Abstract P196: Bidirectional Association Between Hypertension and Gout: The Singapore Chinese Health Study

Circulation ◽  
2015 ◽  
Vol 131 (suppl_1) ◽  
Author(s):  
An Pan ◽  
Gim Gee Teng ◽  
Jian-Min Yuan ◽  
Woon-Puay Koh

Introduction: Although it has been hypothesized that the hypertension-gout relation is bidirectional, few studies have addressed this hypothesis in a prospective setting, particularly in the Asian populations. Methods: We analyzed data from the Singapore Chinese Health Study (SCHS), a cohort of 63,257 Chinese aged 45-74 years at recruitment from 1993-98. The information about self reports of physician-diagnosed hypertension and gout was enquired at follow-ups I (1999-2004) and II (2006-2010). We included participants with complete data for both follow-ups and who were free of heart disease, stroke and cancer at follow-up I. For the analysis of hypertension and risk of incident gout, participants with prevalent gout were further excluded and the final analysis included 31,694 participants. For the analysis of gout and risk of incident hypertension, participants with prevalent hypertension were further excluded and the final analysis included 20,490 participants. Cox proportional hazards models were used to estimate multivariable-adjusted relative risks (RRs) and 95% confidence intervals (CIs) with adjustment for age, sex, years of interview, dialect group, education, smoking status, alcohol intake, physical activity, body mass index (BMI) and history of diabetes. Results: The mean age of the participants at baseline was 60.1 (SD 7.3) years, and the average follow-up year was 6.8 (SD 1.4) years. In the analysis of hypertension and risk of gout, 836 incident cases were identified. Compared to normotensive participants, hypertensive patients had a 93% increased risk of developing gout (RR 1.93; 95% CI 1.66-2.24). The association was slightly stronger in women (RR 2.09; 95% CI 1.69-2.58) compared to men (RR 1.72; 95% CI 1.39-2.14; P for interaction=0.056). The association was also stronger in normal weight adults (BMI <24 kg/m2; RR 2.25; 95% CI 1.82-2.77) compared to overweight/obese individuals (BMI ≥24 kg/m2; RR 1.66; 95% CI 1.34-2.04; P for interaction=0.03). In the parallel analysis of gout and risk of hypertension, 5491 participants reported to have newly diagnosed hypertension during the follow-up. Compared to participants without gout, those with gout had a 17% increased risk of developing hypertension (RR 1.17; 95% CI 1.01-1.35). The association was evident in men (RR 1.29; 95% CI 1.07-1.55) but not in women (RR 0.94; 95% CI 0.73-1.20; P for interaction=0.03). The association was present in normal weight adults (RR 1.34; 95% CI 1.09-1.64) but not among overweight/obese individuals (RR 0.99; 95% CI 0.80-1.23; P for interaction=0.03). Conclusions: Our results provide compelling evidence that the hypertension-gout association is bidirectional in Chinese population. The potential interactions of the bidirectional association with sex and obesity deserve further investigations.

2021 ◽  
Author(s):  
C R Langton ◽  
B W Whitcomb ◽  
A C Purdue-Smithe ◽  
L L Sievert ◽  
S E Hankinson ◽  
...  

