Table 1.

Conditions associated with reduced neural DHA levels.

	Condition	Description
1	Dietary deficiency of ALA	Dietary insufficiency of ALA which would be expected to result in decreased DHA synthesis in the liver and increased 22:5n-6 synthesis from LA, and hence less DHA and more 22:5n-6 transported to brain via plasma lipoproteins.
2	Brain DHA uptake receptors	Polymorphisms in brain fatty acid transport proteins such as fatty acid binding proteins (FABP), fatty acid transport proteins (FATP), fatty acid translocase FAT/CD36, DHA uptake receptors Mfsd2a, and APOE4, and hence less uptake of DHA into the brain from the circulation [7,8].
3	Brain DHA metabolism	Acyl CoA synthetase 6 controls neuronal DHA levels independent of diet by ligating CoA to free DHA, and hence polymorphisms could reduce brain DHA levels [9]
4	Brain PUFA peroxidation	Increased peroxidation of PUFA in brain, where it would be expected to result in increased indices of lipid peroxidation, resulting peroxidation/loss of DHA in the brain [10].
5	Liver ALA metabolism	Polymorphisms in liver FADS1/2 desaturases and elongases [11,12,13] resulting in reduced DHA synthesis from ALA, and hence less DHA transported to brain via plasma lipoproteins.
6	Liver function	Liver damage, such as fatty liver induced by diet, alcohol, or liver diseases, which might impact on the capacity of the liver to synthesise DHA from ALA, and hence less DHA transported to brain via plasma lipoproteins [14,15].