulin and, in my fear, I accepted unquestioningly the prescribed (at the time) low-fat high-carbohydrate American Diabetes Association “heart-healthy” diet. I quickly began to suffer brutal hypoglycemic episodes. No matter how often I tested my blood sugar, it would get away from me and I lived in fear that I’d wake up in the emergency room. My HbA_1c (glycosylated hemoglobin) score, which indicates the risk of diabetic complications, remained obstinately high no matter how hard I worked at the diet. Eventually, I was shocked to realize that my doctor believed the diet wasn’t working because I was cheating. He was wrong. I was never more serious about anything in my life.

Eventually, I learned of Dr Richard Bernstein. This brilliant diabetic engineer learned by self-experimentation that eating a high-carbohydrate diet is the height of folly when one has to depend on injected insulin because carbohydrates quickly elevate glucose in the bloodstream which insulin acts slowly. Dr Berstein pioneered the idea that good blood-sugar control controls diabetic complications, an idea since validated by the Diabetic Control and Complications clinical trial (DCCT/EDIC). He reversed his own diabetic complications, and he had most of them, by normalizing his blood sugar with a low-carbohydrate diet. Amazingly, he couldn’t get the medical profession to listen to him so he qualified as a doctor himself at the age of 49. He now has a diabetes practice in Mamaroneck, New York, and although the mainstream medical profession still doesn’t listen to him, he has established a strategy for surviving diabetes without complications which he has laid out in his books Dr Bernstein’s Diabetes Solution and The Diabetes Diet.

I quickly found that the low-carbohydrate diet restored my “hypoglycemic awareness” (insulin-using diabetics often don’t know when their blood sugar is falling to dangerous levels), and put an end to my hypoglycemic episodes. In addition, the new regime and dramatically improved my HbA_1c score. The American Diabetes Association’s low-fat, high-carbohydrate diet had caused sudden, violent blood-sugar excursions, which I tried to control with slow-acting insulin injections. I might as well have tried to nail jelly to the ceiling.

A graph of my HbA1_c scores before and after I adopted a low-carbohydrate diet

The HbA_1c score predicts the likelihood of diabetic complications: “patients … will accrue substantial benefit from almost-normal glycemic control. In patients with later onset, moderate glycemic control prevents most end-stage complications caused by microvascular disease” (Vijan 1997). However, in the Diabetes Control and Complications Trial, the “Intensive Treatment” group ended the trial with an average HbA_1c of 7.4%, while the “Conventional Care” group’s average was 9.1% (DCCT/EDIC). You can see my HbA_1cscore was in the Intensive Treatment range, and fell 2 full percentage points after I began to avoid starches. When the HbA_1cscores of 4,662 men aged from 45 to 79 years were measured, those who died during the two-to-four years of follow-up were found to have had the highest scores. The researchers calculated that for each 0.1% reduction in HbA_1c risk of death fell by 5%, so my low-carbohydrate diet has therefore likely reduced my risk of death by 20% (Khaw 2001):

Recently, the National Institutes of Health funded a ground-breaking study in which a low-carbohydrate diet was shown to normalize the blood sugars of Type 2 Diabetics after just two short weeks. The HbA_1c score of the participants averaged 7.3% at the start, and was projected to end at a normal 5.6% had the experiment continued for two months (Boden 2005). This is just as Dr Bernstein suggests in his book, and exactly what I experienced. There’s no room left for doubt: the conventional dietary treatment of diabetes guarantees that diabetics, especially insulin-dependent diabetics, will contract life-threatening complications, no matter how hard they try to control their blood sugar.

So, anyway, it came as no surprise to me that key American Diabetes Association donors included General Mills, Kraft Foods, Nestlé, Coca Cola, Hershey Foods and Frito-Lay. The biggest sugar and refined-carbohydrate purveyors on the planet have contrived to encourage those who are least able to handle their products to consume them! My doctor is thrice deceived, this time by food manufacturers. With the drug companies, the food manufacturers have made my doctor their cat’s paw, a person used by another as a dupe or tool.

I thought I was out of the woods: by avoiding refined foods and starchy vegetables, I could keep my blood sugar from wandering into dangerous territory, and, in fact, my blood tests were better than ever before with my LDL-cholesterol down to 111. But my doctor pointed out that the American Heart Association guidelines on the Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults suggests that diabetes be treated aggressively, and that the lower my LDL-cholesterol level, the better. He suggested I adopt the low-fat American Heart Association “Therapeutic Lifestyle Changes” (TLC) Diet to lower my LDL-cholesterol level; and if the diet hasn’t achieved this after three months, that I should take a cholesterol-lowering statin drug.

Now I was as frightened of heart disease as I had been of diabetic complications, so frightened that I actually read the entire 284-page report! I was startled to learn that AModification of blood pressure and lipids in people with diabetes, however, does not reduce CHD risk@ (p. II -15). But I quickly recognized the TLC diet as a retread of my old nemesis, the American Diabetes Association diet, with a few minor differences (such as just 10% of calories from refined vegetable oil instead of 22%). This time, as I researched it as a tool to lower my LDL-cholesterol, I could find almost no benefit except for the manufacturers of the foods and drugs involved. Furthermore, it became clear from the studies I read that cholesterol isn’t even a primary cause of heart disease! But first of all, what is this coronary heart disease of which I’m so at risk?

CHD: Coronary Heart Disease

Coronary heart disease is a frequent complication of diabetes, and diabetics have about 4 times the risk; a male who contracts diabetes early in life may lose up to twelve years of life. A condition which often precedes it is atherosclerosis (from the Greek for porridge and stone), which is found to a greater or lesser extent in the arteries of people all over the world. It may start as early as infancy, with fatty streaks forming at points in the arteries subject to the greatest mechanical stresses from turbulent blood flow, or from distension from the blood-pressure pulses. Although some 35% of people have “clinically significant” atherosclerosis, others are entirely free of it (Enriquez-Sarano 1996).

Atherosclerosis was found in Egyptian mummies dating from 100BC, and was first described at autopsy by Leonardo da Vinci in about 1520. The 17^th Century English physician Thomas Sydenham wrote that “A man is as old as his arteries” because atherosclerosis eventually constricts the coronary arteries so that the blood supply to the heart muscle is inadequate, causing the agonizing pain of angina. However, according to the AHA, “only 20% of coronary attacks are preceded by long-standing angina.” Interestingly, the first heart attack to be described in the medical literature was in 1912. In a heart attack, a blood clot may block an artery narrowed by atherosclerosis, cutting off the blood supply to the heart muscle and resulting in myocardial infarction (which is a heart attack). Unstable plaque (inflamed atherosclerotic plaque) is often found in those who eat a Western diet, and should it rupture, the plaque contents cause a massive clot and an immediate heart attack (Forrester 2002).

Interestingly, coronary heart disease doesn’t always involve atherosclerosis. One in five heart victims have clean arteries, and these deaths are thought to be caused by spasms of the coronary artery or some form of arrhythmia, in which the heartbeat becomes uncoordinated and the heart fails to pump blood. So “Coronary Heart Disease” includes angina, heart attack and sudden heart death, and is included in the more general term “Cardiovascular Disease” which itself includes high blood pressure, cardiomyopathy (in which the heart swells and pumps inefficiently), stroke and various other circulatory problems. The incidence of heart disease increases with age, and is truly epidemic: by 75 years of age, about 78% of men and 86% of women have cardiovascular disease, and 17% of men and 10% of women have CHD.

