Natural aging as as a sequential poly-systemic syndrome.

We review the progression of aging as a sequential development of multiple syndromes analogous to other diseases. This generalized approach may allow practicing physicians to consider the signs of aging as manifestations of a poly-syndrome disease and facilitate prevention, diagnosis and treatment of common aging-related dysfunctions.

How regularities of mortality statistics explain why we age despite having potentially ageless somatic stem cells.

Researchers working in the area of ageing have found numerous manifestations of this process at the molecular biological level, including DNA and protein damage, accumulation of metabolic by-products, lipids peroxidation, macromolecular cross-linking, non-enzymatic glycosylation, anti-oxidant/pro-oxidant misbalance, rising of pro-inflammatory cytokines, etc. This results in an increase in the proportion of cells in growth arrest, reduction of the rate of information processing, metabolic rate decrease, and decrease in rates of other processes characterizing dynamic aspects of the organism's interaction with its environment. Such staggering multilevel diversity in manifestation of senescence precludes (without methodology of systems biology) development of a correct understanding of its primary causes and does not allow for developing approaches capable of postponing ageing or reducing organisms' ageing rate to attain health preservation.

The updated view concerning the possibility of growing old without senescence.

New findings paradoxically highlight the capability of old mitochondria, precursor cells, tissues, and organs for rejuvenation during vital activity at appropriate conditions and modes. But most studies of aging are conducted in living beings situated in rather artificial conditions. Such external conditions are less adequate to the evolutionarily adjusted genetic construction of an organism and lead to the appearance of senescence due to incomplete self-maintenance processes.

Nonpathological senescence arises from unsuitable external influences.

One of the most exciting events in current biogerontology is the elucidation of environmental control over the rate of aging. Many observations suggest that appropriate external stimuli can ameliorate the state of various biological entities and even rejuvenate them. Recent findings support the possibility that nonpathological aging of cells may be caused solely by external signals and moreover that this aging might be reversible.

Inadequate intensity of various components of total environmental signals can lead to natural aging.

We suppose that natural aging derives from an inevitable shift in certain parameters of physiological control systems under the influence of inadequate environmental conditions, which are not able to fully induce an organism's "optimal" existence in the self-maintenance mode. In this case the rate of aging is proportional to the multidimensional difference between the cues from evolutionarily designed adequate habitat and signals from the real environment. The negative correlation between parameters of Gompertzian mortality (and some other published findings) is compatible with this view.