At the World Congress of Gerontology and Geriatrics later this week in Paris, amid sessions on Alzheimer’s disease, elderly care, and osteoporosis is a session provocatively titled “Ageing Is No Longer an Unsolved Biological Problem.” It’s organized by Leonard Hayflick, a professor of anatomy at the University of California, San Francisco.

In the 1960s, Hayflick discovered that human cells grown in a dish will multiply a finite number of times–a property now known as the Hayflick Limit. These cells later helped ignite the search for the cellular sources of aging, and Hayflick, a former president of the Gerontological Society of America, has since become well known for his skepticism toward claims that human longevity can be significantly lengthened through science.

Hayflick spoke with Technology Review about his theory for the biological causes of aging and explains why he thinks that research directed at the fundamental processes of aging will yield greater returns than studying diseases of aging, such as Alzheimer’s and cardiovascular disease.

Technology Review: What do you mean when you say “Aging is no longer an unsolved biological problem”?

Leonard Hayflick: What it means is precisely what it says. Several people in this field believe we do understand the biological cause of aging, which is the same as the cause of nonbiological aging. It’s the second law of thermodynamics. Like all molecules, biological molecules dissipate energy, losing structural integrity and functional capacity. Our bodies have enormous repair capacity, which evolved to repair dysfunctional molecules until reproductive maturation, after which the accumulation of these molecules exceeds repair capacity. Otherwise, the species would vanish. The accumulation over time of dysfunctional molecules leads to the properties of aging at the clinical level that we all recognize.

TR: So it doesn’t imply that there is a solution to aging?

LH: Why would you want to do that?

TR: Some people would like to slow or halt the aging process.

LH: They haven’t thought about the consequences. We relate to each other by perceptions of differences in age, which would be destroyed if some chose to increase their longevity and some did not. The social, political, and economic discontinuities that would occur would be enormous. People who say they want extended longevity say they want it to be so when life satisfaction is greatest. Yet they won’t know [when that is] until late in life. If you’re in your eighties and you decide you want life extended when you were happier, at fifty, it’s no longer possible.

TR: So you don’t want to extend life span. But do you think it’s theoretically possible?

LH: I think it’s highly improbable. Let’s take something infinitely simpler than your body and mine: automobiles. Even if you put the car in a garage and don’t use it, it won’t stand there forever. Eventually, it will age and disintegrate. This is an inevitable law of physics. Some people have proposed changing the parts as they wear out. But when is the original no longer the original? Replacing your brain becomes an insurmountable problem.

TR: You have often pointed out that even in the research world, there is great confusion over the meaning of the term “aging.” What is the confusion?

LH: The facts are these. There are four aspects to the finitude of life: aging, longevity determination, age-associated diseases, and death. Aging is what we call a catabolic process–the breakdown of molecules. Longevity determination is the reverse–the repair or maintenance of molecules. Aging gets confused with longevity determination. The aging process increases vulnerability to age-associated diseases. These concepts are distinguishable from each other and fundamentally different.

TR: Why is it so important to distinguish between aging and the diseases of aging?

LH: You cannot learn about the fundamental biology of aging by studying disease processes. Resolving age-associated diseases tells us nothing about the fundamental biology of aging, just as the resolution of childhood diseases, such as polio and childhood anemia, did not tell us one iota about childhood development.

TR: Why, then, is it important to do research on the fundamental processes of aging?

LH: Because the fundamental processes of aging increase vulnerability to all age-associated diseases. That is why cancer, cardiovascular disease, and stroke, the three leading causes of death in developed countries, occur in older age. The root cause of age-associated diseases implies–demands, even–that for anyone to understand the causes of age-associated diseases, they should know something about the fundamental processes of aging. Learning something about why old cells are more vulnerable to pathology is a key question for which we have little research being conducted.

TR: Really? Little research is being conducted in this area?

LH: Essentially, less than 3 percent of the budget of the National Institute on Aging, the key source of major funding in this country for research on aging, is spent on studying the fundamental biology of aging–and that’s a liberal estimate. Over 50 percent of its budget is devoted to Alzheimer’s-disease research. I am not arguing that we stop research on Alzheimer’s. I’m simply pointing out the fact that there is an enormous difference between research on aging and age-related diseases. If you cured Alzheimer’s tomorrow, it would add about three weeks on to the average life expectancy in this country.

TR: Would focusing more funding on research on the fundamental process of aging bring a greater return on the investment?

LH: Absolutely.