Lab result explainedHormonesLast updated November 8, 2026

IGF-1 blood test: what high and low insulin-like growth factor 1 levels mean

Insulin-like growth factor 1 (IGF-1) · Pituitary and growth hormone panel (often with GH, prolactin, TSH, cortisol) · reported in ng/mL (1 ng/mL = 0.131 nmol/L); often also reported as a z-score or SDS for age

Insulin-like growth factor 1 (IGF-1) is a hormone the liver makes in response to growth hormone (GH), and it carries out most of growth hormone's effects on bone, muscle and metabolism. Because growth hormone itself is released in short bursts, mostly during deep sleep, and is undetectable for much of the day, a single GH level is almost useless; IGF-1 stays steady over 24 hours and gives a reliable picture of average growth hormone output. An IGF-1 blood test is ordered to screen for growth hormone excess (acromegaly in adults, gigantism in children), to help diagnose growth hormone deficiency, to monitor growth hormone treatment, and to investigate short stature or slow growth in children.

Like several hormones, IGF-1 is defined by age. It rises through childhood, peaks during puberty at values of 300 to 900 ng/mL, then falls steadily through adult life: a typical range is about 115 to 360 ng/mL in the 20s, 100 to 270 in the 40s and 70 to 200 in the 60s, with men and women similar. A result is only interpretable against the range for your age and, ideally, as a z-score (how many standard deviations from the mean for age), which is how specialists read it. Nutrition, liver function, thyroid status, insulin, estrogen and kidney function all shift it independently of growth hormone.

The result people most often search for is a high IGF-1, usually found when acromegaly is suspected because of enlarging hands, feet or facial features, or incidentally on a wellness panel. A clearly raised age-adjusted IGF-1 is the single best screening test for acromegaly, and is confirmed by showing that growth hormone fails to suppress after a glucose drink. A low IGF-1 is less specific: it occurs in genuine growth hormone deficiency, but also with under-eating, liver disease, poorly controlled diabetes, hypothyroidism and oral estrogen, and around a third of adults with proven GH deficiency have a normal IGF-1, so a normal result does not exclude it.

IGF-1 at a glance

  • What it is: a liver-made hormone that mediates growth hormone's effects; stable through the day, so it reflects average GH output where a single GH level does not.
  • Normal depends on age (approximate adult ranges): 20s 115–360 ng/mL, 30s 110–300, 40s 100–270, 50s 85–240, 60s 70–200, 70s and over 60–180. Children peak at 300–900 in puberty. Labs and assays differ; use the age-matched range or z-score on your report.
  • High IGF-1: acromegaly (confirmed by a glucose suppression test), puberty, pregnancy, growth hormone or IGF-1 use; mild rises also with hyperthyroidism and some assay variation.
  • Low IGF-1: growth hormone deficiency, under-nutrition or anorexia, liver disease, poorly controlled type 1 diabetes, hypothyroidism, oral estrogen, kidney failure, severe illness; a normal result does not rule out adult GH deficiency.
  • An IGF-1 above the age range with typical features makes acromegaly likely; an IGF-1 below the age range in someone with pituitary disease and two or more other hormone deficiencies is usually enough to diagnose GH deficiency without stimulation testing.
  • Next step: repeat on the same assay, check TSH, liver tests, glucose and nutrition, then a glucose suppression test (if high) or GH stimulation test and pituitary MRI (if low) as indicated.

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What IGF-1 measures

Growth hormone is released by the pituitary in six to twelve pulses a day, the largest soon after falling asleep, with levels between pulses that are often below the detection limit of the assay and a half-life of only about 20 minutes. Exercise, fasting, stress and low blood sugar all trigger extra pulses. A random GH level can therefore be anything from undetectable to 30 ng/mL in a healthy person on the same day, which is why it is not used on its own. Growth hormone acts on the liver (and locally in many tissues) to produce IGF-1, which circulates bound to IGF-binding protein 3 and an acid-labile subunit in a complex that gives it a half-life of 12 to 15 hours and a near-constant level across the day. IGF-1 is therefore the integrated signal of GH secretion over the preceding day or two.

