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Lifestyle Induced Addictive Habits: A Socio-Physiological Issue of Kolkata, West Bengal

Authors:
  • Rammohan College, University of Calcutta
  • Rammohan College, Kolkata, West Bengal
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Somatotyping is a method of description and assessment of the body on three shape and composition scales: endomorphy (relative fatness), mesomorphy (relative musculoskeletal robustness), and ectomorphy (relative linearity). This book (the first major account of the field for thirty years) presents a comprehensive history of somatotyping, beginning with W. J. Sheldon's introduction of the method in 1940. The controversies regarding the validity of Sheldon's method are described, as are the various attempts to modify the technique, particularly the Heath-Carter method, which has come into widespread use. The book reviews present knowledge of somatotypes around the world, how they change with growth, ageing and exercise, and the contributions of genetics and environment to the rating. Also reviewed are the relationships between somatotypes and sport, physical performance, health and behaviour. Students and research workers in human biology, physical and biological anthropology and physical education will all find valuable information in this book.
Article
Background: Cigarette smoking remains the leading avoidable cause of disease burden worldwide, and observational studies have linked various smoking behaviours (active smoking, passive smoking, and smoking cessation) with risk of type 2 diabetes. We did a meta-analysis of prospective studies to investigate the associations between various smoking behaviours and diabetes risk. Methods: We systematically searched MEDLINE (up to May 3, 2015) and Embase (up to April 16, 2014) for reports of prospective studies, using search terms related to smoking, diabetes mellitus, and studies with a prospective design. We supplemented this strategy with manual searches of the reference lists of retrieved publications and relevant reviews. We included prospective studies that reported risk of type 2 diabetes by baseline smoking status. We calculated pooled relative risks (RRs) with 95% CIs using random-effects models, and did subgroup analyses by participant and study characteristics. Findings: We identified 88 eligible prospective studies with 5 898 795 participants and 295 446 incident cases of type 2 diabetes. The pooled RR of type 2 diabetes was 1·37 (95% CI 1·33-1·42) for comparing current smoking with non-smoking (84 studies with 5 853 952 participants), 1·14 (1·10-1·18) for comparing former smoking with never smoking (47 studies with 2 930 391 participants), and 1·22 (1·10-1·35) for comparing never smokers with and without exposure to passive smoke (seven studies with 156 439 participants). The associations persisted in all subgroups, and we identified a dose-response relation for current smoking and diabetes risk: compared with never smokers, the RRs were 1·21 (1·10-1·33) for light smokers, 1·34 (1·27-1·41) for moderate smokers, and 1·57 (1·47-1·66) for heavy smokers. Based on the assumption that the association between smoking and diabetes risk is causal, we estimated that 11·7% of cases of type 2 diabetes in men and 2·4% in women (ie, about 27·8 million cases in total worldwide) were attributable to active smoking. Compared with never smokers, the pooled RR from ten studies with 1 086 608 participants was 1·54 (95% CI 1·36-1·74) for new quitters (<5 years), 1·18 (1·07-1·29) for middle-term quitters (5-9 years), and 1·11 (1·02-1·20) for long-term quitters (≥10 years). Interpretation: Active and passive smoking are associated with significantly increased risks of type 2 diabetes. The risk of diabetes is increased in new quitters, but decreases substantially as the time since quitting increases. If the association between smoking and risk of type 2 diabetes is causal, public health efforts to reduce smoking could have a substantial effect on the worldwide burden of type 2 diabetes. Funding: Chinese National Thousand Talents Program for Distinguished Young Scholars, US National Institutes of Health, the Chinese National 111 Project, and the Program for Changjiang Scholars and Innovative Research Team in University from the Chinese Ministry of Education.
