Current Nutrition & Food Science - Volume 1, Issue 3, 2005

A close relationship exists between inflammation and cancer. It is suggested that resveratrol exerts its antiinflammatory and anti-neoplastic actions by modulating the expression genes and second messengers concerned with inflammation and neoplastic processes.

Epidemiologic and preclinical studies provide evidence that the essential nutrient selenium has cancer protective properties. The mammalian genome encodes 25 selenoprotein genes that contain one or more molecules of selenium in the form of the amino acid selenocysteine, which is translationally inserted into the growing peptide at the UGA codon. Most of the known metabolic functions of selenium are associated with these selenoprotens, and there is evidence that polymorphisms in some selenoproteins, may be associated with increased cancer risk. However, it is not currently known whether selenoproteins or low molecular weight selenium compounds mediate the cancer protective effects of dietary selenium. The anti-carcinogenic effects of selenium occur at much greater levels of intake than is necessary to maximize glutathione peroxidase activity, while thioredoxin reductase activity can be influenced by supranutritional levels of intake. Also, there is increasing evidence that many of the putative effects of selenium on cell cycle control and apoptosis are mediated via reactive oxygen species, and intracellular reactive oxygen species are regulated by several selenoproteins. The development of transgenic and knockout mice with altered selenoprotein expression provides a model system to evaluate the importance of selenoproteins in mediating the cancer protective effects of selenium.

Alzheimer's disease (AD) is the most common cause of dementia in patients over 60 years of age. It is characterized by progressive degradation of cognitive function. It is a disease that affects one of every 10 individuals over the age of 65 and 50% of individuals over the age of 85. The estimated number of people with AD could be well over 14 million by the year 2050, unless a clear understanding of AD pathogenesis is gained and new AD prevention and/or treatment is developed. Concomitantly, the proportion of elderly, nondemented individuals is growing at a rapid rate. It is a well-known fact that reduced amounts of certain dietary nutrients are associated with memory loss and other thinking problems, especially in older individuals. And reduced levels of vitamins C and E have been associated with increased severity of AD. High intake of cholesterol and saturated fats is also associated with an increased risk of AD. In this review, we consider general dietary essential nutrients and non-essential nutrients, including various resources and their biological functions. Moreover, we discuss how nutrition in terms of various intake doses affects brain function, including "normal" aging, age-related dementia, and AD. We also gather together and present recent evidence on how to retard aging, and perhaps prevent AD by adopting a nutritional approach. We believe that the exciting and intriguing information will stimulate great interest in research on what constitutes a healthy diet and research on healthy aging, and the prevention of AD.

Magnesium is an essential mineral with several dietary sources including whole-grains, green leafy vegetables, legumes, and nuts. The western diets that are characterized by a high intake of processed foods contribute to a high prevalence of inadequate magnesium intake in industrialized countries. Accumulating data from animal models and small trials in humans support a pivotal role of magnesium in glucose homeostasis, insulin secretion and action. In observational studies, magnesium intake has been inversely associated with insulin resistance, type 2 diabetes mellitus (DM), hypertension, and cardiovascular diseases (CVD). Herein we systematically review the current literature from human population studies on dietary magnesium intake and a host of metabolic disorders, focusing primarily on type 2 DM, hypertension, and CVD. The available evidence indicates that dietary magnesium may favorably affect a cluster of metabolic abnormalities including insulin resistance, hypertension, and dyslipidemia, known as metabolic syndrome. The metabolic syndrome is prevalent worldwide and is associated with greater risks of major chronic diseases, particularly type 2 DM and CVD. Further, available epidemiologic data provide strong support for dietary recommendations to increase consumption of magnesium-rich foods for the primary prevention of the metabolic syndrome and associated chronic diseases. Future studies are warranted to assess the efficacy of magnesium supplementation in the prevention and/or treatment of metabolic syndrome and type 2 DM in human populations.

Celiac disease is a genetically determined autoimmune disorder induced by an environmental agent, gluten. The disease involves the development of a T-cell mediated inflammatory reaction to ingested gluten in the small intestine that results in villous atrophy. The manifestations of the disease are varied. Patients may be critically ill due to a severe malabsorption syndrome or asymptomatic. The reason for the varied phenotypic expression of the disease is unclear. The mainstay of therapy is a gluten-free diet that may be a testing endeavor in this culture.

