Exploring dietary changes in an interdisciplinary intervention trial: Application of a dietary guidelines food composition database.

BACKGROUND: Consumption of food groups aligning with dietary guidelines is advised for obesity management and was used in a recent lifestyle intervention trial, the Health Track study. We have conducted a number of dietary pattern analyses on this trial but, with recent access to the new Australian Dietary Guidelines (ADG) food composition database, we can now assess ADG adherence, with the advantage of categorising mixed dishes. The present study aimed to compare changes over time in consumption of ADG food groups. METHODS: Secondary analysis of baseline and three-month diet history data was conducted. Participants received individualised dietary advice (I), individualised dietary advice plus 30 g of walnuts per day (IW) or usual care (C). The ADG database was used to determine food group servings with changes in five food groups used as a measure of dietary quality. RESULTS: Fruit and vegetable intakes increased in the IW (+0.4 and +1.1 serves, P < 0.05) and I (+0.5 and +0.4 serves, P > 0.05) arms. Consumption of meat/protein foods increased in the IW arm (+0.3 serves, P > 0.05) but decreased in the I and C arms (both - 0.4 serves, P < 0.05). Consumption of grains and milk/alternatives decreased in all study arms (P < 0.05). Greater improvements in grain and dairy food quality were observed in the intervention arms. CONCLUSIONS: The ADG database enabled ADG specific food group analysis, addressed food quality and showed the HealthTrack intervention increased adherence to dietary guidelines compared to usual care.

Usual intake of meat in Australians: secondary analysis of the 2011-12 National Nutrition and Physical Activity Survey using the NCI method.

INTRODUCTION: Global public health recommendations advise limiting the intake of red and processed meats. There is a need for more comprehensive information on meat consumption in Australia, specifically usual intake of meat from a nationally representative sample. The aim of this study was to use the National Cancer Institute (NCI) method to examine usual meat intakes in the 2011-12 National Nutrition and Physical Activity Survey (NNPAS). METHODS: This was a secondary analysis of the cross-sectional 2011-12 NNPAS, which contains observations for 12 153 respondents (9341 adults and 2812 children/adolescents). Usual consumption of all meat, red and processed meats was calculated using the NCI method. Consumption of meat was explored by age and gender groups, as well as by household type. RESULTS: Amongst adults and children/adolescents, consumption of all meat was significantly higher in males (adults: 187.1 g day-1 ; children/adolescents: 125.0 g day-1 ) than females (adults: 125.5 g day-1 ; children/adolescents: 95.4 g day-1 ). Similar patterns were observed for red (males: adults 85.5 g day-1 , children/adolescents 42.9 g day-1 ; females: adults 57.1 g day-1 , children/adolescents 34.9 g day-1 ) and processed meat, although intakes of processed meats in children and adolescents (males: 26.5 g day-1 ; females: 16.8 g day-1 ) were found to be similar to those of adults aged ≥19 years (males: 28.3 g day-1 ; females: 15.3 g day-1 ). Patterns of meat consumption across household types appeared to differ between genders. CONCLUSIONS: The present study suggests that Australians are likely to be exceeding population recommendations for meat intakes, with differing patterns observed across gender and household types. These findings highlight a need for targeted dietetic and population strategies aimed at promoting a healthy consumption of meats within the Australian population.

Algal supplementation of vegetarian eating patterns improves plasma and serum docosahexaenoic acid concentrations and omega-3 indices: a systematic literature review.

BACKGROUND: Vegetarians are likely to have lower intakes of preformed docosahexaenoic acid (DHA) than omnivorous populations who consume fish and animal products. As such, vegetarian populations have omega-3 indices up to 60% lower than those who consume marine products. Algae, the primary producer of DHA in the marine food chain, offer an alternative source of DHA for those who do not consume marine or animal products. This systematic review aims to examine the evidence for the relationship between supplementation with algal forms of DHA and increased DHA concentrations in vegetarian populations. METHODS: The SCOPUS, Science Direct and Web of Science scientific databases were searched to identify relevant studies assessing the effect of algal DHA consumption by vegetarian (including vegan) populations. RESULTS: Four randomised controlled trials and two prospective cohort studies met the inclusion criteria. All included studies reported algal sources of DHA significantly improve DHA concentrations (including plasma, serum, platelet and red blood cell fractions), as well as omega-3 indices, in vegetarian populations. An evident time or dose response was not apparent given the small number of studies to date. CONCLUSIONS: Future studies should address long chain n-3 polyunsaturated fatty acid deficiencies in vegetarian populations using algal DHA and explore the potential physiological and health improvements in these individuals.

