Search

OBJECTIVE--To quantify the association of treated diabetes with cancer incidence and cancer mortality as well as cancer case fatality and all-cause mortality in adults who subsequently develop cancer and to [...]

Background: Cigarette smoking is an established predictor of incident type 2 diabetes mellitus, but the effects of smoking cessation on diabetes risk are unknown. Objective: To test the hypothesis that smoking cessation increases diabetes risk in the short term, possibly owing to cessation-related weight gain. Design: Prospective cohort study. Setting: The ARIC (Atherosclerosis Risk in Communities) Study. Patients: 10892 middle-aged adults who initially did not have diabetes in 1987 to 1989. Measurements: Smoking was assessed by interview at baseline and at subsequent follow-up. Incident diabetes was ascertained by fasting glucose assays through 1998 and self-report of physician diagnosis or use of diabetes medications through 2004. Results: During 9 years of follow-up, 1254 adults developed type 2 diabetes. Compared with adults who never smoked, the adjusted hazard ratio of incident diabetes in the highest tertile of pack-years was 1.42 (95% CI, 1.20 to 1.67). In the first 3 years of follow-up, 380 adults quit smoking. After adjustment for age, race, sex, education, adiposity, physical activity, lipid levels, blood pressure, and ARIC Study center, compared with adults who never smoked, the hazard ratios of diabetes among former smokers, new quitters, and continuing smokers were 1.22 (CI, 0.99 to 1.50), 1.73 (CI, 1.19 to 2.53), and 1.31 (CI, 1.04 to 1.65), respectively. Further adjustment for weight change and leukocyte count attenuated these risks substantially. In an analysis of long-term risk after quitting, the highest risk occurred in the first 3 years (hazard ratio, 1.91 [CI, 1.19 to 3.05]), then gradually decreased to 0 at 12 years. Limitation: Residual confounding is possible even with meticulous adjustment for established diabetes risk factors. Conclusion: Cigarette smoking predicts incident type 2 diabetes, but smoking cessation leads to higher short-term risk. For smokers at risk for diabetes, smoking cessation should be coupled with strategies for diabetes prevention and early detection. Primary Funding Source: National Heart, Lung, and Blood Institute and National Institute of Diabetes and Digestive and Kidney Diseases.

OBJECTIVE--The aim of this study was to test the hypothesis that diabetes is independently associated with reduced lung function, both cross-sectionally and longitudinally. RESEARCH DESIGN AND METHODS--We conducted cross-sectional and [...]

OBJECTIVE--To test the hypothesis that lower vital capacity is cross-sectionally associated with features of insulin resistance and is an independent predictor of incident type 2 diabetes. RESEARCH DESIGN AND METHODS--We [...]

OBJECTIVE--Hypertension is known to accompany type 2 diabetes in middle age, but it is unknown how early in life blood pressure (BP) begins to rise among individuals who later develop [...]

Background: Anger can trigger myocardial ischemia and may be an independent risk factor for coronary heart disease, but its effect on early compared with late onset of disease is unclear. Methods: We performed a prospective study of 1055 men followed up for 32 to 48 years to examine the risk of premature and total cardiovascular disease (CVD) associated with anger responses to stress during early adult life. Highest level of anger was defined as a self-report of all 3 possible anger reactions to stress (expressed or concealed anger, gripe sessions, and irritability) on a checklist questionnaire administered in medical school. Premature disease was defined as events before age 55 years. Results: During a median follow-up period of 36 years, 205 men developed CVD (cumulative incidence at 76 years, 34.5%), of whom 77 men developed premature disease (cumulative incidence before 55 years, 7.9%). The highest level of anger was associated with an increased risk of premature CVD (adjusted relative risk, 3.1; 95% confidence interval, 1.1-8.6), including premature coronary heart disease (relative risk, 3.5; 95% confidence interval, 1.1-11.8) and premature myocardial infarction (relative risk, 6.4; 95% confidence interval, 1.8-22.3), compared with lower levels of anger. When CVD events after age 55 years were included, there was no longer a statistically significant association between anger and CVD. Conclusion: High level of anger in response to stress in young men is associated with an increased risk of subsequent premature CVD, particularly myocardial infarction. Arch Intern Med. 2002;162:901-906

