BackgroundPlant-based diets have been recommended to reduce the risk of type 2 diabetes (T2D). However, not all plant foods are necessarily beneficial. We examined the association of an overall plant-based diet and hypothesized healthful and unhealthful versions of a plant-based diet with T2D incidence in three prospective cohort studies in the US.Methods and FindingsWe included 69,949 women from the Nurses’ Health Study (1984–2012), 90,239 women from the Nurses’ Health Study 2 (1991–2011), and 40,539 men from the Health Professionals Follow-Up Study (1986–2010), free of chronic diseases at baseline. Dietary data were collected every 2–4 y using a semi-quantitative food frequency questionnaire. Using these data, we created an overall plant-based diet index (PDI), where plant foods received positive scores, while animal foods (animal fats, dairy, eggs, fish/seafood, poultry/red meat, miscellaneous animal-based foods) received reverse scores. We also created a healthful plant-based diet index (hPDI), where healthy plant foods (whole grains, fruits, vegetables, nuts, legumes, vegetable oils, tea/coffee) received positive scores, while less healthy plant foods (fruit juices, sweetened beverages, refined grains, potatoes, sweets/desserts) and animal foods received reverse scores. Lastly, we created an unhealthful plant-based diet index (uPDI) by assigning positive scores to less healthy plant foods and reverse scores to healthy plant foods and animal foods.We documented 16,162 incident T2D cases during 4,102,369 person-years of follow-up. In pooled multivariable-adjusted analysis, both PDI and hPDI were inversely associated with T2D (PDI: hazard ratio [HR] for extreme deciles 0.51, 95% CI 0.47–0.55, p trend < 0.001; hPDI: HR for extreme deciles 0.55, 95% CI 0.51–0.59, p trend < 0.001). The association of T2D with PDI was considerably attenuated when we additionally adjusted for body mass index (BMI) categories (HR 0.80, 95% CI 0.74–0.87, p trend < 0.001), while that with hPDI remained largely unchanged (HR 0.66, 95% CI 0.61–0.72, p trend < 0.001). uPDI was positively associated with T2D even after BMI adjustment (HR for extreme deciles 1.16, 95% CI 1.08–1.25, p trend < 0.001). Limitations of the study include self-reported diet assessment, with the possibility of measurement error, and the potential for residual or unmeasured confounding given the observational nature of the study design.ConclusionsOur study suggests that plant-based diets, especially when rich in high-quality plant foods, are associated with substantially lower risk of developing T2D. This supports current recommendations to shift to diets rich in healthy plant foods, with lower intake of less healthy plant and animal foods.

Increased fruit and vegetable intake lowers blood pressure in short-term interventional studies. However, data on the association of long-term intake of fruits and vegetables with hypertension risk are scarce. We prospectively examined the independent association of whole fruit (excluding juices) and vegetable intake, as well as the change in consumption of whole fruits and vegetables, with incident hypertension in three large longitudinal cohort studies: Nurses’ Health Study (n=62,175), Nurses’ Health Study II (n=88,475), and Health Professionals Follow-up Study (n =36,803). We calculated hazard ratios and 95% confidence intervals for fruit and vegetable consumption while controlling for hypertension risk factors. Compared with participants whose consumption was ≤4servings/week, the pooled hazard ratios among those whose intake was ≥4servings/day were 0.92(0.87–0.97) for total whole fruit intake and 0.95(0.86–1.04) for total vegetable intake. Similarly, compared with participants who did not increase their fruit or vegetable consumption, the pooled hazard ratios for those whose intake increased by ≥7servings/week were 0.94(0.90–0.97) for total whole fruit intake and 0.98(0.94–1.01) for total vegetable. Analyses of individual fruits and vegetables yielded different results. Consumption levels of ≥4servings/per week (as opposed to <1serving/month) of broccoli, carrots, tofu or soybeans, raisins and apples was associated with lower hypertension risk. In conclusion, our results suggest that greater long-term intake and increased consumption of whole fruits may reduce the risk of developing hypertension.