Abstract STUDY QUESTION What is the association of oral contraceptives (OCs) and tubal ligation (TL) with early natural menopause? SUMMARY ANSWER We did not observe an association of OC use with risk of early natural menopause; however, TL was associated with a modestly higher risk. WHAT IS KNOWN ALREADY OCs manipulate hormone levels, prevent ovulation, and may modify the rate of follicular atresia, while TL may disrupt the blood supply to the ovaries. These mechanisms may be associated with risk of early menopause, a condition associated with increased risk of cardiovascular disease and other adverse health outcomes. STUDY DESIGN, SIZE, DURATION We examined the association of OC use and TL with natural menopause before the age of 45 years in a population-based study within the prospective Nurses’ Health Study II (NHSII) cohort. Participants were followed from 1989 to 2017 and response rates were 85-90% for each cycle. PARTICIPANTS/MATERIALS, SETTING, METHODS Participants included 106 633 NHSII members who were premenopausal and aged 25-42 years at baseline. Use, duration and type of OC, and TL were measured at baseline and every 2 years. Menopause status and age were assessed every 2 years. Follow-up continued until early menopause, age 45 years, hysterectomy, oophorectomy, death, cancer diagnosis, or loss to follow-up. We used Cox proportional hazards models to estimate hazard ratios (HRs) and 95% CIs adjusted for lifestyle, dietary, and reproductive factors. MAIN RESULTS AND THE ROLE OF CHANCE Over 1.6 million person-years, 2579 members of the analytic cohort experienced early natural menopause. In multivariable models, the duration, timing, and type of OC use were not associated with risk of early menopause. For example, compared with women who never used OCs, those reporting 120+ months of OC use had an HR for early menopause of 1.01 (95% CI, 0.87-1.17; P for trend=0.71). TL was associated with increased risk of early menopause (HR = 1.17, 95% CI, 1.06-1.28). LIMITATIONS, REASONS FOR CAUTION Our study population is homogenous with respect to race and ethnicity. Additional evaluation of these relations in more diverse populations is important. WIDER IMPLICATIONS OF THE FINDINGS To our knowledge, this is the largest study examining the association of OC use and TL with early natural menopause to date. While TL was associated with a modest higher risk of early menopause, our findings do not support any material hazard or benefit for the use of OCs. STUDY FUNDING/COMPETING INTEREST(S) The study was sponsored by UO1CA176726 and R01HD078517 from the National Institutes of Health and Department of Health and Human Services. The work was supported by the Intramural Research Program of the Eunice Kennedy Shriver National Institute of Child Health and Human Development. The authors have no competing interests to report. TRIAL REGISTRATION NUMBER N/A


2012 ◽  
Vol 30 (4_suppl) ◽  
pp. 394-394 ◽  
Author(s):  
Amanda Phipps ◽  
Xabier Garcia-Albeniz ◽  
Carolyn Hutter ◽  
Emily White ◽  
Charles S. Fuchs ◽  
...  

394 Background: Beyond clinicopathologic stage, there are few established markers of prognosis in colorectal cancer (CRC). Recent genome-wide association studies have identified 17 germline single nucleotide polymorphisms (SNPs) significantly associated with incident CRC. However, it is unclear if these CRC susceptibility SNPs influence survival after CRC diagnosis. Although the functionality of many of these SNPs remains unknown, a few, including rs4939827 in SMAD7, map to genes with plausible biological mechanisms associated with both cancer risk and prognosis. We examined 17 CRC susceptibility SNPs in relation to survival after CRC diagnosis. Methods: We genotyped 2,611 men and women enrolled in five prospective cohort studies who were diagnosed with invasive CRC during study follow-up: the Physicians’ Health Study (N=281), Health Professionals Follow-up Study (N=268), Nurses’ Health Study (N=367), Vitamins and Lifestyle Study (N=281), and the Women’s Health Initiative (N=1414). Analyses were limited to Caucasians with known vital status, cause of death, and survival time. We used Cox proportional hazards regression to assess associations between each SNP and CRC-specific and overall survival in study-specific models adjusted for age, sex, and stage; SNPs were modeled additively to reflect associations per copy of the minor allele. Study-specific results were combined via fixed-effects meta-analysis. Results: The G allele in rs4939827 was associated with poorer CRC-specific survival [hazard ratio (HR)=1.16, p=0.02] and overall survival (HR=1.13, p=0.03) in CRC patients. The A alleles in rs10795668 and in rs4925386 were associated with a 1.14-fold increased risk of overall mortality (both p-values=0.03) but not CRC-specific mortality. Other evaluated SNPs were not associated with survival. Conclusions: Genetic variation in rs4939827 (SMAD7) is associated with CRC-specific and overall survival. These results suggest that SMAD7 may have a role in CRC progression, and provide proof-of-principle that common germline variation may provide prognostic information beyond traditional considerations such as stage.


