The book posits that aging is a loss of epigenetic information, not an irreversible degradation of our DNA. Our cells' "software" forgets how to read the "hardware" (DNA) correctly. This suggests aging can be rebooted, much like restoring a computer's operating system.

The tech world is fixated on trivial AI uses while monumental breakthroughs in healthcare go underappreciated. Innovations like CRISPR and GLP-1s can solve systemic problems like chronic disease and rising healthcare costs, offering far greater societal ROI and impact on longevity than current AI chatbots.

The Orphan Drug Act successfully incentivized R&D for rare diseases. A similar policy framework is needed for common, age-related diseases. Despite their massive potential markets, these indications suffer from extremely high failure rates and costs. A new incentive structure could de-risk development and align commercial goals with the enormous societal need for longevity.

Contrary to the belief that women have a finite egg supply, experiments showed infertile mice regained fertility after their NAD levels were boosted with NMN. This suggests age-related infertility could be reversible, challenging a core tenet of reproductive biology.

Dr. D'Agostino gives his aging, neutered dogs a Selective Androgen Receptor Modulator (SARM) to stimulate muscle protein synthesis and maintain vitality. This approach is analogous to Testosterone Replacement Therapy (TRT) in humans, aiming to counteract the loss of skeletal muscle mass associated with aging and hormonal changes.

Modern ethical boards make certain human studies, like extended fasting, nearly impossible to conduct. This creates an opportunity to revisit older, pre-regulatory research from places like the Soviet Union. While the proposed mechanisms may be outdated, the raw data could unlock valuable modern therapeutic approaches.

By auditing the "noise" or corruption in a cell's epigenetic settings, scientists can determine a biological age. This "epigenetic clock" is a better indicator of true health than birth date, revealing that a 40-year-old could have the biology of a 30-year-old.

The principle of hormesis shows that stressors like fasting and cold exposure trigger a self-preservation state in cells. This "hunker down" mode activates repair mechanisms like sirtuin proteins, which clean up cellular damage, making these seemingly negative activities profoundly healthy.

The common aversion to living to 120 stems from assuming extra years will be spent in poor health. The goal of longevity science is to extend *healthspan*—the period of healthy, mobile life—which reframes the debate from merely adding years to adding high-quality life.