The Genetics of Obesity

The Genetics of Obesity

Have you ever noticed that some people tend to gain weight more easily than others, despite following similar diets and exercise routines? The answer to this lies in our genes as they play a significant role in determining our susceptibility to obesity and Type 2 Diabetes (T2DM). 

Obesity and T2DM are complex conditions that are influenced by a variety of factors, including genetics. Therefore, it is not uncommon to observe different outcomes in terms of weight gain and susceptibility to T2DM in individuals with similar lifestyles. 

The role of genetics in obesity and T2DM cannot be overstated, as it can influence many key biological systems such as metabolism, appetite, and fat storage tendencies. Over 300 gene mutations associated with obesity have been identified1, with some of these genetic markers being linked to upwards of a 9-fold increased risk of developing T2DM2

Experts estimate that between 40-70% of body weight is influenced by our genetic makeup3. An example of this is the gene FTO, which has been linked to changes in appetite, including cravings for high-calorie dense foods and reduced feelings of fullness after eating4. Furthermore, several genes have been found to cause the accumulation of fat around the waist, which increases the risk of developing T2DM5.

In rare cases, monogenic obesity, caused by single-gene mutations, can lead to severe, early-onset obesity. Mutations in the genes encoding leptin, a hormone essential for the maintenance of healthy weight, have been attributed to 30% of severe obesity in children 6

However, most causes of obesity are polygenic, resulting from an interaction between the environment and hundreds of different genetic variants. 

Therefore, it is important to recognise that while genetics plays a significant role in obesity and T2DM, it is often not the only factor in these conditions. Even if you have a  genetic predisposition to obesity, maintaining a healthy lifestyle can help you to reduce your risk and improve your overall health.

At Roczen, evidence-based treatment plans are designed to address the root causes of T2DM that arise from environmental factors. This is especially important for individuals with a strong genetic risk for this condition, as they can still make significant lifestyle changes that have a positive impact on their health. By taking control of your health and implementing the right lifestyle changes with the help and support of Roczen, you can reduce their risk of T2DM and lead a healthier life.

December 14, 2023
Written by
Dr. Harriet Lester
Reviewed by
Dr. Laura Falvey


  1. Tirthani E, Said MS, Rehman A. Genetics and Obesity. 2022 Aug 1. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing. 2022 Jan–. PMID: 34424641.
  2. Mahajan, A., Taliun, D., Thurner, M., Robertson, N. R., Torres, J. M., Rayner, N. W., Payne, A. J., Steinthorsdottir, V., Scott, R. A., Grarup, N., Cook, J. P., Schmidt, E. M., Wuttke, M., Sarnowski, C., Mägi, R., Nano, J., Gieger, C., Trompet, S., Lecoeur, C., . . .  McCarthy, M. I. (2018). Fine-mapping type 2 diabetes loci to single-variant resolution using high-density imputation and islet-specific epigenome maps. Nature Genetics, 50(11), 1505-1513.
  3. Elks, C. E., Zhao, J. H., Sharp, S. J., Wareham, N. J., F. Loos, R. J., & Ong, K. K. (2012). Variability in the Heritability of Body Mass Index: A Systematic Review and Meta-Regression. Frontiers in Endocrinology.
  4. Cecil JE, Tavendale R, Watt P, Hetherington MM, Palmer CN. (2008). An obesity-associated FTO gene variant and increased energy intake in children. N Engl J Med. 11;359(24).
  5. Yaghootkar, H., Lotta, L. A., Tyrrell, J., J. (2016). Genetic evidence for a link between favorable adiposity and lower risk of type 2 diabetes, hypertension and heart disease. Diabetes, 65(8), 2448.
  6. Obradovic, M., Sudar-Milovanovic, E., Soskic, S., Essack, M., Arya, S., Stewart, A. J., Gojobori, T., & Isenovic, E. R. (2021). Leptin and Obesity: Role and Clinical Implication. Frontiers in Endocrinology, 12. 

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