Consumption of a healthy dietary pattern results in significant reductions in C-reactive protein levels in adults: a meta-analysis.

Consumption of healthy dietary patterns has been associated with reduced risk of cardiovascular disease and metabolic syndrome. Dietary intervention targets disease prevention, so studies increasingly use biomarkers of underlying inflammation and metabolic syndrome progression to examine the diet-health relationship. The extent to which these biomarkers contribute to the body of evidence on healthy dietary patterns is unknown. The aim of this meta-analysis was to determine the effect of healthy dietary patterns on biomarkers associated with adiposity, insulin resistance, and inflammation in adults. A systematic search of Scopus, PubMed, Web of Science, and Cochrane Central Register of Controlled Trials (all years to April 2015) was conducted. Inclusion criteria were randomized controlled trials; effects of dietary patterns assessed on C-reactive protein (CRP), total adiponectin, high-molecular-weight adiponectin, tumor necrosis factor-α, adiponectin:leptin, resistin, or retinol binding protein 4. Random effects meta-analyses were conducted to assess the weighted mean differences in change or final mean values for each outcome. Seventeen studies were included in the review. These reflected research on dietary patterns associated with the Mediterranean diet, Nordic diet, Tibetan diet, and the Dietary Approaches to Stop Hypertension diet. Consumption of a healthy dietary pattern was associated with significant reductions in CRP (weighted mean difference, -0.75 [-1.16, -0.35]; P = .0003). Non-significant changes were found for all other biomarkers. This analysis found evidence for favorable effects of healthy dietary patterns on CRP, with limited evidence for other biomarkers. Future research should include additional randomized controlled trials incorporating a greater range of dietary patterns and biomarkers.

Protein synthesis-dependent and -independent regulation of hippocampal synapses by brain-derived neurotrophic factor.

A fundamental difference between short-term and long-term forms of synaptic plasticity is the dependence on transcription and translation of new genes. Using organotypic cultures of hippocampal slices, we have investigated whether the modulation of synapses by brain-derived neurotrophic factor (BDNF) also requires protein synthesis. Long-term treatment of hippocampal slice cultures with BDNF increased the number of docked vesicles, but not that of reserve pool vesicles, at CA1 excitatory synapses. BDNF also increased the levels of the vesicle proteins synaptophysin, synaptobrevin, and synaptotagmin, without affecting the presynaptic membrane proteins syntaxin and SNAP-25, or the vesicle-binding protein synapsin-I. The increase in synaptophysin and synaptobrevin expression was moderate (2-fold) and occurred within 6 h after BDNF application. In contrast, synaptotagmin expression took 24 h to reach maximum levels (5-fold). The delayed increase in synaptotagmin was blocked by protein synthesis inhibitors, while the early increase in synaptophysin and synaptobrevin was not. Moreover, the BDNF-induced increase of synaptotagmin was blocked by inhibiting the cAMP/protein kinase A (PKA) pathway. However, BDNF did not activate PKA, and application of a PKA activator did not mimic the BDNF effect. Taken together, these results suggest a novel, protein synthesis-dependent form of BDNF modulation that requires cAMP gating.

The role of the synaptic protein snap-25 in the potency of botulinum neurotoxin type A.

