One familiar Bible passage - Psalm 90, verse 10 - sets the maximum human life span at "three score years and ten." But recent research by two USC scientists indicates that a more obscure biblical estimate - 120 years - may be closer to the physiological mark.

The higher figure might, in fact, represent the average human life expectancy, if medical science could duplicate the only life-extending mechanism known to be effective in lab rodents - extremely low-calorie diets.

In a new analysis published in the May issue of the Journal of Gerontology, gerontologist Caleb E. Finch and preventive-medicine expert Malcolm C. Pike use extensive, updated comparative data from animals, in conjunction with an old, well-known mathematical relation, to recalculate human-life span potential. The analysis also offers an explanation for certain discrepancies scientists have previously found in mortality data.

The study uses the Gompertz model - named after 19th century British actuary Benjamin Gompertz - to predict maximum life expectancies for various species.

The Gompertz rule predicts that the risk of dying accelerates at a constant rate over time for all organisms, be they fruit flies or humans. For humans, for example, the chances of dying increase by approximately 9 percent each year after puberty - meaning risk of dying in any given year doubles with every eight years lived.

What is striking about this relation, noted Finch, is that it seems to hold for humans (and other animals) living under all kinds of environmental conditions, harsh or benign.

To take an extreme example, Australian soldiers living in Japanese prisoner-of-war camps during World War II suffered very high death rates - approximately 30 times higher than Australian men of the same age living at home. However, the rate of increase in deaths between age groups remained the same for both populations: that is, 24-year-olds died in the same ratio to 48-year-olds, regardless of whether they lived in jungle death camps or in Australian towns and farms.

Similar correlations have been observed in other species, even though the rate of aging is drastically faster in insects and mice than in humans.

The Gompertz model, according to Finch, lets scientists express life expectancy as a product of two distinct factors. One is environment - either stressful, as in the prison camp, or benign. This includes infectious diseases.

The other factor, designated by the Greek letter alpha (a), is a measure of a built-in species clock - "something that seems to be part of our design as animals, a burden of aging that keeps accumulating, like interest compounding on a debt," Finch said.

These two factors can be used to calculate a theoretical value for the maximum age that any member of a given population could reach. For humans, this calculation yields a figure of approximately 120 years - which happens to be the age of the oldest living person, Jeanne Calment of Arles, France, born in 1875.

Interestingly, this figure also coincides with the human life span given in another biblical verse (Genesis 6:3): "...for that [man] also is flesh: yet his days shall be an hundred and twenty years."»

According to Finch, the Gompertz model successfully accounts for a large volume of aging data, but seeming anomalies have been reported in some species, especially at the extreme-old-age end of the life span spectrum.

Many invertebrates and some reptiles, for example, exhibit an old-age plateau. After approximately 90 percent of the population has died, the mortality rate seems to become constant rather than continuing the Gompertz compound-interest acceleration.

Finch's and Pike's study attempts to deal with these anomalies, examining the best mortality data from a wide variety of species in the attempt to see what useful conclusions about life span can be drawn from Gompertz modeling - with the goal of possibly extending estimates for human life span.

The researchers analyzed vital statistics from bird and mammal species, including numerous lines of purebred laboratory mice and rats, along with various breeds of dogs, gerbils, hamsters, turkeys, peafowl, finches, pheasants and Japanese quail - covering most birds and mammals, in fact, for which good mortality data exists. All of this animal data, they found, fit the Gompertz curves closely, with no sign of a leveling off in extreme old age.

Thus, while the Gompertz relation may not hold for some species, for those most closely related to humans, it seems universal.

Finch and Pike also analyzed human mortality figures from different areas of the globe. People in economically advanced areas, they noted, show very different - up to 10 times lower - risk of death by disease and other environmental hazards, compared to people living in underdeveloped, disease-ridden areas in Africa and Asia. "Despite this," the authors write, "it is striking how little a differs between human populations."»

In their conclusion, the two scientists discuss the kinds of foreseeable medical advances that would make it possible for half the population to reach the age of 120, the maximum under current medical and environmental conditions.

Either of two routes might accomplish this goal, the scientists say. If environmental risks of death - infectious disease, accident and natural disasters - were reduced to roughly one-fiftieth of the level currently found in the most medically advanced areas of the world, half of 50-year-olds might expect to reach 120.

This would require remarkable advances, they point out. One recent study found that reliable cures for the three leading causes of death after 50 - cancer, heart and vascular diseases and diabetes - would only raise average life expectancy at 50 to approximately 95.

The other possibility is manipulation of a, the mysterious, species-specific, built-in aging clock. Reduction of a by 45 percent, say the researchers, would increase life expectancy to the 120-year threshold.

Only one treatment is currently known to affect the rate of aging. In numerous species, including rats, it has been shown that long-term maintenance on extremely low-calorie diets retards aging in general - by as much as 45 percent. But, the study notes, "while such ... plasticity in human life span is completely plausible from evolutionary perspectives, we do not know the generalizability of diet restrictions from short-lived rodents to the much longer-lived humans."

Finch and Pike's research was supported by the John D. and Catherine T. McArthur Foundation Network in Successful Aging.