Astonishingly, the theory that high-fat foods-such as meat and dairy-raise our cholesterol levels and so cause a buildup of fat in our arteries has never been proven. Yet, it continues to be promulgated today-as it has been since it was first mooted in the mid-1950s. WebMD, one of the world's most popular websites, tells visitors: "LDL (low-density lipoprotein) chol-esterol can't help being bad-it's just its chemical makeup. LDL cholesterol is an important part of the process of narrowing arteries . . . an LDL cholesterol-lowering diet is low in saturated fat and dietary cholesterol. Adding fibre and plant sterols, like cholesterol-lowering margarine, can further lower LDL levels" (www.webmd.com/ cholesterol-management/ldl-cholesterol-the-bad-cholesterol).
The site disregards 40 years of research demonstrating that each of the statements is false. Just in the past two months, two new studies have been published that confirm what a minority of heart specialists have always suspected: high-fat foods don't raise levels of cholesterol.
They are also discovering something that utterly con-tradicts the entire cholesterol theory-cholesterol actually protects us against heart disease. The 'bad' LDL type-as opposed to HDL (high-density lipoprotein) cholesterol, which apparently mops up its evil relation-has a special part to play in this.
There goes the proof
The first part of the hypothesis-that a high-fat diet causes heart disease-has been disproven in a new study involving 3630 middle-aged men and women, who were split into 1815 'cases' who had suffered a heart attack, and the same number of healthy 'controls'.
The researchers from Brown University in Providence, RI, discovered that both groups consumed similar levels of dairy products, such as milk, cheese, yoghurt and butter, which are full of supposedly harmful saturated fats. Some in the healthy group were voracious consumers of high-fat dairy products, eating up to 593 grammes a day, the researchers found in the 10-year study-and yet, none of them had suffered
a heart attack. In conclusion, the researchers stated that "the evidence is not there" to support the high fats-heart disease theory (Nutr Metab Cardiovasc Dis, 2011; doi: 10.1016/ j.numecd.2011.02.003).
In an earlier study, research-ers from Texas A&M University had gone a step further-they discovered that 'bad' LDL cholesterol is actually good for us. In a study of 52 adults aged from 60 to 69 years who were in good health but not physically active, they discovered that only those with high levels of LDL cholesterol developed the most muscle mass after a vigorous workout.
Research team leader Steve Riechman said: "The truth is, cholesterol is all good. You simply can't remove all the 'bad' cholesterol from your body without serious problems occurring. People often say 'I want to get rid of all my bad cholesterol', but the fact is, if you did so, you would die" (J Gerontol A Biol Sci Med Sci; 2007; 62: 1164-71).
Although findings like these have been published in medical journals since the 1960s, they have been invariably dismissed as anomalous or just plain wrong-because they don't fit within the existing paradigm.
A minority of researchers and doctors-including those who have joined groups such as The International Network of Cholesterol Sceptics (Thincs), headed by Danish researcher Dr Uffe Ravnskov-have maintained for years that cholesterol is vital to our heart, our bodies and our mental health. If that is true, it's then not so surprising that statin drugs-which reduce our levels of cholesterol-have been cited as a cause of muscle damage, dementia, general cognitive decline and even cancer.
Yet the elephant still sits in the room. Heart disease is the number-one killer in the West, and fatty deposits are often found in the arteries of heart-attack victims in a process known as 'atherosclerosis'.
So, if it is so wrong, how did the fatty foods-cholesterol- atherosclerosis theory begin?
Back to the 1950s
By 1950, coronary heart disease (CHD) had become the major killer in the West. In the US, it was responsible for a third of all deaths, and most of these were from myocardial infarction, or heart attack. More than 500,000 Americans were dying every year from heart attack compared with just 3000 in 1930.
What had caused this sudden epidemic?
After the deprivations of the Second World War, the subject of diet and nutrition was 'in the air', and researchers quickly latched on to the idea that the food we eat must be responsible. Some scientists suggested that the epidemic was caused by the rise of hydrogenated vegetable oils found in 'newer' foods such as margarine and biscuits, and that heart disease would decline if we returned to the less processed foods, such as butter, that our grandparents ate.
But there was another food theory on the horizon. David Kritchevsky, a researcher at the Wistar Institute in Philadelphia, PA, demonstrated that choles-terol fed to rabbits caused atherosclerosis (Am J Physiol, 1954; 178: 30-2). He also told the American Oil Chemists Society later that year that polyunsat-urated fats-found in vegetable and corn oils, soybeans, safflower and sunflower seeds-could reduce cholesterol levels.
