Obesity and genetics: why can’t I lose weight?
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First of all, we must put some data into context, which shows us where we are. Over the last 30 years, obesity cases have escalated so rapidly that they have set off alarm bells for national and international health regulatory agencies. The World Health Organization has declared this condition “The Epidemic of the 21st Century” in developed countries. Globally, it is estimated that in 2016, 13% of the adult population was obese and 40% was overweight. These figures appear set to worsen, according to scientific estimates, which predict that by 2030, 20% of the global population will be obese.
According to the World Health Organization, in Spain in 2016, 24.6% of men over 18 were obese and 68.9% were overweight, while among women the percentages dropped to 22.8% and 54.1% , respectively. The data does not improve regarding childhood obesity in our country, which sneaks into the podium as the third country with the highest prevalence of overweight worldwide, with 31% in boys and 28% in girls, and would be the fourth country with the highest prevalence of obesity, with 14% in boys and 10% in girls, according to a study conducted by the Childhood Obesity Surveillance Initiative.
The complexity of obesity makes it very important to define it from different perspectives and define exactly what this condition is. In this post, we’ll explore the conceptual and parameter aspects of obesity, and analyze the nature of this disease, its hereditary genetic relationship, and how it affects what we eat and how our body metabolizes food. The relationship between obesity and genetics can often be causal, but it’s necessary to understand what causes it in order to promote specific habits that help generate balanced caloric expenditure and avoid the factors that foster the imbalance that leads to obesity and the increased risk of other metabolic diseases.
Obesity is a nutritional and metabolic disease
Obesity is defined as an excessive accumulation of adipose or fatty tissue caused by a nutritional disorder in which more food is ingested than can be expended as energy. This excess adipose tissue generates chronic inflammation throughout the body (systemic) due to the increased production of cytokines and pro-inflammatory molecules.
Consequences of obesity
This inflammation, as well as the accumulation of cholesterol plaques in the blood vessels and other consequences of obesity, increase the potential risk of developing other associated diseases such as insulin resistance, type 2 diabetes, hypertension, cardiovascular disease, and cancer. These diseases can be fatal if not treated appropriately.
In fact, obesity as a risk factor is estimated to cause nearly 5 million deaths annually from known causes, half as many as hypertension and four times as many deaths from traffic accidents. It is estimated to account for 8% of all deaths globally.
How is obesity measured?
There are several direct and indirect measures to determine the amount of adipose tissue, but the Body Mass Index (BMI) is the most widely used. In the mid-19th century, in a study of what the anatomically ideal human being would look like, mathematician Adolphe Quetelet first introduced this mathematical formula that relates weight to the square of height. However, it wasn’t until the early 1970s that this index began to be used from a medical perspective. Although many experts claim that the BMI is intended to measure population groups rather than individuals, health organizations use this measure arguing that it is an easy and less complex way to estimate an individual’s body fat content and that it is strongly associated with many adverse effects.
Today there is a consensus among international health bodies and obesity is defined as any BMI measurement greater than 30 kg/m 2 and overweight as any measurement greater than 25 kg/m 2 .
| BMI | Condition |
|---|---|
| Under 18.5 | Underweight |
| Between 18.5 and 24.9 | Normal or adequate weight |
| Between 25.0 and 29.9 | Overweight |
| Between 30.0 and 34.9 | Obesity type I |
| Between 35.0 and 39.9 | Obesity type II |
| Over 40.0 | Type III or morbid obesity |
Obesity and genetics .
Regarding the nature of obesity as a disease, scientists affirm that obesity is a complex, chronic, and multifactorial disease. That is, it is affected by a large number of factors, such as environment, behavior, lifestyle, age, socioeconomic status, and genetics, which influence or correlate with all other factors. In our daily lives, we encounter many popular texts about obesity and lifestyle changes; however, in this post, we will attempt to unravel the genetic factor in obesity.
Through twin studies, different research groups have determined that the heritability of obesity is between 45% and 70%, especially in childhood obesity. To study the influence of genetics on obesity , scientists and health systems separate two types of obesity : obesity related to syndromes or syndromic obesity , and non-syndromic obesity.
Syndromic genetic obesity
Syndromic obesity is characterized by being rare, severe, and developing early. It is one of a series of specific characteristics that encompass the diagnosed syndrome. There are more than 25 syndromes that present with obesity along with other clinical features, the most common being Prader-Willi syndrome, Alstrom syndrome, Fragile X syndrome, and Bardet-Biedl syndrome, among others.
Non-syndromic genetic obesity
On the other hand, we find isolated forms of obesity that occur without any other clinical features and are called non-syndromic obesity . In this case, we can find monogenic or Mendelian obesity (if it is caused by a single gene) and polygenic obesity (if it is caused by the additive effect of several genes).
· Monogenic or Mendelian obesity
Monogenic or Mendelian obesity is caused by mutations in a gene related to the leptin-melanocortin signaling pathway expressed in the hypothalamus. The function of this signaling pathway is to regulate appetite and control energy balance, that is, the balance between what we eat and what we expend. Mutations in this pathway cause the development of hyperphagia and a general imbalance in the endocrine system. This type of obesity accounts for only 5% of cases.
· Polygenic obesity
Polygenic obesity is caused by an accumulation of mutations in several genes, the effects of which are amplified by an inadequate lifestyle, leading to excess energy consumption, which results in the characteristic accumulation of fatty tissue. This type of genetic obesity is analyzed by studying the susceptibility of individuals with various groups of mutations to develop obesity. It has been shown that there are mutations that, on their own, explain a very low percentage of BMI variation (2% in the best cases), but which, in conjunction with other mutations, could increase an individual’s susceptibility to becoming overweight when exposed to exogenous “obesogenic” factors.
Genes and overweight
More than 100 SNPs are known in genes related to feeding control pathways, the most important and most cited in the scientific literature being the FTO and MC4R genes:
FTO (Fat Mass and Obesity Associated Gene):
The FTO gene was the first gene implicated in obesity to be detected through genetic association studies. Mutations in this gene have been shown to cause an increase in daily fat intake, increased appetite, and decreased satiety. In population studies, the most studied mutation in this gene is the rs9939609 mutation, which is located in intron 1. These changes generated by the mutation have been detected in studies of both European and Asian populations.
MC4R (Melanocortin Receptor 4):
Melanocortin receptor 4 is a gene involved in the aforementioned leptin-melanocortin signaling pathway and is one of the genes most associated with childhood obesity. In population studies, the most cited and studied variant of MC4R is rs17782313, and it has been shown in several populations to increase BMI, waist circumference, visceral fat, and body fat percentage.
Genetic information to lose weight and stay healthy
Many people have tried every diet and seen no results. The truth is, not everyone is the same, nor do we all respond the same way to every food. Genetic information can provide the keys to ensuring that our efforts to maintain a healthy diet and exercise finally yield results. At the ADN Institut , for people who want to prevent the development of obesity, prevent metabolic diseases, or identify the cause of their weight loss problems and develop an action plan that takes their genetics into account, we offer the AboutMe-Nutrigenomic test , which analyzes a group of more than 80 variants that have been shown to increase susceptibility to increases in Body Mass Index and Body Fat, which can ultimately lead to obesity.
We also provide professional, genetic, and nutritional counseling to analyze results and develop a personalized plan that takes advantage of all clinical and genetic information.
The ADN Institut AboutMe nutrigenetic test consists of 35 different sections divided into six different categories:
Do you have any questions?
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