Cross-referencing clinical data
A pairing appears on this page only when a trial gave both ingredients together and measured the result. Insulin-Like Growth Factor has none that clears that bar.
Stitching two separate single-ingredient studies into a pairing is the one thing this engine will not do. When a study of the combination itself holds up at source, it lands here with its citation.
No invented synergy. Where actives were studied on their own rather than together, the record shows each on its own evidence, never a combined effect no trial measured.
Research strength. Research strength says how much work stands behind the combination. It is never a product score.
Independent record. Every finding is cited to a named trial, dated, and never written by the brand.
20 pairings are live across the library today. Checked 20 July 2026.
No study gave these as a pair, so they are not in the card above. But the reason they belong together is settled biochemistry, not a guess, so it is worth knowing.
Circulating IGF-1 is produced mainly by the liver under growth hormone drive, and that output falls when protein or energy intake is inadequate. Raising protein intake in an under-fed person raises circulating IGF-1. Supplementation trials in older adults and athletes have measured IGF-1 as a biomarker of that response. Note this is a marker of anabolic signalling, not a measured outcome in itself.
IGF-1 activates mTORC1 through the PI3K and Akt arm, while leucine activates the same complex through Rag GTPase and sestrin sensing. Both inputs are required for a full anabolic signal, which is why amino acid availability and hormonal signalling are described as permissive for each other. This is cell-signalling biochemistry. It does not mean that swallowing IGF-1 adds anything, because the peptide does not survive digestion.
Zinc depletion lowers circulating IGF-1 and blunts growth, and repletion restores it in people who were deficient. The relationship runs through growth hormone signalling and hepatic synthesis. This applies to correcting a deficiency. Adding zinc on top of adequate status has not been shown to raise IGF-1 further.
Arginine given intravenously reliably provokes growth hormone release, which is why it is used as a diagnostic stimulus, and growth hormone in turn drives hepatic IGF-1 production. Oral arginine produces a far smaller and less consistent response because of first-pass metabolism by intestinal arginase. The route matters enormously here. A clinical test result does not transfer to a capsule.
Vitamin D status and circulating IGF-1 track together in observational data, and IGF-1 also increases renal conversion of 25-hydroxyvitamin D to its active form. That makes the relationship bidirectional. Association is not causation in either direction, and supplementation work has been inconsistent. Read it as a linked axis rather than a lever.
Dairy protein raises circulating IGF-1 more than would be predicted from its amino acid content alone, an effect seen across age groups. Comparisons of yoghurt against isolated whey have used IGF-1 among their markers. Whether a higher IGF-1 level is desirable depends entirely on the person and the goal, since the same signal that supports tissue building is not universally wanted across a lifespan.
HMB is a leucine metabolite associated with reduced muscle protein breakdown, while IGF-1 signalling drives synthesis through Akt and mTOR and suppresses the same atrophy-associated ubiquitin ligases. The two act on opposite sides of the same balance in principle. Evidence for the combination in people is thin and mostly in older or clinically compromised groups.
Citrulline raises plasma arginine more effectively than oral arginine does, because it bypasses intestinal arginase, which is the mechanistic argument for using it as a growth hormone stimulus. In the trial setting it was combined with interval training and muscle adaptation markers were followed. The signal is preliminary and confounded by the exercise stimulus, which is by far the stronger input.
Creatine loading increases training volume and cell hydration, both of which sit upstream of the anabolic signalling that IGF-1 participates in. Some resistance training work has reported higher muscle IGF-1 expression with creatine than with training alone. Muscle IGF-1 expression is a marker, and the outcome people care about is measured in strength and lean mass, where creatine has its own direct evidence.
Nothing specific on file for Insulin-Like Growth Factor. Match the label to the daily amount above, and tell your doctor what you take.
Not medical advice. Show the label to your pharmacist.These are the studies our verdict leans on, chosen from the 8 we read for Insulin-Like Growth Factor. The full linked list is below.
12 sources behind our Insulin-Like Growth Factor verdict: peer-reviewed studies and registered clinical trials. Every one links straight to PubMed, the journal, or ClinicalTrials.gov. Read them yourself.
Evidence surfaced via Semantic Scholar (Allen Institute for AI) and ClinicalTrials.gov. Ranked by study type and citation weight, not cherry-picked.
Read this carefully. These are 1,068 voluntary, unverified reactions reported to the FDA (openFDA). The number mostly reflects how popular Insulin-Like Growth Factor is, not how risky it is. A report is not proof Insulin-Like Growth Factor caused anything. It is a signal of what to watch for, nothing more.
Source: openFDA adverse-event reports. Voluntary reporting, not an incidence rate.
FDA Disclaimer: These statements have not been evaluated by the Food and Drug Administration. This information is for educational purposes only and is not intended to diagnose, treat, cure, or prevent any disease. Consult your healthcare provider before starting any supplement regimen.