Botulinum neurotoxin serotype A (BoNT/A) is distinguished from BoNT/E by longer duration of paralysis and greater potency. The proteolytic activity of BoNT/A in cultures of dissociated spinal cord neurons persists beyond 80 days, whereas BoNT/E activity persists for less than 1 day (Keller, J. E., Neale, E. A. Oyler, G., and Adler, M. (1999) FEBS Lett. 456, 137-142). This single quality of toxin activity can account for the differences observed in the duration of muscle block. In the present work we sought to understand the basis for the apparent greater potency of BoNT/A. BoNT/E cleaves a 26-amino acid fragment from the C terminus of the synaptic protein SNAP-25 whereas BoNT/A removes only nine residues creating a 197-amino acid fragment (P197) that is 95% the length of SNAP-25. We show that inhibition of neurotransmitter release by BoNT/E is equivalent to the damage caused to SNAP-25. However, synaptic blockade by BoNT/A is greater than the extent of SNAP-25 proteolysis. These findings can be explained if P197 produces an inhibitory effect on neurotransmitter release. A mathematical model of the experimentally determined relationship between SNAP-25 damage and blockade of neurotransmission supports this interpretation. Furthermore, neurotransmitter release following complete cleavage of SNAP-25 can be achieved by P197, but with about 5-fold less sensitivity to external Ca(2+). In this case, vesicular release is restored by increasing intracellular Ca(2+). These data demonstrate that P197 competes with intact SNAP-25, but is unable to initiate normal synaptic vesicle fusion in physiological concentrations of Ca(2+).

Botulinum neurotoxin A blocks synaptic vesicle exocytosis but not endocytosis at the nerve terminal.

The supply of synaptic vesicles in the nerve terminal is maintained by a temporally linked balance of exo- and endocytosis. Tetanus and botulinum neurotoxins block neurotransmitter release by the enzymatic cleavage of proteins identified as critical for synaptic vesicle exocytosis. We show here that botulinum neurotoxin A is unique in that the toxin-induced block in exocytosis does not arrest vesicle membrane endocytosis. In the murine spinal cord, cell cultures exposed to botulinum neurotoxin A, neither K(+)-evoked neurotransmitter release nor synaptic currents can be detected, twice the ordinary number of synaptic vesicles are docked at the synaptic active zone, and its protein substrate is cleaved, which is similar to observations with tetanus and other botulinal neurotoxins. In marked contrast, K(+) depolarization, in the presence of Ca(2+), triggers the endocytosis of the vesicle membrane in botulinum neurotoxin A-blocked cultures as evidenced by FM1-43 staining of synaptic terminals and uptake of HRP into synaptic vesicles. These experiments are the first demonstration that botulinum neurotoxin A uncouples vesicle exo- from endocytosis, and provide evidence that Ca(2+) is required for synaptic vesicle membrane retrieval.

Persistence of botulinum neurotoxin action in cultured spinal cord cells.

Primary dissociated fetal mouse spinal cord cultures were used to study the mechanisms underlying the differences in persistence of botulinum neurotoxin A (BoNT/A) and botulinum neurotoxin/E (BoNT/E) activities. Spinal cord cultures were exposed to BoNT/A (0.4 pM) for 2-3 days, which converted approximately half of the SNAP-25 to an altered form lacking the final nine C-terminal residues. The distribution of toxin-damaged to control SNAP-25 remained relatively unchanged for up to 80 days thereafter. Application of a high concentration of BoNT/E (250 pM) either 25 or 60 days following initial intoxication with BoNT/A converted both normal and BoNT/A-truncated SNAP-25 into a single population lacking the final 26 C-terminal residues. Excess BoNT/E was removed by washout, and recovery of intact SNAP-25 was monitored by Western blot analysis. The BoNT/E-truncated species gradually diminished during the ensuing 18 days, accompanied by the reappearance of both normal and BoNT/A-truncated SNAP-25. Return of BoNT/A-truncated SNAP-25 was observed in spite of the absence of BoNT/A in the culture medium during all but the first 3 days of exposure. These results indicate that proteolytic activity associated with the BoNT/A light chain persists inside cells for > 11 weeks, while recovery from BoNT/E is complete in < 3 weeks. This longer duration of enzymatic activity appears to account for the persistence of serotype A action.

Neuronal sensitivity to tetanus toxin requires gangliosides.

