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AIs, Superflies, and the Path to Immortality

Interpretation of genetic data from fruit flies bred for longevity suggests the major culprit [behind poor health, disease and limited healthspan] may not be accumulated damage, or any particular mechanism, but rather the intersection of biological complexity with evolutionary adaptation
By Ben Goertzel
August 10, 2010

Excerpt from the August 10, 2010 H+ Magazine Editor’s Blog H+ Magazine (published online August 12, 2010)

Photo: michael*
Drosophila Melanogaster Photo: michael*

. . . Genescient’s . . . Chief Scientist (and professor at the University of California at Irvine), the evolutionary geneticist Michael Rose, advocates a perspective that takes biological complexity even more seriously. Like de Grey, he views health at a systems level, rather than looking for a single core mechanism underlying aging. But he doubts whether accumulated damage is the critical factor we should be examining.

Rose likes to highlight results showing that, after a certain age has passed, an organism’s death rate (its odds of dying during a given year) stop increasing. During this “late life” period, in a fundamental sense, the organism’s health may not be wonderful, but it’s not getting any worse. Of course, some body systems like human teeth might keep degenerating even during late life, but the point is that the apparent existence of a “late life” period with a constant (or near constant) death rate argues against the notion that accumulating damage gradually kills an old organism off.

In Rose’s view, as organisms evolve different genetic mutations arise to adapt the organism’s functionality at different stages of its life. But genes (considered as biological actors, not just sequences of amino acids) are complicated things. Each gene may carry out multiple functions, and in each of these functions, it’s subtly interlinked with other genes. So various adaptations, focused on different stages of life, may interfere with each other in complex ways — an instance of a phenomenon known in genetics lingo as “antagonistic pleiotropy.” And antagonistic pleiotropy causes the organism all sorts of problems. The more different life-stages worth of adaptations get piled on top of each other, the more confusion occurs in the body’s various interlocking systems, causing the problems we all experience as we age. When an organism gets old enough, it reaches an age for which there hasn’t yet been much evolutionary adaptation in its history. Few organisms in its species have lived that long, so the genes of the species haven’t adapted much to the requirements of life at that age. ‘

For instance, not many people have lived to age 100, so the human genome has not adapted much to the particular requirements of life at age 100. Because of this, the human body at age 100 doesn’t have a lot of new problems due to conflicting adaptations, beyond the problems already present in the body at age 90. On the other hand, many people have lived to age 50, and 40, and 30, etc. So a 50 year old human’s body is full of adaptations specialized to improve life at age 50, along with some specialized to improve life at age 40, and some specialized to improve life at age 30, etc. These different adaptations, specialized to improve life at different ages, often conflict with each other (e.g. because the same gene often serves multiple functions and plays roles in multiple networks), creating problems for the 50 year old, including many of the phenomena we describe as “aging.” In other words, at a certain age (somewhere between 50 and 100 years for humans), the problems experienced earlier in life stop compounding, and the death rate levels off.

If this is correct, then accumulated damage of the sort SENS seeks to address isn’t exactly irrelevant, but it no longer assumes a central role. Some accumulated damage may continue into late life, but it’s not a star in the drama of mortality. Rather, it is a bit player at best . . .

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