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Benjamin W. Chaffee

Bio: Benjamin W. Chaffee is an academic researcher from University of California, San Francisco. The author has contributed to research in topics: Smokeless tobacco & Population. The author has an hindex of 23, co-authored 94 publications receiving 2011 citations. Previous affiliations of Benjamin W. Chaffee include Massachusetts Institute of Technology & University of California, Berkeley.


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Journal ArticleDOI
TL;DR: A positive association was consistent and coherent with a biologically plausible role for obesity in the development of periodontal disease, however, with few quality longitudinal studies, there is an inability to distinguish the temporal ordering of events, limiting the evidence that obesity is a risk factor for periodonta disease or that periodontitis might increase the risk of weight gain.
Abstract: Background: Obesity is increasing in prevalence and is a major contributor to worldwide morbidity. One consequence of obesity might be an increased risk for periodontal disease, although periodontal inflammation might, in turn, exacerbate the metabolic syndrome, of which obesity is one component. This review aims to systematically compile the evidence of an obesity–periodontal disease relationship from epidemiologic studies and to derive a quantitative summary of the association between these disease states. Methods: Systematic searches of the MEDLINE, SCOPUS, BIOSIS, LILACS, Cochrane Library, and Brazilian Bibliography of Dentistry databases were conducted with the results and characteristics of relevant studies abstracted to standardized forms. A meta-analysis was performed to obtain a summary measure of association. Results: The electronic search identified 554 unique citations, and 70 studies met a priori inclusion criteria, representing 57 independent populations. Nearly all studies matching inclusion criteria were cross-sectional in design with the results of 41 studies suggesting a positive association. The fixed-effects summary odds ratio was 1.35 (Shore-corrected 95% confidence interval: 1.23 to 1.47), with some evidence of a stronger association found among younger adults, women, and non-smokers. Additional summary estimates suggested a greater mean clinical attachment loss among obese individuals, a higher mean body mass index (BMI) among periodontal patients, and a trend of increasing odds of prevalent periodontal disease with increasing BMI. Although these results are highly unlikely to be chance findings, unmeasured confounding had a credible but unknown influence on these estimates. Conclusions: This positive association was consistent and coherent with a biologically plausible role for obesity in the development of periodontal disease. However, with few quality longitudinal studies, there is an inability to distinguish the temporal ordering of events, thus limiting the evidence that obesity is a risk factor for periodontal disease or that periodontitis might increase the risk of weight gain. In clinical practice, a higher prevalence of periodontal disease should be expected among obese adults. J Periodontol 2010;81:1708-1724.