IGF-1 stimulates cell growth and division, bone lengthening at the growth plates in children, muscle protein synthesis and cartilage growth, and has insulin-like effects on glucose uptake. It feeds back on the pituitary and hypothalamus to restrain GH release. Production depends on more than GH: it needs adequate calories and protein, a functioning liver, normal thyroid hormone and adequate insulin action. Oral estrogen reduces liver IGF-1 production by around 20 to 30 percent (transdermal estrogen much less), and hepatic insulin resistance or portal insulin deficiency, as in poorly controlled type 1 diabetes, lowers it despite normal or high GH.

The lab measures total IGF-1 by immunoassay after separating it from its binding proteins, or by mass spectrometry, in ng/mL (multiply by 0.131 for nmol/L). Different assays give systematically different results, sometimes by 20 to 30 percent, so a result should be compared with that assay's own age-specific range and follow-up tests should use the same lab. Specialists express the result as a z-score or standard deviation score (SDS) for age and sex; a z-score above +2 or below -2 is outside the 95 percent reference interval. Because IGF-1 is stable, it does not need fasting or a particular time of day, although a fasting morning sample is conventional when GH is drawn at the same time.

Normal range for IGF-1

Reference ranges vary between labs and by age, sex and pregnancy. Use the range printed on your own report.

GroupTypical range (ng/mL (1 ng/mL = 0.131 nmol/L); often also reported as a z-score or SDS for age)Notes
Adults 21 to 30About 115–360 ng/mLApproximate; ranges differ by assay. A z-score (standard deviations from the age mean) is the most reliable way to compare results.
Adults 31 to 40About 110–300 ng/mLIGF-1 falls about 1 to 1.5 percent a year through adulthood.
Adults 41 to 50About 100–270 ng/mL
Adults 51 to 60About 85–240 ng/mL
Adults 61 to 70About 70–200 ng/mL
Adults over 70About 60–180 ng/mLLow-normal values are expected; an isolated low result in a well older adult is not GH deficiency.
Children and adolescentsRises from about 50–200 ng/mL in early childhood to a pubertal peak of 300–900 ng/mLInterpreted by age and pubertal stage, not chronological age alone; a child in puberty can have a value that would mean acromegaly in an adult.
PregnancyRises up to about 2 fold in the second and third trimestersPlacental growth hormone drives IGF-1; values return to baseline after delivery.
AcromegalyAbove the age-specific upper limit (z-score over +2), often 2 to 5 times normalConfirmed when GH fails to fall below 1 ng/mL (0.4 with ultrasensitive assays) two hours after a 75 g glucose drink.

High IGF-1

A high IGF-1 for age means growth hormone output is, or recently has been, higher than normal. The important diagnosis is acromegaly, in which a benign pituitary tumour secretes excess GH, usually for a decade or more before it is recognised. Typical features are gradual enlargement of the hands and feet (rings and shoes no longer fit), coarsening of facial features, a widening jaw with spreading teeth, excessive sweating, oily skin and skin tags, carpal tunnel syndrome, joint pain, sleep apnea, headaches and, in women, irregular periods. Acromegaly affects about 6 per 100,000 people; an age-adjusted IGF-1 above the reference range is the recommended screening test, with a sensitivity above 95 percent, and is confirmed by an oral glucose tolerance test in which GH fails to suppress below 1 ng/mL (or 0.4 with newer assays). A pituitary MRI follows a positive biochemical result, never the other way round.

Not every raised IGF-1 is acromegaly. Normal puberty produces values that exceed any adult range, pregnancy raises IGF-1 up to two fold through placental growth hormone, and treatment with growth hormone, or misuse of GH or IGF-1 for sport or anti-ageing, raises it directly. Hyperthyroidism can push IGF-1 modestly above the range, and uncontrolled type 1 diabetes occasionally produces a transiently high GH with a variable IGF-1. Assay differences of 20 to 30 percent between laboratories mean that a value just over the upper limit, with no symptoms, is often repeated on the same assay before anything further is done.

