Understanding the Connection Between the Brain and Our Set Point

It has been established that in the basomedial hypothalamus in the brain, there is a heightened sensitivity to nutrient availability. This includes the signal leptin, a hormone responsible for regulating hunger. Both leptin and insulin bind to receptors in the brain, including the prefrontal regions, amygdala, and hippocampus.

The arcuate nucleus of the hypothalamus, is responsible for food intake and metabolism, and has been established as the most important for the transfer of energy.1

It is now known that these neural circuits in the brain have evolved to process information about food and food-related cues to control feeding behavior.1 Recent research has revealed that other neurotrophins, such as brain-derived neurotrophin factor (BDNF) plays a significant role in the brain’s homeostasis. In order for the brain’s set point to occur, there are feedforward and feedback signals sent from the environment to ensure that the body consumes the appropriate amount of calories and energy expenditure.2 Essentially, the brain controls how much food is consumed, and how much movement is utilized in our day-to-day lives, to maintain a baseline that has been established as the homeostastic 'set point'.

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Certain pharmaceutical drugs, such as antidepressants, have been theorized to influence the body’s set point. Different mechanisms can affect the set point, including the disruption of satiety signals through changes in serotonin and dopamine. Additionally, antidepressants have been reported to increase appetite. 

Recently, GLP-1s have been utilized more in clinical settings to influence the body’s weight set point. These include Ozempic (semaglutide) and Victoza (liraglutide). GLP-1 is an incretin hormone that is made naturally in the intestines. The main functions of the GLP-1s are decreasing caloric intake and increasing satiety. Natural GLP1 stimulators that can be utilized in diet are fiber and whey protein. 

References 

1. Barakat, G. M., Ramadan, W., Assi, G., & El Khoury, N. B. (2024). Satiety: a gut–brain–relationship. The Journal of Physiological Sciences, 74(1), 11.

2. Podyma, Brandon et al. 

Trends in Endocrinology & Metabolism, Volume 32, Issue 7, 488 - 499