Insulin-like growth factor 1, IGF-1, is one of a number of items of great interest for the mainstream of gerontology, those researchers focused on the workings and manipulation of metabolism. It also remains an area of uncertainty at this time, with apparently contradictory results abounding:
it has become apparent that single gene mutations in the insulin and insulin-like growth-factor signalling pathways can lengthen lifespan in worms, flies and mice, implying evolutionary conservation of mechanisms. Importantly, this research has also shown that these mutations can keep the animals healthy and disease-free for longer and can alleviate specific ageing-related pathologies. These findings are striking in view of the negative effects that disruption of these signalling pathways can also produce. ... The underscored passage brings up an issue that we've discussed here previously: Why is it that IGF-I pathway mutations can confer long healthy lives on organisms, even though supplementation with IGF-I is often quite beneficial, and depletion of IGF-I is often bad for individual organ systems? Indeed, according to another recent study, low doses of IGF-I appear to protect the mitochondria in aging rodents - why then do completely IGF-I-deficient animals enjoy extended and healthy lives?
Adding more IGF-1 in an unmodified metabolism seems to be good, but modifying metabolism to completely remove it seems to be much better. To add to these results in animals, an improved testing methodology for humans shows that more IGF-1 activity is apparently better in the elderly:
Elderly men with higher activity of the hormone IGF-1 - or insulin-growth factor 1 - appear to have greater life expectancy and reduced cardiovascular risk
In this study, researchers evaluated 376 healthy elderly men between the ages of 73 and 94 years. A serum sample was taken from each subject at the beginning of the study and researchers were contacted about the status of the participants over a period of eight years.
Subjects with the lowest IGF-1 function had a significantly higher mortality rate than subjects with the highest IGF-1 bioactivity. These results were especially significant in individuals who have a high risk to die from cardiovascular complications.
These new findings come as a result of a new form of testing for IGF-bioactivity. Researchers in this study used a new method, a bioassay, to measure the function of IGF-1 in the blood. Compared to commonly used methods to measure IGF-1, the IGF-1 bioassay gives more information about the actual function (bioactivity) of circulating IGF-1 in the body.
What this doesn't tell us is whether IGF-1 activity is a cart or a horse in this correlation - cause, consequence, or a little of both? I suspect that levels of IGF-1 activity are greatly influenced by obesity, metabolic syndrome, diabetes, general aerobic fitness, risk of atherosclerosis, levels of oxidative stress, and other line items of biochemical damage and poor choice that correlate with a lowered life expectancy.
So eating yourself into an early grave and hoping to dig your way out with hormone supplementation is not the way to go, as always. Neither life nor your metabolism works that way.