Important facts to remember
In the 1920s, the early days of research into the effect of dietary restriction on life extension, it was thought by pioneers of this method, such as Clive McCay of Cornell University, that the increase seen in life span was due to a slowing down of the maturing process, and/or by a slowing of the rate of growth. This is now known not to be the case, since adult animals placed on dietary restriction have regularly achieved lengthened life spans with no signs at all of delayed maturity (because they were already mature when the diet began).
Other theories have suggested that reduction in excess body weight, resulting from dietary restriction, could account for longevity. This, too, is now seen to be inaccurate, since in free feeding animals there is no connection between the amount of body fat the animal has and its life expectancy and, as shown by the research referred to in the previous chapter, those animals which achieve increased life span by dietary restriction are in fact the heavier animals. Weindruch and Walford elaborate on this fact by pointing out that when rats are kept slim by exercise, no increase in their maximum life span is seen, but when animals are kept at a similar weight level to that achieved by exercise, by using dietary restriction, there is indeed an increased life span.
Incidentally, this highlights a repetitive finding in research, that exercise has little if any effect on life expectancy, even though it certainly does influence overall well-being.
These major researchers ask us to keep a few very important facts in mind as we consider how dietary restriction works. The first is that calorie restriction (as part of an otherwise optimal diet) achieves its results in practically all species tested to date, whether cows, fruit flies, mosquitoes, rats, mice or protozoans (and of course humans if we accept the results of the Okinawa experience as evidence from a self-generated trial). In all these creatures one indicator is constant: as dietary restriction continues so is there a reduction in accumulations of the fat/protein complex lipofuscin (see Chapter 3 for comments on the build-up of age pigments in cells with age). As an increase of lipofuscin in cells is seen as a major sign of accelerating aging, and as a reduction in its presence occurs in ALL species to which dietary restriction is applied, and as a 'side-effect' of dietary restriction is life extension, the removal or reduction of lipofuscin is of some considerable importance in understanding the mechanisms involved.
We are also asked to consider the connection, or lack of it, between life extension and benefits to the immune system (achieved by dietary restriction), important as this may be. The reason for dismissing the idea that improvements in immune function are central to the life extension process is because creatures such as protozoa have no immune systems, and yet they, like all other creatures to which dietary restriction is applied respond by living longer.
Reducing disease incidence in itself, does not seem to have much effect on increasing Life expectancy overall, and so improving immune function seems not to be involved in life extension. As Weindruch and Walford point out, a number of other dietary strategies such as protein restriction, can dramatically cut down incidence of auto-immune diseases (chronic nephropathy in rats, for example) but this hardly contributes at all to an increase in life span in animals so treated. The message they repeat is that only calorie restriction achieves life extension in mammals.