Someone posts that their IGF-1 went from 243 to 306 ng/mL on a GH secretagogue. It reads like a result. It might be one — or it might be the same person, the same vial, and two draws that happened to land on different sides of ordinary week-to-week variation. The difference between those two readings is not in the lab report. It’s in whether there was a baseline, whether the interval was long enough for anything to have moved, and whether one compound changed at a time.
Bloodwork is the only feedback loop in peptide research that returns a number instead of a feeling. That makes it valuable and makes it easy to over-read. This article covers which markers are worth running for which class of compound, when to draw them, and the specific ways a single reading lies to you.
Baseline first, or don’t bother
This is the whole article in one line: a number taken during a protocol is meaningless without a number taken before it.
The reason is that lab reference ranges are population-wide, not personal. An IGF-1 of 306 ng/mL sits comfortably inside the range for a 30-year-old man. So does 180. If you were a 180 person and you are now a 306 person, something moved a long way. If you were always a 300 person, nothing happened. The reference range cannot tell those apart, and neither can you, retrospectively.
Private lab panels are straightforward and inexpensive to order across most of Europe without a referral — which means the baseline draw is a small, cheap action that determines whether every subsequent draw is interpretable. Skipping it is the single most common and least recoverable mistake in this area. You cannot go back and take it later.
Match the panel to the mechanism
There is no universal peptide panel, because a peptide is not a category of action. The useful markers are the ones downstream of what the compound actually does. Two classes cover most of what people run.
GH secretagogues: IGF-1 is the workhorse
For CJC-1295, ipamorelin, sermorelin, tesamorelin and the GHRPs, IGF-1 is the marker that matters — and the reason is a nice piece of physiology.
Growth hormone itself is released in pulses. Levels swing across an order of magnitude within a single day, with most of the output concentrated in bursts during slow-wave sleep. A random serum GH draw catches you at an arbitrary point on that curve. It is close to useless as a monitoring tool: a low reading may mean nothing is happening, or it may mean you drew between pulses.
IGF-1 solves this by integrating. It is produced largely in the liver in response to GH exposure, and it has a long enough circulating half-life that its level reflects cumulative GH signalling over days rather than a snapshot of one moment. That smoothing is exactly the property you want in a monitoring marker.
Two things to know about reading it:
It is strongly age- and sex-dependent. IGF-1 falls substantially across the adult lifespan. A raw value of 200 ng/mL is unremarkable at 25 and notable at 60. This is why good labs report an age-adjusted Z-score or SDS alongside the raw number, and why the Z-score is the figure worth tracking. Compare your value to people like you, not to the whole population.
Units vary between labs. European labs report IGF-1 in either ng/mL (equivalently µg/L) or nmol/L. The conversion is roughly ng/mL x 0.131 = nmol/L. If you switch labs mid-protocol you can manufacture a dramatic-looking change out of pure arithmetic — one more reason to stay with one lab across a series.
Alongside IGF-1, run fasting glucose (mmol/L) and HbA1c (mmol/mol, or % if your lab reports the older DCCT units). GH signalling opposes insulin action, so sustained GH elevation tends to nudge glucose handling. That is a mechanistic prediction, not a scare — but it is the reason those two markers belong on the same requisition as IGF-1 rather than on a separate one. If they were going to move, this is the class that would move them.
Where a compound sits on the GH-axis spectrum affects how much movement you should expect at all — our MK-677 vs GH secretagogues comparison covers how differently these molecules load the axis.
GLP-1s and incretins: metabolic panel, plus the liver
For semaglutide, tirzepatide and retatrutide, the interesting markers are metabolic:
- HbA1c — integrates glycaemia over roughly the preceding 8-12 weeks. Its slow response is a feature: it is essentially immune to what you ate yesterday.
- Fasting glucose (mmol/L) — faster-moving, noisier, useful mainly as a companion to HbA1c rather than on its own.
