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ABSTRACT: Consumption of sugar-sweetened beverages (SSBs) is associated with an increased risk of hypertension in cross-sectional studies. However, prospective data are limited.
To examine the associations between SSBs and artificially sweetened beverages (ASBs) with incident hypertension.
Prospective analysis using Cox proportional hazards regression to examine the association between SSBs and ASBs with incident hypertension in three large, prospective cohorts, the Nurses' Health Studies I (n = 88,540 women) and II (n = 97,991 women) and the Health Professionals' Follow-Up Study (n = 37,360 men).
Adjusted hazard ratios for incident clinically diagnosed hypertension.
Higher SSB and ASB intake was associated with an increased risk of developing hypertension in all three cohorts. In a pooled analysis, participants who consumed at least one SSB daily had an adjusted HR for incident hypertension of 1.13 (95 % CI, 1.09-1.17) compared with those who did not consume SSBs; for persons who drank at least one ASB daily, the adjusted HR was 1.14 (95 % CI, 1.09-1.18). The association between sweetened beverage intake and hypertension was stronger for carbonated beverages versus non-carbonated beverages, and for cola-containing versus non-cola beverages in the NHS I and NHS II cohorts only. Higher fructose intake from SSBs as a percentage of daily calories was associated with increased hypertension risk in NHS I and NHS II (p-trend = 0.001 in both groups), while higher fructose intake from sources other than SSBs was associated with a decrease in hypertension risk in NHS II participants (p-trend = 0.006).
Residual confounding factors may interfere with the interpretation of results.
SSBs and ASBs are independently associated with an increased risk of incident hypertension after controlling for multiple potential confounders. These associations may be mediated by factors common to both SSBs and ASBs (e.g., carbonation or cola), but are unlikely to be due to fructose.
Journal of General Internal Medicine 04/2012; 27(9):1127-34. · 2.83 Impact Factor
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ABSTRACT: Never or curtailed lactation has been associated with an increased risk for incident hypertension, but the effect of exclusive breastfeeding is unknown. The authors conducted an observational cohort study of 55,636 parous women in the US Nurses' Health Study II. From 1991 to 2005, participants reported 8,861 cases of incident hypertension during 660,880 person-years of follow-up. Never or curtailed lactation was associated with an increased risk of incident hypertension. Compared with women who breastfed their first child for ≥12 months, women who did not breastfeed were more likely to develop hypertension (hazard ratio (HR) = 1.27, 95% confidence interval (CI): 1.18, 1.36), adjusting for family history and lifestyle covariates. Women who never breastfed were more likely to develop hypertension than women who exclusively breastfed their first child for ≥6 months (HR = 1.29, 95% CI: 1.20, 1.40). The authors found similar results for women who had never breastfed compared with those who had breastfed each child for an average of ≥12 months (HR = 1.22, 95% CI: 1.13, 1.32). In conclusion, never or curtailed lactation was associated with an increased risk of incident maternal hypertension, compared with the recommended ≥6 months of exclusive or ≥12 months of total lactation per child, in a large cohort of parous women.
American journal of epidemiology 11/2011; 174(10):1147-58. · 5.59 Impact Factor
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ABSTRACT: Uses of synthetic vitamin A derivatives (e.g., isotretinoin used for severe acne) and high doses of preformed vitamin A have been implicated in the pathogenesis of hyperuricemia and gout, whereas a trial reported that β-carotene may lower serum uric acid (UA) levels. We evaluated the potential population impact of these factors on serum UA in a nationally representative sample of US adults.
Using data from 14,349 participants ages ≥20 years in the Third National Health and Nutrition Examination Survey (1988-1994), we examined the relationship between serum retinol, β-carotene, and UA levels using weighted linear regression. Additionally, we examined the relationship with hyperuricemia using weighted logistic regression.
Serum UA levels increased linearly with increasing serum retinol levels, whereas serum UA levels decreased with increasing serum β-carotene levels. After adjusting for age, sex, dietary factors, and other potential confounders, the serum UA level differences from the bottom (referent) to the top quintiles of serum retinol levels were 0, 0.16, 0.32, 0.43, and 0.71 mg/dl (P for trend <0.001), and for β-carotene were 0, -0.15, -0.29, -0.27, and -0.40 mg/dl (P for trend <0.001), respectively. Similarly, the multivariate odds ratios of hyperuricemia from the bottom (referent) to top quintiles of serum retinol levels were 1.00, 1.30, 1.83, 2.09, and 3.22 (P for trend <0.001) and for β-carotene were 1.00, 0.85, 0.68, 0.73, and 0.54 (P for trend <0.001), respectively. The graded associations persisted across subgroups according to cross-classification by both serum retinol and β-carotene levels.
