Heart disease is the leading cause of death in the developed world. Although this disease employs more doctors than any other branch of medicine, recent discoveries show some fundamental flaws in our understanding of it-particularly the basic view, held by all of medicine, that fatty foods and high cholesterol are the main culprits.
The established view of coronary heart disease (CHD) rests on three proposi-tions:
1) CHD is mainly the result of a high-fat diet;
2) high fat intakes lead to cholesterol in the blood, which sticks to arterial walls, causing heart disease; 3) cholesterol-reducing drugs (statins) save lives.
These three foundation stones of the heart-disease 'industry' comprise an informal, but mutually reinforcing, alliance of cardiologists, food manu-facturers and drug companies. How-ever, more and more doctors believe that the whole edifice is, if not yet crumbling, then certainly built on unsafe ground, for there's growing evidence that all three propositions are, quite simply, wrong.
The received wisdom is that 'saturated fats'-mainly from animals-are the major culprits in CHD. The origin of the theory goes back to the 1950s, when US nutritionist Ancel Keys did an international comparison of food intake and disease. Focusing on only six countries, he found that the ones with the highest per capita fat consumption had the highest rates of CHD (Lancet, 1957; i: 959).
From these limited data, medicine developed the whole saturated fat ? cholesterol ? atherosclerosis ? CHD hypothesis. But the data were incom-plete. We now know that if Keys had included data from 22 countries (also available at the time), the fat-CHD connection would have disappeared.
Later alerted to the error, Keys tried to retract his earlier conclusions, but to no avail. His theory had already taken root within medicine as well as the food industry, where the low-fat revolution was already in full swing, promoting cheap, low-fat, processed foods as the new 'healthy' way to prevent heart disease.
High fat vs low fat
One piece of evidence often used to support the fat-cholesterol-CHD con-nection is the Framingham Heart Study (from a small town in Massachu-setts where the health records of its 6000 population have been collated every five years for the last half-century). However, the small-print data are often neglected for, although a link between total blood cholesterol and risk of CHD has been found, there is no connection between fat intake and cholesterol-in fact, quite the reverse. As Framingham study director Dr Will-iam Castelli observed, ". . . the more saturated fat and cholesterol one ate, the lower the person's blood choles-terol"(Arch Intern Med, 1992; 152: 1371-2).
That revelation has recently been buttressed by a little-known clinical study that has further blown a hole in the conventional theory. Doctors at Duke University compared the effects of two strict diets on 120 overweight people with high blood-cholesterol levels. For six months, 60 of them followed a low-fat/low-cholesterol diet, the rest followed a low-carbohydrate diet that allowed "unlimited amounts of animal foods . . . and eggs", plus a few selected low-carb vegetables.
On analysis, the researchers found that the low-carb dieters chose to eat so much meat that, on average, they consumed a staggering average of 68 per cent of their daily energy intake from fat. And yet, after six months, their blood triglycerides (fats) were actually lower than before and, even more surprising, lower than those on the low-fat diet. What's more, although their cholesterol levels were higher, it was mainly the 'good' HDL cholesterol that increased, with only insignificant rises in the disease-related, 'bad' LDL cholesterol. The high-fat dieters also managed to lose twice as much weight as the low-fat dieters (12.9 vs 6.7 per cent, respectively) (Ann Intern Med, 2004; 140: 769-77).
The CHD-cholesterol story took another fascinating turn that further twisted the knife in the conventional theory. It's been known for some time that it's not the total cholesterol that's important, but the ratio of HDL (high-density lipoprotein) to LDL (low-density lipoprotein) cholesterol. The higher the relative levels of HDL, the lower the risk of CHD.
A further discovery is that there are two types of LDL, one of which is more CHD-related than the other. The key may not be so much density as size:
the smaller the LDL particle, the deadlier it is. Researchers divided LDL into phenotypes A (big and relatively harmless) and B (small and 'bad').