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Moderate alcohol consumption is associated with a reduced risk of type 2 diabetes. This reduced risk might be explained by improved insulin sensitivity or improved glycemic status, but results of intervention studies on this relation are inconsistent. The purpose of this study was to conduct a systematic review and meta-analysis of intervention studies investigating the effect of alcohol consumption on insulin sensitivity and glycemic status. PubMed and Embase were searched up to August 2014. Intervention studies on the effect of alcohol consumption on biological markers of insulin sensitivity or glycemic status of at least 2 weeks' duration were included. Investigators extracted data on study characteristics, outcome measures, and methodological quality. Fourteen intervention studies were included in a meta-analysis of six glycemic end points. Alcohol consumption did not influence estimated insulin sensitivity (standardized mean difference [SMD] 0.08 [-0.09 to 0.24]) or fasting glucose (SMD 0.07 [-0.11 to 0.24]) but reduced HbA1c (SMD -0.62 [-1.01 to -0.23]) and fasting insulin concentrations (SMD -0.19 [-0.35 to -0.02]) compared with the control condition. Alcohol consumption among women reduced fasting insulin (SMD -0.23 [-0.41 to -0.04]) and tended to improve insulin sensitivity (SMD 0.16 [-0.04 to 0.37]) but not among men. Results were similar after excluding studies with high alcohol dosages (>40 g/day) and were not influenced by dosage and duration of the intervention. Although the studies had small sample sizes and were of short duration, the current evidence suggests that moderate alcohol consumption may decrease fasting insulin and HbA1c concentrations among nondiabetic subjects. Alcohol consumption might improve insulin sensitivity among women but did not do so overall. © 2015 by the American Diabetes Association. Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered.
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The Women’s Empowerment in Agriculture Index (WEAI) measures the empowerment, agency, and inclusion of women in the agricultural sector and comprises two subindexes. The first assesses empowerment of women in five domains, including (1) decisions about agricultural production, (2) access to and decisionmaking power about productive resources, (3) control of use of income, (4) leadership in the community, and (5) time allocation. The second subindex measures the percentage of women whose achievements are at least as high as men in their households. This article documents the development of the WEAI and presents pilot findings from Bangladesh, Guatemala, and Uganda.
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The National Rural Employment Guarantee Act, which entitles rural households to 100 days of casual employment on public works at the statutory minimum wage, contains special provisions to ensure full participation of women. This paper, based on fieldwork in six states in 2008, examines the socio-economic consequences of the NREGA for women workers. In spite of the drawbacks in the implementation of the legislation, significant benefits have already started accruing to women through better access to local employment, at minimum wages, with relatively decent and safe work conditions. The paper also discusses barriers to women's participation.
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Light to moderate alcohol consumption is associated with a reduced risk for cardiovascular diseases. Epidemiologic studies, like our analysis of the European Prospective Investigation into Cancer and Nutrition study, suggest that moderate alcohol consumption is also associated with a reduced risk of type 2 diabetes, reported for various populations. This risk reduction may be explained by an increase in insulin sensitivity after moderate alcohol consumption. Indeed, a positive association between alcohol consumption and insulin sensitivity is consistently reported in cross-sectional studies. Mechanisms for the effect of alcohol on insulin sensitivity may include modulation of changes in the endocrine functioning of fat tissue, modulation of the inflammatory status of several organs, and/or modulation of glucose and fatty acid metabolism.
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Background: Alcohol may affect dietary intake. However, little is known about diets on drinking days in the US population. Objective: We determined whether the diets of drinkers differ on drinking compared with nondrinking days. Design: Data were from the 2003-2008 NHANES Mobile Examination Center interview. We identified 1864 current drinkers (1126 men and 738 women) who completed two 24-h dietary recalls, one of which was on a drinking day and the other of which was on a nondrinking day. Sex-specific repeated-measures analyses that were adjusted for dietary recall order and recall day of the week were used to compare within-individual differences in energy, nutrient, and food-group intakes. Analyses were weighted to produce representative estimates. Results: On their drinking (compared with nondrinking) days, men consumed an excess 168 nonalcohol kcal (P < 0.01), which was reflected in higher intakes of nutrients including total protein (P < 0.001), total fat (P < 0.01), saturated fat (P < 0.01), monounsaturated fat (P < 0.01), potassium (P < 0.001), and sodium (P < 0.05). Men also had higher intakes of food groups including meat (P < 0.001), white potatoes (P < 0.05), and discretionary oil and solid fat (P < 0.05) and lower intakes of total fruit (P < 0.05) and milk (P < 0.05). Women did not consume excess nonalcohol kilocalories but had higher intakes of total fat (P < 0.05), monounsaturated fat (P < 0.05), polyunsaturated fat (P < 0.05), potassium (P < 0.01), and discretionary oil and solid fat (P < 0.05) and lower intakes of milk (P < 0.01) and milk products (P < 0.01). Conclusions: These mostly moderate drinkers had poorer diets on drinking days. Same-day associations between alcohol and diet could be useful targets for public health efforts to improve dietary intake.