These nationally representative data raise concerns that vitamin A supplementation and food fortification may contribute to the high frequency of hyperuricemia in the US population, whereas β-carotene intake may be beneficial against hyperuricemia. The use of β-carotene as a novel preventive treatment for gout deserves further investigation.
Arthritis care & research. 11/2011; 64(3):389-96.
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ABSTRACT: Epidemiologic data suggest that analgesic use increases the risk of renal cell cancer (RCC), but few prospective studies have been published. We investigated the association between analgesic use and RCC in 2 large prospective studies.
We examined the relationship between analgesic use and RCC risk in the Nurses' Health Study and the Health Professionals Follow-up Study. Use of aspirin, other nonsteroidal anti-inflammatory drugs (NSAIDs), and acetaminophen was ascertained in 1990 in the Nurses' Health Study and in 1986 in the Health Professionals Follow-up Study, and every 2 years thereafter. We evaluated baseline and duration of use of analgesics.
During follow-up of 16 years among 77,525 women and 20 years among 49,403 men, we documented 333 RCC cases. Aspirin and acetaminophen use were not associated with RCC risk. However, regular use of nonaspirin NSAIDs was associated with an increased RCC risk; the pooled multivariate relative risk was 1.51 (95% confidence interval, 1.12-2.04) at baseline. The absolute risk differences for users vs nonusers of nonaspirin NSAIDs were 9.15 per 100 000 person-years in women and 10.92 per 100,000 person-years in men. There was a dose-response relationship between duration of nonaspirin NSAID use and RCC risk; compared with nonregular use, the pooled multivariate relative risks were 0.81 (95% confidence interval, 0.59-1.11) for use less than 4 years, 1.36 (0.98-1.89) for 4 to less than 10 years, and 2.92 (1.71-5.01) for use for 10 or more years (P < .001 for trend).
Our prospective data suggest that longer duration of use of nonaspirin NSAIDs may increase the risk of RCC.
Archives of internal medicine 09/2011; 171(16):1487-93. · 11.46 Impact Factor
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Hongmei Nan,
Mousheng Xu,
Jiangwen Zhang,
Mingfeng Zhang,
Peter Kraft,
Abrar A Qureshi,
Constance Chen,
Qun Guo,
Frank B Hu,
Eric B Rimm, Gary Curhan,
Yiqing Song,
Christopher I Amos,
Li-E Wang,
Jeffrey E Lee,
Qingyi Wei,
David J Hunter,
Jiali Han
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ABSTRACT: We conducted a genome-wide association study on the number of melanocytic nevi reported by 9136 individuals of European ancestry, with follow-up replication in 3581 individuals. We identified the nidogen 1 (NID1) gene on 1q42 associated with nevus count (two linked single nucleotide polymorphisms with r(2) > 0.9: rs3768080 A allele associated with reduced count, P = 6.5 × 10(-8); and rs10754833 T allele associated with reduced count, P = 1.5 × 10(-7)). We further determined that the rs10754833 [T] was associated with a decreased melanoma risk in 2368 melanoma cases and 7432 controls [for CT genotype: odds ratio (OR) = 0.86, 95% confidence interval (CI) = 0.75-0.99, P = 0.04; for TT genotype: OR = 0.84, 95% CI = 0.71-0.98, P = 0.03]. Expression level of the NID1 locus was 2-fold higher for the rs10754833 T allele carriers than that with the CC genotype (P = 0.017) in the 87 HapMap CEU cell lines. The NID1 gene is a biologically plausible locus for nevogenesis and melanoma development, with decreased expression levels of NID1 in benign nevi (P = 3.5 × 10(-6)) and in primary melanoma (P = 4.6 × 10(-4)) compared with the normal skin.
