Following the Biochemical Pathways of Aging, Step by Step
The mainstream biogerontology community is engaged in the very, very long and complex process of unpicking all of the detailed changes in biological signaling pathways that occur with aging. The starting points are identified metabolic changes that accompany treatments, lifestyle choices, or environmental circumstances known to extend life. The end result is to fully understand why these low-level biochemical changes lead to longer life span, and replicate or better them. This is a very long term project, which is why many of these researchers do not expect meaningful artificial extension of human life span within their lifetimes, even allowing for accelerating growth in biotechnology and computing power. This article is an example of this sort of research: "researchers have linked hyperactivity in the [mammalian] target of rapamycin complex 1 (mTORC1) cellular pathway to reduced ketone production in the liver, which is a well-defined physiological trait of aging in mice. During sleep or other times of low carbohydrate intake, such as fasting or periods of dieting, the liver converts fatty acids to ketones, which are vital sources of energy during fasting, especially for the heart and brain. As animals age, their ability to produce ketones in response to fasting declines. ... This is the first time that the mTORC1 pathway has been shown to affect a trait associated with aging. This discovery will enable researchers to study the aging process in greater detail, helping them to determine how and why aging suppresses ketone production and activates mTORC1."