A mildly raised IGF-1 in someone who feels well, tall or short, is a common incidental finding and in most cases simply sits at the upper end of normal variation, which is wide: identical twins and families run consistently high or low. Observational studies link higher IGF-1 in the normal range with slightly increased risk of some cancers (prostate, breast, colorectal) and lower IGF-1 with cardiovascular disease, but the absolute effects are small and the relationships are U-shaped; a high-normal IGF-1 is not treated.

Common causes

  1. Acromegaly (growth hormone-secreting pituitary adenoma)

    IGF-1 is typically 2 to 5 times the age-specific upper limit, with GH that fails to suppress on a glucose test. Over 95 percent of cases are pituitary adenomas, most over 1 cm at diagnosis; rare cases come from GHRH-secreting tumours elsewhere.

  2. Gigantism in children and adolescents

    The same tumour before the growth plates have closed produces excessive height and a very high IGF-1 for pubertal stage; it is rare and usually obvious from the growth chart.

  3. Normal puberty

    IGF-1 doubles or triples during the pubertal growth spurt, peaking at 14 to 16 in boys and 12 to 14 in girls, at values that would be abnormal in an adult. Interpretation uses pubertal stage, not just age.

  4. Pregnancy

    Placental growth hormone replaces pituitary GH from mid-pregnancy and raises IGF-1 up to two fold by the third trimester; results in pregnancy are not comparable with standard ranges.

  5. Growth hormone treatment, or GH and IGF-1 misuse

    Prescribed GH for deficiency is dosed to keep IGF-1 in the mid-normal range; higher values indicate over-replacement. GH, IGF-1 and peptide secretagogues used for bodybuilding or anti-ageing raise IGF-1, sometimes to acromegalic levels, with the same long-term risks.

  6. Hyperthyroidism

    Thyroid hormone increases GH action on the liver and can raise IGF-1 10 to 20 percent above baseline; it normalises with treatment.

  7. Assay variation and high-normal variants

    Different immunoassays differ systematically, and families and individuals sit persistently at the top of the range. A borderline value is repeated on the same assay before investigation.

  8. Obesity (occasionally) and high protein or dairy intake

    Obesity usually lowers GH but leaves IGF-1 normal or slightly high because of increased liver sensitivity. High protein and dairy intake raise IGF-1 by around 10 to 15 percent in trials, enough to shift a borderline result.

  9. Poorly controlled type 1 diabetes (variable)

    GH is high but IGF-1 is usually low because of portal insulin deficiency; occasionally IGF-1 reads high during periods of improved control. Mentioned because it confuses interpretation rather than as a common cause of true excess.

Symptoms that can go with it

  • Enlarging hands and feet: rings, gloves and shoes no longer fit
  • Coarsening of facial features, a more prominent brow and jaw, gaps appearing between the teeth, enlarged tongue or nose
  • Excessive sweating, oily thickened skin and skin tags
  • Headaches and, with larger tumours, loss of outer (peripheral) vision
  • Joint pain and stiffness, carpal tunnel syndrome (tingling in the thumb and first fingers), deepening voice
  • Snoring and sleep apnea, fatigue, high blood pressure, new diabetes or prediabetes
  • Irregular or absent periods, milky nipple discharge, reduced libido or erectile difficulty
  • None, when the high value reflects puberty, pregnancy or normal variation

Low IGF-1

A low IGF-1 for age can mean growth hormone deficiency, but more often it reflects something that reduces the liver's response to GH: not eating enough, liver disease, an underactive thyroid, poorly controlled type 1 diabetes, kidney failure, severe illness or oral estrogen. IGF-1 falls within days of fasting or a very low-calorie diet and within weeks of significant weight loss, and it is characteristically low in anorexia nervosa, where it is a marker of under-nutrition rather than of pituitary disease. The first step with a low IGF-1 is therefore to review nutrition, weight change, medicines and liver and thyroid tests before thinking about the pituitary.

