In this episode of the Huberman Lab podcast, Andrew Huberman explores the physiological mechanisms that regulate hunger, eating, and satiety. He reveals how the hypothalamus and insular cortex in the brain, along with gut hormones like ghrelin and cholecystokinin, govern feelings of hunger and fullness.
Huberman also discusses the impact of diet, food processing, emulsifiers, and exercise on appetite and glucose regulation. Listeners will gain insights into how factors like the order of food consumption, processed foods' effects on the gut, and different types of exercise influence the body's hunger signals, satiety responses, and ability to manage blood sugar spikes.
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The hypothalamus plays a key role in regulating hunger and feeding behavior, neuroscientists have found. Within the hypothalamus, the ventromedial hypothalamus contains neurons that either promote or inhibit feeding, Huberman explains. Damaging this region can paradoxically lead to over- or undereating disorders like hyperphagia or anorexia.
Additionally, the insular cortex processes sensory input related to eating, including taste and touch, determining one's enjoyment of foods and feelings of satiety. Its neurons help modulate the relationship with food.
Two key gut hormones regulate appetite: ghrelin and cholecystokinin (CCK). Ghrelin, a "hunger clock", rises before meals, stimulating appetite regardless of blood glucose. Huberman notes its ability to override low glucose signals.
CCK, meanwhile, is released when fatty acids, amino acids, and sugars enter the gut, suppressing appetite. Foods like omega-3s and CLA trigger CCK release, blunting overeating.
Gut sensors can also drive [restricted term] release and sugar cravings. Huberman explains this vagus nerve gut-brain pathway affects desires for certain foods.
Huberman highlights how consumption order impacts glucose response. Eating fibrous foods first can blunt the glucose spike from later carbs.
Processed food emulsifiers, however, damage the gut lining, disrupting CCK release. This impairs satiety signaling, potentially causing overconsumption.
Exercise is beneficial. Cardio improves glucose regulation and [restricted term] sensitivity, Huberman states. Simply walking can moderate blood sugar spikes. Consistent "zone two" cardio enhances the body's ability to handle high-sugar foods.
1-Page Summary
Recent research into the neural and hormonal aspects of hunger and satiety has illuminated the various complex mechanisms the brain uses to regulate appetite and feeding behavior.
Neuroscientists have found that the hypothalamus is integral to controlling hunger and feeding behavior. Within the hypothalamus, researchers highlight the role of the ventromedial hypothalamus.
The function of the ventromedial hypothalamus can be paradoxical. When lesions are made in this region, it can lead to two distinctly opposite eating disorders: hyperphagia, characterized by excessive eating, and anorexia, characterized by a lack of eating. This paradox arises because the ventromedial hypothalamus houses multiple neuron populations that can promote or inhibit feeding. A classic experiment with parabiosed rats—rats surgically united to share a blood supply but with independent brains and mouths—has shown that if the ventromedial hypothalamus is lesioned in one rat, that rat will become obese while its partner loses weight. This suggests that the ventromedial hypothalamus interacts with hormone or endocrine signals that help regulate appetite.
Beyond the hypothalamus, the insular cortex is known to process i ...
Neural and Hormonal Mechanisms Regulating Hunger and Satiety
Understanding how our bodies regulate hunger and satiety involves a complex dialogue between gut hormones and the brain, an interplay that is key to maintaining a healthy balance.
Ghrelin is a peptide hormone released from the GI tract, stands at the forefront of triggering hunger. It primarily stimulates brain areas that increase appetite and creates signs that tell us when to anticipate food.
Huberman explains that the timing of ghrelin’s release is indicative of its nickname as a "hunger clock," because it is linked to a cycle that anticipates regular meal times, regardless of blood glucose levels. This sophisticated mechanism allows ghrelin to override signals of low glucose and prompt hunger at times when we are accustomed to eating.
While ghrelin works to increase hunger, another hormone named cholecystokinin (CCK) serves as its counterbalance by suppressing appetite.
CCK is released in the GI tract in response to certain nutrients like fatty acids, amino acids, and sugars that enter the gut. Huberman highlights that omega-3 fatty acids and conjugated linoleic acid (CLA) are particularly effective at stimulating CCK release. The release of CCK reduces appetite and helps signal the brain that enough food has been ingested, protecting against overeating.
Amino acids derived from dietary intake also play a role in triggering CCK release, again clamping down on the appetite. The presence of these nutrients informs the brain, mainly through CCK, when sufficient nutrients have made their way into the system.
Gut Hormones and Brain in Appetite Regulation
Huberman clarifies how different lifestyle factors such as diet, food processing, and physical activity significantly influence hunger and satiety along with the body's ability to manage blood sugar and [restricted term] levels.
Huberman discusses the impact of the consumption order of macronutrients on the body’s blood glucose and [restricted term] responses. He notes that consuming fibrous foods first can mitigate the glucose spike typically caused by carbohydrates eaten later in a meal. To moderate blood sugar increases and reach satiety sooner, it is advised to eat fiber-rich foods first, followed by proteins, and then carbohydrates, resulting in a steadier rise in blood sugar.
Huberman talks about the presence of emulsifiers in processed foods and their detrimental effect on the gut lining and appetite regulation. Emulsifiers extend food shelf life but also damage the mucosal lining of the gut, causing neurons in the gut to retract. This prevents the release of hormones like cholecystokinin (CCK), impeding the triggering of satiety signals and potentially leading to overeating. Highly processed foods containing emulsifiers can cause significant weight gain and disrupt the gut lining, affecting CCK release and interfering with proper satiety signals.
On the exercise front, Huberman explains the benefits of physical activity for glucose regulation and [restricted term] sensitivity. He elucidates that engaging in high-intensity interval training or weightlifting can lead to lasting increases in basal metabolic rate. Additionally, he mentions that move ...
Diet, Food Processing, and Activity Impact on Hunger and Satiety
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