In a Nutshell
"Does sermorelin work" contains two questions, and they have different answers.
Does it raise growth hormone? Broadly yes — that is what a GHRH analog does, and it is why sermorelin was historically used as a diagnostic agent to test whether a pituitary could respond at all.
Does raising growth hormone that way produce the results it is marketed for in adults — better sleep, more energy, less fat, better recovery, better skin? That has not been established. Two randomized placebo-controlled trials of the drug itself do exist in adults — one reporting improvements on selected cognitive measures, one on body composition in men with HIV-associated lipodystrophy — so the evidence is narrow rather than absent. Neither tested a present-day compounded preparation, and neither examined the sleep, energy, recovery or skin claims. Controlled evidence for chronic compounded adult use remains limited, and no reliable onset timeline has been established.
Almost every confident claim you will read collapses the second question into the first. A measurable change in a blood marker is presented as though it were the outcome you actually want. It is not the same thing, and the gap between them is where this entire question lives.
Sermorelin is supplied today as a compounded preparation rather than an FDA-approved finished drug. Its historical approvals as GEREF® covered diagnostic use and pediatric growth hormone deficiency; the products were discontinued in 2008 and those approvals withdrawn effective June 18, 2009 1. Mayo Clinic's monograph still describes it in those terms — a medicine for children who are not producing enough growth hormone 2.
What Sermorelin Itself Has Been Tested In
Start here, because almost everything else written about sermorelin is either about a different molecule or about what people hope it does.
Two randomized placebo-controlled trials are directly relevant, and both are narrow. A six-month randomized, double-blind, placebo-controlled study of sermorelin acetate — the GEREF product itself — randomized 100 healthy adults aged 60 to 85, of whom 89 completed. It reported improvements on several cognitive measures, the largest being about a five-point rise in WAIS performance IQ 7.
That number is worth sitting with, because the authors did. They devote a passage to whether a five-point gain is clinically meaningful, and conclude that defining clinical meaningfulness for cognitive function is "problematic at best and certainly not at all straightforward." The people who ran the trial declined to tell you it mattered. That is the most honest answer available to "does sermorelin work," and it comes from the larger of the two randomized trials of the drug in adults.
Its drug and placebo were supplied without charge by Serono, which manufactured GEREF, and two of its authors held consulting or research relationships with the company — worth knowing when weighing a positive result. And it tested a specific historical product, dose, population and cognitive endpoint: it establishes nothing about what a present-day compounded preparation would do, or about sleep, energy, recovery, skin or fat loss.
The second trial measured body composition. Twelve weeks of GHRH in 31 men with HIV-associated lipodystrophy — a population with documented reduced growth hormone secretion — increased lean mass and reduced trunk fat. The absolute reduction in abdominal visceral fat did not reach statistical significance 11 — and that is the endpoint most of the marketing is about. The dose was twice daily rather than the nightly regimen usually sold, and the population was one with a documented deficiency rather than healthy adults seeking enhancement.
Neither trial was designed to test the sleep, energy, recovery, skin or general fat-loss claims now made for compounded preparations, and neither used one. Both are small, decades old, and tested historical GHRH(1-29) preparations at specified doses in specified populations. The record is thin and narrow. It is not empty — and most of what follows on this page is about the gap between that record and what is claimed from it.
For context on the wider class, tesamorelin has been trialed against placebo in non-alcoholic fatty liver disease 9, and the ROMANA 3 extension study in cancer cachexia tested anamorelin, a ghrelin-receptor agonist reaching the same axis by a different mechanism 10. Those are other molecules in defined disease states — useful for understanding where the research money has gone, not evidence about sermorelin.
What Happens When You Give Growth Hormone Directly
The largest body of relevant evidence is not about sermorelin at all — it is about growth hormone itself, and it is worth understanding because it sets the necessary context.
In 2007, Annals of Internal Medicine published a systematic review by Liu and colleagues covering 31 articles that described 18 unique study populations of growth hormone therapy in healthy older adults, the population most "anti-aging" marketing is aimed at — 220 treated participants in all, mean age 69, mean treatment 27 weeks 3.
