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The Scientific Theory Behind Aging – The Science of Aging

Even with the recent advancements in genetics and molecular biology the mystery behind human lifespans, for the most part, still remains just that – a mystery. There are numerous theories that have been proposed about aging and they fall into two categories – programmed theories and error theories. Neither one of these categories does a great job of explaining the process of aging. The process tends to be far more complex than that. The science of aging is still based mostly on theory. Let’s delve into this further.telomere

Why do we start to age? What are age markers? Is there a limitation on just how old we can grow? These are questions that mankind has long asked. In spite of the advances the mystery of life has yet to be solved. The traditional theories about aging are not considered satisfactory. Traditional theories of aging said it was neither genetically programmed or adaptation that causes aging. Modern theories fall into two main categories1. Programmed theory and 2. Error/Damage Theory.

The programmed theory implies that aging follows a biological timetable that is likely linked to childhood growth and development regulation, which depends on the genes to maintain, repair and defend themselves. This is different than the damage or error theory, which puts the emphasis on environmental attacks that result in various levels of damage that cause aging.

There are three sub-categories in the programmed theory. They are:

  1. Programmed Longevity – Aging is caused by a sequential switching on/off of specific genes. Senescence is defined as the era that deficits associated with aging are evident. Dr. Davidovic et al talks about genetic instabilities role in aging and aging process dynamics.[1]
  2. Endocrine Theory – It is believed that hormones control the speed at which we age. Recent studies have confirmed that aging is regulated through hormones and that the proof is in the conservation of insulin/IGF-1 signaling (IIS) pathways and the major role they play in the hormonal regulation of aging. Dr. van Heemst talks about the potential mechanism that is primary to IIS and the aging process.[2]
  3. Immunological Theory –The theory is the programming of your immune system is designed to decline over time, which will increase your susceptibility to infectious disease, cause you to age and eventually lead to death. The science shows that the immune system effectiveness peaks at puberty and from there it will gradually decline as one ages.[3] The regulated immune system response has been linked to inflammation, cancer, cardiovascular disease and Alzheimer’s disease.[4]

The error theory includes:

  1. Wear & Tear Theory – Your cells/tissues have key parts and as we age they wear out. It’s a bit like equipment wearing out from use. In 1882, a German biologist by the name of Dr. August Weismann, introduced this theory. Even today, many feel it makes sense.
  2. Rate of Living Theory – This theory believes that the higher your rate of oxygen basal metabolism is the shorter your life span is going to be.[5] While it helps somewhat it isn’t enough to explain maximum life span.[6] Rollo suggests a verion of the living theory that has been modified. It emphasizes the hard wired antagonism of growth and stress resistance.[7]
  3. Cross Linking Theory – In 1942 this was suggested by Johan Bjorksten whose theory was cross linked proteins accumulated and damaged cells/tissues, which in turn slowed down the body’s process of aging. Some studies that are more recent have confirmed the role of cross linking.[8]
  4. Free Radical Theory – In 1954 Dr. Gershman introduced this theory, but actually Dr. Denham Harman developed it, proposing that superoxide along with free radicals caused damage to cells and this damage was cumulative, eventually affecting organs that could stop functioning.[9] It was as far back as the 1930s that it was discovered calorie restricting can extend one’s life. At least, that’s what was found in animals in the lab. [10,11] A number of studies tried to clarify the mechanisms that were underlying in this model; however, that knowledge was not forthcoming until 1990.[12] Recently there has been evidence that this happens because of an increase in free radical formation within the mitochondria that lead to a secondary induction of an increase in the capacity of antioxidant defense
  5. Somatic DNA Damage Theory – DNA damage is continuous in all cells. Most damage is repaired, but some does accumulate and other repaired mechanisms become defective. Genetic mutation happens as you age, which causes the cells to deteriorate and eventually manfunction. [10]
  6. Telemore Theory – Interestingly, there are some neurological diseases that are thought to become high risk as we age, such as Alzheimer’s, which is largely diagnosed in those that are over the age of 65. Creating aging model systems could help to better understand the aging process. In the earliest stages the inability to develop new memories is one of the most common symptoms seen. Recent studies have shown the endogenous neural stem cells located in the hippocampus of the brain could entail the memory function. [13,14] Time and again the hippocampus neural stem cell function decreases with age.[15] It is established that telomere maintenance seems to be necessary for the extended perseverance of the stem cell function in organs where the cells turn over extensively. [16]Back in 1961, a doctor by the name of Dr. Hayflick had a theory that the ability of the cells to divide is limited to approx. 50 times, and that after that they no longer divide. The telomere theory believes telomeres have been shown to shorten each time the cell divides. Some cells, such as sperm and egg cells, use telomerase in order to be able to restore telomeres to the end of their chromosome, which insures these cells are able to keep reproducing and promoting the survival of the species. However, most cells do not have this capacity. Once the critical length is reached by the telomeres, the cells will stop replicating at a significant rate and so they die off, which then leads to death. [17]

    A recent study showed that telomeres do shorten with age in the neural stem cells of the hippocampus and that mice that are telomerase-deficient show reduced neurogenesis and impaired neuronal differentiation and neuritogenesis. [18]

Conclusion – What’s the Meaning of all This?

