Caloric restriction (CR), undernutrition without malnutrition, remains the only experimental paradigm that has been shown consistently to extend lifespan and slow aging in short-lived species. Decades of research, mostly in laboratory rodents, have shown that CR consistently extends lifespan, reduces or delays the onset of many age-related diseases and slows aging in many physiological systems. In recent years gerontologists interested in CR have focused on two unanswered questions. 1) What is the relevance of this nutritional paradigm to human aging?
Organisms have evolved neuroendocrine and metabolic response systems to enhance survival during periods of food shortage, which occur frequently in nature. The anti-aging effect of caloric restriction (CR) might derive from these adaptive responses to maximize organism survival. The present article discusses the potential role for leptin, a hormone secreted from adipocytes, as a key signal that induces the adaptive responses relevant to CR.
It is widely held that caloric restriction (CR) extends lifespan by preventing or reducing the age-related accumulation of irreversible molecular damage. In contrast, our results suggest that CR can act rapidly to begin life and health span extension, and that its rapid genomic effects are closely linked to its health effects. We found that CR begins to extend lifespan and reduce cancer as a cause of death within 8 weeks in older mice, apparently by reducing the rate of tumor growth.
Dietary restriction extends lifespan in many organisms, but little is known about how it affects hematophagous arthropods. We demonstrated that diet restriction during either larval or adult stages extends Aedes aegypti lifespan. A. aegypti females fed either single or no blood meals survived 30-40% longer than those given weekly blood meals. However, mosquitoes given weekly blood meals produced far more eggs.
Dietary restriction (DR) has been used for decades to retard aging in rodents, but its mechanism of action remains an enigma. A principal roadblock has been that DR affects many different processes, making it difficult to distinguish cause and effect. To address this problem, we applied a quantitative genetics approach utilizing the ILSXISS series of mouse recombinant inbred strains. Across 42 strains, mean female lifespan ranged from 380 to 1070days on DR (fed 60% of ad libitum [AL]) and from 490 to 1020days on an AL diet.
OBJECTIVES: To assess the associations among age, health status, and resting metabolic rate (RMR) in a large population of older adults. DESIGN: Cross-sectional analysis. SETTING: Community-dwelling volunteers from the Baltimore Longitudinal Study of Aging (BLSA). PARTICIPANTS: Persons aged 40 to 96 (mean 68.2 ± 11.0) who underwent a comprehensive physical examination, cognitive assessment, RMR testing, body composition assessment, and physical function testing during a 3-day clinic visit (N = 420).
Dietary restriction (DR), typically a 20%-40% reduction in ad libitum or "normal" nutritional energy intake, has been reported to extend life span in diverse organisms, including yeast, nematodes, spiders, fruit flies, mice, rats, and rhesus monkeys. The magnitude of the life span enhancement appears to diminish with increasing organismal complexity. However, the extent of life span extension has been notoriously inconsistent, especially in mammals. Recently, Mattison et al. reported that DR does not extend life span in rhesus monkeys in contrast to earlier work of Colman et al.
Calorie restriction (CR), or a diet modification aiming to reduce the total intake of calories by 20%-40%, has been shown to increase longevity across multiple species. Recently, there has been growing interest in investigating the potential role of CR as a treatment intervention for age-related diseases, such as cancer, because an increasing body of literature has demonstrated a metabolic component to both carcinogenesis and tumor progression. In fact, many of the molecular pathways that are altered with CR are also known to be altered in cancer.
Climacteric: The Journal of the International Menopause Society
Interactions between genetic (genome) and environmental factors (epigenome) operate during a person's entire lifespan. The aging process is associated with several cellular and organic functional alterations that, at the end, cause multi-organic cell failure. Epigenetic mechanisms of aging are modifiable by appropriate preventive actions mediated by sirtuins, caloric input, diet components, adipose tissue-related inflammatory reactions, and physical activity.