Why claims of coronary heart disease caused by saturated fat and cholesterol is false?


Over the last forty years, billions of dollars have been allocated to research examining the link between , and heart disease. Despite the staggering amounts of money and time that have been poured into this undertaking, no direct role for these substances in the causation of cardiovascular disease has ever been established. The saturated fat and hypothesis remains just that a hypothesis.

As you shall learn throughout this article, there exists a massive volume of scientific evidence that completely absolves dietary cholesterol, saturated fat, and elevated blood cholesterol of any harmful role in heart disease. This evidence does not stern from a small group of ax-grinding fringe lunatic researchers; some of the most damning evidence against the mainstream anti-cholesterol dogma comes from research that has actually been funded and conducted by the mainstream itself.

Despite the fact that this contradictory research has been published in prestigious, peer-reviewed medical journals, and despite the complete failure of the massive low-fat, anti-cholesterol campaign to lower the overall incidence of heart disease, the cholesterol/saturated fat theory of coronary disease enjoys almost unanimous acceptance among health authorities. These are the same “experts” that most of us look to for credible, scientifically-sound advice on matters pertaining to diet and health; the same experts who design nutrition guidelines, who tell us whether a particular is “heart-healthy” or harmful, and who set the prescribing guidelines for cholesterol-lowering drugs.

The Decline in Heart Disease that Never Was

It is these same authorities who repeatedly tell us that the death rate from () climbed rapidly during the twentieth century, reached a peak in the late 1960s, then began a gradual decline that continues to this day. The rise in mortality, so the story goes, was primarily a result of America’s predilection for fatty foods-especially those high in “artery-clogging” saturated fats. While the increase in has been attributed to the nation’s gluttony, the subsequent fall in heart disease mortality was, allegedly, a direct result of public awareness campaigns that steered people away from saturated fats and towards “healthy” low-fat foods.

These promotional efforts lowered the population’s blood cholesterol and blood pressure levels, reduced the rate of smoking, and provided a shining example of how both government and private health agencies could work together in harmony and save millions of lives in the process.

That is the official version of events. It is, quite frankly, a self-serving fantasy.

It is only natural that health authorities would like us to believe that they were the prime movers behind any drop in CHD because they have spent astounding amounts of our money researching and promoting dietary measures purported to fight this ubiquitous killer. The National Institutes of Health, the government’s foremost diet, and medical research agency is without question the world’s biggest spender on diet-heart disease research. The NIH has fervently spent well in excess of a billion taxpayer dollars trying to implicate saturated fat and cholesterol in the causation of heart disease, so far without any success whatsoever.

The American Heart Association (AHA), the first prominent health organization to officially embrace the lipid hypothesis, is an incorporated entity with assets totaling over one billion dollars and revenue that exceeds 650 million dollars per year(l). Of this, 540 million dollars is derived from public support, while another 115 million dollars is earned through activities that include the sale of educaţional materials and the lucrative ‘heart check’ program.

The latter is a licensing agreement in which food manufacturers can capitalize on the AHA’s ‘credibility’ by paying a first-year fee of $7,500 per product, and a subsequent annual renewal fee of $4,500 per year. This permits them to display the Association’s logo on their product labels and to market their wares as ‘heart-healthy'(2). Despite its ‘non-profit’ status, top-level executives at the AHA receive six-figure salaries that would be the envy of many CEOs heading for-profit firms; during the 2005 fiscal year, the AHA’s CEO, M. Cass Wheeler, received a hefty $656,608 in compensation. Remuneration to the AHA’s five Vice-Presidents ranged from $249,235 to $414,928(3).

Clearly, fighting CHD is a big business. And there is nothing worse for business than the realization by customers that one’s products and services are ineffective. Imagine the potenţial financial repercussions for an organization that has invested heavily in a product or service of questionable worth, that has unwisely promoted the new offering with unbridled enthusiasm, and has begun to draw criticism from some quarters that it acted prematurely.

To compound this organization’s woes, published scientific findings have emerged which strongly suggest these critics are correct. Imagine further that this entity has no foreseeable way of improving upon this product or service. Impending doom, in terms of prestige and financial loss, is a very real possibility—unless of course, the entity in question can prevent the paying public from ever discovering that there was anything wrong with its offering in the first instance.

This is the exact situation in which promoters of the saturated fat and cholesterol theory of CHD have found themselves for the last four decades. Despite massive propaganda efforts to convince the medical profession and public alike of the validity of their theory, numerous independent commentators over the years have questioned its scientific tenability. In order to counter such concerns, the reigning health orthodoxy has formulated several key arguments that have been repeated with such prolific frequency they are now deeply ingrained in the public psyche. As a result, they have come to be accepted by much of the population as self-evident facts.

The notion that increasing saturated fat consumption precipitated an ‘epidemic’ of CHD, and that the low-fat, anti-cholesterol campaign has played a major role in reversing this epidemic, is one such ’fact’. The ubiquity of this myth is sad testimony to the ease with which so many of us uncritically accept the information presented to us from authoritative-sounding figures. It can readily be disrobed using naţional vital statistics data freely available to anyone with an internet connection.

