Cracking the Aging Code

October 10, 2016
Mitteldorf, a theoretical biologist, and Sagan, a science writer (and the son of science educators Carl Sagan and Lynn Margulis), argue that genes are programmed to promote their own long-term survival as well as to die for group survival and population stability. The existence of cellular death programs could be seen as supporting the group selection theory of evolution, in addition to the far more accepted kin selection theory. Yet this notion is far from proven. The authors’ contention that caloric restriction can lead to prolonged life is widely accepted, but the same is not true of their assertion that predators control their own numbers so they won’t overwhelm their prey. Furthermore, too many unsupported statements erode the reader’s confidence in the authors’ thesis. The book states that “people who are most prominent in telomere research tend to believe that telomerase will prove to be the philosopher’s stone, the fountain of youth, the elixir of Gilgamesh about which humanity has dreamed for thousands of years.” However, the authors identify neither those prominent people nor the research leading them to that ostensible belief. This is unquestionably a fun, provocative read, but it is marred by too much hyperbole and too little support. Agent: Gillian MacKenzie, Gillian MacKenzie Agency.

May 1, 2016
An advancement of the challenging theory that, along with growth and puberty, aging also unfolds "on a schedule programmed into the regulatory portion of our DNA."At first glance, this would appear to contradict "the fundamental premise of Darwinian evolution," survival of the fittest, the principle of natural selection epitomized by the "selfish gene," a term coined by Richard Dawkins in The Selfish Gene (1976). Theoretical biologist Mitteldorf and ecological philosopher Sagan (Cosmic Apprentice: Dispatches from the Edges of Science, 2013, etc.) make a convincing case for broadening the generally accepted neo-Darwinian framework, which incorporates the role of the genome in shaping the individual, to include species evolution and the relationship between individual survival and survival of the ecosystem on which it depends. They address the seeming paradox that "genes for aging have been fixed in the genome, despite the fact that these genes work against themselves." By limiting the reproductive potential of the aging individual, they play an important role in evolution. The authors contend that death and aging are crucial to the existence of "stable ecosystems in nature." Without them, unchecked reproduction would lead to major extinction events and the destruction of ecosystems. Mitteldorf and Sagan suggest that aging and death have evolved to moderate what might otherwise be untrammeled reproduction by predators, leading to the destruction of their prey and their own extinction. Natural selection operates to create a balance between longer life expectancy and greater fertility. Death and aging play a necessary role by regulating population growth in order to create the space for "populations of living things to evolve rapidly and efficiently." This leads the authors to the provocative conclusion that if we accept the goal of increasing longevity and the long-term survival of the human species, we must also accept the idea of zero population growth. A thoughtful examination of the role of aging and death in supporting life.

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May 1, 2016

Mitteldorf (Ctr. for Connected Learning, Northwestern Univ.) and Sagan (Cosmic Apprentice; Death and Sex) assert that aging, which is preprogrammed at the cellular level, provides ecosystems with stability and survival. They detail aging's molecular mechanisms and origins in protozoans, from which multicellular life descends. The authors also demonstrate the shortcomings of other aging theories. Their theory that aging results in population stability is plausible but needs more research. However, Mitteldorf and Sagan do not explain how aging works alongside coevolution and infant mortality or its place in ecosystems with boom-bust cycles. And the authors never tackle the arguments against life extension nor seriously consider competing funding priorities or extended lifetimes with depleted savings. They anticipate unlocking cellular telomerase to reverse senescence without mentioning that cells regulate this enzyme's production with multiple triggers because it runs amok in tumors. Maxine Weinstein and Meredith Lane's Sociality, Hierarchy, Health is a current, scholarly alternative; Sonia Arrison's 100 Plus tackles longevity, while David Stipp's The Youth Pill covers life extension. VERDICT Despite some flaws, this accessible science is the first worthwhile popular book on the evolution and biology of aging in years.--Eileen H. Kramer, Georgia Perimeter Coll. Lib., Clarkston

Copyright 2016 Library Journal, LLC Used with permission.

May 15, 2016
Evolution and ecology have inscribed a death sentence in our genes. And while that proclamation portends bad news for individuals, aging and a programmed span of life stabilize the ecosystem by smoothing out the death rate, providing an opportunity for the next generation to mature, and encouraging population diversity. Theoretical biologist Mitteldorf and writer Sagan (Dazzle Gradually, 2007) explain how aging has evolved as part of nature's four-billion-year construction kit and is controlled by our genes. For proof, they cite research in which the life span of a simple organism is extended by knocking out specific genes. A dash of Dorian Gray, royal jelly (which suspends the aging of queen bees), and trees that survive thousands of years enliven the discussion, along with hormesis, the noteworthy concept that a life span can be lengthened by moderate stress. Calorie restriction, exercise, and even exposure to low doses of radiation appear to impede aging. Suggestions for adding years to one's life are included, but the authors eagerly await imminent advances in telomerase activation, stem-cell therapy, and epigenetics that promise much greater gains.(Reprinted with permission of Booklist, copyright 2016, American Library Association.)