A healthy weight is maintained during a state of energy balance- when the energy intake of an individual matches the energy expenditure. Weight can accrue over a long period of time if the intake is higher than expenditure. Besides intake and expenditure, other factors such as age, basal metabolism, hormonal imbalance, and genetics also influence weight gain or weight loss.
Many humans have inherited genetic adaptations, which evolved to mitigate the ancestral exposure to cycles of feast and famine. Hence, the human body is very good at storing excess energy as fat and reluctant to lose valuable stores (fat) of energy. This is the basis of the  ‘thrifty gene’  hypothesis, which explains why people easily put on weight on an excess calorie diet and find it very hard to lose it.
The heritability associated with energy intake among children is found to be between 47-69%. Twin studies showed that there was a genetic influence on the type of food consumed, along with satiety and food cue response.
FTO and Increased food intake
There are many genes that have been shown to be associated with obesity and energy intake. Of particular significance is the FTO gene. Studies have shown that certain variants of this gene were associated with increased energy intake and increased hunger. Individuals with the abnormal FTO gene weigh at least 3kgs more than individuals who have the normal copy of the gene.
Individuals with an abnormal copy of the FTO gene eat more frequently, with a tendency to prefer calorie-dense foods and larger portions of food. People with the highest risk variant should exert portion control and eat a lot of food rich in fiber which would help quell the hunger. Â They should also consider frequent snacking in small quantities of low calorie, high protein, and high fiber foods to counteract the perpetual hunger they may be experiencing to maintain a stable glycemic index and stable levels of hunger and satiety hormones.
FTO and the Hunger Hormone Grehlin
A hormone that plays a key role in satiety is ghrelin. Ghrelin is responsible for ‘hunger pangs’ as it signals the brain to eat. After a meal, the level of ghrelin is lowered and levels of another hormone, Leptin, are elevated resulting in a feeling of fullness. In an individual with the high risk variant of the FTO gene, the level of ghrelin remains high even after a meal, re
sulting in over eating. In such individuals, exercise has been shown to restore the level of ghrelin to normal levels.
Individuals with the abnormal FTO gene should be encouraged to follow a regular exercise pattern which will aid in lowering ghrelin levels and provide better satiety response.
MC4R gene and Overeating
Another important gene that affects meal size and meal choice but not meal frequency is MC4R. When the energy levels drop in our body, the hunger center sends signals that inhibit MC4R and there is an increase in appetite. When the stomach is full after eating, satiety signals are sent by the satiety center that stimulates the MC4R to send signals to stop eating.
DRD2 and Binge Eating
Overeating that is induced by distress, emotional eating, leads to binge eating which is highly prevalent in adults who are binge eaters or obese. Binge eating disorder is due to hypersensitivity to reward which results in overeating. The tendency to overeat or binge eat can be determined relatively strongly by analyzing the dopamine D2 receptor gene.
Dopamine is a neurotransmitter and its secretion is increased during emotional upheavals. Â From an evolutionary aspect, this hormone is released in response to some adverse condition, to prepare the body for a flight or fight response. Under normal circumstances, when dopamine binds to the DRD2 receptor, it should lower feelings of hunger and increase satiety. However, mutations in the DRD2 gene lead to a lower amount of DRD2 in the brain, which could lead to binge eating or overeating.
Individuals who carry the abnormal gene should consciously avoid overeating when feeling distressed or should store healthy snacks to eat at times of distress. Another study showed that deficits in the dopamine D2 receptor led mice to be inactive, which in turn lead to weight gain. Therefore, people with an abnormal gene should consciously stay active. Â
Regulating energy intake can moderate susceptibility to weight gain and obesity and is essential for people with a higher propensity to gain weight. Interventions that promote self-regulation of energy intake have the potential to control weight gain and also encourage healthy dietary habits. When designing intervention strategies, it is important to understand the genetic aspects involved as nearly 30% of obese individuals underreport their energy intake. The most effective way to fight obesity is through calorie restriction or lowering energy intake. People who carry abnormal genes for energy intake should follow mindful eating to ensure a balance in energy homeostasis.
Individuals who carry the abnormal gene should consciously avoid overeating when feeling distressed or should store healthy snacks to eat at times of distress. Another study showed that deficits in the dopamine D2 receptor led mice to be inactive, which in turn lead to weight gain. Therefore, people with an abnormal gene should consciously stay active. Â
Regulating energy intake can moderate susceptibility to weight gain and obesity and is essential for people with a higher propensity to gain weight. Interventions that promote self-regulation of energy intake have the potential to control weight gain and also encourage healthy dietary habits. When designing intervention strategies, it is important to understand the genetic aspects involved as nearly 30% of obese individuals underreport their energy intake. The most effective way to fight obesity is through calorie restriction or lowering energy intake. People who carry abnormal genes for energy intake should follow mindful eating to ensure a balance in energy homeostasis.
Find out which variations of these genes you carry and more at www.xcode.life
Nutrigenetics, fitness genetics, health genetics are all nascent but rapidly growing areas within human genetics. The information provided herein is to be read and understood in that context.
