American Scientist

A Means to an End: The Biological Basis of Aging and Death. William R. Clark. 240 pp. Oxford University Press, 1999. $27.50.

Aging and death have fascinated and frightened humanity at least since the inception of recorded history. Very, very recently, however, science has offered a glimmer of hope that we might truly understand—and possibly control—aging.

Most modern gerontologists know too well that despite remarkable recent insights into the genetic and environmental bases of aging, controlling aging, much less reversing it, remains an elusive yet optimistic goal. We now understand that aging is complex, but probably not so complex as to be intractable and that evolutionary forces may constrain the extent to which we can control or reverse aging. The lay public, unfortunately, is largely unaware of the complexities of many biological processes, especially aging. Consequently, they are vulnerable to claims by pop cultists and commercial enterprises that aging can be reversed and life span extended to mammoth extents and by simple interventions.

There is a real need for books that can educate the pubic about complex biological processes and present the promise of modern aging research with all the hope that drives contemporary gerontologists—and with all the caveats and unknowns that temper their optimism. In this respect, A Means to an End is largely a success. Much to his credit, the author does not shy away from biological complexity. He clearly and concisely explains basic facts and concepts so that complexities can be understood and appreciated. Occasionally he errs on the side of oversimplification and assumes a bit too much. But the final product is, in all, an illuminating and honest description of the biology and genetics of how and why we age.

One of the major strengths of this book is that it doesn't promise anything. Rather, it simply explains what is known about certain processes thought to be important determinants of aging. This attribute may discourage the reader in search of a simple answer to the problem of aging. But it should encourage the reader in search of candid insights on the struggles and challenges of modern biological research and on the possibilities and limits it offers for retarding aging and extending life.

There are two main weaknesses in this book.

First, it emphasizes cellular replicative senescence, the process that limits the number of cell divisions. It is an important hypothetical cause of aging but one that remains unproven. Moreover, it assumes that replicative senescence is causally linked to aging but offers nothing about why it should contribute to the decline in tissue function and integrity and cancer, all hallmarks of aging. There are ideas out there, but they are not discussed. Moreover, some ideas are largely ignored, although they could be tied, in theory, to replicative senescence.

Second, gene action is sometimes described in confusing or misleading ways. Early on, there should have been a clear definition of genes, mutations and polymorphisms, or minor variations in the DNA sequence. This would have avoided confusion about the nature of aging "genes" that occurs sporadically throughout the book. For example, WRN, the gene defective in the premature–aging Werner syndrome, is referred to as a potential human senescence effector gene when, in fact, it is a senescence resistor gene.

Who should read this book? Those curious about the promise and limits of modern gerontological research who do not need or want oversimplified or unrealistic promises. These readers, if inclined to really think about the problem, will likely find some of the contents lacking but will gain a very good introduction into the problem of aging and the basic biological processes that govern it.—Judith Campisi, Cell and Molecular Biology, Lawrence Berkeley National Laboratory