IGF-1 Bloodwork: What the Number Means and Why There Is No Target Range

A raw IGF-1 value carries almost no information on its own. It needs an age, a sex, and the name of the lab that ran it, because all three change what the same blood would be called. Two people can post the same figure and be in different positions, and neither of them is reading a scale that runs from worse to better.

That last part is where most of the confusion sits. People treat the number as a score. Nothing in the sources behind this page sets an IGF-1 value as a goal for muscle or fat loss. Medicine does set an IGF-1 target in one place, and there it aims at bringing a high number down.

What does an IGF-1 number actually measure?

An IGF-1 number measures a hormone made largely in the liver in response to growth hormone. Because it reflects growth hormone exposure over time instead of a single moment, it behaves as a downstream marker of that axis and not a direct reading of it.

Approved labels use it that way. Somapacitan's label measures IGF-1 to assess the drug's pharmacodynamic properties, and its dosing section titrates on clinical response together with the serum IGF-1 concentration.¹ So it serves as a marker of drug effect, used alongside clinical response and not in place of it.

Injectable analogs share the name and are a different thing, set apart in our comparison of IGF-1 LR3 and IGF-1 DES. What the test does not measure is anything about muscle, strength or body fat. No source cited here connects a particular IGF-1 value to a particular body composition outcome, and body composition is measured separately.

Why is IGF-1 measured instead of growth hormone?

Growth hormone appears on labels as somatropin and in conversation as HGH. It is released in pulses, so a single blood draw catches whatever part of the cycle happened to be running. IGF-1 moves more slowly and integrates that signal, so one sample can carry useful information.

That convenience has a cost, and the acromegaly consensus names it. Growth hormone and IGF-1 results can disagree in the same patient.² The authors suggest assay discrepancies as the probable cause, or biological factors including sex, glucose metabolism and growth hormone receptor polymorphism.² The consensus recommends monitoring both rather than either alone.²

Our comparison of the growth hormone secretagogues sets the compounds apart, since a rise does not say which one caused it. Two markers that can disagree put you in a different position from one marker that settles the question. With one draw you get a cheap approximation, not an answer.

What is an IGF-1 Z-score, and where does it come from?

A Z-score, usually printed as SDS for standard deviation score, says how far a result sits from the median for that age, counted in standard deviations. Zero is the age median. Minus two sits near the bottom of the reference population and plus two near the top.

Scores come from a reference population and a curve-fitting method. One 2025 normative study built age-specific centile curves using "the LMS (Lambda, Mu, Sigma) method," then calculated the standard deviation score from the age-specific L, M and S parameters.³ So an SDS is a position within one particular reference group, computed from one particular set of curves.

Approved labels report it this way too. Its pharmacodynamics section tracks IGF-1 SDS instead of raw concentrations.¹ That section records an IGF-1 SDS of -2.03 at baseline and a change from baseline of 2.36.¹

Why does the same blood give different numbers at different labs?

Different assays measure IGF-1 differently. The gap between them is large enough to change conclusions. Akirov and colleagues, reviewing acromegaly diagnosis in 2021, report that several factors influence IGF-1 assays and produce wide variability between them.⁴ Their review describes notable discrepancies in results between different assays.⁴

The size of the problem is on record. Their review cites a study finding "more than a 2-fold variation in IGF-1 cut-off for the ULN range measured in different laboratories."⁴ The upper limit of normal is the line that decides whether a result is called high. It differed by more than a factor of two depending on who ran the test.

The acromegaly consensus reaches the same place from the clinical side. The consensus records large variability between the different IGF1 assays.² Differences in normative data and reference ranges, the consensus adds, make results difficult to compare across assays.²

Can the assay itself be wrong about you?

For a small number of people the assay can be wrong, and re-drawing will not fix it. Immunoassays for IGF-1 are prone to interference from IGF binding proteins, the IGFBPs that appear on some lab panels.⁵ One 2024 study makes that point as background and not as a finding of its own.⁵ Binding proteins carry most circulating IGF-1, so a method's handling of them shapes the result.

