Fight Aging!

Unintentional poetry can sometimes be found amidst the drudgery of translating literature from one language to another. Spanish to English gifts us with "consumers of drugs of abuse," which serves as the point of attraction to here consider the relationship between aging and damaging ourselves, both proactively and through neglect. The full PDF is also freely available in both Spanish and English, lined up in parallel.

The aging or senescence process that follows maturation is characterized by time-related functional decline due to genetic, biochemical, physiological and anatomical degeneration in tissues and organ systems with time. Oxidative damage to mitochondrial DNA (mtDNA) in the heart and brain is inversely related to maximum life span of mammals, suggesting that accumulation of mtDNA damage is involved in the various disorders associated with aging, cancer and neurodegeneration. The suppression of stem/progenitor cell proliferation also contributes to the aging process, by reducing tissue regeneration and repair and ultimately reducing longevity. Another important factor is the intracellular deposition of lipofuscin granules (age pigment), a non-degradable polymeric material accumulated within lysosomes, which ultimately exacerbate oxidative stress levels in senescent cells.

Drugs of abuse can strongly contribute to these senescence accelerating factors in the brain. Methylenedioxymethamphetamine ('ecstasy') and methamphetamine were shown to promote deletions in brain mtDNA. Concerning stem/ progenitor cells, it has been shown that several opiates and psychostimulants, including ecstasy, decrease the self-renewal capacity of the hippocampus by diminishing the rate of proliferation of neural progenitors and/or by impairing the long-term survival of neural precursors. Chronic alcohol consumption induces lipofuscin deposition in neurons and heart cells. These facts provide interesting hints on the potential of these drugs in accelerating brain senescence.

Degenerative aging is no more than molecular and cellular damage and the (increasingly flailing) reactions of our biochemistry to adapt to, repair, or work around that damage. That we degenerate with age is a function of our present inability to repair the damage produced over a long life. This will change in years ahead with the inexorable advance of biotechnology, but even now we have a fair degree of control over some aspects of aging - over how fast we choose to damage ourselves. Exercise or lack of same looks likely to move life expectancy by a decade, for example.

A useful concept here is the division of aging into primary aging and secondary aging:

Primary aging is the gradual - and presently inevitable - process of bodily deterioration that takes place throughout life: the accumulation of biochemical damage that leads to slowed movements, fading vision, impaired hearing, reduced ability to adapt to stress, decreased resistance to infections, and so forth. Secondary aging processes result from disease and poor health practices (e.g. no exercise, smoking, excess fat and other forms of self-damage) and are often preventable, whether through lifestyle choice or modern medicine. The two categories are somewhat fuzzy at the borders by these definitions; we hope that advancing medical and biotechnology will move the known and understood aspects of primary aging into the secondary aging category as rapidly as possible.

Habitual use of strange chemicals falls under secondary aging, though I would not be surprised to learn that much of the damage of addiction stems from very poor health practices rather than the chemicals themselves - self-neglect that goes beyond mere lack of exercise and overeating.

Carvalho F. (2009). How bad is accelerated senescence in consumers of drugs of abuse? Adicciones, 21 (2) DOI: ADICCIONES, 2009 - VOL. 21 NUM. 2 - PAGES. 99-104