The following study makes the point that when doing an epidemiological study on the effects of "saturated fat," one must take the other food constituents into account. As I've said in the other essays, failure to do so is a violation of the scientific method and should not be considered science.

J Natl Cancer Inst. 2005 Oct 5;97(19):1458-65.

"Intake of total and saturated fat from meat was associated with statistically significant increases in pancreatic cancer risk but that from dairy products was not. CONCLUSION: Red and processed meat intakes were associated with an increased risk of pancreatic cancer. Fat and saturated fat are not likely to contribute to the underlying carcinogenic mechanism because the findings for fat from meat and dairy products differed. Carcinogenic substances related to meat preparation methods might be responsible for the positive association.

In a study entitled "The fish nobody knows," it was found that those who rarely ate fish had a much lower heart attack risk that those who did, apparently because the people in the study usually ate fried fish. Source: Barnett and Barone, 1989.

But it's important not to miss all the important factors involved here. While it's true that studies have demonstrated how dangerous cooked meat can be, one should ask if there is any way of minimizing the danger. First, let's take a look at one study that is clear about the dangers of cooked meat:

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.

Now let's take a look at a study that examines the role that the kinds of fat in one's diet can play:

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...

Fat consumption patterns are well documented, and correlate very well to what is known about molecular-level mechanisms, for example:

"Fat available in the food supply increased from an average of 124 g/day per capital in 1909 to 172 g/day in 1985. Although the chief sources of fat during that time have been fats and oils; meat, poultry, and fish; and dairy products, great changes within each of these groups have occurred. The proportion of animal fat declined from 83 to 58% as butter and lard use declined, whereas the proporion of vegetable fat (in margarinesand in salad and cooking oils) rose from 17 to 42%."

Source: The book, "Diet and Health," by the National Research Council, page 160.

I would further add that the lard of 1909 was considerably higher in saturated fatty acid content than most lard sold in a nation like the USA is today.

Here are some more frightening statistics from this book: "The percentage of calories contributed by linoleic acid [the most common form of dietary omega 6 polyunsaturated fatty acid - also called PUFAs] to total fat fat itake increased from 7% during 1909-1913 to about 16% in 1985... In 1985, linoleic acid was available at 7% of total calories..." Also from page 160. This is important, because the statistics also tell us that: "The requirements for omega-6 PUFAs in mamary 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. In the early 1900s, these kinds of cancers, common today, were rare. Thus, both the molecular-level evidence and all the statistics point to the same "culprit." I can't tell you why this receives so little attention in the "mainstream media," but you are certainly free to contact some "science reporters" and ask. Please post your experiences in this endeavor in the newsgroup section of this site if you do.

As I've pointed out in other essays, having AA in your cells makes you more susceptible to "diseases" thought to be caused by something like excess alcohol consumption. For example:

Toxicol Appl Pharmacol. 2006 Jul 1.  "Nitric oxide donors prevent while the nitric oxide synthase inhibitor l-NAME increases arachidonic acid plus CYP2E1-dependent toxicity."  Wu D, Cederbaum A.

QUOTE:  Polyunsaturated fatty acids such as arachidonic acid (AA) play an important role in alcohol-induced liver injury. AA promotes toxicity in rat hepatocytes with high levels of cytochrome P4502E1 and in HepG2 E47 cells which express CYP2E1. Nitric oxide (NO) participates in the regulation of various cell activities as well as in cytotoxic events. NO may act as a protectant against cytotoxic stress or may enhance cytotoxicity when produced at elevated concentrations�?These results indicate that NO can be hepatoprotective against CYP2E1-dependent toxicity, preventing AA-induced oxidative stress.  UNQUOTE.

Notice how one event follows another, creating a "pathway," which might not have to be therre in the first place. In the above example, NO may be a "protectant," but it can also cause harm if too much is produced, or if it is produced too often. Again, without AA in your cells, this will either not happen, or else it will take more of an insult for it to be triggered, and even then less damage will likely result. Below is a report that is best summed up by a quotation from it:

QUOTE: "What happens four hours after that high-fat meal is that your artery looks just like the arteries of a person who has heart disease," said co-author Janet P. Wallace... UNQUOTE.

The title of this report, however, is as misleading as one could imagine: "A Serving Of Exercise After That Saturated Fat."  Why is it so misleading? Because we are not told what the fatty acid content of the meals was, and worse, as the researchers themselves point out: "Wallace said the oxidation of high-fat meals causes oxidative stress markers that harm the arteries and contribute to such conditions as heart disease, diabetes, Alzheimer's and cancer..."  Now it is biochemical fact that saturated fatty acids in the form of food do not have this effect - something like fresh coconut oil could be used as the only form of fat in a high-fat meal in order to demonstrate this experimentally, something that obviously should have been done by these researchers. However, as is usual, they simply accept linguistic conventions about "saturated fat" and probably don't even know about the low rates of the diseases Wallace mentioned among those who eat very large amounts of SFAs but very low amounts of unsaturated fatty acids.

