Perinatal Supplementation of Long-Chain Fatty Acids as a Strategy to Prevent Hypertension, Diabetes Mellitus and Coronary Heart Disease

by | Jul 2, 2008 | NHRI

By Dr. Undurti Das, EFA Sciences LLC, USA. Conference paper presented at the American Oil Chemists Society (AOCS) Annual Meeting & Expo, May 2004.  Theme: Cost-Effective Methods to Address the Leading Causes of Death & Chronic Diseases

It is interesting to note that exclusive breast-feeding protects against the development hypertension and type 2 diabetes mellitus, and decreases the risk of CHD in later life (1-3). The exact reason for this beneficial action of breast-feeding is not known. Breast milk is rich in linoleic acid (LA, 18:2 ω-6), gamma-linolenic acid (GLA, 18:3 ω-6), arachidonic acid (AA, 20:4 ω-6), α-linolenic acid (ALA, 18:3 ω-3), EPA (eicosapentaenoic acid) and DHA (docosahexaenoic acid (see table 1 for fatty acid composition of breast milk). I suggest that the decreased incidence of adult diseases in breast-fed subjects can be attributed to its high content of both ω-6 and ω-3 long-chain polyunsaturated fatty acids (ω-6 and ω-3 LCPUFAs).

Breast-fed subjects showed lower blood pressure in later life (2, 4). It is possible that the unique LCPUFA content of human milk may have caused structural and/or metabolic changes that influenced blood pressure. This is supported by the observation that in Sprague-Dawley rats ω-3 PUFA deficiency (especially DHA) induced during the perinatal period resulted in raised blood pressure later in life, even when animals were subsequently repleted with this fatty acid (5). There appears to be a critical period with regard to the functionality of neural-PUFAs (especially DHA) and suggests that perinatal supplementation of LCPUFAs (AA, EPA, and DHA) prevents hypertension in adult life (6).

Several case-control studies reported a negative correlation between frequency and duration of breast-feeding and type 1 diabetes (7). Bottle-fed subjects had a higher plasma glucose concentration after a standard oral glucose tolerance test compared to those who were breast-fed (8). In Pima Indians, type 2 diabetes in the next generation was less common among breast-fed children (6.9 and 30.1% among offspring of non-diabetic and diabetic women respectively) than among bottle-fed children (11.9 and 43.6% respectively) (9). Subjects who were exclusively breast-fed for the first 2 months had significantly lower rates of type 2 diabetes compared with those exclusively bottle-fed (96). This decreased incidence of diabetes in breast-fed subjects can be related to the presence of LCPUFAs in human milk.

Hypertension, and type 2 diabetes mellitus influence cardiovascular disease. Compared with men weaned before one year, men not weaned had higher mean serum concentrations of cholesterol, LDL, and apolipoprotein B (10). Men who had been breast-fed had a high mean serum concentrations of total cholesterol, LDL and apolipoprotein B. Standardized mortality ratios for CHD were 97 in men who had been breast-fed and had not been weaned at 1 year, 79 in breast-fed men who had been weaned at 1 year, and 73 in men who had been breast-fed and bottle-fed (10). This indicates that age of weaning and method of infant feeding influences adult serum lipid levels and mortality from CHD. The best results were seen in men who had been breast-fed and had been weaned at 1 year. Although the exact reason for this apparent adverse outcome in terms of abnormal lipid profile and higher incidence of CHD in people who had prolonged breast-feeding (10) is not clear, it can be attributed to programming of cholesterol metabolism in response to the unique lipid and/or hormone contents of breast milk. It is known that the expression of hepatic enzymes or low-density lipoprotein receptors is adversely affected by the high fat diet in later life (11-14). Breast-fed baboons when given a Western style high saturated fat diet had more early atherosclerotic changes in adulthood than formula-fed animals. It was also reported that the longer the period of breast-feeding the less distensible the artery wall in early adult life and these vascular changes were not explained by alterations in plasma cholesterol concentration (15). Decrease in arterial distensibility is an index of vascular elastic behavior as a result of arterial cholesterol accumulation (16). This suggests that breast-feeding programmes baboons and humans to be conservative with cholesterol-perhaps appropriately for their normal diet (breast milk)-but it is the high fat Western diet that leads to arterial disease. This suggests that to continue to derive the benefits of breast-feeding it is necessary to consume the same type and amounts of lipids that are present in breast milk, namely the LCPUFAs.

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