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A cross-sectional study was undertaken to determine anthropometric profile and the prevalence of chronic energy deficiency (CED), based on body mass index (BMI) of adult Santals, a tribal population of Jhargram, West Medinipur District, West Bengal, India. A total of 410 adult (aged > 18 years) Santals of six villages (Jharagaria, Jamiderdanga, Jamda, Jaynagar, Chapashol, and Lukudahi) near Jhargram town of West Medinipur District, West Bengal, India, were studied. These villages are located within 15 km. (approximately) from Jhargram town and 150 km. from Kolkata, the provincial capital of West Bengal. Anthropometric measurements including height, weight, and circumferences as well as BMI were measured using standard protocol. Overall, the extent of CED (BMI < 18.5) was found to be very high (36.8%). The prevalence of CED was higher in women (41.8%) compared to men (31.5%), although this difference was statistically not significant. Using the World Health Organization criterion (WHO, 199528. World Health Organization (WHO). 1995. Physical Status: The Use and Interpretation of Anthropometry, Geneva: World Health Organization. Technical Report Series no. 854 View all references) the prevalence of CED was high and the situation was serious in men. Among women, CED prevalence was very high and the situation was critical. However, compared to some other tribes of eastern India, adult Santals had better anthropometric and nutritional profile. In conclusion, this study provided evidence that although the anthropometric and nutritional profile of adult Santals was better than some of the other tribal populations of eastern India, immediate appropriate nutritional intervention programs are needed for implementation among Santals.
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J Clin Hypertens (Greenwich). 2012;14:792–798. ©2012 Wiley Periodicals, Inc. Heavy alcohol intake increases the risk of hypertension, but the relationship between light to moderate alcohol consumption and incident hypertension remains controversial. The authors sought to analyze the dose-response relationship between average daily alcohol consumption and the risk of hypertension via systematic review and meta-analysis. Electronic databases were searched for prospective control studies examining quantitative measurement of alcohol consumption and biological measurement of outcome. The primary endpoint was the risk of developing hypertension based on alcohol consumption. The level of alcohol consumption from each study was assigned to categorical groups based on the midpoint of their alcohol consumption classes to make possible the comparison of heterogeneous classification of alcohol intake. A total of 16 prospective studies (33,904 men and 193,752 women) were included in the analysis. Compared with nondrinkers, men with alcohol consumption with <10 g/d and 11 to 20 g/d had a trend toward increased risk of hypertension (relative risk [RR], 1.03; 95% confidence interval [CI], 0.94–1.13; P=.51) and (RR, 1.15; 95% CI, 0.99–1.33; P=.06), respectively, whereas a significantly increased risk of hypertension was found with heavy alcohol consumption of 31 to 40 g/d (RR, 1.77; 95% CI, 1.39–2.26; P<.001) and >50 g/d (RR, 1.61; 95% CI, 1.38–1.87; P<.001). Among women, the meta-analysis indicated protective effects at <10 g/d (RR, 0.87; 95% CI, 0.82–0.92; P<.001) and a trend toward decreased risk of hypertension with alcohol consumption 11 to 20 g/d (RR, 0.9; 95% CI, 0.87–1.04; P=.17), whereas a significantly increased risk of hypertension was indicated with heavy alcohol consumption of 21 to 30 g/d (RR, 1.16; 95% CI, 0.91–1.46; P=.23) and 31 to 40 g/d (RR, 1.19; 95% CI, 1.07–1.32; P=.002). In men, heavy alcohol consumption is associated with increased risk of hypertension, whereas there is a trend toward increased risk of hypertension with low and moderate alcohol consumption. The relationship between alcohol consumption and hypertension is J-shaped in women. Limiting alcohol intake should be advised for both men and women.