What it found: fat mass fell by roughly 2.1 kg (95% CI 1.35–2.8) and lean body mass rose by roughly 2.1 kg (95% CI 1.3–2.9). Those are real, measurable changes. But the treated groups experienced significantly more adverse effects than placebo — soft-tissue swelling, joint pain, carpal tunnel syndrome and gynecomastia.
Now consider what that means for sermorelin. Liu reviewed growth hormone itself — given directly, at therapeutic doses. That is a stronger intervention than prompting your own pituitary to release more. If the direct approach produced about two kilograms of body recomposition with no functional gain and more side effects, it is difficult to argue that the indirect approach should be expected to do more.
That is context, not a substitute trial and not a ceiling. Growth hormone given directly and growth hormone released by stimulating your own pituitary produce different exposure patterns, doses and pharmacokinetics — so the Liu figures do not set a mathematical upper limit on what sermorelin can do. Treating them that way would be the same product-and-mechanism substitution this page criticizes elsewhere. What the review does show is that even the direct approach, in this population, produced modest average body-composition change without consistent functional gain and with more adverse effects.
Where the "It Works" Case Comes From
Search this question and, when we checked on July 26, 2026, the fourth result was a 2006 paper in Clinical Interventions in Aging — a frequently cited pro-sermorelin editorial and the source of many of the mechanistic arguments still circulating 4.
It is worth reading it properly, because it is not what its ranking implies.
It is a two-page opinion piece. It reports no patients, no measurements and no trial. Its seven references include a Pittsburgh Post-Gazette newspaper article, a trade magazine feature, the author's own study in rats, and a laboratory paper on isolated pituitary cells.
Most importantly, the piece is transparent about what it is doing. It proposes that sermorelin might be a better option than recombinant growth hormone, describes the open questions as "speculative," and closes by offering sermorelin free of charge to practitioners willing to study it under protocol and publish the outcomes.
That is a legitimate thing to publish. It is a hypothesis and a call for research, and the author was straightforward about it being exactly that.
The problem is what happened next. Some controlled adult research exists — the two trials described above, one published two years before the editorial and one the same year — but not the broad outcome program the editorial asked for. What has never arrived is the body of adult trials that would establish the sleep, energy, recovery, skin and body-composition benefits now marketed. Meanwhile the editorial's mechanistic arguments have been repeated across clinic marketing, gradually shedding the uncertainty they were originally stated with — so a 2006 request for evidence has been recycled into a claim that the evidence exists.
When you read that sermorelin works with your body's own feedback systems, or produces a more natural pattern of release, you are reading a restatement of that editorial's hypothesis. The mechanism may well be correct. It has not been shown to produce the outcomes.
The Same Journal Answered the Question Two Years Later
This part of the story rarely travels with the rest, and it is worth following because it is the field's own literature talking to itself.
The 2006 editorial cited, in support of its proposal, a researcher named George Merriam — one of the small number of scientists who actually ran growth hormone-releasing hormone studies in older adults.
In 2008, Merriam co-authored a review in the same journal, Clinical Interventions in Aging, surveying exactly this question: what GHRH and growth hormone secretagogues do in normal aging. Its title is "Fountain of Youth or Pool of Tantalus?" 5
Tantalus is the figure in Greek myth condemned to stand in water that drains away whenever he bends to drink. The title is doing real work: it names a field where the thing being reached for keeps receding.
That review found what the evidence still shows — growth hormone and IGF-1 rise, some body-composition changes appear in some studies, and the functional outcomes people actually want are inconsistent or absent 5.
And here is the detail that makes the review worth taking seriously. Two years earlier, in 2006, Merriam had been an author on the one randomized, double-blind adult trial of sermorelin in this area — six months against placebo in adults aged 60 to 85, reporting improvements on selected cognitive measures 7. He was not a distant co-author either: the paper names him as the single un-blinded investigator, the one person who saw the IGF-1 results as they came in.
As noted above, that trial's drug and placebo were supplied without charge by Serono, which manufactured GEREF, and two of its authors held consulting or research relationships with the company. He was not a skeptic looking in from outside. He had co-authored a manufacturer-supported study with a positive result, and then co-wrote the cautious review anyway.
