Adventure yes, breakthrough no

Originally published 26 January 1998

John Glen­n’s pro­posed return to space in Octo­ber at age 77 is pure grand­stand­ing on the part of NASA and the sen­a­tor. The osten­si­ble jus­ti­fi­ca­tion for the trip is a bit of a stretch: to study aging.

Thir­ty-six years after he became the first Amer­i­can to orbit Earth, Glenn says: “I want to con­tribute to learn­ing about the ‘whys’ of aging.”

It is cer­tain­ly true that both space flight and aging cause mus­cle dete­ri­o­ra­tion and sleep dis­tur­bances, but the pos­si­bil­i­ty that any sig­nif­i­cant sci­ence is going to be done on this 300-mile-high jun­ket is pret­ty slim.

One thinks of Lewis Car­rol­l’s verse:

"You are old, Father William," the young man said, "And your hair has become very white; And yet you incessantly stand on your head---Do you think, at your age, it is right?"

Well, why not? John Glenn is a true Amer­i­can hero, and if any­one deserves a Shut­tle free­bie, he does. But don’t hold your breath for a big break­through in gerontology.

Glen­n’s announce­ment coin­cid­ed with word from sci­en­tists at the Uni­ver­si­ty of Texas South­west­ern Med­ical School and the Geron Cor­po­ra­tion of Cal­i­for­nia of a real break­through in geron­tol­ogy. The researchers used a nat­ur­al enzyme, called telom­erase, to slow or halt the aging process in human cells.

They have appar­ent­ly found a way to evade the so-called “Hayflick lim­it,” named after the researcher Leonard Hayflick, who dis­cov­ered that human cells cul­tured in a test tube (repro­duc­ing them­selves by split­ting down the mid­dle) nor­mal­ly stop divid­ing and die after about 50 divi­sions. Jer­ry Shay, lead­ing researcher of the Texas group, says: “[Our] cells are now up over 100 pop­u­la­tion dou­blings and they show no evi­dence that they will slow down.”

Shay was appro­pri­ate­ly coy when talk­ing to the press: “We’re not say­ing that this will give peo­ple some­thing to make them live longer.” Nev­er­the­less, the stock price of Geron soared. News­pa­pers her­ald­ed a “foun­tain of youth.”

I hap­pened to be sit­ting in a restau­rant filled with folks on the gray side of 50 on the day the enzyme sto­ry broke, and it was on every­one’s lips. “Reverse aging!” some­one gushed, and a flur­ry of hands moved opti­misti­cal­ly to wrin­kled cheeks.

The sci­en­tif­ic study of aging has had its share of booms and busts, and any “foun­tain-of-youth” break­through should be tak­en with a heap­ing tea­spoon of salt. How­ev­er, this new work with telom­erase looks promising.

Of course, some aspects of aging may be caused by nor­mal wear and tear, and there is not much one can do about that. But evi­dence is grow­ing that many organ­isms, includ­ing humans, are genet­i­cal­ly pro­grammed to age and die, and that’s the sort of thing that appeals to the new breed of genet­ic engi­neers, who have devel­oped the skills to move genes about and turn them on and off.

The big ques­tion is why nat­ur­al selec­tion should have pro­duced genes that are so obvi­ous­ly dis­ad­van­ta­geous. If fit­ness is the goal of evo­lu­tion, then where do gray hair, wrin­kles, mus­cle dete­ri­o­ra­tion, and sleep­less nights come from? Not to men­tion death.

One answer may be the short lifes­pans of ani­mals in the wild. Exter­nal threats to life are nor­mal­ly so severe that few indi­vid­u­als live to old age. Genes that cause aging, what­ev­er their source, will not be strong­ly select­ed against.

For anoth­er thing, it can be dis­ad­van­ta­geous for a species if indi­vid­u­als live long past their peak breed­ing peri­ods, using up resources that could go to more sex­u­al­ly active mem­bers of the pop­u­la­tion. A rapid decline and death might be just the tick­et for breed­ers past their prime — at least as far as the group is concerned.

All of this is some­what spec­u­la­tive, and the sit­u­a­tion is prob­a­bly more com­pli­cat­ed than any­one sup­pos­es, but one thing seems utter­ly cer­tain from an evo­lu­tion­ary point of view: Repro­duc­tion and death are inseparable.

If you’re gonna be mak­ing babies, then some­one’s got­ta die to make room for them.

At one end of the equa­tion of repro­duc­tion and death is the brown mar­su­pi­al mouse of Aus­tralia, a shrew-like crea­ture that does it and dies with remark­able alacrity.

At the appro­pri­ate time of year, bio­log­i­cal clocks tell male mar­su­pi­al mice that it is time to mate. Hor­mones gush, not a now-and-then trick­le, as in humans, but a sud­den flood. Docile juve­niles, less than a year old, are turned into sex-crazed ado­les­cents. Their appetite for sex dis­places all oth­er con­cerns, includ­ing food, drink, groom­ing, sleep, and the avoid­ance of predators.

After a few fren­zied days of non-stop cop­u­la­tion, the hag­gard male mar­su­pi­al mice expire — every one of them! — hav­ing essen­tial­ly gone from youth to old age in a flash. Their work is done. The next gen­er­a­tion is assured. The females of the species can now man­age quite well with­out them, thank you.

At the oth­er end of the equa­tion are humans, who with increas­ing suc­cess — and the expen­di­ture of a hefty por­tion of our col­lec­tive resources — man­age to keep on kick­ing long past our peak repro­duc­tive years.

We latch enthu­si­as­ti­cal­ly onto every bit of news that promis­es even mar­gin­al delay of aging and death. We may not all get the chance to go into space at age 77, like the white-maned but still fit Glenn, but we’ll do our best to thwart the Hayflick lim­it if the gene engi­neers give us half a chance.