A matter of fat

This is an essay I wrote about fat (well, the lipid hypothesis, etc.) for an honours directed study.  I'm changing it slightly, but using a lot of the same material in my thesis.

The Lipid Hypothesis: Science, Politics and Profit.

It is common knowledge that eating saturated fat causes heart disease and that high cholesterol levels are unhealthy.  These things are considered to be scientifically proven, yet there are many historical and cultural exceptions that continue to defy this knowledge.  The Masai tribe in Kenya who consume only blood, milk and meat have a diet high in saturated fat and yet have no evidence of coronary heart diesase, as do the French on their notoriously fatty diet.  Despite these exceptions mainstream medical and scientific opinion has been convinced that saturated fat is unhealthy.  This essay will explore the history and science behind the lipid hypothesis as well as the social issues influenced by it.  Firstly, by explaining the lipid hypothesis, the diet-heart idea, and cholesterol.  Secondly, by looking at the history of the scientific and political 'cholesterol wars'.  Thirdly, by exploring the social evolution of this widely held theory and the industries and agendas that surround it and, finally, this essay will critically examine the scientific approach that has been taken in order to establish this theory.

The Lipid Hypothesis:

The lipid hypothesis is the idea that high levels of cholesterol in the blood leads to coronary heart disease.  The diet-heart hypothesis, considered a partner to the lipid hypothesis, claims that saturated fat in the diet causes raised blood cholesterol and therefore, leads to coronary heart disease (Ravnskov, 2000).  Many scientific studies have been designed and run in order to prove this hypothesis, and despite its current popularity there still exists a group of outspoken critics who claim the evidence fails short of proving anything[1]. As Gurr (1991 B) states “Critical examinations of the literature reveals that the 'Lipid Hypothesis' is not as simple or as well-founded as it apears” (p.1)

What is Cholesterol?

Cholesterol  is a fatty substance found in every human cell.  It is used by the body to repair damaged cells and involved in many necessary bodily functions (Gurr, 1991).  According to the Merck Manual of Medical Information[2]

            Cholesterol and triglycirides are very important fats (lipids) in the blood.    Cholesterol is an essential component of cell membranes, brain and nerve          cells, and bile which helps the body absorb fats and fat-soluble vitamins.  The body uses cholesterol to make vitamin D and various hormones such as       estrogen, testosterone, and cortisol. (Beers, 2003, p. 836)

Despite its many essential, health promoting properties, cholesterol has a bad reputation.  Because of the lipid hypothesis and its publicity, cholesterol has negative connotations associated with heart disease.  The very low levels of cholesterol recommended by the dominant medical system and the cholesterol lowering drugs that achieve these low levels may be depriving the body of the valuable substance necessary for self-repair.  This may be the reason why elderly people are much more likely to die from all causes if they have low levels of cholesterol (Ravnskov, 2000).  Conversely, high colesterol levels measured in the body might be a sign that the body is trying to repair damage, rather than the forwarding of altherosclerosis.

Good and bad cholesterol

Recently the idea has been circulated that some cholesterol, LDL, is bad while HDL cholesterol is good (Ravnskov, 2000).  Neither LDL or HDL are actually cholesterol, both are proteins (lipoproteins) that transport fats around the blood stream (Ravnskov, 2000).  LDL cholesterol transports fat into the blood stream, it is called low density lipoprotein because it has less protein density and more fat.  HDL transports fat back from the blood stream and as some of the fat has been stored in cells it has a higher ratio of protein to fat (Merck, 2003).  Because LDL transports protein into the blood stream it is considered to be bad, the returning HDL is considered to be good (Ravnskov, 2000).  This might seem an unscientific distiction[3] but it is helpful in marketting a drug which is known to lower the 'bad' cholesterol.  The industries involved will be explored later in this essay.

The Cholesterol Wars:

Before the lipid hypothesis eventuated, a young scientist mamed Ignatowski  began working towards proving the hypothesis by Metschnikow that an excess of dietary protein was toxic and accelerated the aging process (Steinberg, 2004). Ignatowski fed rabbits a protein-rich diet  (large amounts of meat, eggs, and milk)  which had the affect of causing arterial lesions like those of human atherosclerosis. Later, Anitschkow and Chalotow found that a diet high in fat without the protein also caused these lesions.  Steinberg (2004) refers to this as “Another instance of an unpleasant fact destroying a beautiful hypothesis” (p.11). However, from these experiments the lipid hypothesis emerged.  Critics of Anitschkow argued that the digestive systems of rabbits were not designed for a diet high in animal fat and demonstrated the limits of this research by running similar trials on dogs and rats which resulted in no arterial lesions.  Dogs and rats produce bile which breaks down fats during digestion, as do humans (Masterjohn, 2008).  This was seen as sufficient evidence, at the time, to disprove the theory, however, devotees remained (Steinberg, 2004).

