There is no doubt that genetics plays some role in obesity. However, this role should be considered relatively small. It is estimated that there are about 100 obesity genes. Most of these genes act on the brain. In general, person-to-person genetic differences come in two categories:
- There is a variation in the number of copies of a particular gene.
- There are minor changes in a specific gene, defined as single nucleotide polymorphisms (SNPs). About 20 million SNPs have been identified. It has been suggested that if you inherit greater than 10 of these so-called obesity genes, then you may be susceptible for sugary (Q. Qi.; New England Journal of Medicine, 2012).
An excellent example of genetics and obesity involves the amylase gene. Amylase is an enzyme that breaks down starches and glycogen into simple sugars. It is secreted by our salivary glands and pancreas. Humans vary in how many copies they have of the gene responsible for synthesizing amylase. Those with more copies of the amylase gene produce more amylase and are less or more prone to obesity (Falchi, M.; Nature Genetics, 2014). Those with fewer copies are more prone to obesity.
As alluded to above, genetics cannot explain our obesity epidemic. Genetics take many, many generations to have a significant effect on a population. Since 1980, American obesity has increased too dramatically to be explained by genetics. Instead, like many things in life, our zip code is more important that our genetic code.