Clearly, several disease processes at work. For starters, there’s whatever causes fatty streaks and atheroma (porridge before it turns to stone), then there’s whatever causes calcium to enter the atheroma to cause atherosclerosis, whatever causes the blood to clot, whatever causes arrhythmias, and whatever causes arterial spasms. As we shall see, nutritional factors are strong modifiers of all these disease processes.

However, it is generally believed that high blood cholesterol is bad for the heart, LDL-cholesterol particularly so. We are told, and we believe, that we are helping ourselves by lowering cholesterol and saturated fat in what we eat. The American Heart Association has made the Therapeutic Lifestyle Changes Diet and statin cholesterol-lowering drugs cornerstones of their strategy for lessening risk of CHD by lowering “bad” LDL-cholesterol. The TLC diet lowers cholesterol and saturated fat in the diet in order to lower cholesterol and LDL-cholesterol in the bloodstream. But I quickly found that almost every tenet of the Therapeutic Lifestyle Changes Diet is speculative. First of all, cholesterol in the diet has little to do with cholesterol in the bloodstream!

Lowering dietary cholesterol hardly affects cholesterol in the bloodstream

Even Dr Ancel Keys, who wrote the mammoth Seven Countries Study which investigated heart disease risk factors in seven countries and started the whole cholesterol scare, didn’t believe dietary cholesterol was important. He wrote:

In the adult man the serum cholesterol level is essentially independent of the cholesterol intake over the whole range of human diets (1956). 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 (1997). I’ve come to think cholesterol is not as important as we used to think it was (1987).

Few know that the diet-cholesterol question was studied in the Framingham Heart Study before the cholesterol spin-doctors took over. At 22 years, the results showed that the average blood levels of cholesterol were essentially the same in men and women consuming less than and more than the average intake. This means, in the words of the researchers, that “There is considerable range of cholesterol levels within the Framingham study group. Something explains this inter-individual variation, but it is not diet”:

		Blood cholesterol (mg/dL)	in those consuming:-
	Average Cholesterol Intake, mg/day	Less than the average:	More than the average:
Men	704	240	240
Women	492	248	244

(Kannel, William B, Gordon, Tavia, The Framingham Diet Study: Diet and the regulation of serum cholesterol.

In The Framingham Study: An Epidemiological Investigation of Cardiovascular Disease. Section 24. US Government Printing Office, Washington, D.C., 1970)

Interestingly, data from the same source compared cholesterol intakes of healthy Framingham subjects and those with CHD:

Cholesterol intake (mg/day) of:	Healthy subjects	Patients with CHD
Men	716	708
Women	477	520

Their conclusion was the only conclusion possible from this data: “There is, in short, no suggestion of any relation between diet and the subsequent development of CHD in the study group."

Lowering dietary cholesterol hardly affects “bad” LDL-cholesterol in the bloodstream

We know this because it took a meta-analysis of locked-ward metabolic studies to show that cholesterol in the diet raises “bad” LDL-cholesterol because the effect is small:

Dietary cholesterol causes marked hypercholesterolemia in many laboratory animals, including non-human primates. High intakes of cholesterol in humans, however, do not cause such a marked increase in serum cholesterol. Nonetheless, controlled metabolic studies in humans indicate that high cholesterol intakes raise LDL cholesterol. The degree of rise varies from person to person as is true for all nutrients. Meta-analysis of studies done in controlled settings confirm the LDL-raising action of dietary cholesterol. (652, 653). (page V-9 of the 3^rd Report of the National Cholesterol Education Program Expert Panel on Detection, Evaluation and Treatment of High Blood Cholesterol in Adults)

In fact, although there seems to be a relationship when different countries are compared, the effect has not been found in within-population studies. As is so typical in the cholesterol-heart disease field, this finding was blamed on confounding factors, and dismissed (Jacobs 1979). Meta-analyses are used when effects are so small that huge numbers of subjects are necessary for a study to achieve statistical significance. The first study says that if I replace 60% of saturated fats with other fats, and avoid 60% of dietary cholesterol, I may lower my LDL-cholesterol by 8 to 12% (Clarke 1997). This is a draconian, near-vegetarian prescription for a small benefit! The second study concludes that “People desiring maximum reduction of serum cholesterol by dietary means may have to reduce their dietary cholesterol to minimal levels (less than 100-150mg/day) to observe modest serum cholesterol reductions ….” (Hopkins 1992).

I see that the National Cholesterol Education Committee has told a half-truth. I can expect little further lowering of my already-low LDL-cholesterol by restricting my cholesterol intake because the TLC diet advocates only about half of the reduction in cholesterol which was found to be effective in the locked-ward studies.

Lowering saturated fat hardly affects cholesterol in the bloodstream either

In the Tecumsheh study of 957 free-living adults in Tecumseh, Michigan, those with the lowest cholesterol levels and those with the highest cholesterol levels were found to eat the same amount of saturated fat, so the TLC diet with its lesser amount of saturated fat will likely not lower my blood cholesterol by much.

Most importantly, lowering cholesterol in the bloodstream doesn’t lower CHD!

Incredibly, an analysis of 22 cholesterol-lowering studies prior to the advent of statins, in which 114,000 people participated, showed almost no change! There were only 0.3% fewer nonfatal heart attacks, the same number of fatal heart attacks, and, worryingly, 0.3% more deaths from all causes in the treatment groups whose cholesterol was lowered:

	Treatment groups	Control groups	Change
Nonfatal heart attacks	2.8%	3.1%	-0.3%
Fatal heart attacks	2.9%	2.9%	0
Total deaths	6.1%	5.8%	*+0.3%*

(Ravnskov 1992)

Cholesterol is a lousy risk factor

And cholesterol in the bloodstream is a very poor predictor of heart risk. An analysis of the Framingham results published in 1980 showed that the 10% of the population with the highest risk according to the cholesterol measures experienced less than 25% of the CHD (Orchard 1980). If cholesterol was as dangerous as it has been represented to be, this percentage would be far higher. The curves for the distribution of cholesterol in those with and without CHD overlap so closely that it is obvious that cholesterol’s predictive power is weak (Ebrahim 1998):

In fact, only 42% of these British men who had a blood cholesterol level above 6.5 mmol/l (253 mg/dl) went on to have heart trouble in the next 15 years. They might as well have tossed a coin – in fact, tossing a coin would have “predicted” 50% of the men at risk!

Lowering “bad” LDL-cholesterol doesn’t necessarily lower heart risk

Suppose the TLC Diet did work and lowered my LDL-cholesterol, will it lower my risk of CHD? A study of an aging Italian population has shown that risk of both heart death and all-cause mortality actually increased dramatically as LDL-cholesterol fell:

Figure 1. Sex-specific and age-adjusted rates of total and cardiovascular mortality by quartiles of serum low-density lipoprotein cholesterol at baseline. The number of deaths is given for each quartile. Conversion factor to conventional units is 38.6 (Tikhonoff 2005).

