December 12, 2008; While the observed growth in the numbers of centenarians is growing exponentially in the world population, the numbers of Supercentenarians (one demographic decade above) has remained relatively flat. Nevertheless, as the base of our population pyramid expands, one should expect to observe the "pyramidal apex" rise, at least somewhat, so long as it doesn't hit a "biological glass ceiling." What's going on here?
The fundamental limits on the maximum-lifespan phenotype of any given mammalian species has not been successfully modeled mathematically (whether in a zoo or in the wild), as the interaction of dozens of gerontic (longevity-determining) genes in the genome of each species leads to prohibitive combinatorial complexity. (Teasing out these relations in a graphical manner has become the task of Systems Biology that is just getting underway as a separate discipline.)
There appears to be a separate master circadian clock within each organ system that is synchronized by the Pineal Gland/Super Chiasmatic Nucleus (SCN) [in the brain] which is in turn synchronized to the day/night cycle of the 24-hour rotation of the Earth. The mechanism by which this happens is speculated to be by some unknown low-concentration protein-signal circulating in the blood that derives from the Pituitary Gland of the NeuroEndocrine Axis [as modulated by the anterior hypothalamus].
There are a wide variety of aging phenotypes for each individual organ (liver, lungs, heart, kidneys, etc.) that stochastically undergo critical failure points (in a synchronized fashion) once the Prime Directive to "Go forth and multiply" has been satisfied (which definitively ends with female menopause in women at ~52 yo and male andropause in men at ~65 yo). The tradeoff in the ability of gerontic genes to be helpful in early life while being deleterious in later life is sometimes referred to as antagonistic pleotropy. However, in Systems Engineering terminology, the synchronization of failure points is called a multiple lock-in phenomenon . This has been compared metaphorically to the customer warranty period provided by automobile manufacturers (of, say, three years or 25,000 miles).
After the age of menopause/andropause, the Darwinian pressure on our genome to facilitate growth and/or repair weakens significantly (modulo the "grandparenting effect," which has value in circumventing the extinction of isolated tribes that have at least a few remaining elders when a limiting environmental resource becomes scarce), during which the aging of individual organ systems becomes systematically desynchronized. Many older organs have a broad spinning reserve that conceals their functional decline, even though this occurs in the background in a relentlessly time-linear fashion. By definition, when the functional capacity of one of the subsystems falls below a threshold compatible with life, this becomes named by epidemiologists/pathologists as the "primary cause of death" written on the Death Certificate. What has not been addressed adequately by public-health experts, in our view, is the clear distinction between intrinsic (molecular/senescent) causes of death and extrinsic causes of death (accidents, suicide, homicide, war, infection by parasites, pandemics, etc.)
This distinction is well understood by actuaries who advise life insurance companies on how to price their term-life premiums. The extrinsic causes of aging rapidly become invisible in geriatric populations (>50 yo) compared with the now dominant intrinsic causes. Mortality life tables plotted on semi-log paper form nearly perfect straight lines after the age of 30 (which can be further refined by gender, age, and race as desired, and are revised weekly by the CDC in Atlanta, GA on their Morbidity and Mortality Weekly Report website for the US population). These straight lines on semi-log paper demonstrate that human mortality (and probably for all mammals) increases exponentially with age (i.e., in a Gompertz/Makeham fashion). With respect to minor influences on mortality such as a family history of certain diseases or admittedly poor life-style choices (such as heavy smoking, heavy drinking, or watching television all day like a couch potato with negligible exercise), the slopes of these lines don't change much. So, life insurance companies tweak their premiums to earn a substantial profit on policies they issue. But they are frequently deluded by the belief that by refining their bets (by excluding people with a family history of x or y or z), as though these other parameters-of-insurability (besides age) were so inherently valuable to their enterprise, they could earn even more. Thus, many companies work hard to compete in this marketplace giving premiums to non-smokers as though this were the only thing that mattered.
We should appreciate that the really-important parameters of longevity operate at the molecular level, such as the accumulation of sticky amyloid compounds which relentlessly infiltrate all our organs, the mechanism for which we have yet to decipher. When we do figure it out (science) and when we learn what to do about it (medicine), "all bets (on life-insurance-policy planning) will be off." We will be on the road to a real revolution in the human condition.
- - L. Stephen Coles