T-03

IGF-1 monitoring guide

Q: What does IGF-1 actually measure?

Insulin-like growth factor 1: the liver's integrated response to GH exposure. GH itself pulses, mostly at night, and is hard to catch in one draw; IGF-1 stays stable across the day, so trials and drug labels use it as the axis readout.

Q: What should sermorelin realistically do to IGF-1?

Schedule-dependent, modest, possibly transient: twice-daily dosing raised it clearly; a single 2 mg nightly dose did not move it in 6 weeks; nightly analog dosing raised it early with fade by week 16. Promised percentages outrun the data.

Q: Is a higher IGF-I level better?

No. IGF-1 confirms the axis responded; it is not an outcome. The approved GHRH analog's label directs IGF-1 monitoring during therapy and flags elevations as a signal to manage; somatropin labels titrate against IGF-1. Above range means a dose conversation.

IGF-1 is the lab everyone argues about.

IGF-1 is the lab everyone argues about. It is the stable downstream marker of GH-axis activity, it is what the sermorelin trials measured, and it is what the labels of approved GH-axis drugs tell clinicians to monitor. This guide explains what IGF-I can and cannot tell you, what sermorelin actually did to it, and the questions worth bringing to the clinician who orders the lab.

Worked example

Trial-calibrated expectations: with twice-daily dosing over two weeks, older men's IGF-1 rose into young-adult ranges (Corpas 1992). With a single 2 mg nightly dose over 6 weeks, IGF-1 did not change (Vittone 1997). With nightly analog dosing over 16 weeks, IGF-1 rose by week 2 and drifted back toward baseline by week 16 (Khorram 1997). Same molecule family, three curves: schedule and duration decide.

Step by step

Before starting anything, discuss a baseline IGF-I with the prescriber, drawn fasting in the morning for consistency.
Ask which assay and age-adjusted reference range the lab uses, and keep later draws on the same assay.
Recheck on the schedule the prescriber sets; the trial data show early rises can fade with continued use, so a single early value overstates durability.
Bring symptoms to every review: edema, joint aches, carpal tunnel symptoms, and glucose changes are the class signals labels flag.
If IGF-I rises above the age-adjusted range, that is a dose conversation with the prescriber, not a victory.

IGF-1 in the sermorelin trials

Regimen	Duration	IGF-1 result	Source	Source
1.0 mg SC twice daily	14 days	Rose; no longer different from young men (P<0.005)	Corpas 1992	source
2 mg SC nightly	6 weeks	No change (GH rose)	Vittone 1997	source
10 mcg/kg analog SC nightly	16 weeks	Up by week 2 (P<0.05); toward baseline by week 16	Khorram 1997	source
Continuous SC GHRH(1-44), 1-2 mg/day	14 days	Increased (P<0.001), pulsatility preserved	Corpas 1993	source

Frequently asked questions

What does IGF-1 actually measure?

Insulin-like growth factor 1: the liver's integrated response to GH exposure. GH itself pulses, mostly at night, and is hard to catch in one draw ^{Van Cauter 1996}; IGF-1 stays stable across the day, so trials and drug labels use it as the axis readout ^{Egrifta label}.

IGF-1 (insulin-like growth factor 1) is produced mainly by the liver in response to growth hormone and mediates much of GH's growth signaling. GH itself is secreted in short pulses, mostly at night, so a random GH draw is nearly meaningless ^{Van Cauter 1996}; IGF-1 integrates exposure over time and stays stable across the day.

That is why the sermorelin trials tracked it, why the tesamorelin label directs monitoring it during therapy ^{Egrifta label}, and why somatropin labels titrate dose against it ^{Norditropin label}. It is a proxy, not a goal: no study ties pushing IGF-I higher in healthy adults to better outcomes.

What should sermorelin realistically do to IGF-1?

Schedule-dependent, modest, possibly transient: twice-daily dosing raised it clearly ^{Corpas 1992}; a single 2 mg nightly dose did not move it in 6 weeks ^{Vittone 1997}; nightly analog dosing raised it early with fade by week 16 ^{Khorram 1997}. Promised percentages outrun the data.

The three adult datasets disagree in an instructive way. Twice-daily injections for 14 days restored IGF-1 in older men to young-adult ranges ^{Corpas 1992}. A single 2 mg nightly dose for 6 weeks raised overnight GH but left IGF-1 unchanged ^{Vittone 1997}. Nightly analog dosing for 16 weeks raised IGF-1 within 2 weeks, after which it drifted back toward baseline despite continued injections ^{Khorram 1997}.

So the honest expectation is schedule-dependent, modest, and possibly transient. A baseline value plus a recheck on the prescriber's schedule beats any promised percentage, and a vendor who quotes one number for everyone is quoting past the evidence.

Is a higher IGF-I level better?

No. IGF-1 confirms the axis responded; it is not an outcome. The approved GHRH analog's label directs IGF-1 monitoring during therapy and flags elevations as a signal to manage ^{Egrifta label}; somatropin labels titrate against IGF-1 ^{Norditropin label}. Above range means a dose conversation.

No, and this is where marketing and medicine part ways. In the approved world IGF-1 elevation is something to watch, not chase: the tesamorelin label directs IGF-1 monitoring during therapy and handles sustained elevations as a management signal ^{Egrifta label}, and somatropin labels titrate dose against serum IGF-1 rather than maximizing it ^{Norditropin label}.

No trial links pushing IGF-1 above age-normal in healthy adults to any benefit, while the GH-therapy literature in healthy elderly adults links stronger axis stimulation to edema, joint symptoms, and glucose problems ^{Liu 2007}. If a draw comes back above the age-adjusted range, the evidence-consistent response is a prescriber conversation about dose.

Tools: educational calculators and references only.