Why can’t I live forever

Why can’t I live everlastingly?

Why can’t I live everlastingly? Is it a positive thing to be able to make? What will enable me to make so? What will forestall me? The literature on the topic is voluminous, but some definitions foremost. Ripening: – this may be defined as “the progressive loss of map accompanied by diminishing birthrate and increasing mortality with progressing age.” ( Kirkwood & A ; Austad, 2000 ) , or “the accretion of diverse inauspicious alterations that increase the hazard of death” ( Harman, D. 1998 ) . Aging, nevertheless, can be divided into two types: – cell aging which occurs when cells lose the ability to split, and organismic aging which refers to whole organic structure impairment, and as such is similar to ageing ( Anon 1, 2006 ) .

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Some theories of ageing/senescence found in assorted articles, with most being taken from “Theories of Ageing” ( Anon, 2 ) are listed below. Other mentions used to roll up this include Anon 3, ( 2006 ) , Beckman & A ; Ames, ( 1998 ) and Kirkwood, ( 1997 ) .

  • Stress – Calorie limitation theory
  • Mitochondrial theory and disease
  • Free groups
  • Evolutionary theories, emphasis and length of service
  • Network theory of ageing
  • Mutation burden and accretion
  • Disposable haoma theory
  • Neuroendocrine theory
  • Wear and rupture theory
  • Familial control theory
  • Waste accretion theory
  • Limited figure of cell divisions theory ( associate to telomere lengths )
  • Hayflick Limit theory
  • Death Hormone theory
  • Thymic-stimulating theory
  • Mistakes and fixs theory
  • Excess DNA theory
  • Cross-link theory
  • Autoimmune theory
  • Rate of life theory
  • Telomerase theory of ageing
  • Bodily mutant theory
  • Antagonistic pleiotropy theory
  • Chemical harm
  • Reliability theory

Ripening is common to virtually all multi-cellular beings, but non to all unicellular beings. Many such as bacteriums simply have to maintain dividing to get away ageing and decease, the causes of their eventual deceases being such as environmental alteration or predation. One of the few multicellular beings to portion possible immortality with bacteriums is the cnidarian,Hydra( Gems, 2005 ) . Another is the sea windflower ( Kirkwood, 1997 ) and perchance several more. But how can we worlds extend our allotted clip to embrace immortality?

Harmonizing to Hughes & A ; Reynolds ( 2004 ) theories of ageing can be divided into two chief types, evolutionary and mechanistic. The former includes such as the mutant accretion, disposable haoma and counter pleiotropy theories, while the mechanistic attack includes for case oxidative emphasis opposition, cellular signalling and dietetic control methods in efforts to widen the normal life-span. The last of these, dietetic control in the signifier of Calorie limitation has moved from the pages of the scientific discipline diary to the popular imperativeness, where it is presented as a agency to widen life. Much of the work in this field has been on gnawers, nevertheless Roth, Ingram & A ; Lane ( 2001 ) used Primatess, with their work proposing similar benefits to that obtained with mice, such as a lower hazard of cardiovascular jobs, diabetes and other age-related diseases. However Roth et Al ( 2001 ) do non anticipate the usage of this method in worlds as they suggest that the 30 % decrease in nutrient consumption required for most of the grownup life span to be mostly unwieldy. A ulterior paper by de Grey, ( 2005 ) , concludes that dietetic limitations in worlds are merely likely to supply for 2-3 excess old ages of life at most. Therefore this does non look to be a really promising manner to increase human length of service.

But possibly we should inquire why we age at all – what the benefit is in increasingly deteriorating, frequently for many old ages, before deceasing? It helps prevent overcrowding of the planet, but how has development managed to bring forth a characteristic such as ageing with all its jobs for the person? One of the suggestions is that ageing is caused by the accretion of late-acting hurtful mutants. Mutants merely expressed in older persons past their generative prime are improbable to impact the population as a whole, plus the Numberss of older persons will be less ( due to extrinsic mortality factors such as disease, accidents and predation. Therefore these late playing hurtful mutants are improbable to be removed by natural choice, and over clip will distribute into the general population and be one of the chief causes of ageing. ( Peter Medawar’s Mutation Accumulation theory of ageing, as in Anon 1, 2006 ) .

Extrinsic mortality factors such as predation and disease will impact the life-span of persons, in that high extrinsic mortality equates to faster ageing and shorter life-spans. Thus 1 might anticipate worlds, populating as they do in controlled environments with no marauders to be longer lived than they are. Another factor, which affects age cohorts otherwise, is counter pleiotropy, a theory proposed by Wlliams ( 1957, cited by Anon, 1, 2006 ) . This states that a cistron may hold different affects depending on age, ie a cistron that has a good consequence early in life may be harmful when older, or vice-versa.

The list above of causes of ageing gives 25 factors ( out of a possible 300+ ) of greater or lesser importance. Several are based on stochastic, ie random events. This applies to for illustration the cross-linking theory of ageing, free extremist and rate of populating theories of ripening, and the bodily theory of ageing. Of these the rate of populating theory ab initio proposed by Pearl in 1928 ( cited by Anon 1, 2006 ) is the least plausible harmonizing to Anon 3 ( 2006 ) It suggests for case that all species take the same approximative figure of breaths, have a similar figure of pulses etc. However there is small if any solid grounds for this, and experimental consequences may demo otherwise. For case Le Bourg ( 1987 ) conducted experiments over the complete life span ofDrosophila melanogastor, and found that there was no correlativity between length of service and activity degrees. One might anticipate the less active flies to hold significantly increased length of service, but this was non the instance.

