Benefits of Omega-3s and Diabetes

Increased diabetes rates parallel a rise in consumption of Omega-6 relative to Omega-3

By: Eric S. Freedland, MD, Boston University School of Medicine

(Note by Cheryl: n-6 = Omega-6 and n-3 = Omega-3)

The increased prevalence of diabetes has paralleled a rise in consumption of n-6 (relative to n-3) fatty acids and trans fatty acids found in partially hydrogenated oil. Both can change cellular membrane phospholipid composition and decrease fluidity—a state associated with altered insulin receptors, decreased insulin sensitivity, and subsequent insulin resistance and hyperinsulinemia.  A large dietary glycemic load exacerbates the hyperinsulinemia.

Since 1850, the n-6 to 3 ratio in the Western diet has risen from 4:1 to greater than 20:1 as fats from fish, wild game, and leaves were replaced by the consumption of linoleic acid (LA)-rich oils from seeds.  Changes in feeding poultry and livestock have altered the n-6 and n-3 content of the animal protein consumed.

This imbalance leads to a high proportion of arachidonic acid (AA)-derived eicosanoids such as thromboxane A2, leukotrienes, and the production of inflammatory mediators, e.g., cytokines and interleukins.  One of the most important functions of the vascular endothelium is to regulate inflammatory reactions, and too much linoleic acid can induce marked injury to endothelial cells. 78.

Excessive intake of the n-6 linoleic acid and relative n-3 deficiency have been postulated to be the major causes of the increasing western-type cancers, cardiovascular and cerebrovascular diseases and allergic hyperreactivity.

Several studies show an association between low intake of n-3 (relative to n-6) and a decrease in mortality from all causes, especially CHD.  Populations that consume a diet rich in Omega 3s have a lower prevalence of diabetes.

Epidemiological evidence from the Multiple Risk Factor Intervention Trial (MRFIT) of 12,866 American males revealed significant inverse relationships between dietary n-3 PUFA and mortality from CHD, cancer, and all-causes.  These effects could be improved by simply lowering the n-6 to n-3 ratio.  A study of 43,757 U.S. health care professionals followed for six years from 1986 found that diets high in n-3 acids are associated with a reduced risk of CHD independently of other dietary and non-dietary risk factors.  Prior to the last world war the prevalence of diabetes and CHD was climbing in Norway paralleling a rise in the n-6/n-3 ratio and consumption of more highly processed high glycemic foods.  Following a significant reduction in n-6/n-3 fat ratio during the war Norway recorded a sharp decrease of almost fifty percent in the incidence of diabetes and cardiovascular mortality.  Unfortunately, reversion to the previous dietary fat intake and n-6/n-3 fat ratio was followed by an equally rapid rise in both diabetes and CHD.

In the last 20 years, there has been a dramatic increase in the prevalence of type 2 diabetes and CHD in urban and upper socioeconomic groups in India.  This rise has paralleled an increase in the consumption of n-6 fatty and the n-6 to n-3 ratio.  Simply changing the composition of the dietary fat to increase the n-3 while decreasing the n-6 PUFA in patients with type 2 Diabetes had a significant impact.  This improved insulin action and reduced the required dosage of hypoglycemic agents.  The response was maximal when the n-6/n-3 ratio in dietary lipids was adequately lowered.

The United States has experienced a sharp and sustained fourfold rise in the number of diagnosed cases of diabetes since 1960.  This rise has paralleled the increased consumption of n-6 fats mostly in the form of seed oils which has risen after reports that n-6 PUFA lowered plasma cholesterol.  Adequate n-6 fatty acids are critical, especially in patients with type 2 diabetes who have an impaired delta 6 desaturase which is key in the first step of n-6 metabolism to eicosanoids.  However, Toborek et al provide compelling evidence that too much linoleic acid can induce profound inflammatory responses in cultured human endothelial cells—most markedly among all the unsaturated fatty acids studied.

Greater than eighty percent of insulin mediated glucose disposal takes place in skeletal muscle. In adult humans, insulin resistance is associated with low proportions of polyunsaturated fatty acids (PUFAs) in muscle membrane structural lipid whereas a higher percentage unsaturated fat, especially long-chain polyunsaturated fatty acids (the Omega-3s), is associated with greater insulin sensitivity 69, 71, 91, 92. N-3 PUFAs may improve insulin sensitivity by increasing membrane fluidity.

Dietary intake has been shown to influence the adipose and muscle membrane phospholipid fatty acid (FA) composition 93, however endogenous factors also play a role. Some adult populations with similar diets demonstrate wide ranges in muscle membrane FA profiles, and mothers at higher risk of the metabolic syndrome (as determined by fasting insulin and triglyceride levels) have children with a muscle membrane characterized by a lower proportion of n-3 PUFAs 94. This suggests there may be genetic differences in the ability to incorporate n-3s into membranes, or perhaps the concurrent ingestion of trans and saturated fats along with other environmental factors is preventing the incorporation of n-3s. This underscores the importance of increasing the amount of n-3s in the diet relative to n-6s to ensure optimal FA muscle membrane composition and insulin sensitivity.

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