How to Increase IGF-1: Practical Approaches for Health
Discover practical strategies to support IGF-1 levels through nutrition, exercise, sleep, and hormonal balance for overall health and well-being.
Discover practical strategies to support IGF-1 levels through nutrition, exercise, sleep, and hormonal balance for overall health and well-being.
Insulin-like growth factor 1 (IGF-1) plays a key role in growth, metabolism, and overall health. Optimizing IGF-1 levels can support muscle development, cognitive function, and recovery, but imbalances—either too high or too low—may have drawbacks.
Lifestyle factors such as diet, exercise, sleep, genetics, and hormone interactions influence IGF-1 production. Understanding these elements can help individuals make informed choices to optimize IGF-1 levels.
IGF-1 is primarily produced in the liver in response to growth hormone (GH) stimulation. This process is governed by the GH/IGF-1 axis, involving the hypothalamus, pituitary gland, and liver. When GH is secreted by the anterior pituitary, it binds to receptors on liver cells, triggering IGF-1 synthesis and release into circulation. IGF-1 then interacts with its receptor (IGF-1R) on target tissues, activating signaling pathways that influence cell growth, differentiation, and survival. These effects are mediated through the PI3K/Akt and MAPK pathways, which regulate tissue growth and metabolism.
Beyond systemic circulation, IGF-1 also functions locally in tissues such as muscle, bone, and the brain. In muscle, it promotes protein synthesis via the mTOR pathway, facilitating growth and repair. Studies in animal models show that IGF-1 overexpression leads to increased muscle mass and strength. In bone, IGF-1 stimulates osteoblast activity and collagen synthesis, contributing to bone density. Research in The Journal of Clinical Endocrinology & Metabolism has linked higher IGF-1 levels to greater bone mineral density.
IGF-1 also plays a role in metabolic regulation, particularly glucose and lipid metabolism. While structurally similar to insulin, IGF-1’s glucose-regulating effects are more tissue-specific. It enhances glucose uptake in skeletal muscle by upregulating GLUT4 translocation while reducing hepatic glucose production. A 2023 Diabetes Care meta-analysis found moderate IGF-1 levels were associated with improved insulin sensitivity. Additionally, IGF-1 promotes lipolysis in fat tissue and lipid oxidation in muscle, supporting energy balance.
In the brain, IGF-1 supports neuroprotection, synaptic plasticity, and myelination, which are particularly important in aging and neurodegenerative conditions. A 2024 Nature Aging study found higher IGF-1 levels correlated with better cognitive performance in older adults, likely due to its role in enhancing brain-derived neurotrophic factor (BDNF) expression.
Diet affects IGF-1 regulation by influencing GH secretion, insulin levels, and metabolic pathways. The balance of carbohydrates, proteins, and fats impacts IGF-1 production through mechanisms such as insulin signaling and amino acid availability.
Carbohydrates influence IGF-1 primarily through insulin secretion. Insulin enhances hepatic sensitivity to GH, promoting IGF-1 synthesis. A 2023 American Journal of Clinical Nutrition study found that diets with 50–60% of total energy from carbohydrates were associated with higher IGF-1 levels.
The type of carbohydrate matters. Diets high in refined sugars and processed carbohydrates may lead to insulin resistance, dampening IGF-1 signaling. In contrast, whole grains, legumes, and fiber-rich foods promote a stable insulin response, supporting IGF-1 production. Very low-carbohydrate diets, such as ketogenic diets, have been shown to reduce IGF-1 levels. A 2022 Cell Metabolism study reported a 20–30% decline in IGF-1 among individuals following a ketogenic diet for six weeks.
Protein intake significantly influences IGF-1 levels. Amino acids like leucine, arginine, and methionine stimulate GH release and provide substrates for IGF-1 synthesis. A 2023 Journal of Nutrition meta-analysis found that individuals consuming at least 1.2 grams of protein per kilogram of body weight per day had higher IGF-1 levels.