Apparently, an LDL-cholesterol level of about 154mg% (4mmol/L in the units of the figure) conferred a considerable survival advantage over the supposedly more desirable under-100mg% (2.6mmol/L) level. This seems to fly in face of conventional wisdom, but when Dr Uffe Ravsnkov (Ravnskov 2000) actually read the references of the National Research Council’s massive Diet and Health: Implications for Reducing Chronic Disease Risk report, which established LDL-cholesterol as a risk factor for heart disease, he found the voluminous literature relies, at bottom, on a single study of the Framingham population which concluded that: “Under age 50 years, [LDL-]cholesterol levels are directly related with 30-year overall and CVD mortality … after age 50 years there is no increased overall mortality with either high or low serum cholesterol levels (Kannel 1979). But I’m 60 years of age, so my LDL-cholesterol level is beside the point!

So the extraordinary conclusion is forced upon me:

Cholesterol doesn’t cause heart disease!

For every complicated problem there is a solution that is simple, direct, understandable, and wrong

HL Menken

There is no nonsense too arrant to become policy with sufficient interference by the government

Bertrand Russel

I was so intrigued that I researched the matter further, and found that the low-fat preoccupation was started by Dr Ancel Keys. Keys was a prolific researcher, and we have him to thank for K-rations, the first scientifically-formulated provisions for the American fighting man. In researching the causes of heart disease, Keys demonized all fats at first, then saturated fat. His research was incredibly sloppy. For example, he cherry-picked among the available data to make a convincing graph, which needless to say is a deeply bogus practice:

The left graph is from Keys, showing data from 6 countries which promise a close relationship between fat in the diet and heart deaths. The right graph is from contemporary data for 22 countries, and shows that Keys cherry-picked his data to make his graph more convincing (Yerushalmy 1957). You don’t need statistics to see the Key’s persuasive relationship disappears when the data for all 22 countries are plotted, or that picking (say) Japan, Ceylon, Chile and France would seem to show that fat protects against heart death.

Keys almost certainly knew from his own investigations that although between-population studies show an association between fat and CHD mortality, within-population studies generally do not (Khor 2004). This implies that it’s not fat that causes CHD mortality, but rather some fellow-traveler such as, for example, the degree of refinement of the diets. In fact, sugar consumption correlates very closely indeed with fat consumption in 30 different countries, and the correlation between heart deaths and sugar consumption has actually been found to be stronger than that between fat and heart deaths. The authors of the study from which the graph below of sugar consumption vs. heart deaths concluded “These results suggest that associations identified in this type of investigation should be interpreted with great caution and need not necessarily reflect causal relationships, but rather suggest avenues along which further research might proceed” (Armstrong 1975):

Sugar consumption in 30 countries plotted against the heart-attack death rates. The relationship is obviously stronger than that between fat and heart death (compare Key’s graph above), yet Keys dismissed it with scorn: “ … the correlation between sugar and CHD does not remotely approach significance” (Keys 1973).

It is long yet vigorous, like the penis of a jackass

Sydney Smith

The Reverend Sydney Smith was talking about the quality of his sermon, but the description fits Key’s writings: one does not get the chance to be won over by the persuasiveness of the argument, but is rather browbeaten into submission. Few know that Keys was on the American Heart Association nutrition advisory committee, or that grants from the American Heart Association Minnesota Affiliate paid for much of his research. Dr Key’s low-fat, low-cholesterol dietary prescription became the official AHA dietary guidelines in 1961. I imagine that the farmers of Minnesota and the refined food manufacturers chortled with glee, for patterns of consumption changed dramatically in their favor. People began to avoid fat in favor of refined carbohydrates:

Since 1963, the consumption of carbohydrates steadily increased back to 500 g/d; however, fiber consumption did not increase proportionately. This finding reflects an increased consumption of refined carbohydrates over this time period (Gross 2004).

My conclusion? The Therapeutic Lifestyle Changes Diet would be useless for me. I believe it would likely be useless for anybody else, unless they ate nothing but fast foods. This is so reminiscent of my attempt to use the very similar American Diabetes Association diet to help my diabetic control: it worsened my blood sugar control because it had too many carbohydrates. Substituting fat for the starchy vegetables and whole grains in my diet returned my HbA_1c test result to the normal range, indicating my risk for diabetic complications is at a minimum. And as an insulin-dependent diabetic, I simply don’t have a choice about eating fat; the calories have to come from somewhere, so I can’t be both low-fat and low-carbohydrate! Since carbohydrates send my blood sugar into orbit, I eat eggs and snack on almonds and Brazil nuts instead, and the consequence is that my cholesterol risk factors are better than they have ever been in my life. My experience utterly refutes the conventional prescription in diabetes management, and the scientific literature suggests that the cholesterol hypothesis is a porky.

But why don’t I use refined vegetable oils and avoid saturated fats? Because studies show that this approach has risks of its own. In the UCLA Veterans Administration trial, saturated fat was replaced by polyunsaturated soybean oil in a 40% calories-from-fat diet and there was a small decrease in the number of deaths from heart disease, but this decrease was completely offset by a robust, 15% increase in deaths from cancer in the treatment group (Dayton 1969). This is not a rogue result, for an analysis of 8 trials employing this strategy (including some low-fat diet trials) shows that it carries with it a 0.1% absolute increased risk of death, meaning that it is at least ineffectual, and probably dangerous (Ravnskov 2003). And, amazingly:

Saturated fat is protective!

Even in Key’s time, there was data which suggested that saturated fat rendered some benefits. Before dismissing saturated fat as a dietary fiend with no redeeming features, it’s necessary to explain the high rate of stroke in Japan, where the saturated fat consumption is among the lowest in the world:

Saturated fat (or something else) protects the peoples of France, Austria, Switzerland, Norway and the Netherlands from stroke, while Japan eats very little and has a high rate of stroke (Yerushalmy 1957).

The relative risk of stroke between the highest and lowest quintiles of saturated fat intake in a 20-year follow-up of the male Framingham population was 0.43, a “robust association” according to the researchers (Gillman 1997). The increment of relative risk of heart problems between the highest and lowest quintiles of saturated fat intake was only 1.03 in this study. The jargon means that those who ate the most saturated fat in Framingham were at 57% less risk of stroke and had a 3% increased risk of heart problems.

Men of Japanese descent living in Hawaii experienced similar outcomes and the researchers concluded with this ringing endorsement of the lipid-heart hypothesis: “This increased risk [of eating a diet low in fat], due to an excess risk of death from stroke and cancer, indicates that there is no overall beneficial effect from a low fat diet in this cohort” (McGee 1985).

More recently, saturated fat in the diet was found to protect post-menopausal women against progression of their atherosclerosis. The study concluded that “In postmenopausal women with relatively low total fat intake, a greater saturated fat intake is associated with less progression of coronary atherosclerosis, whereas carbohydrate intake is associated with a greater progression” (Mozaffarian 2004). In this study, sugars (carbohydrates) were found to be dangerous, and saturated fats were found to be protective!

This raises doubt in my mind about the population studies in which saturated fat intake appears to elevate the risk of heart disease, for most were not controlled for carbohydrate intake. In one such oft-quoted investigation of saturated-fat intake in the Nurses Health Study, fiber intake (which is lowered by sugar intake, and raised by fruit and vegetable intake) was 17 grams per day in the lowest-risk group and 10 grams in the highest-risk group (Hu 1999). But in this study, no distinction is made between “carbohydrates” and “refined carbohydrates”, and low fiber implies a high intake of refined carbohydrates which are low in fiber. So was it the saturated fat that raised their risk of CHD, or was it sugar? Another study which compared the diets of lean and obese individuals concluded that “Obesity is maintained primarily by a diet that is high in fat and added sugar and relatively low in fiber” (Miller 1994).