Ancel Keys is known as the founder of the lipid hypothesis.  He used data collected from six countries to show an obvious correlation between the consumption of fat and the rates of death from coronary heart disease (Ravnskov,2000).  Keys has been criticized for excluding data[4] from countries that did not support his theory (Ravnskov,2000).  A graph constructed with all the available data would show no obvious correlation.

(Ravnskov, 2000, p.18-19)

Over the next few decades after Keys published his Seven Countries Study a serious debade ensued between the converts[5] of the lipid hypothesis and those who remained unconvinced (Steinberg, 2004).  Many new studies were funded, aiming to demonstrate the validity of the diet-heart idea and the lipid hypothesis, but each study was met with criticism.  One such experiment, the Oslo Study, showed reoccurrence of heart attacks were lower on a diet high in polyunsaturated fats (soybean oil), however, the overall mortality was the same for both the control and the diet group (Steinberg, 2004). This could indicate that within the diet group participants died from other causes before a heart attack could kill them.  This demonstrates that the narrow focus on heart disease excludes the possibilities that other conditions may be occurring from following diets low in saturated fat or high in polyunsaturated fats.

Steinberg (2004) has written articles and a book covering this epic debate in which he covers many influential studies, lamenting their flaws, but still convinced of the validity of their cause.  The Oslo Study, which replaced saturated fat with polyunsaturated fat,[6] lasted five years and produced no difference in all-cause mortality but decreased the incidence of second heart attacks. This could be accounted for by the inconsistencies in the control group[7] (Masterjohn, 2008). As Masterjohn states: “There are far too many confounding variables to suggest this study actually indicts saturated fat” (para. 53).

The Wadsworth Veterans Administration Hospital Study fed one group meals made with saturated animal fats and another group meals made with polyunsaturated vegetable oils for eight years (Steinberg, 2004, Masterjohn, 2008). The result was a reduction in cardiovascular events, but an increase in cancer of the same magnitude (Masterjohn, 2008).  Autopsies showed similar atherosclerosis in both groups and more aortal plaque in the group that ate the vegetable oil (Masterjohn, 2008). The difference in the rate of cardiovascular events could be due to the higher rate of heavy smoking[8] in the control group (Masterjohn, 2008).  Members of the treatment group may have had a lower rate of cardiovascular events because they smoked less, “but had more atherosclerosis and cancer despite smoking less -- probably because of the vegetable oil they were eating!” (Masterjohn, 2008, para. 55).

Many other similar studies could be considered part of the lipid anthology.  Steinberg sites seven and leaves out two which would damadge his argument. Rose, et al. (1965, cited in Masterjohn, 2008) replaced animal fat with corn oil over two years lowering serum cholesterol by 23 mg/dL but, unfortunately the cardiac and total mortality quadrupled. The Sydney Diet-Heart Study (1978, cited in Masterjohn, 2008) replaced animal fat with vegetable fat over five years, lowering cholesterol by five percent but increasing total mortality by 50 percent. 

In examining any long-running controversy, it is important to determine whether the skeptics are just having trouble adapting to a new paradigm or whether their doubts are well founded (Taubes, 2004).  Because this issue has two seperate hypotheses, both must be taken into account seperately.  Firstly, the idea that lowering cholesterol prevents heart disease.  This idea has been supported by the evidence that cholesterol lowering drugs such as statins prevent heart attacks (Taubes, 2004).  Although it is conceivable that statins have some other function that prevents heart attacks.  

Masterjohn (2008) explores this possibility by looking at  another function statins are likely to have; reducing the activation of the Rho enzyme which inhibits nitric oxide “a gas that protects against heart disease at every level -- it increases blood flow and vessel dilation, decreases the adhesion of white blood cells to the vessel wall, inhibits the migration of smooth muscle cells to the site of an atherosclerotic lesion, and decreases the formation of blood clots.” (Masterjohn, 2008, para. 40).  This theory has so far been untested.  It still links high levels of LDL cholesterol with atherosclerosis, because the more LDL is in the blood, the smaller the ratio of antioxidants to protect it from oxidisation.   Oxidised LDL is known to cause damadge to the arteries (Masterjohn, 2008).  Oxidised LDL also inhibits nitric oxide prodiction, further reducing the protection from atherosclerosis.  If this is the reason statins reduce cardiac incidents it may be wise to take into account the other main affect statins have; lowering the levels of cholestrol, a very important substance that repairs cells and precurses hormones.  Rather than taking statins, a better approach may be to increase the antioxidants in the blood which will also protect against LDL oxidisation (Masterjohn, 2008).

