Susan A. Hall

Association of Lower Urinary Tract Symptoms and the Metabolic Syndrome: Results From the Boston Area Community Health Survey

PURPOSE In this study we investigated the relationship between lower urinary tract symptoms as defined by the American Urological Association symptom index and the metabolic syndrome, and determined the relationship between individual symptoms comprising the American Urological Association symptom index and the metabolic syndrome. MATERIALS AND METHODS The Boston Area Community Health Survey used a 2-stage cluster design to recruit a random sample of 2,301 men 30 to 79 years old. Analyses were conducted on 1,899 men who provided blood samples. Urological symptoms comprising the American Urological Association symptom index were included in the analysis. The metabolic syndrome was defined using a modification of the Adult Treatment Panel III guidelines. The association between lower urinary tract symptoms and the metabolic syndrome was assessed using odds ratios and 95% confidence intervals estimated using logistic regression models. RESULTS Increased odds of the metabolic syndrome were observed in men with mild to severe symptoms (American Urological Association symptom index 2 to 35) compared to those with an American Urological Association symptom index score of 0 or 1 (multivariate OR 1.68, 95% CI 1.21-2.35). A statistically significant association was observed between the metabolic syndrome and a voiding symptom score of 5 or greater (multivariate adjusted OR 1.73, 95% CI 1.06-2.80) but not for a storage symptom score of 4 or greater (multivariate adjusted OR 0.94, 95% CI 0.66-1.33). Increased odds of the metabolic syndrome were observed even with mild symptoms, primarily for incomplete emptying, intermittency and nocturia. These associations were observed primarily in younger men (younger than 60 years) and were null in older men (60 years old or older). CONCLUSIONS The observed association between urological symptoms and the metabolic syndrome provides further evidence of common underlying factors between lower urinary tract symptoms and chronic conditions outside the urinary tract.

Does Erectile Dysfunction Contribute to Cardiovascular Disease Risk Prediction beyond the Framingham Risk Score

OBJECTIVES This study was designed to determine whether erectile dysfunction (ED) predicts cardiovascular disease (CVD) beyond traditional risk factors. BACKGROUND Both ED and CVD share pathophysiological mechanisms and often co-occur. It is unknown whether ED improves the prediction of CVD beyond traditional risk factors. METHODS This was a prospective, population-based study of 1,709 men (of 3,258 eligible) age 40 to 70 years. The ED data were measured by self-report. Subjects were followed for CVD for an average follow-up of 11.7 years. The association between ED and CVD was examined using the Cox proportional hazards regression model. The discriminatory capability of ED was examined using C statistics. The reclassification of CVD risk associated with ED was assessed using a method that quantifies net reclassification improvement. RESULTS Of the prospective population, 1,057 men with complete risk factor data who were free of CVD and diabetes at baseline were included. During follow-up, 261 new cases of CVD occurred. We found ED was associated with CVD incidence controlling for age (hazard ratio [HR]: 1.42, 95% confidence interval [CI]: 1.05 to 1.90), age and traditional CVD risk factors (HR: 1.41, 95% CI: 1.05 to 1.90), as well as age and Framingham risk score (HR: 1.40, 95% CI: 1.04 to 1.88). Despite these significant findings, ED did not significantly improve the prediction of CVD incidence beyond traditional risk factors. CONCLUSIONS Independent of established CVD risk factors, ED is significantly associated with increased CVD incidence. Nonetheless, ED does not improve the prediction of who will and will not develop CVD beyond that offered by traditional risk factors.

Erectile Dysfunction and Mortality

INTRODUCTION Erectile dysfunction (ED) and cardiovascular disease (CVD) share pathophysiological mechanisms and often co-occur. Yet it is not known whether ED provides an early warning for increased CVD or other causes of mortality. AIM We sought to examine the association of ED with all-cause and cause-specific mortality. METHODS Prospective population-based study of 1,709 men (of 3,258 eligible) aged 40-70 years. ED was measured by self-report. Subjects were followed for a mean of 15 years. Hazard ratios (HR) were calculated using the Cox proportional hazards regression model. MAIN OUTCOME MEASURES Mortality due to all causes, CVD, malignant neoplasms, and other causes. RESULTS Of 1,709 men, 1,284 survived to the end of 2004 and had complete ED and age data. Of 403 men who died, 371 had complete data. After adjustment for age, body mass index, alcohol consumption, physical activity, cigarette smoking, self-assessed health, and self-reported heart disease, hypertension, and diabetes, ED was associated with HRs of 1.26 (95% confidence interval [CI] 1.01-1.57) for all-cause mortality, and 1.43 (95% CI 1.00-2.05) for CVD mortality. The HR for CVD mortality associated with ED is of comparable magnitude to HRs of some conventional CVD risk factors. CONCLUSIONS These findings demonstrate that ED is significantly associated with increased all-cause mortality, primarily through its association with CVD mortality.