434 citations

Journal ArticleDOI
TL;DR: Any use of e-cigarettes, hookah, noncigarette combustible tobacco, or smokeless tobacco was independently associated with cigarette smoking 1 year later, and use of more than 1 product increased the odds of progressing to cigarette use.
Abstract: Importance Approximately 90% of adult smokers first tried a cigarette by 18 years of age, and even infrequent smoking in adolescence is associated with established adult smoking. Noncigarette tobacco use is increasing and could stimulate subsequent conventional cigarette smoking in youths. Objective To estimate the longitudinal association between noncigarette tobacco use and subsequent cigarette smoking initiation among US youth. Design, Setting, and Participants In this prospective cohort study of the Population Assessment of Tobacco and Health (PATH) waves 1 (September 12, 2013, to December 14, 2014) and 2 (October 23, 2014, to October 30, 2015), a nationally representative sample of youths who never smoked a conventional cigarette at baseline and completed wave 2 follow-up (N = 10 384) was studied. PATH retention at follow-up was 87.9%. Exposures Ever use and past 30-day use of electronic cigarettes (e-cigarettes), hookah, noncigarette combustible tobacco, or smokeless tobacco at baseline. Main Outcomes and Measures Ever use and past 30-day use of cigarettes at follow-up. Results The present analysis was based on the 10 384 PATH youth respondents who reported never having smoked a cigarette in wave 1 and whose cigarette ever or past 30-day use was reported in wave 2 (mean [SD] age, 14.3 [1.7] years; age range, 12-17 years; 5087 [49.1%] female; 4829 [52.5%] white). At 1-year follow-up, 469 (4.6%) of all baseline never-smoking youths had tried a cigarette and 219 (2.1%) had smoked a cigarette within the past 30 days. Cigarette ever use at follow-up was higher among youths who had ever used e-cigarettes (78 [19.1%]), hookah (60 [18.3%]), noncigarette combustible tobacco (45 [19.2%]), or smokeless tobacco (29 [18.8%]) at baseline. After adjusting for sociodemographic, environmental, and behavioral smoking risk factors and for baseline ever use of other tobacco products, the odds of past 30-day cigarette use at follow-up were approximately twice as high among baseline ever users of e-cigarettes (odds ratio [OR], 1.87; 95% CI, 1.15-3.05), hookah (OR, 1.92; 95% CI, 1.17-3.17), noncigarette combustible tobacco (OR, 1.78; 95% CI, 1.00-3.19), and smokeless tobacco (OR, 2.07; 95% CI, 1.10-3.87). Youths who had tried more than 1 type of tobacco product at baseline had 3.81 (95% CI, 2.22-6.54) greater adjusted odds of past 30-day cigarette smoking at follow-up than did baseline never tobacco users. Conclusions and Relevance Any use of e-cigarettes, hookah, noncigarette combustible tobacco, or smokeless tobacco was independently associated with cigarette smoking 1 year later. Use of more than 1 product increased the odds of progressing to cigarette use.

181 citations

Journal ArticleDOI
TL;DR: Dental caries was associated with negative child and family experiences and lower OHRQoL across all social groups; yet, families facing greater disadvantage may report lesser quality-of-life impact at the same level of disease experience.
Abstract: Objectives (i) Quantify the relative association between child dental caries experience and maternal-reported child oral health-related quality of life (OHRQoL); (ii) examine whether that association differed according to family socioeconomic status (SES); and (iii) explore whether absolute OHRQoL varied by family SES at similar levels of child caries experience. Methods This study was a cross-sectional analysis of children in southern Brazil (n=456, mean age: 38 months) participating in an existing health centre-based intervention study. OHRQoL impact was quantified as mean score on the Brazilian Early Childhood Oral Health Impact Scale (ECOHIS) and compared over categories of caries experience (dmft: 0, dmft: 1-4, dmft: ≥5). Adjusted ECOHIS ratios between caries categories were calculated using regression modelling, overall and within socioeconomic strata defined by maternal education, social class and household income. Results Caries prevalence (dmft >0) was 39.7%, mean ECOHIS score was 2.0 (SD: 3.5), and 44.3% of mothers reported OHRQoL impact (ECOHIS score >0). Increasing child caries experience was associated with worsening child and family quality of life: ECOHIS scores were 3.0 times greater (95% CI: 2.0, 4.4) for children with dmft ≥5 vs dmft=0, a pattern that persisted regardless of family socioeconomic status (P for interaction: all >0.3). However, adjusted for dental status and sociodemographic characteristics, mean ECOHIS scores were lower when reported by mothers of less educational attainment (ratio: 0.7; 95% CI: 0.5, 1.0), lower social class (ratio: 0.7; 95% CI: 0.5, 1.0) or in lower income households (ratio: 0.8; 95% CI: 0.6, 1.3). Conclusion Dental caries was associated with negative child and family experiences and lower OHRQoL across all social groups; yet, families facing greater disadvantage may report lesser quality-of-life impact at the same level of disease experience. Thus, subjective quality-of-life measures may differ under varying social contexts, with possible implications for service utilization, evaluating oral health interventions, or quantifying disease morbidity in low-SES groups.

