Docosahexanoic acid (DHA, C22:6 (n-3)) is a metabolite of the essential fatty acid alpha-linolenic acid (ALA, C18:3 (n-3)) and is the most abundant n-3 fatty acid in mammalian brain tissue. A source of DHA in the diet is essential to proper brain development and function, and this can be obtained by consumption of cold water fish. Trout, salmon, herring, tuna, mackerel and sardines all contain high levels of DHA. In addition these fish contain high amounts of eicosapentanoic acid (EPA, C20:5 (n-3)) which can be metabolised in humans to form DHA via elongase and desatuarse enzymes. Docosahexanoic acid can also be obtained from ALA through a series of elongation and desaturation reactions, although the conversion rate is perhaps less than 1 % (higher in women and during pregnancy). Good sources of ALA include flax and walnut oils, but these oils are not generally consumed in high amounts in Western diets.
The DHA levels of the brain change based on the fatty acids present in the diet as well as the age of the individual. Generally, DHA levels increase in early life during times of brain development but decrease with age. Deficiencies of DHA in the diet result in an increased desaturation of n-6 fatty acids to their 22 carbon metabolites docosapentanoic acid (DPA, C22:5 (n-6)). This results in increased brain concentrations of DPA, which is unable to allow proper brain function because of its structural differences with DHA. Conversion of ALA to DHA is generally poor in humans with the slowest step being the conversion of EPA to DHA. In contrast, dietary absorption of DHA is high and DHA is readily incorporated into phospholipids membranes and rapidly increases plasma levels. Dietary DHA is also rapidly incorporated into brain lipids.
During pregnancy DHA is transported from the mother to the foetus via the placenta and studies suggest that higher maternal intakes of DHA result in higher foetal levels. Once the child is born their DHA intake must come from mother’s milk. The amount of DHA consumed by the new born is therefore completely dependent on the fatty acid profile of the mother’s diet, with higher intakes of DHA resulting in higher milk levels of DHA. However, because of the poor conversion rate, high level of ALA in the mothers milk do not result in higher phospholipids levels of DHA in the infant. Deficiency of DHA in the mother’s diet results in a lower level of DHA in the infant and this can effect brain development and function. In animals, deficiency of DHA results in brain levels of DHA that are 50 to 80 % lower than control animals.
Levels of DHA in the brain can reach 35 % of fatty acids in synaptic membranes, but levels are relatively low in plasma phospholipids. This suggests that the brain is able to concentrate DHA to the detriment of the plasma. The rapid turnover of fatty acids within the membranes of the brain ensures that the DHA concentration remains high if present in the diet. Esterified DHA in phospholipids of the neuronal membranes are theorised to increase signal transduction because they increase membrane fluidity and allow greater interaction of membrane and cytosolic proteins. The increased membrane fluidity may also increase speed of synaptic communications and thus improve brain efficiency. Unesterified DHA appears to cause regulation of gene expression and may also be metabolised to compounds that may have neuroprotective properties. Unesterified DHA may also allow the formation of new neurones in the brain.
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