Potentially Treatable Common Factors in Age Related Diseases
Everybody agrees that age (time since birth) is a factor linking the age-related diseases such as cancer, heart disease, stroke, arthritis, cataracts, etc. However, time, per se, is not a treatable (medically alterable) factor. The central question surrounding aging is whether there exist potentially medically alterable factors that are common to many or most manifestations of aging including the major age-related diseases. Programmed and non-programmed theories of aging differ dramatically on this point.
Medical Implications of Non-Programmed Aging Theories
For a variety of reasons non-programmed theories generally suggest that treatable common factors do not exist. Williams (an author of the non-programmed antagonistic pleiotropy theory) went so far as to say that treatable common factors were a "logical impossibility." This leads to the conclusion that the only way to approach treatment or prevention of age-related diseases is to attempt to interfere with processes that are unique to each individual disease, a continuation of the existing main-line medical research paradigm.
According to non-programmed theories, human aging is ultimately caused by universal deteriorative processes that cause damage to living tissues. Many non-programmed theories recognize that humans and other organisms have maintenance and repair functions (we could say anti-aging functions) that act to delay damage but contend that eventually each of those functions is inadequate and accumulated unrepaired damage causes manifestations of aging.
Researchers following non-programmed theories are consequently looking for ways to assist the maintenance and repair functions. Anti-oxidants, and agents to assist in repair of telomeres (specific structures in DNA molecules implicated in aging) are typical of these efforts. Non-programmed theories tend to suggest that there are many repair functions that are independent of each other and that therefore assisting any one function might have limited value. Some theorists think (despite Williams) that one or another of the functions is key (e.g. telomere repair) and that therefore aiding that function would significantly delay or reduce many aging manifestations.
Medical Implications of Programmed Aging Theories
Programmed theories explicitly propose the existence of potentially alterable common factors in the aging process, i.e. the "program." Further, since a limited life span conveys evolutionary benefit, aging can be controlled by a complex evolved biological mechanism similar to other evolved mechanisms that provide for beneficial biological functions such as digestion, sugar metabolism, or growth.
Many observations suggest commonality between manifestations of aging including caloric restriction effect, stress effect, and progeria. Other discoveries provide explicit evidence of evolved mechanisms in various organisms that limit life span or restrain reproduction. See Experimental Evidence. The diagram below is an attempt to produce a candidate or "straw man" concept for the design of a complex evolved life span regulation system that would satisfy all of the observations.
Most genetically programmed biological functions are designed to be capable of at least some adjustment within the life of an individual organism in order to adapt to local or temporary conditions. Obvious examples include the ability of muscles to grow or shrink in response to demand for their activity, the ability of organisms to alter their genetically programmed behavior in response to acquired information, the ability of organisms to adapt their genetically programmed reproductive behavior based on planetary cycles, and many others. If life span regulation is indeed a genetically programmed bodily function, we would expect that it would also be capable of some adjustment in order to optimize life span to external conditions. A programmed aging mechanism might therefore look like the figure below. In this concept, maintenance functions are slowed or disabled by a species-unique genetically programmed biological clock that in turn can be adjusted by sensing of external conditions. In other words, aging is controlled by a mechanism similar to the one that controls age of sexual maturity and mating seasons.
This concept has both empirical and theoretical support. Theorists have suggested reasons why increasing life span in response to stress or reduced food supply would create group benefit. Experimentalists have found that both caloric restriction and many forms of stress increase life span in many animals. Non-programmed theories have difficulty with these and other observations. Further, evolvability theory suggests that there is a special relationship (beyond Medawar's hypothesis) between age of sexual maturity and life span, which in turn suggests commonality between the controlling mechanisms.
The complex programmed mechanism theory described here has exciting implications for medical intervention in the prevention and treatment of age-related diseases. In addition to approaches attempted by non-programmed researchers, pro-programmed researchers can attempt to interfere with clock, sensing, or signaling functions to, in effect, "fool" the aging mechanism. Some efforts in this direction such as "caloric restriction mimetics" are underway.
For more detail on the history and status of the programmed vs. non-programmed aging theory controversy see Aging Theories.
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