Age-Related Dysfunctions: Evidence and Relationship with Some Risk Factors and Protective Drugs

The theories interpreting senescence as a phenomenon favored by natural selection require the existence of specific, genetically determined and regulated mechanisms that cause a progressive age-related increase in mortality. The mechanisms defined in the subtelomere–telomere theory suggest that progressive slackening of cell turnover and decline in cellular functions are determined by the subtelomere–telomere–telomerase system, which causes a progressive “atrophic syndrome” in all organs and tissues. If the mechanisms underlying aging-related dysfunctions are similar and having the same origin, it could be hypothesized that equal interventions could produce similar effects. This article reviews the consequences of some factors (diabetes, obesity/dyslipidemia, hypertension, smoking, moderate use and abuse of alcohol) and classes of drugs [statins, angiotensin-converting enzyme (ACE) inhibitors, sartans] in accelerating and anticipating or in counteracting the process of aging. The evidence is compatible with the programmed aging paradigm and the mechanisms defined by the subtelomere–telomere theory but it has no obvious discriminating value against the theories of non-programmed aging paradigm. However, the existence of mechanisms, determined by the subtelomere–telomere–telomerase system and causing a progressive age-related decline in fitness through gradual cell senescence and cell senescence, is not justifiable without an evolutionary motivation. Their existence is expected by the programmed aging paradigm, while is incompatible with the opposite paradigm.