2016 ◽  
Vol 34 (2_suppl) ◽  
pp. 588-588
Author(s):  
Mark A Preston ◽  
Xuehong Zhang ◽  
Rebecca E Graff ◽  
Alejandro Sanchez ◽  
Steven L Chang ◽  
...  

588 Background: The relationship between the widely used analgesics (i.e., aspirin, other nonsteroidal anti-inflammatory drugs (NSAID), and acetaminophen) and risk of total and lethal renal cell cancer remains unclear. Methods: We examined the associations between analgesic use and risk of renal cell cancer overall and by subtypes, in the Nurses’ Health Study (NHS) and the Health Professionals Follow-up Study (HPFS). We collected information on aspirin, other non-aspirin NSAIDs, and acetaminophen in 1990 in the NHS and in 1986 in the HPFS, and every 2 years thereafter. We used Cox proportional hazards models, controlling for other known and suspected risk factors, to examine the associations between baseline and duration of use of each analgesic and risk of total renal cell cancer, lethal renal cell cancer (resulted in death due to disease), as well as clear cell renal cell cancer. We pooled results using a random-effects model. Results: During follow-up of 22 years among 77,527 women and 26 years among 45,913 men, we documented 438 cases of renal cell cancer (230 in women and 208 in men), of which 106 were fatal (56 in women and 40 in men) and 300 were clear cell (165 in women and 135 in men). The pooled multivariable relative risks (RRs) for total renal cell cancer were 1.13 (95% CI: 0.91-1.39) for aspirin use, 1.34 (95% CI: 1.03-1.75) for non-aspirin NSAID use, and 1.07 (95% CI: 0.80-1.44) for acetaminophen use. Similar results were observed for lethal renal cell cancer and clear cell renal cell cancer. Importantly, longer duration of non-aspirin NSAID use was associated with an increased risk of renal cell cancer. The pooled (all p-heterogeneity > 0.05) multivariable RRs for total renal cell cancer were 1.23 (95% CI: 0.94-1.62) for non-aspirin NSAID users of 4-10 years and 1.81 (95% CI: 1.21-2.72) for over 10 years. The corresponding RRs were 1.91 (95% CI: 1.04-3.49) and 3.97 (95% CI: 1.46-10.83) for lethal renal cell cancer, and 1.36 (95% CI: 0.99-1.88) and 1.58 (95% CI: 0.94-2.63) for clear cell renal cell cancer. Conclusions: Our findings support a significant positive association between non-aspirin NSAID use and risk of developing renal cell cancer, especially the lethal form.


2021 ◽  
Author(s):  
Zobida Islam ◽  
Shamima Akter ◽  
Yosuke Inoue ◽  
Huan Hu ◽  
Keisuke Kuwahara ◽  
...  

<b>Objective:</b> Prediabetes has been suggested to increase mortality risk; however, the definitions of prediabetes that can predict mortality remain elusive. We prospectively investigated the association of multiple definitions of prediabetes with the risk of mortality from all-causes, cardiovascular disease (CVD), and cancer in Japanese workers. <p> </p> <p><b>Research</b> <b>design</b> <b>and</b> <b>methods:</b> The study included 62,785 workers who underwent a health checkup in 2010 or 2011 and were followed up for mortality from 2012 to March 2019. <a>Prediabetes was defined according to fasting plasma glucose (FPG) or glycated hemoglobin (HbA1c) level or a combination of both using the American Diabetes Association (ADA) or World Health Organization (WHO)/International Expert Committee (IEC) criteria. </a>The Cox proportional hazards regression model was used to investigate the associations.</p> <p> </p> <p><b>Results:</b> Over a 7-year follow-up, 229 deaths were documented. <a>Compared with normoglycemia, prediabetes defined according to ADA criteria was associated with a higher risk of all-cause (hazard ratio [HR] 1.53; 95% confidence interval [CI] 1.12–2.09) and cancer (HR 2.37; 95% CI 1.45–3.89) mortality but not with CVD mortality. </a>The results were materially unchanged when prediabetes was defined according to ADA FPG, ADA HbA1c, WHO FPG, or combined WHO/IEC criteria. Diabetes was associated with the risk of all-cause, CVD, and cancer mortality.</p> <p> </p> <p><b>Conclusion:</b> In a cohort of Japanese workers, FPG- and HbA1c-defined prediabetes according to ADA or WHO/IEC was each associated with a significantly increased risk of mortality from all-causes and cancer but not CVD. </p>


Author(s):  
Blake Niccum ◽  
Kevin Casey ◽  
Kristin Burke ◽  
Emily W Lopes ◽  
Paul Lochhead ◽  
...  