Within two years, the 'lipid hypothesis' had gained momen-tum. The American Heart Association launched the so-called 'Prudent Diet' in 1956-
in which corn oil, margarine, chicken and cold cereal replaces butter, lard, beef and eggs-in a nationwide television broadcast across the US. One of the expert panellists on the show was Ancel Keys, a researcher at the University of Minnesota, whose name was to become syn-onymous with the cholesterol hypothesis.
In 1958, Keys launched the hugely influential Seven Countries Study, which gave birth to the idea of the 'Mediterranean Diet' and added further credence to the lipid theory. The study demonstrated a direct correlation between heart disease and the amount of animal fat in the diets of the populations of seven countries, including Japan, Finland and the old Yugoslavia (Keys A. Seven Countries: A Multivariate Analysis of Death and Coronary Heart Disease. Cambridge, MA/London: Harvard University Press, 1980).
Later analyses of the study by Ravnskov and others demon-strated that Keys had been highly selective in his data, and had chosen only that which support-ed the high-fats hypothesis. In fact, he had gathered data from 22 countries, and so had ignored the results of 15 nations. If
Keys had included all of the data he had collected, the diet- cholesterol link would have disappeared, says Ravnskov in his book The Cholesterol Myths (Washington, DC: New Trends Publishing, 2000)-a book so reviled by the medical establish-ment that a copy was burned during a live television show in Finland.
Where's the connection?
However, Ravnskov wasn't the only one having difficulties in finding a connection between high-fat foods and heart disease. To its embarrassment and cost, the US Surgeon General's Office had the same problem. For 11 years-from 1988 to 1999-four project officers worked on the definitive report on fats and heart disease, assured that the science was there. Finally, the office issued a letter, written by the last project officer, which announced that the report would never be issued.
Bill Harlan, associate director of the Office of Disease Prevention (ODP) of the US National Institutes of Health (NIH), who helped oversee the project, said: "The report was initiated with a preconceived opinion of the conclusions", but admitted that the science behind those opinions was not supportive (Science, 2001; 291: 2536-45).
Not only doesn't a high-fat diet raise our levels of choles-terol, the next part of the theory-that cholesterol causes CHD and heart attack-also doesn't stack up. Ravnskov has identified around 15 studies that clearly demonstrate that cholesterol plays no role in the development of CHD (Quart J Med, 2003; 96: 927-34).
Even the prestigious Framingham study, which has tracked the heart health of the population of the small town in Massachusetts since 1948, concluded that high cholesterol levels did not predict fatal heart attacks. In fact, the researchers found quite the reverse-people with low cholesterol levels were more likely to die from heart disease (JAMA, 1987; 257: 2176-80).
A study of 997 people aged 70 years and older also couldn't find a connection. High cholesterol levels weren't associated with any increased risk of death from any cause, CHD death or heart attack, the researchers con-cluded (JAMA, 1994; 272: 1335-40).
The statistics are as non-supportive as the science. The percentage of men in the UK who have 'dangerous' levels of cholesterol-in other words, 5 mmol/L or above-has fallen from 75 per cent in 1994 to 58 per cent in 2008 (see box, page 13). The biggest drop is in the 75-plus age range, with just 39 per cent of the male population found to have dangerously high levels compared with 79 per cent in 1994.
Yet, despite this dramatic decrease in the numbers of people with high cholesterol levels, the incidence of CHD has remained stubbornly fixed over the 10 years leading up to 2008. Indeed, the level of CHD has risen slightly in the over-75s-the group that has also seen the most dramatic reduction in the extent of high cholesterol-from 24 per cent in 1988 to around 30 per cent in 2008 (Coronary Heart Disease Statistics, 2010. London: British Heart Foundation).
Nevertheless, the same statistics still point back to the elephant in the room: CHD remains the major killer in the West, responsible
for one in three of all deaths. Atherosclerosis is the major cause of CHD, and continues its relent-less rise. Angioplasty procedures -where the artery is opened up by the insertion of a catheter and 'balloon', which smashes fatty deposits against the artery wall-are now more common than
ever; in the UK, 80,000 of the procedures are carried out every year, three times the level of a decade ago.
So, if fatty foods are not the cause of our clogged arteries, what is?
Medicine accepts that inflam-mation may be a cause of CHD and atherosclerosis. Even conser-vative groups such as the American Heart Association (AHA) are recognizing the role of inflammation in CHD, and several studies have proved the association. In one, which compared 506 men who had suffered a heart attack with 1025 healthy controls, inflammation was a significant indicator of CHD. Those men who had the highest levels of C-reactive protein in their blood-a recognized marker of inflamma-tion-were more than twice as likely to suffer from CHD (BMJ, 2000; 321: 199-204).
