How to Increase IGF-1 Naturally

IGF-1 production depends on growth hormone, but also on age, nutrition, sleep, exercise, liver function, and metabolic health. Adequate calories and protein, resistance training, good sleep, and correcting nutritional deficiencies can support normal levels. Fasting is the exception that often causes confusion: it may raise growth hormone while lowering circulating IGF-1. Higher levels are not automatically healthier, so the goal is normal regulation rather than maximum production.

Growth hormone gets most of the attention in conversations about muscle growth, recovery, and healthy aging, but it is only half of the story. Many of its growth-related effects happen downstream through insulin-like growth factor 1, better known as IGF-1. That relationship also creates a common misconception. If something raises growth hormone, it seems reasonable to assume that IGF-1 will rise with it. In practice, the two can move in opposite directions. A prolonged fast is one of the clearest examples: growth hormone secretion increases while circulating IGF-1 falls. Understanding why makes it much easier to separate habits that support normal production from attempts to simply push a hormone level higher.

Note: This article is for educational purposes only. Research peptides sold by BioHub Peptides are intended for laboratory research and are not approved for human or veterinary use. Nothing in this article should be interpreted as medical advice or instructions for peptide use.

What Is IGF-1?

Insulin-like growth factor 1 is a peptide hormone involved in growth, tissue repair, bone development, protein metabolism, and cell signaling. Although many tissues can produce it locally, the liver is responsible for most of the IGF-1 found in the bloodstream.

Growth hormone, or GH, provides one of the major signals for that production. GH is released from the pituitary gland in pulses and binds to receptors in the liver and other tissues, prompting them to produce IGF-1. The hormone then circulates primarily bound to IGF-binding proteins, which help regulate its availability and activity.

That is why GH and IGF-1 are usually discussed together as the GH–IGF-1 axis. They are closely connected, but they are not interchangeable measurements of the same process.

A medical professional closely examines a leg X-ray, pointing out details with a pen
IGF-1 connects growth hormone signaling with processes involved in growth, tissue repair, and bone development.

What Controls IGF-1 Levels?

Growth hormone may provide the signal, but the body still needs the right conditions to respond to it:

  • Age is one of the strongest influences. Levels rise through childhood, peak around puberty and early adulthood, and generally decline with age.
  • Nutrition also matters because liver production depends partly on sufficient energy, protein, and insulin signaling.
  • Sleep, exercise, sex hormones, body composition, and overall metabolic health can influence different points along the same pathway.

Liver function deserves particular attention because the liver supplies most circulating IGF-1. A strong GH signal cannot produce a normal downstream response if the liver is unable to respond appropriately. The number seen on a blood test is therefore the end result of several interacting systems, not simply a measure of how much growth hormone the pituitary released that day.

Why Might IGF-1 Be Low?

A low result can reflect something as straightforward as inadequate energy intake, but it can also have causes that cannot be fixed by eating more protein or sleeping an extra hour:

  • Malnutrition and prolonged fasting are established causes of reduced circulating levels.
  • Liver disease can interfere with production, while poorly controlled diabetes and hypothyroidism can also affect the GH–IGF-1 axis.
  • Growth hormone deficiency and abnormalities affecting GH receptors or downstream signaling represent another group of possible causes.

Because concentrations naturally change with age, an IGF-1 result is normally considered against an age-adjusted reference range rather than one universal “optimal” number. However, a low value also does not diagnose growth hormone deficiency by itself. Clinical interpretation may require additional testing, particularly when another medical condition or nutritional problem could explain the result.

Does More IGF-1 Mean Better Health?

Not necessarily. It is easy to see how IGF-1 developed a reputation as something worth maximizing. It is studied across research areas such as muscle and bone biology, supports growth during development, and has anabolic effects in multiple tissues. Those functions are real, but they do not turn the hormone into a simple more-is-better marker.

IGF-1 levelWhat it may reflectWhy the context matters
Lower than expectedInadequate nutrition, aging, liver disease, poorly controlled diabetes, thyroid dysfunction, GH deficiency, or other problems affecting the pathwayThe appropriate response depends on the cause. A lifestyle change cannot correct every reason for a low result.
Within the age-adjusted rangeNormal regulation of GH signaling, nutrition, liver function, and other contributing factorsThere is no established health advantage to pushing a normal value toward the top of the range simply for the sake of having more.
Persistently elevatedExcess GH signaling or another abnormal influence on the pathwayChronic excess is not the same as enhanced recovery or healthier aging and warrants medical evaluation.

