Hypertension induced by omega-3 polyunsaturated fatty acid deficiency is alleviated by alpha-linolenic acid regardless of dietary source.

Key Findings:

n-3 fatty acids in the prenatal diet are important in the development of the cardiovascular system and blood pressure control. In this research, hypertension induced by n-3 fatty acid deficiency from a safflower oil-based diet was prevented by canola oil or flaxseed oil diets rich in ALA. Both groups of animals showed lower body fat. Elevated leptin levels were noted in control animals and were associated with hypertension. DHA levels in the prefrontal cortex were related to the n-3 fatty acid deficiency/sufficiency of the diet the animals were fed. ALA contents differed in the flax (1.8%) and canola (0.8%) diets, but no differences DHA levels were found in the frontal cortex of animals. Hypertension caused by n-3 fatty acid deficiency can be prevented by ALA. Hypertension induced by the n-3 fatty acid deficiency was related to higher body weight, body fat and plasma leptin levels.

ABSTRACT:

n-3 polyunsaturated fatty acid deficiency, particularly during the prenatal period, can cause hypertension in later life. This study examined the effect of different sources of alpha-linolenic acid (canola oil or flaxseed oil) in the prevention of hypertension and other metabolic symptoms induced by an n-3 fatty acid-deficient diet. Dams were provided one of three experimental diets from 1 week before mating. Diets were either deficient (10% safflower oil-DEF) or sufficient (7% safflower oil+3% flaxseed oil-SUF-F; or 10% canola oil-SUF-C) in n-3 fatty acids. The male offspring were continued on the maternal diet from weaning for the duration of the study. Body weight, ingestive behaviors, blood pressure, body composition, metabolic rate, plasma leptin and brain fatty acids were all assessed. The DEF animals were hypertensive at 24 weeks of age compared with SUF-F or SUF-C animals; this was not evident at 12 weeks. These results suggest that different sources of ALA are effective in preventing hypertension related to n-3 fatty acid deficiency. However, there were other marked differences between the DEF and, in particular, the SUF-C phenotype including lowered body weight, adiposity, leptin and food intake in SUF-C animals. SUF-F animals also had lower, but less marked reductions in adiposity and leptin compared with DEF animals. The differences observed between DEF, SUF-F and SUF-C phenotypes indicate that body fat and leptin may be involved in n-3 fatty acid deficiency hypertension. (Author’s abstract)