LETTERS TO THE EDITORS
To the Editors:
I read the article "Aging: A Biological Perspective" by Robert Arking (November–December) with interest.
At one point, in a side comment, he says: "Nevertheless, people should mistrust the nonscientific claims and blarney put out by the present antiaging industry. For example, at least 250,000 Web sites sell human growth hormone [HGH], and many tout it as a cure for aging . . . . In the original study behind antiaging claims for growth hormone [not cited], a dozen men showed positive effects at first, but then suffered deleterious side effects that cancelled the study."
Of studies of HGH in humans, I am aware of an early one, by D. Rudman et al. in the New England Journal of Medicine. No human study can assess the effect of any drug on human lifespan in a short time; however, there is also a study in mice. They gave the mice injections of HGH; their experiment shows that their mice quite clearly lived significantly longer on these injections, even though they had to stop their experiment for four weeks and finally stopped it entirely after 23 weeks due to the cost of HGH.
No animal experiment can truly substitute for a long-term experiment in human beings. Moreover, many Web sites do sell a substitute for HGH that apparently can be taken by mouth, currently an unlikely route. However, for animal experiments justifying use of IG F-1 inhibitors, Arking cites in his article only experiments with fruit flies. It seems unlikely that the metabolism of fruit flies will be closer to that of human beings than that of mice. Even for unfavorable effects in human subjects, one author (Rudman, in a subsequent paper) points out that reducing the dose of HGH resolved these problems.
To dismiss this work as simple blarney seems extreme. Moreover, HGH has successful experiments with mammals to support it, while Arking has not provided any lifespan study with healthy mammals of any kind, only with fruit flies. What’s happening here looks to me much more like a problem to be resolved than “simple blarney.” Nor is there any obvious contradiction between the effects of HGH and IGF-1.
To the Editors:
Robert Arking's stimulating article perpetuates a common misinterpretation of life expectancy. When unqualified by a specified age, such as zero or 45 years, life expectancy is shorthand for the average number of years a newborn can be projected to live assuming a constant mortality regime from the time of birth. While Figure 2 indicates that the author comprehends life expectancy, this understanding is regrettably not reflected in the text.
The source of human population life expectancies is the current life table, an actuarial and demographic tool that utilizes cross-sectional, annualized fertility and age-specific mortality data. Revisiting an example in the article, it was a white American female newborn, not the average white American female, that had a life expectancy of 48 years in 1900.
West Virginia University
Dr. Arking replies:
In science, as in life, the truth lies in the details. The insulin-like signaling pathway (ISP) is a longevity-regulating mechanism found in all organisms, as I wrote in the article. Do not deride flies—the evolutionary conservation of a particular process in all species assayed and over approximately 500 million years of evolution bespeaks the existence of a fundamentally important mechanism. However, the only article I specifically cited is the one by Holzenberger et al., which was done with mice.
That article is important for two reasons: First, it provides the proof of concept for the role of IGF-1 on longevity; second, reading that article would lead one to a substantial amount of work done with mutant mice having genetic deficiencies of growth hormone (GH) secretion (which leads to low IGF-1 levels as well), as well as to mice whose GH-receptor gene was deliberately knocked out. These “GHR-KO” mice have a 50 percent reduction in their effective growth hormone levels and live long, a fact consistent with the idea that high GH levels are not associated with extended longevity.
There is a fair amount of information in the primary literature pointing out the dangers associated with high levels of exogenous GH intake. All these experiments were also costly to do, but their data have meaning because the experiments were in fact completed. Data from incomplete experiments may or may not have useful clues, but to maintain that one incomplete experiment has more scientific value than a number of independent experiments using different approaches on mice and rats and flies and worms sounds to me more like cognitive dissonance (that is, a maintenance of opinion in opposition to the facts) than a scientific conclusion. I mean no disrespect, but I will stand by my words.
I agree that it would have been best had I used the correct terminology by including the word "newborns" in the text as well as in the figure. As for the insurance companies, perhaps the interventions alluded to in the article will once again decrease the magnitude of the constant mortality regime in the future and thus allow both people and businesses to "live long and prosper," for another while at least.