As I mentioned yesterday, the biology of aging, the actual dance of proteins and mechanisms and environment that progressively kills us, is enormously complex in its progression from day to day and year to year. Decades and billions of dollars have only scratched the surface, even in this age of rapidly advancing biotechnology. Researchers have focused on a handful of starting point proteins and their roles and are making painstaking inroads into greater understanding, year by year, but we stand a very long way from being able to use modern medicine safely and effectively adjust the operation of metabolism to slow aging - because that would require reproducing or at least understanding a fair fraction of the great complexity of the ongoing dance. Exercise and calorie restriction remain by far the best presently available options if slowing aging is your goal, and I don't expect to see them greatly improved on for a good fifteen to twenty years yet.
Fortunately there is an entirely different and much better path towards lengthening healthy life, which is to identify and repair the forms of cellular and molecular damage that cause aging. Researchers know what these forms of damage are because comparing the detailed structure of old and young tissue has been well within our capabilities for several decades. Remove all the differences between old flesh and young flesh and old cells and young cells and what you have is young flesh and young cells: a process of rejuvenation by biochemical repair. The old could be restored to youthful health and function, and young never become damaged by age. The big deal about this approach is that (a) we know very well how to go about building treatments to do it, and (b) it doesn't require any further understanding of how aging actually happens at the detail level. We know enough now.
But I'm not talking about that today. Today is a return to one of the proteins under investigation by researchers whose primary goal is understanding, and whose slowly growing secondary goal is to try to build some sort of treatment to slow aging that looks enough like a drug to be palatable to the FDA - where the bureaucrats don't accept treatment of aging as a valid activity and will not presently approve any sort of approach to lengthening life through tackling the aging process itself. That is well known and echoes all the way back down the funding chain from commercial development to primary research. What this means in practice is that it is much harder to try to build a great way of preventing age-related disease by tackling aging than it is to try to build yet another mediocre advance in patching over the consequences of age-related disease after the fact. It's a messed-up world that we live in.
The protein of interest is IGF-1, long known to be involved in a range of mechanisms of interest to aging. As for most such culprit proteins it has many roles, as evolution likes reuse. The picture is very complex and challenging to pick apart into its component pieces, but here is a representative human study in which researchers identify a correlation between IGF-1 levels and remaining life expectancy in the elderly. As for most such things it isn't a straightforward correlation, however, and in this case it exists for women only.
Individuals with exceptional longevity comprise an advantageous group for the study of mechanisms that promote healthy aging, as many of them have delayed onset or have been spared from age-related diseases. Diminished IGF-1 signaling may be one such mechanism. Our group showed that a functional mutation in the IGF-1 receptor, which confers partial IGF-1 resistance, was more prevalent in centenarians, as compared to controls without familial longevity. Based on these observations in humans and other species, we hypothesized that lower IGF-1 levels are predictive of extended survival in generally healthy nonagenarians.
We tested the hypothesis that IGF-1 levels in nonagenarians (n = 184), measured at study enrollment, predict the duration of their incremental survival. In the Kaplan-Meier analysis, females with IGF-1 levels below the median had significantly longer survival compared with females with levels above the median. However, this survival advantage was not observed in males.
If you look back in the Fight Aging! archives you'll find a paper showing a correlation between high IGF-1 and increased survival in old men:
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.
But in general, yes, the bulk of animal studies on IGF-1 lean the other way: less is better. Still, is this simple, clear, and well understood? No, of course not. Don't hold your breath waiting for ways to significantly extend life to emerge from this field - most of the participants are not interested in that outcome, and even if they were this is an expensive, long, confusing road to the poor end result of merely slowing aging, not reversing it.