Topic 2 Genes and Obesity

Genes influence every aspect of human physiology, development, and adaptation. Obesity is no exception. 

  • Several genetic factors are responsible for very rare, single-gene forms of obesity
  • “Common” obesity is influenced by dozens, if not hundreds, of genes

But genetic factors identified so far make only a small contribution to obesity risk: many people who carry these so-called “obesity genes” do not become overweight, and healthy lifestyles can counteract these genetic effects.

OUR GENES ARE NOT OUR DESTINY

Nutrition also plays a role in the duration and quality of life.

  • The age-1 gene is the first aging gene to be identified
  • Sirt is the first longevity gene
  • About twenty gerontogens and longevity genes have been identified in different species
  • The hypothesis is that in humans there are about a hundred
  • Those stretches of DNA all have the same function: they control energy metabolism

  • Nutrition has a large share of responsibility for the state of health: genes affect the way our body assimilates nutrients while some substances influence the expression of our genes.

Epigenetics is a rapidly evolving area of research and the first steps are already being made in identifying potential biomarkers for obesity that could be detected at birth.

There is compelling evidence that an adverse prenatal and early postnatal environment can increase obesity risk in later life. Diet and weight loss interventions in obese mothers may lead to a decreased risk of obesity in the offspring, possibly mediated through changes in insulin signalling, fat storage, energy expenditure or appetite control pathways.

These findings may help in predicting an individual’s obesity risk at a young age, before the phenotype develops, and opens possibilities for introducing targeted strategies to prevent the condition.

It is also now clear that several epigenetic marks are modifiable, not only by changing the exposure in utero, but also by lifestyle changes in adult life, which implies that there is the potential for interventions to be introduced in postnatal life to modify or rescue unfavourable epigenomic profiles.