Nutrition plays a significant role in the human lifecycle because it provides energy, helps prevent diseases and promotes growth. The first documented evidence associating dietary restriction and aging came in 1935 in a study conducted by McCay et al that found that reducing the amount of calories consumed by 20% without causing malnourishment increased the lifespan and resistance to age related diseases in a rodent model (Colman et al., 2009; Sinclair, 2005). Typically a reduction of 10-40% of calorie intake is suggested by several authors as being effective in lengthening life, although a recent study using 30% dietary restriction was found to be ineffective in doing so in rhesus monkeys (Mattison et al., 2012).
Several hypotheses exist to explain the mechanism behind life extension due to caloric restriction (CR). Some of the earliest theories that never gained much support include the following: McCay’s original hypothesis that CR reduced the rate of growth and development and thereby increased lifespan; CR reduced metabolic rate which resulted in slower aging; and that the control animals used in the experiments eat significantly more than normal, which makes them age quicker than CR animals (Sinclair, 2005). It has since then been found that CR at any stage of life extends lifespan, and animals on CR show similar or greater metabolic rates than control animals, and the extension of life by CR is significant even when the study controls are fed a normal (not ad libitum) diet (Sinclair, 2005).
Another study proposed that CR slowed aging process by increasing resistance to hyperoxidation. As aging progressed in yeast and other animals, the presence of free radicals increased in the cells. Usually, the levels of these radicals are kept low by a redox system involving peroxiredoxin and sulfiredoxin. Peroxiredoxin reacts with the radicals and gets oxidized and inactive. Sulfiredoxin in turn activates the former by reducing it. Molin et al. (2011) found that CR increased levels of sulfiredoxin in yeast cells, which enabled these cells to keep peroxiredoxin activated for an extended period of time, thereby reducing free radicals and increasing lifespan. In addition, peroxiredoxin inhibited protein damage, which, also contributed to aging via age-related diseases such as Alzheimer’s and Parkinson’s (Molin et al., 2011).
More recently, theories that focus on biochemical mechanisms related to aging have tried to explain the mechanisms of CR mediated lifespan increase. In a study conducted by Berg & Simons in 1960, it was found that reducing fat in the diet increased lifespan. However, this finding does not seem to apply under all situations. Mair, Piper, and Partridge (2005) found that reducing yeast (that supplied proteins and fats) without altering the total calorie content of the diet extended the lifespan of Drosophila melanogaster. This finding suggests that it is not just the restriction of calories, but particular types of...