Vitamin D is widely known to regulate bone health, but there is increasing evidence that it may also ameliorate colitis through inflammation, cell proliferation and apoptosis, and the microbiota. The purpose of this review is to systematically examine the mechanisms by which vitamin D reduces colitis. PubMed and Web of Science were searched for articles published between 2008 and 2019 using key words such as “vitamin D,” “colitis,” “inflammatory bowel disease,” “inflammation,” “apoptosis,” “cell proliferation,” and “gut bacteria”. Retrieved articles were further narrowed and it was determined whether their title and abstracts contained terminology pertaining to vitamin D in relation to colitis in human clinical trials, animal studies, and cell culture/biopsy studies, as well as selecting the best match sorting option in relation to the research question. In total, 30 studies met the established criteria. Studies consistently reported results showing that vitamin D supplementation can downregulate inflammatory pathways of COX-2, TNF-α, NF-κB, and MAPK, modify cell kinetics, and alter gut microbiome, all of which contribute to an improved state of colitis. Although vitamin D and vitamin D analogs have demonstrated positive effects against colitis, more randomized, controlled human clinical trials are needed to determine the value of vitamin D as a therapeutic agent in the treatment of colitis.

Postprandial blood glucose (PBG) is an independent predictor of disease and mortality risk. To date, the shortest, single, moderate-intensity exercise intervention to reduce PBG is a 1 min bout of stair stepping during an oral glucose tolerance test. Whether this effect translates to real meal consumption is unknown. Subjects (N = 30) participated in a randomized controlled crossover trial performing 0 min (seated control), 1 min, 3 min or 10 min of stair climbing and descending bouts (SCD) at a self-selected pace after consumption of a mixed meal on four separate visits. Compared to control, all SCD reduced PBG at least one timepoint: at 30-min the 3 min (-10.8 (-18.7 to -2.8) mg/dL, p = 0.010) and 10 min (-36.3 (-46.4 to -26.3) mg/dL), p < .001), and at 45-min the 1 min (-7.3 (-13.9 to -0.7) mg/dL, p = 0.030, 3 min (-8.7 (-13.9 to -3.6) mg/dL, p = 0.002 and 10 min SCD (-12.2 (-18.2 to -6.1)mg/dL, p < 0.000) reduced PBG. The area under the curve (AUC) for PBG was lower following the 3 min (-4.4% (-7.5 to -1.4%), p = 0.006) and 10 min (-8.9% (-12.4 to -5.3%), p < 0.001), while the incremental AUC (iAUC) was reduced only following the 10 min (-38.0% (-63.7 to -12.3%), p = 0.005) SCD. All SCD were rated by subjects as very light to light intensity. Single, subjectively "light" intensity stair climbing and descending bouts as short as 1 min in duration attenuate the postprandial glucose response in normal weight individuals following consumption of a mixed meal. More pronounced effects require longer bouts in a dose-dependent manner.

The history and trends in use of dietary supplements as documented in the National Health and Nutrition Examination Survey are summarized. The safety and efficacy of selected supplements are discussed. The current regulation of dietary supplements is not robust because legislation governing enforcement is weaker than it is for drugs.

This study examined the effect of moderate intensity stair stepping exercise on the glycemic response, and antioxidant capacity (TAC) during an oral glucose tolerance test (OGTT). Thirty participants (women = 12) completed 4 OGTTs during rest or stair walking bouts of 1, 3, and 10 min in a randomized order. Blood was collected at baseline and 30 min during the OGTTs and analyzed for glucose, insulin, TAC, and lactate. Glucose concentrations were decreased following the 10 min (-22.69 (-34.66 to -10.72) mg/dL, p < 0.002) and 3 min (-15.37 (-25.05 to -5.69) mg/dL, p < 0.004) bouts but not the 1 min bout (-6.18 (-19.54 to 7.18) mg/dL, p = 0.352). Insulin concentrations were decreased following the 10 min (-6.11 (-8.86 to -3.36 μIU/dL), p < 0.001) and 3 min (-2.589 (-4.54 to -0.63) μIU/dL, p < 0.012) bouts but not the 1 min bout (-0.37 (-1.87 to 1.13) μIU/dL, p = 0.616). Insulin sensitivity index values showed a significant increase in the 10-min trial (1.81 (0.03-3.58), p < 0.048), but not during the 3 min (0.65 (-0.66 to 1.96) p = 0.317) or 1 min trial (0.13 (-1.58 to 1.84) p = 0.878). There was no omnibus effect for trial in TAC (p = 0.132, η² = 0.07). There was no interaction between trial and time for blood lactate (p = 0.621, η² = 0.02). This study provides evidence bouts as short as 3 min decrease postprandial blood glucose and insulin levels but longer bouts are needed to affect insulin sensitivity.

Background: Systemic lupus erythematosus (SLE) and rheumatoid arthritis (RA) are associated with a high incidence of cardiovascular disease. Coronary atherosclerosis, particularly total plaque and noncalcified plaque on coronary computed tomography angiography (CCTA) has been correlated with cardiovascular events. We compared baseline coronary plaque burden and progression by serial CCTA in SLE and RA patients. Methods: We prospectively evaluated 44 patients who underwent serial CCTA examinations to quantify coronary plaque progression, 22 SLE patients, and 22 age- and sex-matched RA patients. Semiautomated plaque software was used for quantitative plaque assessment. Linear regression examined the effect of SLE diagnosis (versus RA) on annualized change in natural log-transformed total normalized atheroma volume (ln-TAV_norm) for low-attenuation, fibrofatty, fibrous, total noncalcified, densely calcified, and total plaque. Results: No quantitative differences for any plaque types were observed at baseline between SLE and RA patients (P = 0.330–0.990). After adjustment for baseline plaque and cardiovascular risk factors, the increase in ln-TAV_norm was higher in SLE than RA patients for fibrous [Exp-β: 0.202 (0.398), P = 0.0003], total noncalcified [Exp-β: 0.179 (0.393), P = 0.0001], and total plaque volume [Exp-β: 0.154 (0.501), P = 0.0007], but not for low-attenuation, fibrofatty, or densely calcified plaque (P = 0.103–0.489). Patients with SLE had 80% more fibrous, 82% more noncalcified, and 85% more total plaque increase than those with RA. Conclusion: Coronary plaque volume was similar in RA and SLE at baseline. Progression was greater in SLE, which may explain the greater cardiovascular risk in this disease. Further research to evaluate screening and management strategies for cardiovascular disease in these high-risk patients is warranted.