CiteULike: omalbam's epidemiology

What is missing from descriptions of treatment in trials and reviews?

Paul Glasziou — 2008-07-03T22:33:34-00:00

BMJ, Vol. 336, No. 7659. (28 June 2008), pp. 1472-1474.

10.1136/bmj.39590.732037.47

Prevalence of symptomatic androgen deficiency in men.

AB Araujo — 2008-01-25T20:09:48-00:00

J Clin Endocrinol Metab, Vol. 92, No. 11. (November 2007), pp. 4241-4247.

CONTEXT: Despite recognition that androgen deficiency in men should be defined according to biochemical and clinical criteria, most prevalence estimates are based on low testosterone levels alone. OBJECTIVE: The objective of this study was to examine the association between symptoms of androgen deficiency and low total and calculated free testosterone levels and estimate the prevalence of symptomatic androgen deficiency in men. DESIGN: This study was a population-based, observational survey. PARTICIPANTS: A total of 1,475 Black, Hispanic, and white men, between the ages of 30-79 yr, with complete data on testosterone, SHBG, and symptoms of androgen deficiency, and who are not taking medications that impact sex steroid levels were randomly selected from the Boston Area Community Health Survey. OUTCOME: Outcomes were measured as symptomatic androgen deficiency, defined as low total (<300 ng/dl) and free (<5 ng/dl) testosterone plus presence of low libido, erectile dysfunction, osteoporosis or fracture, or two or more of following symptoms: sleep disturbance, depressed mood, lethargy, or diminished physical performance. RESULTS: Mean age of the sample was 47.3 +/- 12.5 yr. Approximately 24% of subjects had total testosterone less than 300 ng/dl, and 11% of subjects had free testosterone less than 5 ng/dl. Prevalence of symptoms were as follows: low libido (12%), erectile dysfunction (16%), osteoporosis/fracture (1%), and two or more of the nonspecific symptoms (20%). Low testosterone levels were associated with symptoms, but many men with low testosterone levels were asymptomatic (e.g. in men 50+ yr, 47.6%). Crude prevalence of symptomatic androgen deficiency was 5.6% (95% confidence interval: 3.6%, 8.6%), and was not significantly related to race and ethnic group. Prevalence was low in men less than 70 yr (3.1-7.0%) and increased markedly with age to 18.4% among 70 yr olds. Projection of these estimates to the year 2025 suggests that there will be as many as 6.5 million American men ages 30-79 yr with symptomatic androgen deficiency, an increase of 38% from 2000 population estimates. CONCLUSIONS: Prevalence of symptomatic androgen deficiency in men 30 and 79 yr of age is 5.6% and increases substantially with age. The aging of the U.S. male population will cause a large increase in the burden of symptomatic androgen deficiency. Future work should address the clinical significance of low testosterone levels in asymptomatic men.

Assessing the probability that a positive report is false: an approach for molecular epidemiology studies.

S Wacholder — 2007-03-10T13:50:49-00:00

J Natl Cancer Inst, Vol. 96, No. 6. (17 March 2004), pp. 434-442.

Too many reports of associations between genetic variants and common cancer sites and other complex diseases are false positives. A major reason for this unfortunate situation is the strategy of declaring statistical significance based on a P value alone, particularly, any P value below.05. The false positive report probability (FPRP), the probability of no true association between a genetic variant and disease given a statistically significant finding, depends not only on the observed P value but also on both the prior probability that the association between the genetic variant and the disease is real and the statistical power of the test. In this commentary, we show how to assess the FPRP and how to use it to decide whether a finding is deserving of attention or "noteworthy." We show how this approach can lead to improvements in the design, analysis, and interpretation of molecular epidemiology studies. Our proposal can help investigators, editors, and readers of research articles to protect themselves from overinterpreting statistically significant findings that are not likely to signify a true association. An FPRP-based criterion for deciding whether to call a finding noteworthy formalizes the process already used informally by investigators--that is, tempering enthusiasm for remarkable study findings with considerations of plausibility.

Physical Activity and Mortality: Is the Association Explained by Genetic Selection?

Sofia Carlsson — 2008-01-08T22:34:30-00:00

Am. J. Epidemiol., Vol. 166, No. 3. (1 August 2007), pp. 255-259.