Rare sequence variants are the sharper case. Screening 243,808 patients, that study identified 1,099 carrying IGF-1 variants.⁵ A variant may change binding to the receptor or to the binding proteins.⁵ For heterozygous carriers the authors note that their mass-spectrometry concentrations account for only half the total IGF-1, and that z-scores for those patients shifted toward negative levels.⁵

One number in that paper is inconsistent with itself. Its abstract reports that 98% of variants sat at the C-terminus while its results section says 95%.⁵ The discrepancy is small and the direction is unaffected. Of the two, the abstract figure is weaker, since a results section is where the count is derived.

Can I compare my result to someone else's?

No, and the consensus documents effectively say so. Both sources recommend staying on one assay for exactly this reason. Their strong recommendation is that "endocrinologists use the same assay when monitoring IGF1 levels over time."² Akirov's review puts it as advice to use the same well-validated assay throughout a patient's follow-up.⁴

Advice to hold the assay constant within one person is also a statement about comparing across people. If two draws from the same patient on different assays cannot be lined up, two numbers from two strangers on unknown assays cannot either.

Reference intervals add a second layer. One 2025 study notes that "IGF-1 levels are highly specific to ethnicity" and cites a stated requirement for ethnicity-specific reference ranges.³ Two people with the same raw value can sit at different positions in their own reference populations.

Why does age change what counts as normal?

What counts as normal changes with age, because IGF-1 falls across adult life and the same value means something different at 25 and at 55. The 2021 review describes values rising from birth until puberty, then declining with advancing age.⁴

The 2025 normative study puts numbers on the adult decline. Their data put median IGF-1 highest at 20 years of age, falling with each successive age stratum, at 30.1 ng/ml per decade.³ Over twenty years of adult life that is a substantial shift in the middle of the distribution.

Age adjustment is therefore not a formality. Somebody at the top of the range at 45 could sit mid-range in their twenties, with an identical raw figure.

Is there a target IGF-1 for muscle or fat loss?

Nothing in the sources behind this page sets one. No label, consensus statement or study cited here names an IGF-1 concentration or SDS as a goal for muscle gain, fat loss or body composition. Nothing was missed in the search; that question has not been answered in a form anyone could cite.

What exists instead is a marker used to assess drug effect and safety. Novo's label titrates to "clinical response and serum insulin-like growth factor-1 (IGF-1) concentrations," which puts the clinical result first and the number second.¹

So the question "what should I aim for" has no sourced answer. Confident figures from anywhere are somebody's opinion until a document is attached. Whoever ordered the test owns the interpretation of a specific result. Our guide to talking to your doctor covers that conversation.

Where does a validated IGF-1 target actually exist?

One place qualifies. It runs the other way. In acromegaly, a disease of growth hormone excess, the consensus states that "Treatment is aimed at normalizing IGF1 levels, as doing so usually reflects adequate disease control."² The same statement recommends "that normalizing levels of IGF1 is a key goal, as it is the best reflection of disease control."²

Normalizing means bringing a high value into the reference range. The only well-documented IGF-1 target in medicine is a target for reduction, set because a sustained high value is the problem being treated.

People bring the opposite intuition to the number. In the one clinical context with a validated target, what some describe as a goal is what the target exists to remove.

What does an approved label say to do with a high IGF-1?

An approved label says to reduce the exposure. Section 2.4 instructs a prescriber to "Decrease the dosage as necessary on the basis of adverse reactions and/or serum IGF-1 concentrations above the age- and sex-specific normal range."¹ Above the age and sex specific normal range is the trigger, and a decrease is the response.

Nothing in that instruction treats a higher number as progress. The direction of the approved response to a value above normal is downward, in a population treated for deficiency, under supervision.

Our guide to peptide bloodwork covers which tests get run before starting and what a baseline is for. This page is about reading one of those results afterward.