Human Molecular Genetics 07/2011; 20(13):2673-9. · 7.64 Impact Factor
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Hongmei Nan,
Mousheng Xu,
Peter Kraft,
Abrar A Qureshi,
Constance Chen,
Qun Guo,
Frank B Hu, Gary Curhan,
Christopher I Amos,
Li-E Wang,
Jeffrey E Lee,
Qingyi Wei,
David J Hunter,
Jiali Han
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ABSTRACT: We conducted a genome-wide association study on cutaneous basal cell carcinoma (BCC) among 2045 cases and 6013 controls of European ancestry, with follow-up replication in 1426 cases and 4845 controls. A non-synonymous SNP in the MC1R gene (rs1805007 encoding Arg151Cys substitution), a previously well-documented pigmentation gene, showed the strongest association with BCC risk in the discovery set (rs1805007[T]: OR (95% CI) for combined discovery set and replication set [1.55 (1.45-1.66); P= 4.3 × 10(-17)]. We identified that an SNP rs12210050 at 6p25 near the EXOC2 gene was associated with an increased risk of BCC [rs12210050[T]: combined OR (95% CI), 1.24 (1.17-1.31); P= 9.9 × 10(-10)]. In the locus on 13q32 near the UBAC2 gene encoding ubiquitin-associated domain-containing protein 2, we also identified a variant conferring susceptibility to BCC [rs7335046 [G]; combined OR (95% CI), 1.26 (1.18-1.34); P= 2.9 × 10(-8)]. We further evaluated the associations of these two novel SNPs (rs12210050 and rs7335046) with squamous cell carcinoma (SCC) risk as well as melanoma risk. We found that both variants, rs12210050[T] [OR (95% CI), 1.35 (1.16-1.57); P= 7.6 × 10(-5)] and rs7335046 [G] [OR (95% CI), 1.21 (1.02-1.44); P= 0.03], were associated with an increased risk of SCC. These two variants were not associated with melanoma risk. We conclude that 6p25 and 13q32 are novel loci conferring susceptibility to non-melanoma skin cancer.
Human Molecular Genetics 06/2011; 20(18):3718-24. · 7.64 Impact Factor
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Marilyn C Cornelis,
Keri L Monda,
Kai Yu,
Nina Paynter,
Elizabeth M Azzato,
Siiri N Bennett,
Sonja I Berndt,
Eric Boerwinkle,
Stephen Chanock,
Nilanjan Chatterjee, [......],
Eric B Rimm,
Lynda M Rose,
Nathaniel Rothman,
Debra Silverman,
Rachael Stolzenberg-Solomon,
Amy Subar,
Meredith Yeager,
Daniel I Chasman,
Rob M van Dam,
Neil E Caporaso
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ABSTRACT: We report the first genome-wide association study of habitual caffeine intake. We included 47,341 individuals of European descent based on five population-based studies within the United States. In a meta-analysis adjusted for age, sex, smoking, and eigenvectors of population variation, two loci achieved genome-wide significance: 7p21 (P = 2.4 × 10(-19)), near AHR, and 15q24 (P = 5.2 × 10(-14)), between CYP1A1 and CYP1A2. Both the AHR and CYP1A2 genes are biologically plausible candidates as CYP1A2 metabolizes caffeine and AHR regulates CYP1A2.
