Effect of point-of-purchase calorie labeling on restaurant and cafeteria food choices: A review of the literature

<p>Abstract</p> <p>Background</p> <p>Eating away from home has increased in prevalence among US adults and now comprises about 50% of food expenditures. Calorie labeling on chain restaurant menus is one specific policy that has been proposed to help consumers make better food choices at restaurants. The present review evaluates the available empirical literature on the effects of calorie information on food choices in restaurant and cafeteria settings.</p> <p>Methods</p> <p>Computer-assisted searches were conducted using the PUBMED database and the Google Scholar world wide web search engine to identify studies published in peer-review journals that evaluated calorie labeling of cafeteria or restaurant menu items. Studies that evaluated labeling only some menu items (e.g. low calorie foods only) were excluded from the review since the influence of selective labeling may be different from that which may be expected from comprehensive labeling.</p> <p>Results</p> <p>Six studies were identified that met the selection criteria for this review. Results from five of these studies provide some evidence consistent with the hypothesis that calorie information may influence food choices in a cafeteria or restaurant setting. However, results from most of these studies suggest the effect may be weak or inconsistent. One study found no evidence of an effect of calorie labeling on food choices. Each of the studies had at least one major methodological shortcoming, pointing toward the need for better designed studies to more rigorously evaluate the influence of point-of-purchase calorie labeling on food choices.</p> <p>Conclusion</p> <p>More research is needed that meets minimum standards of methodological quality. Studies need to include behavioral outcomes such as food purchase and eating behaviors. Also, studies need to be implemented in realistic settings such as restaurants and cafeterias.</p

Work hours, weight status, and weight-related behaviors: a study of metro transit workers

<p>Abstract</p> <p>Background</p> <p>Associations between hours worked per week and Body Mass Index (BMI), food intake, physical activity, and perceptions of eating healthy at work were examined in a sample of transit workers.</p> <p>Methods</p> <p>Survey data were collected from 1086 transit workers. Participants reported hours worked per week, food choices, leisure-time physical activity and perceptions of the work environment with regard to healthy eating. Height and weight were measured for each participant. Multivariate linear and logistic regressions were conducted to examine associations between work hours and behavioral variables. Associations were examined in the full sample and stratified by gender.</p> <p>Results</p> <p>Transit workers working in the highest work hour categories had higher BMI and poorer dietary habits, with results differing by gender. Working 50 or more hours per week was associated with higher BMI among men but not women. Additionally, working 50 or more hours per week was significantly associated with higher frequency of accessing cold beverage, cold food, and snack vending machines among men. Working 40 or more hours per week was associated with higher frequency of accessing cold food vending machines among women. Reported frequency of fruit and vegetable intake was highest among women working 50 or more hours per week. Intake of sweets, sugar sweetened beverages, and fast food did not vary with work hours in men or women. Physical activity and perception of ease of eating healthy at work were not associated with work hours in men or women.</p> <p>Conclusions</p> <p>Long work hours were associated with more frequent use of garage vending machines and higher BMI in transit workers, with associations found primarily among men. Long work hours may increase dependence upon food availability at the worksite, which highlights the importance of availability of healthy food choices.</p

Paradoxical augmented relapse in alcohol-dependent rats during deep-brain stimulation in the nucleus accumbens

Case reports indicate that deep-brain stimulation in the nucleus accumbens may be beneficial to alcohol-dependent patients. The lack of clinical trials and our limited knowledge of deep-brain stimulation call for translational experiments to validate these reports. To mimic the human situation, we used a chronic-continuous brain-stimulation paradigm targeting the nucleus accumbens and other brain sites in alcohol-dependent rats. To determine the network effects of deep-brain stimulation in alcohol-dependent rats, we combined electrical stimulation of the nucleus accumbens with functional magnetic resonance imaging (fMRI), and studied neurotransmitter levels in nucleus accumbens-stimulated versus sham-stimulated rats. Surprisingly, we report here that electrical stimulation of the nucleus accumbens led to augmented relapse behavior in alcohol-dependent rats. Our associated fMRI data revealed some activated areas, including the medial prefrontal cortex and caudate putamen. However, when we applied stimulation to these areas, relapse behavior was not affected, confirming that the nucleus accumbens is critical for generating this paradoxical effect. Neurochemical analysis of the major activated brain sites of the network revealed that the effect of stimulation may depend on accumbal dopamine levels. This was supported by the finding that brain- stimulation-treated rats exhibited augmented alcohol-induced dopamine release compared with sham-stimulated animals. Our data suggest that deep-brain stimulation in the nucleus accumbens enhances alcohol-liking probably via augmented dopamine release and can thereby promote relapse