In children, a low IGF-1 with poor growth velocity (falling across height centiles) raises the question of growth hormone deficiency, which is then confirmed with GH stimulation tests. In adults, growth hormone deficiency almost always occurs in people with known pituitary disease (a pituitary tumour, surgery or radiation to the pituitary, head injury, Sheehan syndrome, or childhood-onset GH deficiency), and the symptoms (fatigue, increased abdominal fat, reduced muscle and bone mass, low mood, poor exercise capacity, high LDL) are non-specific. Guidelines recommend testing only people with a reason to suspect pituitary disease. In that group, a low IGF-1 with deficiencies of three other pituitary hormones is diagnostic on its own; otherwise a stimulation test (insulin tolerance, glucagon or macimorelin) is required because around 30 to 40 percent of adults with proven GH deficiency have an IGF-1 within the normal range.

A low-normal or mildly low IGF-1 in an otherwise healthy adult who feels well, is not losing weight and has no pituitary history is almost never GH deficiency and is not a reason for growth hormone treatment, which is not approved for ageing or for low IGF-1 alone and carries risks of fluid retention, joint pain, insulin resistance and, in theory, tumour growth. IGF-1 falls by about 1 to 1.5 percent a year through adult life, and low-normal values are expected after 60.

Common causes

  1. Under-nutrition, fasting and anorexia nervosa

    Calorie and protein restriction lowers IGF-1 within days even though GH rises (the liver becomes GH-resistant); in anorexia IGF-1 is often below 100 ng/mL and recovers with refeeding. A low IGF-1 in someone who has lost weight is nutritional until proven otherwise.

  2. Growth hormone deficiency in adults

    Pituitary adenomas and their treatment (surgery, radiotherapy), craniopharyngioma, traumatic brain injury, Sheehan syndrome, infiltrative disease and childhood-onset deficiency cause it. GH is the first pituitary hormone lost, so deficiency often coexists with low TSH, ACTH or gonadotropin output.

  3. Growth hormone deficiency in children

    Congenital or acquired, presenting as slow growth (crossing height centiles downward), a young appearance for age, central fat and, in infants, low blood sugar. Confirmed with GH stimulation tests, not IGF-1 alone, since IGF-1 is naturally low in young children.

  4. Liver disease

    Cirrhosis and significant chronic hepatitis reduce the liver's capacity to make IGF-1; levels fall in proportion to liver function and are used in some prognostic scores.

  5. Hypothyroidism

    Thyroid hormone is needed for GH to drive IGF-1 production; untreated hypothyroidism lowers IGF-1 by 20 to 40 percent, and it rises again on thyroxine.

  6. Poorly controlled type 1 diabetes

    The liver needs insulin from the portal vein to respond to GH; with insulin deficiency IGF-1 is low despite high GH, a pattern that contributes to poor growth in children with uncontrolled diabetes.

  7. Oral estrogen

    The combined pill and oral estrogen HRT reduce hepatic IGF-1 production by 20 to 30 percent; transdermal estrogen does not. Women on GH replacement who take oral estrogen need higher GH doses.

  8. Chronic kidney disease, critical illness and chronic inflammation

    Advanced kidney disease, sepsis, major surgery, heart failure and active inflammatory disease all induce GH resistance and lower IGF-1 temporarily or persistently.

  9. Laron syndrome and other GH insensitivity

    Rare inherited defects in the GH receptor or signalling cause very low IGF-1 with high GH and severe short stature; diagnosed in childhood.

  10. Normal ageing

    IGF-1 declines by 1 to 1.5 percent a year from the 30s, so values of 70 to 120 ng/mL are typical and normal in the 70s and 80s.

Symptoms that can go with it

  • Often none; a low IGF-1 from ageing, diet or medication produces no symptoms of its own
  • In children: slow growth, falling across height centiles, a younger appearance than peers, increased central fat, delayed tooth eruption
  • In adults with pituitary GH deficiency: fatigue, reduced exercise capacity, increased abdominal fat with reduced muscle, low mood and poor concentration, thin dry skin, reduced sweating
  • Low bone density or fractures with long-standing deficiency
  • Low blood sugar in infants and young children with GH deficiency
  • Symptoms of the underlying cause: weight loss and cold intolerance in under-nutrition, tiredness and weight gain in hypothyroidism, jaundice or bruising in liver disease
  • Headaches, visual loss or other pituitary hormone symptoms (thirst, intolerance of cold, dizziness on standing, absent periods) when the cause is pituitary disease