Public health recommendations promote physical activity to improve health and longevity. Recent data suggest that the association between physical activity and mortality may be due to genetic selection. Using data on twins, the authors investigated whether genetic selection explains the association between physical activity and mortality. Data were based on a postal questionnaire answered by 13,109 Swedish twin pairs in 1972. The national Cause of Death Register was used for information about all-cause mortality (n = 1,800) and cardiovascular disease mortality (n = 638) during 1975-2004. The risk of death was reduced by 34% for men (relative risk = 0.64, 95% confidence interval: 0.50, 0.83) and by 25% for women (relative risk = 0.75, 95% confidence interval: 0.50, 1.14) reporting high physical activity levels. Within-pair comparisons of monozygotic twins showed that, compared with their less active co-twin, the more active twin had a 20% (odds ratio = 0.80, 95% confidence interval: 0.65, 0.99) reduced risk of all-cause mortality and a 32% (odds ratio = 0.68, 95% confidence interval: 0.49, 0.95) reduced risk of cardiovascular disease mortality. Results indicate that physical activity is associated with a reduced risk of mortality not due to genetic selection. This finding supports a causal link between physical activity and mortality. 10.1093/aje/kwm132

Early adult risk factor levels and subsequent coronary artery calcification: the CARDIA Study.

CM Loria — 2008-01-08T18:45:16-00:00

J Am Coll Cardiol, Vol. 49, No. 20. (22 May 2007), pp. 2013-2020.

OBJECTIVES: We sought to determine whether early adult levels of cardiovascular risk factors predict subsequent coronary artery calcium (CAC) better than concurrent or average 15-year levels and independent of a 15-year change in levels. BACKGROUND: Few studies have used multiple measures over the course of time to predict subclinical atherosclerosis. METHODS: African American and white adults, ages 18 to 30 years, in 4 U.S. cities were enrolled in the prospective CARDIA (Coronary Artery Risk Development in Young Adults) study from 1985 to 1986. Risk factors were measured at years 0, 2, 5, 7, 10, and 15, and CAC was assessed at year 15 (n = 3,043). RESULTS: Overall, 9.6% adults had any CAC, with a greater prevalence among men than women (15.0% vs. 5.1%), white than African American men (17.6% vs. 11.3%), and ages 40 to 45 years than 33 to 39 years (13.3% vs. 5.5%). Baseline levels predicted CAC presence (C = 0.79) equally as well as average 15-year levels (C = 0.79; p = 0.8262) and better than concurrent levels (C = 0.77; p = 0.019), despite a 15-year change in risk factor levels. Multivariate-adjusted odds ratios of having CAC by ages 33 to 45 years were 1.5 (95% confidence interval [CI] 1.3 to 1.7) per 10 cigarettes, 1.5 (95% CI 1.3 to 1.8) per 30 mg/dl low-density lipoprotein cholesterol, 1.3 (95% CI 1.1 to 1.5) per 10 mm Hg systolic blood pressure, and 1.2 (95% CI 1.1 to 1.4) per 15 mg/dl glucose at baseline. Young adults with above optimal risk factor levels at baseline were 2 to 3 times as likely to have CAC. CONCLUSIONS: Early adult levels of modifiable risk factors, albeit low, were equally or more informative about odds of CAC in middle age than subsequent levels. Earlier risk assessment and efforts to achieve and maintain optimal risk factor levels may be needed.

Mortality trends in men and women with diabetes, 1971 to 2000.

EW Gregg — 2007-12-06T09:59:48-00:00

Ann Intern Med, Vol. 147, No. 3. (7 August 2007), pp. 149-155.

