Condition
Excess food intake
18 compounds were checked against excess food intake, and every one of them earned a row.
Last updated
Recorded under Weight, alongside 4 other indications.
Compounds with a graded row
Ordered by rung, strongest first. The rung rates the study design; the chip beside it says what the study measured. Both are needed.
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Cholecystokinin (CCK)
human RCT Direct outcome Not approved for this condition
- Who was studied
- healthy men, n=15, double-blind placebo-controlled crossover, 20-minute intravenous CCK-8 infusion at 4 ng/kg/min before one ad libitum test meal
Energy intake at a single ad libitum test meal fell during CCK-8 infusion relative to saline, by 56.6 percent in the eight subjects reporting gastrointestinal disturbance and 44.6 percent in the seven without; meal duration and eating rate also fell. The reduction was measured at one meal in healthy volunteers, and the paper's own question was how far nausea and anxiety account for it. An earlier double-blind crossover in eight obese men found six of eight ate less on the same infusion rate.
Source PubMed 2 primary sources read for this row
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Ghrelin
human RCT Direct outcome Not approved for this condition
- Who was studied
- healthy adults, n=9, randomised double-blind crossover, single intravenous infusion at 5.0 pmol/kg/min
Ghrelin increases food intake: every participant ate more from a free-choice buffet during ghrelin infusion than during saline, a mean rise of 28 percent, with higher appetite scores. It was administered to stimulate eating, and this row records an orexigenic effect, the opposite direction to the subject of this page.
Source PubMed 1 primary source read for this row
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GHRP-2
human RCT Direct outcome Not approved for this condition
- Who was studied
- 19 healthy weight-stable adults, 10 lean and 9 obese; subcutaneous infusion at 1 microgram/kg/hour, 0.1 microgram/kg/hour or placebo for 270 minutes across three visits, with an ad libitum buffet lunch as the endpoint
The direction of this result is towards more eating, not less. GHRP-2 raised ad libitum food intake by 10.2 per cent at the low dose and 33.5 per cent at the high dose against placebo, and obesity status did not blunt the response. Appetite ratings before the meal rose; fullness after the meal did not differ. A compound recorded here against excess food intake because it was measured against that endpoint and moved it upward; nothing in the record supports it as a treatment for the condition. The exposure was a single infusion in a laboratory meal paradigm, so no weight outcome over time is on file. Rung set from the study's own design wording, "double-blind randomized".
Source PubMed 1 primary source read for this row
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PYY3-36
human RCT Direct outcome Not approved for this condition
- Who was studied
- 12 obese and 12 lean adults, double-blind placebo-controlled crossover, single intravenous infusion; buffet lunch offered two hours later
Measured calories eaten at a free-choice buffet lunch after a single infusion: down 30 percent in the obese subjects and 31 percent in the lean subjects, with 24-hour calorie intake also reduced in both groups. This is a one-day intake measurement; the study did not follow body weight, so nothing here shows a change in weight.
Source PubMed 1 primary source read for this row
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Leptin
human case series Direct outcome Not approved for this condition
- Who was studied
- women with lipodystrophy and hypoleptinaemia, n=8, open-label recombinant methionyl human leptin for 4 months; no control group
Energy consumed to reach satiation from a standardised food array fell from 2034 to 1135 kcal over four months of leptin injections, with satiation reached sooner and satiety lasting longer. All eight participants were leptin-insufficient, which is the condition being corrected; no measured-intake study on file in people with normal leptin. Metreleptin is approved for the metabolic complications of generalised lipodystrophy and congenital leptin deficiency, not for reducing food intake.
Source PubMed 1 primary source read for this row
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Setmelanotide
human case series Direct outcome Approved for this condition
- Who was studied
- participants aged 6 years or older with severe obesity due to biallelic pro-opiomelanocortin or leptin receptor deficiency, n=10 (POMC trial) and n=11 (LEPR trial), across ten hospitals in seven countries; 12 weeks open-label, an 8-week placebo-controlled withdrawal sequence, then 32 further open-label weeks. The hunger endpoint was assessed in 7 participants per trial aged 12 or over
Hunger was measured directly on the most-hunger item of an 11-point Likert-type scale. Mean change at approximately one year was -27.1% in the POMC trial (n=7, 90% CI -40.6 to -15.0, p=0.0005) and -43.7% in the LEPR trial (n=7, -54.8 to -29.1, p<0.0001). Seven participants per trial is the whole hunger dataset, and there is no placebo comparison for it: the withdrawal sequence was blinded, but the reported hunger figure is the change from baseline on treatment. Injection site reaction was reported in every participant in both trials. Rung set by review: the pivotal POMC and LEPR trials are single-arm and open-label, and the hunger figure is a change from baseline in seven participants per trial with no placebo comparison.
