EPA AND DHA AND THE BRAIN

Long-chain polyunsaturated fatty acids are important structural components in cell membrane phospholipid bilayers, with EPA and DHA concentrated in synaptic membranes in the brain and in the retina (Dyall and Michael-Titus, 2008). Variations in the ratio of n-3:n-6 composition may affect membrane fluidity, thickness, or other characteristics, as well as influence how proteins embedded in the membrane move and function (Lauritzen et al., 2001). There is evidence that n-3 fatty acids protect normal mitochondrial function and reduce excitotoxicity (reviewed in Dyall and Michael-Titus, 2008). Human studies (years 1990 and later) addressing the influence of EPA/DHA on resilience or treatment of central nervous system (CNS) injuries or disorders, such as stroke, epilepsy, and subarachnoid hemorrhage, are presented in Table 13-1. Likewise, Table 13-1 also lists animal studies on the effects of EPA/DHA on TBI.

There are various models that explain the transportation of fatty acids through the blood-brain barrier, most of them involving complexes with albumin and circulating lipoproteins. Other models propose that there are no specific transporters that participate in this process (Hamilton and Brunaldi, 2007).

USES AND SAFETY

There are insufficient data to correlate reduced concentrations of n-3 fatty acids with functional impairments; therefore, no Estimated Average Requirements (EARs) have been established. An Adequate Intake (AI) for alpha-linolenic acid, based on the average daily intake by apparently healthy people that is therefore assumed to be adequate, has been set at 1.6 g/day for adult men and 1.1 g/day for adult women (IOM, 2005). Any intake of EPA and DHA, which normally accounts for about 10 percent of total n-3 fatty acids in the diet, is considered to contribute to the AI for ALA. The most effective way to increase body stores of EPA and DHA is through increased dietary intake of oil from cold-water fish species and from krill.

Intake of up to 1 g/day of n-3 fatty acids from dietary fish intake is generally regarded as having very low risk, but higher intakes can increase the risk of gastrointestinal upset as well as increases in blood glucose and concentrations of low-density lipoprotein (LDL) cholesterol (Kris-Etherton et al., 2002). Increased intake of n-3 fatty acids will decrease the synthesis of the eicosanoid thromboxane A2, which promotes platelet aggregation (Kramer et al., 1996). Excessive intake can therefore increase the risk of bleeding, although this was not generally observed in a number of randomized clinical trials of fish-oil supplementation (Huang et al., 2007; Javierre et al., 2006). Environmental contaminants such as mercury and polychlorinated biphenyls can accumulate in certain species of fish, presenting another potential risk. The risk from mercury toxicity can be diminished, however, by avoiding some fish species (e.g., swordfish, mackerel), and ingestion of other contaminants can be diminished by removing the skin and fat from fish before cooking. Alternatively, purified EPA and DHA can be taken in capsule form.

Although increased dietary n-3 fatty acid intake reduces cellular production of ROS, the increased desaturation (double bonds) of these fatty acids increases susceptibility to lipid peroxidation, which may have detrimental effects on specific cellular processes, such as T cell–mediated immune function (Wu and Meydani, 1998). This can be ameliorated, however, by adequate supplementation with the antioxidant vitamin E (Wu and Meydani, 1998).



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