Up until recently, genes and epigenetic variations have dictated how the inheritance of obesity works. Sure, they “contribute to obesity by influencing the function of metabolic pathways in the body and regulating neural pathways and appetite centers.” Certainly, they “influence insulin resistance, dyslipidemia, inflammation, hypertension, and ectopic fat deposition.”
Of course, genetic mutations “can be inherited in an autosomal dominant or autosomal recessive manner and are influenced by genetic mechanisms of deletion, genetic imprinting, and translocation.” So far all these factors, as described in the book Genetics and Obesity, have been unrelentingly true.
Multiplicity of causation
But, as previously discussed, genes and their complex epigenetic mutations no longer hold the monopoly on defining or deciding fate for all humans, all the time.
First, science learned a lot about how epigenetic modifications happen during the development of the fetus. Of course, such a possibility had been suspected. But we have come a long way from the days when, for instance, the grotesque physique of the so-called Elephant Man was blamed on his pregnant mother having been frightened by the sight and behavior of an elephant.
The advance of science caused such beliefs to be dismissed as mere superstition. Then, science progressed even further to discover that disorders actually can grow from the horrors of war and other emotionally devastating roots.
Things that can happen
Epigenetic development, including changes to the insulin metabolism of a fetus, can be influenced by maternal over-nutrition and also by maternal under-nutrition. For the unborn child such disturbance can be a survival adaptation, but once born and exposed to other nutrition sources, it can lead to inescapable difficulty in survival.
The authors of Genetics and Obesity mention how…
The rising prevalence of obesity and type 2 diabetes in developing countries like India and sub-Saharan Africa confounded epidemiologists for the longest time and is now known to have its origins explained by the theory of fetal programming.
Another source of trouble, quite understandably, is maternal exposure to toxins like those introduced by cigarette smoking, and other endocrine-disrupting chemicals now recognized as obesogens. Maternal stress, caused by such events as natural disasters and their grievous consequences, is strongly suspected. Fetal metabolic derangement can stem from the mother being very young, or seriously underweight, or suffering from diabetes.
Multifactorial, again
The nourishment absorbed by a person as a baby and as a small child are both, of course, very influential in either a positive or negative way. Treatment with antibiotics in the first year of life has been linked to subsequent obesity, as well as non-alcoholic fatty liver disease and other conditions later in life. Even paternal over-nutrition, low protein intake, pre-diabetes, and other conditions can affect a child’s development. Mind you, this is the father! These causes have recently been looked at much more closely than ever before.
Then, there is syndromic obesity, so named because it results from syndromes with such distinctive names as Prader-Willi, WAGR, SIM1, Bardet-Biedl, and Fragile X. Also, there is monogenic obesity, which “generally involves mutations in the leptin signaling pathway leading to suppression of anorexigenic and activation of orexigenic pathways.” Furthermore, around 60% of inherited obesity is now understood to be of polygenic origin, affecting appetite control, energy balance, and many other factors.
Your responses and feedback are welcome!
Source: “Genetics and Obesity,” NIH.gov, 07/31/23
Source: “Joseph Merrick — The Elephant Man,” LondonMuseum.org, undated
Image by Cory Doctorow/Attribution-ShareAlike 2.0 Generic
FAQs and Media Requests: 