Background: Whether the increase in blood pressure with coffee drinking seen in clinical trials persists over time and translates into an increased incidence of hypertension is not known. Methods: We assessed coffee intake in a cohort of 1017 white male former medical students (mean age, 26 years) in graduating classes from 1948 to 1964 up to 11 times over a median follow-up of 33 years. Blood pressure and incidence of hypertension were determined annually by self-report, demonstrated to be accurate in this cohort. Results: Consumption of 1 cup of coffee a day raised systolic blood pressure by 0.19 mm Hg (95% confidence interval, 0.02-0.35) and diastolic pressure by 0.27 mm Hg (95% confidence interval, 0.15-0.39) after adjustment for parental incidence of hypertension and time-dependent body mass index, cigarette smoking, alcohol drinking, and physical activity in analyses using generalized estimating equations. Compared with nondrinkers at baseline, coffee drinkers had a greater incidence of hypertension during follow-up (18.8% vs 28.3%; P=.03). Relative risk (95% confidence interval) of hypertension associated with drinking 5 or more cups a day was 1.35 (0.87-2.08) for baseline intake and 1.60 (1.06-2.40) for intake over follow-up. After adjustment for the variables listed above, however, these associations were not statistically significant. Conclusion: Over many years of follow-up, coffee drinking is associated with small increases in blood pressure, but appears to play a small role in the development of hypertension.

Background: Knee and hip injuries have been linked with osteoarthritis in cross-sectional and case-control studies, but few prospective studies have examined the relation between injuries in young adults and risk for later osteoarthritis. Objective: To prospectively examine the relation between joint injury and incident knee and hip osteoarthritis. Design: Prospective cohort study. Setting: Johns Hopkins Precursors Study. Participants: 1321 former medical students. Measurements: Injury status at cohort entry was recorded when the mean age of participants was 22 years. Injury during follow-up and incident osteoarthritis were determined by using self-administered questionnaires. Osteoarthritis was confirmed by symptoms and radiographic findings. Results: Over a median follow-up of 36 years, 141 participants reported joint injuries (knee alone [n = 111], hip alone [n = 16], or knee and hip [n = 14]) and 96 developed osteoarthritis (knee alone [n = 64], hip alone [n = 27], or knee and hip [n = 5]). The cumulative incidence of knee osteoarthritis by 65 years of age was 13.9% in participants who had a knee injury during adolescence and young adulthood and 6.0% in those who did not (P = 0.0045) (relative risk, 2.95 [95% CI, 1.35 to 6.45]). Joint injury at cohort entry or during follow-up substantially increased the risk for subsequent osteoarthritis at that site (relative risk, 5.17 [CI, 3.07 to 8.71] and 3.50 [CI, 0.84 to 14.69] for knee and hip, respectively). Results were similar for persons with osteoarthritis confirmed by radiographs and symptoms. Conclusions: Young adults with knee injuries are at considerably increased risk for osteoarthritis later in life and should be targeted in the primary prevention of osteoarthritis.

Background: Several studies have found that depression is an independent predictor of poor outcome after the onset of clinical coronary artery disease. There are few data concerning depression as a risk factor for the development of coronary artery disease. Objective: To determine if clinical depression is an independent risk factor for incident coronary artery disease. Patients and Methods: The Johns Hopkins Precursors Study is a prospective, observational study of 1190 male medical students who were enrolled between 1948 and 1964 and who continued to be followed up. In medical school and through the follow-up period, information was collected on family history, health behaviors, and clinical depression. Cardiovascular disease end points have been assessed with reviews of annual questionnaires, National Death Index searches, medical records, death certificates, and autopsy reports. Results: The cumulative incidence of clinical depression in the medical students at 40 years of follow-up was 12%. Men who developed clinical depression drank more coffee than those who did not but did not differ in terms of baseline blood pressure, serum cholesterol levels, smoking status, physical activity, obesity, or family history of coronary artery disease. In multivariate analysis, the men who reported clinical depression were at significantly greater risk for subsequent coronary heart disease (relative risk [RR], 2.12; 95% confidence interval [CI], 1.243.63) and myocardial infarction (RR, 2.12; 95% CI, 1.11-4.06). The increased risk associated with clinical depression was present even for myocardial infarctions occurring 10 years after the onset of the first depressive episode (RR, 2.1; 95% CI, 1.1-4.0). Conclusion: Clinical depression appears to be an independent risk factor for incident coronary artery disease for several decades after the onset of the clinical depression. Arch Intern Med. 1998;158:1422-1426