There is, in fact, an immense body of evidence to suggest that saturated fat in the diet is, at the least, not harmful:

To date, some 26 long-term follow-up studies, ranging in length from 4 to 23 years, have examined the relationship between saturated fat intake and cardiovascular disease.[1-26] We are constantly told that saturated fat is a toxic "artery-clogger", yet only four of these studies have managed to detect even desperately weak statistical associations between saturated fat and CHD/CVD mortality. One study observed a protective relationship, while all the rest found no association at all.

Even more importantly, controlled clinical trials – which represent far more reliable evidence than confounder-prone epidemiological studies – have completely failed to show any CVD or total mortality benefit for individuals randomized to saturated fat restricted diets (Anthony Colpo, TheOmnivore.com 2005).

In the reference supporting the last assertion, Dr MF Oliver wrote that “The commonly-held belief that the best diet for prevention of coronary heart disease is a low-saturated fat, low-cholesterol diet is not supported by the available evidence from clinical trials. In primary prevention, such diets do not reduce the risk of myocardial infarction or coronary or all-cause mortality (Oliver 1997).

Worse still, I learn that:

Low blood cholesterol is itself not without risk

Other than that, Mrs. Lincoln, how did you enjoy the play?

Low cholesterol is associated with a much higher risk of violent death and suicide, so much so that six studies in which cholesterol was lowered and deaths from heart disease reduced showed no change in the death rate from all causes between the treatment and control groups because of increased death by violence and suicide. The study concluded that “The association between reduction of cholesterol concentrations and deaths not related to illness warrants further investigation. Additionally, the failure of cholesterol lowering to affect overall survival justifies a more cautious appraisal of the probable benefits of reducing cholesterol concentrations in the general population” (Muldoon 1990).

Even more disquieting is the outcome of a huge study of 149,650 men and women which concluded that:

In men, across the entire age range, although of borderline significance under the age of 50, and in women from the age of 50 onward only, low cholesterol was significantly associated with all-cause mortality, showing significant associations with death through cancer, liver diseases, and mental diseases. (Ulmer 2004)

Studies suggesting a link between low cholesterol and all-cause mortality are thick on the ground. In New Zealand Maoris, low cholesterol predicted death, raising the relative risk of death by 2.3 in men and 1.9 in women (Beaglehole 1980), and in Korean men, “The cholesterol level associated with the lowest mortality ranged from 211 to 251 mg/100ml …” (Song 2000), well above the American Heart Association’s upper limit of normal, which is 200mg%. After age 72, the Honolulu Heart Program study suggests that low cholesterol is associated with increased risk of death from all causes (Schatz 2001):

Quartile 1 had the lowest average cholesterol and the highest mortality:

Quartile 1: 149mg%

Quartile 2: 178mg%

Quartile 3: 199mg%

Quartile 4: 232mg%

And Quartile 4 had the highest cholesterol and the lowest mortality! The dose-response relationship is present in each quartile (see table) which suggests that the findings are valid.

The red line represents the group with the lowest average cholesterol, 149mg%. This group had the lowest probability of survival at all times during the 6 years of follow-up, indicating that, after age 72, higher cholesterol is protective!

One reason may be that low cholesterol is associated with low immunity. This is a robust effect which has been found in any number of studies, although it is usually dismissed as an artifact:

Men occasionally stumble over the truth, but most of them pick themselves up and

hurry off as if nothing ever happened.

Winston Churchill

For example, a 15-year Kaiser Permanente study of 61,827 patients found “an inverse association … between total cholesterol and incidence of infections either requiring hospitalization or acquired in the hospital” (Irribarren 1998).

Triglycerides and VLDL-cholesterol: the plot thickens

In the confusing maze of blood fats, there is a pattern which is associated with increased risk of heart disease: elevated triglycerides raise the relative risk of CHD considerably. “… an 88 mg/dl (1.0 mmol/L) increase in plasma triglyceride levels significantly increased the relative risk of cardiovascular disease by approximately 30% in men and 75% in women” (Cullen 2001). It is by now generally accepted that triglycerides are elevated by refined carbohydrates in the diet (Parks 2000), and that fasting triglycerides are a risk factor for heart disease. Ancel Keys, wrong in this as in so much else, heatedly dismissed these finding when they first appeared (Keys 1963). Right for the wrong reasons, he adopted the Cretan diet, retired to Tuscany and died in 2004 at 100 years of age (VanItallie 2005). Irritatingly, his flawed ideas live on, causing misery and premature death the world over.

High triglycerides combined with low HDL-cholesterol were found in heart-attack survivors, showing that “the ratio of triglycerides to HDL was a strong predictor of myocardial infarction … RR in the highest compared with the lowest quartile=16.0 …” (Gaziano 1997). Dr Gaziano is saying that our relative risk of heart attack is 16 times greater if we have both high triglycerides and low HDL-cholesterol. This pattern of blood fats is associated with insulin resistance.

It may help to understand how these different blood fats are related:

Total cholesterol = LDL-cholesterol + HDL-cholesterol + (triglycerides ÷ 5)

Triglycerides are themselves one-fifth cholesterol! LDL-cholesterol is actually a triglyceride- and cholesterol-delivery system, and LDL-cholesterol is what remains after very-low-density cholesterol, VLDL-cholesterol which is made in the liver, releases most of its triglycerides. This confusing naming system complicates matters until one is ready to throw up one’s hands – but to do this is to trust one’s health to people who don’t have our best interests at heart, so to speak. The point here is that elevated triglycerides, especially when combined with low HDL-cholesterol, pose an exceedingly serious threat to heart health, apparently considerably greater that any form of cholesterol, assuming that cholesterol is, in truth, any threat at all.

A further threat, one which is increased considerably by low-fat diets containing refined carbohydrates, is posed by remnant lipoproteins, which are what’s left after the triglyceride part of the lipoprotein has been taken up by cells (Jialal 2002). These so-called “small, dense” LDL remnants are elevated by high carbohydrate, low fat diets:

These results indicate that the effects of low-fat diets on lipoprotein metabolism are not limited to higher fasting plasma triglyceride and lower HDL cholesterol concentrations, but also include a persistent elevation in “remnant lipoproteins”. 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 CHO [carbohydrates] (Abbasi 2000).

It’s worth repeating: low-fat diets containing refined carbohydrates worsen atherogenic remnant lipoproteins. Dr Abbasi’s study compared low-fat diets (like the American Heart Association Therapeutic Lifestyle Changes Diet, which is prescribed to lower high cholesterol) with low-carbohydrate diets (like the Atkins diet). The main finding was that the low-fat diet actually elevated risk of heart disease. Oddly, we don’t hear much about this pattern of increased heart risk from low-fat diets, although, as we shall see, it is a consistent finding in studies which use refined foods among their carbohydrate sources. Remnant lipoproteins are violently atherogenic (Koba 2006) unless quickly removed from the circulation by the liver, and what’s important about this study is that it points out that carbohydrate in the diet causes a persistent elevation of these small, dense atherogenic remnant lipoproteins.

