Genetic study of obesity

The main cause of obesity is the imbalance that occurs between the intake of calories, with a greater consumption of hypercaloric foods, that is, with a high content of fats and carbohydrates, and the consumption of these calories, to a large extent due to less physical activity, both at work and social level. Anyway, as in many other pathologies, obesity has a multifactorial origin, coming into play, in addition to those already mentioned, genetic, metabolic, hormonal, psychological, nervous and environmental factors that predispose to it.

Multiple studies have estimated that the genetic influence on that of people ranges between 40% and 70%, figures that are not inconsiderable. From a genetic point of view, there is no single gene or a specific set of genes that determine whether a person is obese or not, but it is true that there are a series of genes that regulate satiety and energy consumption in the processes metabolic that can present variations within the normality that predispose to overweight and obesity.

These normal variations in the structure of the same gene are what in genetics are called polymorphisms, small nuances that make, if present, a tendency to gain or lose weight is established naturally. More than 30 genetic markers (normal variations of certain genes) that genetically predispose to obesity have been detected.

How is the genetic study of obesity carried out?

Performing a genetic profile of obesity (PGO) is quite simple. It can be carried out by simply taking one and with it a genetic study is carried out where the presence of 5 or 6 of these genes with variations that predispose to obesity is assessed. It has been observed that 86% of the women and 64% of the men who underwent a PGO had one or more of these polymorphisms. Another way to obtain cells to perform PGO is by scraping the oral mucosa (the inside of the cheek) with a cotton swab.

The PGO assesses a series of genes that control appetite and satiety, the formation of fatty tissue, the regulation of body temperature or blood insulin levels, among other factors. Some of these genes studied are:

• MC4R, which encodes the melanocortin receptor 4. This substance acts at the level of the hypothalamus, a part of the brain, and controls appetite by reducing intake. The polymorphism studied has been shown not to have its effect, with what is eaten more and through metabolic changes energy consumption is decreased.
• NPY, which creates neuropeptide Y, a neurotransmitter that also acts at the level of the hypothalamus and is responsible for stimulating intake and acting on fatty tissue, thereby raising blood triglyceride levels and increasing appetite.
• LEPR, which encodes leptin, a substance produced by the cells of fatty tissue and which is responsible for reducing the sensation of appetite at the brain level; the studied polymorphism of this gene causes leptin not to take effect and therefore costs more to satisfy the appetite.
• PPARG, which is responsible for regulating insulin sensitivity, in such a way that a variation in this gene causes insulin resistance to increase and therefore part of the ingested carbohydrates are transformed into fats and accumulate in the tissue adipose.
• ADRB2 and ADRB3, two genes that encode types beta 2 and 3 of adrenergic receptors, especially at the level of fat tissue, which allows the consumption of fat when performing physical activity; one type of polymorphism in these genes does not cause fats to be "burned" during physical activity.

• FTO, encodes another protein that regulates intake in the hypothalamus by reducing it, so that those who present a specific variation of this gene see their need to consume food increased.
• UCP2, a gene that regulates weight and body temperature, allowing fat to be consumed and energy released in the form of heat; its variation from normality means that this does not occur, so that by not consuming fat there is a greater risk of it accumulating.
• INSIG2, a gene that, if it presents a certain polymorphism, favors the formation of cholesterol.
• GNB3, regulator of the formation of adipocytes, the cells of fatty tissue, so that if it presents a certain polymorphism its activity is increased and the number of adipocytes and, consequently, of fatty tissue increases.

Thus, the PGO makes it possible to determine the existence of some of these forms of certain genes that predispose to obesity and, depending on which they are, to adapt the obesity treatment to each patient in particular, assessing whether the polymorphisms present are related to the metabolism of carbohydrates, fats or the response to physical activity or calorie restriction. A person with modifications in genes that regulate carbohydrates will benefit from a diet low in carbohydrates, while if the polymorphisms present are related to lipid metabolism, the patient will respond better to a diet of restriction of fats.

Likewise, the PGO and the knowledge of the presence of these genetic alterations helps to disprove the idea of ​​"miracle diets" that promise to lose weight with little effort, as well as to predict the response to the pharmacological treatment of obesity in the event that this was precise.

weight loss in case of overweight or obesity should always be based on the two essential pillars to achieve it, dietary modifications and the practice of. However, by performing a PGO and knowing the “weak points” of the patient, these interventions could be adjusted to obtain optimal effectiveness from them.

If you have insurance, you have access to preferential prices for the Genetic Study of Obesity service.

• Carrying out a Genetic Profile of Obesity (PGO) and knowing the “weak points” of the patient in terms of lifestyle, allows adjusting diet and exercise to obtain optimal effectiveness.
• It is quite simple and can be carried out by simply taking a blood sample to assess the presence of genes with variations that predispose to obesity.
• Another way to obtain cells to perform PGO is by scraping the oral mucosa (the inside of the cheek) with a cotton swab.