IGF-1 (insulin-like growth factor 1) is a hormone that plays a central role in growth, tissue repair, and metabolism throughout your life. It’s a small protein made up of 70 amino acids, produced mainly by the liver in response to growth hormone. Sometimes called somatomedin C on lab reports, IGF-1 acts as the primary messenger that carries out many of growth hormone’s effects on your body.
How Your Body Makes IGF-1
The process starts in your brain. The hypothalamus releases a signal called growth hormone-releasing hormone, which tells the pituitary gland to secrete growth hormone into your bloodstream. Growth hormone then travels to the liver, where it binds to receptors and triggers IGF-1 production. The liver is the largest source, releasing IGF-1 into the blood so it can reach tissues throughout the body. But other tissues, including cartilage and muscle, also produce smaller amounts of IGF-1 locally.
This system has a built-in thermostat. When IGF-1 levels rise high enough, the hormone signals back to the pituitary gland to slow down growth hormone release. This negative feedback loop keeps both hormones in a functional range. Other signals, including the hunger hormones leptin and ghrelin, also fine-tune growth hormone secretion.
What IGF-1 Does in Your Body
IGF-1’s structure is nearly identical to insulin, sharing about 50% of the same amino acid sequence. That similarity lets it interact with insulin receptors, which is why it influences blood sugar in addition to growth. IGF-1 increases glucose uptake in your muscles and other peripheral tissues while reducing glucose production by the liver, both of which improve insulin sensitivity.
Beyond metabolism, IGF-1 drives several core biological processes:
- Bone growth and maintenance. Animal studies show that completely removing the IGF-1 gene leads to shortened bones, increased cartilage cell death, and a 25% reduction in cortical bone size.
- Muscle development. IGF-1 triggers muscle growth by activating satellite cells, the stem cells responsible for repairing and building muscle fibers.
- Nervous system support. IGF-1 promotes nerve sprouting and protects against nerve degeneration, giving it a role in brain health and injury recovery.
These functions are especially important during childhood and adolescence, when rapid growth demands high IGF-1 activity. But the hormone remains active in adults, contributing to tissue maintenance, wound healing, and metabolic regulation.
Normal IGF-1 Levels by Age
IGF-1 peaks in your 20s and declines steadily with age. Levels are measured in nanograms per milliliter (ng/mL) through a simple blood test. Here’s what typical median values look like across adulthood, based on population reference data:
- Ages 21–25: around 265 ng/mL (normal range roughly 158–416)
- Ages 31–35: around 183 ng/mL (range roughly 102–281)
- Ages 41–45: around 148 ng/mL (range roughly 72–237)
- Ages 51–55: around 130 ng/mL (range roughly 72–219)
- Ages 61–65: around 130 ng/mL (range roughly 61–199)
- Ages 76–80: around 109 ng/mL (range roughly 62–211)
These ranges are wide because IGF-1 varies with genetics, nutrition, body composition, and the specific lab assay used. Your doctor will compare your result to age- and sex-matched reference ranges from the testing manufacturer rather than a single universal cutoff.
What Happens When IGF-1 Is Too Low
The most dramatic example of IGF-1 deficiency is Laron syndrome, a genetic condition where the body cannot respond to growth hormone. Children with Laron syndrome are slightly shorter at birth (42–47 cm compared to the typical 49–52 cm) and grow at roughly half the normal rate in early childhood. They develop small organs, weak muscles that delay walking, thin bones prone to breakdown, delayed puberty by three to seven years, and impaired skin, hair, and nail growth.
In adults, low IGF-1 most commonly results from liver disease, since the liver is the primary production site. People with liver cirrhosis show markedly reduced IGF-1 even in early stages, and the hormone is used as an indicator of how well the liver is functioning. Aging itself also causes a natural decline in IGF-1 secretion, contributing to loss of muscle mass, increased body fat, reduced bone density, lower energy, and changes in mood and quality of life.
Severe caloric restriction or malnutrition can also suppress IGF-1. Research on military personnel during simulated field operations found that restricted energy intake combined with weight loss led to measurable drops in IGF-1 concentration.
What Happens When IGF-1 Is Too High
Persistently elevated IGF-1 is the hallmark of acromegaly, a condition usually caused by a benign tumor on the pituitary gland that overproduces growth hormone. Diagnosis involves confirming that IGF-1 is above the age- and sex-appropriate upper limit of normal. Acromegaly causes gradual enlargement of the hands, feet, and facial features, along with joint pain, fatigue, and organ enlargement.
The more concerning long-term risk of excess IGF-1 is cancer. A study of 598 acromegaly patients in New York City found that cumulative exposure to elevated IGF-1 over time was a significant predictor of cancer development. The standardized incidence ratios were notably elevated for thyroid cancer (6.87 times the expected rate), colorectal cancer (2.65 times), and breast cancer (1.67 times). There were also trends toward increased kidney and prostate cancer risk. Importantly, bringing IGF-1 levels back to normal through treatment returned mortality risk to expected levels.
IGF-1 and Longevity
Here’s where IGF-1 gets counterintuitive. While you need adequate IGF-1 for health, having naturally lower levels within the normal range appears to favor a longer life. Research on the children of centenarians (people who lived past 100) found that these offspring had significantly lower IGF-1 bioactivity compared to age-matched controls whose parents had typical lifespans. This wasn’t explained by differences in age, weight, or height. The pattern also showed familial aggregation, meaning IGF-1 bioactivity in centenarians correlated with that of their children, suggesting a genetic component.
Certain genetic variants in the IGF-1 receptor gene are also overrepresented among long-lived individuals. People carrying these variants tend to have lower levels of free IGF-1 in their blood. The takeaway isn’t that less IGF-1 is always better. Rather, the body seems to benefit from a moderate, well-regulated level: enough to maintain tissues and metabolism, but not so much that it accelerates cell growth unchecked.
How Diet and Exercise Affect IGF-1
Protein intake is the strongest dietary lever for IGF-1. Studies show that IGF-1 rises linearly with protein dose over consecutive days of high-protein eating. In one controlled experiment, a single high-protein meal didn’t change IGF-1 within the first five hours, but by 24 hours, levels were 17.5% higher than baseline. This delayed response suggests IGF-1 shifts reflect your overall dietary pattern rather than individual meals.
Resistance training and sprinting both cause a quick spike in IGF-1 immediately after exercise. In one study, free IGF-1 was significantly elevated right after a resistance workout. However, this bump is short-lived. By the next morning, levels had returned to baseline. So a single workout transiently raises IGF-1, but the lasting effects on the hormone likely come from consistent training over weeks and months rather than any one session.
One unexpected finding: combining protein intake with resistance exercise in the same session did not raise IGF-1 at all, not acutely or at 24 hours. The reasons aren’t fully understood, but it suggests the two stimuli may interfere with each other’s signaling rather than stacking their effects. Caloric restriction, on the other hand, reliably lowers IGF-1, which may partly explain why fasting and reduced calorie intake are linked to markers of slower aging in some research.