HealthWorks: results of a multi-component group-randomized worksite environmental intervention trial for weight gain prevention

<p>Abstract</p> <p>Background</p> <p>U.S. adults are at unprecedented risk of becoming overweight or obese, and most scientists believe the primary cause is an obesogenic environment. Worksites provide an opportunity to shape the environments of adults to reduce obesity risk. The goal of this group-randomized trial was to implement a four-component environmental intervention at the worksite level to positively influence weight gain among employees over a two-year period. Environmental components focused on food availability and price, physical activity promotion, scale access, and media enhancements.</p> <p>Methods</p> <p>Six worksites in a U.S. metropolitan area were recruited and randomized in pairs at the worksite level to either a two-year intervention or a no-contact control. Evaluations at baseline and two years included: 1) measured height and weight; 2) online surveys of individual dietary intake and physical activity behaviors; and 3) detailed worksite environment assessment.</p> <p>Results</p> <p>Mean participant age was 42.9 years (range 18-75), 62.6% were women, 68.5% were married or cohabiting, 88.6% were white, 2.1% Hispanic. Mean baseline BMI was 28.5 kg/m²(range 16.9-61.2 kg/m²). A majority of intervention components were successfully implemented. However, there were no differences between sites in the key outcome of weight change over the two-year study period (<it>p </it>= .36).</p> <p>Conclusions</p> <p>Body mass was not significantly affected by environmental changes implemented for the trial. Results raise questions about whether environmental change at worksites is sufficient for population weight gain prevention.</p> <p>Trial Registration</p> <p>ClinicalTrials.gov: <a href="http://www.clinicaltrials.gov/ct2/show/NCT00708461">NCT00708461</a></p

Health Measurement Scales: Methodological Issues

Health scales or indices are composite tools aiming to measure a variety of clinical conditions, behaviors, attitudes and beliefs that are difficult to be measured quantitatively. During the past years, these tools have been extensively used in cardiovascular disease prevention. The already proposed scales have shown good ability in assessing individual characteristics, but had moderate predictive ability in relation to the development of chronic diseases and various other health outcomes. In this review, methodological issues for the development of health scales are discussed. Specifically, the selection of the appropriate number of components, the selection of classes for each component, the use of weights of scale components and the role of intra- or inter-correlation between components are discussed. Based on the current literature the use of components with large number of classes, as well as the use of specific weights for each scale component and the low-to-moderate inter-correlation rate between the components, is suggested in order to increase the diagnostic accuracy of the tool

Fine Mapping of the 1p36 Deletion Syndrome Identifies Mutation of PRDM16 as a Cause of Cardiomyopathy

Deletion 1p36 syndrome is recognized as the most common terminal deletion syndrome. Here, we describe the loss of a gene within the deletion that is responsible for the cardiomyopathy associated with monosomy 1p36, and we confirm its role in nonsyndromic left ventricular noncompaction cardiomyopathy (LVNC) and dilated cardiomyopathy (DCM). With our own data and publically available data from array comparative genomic hybridization (aCGH), we identified a minimal deletion for the cardiomyopathy associated with 1p36del syndrome that included only the terminal 14 exons of the transcription factor PRDM16 (PR domain containing 16), a gene that had previously been shown to direct brown fat determination and differentiation. Resequencing of PRDM16 in a cohort of 75 nonsyndromic individuals with LVNC detected three mutations, including one truncation mutant, one frameshift null mutation, and a single missense mutant. In addition, in a series of cardiac biopsies from 131 individuals with DCM, we found 5 individuals with 4 previously unreported nonsynonymous variants in the coding region of PRDM16. None of the PRDM16 mutations identified were observed in more than 6,400 controls. PRDM16 has not previously been associated with cardiac disease but is localized in the nuclei of cardiomyocytes throughout murine and human development and in the adult heart. Modeling of PRDM16 haploinsufficiency and a human truncation mutant in zebrafish resulted in both contractile dysfunction and partial uncoupling of cardiomyocytes and also revealed evidence of impaired cardiomyocyte proliferative capacity. In conclusion, mutation of PRDM16 causes the cardiomyopathy in 1p36 deletion syndrome as well as a proportion of nonsyndromic LVNC and DCM