Pediatricians' weight assessment and obesity management practices

<p>Abstract</p> <p>Background</p> <p>Clinician adherence to obesity screening guidelines from United States health agencies remains suboptimal. This study explored how personal and career demographics influence pediatricians' weight assessment and management practices.</p> <p>Methods</p> <p>A web-based survey was distributed to U.S. pediatricians. Respondents were asked to identify the weight status of photographed children and about their weight assessment and management practices. Associations between career and personal demographic variables and pediatricians' weight perceptions, weight assessment and management practices were evaluated using univariate and multivariate modeling.</p> <p>Results</p> <p>3,633 pediatric medical providers correctly identified the weight status of children at a median rate of 58%. The majority of pediatric clinicians were white, female, and of normal weight status with more than 10 years clinical experience. Experienced pediatric medical providers were less likely than younger colleagues to correctly identify the weight status of pictured children and were also less likely to know and use BMI criteria for assessing weight status. General pediatricians were more likely than subspecialty practitioners to provide diverse interventions for weight management. Non-white and Hispanic general practitioners were more likely than counterparts to consider cultural approaches to weight management.</p> <p>Conclusion</p> <p>Pediatricians' perceptions of children's weight and their weight assessment and management practices are influenced by career and personal characteristics. Objective criteria and clinical guidelines should be uniformly applied by pediatricians to screen for and manage pediatric obesity.</p

Human malarial disease: a consequence of inflammatory cytokine release

Malaria causes an acute systemic human disease that bears many similarities, both clinically and mechanistically, to those caused by bacteria, rickettsia, and viruses. Over the past few decades, a literature has emerged that argues for most of the pathology seen in all of these infectious diseases being explained by activation of the inflammatory system, with the balance between the pro and anti-inflammatory cytokines being tipped towards the onset of systemic inflammation. Although not often expressed in energy terms, there is, when reduced to biochemical essentials, wide agreement that infection with falciparum malaria is often fatal because mitochondria are unable to generate enough ATP to maintain normal cellular function. Most, however, would contend that this largely occurs because sequestered parasitized red cells prevent sufficient oxygen getting to where it is needed. This review considers the evidence that an equally or more important way ATP deficency arises in malaria, as well as these other infectious diseases, is an inability of mitochondria, through the effects of inflammatory cytokines on their function, to utilise available oxygen. This activity of these cytokines, plus their capacity to control the pathways through which oxygen supply to mitochondria are restricted (particularly through directing sequestration and driving anaemia), combine to make falciparum malaria primarily an inflammatory cytokine-driven disease