Lifespan is somehow related to the amount of food energy consumed: this was first systematically investigated in the seminal study by Weidruch et al (1986). A simplistic pursuit of this principle of caloric restriction followed, involving research into longevity of those who simply reduced their food energy intake. Perhaps not suprisingly, people found that cutting down on food reduced their quality of life so considerably as to negate any possible advantages of lengthening their lives.
Underlying this research was the hypothesis that oxidative damage was the agent which accelerated aging, and that aging was retarded when the amount of carbohydrates (and thereby insulin release) was reduced through dietary restriction.
However, recent research has produced increased longevity in animals (and shows promise for increased human longevity) through the use of insulin uptake retardation. This was done through altering an animal’s metabolism to allow it to consume similar food-energy levels to other animals, but without building up fatty tissue. (Bluher et al, 2003)
This has set researchers off on a line of study which presumes that it is not low food energy consumption which increases longevity. Instead, longevity may depend on an efficient fat processing metabolism, and the consequent long term efficient functioning of our organs free from the encumbrance of accumulating fatty deposits. (Das et al, 2004) Thus, longevity may be related to maintained insulin sensitivity. However, several other factors including low body temperature seem to promote longevity also and it is unclear to what extent each of them contribute
|