Animal-based proteins, particularly dairy, meat, and fish, have a stronger effect on IGF-1 than plant-based proteins due to their higher bioavailability of essential amino acids. Dairy, in particular, has been linked to elevated IGF-1 levels. A 2022 British Journal of Nutrition study found daily milk consumption increased IGF-1 concentrations by 10–15% over 12 weeks.
Fats influence IGF-1 through hormone signaling and metabolism. While total fat intake has a less direct impact, fat type plays a role. Saturated fats, found in animal products and tropical oils, have been linked to higher IGF-1 levels. A 2023 Lipids in Health and Disease study found that diets high in saturated fats were associated with an 8–12% increase in IGF-1.
Conversely, polyunsaturated fats (PUFAs), particularly omega-3 fatty acids from fish, flaxseeds, and walnuts, have been linked to lower IGF-1 levels. A 2022 Journal of Clinical Endocrinology & Metabolism trial found omega-3 supplementation reduced IGF-1 concentrations by 10% over 12 weeks. Monounsaturated fats, found in olive oil, avocados, and nuts, appear to have a neutral or slightly positive effect.
Exercise influences IGF-1 production, bioavailability, and effects, with variations based on intensity, duration, and training type. While acute exercise temporarily increases circulating IGF-1, long-term training adaptations vary.
Resistance training has a strong effect on IGF-1, particularly in muscle hypertrophy and repair. Mechanical tension and muscle fiber microdamage stimulate local IGF-1 expression, enhancing protein synthesis via the mTOR pathway. Compound movements like squats and deadlifts elicit robust IGF-1 responses due to high mechanical stress.
Moderate-intensity aerobic exercise maintains or slightly elevates IGF-1 levels, particularly with proper nutrition. However, prolonged endurance training, such as marathon running, can reduce IGF-1 due to energy deficits and increased cortisol. Balancing endurance training with recovery and nutrition helps sustain IGF-1.
High-intensity interval training (HIIT) combines resistance and endurance elements, promoting IGF-1 while improving insulin sensitivity. A Journal of Applied Physiology study found that HIIT three times per week increased IGF-1 levels by 15–20% over eight weeks.
Most GH secretion, which drives IGF-1 production, occurs during deep sleep. Slow-wave sleep (SWS) in the first half of the night is associated with the highest GH pulses. Disruptions in sleep duration or quality impair this process, leading to lower IGF-1 levels. A Journal of Clinical Endocrinology & Metabolism study found individuals sleeping fewer than six hours per night had significantly lower IGF-1 concentrations.
Sleep disorders such as sleep apnea, characterized by nocturnal awakenings and intermittent hypoxia, have been linked to reduced IGF-1 levels due to disrupted GH release and increased inflammation. Improving sleep quality through optimizing the sleep environment, reducing blue light exposure, and maintaining a consistent schedule supports IGF-1 production.
Genetics influence IGF-1 levels, with polymorphisms in genes related to the GH/IGF-1 axis affecting baseline concentrations and responsiveness to diet and exercise. A well-documented IGF1 gene variant involves a cytosine-adenine (CA) repeat polymorphism, where shorter repeats are linked to higher IGF-1 levels.
Variations in the growth hormone receptor (GHR) gene also impact IGF-1 synthesis. A common exon 3 deletion variant in GHR enhances GH sensitivity, leading to increased IGF-1 production. This variant is more prevalent among elite athletes, suggesting a genetic link to physical performance. Genome-wide association studies (GWAS) have also identified IGFBP-related loci affecting IGF-1 bioavailability.
IGF-1 regulation occurs within a network of hormonal interactions. GH is the primary driver, but insulin, thyroid hormones, and sex steroids also play roles. Insulin enhances hepatic IGF-1 production by increasing GH receptor expression on liver cells, linking metabolic status to IGF-1 availability.
Testosterone increases IGF-1 synthesis, contributing to muscle growth and recovery, while estrogen modulates IGFBP expression, influencing IGF-1 bioavailability. Thyroid hormones affect GH secretion and liver sensitivity to GH, with hypothyroidism often linked to lower IGF-1 levels. Maintaining overall endocrine balance is crucial for optimal IGF-1 function.