Read it alongside

  • Growth hormone (GH) — only meaningful as a suppression test (after 75 g glucose) for acromegaly or a stimulation test for deficiency; a random GH is not interpretable.
  • IGFBP-3 — the main IGF-1 binding protein; less affected by nutrition and sometimes used alongside IGF-1 in children.
  • TSH and free T4 — hypothyroidism lowers IGF-1 and hyperthyroidism raises it; thyroid status must be known before interpreting.
  • Prolactin — co-secreted by about a third of GH-producing tumours and raised by pituitary stalk compression; part of any pituitary assessment.
  • Morning cortisol, LH, FSH and testosterone or estradiol — show whether other pituitary hormones are affected, which both supports GH deficiency and determines treatment priorities.
  • Glucose and A1C — acromegaly causes insulin resistance and diabetes; poorly controlled diabetes lowers IGF-1.
  • ALT, AST, albumin and bilirubin — liver disease lowers IGF-1 independently of GH.
  • Albumin, prealbumin and weight history — under-nutrition is the commonest cause of a low IGF-1 and should be assessed before pituitary testing.

What usually happens next

  1. If IGF-1 is above the age range, expect a repeat on the same assay, then an oral glucose tolerance test with GH measured at 0, 30, 60, 90 and 120 minutes; failure of GH to fall below 1 ng/mL (0.4 on ultrasensitive assays) confirms acromegaly and a pituitary MRI follows.
  2. If IGF-1 is below the age range, expect a review of weight, diet, alcohol, medicines (oral estrogen in particular), TSH, liver tests and glucose first; correcting those and retesting in 2 to 3 months often normalises it.
  3. Adult GH deficiency is only pursued in people with pituitary disease or a history that puts it at risk (tumour, surgery, radiation, head injury, childhood GH deficiency); in that setting a low IGF-1 with three or more other pituitary deficiencies is diagnostic and otherwise a stimulation test is arranged by an endocrinologist.
  4. For a child with a low IGF-1, the key data are height measurements over 6 to 12 months and a bone-age X-ray; GH stimulation tests follow if growth velocity is low.
  5. Use the same laboratory for follow-up tests, because assays differ by 20 to 30 percent and a change between labs can masquerade as a real change.
  6. Ask for the result as a z-score or SDS for age if it is not shown; it is the clearest way to see how far from normal the value really is.

Diet, lifestyle and natural levers with evidence

What can move IGF-1 once the cause is known. Nothing here replaces finding the cause.

Adequate calorie and protein intake

Strong evidence

Nutrition is the strongest non-hormonal determinant of IGF-1. Fasting for 5 days lowers IGF-1 by 30 to 50 percent and refeeding restores it within a week; in anorexia nervosa it rises steadily with weight gain. Protein matters specifically: in intervention studies, raising protein intake from low to adequate (around 1 to 1.2 g/kg a day) in older adults increased IGF-1 by about 10 to 20 percent, and a meta-analysis of 8 trials found milk or dairy intake raised IGF-1 by around 13 ng/mL on average. People eating vegan diets have IGF-1 about 10 to 15 percent lower than omnivores in cohort studies.

Raising IGF-1 is not a goal in itself; higher-normal values are linked in observational studies with modestly higher risk of some cancers, so protein intake should aim at adequacy, not excess.

Resistance and aerobic exercise

Moderate evidence

A single bout of intense exercise triggers a large GH pulse, but the effect on resting IGF-1 is modest and inconsistent. Meta-analyses of training trials in older adults report small rises in IGF-1 (roughly 5 to 10 percent, or 10 to 20 ng/mL) after 12 or more weeks of resistance training, with larger effects in people who were sedentary or under-muscled, while aerobic training alone shows little change. The muscle, bone and metabolic benefits of exercise occur regardless of whether blood IGF-1 moves, partly through local IGF-1 production in muscle.

Sleep, particularly deep (slow-wave) sleep

Moderate evidence

The largest GH pulse of the day occurs in the first hours of slow-wave sleep, and total sleep deprivation abolishes it. Studies of chronic sleep restriction (4 to 6 hours a night for a week) show reduced GH output and, in some, lower IGF-1, with obstructive sleep apnea similarly suppressing nocturnal GH; treating sleep apnea with CPAP raises IGF-1 in trials. Effects on IGF-1 are modest in people who already sleep adequately.

