Linoleic acid is an essential fatty acid. People carrying different variants of the FADS1 gene had a different inflammatory response and different changes in their fasting glucose levels when supplementing their diet by linoleic acid rich sunflower oil. This was the first time these associations were studied in humans. A new study from the University of Eastern Finland shows how the effects of linoleic acid on the human body are largely dependent on genes. According to Postdoctoral Researcher Maria Lankinen from the University of Eastern Finland, the findings warrant speculation on whether the recommended intake of linoleic acid – and possibly other fatty acids, too – should be tailored to match a person’s genes. The FADS1 gene regulates the body’s fatty acid metabolism and also plays a role in glucose metabolism. A person’s diet, in turn, has a major impact on the concentrations of different fatty acids in the body. Linoleic acid is found in plant-based oils, nuts and seeds, and it is the most common polyunsaturated omega-6 fatty acid. A high intake and high levels of linoleic acid in the blood have been associated with a reduced risk of type 2 diabetes and cardiovascular disease.
On the other hand, however, the metabolites of linoleic acid can mediate inflammation, which is why a high intake of linoleic acid is regarded as a plausible factor contributing to low-grade inflammatory state. According to the newly published study, these contradictory observations could be explained by genetic differences. The study explored whether point mutations in rs174550 of the FADS1 gene modify the effects of linoleic acid on serum fatty acid composition and on fasting glucose, insulin and CRP levels. These were analysed in more than 1,300 middle-aged men participating in the METSIM (Metabolic Syndrome in Men) Study. In addition, 60 men participated in the FADSDIET intervention for carriers of two different gene variants. Over the course of four weeks, they supplemented their daily diet by 30-50 ml of linoleic acid rich sunflower oil. Selecting the participants on the basis of their genes makes this a unique research setting, which provides information on the interactions of diet with genes. The findings indicate that the effects of linoleic acid on the human body are largely dependent on which variant of the FADS1 gene a person is carrying.
This has an effect on, for example, how effectively a linoleic acid supplement can lower fasting glucose levels. Moreover, depending on the gene variant, increased intake of linoleic acid can make a person’s CRP levels go either up or down. The FADS1 gene variant also had an effect on the levels of inflammation mediators, which are created from the metabolites of linoleic acid and other omega-6 fatty acids. In addition to dietary intakes, which are low for many individuals, tissue EPA and DHA are also influenced by the rate of bioconversion from α-linolenic acid (α-LNA). Δ-5 and Δ-6 desaturase enzymes, encoded for by FADS1 and FADS2 genes, are key desaturation enzymes involved in the bioconversion of essential fatty acids (α-LNA and linoleic acid (LA) to longer chained PUFA. In general, carriers of FADS minor alleles tend to have higher habitual plasma and tissue levels of LA and αLNA, and lower levels of arachidonic acid, EPA and also to a lesser extent DHA. In conclusion, available research findings suggest that FADS minor alleles are also associated with reduced inflammation and cardiovascular risk, and that total dietary fat and fatty acid intake have the potential to modify relationships between FADS gene variants and circulating fatty acid levels.
However to date, neither the size-effects of FADS variants on fatty acid status, nor the functional single nucleotide polymorphisms in FADS1 and 2 have been identified. Such information could contribute to the refinement and targeting of EPA and DHA recommendations, whereby additional log chain n-3 PUFA intakes could be recommended for those carrying FADS minor alleles.
- Edited by Dr. Gianfrancesco Cormaci, PhD, specialist in Clinical Biochemistry.
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