The role of fish in food-based strategies to combat vitamin A and mineral deficiencies in developing countries

Fish is important in the diets and livelihoods of many poor people suffering from vitamin and mineral deficiencies. In this article, fish intake in rural Bangladesh and Cambodia and the vitamin A, calcium, iron, and zinc contents and nutrient bioavailability of commonly consumed species are presented. The contribution of these species to nutrient intakes as well as their potential to meet dietary recommendations are presented and discussed. Data from consumption surveys were analyzed to obtain fish intake by species. Commonly consumed species were analyzed for nutrient contents, and studies on nutrient bioavailability were conducted. In poor, rural, Bangladeshi households, mean fish intake was 13-83 g raw, whole fish per person/d. Frequency of intake of small fish was high, and small fish made up 50-80% of all fish eaten during the fish production season in rural Bangladesh and Cambodia. Many small fish are eaten whole and therefore are a rich calcium source; some are also rich in vitamin A, iron, and zinc. Even small production of the vitamin A-rich fish mola in ponds in Bangladesh can meet the annual vitamin A recommendation of 2 million children, and a traditional daily meal with the iron-rich fish trey changwa plieng can meet 45% of the daily median iron requirement of Cambodian women. Fish consumption data on the species level, nutrient analyses, awareness of the nutritional value of fish, as well as promotion of the production and accessibility of nutrient-dense species can lead to the use of fish in food-based strategies to combat nutrient deficiencies in poor people in Asia and Africa.     

Validation study of the acute biotic ligand model for silver

An important final step in development of an acute biotic ligand model for silver is to validate predictive capabilities of the biotic ligand model developed for fish and invertebrates. To accomplish this, eight natural waters, collected from across North America, were characterized with respect to ionic composition, pH, dissolved organic carbon, and sulfide. Tests were conducted with the cladoceran Ceriodaphnia dubia (48-h static) and the fish Pimephales promelas (96-h static renewal) to determine the concentrations causing lethality to 50% of the organisms (LC50s) for silver in each of these waters. Overall, the biotic ligand model adequately predicted silver toxicity to C. dubia; however, in some cases, predicted LC50 values exceeded measured values. The accuracy of the biotic ligand model predictions was less convincing for silver toxicity to P. promelas with pronounced problems in low-ionic strength waters. Another issue was the use of acclimated organisms in toxicity studies because the biotic ligand model has been developed with the use of a mix of studies with acclimated and nonacclimated test organisms of varying ages and sizes. To evaluate whether effects of acclimation to test waters influence biotic ligand model predictions, a subset of the natural waters were also tested with P. promelas that had been acclimated to the natural water for 7 d before testing. These experiments revealed no differences in toxicity between acclimated and nonacclimated P. promelas. To determine the influence of organism size, which has been previously correlated to Na(+) turnover and acute silver toxicity across multiple species, Na(+) and Cl(-) influx rates were measured in P. promelas of different sizes. Our results show that Na(+) and Cl(-) influx rates were inversely related to fish mass and positively correlated with silver sensitivity.     

Increase in cardiovascular pathology in female sprague-dawley rats following chronic treatment with 2,3,7,8-tetrachlorodibenzo-p-dioxin and 3,3′,4,4′,5-pentachlorobiphenyl

The effects of chronic exposure to dioxin (2,3,7,8,-tetrachlorodibenzo-p-dioxin [TCDD]) and a dioxin-like compound (3,3′,4,4′,5-pentachlorobiphenyl [PCB126]) on the cardiovascular system were evaluated in female Harlan Sprague-Dawley rats as part of an ongoing National Toxicology Program investigation. The animals were gavage treated 5 d per week with up to 1000 ng of PCB126 per kilogram of body weight per day or up to 100 ng of TCDD per kilogram of body weight per day for up to 2 yr. The control animals received only a corn oil/acetone vehicle (99:1 mixture). The corresponding stop-study groups received the highest doses for 31 wk and then received only the vehicle for the remainder of the study. After a full necropsy of all animals, a complete set of tissues was examined microscopically. Administration of each compound was associated with treatment-related increases in the incidences of degenerative cardiovascular lesions. Cardiomyopathy and chronic active arteritis increased in a dose-related manner in all groups treated with PCB126 or with TCDD. Increased incidences were also observed in the stop-study groups, indicating that a shorter term exposure may produce some effects. The average severity of cardiomyopathy was minimal or slightly greater in all dose groups, including the controls. Chronic active arteritis occurred primarily in the mesentery and pancreas, although the rectum, liver, heart, ovary, uterus, and glandular stomach in the PCB126 study and the liver and ovary in the TCDD study were affected in a few of the dosed animals. The authors’ investigations indicate that the rat cardiovascular system is a target for dioxin toxicity, which increases the incidence of spontaneous cardiomyopathy and arteritis.     

Chronic obstructive pulmonary disease and asthma-associated Proteobacteria,but not commensal Prevotella spp., promote Toll-like receptor 2-independent lung inflammation and pathology

Recent studies of healthy human airways have revealed colonization by a distinct commensal bacterial microbiota containing Gram-negative Prevotella spp. However, the immunological properties of these bacteria in the respiratory system remain unknown. Here we compare the innate respiratory immune response to three Gram-negative commensal Prevotella strains (Prevotella melaninogenica, Prevotella nanceiensis and Prevotella salivae) and three Gram-negative pathogenic Proteobacteria known to colonize lungs of patients with chronic obstructive pulmonary disease (COPD) and asthma (Haemophilus influenzae B, non-typeable Haemophilus influenzae and Moraxella catarrhalis). The commensal Prevotella spp. and pathogenic Proteobacteria were found to exhibit intrinsic differences in innate inflammatory capacities on murine lung cells in vitro. In vivo in mice, non-typeable H. influenzae induced severe Toll-like receptor 2 (TLR2)-independent COPD-like inflammation characterized by predominant airway neutrophilia, expression of a neutrophilic cytokine/chemokine profile in lung tissue, and lung immunopathology. In comparison, P. nanceiensis induced a diminished neutrophilic airway inflammation and no detectable lung pathology. Interestingly, the inflammatory airway response to the Gram-negative bacteria P. nanceiensis was completely TLR2-dependent. These findings demonstrate weak inflammatory properties of Gram-negative airway commensal Prevotella spp. that may make colonization by these bacteria tolerable by the respiratory immune system.     

A review of the evidence for and against increased mortality in hypothyroidism

The lifetime risk of overt hypothyroidism is around 5%, and this disease is usually preceded by subclinical hypothyroidism, which has an even higher prevalence (estimated to be up to 9%). Hypothyroidism has been linked with cardiac dysfunction, atherosclerosis, hypertension and coagulopathy. Intuitively, this increased morbidity is expected to shorten patients' lifespan, but definitive data are lacking on whether either of these hypothyroid states (particularly overt hypothyroidism) increase mortality. Study findings are inconsistent and, overall, the pooled data do not demonstrate increased mortality in patients with either subclinical or overt hypothyroidism. However, none of the available studies was adequately designed to answer this question. This Review discusses major shortcomings in those studies, such as population dissimilarities, hypothyroid state classification and misclassification, the inclusion of nonthyroidal illness, drug interference from concurrent therapies, serious comorbidities (for example, cardiovascular disease), differences in duration of follow-up and the number of levothyroxine-treated individuals. Taken together, the data exhibit little evidence of systematic bias and no strong scientific proof of increased mortality related to either subclinical or overt hypothyroidism. Future studies, however, should take the above-mentioned shortcomings and potential genetic confounding into consideration.