There is another reason to be cautious about treating a higher number as the goal. The pathway influences cell growth and survival, which is useful where normal growth and repair are concerned but becomes more complicated when signaling is chronically excessive.

That makes normal regulation a more defensible objective than maximizing IGF-1.

Why Using Peptides to Raise IGF-1 Is a Different Question

Once the GH–IGF-1 relationship is understood, research peptides that stimulate growth hormone can sound like an obvious shortcut. Increase the upstream signal, and the downstream hormone should follow. But the biology is not that predictable.

Growth hormone-releasing peptides and related compounds can alter GH secretion, but the eventual IGF-1 response still depends on nutrition, insulin signaling, liver responsiveness, dose, timing, individual physiology, and the specific compound being studied. Increasing one signal does not provide precise control over the entire axis.

More importantly, experimental effects observed in controlled research do not establish safety for unsupervised human use.

Flat lay of various educational plastic anatomy models including organs and bones for study
Peptide research can reveal how the GH–IGF-1 axis responds to stimulation, but experimental findings do not establish safe human use.

Human Safety Data Are Often Limited

Several compounds discussed online for GH or IGF-1 manipulation are not approved treatments for increasing either hormone in otherwise healthy people. The FDA has specifically identified safety concerns around a number of substances used or proposed for compounding. Its current safety information notes concerns involving CJC-1295, GHRP-2, GHRP-6, and Ipamorelin, including limited human safety data, potential immunogenicity, metabolic effects, peptide-related impurities, and reported serious adverse events in some settings.

Those concerns are not interchangeable across every peptide, but they illustrate why “it raises GH” is not enough information to establish safe human use.

Product Quality Adds Another Variable

Peptides also present manufacturing and analytical challenges that do not exist in the same way with ordinary diet or exercise. Identity, purity, peptide-related impurities, degradation, aggregation, storage conditions, and handling can all affect what is actually present in a sample. A research finding involving a characterized compound under laboratory conditions therefore cannot simply be transferred to an unknown product purchased for self-administration.

For a person trying to support normal hormone physiology, that makes experimental peptide use a fundamentally different proposition from addressing sleep, nutrition, training, or another modifiable lifestyle factor.

How to Increase IGF-1 Naturally

There is no food, workout, or sleep schedule that guarantees a particular increase. The natural factors with the strongest rationale work by supporting the conditions under which the GH–IGF-1 axis normally operates. That means the focus shifts away from trying to trigger a short-lived hormonal response and toward the broader conditions that allow normal signaling to take place. Some of those factors influence growth hormone release, while others affect how well the liver and other tissues respond to it. The most useful strategies, therefore, are the ones that support the system as a whole rather than trying to force one number upward.

Eat Enough Protein and Total Calories

The body is unlikely to prioritize growth-related signaling when it does not have enough energy or raw material available to support it. Human research has linked higher protein intake with modest increases in circulating IGF-1, while severe energy restriction tends to move levels in the opposite direction. The relationship is not unlimited: once nutritional needs are met, adding progressively more protein does not mean production will continue rising proportionally.

This makes adequate intake more important than chasing individual “IGF-1 foods.” Protein-rich foods can contribute, but the broader dietary pattern matters because protein intake cannot fully compensate for chronic under-fueling. So, for someone who is already meeting energy and protein needs, eating more solely to manipulate one hormone is unlikely to offer the same benefit as correcting an actual deficiency.

Use Resistance Training Consistently

Resistance exercise has a more convincing place in the discussion, although its effects are frequently oversimplified. Training influences both growth hormone secretion and growth-related signaling within muscle. Meta-analyses of resistance-training trials have found increases in circulating IGF-1 overall, but the response varies considerably between studies and appears to differ by age, sex, training duration, and baseline characteristics.