That is the opposite of cherry-picking. It is a researcher declining to over-read his own finding — and he is the throughline of this whole field, cited by the 2006 editorial, an author of the positive adult trial, an author of the skeptical review, and later an author of the tesamorelin cognition trial 6.
So the sequence runs: a 2006 editorial proposes a hypothesis and asks for trials; in the same year a separate research group that included Merriam publishes a positive but narrow cognitive result; that group publishes a skeptical review in the same journal two years later; and clinic marketing has gone on repeating the editorial's mechanistic arguments, generally without the uncertainty the author attached to them, and generally without either study.
What Has and Has Not Been Studied, by Outcome
| Marketed outcome | What controlled human evidence exists for sermorelin in adults |
|---|---|
| Deeper sleep | Not established. Physiologically plausible — GH release peaks in early deep sleep — but reviews of GHRH studies in normal aging describe mixed effects with no dependable general sleep benefit 5. Reports for sermorelin specifically are anecdotal |
| More energy / vitality | Not established. No controlled trial has evaluated this as an endpoint in adults |
| Less body fat | Not established for general adult fat loss. A randomized GHRH trial in men with HIV-associated lipodystrophy reduced trunk fat, but absolute visceral fat did not reach significance 11. See sermorelin and belly fat |
| Lean mass / muscle | Not established. Controlled studies have not shown that compounded sermorelin preserves skeletal muscle or lean mass during GLP-1 treatment, calorie restriction or weight loss |
| Faster exercise recovery | Not established. No controlled trial has evaluated this as an endpoint in adults |
| Skin and collagen | Not established. No sermorelin trial has evaluated skin outcomes in adults |
| Cognitive clarity / mood | One of two adult outcomes with randomized controlled evidence (see also body fat). A six-month randomized, double-blind, placebo-controlled trial of sermorelin acetate (GEREF) in adults aged 60–85 reported improvements on selected cognitive measures 7; a separate controlled trial in this class used tesamorelin 6. Neither establishes a general cognitive indication, and neither tested today's compounded preparation. See below |
| Raising IGF-1 as a marker | Measurable — but a laboratory change, not a clinical outcome. See below |
| Diagnostic pituitary testing | Tier B — the historical, evidenced use |
| Pediatric growth hormone deficiency | Tier B — the historical approved indication, in children |
The pattern is consistent, with a couple of exceptions. The two things with the strongest evidence — diagnostic testing and pediatric growth hormone deficiency — are the two nobody markets. Controlled adult evidence exists in two narrow places: selected cognitive measures in healthy older adults, and selected body-composition measures in men with HIV-associated lipodystrophy and reduced growth hormone secretion. Neither establishes predictable benefit from a present-day compounded preparation for general adult wellness or fat loss — and cognition, the better-evidenced of the two, is largely absent from the marketing.
The cognition trial is worth knowing about, because of how it gets used
The largest and most recent controlled cognition trial in this drug class tested a different molecule. In 2012, Archives of Neurology published a randomized trial in 152 adults aged 55 to 87, 66 of them with mild cognitive impairment. After 20 weeks it reported a favorable effect on a composite cognitive measure, particularly executive function 6.
The drug tested was tesamorelin, not sermorelin.
Now look at that paper's title: "Effects of growth hormone-releasing hormone on cognitive function in adults with mild cognitive impairment and healthy older adults." It says growth hormone-releasing hormone — the class — because that is what the researchers were studying. Sermorelin is also a growth hormone-releasing hormone analog. So the trial can be cited, accurately by the letter, in a sentence about "GHRH" and read by a patient as being about the drug they were just offered.
This is the single cleanest example of the substitution this whole page is about. The trial is real, the finding is real, and it is evidence about tesamorelin — a different molecule, with different pharmacokinetics, in a defined population, over 20 weeks. It does not establish that compounded sermorelin improves cognition, prevents dementia, or has a cognitive effect in younger adults.
See sermorelin vs tesamorelin.
The same move happens with body composition
Cognition is the clearest illustration because the molecule swap is so exact. The more common substitution concerns body composition.
