of the two ends, either excessive weight loss or weight gain occurs. Obesity occurs when the body stores food or energy much more than it consumes as is encoded in the body's DNA. Scientists have attempted to explain the widespread occurrence of this imbalance in favor of energy storage that leads to obesity between individuals with the “Thrifty Gene” hypothesis. This hypothesis explains how nature has favored, since ancient times, those individuals who can store energy more than the others who don't as the former are able to overcome times of famine and environmental challenges, and so are better at survival(“Obesity”). Therefore, through natural selection, these individuals that store more than they release reproduced more and passed on their genes to their offspring, causing a shift towards individuals carrying genes that lead to energy storage between humans (“Obesity”). However, now that we are living in societies where food is abundant, such tendency to store energy that is found within some people's genetic makeup is pushing us towards obesity, and genetic changes within a population occur too slowly to change such a phenomenon.
In addition to the previous hypothesis, mutations in specific genes are now associated with obesity. In a paper published in the Journal Science, by researchers at Boston Children's Hospital, the researchers found four mutations in a gene (Mrap2) in a group of 500 obese people who possessed only one mutated version of this gene each; this gene prevented them from burning off fat calories, leading to excessive weight gain even when these people cut off their food consumption (Sifferlin). A mutated form of the FTO gene was discovered to increase cravings for high fat foods and a greater appetite in a study published in the Journal of Clinical Investigation (JCI). In this study, a group of 359 normal weight men were classified according to their FTO genes and 45 of them turned out to have the mutated form of FTO; these 45 didn't experience the drop in ghrelin levels, the hormone associated with hunger, after eating, in contrast to the others who had the normal version of the gene which means that these men won't feel full and will consume more food (Sifferlin). Also, we now even have evidence to believe that some syndromes caused by genetic defects are characterized by obesity. For example, PWS (Prader – Willi Syndrome) is a genetic disorder that causes mental retardation, weakened muscular activity, endocrine abnormalities, and hypothalamic deterioration which all cause obesity (Bell).
Now that we have evidence that genes are responsible for obesity or weight in general, we expect that families will exhibit similar body sizes due to their common DNA structures. It turns out that heritability does manifest itself in one's BMI as chances that one inherits susceptibility towards a certain body size is between 50 % to 70 % (“Genetics”). Also, further investigation into the matter demonstrates how adopted children are more likely to have body size similar to their biological parents more than their adopted parents (Bell), revealing how genetics plays a more important role in determining weight and size.