Abstract Background No dietary factors have yet been shown to conclusively impact the incidence of microscopic colitis (MC). Here, we sought to examine the relationship between alcohol intake and the risk of MC. Methods We conducted a prospective cohort study of 209,902 participants (age range, 28.5–66.7 years) enrolled in the Nurses’ Health Study (NHS) and Nurses’ Health Study II (NHSII). Validated data on alcohol consumption were collected at baseline in 1986 in the NHS and 1991 in the NHSII and updated every 4 years. Diagnoses of MC were confirmed via review of histopathology data. We used Cox proportional hazards modeling to estimate adjusted hazard ratios (aHRs) and 95% confidence intervals (CIs). Results Through 2016 in the NHS and 2017 in the NHSII, we confirmed 352 incident cases of MC over 4,994,324 person-years. Higher alcohol consumption was associated with an increased risk of MC (Ptrend &lt; .001). Compared to non-users, the aHRs of MC were 1.20 (95% CI, 0.86–1.67) for consumers of 0.1–4.9 g/day of alcohol, 1.90 (95% CI, 1.34–2.71) for consumers of 5–14.9 g/day, and 2.31 (95% CI, 1.54–3.46) for consumers of ≥15 g/day. The associations were consistent across the histologic subtypes of collagenous and lymphocytic colitis (Pheterogeneity = .523). When stratified by alcohol type, the risk according to every 2 servings/week appeared to be strongest with consumption of wine (aHR, 1.08; 95% CI, 1.04–1.12) as compared to beer (aHR, 1.01; 95% CI, 0.91–1.12) or liquor (aHR, 1.00; 95% CI, 0.92–1.09). Conclusions Alcohol consumption was associated with an increased risk of MC. Further studies are needed to determine the mechanism underlying these associations, as well as the impact of reducing alcohol intake in patients with MC.


Circulation ◽  
2014 ◽  
Vol 129 (suppl_1) ◽  
Author(s):  
Lyanne M Kieneker ◽  
Ron T Gansevoort ◽  
Edith J Feskens ◽  
Johanna M Geleijnse ◽  
Gerjan Navis ◽  
...  

Background: Potassium supplementation lowers blood pressure (BP) in randomized controlled trials, but the long-term effect of dietary potassium intake on risk of hypertension has not yet been established. Objective: To examine the association of 24h urinary excretions of potassium, reflecting dietary uptake, with risk of hypertension. Methods: We used data from the Prevention of Renal and Vascular End-Stage Disease (PREVEND) study, a prospective, community-based, observational cohort of Dutch men and women aged 28-75 years. Potassium excretion was measured at baseline (1997-98) and during follow-up (2001-03) in two consecutive 24h urine specimens. Risk of hypertension (defined as BP ≥140/90 mmHg, or initiation of BP-lowering drugs) was studied in 5,511 normotensive subjects not using BP-lowering drugs at baseline. We used Cox proportional hazards regression analysis with time-dependent covariates. Results: Baseline median potassium excretion was 72 mmol/24h (Q1-Q3: 57-85 mmol/24h). During a median follow-up of 7.6 years (Q1-Q3: 5.0-9.3 years), 1172 subjects developed hypertension. We observed a nonlinear association between potassium excretion and risk of hypertension (P=0.005; Figure ). This association was in such a way that the lowest sex-specific tertile of potassium excretion (men: <68 mmol/24h; women: <58 mmol/24h) had an increased risk of hypertension (hazard ratio [HR], 1.22; 95% confidence interval [CI], 1.08-1.37) after adjustment for age and sex, compared to the upper two tertiles. Further adjustment for body mass index, smoking status, alcohol intake, parental history of hypertension (HR, 1.25; 95% CI, 1.11-1.41), and additionally for 24h urinary excretions of sodium, magnesium, and calcium (HR, 1.23; 95% CI, 1.08-1.40) did not materially affect the association. Conclusions: In this population-based cohort, low potassium excretion was associated with an increased risk of developing hypertension. Figure: Association between 24h urinary potassium excretion and risk of hypertension.