Muscle dysfunction is a common occurrence in malnutrition resulting in poorer functional status, delayed recovery and impaired outcome in chronic and acute disease. Although it is a well-known phenomenon, its pathogenesis is not yet completely understood. Loss of muscle mass undeniably contributes to impaired function, but is not the only factor. Muscle function is known to respond earlier to food deprivation than other nutritional indices, implying further factors to be responsible of the muscle weakness observed in malnutrition. Many recent studies have contributed to shed light on the alterations in muscle cell energetics occurring in malnutrition (i.e. enzyme depletion, mitochondrial dysfunction, impaired oxidative phosporylation and electrolyte disturbances and altered cell membrane potential), suggesting several mechanisms leading to impaired muscle function.

The present review evaluates the effect of pre- and postnatal supplementation of nutrition with long-chain polyunsaturated fatty acids (LCPUFA) on neurodevelopmental outcome of term infants. The few studies which have been performed on the role of prenatal LCPUFA status or prenatal LCPUFA supplementation in neurodevelopmental outcome suggest that a better prenatal arachidonic acid (AA) and doxosahexaenoic acid (DHA) status might be related to a better neurodevelopmental outcome in early infancy. A review of the randomised controlled trials on postnatal formula supplementation with LCPUFA in term infants revealed that supplementation with LCPUFA, in particularly supplementation with ≥0.30% DHA, has a beneficial effect on neurodevelopmental outcome till 4 months of age. The studies could not demonstrate a consistent positive effect beyond that age. However, in the majority of studies neurodevelopmental outcome was assessed at 6 to 24 months, i.e. at an age where there is a 'latency' in the expression of minor neurological dysfunction. This may mean that it is possible that LCPUFA may have a long lasting beneficial effect on neurodevelopmental outcome at school-age and beyond. This hypothesis urgently needs testing in nutritional intervention studies in which children are followed till at least school-age.

Factors adversely affecting bone accrual during adolescence may be risk factors for developing osteoporosis later in life. The present review discusses pregnancy and lactation during adolescence as potential conditions negatively affecting bone mass acquisition in women. The physiological adaptations of calcium homeostasis during pregnancy and lactation have been extensively studied in adult women and include a temporary bone loss that is recovered after weaning. Much less is known about the ability of adolescent women to adapt to the high calcium demands of pregnancy and lactation while preserving maternal bone mass. Physiological adaptations of calcium and bone metabolism during adolescence, and during pregnancy and lactation in adolescents are reviewed in this work, with emphasis on intestinal absorption, urinary excretion, bone turnover and hormonal regulation. Comparisons between adult and adolescent women are included. Genetic and nutritional factors potentially affecting bone acquisition during adolescence are considered. The available evidence suggests that pregnancy and lactation adversely affect bone mass acquisition of adolescent women, particularly when calcium intake is low. However, more studies are needed to evaluate the impact of pregnancy and lactation during adolescence on maternal bone mass later in life.

Increasing evidence suggests that the diminution of cereals consumption and the increase of more refined products consumption are associated with the apparition of marginal deficiencies in micronutrients such as thiamin. The phosphorylated form of thiamin (TDP) is an important co-enzyme involved in several metabolic reactions, and the consequences of thiamin deficiency (TD) depend on its severity. For example, TD leads to alteration in brain metabolism with a decrease in brain concentrations of TDP, a reduction in activities of TDP-dependent enzymes, an increase of lactate concentration, a reduced tissue pH and a selective loss of neurons. An optimised thiamin supply could also prevent the formation of radical species, protect against metabolic stress and prevent the formation of Advanced Glycation End Products. These observations emphasise the importance of whole cereals, and particularly whole bread, in the prevention of thiamin deficiency. In this view, to get whole bread with maximal nutritional density, several steps of the transformation of grain into bread should be further examined: selection of cultivars with a high thiamin level, use of less refined flours and optimisation of the fermentation process during bread making.

The traditional Mediterranean diet is suggested to be associated with the lowest prevalence of metabolic syndrome, coronary heart disease, and type 2 diabetes and is suggested to be the optimal diet for the general public. This diet is considered to be a moderate protein diet. It has been suggested that the Mediterranean diet's protein content is partly responsible for the beneficial effects on health, but the level of protein intake to induce a cardioprotective effect is not yet well known. Nevertheless, there are current studies that support the hypothesis that high protein intake, particularly of plant origin, may have beneficial health effects, which provides some insight on the role of protein in modulating cardiovascular disease risk factors. Therefore, in this work current information about the role of the adoption of the traditional Mediterranean diet on the prevalence of Metabolic Syndrome as a risk factor for coronary heart disease is reviewed. Also special attention is given on the influence of protein intake in relation to the incidence of this syndrome.