In this article, we introduce the concept of cellular hyperfunctionality, which posits that age-related diseases are caused by excessive cellular activity rather than loss of function or damage to tissues. The theory, popularized by Dr. Mikhail Blagosklonny, challenges the long-held belief that aging is a result of wear and tear, and instead suggests that cellular overactivity is the primary driver of aging.
Three hyperfunctional features characterize dysfunctional cells: hyperplasia, hypertrophy, and hyperfunctionality. These features lead to tissue dysfunction and acceleration of the aging process. As we age, our cells are unable to effectively slow down the functions needed for growth, causing inappropriate cellular hyperactivity and leading to age-related diseases like cancer and osteoporosis.
Senescent cells, which are increasingly prevalent as we age, can be particularly problematic due to their inability to divide and their release of pro-inflammatory and growth-promoting molecules. These cells contribute to the development of various age-related diseases and are difficult to remove from the body as we age.
The article also highlights the potential benefits of caloric restriction and the drug rapamycin in addressing cellular hyperfunctionality. Caloric restriction can help promote autophagy, a cellular process that helps maintain healthy cell function, while rapamycin inhibits the mTOR pathway, which is involved in cell senescence and aging. By targeting and suppressing the mTOR pathway, rapamycin can mitigate the release of harmful molecules from senescent cells, protect neighboring tissues, and encourage the elimination of aging cells through autophagy.
The article suggests that by inhibiting mTOR and using molecules like rapamycin, we can reduce cellular hyperfunction, increase autophagy, and decrease senescent cell pathology to decelerate the aging process. This shift in understanding aging as a phenomenon of cellular overactivity has profound implications for how we approach aging and age-related diseases.