Circulation ◽  
2013 ◽  
Vol 127 (suppl_12) ◽  
Author(s):  
Elizabeth J Bell ◽  
Pamela L Lutsey ◽  
Vijay Nambi ◽  
Mary Cushman ◽  
Elizabeth Selvin ◽  
...  

Introduction— Diabetes has been inconsistently associated with increased risk of venous thromboembolism (VTE). Glycemia is positively associated with coagulation activation and hypofibrinolysis, resulting in a procoagulant state. However, there is little direct evidence on associations of glycemia with VTE. Hypothesis— Glycemia, as measured by hemoglobin A 1c (A 1c ), is positively associated with incident VTE over a follow-up period of 15 years. Methods— The Atherosclerosis Risk in Communities (ARIC) study is a population-based cohort study of middle-aged adults followed for 15 years after visit 2, when A 1c was measured. Because A 1c is affected by treatment in diagnosed diabetics, separate analyses were conducted for individuals with diagnosed diabetes. Diagnosed diabetes was defined as taking diabetes medication or a history of diabetes (self-report). We assessed the relation between A 1c and incident VTE during follow-up using Cox proportional hazards models, controlling for potential confounders: age, sex, race, smoking status and amount, hormone use, body mass index, and waist-to-hip ratio. Results— The cohort free of VTE and/or anticoagulant use in 1990-1992 included 11,976 participants without a diagnosis of diabetes (317 VTE events) and 1,040 participants with a diagnosis of diabetes (45 VTE events). As shown in the figure, the adjusted hazard ratio estimates, using participants with an A 1c < 5.70 % and without diagnosed diabetes as the referent, were close to 1, regardless of A 1c level and diabetes diagnosis status. Further, there was no relation in analyses conducted by VTE type (provoked and unprovoked) or in participants with diabetes (both diagnosed and undiagnosed) relative to those without diabetes. Conclusions— In conclusion, although a modest association cannot be ruled out, our findings do not support an association between A 1c and VTE.


Gut ◽  
2020 ◽  
pp. gutjnl-2020-322557 ◽  
Author(s):  
Jinqiu Yuan ◽  
Qiangsheng He ◽  
Long H Nguyen ◽  
Martin C S Wong ◽  
Junjie Huang ◽  
...  

ObjectiveThe association between the regular use of proton pump inhibitors (PPIs) and the risk of type 2 diabetes remains unclear, although a recent randomised controlled trial showed a trend towards increased risk. This study was undertaken to evaluate the regular use of PPIs and risk of type 2 diabetes.MethodThis is a prospective analysis of 204 689 participants free of diabetes in the Nurses' Health Study (NHS), NHS II and Health Professionals Follow-up Study (HPFS). Type 2 diabetes was confirmed using American Diabetes Association (ADA) diagnostic criteria. We evaluated hazard ratios (HRs) adjusting for demographic factors, lifestyle habits, the presence of comorbidities, use of other medications and clinical indications.ResultsWe documented 10 105 incident cases of diabetes over 2 127 471 person-years of follow-up. Regular PPI users had a 24% higher risk of diabetes than non-users (HR 1.24, 95% CI 1.17 to 1.31). The risk of diabetes increased with duration of PPI use. Fully adjusted HRs were 1.05 (95% CI 0.93 to 1.19) for participants who used PPIs for >0–2 years and 1.26 (95% CI 1.18 to 1.35) for participants who used PPIs for >2 years compared with non-users.ConclusionsRegular use of PPIs was associated with a higher risk of type 2 diabetes and the risk increased with longer duration of use. Physicians should therefore exercise caution when prescribing PPIs, particularly for long-term use.


