Mammal Aging as a Programmed Life Cycle Function - Resolving the Cause and Effect Conundrum.

Because aging and internally determined lifespan vary greatly between similar species it is now widely accepted that aging is an evolved trait, resulting in two classes of evolutionary aging theories: aging is programmed by complex biological mechanisms, and aging is not programmed. As recently as 2002 programmed aging is thought to be theoretically impossible. However, genetics discoveries, results of selective breeding, and other direct evidence strongly support the idea that aging creates an evolutionary advantage and that therefore complex biological mechanisms evolved that control aging in mammals and other multiparous organisms. Like life-cycle programs that control reproduction, growth, and menopause the aging program can adjust the aging trait during an individual's life to compensate for temporary or local changes in external conditions that alter the optimum lifespan for a particular species population. Genetics discoveries also strongly support the evolvability concept to the effect that sexually reproducing species can evolve design features that increase their ability to evolve, and that aging is one such feature. Genetics discoveries also prove that biological inheritance involves transmission of organism design information in digital form between parent and descendant of any organism. This has major implications for the evolution process.

Mammal Aging is Controlled by an Evolvability-Based Adaptive Program.

As recently as in 2002 gerontologists widely thought that an aging program that purposely caused aging in mammals was impossible and therefore scientifically ridiculous because it violated widely accepted concepts regarding the nature of the evolution process. However, a number of modern evolutionary mechanics concepts such as group selection and evolvability suggest that an individually adverse trait like aging can evolve if it creates an advantage (reduced probability of extinction) for a population. Genetics discoveries suggest that aging creates multiple population advantages and, therefore, aging programs that purposely cause and regulate aging evolved in mammals. This led to various concepts regarding the nature of the program. One such concept is that aging is a completely genetically specified function of age, essentially a biological clock. However, this article presents evidence and theoretical basis for the idea that the programmed aging function is controlled by an adaptive mechanism that can sense local or temporary conditions that affect the optimum aging function and adjust it to compensate for those conditions. This issue is important for medical research because the sensing mechanisms and associated signaling provide additional points at which intervention in the aging process and associated highly age-related diseases could be attempted.

Emerging programmed aging mechanisms and their medical implications.

For many generations programmed aging in humans was considered theoretically impossible and medical attempts to treat or delay age-related diseases were based on non-programmed aging theories. However, there is now an extensive theoretical basis for programmed mammal aging and substantially funded medical research efforts based on programmed aging theories are underway. This article describes the very different disease mechanism concepts that logically result from the theories and the impacts emerging programmed aging mechanisms will have on funding and performing medical research on age-related conditions.

Evolution of Aging Theories: Why Modern Programmed Aging Concepts Are Transforming Medical Research.

Programmed aging refers to the idea that senescence in humans and other organisms is purposely caused by evolved biological mechanisms to obtain an evolutionary advantage. Until recently, programmed aging was considered theoretically impossible because of the mechanics of the evolution process, and medical research was based on the idea that aging was not programmed. Theorists struggled for more than a century in efforts to develop non-programmed theories that fit observations, without obtaining a consensus supporting any non-programmed theory. Empirical evidence of programmed lifespan limitations continued to accumulate. More recently, developments, especially in our understanding of biological inheritance, have exposed major issues and complexities regarding the process of evolution, some of which explicitly enable programmed aging of mammals. Consequently, science-based opposition to programmed aging has dramatically declined. This progression has major implications for medical research, because the theories suggest that very different biological mechanisms are ultimately responsible for highly age-related diseases that now represent most research efforts and health costs. Most particularly, programmed theories suggest that aging per se is a treatable condition and suggest a second path toward treating and preventing age-related diseases that can be exploited in addition to the traditional disease-specific approaches. The theories also make predictions regarding the nature of biological aging mechanisms and therefore suggest research directions. This article discusses developments of evolutionary mechanics, the consequent programmed aging theories, and logical inferences concerning biological aging mechanisms. It concludes that major medical research organizations cannot afford to ignore programmed aging concepts in assigning research resources and directions.

Solving the programmed/non-programmed aging conundrum.

For more than 150 years there has been some level of scientific argument regarding whether aging in humans and other mammals is purposely genetically programmed because living too long produces an evolutionary disadvantage, or whether aging in mammals is non-programmed because there is no such disadvantage. Although for many decades it was very widely thought that programmed aging in mammals was theoretically impossible, new evolutionary mechanics theories and new discoveries support programmed mammal aging as well as programmed lifespan limitation in non-mammals. The emergence of modern programmed aging theories has created a schism in the bioscience community regarding the programmed/ non-programmed issue. Because the two theories have radically different predictions regarding the fundamental nature of aging and consequently the nature of highly age-related diseases like cancer, stroke, and heart disease, resolving this issue is critical to medical research. This article summarizes the evolutionary mechanics basis of modern programmed and non-programmed aging theories, describes some of the many ancillary circumstances that continue to prevent resolution of this issue, and recommends steps that could be taken to rapidly resolve the programmed/ non-programmed conundrum.

Is the evolutionary programmed/ non-programmed aging argument moot?

