HOME Previous Columns Email Contacts Advertising

A sample of actual research studies acquired through Pub/Med/ There are over 120 such studies that prove the harmful effects of trans fatty acids, trans-isomers on the body that cause diabetes, coronary heart disease, breast cancer, other cancers, auto-immune disorders, attention deficit disorders and more! You can only pull the full studies if you have a logon ID from a Medical University Library on Pub/Med. You can get this by going in to a University Medical Library and acquiring one.

Isr J Med Sci 1996 Nov;32(11):1134-43
Diet and disease--the Israeli paradox: possible dangers of a high omega-6
polyunsaturated fatty acid diet.
Yam D, Eliraz A, Berry EM
Department of Membrane Research and Biophysics,
Weizmann Institute of Science, Rehovot, Israel.

Israel has one of the highest dietary polyunsaturated/saturated fat ratios in the world; the consumption of omega-6 polyunsaturated fatty acids (PUFA) is about 8% higher than in the USA, and 10-12% higher than in most European countries. In fact, Israeli Jews may be regarded as a population-based dietary experiment of the effect of a high omega-6 PUFA diet, a diet that until recently was widely recommended. Despite such national habits, there is paradoxically a high prevalence of cardiovascular diseases, hypertension, non-insulin-dependent diabetes mellitus and obesity-all diseases that are associated with hyperinsulinemia (HI) and insulin resistance (IR), and grouped together as the insulin resistance syndrome or syndrome X. There is also an increased cancer incidence and mortality rate, especially in women, compared with western countries. Studies suggest that high omega-6 linoleic acid consumption might aggravate HI and IR, in addition to being a substrate for lipid peroxidation and free radical formation. Thus, rather than being beneficial, high omega-6 PUFA diets may have some long-term side effects, within the cluster of hyperinsulinemia, atherosclerosis and tumorigenesis.

J Physiol Pharmacol 1993 Dec;44(4):391-8
Effects of saturated and polyunsaturated fat enriched diet on the skeletal
muscle insulin sensitivity in young rats.
Budohoski L, Panczenko-Kresowska B, Langfort J, Zernicka E, Dubaniewicz A,
Ziemlanski S, Challiss RA, Newsholme EA
Department of Applied Physiology, Polish Academy of Sciences, Warsaw.

The purpose of this study was to evaluate the effect of diets enriched with fat containing different amounts (30% or 60% total energy) of either saturated (SF) or polyunsaturated fatty acids (PUFA) on glucose tolerance in vivo and insulin sensitivity of glucose utilisation by the soleus muscle in vitro. Young rats were maintained for 28 days after weanling on diets containing either sunflower oil (PUFA), animal fat (butter+lard - SF) or the standard laboratory chow (controls). The sunflower oil added to a diet in moderate quantities (30% total energy) improved the total glucose tolerance, while the diets containing high percentage of PUFA (60%) and moderate or high contents of SF caused impairment of glucose tolerance. The diet with 30% of total energy derived from sunflower oil increased the in vitro sensitivity of glucose utilisation to insulin by the soleus muscle, while in contrast, higher proportions of energy given in a form of PUFA as well as the diets enriched with animal fat impaired the sensitivity of this process to insulin. It is also important to note that the synthesis of glycogen in muscles taken from the rats fed high percentage of saturated fatty acid was found unresponsible to insulin. It is concluded that composition of dietary fat has a profound effect on carbohydrate tolerance and the response of muscle glucose metabolism to insulin. It seems likely that this effect may be at least partly mediated by changes in locally produced prostaglandins.

Lipids 1996 Mar;31 Suppl:S33-6
Polyunsaturated fatty acids inhibit hepatic stearoyl-CoA desaturase-1 gene in
diabetic mice.
Waters KM, Ntambi JM
Department of Biochemistry, University of Wisconsin-Madison 53706, USA.