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Background: Transthoracic echocardiography was used in a rodent animal model to determine whether long-term alcohol consumption (8 and 12 months) was associated with the development of a dilated cardiomyopathy. We also investigated whether alcohol-induced changes in cardiac structure corresponded to activation of the renin-angiotensin system and the natriuretic peptide (NP) system. Methods: Male rats received either the Lieber-DeCarli liquid alcohol diet (EtOH) (9%v/v) (n= 8) or control diet (CON) (n= 8). Echocardiography (echo) was used to determine left-ventricular (LV) dimensions, and isolated heart studies (Langendorff and atrium) were used to assess ex vivo contractility. Plasma and tissue angiotensin-I converting enzyme (ACE) activity was measured. Gene expression, plasma, and tissue levels of the NPs were determined by northern blot analysis and radioimmunoassay, respectively. Results: After 8 months of alcohol consumption, there was a trend for the end diastolic dimension, end systolic dimension, and LV mass to be greater in the 8 month EtOH group compared with the CON group. However, after 12 months of alcohol consumption, significant increases were found between the groups in several echo parameters. Tissue ACE activity (nmoles/min/mg protein) was greater in the 12 month EtOH group compared with the 12 month CON and 8 month EtOH group (p < 0.05). We found no differences between groups in gene expression (messenger RNA), plasma, and tissue levels of the NPs. Conclusions: Echocardiography revealed that 8 to 12 months of alcohol consumption was associated with the development of a dilated cardiomyopathy. However, this was not preceded by an increase in tissue ACE activity, and these changes occurred in the absence of increased plasma and LV tissue levels of the NPs.
Article
Alcohol and nicotine, in the form of tobacco, are commonly co-abused. Nicotinic receptors also have been implicated in alcohol action. We designed the present study to examine the possible involvement of nicotinic receptors in alcohol self-administration. Pretreatment with lower doses (0.1–0.4 mg/kg) of nicotine, administered acutely or chronically, did not affect alcohol consumption, whereas a higher dose (0.8 mg/kg) initially suppressed alcohol consumption but stimulated alcohol consumption on repeated treatment. We observed the same pattern of nicotine effects on alcohol self-administration using an operant procedure. A dose of 0.8 mg/kg of nicotine initially suppressed operant responding for alcohol. Such suppression of alcohol self-administration was more pronounced during the first 20 min of the 60 min operant session. Responding for alcohol in the nicotine treated group, however, was significantly increased above the saline treated group by the 5th day of treatment. Mecamylamine, a noncompetitive nicotinic receptor antagonist, reduced alcohol consumption, whereas dihydro-β-erythroidine (DHβE), a competitive nicotinic receptor antagonist, did not modify alcohol consumption. The stimulation of alcohol intake induced by nicotine treatment and the suppression of alcohol intake induced by mecamylamine provide evidence for the involvement of nicotinic receptors in alcohol consumption and/or self-administration. The failure of DHβE to reduce alcohol consumption, however, suggests that ethanol-nicotine interaction is mediated by other nicotinic receptor subtypes rather than α4β2 receptor subtype, or that mecamylamine acts through a nonnicotinic mechanism.
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To evaluate the association between current and lifetime alcohol consumption, and overall and central obesity in adults of an urban Portuguese population. Participants were randomly selected from the non-institutionalized Porto inhabitants, aged ≥18 years (EPIPorto Study: 1999-2003). The study included 2366 participants for evaluating current alcohol consumption and overall obesity, and 2377 participants for central obesity. A trained interviewer applied a questionnaire and anthropometrics were measured. Data on alcohol intake were obtained by using a food frequency questionnaire. Overall obesity was considered when body mass index was ≥30.0 kg/m(2), and central obesity when waist circumference (WC) was ≥88 cm in women and ≥102 cm in men. Odds ratios (OR) and 95% confidence intervals (95% CI) were calculated, separately by sex, using unconditional logistic regression models. After adjustment for age, education, smoking, energy intake and regular physical exercise, men who consumed >60g/day of alcohol were more frequently obese compared with non-drinkers (OR=2.26, 95% CI: 1.17-4.35). When considering lifetime alcohol consumption, the magnitude of the association was stronger in both women (OR=2.41, 95% CI: 1.28-4.56) and men (OR=4.22, 95% CI: 1.93-9.24). For central obesity, women consuming 15.1-30 g/day and >30 g/day had higher probability of being obese, considering both current and lifetime alcohol consumption. In men, the same positive associations were observed, which were particularly stronger between lifetime alcohol consumption and central obesity (>60g/day vs non-drinkers: OR=4.02, 95% CI: 1.80-8.98). Independently of social and behavioural features, current and lifetime alcohol consumption were positively associated with overall and central obesity, in both women and men.
