What these peptides actually do
Growth-hormone secretagogues don't supply growth hormone — they provoke your own pituitary to release more of it, which raises IGF-1, the downstream hormone that mediates most of GH's effects on tissue repair and body composition. They come in two families that pair together: GHRH analogs (tesamorelin, CJC-1295) and ghrelin-receptor agonists (ipamorelin), the latter working partly by leaning against somatostatin, the brake on GH release. IGF-1 is the marker you track to confirm the protocol is doing anything at all.
The depth of evidence varies — know where each one stands
The three aren't equally studied, and that's worth knowing. Tesamorelin has the deepest clinical data — controlled trials in visceral-fat reduction showing clear IGF-1 elevation and fat loss — so it's the most characterized of the GH-axis peptides. CJC-1295 and ipamorelin run more on mechanism and practitioner experience than on large human trials. All three work on a well-understood axis and are widely used; just calibrate your confidence to the evidence behind each, and — as always in this course — source quality matters as much as the compound choice.
The metabolic cost: GH opposes insulin
Growth hormone is counter-regulatory to insulin — it raises hepatic glucose output and antagonizes insulin's action at the tissues. So GH-class protocols predictably drift fasting glucose and insulin upward, and the regulatory record on tesamorelin flagged a real signal: a higher rate of new diabetes over longer-term use, even though short-term group glucose changes were modest. The practical consequence: watch HOMA-IR and HbA1c, not just glucose, and do not stack a GH protocol onto an already insulin-resistant metabolism without addressing that first. This is the cost side of the ledger, and it is silent without bloodwork.
IGF-1 and the longevity tradeoff — get the shape right
Here the popular framing is usually imprecise, and the correction matters. IGF-1 and all-cause mortality follow a U-shaped relationship: both low and high IGF-1 associate with higher mortality, with the lowest-risk zone around 120–160 ng/mL in the meta-analytic data. That is the "don't crush it, don't blow it out" logic — but it is not a clean "J-curve," and cancer behaves differently. For cancer specifically, higher IGF-1 shows a more linear adverse association — elevated IGF-1 tracks with higher prostate and breast cancer risk, with no protective benefit at the low end. So the honest summary is: target upper-normal-for-age for repair if you're running these peptides, but understand that pushing IGF-1 supraphysiologic is the longevity-adverse tail, and the cancer arm of that tradeoff doesn't have a reassuring floor. There is no clinical guideline target for IGF-1 in secretagogue users; treat these as ranges to respect, not numbers to maximize.
Timing and the bloodwork that grades it
The dosing-window nutrition (a low-insulin window around the dose, often pre-bed) is covered in the Dieting course — the physiology is real, the exact clock is practitioner practice. What anchors the protocol is the bloodwork: IGF-1 to confirm it's working and stay out of the supraphysiologic tail, and fasting insulin / HOMA-IR / HbA1c to confirm you're not buying body composition with your glucose metabolism. Run a peptide you can't measure the effect of, and you're guessing in both directions — whether it works and whether it's costing you.
Educational content, not individual medical advice.