Insulin and dietary fructose independently induce stearoyl-CoA desaturase 1 (SCD1) gene expression in diabetic mouse liver. In the present study, we again used diabetic mice and supplemented a high fructose diet with polyunsaturated fatty acids (PUFA) to determine the selective repression of SCD1 gene expression by dietary PUFA, as previously shown in normal mice. We saw dramatic repression of SCD1 mRNA expression, with trilinolenin at 3% and triarachidonin at 1% supplementation. We also observed significant repression of insulin-induced SCD1 mRNA upon supplementation of the noninducing starch diet with PUFA. In conclusion, our data demonstrate that PUFA negatively regulate hepatic gene expression through an insulin-independent mechanism.

J Am Coll Nutr 1993 Jun;12(3):274-80
Influence of dietary fat quantity and composition on insulin binding to rat
MacDonald RS, Thornton WH Jr
Department of Food Science and Human Nutrition, University of Missouri,
Columbia 65211.

It is presently recommended that the general US population reduce the consumption of dietary lipid in order to reduce the risk of several chronic diseases, although the mechanism(s) through which dietary factors alter cellular function remain unclear. Dietary lipid composition has been shown to alter the plasma membrane lipid composition of adipocytes, muscle and other tissues. These changes in membrane lipid composition have been correlated with altered insulin receptor binding and signal transduction. Insulin receptors are present on mucosal cells of the intestinal tract, although their role in this tissue is not fully understood. We have fed rats diets containing 6, 31.4 or 76% of calories from lard (Protocol 1) and found insulin binding to be increased in the duodenum and decreased in the colon of rats fed the high-fat diet. Additionally, we compared diets containing either 12 or 37.6% of calories from beef tallow (saturated fatty acids or SFA) or corn oil (polyunsaturated fatty acids or PUFA; Protocol 2) and found insulin binding in the jejunum to be significantly decreased by a low SFA or high PUFA diet relative to the low PUFA diet. These results suggest that intestinal insulin receptors are responsive to dietary lipid quantity and quality which may have implications as to the role of dietary factors in modifying nutrient transport and/or risk of intestinal disease.

Diabetes Care 1996 Apr;19(4):394-5
Fatty acids and insulin resistance.
Boden G
Division of Endocrinology/Metabolism and Diabetes, Temple University
School of Medicine, Philadelphia, Pennsylvania, USA.

We have demonstrated that physiological elevations in plasma free fatty acid concentrations inhibit insulin-stimulated glucose uptake in a dose-dependent manner in normal control subjects and in patients with NIDDM. Two possible mechanisms were identified: 1) a fat-related inhibition of glucose transport or phosphorylation that appeared after 3-4 h of fat infusion and 2) a decrease in muscle glycogen synthase activity that appeared after 4-6 h of fat infusion. We conclude that elevations of plasma FFAs caused insulin resistance and hence may play a significant role in the pathogenesis of insulin resistance in obesity and NIDDM.

Diabetes 1991 Feb;40(2):280-9
Influence of dietary fat composition on development of insulin resistance in rats. Relationship to muscle triglyceride and omega-3 fatty acids in muscle phospholipid.
Storlien LH, Jenkins AB, Chisholm DJ, Pascoe WS, Khouri S, Kraegen EW
Garvan Institute of Medical Research, St. Vincent's Hospital, Darlinghurst, New
South Wales, Australia.

High levels of some but not all dietary fats lead to insulin resistance in rats. The aim of this study was to investigate the important determinants underlying this observation. Insulin action was assessed with the euglycemic clamp. Diets high in saturated, monounsaturated (omega-9), or polyunsaturated (omega-6) fatty acids led to severe insulin resistance; glucose infusion rates [GIR] to maintain euglycemia at approximately 1000 pM insulin were 6.2 +/- 0.9, 8.9 +/- 0.9, and 9.7 +/- 0.4 mg.kg-1. min-1, respectively, versus 16.1 +/- 1.0 mg.kg-1.min-1 in chow-fed controls. Substituting 11% of fatty acids in the polyunsaturated fat diet with long-chain omega-3 fatty acids from fish oils normalized insulin action (GIR 15.0 +/- 1.3 mg.kg-1.min-1). Similar replacement with short-chain omega-3 (alpha-linolenic acid, 18:3 omega 3) was ineffective in the polyunsaturated diet (GIR 9.9 +/- 0.5 mg.kg-1.min-1) but completely prevented the insulin resistance induced by a saturated-fat diet (GIR 16.0 +/- 1.5 mg.kg-1.min-1) and did so in both the liver and peripheral tissues. Insulin sensitivity in skeletal muscle was inversely correlated with mean muscle triglyceride accumulation (r = 0.95 and 0.86 for soleus and red quadriceps, respectively; both P less than 0.01). Furthermore, percentage of long-chain omega-3 fatty acid in phospholipid measured in red quadriceps correlated highly with insulin action in that muscle (r = 0.97). We conclude that 1) the particular fatty acids and the lipid environment in which they are presented in high-fat diets determine insulin sensitivity in rats; 2) impaired insulin action in skeletal muscle relates to triglyceride accumulation, suggesting intracellular glucose-fatty acid cycle involvement; and 3) long-chain omega-3 fatty acids in phospholipid of skeletal muscle may be important for efficient insulin action.