However, inflammation is not a cause-it is the body's immune system response to stress and infection. In medicine, the concept of stress refers to any 'insult' to the body, such as a poor diet of 'fast food' and processed foods or exposure to environmental pollutants, as well as tension and depression, or feeling alone or separate and helpless.
But what role does cholesterol in general-and the LDL variety in particular-play in all of this? Although medicine accepts a link between inflammation and CHD, the conventional view remains that LDL cholesterol serves no useful purpose. As the AHA website maintains: "When too much LDL (bad) cholesterol circulates in the blood, it can slowly build up in the inner walls of the arteries that feed the heart and brain . . . [and] can form plaque, a thick, hard deposit that can narrow the arteries . . ." (www.heart.org/HEARTORG/ Conditions/Cholesterol/ AboutCholesterol/Good-vs-Bad Cholesterol_UCM_305561_Article.jsp). And we get "too much" LDL cholesterol when we eat fatty foods, among other things.
Cholesterol, the good guy
A new school of thought believes that LDL cholesterol plays a positive role in our health and wellbeing.
It may be a marker of inflammation, or it may be an infection-fighter that's trying to repair inflamed arteries. If so, 'bad' cholesterol is like the good guy trying to help out at the scene of the crime when the police barge in and accuse the wrong man.
If this theory is right, LDL cholesterol starts to form in our arteries to point to or repair damage caused by inflammation -following infection or stress-and not because we have eaten too much fatty food.
The importance of LDL cholesterol has been borne out in a variety of studies. In one meta-analysis of 19 studies from the US, Europe, Israel and Japan including 68,406 deaths, most of those who died from either respiratory or gastrointestinal disease-usually as the result of infection-had very low levels of cholesterol (Circulation, 1992; 86: 1046-60).
In another study, the chances of survival in patients with chronic heart failure were related to their levels of choles-terol. Those who had high concentrations were far more likely to live than did those with low levels (Lancet, 2000; 356: 930-3).
Other research suggests a link between low levels of LDL cholesterol and certain cancers, such as multiple myeloma and gastrointestinal cancer (Ann Hematol, 2008; 87: 223-8; J Exp Clin Cancer Res, 2004; 23: 233-40). However, it is not clear whether low cholesterol levels are a cause or a result of the disease.
The health-keeping role of cholesterol becomes even more important as we get older. In one study of 724 participants with an average age of 89 years, the researchers discovered that each 1-mmol/L increase in total cholesterol equated to a 15-per-cent drop in mortality (death rate). In other words, those who had the highest cholesterol levels lived longer. Overall, cholesterol apparently had a protective effect against cancer and infection (Lancet, 1997; 350: 1119-23).
Cholesterol also helps to keep us mentally sharp as we get older, and protects us against dementia and cognitive decline. One study of 1051 people aged 65 and older discovered that dementia particularly affected those who had low cholesterol levels (J Gerontol A Biol Sci Med Sci, 2010; 65: 559-64).
Not the end of an era
In the 1970s, Dr George Mann of Vanderbilt University in Nashville, TN, studied the diets and health of the Masai tribe
in East Africa. Their diet was almost entirely made up of meat, blood and milk from their cattle-and yet their cholesterol levels were low, and CHD was almost unheard of.
In conclusion, he described the cholesterol-heart disease theory as "the greatest scam in the history of medicine" (N Engl J Med, 1977; 297: 644-50). It was a scam because the food industry-and, later, the drugs industry-made a fortune from the theory, and continues to do so.
Sadly, it is also a tragedy. By attacking LDL cholesterol, we are depleting our body's stores of a vital fat that is one of our greatest allies in the fight against inflammation and infection. It is especially needed as we age, and it protects us against dementia and cognitive decline-and yet, the elderly
are especially targeted for cholesterol-lowering statins, as they are for most every drug going.
Dementia may not only be a symptom of old age, but the legacy of the greatest scam in the history of medicine.
Factfile: Cholesterol keeps us alive
All of our cells, apart from our neurones, produce cholesterol, which is synthesized by the liver. Cholesterol is needed:
u to create brain synapses, which connect our nerve cells together;
u for the synthesis of vitamin D from sunlight, which creates healthy bones and protects us from several cancers;
u to keep our cells alive;
u for our sex hormones; and
u for the creation of bile, which helps us to digest our food.
You need so much cholesterol to stay alive that the liver produces between four to five times the amounts of cholesterol that you eat. In a biological process known as 'down-regulation', the liver produces less cholesterol if your diet is high in fatty foods.
