Hope I Die When I’m Really Old

Hope I Die When I’m Really Old

New Discovery Make Sense of Long Life Spans in Genesis 5 and 11

The other day I was shopping in the used CD section of my favorite local independent record store and I came across a compendium of songs by The Who.

Perhaps the one song most closely identified with this particular quartet of British rockers is “My Generation.” The song became an anthem for the rebellious British youth of the 1960s, decrying the older generation with the familiar chorus, “Hope I die before I get old.”

Now that I’m part of the older generation I can’t help thinking about the irony of the lyrics whenever I listen to this song. I hope I die when I’m really old. Amazingly, advances in the biology and the biochemistry of aging continue to make my hope a distinct possibility. And not only do these breakthroughs hold the promise for extending human life expectancy, they also provide a response to one of the greatest difficulties that skeptics have with the early chapters of Genesis: the long life spans of the patriarchs.

In the past decade or so, biomedical researchers have made significant progress toward comprehending aging. Scientists have identified a number of distinct biochemical mechanisms that play a role in senescence (aging). In most cases, when researchers subtly manipulate these processes, they can dramatically increase the life expectancy of model laboratory organisms, such as fruit flies, nematodes (worms), yeast, and mice. (See Who Was Adam? for a detailed description of some of these advances.)

Caloric Restriction

Scientists have discovered that caloric restriction extends life span. Reducing food intake by 30 to 70% can extend life expectancy by up to 40% for a wide range of organisms from yeast to mammals—assuming a nutritious diet. In humans, long-term calorie restriction reduces the risk of atherosclerosis.

Biochemists now have some understanding of how caloric restriction works. It appears that reduced intake of calories increases the activity of enzymes called sirtuins. This family of enzymes occurs in a wide range of organisms, including humans. Sirtuins become active inside the cell when the levels of nicotinamide adenine dinucleotide (NAD+) increase. The amount of this compound in the cell varies in response to the cell’s energy status. When in an energy-rich state, NAD+ levels fall off. When in an energy-poor state, NAD+ levels rise. Caloric restriction causes the cell to enter into an energy-poor state and, hence, ups the NAD+ levels and the sirtuin activity.

When sirtuins are active, genes become “turned off” or silenced. This presumably limits the “wear-and-tear” on DNA that normally takes place during the normal course of metabolism. The result is a delay in the aging process. Researchers note that when they inhibit sirtuin activity, the cell displays a biochemical profile that resembles those changes that take place during senescence.

Scientists have begun to manipulate sirtuin activity in an attempt to lengthen the life expectancy of model laboratory organisms. For example, investigators observe that when they add an additional sirtuin gene to yeast and nematodes, it extends their lifespan. Recently, a team of pharmacologists discovered a number of compounds that activate sirtuins in yeast and mimic the benefits of caloric restriction. One of the most potent, resveratrol, is found in red wine. When administered to yeast, this compound increases life expectancy by 70%! Follow-up studies demonstrated similar benefits for nematodes and fruit flies. Researchers have also extended the life span of mice that were fed high-fat diets by including resveratrol in their daily regime.

A new study extends our understanding of the impact of resveratrol action. Researchers fed three groups of mice different diets. One group received a control diet, one included low doses of resveratrol, and one a calorie-restricted diet. They evaluated the effects of these diets by monitoring gene expression profiles for the entire genome in a number of tissues. The team observed that the gene expression profiles for brain, cardiac, and skeletal muscles of mice that were fed resveratrol and a calorie-restricted diet overlapped. They also noted that both types of diets prevented changes in gene expression profiles associated with aging. They also noted that resveratrol feeding and reduced calories didn’t show age-related losses in cardiac function. This study provides the most comprehensive work to date documenting the positive effects of resveratrol in mammals, and opens the way for similar studies in humans.

This and other discoveries clearly indicate that aging results from rather subtle changes in cellular chemistry. (In this case, altering the activity level of sirtuins retards aging.) These changes are so slight that investigators studying the aging phenomenon are gaining hope and confidence that, in the near future, they will be able to partly interrupt the aging process by direct intervention through altered diet, drug treatment, and gene manipulation. It is not out of the question to extend human life expectancy to several hundred years—about the length of time the Bible claims that the patriarchs lived.

Biochemists’ success in altering the life span of model organisms in the laboratory and the encroaching ability to increase human life expectancy through biochemical manipulation makes the long life spans in Genesis 5 and 11 scientifically plausible. If humans can alter life spans, how much easier must it be for God to do so?

Varying sirtuin activity represents one possible method that God could have used to permit early humans to live several hundred years at the time of their creation, and then subtly adjust it to shorten life spans to no more than 120 years after the Flood event.

I may be singing along to “My Generation” for a long time.

Back to the used CD bins. Maybe I’ll find a Janis Joplin album. “Lord won’t you buy me a Mercedes Benz?”