A study was conducted to assess whether older physicians discuss their preferences for medical care at the end of life with their physicians and the life-sustaining treatment they wish in the event of incapacity to make these decisions for themselves. It was found that nearly two-thirds of physicians had completed an advance directive and that most physicians believed that their families were aware of preferences for medical treatment in the event of future incapacity.

PURPOSE: Obesity in middle age is associated with an increased risk of osteoarthritis of the knees in later life. We sought to determine whether body mass index in young men was a risk factor for the subsequent development of osteoarthritis of the knee and hip. SUBJECTS AND METHODS: Body mass index was assessed in 1,180 male medical students at age 23 [+ or -] 2 (mean [+ or -] SD) years and at several times during follow-up. The incidence of knee and hip osteoarthritis was ascertained by self-report and corroborated with information on symptoms and radiographic findings. RESULTS: During a median follow-up of 36 years, 62 participants developed knee osteoarthritis and 27 developed hip osteoarthritis. The incidence of knee, but not hip, osteoarthritis was strongly associated with body mass index assessed at ages 20 to 29 years and 30 to 39 years (both P [is less than] 0.001). For body mass index assessed at ages 20 to 29 years, the incidence of knee osteoarthritis at age 65 years was 12.8% among the heaviest subjects (range 24.7 to 37.6 kg/[m.sup.2]), threefold greater than the incidence of 4.0% in the leanest (15.6 to 22.8 kg/[m.sup.2]) category of body mass index (P = 0.0001). Thus, for a man who was 180 cm (5' 11') tall, each 8 kg (18 lb) greater weight at ages 20 to 29 years was associated with an increased risk of subsequent knee osteoarthritis (relative risk = 1.7, 95% confidence interval 1.3 to 2.1), after adjustment for year of birth, physical activity, and knee injury. Body mass index at ages 20 to 29 years was more predictive of future osteoarthritis than at ages 30 to 39 or 40 to 49 years. CONCLUSION: Greater body mass index in young men ages 20 to 29 years is associated with an increased risk of subsequent knee, but not hip, osteoarthritis, suggesting that cumulative exposure to greater weight during young adult life is an important cause of osteoarthritis. Am J Med. 1999;107:542-548. [C] 1999 by Excerpta Medica, Inc.

Background: Obesity in middle age is a well-known risk factor for the development of type 2 diabetes mellitus. However, the importance of weight and weight gain at younger ages is less certain. Objective: To determine the relationship of body weight patterns from 20 to 49 years of age with the subsequent risk for type 2 diabetes mellitus. Setting: An ongoing longitudinal study of former medical students. Participants: Nine hundred sixteen white men without diabetes at 50 years of age. Measurements: Weight and height measured in medical school, then assessed by mailed questionnaire to 49 years of age. Main Outcome: Incident type 2 diabetes mellitus based on physician self-report. Results: During 14 255 person-years of follow-up, there were 35 incident cases of type 2 diabetes mellitus (2.5 per 1000 person-years). After simultaneous adjustment for age, physical activity, lifetime maternal history of diabetes, and smoking, body mass indexes (BMIs; calculated as weight in kilograms divided by the square of height in meters) at 25, 35, and 45 years of age were all strongly associated with diabetes risk (relative risks for overweight [BMI [is greater than or equal to] 25.0] vs not overweight, [is greater than] 3.0; all Ps [is less than] .05), as were maximum and average BMI to 49 years of age. The relationship of BMI at 25 years of age to diabetes risk was substantially attenuated by adjustment for BMI at 45 years of age and average BMI, but was independent of weight change, weight variability, or maximum BMI. Conclusion: In men, overweight at 25 years of age strongly predicts diabetes risk in middle age, largely through its association with overweight at 45 years of age and high average BMI to 49 years of age. Arch Intern Med. 1999; 159:957-963