Weight loss in obesity

Moderate evidence

Obesity blunts GH secretion markedly while IGF-1 stays roughly normal, because insulin increases liver GH sensitivity. Weight loss of 10 percent or more restores GH pulses, and bariatric surgery studies show IGF-1 rising modestly over the following year. This mainly matters for interpreting GH stimulation tests, which give falsely low results in obesity, rather than as a way of changing IGF-1 for its own sake.

Zinc repletion where deficient

Preliminary evidence

Zinc is needed for GH signalling and IGF-1 synthesis. In zinc-deficient children in low-income settings, supplementation (typically 10 to 20 mg a day for 6 to 12 months) raised IGF-1 and growth velocity in several randomised trials, and small trials in older adults with low zinc intake reported rises in IGF-1. There is no evidence that zinc raises IGF-1 in people who are already replete.

Doses above 40 mg a day long-term cause copper deficiency and can lower HDL; zinc interferes with absorption of some antibiotics.

When to see a clinician promptly

  • A high IGF-1 for age with enlarging hands, feet or facial features, new snoring or sleep apnea, headaches or visual field loss: acromegaly shortens life expectancy if untreated and needs an endocrinology referral.
  • Sudden severe headache with visual loss, double vision or collapse in anyone with a known or suspected pituitary tumour: pituitary apoplexy is an emergency.
  • A child whose height is falling across centiles on the growth chart, or who is growing less than about 4 cm a year after age 4, whatever the IGF-1 value.
  • A low IGF-1 with a history of pituitary tumour, surgery, radiation or significant head injury, or with other signs of pituitary failure (fatigue, dizziness on standing, cold intolerance, absent periods, loss of libido, excess thirst).
  • A low IGF-1 with ongoing weight loss, which may indicate an eating disorder, malabsorption, liver disease or another illness needing assessment.
  • Anyone using growth hormone, IGF-1 or peptide secretagogues bought without prescription, given the risks of diabetes, joint and heart problems and the possibility of acromegaly-like complications.

Frequently asked questions

What is a normal IGF-1 level by age?

Approximately 115 to 360 ng/mL in your 20s, 110 to 300 in your 30s, 100 to 270 in your 40s, 85 to 240 in your 50s, 70 to 200 in your 60s and 60 to 180 over 70, with children peaking at 300 to 900 during puberty. These are approximate: different assays differ by 20 to 30 percent, so use the age-specific range printed on your report, or the z-score if given. A z-score between -2 and +2 is within the normal 95 percent range.

Why test IGF-1 instead of growth hormone?

Growth hormone is released in brief pulses, mainly in deep sleep, with a half-life of about 20 minutes, so a random GH can be undetectable or 20 ng/mL in the same healthy person on the same day. IGF-1 is made by the liver in response to GH and stays steady over 24 hours with a half-life of 12 to 15 hours, so it reflects average GH output. GH is only useful in dynamic tests: a glucose suppression test for acromegaly or a stimulation test for deficiency.

What IGF-1 level indicates acromegaly?

Any value above the age- and sex-specific upper limit (a z-score above +2) is a positive screen, and most people with acromegaly have IGF-1 two to five times the upper limit. The diagnosis is confirmed when GH fails to fall below 1 ng/mL (0.4 with ultrasensitive assays) two hours after a 75 g glucose drink, after which a pituitary MRI locates the tumour. A normal age-adjusted IGF-1 makes acromegaly very unlikely.

What does low IGF-1 mean?

Usually that the liver is not responding fully to growth hormone, because of under-eating or weight loss, liver disease, an underactive thyroid, poorly controlled type 1 diabetes, kidney disease, oral estrogen or severe illness; these are checked first. True growth hormone deficiency in adults almost always occurs with known pituitary disease, and around a third of those people have a normal IGF-1, so a stimulation test, not IGF-1 alone, makes the diagnosis. In children a low IGF-1 matters if growth is slow.

Does a low IGF-1 mean I need growth hormone?

