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Does omega status depend on your genes?

Genetic data could end up rewriting some aspects of nutrition literature. This study looked at people from different locales around the world, to see if they metabolize certain fats differently depending on their genes

Study under review: Positive selection on a regulatory insertiondeletion polymorphism in FADS2 influences apparent endogenous synthesis of arachidonic acid

Introduction

Anatomically modern humans first appeared in East Africa nearly 200,000 years ago. Since then, humans have spread out to colonize most of the Earth, forcing adaptation to a wide range of new habitats and climates. These new environments and challenges to our survival likely resulted in powerful selective pressures (the driving forces of evolution and natural selection that alter the survival ability of an organism) on our DNA, leading to new gene variants, and combinations thereof, that were better suited for survival. These gene variants are called alleles, while specific combinations of alleles are called a genotype.

Recent examples of human evolution through natural selection include genetic changes in response to malaria[1], changes that favor lactose[2] (milk sugar) consumption in adulthood, and changes that regulate brain size[3]. For malaria, the selective pressure was the malaria virus, which increased the survivability of individuals who carried a mutation for sickle cell anemia because this mutation is highly protective against dying from malaria. While selective pressure has occurred throughout human evolution, the agricultural revolution and greater population sizes that began 10,000 years ago have accelerated[4] the rate at which we are able to observe evolutionary changes. The process of natural selection at a genetic level works in two ways. A random mutation could appear that is beneficial in the current environment, or a new environmental stress appears that makes an already existing genotype beneficial to have. In either case, the organism carrying the beneficial allele (whether new or preexisting) has a survival advantage and is likely to reproduce and pass it on to offspring. The chunks of DNA containing a specific set of alleles that tend to be inherited as a unit are called haplotypes, as pictured in Figure 1.

Figure 1: Alleles, genotypes, and haplotypes

Some of the many genes being explored for variation in modern humans are the fatty acid desaturase (FADS) genes, which code for the enzymes responsible for transforming the shorter-chained omega-3 and omega-6 fatty acids into their long-chained derivatives. Specifically, FADS1 codes for Δ5-desaturase and FADS2 codes for Δ6-, Δ8-, and Δ4-desaturases.

Research has also demonstrated marked genetic variation in the FADS gene cluster between populations. Individuals living in Africa[5] appear to have a FADS genotype that promotes more efficient conversion of shorter-chained polyunsaturated fatty acids into their long-chained derivatives, whereas the Greenlandic Inuit[6] show a genotype that reduces conversion ability. One proposed hypothesis[7] about the mechanisms responsible for these genetic differences is diet. Populations with low consumption of the long-chained polyunsaturated fatty acids, such as Africans, would need enhanced conversion ability to supply the body’s demands. By contrast, the Inuit consume a diet rich in seafood that contains preformed long-chained fatty acids, thus reducing the need for conversion.

The authors of the current study have previously identified[8] a genetic variant in the haplotype called rs66698963. This variation can come in two flavors: with some code inserted (the “I” version) or that code deleted (D). Carriers of two “D” alleles (D/D genotype) displayed significantly lower levels of the FADS1 enzyme than carriers of two “I” alleles (I/I genotype).

Collectively, the above information led the authors of the current study to hypothesize that individuals carrying the D/D genotype of rs66698963 would have a lower metabolic capacity to produce long-chained polyunsaturated fatty acids from precursors than individuals carrying I/I. They were also interested in exploring how global populations differed in their genotype frequency distribution. This is important because if this hypothesis is true, then some people may have to eat more long-chained omega-3 and omega-6 polyunsaturated fatty acids due to a lower capacity to make it themselves. This need may depend on the diet history of your ancestors.

To this day, humans continue to evolve in response to environmental stressors and changes in habitat. One such adaptation is our ability to produce long-chained polyunsaturated fatty acids from dietary precursors, which is influenced by the FADS gene cluster. The study under review sought to determine whether genetic variation in FADS would be associated with long-chained polyunsaturated fat concentrations and how variation differed by population.

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