PURPOSE OF THE REVIEW: The present review discusses the current state of knowledge regarding the effects of calorie restriction in modulating metabolism and aging. RECENT FINDINGS: There are currently no interventions or gene manipulations that can prevent, stop or reverse the aging process. However, there are a number of interventions that can slow down aging and prolong maximal lifespan up to 60% in experimental animals.
Dietary restriction (DR) delays or prevents age-related diseases and extends lifespan in species ranging from yeast to primates. Although the applicability of this regimen to humans remains uncertain, a proportional response would add more healthy years to the average life than even a cure for cancer or heart disease. Because it is unlikely that many would be willing or able to maintain a DR lifestyle, there has been intense interest in mimicking its beneficial effects on health, and potentially longevity, with drugs.
Caloric restriction (CR) is the only non-genetic intervention known to date to slow the onset of age-related diseases and increase average and maximum lifespan in several species. Its interest is continually growing, particularly for the identification of mechanisms involved in increasing longevity. Unlike studies in invertebrate and rodent models have provided some indication about the mechanisms of the CR, the efficacy of CR as an anti-aging protocol in primates has not yet been fully established.
Traditionally, thick enamel has often been used to infer durophagy (i.e., hard nut and seed consumption) in extinct hominins. These inferences are based on the hypothesis that thick enamel is primarily an adaptation to prevent tooth fracture or chipping resulting from high-stress loads produced during the mastication of large hard foods. An alternative view argues that thick enamel may aid in maintaining tooth function in the face of gradual dental wear from grit, phytoliths and acid, which may be found in foods of widely varying hardness.
The SMARCA2 gene, which encodes BRM in the SWI/SNF chromatin-remodeling complex, was recently identified as being associated with schizophrenia (SZ) in a genome-wide approach. Polymorphisms in SMARCA2, associated with the disease, produce changes in the expression of the gene and/or in the encoded amino acid sequence. We show here that an SWI/SNF-centered network including the Smarca2 gene is modified by the down-regulation of REST/NRSF in a mouse neuronal cell line. REST/NRSF down-regulation also modifies the levels of Smarce1, Smarcd3 and SWI/SNF interactors (Hdac1, RcoR1 and Mecp2).
[I]nterest in animals as a source of organs and tissues for human beings remains strong. New developments in immunosuppression technology promise to lower the technical barriers to a routine use of nonhumans as organ donors, and the image of colonies of animals kept at the ready for supplying the growing human need for new organs seems a much more plausible scenario now than it did when broached by transplantation specialists in the Sixties. As Arthur Caplan has powerfully argued, the prospects that other sources of organs may resolve the supply problem are grim....
The well-known ethologist and Nobel Price Konrad Lorenz said that, according to the evolution, the human mental capacities, and therefore the morality, ought to have had forerunner in the animals which have preceded us: he call them <ratiomorphe structures>, i.e. forerunners of our reason. Recently, the social life of non human primates has been intensely studied with the conclusions that there are rules which can be considered as rudiments of a moral behaviour.
The goal of the International Alt/Self Project (IASP) is to determine the molecular basis of societal altruistic and selfish behaviour in primate societies. In order to solve this difficult problem, an International Consortium comprising genomists and psycho-biologists from the G-8 countries has been created. In a first step it was decided to concentrate on extreme opposite phenotypes manifesting in Homo sapiens sapiens: the hyper-altruism syndrome (HAS) and the hyper-selfishness syndrome (HSS).