And once again, a high-fat diet is the winner. In a study by the prestig-ious Lawrence Berkeley National Laboratory in California, researchers found that a 20-per-cent-fat diet given to healthy men produced around 50 per cent LDL(B)s in the blood, but this fell to 20 per cent when the diet was 45-per-cent fat. So, there's a clear inverse relationship between dietary fat and 'bad' LDL(B)s. They also found that the lower-fat diets converted many of the men's harmless As into deadly Bs (Am J Clin Nutr, 1999; 69: 411-8).
It's evident that cholesterol is not the simple story we've been led to believe it is-nor is the idea that 'fat leads to heart disease'. The most crushing blow so far was delivered by Swedish doctors, on announcing the results of a five-year study of nearly 30,000 middle-aged people in Malmo. Looking at fat intake and deaths-particularly from cancer and heart disease-the only correlation they found was with female cancers, where a high-fat diet appeared to be harmful.
But with heart disease or deaths in general, no links were found. High fat intakes were not associated with higher death rates-in fact, quite the reverse. The highest fat intakes resulted in the fewest deaths-and vice versa. "Cur-rent dietary guidelines concerning fat intake are generally not supported by our results," they concluded-in other words, the official advice to keep total dietary fat below 30 per cent and saturated fats below 10 per cent is sim-ply wrong (J Intern Med, 2005; 258: 153-65).
The Swedish experience is mirrored in many other countries and popula-tions, with high-fat diets showing either beneficial health effects or, at least, no adverse ones (see box, page 8).
Clearly, a total rethink is needed regarding fats, cholesterol and health.
High fat and healthy
A few enlightened doctors are already speaking out in defence of fats, recognizing that the conventional anti-fat health message is topsy-turvy. "We need a lot of fat," says neurologist Dr Russell Blaylock. "Fats form many of our hormones, allow our cells to com-municate, make up cell membranes, comprise 60 per cent of the brain and enhance immunity, just to name a few of their benefits."
In fact, the kind of fat the body itself makes is saturated; it's used as a vital store of energy, and some recent research has shown that the body needs an intake of saturated fats to help utilize its own fat stores (FASEB J, 1988; 2: A852).
There's also new evidence that high-fat diets can help neurodegenerative disorders such as Alzheimer's and Parkinson's-in fact, in a "broad range of disorders involved with the death of brain cells" (Behav Pharmacol, 2006; 17: 431-9). Conversely, low saturated-fat levels can cause fatigue, poor concen-tration and depression. The reason is thought to be a lack of cholesterol, as the serotonin receptors in the brain need cholesterol to function properly (Br J Psychiatry, 2000; 176: 398-400).
Cholesterol too, like fat, has many other important functions. Far from being an enemy to the body, as conventional thinking holds, choles-terol is a valuable substance made by the body itself. Little of the cholesterol in our blood comes directly from food; most of it is made in the liver. That's because cholesterol strengthens cell membranes and intestinal walls, makes bile, and is vital for hormone and vita-min production. It may even act as an antioxidant and boost immunity.
Small wonder that "people with high cholesterol live the longest," says medical researcher Dr Uffe Ravnskov. "This statement seems incredible, but its truth emerges clearly from many scientific papers-particularly studies of the elderly." One was done by Yale University, and found that old people with high cholesterol had half the number of deaths from heart attack as their low-cholesterol peers (JAMA, 1994; 272: 1335-40).
In another first-class study, doctors from London's Imperial College found that high cholesterol levels protected people with chronic heart failure, leading to dramatic reductions in death rates. "The chance of survival increases by 25 per cent for each mmol/L [38.6 mg/dL] increment in total cholesterol," they reported (J Am Coll Cardiol, 2003; 42: 1933-40).
In Holland, scientists have been studying the 200-year-long records of two families with genetically high levels of cholesterol, and found no increase in deaths compared with those without the condition (BMJ, 2001; 322: 1019-23).
