Biologist Ray Peat has written about experiments done on animals decades ago, and basically what one learns is that animals on a high omega 6 and/or 3 diet die of cancer at alarming rates while those on a fat free diet hardly ever develop cancers and live longer in general.

Such experiments are straightforward and can be repeated when new variables are considered or discovered. There is no need for "models," "markers," "surrogate endpoints," "correlations," "associations," or "further investigations." That is, if a species of animal such as a dog lives a long and healthy life on a diet that a humans have eaten and found to be tasty and satisifying, then one is in a position to give advice to those interested, especially in light of such experiments as the following:

Blood Coagul Fibrinolysis. 2006 Jun;17(4):259-64.

Inhibitory effects of cardiotonic pills on platelet function in dogs fed a high-fat diet.

Zhang L, Zheng J, Li HM, Meng YX.

Department of Cardiology, Tianjin 254th Hospital (Affiliated Hospital of the Medical College of Nankai University), China bInstitute of Research and Development, Tasly Pharmaceutical Company, Tianjin, China.

Insulin resistance and the consequent metabolic disorders are associated with a state of platelet hyperactivity. Oxidative stress is responsible for the persistent platelet activation. We sought to study the inhibitory effect of cardiotonic pills, an oral herbal component, on platelet function in a dog model with insulin resistance induced by high-fat feeding. We fed 18 dogs with a high-fat diet and six dogs with normal chow as control for 6 months. Then, six dogs were fed with a high-fat diet and received additional aspirin (250 mg/day), and another six dogs received additional cardiotonic pills (1000 mg/day) for 4 months. Time-course changes in metabolic parameters and platelet function were detected. After high-fat feeding for 6 months, In addition, a platelet hyperactivity state, characterized by increased agonist 18 dogs developed a series of metabolic disorders including obesity, dyslipidemia, oxidative stress and insulin resistance.(arachidonic acid, ADP and collagen) induced platelet aggregation, platelet expression of adhesion molecules (P-selectin and GP IIb/IIIa), and platelet intracellular calcium concentration, was indicated. Cardiotonic pills showed a significant antioxidative activity by presenting an increase in plasma superoxide dismutase and decrease in erythrocyte glutathione, as well as a lipid-lowering effect (decrease in both plasma cholesterol and triglyceride). Either aspirin or cardiotonic pills could significantly reverse the platelet hypersensitivity and hyperfunction. Compared with aspirin, cardiotonic pills showed a more exaggerated inhibitory effect on platelet function (a significantly decreased collagen-stimulated platelet aggregation, and expression of adhesion molecules). In conclusion, cardiotonic pills inhibited platelet hyperfunction in dogs with insulin resistance. This inhibitory effect may mainly be explained by antioxidative activity and metabolic control.

Note that we do not know what kind of fat was used in the "high fat diet." The researchers are assuming, apparently, that any fat source, when fed in such amounts as they do here, will result in: "...a series of metabolic disorders including obesity, dyslipidemia, oxidative stress and insulin resistance."

My modest proposal is to repeat this experiment, except to substitute fresh coconut oil for whatever fat source they used here, and see if such "disorders" result. In light of the rarity of these disorders among peoples who eat large amounts of coconut products, it seems highly unlikely, but the important point is that it would be conclusive, because the basic chemistry is known. That is, unsaturated fatty acids can cause damage in the oxidative stress context whereas saturated ones cannot, so if the dogs are fine on the high fat/coconut oil diet, then we know that unsaturated fatty acids are the "culprit," and people should be told to avoid such "food" products.

Experiments in alcohol related liver injury, interestingly, have demonstrated this point, though you don't hear about this in the media, for example:

Clin Biochem. 1989 Feb;22(1):41-9.

Biochemical basis for alcohol-induced liver injury.

French SW.

Department of Pathology, Faculty of Health Sciences, University of Ottawa, Ontario, Canada.

