Background Type 2 diabetes affects approximately 8 percent of adults in the United States. Some risk factors — elevated plasma glucose concentrations in the fasting state and after an oral glucose load, overweight, and a sedentary lifestyle — are potentially reversible. We hypothesized that modifying these factors with a lifestyle-intervention program or the administration of metformin would prevent or delay the development of diabetes. Methods We randomly assigned 3234 nondiabetic persons with elevated fasting and post-load plasma glucose concentrations to placebo, metformin (850 mg twice daily), or a lifestyle modification program with the goals of at least a 7 percent weight loss and at least 150 minutes of physical activity per week. The mean age of the participants was 51 years, and the mean body-mass index (the weight in kilograms divided by the square of the height in meters) was 34.0; 68 percent were women, and 45 percent were members of minority groups. Results The average follow-up was 2.8 years. The incidence of diabetes was 11.0, 7.8, and 4.8 cases per 100 person-years in the placebo, metformin, and lifestyle groups, respectively. The lifestyle intervention reduced the incidence by 58 percent (95 percent confidence interval, 48 to 66 percent) and metformin by 31 percent (95 percent confidence interval, 17 to 43 percent), as compared with placebo; the lifestyle intervention was significantly more effective than metformin. To prevent one case of diabetes during a period of three years, 6.9 persons would have to participate in the lifestyle-intervention program, and 13.9 would have to receive metformin. Conclusions Lifestyle changes and treatment with metformin both reduced the incidence of diabetes in persons at high risk. The lifestyle intervention was more effective than metformin.

Reduction in the incidence of type 2 diabetes with lifestyle intervention or metformin.

Objective. —To identify and quantify the major external (nongenetic) factors that contribute to death in the United States. Data Sources. —Articles published between 1977 and 1993 were identified through MEDLINE searches, reference citations, and expert consultation. Government reports and compilations of vital statistics and surveillance data were also obtained. Study Selection. —Sources selected were those that were often cited and those that indicated a quantitative assessment of the relative contributions of various factors to mortality and morbidity. Data Extraction. —Data used were those for which specific methodological assumptions were stated. A table quantifying the contributions of leading factors was constructed using actual counts, generally accepted estimates, and calculated estimates that were developed by summing various individual estimates and correcting to avoid double counting. For the factors of greatest complexity and uncertainty (diet and activity patterns and toxic agents), a conservative approach was taken by choosing the lower boundaries of the various estimates. Data Synthesis. —The most prominent contributors to mortality in the United States in 1990 were tobacco (an estimated 400000 deaths), diet and activity patterns (300 000), alcohol (100 000), microbial agents (90 000), toxic agents (60 000), firearms (35 000), sexual behavior (30 000), motor vehicles (25 000), and illicit use of drugs (20 000). Socioeconomic status and access to medical care are also important contributors, but difficult to quantify independent of the other factors cited. Because the studies reviewed used different approaches to derive estimates, the stated numbers should be viewed as first approximations. Conclusions. —Approximately half of all deaths that occurred in 1990 could be attributed to the factors identified. Although no attempt was made to further quantify the impact of these factors on morbidity and quality of life, the public health burden they impose is considerable and offers guidance for shaping health policy priorities. (JAMA. 1993;270:2207-2212)

https://jamanetwork.com/journals/JAMA/articlepdf/409171/jama_270_18_038.pdf

Actual causes of death in the United States.

OBJECTIVE To assess predictors of CVD mortality among men with and without diabetes and to assess the independent effect of diabetes on the risk of CVD death. RESEARCH DESIGN AND METHODS Participants in this cohort study were screened from 1973 to 1975; vital status has been ascertained over an average of 12 yr of follow-up (range 11–13 yr). Participants were 347,978 men aged 35–57 yr, screened in 20 centers for MRFIT. The outcome measure was CVD mortality. RESULTS Among 5163 men who reported taking medication for diabetes, 1092 deaths (603 CVD deaths) occurred in an average of 12 yr of follow-up. Among 342,815 men not taking medication for diabetes, 20,867 deaths were identified, 8965 ascribed to CVD. Absolute risk of CVD death was much higher for diabetic than nondiabetic men of every age stratum, ethnic background, and risk factor level—overall three times higher, with adjustment for age, race, income, serum cholesterol level, sBP, and reported number of cigarettes/day ( P CONCLUSIONS These findings emphasize the importance of rigorous sustained intervention in people with diabetes to control blood pressure, lower serum cholesterol, and abolish cigarette smoking, and the importance of considering nutritional-hygienic approaches on a mass scale to prevent diabetes.

https://www.siditalia.it/pdf/Diabete-ed-Arterosclerosi/MRFIT_Diab_care_1993.pdf

Diabetes, other risk factors, and 12-yr cardiovascular mortality for men screened in the Multiple Risk Factor Intervention Trial.

