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The fight against obesity continues. All the while, health professionals and researchers continue to explore the cause and the prevention of obesity to reduce the negative impact on society and individuals alike.

Genetic studies have begun to unpick how DNA, in conjunction with environmental stimuli may be a key driver in BMI and eating behaviours. This connection is rapidly growing and recent studies may have identified a genetic disposition to preferring food with a high fat content. Could this mean, therefore, that some possess a subconscious preference for high fat, therefore, high calorie food – putting them at an increased risk of obesity?

Specifically, genetic variants in melanocortin-4 receptor (MC4R) and CD36 have gained attention for possibly providing a fatty acid preference in individuals.

A link between MC4R – found in the hypothalamus – and appetite regulation is well founded (Z Yilmaz, 2015). Genetic studies have clearly shown an association between some variants and increased BMI – suggesting possible alterations in appetite regulation causing weight gain (Loos RJ, 2008). Although concrete mechanisms have not been established, a recent study hitting the headlines (Wanjeck, 2016) found that carriers of a MC4R polymorphism consumed 95% more of a Chicken korma dish with a higher fat content compared to non-carriers. Two dishes identical in taste, texture and appearance but lower in fat content were consumed at a lower quantity in the MC4R variant carriers (Agatha A. van der Klaauw, 2016). The first study of its kind in human subjects, suggests that genetics may in part explain a preference for fatty foods and therefore an increased risk of obesity.

Other research has investigated variants of the gene CD36 – a fatty acid translocase expressed in many sites, including taste cells, and possessing a functional role in fatty acid metabolism (Kathleen L. Keller, 2012). Studies suggest that it may also influence fat preference in carriers, and therefore BMI. A relatively small study of African American obese subjects found that variants of CD36 noted a high fat salad cream as ‘creamier’ than a lower-fat version – suggesting an increased sensitivity to fatty acids (Kathleen L. Keller, 2012). Interestingly, however, linking this to a higher BMI has not been conclusive (Dongli Liu, 2016). It has been noted that a hypersensitivity to fatty acids may enable individuals to consumer a lower amount of that food (Kathleen L. Keller, 2012).

Although research continues to grow, such information contributes to the idea of personalised nutrition. We might be just that bit closer to identify individuals with a higher affinity for fatty foods  which could help you tailor advice to your clients. Do clients with a preference to fatty foods therefore consume too much and require coaching to reduce intake, or in fact does this mean they could be supported to switch the type of fats they are consuming? Knowing which genotype your client has inherited could steer your approach in the right direction and empower them in turn with useful and actionable information.



Agatha A. van der Klaauw, J. M. (2016). Divergent effects of central melanocortin signalling on fat and sucrose preference in humans. Nature communications, DOI: 10.1038/ncomms13055.

Dongli Liu, N. A. (2016). Mechanism of fat taste perception: Association with diet and obesity. Progress in Lipid Research, 63: 41-49.

Kathleen L. Keller, L. C. (2012). Common Variants in the CD36 Gene Are Associated With Oral Fat Perception, Fat Preferences, and Obesity in African Americans. Obesity (Silver Spring), 20(5): 1066–1073.

Loos RJ, L. C. (2008). Common variants near MC4R are associated with fat mass, weight and risk of obesity. Nature Genetics, 40(6): 768–775.

Wanjeck, C. (2016, October 4). Like Fatty Foods? There’s a Gene for That. Retrieved from Live Science:

Z Yilmaz, C. D. (2015). Association between MC4R rs17782313 polymorphism and overeating behaviors. International Journal of Obesity, 39, 114–120.