There is a profoundly important distinction here between simple carbohydrates, which are sugars, and starchy (complex) carbohydrates from, for example, whole grains. Starches are actually long chains of glucose molecules, and most starches are quite resistant to digestion so that their glucose enters the bloodstream more slowly than sugars. It’s quite clear that simple carbohydrates elevate triglycerides and small, dense LDL-cholesterol and lower HDL-cholesterol (Parks 2000), and that this pattern of fat in the blood is a virulent risk factor for heart disease (Wilson 2005). Starchy carbohydrates simply do not cause these blood-lipid changes at any level of consumption, no doubt in part because they come with the full complement of nutrients such as magnesium which are well-known to be protective.

It looks like “three strikes” for sugars. It’s worth repeating here, to underline the point, that a prospective study has found that the pattern of high triglycerides and low HDL-cholesterol (which can be caused by eating refined carbohydrates) confers a remarkable 16 times greater risk of heart attack (Abbasi 2000)! Interestingly, one way a sugary diet worsens this disturbance in the blood fats is via alterations of mineral levels within cells, which are also associated with insulin resistance. Now this is a worthwhile observation, for, as we shall see, there are simple dietary remedies. But I’m getting ahead of myself.

What the literature really shows

In the first actual clinical test of the low-fat diet (the Therapeutic Lifestyle Changes Diet is a low-fat diet) ever performed in its thirty-plus years, no benefit was found. This $415,000,000 study (funded with tax dollars) revealed that, after eight years:

The intervention was associated with increased risk in the 3.4% of women with baseline CVD [cardiovascular disease] … In conclusion, this long-term dietary intervention in postmenopausal women, intended to reduce fat intake and increase intake of vegetables, fruits, and grains, achieved an 8.2% of energy decrease in total fat intake but only a 2.9% of energy decrease in saturated fat intake and only modest increases in intakes of vegetables, fruits, and grains. The intervention did not reduce risk of CHD or stroke (Howard 2006).

In other words, the low-fat diet my doctor has prescribed for me neither increased nor decreased the risk of heart disease among most of the study participants, but for the 3.4 percent of trial participants with pre-existing cardiovascular disease, the relative risk of non-fatal and fatal CHD was actually increased by 26%!

Despite of the slick PR of the American Heart Association, there are many in the scientific community who simply do not subscribe to the cholesterol hypothesis. One such is Dr Uffe Ravnskov, an independent researcher who wrote The Cholesterol Myths. How is it that the world believes that cholesterol kills? Because the American Heart Association and the National Heart Lung and Blood Institute (one of the National Institutes of Health) between them fund over 90% of heart research, and they fund cholesterol research almost exclusively. Instead of dying a natural death, as defective hypotheses must for science to progress, cholesterol and its researchers are propped up on the life-support of practically unlimited funds! Science is very much like evolution in the sense that science depends on the survival of the fittest hypothesis. If defective hypotheses are favored for commercial reasons over fitter hypotheses, some may achieve commercial success but provide little in the way of useful strategies for preventing heart disease. This is to say that the cholesterol hypothesis is 100% wrong, but it lives because it sells a phenomenal amount of sugar-fortified low-fat foods and statin drugs.

What raises cholesterol?

Studies through the years have revealed what really causes high cholesterol: sugar, hypothyroidism, stress, and nutrient deficiencies.

A study funded by NASA to discover the best diet for astronauts found that sugar (but not glucose) profoundly elevated serum cholesterol:

Twenty-four felons aged from 24 to 43 years in the California prison system at Vacaville were fed a low-fat, 14% protein, chemically-defined diet containing carbohydrate calories either from 100% glucose, or 75% glucose with 25% sucrose. The decreases in serum cholesterol levels at the end of the first 4 weeks on the 100% glucose diet ranged from 9 to 49% of the baseline values, an average of 76mg%, and a significant change in the opposite direction occurred when the sucrose-containing diet resumed. There was very little fat in the diet, so that the experiment “unequivocally demonstrates an important relationship between the nature of the dietary carbohydrate and serum cholesterol levels” (Winitz 1970, Winitz 1964). This sugar-raises-cholesterol effect was confirmed in a more recent study which used an American-style diet containing 42% fat – cholesterol rose with time in a dose-dependent fashion when sugar was fed, but remained at baseline levels when carbohydrate was given as starch (Reiser 1979). A low glycemic index diet (meaning low in simple sugars (Wolever 1994) lowered cholesterol by 15% in six healthy male volunteers (Jenkins 1989).

Stress raised the cholesterol of tax accountants by an average of 20% around April 15^th(Friedman 1958), and all manner of emotionally-arousing events, from race-car driving to examinations provoke the same reaction (Dimsdale 1982). Correcting sub clinical hypothyroidism lowered LDL-cholesterol by an average of 8% in one study (Kahaly 2000). “Chronic magnesium supplementation produced a significant reduction of plasma cholesterol and LDL cholesterol, and an increase of HDL cholesterol” in Type 2 diabetics (Corica 1994). Taking vitamin C varied an experimenter’s cholesterol level between 230 and 140 mg% (Spittle 1971), and chromium given with niacin lowered LDL-cholesterol by 27% (Gordon 1991).

In summary, for 24 California felons, replacing sugar with starch lowered cholesterol, on average, by 76mg%. That this is likely an important determinant of our cholesterol levels because we eat, on average, 160 pounds of sugars annually – most of us eat our own weight in sugars each year! And since between 10% and 40% of us are sub clinically hypothyroid, most of us feel stressed, 56% of us eat diets with insufficient magnesium (USDA 2005), 30% suffer vitamin C-depletion (Hampl 2004) and almost all of us are depleted of chromium (because sugar causes both chromium and magnesium to be lost in the urine), it’s really not a surprise that many of us have high cholesterol. The really surprising thing is that we are not advised to abstain from sugar, neither are we tested for thyroid deficiency, nor are we prescribed vitamin C, magnesium, chromium, niacin or even prescribed security blankets for our stress when we consult doctors because of high cholesterol.

So does cholesterol really matter?

Dr William Castelli, director of the Framingham study, revealed in a moment of candor what he’d really found in the Framingham population. The Framingham study followed most of the residents of Framingham, Massachusetts, for many years, and revealed much of what we know, or think we know, about heart-disease risk factors. In 1992, Dr Castelli wrote to an obscure journal in response to a study (Fraser 1992) which had found raw nuts to be powerfully cardio-protective. The tone of the letter is tongue in cheek, and a careful reading of the letter itself suggests to me that he is bemoaning the tendency of epidemiological studies to throw up results which fly in the face of reason, such as, in his mind, findings which contradict the cholesterol-causes-heart-disease notion (Castelli 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 ... we found that the people who ate the most cholesterol, ate the most saturated fat, ate the most calories weighed the least and were the most physically active. ... In view of this, this study fails to describe a relationship of those traditional dietary constituents, saturated fat and cholesterol, known to have an adverse effect on blood lipids, and thereby, on the subsequent development of coronary disease end points.

Dr Castelli actually found no relation whatsoever between cholesterol or saturated fat and heart disease in the Framingham study, but he has the conviction of a religious zealot that the relationships exist! You can see the danger of funding research projects headed by a guy like this: No matter what he finds, cholesterol is the cause. It seems the entire cholesterol preoccupation and the dietary advice based upon it are nothing more than a marketing scheme employing the supposedly-disinterested American Heart Association as a mouthpiece to plant an erroneous belief so deeply in the minds of a generation that it has become the conventional wisdom.