Hormones definitely have an impact on aging. No matter what theory you believe, most agree on this point. However, how they control the rate at which we age or isn’t quite understood yet. Some anti aging doctors prescribe HGH to slow the aging process. HGH research has proven that HGH can reverse some signs of aging such as reducing/eliminating fine lines and wrinkles, increased energy, increased libido, decreased body fat, increase lean muscle mass, and the list goes on. What has not been studies is the long term affects of taking HGH.

References

[1] Eriksson PS, Perfilieva E, Bjork-Eriksson T, Alborn AM, Nordborg C, Peterson DA, Gage FH. Neurogenesis in the adult human hippocampus. Nat Med. 1998;4:1313–7. [PubMed]

[2] Davidovic M, Sevo G, Svorcan P, Milosevic DP, Despotovic N, Erceg P. Old age as a privilege of the “selfish ones” Aging and Disease. 2010;1:139–146. [PMC free article] [PubMed]

[3] van Heemst D. Insulin, IGF-1 and longevity. Aging and Disease. 2010;1:147–157. [PMC free article] [PubMed]

[4] Cornelius E. Increased incidence of lymphomas in thymectomized mice–evidence for an immunological theory of aging. Experientia. 1972;28:459. [PubMed]

[5] Rozemuller AJ, van Gool WA, Eikelenboom P. The neuroinflammatory response in plaques and amyloid angiopathy in Alzheimer’s disease: therapeutic implications. Curr Drug Targets CNS Neurol Disord. 2005;4:223–233. [PubMed]

[6] Brys K, Vanfleteren JR, Braeckman BP. Testing the rate-of-living/oxidative damage theory of aging in the nematode model Caenorhabditis elegans. Exp Gerontol. 2007;42:845–851. [PubMed]

[7] Hulbert AJ, Pamplona R, Buffenstein R, Buttemer WA. Life and death: metabolic rate, membrane composition, and life span of animals. Physiol Rev. 2007;87:1175–1213. [PubMed]

[8] Rollo CD. Aging and the Mammalian Regulatory Triumvirate. Aging and Disease. 2010;1:105–138. [PMC free article] [PubMed]

[9] Gerschman R, Gilbert DL, Nye SW, Dwyer P, Fenn WO. Oxygen poisoning and x-irradiation: a mechanism in common. Science. 1954;119:623–626. [PubMed]

[10] Harman D. Aging: a theory based on free radical and radiation chemistry. J Gerontol. 1956;11:298–300. [PubMed]

[11] Li Y, Mu Y, Gage FH. Development of neural circuits in the adult hippocampus. Curr Top Dev Biol. 2009;87:149–74. [PubMed]

[12] Ma DK, Bonaguidi MA, Ming GL, Song H. Adult neural stem cells in the mammalian central nervous system. Cell Res. 2009;19:672–82. [PMC free article] [PubMed]

[13] Querfurth HW, LaFerla FM. Alzheimer’s disease. N Engl J Med. 2010;362:329–44. [PubMed]

[14] Potter H, Geller LN. Alzheimer’s disease, Down’s syndrome, and chromosome segregation. Lancet. 1996;348:66. [PubMed]

[15] Potter H, Geller LN. Alzheimer’s disease, Down’s syndrome, and chromosome segregation. Lancet. 1996;348:66. [PubMed]

[16] Geller LN, Potter H. Chromosome missegregation and trisomy 21 mosaicism in Alzheimer’s disease. Neurobiol Dis. 1999;6:167–79. [PubMed]

[17] Johnson LV, Leitner WP, Rivest AJ, Staples MK, Radeke MJ, Anderson DH. The Alzheimer’s A beta -peptide is deposited at sites of complement activation in pathologic deposits associated with aging and age-related macular degeneration. Proc Natl Acad Sci U S A. 2002;99:11830–5. [PMC free article] [PubMed]

[18] Anderson DH, Talaga KC, Rivest AJ, Barron E, Hageman GS, Johnson LV. Characterization of beta amyloid assemblies in drusen: the deposits associated with aging and age-related macular degeneration. Exp Eye Res. 2004;78:243–56. [PubMed]

 

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