Chronic kidney disease1 (CKD) is a worldwide public health problem. In the United States, there is a rising incidence and prevalence of kidney failure, with poor outcomes and high cost. The number of individuals with kidney failure treated by dialysis and transplantation exceeded 320 000 in 1998 and is expected to surpass 650 000 by 2010.1,2 There is an even higher prevalence of earlier stages of CKD (Table 1).1,3 Kidney failure requiring treatment with dialysis or transplantation is the most visible outcome of CKD. However, cardiovascular disease (CVD) is also frequently associated with CKD, which is important because individuals with CKD are more likely to die of CVD than to develop kidney failure,4 CVD in CKD is treatable and potentially preventable, and CKD appears to be a risk factor for CVD. In 1998, the National Kidney Foundation (NKF) Task Force on Cardiovascular Disease in Chronic Renal Disease issued a report emphasizing the high risk of CVD in CKD.5 This report showed that there was a high prevalence of CVD in CKD and that mortality due to CVD was 10 to 30 times higher in dialysis patients than in the general population (Figure 1 and Table 2).6–18 The task force recommended that patients with CKD be considered in the “highest risk group” for subsequent CVD events and that treatment recommendations based on CVD risk stratification should take into account the highest-risk status of patients with CKD. 

View this table:

TABLE 1. Stages of CKD 





Figure 1. Cardiovascular mortality defined by death due to arrhythmias, cardiomyopathy, cardiac arrest, myocardial infarction, atherosclerotic heart disease, and pulmonary edema in general population (GP; National Center for Health Statistics [NCHS] multiple cause of mortality data files International Classification of Diseases, 9th Revision [ICD 9] codes 402, 404, 410 to 414, and …

Kidney disease as a risk factor for development of cardiovascular disease: a statement from the American Heart Association Councils on Kidney in Cardiovascular Disease, High Blood Pressure Research, Clinical Cardiology, and Epidemiology and Prevention.

Body-mass index and cause-specific mortality in 900 000 adults: collaborative analyses of 57 prospective studies

Background. Many believe that the prospect of weight gain discourages smokers from quitting. Accurate estimates of the weight gain related to the cessation of smoking in the general population are not available, however. Methods. We related changes in body weight to changes in smoking status in adults 25 to 74 years of age who were weighed in the First National Health and Nutrition Examination Survey (NHANES I, 1971 to 1975) and then weighed a second time in the NHANES I Epidemiologic Follow-up Study (1982 to 1984). The cohort included continuing smokers (748 men and 1137 women) and those who had quit smoking for a year or more (409 men and 359 women). Results. The mean weight gain attributable to the cessation of smoking, as adjusted for age, race, level of education, alcohol use, illnesses related to change in weight, base-line weight, and physical activity, was 2.8 kg in men and 3.8 kg in women. Major weight gain (>13 kg) occurred in 9.8 percent of the men and 13.4 percent of the women who qui...

https://www.nejm.org/doi/pdf/10.1056/NEJM199103143241106

Smoking cessation and severity of weight gain in a national cohort.

Background: It is widely claimed that racial and ethnic minorities, especially in the US,are less willing than non-minority individuals to participate in health research. Yet,there is a paucity of empirical data to substantiate this claim. Methods and Findings: We performed a comprehensive literature search to identify all puublished health research studies that report consent rates by race or ethnicity. We found 20 health research studies that reported consent rates by race or ethnicity. These 20 studies reported the enrollment decisions of over 70,000 individuals for a broad range of research,from interviews to drug treatment to surgical trials. Eighteen of the twenty studies were single-site studies conducted exclusively in the US or multi-site studies where the majority of sites (i.e., at least 2/3) were in the US. Of the remaining two studies, the Concorde study was conducted at 74 sites in the United Kingdom, Ireland, and France, while the Delta study was conducted at 152 sites in Europe and 23 sites in Australia and New Zealand. For the three interview or non-intervention studies, African-Americans had a nonsignificantly lower overall consent rate than non-Hispanic whites (82.2% versus 83.5%; odds ratio [OR] ¼ 0.92; 95% confidence interval [CI] 0.84–1.02). For these same three studies, Hispanics had a nonsignificantly higher overall consent rate than non-Hispanic whites (86.1% versus 83.5%; OR ¼ 1.37; 95% CI 0.94–1.98). For the ten clinical intervention studies, African-Americans’ overall consent rate was nonsignificantly higher than that of non-Hispanic whites (45.3% versus 41.8%; OR¼1.06; 95% CI 0.78–1.45). For these same ten studies, Hispanics had a statistically significant higher overall consent rate than non-Hispanic whites (55.9% versus 41.8%; OR¼1.33; 95% CI 1.08–1.65). For the seven surgery trials, which report all minority groups together, minorities as a group had a nonsignificantly higher overall consent rate than non-Hispanic whites (65.8% versus 47.8%; OR ¼ 1.26; 95% CI 0.89–1.77). Given the preponderance of US sites, the vast majority of these individuals from minority groups were African-Americans or Hispanics from the US. Conclusions We found very small differences in the willingness of minorities, most of whom were African-Americans and Hispanics in the US, to participate in health research compared to non-Hispanic whites. These findings, based on the research enrollment decisions of over 70,000 individuals, the vast majority from the US, suggest that racial and ethnic minorities in the US are as willing as non-Hispanic whites to participate in health research. Hence, efforts to increase minority participation in health research should focus on ensuring access to health research for all groups, rather than changing minority attitudes.

