Progress in food & nutrition science最新文献

Iron deficiency has far reaching consequences on systemic functions apart from the well known feature of anemia. Because iron deficiency anemia is easy to recognize and treat, the non-hematological manifestations of this trace element deficiency have been overlooked. There is a large body of evidence accumulated from animal and human studies to indicate that iron deficiency states are associated with alterations in cellular function, growth, motor development, behaviour and cognitive function. There are consequences for the host's level of immunocompetence against infection, for physical work and metabolic stress, for altered fetal outcome and premature labour in pregnant women. The gastrointestinal functions and other organ systems are also affected as a result of iron deficiency. The purpose of this review is to emphasize the importance of the non-hematological manifestations of iron deficiency and to highlight areas of interest, both to basic scientists and health care professionals.

Record linkage in the context of epidemiology refers to the putting together of information (records) on the same person which may have been recorded on different occasions and became part of different data collections. The objective of this article is to provide an overview of the use of record linkage in epidemiology, particularly as it pertains to nutrition and food studies. A short description of epidemiological methodology is provided in order to clarify what epidemiologists expect to achieve by record linkage. A general description of the mechanics of record linkage explains how the methodology relates to the quality of the resulting data sets. The potential impact of the approach of record linkage on epidemiological research is discussed, particularly as it relates to nutritional and other food related studies. Ethical considerations related to record linkage are discussed, and in conclusion the future of record linkage is considered.

A new retinoic acid-related receptor has been identified. It is called the retinoid X receptor and is distinct from the retinoic acid receptors, alpha, beta and gamma. It represents an "orphan" receptor because its function and ligand are unknown. What is known is that it is structurally related to the steroid receptor genes. The ligand to which the retinoic acid X receptor binds has recently been determined to be either retinoic acid itself or another metabolically derived molecule. It is speculated that retinoic acid could serve as a precursor that is metabolized to a more active form as is the case for vitamin D and estrogen (24). The elucidation of an alternative pathway in retinoid metabolism will increase our understanding of the scope of retinoid action.

Consumption of saturated fats contributes to elevated circulating cholesterol levels, whilst either polyunsaturated or monounsaturated fats are linked to depressed levels. Since elevated serum cholesterol is a risk factor for coronary heart disease, it is of interest to understand the factors responsible for the responses elicited by dietary fat quality. Changes in faecal sterol excretion, exogenous cholesterol absorption, lipoprotein composition, and lipoprotein catabolism can coincide with changes in fat intake but may not necessary cause them. Whether or not rates of whole-body cholesterol synthesis respond to dietary fat quality is not known. To date, animal studies suggest that shifts in LDL receptor-mediated cholesterol transport are to blame for responses of circulating cholesterol levels to dietary fat.

Folic acid plays a crucial role in DNA and protein synthesis, suggesting that every mechanism in which cell proliferation intervenes may be altered. Cell-mediated immunity is especially affected by folate deficiency: the blastogenic response of T lymphocytes to certain mitogens is decreased in folate-deficient humans and animals, and the thymus is preferentially altered. The effects of folic acid deficiency upon humoral immunity have been more thoroughly investigated in animals than in humans, and the antibody responses to several antigens have been shown to decrease. Conversely, the phagocytic and bactericidal capacities of polymorphonuclear cells have been studied mainly in folate-deficient humans. However results in this field are controversial. Alterations in immune system functions could lead to decreased resistance to infections, as commonly observed in folate-deficient humans and animals.

Foods rich in nucleic acids, which elevate serum uric acid levels, are restricted in the diets of hyperuricemic individuals. This restriction has been based on the amount of total dietary nucleic acids or all purines, assuming no differences in uricogenic effects of individual purines (adenine, guanine, hypoxanthine, and xanthine). However, inspite of their biochemical similarity, purines are metabolized differently and produce different uricogenic effects in animals and humans. Among the four purine bases, adenine and hypoxanthine have been reported to be more uricogenic than guanine and xanthine. Moreover, free adenine has been shown to be more uricogenic than its nucleoside or nucleotide when fed to animals. Changes in the contents of purines and release of free bases have been reported to occur during various cooking procedures such as stewing, roasting, boiling, and broiling of meat, poultry, and fish products. The differences in metabolic effects of individual purines, and modification in the amount and form of purines caused by processing would suggest that the uricogenic potential of processed foods should be based on the nature and quantity of dietary purines. Recent data on purine contents of processed foods, and information on metabolic effects of dietary purines are reviewed to assess the uricogenic potential of processed foods.

Recent nutrition recommendations are directed towards prevention of chronic degenerative diseases, particularly coronary heart disease and cancer. This focus is in response to morbidity and mortality trends during this century. The evidence supporting such dietary changes remains inconclusive because of difficulties inherent in the measurement of usual dietary intake. The association between dietary fat and breast cancer is reviewed as an example of the problems faced in assessing whether a dietary component does alter the risk of disease. Current recommendations suggest a population-based approach to dietary modifications; the public health implications of this approach are discussed.

The ability of insulin-dependent diabetic (IDDM) women to breast-feed has been documented, however, there is little information concerning milk composition or factors that influence successful breastfeeding. Placental lactogen and prolactin levels can be normalized during pregnancy with good metabolic control. These hormones affect the readiness of the mammary gland for lactation. Prolactin maintains mammary gland insulin receptors to ensure anabolism. Lactation in IDDM women may be influenced by hyper- or hypoglycemia as women balance their insulin needs. Milk from diabetic animals has decreased lactose, fat, protein and volume and these effects can be reversed with insulin administration. Mature breast milk of IDDM women has increased glucose and sodium and mammary gland lipid metabolism may be impaired. Milk lactose and citrate, markers of lactogenesis II, suggest delayed lactation occurs in diabetic women. Many factors may influence lactation success and breast milk composition of IDDM women. Some of these include: method of delivery, feeding frequency, fetal condition, gestational age, mastitis incidence, metabolic control and maternal dietary intake. Lactation management of the IDDM woman must address these factors.

Reviewing the medical literature since 1981 show that patients with acquired immunodeficiency syndrome (AIDS) usually suffer from poor ingestion and absorption, increased excretion of nutrients, metabolic and endocrine abnormalities and immunologic abnormalities which impair nutrition. Human immunodeficiency virus (HIV) and associated opportunistic infections stimulate a broad and complex array of responses which include fever, hypermetabolism, leukocytosis, proteolysis of skeletal muscle, and synthesis, by the liver, of acute-phase reactant proteins and various intracellular enzymes. These responses increase gluconeogenesis and lipogenesis, decrease albumin synthesis, and redistribute and/or sequester various trace elements. Infection-induced depletion of body nutrients serves to weaken host resistance. The deterioration of the nutritional status of these patients is likely to have an important effect on the course of the disease. It is thus evident that comprehensive management of HIV infection must include nutritional evaluation and treatment. When oral nutrition proves to be insufficient to maintain adequate intake, alternative routes must be considered. Selection of an appropriate nutritional support formula requires an evaluation of the absorptive capacity of the gastrointestinal (GI) tract, the length of time required for nutritional repletion, costs, patient acceptance, and feasibility of at-home use. Nutritional support maximizes the ability of the AIDS patient to resist infection, may favor the response to medication by decreasing the incidence of adverse drug reactions, and may prolong the quality and productivity of life.