That variation matters because muscle adaptation is not determined solely by how much circulating IGF-1 changes after a workout. Mechanical loading stimulates local signaling inside muscle as well, so a successful training program does not need to produce a dramatic change on a blood test to be effective. The more useful takeaway is that regular resistance exercise supports the physiology associated with muscle maintenance and healthy aging. Treating a temporary hormone response as the objective misses most of the reason training works.

Elderly man exercising on a track with a resistance band
Resistance training can influence growth-related signaling even when changes in circulating IGF-1 are modest.

Protect Sleep and Recovery

Growth hormone is released in pulses rather than at a steady rate throughout the day, and one of the most reproducible pulses occurs after sleep begins. As such, slow-wave sleep has a particularly close relationship with nocturnal GH secretion. That makes sleep relevant to the upstream part of the pathway even though it would be too simplistic to claim that an extra hour in bed directly translates into a predictable rise in circulating IGF-1.

Consistency matters here more than trying to identify a perfect “growth hormone window.” Regularly cutting sleep short or disrupting sleep changes the environment in which normal endocrine rhythms operate. Sleep also overlaps with training recovery, appetite regulation, and metabolic health, giving it a wider role than a single hormone measurement suggests.

Correct Deficiencies Instead of Chasing Supplements

The supplement conversation becomes confusing because evidence that a nutrient is necessary for normal physiology is often presented as evidence that taking more of it will increase hormone production. Those are different claims.

Micronutrient deficiencies can interfere with normal growth and endocrine function, and correcting a genuine deficiency may restore a process that was being limited. Once nutritional requirements are already being met, however, there is no general rule that progressively larger doses will continue raising IGF-1.

The same can be applied to amino acids promoted as “GH boosters.” An acute effect on growth hormone secretion does not automatically establish a meaningful or sustained rise downstream. Instead, a diet that reliably covers energy, protein, vitamins, and minerals is a more defensible starting point than building a supplement stack around one laboratory marker.

Keep Metabolic Health in the Picture

The GH–IGF-1 axis is closely tied to the body’s overall metabolic state, which helps explain why the relationship between the two hormones is not always straightforward. Obesity, particularly excess visceral fat, is associated with lower spontaneous GH secretion, while prolonged undernutrition can produce the opposite pattern: GH rises even as circulating IGF-1 falls.

These apparently opposite responses show why the pathway cannot be reduced to a simple rule such as “more GH equals more IGF-1.” Insulin signaling, liver function, body composition, and energy availability all influence what happens after growth hormone is released.

For that reason, supporting metabolic health as a whole is more meaningful than trying to manipulate one hormone in isolation.

What About Fasting?

Fasting is where the usual explanation breaks down most clearly. During a prolonged fast, growth hormone secretion can increase substantially. On the surface, that sounds like it should stimulate more IGF-1. Instead, human studies show that fasting tends to reduce circulating levels.

The reason lies largely in the liver. Lower nutrient and insulin availability reduces the liver’s responsiveness to the GH signal. This state is often described as hepatic GH resistance: the pituitary continues releasing growth hormone, but the usual downstream production no longer follows in proportion.

A 2019 systematic review and meta-analysis found that fasting significantly reduced circulating IGF-1, while ordinary calorie restriction produced less consistent changes. More severe energy restriction was more likely to produce a reduction. So fasting may be useful to study precisely because it separates the two hormones so clearly. It is not strong evidence for using fasting as a way to increase IGF-1.

a minimalist setup with a fork centered on a white plate
Fasting is a useful reminder that higher growth hormone does not automatically mean higher IGF-1.

Support the System, Not Just the Number

There is no natural trick that overrides the way this pathway is regulated. Enough food and protein provide the resources for normal production. Resistance training supplies a meaningful physiological stimulus. Sleep supports normal GH rhythms, while good metabolic and nutritional health allows the signal to travel downstream as intended.

Those habits may help when lifestyle factors are holding levels back, but they are not tools for pushing an already normal result indefinitely higher. IGF-1 is part of a regulated growth system, not a score where the highest number wins. Supporting the conditions in which that system functions normally makes far more physiological sense than trying to maximize one endpoint.

