In what way might a CC diet slow the aging process?

Low insulin levels, maintained by the CC diet, decreases the effective bioactivity of a hormone IGF-I that, in rodent studies has emerged as a key driver of the aging process.

Keeping insulin levels low may also have potential for literally slowing the aging process. Low insulin decreases the effective bioactivity of a closely related hormone, insulin-like growth factor-I (IGF-I), which in rodent studies has emerged as a key driver of the aging process. In rodents that have been genetically altered to reduce the level or bioactivity of IGF-I, many aspects of aging are slowed, cancer is prevented or postponed, and maximal achievable lifespan is notably increased. Similar effects are seen in rodents subjected to chronic caloric restriction or intermittent fasting, in part owing to the reduction in insulin/IGF-I activity associated with these measures. However, reduced cellular fuel availability also contributes to the impact of caloric restriction on the aging process, by activating certain key enzymes (AMPK, Sirt1) which detect fuel deficit. Although the ways in which low activity of insulin/IGF-I and high activity of AMPK/Sirt1 slow the aging process are complex and still imperfectly defined, activation of a cellular process known as macroautophagy appears to play a very key role. This process causes the degradation of long-lived intracellular proteins and membranes — thereby enabling proteins and membranes that have been damaged by oxidative stress or other types of “wear and tear” to be replaced by newly synthesized, functionally competent proteins and membranes, effectively renewing and “rejuvenating” the contents of the cell.

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