A trial frequently reached for here was published in 2009 in the Journal of Clinical Endocrinology & Metabolism, under the title "Testosterone and growth hormone improve body composition and muscle performance in older men" 8. It is a real randomized trial in 122 men around age 70, and it reports real gains in lean mass, strength and fat loss over 16 weeks.
But every participant received testosterone. The randomization was to two testosterone doses crossed with three growth hormone doses — one of which was zero — so there was no growth-hormone-only group and no untreated group. The authors' own conclusion assigns the gains to testosterone, with outcomes that "appeared to be further enhanced" by growth hormone. And the growth hormone arm received growth hormone itself, not sermorelin and not any secretagogue.
Placed in a sentence about "growth hormone optimization," a trial like this reads as support for a drug it never administered, in a combination that is not what is being sold, with the credit assigned to the wrong hormone.
The tell is the same one as before: the citation is accurate about the axis and silent about the molecule. So whenever evidence is offered for sermorelin, the useful question is the simplest one — which drug did the participants actually receive, and at what dose, for how long?
"Not established" does not mean "disproven." For most of the outcomes in the table above, the trial has not been run. Absence of evidence is not proof that nothing happens — but it is a thin basis for an ongoing course of injections, and it is very different from what the marketing implies.
What Is the Success Rate of Sermorelin?
There is no published one, and there cannot be until outcome trials define what success is and measure how often it occurs.
Any percentage you encounter is not derived from controlled data. The same applies to week-by-week results timelines: those describe what patients commonly report, which is a different kind of claim from a measured endpoint. In an unblinded, paid-for treatment, expectation, self-selection and simultaneous changes in diet, training or sleep all shape what gets reported — which is why attribution needs a control group.
Does a Rising IGF-1 Prove It Is Working?
This deserves care, because it is the most persuasive-seeming evidence a patient is usually shown.
IGF-1 testing and body-composition scanning may reasonably inform safety and continuation decisions. What they do not do is establish that sermorelin caused a change you have noticed, directly measure skeletal muscle or visceral fat, or convert an unvalidated adult outcome into a validated one.
A rising IGF-1 tells you the axis responded to the stimulus. It does not tell you that your sleep, body composition or recovery will improve as a result. Treating a marker as a proxy for a benefit is the same move as collapsing the second question into the first — just with a number attached.
Note also that lean mass is not the same as skeletal muscle. It includes body water, organs, connective tissue and bone. Since growth hormone can cause fluid retention, an increase in estimated lean mass can partly reflect retained fluid.
There is a telling detail in how this is monitored in practice. On this axis, IGF-1 and fasting insulin are commonly treated as discretionary measurements — taken at the clinician's judgment rather than routinely. The number most often presented to patients as proof that sermorelin is working is one the clinicians who prescribe on this axis do not necessarily measure at all. That is worth more than any argument on this page: the people best placed to treat a rising IGF-1 as the goal do not treat it that way. See dosing and monitoring.
What About Reviews and Testimonials?
Patient reports are real experiences and worth taking seriously — but they cannot answer this question, for reasons that have nothing to do with honesty.
Sermorelin is typically started alongside other changes: a clinic visit, lab work, sleep and nutrition advice, sometimes a training program. It is usually paid for out of pocket, which raises expectation. It is rarely blinded. Improvements reported under those conditions cannot be attributed to the injection rather than to everything else that changed at the same time.
That is precisely what controlled trials exist to separate, and it is why the missing trials matter more than the volume of positive testimonials.
Is It Safe?
Safety and efficacy are separate questions. Historical GEREF data and growth-hormone-axis pharmacology identify the concerns to watch — injection-site reactions, fluid retention, joint pain and effects on glucose regulation — but how often they occur during chronic adult use of today's compounded preparations, and what they mean long term, has not been well characterized. Screening and monitoring reduce identifiable risk; they do not establish long-term safety. And "fewer reported problems" is not the same as "demonstrated benefit": a reassuring safety picture is not a reason to take something whose benefit for the intended adult outcome has not been established.
