- Dieting and physical activity are not effective in the long term for individuals who are obese.
- Neuroplasticity alterations occur in the brain after calorie restriction and exercise.
- Treatment of obesity essentially requires psychological and neurological methods.
Nutritionists and diet therapists may be discouraged, but epidemiological and clinical studies have revealed that dieting for weight loss is not effective in the long term. The most common treatment for obesity at present is calorie restriction and increased physical activity.
Many individuals who have tried low-calorie diets, especially non-standard ones, have reported experiencing serious issues over time. These issues include increased appetite, loss of muscle mass, weight regain, stress, and anger. For these reasons, many people often abandon these diets due to these side effects.
After harsh or rapid calorie restriction and an unusual increase in physical activity, the brain utilizes certain evolutionary mechanisms to compensate for them. This is mainly achieved by impairing hunger and satiety signaling and decreasing the basal metabolic rate (BMR).
An increase in appetite helps people consume more high-energy food than usual, while a decline in BMR maintains the body's energy stores. BMR is the minimum energy required to maintain vital body functions and accounts for the majority of energy expenditure in the body.
It mostly depends on body size and muscle mass. These mechanisms were useful for our ancestors who faced long periods of food scarcity. The hypothalamus plays a critical role in controlling both appetite and the production of heat by thermogenic tissues .
Some mechanisms are involved in controlling appetite and satiety in the brain. AgRP neurons in the hypothalamus are the strongest regulators of hunger, satiety, and food-seeking behaviors. It seems that this system is an evolutionarily conserved mechanism during food scarcity and plays a similar role during calorie-restriction diets.
A recent study has revealed that a synaptic amplifier, in the hypothalamus, may play a role in disrupting normal hunger control. The researchers found that TRH-releasing neurons synapse with AgRP neurons and amplify these synapses during food deprivation. This synaptic amplification leads to an increase in food intake and weight gain in mice.
The findings suggest that targeting the synaptic amplifier in the hypothalamus could be a promising strategy for treating obesity. However, further research is needed to confirm these findings and determine the effectiveness and safety of this approach in humans.
The hypothalamus also controls thyroid hormones, which play a significant role in regulating metabolism. Additionally, it directly influences appetite by sending and receiving signals related to leptin, insulin, and ghrelin .
BMR is influenced by the number of calories consumed in the diet compared to energy expenditure. Excessive energy consumption seems to increase BMR, while very low-calorie dieting leads to a decrease in BMR. Since the basal metabolic rate is the main factor in daily energy expenditure, reducing it through caloric restriction makes it challenging for obese individuals to lose weight and maintain the weight they have lost.
In a study, it has been shown that AgRP neurons are necessary to shift metabolism toward energy conservation and lipid storage. This is achieved, in part, by reducing energy expenditure in thermogenic tissues.
The hypothalamus controls the production of thyroid hormones, which also play a role in mitochondrial thermogenesis in peripheral tissues, especially muscles. This thermogenesis decreases during fasting and dieting due to a decrease in thyroid hormone release.
Most of our behavior and decisions in daily life are influenced by unconscious brain functions. These unconscious systems occur during repetitions of specific behaviors and feedback signals perceived over the long term. These repeated behaviors create new neural connections in specific regions of the brain and serve as automatic circuits that control daily decisions and behavioral habits.
The brain requires less energy for unintentional and automatic decision-making and behaviors than it does for conscious mechanisms. Breaking these circuits requires significant conscious and intentional efforts to establish new neural connections to address the existing circuits.
Amplifying AgRP neurons in the hypothalamus is achieved through a process called neuroplasticity. This passive mechanism involves unconsciously reinforcing the act of eating repeatedly, thereby promoting increased food consumption. These mechanisms also decrease energy expenditure to conserve our energy stores.
Acute exercise also promotes the activation of the AgRP pathway. Aerobic exercise increased the activity of several neuron populations that stimulate appetite, including AgRP and TH neurons. Activation of AgRP neurons stimulates food intake, and the activity of this group of neurons is heightened immediately following moderate- and high-intensity treadmill exercise.
However, the good news is that the field of habit formation and behavioral change has made significant progress in recent years. We now have a better understanding of how our brains function and how to use that knowledge to overcome harmful habits.
Self-directed neuroplasticity refers to intentionally rewiring your brain to develop positive habits. People primarily achieve this through active reflection.
- Replace the habit with a different one
- Avoid tempting situations
- Practice mindfulness
- Participate in group therapy
- Reward oneself to stay motivated for further actions
These are some techniques to prevent breaking a diet. Pharmacological approaches to target brain rewiring may be helpful for patients in managing brain compensation mechanisms during a calorie-restricted diet. However, it seems that a psychiatrist should be part of the obesity treatment team, similar to other addictions.
1. Molé, P. A. (1990). Impact of energy intake and exercise on resting metabolic rate. Sports Med, 10(2), 72-87.
2. Grzelka, K., Wilhelms, H., Dodt, S., Dreisow, M. L., Madara, J. C., Walker, S. J., . . . Fenselau, H. (2023). A synaptic amplifier of hunger for regaining body weight in the hypothalamus. Cell Metab, 35(5), 770-785.e775.