Quintessence International (Berlin, Germany: 1985)
The basic mechanism of dental amalgam corrosion has been thoroughly studied during the last 50 years by various experimental techniques, most often carried out in vitro. Electrochemical methods were extensively employed, and it was recognized that a gradual dealloying of the more electroactive components, Zn, Sn, and to a lesser extent Cu, contributed to change the surface composition. It is also well known that, in all circumstances, galvanic coupling threatens the longevity of the restoration.
As the elderly population is increasing rapidly, there is a lot of scientific interest in clarifying the differential life-style, genetic, biochemical and molecular factors contributing to mortality or exceptional longevity. Within the framework of the ZINCAGE project, 249 old (60-85 years) and nonagenarian Greek subjects (>/=85 years old) were recruited and anthropometrical, blood and biochemical indices as well as blood pressure measurements were obtained.
A common cause of amyotrophic lateral sclerosis is mutations in superoxide dismutase-1, which provoke the disease by an unknown mechanism. We have previously found that soluble hydrophobic misfolded mutant human superoxide dismutase-1 species are enriched in the vulnerable spinal cords of transgenic model mice. The levels were broadly inversely correlated with life spans, suggesting involvement in the pathogenesis.
BACKGROUND: Zinc deficiency due to poor nutrition or genetic mutations in zinc transporters is a global health problem and approaches to providing effective dietary zinc supplementation while avoiding potential toxic side effects are needed. METHODS/PRINCIPAL FINDINGS: Conditional knockout of the intestinal zinc transporter Zip4 (Slc39a4) in mice creates a model of the lethal human genetic disease acrodermatitis enteropathica (AE).
Despite all that has been written, little evidence supports the notion that the American diet for the elderly needs major modifications (table 3). Particularly in counseling and assessing the elderly, physicians must keep in mind that whatever technique older patients used to reach their present age is probably better than what we can recommend.
Four classes of etiologic agents that cause human illness have been discovered. Sometimes members of two or more classes of agents cooperate to cause illness. Knowledge of etiology is necessary if a disease is to be eradicated. The leading causes of death in the United States have changed dramatically in the last century. Infection has been replaced by chronic illnesses of obscure etiology. Ischemic heart disease is the leading cause of death in middle age and is the major obstacle to becoming old.
Approximately 40 micronutrients are required in the human diet. Deficiency of vitamins B12, folic acid, B6, niacin, C, or E, or iron, or zinc, appears to mimic radiation in damaging DNA by causing single- and double-strand breaks, oxidative lesions, or both. The percentage of the US population that has a low intake (< 50% of the RDA) for each of these eight micronutrients ranges from 2% to > or = 20%; half of the population may be deficient in at least one of these micronutrients.
The pivotal role played by zinc-gene interaction in affecting the inflammatory response mediated by IL-6 in ageing, successful ageing (nonagenarians) and the most common age-related diseases is now recognized. Contradictory data emerging from association studies of IL-6 polymorphisms with longevity and chronic age-related diseases seem to arise from the interaction of this inflammatory pathway with dietary habits. Similar conclusions are expected to arise from association studies with the frailty syndrome.
In ageing, alterations in inflammatory/immune response and antioxidant capacity lead to increased susceptibility to diseases and loss of mobility and agility. Various essential micronutrients in the diet are involved in age-altered biological functions. Micronutrients (zinc, copper, iron) play a pivotal role either in maintaining and reinforcing the immune and antioxidant performances or in affecting the complex network of genes (nutrigenomic approach) involved in encoding proteins for a correct inflammatory/immune response.