Thus, I agree with them on their findings. They appear to have fed the subjects meals featuring a lot of lard (which is 39% saturated) as well as highly unsaturated oils (used for the cooking). And I would expect such findings, and I agree with their interpretation up to this point. I disagree that lard should be called a "saturated fat," however, because they also call coconut oil a "saturated fat," and fresh coconut oil will not have this effect. It is therefore appropriate for them to repeat the experiment using fresh coconut oil instead of whatever fat source they used, and then report on the results (I am assuming the coconut oil would be consumed fresh, so that other factors will not be in play). However, they probably cannot even conceive of this possibility, which is ne reason owhy I am writing these essays.  Another major problem is that the "high-fat" meals served to the subjects were high in cholesterol cooked while exposed to air. The scientific method requires that factors be isolated, so we don't know if the animal fat used plus the oxidized cholesterol was mostly to blame, or if it was one or the other.  Here is the meal in question: "The high-fat breakfast included eggs, sausage and hash browns. It included 48 grams of fat (16.5 grams saturated fat and 4.5 grams trans fat), 33 grams protein, 91 grams carbohydrates, 280 milligrams of cholesterol and 2,220 milligrams of sodium."  As to the "exercise," it was desribed as follows: "...all 25-year-olds who were determined to be physically active and apparently healthy, walked on a treadmill for 45 minutes two hours after eating..." It's difficult to know what this accomplished, as it's known that at least some forms of "exercise" cause a great deal of oxidative stress, so at the very least, the claim is as tentative as can be.

Source of this report: http://www.sciencedaily.com/releases/2006/09/060901192519.htm

And here's a passage from a recent study supporting the point made above about how PUFAs cause damage: "Arachidonic acid epoxides, previously suggested to be involved in apoptosis, oncogenesis and cell proliferation, are generated by cytochrome P450 epoxygenases..."

Source: J Mol Histol. 2006 Sep 7.

Finally, here is Lancet study that has received almost no attention:  Lancet. 1994 Oct 29;344(8931):1195-6.

"Dietary polyunsaturated fatty acids and composition of human aortic plaques."  Felton CV, Crook D, Davies MJ, Oliver MF.

QUOTE:  How long-term dietary intake of essential fatty acids affects the fatty-acid content of aortic plaques is not clear. We compared the fatty-acid composition of aortic plaques with that of post-mortem serum and adipose tissue, in which essential fatty-acid content reflects dietary intake. Positive associations were found between serum and plaque omega 6 (r = 0.75) and omega 3 (r = 0.93) polyunsaturated fatty acids, and monounsaturates (r = 0.70), and also between adipose tissue and plaque omega 6 polyunsaturated fatty acids (r = 0.89). No associations were found with saturated fatty acids. These findings imply a direct influence of dietary polyunsaturated fatty acids on aortic plaque formation and suggest that current trends favouring increased intake of polyunsaturated fatty acids should be reconsidered.  UNQUOTE.

On the other hand:  American Journal of Clinical Nutrition, Vol. 82, No. 4, 894-900, October 2005.  © 2005 American Society for Clinical Nutrition

QUOTE: High-fat dairy foods contain many potentially anticarcinogenic factors, including conjugated linoleic acid (CLA). However, few epidemiologic studies have specifically evaluated high-fat dairy food consumption, and none have evaluated CLA intake, in relation to colorectal cancer risk... These prospective data suggest that high intakes of high-fat dairy foods and CLA may reduce the risk of colorectal cancer. UNQUOTE.

And this is excellent:  Mutat Res. 2002 Sep 30;506-507:9-20.  "Comments on the history and importance of aromatic and heterocyclic amines in public health."  Weisburger JH.<o:p></o:p>

QUOTE: The carcinogenic risk of aromatic amines in humans was first discovered when a physician related the occurrence of urinary bladder cancer to the occupation of his patients. They were employed in the dyestuff industry, chronically exposed to large amounts of intermediate arylamines�?Epidemiological data suggest that meat eaters may have a higher risk of breast and colon cancer. HCAs induced cancer in rats in these organs and also in the prostate and the pancreas. In addition, there is some evidence that they affect the vascular system. The formation of HCAs during cooking can be decreased by natural and synthetic antioxidants, by tryptophan or proline, or by removing the essential creatine through brief microwave cooking prior to frying or broiling. The amounts of HCAs in cooked foods are small, but other components in diet such as omega-6-polyunsaturated oils have powerful promoting effects in target organs of HCAs. On the other hand, the action of HCAs may be decreased by foods containing antioxidants, such as vegetables, soy, and tea�?Possibly, the carcinogenic effect of HCAs is accompanied by the presence of reactive oxygen species (ROS), which are also inhibited by antioxidants..  UNQUOTE.

Finally, from a recent report:  QUOTE: ...The researchers couldn't explain why eating more animal fat was associated with breast cancer risk. It may be that factors other than fat are involved. For instance, grilling red meat can create cancer-causing chemicals�?Earlier studies had suggested one reason for the increased cancer risk, relating this to the heterocyclic amines (HCAs) that form when red meat is cooked at high temperatures (like frying and grilling), especially well-done. In laboratory studies, HCAs bond to estrogen receptors and create estrogen-like effects. In earlier research with
women past menopause, those who consistently ate hamburger, beef steak and bacon very well done thus getting high levels of HCAs -had more
than four times the breast cancer risk in comparism with women who consumed these meats raw or medium done�?Like many carcinogens, HCAs have to be activated to be able to damage our DNA and pose cancer risk...  UNQUOTE.<o:p></o:p>

Source: http://www.tribune.com.ng/22032007/hlt2.html