In spite of the significant advancement in science and technology, the science behind lifespan is still a mystery. The theories that explain the process of aging and life span, are broadly divided into programmed and error theories (Jin, 2010). Though none of these theories are completely satisfactory, they do help to enhance one’s understanding in the area. According to the programmed longevity theory, aging follows a biological timetable, which is innate and heritable. The theory was first suggested by August Weismann. He theorized that; there is an actual limit to the extent of somatic cell division in a species, and this is innately programmed. The number of cell generations varies from species to species and this determines their average lifespan.
Though Weismann’s theory was initially criticized for the lack of experimental evidence; later, scientists were able to demonstrate experimentally, that generations of long lived fruit flies lived longer like their regenerators and generations of short lived fruit flies lived shorter. The switching on and off of certain genes with time could be the reason behind the programming process. Environmental factors also determine a species life span. Placing animals in a dangerous environment, decreased lifespan in both the animals and its progeny.
In support of Weismann’s theory, scientists have discovered in lower eukaryotes like yeast, worms, flies, mice and salmon; the evidence for a molecular pathway that regulates aging (Longo, Mitteldorf & Skulachev, 2005) . This raises the possibility for such gene controlled programming in higher eukaryotes as well. Thus scientist were able to establish through experiments the evolutionary plasticity of aging and longevity as predicted by Weismann.
Benefits of using programmed longevity theory to describe longevity: According to Weismann’s theory of programmed longevity, every organism has a suicidal program that is triggered after a set time. Scientists have discovered an evolutionarily conserved insulin/IGF-1 signaling pathway, which plays an important role in hormonal regulation of aging. A mutation in this signaling pathway increased active lifespan in Caenorhabditis elegans. Likewise the immune system is programmed to decline with time, and this increases the susceptibility to infection and diseases. Though programmed longevity theory is not an ultimate theory to explain lifespan, it has set a platform for further elaborative studies and advanced theories. (Gavrilov & Gavrilova, 2002)
Currently, mutation accumulation theory and antagonistic pleiotropy theory are widely accepted theories to explain aging and lifespan. Both these theory support, the initial evolutional conservation of longevity proposed by the programmed longevity theory. On the other hand, the claim that; aging is an essential and innate part of an individual’s biology is contradicted by accumulation of mutation theory. Nevertheless, programmed longevity theory supports the role played by genes in the control of aging. All the later programmed theories of aging, evolved from the original idea of programmed longevity theory.
Programmed longevity theory, supports the presence of an inbuilt cell program, which determines the point when the cell loses its ability to replicate and initiates apoptosis process. This point is described as “growing old” point. Leonard Hayflick demonstrated through human cells culture experiments, that cell did stop to multiple after a finite number of cell divisions. He determined that fetal cells multiplied close to 100 times, and cells of 70year old multiplied only 20 times before undergoing cell death. Later the discovery of shortening of the telomeres with each cell division, provided molecular explanation for this observation.
Limitation of programmed longevity theory: According to Weismann’s programmed longevity theory, all somatic cells have a limited number of generation cycle and this limitation decides the onset of aging. However, Alex Carrel and Albert Ebeling, showed by experimental evidence that chicken fibroblast like cells can be cultivated in cell culture flask, indefinite number of time. Researchers argue that, cell death is not a result of an inherent program, but by an environmental induced cell programming that triggers cell death. Programmed longevity theory is further limited by the lack of identifying a clear pathway that supports the inherent quality of a cell to die after a set time duration. The cause and effect relations that will provide evidence for this theory is still lacking. (Gavrilov & Gavrilova, 2002)
According to the programmed longevity theory, a given species must have similar average lifespan, irrespective of the environment. Ignoring environmental influence, is one of the greatest limitation of this theory. Average lifespan of Chaffinch in captivity was 29 years, while in the wild it was 1.2 to 1.5 years. Similar observations were made for other species as well. To date no one has determined the age of programmed cell death for any species.
Conclusion: Selective deterioration or cell death specific to a tissue is not considered aging. Aging is a generalized process and programmed longevity theory has helped bio gerontologist to conceive the fundamental idea behind the evolutionary nature of aging. It was the first theory to explain aging and lifespan from an evolutionary viewpoint. Though it was later abandoned for the lack of experimental evidence, current molecular biology findings on the pathways that regulate aging has helped to revive the theory back into main stream.
Bio-gerontology research has been completely transformed by the identification of single gene mutations that were able to reverse the aging process. Single gene mutations of daf-2 gene and methuselah gene in nematode and fruit flies respectively, were able to reveres aging by about 30-35% (Gavrilov & Gavrilova, 2002). The present challenges in bio-gerontology, is to determine genes that control aging in humans and to control the time of onset of aging.
References
Gavrilov, L., & Gavrilova, N. (2002). Evolutionary Theories of Aging and Longevity. The Scientific World JOURNAL, 2, 339-356. doi:10.1100/tsw.2002.96
Jin, K. (2010). Modern Biological Theories of Aging. Aging Dis., 1(2), 72–74.
Longo, V., Mitteldorf, J., & Skulachev, V. (2005). Opinion: Programmed and altruistic ageing. Nat Rev Genet, 6(11), 860-866. doi:10.1038/nrg1706