BACKGROUND: Whether mortality rates among diabetic adults or excess mortality associated with diabetes in the United States has declined in recent decades is not known. OBJECTIVE: To examine whether all-cause and cardiovascular disease mortality rates have declined among the U.S. population with and without self-reported diabetes. DESIGN: Comparison of 3 consecutive, nationally representative cohorts. SETTING: Population-based health surveys (National Health and Nutrition Examination Surveys I, II, and III) with mortality follow-up assessment. PATIENTS: Survey participants age 35 to 74 years with and without diabetes. MEASUREMENTS: Diabetes was determined by self-report for each survey (1971-1975, 1976-1980, and 1988-1994), and mortality rates were determined through 1986, 1992, and 2000 for the 3 surveys, respectively. RESULTS: Among diabetic men, the all-cause mortality rate decreased by 18.2 annual deaths per 1000 persons (from 42.6 to 24.4 annual deaths per 1000 persons; P = 0.03) between 1971 to 1986 and 1988 to 2000, accompanying decreases in the nondiabetic population. Trends for cardiovascular disease mortality paralleled those of all-cause mortality, with 26.4 annual deaths per 1000 persons in 1971 to 1986 and 12.8 annual deaths per 1000 persons in 1988 to 2000 (P = 0.06). Among women with diabetes, however, neither all-cause nor cardiovascular disease mortality declined between 1971 to 1986 and 1988 to 2000, and the all-cause mortality rate difference between diabetic and nondiabetic women more than doubled (from a difference of 8.3 to 18.2 annual deaths per 1000 persons). The difference in all-cause mortality rates by sex among people with diabetes in 1971 to 1986 were essentially eliminated in 1988 to 2000. LIMITATIONS: Diabetes was assessed by self-report, and statistical power to examine the factors explaining mortality trends was limited. CONCLUSIONS: Progress in reducing mortality rates among persons with diabetes has been limited to men. Diabetes continues to greatly increase the risk for death, particularly among women.

Associations of diabetes mellitus with total life expectancy and life expectancy with and without cardiovascular disease.

OH Franco — 2008-01-08T00:25:43-00:00

Arch Intern Med, Vol. 167, No. 11. (11 June 2007), pp. 1145-1151.

BACKGROUND: Diabetes mellitus is a recognized risk factor for cardiovascular disease (CVD) and mortality. However, limited information exists on the association of diabetes with life expectancy with and without CVD. We aimed to calculate the association of diabetes after age 50 years with life expectancy and the number of years lived with and without CVD. METHODS: Using data from the Framingham Heart Study, we built life tables to calculate the associations of having diabetes with life expectancy and years lived with and without CVD among populations 50 years and older. For the life table calculations, we used hazard ratios for 3 transitions (healthy to death, healthy to CVD, and CVD to death), stratifying by the presence of diabetes at baseline and adjusting for age and confounders. RESULTS: Having diabetes significantly increased the risk of developing CVD (hazard ratio, 2.5 for women and 2.4 for men) and of dying when CVD was present (hazard ratio, 2.2 for women and 1.7 for men). Diabetic men and women 50 years and older lived on average 7.5 (95% confidence interval, 5.5-9.5) and 8.2 (95% confidence interval, 6.1-10.4) years less than their nondiabetic equivalents. The differences in life expectancy free of CVD were 7.8 and 8.4 years, respectively. CONCLUSIONS: The increase in the risk of CVD and mortality from diabetes represents an important decrease in life expectancy and life expectancy free of CVD. Prevention of diabetes is a fundamental task facing today's society in the pursuit of healthy aging.

Increasing cardiovascular disease burden due to diabetes mellitus: the Framingham Heart Study.

CS Fox — 2008-01-08T00:20:23-00:00

Circulation, Vol. 115, No. 12. (27 March 2007), pp. 1544-1550.

BACKGROUND: Marked reductions in cardiovascular disease (CVD) morbidity and mortality have occurred in the United States over the last 50 years. We tested the hypothesis that the relative burden of CVD attributable to diabetes mellitus (DM) has increased over the past 5 decades. METHODS AND RESULTS: Participants aged 45 to 64 years from the Framingham Heart Study, who attended examinations in an "early" time period (1952 to 1974), were compared with those who attended examinations in a later time period (1975 to 1998). The risk of CVD events (n=133 among those with and 1093 among those without DM) attributable to DM in the 2 time periods was assessed with Cox proportional hazards models; population attributable risk of DM as a CVD risk factor was calculated for each time period. The age- and sex-adjusted hazard ratio for DM as a CVD risk factor was 3.0 (95% CI, 2.3 to 3.9) in the earlier time period and 2.5 (95% CI, 1.9 to 3.2) in the later time period. The population attributable risk for DM as a CVD risk factor increased from 5.4% (95% CI, 3.8% to 6.9%) in the earlier time period to 8.7% (95% CI, 5.9% to 11.4%) in the later time period (P for attributable risk ratio=0.04), although multivariable adjustment resulted in attenuation of these findings (P=0.12); most of these observations were found among men. CONCLUSIONS: The proportion of CVD attributable to DM has increased over the past 50 years in Framingham. These findings emphasize the need for increased efforts to prevent DM and to aggressively treat and control CVD risk factors among those with DM.