The brain plays a crucial role in regulating body weight. Through a process known as set point theory, each person has a specific weight that their brain aims to maintain.
This set point is akin to the brain’s ability to regulate body temperature within certain limits. Evolutionarily, individuals who maintained a constant body fat level were more likely to survive periods of food scarcity and avoid health issues associated with being overweight.
Diets often fail because the brain wants to keep people at a higher weight than average. It sends out chemical signals that increase hunger and other cues that make it challenging to shed pounds. Even if someone manages to lose weight, the brain’s defense of the set point makes it difficult to maintain the weight loss in the long term.
The hypothalamus, a key brain structure involved in appetite control, plays a crucial role in the brain’s regulation of body weight. It sits above the pituitary gland and below the thalamus. When we eat, the gut secretes hormones and small peptides into the bloodstream, including glucagon-like peptide 1 (GLP-1) and ghrelin, which help regulate hunger. These chemicals travel through the gut-brain axis, a communication pathway between the gut and brain, to reach the brainstem.
Once in the brainstem, signals are sent to the hypothalamus, which is responsible for making people feel full. The hypothalamus monitors both food intake and stored body fat. It detects the hormone leptin, which is released in proportion to the percentage of body fat. If leptin levels fall below what is determined by the set point, the hypothalamus sends signals to the rest of the brain that increase hunger, make food more rewarding, and reduce sensitivity to pain, distracting individuals from eating less.
Obesity arises when this set point regulation is disrupted. One possible theory involves a cluster of brain cells called AgRP neurons in the hypothalamus, which have a powerful role in appetite regulation. When these neurons are inhibited, mice ignore food to the point of starvation, while stimulation of these neurons triggers uncontrollable eating.
Under normal circumstances, AgRP neurons are suppressed by hormones and nutrients that indicate an energy surplus, such as leptin, insulin, and glucose. Even the sight of food can dampen the activity of AgRP neurons. However, a high-fat diet can activate and increase the number of support cells called glia that surround the AgRP neurons. This response, known as gliosis, is usually seen when neurons are damaged and has been observed in brain scans of people with obesity. It is believed that gliosis prevents AgRP neurons from detecting the body’s inhibitory signals, leading to reduced sensitivity. If the hypothalamus only detects half of the body’s leptin levels, it miscalculates stored fat levels as lower than the set point, triggering signals that increase cravings and promote weight gain.
The diabetes drug Ozempic, which has been effective in weight loss treatment, works by altering the brain’s response to food. The drug contains semaglutide, which mimics GLP-1 and binds to GLP-1 receptors in the brainstem. This stimulation of neural circuits results in a feeling of fullness and counteracts the appetite-inducing signals from AgRP neurons. As a result, cues from the hypothalamus that would typically trigger more eating are suppressed.
– The brain has a set point for body weight that it aims to maintain
– Diets often fail because the brain defends this set point by increasing hunger signals
– The hypothalamus is a key brain structure responsible for appetite control
– AgRP neurons in the hypothalamus play a powerful role in appetite regulation
– Gliosis, the activation of support cells, can lead to reduced sensitivity to inhibitory signals and weight gain
– The drug Ozempic, which contains semaglutide, alters the brain’s response to food by mimicking GLP-1 and stimulating neural circuits that promote feelings of fullness.
Source Article: https://www.livescience.com/health/how-does-the-brain-regulate-body-weight