- A lipid panel — total cholesterol, LDL, HDL, triglycerides. Triglycerides are typically the most responsive of the four and the most sensitive to whether you actually fasted.
- Liver enzymes (ALT and AST) — the genuinely interesting one.
That last item deserves a moment, because it inverts the usual framing. Liver enzymes are normally watched as a damage signal. On incretins they frequently move downward, and that direction is the point: hepatic fat is highly responsive to these compounds, and falling ALT tends to track falling liver fat. A baseline ALT of 48 U/L dropping to 26 over a few months is one of the more informative things this class of bloodwork can show you — and it is completely invisible without the baseline. We covered the underlying mechanism in GLP-1s and fatty liver.
The panel worth having regardless
Independent of compound class, a general panel earns its cost:
| Panel | What it covers | Why it’s worth it |
|---|---|---|
| Full blood count | Haemoglobin, white cells, platelets | Cheap, broad, catches unrelated things |
| Comprehensive metabolic panel | Electrolytes, kidney markers, liver enzymes | The backbone of any baseline |
| Lipids | Cholesterol fractions, triglycerides | Slow-moving, worth a starting point |
| HbA1c | Glycaemia over ~3 months | Relevant to nearly every metabolic compound |
| Ferritin | Iron stores | Low ferritin explains fatigue |
| Vitamin D | 25-OH-D, nmol/L | Widely low at European latitudes |
Those last two are on the list for a specific reason: they explain fatigue that otherwise gets attributed to a peptide. Low ferritin and low vitamin D are both common and both produce exactly the vague tiredness that people notice three weeks into a protocol and blame on the compound. If you have a baseline showing ferritin at 18 µg/L, you know where to look. If you don’t, you spend a month adjusting a dose that was never the problem.
Timing: why week 2 tells you nothing
- 1
Baseline — before the first dose
The comparator for everything that follows. Fasted, morning, well hydrated, no hard training in the preceding 24-48 hours. Note the conditions; you will be reproducing them.
- 2
Weeks 1-6 — don't draw
Most markers integrate over weeks. HbA1c reflects roughly three months of glycaemia; IGF-1 needs sustained exposure to shift. Testing here mostly measures assay noise and day-to-day variation, and a null result invites a dose change that wasn't warranted.
- 3
8-12 weeks — the first informative draw
Long enough for slow markers to have responded, short enough to catch a meaningful move early. Same lab, same conditions, same time of day as baseline.
- 4
Periodically thereafter
Every 3-6 months, or after any deliberate change to the protocol. The third draw is the one that converts two points into a direction.
The interval is not arbitrary. It is set by the biology of the markers themselves. HbA1c is a measure of how much glucose has stuck to haemoglobin over the lifespan of the red cells carrying it — it physically cannot reflect the last fortnight. IGF-1 responds faster, but still needs sustained GH exposure to settle at a new level. Drawing at week 2 asks a question the marker is not built to answer, and gets back the only thing it can supply: noise.
The other half of the cadence is repeatability. Same lab, same assay, same conditions. Different labs use different assay platforms with different calibration, and the between-lab difference can rival the effect you are trying to detect. This matters more than most people expect, and it costs nothing to control for.
The interpretation trap
This is where most of the value is lost, so it deserves more than a footnote.
A blood test does not measure a marker. It measures a marker at one moment, under one set of conditions, on one machine. Every one of those introduces variation that has nothing to do with your protocol:
- Diurnal variation. Plenty of markers swing across the day on their own schedule. A morning draw and an afternoon draw are not the same measurement.
- Hydration. Dehydration concentrates everything in the sample. Haemoglobin, haematocrit and albumin move first. A hard sauna or a long flight before a draw shows up as numbers.
- Recent training. A heavy session raises creatine kinase, and can move liver enzymes — AST especially, which is not liver-specific and leaks from skeletal muscle. An ALT/AST flag 24 hours after a hard leg day is very often the leg day.
