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Is CBG an Appetite Suppressant? Unpacking the Complex Science of Cannabinoids and Hunger

5 min read

A 2016 study published in a prominent pharmacology journal found that oral administration of cannabigerol (CBG) stimulated appetite in rats, significantly increasing their food intake without causing adverse neuromotor side effects. This discovery directly challenges the common, albeit unsubstantiated, claim that is CBG an appetite suppressant and instead positions it as a potential non-intoxicating appetite stimulant.

Quick Summary

Cannabigerol (CBG) is not an appetite suppressant; multiple animal studies indicate it stimulates appetite, a stark contrast to popular belief. Unlike intoxicating THC, CBG's hunger-inducing effects are non-psychoactive and dose-dependent. More human research is needed to confirm these findings, especially concerning long-term use and individual differences.

Key Points

  • CBG Is an Appetite Stimulant in Studies: Early research, primarily in rats, shows that CBG increases food intake and meal frequency in a dose-dependent manner.

  • Non-Psychoactive Hunger Boost: Unlike THC, CBG stimulates appetite without causing intoxication, making it a potentially valuable option for conditions causing appetite loss.

  • Mechanism Is Complex: CBG's effect on appetite is likely mediated by its interaction with receptors outside the primary endocannabinoid system, such as α2-adrenoceptors.

  • Human Data Is Mixed: Human anecdotal reports and limited studies show inconsistent effects, with some users reporting increased appetite and others noting no change or even suppression.

  • Not for Weight Loss: Based on scientific evidence, CBG is not an appetite suppressant and should not be used as a weight-loss aid.

  • More Research is Needed: The full scope of CBG's effects on human appetite is still being explored, and further clinical trials are required.

In This Article

Understanding the Endocannabinoid System's Role in Appetite

To understand how cannabigerol (CBG) affects appetite, one must first grasp the function of the endocannabinoid system (ECS). The ECS is a complex cell-signaling system that plays a crucial role in regulating various bodily functions, including appetite, mood, memory, and pain sensation. It is composed of endogenous cannabinoids (endocannabinoids), receptors (CB1 and CB2), and enzymes that synthesize and break down these compounds.

Appetite regulation is primarily mediated by the CB1 receptors, which are highly concentrated in the brain areas that control hunger, such as the hypothalamus. Cannabinoids, whether produced by the body (endocannabinoids) or derived from plants (phytocannabinoids like CBG and THC), can interact with these receptors to modulate eating behaviors. While THC is notorious for binding directly to CB1 receptors and causing the intense hunger known as "the munchies," CBG's interaction is different and more subtle.

Animal Studies: A Clear Signal for Appetite Stimulation

Early scientific research, predominantly on animal models, has provided the strongest evidence regarding CBG's effect on appetite. The 2016 study mentioned in the introduction administered varying doses of CBG to pre-satiated rats. The researchers observed a dose-dependent increase in food intake, with higher doses (120-240 mg/kg) more than doubling the amount of food consumed.

  • Increased Meal Frequency: The study's detailed analysis of meal patterns showed that CBG increased the number of meals the rats consumed.
  • Reduced Latency to Feed: CBG was also found to reduce the time it took for the animals to begin eating.
  • No Psychoactive Side Effects: Crucially, these effects occurred without causing any intoxicating or adverse neuromotor side effects, unlike THC.

Another pre-clinical study also noted that CBG was able to reduce the anorexia and weight loss caused by the chemotherapy drug cisplatin in rats, further highlighting its potential as an appetite stimulant. These animal studies provide a strong scientific basis for CBG's appetite-stimulating properties, suggesting it could be a valuable therapeutic agent for conditions involving appetite loss, such as cachexia.

Conflicting Human Evidence and Anecdotal Accounts

Despite the consistent findings in animal models, the picture is less clear when it comes to human experiences. Anecdotal reports and some preliminary human studies paint a more mixed and sometimes contradictory view of CBG's effects on appetite.

  • A 2024 survey of CBG users, while focusing on anxiety and mood, noted that only a minority (11.8%) reported an increase in appetite, with 16.5% reporting dry mouth and 15% reporting sleepiness. This contrasts sharply with the robust appetite stimulation seen in animal studies.
  • Another recent human study exploring the effects of CBG on anxiety reported "minimal changes" in appetite among participants, though the dose used was modest.
  • Some anecdotal reports from users describe CBG as having a neutral or slightly suppressive effect on appetite, sometimes attributing it to improved mood and reduced stress-induced eating.

This discrepancy between animal and human data may be due to several factors, including dosage differences, individual metabolism, product composition (e.g., isolate vs. broad-spectrum), and the fact that animal results do not always translate perfectly to humans. The animal studies used relatively high doses of CBG, whereas human consumption often involves much lower concentrations.

