Integrative and Comparative Biology Advance Access originally published online on June 22, 2007
Integrative and Comparative Biology 2007 47(6):892-893; doi:10.1093/icb/icm068
| ||||||||||||||||||||||||||||||||||||||||||||||||
Book Review |
The Evolution of Death: Why We Are Living Longer. Stanley Shostak.
Department of Biological Science
Northern Illinois University
Correspondence: E-mail: neilb{at}niu.edu
The Evolution of Death: Why We Are Living Longer.Stanley Shostak.
SUNY series in Philosophy and Biology. Albany, NY: State University of New York, 2006. 246 pp. ISBN 0-7914-6946-8, $80.50.
Stanley Shostak has studied cnidarians such as Hydra for a number of years. Like many biologists who study these seemingly immortal animals, Shostak has thought more generally about aging and senescence. He elaborates on these themes in The Evolution of Death. The book is divided into two parts, Part I (four chapters), "How biology makes sense of death," and Part II (two chapters), "How death evolves and where it is heading." Overall, I would say that while the book begins inauspiciously in Part I, Shostak more than redeems himself in Part II.
Most biologists will find Chapter 1 of Part I somewhat frustrating. As described by Shostak (p. 5): "Chapter 1 emphasizes evolution as the principle that unifies death with life while dismissing some of the false clues that have misled scientists in their quest to make sense of death." Nevertheless, most biologists seem fairly comfortable with the notion that life history (including senescence) evolves. Indeed, Peter Medawar's "test tube" model of the evolution of senescence uses a compelling verbal model to effectively capture the basic notion—in a dangerous environment, there is little cost to senescence. Along with subsequent mathematical elaborations by a number of other workers, these models arguably represent some of the most successful predictive efforts of evolutionary biology. Shostak's position is thus difficult to understand. He does mention Medawar (p. 9), but does not clearly describe his model. He writes (p. 17): "The evolutionary biologist George William's ‘theory of antagonistic pleiotropy’ is a theory of genetic deception." The basis for these criticisms is not clearly articulated. For instance, in the chapter summary (p. 39) one sentence reads: "Chapter 1 has shown that life span, aging, and dying are not adapted to making room for variants, not determined by genes, not required by the environment, and not decreed by entropy." The passage then continues: "Death is shaped by life. Survivorship distributions illustrate the sensitivity of aging, dying, and death to both randomness—accidents and encounters with environmental hazards—and determinism—biologically built-in and genetic effectors." On one hand, Shostak seems to be rejecting the generally accepted evolutionary view of senescence, while on the other hand, much of his argument seems compatible with this view.
Chapters 2–4 are more clearly articulated, consisting of mostly background material on organismal aging and life cycle evolution. Shostak nicely connects the latter to underlying cellular processes, e.g., (p. 83): "... lifecycles move from germ cells capable of reprogramming to stem cells capable of proliferating and initiating the programs of precursor and transit cells, interacting with other tissue and with the external environment, and differentiating in tissues and organs. Mortality represents an end to these processes; negligible senescence and indefinite life span represent their continuation." Toward the end of Chapter 4, Shostak really begins to find his footing when discussing the cellular mechanisms of aging. For instance (p. 102), "... we suffer from aging and ‘natural death’ because we have run out of the normal replacement cells that previously maintained our body's working tissues." Shostak thus introduces (p. 103) the "cellular theory of aging" that will be the focus of Part II. While not an alternative to evolutionary theories of aging, this cellular theory does provide considerable mechanistic rigor that is lacking from some other discussions.
Part II picks up this theme with Chapter 5, titled "Putting cells in the picture." This chapter provides a comprehensive overview of the role of cells in development, maintenance, and regeneration. Shostak points out the limitations of viewing the activity of the enzyme telomerase as an arbiter of aging. Shostak then puts modern discussions of embryonic stem cells in the appropriate historical and biological context. While he recognizes that (p. 126) "Pluripotential cells ... would be enormously valuable for therapeutic purposes," he also points out the potential risks (p. 130): "One must also bear in mind that ES [embryonic stem] cells are first cousins of EC [embryonic carcinoma] cells that become metastatic, invasive, and destructive cancer cells in a dose-dependent way upon introduction to blastocysts, neonates, and adults."
In Chapter 6, "Neoteny and longevity," the central themes of the book—the evolution of human development and aging—come together. As the environment becomes permissive, humans may evolve longer lifespan via neoteny. Shostak argues persuasively that these changes will be based on (p. 141) "... instead of more cell divisions, the acquisition of more stem and cognate cells ...." He continues (p. 141): "The lynchpin connecting neoteny with an expanded life span would seem to be the embryonic addition of SR [self-renewing] cells to tissues, thus tipping the scale in favor of extended cellular replacement in adult organisms." Further, these stem cells have to come from somewhere (p. 142): "One embryonic compartment comes to mind as the most likely source of these somatic SR cells. In fact, it is the only compartment that could suffer a loss of cells without the organism paying too high an anatomical or physiological price—and that compartment is the normal source of primordial germ cells (PGCs)!"
Shostak outlines in some mechanistic detail how this reallocation of cells could occur and links it to declining fertility in human populations. In many ways, this is the most detailed and convincing argument I have seen for potential evolutionary increases in human life span. Some assumptions nevertheless remain, for instance that all human somatic cells (in particular those of the heart and brain) are replaceable, but the general ideas here are well worth considering. Overall, perhaps the best way to sum up the book in its entirety is that Shostak unnecessarily burdens an otherwise very interesting discussion with some unfounded criticism of evolutionary theory. In evolutionary terms, he has clearly identified a potential cellular basis for the trade-off between reproduction and somatic maintenance—the allocation of cells to different embryonic compartments. Certainly, these cellular mechanisms of development have some basis in the gene activity of component cells. This trade-off may thus exemplify the concept of antagonistic pleiotropy: activity of an allele that leads a cell to settle in one embryonic compartment precludes its settlement in another. In a dangerous environment, this trade-off can lead to early reproduction and rapid senescence, while in a more benign environment delayed reproduction and greater longevity can evolve. In either case, the underlying cellular mechanisms are important, and Shostak's clear discussion of these mechanisms is to be commended.
CiteULike 
Connotea 
Del.icio.us What's this?
| ||||||||||||||||||||||||||||||||||||||||||||||||