Specifically, our findings indicate that any benefits of Cr supplementation on hypertrophy gains during resistance training may not be attributed to a direct anabolic effect on the skeletal muscle. The authors acknowledge the grant support of São Paulo Research Foundation (FAPESP), Proc. 04/08627-3. “
“See Covering the Cover synopsis on page 1327. Helicobacter pylori infection,

nonsteroidal anti-inflammatory medications (NSAIDs), and aspirin are believed selleck chemicals to be the main causes of nonvariceal upper gastrointestinal bleeding,1 and with the discovery of proton pump inhibitors (PPIs) and H pylori eradication therapy, the burden of peptic ulcer disease has been decreasing. 2 Despite this, upper gastrointestinal hemorrhage

remains the most common acute severe medical admission for gastroenterology, 3 and 4 and its incidence in population-based studies remains virtually unchanged. 5 and 6 This suggests that other (previously unidentified) risk factors are contributing to its population burden. Historically, nongastrointestinal comorbidity was believed to be associated with stress ulceration7 but, currently, the role of comorbidity in the etiology of gastrointestinal bleeding (GIB) is selleck products not recognized apart from in severe illness; for example, sicker cirrhotic patients are known to have an increased risk of variceal bleeding,8 and sicker patients in intensive therapy units (ITUs) have an increased risk of nonvariceal bleeding.9 However, as the proportion of bleed patients with comorbidity has increased during the last decade,5 we wondered if exposure to less severe but chronic comorbidity could itself be responsible for the persisting incidence of bleeding. Outside of ITU though, the effect of comorbidity has only been assessed as a confounder in studies that focused on the effect of

medications on gastrointestinal bleeds.10 Although these studies do support a role for comorbidity, they do not allow us to understand whether it is an important independent contributor to the persisting burden of upper GIB. We have therefore conducted a study aimed primarily at assessing whether comorbidity 4��8C might have an important role in the etiology of upper GIB. To do this we have conducted a case-control study and formed a model fully corrected for known measured risk factors of upper GIB. We have then calculated the additional explanatory effect of adding comorbidity to our model to understand its effect on bleeding incidence in the general population. We conducted a matched case control study. To provide the detailed longitudinal data and necessary power for this study, we have used the recently linked English Hospital Episodes Statistics data (secondary care data) and General Practice Research Database (GPRD) (primary care data).