So, is there no connection between heart disease and cholesterol levels? Yes, there is, but the data are not nearly as consistent as the established view makes out, with a substantial minority of clinical studies showing an inverse relationship: less cholesterol, more heart attacks. In fact, over 60 per cent of all heart attacks occur in people with normal cholesterol, and most of those with high cholesterol never suffer heart attacks at all. "Consider the fact that more than 90 per cent of all cardiovascular disease occurs in people above age 60," says Dr Ravnskov, " and that almost all studies have found that high cholesterol is not a risk factor for either women or old people. This means that high cholesterol is only a risk factor for less than 5 per cent of those who die from a heart attack."
And yet, CHD is increasing, and has been for nearly a century. So, if neither fat nor cholesterol is the culprit, then what is?
A processing problem
Many nutritionists are now pointing the finger at modern processed food. "It's a little known fact that, before 1920, coronary heart disease was rare in developed countries like America," says pioneering nutritionist Dr Mary Enig, of the Weston Price Foundation, "but it rose dramatically over the next 40 years. If, as we have been told, heart disease results from the consumption of saturated fats, one would expect to find a corresponding increase in animal-fat consumption. Actually, the reverse is true. In America, for exam-ple, during the period from 1910 to 1970, there was a significant decline in the proportion of traditional animal fat in the national diet."
Enig has shown that the rise of heart disease corresponds with the intro-duction of polyunsaturated plant oils into foodstuffs. Invented in 1916, margarine was the earliest and best-known example, but thousands of common foods soon followed suit. "One reason the polyunsaturates cause health problems is that they become oxidized when subjected to heat, as in food processing, and produce free rad-icals," says Enig. "These are extremely reactive chemically, causing damage to blood vessels and initiating athero-sclerosis."
The most harmful industrial food-processing technique is thought to be hydrogenation, a procedure designed to transform polyunsaturated plant oils into compounds resembling animal fats (see box, page 8). The problem is that hydrogenated oils contain large quantities of toxic trans fatty acids (TFAs), ubiquitous in processed foods of all kinds.
Enig believes it's not animal fats, but hydrogenated oils and their TFAs that are primarily responsible for the rise in heart disease, a conclusion at least partially endorsed by a recent top-level survey. Nine months ago, researchers at the Harvard School of Public Health reported on their analy-sis of at least a decade's worth of data on trans fats intake and heart disease, and dropped a bombshell on both the food industry and CHD research.
"TFAs have a major role in heart disease," announced survey director Professor Walter Willetts. "The magni-tude of the association with CHD is considerably stronger than for satura-ted fat."
TFAs, he showed, have particularly nasty effects: raising triglycerides and 'bad' LDL cholesterol; reducing 'good' HDL cholesterol; and causing inflam-mation in the arteries-all of which are known to provoke CHD (N Engl J Med, 2006; 354: 1601-13).
What's more, there's now objective physical evidence of the damage TFAs can do to the arteries. In a little-publicized study, British researchers examined the arteries of people who had died of CHD, and found the tell-tale fatty deposits on the artery walls.
But their analyses of these deposits were another blow to the high-fat-CHD theory as it was revealed that the plaques contained no saturated fats at all and hardly any cholesterol, but were filled with masses of polyun-saturated fats and TFAs (Lancet, 1994; 344: 1195-6)-findings that have been confirmed by researchers in Poland (Eur J Nutr, 2004; 43: 313-8).
There's one more crucial piece of the jigsaw. After some painstaking detective work in the heart-disease research archives, Dr Enig discovered that, until the mid-1980s, researchers didn't discriminate between saturated fats and TFAs, lumping them both together in their diet analyses (J Am Coll Nutr, 1990; 9: 471-86). "Thus, histori-cally, natural saturated fats have been tarred with the black brush of un-natural hydrogenated vegetable oils," she says. So, the circle can now be squared, and puzzling paradoxes answered. Why do so many recent studies find no correlation between high saturated-fat intake and CHD, or why do many populations with high fat intakes have such little heart disease? The answer is simple: no TFAs = no CHD . . . QED.