Marketing disguised as science?

The fact is that some form of the worthless low-fat Therapeutic Lifestyle Changes Diet is the medical prescription for weight loss (66% of Americans are overweight), diabetes (7% have diabetes, and a further 40% have “pre-diabetes”) and heart disease (24%), and it is even suggested to healthy people for the prevention of disease! For example, the new, 2005 USDA Food Pyramid strongly promotes the low-fat diet to the public, but few of us have read the USDA mission statement: … a strategic plan [for] expanding markets for agricultural products [and] … further developing alternative markets for agricultural products. It is bizarre that the USDA should also be given responsibility for advising the nation on what to eat when it is also responsible for subsidizing corn, wheat, soybeans and cotton crops to the tune of $20bn per year and finding markets for all this bounty!

In the Food Pyramid fine print, I learn that if I follow this diet, I have 217 “discretionary” calories left over after I have achieved all the Recommended Daily Allowances for vitamins, minerals and the essential fatty acids. Discretionary calories are, according to the USDA, from refined foods, and 217 calories is equivalent to about 12 teaspoons of sugar which is the amount in one can of Coca Cola. Vanishingly few people in America eat as little sugar as this, for the average American eats about 50 teaspoons of sugar daily. But Heaven forbid that we should restrict a market for agricultural products! The USDA Food Pyramid fails us because it doesn’t explicitly condemn refined carbohydrates; it only advises that half one’s grain intake should be unrefined. And we are not warned that eating more than trivial amounts of sugar negates the benefit of the diet by guaranteeing nutritional deficiencies.

The low-fat Therapeutic Lifestyle Changes Diet has too many carbohydrates to work for insulin-dependent diabetes, or Type 2 Diabetes. And such diets do not work very well for weight loss: “within the United States, a substantial decline in the percentage of energy from fat consumed during the past two decades has corresponded with a massive increase in obesity” (Willett 1998), although low-carbohydrate diets probably do: “consumption of high-GI carbohydrates may increase hunger and promote overeating” (Roberts 2000). Low-fat diets provoke too much insulin secretion to be healthy in heart disease or, in fact, for anybody at any time. But what a clever way to market refined grain products, sugar and refined vegetable oils to the overweight, diabetics, heart victims and in fact the entire population: low-fat diets are prescribed for the very problems they cause! And, in a truly diabolical twist, the money that the food refiners have given to the various disease Associations to establish this useless diet as the standard of care is tax-deductible to them as a charitable contribution!

Nutrients: The missed clue

Dr Ancel Key’s original paper on total fat consumption and mortality from coronary heart disease cherry-picked among the countries for which data was available, apparently because this misrepresentation fit his graph more convincingly. Tragically, it is apparent from a plot of all the countries for which data was available that something other than fat consumption was affecting mortality. The countries with the lowest mortality were Ceylon, Japan, Mexico, Chile, Portugal and France, and their percentages of calories from fat ranged from 7% in Japan to 30% in France. What do these countries have in common? There are two island nations and Portugal (which has a very long coastline relative to its area) in which fish are prominent in the diet, four relatively undeveloped nations with largely unrefined diets, and one Western nation which prefers butter over refined vegetable oils. It begins to look as thought fish and unrefined foods could be important in the prevention of heart disease. The countries with the highest mortality were the United States, Finland, Australia, Canada, New Zealand and Israel; that these countries are among those with the most refined diets in the world (check out their sugar consumption) lends strength to the idea that refined foods contribute to heart disease.

The true tragedy of the entire cholesterol fiasco is that, buried in Key’s Seven Countries Study (in which Keys blamed saturated fat rather than total fat), there is the fascinating information that the heart death rate in Corfu is five times that of Crete. These neighboring Greek islands had diets which were identical according to laboratory assessments of the time. A similar disparity existed in neighboring counties in Finland, where the heart death rate in North Karelia was much higher than that of counties to the south which have the same demographic and diet. Keys obscured this clue by choosing the high death rate of North Karelia to represent Finland, and the low death rate of Crete to represent Greece. Had this intriguing hint been followed up, millions of lives might have been saved. It is quite certain that all this was not lost on Keys for he adopted the Cretan diet, as related in his book Eat Well and Stay Well (Doubleday 1959), and lived to be 100 years old.

Studies which have passed unnoticed since then reveal that the diet of Crete, but not that of Corfu, contains abundant purslane, a salad leaf which is rich in cardio-protective omega-3 fatty acids. And in North Karelia, the blood lipoproteins which transport cholesterol contain less vitamin E than those of the inhabitants of the southern counties, so that their LDL-cholesterol is at greater risk of oxidation. And the water supply of North Karelia is softer, meaning that it contains less cardio-protective magnesium than the water in the south. It remains to be seen whether these nutrient differences explain the difference in heart deaths. But I’m getting ahead of myself again.

Albert Einstein

Yet there is dissent. The prestigious magazine Science published an article by journalist Gary Taubes entitled The Soft Science of Dietary Fat in 2001, and the Journal of American Physicians and Surgeons published Anthony Colpo’s LDL Cholesterol: “Bad” Cholesterol, or Bad Science? in 2005. The articles question the science behind current dietary recommendations and outline their commercial motivations, and indeed question the motives of the organizations promulgating the recommendations. Although these are scientific journals, these men are not researchers and therefore do not rely on the research funding sources which, in effect, gag researchers who must obtain future funding. It seems that scientists must let others speak for them if they wish to stay in the game.

I think statins and the Therapeutic Lifestyle Changes Diet are dangerously stupid. But I’m intrigued by the Kitava Islanders freedom from heart disease, and with Dr Weston Price’s observation that diverse healthy populations lived on wildly different diets having in common only that each was composed of whole foods. The industrial revolution started a migration to the cities, which, in turn, created a demand for foods with “shelf-life”, foods which can be transported and stored without spoilage. Whole foods, fresh from the fields or the sea, were replaced by processed and preserved foods of lesser nutritional quality: refined foods. What happens to a food when it’s refined?

Food refining causes nutrient losses

Since at least 20% of the average citizen=s calories come from sugar, with perhaps another 30% from refined flour and alcohol which have much or all of their vitamins and minerals refined out of them, few of us actually consume a balanced diet. The amounts of 21 nutrients lost in the refining of the 1200 calories of sugar and refined flour in the average citizen’s diet are easily calculated to lie between 95% (magnesium) and 58% (selenium). We’ve thrown away the wrong parts of the food!

Comparing the National Center for Health Statistics dietary data to the government’s suggested Dietary Reference Intakes suggests that many of us don=t achieve even the Recommended Dietary Allowance of calcium, folic acid, fiber, or magnesium. One in three of those surveyed had vitamin C deficiency or depletion, and between 20% and 90% (depending which study you favor) don’t take in sufficient vitamin B6. Refining removes twice the RDA for magnesium, and fully 56% of us don’t get even the RDA from our diets. Five times the RDA of folate is lost (the “enrichment” of the flour does not replace all that is taken out), and the elevated homocysteine level of half the population tells us they don’t get enough folate, even if we’re technically not deficient in it. The list goes on.

