Insulin-like growth factor 1 (IGF-1) has long been recognized for its role in growth, development, and tissue repair. But as science evolves, so does the conversation—especially when it comes to aging and lifespan. Mounting evidence suggests that while IGF-1 is essential for regeneration and recovery, chronically high levels may accelerate aging and increase the risk of chronic disease, including cancer.
Researchers are now asking: Could less IGF-1 be the key to living longer?
IGF-1 is a powerful anabolic hormone. It promotes cell growth, supports tissue healing, and plays a central role in metabolic balance. However, this same potency can be a liability. Elevated IGF-1 has been linked to increased cellular proliferation and reduced apoptosis, two hallmarks of cancer progression. As such, it has emerged as a possible risk factor in age-related diseases, including breast, prostate, and colorectal cancers.
In the context of aging, it appears that higher isn’t always better. Both animal and human studies suggest an inverse relationship between IGF-1 activity and lifespan—particularly when IGF-1 remains elevated over time.
"For individuals aged 50–65, consuming a high-protein diet was linked to a 75% higher overall mortality rate and a fourfold increase in cancer-related deaths over 18 years. Each 10 ng/mL rise in IGF-I levels increased cancer mortality risk by an additional 9% in the high-protein group compared to those with lower intake." - IGF-I and the endocrinology of aging, https://doi.org/10.1016/j.coemr.2018.11.001
In species ranging from worms to rodents, downregulating the insulin/IGF-1 pathway has been shown to extend lifespan and enhance metabolic resilience. These organisms often display delayed aging, improved stress resistance, and fewer degenerative changes over time.
In mice, lower IGF-1 activity has been associated with longer life and reduced incidence of age-related disease. These findings suggest that IGF-1 is more than a growth factor—it’s a regulator of biological pace.
What about people?
Studies of long-lived human populations—particularly those with familial longevity—reveal a similar trend. Many exhibit mild insulin resistance and lower IGF-1 bioactivity, particularly in midlife. This pattern may support healthy aging by slowing tissue turnover and minimizing DNA damage.
Interestingly, this doesn’t reflect a state of deficiency. It reflects metabolic adaptation—the body maintaining enough IGF-1 to repair tissue while avoiding levels that may fuel overgrowth.
"Humans with more stable circulating IGF-I levels over time show better survival. Changes in IGF-I levels over time within an individual may provide more insight into its relevance for lifespan than a single baseline measurement"
- IGF-I and the endocrinology of aging, https://doi.org/10.1016/j.coemr.2018.11.001