Veroudering alegemeen
- Latest advances in antiaging medicine
Rapid progress is being made in our ability to modify the aging process. Rather than serving as a period of debility and decreasing health, for many people, the later years of life are becoming a period of continued productivity, independence and good health. Progress is also being made in increasing average lifespan. The leading causes of death (cardiovascular disease, cancer, lung disease, diabetes) are the end result of decades-long processes. With current knowledge, it is possible to delay the onset of these diseases. This can be assisted by lifestyle choices incorporating healthful diet, exercise, stress management, and nutritional supplementation. Emerging genomics technology will allow individuals to establish personalized programs, while early detection of heart disease and cancer will contribute to longevity. Biotechnological therapies involving stem cells, recombinant DNA, proteomics, therapeutic cloning and gene-based therapies are expected to play major roles in promoting successful aging. We are at the threshold of artificial intelligence (AI) and nanotechnology (NT). AI will allow for a merging of our biological thinking with advanced forms of non-biological intelligence to vastly expand our ability to think, create and experience. NT will ultimately allow us to build devices able to build molecules much like our current cellular machinery does, one atom at a time. It is the goal of today's antiaging medicine to forestall disease and aging long enough for people to utilize the powerful biotechnology and nanotechnology therapies that will be developed over the decades ahead. These future therapies have the potential to greatly extend longevity. - The biology of aging
In humans, aging is inexorable. The progressive decrease in physiological capacity and the reduced ability to respond to environmental stresses lead to increased susceptibility and vulnerability to disease. Consequently, mortality due to all causes increases exponentially with aging. Attempts at understanding the causes of aging are limited by the complexity of the problem. Aging changes are manifest from the molecular to the organismic level; environmental factors affect experimental observations; secondary effects complicate elucidation of primary mechanisms; and precisely defined, easily measurable biomarkers are lacking. No one unifying theory may exist, since the mechanisms of aging could be quite distinct in different organisms, tissues, and cells. Evolutionary pressures have selected for successful reproduction, making it likely that the post-reproductive physiology of an organism (i.e., aging) is an epigenetic and pleiotropic manifestation of the optimization for early fitness. Indeed, antagonistic pleiotropy, wherein genes that enhance early survival and function but are disadvantageous later in life, may play an overriding role in aging. Theories of aging can be divided into two general categories: stochastic and developmental-genetic. These are not mutually exclusive, particularly when considering the free radical/mitochondrial DNA theory of aging. Increasing evidence suggests that cellular senescence and organismic aging are antagonistically pleiotropic manifestations of evolutionary pressures to prevent malignant transformation. In other words, aging may be the price we pay to avoid cancer. The beneficial paradox may be that the maximum lifespan potential of humans may have been achieved, in part, due to our ability to grow old. - A forkhead in the road to longevity: the molecular basis of lifespan becomes clearer
OBJECTIVE: Although the quest for longevity is as old as civilization itself, only recently have technical and conceptual advances in genomics research brought us to the point of understanding the precise molecular events that make us age. This heralds an era when manipulations of these will enable us to live longer, healthier lives. The present review describes how recent experimental strategies have identified key genes and intracellular pathways that are responsible for ageing and longevity. FINDINGS: In diverse species transcription factors belonging to the forkhead/winged helix box gene, group O (FOXO) subfamily have been found to be crucial in downstream suppression of the life-shortening effects of insulin/insulin-like growth factor-I receptor signalling pathways that, when upregulated, accelerate ageing by suppression of FOXO. The various adverse processes activated upon FOXO suppression include increased generation of reactive oxygen species (ROS). ROS are pivotal for the onset of various common conditions, including hypertension, atherosclerosis, type 2 diabetes, cancer and Alzheimer's disease, each of which shortens lifespan. In humans, FOXO3a, as well as FOXO1 and -4, and their downstream effectors, could hold the key to counteracting ageing and common diseases. An understanding of the processes controlled by these FOXOs should permit development of novel classes of agents that will more directly counteract or prevent the damage associated with diverse life-threatening conditions, and so foster a life of good health to a ripe old age. Just like caloric restriction, lifespan can be increased in various species by plant-derived polyphenols, such as resveratrol, via activation of sirtuins in cells. Sirtuins, such as SIRT1 in mammals, utilize FOXO and other pathways to achieve their beneficial effects on health and lifespan. CONCLUSION: Lifespan is tractable and basic mechanisms are now known. Longevity research complements and overlaps research in most major medical disciplines. Current progress bodes well for an ever-increasing length of healthy life for those who adapt emerging knowledge personally (so-called 'longevitarians'). - Genetic and Environmental Influences on Exceptional Longevity and the AGE Nomogram
To live beyond the octogenarian years, population and molecular genetic studies of centenarian sibships indicate that genetic factors play an increasingly important role as the limit of life span is approached. These factors are likely to influence basic mechanisms of aging that in turn broadly influence susceptibility to age-related illnesses. Lacking genetic variations that predispose to disease as well as having variations that confer disease resistance (longevity enabling genes) are probably both important to achieving exceptional old age. The AGE (aging, genetics, environment) nomogram is introduced as an illustrative construct for understanding the influence of environmental and genetic factors on survival to various ages, depending on variations in the hypothesized relative importance of genes and environment to longevity. The rapid rise in the incidence of centenarians could indicate that many more people than we originally thought have the optimal set of genetic factors necessary to get to 100 and beyond. Recent studies indicate the likelihood that such factors will be elucidated in the near future. - Replicative Aging, Telomeres, and Oxidative Stress