To illustrate the importance of cholesterol, a sufferer of Smith-Lemli-Opitz syndrome (SLOS), a rare developmental disorder that causes very low cholesterol levels, can suffer from spontaneous abortion, multiorgan system failure and immediate death, congenital heart disease, frequent vomiting, blindness or visual impairment, deafness and/or pneumonia, heart failure or liver failure resulting in death.
Factfile: Your cholesterol levels
'Healthy' cholesterol levels vary according to the latest medical fashion. The average total cholesterol level in the UK is 6.1 mmol/L (millimoles per litre of blood), although medicine currently believes that the 'healthy' total is
Of that quantity, our HDL or 'good' cholesterol level constitutes about 1.3 mmol/L, although the optimal level according to your doctor is anything above 2 mmol/L. Our 'bad' LDL level is typically 3.5 mmol/L, although any reading above 4 mmol/L will trigger a prescription for a statin drug.
Around 20 years ago, a healthy total cholesterol level was considered to be 7 mmol/L, but this fell to
6.5 mmol/L 10 years ago. Nowadays, the drive is relentlessly downwards, and some experts are calling for a
new 'healthy' total cholesterol level of just 2.5 mmol/L.
Researchers at the prestigious Harvard Medical School want to see the average LDL cholesterol level halved in the US. "Perhaps someday there will be a consensus that nearly everyone should make aggressive attempts to lower their LDL cholesterol with statins," they say (www.health.harvard.edu/fhg/updates/ update1104b.shtml).
However, researchers at the University of Michigan say that the current low LDL levels are entirely arbitrary, and have no scientific validity (Arch Intern Med, 2006; 145: 520-30).
So, not only is your cholesterol level the subject of medical fashion, but it also changes according to the seasons and even during the course of a single day. For example, cholesterol levels rise in the winter months and fall during the summer; they also rise when you have an infection or when you're stressed, and during and after a heart attack (Townsend Letter, 2009; 311: 61).
Factfile: The age of the statin
Cholesterol-lowering statins are among the great 'lifestyle drugs'. Zocor (simvastatin) can be bought at your local pharmacy in the UK without a prescription, and so good are they for all of us that they could even be added to the public water supply, says Dr John Reckless, chairman of Heart UK (http://news.bbc.co.uk/2/hi/health/ 3931157.stm).
Such exuberance-and prolific prescribing by doctors-has made statins the world's most profitable drug family, with annual sales of around $26 billion ('Statins: The World Market, 2009-2024', LeadDiscovery, at www.leaddiscovery.co.uk/reports/1421/Statins_The_World_Market_ 20092024/).
Most doctors see statins as the perfect drug: they are life-savers, and come with virtually no side-effects. Unfortunately, the data support neither of these claims.
u Statins as life-savers. Just one group of people appear to benefit from statins-
men who have had a previous heart attack. Healthy men and women will not see their life expectancy improved whatsoever, even if they have taken a statin every day for five years. The Scandinavian Simvastatin Survival Study (4S study) found that statins can achieve a 0.66-per-cent reduction in overall mortality per year, while the West of
Scotland Coronary Prevention Study (WOSCOPS) calculated a 0.18-per-cent reduction in overall mortality.
Such marginal gains are offset by other studies, such as the Expanded Clinical Evaluation of Lovastatin (EXCEL) trial, which revealed that people taking statins were
0.3-per-cent more likely to die than someone not taking the drug (Ravnskov U. The Cholesterol Myths. Washington, DC: New Trends Publishing, 2000).
The manufacturer of one statin, Zetia (ezetimibe), withheld data-until pressed to reveal its findings by the US Congress-demonstrating that the drug was ineffective (BMJ, 2008; 336: 180-1).
u No side-effects. Common problems include muscle tenderness and weakness, a condition known as myopathy. One statin-cerivastatin (Baycol)-was taken off the market because it was found to cause the condition (Ann Intern Med, 2002; 137: 581-5). It was also found that 31 people died while taking this statin.
These drugs can also cause Parkinson's, the disease of the central nervous system. In one study, statin users who developed Parkinson's had levels of LDL cholesterol that were three times lower than the average (Mov Disord, 2007; 22: 377-81).
The drugs can also lead to memory loss, depression, confusion, irritability and dizziness, and major birth defects of a scale such as seen with thalidomide. There is also growing concern that they can cause cancer and heart failure (Kendrick M. The Great Cholesterol Con. London: John Blake Publishing, 2007).
WDDTY VOL. 22 NO. 4