PLoS Genetics 04/2011; 7(4):e1002033. · 8.69 Impact Factor
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Ron T Gansevoort,
Kunihiro Matsushita,
Marije van der Velde,
Brad C Astor,
Mark Woodward,
Andrew S Levey,
Paul E de Jong,
Josef Coresh,
Meguid El-Nahas,
Kai-Uwe Eckardt, [......],
Salim Yusuf,
Koon K Teo,
Peggy Gao,
Robert G Nelson,
William C Knowler,
Priscilla Auguste,
Kasper Veldhuis,
Laura Camarata,
Beverly Thomas,
Tom Manley
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ABSTRACT: Both a low estimated glomerular filtration rate (eGFR) and albuminuria are known risk factors for end-stage renal disease (ESRD). To determine their joint contribution to ESRD and other kidney outcomes, we performed a meta-analysis of nine general population cohorts with 845,125 participants and an additional eight cohorts with 173,892 patients, the latter selected because of their high risk for chronic kidney disease (CKD). In the general population, the risk for ESRD was unrelated to eGFR at values between 75 and 105 ml/min per 1.73 m2 but increased exponentially at lower levels. Hazard ratios for eGFRs averaging 60, 45, and 15 were 4, 29, and 454, respectively, compared with an eGFR of 95, after adjustment for albuminuria and cardiovascular risk factors. Log albuminuria was linearly associated with log ESRD risk without thresholds. Adjusted hazard ratios at albumin-to-creatinine ratios of 30, 300, and 1000 mg/g were 5, 13, and 28, respectively, compared with an albumin-to-creatinine ratio of 5. Albuminuria and eGFR were associated with ESRD, without evidence for multiplicative interaction. Similar associations were found for acute kidney injury and progressive CKD. In high-risk cohorts, the findings were generally comparable. Thus, lower eGFR and higher albuminuria are risk factors for ESRD, acute kidney injury and progressive CKD in both general and high-risk populations, independent of each other and of cardiovascular risk factors.Keywords: acute kidney injury; albumin-to-creatinine ratio (albuminuria); dipstick (proteinuria); eGFR (kidney function); ESRD (end-stage renal disease); meta-analysis
Kidney International 02/2011; 80(1):93-104. · 6.61 Impact Factor
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Carsten A Böger,
Ming-Huei Chen,
Adrienne Tin,
Matthias Olden,
Anna Köttgen,
Ian H de Boer,
Christian Fuchsberger,
Conall M O'Seaghdha,
Cristian Pattaro,
Alexander Teumer, [......],
Peter P Pramstaller,
L Adrienne Cupples,
Jacques S Beckmann,
Qiong Yang,
Iris M Heid,
Rainer Rettig,
Albert W Dreisbach,
Murielle Bochud,
Caroline S Fox,
W H L Kao
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ABSTRACT: Identification of genetic risk factors for albuminuria may alter strategies for early prevention of CKD progression, particularly among patients with diabetes. Little is known about the influence of common genetic variants on albuminuria in both general and diabetic populations. We performed a meta-analysis of data from 63,153 individuals of European ancestry with genotype information from genome-wide association studies (CKDGen Consortium) and from a large candidate gene study (CARe Consortium) to identify susceptibility loci for the quantitative trait urinary albumin-to-creatinine ratio (UACR) and the clinical diagnosis microalbuminuria. We identified an association between a missense variant (I2984V) in the CUBN gene, which encodes cubilin, and both UACR (P = 1.1 × 10(-11)) and microalbuminuria (P = 0.001). We observed similar associations among 6981 African Americans in the CARe Consortium. The associations between this variant and both UACR and microalbuminuria were significant in individuals of European ancestry regardless of diabetes status. Finally, this variant associated with a 41% increased risk for the development of persistent microalbuminuria during 20 years of follow-up among 1304 participants with type 1 diabetes in the prospective DCCT/EDIC Study. In summary, we identified a missense CUBN variant that associates with levels of albuminuria in both the general population and in individuals with diabetes.
Journal of the American Society of Nephrology 02/2011; 22(3):555-70. · 9.66 Impact Factor
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Marije van der Velde,
Kunihiro Matsushita,
Josef Coresh,
Brad C Astor,
Mark Woodward,
Andrew Levey,
Paul de Jong,
Ron T Gansevoort,
Andrew S Levey,
Paul E de Jong, [......],
Henk J Bilo,
Hanneke Joosten,
Nanno Kleefstra,
K H Groenier,
Priscilla Auguste,
Kasper Veldhuis,
Yaping Wang,
Laura Camarata,
Beverly Thomas,
Tom Manley
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ABSTRACT: Screening for chronic kidney disease is recommended in people at high risk, but data on the independent and combined associations of estimated glomerular filtration rate (eGFR) and albuminuria with all-cause and cardiovascular mortality are limited. To clarify this, we performed a collaborative meta-analysis of 10 cohorts with 266,975 patients selected because of increased risk for chronic kidney disease, defined as a history of hypertension, diabetes, or cardiovascular disease. Risk for all-cause mortality was not associated with eGFR between 60-105 ml/min per 1.73 m², but increased at lower levels. Hazard ratios at eGFRs of 60, 45, and 15 ml/min per 1.73 m² were 1.03, 1.38 and 3.11, respectively, compared to an eGFR of 95, after adjustment for albuminuria and cardiovascular risk factors. Log albuminuria was linearly associated with log risk for all-cause mortality without thresholds. Adjusted hazard ratios at albumin-to-creatinine ratios of 10, 30 and 300 mg/g were 1.08, 1.38, and 2.16, respectively compared to a ratio of five. Albuminuria and eGFR were multiplicatively associated with all-cause mortality, without evidence for interaction. Similar associations were observed for cardiovascular mortality. Findings in cohorts with dipstick data were generally comparable to those in cohorts measuring albumin-to-creatinine ratios. Thus, lower eGFR and higher albuminuria are risk factors for all-cause and cardiovascular mortality in high-risk populations, independent of each other and of cardiovascular risk factors.