Left: Nutrient loss during flour refining; Right: One in three of us are low in vitamin C! (Figure from Hampl)

Incredibly, this is not news. Although it seems scandalous to me, I did not learn of it on CNN. It is not even new, for it was remarked on in the 1939 US Department of Agriculture Yearbook:

The chief fault of many American diets is that they provide too little of the essential minerals and vitamins. This fault is due in large measure to the fact that refined foods are consumed in such amounts that the intake of mineral and vitamin rich natural foods is lower than it should be (Food and Life, USDA Yearbook, 1939)

What effect does this have on us? If whole foods carry with them the nutrients needed for their metabolism and refined foods do not, common sense suggests Dr Weston Price was right in his belief that it’s the lack of the missing nutrients that causes disease. With this organizing principle in mind, let us look to the scientific literature. This is really easy to do this, by the way, thanks to your tax dollars at work. I simply enter the query in the National Library of Medicine database and it returns the abstract of the article. If I want to read the whole article, I can order it through the delightfully-named Loansome Doc service.

I particularly like Harvard epidemiologist Dr Walter C Willett’s population studies because they look at what people are eating (or not eating), and if they get, say, heart disease in the following years. Of course, such studies cannot prove that dietary deficiencies cause heart disease, but they can show if they are fellow travelers with some unknown cause. So I enter “Willett WC, vitamin E CHD” (or whatever the current nutrient of interest may be) and discover a wealth of information.

Often, the results of these studies are presented as “relative risk” of heart disease, which is the ratio of the incidence of whatever’s being investigated in the groups taking in the highest and lowest levels of a nutrient (Barratt 2004). Thus, in Dr Eric Rimm’s study (in which Dr Willett participated) of “Vitamin E Consumption and the Risk of Coronary Heart Disease in Men”, the study participants were divided into five groups. Over the four years of the study, the quintile taking in the least vitamin E developed coronary heart disease at the rate of 19.4 per 1000 people, while the incidence among those taking the most was 14.4 per 1000 people. The relative risk is the ratio of 14.4 ¸ 19.4, which is 0.74 (which may also be stated as a relative risk reduction of 26%).

Individuals poorly nourished in E developed CHD at the rate of 0.49%, close to the 0.5% rate found by the American Heart Association for a 60-year-old male, which is perhaps unsurprising since 93% of the population consumes less than the RDA for vitamin E (USDA 2005). The absolute risk reduction was that 5 fewer people per 1000 developed CHD over the four years of the study in the high intake group compared with the low intake group; thus, individuals well-nourished in vitamin E had an absolute risk reduction of (5 ÷ 4) or 0.13% per year. This absolute risk reduction of 0.13% therefore represents about one third of the risk of CHD for a 60-year-old male, a considerable proportion.

Thus, the absolute risk says whether the problem is clinically significant in the study population, and the relative risk indicates how effective the intervention is. The relative risk reduction of 26% looks impressive, but is essentially meaningless without the absolute risk figure of 0.49% which means being well-nourished in vitamin E halves the risk of CHD. Together, they answer the question: is the effect of vitamin E large enough to be clinically important? When the absolute risk reduction is small, as in the statin studies, the relative risk reduction numbers have little clinical significance, however large they may be. But when the absolute risk is large, the relative risk reduction is meaningful and provides guidance on how effective the intervention is.

I have listed a number of such studies in order of their clinical relevance. Why these particular Rag, Tag and Bobtail studies? Mainstream studies play down the risks and exaggerate the benefits of drugs, advocating almost useless cholesterol treatments on study outcomes which failed to reach significance; drugs which do not offer a remedy for what ails me. Mainstream nutritional recommendations have clearly done more harm than good; but, by contrast, I believe these few studies actually show which way the wind blows.

Nutrients lower Cardiovascular Disease risk

Nutrient

How many have

“low nutrient

status”?

Amount,

Study population;

Study duration

Absolute Risk

high-intake group (hi)/year

Absolute Risk

low-intake group (lo)/year

Relative Risk

(hi/lo)

Absolute Risk Reduction/year

(hi – lo)/duration

Carotenoids

(Gaziano 1995)

44%

(USDA 2005)

<0.8βcarotene foods>2.05/svgs/day

Elderly subjects; 4.75 years

2.23%

4.53%

0.54

(0.49)

2.3%

CVD death

Magnesium

(Singh 1990)

67% of adults

(USDA 2005)

1142mg vs. 418mg

High-risk adults; 10 years

0.93%

1.6%

0.6

(0.6)

0.63%

CHD death

Vitamin C

(Enstrom 1992)

40%(M) 32%(F)

(Hampl 2004)

>800 vs. <50mg

Adults; 10 years

0.91%

1.3%

0.65(M)

(0.69%)

0.42%

CVD death

Omega-3 fish oils

(Mozaffarian 2003)

US: 0.01- 0.02g/day Desirable: 0.65g/day

(Kris-Etherton 2000)

≥3/wk Fish meals <1/mo

(not fried or fish sandwich)

Subjects ≥ 65 years; 9.3 years

0.35%

1.1%

0.28

(0.32)

0.76%

Sudden CHD death

Sodium

(Tuomilehto 2001)

90% > UL* of 2.3g

(FNB 2004)

<3.64 vs. >6g/day in urine

Finnish men; 10 years

0.72%**

0.5%**

1.38

(1.43)

0.22%**

CVD death

Potassium

(Bazzano 2001)

>97%

(USDA 2005)

>2.67 vs. <1.37 g/day

Adults; 19 years (AI=4.7 g)

0.38%

0.62%

0.72

(0.61)

0.27%

Stroke

Vitamin E

(Rimm 1993)

93%

(USDA 2005)

>60IU vs. <7.5IU (M)

Adult men; 4 years

0.36%

0.49%

0.64(M),

(0.74)

0.13%

New CHD

Sedentary lifestyle

(Tanasescu 2002)

88% are sedentary

(Reeves 2005)

Most vs. least exercise

Adult men; 12 years

0.25%

0.41%

1.72(M)

(1.62)

0.17%

New CHD

trans-fats

(Ascherio 1996)

US 5.8g/day

(USDA 2006)

4.3 vs. 1.5g/day (M)

Adults; 6 years

0.38%

0.25%

1.43(M)

(1.5)

0.13%

New CHD

Hypothyroidism

(Barnes 1972)

10-40%

(Barnes 1972)

1-4gr vs. 0gr Armour thyroid vs. Framingham pop.; 20 years

0.01%

0.22%

0.06

0.9%

New CHD

Glycemic Load

(Liu 2000)

US sugar: 146lb/yr

(USDA 2004)

206 vs. 117

Adult women; 10 years

0.09%

0.13%

1.98(F)

(1.37)

0.04%

New CHD

Folate

(Rimm 1998)

88%

(Subar 1998)

696 vs. 158µgm

Adult women; 14 years

0.06%

0.11%

0.69(F)

(0.58)

0.05%

New CHD

Folate and B6

(Rimm 1998)

High folate and B6 give lowest RR

Folate 696 vs. 158µgm +

B6 4.6 vs. 1.1mg/day

0.55(F)

New CHD

Vitamin B6

(Rimm 1998)

71%(M) 90%(F)

(Kant 1990)

4.6 vs. 1.1mg/day

Adult women; 14 years

0.06%

0.09%

0.67(F)

(0.62)

0.04%

New CHD

6.1%

Relative Risks are controlled for age, smoking and other risk factors in most studies and may therefore differ from “(hi/lo)”. Absolute Risks are from the raw data, the number of deaths or new cases in each group. *Tolerable Upper Intake Level. **Estimated assuming a linear dose-response relationship.