The Real Story Behind the Rise and Fall of CHD

Before we begin to dismantle the ‘Big Fat Lie’, it is important to define the difference between coronary and non-coronary heart disease. When we talk of CHD, also known as ischemic heart disease, we are referring to the blockage of a coronary artery that impairs or completely blocks blood flow to the heart.

This blockage can be caused by the build-up of arterial plaque, the formation of blood clots, or arterial spasm, and if severe enough causes a heart attack, also referred to as a myocardial infarction.

Non-CHD heart stoppage is most commonly referred to as heart failure and can occur from such conditions as cardiac arrhythmia, cardiomyopathy, endocarditis, myocarditis, and pericarditis. It is CHD that is invariably the focus of diet-heart theories, for heart failure has long been attributed mostly to non-dietary causes such as viral infection, aging, and genetic defects of the heart.

Having made this vital distinction, let us now cast our eyes upon Figure 1 a. It presents the death rate from CHD, non-coronary heart disease and all heart conditions combined, for the period 1900-1993. When we glance at the plotted line for CHD, we see that it does indeed travel an upward path throughout most of the twentieth century, sometimes swinging violently skyward, before reversing direction in 1968.

Unadjusted CHD, all heart disease except CHD, and all heart deasease mortality between 1900-1993
Fig. 1a. Unadjusted CHD, all heart disease except CHD, and all heart disease mortality between 1900-1993

The death rates depicted in Figure 1a are derived from the National Center for Health Statistics and are based on the International Classification of Diseases (ICD). The ICD provides a standardized System for classifying causes of death in an effort to ensure uniformity of reporting amongst different regions and nations. The first ICD came into effect in 1900 and has since been modified about once every ten years, the last revision occurring in 1999. These frequent revisions are necessary to keep the ICD current with rapidly growing scientific knowledge about life-threatening diseases.

At the beginning of the 1900s, doctors and scientists knew very little about CHD. It was not until 1912 that a Dr. James B. Herrick first described an unusual form of heart disease resulting from hardening of the arteries(4). The paucity of knowledge surrounding this ‘new’ condition was reflected in the ICD System, where deaths attributable to CHD were classified as “Anginapectoris”. Angina is actually a symptom of CHD and not the disease itself (angina pectoris literally means ‘pain in the chest’ and results from inadequate blood flow to the heart).

It was not until 1929 that the classification was changed to “Diseases of the coronary arteries, Anginapectoris”, and it was at this point that the number of recorded CHD deaths, which had shown little change since 1900, underwent a sudden and sharp increase. This increase was accompanied by a leveling-off in the number of recorded non-coronary heart disease deaths, as can be seen in Figure 1 a.

In 1948, the sixth ICD introduced a major new category, entitled “Arteriosclerotic heart disease, including coronary disease”. This new classification included three subcategories; 1) “Arteriosclerotic heart disease so described”, 2) “Heart disease specified as involving coronar}’ arteries”, and 3) “Angina pectoris without mention of coronary disease”. As you can see in Figure 1a, this new addition was accompanied by a massive vertical leap in CHD death rates and a similarly massive drop in non-coronary heart disease deaths.

In 1968, the eighth ICD came into effect. For the first time ever, the heart attack was given an explicit listing, under the category “Acute myocardial infarction”. This landmark change was immediately followed by yet another abrupt jump in the CHD mortality curve.

The ninth ICD update in 1979 introduced five new sub-categories to the “AII other forms of heart disease” category. This is the umbrella classification into which all non-CHD categories of heart disease are placed. Among the new arrivals were heart failure and arrhythmia, which refers to a disturbance in the normal rhythm of the heartbeat. Nowadays, both heart failure and arrhythmia are known to be major causes of cardiac death. The establishment of specific categories for these was accompanied by a sudden downturn in CHD mortality and an instantaneous upswing in non-CHD deaths.

There are two possible explanations for the CHD mortality pattern shown in Figure 1a. The first one is that, during the twentieth century, coronary and non- coronary heart disease victims were doing an outstanding job of timing their deaths to correspond precisely with the new ICD classification changes-a highly unlikely occurrence, to say the least. The second and far more realistic explanation is simply that doctors were increasingly classifying victims into CHD- and non-CHD-related categories as the classifications became more specific, ECG machines became more widely used, and medical knowledge of heart disease increased. When the 1968 additions to the ICD criteria allowed doctors to assign the maximum possible percentage of heart disease deaths to the CHD category, CHD mortality hit its ‘peak’ then immediately began to decline in line with the overall heart disease trend(5,6).

Adjusted Versus Unadjusted Data

CHD fatalities occur most commonly in old age. In 1900, the average life expectancy in the US was only forty-nine years, due in no small part to a rate of infant mortality far higher than that seen today. As ninety-four percent of CHD deaths occur after the age of fifty-five, and because average life expectancy in the US had increased to seventy-seven years by the year 2000, one need not be a genius to identify a major reason why so many more people began dying of CHD throughout the last century. Quite simply, many more people were living long enough to die of CHD.