Kidney International 02/2011; 79(12):1341-52. · 6.61 Impact Factor
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ABSTRACT: To evaluate the independent association between alcohol consumption and risk of developing psoriasis and to determine if this risk is associated with different types of alcoholic beverages.
A prospective study of female nurses who were followed up from 1991 to 2005.
Nurses' Health Study II, a cohort of 116,671 US women aged 27 to 44 years in 1991.
The study population included 82,869 women who reported amount and type of alcohol intake on biennial questionnaires. We excluded participants with a history of psoriasis prior to 1991.
Self-report of incident physician-diagnosed psoriasis. For a sensitivity analysis, we had a subset of confirmed psoriasis cases.
There were 1150 cases of incident psoriasis, 1069 of which were used for analysis. Compared with women who did not drink alcohol, the multivariate relative risk (RR) of psoriasis was 1.72 (95% confidence interval [CI], 1.15-2.57) for an alcohol consumption of 2.3 drinks/wk or more. When examined by type of alcoholic beverage, there was an association between psoriasis and nonlight beer intake (multivariate RR for ≥ 5 drinks/wk, 1.76; 95% CI, 1.15-2.69); light beer, red wine, white wine, and liquor were not significantly associated with psoriasis risk. The association with nonlight beer intake became stronger in a subset of confirmed psoriasis cases (multivariate RR for ≥ 5 drinks/wk, 2.29; 95% CI, 1.36-3.85).
Nonlight beer intake is associated with an increased risk of developing psoriasis among women. Other alcoholic beverages did not increase the risk of psoriasis in this study.
Archives of dermatology 12/2010; 146(12):1364-9. · 4.76 Impact Factor
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ABSTRACT: Fructose-rich beverages such as sugar-sweetened soda and orange juice can increase serum uric acid levels and, thus, the risk of gout, but prospective data on the relationship are limited.
To examine the relationship between intake of fructose-rich beverages and fructose and the risk of incident gout among women.
In the Nurses' Health Study, a US prospective cohort study spanning 22 years (1984-2006), we analyzed data from 78,906 women with no history of gout at baseline who provided information on intake of beverages and fructose through validated food frequency questionnaires.
Incident cases that met the American College of Rheumatology survey criteria for gout.
During 22 years of follow-up, we documented 778 confirmed incident cases of gout. Increasing intake of sugar-sweetened soda was independently associated with increasing risk of gout. Compared with consumption of less than 1 serving per month of sugar-sweetened soda, the multivariate relative risk of gout for 1 serving per day was 1.74 (95% confidence interval [CI], 1.19-2.55) and for 2 or more servings per day was 2.39 (95% CI, 1.34-4.26) (P<.001 for trend). The corresponding relative risks for orange juice were 1.41 (95% CI, 1.03-1.93) and 2.42 (95% CI, 1.27-4.63) (P = .02 for trend). The absolute risk differences corresponding to these relative risks were 36 and 68 cases per 100,000 person-years for sugar-sweetened soda and 14 and 47 cases per 100,000 person-years for orange juice, respectively. Diet soft drinks were not associated with the risk of gout (P = .27 for trend). Compared with the lowest quintile of fructose intake, the multivariate relative risk of gout in the top quintile was 1.62 (95% CI, 1.20-2.19; P = .004 for trend) (risk difference of 28 cases per 100,000 person-years).
Among this cohort of women, consumption of fructose-rich beverages is associated with an increased risk of incident gout, although the contribution of these beverages to the risk of gout in the population is likely modest given the low incidence rate among women.
