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Dieta y factores genéticos que interfieren
Nutrigenetics

06/06/2023

Obesity and genetics; why don’t I lose weight?

First of all, we need to put some facts and figures into context, which show where we stand. In the last 30 years, cases of obesity have escalated so rapidly that they have set off alarm bells for health regulators at national and international levels. The World Health Organisation has declared this condition to be “The Epidemic of the 21st Century” in developed countries. Globally, in 2016, an estimated 13% of the adult population was obese and 40% was overweight. These figures look set to get worse, with scientists estimating that 20% of the world’s population will be obese by 2030.

According to the World Health Organisation, in Spain in 2016, 24.6% of men over the age of 18 were obese and 68.9% were overweight, while in women the percentages dropped to 22.8% and 54.1%, respectively.. The data do not improve with regard to childhood obesity in our country, which is on the podium as the third country with the third highest prevalence of overweight in the world with 31% in boys and 28% in girls, and the fourth country with the highest prevalence of obesity with 14% in boys and 10% in girls, according to a study carried out by the Childhood Obesity Surveillance Initiative.

Data on the progression of obesity in adults in Spain.

Data on the progression of childhood obesity in 40 years in Spain.

The complexity of obesity makes it very important to define it from different points of view and to delimit what exactly this condition is. In this post we will look at what obesity is conceptually, in parameters and analyse the nature of this disease, the hereditary genetic relationship and how it interferes with what we eat and how our body metabolises food. The relationship between obesity and genetics may in many cases be cause and effect, but it is necessary to know what causes it in order to encourage specific habits that help to generate balanced calorie expenditure and avoid the imbalance that fosters obesity and 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 energetically. This excess adipose tissue leads to chronic inflammation throughout the body (systemic) due to increased production of cytokines and pro-inflammatory molecules.

Consequences of obesity

This inflammation, as well as the accumulation of cholesterol plaques in blood vessels or other consequences of obesity lead to an increase in the potential risk of developing other associated diseases such as insulin resistance, type 2 diabetes, hypertension, cardiovascular accidents or cancer. These diseases could lead to fatal consequences if appropriate intervention is not taken.

Risk factors for obesity, diseases such as diabetes, cancer or cardiovascular diseases

In fact, it is estimated that obesity as a risk factor causes nearly 5 million deaths with a known cause each year, half as many as hypertension and four times as many deaths in traffic accidents. It is estimated to account for 8% of deaths globally.

How is obesity measured?

There are several direct and indirect measures to determine the amount of adipose tissue, but mostly the Body Mass Index (BMI) is used. In the mid-19th century, in a study of what the ideal human being would look like anatomically speaking, the mathematician Adolphe Quetelet first introduced this mathematical formula relating weight to the square of height. But it was not until the early 1970s that this index started to be used from a medical perspective. Although many experts claim that BMI is meant to measure population groups and not individuals, health agencies 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 of the adverse effects.

There is now a consensus among international health bodies that obesity is defined as any BMI greater than 30 kg/m2 and overweight as any BMI greater than 25 kg/m2.

BMICondition
Under 18.5Underweight
Between 18.5 and 24.9Normal or adequate weight
Between 25.0 and 29.9Overweight
Between 30.0 and 34.9Obesity type I
Between 35.0 and 39.9Obesity type II
Greater than 40.0Type III or morbid obesity

Obesity and genetics.

Regarding the nature of obesity as a disease, scientists state that obesity is a complex, chronic and multifactorial disease, i.e. it is affected by a large number of factors such as environment, behaviour, lifestyle, age, socio-economic status and genetics that influence or correlate with all other factors. In everyday life we find many popular texts about obesity and lifestyle changes, however, in this post we are going to try to unravel the genetic factor of 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 care systems separate two types of obesity either syndromic obesity or syndromic obesity, and non-syndromic obesity.

Syndromic genetic obesity

Syndromic obesityis characterised by being rare, severe and developing early, and falls within a set of defined characteristics that encompasses the syndrome being diagnosed. There are more than 25 syndromes with obesity and 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, there are isolated obesities that occur without any other clinical features and are called non-syndromic obesity.. In this case we can findmonogenic 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 is caused by mutations in a gene related to the leptin-melanocortin signalling pathway that is expressed at the level of the hypothalamus. The function of this signalling pathway is to regulate appetite and control energy balance, i.e. the comparison between what we eat and what we expend. Mutations in this pathway lead to the development of hyperphagia and a general imbalance of 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 whose effects are amplified by an inappropriate lifestyle, leading to an excess of energy which results in the characteristic accumulation of fatty tissue. This type of genetic obesity is analysed by studying the susceptibility of individuals with various groups of mutations to develop obesity, in this way it has been seen that there are mutations that alone explain a very low percentage of variation in BMI (2% in the best cases), but that in conjunction with other mutations could increase the susceptibility of the individual to develop overweight when exposed to exogenous “obesogenic” factors.

