The Problem with Linear Projections of the Future

By Sally Morem

While rummaging through an old file folder stuffed in a box, I stumbledupon a copy of Marvin Cetron and Owen Davies’ article on extended life-spans, originally published in

The Futurist

in April 1998. I was simplyastounded at how dated their scenarios seemed after a mere 11 years. Youmay be wondering why I’m responding to such an old article. Two reasons:I’d like to address the reason why this kind of thinking, “The future thatnever was and never could be,” seems to crop up so often in science fictionand futurism. And I’d like to suggest some fixes.Cetron and Davies discussed at some length the discovery made by medicalresearchers that melatonin acted to slow down aging in mice. It seemed atthe time to be the key to solving the mystery of aging. This really rocked theworld of medicine in 1995. It seemed to cut through all the noise. Therewere at that point some 50 distinct theories on why we age. If melatonin proved to be the key to finding a technological fountain of youth, a lot of conceptual clutter could be cleared out of the medical profession.For instance, earlier researchers found that when rats are placed on severelyrestrictive diets (just above starvation level), they live almost twice as longas rats fed a normal diet. By 1995, doctors thought this might prove to bethe result of some subtle effect starvation has on melatonin levels. Agingaffects every aspect of our body, and it seemed nearly impossible to tellwhich changes were causes and which were effects.All research on mice and rats seemed merely to show how to slow downaging in those animals. But, they told researchers little about why rats, miceand humans age in the first place, and what factors in the treatments thatcause slowdown in aging actually caused the change, not to mention howthey do so.

Diet, exercise, vitamin pills, meditation, and so on turn out to have onlytemporary meliorative effects on aging. Every one of these treatments wasessentially an attempt to keep an old engine running with bailing wire andScotch tape. Partially effective in the short term, but in the long run, provingto be full-fledged failures. None of us it seems, at least as of 1995, wouldever “get out alive.” Death would eventually claim us all.We seemed no closer to an answer to the riddle than when W. Donner Denkla promoted his “death clock” theory of aging. He believed that ahormone worked by shutting down energy production processes in the cells.He found that by removing the pituitary glands from rats their rate of agingslowed down dramatically, and in some cases aging seemed to reverse, atleast for awhile. Near the end of their comparatively long lives, the rats (uptill then quite healthy) suddenly collapsed and died.The authors said that as of 1995, Denkla’s explanation appeared simplistic.Preventing any of the destructive changes in the body will stave off further decay, at least for a time. Okay. Fine. But why? Simply because thosechanges were somehow prevented from weakening the body, which prevented cascading further destruction. But again, why? Why would the pituitary, the source of growth hormone cause such havoc. And why, evenafter removing it, would the body still die after enjoying a longer thannormal lifespan?The authors correctly label Denkla’s “death hormone” as a secondary effectof a much deeper cause. And the starvation treatment of rats didn’t bring usany closer to answers.Cetron and Davies believed the root cause had finally been identified: thelack of melatonin in the adult body. They further believed that the answer lay in how melatonin worked in the body. Melatonin floods our organswhen we are young, and drops sharply when we hit our teens. It restrainssexual maturation till then. Is it the Never Never Land “won’t grow up”hormone? It helps us sleep (levels rise at night); it helps protect us fromdisease; it may govern aging itself. But perhaps, melatonin levels might begoverned by an even deeper cause.The pineal gland produces melatonin. When young glands weretransplanted into old mice, those mice that survived the operation lived theequivalent of the human life span of 125 years. But the mice still aged, even

though much more slowly than normal. They then died quite abruptly, in amanner similar to that described in Oliver Wendell Holmes’s poem, “TheOne Hoss Shay.” This fact suggested that there was indeed a still deeper cause of aging, something that all the studies of hormone levels, healthy or unhealthy lifestyle, and the activities of glands were glossing over.Whatever was going wrong, we can logically assume that it underlies everysingle symptom detected in the aging body.Clearly, researchers hadn’t dug deep enough. Cetron and Davies werewrong. Metatonin wasn’t

. Their article didn’t mention anything about thetelomeres, regions of repetitive nucleotides at the end of chromosomes that protect them from unraveling during cell division. When they get too short,cells no longer divide. After 50 divisions, the cell reaches the Hayflick limit.A major article on this discovery appeared in

Scientific American

in 1998,the very year Cetron and Davies wrote their article. I’m surprised theydidn’t mention it.The problems with Cetron and Davies’ article would be simple to fix if their assertions about the effects of melatonin had been updated to account for thetelomeres. But that’s the least of their problems. They riffed on all thisexcitement over melatonin, speculating on all the changes they wereexpecting in society in response to the development of some serious lifeextension technologies. And here’s the key problem:

They did so in a linear fashion

.It didn’t help when they said future generations

would have to devise new mechanisms for allocating society’s resources

. I knew when I read that line —as pure a representative statement of belief in zero-sum social games ascan be found anywhere—that Cetron and Davies were missing an even bigger trend: The massive enlargement of the set known to us today as“natural resources.”In order to show the real problem with linear projections, let’s sayresearchers discovered that the ultimate cause of all apparent causes of aging, and all the dreadful effects we experience, is so basic it can no longer be questioned. Perhaps it’s telomeres or something even deeper. Let’s saythe cause has been demonstrated fully. Let’s say all medical researchers aresatisfied that they’ve found

the

answer. Let’s state further that fixing the problem will prove to be relatively simple as treatment would merely consistof a basic mechanical process.