In order to be able to slow, interrupt or reverse the aging process, we need to understand the actual processes that occur in the body as we age.

Hormonal Decline

A number of the manifestations of aging are a result of hormonal decline (the natural age-related decline in the production of the sex hormones Estrogen, Progesterone, Testosterone, adrenal hormones such as DHEA, and pituitary hormones such as Growth Hormone). The decline in these hormones has widespread effects on body composition, bone integrity, skeletal and heart muscle strength, ability to regenerate and repair cells, cognitive functions and mood, as well as on our reproductive capacity.

Inflammatory status, immune function and mutations in cellular DNA

The immune system is programmed to decline over time, which leads to an increased vulnerability to infectious disease and thus aging. In addition to combating infectious agents, an intact immune system is required for the recognition of cancer cells and the recognition of foreign proteins. Dysregulation of the immune response has been linked to the development of autoimmune disorders, cancer, inflammation and Alzheimer’s disease.

DNA damage occurs continuously in cells of living organisms. While most of these damages are repaired, some accumulate, causing cells to deteriorate and malfunction. Therefore, ageing also results from damage to the genetic integrity of the body’s cells.

Mitochondrial Dysfunction and the production of intracellular energy

Free Radicals – are responsible for accumulated damage to intracellular components,  causing cells and eventually organs, to stop functioning. Reactive oxygen species (ROS) signalling is recognised to be an important enzyme/gene pathway responsible for the development of cell deterioration and organismal aging. This has been the rationale for the promotion of antioxidants as part of an anti-aging regime. The body itself produces some antioxidants, which help “mop up” these damaging molecules.

Mitochondria are the energy factories of cells.  Increasing age in mammals correlates with accumulation of mitochondrial DNA (mtDNA) mutations. and can directly cause manifestations of aging, such as osteoporosis, hair loss, greying of the hair, weight (muscle) reduction and decreased fertility. Vulnerable cells in humans include heart, skeletal muscle, colonic crypts and neurons. Mitochondrial dysfunction has also been linked in humans to the development of Alzheimer’s disease, insulin resistance, and chronic fatigue syndrome, as well as the overall aging process.

Telomeres and the Hayflick theory of limited cell division

Dr. Hayflick demonstrated that there is a definitive upper limit to the chronological age that human beings can attain (probably around 120 years). The limiting factor being the number of divisions or replications that human cells can undergo while still retaining their functionality. The mechanism of this limitation was further elucidated by the discovery of telomeres – redundant lengths of nucleotides that occupy the ends of the DNA molecules – these have a protective role to play in keeping our genomic sequence intact – or, in pictorial terms stop “fraying” of the ends of the DNA molecules. Each time a cell divides, small pieces of the telomeres are lost in the replication process, until a critical length is reached, at which time further division threatens the integrity of the genome itself  – hence, further division is halted, and the cell line comes to an end.

Truly immortal cells (e.g. cancer cells) produce an enzyme called telomerase, which repairs the shortened telomere, and allows replication to continue indefinitely: hence one theoretical way of extending the human lifespan would be to incorporate telomerase or a like substance, into our genetic code. In experiments on mice, scientists have been able to simulate the action of telomerase and achieved demonstrable reversal of the aging process.