Baillieres Clin Endocrinol Metab 1990 Dec;4(4):877-94
Polyunsaturated fatty acids and coronary heart disease.
Sanders TA

Polyunsaturated fatty acids can be used to replace saturated fatty acids in the diet in order to decrease plasma cholesterol concentrations. Intakes of up to 12% of the energy intake as linoleic do not decrease HDL cholesterol. Animal studies show a decreased incidence of atherosclerosis in animals fed polyunsaturated fats compared with saturated fats. Linoleic acid is required for the synthesis of eicosanoids, which are important in the regulation of platelet aggregation, blood pressure and coronary flow. Small amounts of linoleic acid are required for normal eicosanoid synthesis but larger intakes may lead to overproduction of eicosanoids. Dietary eicosapentaenoic and docosahexaenoic acids, which are provided by fish oils, have a protective effect on experimental myocardial infarction. Epidemiological evidence and secondary prevention trials suggest that these marine-derived polyunsaturates offer protection from CHD. Current advice on fat intake needs to be revised to take into account the neutrality of monounsaturated fatty acids and the need to balance the different types of polyunsaturated fatty acids.

J Nutr Sci Vitaminol (Tokyo) 1995 Apr;41(2):207-16
Polyunsaturated fatty acid-mediated suppression of insulin-dependent
gene expression of lipogenic enzymes in rat liver.
Iritani N, Fukuda H
Tezukayama Gakuin College, Sakai, Japan.

The effects of dietary polyunsaturated fat on insulin-dependent gene expression of lipogenic enzymes and a possible mechanism for PUFA-mediated suppression of the gene expression have been investigated in rat livers. When diabetic rats were injected with insulin, the insulin dose-dependent induction of lipogenic enzyme mRNAs were markedly reduced with increasing dietary corn oil. On the other hand, the PUFA-mediated suppression of the mRNA concentrations was partially restored by treatment with pioglitazone, a candidate for increasing insulin receptor phosphorylation. Moreover, insulin binding to receptors of liver, receptor autophosphorylation, and kinase activity toward exogenous substrate were lower in the corn oil diet group than in the hydrogenated fat group. The PUFA-mediated suppression of insulin binding was somewhat restored by pioglitazone, and the suppression of insulin receptor phosphorylation was significantly restored. It is suggested that the PUFA-mediated suppression of insulin-dependent gene expression of lipogenic enzymes can be ascribed to a decrease in insulin receptor binding primarily and also to receptor phosphorylation. Thus, PUFA appears to suppress the lipogenic enzyme gene expression stimulated by insulin.

J Nutr 1997 Jun;127(6):1077-83
Dietary soybean protein increases insulin receptor gene expression in
Wistar fatty rats when dietary polyunsaturated fatty acid level is low.
Iritani N, Sugimoto T, Fukuda H, Komiya M, Ikeda H
Tezukayama Gakuin College, Osaka, Japan.