Does any approved label name a number to stop at?

One does, and it is a ceiling and not a floor. The tesamorelin label tells prescribers to "Consider discontinuing EGRIFTA SV in patients with persistent elevations of IGF-1 levels (e.g., >3 SDS), particularly if the efficacy response is not robust."⁶ Greater than 3 SDS is the only numeric IGF-1 threshold in any document cited on this page, and crossing it is a reason to stop.

Frequencies sit on the same label. Among patients treated for 26 weeks, "47% had IGF-1 levels greater than 2 standard deviation scores (SDS), and 36% had SDS >3."⁶ That effect appeared as early as 13 weeks.⁶ A drug that raises IGF-1 pushed nearly half its patients past 2 SDS inside six months, and the label records it under warnings.

Those proportions fell with longer treatment. At 52 weeks, "34% had IGF-1 SDS >2 and 23% had IGF-1 SDS >3."⁶ Why the share dropped is not explained on the label. One mechanism would produce the same pattern: the discontinuation the label itself advises removes the highest values from the group still being counted. That reading is mine and not the label's.

Does a rising IGF-1 prove the product is real?

A rise is consistent with activity and does not prove the product is real, let alone its purity or quantity. An IGF-1 increase shows that something raised IGF-1. It does not say what the vial contained, how much of it, or whether anything else was in there.

Arithmetic also does not run the way people expect. Novo's label reports a less than dose proportional IGF-1 response at steady state in 26 adult patients with growth hormone deficiency.¹ A less than proportional response means a change in exposure produces a smaller change in the number. So the size of a rise is a poor proxy for the size of a dose.

Identity questions need identity tests. A certificate of analysis reports what a lab found in a sample of the material, and a blood result cannot substitute for one.

Does a flat IGF-1 prove the product is fake?

Several ordinary explanations come before a fake product, and the label names some of them. Timing is one. The label says to "Draw IGF-1 samples 3 to 4 days after the prior dose," and reports maximum concentrations "within 2 to 4 days after dosing."¹ Blood drawn at the wrong point in a weekly cycle measures a different part of the curve.

Other factors sit on the same label. "Oral estrogens may reduce the serum IGF-1 response to SOGROYA," and altered levels were observed in hepatic and renal impairment.¹ Assay change between draws is another, given the two-fold spread in reference limits.⁴

The less than proportional response applies here too.¹ A small measured change can follow from a real effect, so a flat result is weak evidence either way.

When in the week should blood be drawn?

Blood should be drawn at a consistent point in the week, and the label specifies timing for one product because it matters. Somapacitan samples are drawn three to four days after the prior dose, when concentrations peak.¹ Draw early or late against that and the comparison with a previous result breaks.

Consistency across draws is the usable principle. Two results collected at different points in a dosing cycle, on different assays, are two measurements of different things presented in the same units.

For any other compound, this page cannot supply the right moment. Labels that specify timing do so for their own product and schedule. That question belongs with whoever ordered the test.

What else moves an IGF-1 result?

More things move an IGF-1 result than most people account for. Novo's label names oral estrogens as reducing the IGF-1 response, and records altered IGF-1 exposure in hepatic and renal impairment.¹ The consensus adds sex, glucose metabolism and growth hormone receptor polymorphism as biological contributors to discordant results.²

Assay and reference population sit underneath all of it. The two-fold spread in upper limits between laboratories, and the ethnicity specificity of reference intervals, both change the interpretation without changing the person.³⁴

A single number therefore arrives carrying several unknowns at once. One assay, a consistent draw time, and a clinician who knows the rest of the picture all help.

Does being in a calorie deficit lower IGF-1?

A calorie deficit does lower IGF-1, and a 2021 review calls nutritional status "a key regulator of IGF-I synthesis and secretion."⁷ Somebody cutting hard while tracking IGF-1 is changing two things at once.