Not unless you have confirmed growth hormone deficiency from pituitary disease. GH treatment is approved for diagnosed deficiency, not for low IGF-1 alone, and not for ageing, fatigue or body composition in people with a normal pituitary. In healthy older adults, trials of GH produced small gains in lean mass but no gain in strength or function, with frequent fluid retention, joint pain, carpal tunnel syndrome and raised blood sugar.

Can diet or exercise raise IGF-1 naturally?

Eating enough calories and protein is the biggest lever: fasting lowers IGF-1 by 30 to 50 percent within days and adequate protein (around 1 to 1.2 g/kg a day) restores it; dairy and animal protein raise it by about 10 to 15 percent in trials. Resistance training over 12 or more weeks produces small rises of 5 to 10 percent in older adults, and deep sleep is when most GH is released. These changes bring a nutritionally low IGF-1 back to normal; they do not correct pituitary deficiency.

Is a high IGF-1 linked to cancer?

In large cohort studies, people with IGF-1 in the upper part of the normal range have a modestly higher risk of prostate, breast and colorectal cancer than those in the lower part, with about a 10 to 25 percent relative difference per standard deviation, and people with acromegaly have a higher rate of colon polyps and are offered colonoscopy. Very low IGF-1 is associated with cardiovascular disease, so the relationship is U-shaped. A high-normal IGF-1 is not treated; the finding informs screening discussions rather than action.

Do I need to fast for an IGF-1 test?

Not strictly, because IGF-1 is stable through the day and barely changes after a meal, but a morning fasting sample is conventional, especially when GH, glucose or a lipid panel is drawn at the same time. Avoid testing within a few days of a very low-calorie diet or prolonged fast, which lower it, and tell the lab about oral estrogen, thyroid medication, growth hormone or any peptide products, all of which shift the result.

References

  1. Insulin-like growth factor 1 (IGF-1) test. MedlinePlus, US National Library of Medicine (2023)
  2. Insulin-like growth factor 1 (IGF-1), serum: clinical and interpretive information. Mayo Clinic Laboratories (2024)
  3. Katznelson L, Laws ER, Melmed S, et al.. Acromegaly: an Endocrine Society clinical practice guideline. Journal of Clinical Endocrinology and Metabolism (2014)
  4. Giustina A, Barkan A, Beckers A, et al.. A consensus on the diagnosis and treatment of acromegaly comorbidities: an update. Journal of Clinical Endocrinology and Metabolism (2020)
  5. Molitch ME, Clemmons DR, Malozowski S, Merriam GR, Vance ML. Evaluation and treatment of adult growth hormone deficiency: an Endocrine Society clinical practice guideline. Journal of Clinical Endocrinology and Metabolism (2011)
  6. Yuen KCJ, Biller BMK, Radovick S, et al.. American Association of Clinical Endocrinologists and American College of Endocrinology guidelines for management of growth hormone deficiency in adults and patients transitioning from pediatric to adult care. Endocrine Practice (2019)
  7. Bidlingmaier M, Friedrich N, Emeny RT, et al.. Reference intervals for insulin-like growth factor-1 (IGF-I) from birth to senescence: results from a multicenter study using a new automated chemiluminescence IGF-I immunoassay conforming to recent international recommendations. Journal of Clinical Endocrinology and Metabolism (2014)
  8. Clemmons DR. Consensus statement on the standardization and evaluation of growth hormone and insulin-like growth factor assays. Clinical Chemistry (2011)
  9. Melmed S. Medical progress: acromegaly. New England Journal of Medicine (2006)
  10. Qin LQ, He K, Xu JY. Milk consumption and circulating insulin-like growth factor-I level: a systematic literature review. International Journal of Food Sciences and Nutrition (2009)
  11. Fontana L, Weiss EP, Villareal DT, Klein S, Holloszy JO. Long-term effects of calorie or protein restriction on serum IGF-1 and IGFBP-3 concentration in humans. Aging Cell (2008)
  12. Acromegaly and gigantism. Merck Manual Professional Version (2024)

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This page is educational and is not medical advice or a diagnosis. Lab results have to be interpreted together with your history, symptoms and other results by a clinician who knows you. Do not start or stop a supplement to change a lab value before the cause is known.