Breast-feeding and risk for childhood obesity: does maternal diabetes or obesity status matter?

OBJECTIVE: We sought to evaluate whether maternal diabetes or weight status attenuates a previously reported beneficial effect of breast-feeding on childhood obesity. RESEARCH DESIGN AND METHODS: Growing Up Today Study (GUTS) participants were offspring of women who participated in the Nurses' Health Study II. In the present study, 15,253 girls and boys (aged 9-14 years in 1996) were included. Maternal diabetes and weight status and infant feeding were obtained by maternal self-report. We defined maternal overweight as BMI > or = 25 kg/m2. Childhood obesity, from self-reported height and weight, was based on the Centers for Disease Control and Prevention definitions as normal, at risk for overweight, or overweight. Maternal status categories were nondiabetes/normal weight, nondiabetes/overweight, or diabetes. Logistic regression models used generalized estimating equations to account for nonindependence between siblings. RESULTS: For all subjects combined, breast-feeding was associated with reduced overweight (compared with normal weight) in childhood. Compared with exclusive use of formula, the odds ratio (OR) for exclusive breast-feeding was 0.66 (95% CI 0.53-0.82), adjusted for age, sex, and Tanner stage. Results did not differ according to maternal status (nondiabetes/normal weight OR 0.73 [95% CI 0.49-1.09]; nondiabetes/overweight 0.75 [0.57-0.99]; and diabetes 0.62 [0.24-1.60]). Further adjustment for potential confounders attenuated results, but results remained consistent across strata of maternal status (P value for interaction was 0.50). CONCLUSIONS: Breast-feeding was inversely associated with childhood obesity regardless of maternal diabetes status or weight status. These data provide support for all mothers to breast-feed their infants to reduce the risk for childhood overweight.     

Pediatric rheumatology: what does the future hold?

Effectiveness of the traditional rehabilitation approaches used in pediatric rheumatology has been difficult to prove and, in times of cost containment, this lack of evidence may lead to undertreatment with physical and occupational therapies. Quantitative methods such as those described in this issue by Brostr?m and colleagues can be used to validate those approaches and to reinforce the need for careful attention to the effects of even minor loss of range and strength in children with juvenile arthritis. Historically, up to half of the children affected by polyarticular juvenile arthritis became disabled. Some factors that have led to improved outcomes for childhood rheumatic diseases are discussed, including medications (use of weekly low-dose methotrexate, intra-articular steroid injections, new biologic agents that specifically block mediators of inflammation, for example, tumor necrosis factor and interleukin-1), surgery (joint replacements), and psychosocial interventions (with schools and families). The importance of maintaining range of movement, strength, weight bearing, and ambulation, in an effort to prevent sequelae such as osteoporosis and wheelchair dependence, is emphasized. Early identification of children with rheumatic diseases and aggressive intervention, with a combined medical, rehabilitation, psychosocial, and, rarely, surgical approach, should now allow most affected children to reach adulthood with little or no disability.     

Diagnosing sepsis: does the microbiology matter?

Sepsis is caused by infection, and knowing what type of organism is causing the infection certainly matters in terms of both epidemiology and selecting antibiotic therapy. Although there is considerable laboratory evidence that micro-organisms initiate sepsis in different ways, the clinical consequences are usually indistinguishable. New drugs that target specific points in the activation pathway are starting to emerge, and these will require us to be much more accurate in how we diagnose sepsis.     

Progressive renal disease: does the quality of the proteinuria matter or only the quantity?

Proteinuria is now accepted to be not just a sign of renal disease but also a contributory factor to the development of progressive tubulointerstitial fibrosis. Excellent correlations between the degree of proteinuria and rate of decline of glomerular filtration rate have been demonstrated. What has been investigated less is whether the type of protein found in the urine is important. Using transformed and primary human proximal tubular epithelial cells, we have investigated the binding of albumin and retinol binding protein to plasma membrane preparations and studied the response of the intact cells to increasing concentrations of these same proteins. We have preliminary evidence for differences in the pattern of binding of these two proteins to the plasma membrane receptors and also for differential release of pro-inflammatory cytokines from intact cells. These in vitro results, along with those of other groups, and some recent clinical findings suggest that the quality of proteinuria may play a role in the early development of interstitial fibrosis. Furthermore, the use of such in vitro model systems based on human proximal epithelial cell culture can provide a means of evaluating the potential significance of different markers of tubular damage.     

The diagnosis of adrenal insufficiency in the critically ill patient: does it really matter?

The definition of what constitutes a 'normal' adrenal response to critical illness is unclear. Consequently, published studies have used a variety of biochemical criteria to define 'adrenal insufficiency'. These criteria have been based on the baseline cortisol level or the increment in cortisol following corticotropin administration. However, in critically ill patients there are a number of confounding factors that make interpretation of these tests difficult. Furthermore, in those patients who are most likely to benefit from treatment with low-dose glucocorticoids, there is no evidence that treatment should be based on adrenal function testing. In those patients in whom the diagnosis of adrenal insufficiency may be important, this diagnosis may best be made based on the free cortisol level or the total cortisol level stratified by serum albumin.     

Women's prehospital delay associated with myocardial infarction: does race really matter?

