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Life expectancy at birth increased by more than 30 years during the last
century. However, maximal life span increased little during the last centuries
indicating that there is a limit in the maximal life expectancy of the human
species. The respective roles of and interactions between genes,
environment and stochastic factors determine the pace of the aging
process. The important progress in the biomedical domain contributes in the
development of strategies for the prevention of the functional decline and
the frailty process, thereby increasing the probability of successful aging.
However, it is rather illusory that these actions may alter the limits of human
maximum longevity and stop the ageing process.
The progressive increase of aortic stiffness with age contributes to the development of systolic hypertension, and several cardiovascular alterations often leading to the heart failure, which is one of the most common causes of not only death, but also loss of autonomy, poor quality of life and repeated hospitalization in older adults. In addition, age-related vascular changes play an important role in the development of kidney and brain abnormalities as observed in chronic kidney disease, vascular dementia and also Alzheimer’s disease. Using methods that can measure non-invasively arterial stiffness is has been shown that this parameter is an independent strong determinant of cardiovascular complications, cognitive decline, and other age-related diseases. Clinical trials should determine and predict to what extent non-drug and drug therapeutic strategies might attenuate the increase of aortic stiffness with age. Non-pharmacological prevention, including dietary interventions and increased physical activity may have some effects on this process. Drug therapy requires further research on the mechanisms of systolic hypertension and the possible role of vascular smooth muscle and extracellular matrix. All treatments require investigations on the potential new goal of reducing the age-related increase in aortic stiffness.
Telomeres are specialised non-coding repetitive DNA-protein structures that form protective caps at the ends of eucaryotic chromosomes. They safeguard the chromosome ends, maintain genomic integrity and play a crucial role in replicative senescence, one of the main mechanisms of aging in cultured somatic cells. In epidemiological studies, short telomere length (TL) has been associated with increased risk of degenerative diseases and diminished survival. TL at birth, which is strongly determined genetically, and TL attrition during growth are seemingly the main explanation for inter-individual variation in TL across adults. This implies that the association between TL and adult-onset diseases largely reflects elements that have fashioned TL during early life.
Recent studies show that more people than ever before are reaching old age in better health and enjoying that health for a longer time. This Handbook outlines the latest discoveries in the study of aging from bio-medicine, psychology, and socio-demography. It treats the study of aging as a multidisciplinary scientific subject, since it requires the interplay of broad disciplines, while offering high motivation, positive attitudes, and behaviors for aging well, and lifestyle changes that will help people to stay healthier across life span and in old age. Written by leading scholars from various academic disciplines, the chapters delve into the most topical aspects of aging today - including biological mechanisms of aging, aging with health, active and productive aging, aging with satisfaction, aging with respect, and aging with dignity. Aimed at health professionals as well as general readers, this Cambridge Handbook offers a new, positive approach to later life.
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