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Our eating behavior is driven by a physiological need to satisfy hunger and provide energy, as well as a neurological desire to consume foods we want or like. These drivers are common to al humankind, however, differences in BMI and the obesity epidemic show that some respond to these needs and desires differently to others.

Many experts agree that we all have a weight ‘set-point’ which is largely determined by our genetics and of which should be kept relatively constant by an ‘energy homeostasis system’ including the hypothalamus, appetite hormones and digestive system to regulate appetite and food intake according to our physical needs (Yu, 2015) The rise of obesity, however, suggests that one is able to override their weight set-point, and researchers are investigating the role of the brain driving eating behavior beyond physical needs and leading to what is being called ‘hedonistic obesity’.

The study of hedonistic obesity looks at the neuronal pathways involved in the reward system of the brain. Through functional MRI (fMRI) scans, images have shown higher activity in the reward regions of the brain in response to food cues among obese individuals, compared to healthy weight controls (Stice, 2008).

Recently emerging is the role of genetics in susceptibility to hedonistic obesity. Commonly known variants such as; FTO and MTHFR, play a significant role in the hypothalamus and can therefore be argued as highly influential to eating behavior. Furthermore, genetic variants for taste receptors and appetite hormones may also play an important role in individuals ‘liking’ and ‘wanting’ food beyond their physical satiety signals (Grimm, 2011)

A recent study on school children used fMRI to measure the response of food stimuli in the reward-related area of the brain – nucleus accumbency (NAcc) and correlated their findings with BMI and the obesity risk polymorphism FTO rs9939609. It was found that those with the risk ‘A’ allele had a larger NAcc volume and also showed higher brain activity in response to being shown a food commercial in a controlled environment. The study concluded that risk of hedonistic obesity may be apparent from a very early age dependent on genetic variants affecting the development and growth of reward-related regions of the brain (Rapuano, 2017).

Also interesting is the correlation between low levels of dopamine and dopamine receptors and obesity. It has been suggested that those affected may display more frequent eating behavior and likely to eat larger portions in order to receive reward signals similar to those with normal dopamine levels (Grimm,2011). Whilst nutritional neuroscience is growing, so is the genetic influence to such, and this is therefore a key area for health professionals to watch. If we can begin to understand the underlying mechanism which dictate eating behavior, then we are much closer to understanding how to tackle hedonistic obesity in susceptible individuals.

As a practitioner, you might want to get further insight on environmental triggers and ask questions such as;

“where do you eat your meals when at home?”

“How do you spend your lunch time?”

“Describe how you would spend family time with your children”

“Do you feel satisfied after finishing your meal?”

Looking into the future, nutritional neuroscience will play a bigger role in the treatment plans as we learn more about the brain and neuronal pathways. By knowing which genotype clients have inherited, this may provide clues as to the best nutritional intervention strategy to employ. We are certainly watching this area closely!

 

The GenoVive Team

 

 

References

Felsted, J. A.-D. (2010). Genetically determined differences in brain response to a primary food

reward. Journal of Neuroscience,30(7): 2428-32.

Grimm, E. R. (2011). Genetics of Eating Behavior: Established and Emerging Concepts. Nutrition

Reviews, 69(1): 52-60.

Rapuano, K.M.-D. (2017). Genetic risk for obesity predicts nucleus accumbens size and

responsivity to real-world food cues. PNAS, 114(1)160-165.

Stice, E.S. (2008). Relation between obesity and blunted striatal response to food is moderated

by TaqIA A1 allele. Science, 322(5900): 449-452.

Stice, E.S. (2008). Relation of reward from food intake and anticipated food intake to obesity; a

functional magnetic resonance imaging study. Journal of Abnormal Psychology, 117(4):

924-935.

Yu, Y.-H. V. (2015). Metabolic vs. hedonic obesity: a conceptual distinction and its clinical

Implications. Obesity Reviews, 16: 234-247.