Background and objectives: Nearly 30% of renal transplant recipients develops BK viremia, a prerequisite for BK nephropathy. Case reports have evaluated treatment options for BK virus, but no controlled studies have assessed prophylactic therapies. Fluoroquinolone antibiotics were studied for prevention of BK viremia after renal transplantation.Design, setting, participants, & measurements: This retrospective analysis evaluated adult renal transplant recipients with at least one BK viral load (blood) between 90 and 400 days after transplantation. Six to 12 months of co-trimoxazole was used for Pneumocystis prophylaxis. In sulfa-allergic/-intolerant patients, 6 to 12 months of atovaquone with 1 month of a fluoroquinolone was used. Fluoroquinolones can inhibit BK DNA topoisomerase. The two groups studied were those that received 30 days of levofloxacin or ciprofloxacin after transplantation and those that did not. The primary endpoint was BK viremia rates at 1 year. Of note, of the 160 patients not receiving fluoroquinolone prophylaxis, 40 received a fluoroquinolone for treatment of a bacterial infection within 3 months after transplantation. Subgroup analysis evaluating these 40 patients against the 120 who had no exposure to fluoroquinolones was completed.Results: A 1-month fluoroquinolone course after transplantation was associated with significantly lower rates of BK viremia at 1 year compared with those with no fluoroquinolone. In the subgroup analysis, exposure to fluoroquinolone for treatment of bacterial infections within 3 months after transplantation was associated with significantly lower 1-year rates of BK viremia.Conclusions: This analysis demonstrates that fluoroquinolones are effective at preventing BK viremia after renal transplantation.

Objective To determine whether higher intake of baked or boiled potatoes, French fries, or potato chips is associated with incidence of hypertension.Design Prospective longitudinal cohort studies.Setting Healthcare providers in the United States.Participants 62 175 women in Nurses’ Health Study, 88 475 women in Nurses’ Health Study II, and 36 803 men in Health Professionals Follow-up Study who were non-hypertensive at baseline.Main outcome measure Incident cases of hypertension (self reported diagnosis by healthcare provider).Results Compared with consumption of less than one serving a month, the random effects pooled hazard ratios for four or more servings a week were 1.11 (95% confidence interval 0.96 to 1.28; P for trend=0.05) for baked, boiled, or mashed potatoes, 1.17 (1.07 to 1.27; P for trend=0.001) for French fries, and 0.97 (0.87 to 1.08; P for trend=0.98) for potato chips. In substitution analyses, replacing one serving a day of baked, boiled, or mashed potatoes with one serving a day of non-starchy vegetables was associated with decreased risk of hypertension (hazard ratio 0.93, 0.89 to 0.96).Conclusion Higher intake of baked, boiled, or mashed potatoes and French fries was independently and prospectively associated with an increased risk of developing hypertension in three large cohorts of adult men and women.

Objective Disruption of vitamin D signaling in rodents causes activation of the renin angiotensin system (RAS) and development of hypertension. Observational studies in humans found lower circulating 25-hydroxyvitamin D (25[OH]D) is associated with increased RAS activity and blood pressure (BP). We performed the first randomized control trial to investigate the effects of vitamin D supplementation on the RAS in humans. Methods Vitamin D deficient, (25[OH]D ≤20 ng/mL), overweight individuals without hypertension were randomized into a double-blind, placebo-controlled trial of 8 weeks treatment with ergocalciferol or placebo. Kidney-specific RAS activity, measured using renal plasma flow (RPF) response to captopril in high sodium balance, was assessed at baseline and 8 weeks, as was systemic RAS activity and 24-hour ambulatory BP. Results 84 participants completed the study. Mean 25[OH]D levels increased from 14.7 to 30.3 ng/mL in the ergocalciferol group, p-value < 0.0001, and from 14.3 to 17.4 ng/mL in the placebo group, p-value = 0.3. The RPF response to captopril was 33.9±56.1 mL/min/1.73m2 at baseline and 35.7±47.7 mL/min/1.73m2 at 8 weeks in the ergocalciferol group (p-value=0.83); and was 37.3±46.9 mL/min/1.73m2 at baseline and 35.9±26.2 mL/min/1.73m2 at 8 weeks in the placebo group (p-value=0.78). Ergocalciferol had no effect on PRA, AngII, or 24-hour BP measurements. Conclusions This trial found no benefit from correcting vitamin D deficiency on RAS activity or BP after 8 weeks. These findings are not consistent with the hypothesis that vitamin D is a modifiable target for lowering blood pressure in vitamin D deficient individuals.