To investigate the effects of different dietary fatty acids and proteins on glucose tolerance and insulin receptor gene expression, Wistar fatty rats (genetically obese, noninsulin-dependent diabetes mellitus) and their lean littermates (8 wk old) were fed a casein or soybean protein diet containing 9% partially saturated beef tallow (plus 1% corn oil), 10% corn oil or 10% fish oil for 3 wk. In glucose tolerance tests, plasma insulin concentrations were significantly higher in obese rats fed corn oil or fish oil than in those fed partially saturated beef tallow, particularly in the soybean protein groups. However, plasma glucose concentrations were not significantly affected by dietary protein or fat. The insulin receptor mRNA concentrations in livers and adipose tissues were higher in rats fed soybean protein/partially saturated beef tallow than in those fed any other protein/fat combination. Dietary soybean protein may help to reduce the insulin resistance, but only when a diet low in polyunsaturated fatty acids is consumed. On the other hand, the insulin receptor mRNA concentrations in adipose tissue were generally lower in the obese rats of all dietary groups than in the lean rats, suggesting that insulin resistance may be due to a defect of insulin receptor gene expression.

Other Studies that particularly prove that trans fatty acids and trans-isomers are the culprits. You will have to pull these up yourself on Pub/Med for they are quite long.

Diet-induced insulin resistance preceds other aspects of
the metabolic syndrome
Journal of Applied Physiology April 1998
Depart of phyiological Science
University of California
Barnard RJ, Roberts CK, Varon SM, Berge JJ

Title: Is Insulin resistance influenced by dietary linoleic acid
and trans fatty acid?
* the above shows the direct evidence that hydrogenated oils which produce trans fatty acids and trans-isomers have a direct influence on the pancreas and effectiveness of insulin and production.

Journal of Biology Medicine Oct. 1994M
Center for Genetics, Nutrition and Health, Washington DC
Simopoulous AP

* This study defintely shows that linoleic acid is positively related to insulin resistance, insulin-dependent diabetes IDDM and that trans fatty acids caused not only a significant reduction in the effectiveness of insulin but suppressing the pancreas from producing insulin.
Prostaglandins, Leukotcytes, Essential Fatty Aacids Oct. 1997
Metabolic Research Centre and Dpart. of Biomedical Science,
University of Australia.

Title: Fatty Acids, Triglecerides and sydromes of insulin resistance * this study shows that trans-fatty acids cause insulin resistance*

Other References:


1) Flax as a True Aid Against Arthritis, Heart Infarction, Cancer, and other Diseases, Dr. Johanna Budwig. (Apple Publishing Company, 1992),

2) The Kellogg Report, Joseph D. Beasley, M.D., Jerry J. Swift, M.A. (The Institute of Health Policy and Practice, U.S.A. 1989),

3) Potential Uses of Flax in Human Nutrition, Stephen C. Cunnane, Ph.D., Thomas M.S. Wolever, M.D., Ph.D. (Dept. of Nutritional Sciences, Faculty of Medkine, University of Toronto),

4) Improving Atherogenic Risk in Hyper-lipidemic Humans with Flax Seed Supplementation, Marvin L Bierenbaum, M.D., Tom R. Watkins, Ph.D. (Kenneth L. Jordan Heart Fund, U.S.A.)

5) Does Dietary Linolenic Acid Influence Blood Pressure?, E.M. Barry, J. Hirsch (Am. J. Clin. Nutr. 44:436-440,1989),

6) Effect of Flax and Dietary Alpha-Linolenic Acid on Blood Platelets in Human Subjects, B.J. Holub (Proceedings of the 53rd Flax Institute, U.S.A., 1990),

7) Use of Flaxseed as a Source of Omega-3 Fatty Acid in Human Nutrition, Molly A. Dieken (Proceedings of the 54th Flax Institute, U.S.A. 1992),

8) The Omega-3 Phenomenon, D. Ruden and C. Felix (Avon, 1987),

9) Beyond Pritiken, A.L.G. (Bantam U.S.A. 1988),

10) Fats and Oil, Udo Erasmus (Alive: Vancouver, 1986), 11) Healing Fats, Killing Fats, Udo Erasmus (1990).

Read DL Dewey's column
Hydrogenated Oils - Silent Killers

© 1996 - 1997 - 1998 ~ ~ David Lawrence Dewey

READ DL Dewey's
Previous Column
Hydrogenated Oils Are Silent Killers

HOME Previous Columns Email Contacts Advertising

©1997, 1998, 1999 Rocky Mountain Publicity
Updated October 7th, 1999
Email Contacts