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1.  STATE EXPENDITURES FOR TOBACCO-CONTROL PROGRAMS AND THE TOBACCO SETTLEMENT 
The New England journal of medicine  2002;347(14):1080-1086.
Background
Despite controversy surrounding the use of funds arising from settlement agreements with the tobacco industry, little is known about the role of these funds in expenditures for state tobacco-control programs.
Methods
We evaluated state expenditures for tobacco-control programs in fiscal year 2001 in the context of the amount of tobacco-settlement funds received and allocated to tobacco-control programs and in the context of other state-level economic and health data.
Results
In 2001 the average state received $28.35 per capita from the tobacco settlement but allocated approximately 6 percent of these funds to tobacco-control programs. The average state dedicated $3.49 per capita (range, $0.10 to $15.47) to tobacco-control programs. The proportion of settlement funds allocated to tobacco-control programs varied from 0 to 100 percent and was strongly related to levels of tobacco-control funding (P<0.001). States with higher smoking rates tended to invest less per capita in tobacco-control programs (P=0.007), as did tobacco-producing states (the mean per capita expenditure was $1.20, as compared with $3.81 in non–tobacco-producing states; P<0.008). In a multivariate analysis, the proportion of the settlement revenue allocated to tobacco-control programs was the primary determinant of the level of total funding; the state tobacco-related health burden was unrelated to program funding.
Conclusions
State health needs appear to have little effect on the funding of state tobacco-control programs. Because only a very small proportion of the tobacco settlement is being used for tobacco-control programs, the settlement represents an unrealized opportunity to reduce morbidity and mortality from smoking.
doi:10.1056/NEJMsa012743
PMCID: PMC3535289  PMID: 12362010
2.  PRIMARY CHEMOPREVENTION OF FAMILIAL ADENOMATOUS POLYPOSIS WITH SULINDAC 
The New England journal of medicine  2002;346(14):1054-1059.
Background
Familial adenomatous polyposis is caused by a germ-line mutation in the adenomatous polyposis coli gene and is characterized by the development of hundreds of colorectal adenomas and, eventually, colorectal cancer. Nonsteroidal antiinflammatory drugs can cause regression of adenomas, but whether they can prevent adenomas is unknown.
Methods
We conducted a randomized, double-blind, placebo-controlled study of 41 young subjects (age range, 8 to 25 years) who were genotypically affected with familial adenomatous polyposis but phenotypically unaffected. The subjects received either 75 or 150 mg of sulindac orally twice a day or identical-appearing placebo tablets for 48 months. The number and size of new adenomas and side effects of therapy were evaluated every four months for four years, and the levels of five major prostaglandins were serially measured in biopsy specimens of normal-appearing colorectal mucosa.
Results
After four years of treatment, the average rate of compliance exceeded 76 percent in the sulindac group, and mucosal prostaglandin levels were lower in this group than in the placebo group. During the course of the study, adenomas developed in 9 of 21 subjects (43 percent) in the sulindac group and 11 of 20 subjects in the placebo group (55 percent) (P=0.54). There were no significant differences in the mean number (P=0.69) or size (P=0.17) of polyps between the groups. Sulindac did not slow the development of adenomas, according to an evaluation involving linear longitudinal methods.
Conclusions
Standard doses of sulindac did not prevent the development of adenomas in subjects with familial adenomatous polyposis.
doi:10.1056/NEJMoa012015
PMCID: PMC2225537  PMID: 11932472
4.  REDUCTION IN THE INCIDENCE OF TYPE 2 DIABETES WITH LIFESTYLE INTERVENTION OR METFORMIN 
The New England journal of medicine  2002;346(6):393-403.
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, over-weight, 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.
doi:10.1056/NEJMoa012512
PMCID: PMC1370926  PMID: 11832527

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