JAMA The Journal of the American Medical Association 11/2010; 304(20):2270-8. · 30.03 Impact Factor
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ABSTRACT: Coffee is one of the most widely consumed beverages in the world and may affect the risk of gout via various mechanisms, but prospective data on the relation between coffee intake and the risk of incident gout are limited.
Over a 26-y period, we prospectively examined the relation between coffee intake and risk of incident gout in 89,433 female participants in the Nurses' Health Study. We assessed the consumption of coffee, decaffeinated coffee, tea, and total caffeine in participants every 2-4 y through validated questionnaires. We used a supplementary questionnaire to ascertain whether participants met the survey criteria of the American College of Rheumatology for gout. Results: During the 26 y of follow-up, we documented 896 confirmed incident cases of gout. There was an inverse association between higher coffee intake and the risk of gout. The multivariate relative risks (RRs) for incident gout according to coffee-consumption categories [ie, 0, 1-237, 238-947, and ≥948 mL coffee/d (237 mL = one 8-ounce cup)] were 1.00, 0.97, 0.78 (95% CI: 0.64, 0.95), and 0.43 (95% CI: 0.30, 0.61; P for trend < 0.0001), respectively. For decaffeinated coffee, the multivariate RRs according to consumption categories (0, 1-237, and ≥237 mL decaffeinated coffee/d) were 1.00, 1.02, and 0.77 (95% CI: 0.63, 0.95; P for trend = 0.02), respectively. There was an inverse association between total caffeine from all sources and the risk of gout; the multivariate RR of the highest quintile compared with the lowest quintile was 0.52 (95% CI: 0.41, 0.68; P for trend <0.0001).
These prospective data suggest that long-term coffee consumption is associated with a lower risk of incident gout in women.
American Journal of Clinical Nutrition 10/2010; 92(4):922-7. · 6.67 Impact Factor
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ABSTRACT: Higher levels of serum alkaline phosphatase (AlkP) are associated with excess mortality in dialysis patients, but whether AlkP is associated with adverse outcomes among people without kidney failure is unknown.
We first analyzed the association between AlkP and cardiovascular outcomes among 4115 participants with a previous myocardial infarction (the Cholesterol And Recurrent Events [CARE] study). Results were validated by analyzing the association between AlkP and mortality in an independent sample of 14,716 adults from the general US population (the Third National Health and Nutrition Examination Survey). A graded, independent association was noted between baseline tertile of AlkP and the adjusted hazard ratio of all-cause mortality in CARE participants (P(trend)=0.02). After adjustment for serum phosphate, hepatic enzymes, and other potential confounders, participants with AlkP in the highest tertile had an adjusted hazard ratio of 1.43 (95% confidence interval 1.08 to 1.89) compared with those in the lowest tertile. Multivariable-adjusted associations between higher AlkP and all-cause and cardiovascular mortality were present in the Third National Health and Nutrition Examination Survey (P(trend) across tertiles of AlkP=0.006 and 0.038, respectively). Findings from both CARE and the Third National Health and Nutrition Examination Survey were similar among individuals with and without evidence of kidney disease, defined by estimated glomerular filtration rate <60 mL min(-1) 1.73 m(-2).
We found an independent relation between higher levels of AlkP and adverse outcomes among survivors of myocardial infarction and in a general population sample. The excess risk of death was present in people without evidence of kidney disease and was particularly high among people with higher levels of both AlkP and serum phosphate.
Circulation 11/2009; 120(18):1784-92. · 14.74 Impact Factor
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ABSTRACT: To prospectively study the relation between menopause, postmenopausal hormone use and risk of gout, since female sex hormones have been postulated to decrease gout risk among women.
In the Nurses' Health Study, the association between menopause, age at menopause, postmenopausal hormone use and risk of self-reported physician-diagnosed incident gout among 92 535 women without gout at baseline was examined. Multivariate proportional hazards regression analysis was used to adjust for other risk factors for gout such as age, body mass index, diuretic use, hypertension, alcohol intake and dietary factors.
During 16 years of follow-up (1 240 231 person-years), 1703 incident gout cases were recorded. The incidence rate of gout increased from 0.6 per 1000 person-years in women <45 years of age to 2.5 in women > or =75 years of age (p for trend <0.001). Compared with premenopausal women, postmenopausal women had a higher risk of incident gout (multivariate-adjusted relative risk (RR)=1.26; 95% confidence interval (CI) 1.03 to 1.55). Among women with a natural menopause, women with age at menopause <45 years had a RR of 1.62 (95% CI 1.12 to 2.33) of gout compared with women with age at menopause 50-54 years. Postmenopausal hormone users had a reduced risk of gout (RR=0.82; 95% CI 0.70 to 0.96).