Tetanus toxin produces spastic paralysis in situ by blocking inhibitory neurotransmitter release in the spinal cord. Although di- and trisialogangliosides bind tetanus toxin, their role as productive toxin receptors remains unclear. We examined toxin binding and action in spinal cord cell cultures grown in the presence of fumonisin B(1), an inhibitor of ganglioside synthesis. Mouse spinal cord neurons grown for 3 weeks in culture in 20 microM fumonisin B(1) develop dendrites, axons, and synaptic terminals similar to untreated neurons, even though thin layer chromatography shows a greater than 90% inhibition of ganglioside synthesis. Absence of tetanus and cholera toxin binding by toxin-horseradish peroxidase conjugates or immunofluorescence further indicates loss of mono- and polysialogangliosides. In contrast to control cultures, tetanus toxin added to fumonisin B(1)-treated cultures does not block potassium-stimulated glycine release, inhibit activity-dependent uptake of FM1-43, or abolish immunoreactivity for vesicle-associated membrane protein, the toxin substrate. Supplementing fumonisin B(1)-treated cultures with mixed brain gangliosides completely restores the ability of tetanus toxin to bind to the neuronal surface and to block neurotransmitter release. These data demonstrate that fumonisin B(1) protects against toxin-induced synaptic blockade and that gangliosides are a necessary component of the receptor mechanism for tetanus toxin.

Women's satisfaction with medical termination.

One hundred women aged between 14 and 43 completed a questionnaire regarding their experience and satisfaction with medical termination of pregnancy at Bedford Hospital. A visual analogue score from 0-10 was used. Age, occupation, marital status, parity, previous terminations and awareness of the medical method were recorded. Additional comments were also invited. Overall satisfaction with the method was good, with a mean score of 8.19 and women were very appreciative of the care given by nursing staff. Counselling and choice of method offered scored less well and need improvement. Eighty five per cent of this sample had already had a previous termination of pregnancy, with 30 per cent having had two or more, indicating a need for improved contraceptive counselling both before and after the termination.

PIP: Women's satisfaction with medical abortion was assessed in a survey of 100 women 14-43 years of age (mean age, 24.6 years) who undergone this procedure at Bedford Hospital (UK). 45 women had not heard of medical abortion before presentation to the hospital. 30 women stated they were not given a choice between medical and surgical abortion. 85 women had already had at least 1 prior pregnancy termination and 30 reported 2 or more prior procedures. Women were given 200 mg of oral mifepristone and returned to the gynecology ward 48 hours later for a 1 mg gemeprost vaginal pessary. A satisfaction questionnaire was distributed before discharge. Women used a visual analogue scale with scores from 0 to 10 to assess staff helpfulness, the appropriateness of the information they received, and overall satisfaction. The amount of bleeding was deemed heavy by 51 women and acceptable by another 42 women. 70 women did not require pain killers. The mean score for overall satisfaction was 8.19 out of a possible 10. When women with a previous surgical abortion were asked to compare it with the medical procedure, the mean value was 7.63, favoring the medical option. Satisfaction with the staff and the informational leaflet was high. The greatest dissatisfaction centered around the adequacy of the counseling women received. The high rate of repeat abortion indicates a need for improved contraceptive counseling before and after pregnancy termination.

Syntaxin and 25-kDa synaptosomal-associated protein: differential effects of botulinum neurotoxins C1 and A on neuronal survival.

The Clostridium botulinum neurotoxins (BoNTs) A and C1 cleave specific proteins required for neuroexocytosis. We demonstrated that, in intact neurons, BoNT A cleaves 25-kDa synaptosomal-associated protein (SNAP-25), and BoNT C1 cleaves both syntaxin and SNAP-25 (Williamson et al.: Mol Biol Cell 6:61a, 1995; J Biol Chem 271:7694-7699, 1996). Here, we compare the actions of BoNT A and BoNT C1 on mature and developing mouse spinal cord neurons in cell culture and demonstrate that BoNT C1 is severely neurotoxic. In mature cultures, synaptic terminals become enlarged shortly after BoNT C1 exposure, and, subsequently, axons, dendrites, and cell bodies degenerate. Electron microscopy confirms that early degenerative changes occur in synaptic terminals when the somatic cytoplasm appears normal. In newly plated cultures, few neurons survive exposure to BoNT C1. Whereas both BoNT A and BoNT C1 cleave SNAP-25, BoNT A has no adverse effect on neurite outgrowth, synaptogenesis, or neuron survival. This cytotoxicity is unique to BoNT C1, is specific to neurons, and is initiated at the synaptic terminal, suggesting either a novel role for syntaxin or additional actions of BoNT C1. The neurodegeneration induced by BoNT C1 may be significant in terms of its efficacy for the clinical treatment of dystonia and spasticity.