Omega-3 fatty acids form the basis of many treatment protocols due to the prevalence of deficiency in the western diet and their being indicated in a plethora of disease states. In the age of nutrigenomics, further evidence is coming to light that suggests a greater need for omega-3 supplementation in individuals with certain single nucleotide polymorphisms (SNPs), as revealed in DNA testing. The protective benefits of omega-3 fatty acids have been thoroughly demonstrated in many major conditions - well known among them are Alzheimer’s disease (AD), non-alcoholic fatty liver disease (NAFLD) and cardiovascular disease (CVD). SNPs relating to these diseases are also linked to altered fatty acid metabolism and therefore omega-3 requirements are likely to be greater in in these individuals. 
DHA is known to be depleted in brain regions associated with AD. This may be as a result of more than just inadequate dietary intake – the genetic variability on the APOE4 gene is also believed to contribute. Omega-3 DHA offers protection against mechanisms that drive the pathology of AD, such as anti-inflammatory and anti-amyloidogenic effects, as well as the ability to reduce phosphorylation.
In NAFLD, omega-3 aids in reducing inflammation and hepatic lipogenesis, preventing triglyceride accumulation. More specific processes in which omega-3 may affect NAFLD include acting via the downregulation of sterol-regulatory-element-binding protein 1c (SREBP-1c) and up-regulation of peroxisome-proliferator-activated receptor a (PPAR-a), consequently favouring fatty acid oxidation and reducing hepatic steatosis.
Omega-3s also influence CVD risk via several mechanisms – interacting with and modulating membrane channels and proteins, altering cellular membrane properties, affecting eicosanoid profiles and regulating gene expression. A range of genetic SNPs have been associated with CVD risk, chief among them are the APOA1 and NOS3. A recent meta-analysis concluded that omega-3 may be associated with lowered inflammatory biomarkers and lipid profiles in patients with CVD as well as in diabetic patients.
Genes associated with disease and the effects of omega-3 fatty acid:
|Gene||Associated Condition||The Role of n-3 PUFAs|
Apolipoprotein A-I is a crucial constituent of HDL and the consumption of omega-3 fatty acids may influence APOA1 gene expression.
|NOS3||Risk markers of CVD||
Carriers of a minor allele in the NOS3 gene have plasma triacylglycerol (TAG) concentrations which are more responsive to n-3 PUFAs, thus may benefit from its consumption to reduce plasma TAG.
Omega-3 activates PPAR-α, altering lipid metabolism to increase fat catabolism, leading to reduced hepatic steatosis and triglycerides.
DNA testing for SNPs can prove to be a useful clinical tool when individualising client protocols as it offers a deeper insight into specific areas of a client’s health and how best to target your approach.
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