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Longevity
Octogenarians on dialysis: lessons in longevity and quality of life. A biological age of 20+?
Rogers S, Omilian J, Holcomb J, Long Y.
Greenfield Health Systems (GHS), Detroit, USA.
A review of literature indicates that people who experience longevity have certain characteristics and personality traits in common. While family history and health habits play an important role, centenarian research reveals that family support, an optimistic attitude, a sense of purpose, and an ability to manage stress, all can contribute to longevity. Social workers conducted intensive life review interviews with 17 octogenarians receiving dialysis at a clinic in the Detroit suburb Eastpointe, Mich. to learn more about their backgrounds, health habits, and coping styles in order to determine if they shared tendencies found in centenarians, and the implications it had for younger dialysis patients. Our initial findings support our hypothesis: Octogenarians on dialysis often share characteristics with centenarians, something that may help them to stave off or ameliorate the effects of chronic illness until later in life.
Reduced telomerase activity in human T lymphocytes exposed to cortisol; reduce stress to live longer!
Choi J, Fauce SR, Effros RB.Brain Behav Immun. '08 May;22(4):600-5. Epub 2008 Jan 25.
Department of Pathology and Laboratory Medicine, David Geffen School of Medicine at UCLA, 10833 Le Conte Avenue, Los Angeles, CA 90095-1732, USA.
Accelerated telomere shortening in lymphocytes has been associated with a variety of human pathologies, including HIV disease, Down syndrome, and cardiovascular disease. Recent findings indicate that reduced telomere length is also associated with chronic psychological stress and mood disorders. Telomerase, which prevents telomere shortening, can be upregulated in T lymphocytes in concert with activation, thereby retarding telomere shortening. Here, we demonstrate that exposure of human T lymphocytes to cortisol is associated with a significant reduction in telomerase activity both during primary stimulation of resting cells and secondary stimulation of previously activated cells. The effect is observed in both CD4 and CD8 T lymphocytes, and is associated with reduced transcription of hTERT, the telomerase catalytic component. These findings provide a potential mechanism for stress-associated telomere length attrition, and suggest that strategies to enhance T lymphocyte telomerase activity may provide beneficial effects on immune function in situations of chronic emotional stress.
The GH/IGF-I axis and longevity.
Holzenberger M. Eur J Endocrinol. 2004 Aug;151 Suppl 1:S23-7.
Inserm U515, Hopital Saint-Antoine, 184 rue Fbg St-Antoine, 75571 Paris 12, France. holzenberger@st-antoine.inserm.fr
Several converging lines of evidence obtained over the last years in a wide variety of experimental model organisms suggest that the ageing process is regulated by genes that encode proteins from the somatotroph axis: longevity genes like daf-2, which were identified using mutant Caenorhabditis elegans strains, turned out to be orthologues of the mammalian genes encoding insulin-like signalling cascade proteins. Transgenic flies with mutations in the corresponding insect genes showed a similar pattern of increased lifespan. Finally, mice with spontaneous mutations leading to pituitary hormone deficiency significantly outlived controls.
While these and other genetic models suggest that the downregulation of the somatotroph axis can slow the ageing process, other results from studies using pharmacological administration of growth hormone suggest that such stimulating treatment can restore some of the phenotypic traits associated with youth. To better understand the role of the insulin-like receptors in mammalian lifespan regulation and ageing, we explored the phenotype of heterozygous IGF-I receptor (IGF1R) knockout mice. Compared with control littermates these mutants live longer without any obvious impairment of their health and physiology, except a reduced glucose tolerance that we observed in males. These IGF1R(+/-) mutants were also more resistant to oxidative stress in vivo, and we identified a possible molecular pathway linking underphosphorylation of IGF-I receptors to the lack of activation of p66Shc, a protein capable of increasing resistance to oxidative stress through regulation of a set of downstream genes.
These and other results suggest that in mammals too, lifespan can be increased by continuous, long-term downregulation of IGF signalling. Since growth hormone administration normally stimulates IGF production in tissues, the question arises whether the beneficial effects of GH, as reported by others, could be IGF independent. This hypothesis can be addressed, for example, by adequately combining existing transgenic mouse models.
Is there such thing as "vaccine against aging"?
Davidovic M, Milosevic DP, Despotovic N, Sekularac N, Erceg P.
Center of geriatrics, KBC Zvezdara, 11000 Beograd, Presevska 31, Serbia. davidovi@eunet.yu Adv Gerontol. 2007;20(2):56-9.
Problem could be found in the fact that very often we look for one deciding, definitive reason for the process of aging. It is a sort of search for a big discovery, like a fountain of youth or such. More and more authors are trying to explain the unknowns in the understanding of these observations about ageing, by adding the statement that there are two subgroups in the general population. This acknowledgement of two subpopulations explains why there are numerous cases that can not be explained or defined or fitted in these basic observations about caloric restrictions and the delay of reproduction. The identification of those two groups would allow us to find more realistic results in studies, and therefore a more efficient therapy of certain diseases. This hypothesis does not contradict theories of aging that we have accepted (at least not the majority of accepted theories), and this hypothesis also does not contradict the fact that there is a large interindividual variability. This hypothesis doubts, and claims there are exceptions to the starting assumption of geriatrics and gerontology's that: "parallel to the aging process the functions of all organs and organ systems lessen". In future we could use one of these screening tools to detect genetic instable population: the cytokinesis-block micronucleus assay, expression of hTERT, the component of the enzyme telomerase, identification of the "longevity" genes like daf-16, p53, THO, HSP70 or the level of insulin-growth factor-I. This would enable us to correct genetic instability in this population with "vaccine of youth", making the human race living 30 years longer with excellent life quality.