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Mechanism

Leptin and Ghrelin

A pair of opposing appetite hormones. Leptin (produced by adipose tissue) signals satiety to the hypothalamus. Ghrelin (produced in the stomach) signals hunger. Their dysregulation (leptin resistance in obesity, high ghrelin in anorexia) contributes to weight and appetite disorders.
Category
Scientific evidence
Very high
Number of findings
4
Sources
Our own summaries · Cited studies

Effect by goal · level of evidence

Satiety and hunger

regulate Very high physiology (A)
Appetite regulation

High leptin = satiety; high ghrelin = hunger. In obesity, despite high leptin, there is leptin resistance in the hypothalamus: people eat without perceiving satiety.

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Leptin resistance

dysregulates Very high physiology (A)
Target in obesity

A chronic inflammatory state and excess adiposity cause leptin resistance. Reducing inflammation (omega-3, exercise, sleep) restores sensitivity.

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Sleep and appetite

modulates Very high cohorts + RCTs (AA)
Sleep-appetite pathway

Lack of sleep raises ghrelin and lowers leptin: you eat more the next day. Sleeping 7-9 h is one of the most effective interventions for regulating appetite.

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Intermittent fasting

modulates Moderate RCT (AA)
Adaptation to fasting

Intermittent fasting reduces baseline ghrelin in the medium term after adaptation (2-4 weeks). It explains why, a few weeks after starting, you are 'no longer hungry at noon'.

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Information, not medical advice. Scientific evidence reflects the quality of the studies.

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