Correlates of low testosterone and symptomatic androgen deficiency in a population-based sample.

CONTEXT Risk factors for low testosterone and symptomatic androgen deficiency (AD) may be modifiable. OBJECTIVE Our objective was to examine demographic, anthropometric, and medical correlates of low testosterone and symptomatic AD. DESIGN Data were used from the Boston Area Community Health Survey, an epidemiological study conducted from 2002-2005. SETTING Data were obtained from a community-based random sample of racially and ethnically diverse men. PATIENTS OR OTHER PARTICIPANTS Data were available for 1822 men. MAIN OUTCOME MEASURES Multivariate logistic regression was used to estimate odds ratios (OR) and 95% confidence intervals (CI) for associations of covariates with 1) low testosterone and 2) symptomatic AD. The operational definition of low testosterone was serum total testosterone less than 300 ng/dl and free testosterone less than 5 ng/dl; symptomatic AD was defined as the additional presence of symptoms: any of low libido, erectile dysfunction, or osteoporosis or two or more of sleep disturbance, depressed mood, lethargy, or diminished physical performance. RESULTS Factors associated with low testosterone included age (OR = 1.36; 95% CI= 1.11-1.66, per decade), low per-capita income (

The safety of artemisinins during pregnancy: a pressing question

6000 or less per household member vs. more than

The Natural History of Symptomatic Androgen Deficiency in Men : Onset, Progression, and Spontaneous Remission

30,000; OR = 2.86; 95% CI = 1.39-5.87), and waist circumference (per 10-cm increase; OR = 1.75; 95% CI = 1.45-2.12). Only age (OR = 1.36; 95% CI = 1.04-1.77), waist circumference (OR = 1.88; 95% CI = 1.44-2.47), and health status (OR = 0.21; 95% CI = 0.05-0.92, excellent vs. fair/poor) were associated with our construct of symptomatic AD. Of all variables, waist circumference was the most important contributor in both models. CONCLUSIONS Waist circumference is a potentially modifiable risk factor for low testosterone and symptomatic AD. Manifestation of symptoms may be a consequence of generally poor health status.

Low dietary or supplemental zinc is associated with depression symptoms among women, but not men, in a population-based epidemiological survey

BackgroundAn increasing number of countries in sub-Saharan Africa are changing to artemisinins combination therapy (ACT) as first or second line treatment for malaria. There is an urgent need to assess the safety of these drugs in pregnant women who may be inadvertently exposed to or actively treated with ACTs.ObjectivesTo examine existing published evidence on the relationship between artemisinin compounds and adverse pregnancy outcomes and consider the published evidence with regard to the safety of these compounds when administered during pregnancy.MethodsStudies on ACT use in pregnancy were identified via searches of MEDLINE, EMBASE, Cochrane and Current Contents databases. Data on study characteristics, maternal adverse events, pregnancy outcomes and infant follow up were extracted.ResultsFourteen relevant studies (nine descriptive/case reports and five controlled trials) were identified. Numbers of participants in these studies ranged from six to 461. Overall there were reports on 945 women exposed to an artemisinin during pregnancy, 123 in the 1st trimester and 822 in 2nd or 3rd trimesters. The primary end points for these studies were drug efficacy and parasite clearance. Secondary endpoints were birth outcomes including low birth weight, pre-term birth, pregnancy loss, congenital anomalies and developmental milestones. While none of the studies found evidence for an association between the use of artemisinin compounds and increased risk of adverse pregnancy outcomes, none were of sufficient size to detect small differences in event rates that could be of public health importance. Heterogeneity between studies in the artemisinin and comparator drugs used, and in definitions of adverse pregnancy outcomes, limited any pooled analysis.ConclusionThe limited data available suggest that artemisinins are effective and unlikely to be cause of foetal loss or abnormalities, when used in late pregnancy. However, none of these studies had adequate power to rule out rare serious adverse events, even in 2nd and 3rd trimesters and there is not enough evidence to effectively assess the risk-benefit profile of artemisinin compounds for pregnant women particularly for 1st trimester exposure. Methodologically rigorous, larger studies and post-marketing pharmacovigilance are urgently required.