Chronic ethanol ingestion leads to hepatocellular injury and alcoholic liver disease (ALD) only if multiple factors combine to favor centrilobular hepatocellular hypoxia. It is hypothesized that these factors include a shift in the redox state, the induction of the microsomal ethanol oxidizing system (MEOS), a high blood alcohol level (BAL), a high polyunsaturated fat diet and episodic decreased O2 supply to the liver. The shift in the redox state favors a low cellular pH, decreased fatty acid oxidation and increased triglyceride formation. The increased MEOS activity increases O2 consumption and portal-central O2 gradient as well as favors acetaldehyde toxic effects including retention of hepatic lipids and export proteins causing cell swelling. The resultant increase in the concentration of acetaldehyde and lactate may stimulate fibrosis as they stimulate collagen synthesis in vitro. The resultant fatty liver narrows the sinusoids slowing sinusoid blood flow. The combination of events reduces available O2 leading to decreased levels of ATP and cellular pH making the liver vulnerable to episodes of systemic hypoxia. The role of membrane changes are reviewed, i.e., 1) membrane fluidity as related to changes in the species of phospholipids, 2) mitochondrial function as related to the changes in the lipid environment of the electron transport chain, and 3) linoleic acid-prostaglandin metabolism. Acute ethanol in vitro has been shown to affect liver cell metabolism regulation by triggering and increasing protein phosphorylation through the Ca2+-phospholipase C pathway. A high fat diet enhances the liver injury caused by chronic ethanol ingestion.

J Nutr. 2004 Apr;134(4):904-12.

And:

Dietary saturated fat reduces alcoholic hepatotoxicity in rats by altering fatty acid metabolism and membrane composition.

Ronis MJ, Korourian S, Zipperman M, Hakkak R, Badger TM.

Arkansas Children's Nutrition Center, Department of Pharmacology/Toxicology, University of Arkansas for Medical Sciences, Little Rock, AR 72205, USA. [email protected]

Rats fed a saturated fat diet are protected from experimentally induced alcoholic liver disease, but the molecular mechanisms underlying this phenomenon remain in dispute. We fed male Sprague-Dawley rats intragastrically by total enteral nutrition using diets with or without ethanol. In 1 control and 1 ethanol group, the dietary fat was corn oil at a level of 45% of total energy. In other groups, saturated fat [18:82 ratio of beef tallow:medium-chain triglyceride (MCT) oil] was substituted for corn oil at levels of 10, 20, and 30% of total energy, while keeping the total energy from fat at 45%. After 70 d, liver pathology, serum alanine aminotransferase (ALT), biochemical markers of oxidative stress, liver fatty acid composition, cytochrome P450 2E1 (CYP2E1) expression and activity and cytochrome P450 4A (CYP4A) expression were assessed. In rats fed the corn oil plus ethanol diet, hepatotoxicity was accompanied by oxidative stress. As dietary saturated fat content increased, all measures of hepatic pathology and oxidative stress were progressively reduced, including steatosis (P < 0.05). Thus, saturated fat protected rats from alcoholic liver disease in a dose-responsive fashion. Changes in dietary fat composition did not alter ethanol metabolism or CYP2E1 induction, but hepatic CYP4A levels increased markedly in rats fed the saturated fat diet. Dietary saturated fat also decreased liver triglyceride, PUFA, and total FFA concentrations (P < 0.05). Increases in dietary saturated fat increased liver membrane resistance to oxidative stress. In addition, reduced alcoholic steatosis was associated with reduced fatty acid synthesis in combination with increased CYP4A-catalyzed fatty acid oxidation and effects on lipid export. These findings may be important in the nutritional management and treatment of alcoholic liver disease.

UPDATE: In recent study (Prostaglandins Other Lipid Mediat. 2006 Jul;80(1-2):1-14. Epub 2006 Jun 23.), the researchers state: "In this regard, we have shown that COX nitration occurs in human atherosclerotic tissue and in aortic lesions from ApoE(-/-) mice kept on a high fat diet." Again, we are not told what the fat source is, and it's likely that if the mice were raised on something like coconut oil as their primary fat source, this result would not occur. If only such experiments were properly controlled, in accordance with the scientific method - this is so obvious that it is quite frightening that the "brightest minds" (the ones most people trust their lives to) seem totally unaware of relevant factors that need to be taken into account.

And then there is more of the same: "Polyunsaturated free fatty acids (PUFAs) participate in normal functioning of the cell, particularly in control intracellular cell signalling. As nutritional components they compose a human diet with an indirect promoting influence on tumourogenesis... free AA levels are elevated in colon cancer, as AA is the precursor to biologically active eicosanoids." Those like myself who do the research with an open mind find these kinds of statements boring at this point, because there are so many of them in the literature, and yet mainstream media "journalists" appear to be completely ignorant of these matter-of-fact remarks about PUFAs.

Source: Mol Cell Biochem. 2006 Jul 21; [Epub ahead of print]

Title: "Altered membrane free unsaturated fatty acid composition in human colorectal cancer tissue."

Authors: Szachowicz-Petelska B, Sulkowski S, Figaszewski ZA.