132 citations

Journal ArticleDOI
TL;DR: Among adolescent cigarette experimenters, using e-cigarette was positively and independently associated with progression to current established smoking, suggesting that e-cigarettes do not divert from, and may encourage, cigarette smoking in this population.
Abstract: BACKGROUND: It has been shown that never-smoking adolescents who try electronic cigarettes (e-cigarettes) are at increased risk of subsequent conventional cigarette smoking. We evaluated associations between e-cigarette use and progression to established smoking among adolescents who had already tried cigarettes. METHODS: Among participants (age 12–17 years) in the nationally representative Population Assessment of Tobacco and Health survey who had smoked a cigarette (≥1 puff) but not yet smoked 100 cigarettes ( N = 1295), we examined 3 outcomes at 1-year follow-up as a function of baseline e-cigarette use: (1) having smoked ≥100 cigarettes (established smoking), (2) smoking during the past 30 days, and (3) both having smoked ≥100 cigarettes and past 30-day smoking (current established smoking). Survey-weighted multivariable logistic regression models were fitted to obtain odds ratios (ORs) and 95% confidence intervals (CIs) adjusted for smoking risk factors. RESULTS: Versus e-cigarette never use, having ever used e-cigarettes was positively associated with progression to established cigarette smoking (19.3% vs 9.7%), past 30-day smoking (38.8% vs 26.6%), and current established smoking (15.6% vs 7.1%). In adjusted models, e-cigarette ever use positively predicted current established smoking (OR: 1.80; 95% CI: 1.04–3.12) but did not reach statistical significance (α = .05) for established smoking (OR: 1.57; 95% CI: 0.99–2.49) and past 30-day smoking (OR: 1.32; 95% CI: 0.99–1.76). CONCLUSIONS: Among adolescent cigarette experimenters, using e-cigarettes was positively and independently associated with progression to current established smoking, suggesting that e-cigarettes do not divert from, and may encourage, cigarette smoking in this population.

130 citations

Journal ArticleDOI
TL;DR: The overall public health benefit of zinc supplementation in pregnancy appears limited and might reflect a reduction in maternal infection, a primary cause of prematurity, while further study would be needed to explore this possibility in detail.
Abstract: Poor maternal zinc status has been associated with foetal loss, congenital malformations, intra-uterine growth retardation, reduced birth weight, prolonged labour and preterm or post-term deliveries. A meta-analysis completed in 2007 showed that maternal zinc supplementation resulted in a small but significant reduction in preterm birth. The purposes of this analysis are to update that previous review and expand the scope of assessment to include maternal, infant and child health outcomes. Electronic searches were carried out to identify peer-reviewed, randomised controlled trials where daily zinc supplementation was given for at least one trimester of pregnancy. The co-authors applied the study selection criteria, assessed trial quality and abstracted data. A total of 20 independent intervention trials involving more than 11,000 births were identified. The 20 trials took place across five continents between 1977 and 2008. Most studies assessed the zinc effect against a background of other micronutrient supplements, but five were placebo-controlled trials of zinc alone. The provided dose of supplemental zinc ranged from 5 to 50 mg/day. Only the risk of preterm birth reached statistical significance (summary relative risk 0.86 [95% confidence interval 0.75, 0.99]). There was no evidence that supplemental zinc affected any parameter of foetal growth (risk of low birth weight, birth weight, length at birth or head circumference at birth). Six of the 20 trials were graded as high quality. The evidence that maternal zinc supplementation lowers the risk of preterm birth was graded low; evidence for a positive effect on other foetal outcomes was graded as very low. The effect of zinc supplementation on preterm birth, if causal, might reflect a reduction in maternal infection, a primary cause of prematurity. While further study would be needed to explore this possibility in detail, the overall public health benefit of zinc supplementation in pregnancy appears limited.

