Fries' hypothesis is that the burden of lifetime illness may be compressed into a shorter period before the time of death, if the age of onset of the first chronic infirmity can be postponed before the age of death. In order to confirm this hypothesis, the evidence must show that it is possible to delay the onset of infirmity, and that corresponding increases in longevity will be modest.
On the one side:
Longevity will continue to increase under hopeful scenarios for the human future, and morbidity will continue to decrease. The question is the relative rate of those, and I’m just telling you and anybody else who would make such an argument that in fact the data is in. The mortality rates are going down 1 percent a year. That’s a substantial decline in mortality rates. That’s been continuing for a century, that’s almost a straight line, at 1 percent a year. The morbidity rates are going down 2 percent a year. It’s the story.
And on the other side:
KYLE JENSEN: Now do you feel that the compression of morbidity theory should be the focus of biomedical gerontology?
AUBREY DE GREY: No, not really I don’t. It’s important first of all to remember that the original description of compression of morbidity by Jim Fries in 1990 did not even propose this. What he proposed was that actually it would be easier to implement changes in lifestyle that would postpone the onset of morbidity than it would be to develop medical technologies to postpone death. In other words, he felt that by changes of lifestyle we could compress the period between the two, but he never suggested that we would actually compress morbidity by intervening in the biology of aging. Indeed, he felt that intervening in the biology of aging was essentially impossible. What we are actually seeing is failure to implement those changes of lifestyle that Jim Fries suggested. We are seeing increase in lifespan and also [delay in] onset of morbidity. Not much change in the rates of those two so the interval between the two [remains the same]. There is not progress being made in compressing morbidity. There is a bit of variation. In some statistics we see a little bit of compression in some people; in some places we see a little bit of expansion. By in large what we are seeing is exactly what you would expect from postponing aging. In other words, you postpone the onset of morbidity and you also postpone death by about the same amount.
As they say, you can do all sorts of things with statistics and definitions, and I'm far from qualified to put forward any sort of firm opinion as to whether present statistics better support one side or another. Compression of morbidity is something of the declared goal of those in the mainstream of aging research who don't want to talk about extending life span, however, which makes it a little more than a matter of statistical interpretation. When a researcher talks about compression of morbity, that is something of a cipher, an identifying mark as to where he stands on the topic of engineered longevity: possibly in favor, but not willing to risk offending conservative funding organizations, possibly against. Either case has much the same result - a researcher who isn't working as freely as he might to extend human longevity.
From my reductionist viewpoint, I find it hard to reconcile an existence of compression of morbidity with the performance of reliability theory as applied to aging, amongst other things. Theories of aging based upon accumulation of biochemical damage and incremental system failure are very convincing, and have a great deal of experimental support, but don't predict that compression of morbidity is possible to any great degree. The only way to push out health life span is to prevent or repair damage, and that will also push out overall life span.