Effects associated with growth hormone excess are dose-related. Separately, historical GEREF evidence concerned specified products, formulations, routes, doses and populations — it does not establish the quality, stability or safety of every present-day compounded preparation.
There is one piece of controlled adult tolerability data, and it is small. In the six-month randomized trial described earlier, 11 of 100 participants were excluded or dropped out. Two — 2% — did so for reasons the investigators judged likely related to the study drug: one urticarial rash at the injection site, and one general feeling of malaise after starting injections 7. That is genuine controlled evidence rather than clinic anecdote, and it is reassuring as far as it goes. What it does not do is characterize what happens over years, or in people taking a present-day compounded preparation rather than the GEREF product that trial used.
Speak to a clinician promptly about new or worsening swelling, persistent joint pain, numbness or tingling in the hands, or new blood sugar problems.
And separately: who it is not for
A question about whether something works is incomplete without who should not take it, and compounded sermorelin has no FDA-approved label carrying a formal contraindication list. Clinicians prescribing on this axis treat the following as absolute: a prior allergic reaction to sermorelin, particularly anaphylaxis; pregnancy, planned near-term pregnancy or breastfeeding; active malignancy; and significant hypothalamic-pituitary structural disease or an intracranial lesion. Uncontrolled thyroid disease, diabetes or prediabetes, significant liver or kidney disease, and cancer in remission are treated as calling for individual assessment rather than a blanket rule.
Sermorelin is also prohibited by the World Anti-Doping Agency — a disqualifier for anyone competing under an anti-doping code, whatever the clinical reasoning.
Full list and the monitoring that goes with it: dosing and monitoring. Full detail on adverse effects: sermorelin side effects.
Red Flags
- A specific success rate or results timeline — no controlled outcome data supports either
- A mechanism described as though it were a result — "works with your natural feedback," "restores youthful secretion." These are hypotheses about how it might act, not findings about what it does
- Evidence from growth-hormone-deficient patients, or from GH itself, presented as evidence for sermorelin in adults without a deficiency
- A rising IGF-1 offered as proof the treatment is working
- Before-and-after photographs — see what before-and-after photos actually tell you
- An injectable peptide shipped directly to you for self-treatment, with no prescriber and no documented clinical pathway — see peptide sourcing and quality
What You Can Do About It
Start from the symptom, not the molecule. Poor sleep, low energy, stubborn abdominal fat and slow recovery are all worth taking seriously — and all have common, treatable causes that are established rather than hypothesized. Untreated sleep apnea, thyroid dysfunction, insulin resistance, low testosterone, perimenopausal change, iron deficiency and medication effects account for a large share of these complaints, and identifying one changes the outcome far more reliably than any peptide currently on the market.
Ask what specifically would count as this working, and how you would know. If the answer is a lab marker rather than a symptom or a function, that is worth noticing.
Ask what the evidence is for that preparation, in your population, for your goal — not for growth hormone, not in deficient patients, not in children.
Set a review point before starting anything. An open-ended course with no defined endpoint and no stopping criteria is not a treatment plan.
Get Started with JumpstartMD
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Every visit includes clinical review and body-composition assessment, and treatment follows from what the assessment finds rather than from a product chosen in advance.
Clinician-guided peptide therapy may be considered after an individualized clinical evaluation. Certain therapies may use compounded medications, which are not FDA-approved, and evidence, risks and expected outcomes vary by treatment. See peptide therapy.
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Related Articles
- Sermorelin — mechanism, evidence and current regulatory status
- Does sermorelin burn belly fat?
- Sermorelin before and after — what the photos tell you
- Sermorelin side effects
- Sermorelin vs tesamorelin
- Sermorelin vs HGH
- Where peptides stand with the FDA
Frequently Asked Questions
Does sermorelin work?
It raises growth hormone — that is established, and it is why sermorelin was historically used as a diagnostic agent. Whether that produces the adult outcomes it is marketed for, such as better sleep, less body fat or improved recovery, has not been established in controlled studies. The two questions are routinely presented as one.
What is the success rate of sermorelin?
No published success rate exists. The small adult trials that have been run measured specific endpoints in specific populations rather than defining and measuring "success," so any percentage quoted is not derived from controlled data.