2021 ◽  
Vol 5 (Supplement_2) ◽  
pp. 459-459
Author(s):  
Tyler Titcomb ◽  
Buyun Liu ◽  
Linda Snetselaar ◽  
Terry Wahls ◽  
Wei Bao

Abstract Objectives To evaluate the association of the ketogenic ratio of macronutrients (KR) with incidence of diabetes (DM). Methods Dietary information was obtained at baseline from postmenopausal women enrolled in the Women's Health Initiative (WHI) clinical trials (not including the intervention arm of dietary modification trial) and observational study. Participants were excluded if they had prevalent diabetes or unknown status of diabetes at baseline or reported energy intakes &lt;600 or &gt;5000 kilocalories. The KR was calculated as follows: (0.9*grams fat + 0.46*grams protein) divided by (0.1*grams fat + 0.58*grams protein + grams total carbohydrate – grams total fiber). A KR value 1.5 is considered the minimum threshold to predict a ketogenic diet. Cox proportional hazards models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for associations between KR and risk of DM. Follow-up time was the number of days from enrollment to the first instance of incident DM. Results Among 128 752 participants, there were 19 439 incident cases of DM with median follow-up time of 20.7 years. The median KR was 0.36 and 12 participants (&lt;0.0001%) exceeded the KR threshold for a ketogenic diet. After adjustment for age, race/ethnicity, comorbidities, education, income, marital status, health insurance, smoking, DM family history, hormone use, energy intake, HEI scores, physical activity, region, and WHI arm, each KR quintile was associated with increased risk of DM. Comparing extreme quintiles of KR, the adjusted HR (95% CI) for diabetes was 1.32 (1.26–1.39; Ptrend &lt; 0.0001). The association remained significant after further adjustment for BMI, with an adjusted HR (95% CI) of 1.22 (1.16–1.29; Ptrend &lt; 0.0001) comparing the highest with lowest quintile of KR. We were unable to show an association of exceeding the KR threshold with DM due to the small number of participants who exceeded the KR threshold. Conclusions The KR was positively associated with incidence of DM. However, we are unable to draw conclusions about ketogenic diets because the majority of participants were below the KR threshold for a ketogenic diet. Funding Sources This work was supported by the Fraternal Order of Eagles Diabetes Research Center with funding from the National Institutes of Diabetes and Digestive and Kidney Diseases.


2021 ◽  
Vol 10 (6) ◽  
Author(s):  
Bin Yan ◽  
Ruohan Li ◽  
Jiamei Li ◽  
Xuting Jin ◽  
Fan Gao ◽  
...  

Background Previous studies have suggested that sleep timing is associated with cardiovascular risk factors. However, there is no evidence on the relationship between sleep timing and congestive heart failure (CHF). We aimed to examine this relationship in this study. Methods and Results We recruited 4765 participants (2207 men; mean age, 63.6±11.0 years) from the SHHS (Sleep Heart Health Study) database in this multicenter prospective cohort study. Follow‐up was conducted until the first CHF diagnosis between baseline and the final censoring date. Sleep timing (bedtimes and wake‐up times on weekdays and weekends) was based on a self‐reported questionnaire. Cox proportional hazard models were constructed to investigate the association between sleep timing and CHF. During the mean follow‐up period of 11 years, 519 cases of CHF (10.9%) were reported. The multivariable Cox proportional hazards models revealed that participants with weekday bedtimes >12:00  am (hazard ratio [HR], 1.56; 95% CI, 1.15–2.11; P =0.004) and from 11:01  pm to 12:00  am (HR, 1.25; 95% CI, 1.00–1.56; P =0.047) had an increased risk of CHF compared with those with bedtimes from 10:01  pm to 11:00  pm . After stratified analysis, the association was intensified in participants with a self‐reported sleep duration of 6 to 8 hours. Furthermore, wake‐up times >8:00  am on weekdays (HR, 1.53; 95% CI, 1.07–2.17; P =0.018) were associated with a higher risk of incident CHF than wake‐up times ≤6:00  am . Conclusions Delayed bedtimes (>11:00  pm ) and wake‐up times (>8:00  am ) on weekdays were associated with an increased risk of CHF.


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