Vitetta and Anton Concluding remarks The purest use of the term “biological aging” conﬁnes it exclusively to molecular changes. Hayﬂick (2003) deﬁnes aging in biological systems as a stochastic process that occurs systemically after reproductive maturity in animals that reach a ﬁxed size in adulthood and that it is then caused by the esca- lating loss of molecular ﬁdelity that ultimately exceeds repair capacity. This then increases the vulnerability to pathology or age-associated diseases. Further, that there is a ﬁnitude associated with aging that eventually leads to death (Hayﬂick 2003). Grimley Evans (2000) deﬁned senescent changes as de novo structural and functional alterations that are not part of the developmental program. In this selective and brief review we have summarized the scientiﬁc evidence that may prevent disease and maintain the molecular integrity of the organism, thus expanding the mean life expectancy whilst operating within the framework of normal physiological function and repair. We ﬁnd that whilst aging is not irreversible and inevitable, certain key factors may add signiﬁcant beneﬁts to human mean life expectancy. There is a vast array of scientiﬁc literature that concludes that lifestyle modiﬁcation factors that optimize nutrition, physical activity and mental health have signiﬁcant correlates with reducing the risks of disease in later life that is translates into an increased mean life expectancy. Further, although the correction of all hormonal deﬁcits by an adequate multiple hormone replacement therapy, is not currently possible, hormone therapy does constitute a viable solution to prevent and treat most hormonal deﬁcits due to pathological aging. Hertogue (2005) recently reported that even though we are not presently able to abrogate senescence by hormone treat- ments because of the unavailability as medications of all hor- mones that decline with age, the future appears promising. As a ﬁnal note; with the onset of the 21st century, it is apparent that we stand on the horizon of a revolution in anti aging therapies and technologies. A promising therapeutic modality, the concept of stem cell treatments, will within the next decade, allow a markedly expanded quality of health and possibly also further increase the mean human life expec- tancy. Recent advances by major corporations, both private and public, have documented that we are already capable of taking stem cells from an individual and selectively copy- ing these cells along with their DNA components. Thus making possible the restoration and rejuvenation properties that human bodies lose as they age. The prospects for use of human embryonic stem cells derivatives in regenera- tive medicine hence are signiﬁcant (Trouson 2006). If, the potential contributions to human regenerative medicine can 542 be realized, signiﬁcant alterations and enhancement of mean life expectancy in humans will be possible. References Ader R. 2003. Conditioned immunomodulation: research needs and directions. Brain Behav Immun, (Suppl 1):S51–7. Review. Anton B, Vitetta L, Cortizo F, Sali A. 2005. Can we delay aging? The biology and science of aging. Ann N Y Acad Sci, 1057:525–35. Balaban RS, Nemoto S, Finkel T. 2005. Mitochondria, oxidants, and aging. Cell, 120:483–95. Baur JA, Sinclair DA. 2006. Therapeutic potential of resveratrol: the in vivo evidence. Nat Rev Drug Discover, 5:493–506. Bennett R. 2005. Growth hormone in musculoskeletal pain states. Curr Pain Headache Rep, 9:331–8. Cheng SY. 2005. Isoform-dependent actions of thyroid hormone nuclear receptors: lessons from knockin mutant mice. Steroids, 70:450–4. Cleare AJ. 2004. The HPA axis and the genesis of chronic fatigue syndrome. Trends Endocrinol Metab, 15:55–9. Cranney A, Papaioannou A, Zytaruk N, et al. 2006. Parathyroid hor- mone for the treatment of osteoporosis: a systematic review. CMAJ, 175:52–9. Crestanello JA, Doliba NM, Doliba NM, et al. 2002. Effect of coenzyme Q10 supplementation on mitochondrial function after myocardial ischemia reperfusion. J Surg Res, 102:221–8. Duan W, Mattson MP. 1999. Dietary restriction and 2-deoxyglucose administration improve behavioral outcome and reduce degeneration of dopaminergic neurons in models of Parkinson’s disease. J Neurosci Res, 57:195–206. Engelman RW, Day NK, Chen RF, et al. 1990. Calorie consumption level inﬂuences development of C3H/Ou breast adenocarcinoma with indif- ference to calorie source. Proc Soc Exp Biol Med, 193:23–30. Fernandes G, Yunis EJ, Good RA. 1976. Suppression of adenocarcinoma by the immunological consequences of calorie restriction. Nature, 263:504–7. Fernandes G, Good RA. 1984. Inhibition by restricted calorie diet of lym- phoproliferative disease and renal damage in MRL/lpr mice. Proc Natl Acad Sci, 81:6144–8. Finkel T, Holbrook NJ. 2000. Oxidants, oxidative stress and the biology of aging. Nature, 408:239–47. Global Population Aging in the 21st Century and Its Economic Implications. 2005. URL: http://www.cbo.gov/ftpdocs/69xx/doc6952/12-12-Global. pdf. Grimley Evans J. 2000. 21st Century: Review: ageing and medicine. J Intern Med, 247:159–67. Guarente l, Kenyon C. 2000. Genetic pathways that regulate aging in model organisms. Nature, 408:255–62. Guarente L, Picard F. 2005. Cell, 120:473–82. Harman D. 1956. Aging: a theory based on free radical and radiation chem- istry. J Gerontol, 11:298–300. Hayﬂick L. 2003. Living forever and dying in the attempt. Exp Gerontol, 38:1231–41. Heilbronn LK, de Jonge L, Frisard MI, et al. 2006. Effect of 6-month calorie restriction on biomarkers of longevity, metabolic adaptation, and oxidative stress in overweight individuals: a randomized controlled trial. JAMA, 295:1539–48. Hertogue T. 2005. The “multiple hormone deﬁciency” theory of aging: is human senescence caused mainly by multiple hormone deﬁciencies. Ann N Y Acad Sci, 1057:448–65. Review. Holloszt JO. 1997. Mortality rate and longevity of food-restricted exercising male rats: a reevaluation. J Appl Physiol, 82:399–403. Howitz KT, Bitterman KJ, Cohen HY, et al. 2003. Small molecule activa- tors of sirtuins extend Saccharomyces cerevisiae lifespan. Nature, 425:191–6. Ingram DK, Weindruch R, Spangler EL, et al. 1987. Dietary restriction beneﬁts learning and motor performance of aged mice. J Gerontol, 42:78–81. Clinical Interventions in Aging 2007:2(4)