Aging is a very complex phenomenon, both in vivo and in vitro. Free radicals and oxidative stress have been suggested for a long time to be involved in or even to be causal for the aging process. Telomeres are special structures at the end of chromosomes. They shorten during each round of replication and this has been characterized as a mitotic counting mechanism. Our experiments show that the rate of telomere shortening in vitro is modulated by oxidative stress as well as by differences in antioxidative defence capacity between cell strains. In vivo we found a strong correlation between short telomeres in blood lymphocytes and the incidence of vascular dementia. These data suggest that parameters that characterise replicative senescence in vitro offer potential for understanding of, and intervention into, the aging process in vivo. - Cell Senescence in Human Aging and Disease
While aging is attributed to "wear and tear," genetic studies show that these effects are avoidable (as is the case in germ cell lines) and occur only when cells down-regulate active (and sufficient) repair mechanisms, permitting degradation to occur. Aging occurs when cells permit accumulative damage by wear and tear, by altering their gene expression rather than vice versa. Using telomerase in laboratory settings, we can currently reset this pattern and its consequences both within cells and between cells. Doing so resets not only cell behavior but the pathological consequences within tissues comprising such cells. We can currently grow histologically young, reconstituted human skin using old human skin cells (keratinocytes and fibroblasts). - The anti-ageing effects of caloric restriction may involve stimulation of macroautophagy and lysosomal degradation, and can be intensified pharmacologically
Caloric restriction (CR) and a reduced growth hormone (GH)-insulin-like growth factor (IGF-1) axis are associated with an extension of lifespan across taxa. Evidence is reviewed showing that CR and reduced insulin of GH-IGF-1 axis may exhibit their effects at least partly by their common stimulatory action on autophagy, the cell repair mechanism responsible for the housekeeping of cell membranes and organelles including the free radical generators peroxisomes and mitochondria. It is shown that the life-long weekly administration of an anti-lipolytic drug may decrease glucose and insulin levels and stimulate autophagy and intensify anti-ageing effects of submaximal CR. - Approaches to anti-aging intervention: the promises and the uncertainties
Humans have long sought the elixir to long life. Today, although advances in our understanding of the aging process have given gerontologists new insights in potential anti-aging interventions, public demand for these interventions is outpacing our current knowledge. My presentation begins with a brief historical background that outlines some of the past and present approaches to anti-aging interventions. Using the dietary restriction paradigm as a prototype, discussions center on a three-pathway model that provides the bases to design effective interventions: (1) retardation of biological aging, (2) suppression of age-related disease, and (3) modulation of cross talk between (1) and (2). One other concept useful for discussion in relation to interventions is the enhancement of an organism's resistance to deter vulnerability to aging and disease. These models are best used to explain the efficacy of currently popular interventions such as antioxidant supplementation and hormone therapies. This presentation further highlights the promises that antioxidant supplements hold in warding off oxidative damage as well as their inherent problems and biological limitations. Also discussed here are the promises and uncertainties of anti-aging interventions by genetic manipulation, as seen in animal model studies, and prophylactic treatments targeted against disease, such as hormonal approaches using estrogen and DHEA, as well as other intervening measures.
SITE MAP
- Candida: Candida infectie - Vaginale infectie - CVS/ME: Chronische vermoeidheid Syndroom - Diabetische complicaties: Behandeling diabetische complicaties - Neuropathie - Retinopathie - Nefropathie - Bloeduiker stabilisatie - Hart en vaatziekten: Behandeling Cardiomyopathie (Hartfalen) - Treatment Cardiomyopathy (Heart Failure) - Hoge bloeddruk - Cholesterol verlaging - Aderverkalking (atherosclerose - arteriosclerose) - Levensverlenging: 100 jaren jong - DHEA - Melatonine - 65+ - Kanker: - Ondersteuningstherapie bij kanker - Artrose en artritis: - Artrose - Artritis - Arthrose und Arthritis - Fibromyalgie: - Behandeling Fibromyalgie: introductie - Urinewegen: - Prostaatklachten - Blaasontsteking - Voeding: Voeding wat is er mis mee - Melk BAH!! - Suiker vergif voor je lichaam - Aanvulling onvolwaardige voeding - Vitamine supplementen: Voedingssupplementen - Overgewicht: - Overgewicht Home page - SLIM Home page - Andere artikelen: - HPU - Astma - Multiple Sclerosis (MS) - Psoriasis - Plus - Depressie - Algemeen behandelingsforum - Orthomoleculaire Geneeskunde -
- Candida: Candida infectie - Vaginale infectie - CVS/ME: Chronische vermoeidheid Syndroom - Diabetische complicaties: Behandeling diabetische complicaties - Neuropathie - Retinopathie - Nefropathie - Bloeduiker stabilisatie - Hart en vaatziekten: Behandeling Cardiomyopathie (Hartfalen) - Treatment Cardiomyopathy (Heart Failure) - Hoge bloeddruk - Cholesterol verlaging - Aderverkalking (atherosclerose - arteriosclerose) - Levensverlenging: 100 jaren jong - DHEA - Melatonine - 65+ - Kanker: - Ondersteuningstherapie bij kanker - Artrose en artritis: - Artrose - Artritis - Arthrose und Arthritis - Fibromyalgie: - Behandeling Fibromyalgie: introductie - Urinewegen: - Prostaatklachten - Blaasontsteking - Voeding: Voeding wat is er mis mee - Melk BAH!! - Suiker vergif voor je lichaam - Aanvulling onvolwaardige voeding - Vitamine supplementen: Voedingssupplementen - Overgewicht: - Overgewicht Home page - SLIM Home page - Andere artikelen: - HPU - Astma - Multiple Sclerosis (MS) - Psoriasis - Plus - Depressie - Algemeen behandelingsforum - Orthomoleculaire Geneeskunde -