The most striking thing about this table is that nutritional deficiencies are so widespread as to constitute a public health scandal. My nutritional status simply hasn’t come up in my medical examinations, yet these studies imply that if I am well-nourished in these eight essential nutrients and avoid unhealthful practices, my risk of the various troubles subsumed under the rubric of cardiovascular disease may be reduced by 6.1% per year.

Carotenoids from vegetables together with magnesium and vitamins B, C and E found in whole foods, along with avoiding hypothyroidism and eating fish, are associated with lowered rates of cardiovascular disease. Of course, the iodine which helps prevent hypothyroidism comes with the package if ocean fish are eaten. Sugar and trans-fats (the man-made fats in margarines and refined vegetable oils), and pursuing a sedentary lifestyle add to the risk of heart disease.

The American Heart Association 2005 Statistical Update shows that the ten-year risk of developing cardiovascular disease (which includes coronary heart disease) for a male aged 60 years is 15.6%, about 1.56% per year. This figure is simply dwarfed by the 6.1% risk reduction afforded by attending to just eight of the 44 essential nutrients, exercising and avoiding junk food. And in the study of folate and vitamin B6, being replete in both nutrients improved the relative risk of developing CHD from 0.67 to 0.55, so synergy is at work here too: the more nutrients we are replete in, the better our chances.

Furthermore, other essential nutrients certainly contribute to CVD risk; vitamin D, for example, is insufficient in about half the population, and low levels are associated with high blood pressure, impaired fasting glucose and overweight (Martins 2007). Nobody has yet performed a prospective population study to discover the strength of its association with heart risk, but there is no question that it exists. Thus, the annual absolute risk reduction from an unrefined diet and healthy lifestyle is at least 6.1%. Can it really this simple? Is this the “secret” of the Kitava Islanders robust good health?

Once you eliminate the impossible, whatever remains, no matter how improbable, must be the truth

Sherlock Holmes

A Note on Causation

These epidemiological studies suggest that attending to nutrition and avoiding refined foods will drastically reduce the risk of CVD, but they cannot prove that poor nutrition causes CVD. In science, a causal relationship is established if there is a plausible mechanism, a dose-response relationship, consistency across populations, and verification by clinical trial. This is a summary of Dr Bradford Hill’s criteria for causation, which were used, for example, by Sir Richard Doll when he established that smoking causes lung cancer.

The studies in the table above support dose-response relationships between nutrients and susceptibility to CVD. Interestingly, the dose-response relationship between impoverished Western food and degenerative disease is relentlessly detailed in the World Health Organization report Diet, Nutrition and the Prevention of Chronic Diseases, which also establishes consistency across populations. As refined foods enter the diets of undeveloped countries, so too does CVD and rest of the Western degenerative diseases. Papua, New Guinea, is an example, with heart disease well established in the capital, Port Moresby (although it was unknown there until 1964), and just beginning to be found in outlying areas. The observations corroborate and extend Dr Weston Price’s 1930s studies referred to earlier.

The great natural experiment of the Kitava Islanders might be said to satisfy the requirement for verification by clinical trial. Here is a population which has not been exposed to Western foods, and which is free of cardiovascular disease and free also from the cancers and dementias which afflict so many in the West.

The final requirement: plausible mechanisms. Many plausible mechanisms are already established. After all, essential nutrients are those we can’t live without. As I read with increasing fascination the obscure research which suggests nutrients may be more effective than drugs, I learned of many plausible mechanisms I’d never dreamed of. Just as pulling a woolen thread can unravel the entire sweater, I found that, far from being the implausible imaginings of wild eccentrics, there is consistent, solid science underlying the links between lousy food and degenerative disease. One such link is insulin resistance in which the muscles, fatty tissue and the liver lose their capacity to take in glucose from the blood when stimulated by insulin. To preserve blood sugar levels in the normal range, the amount of insulin in the circulation rises so that a state of hyperinsulinism follows. The link between heart disease and insulin resistance is that some two thirds of heart patients are insulin resistant

Almost all individuals with Type 2 Diabetes and most with hypertension, cardiovascular disease, and obesity are insulin resistant, and, ominously, more than 40% of the remaining supposedly healthy individuals have it by age 70 (Ford 2002). This means that insulin resistance is a chronic progressive condition that almost all of us are incubating. Worse, the associated high insulin level is a “very good predictor of the development of CHD” (Moller 1995), conferring a relative risk of 2.2 for the development of coronary heart disease (Feskens 1994).

Insulin Resistance

I had always thought that nutritional deficiencies impaired the immune system (say), or crippled the antioxidant defense system, or that they elevated homocysteine that damaged the arterial system – that they affected some bodily system.

However, these various dietary faults all worsen insulin resistance at the level of the cell, the fundamental unit of all bodily systems. Insulin resistance contributes to heart disease: people with Coronary Heart Disease were found to have 64% worse insulin resistance than normal subjects. People with impaired glucose tolerance and Coronary Artery Disease had 98% worse insulin resistance than people with Impaired Glucose Tolerance but no Coronary Artery Disease – the “data suggest that in patients with CAD, insulin-mediated glucose metabolism is significantly impaired, and a significant correlation was noted between insulin resistance and severity of CAD” (Shinozaki 1996). In a study of 154 people referred for coronary angiography, the most insulin-resistant were nearly twice as likely to have CAD as those who retained their sensitivity to insulin (Quadros 2007):

The fasting blood sugar figures on the graph show a continuous relationship between the severity of CAD in this symptomatic population from low-normal (<88mg%) via Impaired Glucose Tolerance (100-125mg%) to diabetic (>126mg%); insulin resistance increases the incidence of CAD.

Moreover, insulin resistance predisposes to the other Western degenerative diseases: hypertension, obesity, diabetes and cancer. Remarkably, pieces of this puzzle rarely come together so the true picture can be seen: degenerative disease usually starts with insulin resistance!

On Kitava, remember, insulin levels actually fall with age. In the figure below, the hatched area shows how insulin rises with age in Swedes while the line shows that the Kitava Islanders’ insulin resistance falls with age. Unlike the Swedes, the Kitava Islanders retain their sensitivity to insulin with age, and have no degenerative disease (Lindeberg 1999):

Another clue is that healthy Western centenarians retain childhood’s high sensitivity to insulin (

	WOSCOPS Pravastatin	CARE Pravastatin	AFCAPS/TexCAPS Lovastatin
	Healthy people; High cholesterol	CHD patients; Normal cholesterol	Healthy people; Normal cholesterol
Non-fatal CHD events: Drug Group/Control Group	143/204	135/173	116/183
Relative Risk of Non-fatal CHD	-22%	-22%	-38%
	Significant	Significant	Significant
Deaths from CHD: Drug Group/Control Group	38/52	96/119	11/15
Relative Risk of CHD death	-27%	-19%	-27%
	Not significant	Not significant	Not significant
Deaths from all causes: Drug Group/Control Group	106/135	180/196	80/77
Change in Absolute Risk of Death (%)	-0.9%	-0.77%	+0.09%
	Not significant	Not Significant	Not Significant