How long does sermorelin take to work?
No reliable onset timeline has been established for adult outcomes. Published week-by-week timelines describe commonly reported experiences rather than measured endpoints.
Is sermorelin worth it?
That depends on what is causing your symptoms, and it is worth answering that question first. The complaints sermorelin is marketed for — poor sleep, low energy, stubborn fat, slow recovery — frequently have identifiable and treatable causes with far better evidence behind their treatments.
Is sermorelin safe?
Injection-site reactions, fluid retention, joint pain and effects on glucose regulation are the recognized concerns; how frequently they occur during chronic adult use of current compounded preparations has not been well characterized. Safety is a separate question from effectiveness, and a manageable profile is not a reason to take something not shown to work.
Is sermorelin the same as HGH?
No. Recombinant growth hormone is the hormone itself; sermorelin prompts the pituitary to release its own. See sermorelin vs HGH.
Does a rising IGF-1 mean sermorelin is working?
It indicates the growth hormone axis responded to the stimulus. It does not establish that sermorelin caused any symptom change, and it does not directly measure muscle or visceral fat.
Is there anything better than sermorelin?
For fat reduction specifically, the medicines with the strongest outcome evidence are the approved GLP-1 and dual-agonist treatments — see peptides for weight loss. For the other complaints, the better step is usually identifying the underlying cause rather than substituting a different peptide.
References
- U.S. Food and Drug Administration, "Determination That GEREF (Sermorelin Acetate) Injection... Were Not Withdrawn From Sale for Reasons of Safety or Effectiveness," Federal Register, vol. 78, pp. 14095-14096, Mar. 4, 2013. [Online]. Available: https://www.govinfo.gov/content/pkg/FR-2013-03-04/pdf/2013-04827.pdf [Accessed: Jul. 26, 2026]. ↩
- Mayo Clinic, "Sermorelin (injection route) — description and brand names." [Online]. Available: https://www.mayoclinic.org/drugs-supplements/sermorelin-injection-route/description/drg-20065923 [Accessed: Jul. 26, 2026]. ↩
- H. Liu, D. M. Bravata, I. Olkin, S. Nayak, B. Roberts, A. M. Garber, A. R. Hoffman, "Systematic review: the safety and efficacy of growth hormone in the healthy elderly," Annals of Internal Medicine, vol. 146, no. 2, pp. 104-115, Jan. 2007, [Online]. Available: https://doi.org/10.7326/0003-4819-146-2-200701160-00005. PMID: 17227934. [Accessed: Jul. 26, 2026]. ↩
- R. F. Walker, "Sermorelin: A better approach to management of adult-onset growth hormone insufficiency?," Clinical Interventions in Aging, vol. 1, no. 4, pp. 307-308, Dec. 2006, [Online]. Available: https://doi.org/10.2147/ciia.2006.1.4.307. PMCID: PMC2699646. PMID: 18046908. [Accessed: Jul. 26, 2026]. ↩
- E. C. Hersch, G. R. Merriam, "Growth hormone (GH)-releasing hormone and GH secretagogues in normal aging: Fountain of Youth or Pool of Tantalus?," Clinical Interventions in Aging, vol. 3, no. 1, pp. 121-129, 2008, [Online]. Available: https://pubmed.ncbi.nlm.nih.gov/18488883/. PMID: 18488883. PMCID: PMC2544358. [Accessed: Jul. 26, 2026]. ↩
