Ketosis — from ketogenic diets or exogenous ketone esters — prevents the surge in the hunger peptide ghrelin that normally follows weight loss, potentially reducing appetite and the risk of weight regain.
30% thresholdAppetite-suppressing effects appeared in rodents when ketone esters provided at least 30% of total dietary energy
What the researchers found
Ketogenic diets prevent the increase in ghrelin secretion that normally accompanies weight loss, while also reducing hunger and preventing hunger increases. The exact threshold of ketosis required for appetite suppression has not been established.
Exogenous ketone esters showed concentration-dependent effects on food intake and body weight in rodent models, with a threshold effect appearing when ketone esters provided 30% of total dietary energy. In a human study, acute consumption of a ketone ester drink reduced feelings of hunger and increased satiety compared to a dextrose (sugar) drink. The mechanisms mediating ketosis-induced appetite suppression remain to be fully elucidated.
Why it matters
Weight regain after dieting is the biggest unsolved problem in obesity treatment. The ghrelin rebound — the body's compensatory hunger increase after weight loss — is a major driver. If ketosis can prevent this peptide hormone surge, it could be the key to sustaining weight loss. Understanding the mechanism could lead to targeted interventions (dietary or supplemental) that suppress appetite without relying solely on willpower.
How the study worked
Narrative review of published literature on ketosis and appetite regulation, covering evidence from ketogenic diet studies, exogenous ketone ester studies (animal and human), ghrelin and appetite hormone measurements, and proposed mechanisms of action.
What this study cannot tell us
The exact level of ketosis needed for appetite suppression is unknown. Most evidence for ghrelin suppression comes from short-term studies — long-term effects are unclear. Ketogenic diets have notoriously poor adherence, limiting their practical utility. Human data on exogenous ketone esters and appetite is limited to acute studies. The review acknowledges that underlying mechanisms are not fully understood.
How to read the evidence
This is a narrative review combining evidence from multiple sources: ketogenic diet clinical studies, animal models of exogenous ketone supplementation, and limited human acute-dosing studies. While the ghrelin-suppressing effect of ketosis is consistently observed, the mechanisms and optimal dosing remain poorly characterized.
When this study was published
Published in 2020, this review captures the state of knowledge during a period of growing scientific and public interest in both ketogenic diets and appetite hormone biology. Research on exogenous ketones has continued to advance since publication.
The bigger picture
This review connects two major trends in metabolic health: the popularity of ketogenic diets and the scientific understanding of gut peptide hormones in appetite regulation. The finding that ketosis specifically modulates ghrelin — a peptide already targeted by GLP-1 drugs and bariatric surgery — suggests that dietary and pharmacological approaches to appetite control may converge on similar hormonal pathways.
Questions still open
- What is the minimum blood ketone level needed to suppress ghrelin and reduce appetite during weight loss?
- Can exogenous ketone supplements provide sustained appetite suppression comparable to a full ketogenic diet?
- Would combining ketosis-induced ghrelin suppression with GLP-1 agonist therapy produce additive appetite-suppressing effects?
Common questions
Why does the body increase hunger after weight loss?
Could ketone supplements replace a ketogenic diet for appetite control?
Read the original research
Impact of ketosis on appetite regulation-a review.
Nutrition research (New York, N.Y.), 77, 1-11
Citation
Deemer, Sarah E; Plaisance, Eric P; Martins, Catia. (2020). Impact of ketosis on appetite regulation-a review.. Nutrition research (New York, N.Y.), 77, 1-11. https://doi.org/10.1016/j.nutres.2020.02.010