On July 19, 2003, a report of a study appeared in New York's "Newsday" newspaper, page A8.  The study in question is typical of the kind of evidence nutritionists and other "experts" cite when they make their claims.  The title of this report was "Cancer, Fatty Foods Linked."  I agree with this title, but in the report, an author of the study is quoted as saying, "The [pro-breast cancer] effect seems to be related particularly to saturated fat found mostly in high-fat milk, meat and some cereals such as biscuits and cakes."

The study was based upon "detalied food diaries of 13,000 older women in Norforlk in eastern England..."

The result of an analysis of these diaries was that:  "The women who were eating 90 grams of fat [a day] had a twofold risk of those who were eating who were eating 40 grams..."

Again, this makes perfect sense to me - I wouldn't be suprised if the risk was higher, actually.  But my question is, why is "saturated fat" being blamed?  First of all, we will assume that by "saturated fat" they mean "saturated fatty acids," and are not discriminating among the many different kinds of saturated fatty acids - this is likely the case and there is nothing else that could be said if these assumptions were not made.  Secondly, most people eating a typical Western diet and 90 grams of fat per day are going to be eating more PUFAs than a person eating a similar diet but containing only 40 grams of fat per day.  Are they assuming that because PUFAs are considered "essential" that they do not have to consider the possibility that the PUFAs may be a major factor?  The author of the report does not say.  Since it is now known that oxidized cholesterol is very dangerous, and since foods typical in Western diets that are rich in saturated fatty acids are also rich in cholesterol (and also that much of this kind of food is cooked at high temperatures), this is a factor that would need to be controlled, but again there is no way to know from this report if it was.  Of course, it is highly unlikely that these elderly British women consumed large amounts of coconut or palm kernel oil - these are products that are rich in saturated fatty acids, low in unsaturated fatty acids, and contain no cholesterol.  A control group consuming one or both of these oils is absolutely essential for this kind of study to be reasonable, scientifically.

Moreover, The National Research Council of the USA published an exhaustive review of the literature up to the late 1980s, and titled this book, "Diet and Health: Implications for Reducing Chronic Disease Risk" (1990).  A key point the authors make is: "Dietary fats increase the yield of mammary tumors only when they contain adequate amounts of omega-6 PUFAs, which are normally present as linoleate in fats derived from plants and land animals.  This probably explains why fats such as butter, coconut oil, and beef tallow have little effect on mammary carcinogenesis (carroll et al., 1981).  The requirements for omega-6 PUFAs in mammary tumor promotion have been explored systematically by Ip et al. (1985), who reported 4 to 5% of total calories as the threshold at which the yield of mammary tumors increased."  Page 213.  Moreover, I would add that both older and recent studies suggest that cooked "meat" is particularly dangerous, and this is now understood down to the molecular level.  Even in "Diet and Health" this point is made: "...some dietary fats, e.g., lard and beef tallow... enhance mammary tumorigenesis when fed only at or before exposure to a carcinogen..."  Page 214.

Here are some studies of note in this context:

Free Radic Biol Med. 1988;5(2):95-111.

"The ways in which dietary polyunsaturated fats and antioxidants affect the balance between activation and detoxification of environmental precarcinogens is discussed, with particular reference to the polycyclic aromatic hydrocarbon benzo(a)pyrene. The structure and composition of membranes and their susceptibility to peroxidation is dependent on the polyunsaturated fatty acid (PUFA) content of the cell and its antioxidant status, both of which are determined to a large degree by dietary intake of these compounds. An increase in the PUFA content of membranes stimulates the oxidation of precarcinogens to reactive intermediates by affecting the configuration and induction of membrane-bound enzymes (e.g., the mixed-function oxidase system and epoxide hydratase); providing increased availability of substrates (hydroperoxides) for peroxidases that cooxidise carcinogens (e.g., prostaglandin synthetase and P-450 peroxidase); and increasing the likelihood of direct activation reactions between peroxyl radicals and precarcinogens. Antioxidants, on the other hand, protect against lipid peroxidation... It has been concluded that dietary factors exert the greatest environmental influence on carcinogenesis and Doll and Pet have estimated that diet is responsible for approximately 35% of the total cancer deaths in the USA�?The polycyclic aromatic hydrocarbon benzo(a)pyrene (BP) is a widely occurring environmental pollutant formed by the combustion of organic materials including cigarettes.  It is present in smoked foods and as a contaminant in a wide range of crops, particularly vegetables�?In 1975, Marnett and coworkers demonstrated the conversion of BP from BP-7,8-diol to BPDEs during the formation of prostaglandins from arachidonic acid�?An increase in both the number of tumour-bearing animals and the multiplicity of respiratory tract tumors induced by BP has been demonstrated when hamsters were fed high fat diets and this effect was most pronounced in the group fed unsaturated fat (sunflower oil)…Taken together, these studies demonstrate that the oxidation of carcinogens catalysed by the MFO system in most tissues studied is dependent upon the presence of dietary EFA [omega 6 and/or omega 3 PUFAs]�?The double bonds of PUFAs are suspectible [sic �?presumably this should be susceptible] to attack by free radicals and this results in the formation of lipid radicals which combine with oxygen to yield peroxy radicals.  These species may then react with another molecule of an unsaturated fatty acid resulting in a chain reaction and the formation of lipid hydroperoxides whicfh break down in the presence of transition metals to a complex mixture of short-chain molecules including aldehydes and hyrdrocarbon gases�?In one study, the increase in the number of DMBA-induced mammary tumours as a result of selenium deficiency was particularly pronounced when the diet was rich in polyunsaturated fats and chemoprevention by increasing the intake of selenium was potentiated by additional vitamin E intake�?Precarcinogens such as BP may oxidised to mutagenic and toxic species in foodstuffs which contain polyunsaturated fatty acids and are subjected to conditions which induce peroxidation�?Unprotected PUFAs undergo peroxidation which can be initiated by intracellular free radicals produced in small quantities under normal circumstances or by a wide variety of environmental toxins…�?/SPAN>

