There has been some discussion of late in the scientific community regarding whether or not there is a maximum human life span, whether that concept is even meaningful, and the scope of improvement in human life expectancy that could be plausibly achieved in the near future. The present round of debate was kicked off by a paper published this time last year in which Jan Vijg's team made a pessimistic argument for a ceiling on human life span based on recent historical data - that the current gentle upward trend in human life expectancy will hit a limit. Since it can take a year to assemble a paper and get it through the peer review process, some of the in-depth responses to this paper are now arriving, such as the one I'll point out here.
Is there a limit to human life span? It is fairly obvious that the answer is both yes and no. It is "yes" in the sense that we don't observe anyone living much past 120, so while aging is the sum of all intrinsic biological processes that increase mortality over time, and whether or not death strikes in any given minute is a roll of the dice, eventually the mortality rate is so high that no-one remains lucky enough to live through it for long. That is in effect a limit. On the other hand, the answer is "no" in the sense that we know what these biological processes are, and modern biotechnology will soon enough build the means to repair and reverse the cell and tissue damage that causes aging and all of its consequences. As soon as any specific form of damage can be reliably repaired, then it will no longer act to increase mortality to lifespan-limiting levels, and people will live longer as a result. The prior limit will be pushed out, and a new limit established.
The present upward trend in life expectancy, about one year every decade for remaining life expectancy at 60, is caused by some mix of (a) better lifestyle choices over time and (b) accidental effects on very late life mortality arising from improvements in medical technology. These modest gains have to be accidental since over the past century next to no-one was deliberately trying to treat the causes of aging as a way to extend healthy life. The research and medical communities have certainly been trying to patch over the sort of age-related disease that kills most people somewhere in the age range of 60 to 90, with limited success. There is, however, no necessary reason for those efforts to correlate well with mortality rates in the tiny remaining cohort who survive into their 110s, most of whom evaded the full-blown age-related diseases that killed their peers decades before that age.
A fair amount of the discussion among scientists is focused around whether or not we can keep on doing whatever it is we've been doing, and see human life span continue to increase at much the same rate, essentially without limit. From my point of view, this is a somewhat pointless activity, as the research community will deploy rejuvenation therapies over the next few decades that will completely change the landscape. What happened as a result of the last fifty years of medical progress has absolutely no relevance to what will happen over the next fifty years of medical progress. In the past, researchers were not attempting to treat aging as a medical condition, and nor were they deliberately targeting mechanisms and causes of aging with that in mind. Now and going forward, they are. The difference will be night and day.
The authors of this paper are more concerned with whether or not animal data on the numerous methods of altering metabolism - those that have been demonstrated to somewhat slow the aging process - can be related to human data from the incidental past trend in life expectancy. They find that there are similarities at the high level. I don't know that this is any better than arguing from first principles as I did above, but it is certainly a great deal more work. The methods of slowing aging used to date, such as calorie restriction and pharmaceuticals intended to recreate some of the beneficial reaction to calorie restriction, are largely known to have much smaller effects on human life span than they do in mice - where they are reliable, and many are not all that reliable. I don't think that this area of research will contribute important gains to human life span in comparison to biotechnologies that repair accumulated cell and tissue damage, such as the rejuvenation therapies of the SENS research programs. So again it is a question mark as to what use the existing data from the past is to us when the best forms of future development will take an entirely different approach.
Israeli scientists are convinced the maximum life span can be increased to 140 years or more, if science treats not only diseases but also specifically tackles the aging processes. That's quite a boast, given that the longest confirmed life span so far is 122 years. As the means of intervening with and holding back the ravages of age increase, scientists are now asking whether our natural genetic makeup is actually limited to a maximum life span of 115 to 120 years, or whether this limit can be breached. As you might expect, the scientific community is home to a lively debate on the subject. Other scientists are convinced that developing ways of delaying the aging process is only a matter of time, and that mankind must not accept 120 years as a limit.
Haim Cohen, head of the Molecular Mechanism of Aging Laboratory at Bar-Ilan University, is one of those who believes the maximum life span can be increased by 30 percent and eventually cross the 140-year threshold (compared to 115 to 120 years today). "In the past century we've experienced a dramatic increase in human life expectancy. In the past 60 years, life expectancy at birth has risen by an average of 72 percent. However, the maximum life expectancy has risen by only 8 percent. In the study, we examined whether the minor increase in maximal life expectancy means humanity has reached its maximum potential. The average rise in life expectancy stemmed mainly from medical solutions dealing directly with disease symptoms, and that increased the number of people who lived to a more advanced age."
Until 100 years ago, dying of old age was a privilege. The new study shows that in 1900, only 30 percent of all deaths were related to age or age-related diseases, while more than half were caused by infections. From the 1950s onward, the picture changed dramatically, as infections became curable and some of the terminal diseases turned into chronic ones. Today, more than 80 percent of deaths are related to diseases that occur mostly among the elderly. These factors certainly contributed to extending the overall life expectancy, but why is that barely reflected in the maximum life expectancy? Cohen and his colleagues say it stems from the approach that has characterized medicine. "The changes in life expectancy have so far stemmed from medical treatments developed in response to various illnesses - but there was no intervention in the basic aging mechanisms. What will happen when we deal directly with those biological mechanisms and metabolic processes responsible for aging?"
To examine whether intervention in the aging processes will affect life expectancy, Cohen and his team gathered and analyzed all the studies made in the last 20 years ("There are hundreds of them," he noted). In them, scientists succeeded in delaying the aging of organisms such as fungi, worms, flies, mice, rats and even monkeys. "We found something interesting in all of them: The increase in the maximum age was almost identical to the rise in the average or median age, reaching up to 30 percent." Cohen believes the findings indicate that focusing on the biological and genetic causes of aging will allow for a further leap in maximal life expectancy in the future. "Aging is a natural biological process whose basic characteristic is decreased functioning. Though the aging process looks different in various organisms, it is based on very similar mechanisms."
While average human life expectancy has increased dramatically in the last century, the maximum lifespan has only modestly increased. These observations prompted the notion that human lifespan might have reached its maximal natural limit of ~115 years. To evaluate this hypothesis, we conducted a systematic analysis of all-cause human mortality throughout the 20th century. Our analyses revealed that, once cause of death is accounted for, there is a proportional increase in both median age of death and maximum lifespan.
To examine whether pathway targeted aging interventions affected both median and maximum lifespan, we analyzed hundreds of interventions performed in multiple organisms (yeast, worms, flies, and rodents). Three criteria: median, maximum, and last survivor lifespans were all significantly extended, and to a similar extent. Altogether, these findings suggest that targeting the biological/genetic causes of aging can allow breaking the currently observed ceiling of human maximal lifespan.