Genetic factors for overweight and obesity

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 (Gen asociado a la masa grasa y la obesidad):

The FTO gene was the first gene implicated in obesity detected by genetic association studies. Mutations in this gene have been shown to cause increased daily fat intake, increased appetite and decreased satiety. In population studies, the most studied mutation in this gene is the rs9939609 mutation found in intron 1. These mutation-generated changes 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 signalling pathway and is one of the genes most associated with childhood obesity. In population studies, the most commonly cited and studied variant of MC4R is rs17782313 and 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 all the diets and see no results. Not all people are the same, nor do we respond in the same way to all foods. Genetic information can give us the keys to ensure that our efforts to maintain a healthy diet and physical exercise finally pay off. At ADN Institut for people who want to prevent the development of obesity, prevent metabolic diseases or detect the reason for their weight loss problems and draw up an action plan that takes into account their genetics, we have available the AboutMe-Nutrigenetic test where we look at a group of over 80 variants that have been shown to increase susceptibility to increased Body Mass Index and Body Fat that can lead to obesity.

We also accompany it with professional, genetic and nutritional advice, both to analyse results and to draw up a personalised plan that takes advantage of all the clinical and genetic information.

El test nutrigenético AboutMe de ADN Institut se compone de 35 secciones diferentes que se dividen en 6 categorías distintas:

Do you have any questions?

 

References.

1. Raskiliene A, Smalinskiene A, Kriaucioniene V, Lesauskaite V, Petkeviciene J. Associations of MC4R, LEP, and LEPR Polymorphisms with Obesity-Related Parameters in Childhood and Adulthood. Genes. 2021; 12(6):949. https://doi.org/10.3390/genes12060949
2. Gabriel Á. Martos-Moreno, Clara Serra-Juhé, Luis A. Pérez-Jurado, Jesús Argente. https://www.endocrinologiapediatrica.org/revistas/P1-E22/P1-E22-S1079-A391.pdf
3. Jiménez, E. G. (2011). Genes y obesidad: una relación de causa-consecuencia. Endocrinología y Nutrición, 58(9), 492-496. https://doi.org/10.1016/j.endonu.2011.06.004
4. Nicora, G., Zucca, S., Bellazzi, R., Bellazzi, R., & Magni, P. (2022). A machine learning approach based on ACMG/AMP guidelines for genomic variant classification and prioritization. Scientific Reports, 12(1). https://doi.org/10.1038/s41598-022-06547-3
5. Panera, N., Mandato, C., Crudele, A., Bertrando, S., Vajro, P., & Alisi, A. (2022). Genetics, epigenetics and transgenerational transmission of obesity in children. Frontiers in endocrinology, 13, 1006008. https://doi.org/10.3389/fendo.2022.1006008
6. Mahmoud, R., Kimonis, V., & Butler, M. G. (2022). Genetics of Obesity in Humans: A Clinical Review. International journal of molecular sciences, 23(19), 11005. https://doi.org/10.3390/ijms231911005
7. Bouchard C. (2021). Genetics of Obesity: What We Have Learned Over Decades of Research. Obesity (Silver Spring, Md.), 29(5), 802–820. https://doi.org/10.1002/oby.23116
8. Singh, R. K., Kumar, P., & Mahalingam, K. (2017). Molecular genetics of human obesity: A comprehensive review. Comptes rendus biologies, 340(2), 87–108. https://doi.org/10.1016/j.crvi.2016.11.007
9. Hurtado A, M. D., & Acosta, A. (2021). Precision Medicine and Obesity. Gastroenterology clinics of North America, 50(1), 127–139. https://doi.org/10.1016/j.gtc.2020.10.005
10. Walley, A. J., Asher, J. E., & Froguel, P. (2009). The genetic contribution to non-syndromic human obesity. Nature reviews. Genetics, 10(7), 431–442. https://doi.org/10.1038/nrg2594
11. Pi-Sunyer F. X. (2002). The obesity epidemic: pathophysiology and consequences of obesity. Obesity research, 10 Suppl 2, 97S–104S. https://doi.org/10.1038/oby.2002.202
12. Hannah Ritchie and Max Roser (2017) – “Obesity”. Published online at OurWorldInData.org. Retrieved from: ‘https://ourworldindata.org/obesity’ [Online Resource]

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