I read with interest the articles by Targher et al. (1), which shows that nonalcoholic fatty liver disease (NAFLD) is extremely common in type 2 diabetes and is associated with a higher prevalence of cardiovascular disease (CVD), and by Hu et al. (2), which shows that type 2 diabetes is associated with an increased risk of Parkinson's disease. Neither is surprising, considering society's excessive use of polyunsaturated n-6–rich vegetable oils (a source of linoleic acid, a short-chain n-6 polyunsaturated fatty acid [PUFA]) in place of saturated fats, in addition to a deficiency of n-3 fat. It is possible to hypothesize that Parkinson's disease, CVD, and diabetes share common ground linked by improper diet.
Svegliati-Baroni et al. (3) have demonstrated that supplementation of n-3 PUFA ameliorates fatty liver and degree of liver injury in rats. In humans, a high-fat intake, particularly of n-6 fat and a high n-6:n-3 ratio, was found in patients of nonalcoholic steatohepatitis (4).
A diabetes prevention study in Eskimos demonstrated that a higher consumption of long-chain n-3 fatty acids was associated with improved glucose tolerance, insulin resistance, and components of the metabolic syndrome (5).
Diabetes, heart disease, and NAFLD appear to be chronic inflammatory conditions in response to inadequate or improper diet. As demonstrated by Julien et al. (6), nutritional intake affects brain fatty acids and is a determinant of Parkinson's disease. The same applies to diabetes (7), and the benefit of n-3 fat in CVD is also well known. Long-chain n-3 PUFAs decrease triglycerides, inflammatory eicosanoids and cytokines, blood pressure, and thrombosis and increase nitric oxide production and endothelial relaxation (8).
A problem in Parkinson's disease is the decrease in dopamine. Studies also show that Parkinson's patients who experienced motor complications due to levodopa had higher arachidonic acid concentrations in the cortex compared with control subjects and levodopa-treated patients devoid of motor complications (6).
PUFAs are required in the ratio of n6:n3 of <5:1. Arachidonic acid and docosahexanoic acid are longer PUFAs of n-6 and n-3, respectively. In proper proportion, their intake determines homeostasis of various body tissues including nervous tissue. Animal studies reveal that n-3 fatty acid deficiency decreases dopamine receptor binding (9) and alters dopamine metabolism (10), and supplementation with long-chain PUFAs prevents the decrease in dopaminergic neurotransmitters in the frontal cortex caused by deficiency in alphalinolenic acid (n-3 fat) (11).
Universal recommendations to correct PUFA imbalance are needed to prevent diabetes and a host of diseases including Parkinson's disease, heart disease, and NAFLD. Implications point to a solution for preventing all the four diseases: correction of inadequate or improper diet; therefore there is an urgent need for large-scale studies in this respect.