Research References

Amiri, N., Fathei, M., & Mosaferi Ziaaldini, M. (2021). Effects of resistance training on muscle strength, insulin-like growth factor-1, and insulin-like growth factor-binding protein-3 in healthy elderly subjects: A systematic review and meta-analysis of randomized controlled trials. Hormones, 20(2), 247–257. https://doi.org/10.1007/s42000-020-00250-6

Ergun-Longmire, B., & Wajnrajch, M. P. (2025). Growth and growth disorders. In Endotext. MDText.com, Inc. https://www.ncbi.nlm.nih.gov/books/NBK279142/

Jiang, Q., Lou, K., Hou, L., Lu, Y., Sun, L., Tan, S. C., Low, T. Y., Kord-Varkaneh, H., & Pang, S. (2020). The effect of resistance training on serum insulin-like growth factor 1 (IGF-1): A systematic review and meta-analysis. Complementary Therapies in Medicine, 50, 102360. https://doi.org/10.1016/j.ctim.2020.102360

Kazemi, A., Speakman, J. R., Soltani, S., & Djafarian, K. (2020). Effect of calorie restriction or protein intake on circulating levels of insulin like growth factor I in humans: A systematic review and meta-analysis. Clinical Nutrition, 39(6), 1705–1716. https://doi.org/10.1016/j.clnu.2019.07.030

Olarescu, N. C., Gunawardane, K., Hanson, T. K., Møller, N., & Jørgensen, J. O. L. (2025). Normal physiology of growth hormone in normal adults. In Endotext. MDText.com, Inc. https://www.ncbi.nlm.nih.gov/books/NBK279056/

Rahmani, J., Varkaneh, H. K., Clark, C., Zand, H., Bawadi, H., Ryan, P. M., Fatahi, S., & Zhang, Y. (2019). The influence of fasting and energy restricting diets on IGF-1 levels in humans: A systematic review and meta-analysis. Ageing Research Reviews, 53, 100910. https://doi.org/10.1016/j.arr.2019.100910

Sassin, J. F., Parker, D. C., Mace, J. W., Gotlin, R. W., Johnson, L. C., & Rossman, L. G. (1969). Human growth hormone release: Relation to slow-wave sleep and sleep-waking cycles. Science, 165(3892), 513–515. https://doi.org/10.1126/science.165.3892.513

U.S. Food and Drug Administration. (n.d.). Certain bulk drug substances for use in compounding that may present significant safety risks. Retrieved September 18, 2026, from https://www.fda.gov/drugs/human-drug-compounding/certain-bulk-drug-substances-use-compounding-may-present-significant-safety-risks

What is a normal IGF-1 level for your age?

There is no single normal IGF-1 level for everyone. Reference ranges vary with age and can also differ by sex, laboratory method, and assay. Levels are generally highest during adolescence and early adulthood, then decline with age. For that reason, results are interpreted against an age-adjusted laboratory range rather than one universal target.

Why does IGF-1 decline with age?

IGF-1 tends to decline as people get older because growth hormone secretion also decreases with age. Changes in sleep, body composition, sex hormones, liver responsiveness, and overall metabolic health may contribute as well. This gradual reduction is part of normal aging, which is why a lower value in an older adult is not automatically considered abnormal.

Do IGF-1 supplements actually work?

Products marketed as “IGF-1 supplements” are not the same as medically prescribed growth hormone or experimental peptides. Nutrients such as protein, zinc, and certain amino acids support normal hormone physiology when intake is inadequate, but taking more than the body needs does not reliably raise IGF-1. Claims that an over-the-counter supplement can meaningfully increase levels should therefore be viewed cautiously.

Can you have low IGF-1 without growth hormone deficiency?

Yes. Low IGF-1 can occur for reasons other than growth hormone deficiency, including inadequate calorie or protein intake, liver disease, poorly controlled diabetes, thyroid disorders, and other metabolic conditions. Because several factors influence the GH–IGF-1 axis, a low result by itself is not enough to diagnose a problem with growth hormone production.

Can IGF-1 levels change quickly?

IGF-1 is generally more stable than growth hormone, which can rise and fall sharply throughout the day in response to sleep, exercise, fasting, and other stimuli. Circulating IGF-1 changes more gradually because it reflects downstream production and is largely carried by binding proteins. That is one reason it is often used to assess longer-term GH activity rather than short-term hormone pulses.

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