The low-fat fallacy

The connection between dietary fat and disease is so entrenched in our thinking that it has spawned a multimillion-dollar processed-foods industry, informed the dietary advice given by doctors to generations of heart patients and permeated our collective consciousness.

Low fat is a mantra so often repeated over so many years that few of us can take a bite of full-fat anything without feeling just a little guilty. 

Indeed, this certainty over the role of fat and heart disease transformed our dairy industry from one that once applauded fresh whole cream to one in which the ‘best’ milk is utterly denuded of its essential components.

We’ve spent decades ripping the fat out of all of our food, only to discover that it is the removal of fat that is the problem.
The latest evidence, from a number of new studies on prostate cancer, shows a link between a high consumption of dairy products and cancer of the prostate. Careful exam-ination of these studies demonstrates that the major culprit, in most instances, is a high consumption of low-fat milk.

Problems with low-fat milk are now surfacing in many quarters, particularly in hormone-related disturbances. Besides prostate cancer, it’s now been linked to infertility and ovarian cancer.

The greatest irony of all is the evidence that low-fat milk is also associated with heart disease in men, the very population first targeted as being the main victims of high-fat foods.

Ancel Keys is credited with first postulating the ‘fat-makes-you-fat’ thesis in the 1950s (Lancet, 1957; i: 959–66). In research now referred to as the ‘Seven Countries Study’, he examined the fat intake of seven countries, and allegedly demonstrated a clear correlation between mortality from coronary heart disease and percentage of calories from dietary fat.

From this extraordinarily limited data, medicine first hypothesized that a high dietary intake of fat caused a high level of cholesterol in the blood which, in turn, furred up arteries, eventually leading to a heart attack or stroke. According to this reasoning, heart disease could largely be prevented by limiting fat intake.

A number of researchers have now demonstrated that the original study was hopelessly flawed. At the time of Keys’ research, data from 22 countries was available. If the fat intake from all those countries had been factored in, no such correlation would have been demonstrated.

Indeed, in 1998, William Grant published a review of all the epidemiological evidence concerning diet and heart disease, and also carried out his own researches, examining heart disease and the dietary habits in 32 countries (Altern
Med Rev, 1998; 3: 281–94). After having done his statistical analyses, he discovered that the food with the highest association with coronary heart disease in men over the age of 45 was non-fat milk. 

Other studies support Grant’s findings. For instance, increased levels of bovine substances have been found in the arteries of people with atherosclerosis. Researchers have determined that arterial plaque is rich in calcium and that, without the softening effects of milk fat, calcium has a deleterious effect. Still others find that lactose, present in high amounts in non-fat milk, also contributes to the formation of arterial plaque. 

Other aspects of the processing of milk may also be implicated in heart disease. One researcher, for instance,  postulated that heat-denatured bovine immunoglobulin could be a risk factor.

In low-fat milk, we have yet another instance of a crime against nature. Once again, in our arrogant insistence on tinkering with natural foodstuffs, we have inadvertently created a health crisis. At some point, perhaps we’ll
learn that whenever we attempt to ‘improve’ on food, we end up paying for it.

Lynne McTaggart