Nutritional and Botanical Approaches to Antiaging

Abstract

A s the human population ages and increases in longevity, study of biological aging is emerging. According to the Centers for Disease Control and Prevention, for 2003, an estimated 35.9 million Americans were over the age of 65 and more than 25 percent of this population was in fair-to-poor health. 1 The mechanism of cellular aging is elusive and many theories have been proposed to explain the decrease in physiologic function that occurs with aging. As a result of increased risks of disease and mortality, decreases in quality of life, and rising health care costs, aging and longevity research is necessary to address problems related to aging. A wide range of nutrients and interventions have been shown to decrease cellular aging and age-related disease. Theories of Aging There are several theories of cellular aging. These theories are not mutually exclusive, and many complement each other. Aging was initially believed to be a result of genetically programmed cell death. Subsequently, it was proposed that aging might be a result of accumulation of cellular damage and mutation. Given that evidence has surfaced suggesting that aging may be a result of cellular damage, this implies that interventions to influence aging are possible. Oxidative Stress and Free Radicals Damage caused by free radicals is the most popular and universal theory of cellular aging. These highly reactive molecules are formed in many biochemical reactions as well as being introduced via exogenous exposures. Free radicals react with molecules causing damage and mutations, and have been implicated in many disease processes. 2 Studies indicate that an increase in the accumulation of oxidative damage increases functional deficits during aging, and treatments that decrease oxidative damage have been shown to delay age-related loss of function. 3 Other evidence suggests that increases in oxidative stress cause increases in inflammatory mediators, leading to age-related inflammatory diseases, such as arthritis, atherosclerosis, osteoporosis, and dementia. 4 Mitochondrial Damage Mitochondria produce most of the energy used by the body in the form of adenosine triphosphate (ATP). Oxidative phosphorylation provides the majority of ATP production via the electron transport chain. Aging has been shown to decrease the efficiency of mitochondrial oxidative phosphorylation. Specifically, aging decreases cellular energy production, impairs substrate oxidation, and increases the production of free radicals. 5 Loss of muscle mass and function seen with aging is associated with mitochondrial damage in muscle cells. 6 Studies indicate that aging is associated with a decrease in number and increase in size of mitochondria, making them less efficient with age. 7 Small amounts of reactive oxygen species (ROS) are formed via energy production that regulates some cellular functions, and that can act as a second messenger for transcription factors. 8 Cells have several antioxidant enzymes to prevent excess ROS from causing damage. Enzymes required for oxidative phosphory...

Metabolismo mitocondrial, radicais livres e envelhecimento

“…Elas foram isoladas e caracterizadas por Sinclair e Guarente em 1997 48 e compreendem proteínas desacetiladoras dependentes da coenzima NAD, envolvidas no controle do metabolismo energético e associadas à longevidade. 49 A restrição calórica estimula as sirtuínas que inibem a expressão do NFkB, reduzindo a inflamação, a imunossenescência e o envelhecimento celular. 30 A redução na produção de espécies reativas pelas mitocôndrias devido a RC diminui os danos às biomoléculas mitocondriais, contribuindo e muito para amenizar o envelhecimento.…”