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Aims/hypothesisType 2 diabetes mellitus has been implicated as a risk factor for hearing loss, with possible mechanisms including microvascular disease, acoustic neuropathy or oxidative stress. A few small studies have examined the longitudinal association between type 2 diabetes and hearing loss, but larger studies are needed. Our objective was to examine whether type 2 diabetes (including diabetes duration) is associated with incident hearing loss in two prospective cohorts: Nurses’ Health Studies (NHS) I and II.MethodsWe conducted a longitudinal study of 139,909 women to examine the relationship between type 2 diabetes and the risk of self-reported incident hearing loss. A physician-diagnosis of diabetes was ascertained from biennial questionnaires. The primary outcome was hearing loss reported as moderate or worse in severity (categorised as a ‘moderate or severe’ hearing problem, or ‘moderate hearing trouble or deaf’) on questionnaires administered in 2012 in NHS I and 2009 or 2013 in NHS II. Cox proportional hazards regression was used to adjust for potential confounders.ResultsDuring >2.4 million person-years of follow-up, 664 cases of moderate or worse hearing loss were reported among those with type 2 diabetes and 10,022 cases among those without type 2 diabetes. Compared with women who did not have type 2 diabetes, those with type 2 diabetes were at higher risk for incident moderate or worse hearing loss (pooled multivariable-adjusted HR 1.16 [95% CI 1.07, 1.27]). Participants who had type 2 diabetes for ≥8 years had a higher risk of moderate or worse hearing loss compared with those without type 2 diabetes (pooled multivariable-adjusted HR 1.24 [95% CI 1.10, 1.40]).Conclusions/interpretationIn this large longitudinal study, type 2 diabetes was associated with a modestly higher risk of moderate or worse hearing loss. Furthermore, longer duration diabetes was associated with a higher risk of moderate or worse hearing loss.

The relation between sodium intake and cardiovascular disease is controversial. This study used individual-participant data from six prospective cohorts of healthy adults. Higher sodium and lower potassium intakes, estimated from multiple 24-hour urine samples, were associated in a dose-dependent manner with a higher cardiovascular risk.

Background Nephrolithiasis is a frequent condition. While it is generally accepted that such condition carries a risk of recurrence over time, the exact risk and its predictors have been rarely quantitated. We aimed to estimate recurrence of kidney stones, overall and in specific subgroups, from randomized controlled trials (RCTs) of calcium stone formers. Methods Systematic review of RCTs of adult patients with idiopathic calcium kidney stones. Recurrence rates analyzed in subgroups based on type of intervention and other characteristics, using Poisson regression models. Results The analysis included 21 RCTs with 2168 participants over a median follow-up of 3.2 years (range 0.5–9.7). The median recurrence of kidney stones was 15 per 100 person–years (range 0–110). Recurrence was higher in those with two or more previous stone episodes compared to those with a single episode at enrolment (16 vs. 6 per 100 person–years, p < 0.001) and in those untreated or treated with dietary changes compared to those treated with drugs (26 vs. 23 vs. 9 per 100 person–years, p < 0.001). The effect of drugs on recurrence seemed to be beneficial only among those with two or more previous stone episodes. Conclusions The overall recurrence rate of stones depends on factors such as previous stone history and type of treatment. Dietary approaches seem to be more effective among single stone formers, whereas drugs seem to be more effective among recurrent stone formers.

To examine the association between ultraviolet radiation (UVR) exposure and the risk of herpes zoster (HZ) in 3 prospective cohorts. We included 205,756 participants from the Health Professionals Follow-up Study (HPFS; 1986-2008), Nurses’ Health Study (NHS; 1996-2012), and Nurses’ Health Study II (NHS II; 1991-2013). Ambient UVR exposure was based on updated geocoded address histories linked with a high-resolution spatiotemporal ultraviolet model. Incident HZ cases were identified by self-reported clinician diagnosis. Sunburn history and medical, lifestyle, and dietary factors were assessed using biennial questionnaires. Multivariable Cox proportional hazards models were used. A total of 24,201 cases of HZ occurred during 3,626,131 person-years. Ambient UVR exposure was associated with a higher risk of HZ in men (HPFS: multivariable-adjusted hazard ratio [MVHR] comparing highest vs lowest quintiles, 1.14; 95% CI, 1.02-1.29; P=.03 for trend) but not in women (NHS: MVHR, 0.99; 95% CI, 0.93-1.05; NHS II: MVHR, 0.96; 95% CI, 0.90-1.03). A higher lifetime number of severe sunburns was associated with a higher risk of HZ in all cohorts (HPFS: MVHR for ≥10 sunburns vs none, 1.08; 95% CI, 0.96-1.20; P=.02 for trend; NHS: MVHR, 1.14; 95% CI, 1.05-1.22; P=.01 for trend; NHS II: MVHR, 1.13; 95% CI, 1.00-1.28; P<.001 for trend). Ambient UVR exposure was associated with a higher risk of HZ in men but not in women. A history of severe sunburn was associated with a modest increased risk of HZ in men and women, possibly because of immunosuppression from overexposure to the sun.

