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In this video we will discuss the antagonistic hallmarks of ageing's response to damage in relation to Growth hormone and Insulin like growth hormone-1.We will focus on the 3 hallmarks : Mitochondrial dysfunction, Deregulation of nutrient sensing and Cellular senescence. Mitochondrial dysfunction is involved in the generation of reactive oxygen species (R O S) .Although age induced mitochondrial dysfunction and overall reductions in the secretion and action of G H and I G F 1 coincide, a clear causality between both processes has not yet been established. The R O S theory gives a clearer explanation about this. Lower levels of R O S are needed to maintain proper mitochondrial function. However, excessive amounts of R O S will promote accelerated ageing. Mitochondrial dysfunctions also influence the somatotropic axis. Alterations in this axis have been linked to unfavourable effects on mitochondrial metabolism in the brain, muscle, and skeletal tissue. Evidence suggests that alternate day fasting has the capability to avoid mitochondrial degeneration. Deregulated nutrient sensing which has different pathways influenced by nutrient levels. We will focus on the Insulin and Insulin-like growth factor signalling, because The I I S is the most conserved age-controlling pathway. The I G F 1 pathway is the same as that elicited by insulin, which informs cells of the presence of glucose. Resulting in an increase in blood glucose, insulin and I G F 1 when we eat. Attenuation of the I I S pathway appears to extend the life span in several model organisms like mice, fruit flies and worms. Moreover, mutations or polymorphisms which limit the functions of G H , I G F 1, and insulin receptors are associated with longevity. Finally, Cellular senescence, defined as irreversible cell cycle arrest is driven by a variety of mechanisms, including telomere shortening, DNA damage, Gene expression, stress, and inflammatory cytokines. With age we have an accumulation of cell damage resulting in lower I I S signalling and therefore lower senescence, inflammation and decreased ageing. This brings us to a Paradox.Low levels of I G F 1 are associated with longevity. However, too low levels of I I S signalling are incompatible with life. There is enough evidence to support the relationship between the antagonistic hallmarks of ageing/I I S signalling and the way they regulate cell balance during the ageing process. When they lose balance, major metabolic pathways could be affected leading to age related diseases and accelerated ageing. This relationship could be seen as biphasic. Supressing growth at the advantage of repair and maintenance.