106 citations


Cited by
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TL;DR: March 5, 2019 e1 WRITING GROUP MEMBERS Emelia J. Virani, MD, PhD, FAHA, Chair Elect On behalf of the American Heart Association Council on Epidemiology and Prevention Statistics Committee and Stroke Statistics Subcommittee.
Abstract: March 5, 2019 e1 WRITING GROUP MEMBERS Emelia J. Benjamin, MD, ScM, FAHA, Chair Paul Muntner, PhD, MHS, FAHA, Vice Chair Alvaro Alonso, MD, PhD, FAHA Marcio S. Bittencourt, MD, PhD, MPH Clifton W. Callaway, MD, FAHA April P. Carson, PhD, MSPH, FAHA Alanna M. Chamberlain, PhD Alexander R. Chang, MD, MS Susan Cheng, MD, MMSc, MPH, FAHA Sandeep R. Das, MD, MPH, MBA, FAHA Francesca N. Delling, MD, MPH Luc Djousse, MD, ScD, MPH Mitchell S.V. Elkind, MD, MS, FAHA Jane F. Ferguson, PhD, FAHA Myriam Fornage, PhD, FAHA Lori Chaffin Jordan, MD, PhD, FAHA Sadiya S. Khan, MD, MSc Brett M. Kissela, MD, MS Kristen L. Knutson, PhD Tak W. Kwan, MD, FAHA Daniel T. Lackland, DrPH, FAHA Tené T. Lewis, PhD Judith H. Lichtman, PhD, MPH, FAHA Chris T. Longenecker, MD Matthew Shane Loop, PhD Pamela L. Lutsey, PhD, MPH, FAHA Seth S. Martin, MD, MHS, FAHA Kunihiro Matsushita, MD, PhD, FAHA Andrew E. Moran, MD, MPH, FAHA Michael E. Mussolino, PhD, FAHA Martin O’Flaherty, MD, MSc, PhD Ambarish Pandey, MD, MSCS Amanda M. Perak, MD, MS Wayne D. Rosamond, PhD, MS, FAHA Gregory A. Roth, MD, MPH, FAHA Uchechukwu K.A. Sampson, MD, MBA, MPH, FAHA Gary M. Satou, MD, FAHA Emily B. Schroeder, MD, PhD, FAHA Svati H. Shah, MD, MHS, FAHA Nicole L. Spartano, PhD Andrew Stokes, PhD David L. Tirschwell, MD, MS, MSc, FAHA Connie W. Tsao, MD, MPH, Vice Chair Elect Mintu P. Turakhia, MD, MAS, FAHA Lisa B. VanWagner, MD, MSc, FAST John T. Wilkins, MD, MS, FAHA Sally S. Wong, PhD, RD, CDN, FAHA Salim S. Virani, MD, PhD, FAHA, Chair Elect On behalf of the American Heart Association Council on Epidemiology and Prevention Statistics Committee and Stroke Statistics Subcommittee

5,739 citations

Journal ArticleDOI
TL;DR: The extent and consequences of oral diseases, their social and commercial determinants, and their ongoing neglect in global health policy are described to highlight the urgent need to address oral diseases among other NCDs as a global health priority.

1,349 citations

Journal ArticleDOI
TL;DR: Emerging evidence to support the existence of a two-way relationship between diabetes and periodontitis, with diabetes increasing the risk for periodontococcal inflammation, andperiodontal inflammation negatively affecting glycaemic control is supported.
Abstract: Periodontitis is a common chronic inflammatory disease characterised by destruction of the supporting structures of the teeth (the periodontal ligament and alveolar bone). It is highly prevalent (severe periodontitis affects 10–15% of adults) and has multiple negative impacts on quality of life. Epidemiological data confirm that diabetes is a major risk factor for periodontitis; susceptibility to periodontitis is increased by approximately threefold in people with diabetes. There is a clear relationship between degree of hyperglycaemia and severity of periodontitis. The mechanisms that underpin the links between these two conditions are not completely understood, but involve aspects of immune functioning, neutrophil activity, and cytokine biology. There is emerging evidence to support the existence of a two-way relationship between diabetes and periodontitis, with diabetes increasing the risk for periodontitis, and periodontal inflammation negatively affecting glycaemic control. Incidences of macroalbuminuria and end-stage renal disease are increased twofold and threefold, respectively, in diabetic individuals who also have severe periodontitis compared to diabetic individuals without severe periodontitis. Furthermore, the risk of cardiorenal mortality (ischaemic heart disease and diabetic nephropathy combined) is three times higher in diabetic people with severe periodontitis than in diabetic people without severe periodontitis. Treatment of periodontitis is associated with HbA1c reductions of approximately 0.4%. Oral and periodontal health should be promoted as integral components of diabetes management.

