How the Endocannabinoid System Drives Both Food Craving and Fat Storage | Research

The takeaway

The endocannabinoid system both stimulates appetite by increasing food craving and enjoyment and promotes fat storage, making CB1 blockers a potential class of anti-obesity drugs.

Read this if you want a quick overview of why cannabis makes you hungry and how that relates to obesity science.

Endocannabinoids drive both appetite (brain CB1) and fat storage (peripheral CB1)

What the researchers found

This brief review outlined how the endocannabinoid system drives overeating through two complementary mechanisms.

First, endocannabinoids acting at CB1 receptors in the brain increase appetite by enhancing both food craving (wanting) and food enjoyment (liking). This explains the well-known "munchies" effect of cannabis.

Second, the endocannabinoid system promotes energy storage as fat in adipose (fat) tissue, meaning it doesn't just increase food intake but also directs where that energy goes.

These dual actions, increasing intake and promoting storage, raised the possibility that CB1 receptor blockers could address obesity from both directions: reducing appetite and decreasing fat deposition.

Why it matters

Understanding that the endocannabinoid system drives both overconsumption and fat storage explained why cannabis users often experience intense food cravings and why the CB1 blocker rimonabant showed weight loss effects in clinical trials.

The numbers in context

Endocannabinoids activate CB1 receptors in brain (appetite) and peripheral tissues (fat storage). CB1 antagonists were identified as potential anti-obesity agents.

How the study worked

Brief narrative review or editorial summarizing the current understanding of endocannabinoid system involvement in appetite regulation and energy storage.

What this study cannot tell us

This is a brief editorial rather than a systematic review. It summarizes the concept without detailed evidence assessment.

How to read the evidence

This is a brief editorial or commentary summarizing established concepts rather than presenting new data.

When this study was published

Published in 2008, around the time rimonabant was being withdrawn from European markets. Peripheral CB1 antagonists are still in development.

The bigger picture

While the specific drug rimonabant was later withdrawn due to psychiatric side effects, the concept of endocannabinoid-driven appetite and fat storage has remained central to obesity research. Newer approaches aim to block peripheral CB1 receptors (in fat tissue) while sparing brain CB1 receptors to avoid psychiatric effects.

Questions still open

Can peripherally restricted CB1 antagonists reduce fat storage without affecting brain appetite circuits? Do chronically obese individuals have elevated endocannabinoid tone?

Common questions

Why does cannabis cause "the munchies"?

Cannabis activates CB1 receptors in brain regions that control appetite, increasing both food craving (wanting food) and food enjoyment (how good it tastes). This makes you want to eat and makes food seem more rewarding.

What happened to CB1-blocking weight loss drugs?

Rimonabant, a CB1 blocker, was approved in Europe for weight loss in 2006 but withdrawn in 2008 due to psychiatric side effects (depression, suicidal thoughts). Researchers are now developing versions that only block CB1 in fat tissue, not the brain.

Read the original research

Endocannabinoids and the neurochemistry of gluttony.

Journal of neuroendocrinology, 20(9), 1099-100

View on PubMed ↗Publisher’s paper ↗

Citation

Kirkham, Tim. (2008). Endocannabinoids and the neurochemistry of gluttony.. Journal of neuroendocrinology, 20(9), 1099-100. https://doi.org/10.1111/j.1365-2826.2008.01762.x