Fasting length matters, and the direction flips. That review reports that fasting under three days increases growth hormone secretion before any IGF-I reduction.⁷ Fasting beyond three days leads to peripheral growth hormone resistance, a state of normal or elevated growth hormone alongside low serum IGF-I.⁷ So growth hormone and IGF-1 can move in opposite directions depending on how long somebody has gone without food.

Protein turns out to be the hinge on calorie restriction. The review states that "In humans, CR reduces the levels of IGF-I, but this happens only if protein intake is also restricted."⁷ Restricting calories while keeping protein up is not the same input. Nothing on this page is dietary advice, and the point is narrower: a falling IGF-1 during a deficit has an explanation that has nothing to do with the vial.

How well does IGF-1 perform as a diagnostic test?

IGF-1 performs less well as a diagnostic test than its reputation suggests, in the one setting with published accuracy figures. In 2021, a Japanese study of 298 children with short stature or reduced growth velocity, median age 4.98 years, tested IGF-1 as a screen for growth hormone deficiency. At its best cutoff it produced a sensitivity of 0.685 and a specificity of 0.417.⁸ Positive and negative predictive values were 0.25 and 0.823, with an area under the curve of 0.517.⁸

Its authors concluded that "IGF-1 level had poor diagnostic accuracy as a screening test for GHD."⁸ Their paper also states that IGF-1 should not be used alone to screen for growth hormone deficiency.⁸ Mean IGF-1 SD did not differ significantly between the GHD and non-GHD groups in that study.⁸

That study was in young children, and it does not transfer to adults. The study is cited for one narrow point: in the clinical setting where IGF-1 screening is formally used and has been measured, performance was poor. No equivalent accuracy study in adults using secretagogues is cited here, because none was found.

What has not been measured?

Nobody has measured the connection between an IGF-1 value and a body composition outcome. No source cited here reports what a given IGF-1 concentration or SDS produces in muscle mass or fat mass in healthy adults. Most people asking what to aim for are asking exactly that.

Long-term safety at a sustained high value in healthy adults is also unmeasured here. The acromegaly literature describes a disease where IGF-1 runs high for years, and treatment aims to normalize it.² Whether a healthy person holding a high value carries related risk is a different question, and no cited source answers it.

Assay harmonization is the third gap, and it is the one with the clearest cost. While upper limits differ more than two-fold between laboratories, every figure anybody quotes is partly a statement about which lab they used.⁴

What would settle it?

Nothing would settle it short of different studies for the different questions. None of them exists in the sources here. A body composition question needs healthy adults, a measured IGF-1 trajectory, and body composition measured by something better than a scale, reported together.

Nobody needs another study for comparability; harmonization work is what is missing. Both consensus documents offer a workaround instead of a fix: stay on one assay so your own numbers can be compared to each other.²⁴

Until then, the defensible reading of an IGF-1 result is narrow. It says roughly where one person sat in one reference population on one assay at one moment. It is useful for tracking against itself, and it is not a scoreboard.

Common questions

What should my IGF-1 level be?

What is an IGF-1 Z-score or SDS?

Is an IGF-1 of 350 high?

Why does my IGF-1 differ between labs?

Can I compare my IGF-1 to someone else's result?

Is there an IGF-1 number at which a label says to stop?

How often do these drugs push IGF-1 above normal?

Does a higher IGF-1 mean more muscle?

What does an approved label do about a high IGF-1?

Does my IGF-1 rising prove my product is genuine?

My IGF-1 barely moved. Is my product fake?

Does IGF-1 change with age?

Does ethnicity affect the reference range?

Does fasting or dieting change my IGF-1?

Could my IGF-1 result be wrong about me?

Why measure IGF-1 instead of growth hormone?

Is IGF-1 a reliable diagnostic test?

Do oral contraceptives or estrogen affect IGF-1?