These prospective findings indicate that menopause increases the risk of gout, whereas postmenopausal hormone therapy modestly reduces gout risk.
Annals of the rheumatic diseases 07/2009; 69(7):1305-9. · 8.11 Impact Factor
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ABSTRACT: Increased activation of the renin-angiotensin system (RAS) may be important in promoting coronary heart disease (CHD) and renal dysfunction, but limited data are available on associations between angiotensin type 1 receptor (AGT1R) and angiotensinogen (AGT) genotypes in type 2 diabetes.
Study participants were diabetics from the Health Professionals Follow-Up Study (HPFS) and the Nurses' Health Study (NHS). We analyzed single nucleotide polymorphisms (SNPs) associated with cardiovascular pathophysiology (including AGT1R T573C, AGT1R A1166C, and AGT M235T) and presence of renal dysfunction (eGFR<60 ml/min/1.73 m2) or history of CHD.
The AGT1R 1166 C-allele was associated with eGFR<60 ml/min/1.73 m2 (multivariable OR 1.63 [1.01, 2.65]) in the HPFS men (n = 733) and in the combined dataset (n = 1566) (OR 1.42 [1.02, 1.98]). The AGT1R 1166 C-allele was also associated with CHD in men (OR 1.57 [1.10, 2.24]). In NHS women (n = 833), AGT 235T-allele was associated with CHD (OR 1.72 [1.20, 2.47]). Removal of hypertension from the fully adjusted models did not influence results, suggesting that the associations may not be mediated by hypertension. There were significant interactions between sex and AGT1R 1166 C-allele (p = 0.008) and AGT M235T (p = 0.03) in models for CHD. No significant associations were seen between AGT1R T573 C-allele and renal dysfunction or CHD.
Polymorphisms in AGT1R and AGT genes are associated with renal dysfunction and CHD in type 2 diabetes and further support the important role of the RAS in these complications. Sex may modify associations between AGT1R 1166 C-allele and AGT 235T and CHD in type 2 diabetes.
BMC Nephrology 04/2009; 10:9. · 2.18 Impact Factor
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ABSTRACT: Several metabolic studies and a recent double-blind, placebo-controlled, randomized trial have shown that higher vitamin C intake significantly reduces serum uric acid levels. Yet the relation with risk of gout is unknown.
We prospectively examined, from 1986 through 2006, the relation between vitamin C intake and risk of incident gout in 46 994 male participants with no history of gout at baseline. We used a supplementary questionnaire to ascertain the American College of Rheumatology criteria for gout. Vitamin C intake was assessed every 4 years through validated questionnaires.
During the 20 years of follow-up, we documented 1317 confirmed incident cases of gout. Compared with men with vitamin C intake less than 250 mg/d, the multivariate relative risk (RR) of gout was 0.83 (95% confidence interval [CI], 0.71-0.97) for total vitamin C intake of 500 to 999 mg/d, 0.66 (0.52-0.86) for 1000 to 1499 mg/d, and 0.55 (0.38-0.80) for 1500 mg/d or greater (P < .001 for trend). The multivariate RR per 500-mg increase in total daily vitamin C intake was 0.83 (95% CI, 0.77-0.90). Compared with men who did not use supplemental vitamin C, the multivariate RR of gout was 0.66 (95% CI, 0.49-0.88) for supplemental vitamin C intake of 1000 to 1499 mg/d and 0.55 (0.36-0.86) for 1500 mg/d or greater (P < .001 for trend).
Higher vitamin C intake is independently associated with a lower risk of gout. Supplemental vitamin C intake may be beneficial in the prevention of gout.
Archives of internal medicine 03/2009; 169(5):502-7. · 11.46 Impact Factor
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ABSTRACT: The presence of parathyroid hormone receptor mRNA in a wide variety of tissues, including the endothelium, suggests that parathyroid hormone has potentially important effects in addition to the maintenance of calcium and phosphate homeostasis. We conducted a prospective study to examine the association between plasma intact parathyroid hormone levels and the subsequent risk of developing hypertension.