The second idea; that eating saturated fat causes heart attacks, is much harder to prove and further experiments have only complicated the issue further (Taubes, 2004).  If indeed saturated fats directly lead to atherosclerosis this affect should be obviously demonstrated in controlled trials.  This is not the case.  There does not appear to be any trials that can clearly demonstrate this theory (Masterjohn, 2008).  Despite a lack of scientific proof, the idea that eating less saturated fat would reduce heart disease became part of a widely publicised public health campaign[9] (Taubes, 2004).  This was followed by a 'Consensus Conference[10]', lead by Steinberg, designed to end the debate.  Most of the experts invited were converts of the lipid hypothesis, although a minority of skeptics argued that equating the effects of drugs with diet was unscientific.  The conference report did not mention any disagreement (Taubes, 2004). “There was "no doubt," it concluded, that low-fat diets "will afford significant protection against coronary heart disease" to every American over 2 years old.” (Taubes, 2004, para. 30).

The Scientific Paradigm:

According to the highly regarded supporter of the lipid hypothesis, Steinberg, “The lack of a well-delineated hypothesis is not necessarily a barrier to the acceptance of new directions in medical practice” (2007, p.89).  In the scientific paradigm quantities are important.  Things that can be measured are given more significance than things that cannot.  This may help to explain the popularity of the idea that something measurable like cholesterol could be considered the main or sole factor in heart disease, as opposed to something unquantifiable like stress, which may also be a factor (Ravnskov, 2000).  It is under this paradigm that reductionism is utilised in order to simplify information.  This has been applied to food science in a way that is described by Scrinis (2008) as nutritionism; where the benefits (or problems) of a food can be reduced to a single identifyable substance, and a synthesised substance of the same name can be added to processed food to suposedly increase it's nutritional value.  In this way food is fragmented, rather than seen in a holistic sense. 

Often in the scientific process a problem is first identified as worthy of investigation.  In this case the problem of heart disease has been identified, since the 1950s, as being of major concern (Ravnskov, 2000).  Theories then emerge which may be based on research showing correlations, for example, the rise of avaliable dietary fat (which is one of many dietary changes), or the correlation between the cholesterol found in arteries and atherosclerosis.  Neither of these things are proof that dietary fat or blood cholesterol cause atherosclerosis, but it is evident that simple solutions are being sought.  A molecule, such as cholesterol or saturated fat is charged with the crime of murder, and a theory of how this happens is constructed.  Then the implicated parties are put on trial.  Correlations found in trials are considered (by some) to be proof (or as good as), and once the theory becomes well recognised it is considered factual.  Once these things have been established researchers look for solutions to the problem, such as cutting down on dietary saturated fat or taking drugs which lower blood cholesterol. 

Although this sounds simple and sensible there are a number of problems with this method.  Firstly, when it comes to human biology and nutrition, the chemistry involved is seldom simple.  There are always factors that are yet to be understood.  To act as if all the avaliable information is complete is naïve.  Cholesterol lowering drugs work against even some of the avaliable information about the importance of cholesterol in health, ignoring the complexity of this molecule and its many functions in the body.  As Taubes points out,

            The catch has been that few involved in this business were prepared to deal             with a complicated story. Researchers initially preferred to believe it was          simple — that a single unwholesome nutrient, in effect, could be isolated from   the diverse richness of human diets... But as contrarian data continued to     accumulate, the complications became increasingly more difficult to ignore or           exclude, and the press began waffling or adding caveats. The scientists then      got the blame for not sticking to the original simple story, which had,           regrettably, never existed. (2004, para. 37)

Another problem with this particular scientific process is due to a well known logical fallacy, called Questionable Cause which is when a correlation is taken to imply causation.  It is possible that a third factor, such as stress, causes both the rise in blood cholesterol and atherosclerosis, or that the rise of blood cholesterol is actually a symptom of atherosclerosis, repairing damadge to the arteries (Ravnskov, 2000).

