Fructose content in popular beverages made with and without high-fructose corn syrup

ObjectiveExcess fructose consumption is hypothesized to be associated with risk for metabolic disease. Actual fructose consumption levels are difficult to estimate because of the unlabeled quantity of fructose in beverages. The aims of this study were threefold: 1) re-examine the fructose content in previously tested beverages using two additional assay methods capable of detecting other sugars, especially maltose, 2) compare data across all methods to determine the actual free fructose-to-glucose ratio in beverages made either with or without high-fructose corn syrup (HFCS), and 3) expand the analysis to determine fructose content in commonly consumed juice products.MethodsSugar-sweetened beverages (SSBs) and fruit juice drinks that were either made with or without HFCS were analyzed in separate, independent laboratories via three different methods to determine sugar profiles.ResultsFor SSBs, the three independent laboratory methods showed consistent and reproducible results. In SSBs made with HFCS, fructose constituted 60.6% ± 2.7% of sugar content. In juices sweetened with HFCS, fructose accounted for 52.1% ± 5.9% of sugar content, although in some juices made from 100% fruit, fructose concentration reached 65.35 g/L accounting for 67% of sugars.ConclusionOur results provide evidence of higher than expected amounts of free fructose in some beverages. Popular beverages made with HFCS have a fructose-to-glucose ratio of approximately 60:40, and thus contain 50% more fructose than glucose. Some pure fruit juices have twice as much fructose as glucose. These findings suggest that beverages made with HFCS and some juices have a sugar profile very different than sucrose, in which amounts of fructose and glucose are equivalent. Current dietary analyses may underestimate actual fructose consumption.     

A Closer Look at Racism and Heterosexism in Medical Students’ Clinical Decision-Making Related to HIV Pre-Exposure Prophylaxis (PrEP): Implications for PrEP Education

Social biases among healthcare providers could limit PrEP access. In this survey study of 115 US medical students, we examined associations between biases (racism and heterosexism) and PrEP clinical decision-making and explored prior PrEP education as a potential buffer. After viewing a vignette about a PrEP-seeking MSM patient, participants reported anticipated patient behavior (condomless sex, extra-relational sex, and adherence), intention to prescribe PrEP to the patient, biases, and background characteristics. Minimal evidence for racism affecting clinical decision-making emerged. In unadjusted analyses, heterosexism indirectly affected prescribing intention via all anticipated behaviors, tested as parallel mediators. Participants expressing greater heterosexism more strongly anticipated increased risk behavior and adherence problems, which were associated with lower prescribing intention. The indirect effect via condomless sex remained significant adjusting for background characteristics. Prior PrEP education did not buffer any indirect effects. Heterosexism may compromise PrEP provision to MSM and should be addressed in PrEP-related medical education.     

Effects of unfractionated heparin on renal osteodystrophy and vascular calcification in chronic kidney disease rats

Unfractionated heparin (UFH) is the most widely used anticoagulant in hemodialysis for chronic kidney disease (CKD) patients. Many studies have verified that UFH can induce bone loss in subjects with normal bone, but few have focused on its effect on renal osteodystrophy. We therefore investigated this issue in adenine-induced CKD rats. As CKD also impairs mineral metabolism systemically, we also studied the impacts of UFH on serum markers of CKD–mineral and bone disorder (CKD–MBD) and vascular calcification. We administered low and high doses of UFH (1 U/g and 2 U/g body weight, respectively) to CKD rats and compared them with CKD controls. At sacrifice, the serum markers of CKD–MBD did not significantly differ among the two UFH CKD groups and the CKD control group. The mean bone mineral densities (BMDs) of the total femur and a region of interest (ROI) constituted of trabecular and cortical bone were lower in the high-dose UFH (H-UFH) CKD group than in the CKD control group (P < 0.05 and P < 0.01, respectively). The BMD of the femoral ROI constituted of cortical bone did not differ between the H-UFH CKD group and the CKD control group. Histomorphometrical changes in the CKD rats indicated secondary hyperparathyroidism, and the femoral trabecular bone volume, but not cortical bone volume, significantly decreased with increasing UFH dose. The same decreasing trend was found in osteoblast parameters, and an increasing trend was found in osteoclast parameters; however, most differences were not significant. Moreover, no distinct statistical differences were found in the comparison of vascular calcium or phosphorus content among the CKD control group and the two UFH CKD groups. Therefore, we concluded that UFH could induce bone loss in CKD rats with secondary hyperparathyroidism, mainly by reducing the trabecular volume and had little effect on cortical bone volume. The underlying mechanism might involve inhibition of osteoblast activity and promotion of osteoclast activity by UFH. We did not find any effect of UFH on vascular calcification in CKD rats with secondary hyperparathyroidism.