Sunday, 18 March 2012

Can we slow down the ageing process? - Nathan Kok (42927611)

Ageing is an inevitable process that occurs in every living being. However, the lifespan of different organisms may differ greatly, e.g. an adult Mayfly has a lifespan of between 30 minutes to 48 hours (CSIRO, 1996) and a tortoise can live up to over 200 years (Wonderquest, 2001). As lifespan differs greatly from species to species, it seems possible that the ageing process can be controlled and used to prolong lives through the modification of genetics. Although the early stages of ageing may provide benefits such as intellectual and physical maturity, it is laced with many long term negatives including physical and mental degradation, as well as an increased susceptibility to diseases (National Institute of Ageing, 2009) and terminal illnesses such as cancer (SEER, 2010).

                                            Incidence of Cancer by Age 2003-2007
                                                                (SEER 2010)
Further, it has been discovered that age-related diseases can be combated by DNA mutations that hinder the ageing process (Kenyon, 2010). This produces an underlying message that humans, as well as other organisms, have the capability to live much longer, and formed the basis of Kenyon's study (2010). Although much about this topic is still undiscovered, there is significant evidence that ageing is in fact genetic based and can be controlled.

                                                      Werner's Syndrome patient (WS)

The relationship between ageing and genetics became notable with Kenyon's experimentation with the Caenorhabditis elegans (nematode). This was achieved through the manipulation of insulin / IGF-1 (Revision History of Insulin-Like Growth Factor 1, 2012). Experiments showed mutations in the DNA which reduces activity of the daf-2 gene in the nematode, that "encode hormone receptors similar to the insulin and IGF-1 receptors" (Kenyon, 2010). This changes gene expression, which is shown to increase the lifespan of the nematode greater than two-fold (Garigan, 2002). Although results were quite convincing for nematodes, it was questionable whether this process would affect more complex animals. It was determined in mice and small dogs that an inverse relationship between IGF-1 receptors and lifespan was prevalent, and supported the basis that IGF-1 was responsible for ageing (Kenyon, 2010), i.e. the lower the level of IGF-1 receptors and insulin, the longer the expected lifespan. Furthermore, it was discovered that the reduced pace of ageing did not commence until growth had stopped (de Magalhaes, 2011). One question remained - whether this IGF-1 receptor had any influence on the speed of ageing in humans (Kenyon, 2010). Studies demonstrated that it was possible, showing a community of Ashkenazi Jewish centenarians, who had deficiencies in the IGF-1 receptor, who possessed extended longevity (Suh et al., 2008). This mutation in the DNA was also prominent in the Japanese, and is linked to their ability to maintain their youthfulness well into their adulthood (Kojima et al., 2004).

If the findings of Kenyon's experimentation in nematodes can be transferable to humans, scientists may be capable of manipulating human life span. Through Kenyon's experimentation with the Caenorhabditis elegans, she has provided evidence of the existence of genetic-based longevity. These prospects give rise to new possibilities and will play a prominent role in society in the future in combating age-related diseases and prolonging life.

CSIRO 1996, Ephemeroptera: Mayflies, viewed 13 March 2012, <>

De Magalhaes, JP 2011, 'Is Ageing Genetic or Is It Wear and Tear?', <>

Garigan, D. et al 2002, 'Genetic analysis of tissue aging in Caenorhabditis elegans: a role for heat shock factor and bacterial proliferation', Genetics161, 1101–1112

Kenyon, CJ March 25 2010, 'The Genetics of Ageing' , Nature Volume 464.

Kojima, T. et al 2004, 'Association analysis between longevity in the Japanese population and
polymorphic variants of genes involved in insulin and insulin-like growth factor 1 signaling
pathways'. Exp. Gerontol. 39, 1595–1598.
National Institute of Aging 2009, 'Sexuality Later in Life', viewed 14 March 2012, <>

Revision History of Insulin-Like Growth Factor 1 2012, viewed 14 March 2012, <>

SEER Cancer Statistics 2010, 'Age-Specific SEER Incidence Rates, 2003-2007', Released April 15, 2010, viewed 13 March 2012, < >.

Suh, Y. et al 2008, 'Functionally significant insulin-like growth factor I receptor mutations in
centenarians'. Proc. Natl Acad. Sci. USA 105, 3438–3442.

Wonderquest 2001, Longest and Shortest Life Span', viewed 13 March 2012, <>

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