Background Fifty years after the first Surgeon General’s report, tobacco use remains the nation’s leading preventable cause of death and disease, despite declines in adult cigarette smoking prevalence. Smoking-attributable healthcare spending is an important part of overall smoking-attributable costs in the U.S. Purpose To update annual smoking-attributable healthcare spending in the U.S. and provide smoking-attributable healthcare spending estimates by payer (e.g., Medicare, Medicaid, private insurance) or type of medical services. Methods Analyses used data from the 2006–2010 Medical Expenditure Panel Survey linked to the 2004–2009 National Health Interview Survey. Estimates from two-part models were combined to predict the share of annual healthcare spending that could be attributable to cigarette smoking. The analysis was conducted in 2013. Results By 2010, 8.7% (95% CI=6.8%, 11.2%) of annual healthcare spending in the U.S. could be attributed to cigarette smoking, amounting to as much as $170 billion per year. More than 60% of the attributable spending was paid by public programs, including Medicare, other federally sponsored programs, or Medicaid. Conclusions These findings indicate that comprehensive tobacco control programs and policies are still needed to continue progress toward ending the tobacco epidemic in the U.S. 50 years after the release of the first Surgeon General’s report on smoking and health.

Objective. To examine the role of genetic variation in the renal urate transporter SLC2A9 in gout in New Zealand sample sets of Māori, Pacific Island, and Caucasian ancestry and to determine if the Māori and Pacific Island samples could be useful for fine-mapping.Methods. Patients (n‫؍‬ 56 Māori, 69 Pacific Island, and 131 Caucasian) were recruited from rheumatology outpatient clinics and satisfied the American College of Rheumatology criteria for gout. The control samples comprised 125 Māori subjects, 41 Pacific Island subjects, and 568 Caucasian subjects without arthritis. SLC2A9 single-nucleotide polymorphisms rs16890979 (V253I), rs5028843, rs11942223, and rs12510549 were genotyped (possible etiologic variants in Caucasians).Results. Association of the major allele of rs16890979, rs11942223, and rs5028843 with gout was observed in all sample sets (P ‫؍‬ 3.7 ؋ 10 ؊7 , 1.6 ؋ 10 ؊6 , and 7.6 ؋ 10 ؊5 for rs11942223 in the Māori, Pacific Island, and Caucasian samples, respectively). One 4-marker haplotype (1/1/2/1; more prevalent in the Māori and Pacific Island control samples) was not observed in a single gout case.Conclusion. Our data confirm a role of SLC2A9 in gout susceptibility in a New Zealand Caucasian sample set, with the effect on risk (odds ratio >2.0) greater than previous estimates. We also demonstrate association of SLC2A9 with gout in samples of Māori and Pacific Island ancestry and a consistent pattern of haplotype association. The presence of both alleles of rs16890979 on susceptibility and protective haplotypes in the Māori and Pacific Island sample is evidence against a role for this nonsynonymous variant as the sole etiologic agent. More extensive linkage disequilibrium in Māori and Pacific Island samples suggests that Caucasian samples may be more useful for fine-mapping.Gout is the most common form of arthritis affecting men, occurring in 1-2% of Caucasian men in Westernized countries. In New Zealand, gout affects 9.3-13.9% of Māori men and 14.9% of Pacific Island men (1,2). Māori and Pacific Island populations also have high rates of severe gout, with frequent tophaceous disease and accelerated joint damage (3,4). The central cause of gout is hyperuricemia, which leads to the deposition of monosodium urate crystals within joints and tissue; in some gout patients this is followed by the development of an inflammatory response to the urate crystals and an attack of acute gout. Renal underexcretion of uric acid has been demonstrated to be a primary gout-determining checkpoint in Māori and Pacific Island people (5-7).

While it is well documented that economic expansions provide widespread and immediate financial benefits, the evidence on how an economic downturn affects individual's health behaviors is surprisingly mixed. In this paper, we take a structural approach to investigate the effects of wages and working hours on health behaviors of low-educated persons using variations in wages and hours caused by changes in local economic activity. In the empirical analysis, we adopt a two-sample instrumental variables approach to combine the data on individual health behaviors from the Behavioral Risk Factor Surveillance System (BRFSS) and the National Health Interview Survey (NHIS) with the data on individual employment from the Current Population Survey (CPS). The total sample size of the combined CPS-BRFSS data for the time period of 1984-2005 is 967,594, while that of the combined CPS-NHIS data for the time period of 1976-2001 is 364,078. We find that increases in wages caused by economic expansions are associated with greater consumption of cigarettes in the United States. We also find that increases in hours of work caused by economic expansions are associated with more cigarette consumption, but less physical activity and physician visits. More importantly, the evidence suggests that most of such effects associated with changes in hours of work can be attributed to the changes at the extensive margin of employment, meaning the changes in employment status, rather than the changes at the intensive margin, meaning changes in hours of work conditional on being employed. These findings imply that changes in employment may have heterogeneous impacts on time-intensive and less time-intensive health behaviors and also provide additional evidence on the importance of time in health production, particularly for time-intensive activities.

Objectives The burden of gout has been increasing globally. However, little is known about the global, regional and national distribution and time trend of this disease. We present a comprehensive analysis of the Global Burden of Disease Study 2017 on gout burden estimates for 195 countries or territories between 1990 and 2017. Methods Age-standardized prevalence and disability-adjusted life-years of gout were reported between 1990 and 2017 in 195 countries and territories, and associations between these estimates and sociodemographic index (SDI) were further explored. Total and annual percent change between 1990 and 2017 were calculated to quantify the time trends of gout burden. Results Age-standardized prevalence rates (95% uncertainty interval) per 100 000 persons were 790.90 (706.10–881.90) and 253.49 (225.69–284.02) in 2017 in males and females, respectively. The annual percent change in age-standardized prevalence (males, 0.22%; females, 0.38%) and disability-adjusted life-years (males, 0.21%; females, 0.38%) of gout increased every year from 1990 to 2017, globally. The highest increase was detected in high-SDI countries, especially in high-income North America. A non-linear association was observed between burden of gout and SDI, with the lowest estimates of gout burden when SDI value was about 0.6. High BMI was the leading risk factor for the burden of gout. Conclusion These study results suggest a globally rising trajectory of gout burden between 1990 and 2017. More effective interventions, such as detailed and intensive dietary managements and other prevention strategies for reducing obesity, should be carried out to reverse this trend, especially in females and high-SDI countries.

Background-Smokers may react to cigarette excise tax increases by engaging in priceminimization strategies (i.e., finding ways to reduce the cost of cigarette smoking) rather than by quitting or reducing their cigarette use, thereby reducing the public health benefits of such tax increases.