/pdf/are-racial-and-ethnic-minorities-less-willing-to-participate-57b1uw0dry.pdf

Are racial and ethnic minorities less willing to participate in health research

Clinical research has established that increases in physical activity cause weight loss among the obese, but less is known about the influence of physical activity on longer-term weight change in the general population. Data from the NHANES-I Epidemiologic Follow-up Study (1971-1975 to 1982-1984) were used to examine the relationship between self-reported recreational physical activity level (low, medium, high) and measured weight change after ten years among 3515 men and 5810 women aged 25-74 years. Cross-sectional analyses at both the baseline and follow-up surveys revealed that recreational physical activity was inversely related to body weight. Low recreational physical activity reported at the follow-up survey was strongly related to major weight gain (> 13 kg) that had occurred during the preceding ten years. The estimated relative risk of major weight gain for those in the low activity level at the follow-up survey compared to those in the high activity level was 3.1 (95% Cl = 1.6-6.0) in men and 3.8 (2.3-6.5) in women. In addition, the relative risk for persons whose activity level was low at both the baseline and follow-up surveys was 2.3 (0.9-5.8) in men and 7.1 (2.2-23.3) in women. However, no relationship was found between baseline physical activity level and subsequent weight gain among either men or women. The lack of a relationship may be due to mis-specification of physical activity because of changes in activity over time. These findings suggest that low physical activity may be both a cause and a consequence of weight gain.(ABSTRACT TRUNCATED AT 250 WORDS)

Recreational physical activity and ten-year weight change in a US national cohort

The authors compare the mortality experience of a national sample of diabetic men and women with their nondiabetic counterparts. The study population consists of respondents from the First National Health and Nutrition Examination Survey (NHANES I), conducted in 1971-1975, who were traced in 1982-1984 through the NHANES I Epidemiologic Follow-up Study. Over the nine-year follow-up period, the age-adjusted death rates for diabetic men and women were twice the rates for nondiabetics. About 75% of the excess mortality among diabetic men and 57% among diabetic women was attributable to cardiovascular disease deaths. After adjustment for age, systolic blood pressure, serum cholesterol, body mass index, and smoking, the relative risk of death was 2.3 for diabetic men and 2.0 for diabetic women. The relative risk for diabetics was highest for ischemic heart disease mortality (2.8 for men and 2.5 for women) and lowest for noncardiovascular disease deaths (1.4 for men and 1.1 for women). When subjects who reported having had a heart attack prior to the baseline examination were excluded, the relative risks for ischemic heart disease mortality among diabetics remained substantial (2.4 for men and 2.6 for women). There was little evidence that the relative risk of death for diabetics compared with nondiabetics differed by age or sex, although 95% confidence intervals around these estimates were wide.

Mortality among diabetics in a national sample

Although maternal cigarette smoking has been shown to reduce the birth weight of an infant, previous findings on the relation between smoking and fetal and infant mortality have been inconsistent. This study used the largest data base ever available (360,000 birth, 2,500 fetal death, and 3,800 infant death certificates for Missouri residents during 1979-1983) to assess the impact of smoking on fetal and infant mortality. Multiple logistic regression was used to estimate the joint effects of maternal smoking, age, parity, education, marital status, and race on total mortality (infant plus fetal deaths). Compared with nonsmoking women having their first birth, women who smoked less than one pack of cigarettes per day had a 25% greater risk of mortality, and those who smoked one or more packs per day had a 56% greater risk. Among women having their second or higher birth, smokers experienced 30% greater mortality than nonsmokers, but there was no difference by amount smoked. The prevalence of smoking in this population was 30%. It was estimated that if all pregnant women stopped smoking, the number of fetal and infant deaths would be reduced by approximately 10%. The higher rate of mortality among blacks compared with whites could not be attributed to differences in smoking or the other four maternal characteristics studied. In fact, the black-white difference was greater among low-risk women (e.g., married multiparas aged 20 and over with high education) than among high-risk women (e.g., unmarried teenagers with low education).

Jennifer H. Madans

Papers

Smoking cessation and severity of weight gain in a national cohort.

Are racial and ethnic minorities less willing to participate in health research

Recreational physical activity and ten-year weight change in a US national cohort

Mortality among diabetics in a national sample

The effects of maternal smoking on fetal and infant mortality