Objectives To assess the relationship between comorbid depression and diabetes and cognitive decline among Mexican Americans age 65 and over. Design Retrospective cohort study with longitudinal analysis. Setting Texas, New Mexico, Colorado, Arizona, and California Participants Hispanic Established Populations for the Epidemiologic Study of the Elderly (H-EPESE). Measurements Cognition was assessed using the Mini Mental State Examination (MMSE). Depression was defined as a score ≥16 on the Center for Epidemiologic Studies Depression Scale. Diabetes was defined as according to self-reported history or taking insulin or oral hypoglycemic medication. Results Participants with depression and diabetes, depression only, diabetes only, and neither condition declined an average of 6.5, 4.4, 7.8, and 4.2 points on the MMSE, respectively, across the six examination waves. Participants with diabetes or comorbid diabetes and depression declined an average of 0.18 points per year (P<0.01) and 0.25 points per year, respectively, on the MMSE compared to participants with neither condition. Depression was associated with significantly greater cognitive decline (β̂ =−0.11, P<0.05) after excluding participants with baseline cognitive impairment (MMSE≤17). The odds for developing severe cognitive impairment among participants with diabetes increased by 1.08 times per year (95% CI=1.03 – 1.122) and by 1.08 times per year (95% CI=1.01 – 1.15) for participants with comorbid depression and diabetes compared to participants with neither of these conditions. Conclusion Diabetes and comorbid depression and diabetes are risk factors for cognitive decline among older Mexican Americans. Interventions that reduce the prevalence of depression and diabetes among Mexican Americans may decrease the number of older adults who experience cognitive decline.

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To define the clinical significance of delayed postsphincterotomy hemorrhage, we reviewed 476 consecutive ERCP procedures performed over a three-year period. Of 250 patients who underwent endoscopic sphincterotomy (ES), five (2%) developed postprocedure hemorrhage, two of whom had immediate, self-limited bleeding that resolved after endoscopic injection of epinephrine and did not require transfusion. The other three had delayed hemorrhage characterized by: onset 20-48 hr after the procedure, melena without hematemesis as the index clinical manifestation of bleeding, and atraumatic balloon extraction of common duct stones. Transfusion of 2-6 units of packed erythrocytes was necessary in each and one patient required surgical hemostasis. Delayed hemorrhage following ERS is an important, frequently severe complication to remember when contemplating performing ERS as an outpatient procedure.

The neurobiological mechanisms that mediate psychiatric comorbidities associated with metabolic disorders such as obesity, metabolic syndrome and diabetes remain obscure. High fructose corn syrup (HFCS) is widely used in beverages and is often included in food products with moderate or high fat content that have been linked to many serious health issues including diabetes and obesity. However, the impact of such foods on the brain has not been fully characterized. Here, we evaluated the effects of long-term consumption of a HFCS-Moderate Fat diet (HFCS-MFD) on behavior, neuronal signal transduction, gut microbiota, and serum metabolomic profile in mice to better understand how its consumption and resulting obesity and metabolic alterations relate to behavioral dysfunction. Mice fed HFCS-MFD for 16 weeks displayed enhanced anxiogenesis, increased behavioral despair, and impaired social interactions. Furthermore, the HFCS-MFD induced gut microbiota dysbiosis and lowered serum levels of serotonin and its tryptophan-based precursors. Importantly, the HFCS-MFD altered neuronal signaling in the ventral striatum including reduced inhibitory phosphorylation of glycogen synthase kinase 3β (GSK3β), increased expression of ΔFosB, increased Cdk5-dependent phosphorylation of DARPP-32, and reduced PKA-dependent phosphorylation of the GluR1 subunit of the AMPA receptor. These findings suggest that HFCS-MFD-induced changes in the gut microbiota and neuroactive metabolites may contribute to maladaptive alterations in ventral striatal function that underlie neurobehavioral impairment. While future studies are essential to further evaluate the interplay between these factors in obesity and metabolic syndrome-associated behavioral comorbidities, these data underscore the important role of peripheral-CNS interactions in diet-induced behavioral and brain function. This study also highlights the clinical need to address neurobehavioral comorbidities associated with obesity and metabolic syndrome.