- Fasting state. Triglycerides and glucose are the obvious ones. Fasted at baseline and fed at follow-up is not a comparison; it’s two different tests.
- Assay variation. Run the same sample twice and you get two slightly different numbers. That coefficient of variation is a property of the instrument and it is nonzero.
The practical version: before you conclude a marker moved, ask what else was different about the draw. Time of day, hydration, training, food, lab. If any of those changed, the marker may not have.
And treat the direction of a surprise as information about your method. A dramatic single reading is more likely to be a measurement artefact than a dramatic biological event, simply because artefacts are common and dramatic biological events are rare.
What bloodwork can’t tell you
Two limits are worth being explicit about, because bloodwork gets asked to do jobs it cannot do.
It cannot verify your vial. A rising IGF-1 tells you GH signalling increased. It does not tell you the vial contained what the label said, at the stated purity, at the stated quantity. Underdosed, mislabelled and degraded material can all produce numbers that look broadly plausible. Bloodwork measures your response; it does not analyse your compound. That job belongs to a certificate of analysis and, ideally, third-party testing — see understanding peptide purity and COAs for what that documentation should contain.
It cannot attribute a change to a compound you started alongside two others. If three things began the same week, a moved marker has three candidate causes and no way to distinguish them — and that’s before counting the diet change, the new sleep schedule and the season. Bloodwork is a measuring instrument, not an experimental design. The design is the part you have to supply, and it’s the subject of running one peptide at a time.
Put together, the discipline is unglamorous and entirely mechanical: baseline before you start, one variable at a time, an interval long enough for the marker to respond, the same lab under the same conditions, and three points before you believe a direction. Do that and the numbers mean something. Skip any of it and you are collecting data you cannot interpret — which is more expensive than collecting none, because it feels like knowing.
Frequently Asked Questions
What bloodwork should I run before starting a peptide protocol?
A general baseline covers most needs: full blood count, comprehensive metabolic panel, lipids, HbA1c, plus ferritin and vitamin D. Add the markers specific to the compound class — IGF-1 for GH secretagogues, or fasting glucose, HbA1c, lipids and liver enzymes for GLP-1s and incretins. The point of the baseline is not to find something wrong. It’s to create the comparator that makes every later draw readable.
Why is IGF-1 measured instead of growth hormone?
Because GH is pulsatile. It is released in bursts, mostly during slow-wave sleep, and levels swing enormously within a single day — so a random draw catches an arbitrary point on that curve and tells you almost nothing. IGF-1 is produced in response to GH exposure and circulates long enough to integrate that signal over days. It’s a smoothed measure of the same axis, which is exactly what monitoring needs.
How long after starting a peptide should I test bloodwork?
Roughly 8 to 12 weeks. Most relevant markers integrate over weeks — HbA1c reflects around three months of glycaemia, and IGF-1 needs sustained exposure to settle at a new level. Drawing at week 2 mostly measures noise, and a null result at week 2 tempts a dose change that the data never supported.
Why did my IGF-1 change without any change in dose?
Several ordinary explanations come before the interesting ones: a different lab or assay platform, a different time of day, hydration state, a hard training session in the preceding 24-48 hours, or plain assay variation. IGF-1 also drifts with age, illness, nutrition and sleep. This is why a trend across three draws beats one dramatic reading, and why keeping the lab and the conditions constant is worth more than it sounds.
Can bloodwork tell me if my peptide is real?
No. It measures your response, not your compound. A moved marker is consistent with a real, correctly dosed vial — and also with an underdosed one, a partially degraded one, or a coincidence. For the compound itself you need a certificate of analysis and, for a supplier you’ll use repeatedly, independent third-party testing.
Related reading
- One Peptide at a Time — the experimental design that makes bloodwork attributable
- Understanding Peptide Purity & COAs — what bloodwork cannot verify about your vial
- MK-677 vs GH Secretagogues — how differently these compounds load the GH axis
- GLP-1s and Fatty Liver — why ALT often falls on incretins