Low-Carb Diets, Ketosis, and Ghrelin: What a Trial Found

A low-carbohydrate diet may reduce one post-meal hunger signal more than an isocaloric low-fat diet. But the best direct trial also leaves a large unanswered question: did ketones change ghrelin, or did the low-carb group's greater weight loss drive the difference?

In an eight-week randomized trial, women with lipedema assigned to 75 grams of carbohydrate per day had a statistically significant reduction in postprandial ghrelin total area under the curve, while the 180-gram-per-day low-fat group did not show the same pattern. The between-group result reached statistical significance, but narrowly: P=0.046. That is an interesting biomarker result, not proof that dietary ketosis reliably makes people feel less hungry or that it will generalize beyond this specific population.

The result: lower post-meal ghrelin on the low-carb diet

Lundanes et al.'s 2025 randomized controlled trial assigned 55 women with lipedema and a mean BMI of 36.8 ± 5.1 kg/m² to low-energy diets for eight weeks. Thirty participants followed a low-carbohydrate diet capped at 75 g of carbohydrate daily; 25 followed a low-fat diet with 180 g daily. The diets had matched calorie targets.

The main hormone finding was specific. The low-carbohydrate group had a reduction in postprandial ghrelin total area under the curve (within-group P=0.002), and its change differed from the low-fat group (P=0.046). Fasting ghrelin did not change significantly in either group. In other words, the signal appeared after eating, rather than as a lower baseline concentration before a meal.

Ghrelin is often called the hunger hormone because it can stimulate appetite, but that label can make it sound more decisive than it is. Eating behavior reflects food preference, habit, sleep, stress, gastrointestinal symptoms, social context, and several hormonal signals. A lower ghrelin response can support an appetite-control hypothesis; it cannot by itself tell us how much less someone will eat.

The trial found a statistically significant difference in a post-meal hormone measure. It did not establish that ketones alone caused the difference, or that participants experienced a clinically meaningful reduction in hunger.

Why ketones are a plausible explanation

The strongest evidence that ketones themselves can affect appetite comes from a different kind of experiment. In a randomized crossover study of healthy young men, Vestergaard et al. in 2021 found that an acute dose of exogenous ketone ester reduced plasma acyl ghrelin and subjective appetite without caloric restriction. That matters because it separates a short-lived pharmacological ketosis experiment from fasting or a diet-induced calorie deficit.

Taken together, the ketone ester study and the lipedema trial make a biologically plausible case: ketone bodies may contribute to lower ghrelin signaling after meals. Proposed routes include signaling by beta-hydroxybutyrate at receptors on ghrelin-producing gastric cells or effects on appetite circuits in the brain. These are hypotheses, not confirmed pathways in the women studied by Lundanes and colleagues. The dietary trial did not directly link beta-hydroxybutyrate concentrations to each participant's ghrelin response.

The distinction matters. A ketone ester creates a rapid, high-amplitude exposure after a single dose. Eight weeks of carbohydrate restriction changes meal composition, body weight, insulin dynamics, and daily energy intake. Those are related metabolic states, but they are not interchangeable experiments.

The biggest problem: the groups did not lose the same amount of weight

The low-carbohydrate group lost 10.3% of body weight, compared with 7.3% in the low-fat group. The difference was statistically significant. That is the central limitation of the trial because weight loss itself can alter appetite hormones.

Body-composition changes may matter as well. Martins et al. in 2023 reported that the amount of fat-free-mass loss was associated with changes in appetite and weight regain among people with obesity. That study does not prove that lean-mass loss explained the ghrelin finding in lipedema, but it shows why macronutrients are not the only plausible explanation when diet groups lose different amounts of weight.

A matched-weight-loss randomized trial would provide a cleaner test: keep weight loss similar in low-carb and low-fat groups, measure ketones and appetite hormones repeatedly, and then ask whether the ghrelin difference remains. No study described here has done that.

The other appetite hormones do not tell a clean ketosis story

If the low-carb diet had broadly strengthened gut-derived satiety signaling, researchers might expect several appetite-related hormones to move in a diet-specific direction. They did not.

Both groups had significant decreases in postprandial cholecystokinin (CCK) across total and incremental area-under-the-curve measures, with P≤0.005, and there was no between-group difference. CCK helps signal meal-related fullness, particularly after fat and protein intake. Its similar decline in both groups points toward a shared consequence of calorie restriction or weight loss rather than a low-carb-specific CCK effect.

GLP-1 and peptide YY also did not show significant diet-specific effects in the lipedema trial. The acute ketone ester experiment likewise found no significant GLP-1 change. That does not rule out every appetite effect of carbohydrate restriction, but it argues against a simple story in which ketosis activates all the usual satiety hormones at once.

Broader evidence remains mixed. A 2024 systematic review and meta-analysis of randomized trials reported that ketogenic diets changed some adipokines, while finding no discernible overall effect on ghrelin. Such pooled findings can differ from a single trial because studies vary in diet duration, calorie restriction, participant health, and how ghrelin is measured. The result is useful context, not a reason to erase the lipedema trial's post-meal finding.

A hormone change may not feel like less hunger

The women on the low-carbohydrate diet reported significant within-group improvements in postprandial fullness: P=0.035 for incremental area under the curve and P=0.005 for total area under the curve. Yet neither improvement differed significantly from the low-fat group (between-group P=0.703 and P=0.365, respectively). The trial therefore did not show a clear subjective fullness advantage for the low-carb diet over its comparator.

That mismatch has appeared elsewhere. In a randomized crossover study of trained competitive cyclists and triathletes, Graybeal et al. found that appetite perceptions did not match hormonal appetite measures after a ketogenic diet compared with high-carbohydrate and habitual diets. The athletes differ sharply from middle-aged women with lipedema, so their results cannot be transferred directly. They do reinforce a basic point: ghrelin is a biomarker, not a direct readout of what a person feels or eats.

Other ketogenic-diet research supports the idea that appetite hormones can shift under non-starvation conditions. Valinejad et al. examined appetite sensations, appetite-regulating hormones, and body composition during a ketogenic diet with and without exercise. A 2025 meta-analysis in women with polycystic ovary syndrome also found meaningful weight, metabolic, and endocrine changes with ketogenic diets. Neither line of research establishes that lipedema responds the same way. PCOS, athletic training, and lipedema each bring different physiology to the table.

Who can use this finding?

The direct dietary evidence applies to women with lipedema, not to men, the general population with obesity, or people seeking an appetite hack while otherwise maintaining their usual diet. The trial's participants had a mean age of 47.9 ± 11.3 years, an age range in which ovarian-hormone transitions may also affect appetite biology. The study did not resolve how menopausal status influenced ghrelin responses.

For someone who finds a lower-carbohydrate pattern easier to sustain, these findings provide a reasonable mechanistic hypothesis for why meals may feel more manageable. They do not justify treating ketones as a proven appetite suppressant or taking ketone esters as a substitute for a workable diet. The human data show an intriguing post-meal ghrelin difference, a plausible ketone mechanism, and several reasons to keep the conclusion modest.

The fairest verdict is practical: low-carb eating may help some people manage hunger, but this trial cannot separate ketosis from greater weight loss, and it did not show a statistically significant advantage in reported fullness over low-fat eating. The next useful study needs matched weight loss, direct ketone measurements, and appetite outcomes that matter outside a blood draw.