Other stochastic mechanisms of ageing have instead more grounds to endorse them up, and will be considered briefly here. For case the consequence of free groups on ripening was considered ( by Harman, cited in Barouki, 2006 ) some fifty old ages ago ( in 1956, Beckman & A ; Ames ) . He proposed that accrued oxidizers were the cause of alterations in cognitive and physical maps as the being aged. These alterations ( harm ) , were caused by O metamorphosis taking to production of free groups, which in bend oxidised nearby protein, lipid and DNA molecules, so changing their operation – DNA is damaged, proteins are cross-linked and age pigments may be formed. Antioxidents are needed to take extra free extremist build-up, and in some instances when fed in big measures to experimental animate beings, appear to decelerate down some of the ripening processes. But harmonizing to Anon 3 ( 2006 ) , animate beings fed big sums of antioxidants restrict their thermal consumption – and a decreased thermal consumption, as the writers point out, is the lone proven method so far of life extension.

A concluding ripening mechanism to be considered is decrease in telomere length, in which shortening of the telomeres occur with each cell division. Thus it is likely to be related to the finite figure of cell divisions an organisms cells can travel through earlier decease, and varies with species, and cell type within species. The terminals of the chromosome signifier a ‘cap’ consisting of DNA repetitions synthesised by the enzyme telomerase. At each cell division the telomeres shorten and finally the cell can no longer divide and so dies. That the telomeres are involved in ageing was eventually accepted in 1990, by the work of Bodner et Al, andVaziri and Benchimol ( cited by Iqbal, 2006 ) . This was demonstrated by the add-on of telomerase to normal bodily cells ( which do non incorporate this enzyme ) , followed by an addition of telomere length and alteration in morphology of the cells to younger looking 1s.

So why can’t I live everlastingly? Presently more is known about causes of ageing with efficaciously nil about its effectual bar.We are cognizant of many things which contribute to ageing, but for its bar all that can be suggested at nowadays is to drastically control 1s appetite for the continuance of 1s big life. So many things play their portion in ageing that one theory, the web theory of ageing ( Kowald & A ; Kirkwood, I996 ) incorporates many of them, so admiting the interaction happening between many of the different mechanisms. Telomere research would look to be the country to concentrate on if any appreciable life extension is the purpose, but of class there is the down side to be considered. Cancer cells have overcome the destiny of normal cells and can go on spliting for countless times – ( see the HeLa cell line used for old ages in malignant neoplastic disease research ) . Thus research on ripening is likely to include and integrate malignant neoplastic disease surveies until the two can be efficaciously separated.

  • Anon. 1 Aging

hypertext transfer protocol: //en.wilkipedia.org/wiki/Senescence accessed 05/11/06

  • Anon 2 Theories of Aging

hypertext transfer protocol: //www.prolonyouth.com/theories.html accessed 05/11/06

  • Anon 3 How do we age? hypertext transfer protocol: //www.healthandage.com/html/min/afar/content/other2_2.htm accessed 05/11/06 )
  • Beckman, K.B. & A ; Ames, B.N. The Free Radical Theory of Aging Matures. Physiol. Rev. ( 1998 ) 78: pp 547-581
  • Gems, D. Lecture 2 – Investigating ageing utilizing carnal theoretical accounts. Biology C339/3a/b, ( 2005 )

Hypertext transfer protocol: //www.ucl.ac.uk/ucbtdag/C339Ageing.html accessed 05/11/06

  • De Grey, A.D. The unfortunate influence of the conditions on the rate of ripening: why human thermal limitation or its emulation may merely widen life anticipation by 2-3 old ages.

hypertext transfer protocol: //www.ncbi.n1m.nih.gov.gov/entrez/wuery.fcgi? db=pubmed & A ; cmd=… accessed 05/11/06

  • Harman, D. Aging: Phenomena and Theories. Annalss of the New York Academy of Sciences ( 1998 ) 854: pp1-7
  • Hughes, K.A. & A ; Reynolds R.M. Evolutionary and Mechanistic Theories of Aging. Ann. Rev. Entomol. ( 2005 ) vol.50: pp421-445
  • Iqbal, M.A. Chromosome Telomeres: The Aging Clock

hypertext transfer protocol: //www.kfshrc.edu.sa/annals/186/98-246ed.html accessed 05/11/06

  • Kirkwood, T.B.L. The beginnings of human ageing. Phil. Trans. R. Soc. Lond. B ( 1997 ) 352: pp1765-1772
  • Kowald, A. & A ; Kirkwood, T.B. A web theory of ripening: the interactions of faulty chondriosomes, deviant proteins, free groups and scavengers in the ripening procedure. Mutat Res. ( 1996 ) 5:316 ( 5-6 ) : pp 209-236
  • Le Bourg, E. The rate of life theory. Spontaneous locomotor activity, aging and length of service inDrosophila melanogastor Exp Gerontol.( 1987 ) :22 ( 5 ) : pp 359-369
  • Roth, G.S. , Ingram, D.K. & A ; Lane, M.A. Caloric Restriction in Primates and Relevance to Humans. Annalss of the New York Academy of Sciences ( 2001 ) 928: pp305-315
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