- L. D. Baker, S. M. Barsness, S. Borson, G. R. Merriam, S. D. Friedman, S. Craft, M. V. Vitiello, "Effects of growth hormone-releasing hormone on cognitive function in adults with mild cognitive impairment and healthy older adults: results of a controlled trial," Archives of Neurology, vol. 69, no. 11, pp. 1420-1429, Nov. 2012, [Online]. Available: https://doi.org/10.1001/archneurol.2012.1970. PMID: 22869065. [Accessed: Jul. 26, 2026]. ↩
- M. V. Vitiello, K. E. Moe, G. R. Merriam, G. Mazzoni, D. H. Buchner, R. S. Schwartz, "Growth hormone releasing hormone improves the cognition of healthy older adults," Neurobiology of Aging, vol. 27, no. 2, pp. 318-323, Feb. 2006, [Online]. Available: https://doi.org/10.1016/j.neurobiolaging.2005.01.010. PMID: 16399214. Full text: https://faculty.washington.edu/vitiello/Recent%20Publications/GHRH%20and%20Cognition%20in%20Aging.pdf [Accessed: Jul. 26, 2026]. ↩
- F. R. Sattler, C. Castaneda-Sceppa, E. F. Binder, E. T. Schroeder, Y. Wang, S. Bhasin, M. Kawakubo, Y. Stewart, K. E. Yarasheski, J. Ulloor, P. Colletti, R. Roubenoff, S. P. Azen, "Testosterone and growth hormone improve body composition and muscle performance in older men," The Journal of Clinical Endocrinology & Metabolism, vol. 94, no. 6, pp. 1991-2001, Jun. 2009, [Online]. Available: https://doi.org/10.1210/jc.2008-2338. PMID: 19293261. PMCID: PMC2690426. [Accessed: Jul. 26, 2026]. ↩
- U.S. National Library of Medicine, "Growth Hormone Releasing Hormone Analog to Improve Nonalcoholic Fatty Liver Disease and Associated Cardiovascular Risk," ClinicalTrials.gov identifier NCT03375788. [Online]. Available: https://clinicaltrials.gov/study/NCT03375788 [Accessed: Jul. 26, 2026]. ↩
- U.S. National Library of Medicine, "Anamorelin HCl in the Treatment of Non-Small Cell Lung Cancer-Cachexia (NSCLC-C): An Extension Study (ROMANA 3)," ClinicalTrials.gov identifier NCT01395914. [Online]. Available: https://clinicaltrials.gov/study/NCT01395914 [Accessed: Jul. 26, 2026]. ↩
- P. Koutkia, B. Canavan, J. Breu, M. Torriani, J. Kissko, S. Grinspoon, "Growth hormone-releasing hormone in HIV-infected men with lipodystrophy: a randomized controlled trial," JAMA, vol. 292, no. 2, pp. 210-218, Jul. 2004, [Online]. Available: https://doi.org/10.1001/jama.292.2.210. PMID: 15249570. [Accessed: Jul. 26, 2026]. ↩
- E. Van Cauter, L. Plat, "Physiology of growth hormone secretion during sleep," The Journal of Pediatrics, vol. 128, no. 5 Pt 2, pp. S32-S37, May 1996, [Online]. Available: https://doi.org/10.1016/s0022-3476(96)70008-2. PMID: 8627466. [Accessed: Oct. 5, 2026]. ↩
- U. G. Kyle, I. Bosaeus, A. D. De Lorenzo, et al., "Bioelectrical impedance analysis — part I: review of principles and methods," Clinical Nutrition, vol. 23, no. 5, pp. 1226-1243, Oct. 2004, [Online]. Available: https://doi.org/10.1016/j.clnu.2004.06.004. PMID: 15380917. [Accessed: Jul. 26, 2026]. ↩
- A. Prakash, K. L. Goa, "Sermorelin: a review of its use in the diagnosis and treatment of children with idiopathic growth hormone deficiency," BioDrugs, vol. 12, no. 2, pp. 139-157, Aug. 1999, [Online]. Available: https://doi.org/10.2165/00063030-199912020-00007. PMID: 18031173. [Accessed: Oct. 5, 2026]. ↩
- (Withdrawn — the statement this reference was to support was reworded instead and no longer needs a citation.) ↩
- S. Bourke, J. M. Morton, P. Williams, "Effect of JumpstartMD, a Commercial Low-Calorie Low-Carbohydrate Physician-Supervised Weight Loss Program, on 22,407 Adults," Journal of Obesity, vol. 2020, art. no. 8026016, Apr. 2020, [Online]. Available: https://doi.org/10.1155/2020/8026016. PMID: 32318289. PMCID: PMC7157789. [Accessed: Jul. 26, 2026]. ↩