Do Statins Affect Androgen Levels in Men? Results from the Boston Area Community Health Survey

OBJECTIVES: To describe the onset, progression, and remission of symptomatic androgen deficiency (SAD) using longitudinal data from the Massachusetts Male Aging Study (MMAS).

Sexual Activity, Erectile Dysfunction, and Incident Cardiovascular Events

BACKGROUND Prior studies indicate that the biochemical alterations of depressive episodes result in decreased serum zinc concentrations. Given these findings, it is plausible that consistently low dietary zinc intakes contribute to depressive symptoms, yet epidemiological data are lacking. The authors tested the hypothesis that low zinc intake is associated with depressive symptoms using cross-sectional data from the population-based Boston Area Community Health survey (2002-2005). METHODS Dietary and supplement use data were collected by validated food frequency questionnaire. Current depressive symptoms were assessed by the abridged validated Center for Epidemiologic Studies Depression scale and analyzed using multivariate logistic regression, adjusting for sociodemographic, health and lifestyle characteristics. RESULTS Results showed an interaction (P=0.03) with gender, whereby zinc was associated with depressive symptoms in women (N=2163), but not men (N=1545). Women with low dietary or supplemental zinc intake were more likely to have depressive symptoms (e.g., dietary zinc quartile 1 vs. 4, OR=1.76, 95% CI: 1.26, 2.45; P-trend=0.004; supplemental zinc P-trend=0.03). Associations were stronger among women using antidepressant medications (e.g., total zinc OR=4.75, 95% CI: 1.98, 11.4; P-trend=0.0005). LIMITATIONS The cross-sectional, observational nature of the study leaves uncertain whether the observed associations represent actual causal relationships between zinc intake and depressive symptoms. CONCLUSIONS These findings suggest: (1) gender-specific pathophysiological mechanisms of depression, (2) inadequate dietary zinc intake contributes to depressive symptoms in women, and (3) supplemental zinc is a beneficial adjunct to antidepressant therapy in women. Additional research on both men and women is needed to verify these novel findings. If confirmed by other studies, the potential importance of adequate zinc intake is underscored by the recognized limitations of pharmacotherapy for depression.

Prevalence and Psychosocial Correlates of Symptoms Suggestive of Painful Bladder Syndrome: Results From the Boston Area Community Health Survey

Background: In 2005, statins were among the most commonly used prescription medications in the United States. Some data suggest statins may affect cancer risk and/or disease severity. Because cholesterol is a required intermediate in sex steroid synthesis, it is possible that statins influence prostate cancer risk through effects on steroid hormone metabolism. We investigated whether levels of circulating androgens and their carrier protein, sex hormone–binding globulin (SHBG), varied by statin exposure among a sample of 1,812 men from a population-based epidemiologic study, the Boston Area Community Health Survey. Methods: We measured serum total testosterone, free testosterone, dehydroepiandrosterone sulfate, luteinizing hormone, and SHBG. Statin exposure was collected through participant self-report and/or interviewer-recorded information. Multivariate linear models were constructed to account for potential confounding. Results: The prevalence of statin use was 12.4% [95% confidence interval (95% CI), 10.3-14.9]. On average, statin users were older, had larger body mass index and more chronic illnesses, and used more medications. We found no relationship between statin use and free testosterone, dehydroepiandrosterone sulfate, or luteinizing hormone. A significant association between statin use and total testosterone was initially observed but was not robust to covariate control in a multivariate model that included age, body mass index, time since awakening, and history of cardiovascular disease and diabetes (−5.5%; 95% CI, −13.2 to 2.9%). In multivariate models adjusted similarly, SHBG levels among statin users were statistically significantly lower compared with nonusers (−10.6%; 95% CI, −18.8 to −1.6%). Conclusion: In this sample, it is unlikely that statins affect circulating androgens and prostate cancer risk through a hormonal mechanism. (Cancer Epidemiol Biomarkers Prev 2007;16(8):1587–94)