Objectives To prospectively assess the joint association of birth weight and established lifestyle risk factors in adulthood with incident type 2 diabetes and to quantitatively decompose the attributing effects to birth weight only, to adulthood lifestyle only, and to their interaction.Design Prospective cohort study.Setting Health Professionals Follow-up Study (1986-2010), Nurses’ Health Study (1980-2010), and Nurses’ Health Study II (1991-2011).Participants 149 794 men and women without diabetes, cardiovascular disease, or cancer at baseline.Main outcome measure Incident cases of type 2 diabetes, identified through self report and validated by a supplementary questionnaire. Unhealthy lifestyle was defined on the basis of body mass index, smoking, physical activity, alcohol consumption, and the alternate healthy eating index.Results During 20-30 years of follow-up, 11 709 new cases of type 2 diabetes were documented. The multivariate adjusted relative risk of type 2 diabetes was 1.45 (95% confidence interval 1.32 to 1.59) per kg lower birth weight and 2.10 (1.71 to 2.58) per unhealthy lifestyle factor. The relative risk of type 2 diabetes associated with a combination of per kg lower birth weight and per unhealthy lifestyle factor was 2.86 (2.26 to 3.63), which was more than the addition of the risk associated with each individual factor, indicating a significant interaction on an additive scale (P for interaction<0.001). The attributable proportions of joint effect were 22% (95% confidence interval 18.3% to 26.4%) to lower birth weight alone, 59% (57.1% to 61.5%) to unhealthy lifestyle alone, and 18% (13.9% to 21.3%) to their interaction.Conclusion Most cases of type 2 diabetes could be prevented by the adoption of a healthier lifestyle, but simultaneous improvement of both prenatal and postnatal factors could further prevent additional cases.

Background Herpes zoster (HZ), commonly known as “shingles,” may contribute to cognitive decline through mechanisms such as neuroinflammation or direct neuronal injury. However, evidence on the longitudinal association between HZ and cognitive decline is conflicting and whether the risk differs by APOE ε4-carrier status has not been studied; prospective cohort studies on the association between HZ vaccination and cognitive decline are also lacking. Methods We included 149,327 participants from three large cohorts—the Nurses’ Health Study (NHS), NHSII, and Health Professionals Follow-Up Study (HPFS)—to prospectively examine the association between HZ and subsequent subjective cognitive decline (SCD). Poisson regression was used to estimate the multivariable-adjusted relative risk (MVRR) of a 3-unit increment in SCD score according to years since HZ compared with participants with no history of HZ. Results Compared with individuals with no history of HZ, the MVRR (95% CI) of a 3-unit increment in SCD score was significantly and independently higher among individuals with a history of HZ, but the duration of time since HZ when the elevated risk of SCD was statistically significant differed among the cohorts. In NHS, HZ was associated with higher long-term risk of SCD; compared with individuals with no history of HZ, the MVRR (95% CI) of a 3-unit increment in SCD score was 1.14 (1.01, 1.32) for ≥ 13 years since HZ. In NHS II, HZ was associated with higher risk of SCD in both the short-term [MVRR 1.34 (1.18, 1.53) for 1–4 years] and long-term [MVRR 1.20 (1.08, 1.34) for ≥ 13 years since HZ]. In HPFS, an elevated risk of SCD was suggested across all time points. Among the subset of participants with information on APOE ε4, there was a suggestion that the association differed by APOE ε4 carrier status, but the results were not consistent between women and men. Among the subset of women with information on HZ vaccination, there was a suggestion that the long-term risk of SCD may be greater among women who were not vaccinated against HZ. Conclusions Data from three large independent cohorts of women and men showed that HZ was associated with higher long-term risk of SCD, and the risk may differ by APOE ε4-carrier status.

The population impact of modifying obesity and other key risk factors for hyperuricemia has been estimated in cross-sectional studies; however, the proportion of incident gout cases (a clinical end point) that could be prevented by modifying such factors has not been evaluated. To estimate the proportion of incident gout cases that could be avoided through simultaneous modification of obesity and other key risk factors. The Health Professionals Follow-up Study is a US prospective cohort study of 51 529 male health professionals enrolled in 1986 and followed up through questionnaires every 2 years through 2012. Self-reported gout cases were confirmed through June 2015. Clean and complete data used for this analysis were available in June 2016, with statistical analyses performed from July 2016 to July 2019. From data collected in the validated questionnaires, men were categorized to low-risk groups according to combinations of the following 4 factors: normal body mass index (BMI [calculated as weight in kilograms divided by height in meters squared]; <25), no alcohol intake, adherence to Dietary Approaches to Stop Hypertension (DASH)-style diet (highest quintile of DASH diet score), and no diuretic use. Population attributable risks (PARs) for incident gout meeting the preliminary American College of Rheumatology survey criteria, overall and stratified by BMI. We analyzed 44 654 men (mean [SD] age, 54.0 [9.8] years) with no history of gout at baseline. During 26 years of follow-up, 1741 (3.9%) developed incident gout. Among all participants, PAR for the 4 risk factors combined (BMI, diet, alcohol use, and diuretic use) was 77% (95% CI, 56%-88%). Among men with normal weight (BMI <25.0) and overweight (BMI 25.0-29.9), we estimated that more than half of incident gout cases (69% [95% CI, 42%-83%] and 59% [95% CI, 30%-75%], respectively) may have been prevented by the combination of DASH-style diet, no alcohol intake, and no diuretic use. However, among men with obesity (BMI ≥30), PAR was substantially lower and not significant (5% [95% CI, 0%-47%]). The findings of this cohort study suggest that addressing excess adiposity and other key modifiable factors has the potential to prevent the majority of incident gout cases among men. Men with obesity may not benefit from other modifications unless weight loss is addressed.

