Higher Ketone Levels During Dieting Suppress Hunger Hormone Ghrelin and Boost GLP-1 and CCK
In 87 people who lost ~18 kg on a very low-calorie diet, higher blood ketone levels were associated with lower ghrelin and higher GLP-1 and CCK satiety hormones.
Quick Facts
What This Study Found
Fasting βHB negatively correlated with ghrelin changes (P=0.003) and positively with GLP-1 (P=0.025) and CCK (P=0.035) after 17.7 kg weight loss, but not with subjective appetite.
Key Numbers
Lost 17.7 kg; BHB 1.24 mmol/L; ghrelin r=-0.315 (p=0.003); GLP-1 r=0.244 (p=0.025); CCK r=0.228 (p=0.035); no PYY correlation
How They Did This
Observational study of 87 adults with obesity (BMI 36.5) on 8-week very low-energy diet. Measured at baseline and week 9: body composition, fasting βHB, active ghrelin, GLP-1, PYY, CCK, insulin; subjective appetite by VAS.
Why This Research Matters
Weight loss typically increases hunger (the body fights back). Ketosis may counteract this by modulating gut hormones, making very low-calorie and ketogenic diets more tolerable.
The Bigger Picture
The appetite-suppressing effect of ketosis may explain the popularity and reported ease of ketogenic diets. Understanding the mechanism (via GLP-1 and CCK) could lead to targeted therapies.
What This Study Doesn't Tell Us
Observational correlations — cannot prove causation; no non-ketotic control group; subjective appetite didn't correlate with βHB; confounders possible; short follow-up.
Questions This Raises
- ?Does exogenous ketone supplementation suppress ghrelin without calorie restriction?
- ?Would maintaining ketosis long-term prevent the appetite rebound that drives weight regain?
- ?What molecular mechanism links βHB to GLP-1 and CCK secretion?
Trust & Context
- Key Stat:
- βHB → lower ghrelin Higher ketone levels correlated with reduced hunger hormone ghrelin (r=-0.315, P=0.003) after major weight loss
- Evidence Grade:
- Moderate — well-designed observational study with 87 participants and validated hormone measurements, but correlational only.
- Study Age:
- Published in 2020; the ketone-appetite connection continues to be actively studied.
- Original Title:
- Association Between Ketosis and Changes in Appetite Markers with Weight Loss Following a Very Low-Energy Diet.
- Published In:
- Obesity (Silver Spring, Md.), 28(12), 2331-2338 (2020)
- Authors:
- Martins, Catia(5), Nymo, Siren(3), Truby, Helen(2), Rehfeld, Jens F, Hunter, Gary R, Gower, Barbara A
- Database ID:
- RPEP-04986
Evidence Hierarchy
Watches what happens naturally without intervening.
What do these levels mean? →Frequently Asked Questions
Why are people less hungry in ketosis?
This study suggests ketones directly influence gut hormones — suppressing ghrelin (hunger) while boosting GLP-1 and CCK (fullness) — creating a hormonal environment that reduces appetite.
Do ketone supplements work the same way?
Unknown. This study involved ketosis from calorie restriction. Whether exogenous ketone supplements have the same appetite hormone effects hasn't been established.
Read More on RethinkPeptides
Cite This Study
https://rethinkpeptides.com/research/RPEP-04986APA
Martins, Catia; Nymo, Siren; Truby, Helen; Rehfeld, Jens F; Hunter, Gary R; Gower, Barbara A. (2020). Association Between Ketosis and Changes in Appetite Markers with Weight Loss Following a Very Low-Energy Diet.. Obesity (Silver Spring, Md.), 28(12), 2331-2338. https://doi.org/10.1002/oby.23011
MLA
Martins, Catia, et al. "Association Between Ketosis and Changes in Appetite Markers with Weight Loss Following a Very Low-Energy Diet.." Obesity (Silver Spring, 2020. https://doi.org/10.1002/oby.23011
RethinkPeptides
RethinkPeptides Research Database. "Association Between Ketosis and Changes in Appetite Markers ..." RPEP-04986. Retrieved from https://rethinkpeptides.com/research/martins-2020-association-between-ketosis-and
Access the Original Study
Study data sourced from PubMed, a service of the U.S. National Library of Medicine, National Institutes of Health.
This study breakdown was produced by the RethinkPeptides research team. We analyze and report published research findings without making health recommendations. All interpretations are based solely on the published abstract and study data.