1,110 citations

Journal ArticleDOI
TL;DR: Many of the systemic risk factors for periodontal disease, such as smoking, diabetes and obesity, and osteoporosis in postmenopausal women, are relatively common and can be expected to affect most patients with periodontals seen in clinics and dental practices.
Abstract: Risk factors play an important role in an individual's response to periodontal infection. Identification of these risk factors helps to target patients for prevention and treatment, with modification of risk factors critical to the control of periodontal disease. Shifts in our understanding of periodontal disease prevalence, and advances in scientific methodology and statistical analysis in the last few decades, have allowed identification of several major systemic risk factors for periodontal disease. The first change in our thinking was the understanding that periodontal disease is not universal, but that severe forms are found only in a portion of the adult population who show abnormal susceptibility. Analysis of risk factors and the ability to statistically adjust and stratify populations to eliminate the effects of confounding factors have allowed identification of independent risk factors. These independent but modifiable, risk factors for periodontal disease include lifestyle factors, such as smoking and alcohol consumption. They also include diseases and unhealthy conditions such as diabetes mellitus, obesity, metabolic syndrome, osteoporosis, and low dietary calcium and vitamin D. These risk factors are modifiable and their management is a major component of the contemporary care of many periodontal patients. Genetic factors also play a role in periodontal disease and allow one to target individuals for prevention and early detection. The role of genetic factors in aggressive periodontitis is clear. However, although genetic factors (i.e., specific genes) are strongly suspected to have an association with chronic adult periodontitis, there is as yet no clear evidence for this in the general population. It is important to pursue efforts to identify genetic factors associated with chronic periodontitis because such factors have potential in identifying patients who have a high susceptibility for development of this disease. Many of the systemic risk factors for periodontal disease, such as smoking, diabetes and obesity, and osteoporosis in postmenopausal women, are relatively common and can be expected to affect most patients with periodontal disease seen in clinics and dental practices. Hence, risk factor identification and management has become a key component of care for periodontal patients.

853 citations

Journal ArticleDOI
TL;DR: Meta-analyses conclude that periodontal therapy in individuals with diabetes mellitus can result in a modest improvement of glycemic control and increased patient awareness of the link between Diabetes mellitus and oral health and collaboration among medical and dental professionals for the management of affected individuals become increasingly important.
Abstract: Diabetes mellitus (a group of metabolic disorders characterized by hyperglycemia) and periodontitis (a microbially induced inflammatory disorder that affects the supporting structures of teeth) are both common, chronic conditions. Multiple studies have demonstrated that diabetes mellitus (type 1 and type 2) is an established risk factor for periodontitis. Findings from mechanistic studies indicate that diabetes mellitus leads to a hyperinflammatory response to the periodontal microbiota and also impairs resolution of inflammation and repair, which leads to accelerated periodontal destruction. The cell surface receptor for advanced glycation end products and its ligands are expressed in the periodontium of individuals with diabetes mellitus and seem to mediate these processes. The association between the two diseases is bidirectional, as periodontitis has been reported to adversely affect glycemic control in patients with diabetes mellitus and to contribute to the development of diabetic complications. In addition, meta-analyses conclude that periodontal therapy in individuals with diabetes mellitus can result in a modest improvement of glycemic control. The effect of periodontal infections on diabetes mellitus is potentially explained by the resulting increase in levels of systemic proinflammatory mediators, which exacerbates insulin resistance. As our understanding of the relationship between diabetes mellitus and periodontitis deepens, increased patient awareness of the link between diabetes mellitus and oral health and collaboration among medical and dental professionals for the management of affected individuals become increasingly important.

702 citations