Fibroblast growth factor 23 (FGF23), parathyroid hormone (PTH), and phosphorus all have been proposed as plasma biomarkers for the development of coronary heart disease (CHD) in individuals with normal renal function. In a nested case-control study of men in the Health Professionals Follow-up Study, free of diagnosed cardiovascular disease at blood draw, we prospectively examined associations between plasma FGF23, PTH, and phosphorus and risk of CHD. During 10 years of follow-up, 422 men developed nonfatal myocardial infarction or fatal CHD. Controls were selected in a 2:1 ratio and matched for age, date of blood collection, and smoking status. Mean estimated glomerular filtration rate was 86 mL/min per 1.73 m 2 in cases and controls. At baseline, there were no statistically significant differences between cases and controls in plasma levels of FGF23, PTH, or phosphorus. After adjusting for matching factors, family history of myocardial infarction, body mass index, alcohol consumption, physical activity, history of diabetes mellitus and hypertension, ethnicity, region, plasma 25-hydroxyvitamin D, and other factors, the odds ratios for incident CHD for participants in the highest, compared with lowest, quartiles were 1.03 (95% CI 0.70-1.52, P for trend 0.84) for FGF23, 1.20 (95% CI 0.82-1.76, P trend 0.99) for PTH, and 0.72 (95% CI 0.51-1.02, P trend 0.13) for phosphorus. Plasma FGF23, PTH, and phosphorus are not associated with the development of incident CHD in men without chronic kidney disease.

To examine the interaction between APOE genotypes and both treated and untreated hypertension on cognitive function in an updated analysis of Nurses' Health Study (NHS) data. At baseline (1995-2001) and 3 biennial follow-up assessments over ~6 years, cognitive function was assessed. 8300 NHS participants aged 70+ years underwent a cognitive battery, which comprised 6 tests including the Telephone Interview for Cognitive Status (TICS) and tests of verbal memory, category fluency, and working memory. We estimated the mean differences in average cognitive scores across up to 4 assessments using multiple linear regression. We also tested for interaction between APOE e4 allele carrier status and hypertension overall, as well as for apparently untreated and treated hypertension. We confirmed that, compared with those with APOE e3/3 genotype, APOE e4 allele carriers scored lower by 0.55 units on the average TICS score (95%CI:-0.67,-0.43). We also observed a significantly worse average TICS score among women with untreated hypertension compared with women without hypertension (difference = -0.23, 95%CI:-0.37,-0.09), while no significant difference was observed for women with treated hypertension. Significant interaction was detected between the APOE e4 allele and untreated hypertension (p-int = 0.02 for the TICS; p-int = 0.045 for global score), but not with treated hypertension. Specifically, compared with normotensive women with the APOE e3/3 genotype, APOE e4 allele carriers with treated hypertension scored lower by 0.50 units (95%CI:-0.69,-0.31); however, the APOE e4 allele carriers with untreated hypertension scored lower by 1.02 units on the TICS score (95%CI:-1.29, -0.76). This interaction of APOE e4 and untreated hypertension was also consistently observed for the global score. Women with hypertension and at least one APOE e4 allele had worse average cognitive function compared with women without hypertension with the e3/3 genotype; this difference was amplified among APOE e4 allele carriers with untreated hypertension.

This study examined the relation between the level of C-reactive protein (CRP) and other inflammatory markers and the risk of coronary heart disease in large cohorts of men and women who were free of cardiovascular disease at baseline. During a follow-up period of six to eight years, men and women with CRP levels of at least 3 mg per liter had a risk of coronary events that was 1.68 times that of those with CRP levels of less than 1 mg per liter. Although lipid levels were better predictors of coronary risk, C-reactive protein was a significant predictor of risk in both sexes. Inflammation plays an essential role in the development of insulin resistance and type 2 diabetes mellitus, the initiation and progression of atherosclerotic lesions, and plaque disruption. 1 , 2 Interleukin-6 and tumor necrosis factor α (TNF-α) are inflammatory cytokines and the main inducers of the secretion of C-reactive protein in the liver. 3 C-reactive protein is a marker of low-grade inflammation, and recent studies suggest that this protein has a role in the pathogenesis of atherosclerotic lesions in humans. 4 The effects of TNF-α are mediated by two receptors, type 1 and type 2 (TNF-R1 and TNF-R2), which circulate in soluble forms (sTNF-R1 and . . .