Sources

1. SOGROYA (somapacitan-beco) injection, US prescribing information, Novo Nordisk, sections 2.4, 7, 12.1, 12.2 and 12.3. Read at source via DailyMed. Quoted for the titration instruction on clinical response and serum IGF-1 concentrations, the instruction to draw IGF-1 samples 3 to 4 days after the prior dose, the statement that maximum IGF-1 concentrations were observed within 2 to 4 days after dosing, the less than dose proportional IGF-1 response at steady state in adult GHD patients (n=26), the reported IGF-1 SDS of -2.03 at baseline with a change from baseline of 2.36, the statement that oral estrogens may reduce the serum IGF-1 response, and the altered IGF-1 levels in hepatic and renal impairment. The instruction to decrease the dosage on the basis of serum IGF-1 concentrations above the age- and sex-specific normal range was additionally verified by exact-phrase query against the openFDA drug label API dosage_and_administration field. That query returned a single record. The DailyMed fetch had truncated the sentence. ↩1 ↩2 ↩3 ↩4 ↩5 ↩6 ↩7 ↩8 ↩9 ↩10 ↩11 ↩12 ↩13 ↩14 ↩15 ↩16 ↩17 ↩18
2. Melmed S, Bronstein MD, Chanson P, Klibanski A, Casanueva FF, Wass JAH, Strasburger CJ, Luger A, Clemmons DR, Giustina A, et al. A Consensus Statement on acromegaly therapeutic outcomes. Nature Reviews Endocrinology 2018;14:552-561. DOI 10.1038/s41574-018-0058-5. Read at source. Quoted for the statements that treatment is aimed at normalizing IGF1 levels and that normalizing IGF1 is a key goal reflecting disease control, that large variability exists between the different IGF1 assays, that differences in normative data and reference ranges make it difficult to compare results across assays, the strong recommendation that endocrinologists use the same assay when monitoring IGF1 over time, the recommendation to monitor both GH and IGF1, and the attribution of discordant GH and IGF1 values to assay discrepancies and biological factors including sex, glucose metabolism and GH receptor polymorphism. This is a consensus statement on a disease of growth hormone excess, not a document about healthy adults. ↩1 ↩2 ↩3 ↩4 ↩5 ↩6 ↩7 ↩8 ↩9 ↩10 ↩11 ↩12 ↩13 ↩14 ↩15 ↩16
3. Shah R, Bansal D, Rastogi P, Sachdev S, Devi N, Sharma RR, Sachdeva N, Agrawal A, Das L, Chanson P, Dutta P, et al. Normative data for insulin-like growth factor-1 and insulin-like growth factor binding protein-3 and their determinants in healthy adult males from India: the INDIIGo study. Scientific Reports 2025;15:41340. DOI 10.1038/s41598-025-25235-6. Read at source. Quoted for the generation of age-specific normative centile curves using the LMS (Lambda, Mu, Sigma) method, the calculation of the standard deviation score from the age-specific L, M and S parameters, median IGF-1 values highest at 20 years of age and decreasing with each successive age-group stratum, the decline of 30.1 ng/ml per decade, the statement that IGF-1 levels are highly specific to ethnicity, and the cited requirement for ethnicity-specific IGF-1 reference ranges. This study was conducted in healthy adult males in India, so its reference intervals are specific to that population. ↩1 ↩2 ↩3 ↩4 ↩5 ↩6 ↩7 ↩8 ↩9
4. Akirov A, Masri-Iraqi H, Dotan I, Shimon I. The Biochemical Diagnosis of Acromegaly. Journal of Clinical Medicine 2021;10(5):1147. DOI 10.3390/jcm10051147. Read at source. Quoted for the statements that several factors may influence IGF-1 assays and result in wide variability between assays, that there could be notable discrepancies in IGF-1 test results between different assays, the cited finding of more than a 2-fold variation in the IGF-1 cut-off for the upper limit of normal measured in different laboratories, the advice to use the same well-validated IGF-1 assay throughout patient follow-up, and the description of values rising from birth until puberty followed by a decline with advancing age. This review does not use the terms Z-score or SDS. ↩1 ↩2 ↩3 ↩4 ↩5 ↩6 ↩7 ↩8 ↩9 ↩10 ↩11 ↩12