There are two modern evolutionary theories of mammal senescence: Programmed theories contend that mammals purposely limit their lifespans because doing so creates an evolutionary advantage. Non-programmed theories contend that each mammal specie only needs a particular lifespan and therefore only evolved and retained the capability for attaining that lifespan. Arguments over the evolutionary nature of aging have now existed for more than 150 years and for reasons described here may never be definitively resolved. The programmed/ non-programmed question is critical to medical research because the theories have grossly different predictions regarding the biological mechanisms associated with the aging process and therefore, the nature of age-related diseases and conditions. This article describes and compares two approaches for avoiding the need to obtain resolution on the evolutionary basis of senescence in order to identify and characterize the biological mechanisms responsible for aging and therefore the nature of highly age-related diseases.

Is the Evolutionary Programmed/ Non-programmed Aging Argument Moot?

There are two modern evolutionary theories of mammal senescence: Programmed theories contend that mammals purposely limit their lifespans because doing so creates an evolutionary advantage. Non-programmed theories contend that each mammal specie only needs a particular lifespan and therefore only evolved and retained the capability for attaining that lifespan. Arguments over the evolutionary nature of aging have now existed for more than 150 years and for reasons described here may never be definitively resolved. The programmed/ non-programmed question is critical to medical research because the theories have grossly different predictions regarding the biological mechanisms associated with the aging process and therefore, the nature of age-related diseases and conditions. This article describes and compares two approaches for avoiding the need to obtain resolution on the evolutionary basis of senescence in order to identify and characterize the biological mechanisms responsible for aging and therefore the nature of highly age-related diseases.

Solving the Programmed/ Non-Programmed Aging Conundrum.

For more than 150 years there has been some level of scientific argument regarding whether aging in humans and other mammals is purposely genetically programmed because living too long produces an evolutionary disadvantage, or whether aging in mammals is non-programmed because there is no such disadvantage. Although for many decades it was very widely thought that programmed aging in mammals was theoretically impossible, new evolutionary mechanics theories and new discoveries support programmed mammal aging as well as programmed lifespan limitation in non-mammals. The emergence of modern programmed aging theories has created a schism in the bioscience community regarding the programmed/ non-programmed issue. Because the two theories have radically different predictions regarding the fundamental nature of aging and consequently the nature of highly age-related diseases like cancer, stroke, and heart disease, resolving this issue is critical to medical research. This article summarizes the evolutionary mechanics basis of modern programmed and non-programmed aging theories, describes some of the many ancillary circumstances that continue to prevent resolution of this issue, and recommends steps that could be taken to rapidly resolve the programmed/ non-programmed conundrum.

Modern evolutionary mechanics theories and resolving the programmed/non-programmed aging controversy.

Modern programmed (adaptive) theories of biological aging contend that organisms including mammals have generally evolved mechanisms that purposely limit their lifespans in order to obtain an evolutionary benefit. Modern non-programmed theories contend that mammal aging generally results from natural deteriorative processes, and that lifespan differences between species are explained by differences in the degree to which they resist those processes. Originally proposed in the 19th century, programmed aging in mammals has historically been widely summarily rejected as obviously incompatible with the mechanics of the evolution process. However, relatively recent and continuing developments described here have dramatically changed this situation, and programmed mammal aging now has a better evolutionary basis than non-programmed aging. Resolution of this issue is critically important to medical research because the two theories predict that very different biological mechanisms are ultimately responsible for age-related diseases and conditions.

Aging, evolvability, and the individual benefit requirement; medical implications of aging theory controversies.

There is a class of theories of aging (variously termed adaptive aging, aging by design, aging selected for its own sake, or programmed death theories) that hold that an organism design that limits life span conveys benefits and was selected specifically because it limits life span. These theories have enjoyed a resurgence of popularity because of the discovery of genes that promote aging in various organisms. However, traditional evolution theory has a core tenet that excludes the possibility of evolving and retaining an individually adverse organism design, i.e. a design characteristic that reduces the ability of individual organisms to survive or reproduce without any compensating individual benefit. Various theories of aging dating from the 1950s and based on traditional evolution theory enjoy substantial popularity. Therefore, any theorist proposing an adaptive theory of aging must necessarily also propose some adjustment to traditional evolution theory that specifically addresses the individual benefit issue. This paper describes an adaptive theory of aging and describes how one of the proposed adjustments (evolvability theory) supports adaptive aging. This issue is important because adaptive theories are generally more optimistic regarding prospects for medical intervention in the aging process and also suggest different approaches in achieving such intervention.

Aging as an evolved characteristic - Weismann's theory reconsidered.

Theories of aging have become significantly more important because of discoveries which indicate that aging is not universal or inevitable and which therefore indicate that major medical intervention in aging is possible. Directions of anti-aging research could be significantly influenced by basic theories of aging. Weismann proposed in 1882 that aging was an evolved genetically programmed adaptation that had a species benefit. Since then this idea has been largely replaced by various theories in which aging is not an adaptation but results from accumulated adverse mutations or is an adverse side effect of some essential process. Arguments are presented to the effect that aging is an evolved beneficial characteristic and is therefore likely to result from a more complex and structured mechanism than if it resulted from more random processes such as mutation accumulation. Further, aging appears to be one of a number of related and interactive life-cycle characteristics including age-at-puberty suggesting that it might be controlled by similar biological mechanisms.