Our study yielded articles regarding impressions of patients with diabetes about their general health and outcomes. However, we did not discover much literature directly concerning attitudes toward catastrophic lower extremity outcomes before they occurred. We also identified that patients lack knowledge of management and complications of diabetes; both of these gaps provide an opportunity to better direct care for such patients.

IntroductionDiabetes self-care practices are less effective outside of controlled research settings, and almost half of patients do not achieve good glycemic control. Qualitative studies suggest some lifestyle strategies may be linked to good control, but those strategies have not been validated. This study provides population-based evidence that dietary strategies identified in qualitative studies are associated with glycemic control in US patients with diabetes.Research design and methodsIn a cross-sectional sample of the National Health and Nutrition Examination Survey (NHANES), qualitative self-management themes were matched to survey questions and used to predict good glycemic control (hemoglobin A1c <7.0% (53 mmol/mol)). Patients were limited to those 50 years of age and older with a diagnosis of diabetes for at least 1 year (N=465).ResultsPatients averaged 65 years of age with a body mass index of 32.56 kg/m2 and 42% reported no physical activity. In logistic regression models controlling for sociodemographic and medical history variables, self-monitoring of blood glucose, weight loss, and physical activity were not significantly associated with glycemic control. Instead, dietary practices such as consuming low-calorie foods (OR=4.05, 95% CI 1.64 to 10.01), eating less fat (OR=2.15, 95% CI 1.03 to 4.47), and reducing sodium (OR=1.94, 95% CI 1.18 to 3.17) were significantly associated with good glycemic control, as was diabetes education or consultation with a dietitian (OR=3.48, 95% CI 1.28 to 9.45). Non-adherence to medications (OR=0.27, 95% CI 0.11 to 0.68) and general dietary descriptions, such as following a ‘diabetic diet’ (OR=0.32, 95% CI 0.17 to 0.57) and ‘changing eating habits for weight loss’ (OR=0.34, 95% CI 0.15 to 0.77), were associated with poorer glycemic control.ConclusionsThe NHANES validation of lifestyle management strategies suggests practices that may be sustainable. In a population that tends to be obese with low physical activity, successful self-care might emphasize specific dietary practices offering concrete touchpoints for patient communication and guidance. These strategies might help maintain glycemic control.

Investigations into the causative role that western dietary patterns have on obesity and disease pathogenesis have speculated that quality and quantity of dietary fats and/or carbohydrates have a predictive role in the development of these disorders. Standard reference diets such as the AIN-93 rodent diet have historically been used to promote animal health and reduce variation of results across experiments, rather than model modern human dietary habits or nutrition-related pathologies. In rodents high-fat diets (HFDs) became a classic tool to investigate diet-induced obesity (DIO). These murine diets often relied on a single fat source with the most DIO consistent HFDs containing levels of fat up to 45-60% (kcal), higher than the reported human intake of 33–35% (kcal). More recently, researchers are formulating experimental animal (pre-clinical) diets that reflect mean human macro- and micronutrient consumption levels described by the National Health and Nutrition Examination Survey (NHANES). These diets attempt to integrate relevant ingredient sources and levels of nutrients; however, they most often fail to include high-fructose corn syrup (HFCS) as a source of dietary carbohydrate. We have formulated a modified Standard American Diet (mSAD) that incorporates relevant levels and sources of nutrient classes, including dietary HFCS, to assess the basal physiologies associated with mSAD consumption. Mice proffered the mSAD for 15 weeks displayed a phenotype consistent with metabolic syndrome, exhibiting increased adiposity, fasting hyperglycemia with impaired glucose and insulin tolerance. Metabolic alterations were evidenced at the tissue level as crown-like structures (CLS) in adipose tissue and fatty acid deposition in the liver, and targeted 16S rRNA metagenomics revealed microbial compositional shifts between dietary groups. This study suggests diet quality significantly affects metabolic homeostasis, emphasizing the importance of developing relevant pre-clinical diets to investigate chronic diseases highly impacted by western dietary consumption patterns.