To gain insight into whether any increase in mortality from a specific disease is real or simply an artifact of increased life expectancy, researchers calculate what is known as ‘age-adjusted’ death rates. These are figures that have been arrived at only after making allowances for any increase in average life spân. The heart disease trend lines are seen in Figure 1a – the same figures cited by health authorities when commenting on the rise and decline of CHD-are, not age-adjusted. Those in figure 1b are.

In Figure 1 b, the plot for CHD mortality (for which age-adjusted data is only available from 1960 onwards) hits a peak in 1968 before turning around and heading southeast, similar to what we saw in Figure la. Take a closer look, though, at the trend line for overall heart disease mortality. It hits a peak, not in the late sixties, but in 1950. We know that the 1968 peak for CHD mortality is simply an artifact of changing diagnostic criteria; that when the maximum possible number of deaths were finally being placed into this category, its trajectory instantly fell into line with that of overall heart disease mortality. We, therefore, have every reason to believe that the historical age-adjusted peak for CHD occurred, not in 1968, but somewhere around 1950. As such, the true decline in CHD appears to have begun over a decade before the health establishment launched its campaign against saturated fat and cholesterol!

Postponing the Inevitable

It is an extremely interesting exercise to sit back and take in all the proffered explanations for the reduction in CHD mortality. While orthodoxy assures us it’s anti-fat, anti-cholesterol efforts have helped instigate the drop in CHD, others have tried to link the decline with the increased or decreased consumption of specific food items, or to food fortification with certain vitamins. There’s just one problem with all these theories, and that’s the little-publicized fact that while CHD deaths have been declining, numerous studies show that the overall age-adjusted incidence of CHD-which includes non-fatal disease is remaining steady or even increasing(1-10). In other words, people are having just as many heart attacks as ever-if, not more-but emergency medical care has become increasingly adept at saving their lives(11-14).


The authors of the famous Framingham study, frequently cited in support of the cholesterol hypothesis, wrote in a 1990 article; “Our data indicate that the decline in mortality was primarily the result of improved survival among persons with new cases of cardiovascular disease, rather than the result of a substanţial decrease in the incidence of the disease”{ 9).

In 1996, a high-ranking member of the health orthodoxy revealed at an annual gathering of his colleagues that deaths from heart disease had not dropped nearly as much as officials had claimed and that the prevalence of the disease may actually be increasing. So why the erroneous assertions about an establishment-led drop in CHD?

“Our philosophy was that to get more money from politicians, we had to show that good things were happening”. The individual responsible for these words, quoted in a 1996 edition of the Wall Street Journal, was none other than Jan L. Breslow, the then newly-appointed president of the AHA(15).

Ambulance and paramedic networks, the development of CPR techniques and electrical defibrillators, anti-clotting drugs, coronary care units, and campaigns to raise awareness of heart attack symptoms are the true stars responsible for the decline in CHD deaths. If highly touted ‘risk factor’ changes were responsible for the decline in CHD mortality, they would surely reduce the incidence of CHD itself.

The Anti-Cholesterol Campaign Has Been Counter-Productive

Throughout the twentieth century, there has been a steady and substanţial decline in the number of people smoking cigarettes(16). Because smoking unarguably contributes to heart disease, the incidence of CHD should, by all rights, have undergone a marked decline during this same period—but it hasn’t! Clearly, some other factor(s) has acted to counter the beneficial impact of this reduction in cigarette smoking. As we will explore in later chapters, a number of the establishment’s recommended dietary modifications actually encourage the onset of CHD (and various other lethal diseases).

The Increase in Saturated Fat that Never Was

Even after adjusting the mortality data for increased life expectancy, a substanţial increase in coronary and overall heart disease mortality is still evident during the first half of the last century. Is this increase in any way due to increasing saturated fat consumption? Absolutely not.

Take a good look at Figure 1c, which shows the consumption of various types of fats during the last century(17). Beginning in the 1920s, total fat consumption increased steadily, due entirely to the accelerating use of vegetable oils, shortenings, and margarines. The increasing popularity of these unsaturated fat-rich vegetable fats also explains the rise in polyunsaturated and monounsaturated fat intake. Saturated fat intake, on the other hand, has remained relatively stable in the face of increasing total fat intake.

While vegetable fats do contain some saturates, the richest source of these in the American diet is animal fats, whose consumption slightly declined during the twentieth century(l 8). As can readily be seen from the graph, saturated fat is the only type of fat whose consumption did not rise during the twentieth century. Whether you choose to believe the historic peak in CHD mortality occurred in 1950 or in 1968, saturated fat intake during the decades prior to either of these dates shows no increase. Neither animal fats nor saturated fat can be logically blamed for any increase in CHD deaths.

Much Ado About Nothing

It seems that, during the last four decades, saturated fats from animal foods have been implicated in just about every health ailment to have ever befallen humankind. However, for the same reason, that animal fats cannot possibly be associated with any increase in CHD, they cannot logically be implicated in any real or imagined increases in , diabetes, obesity, teenage acne, falling sperm counts or global warming.

Source: The Great Cholesterol Con, Anthony Colpo

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