5. Motorykin I, Mu J, Miller BS, Li A, Clarke NJ, McPhaul MJ, Wu Z. Detection rate of IGF-1 variants and their implication to protein binding: study of over 240,000 patients. Clinical Chemistry and Laboratory Medicine 2024;62(3):484-492. DOI 10.1515/cclm-2023-0709. Read at source. Quoted for the identification of 1,099 patients carrying IGF-1 variants out of 243,808 screened, the statement that a variant may change binding to its receptor and/or its binding proteins, the note that concentrations account for only half the total IGF-1 in heterozygous carriers, the z-scores shifted toward negative levels, and the background statement that immunoassays are prone to interference from IGF binding proteins. That last point is background in the paper's introduction and not a finding of the study, and the page says so. The paper reports the share of variants at the C-terminus as 98% in its abstract and 95% in its results section; both figures are printed on the page. ↩1 ↩2 ↩3 ↩4 ↩5 ↩6 ↩7 ↩8
6. EGRIFTA SV (tesamorelin) for injection, US prescribing information, Theratechnologies Inc., section 5.2 Warnings and Precautions. Read at source via the openFDA drug label API (https://api.fda.gov/drug/label.json), warnings_and_cautions field. Quoted for the instruction to consider discontinuing in patients with persistent elevations of IGF-1 levels above 3 SDS particularly if the efficacy response is not robust, the finding that among patients treated for 26 weeks 47% had IGF-1 above 2 SDS and 36% above 3 SDS with the effect seen as early as 13 weeks, and the figures of 34% above 2 SDS and 23% above 3 SDS among patients who remained on treatment for 52 weeks. Tesamorelin is approved for HIV-associated lipodystrophy, so these frequencies come from that population and not from healthy adults. The site's own comparison page reports the 26-week figure as 47.4%, a more precise number than the 47% the label states. The label figure is the one used here. ↩1 ↩2 ↩3 ↩4 ↩5 ↩6 ↩7 ↩8
7. Caputo M, Pigni S, Agosti E, Daffara T, Ferrero A, Filigheddu N, Prodam F. Regulation of GH and GH Signaling by Nutrients. Cells 2021;10(6):1376. DOI 10.3390/cells10061376. Read at source. Quoted for the statement that nutritional status is a key regulator of IGF-I synthesis and secretion, that short-term fasting under three days increases GH secretion before any IGF-I reduction, that prolonged fasting beyond three days leads to peripheral GH resistance characterized by normal or elevated GH with low serum IGF-I, and that in humans calorie restriction reduces IGF-I only if protein intake is also restricted. This is a narrative review, and its caloric restriction section was not fully retrieved, so only the statements quoted here were read. ↩1 ↩2 ↩3 ↩4 ↩5 ↩6 ↩7
8. Iwayama H, Kitagawa S, Sada J, Miyamoto R, Hayakawa T, Kuroyanagi Y, Muto T, Kurahashi H, Ohashi W, Takagi J, Okumura A. Insulin-like growth factor-1 level is a poor diagnostic indicator of growth hormone deficiency. Scientific Reports 2021;11:16159. DOI 10.1038/s41598-021-95632-0. Read at source. Quoted for the reported 0.685 sensitivity, 0.417 specificity, 0.25 positive and 0.823 negative predictive values and 0.517 area under the curve at the best cutoff, the conclusion that IGF-1 level had poor diagnostic accuracy as a screening test for GHD, the statement that IGF-1 should not be used alone for the screening of GHD, and the report that mean IGF-1 SD was not significantly different between the GHD and non-GHD groups. Population: 298 children with short stature or decreased growth velocity at a single Japanese hospital, median age 4.98 years, 60 with growth hormone deficiency and 238 without. This is a pediatric population and the findings are not transferable to adults. ↩1 ↩2 ↩3 ↩4 ↩5 ↩6 ↩7