Oestrogen may have a beneficial affect on the production of docosahexanoic acid (DHA, C22:6 (n-3)) in women. Research has shown that DHA levels in women are 14.6 % higher than in men, but only 10.2% higher when those women taking contraceptive pills were not included in the comparison (here). These results might account for the lower risk of cardiovascular disease seen in pre-menopausal women, because higher DHA plasma phospholipids levels are known to be protective of cardiovascular disease. The DHA needed by humans can be derived either directly from fatty fish such a mackerel, tuna, salmon or sardines, or can be synthesised from the essential fatty acid alpha linolenic acid (ALA, C18:3 (n-3)) which is of vegetable source. This process occurs via a series of elongation and desaturation reactions to produce EPA, and subsequently EPA is metabolised to DHA.
Previously, it was thought that EPA is converted to DHA via elongation to form docosapentanoic acid (DPA, C22:5 (n-3)), and then a subsequent desaturation via the enzyme Δ4-desaturase. However, research2 suggests that Δ4-desaturase does not exist. Therefore it is currently theorised that EPA is twice elongated to a C24:5 fatty acid, which then undergoes a desaturation at position 6 to produce tetracosahexanoic acid (THA, C24:6 (n-3)). β-oxidation of THA then reduces the chain length to produce DHA. Zellweger syndrome is a peroxisome biogenesis disorder (PBD) that is caused by a defect in the PEX genes that are required for normal function of peroxisomes. The disorder that results in a deficiency of functional peroxisomes and the sufferers are known to have lower than normal levels of DHA. It is though that oestrogen can effect on the proliferation of peroxisomes in cells and thus affect the production of DHA
Research1 has demonstrated that women receiving hormone replacement therapy (HRT) have significant reductions in the accumulation of EPA in phospholipids after receiving supplemental DHA free of EPA. Women receiving HRT had higher triglyceride, triglyceride:HDL cholesterol and C-reactive protein levels than controls not taking HRT. The subjects were then fed 2.8 g of DHA per day and all women had significant (20%) reductions in triglyceride levels, significant increases (8%) in HDL cholesterol levels, a significant lower overall ratio of triglycerides to HDL cholesterol (28%) as well as a significant (7%) decrease in resting heart rate. All women receiving the DHA supplements had increases in EPA, presumably caused by retro-conversion from DHA. However, those receiving hormone replacement therapy had a 45% lower increase in EPA and a 42% lower retro-conversion of DHA to EPA
The supplements used in this study were algal DHA which is a good source of DHA for vegetarians. The retro conversion of DHA to EPA has been estimated to be around 7.4% and 11.4% in young adult omnivores and vegetarians, respectively. In this study the retro-conversion of DHA to EPA for non-HRT women was 9.0%. However, in those women receiving HRT it was 5.2%. This would suggest that HRT somehow inhibits the retro-conversion of DHA to EPA. The authors suggest that this might be because HRT increases the β-oxidation of fatty acids in both peroxisomes and mitochondria. While increases the β-oxidation in peroxisomes would increase retro conversion of DHA to EPA, increases in mitochondrial β-oxidation would cause the oxidation of the DHA completely. Other studies confirm that women receiving HRT have altered levels of both EPA and DHA which may alter cardiovascular risk. .
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