We measured intact parathyroid hormone in 481 men without hypertension from the Health Professionals Follow-up Study. During 10 years of follow-up, we observed 142 cases of incident hypertension. Cox proportional hazards regression was used to adjust for age, race, body mass index, alcohol use, smoking, physical activity, predicted plasma 25-hydroxyvitamin D level, and other factors.
Median baseline levels of intact parathyroid hormone were 40.1 pg/ml in individuals who developed hypertension and 36.3 pg/ml in those who did not (P = 0.01). After multivariate adjustment, the relative risk for incident hypertension in men in the highest quartile of parathyroid hormone (median 56.0 pg/ml) compared with the lowest quartile of parathyroid hormone (median 26.3 pg/ml) was 1.83 (95% confidence interval 1.10-3.03; P for trend = 0.01). Analyses restricted to men in the lowest 90th percentage of the parathyroid hormone distribution (< or =58 pg/ml) yielded similar results. Further adjustment for the intake of calcium and sodium, as well as for season and fasting status at time of blood draw, did not materially change the results.
Plasma levels of intact parathyroid hormone, even within ranges considered normal, are positively and independently associated with a higher risk of incident hypertension.
Journal of Hypertension 07/2008; 26(7):1390-4. · 4.02 Impact Factor
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ABSTRACT: The authors examined whether a diet that increases plasma urate level is also related to reduced risk of Parkinson's disease (PD). The study population comprised 47,406 men in the Health Professionals Follow-up Study. The potential effect of diet on plasma urate level was estimated by regressing plasma urate on intakes of selected foods and nutrients in a subsample of 1,387 men. Coefficients of this regression model were then used to calculate a dietary urate index for all cohort participants. Multivariate relative risks of PD were estimated by means of Cox proportional hazards models. After 14 years of follow-up (1986-2000), the authors documented 248 incident cases of PD. A higher dietary urate index was associated with a lower risk of PD (top quintile vs. bottom: relative risk = 0.47, p-trend = 0.0008), after adjustment for age, smoking, caffeine intake, and other potential confounders. This association remained strong and significant after further adjustment for each component of the index individually (p-trend < 0.02 for each). These data support urate as a potentially protective factor in PD and suggest that dietary changes expected to increase plasma urate level may contribute to lower risk of PD. These potential benefits, however, should be weighed against expected adverse effects on risk of gout and other chronic diseases.
American journal of epidemiology 05/2008; 167(7):831-8. · 5.59 Impact Factor
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ABSTRACT: We examined associations between vitamin C intake and serum uric acid in men in a population-based study.
We included 1387 men without hypertension and with body mass index (BMI) < 30 kg/m(2) in the Health Professional Follow-up Study. Dietary intake was assessed with a semiquantitative food frequency questionnaire validated for use in this population. Serum uric acid concentrations were measured.
Greater intakes of total vitamin C were significantly associated with lower serum uric acid concentrations, after adjustment for smoking, BMI, ethnicity, blood pressure, presence of gout, use of aspirin, and intake of energy, alcohol, dairy protein, fructose, meat, seafood and coffee. An inverse dose-response association was observed through vitamin C intake of 400-500 mg/day, and then reached a plateau. Adjusted mean uric acid concentrations across total vitamin C intake categories (< 90, 90-249, 250-499, 500-999, or > or = 1000 mg/day) were 6.4, 6.1, 6.0, 5.7, and 5.7 mg/dl, respectively (p for trend < 0.001). Greater vitamin C intake was associated with lower prevalence of hyperuricemia (serum uric acid > 6 mg/dl). Multivariate odds ratios for hyperuricemia across total vitamin C intake categories were 1 (reference), 0.58, 0.57, 0.38, and 0.34 (95% CI 0.20-0.58; P for trend < 0.001). When we used dietary data, which were assessed 4-8 years before blood collection, as predictors, we observed similar inverse associations between vitamin C intake and uric acid.
These population-based data indicate that vitamin C intake in men is inversely associated with serum uric acid concentrations. These findings support a potential role of vitamin C in the prevention of hyperuricemia and gout.
The Journal of Rheumatology 05/2008; 35(9):1853-8. · 3.69 Impact Factor