Social issues and Industries:

As Taubes (2004) notes, since the 1970's healthy eating in the US has become synonymous with avoiding saturated fat in the diet.  And as a result “The creation and marketting of reduced-fat food products has become big business; over 15,000 have appeared on supermarket shelves” (Taubes, 2004, para. 4). This growth industry has not been confined to food, an entire area of food research has developed to back up the 'healthy' claims of food manufacturers (Taubes, 2004).  This is supported by governmental policy recommending saturated fat be eaten sparingly.  “The low-fat gospel spreads farther by a kind of societal osmosis, continuously reinforced by physicians, nutritionists, journalists, health organisations, and consumer advocacy groups” (Taubes, 2004, para. 4).

Taubes discusses the social and political context of the rise of this phenomena:

            Like the flourishing American affinity for alternative medicine, an antifat      movement evolved independently of science in the 1960s. It was fed by distrust of the establishment — in this case, both the medical establishment   and the food industry — and by counterculture attacks on excessive         consumption, whether manifested in gas-guzzling cars or the classic American   cuisine of bacon and eggs and marbled steaks. And while the data on fat and             health remained ambiguous and the scientific community polarized, the       deadlock was broken not by any new science, but by politicians. (Taubes, 2004, para. 13)

Politics has played a large role in the dissemination of the diet-heart idea.  Taubes explains how the staff working for the US Senator, McGovern, were responsible for the first anti-fat legislation that spread throughout the US and then the rest of the Western world.  “Turning the dietary fat hypothesis into dogma” (Taubes, 2004, para. 14)

Other social and cultural contexts are also important to mention.  Japan has often been claimed as proof of the diet-heart hypothesis because Japanese people eat little saturated fat, have long life-spans and have low rates of coronary heart disease.  What is not noticed by these statistics is that the long life spans in Japan are a fairly recent development, coinciding with higher consumption of animal meat and saturated fat.  Another notable point is that it is considered dishonorable to be declared dead of heart attack in Japan, and for this reason doctors are more likely to write the cause of death as a stroke on death certificates (Ravnskov, 2000).

Upon researching this topic I stumbled upon something that I considered to be a good, succinct example of the industries involved in the promotion of the lipid hypothesis.  This occurred as a sidebar of a google search for 'coronary heart disease' (Google search, 14^th April, 2009).

Coronary Heart Disease

A resource for physicians and

patients about thrombosis!

www.Thrombosisadviser.com

Heart Disease Facts

The Source Of Professional & Up To

Date Info On Cardiovascular Health

www.heartfoundation.org.au

Coronary Heart Disease

Maintain a healthy heart with

Flora pro-active healthy recipes!

www.floraloveyourheart.co.nz

The first of these symbolises the medical industry involved in the promotion of this idea.  Doctors, as experts, have a lot invested (in terms of their reputations) in the information they have been giving out to their patients.  Drug companies make millions of dollars from selling cholesterol lowering drugs (Taubes, 2004).  Heart foundations receive a lot of funding for research based on the lipid hypothesis, much of it from pharmaceutical companies, governments and the diet food industry, represented here by Flora, which also flourishes under this dominant theory.  Each of these industries, both profit and non-profit, have a vested interest in the promotion of this problem and in the theories that support it, regardless of whether they are accurate.  George V. Mann, a physician and nutrition expert at Vanderbilt University suggested that "the dietary dogma was a money-maker for segments of the food industry, a fund-raiser for the Heart Association, and busy work for thousands of fat chemists" (cited in: Steinberg, 2007, p.58).

Truth and science

Despite the many scientists who continue to question the validity of the diet-heart idea and the lipid hypothesis, the supporters of the now dominant theories receive the most credit.  As George V. Mann stated: "to be a dissenter was to be unfunded because the peer-review system rewards conformity and excludes criticism." (Mann, G. V. 1977. cited in Steinberg, 2004, para. 63).  In this self-promoting system disenters are marginalised, regardless of the strength of their criticism and the general public are unlikely to have access to this contrary information. 

Aside from the lucritive industry around this theory, scientists may also choose to cling to it because they have already invested their time and other people's money in it, as Taubes (2004) notes.  This may be why the inability to prove the hypothesis was disregarded and a leap of faith was made, using the positive results of cholesterol lowering drugs reducing heart attacks as if it were proof of the lipid hypothesis (and the diet-heart idea), a process that Steinberg (2004) is supportive of.  After all the money and time put into trials the experts were expected to give advice, regardless of whether it was scientifically proven (Taubes, 2004). A good summary is provided by Masterjohn:

            It is also interesting to contemplate the sheer movement of cash (representing          real economic resources) into these studies and to consider how fruitless the     use of these resources has actually been. The technology developed by private   industry has saved more lives by making heart disease less fatal. Meanwhile,           cattle-herding tribes like the Masai have protected themselves against heart           disease far more effectively than we have, having neither hundreds of millions    of dollars for even a single placebo-controlled trial nor any of the fancy             technology that industrial capitalism produces. (Masterjohn, 2008, para. 79).