How CBG's Unique Pharmacology Explains its Action

CBG's distinct mechanism of action helps to explain its complex effects on appetite and why it differs from other cannabinoids. While it has some affinity for CB1 and CB2 receptors, it is considered a partial agonist, meaning it doesn't activate them as strongly as THC. Its appetite-stimulating effects likely involve other pathways:

  • Activation of α2-adrenoceptors: CBG is a potent agonist at α2-adrenoceptors, which have been shown in animal models to have hyperphagic (appetite-stimulating) effects, particularly in the hypothalamus.
  • Inhibition of Anandamide Reuptake: CBG inhibits the reuptake of anandamide, an endocannabinoid that plays a role in mood and appetite. By increasing the levels of anandamide, CBG might indirectly stimulate hunger, though this effect seems to be less potent than its action on adrenoceptors.
  • Interaction with PPARγ Receptors: CBG acts as an agonist at Peroxisome proliferator-activated receptors (PPARγ), which are involved in energy metabolism and can influence insulin sensitivity. While the exact link to appetite is still being researched, this interaction points to a broader metabolic influence.
  • Modulation of 5-HT1A Receptors: CBG also acts as a moderate antagonist at 5-HT1A receptors, which are involved in mood and anxiety. By reducing anxiety and stress, CBG might indirectly influence eating behaviors in humans, especially for those who experience emotional eating.

CBG vs. Other Cannabinoids: A Comparison

To highlight the unique profile of CBG, it's helpful to compare its effects on appetite with those of its better-known relatives, THC and CBD.

Feature CBG (Cannabigerol) THC (Tetrahydrocannabinol) CBD (Cannabidiol)
Effect on Appetite Stimulant (animal studies), mixed/minimal effects (human reports) Strong stimulant (causes "munchies") Suppressant or no effect (mixed results)
Mechanism Partial agonist of CB1/CB2; potent α2-adrenoceptor agonist Strong agonist of CB1 receptor Modulates ECS, low affinity for CB receptors
Psychoactivity Non-intoxicating Intoxicating (causes a "high") Non-intoxicating
Primary Use for Appetite Investigational for severe appetite loss (e.g., cachexia) Clinical use for anorexia in conditions like AIDS Not typically used for appetite; focus on other benefits
Best For Boosting appetite without a "high" Strong, fast-acting appetite stimulation Those seeking other benefits without appetite changes

Conclusion

While the popular notion that is CBG an appetite suppressant has circulated, the available scientific research, particularly from animal studies, points in the opposite direction. CBG is more accurately described as a potential non-intoxicating appetite stimulant, capable of increasing food intake and meal frequency, likely through its interaction with non-cannabinoid receptors like the α2-adrenoceptor.

However, the lack of extensive, high-quality human clinical trials means the effects in people are not yet fully understood and can vary considerably, with some individuals reporting minimal or no change to their appetite. Therefore, any consumer seeking to use CBG for weight or appetite management should exercise caution and rely on confirmed scientific evidence rather than unsubstantiated claims. As research continues, the nuances of CBG's pharmacology will become clearer, potentially paving the way for safe and effective clinical applications for appetite regulation. In the meantime, consulting a healthcare professional is recommended before using any cannabinoid product for a specific health concern.

For more detailed information on CBG's mechanisms and potential therapeutic uses, you can refer to authoritative sources like the National Center for Biotechnology Information (NCBI).

Key Takeaways

  • Contradictory to Suppression: Contrary to popular claims, scientific evidence, primarily from animal studies, suggests CBG is an appetite stimulant, not a suppressant.
  • Appetite Stimulation without Intoxication: CBG's appetite-boosting effects were observed without the psychoactive "high" associated with THC, making it a unique candidate for medical applications.
  • Different Mechanism of Action: CBG does not act on the endocannabinoid system in the same way as THC, instead interacting with other pathways like α2-adrenoceptors to produce its effects.
  • Variable Human Response: The effects of CBG on human appetite are less clear, with some studies and anecdotal reports showing minimal or mixed results, potentially due to dosage and individual differences.
  • Requires More Research: More rigorous human studies are necessary to fully understand CBG's role in appetite regulation and determine optimal dosing and efficacy.
  • Not a Weight Loss Tool: Because of its potential appetite-stimulating effects, CBG should not be considered a tool for weight loss.

Frequently Asked Questions

No, CBG is not a weight loss supplement. In fact, most animal research indicates that CBG stimulates appetite and increases food intake, which could lead to weight gain rather than loss. A balanced diet and regular exercise remain the most proven methods for weight management.

THC is a potent appetite stimulant known for causing the "munchies." CBG also stimulates appetite, but its effects, as seen in animal studies, are typically less intense and do not involve intoxication, making it a non-psychoactive option for increasing hunger.

Yes, some cannabinoids, most notably THCv (tetrahydrocannabivarin), have shown potential to suppress appetite in animal studies. Additionally, CBD's effect on appetite is debated, with some studies suggesting a suppressive effect, especially in certain populations.

The varying effects of CBG in humans may be due to differences in dosage, product formulation, and individual biology. Some users report that CBG helps manage anxiety, which can reduce emotional eating and indirectly lead to lower overall food intake, but this is not a direct appetite suppression effect.

The appetite-stimulating effects observed in animal studies are believed to be primarily driven by CBG's activity as a potent agonist of α2-adrenoceptors in the brain, rather than direct activation of CB1 receptors like THC.

Yes, combining CBG with other cannabinoids can alter its effects. Some evidence suggests that combining CBG with THC might create a more potent appetite stimulus. Conversely, combining CBG with a cannabinoid like CBD or THCV might modulate or counteract its appetite-stimulating properties.

Most research on CBG's appetite-stimulating effects has been in pre-clinical, animal-based studies. While these findings warrant further investigation, human clinical trials are limited and more research is needed to determine its safety and efficacy for treating appetite loss in humans.

References

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Medical Disclaimer

This content is for informational purposes only and should not replace professional medical advice.