Aging starts at a cellular level

Telomere shortening—Telomeres are particularly susceptible to age-related deterioration. Constant cell division depletes telomerase levels, leading to cell malfunction. While further research is still needed, we do know that the longer our telomeres, the better.3

Mitochondrial senescence—As with telomeric shortening, both intrinsic and partially extrinsic factors play a role in mitochondrial degeneration, with oxidative and inflammatory stress among the key suspects. Physical exercise promotes autophagy and induces mitochondrial neogenesis in many tissues via the activation of adenosine monophosphate-activated protein (AMP)-kinase and exerts additional benefits via the up-regulation of brain-derived neurotrophic factor (BDNF) synthesis.4,5

Reduced expression of mRNA (messenger ribonucleic acid) splicing factors—this subroutine is linked to the accumulation of senescent cells and is susceptible to modulation by lifestyle and specifically dietary factors.6

Extracellular matrix (ECM)—is responsible for the physical maintenance of all cells, and current understanding is that it influences cellular activity and responses. ECM causes the progressive deterioration of tissues and physiological systems.7 Like the other subroutines, this is subject to both intrinsic and extrinsic factors. It is particularly susceptible to chronic inflammation.8

Metabolic deterioration—This subroutine is linked to lifestyle and dietary factors, hence amenable to lifestyle, dietary and supplemental intervention.9

Endocrine decline—The endocrine system consists of a group of glands and organs that regulate and control various body functions by producing and secreting hormones. The endocrine function generally declines with age because hormone receptors become less sensitive.10