Conclusions

The lipid hypothesis has had a long history of failed experiments influenced by financial agandas.  The idea that eating saturated fat causes a build up of fat in the arteries seems logical at first glance, but with further information about the digestive system and dozens of studies with no clear results proving this idea, not to mention the cultural anomalies, even the most dedicated scientists must admit this issue is more complicated that it was first proposed to be.  Using the drug evidence of statins to 'prove' the lipid hypothesis is as unscientific as using a miracle to prove the existence of god.  The idea suggested by Masterjohn that statins appear to work due to another affect (inhibiting the Rho enzyme) is one which seems worthy of further exploration, although with so much riding on the lipid hypothesis, it may be hard to find funding.  This exposes one of the main flaws in modern science.  The funding for research often comes from groups, organisation and corporations with financial agendas.  Research that these parties find unfavourable is not readily released and experiments are designed to deliberately show a desired result.  Scientists who do not support the dominant theory are marginalised, and as a result, their work is considered less credible.  A thoroughly unscientific process.

References

Beers, M. (Ed). (2003). Merck Manual of Medical Information (2^nd ed). New York:            Simon & Schuster.

Gurr, M. (1991A). Cholesterol in the food and Blood. Diet Health Dialogue.         Wellington: Dairy Advisory Bureau.

Gurr, M. (1991B). The lipid hypothesis: A review of the experimental and Epidemiological evidence. Diet Health Dialogue. Wellington: Dairy Advisory           Bureau.

Masterjohn, C. (2008). A review of the cholesterol wars: The skeptics vs. the          preponderance of the evidence.Cholesterol and Health. Retrieved April 18,           2009, from http://www.cholesterol-and-health.com/Daniel-Steinberg- Cholesterol-Wars.html

Ravnskov, U. (2000). The cholesterol myths. Washington: New Trends Publishing.

Scrinis, G. (2008). On the ideology of Nutritionism. Gastronomica: The journal of             food and culture. University of California press. Vol. 8 (1) pp. 38-48

Steinberg, D. (2004) Thematic review series: The Pathogenesis of Atherosclerosis. An       interpretive history of the cholesterol controversy: part I-V. Journal of Lipid     Research, American Society for Biochemistry and Molecular Biology. Vol. 45, pp. 1583-1593,

Steinberg, D. (2007). The Cholesterol Wars. New York NY: Academic       Press/Elsevier, Inc
 

Taubes, G. (2004). The soft science of dietary fat. Science 30 March 2001:
            Vol. 291. no. 5513, pp. 2536 – 2545

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[1]             Many of these critics are well qualified.  Dr. Uffe Ravnskov, author of The Cholesterol Myths (2000) is a medical doctor with a PhD, Mike Gurr (1991A, 1992B), the author of several articles arguing against the role of dietary fats and cholesterol in the blood has a PhD.  Chris Masterjohn (2008) is also a medical doctor with a PhD, but despite their qualifications these critics are marginalised in favor of mainstream science.

[2]    Self proclaimed the world's most widely used medical reference for the twenty-first century.

[3]    Or even a moral or religious one.

[4]    Reliable data from more than twenty countries was avaliable at the time of Keys' research (Ravnskov, 2000)

[5]             Religious terminology is used by Steinberg, supporter of the lipid hypothesis: “The "nonbelievers" were largely confining themselves to the intervention trial data per se. The "believers," if they had had a catechism, might have recited it…” (2004, p.1)

[6]             Including a pint of soybean oil per week

[7]             The control group started out with a higher number of older and overweight participants and by the end of the study it had twice as many heavy smokers. Members of the treatment group were counseled to cut down their intake of margarine and increase their intake of fruits, vegetables, and fish, they were provided with free sardines canned in cod liver oil (Masterjohn, 2008)

[8]             Smoking increases the risk of spasms that can lead to heart attacks

[9]             Even the idea that low fat diets are beneficial to weight loss is not well founded, although it is often held to be a religious truth.  Despite the calorie density of fat being significantly higher than carbohydrate and protein, participants in low fat diet trials were found to lose weight initially and then return to their initial weight (Taubes, 2004).

[10]  At a Consensus Conference a (supposedly unbiased) panel review the evidence given by experts (Taubes)