Source PubMed 1 primary source read for this row
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Amylin
animal in vivo Direct outcome Not approved for this condition
- Who was studied
- rats aged 7-9 weeks, 3 months and 15-18 months, intraperitoneal amylin 0.1-10 mcg/kg, food-deprived before testing
Intraperitoneal amylin reduced food intake dose-dependently in food-deprived rats, mostly within the first two hours, with intake compensated by 24 hours and no effect in non-deprived animals. The human buffet-meal evidence usually attached to amylin was generated with pramlintide, a modified analogue, not with native amylin; no measured-intake study in humans using native amylin is on file.
Source PubMed 1 primary source read for this row
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Nesfatin-1
animal in vivo Direct outcome Not approved for this condition
- Who was studied
- rats, intracerebroventricular injection, acute and chronic dosing; no human study on file
Intracerebroventricular nesfatin-1 decreased food intake in rats dose-dependently, and a neutralising antibody increased it; the effect persisted in leptin-receptor-mutant Zucker rats and was blocked by a melanocortin-3/4 antagonist. Delivery was directly into the brain ventricles of rats, and no study has measured food intake in humans given nesfatin-1.
Source PubMed 1 primary source read for this row
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Obestatin
animal in vivo Direct outcome Not approved for this condition
- Who was studied
- rats, treated with obestatin isolated from rat stomach; no human study on file
The 2005 isolation paper reported that obestatin suppressed food intake and slowed weight gain in rats. That result has repeatedly failed to replicate: a later rat study found no effect on spontaneous intake in either fed or food-restricted animals and no blocking of ghrelin-stimulated intake, and the proposed GPR39 receptor binding also failed to replicate, leaving the receptor unresolved. No human food-intake study is on file.
Source PubMed 2 primary sources read for this row
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Orexin-A
animal in vivo Direct outcome Not approved for this condition
- Who was studied
- rats, single intracerebroventricular injection of 23.4 nmol and 8-day infusion of 18 nmol/day; no human study on file
Orexin-A increases food intake: a single intracerebroventricular dose increased feeding in satiated rats and prolonged it in fasted rats, and an 8-day infusion raised daytime feeding while lowering night-time feeding, leaving 24-hour intake unchanged. It is administered to stimulate feeding, the opposite direction to the subject of this page, and no measured-intake study in humans is on file.
Source PubMed 1 primary source read for this row
Recorded absences
6 compounds are listed here without a rung. Each row exists to mark a distinction a reader would otherwise draw wrongly, and each says what is missing rather than leaving the compound off the page.
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CRH (Corticotropin-Releasing Hormone)
No rung — nothing on file to grade Not approved for this condition
CRH suppresses feeding in rodents, which is a mechanism observation in an animal, not an administered intervention with a human intake outcome. Nothing retrieved supports a row.
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GHRH (Growth Hormone-Releasing Hormone)
No rung — nothing on file to grade Not approved for this condition
No study measured food intake after GHRH. The appetite work in the somatotropic axis is ghrelin and its agonists, which act at a different receptor.
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GHRP-1
No rung — nothing on file to grade Not approved for this condition
No study measured food intake after GHRP-1 in any species. The ghrelin-agonist feeding literature uses GHRP-2 and ghrelin itself.
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GHRP-6
No rung — nothing on file to grade Not approved for this condition
No study measured food intake after GHRP-6 as an endpoint in its own right. Most GHRP-6 appearances in the appetite literature are as the antagonist D-Lys3-GHRP-6, a blocking tool used to test ghrelin, which is the opposite intervention.
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Hexarelin
No rung — nothing on file to grade Not approved for this condition
No study measured food intake after hexarelin. The feeding work in this peptide family was done with GHRP-2 and with ghrelin.
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HGH Frag 176-191
No rung — nothing on file to grade Not approved for this condition
Caloric intake was measured in the obese-mouse study as a control variable, not as an endpoint, and no appetite or hunger measure exists for this compound in any species.
Every compound checked earned a row
Nothing was checked against excess food intake and set aside. That is unusual — most conditions here have a list at the bottom of this page.
What this page does not say
It reports what was measured, in whom, and how directly. It does not say what to take or at what dose, and a row here is a record of a study rather than a reason to use anything. Every rung links to the rubric that assigned it.