BACKGROUND/RESEARCH OBJECTIVE: Well-documented disparities in cardiovascular health account for approximately one third of the difference in life expectancy between blacks and whites. Mortality from cardiovascular disease is greater among black women than among white women, and black women report longer delays in treatment seeking following onset of symptoms of acute myocardial infarction (AMI). Despite this disparate burden, there is little race-specific data on correlates of delay for black or white women. This secondary data analysis compares duration and correlates of delay in treatment seeking by race following onset of AMI symptoms. SUBJECTS/METHODS: We analyzed self-report data from 509 black and 500 white women, interviewed 4 to 6 months after AMI, using multivariable logistic and linear regression. RESULTS/CONCLUSIONS: Median delay time was nonsignificantly shorter for black than for white women (1.0 vs 1.5 hours). Equal proportions of black and white women (57% vs 54%) sought treatment within 2 hours of symptom onset. In multivariable analyses, correct attribution of symptoms to AMI was a significant predictor of treatment seeking within 2 hours of symptom onset for black and white women (odds ratios = 2.79 and 3.86, respectively); eligibility for public insurance was a significant predictor for black women only (odds ratio = 2.3). Common comorbidities, AMI risk factors, and other demographics were not significantly associated with delay time. Insurance coverage and the correct attribution of symptoms to cardiac causes are substantial and modifiable predictors of delay in seeking treatment of AMI.     

What does the public really think?

In this article, the public’s opinion on the veterinary profession and how social media plays a part in how we’re seen in the public eye has been researched. Facebook was used to ask two private groups their opinions not only on how they feel about vets, but also their knowledge on the role of a veterinary nurse.     

The obesity paradox in the ICU: real or not?

The obesity paradox has been used to describe the observed phenomenon described by several studies that indicated improved survival for critically ill patients with mild to moderate obesity when compared with their lean counterparts. The study by Arabi and coworkers challenges the obesity paradox concept for critically ill obese patients with septic shock. Their data indicate that obesity, per se, does not significantly improve mortality when outcomes are adjusted for differences in baseline characteristics and sepsis interventions. Further studies are needed to assess the influence of body weight, lean weight, and fat mass for optimizing fluid resuscitation, pharmacotherapy, and nutritional therapy for critically ill patients with sepsis.In the previous issue of Critical Care, Arabi and coworkers examined the effect of obesity upon clinical outcomes following septic shock in a large multicenter cohort study [1]. The worldwide obesity epidemic has led to numerous studies that examined the impact of obesity upon clinical outcomes during critical illness over the past decade. Although the data are conflicting, the prevailing theme is that increased morbidity is associated with an increasing body mass index (BMI; weight (kg) / height² (m²)) above normal [2] but a U-shaped curve may be present when relating BMI to survival [3]. Malnourished patients with low BMI (<18.5 kg/m²) and those with severe class III obesity (BMI ≥40 kg/m²) would thus be expected to have the worse outcomes. Because obesity has long been established as a causative factor in the development of diabetes, congestive heart failure, and other obesity-related co-morbidities, improved ICU survival for those with class I and class II obesity (BMI = 30 to 39.9 kg/m²) compared with those with a normal BMI (20 to 25 kg/m²) seems incongruent or opposite of what would be expected. The term obesity paradox has therefore been used to describe the observed phenomenon of improved survival for critically ill patients with obesity when compared with their lean counterparts.Etiologies for this presumed paradox are not clear. Emerging research indicates that adipose cells may mediate a range of short-term beneficial functions in response to sepsis or stress despite the chronic inflammatory and detrimental health effects from obesity. Adipose tissue is a functional organ capable of altering metabolism and secreting immune-modulating chemokines, and not just a depot for excess energy as assumed in the past [4]. Leptin, secreted from adipose tissue, augmented the immune response and improved bacterial clearance in animals [5]. Critically ill septic patients who survived from sepsis had threefold higher plasma concentrations of leptin compared with those who died [6]. Lipoproteins, apoproteins, and eicosanoid-derived resolvins and protectins have been shown to neutralize lipopoly saccharide, to stimulate clearance of inflammatory debris, and to exert direct anti-inflammatory actions [7,8].It has been argued that the potential beneficial effect of obesity upon survival for the ICU patient is not a real phenomenon, but is probably reflective of selection biasin the study design without adequately adjusting for confounding factors that may have influenced clinical outcomes. A strength of Arabi and colleagues'' study was that mortality was evaluated using the raw data as well as adjusting for differences in baseline characteristics with or without differences in sepsis interventions [1]. Their raw unadjusted data reflected the obesity paradox paradigm - that obese patients had a lower odds ratio for mortality than normal-weight subjects. However, after adjusting for confounders, the impact of obesity was reduced to, at best, a statistically insignificant trend. Their data would indicate that obesity, per se, did not significantly improve survival from septic shock [1].The investigators postulated that how obese and non-obese patients were managed during resuscitation and antibiotic therapy may have influenced their survival. Since therapeutic interventions did not take into consideration the large variations in BMI among patients, the patients with class III obesity received one-half of the amount of fluid that the underweight group received when normalized to body weight. The investigators implied that lean patients may have been over-resuscitated, which has been shown to have detrimental effects including prolonged duration of mechanical ventilation [9]. Additionally, there is a paucity of literature regarding how pharmacokinetic properties of many drugs are altered during critical illness for patients with obesity [10]. Finally, most studies examining the obesity paradox, including this one, did not closely evaluate nutrition therapy. Early initiation of nutrition therapy decreases infectious morbidity for critically ill surgical and trauma patients [11]. Provision of higher amounts of protein has been associated with improved survival during critical illness [12,13], whereas preliminary evidence indicates that excessive caloric intake worsens morbidity particularly for obese patients [14].In summary, the important work of Arabi and coworkers challenges the validity of the obesity paradox concept for critically ill patients with septic shock [1]. Additionally, their data compel clinician scientists to conduct future research towards better defining optimal fluid resuscitation, pharmacotherapy, and nutrition therapy that considers the wide range in BMI, lean weight, and fat mass observed for these complex patients.