Cancer Res. 2005 Sep 1;65(17):8034-41.

"Cooking meat at high temperatures produces heterocyclic amines (HCAs) and polycyclic aromatic hydrocarbons (PAHs). Processed meats contain N-nitroso compounds... Greater intake of bacon and sausage was associated with increased colorectal adenoma risk... Our study of screening-detected colorectal adenomas shows that red meat and meat cooked at high temperatures are associated with an increased risk of colorectal adenoma."

Thus, the fact that today's meat (from pigs, chickens, and cows especially) is richer in omega-6 PUFAs these days is highly likely to be a very important factor in carcinogenic processes.  Yet all most of us hear about in the "mainstream media" are the same kinds of studies, which make the same kinds of claims, while other (much stronger evidence) is never, or hardly ever even mentioned.  Fortunately, with the resources now available on the internet, one does not need to rely upon newspapers, popular magazines or books, and TV news programs for his or her nutritional information.

Recently, I came across a web site with the following information:

QUOTE: Cholesterol enters the body from saturated fats in animal sources, such as meat, poultry, egg yolks, liver, butter, cheese, and other dairy products. The cholesterol goes to the liver where it joins the cholesterol that is made there. The cholesterol is transported from the liver to the cells by low density lipoproteins (LDL), which acts like a nutritional ferry boat, loading up the cholesterol and navigating through the bloodstream, stopping at cells and depositing cholesterol to the cells that need it. If a cell already has enough cholesterol, it "refuses delivery" of the cholesterol cargo. The excess LDL stays in the blood where the cholesterol is deposited in the walls of arteries, causing atherosclerotic plaque. The more plaque that builds up, the narrower the arteries become, until eventually the blood supply to vital organs is reduced. This is why LDLs are known as the "bad cholesterol."*

But take heart, a nutritional rescuer is also present in the bloodstream, the high density lipoproteins, or HDLs. These are known as "good cholesterol," since they travel like a vacuum cleaner through the bloodstream, picking up excess cholesterol in the bloodstream, and also possibly sucking the cholesterol from the fat-laden plaques. The HDLs carry this excess cholesterol back to the liver, which converts it to bile, which is eliminated into the intestines. How your liver handles cholesterol is determined primarily by genetics, and secondarily by your diet.

While this is an oversimplification of a complicated biochemical process, it helps us understand two conclusions:

• Any diet that raises cholesterol and LDLs and/or lowers HDL is bad.
• Any diet that lowers cholesterol and/or raises HDL is good.   UNQUOTE.

SOURCE:  http://www.askdrsears.com/html/4/T040800.asp

Note how the author assumes that "excess LDL" will be "deposited in the walls of arteries."  Rather, the molecular-level evidence demonstrates that oxidized LDL are "attacked" by macrophages, which can then become dysfunction and lodge in arteries, eventually causing plaque buildup if the process continues.  Also; if, as the author says, HDL takes excess cholesterol bck to the liver and it's converted to to bile, abstructed ducts and gallbladder problems can occur, if too much of the cholesterol is oxidized.  The issue is oxidation of cholesterol.  The idea that "LDL is bad" is based upon an emphasis on "heart disease" in the context of unhealthy Western diets (rich in foods that act as oxidizing agents, like refined and highly polyunsaturated oils).  Low LDL means a higher risk of certain cancers, amongst other unpleasant things.  The author does make a point that many people are not aware of:  QUOTE:  For most people, about eighty percent of the cholesterol in their blood is made by their own body, with the rest coming from their diet. In fact, your body needs cholesterol so much that it makes around 3,000 milligrams per day that's ten times the maximum recommendation for daily dietary cholesterol.  UNQUOTE.