Article
It was hypothesized that both thrombogenic and atherogenic factors may be responsible for premature coronary heart disease (CHD) in young Indians. A case-control study was performed to determine cardiovascular risk factors in young patients with CHD in India. Successive consenting patients <55 yr with an acute coronary event or recent diagnosis of CHD were enrolled (cases, n=165). Age- and gender-matched subjects with no clinical evidence of CHD were recruited as controls (n=199). Demographic, anthropometric, clinical, haematological, and biochemical data were obtained in both groups. Univariate and multivariate logistic regression were performed to identify important risk factors. In cases vs. controls mean systolic BP, diastolic BP, platelet counts, LDL cholesterol, non-HDL cholesterol, triglycerides, and fibrinogen were higher and HDL cholesterol lower (P<0.001). The presence of current smoking, low fruit and vegetables intake, high fat intake, hypertension, diabetes, low HDL cholesterol, and high LDL cholesterol, total:HDL ratio, fibrinogen and homocysteine was significantly higher in cases (P<0.05). Multivariate logistic regression analysis (age adjusted odds ratio, 95% confidence intervals) revealed that smoking (19.41, 6.82-55.25), high fat intake (1.66, 1.08-2.56), low fruit and vegetables intake (1.99, 1.11-3.59), hypertension (8.95, 5.42-14.79), high LDL cholesterol [2.49 (1.62-3.84)], low HDL cholesterol (10.32, 6.30-16.91), high triglycerides (3.62, 2.35-5.59) high total:HDL cholesterol (3.87, 2.35-5.59), high fibrinogen (2.87, 1.81-4.55) and high homocysteine (10.54, 3.11-35.78) were significant. Our results showed that thrombotic (smoking, low fruit/vegetables intake, fibrinogen, homocysteine) as well as atherosclerotic (hypertension, high fat diet, dyslipidaemia) risk factors were important in premature CHD. Multipronged prevention strategies are needed in young Indian subjects.
Article
The body composition of 99 men and 89 women from south India was estimated using hydrodensitometry, bioelectrical impedance and skinfold thickness. Comparisons of the hydrodensitometry (reference method) and skinfold methods showed that there were no significant differences between the methods, for estimates of fat free mass (FFM) and per cent fat. The mean difference between the estimates FFM (bias), from skinfold measurement and hydrodensitometry was small for both groups (+0.16 +/- 1.09 kg in men and +0.67 +/- 0.9 kg in women). The same trend was observed in per cent fat estimates (-0.37 +/- 2.04 in men and -1.49 +/- 2.28 in women), showing that the skinfold method can be used as an accurate and expedient method to determine body composition. The bioelectrical impedance method obtained a significantly lower FFM and higher body fat than the reference (hydrodensitometry) method. This could have been due to the use of an inappropriate equation derived from Western population studies. Hence, a new predictive equation, for the measurement of FFM by the bioelectrical impedance method was derived for this population, using the variables of height2/impedance and FFM measured by underwater weighing. The new equation for the bioelectrical impedance method then gave values of body composition which compared well (0.26 +/- 2.32 kg) in men and (0.36 +/- 2.49 kg) in women with the hydrodensitometry method.
Article
Cigarette smoking is a major independent risk factor for cardiovascular disease. While the association between chronic smoking and cardiovascular disease is well established, the underlying mechanisms are incompletely understood, partly due to the lack of adequate in vivo animal models. Here, we report a mouse model of chronic smoking-induced cardiovascular pathology. Male C57BL/6J mice were exposed to whole body mainstream cigarette smoke (CS) using a SCIREQ "InExpose" smoking system (48 min/day, 5 days/wk) for 16 or 32 wk. Age-matched, air-exposed mice served as nonsmoking controls. Blood pressure was measured, and cardiac MRI was performed. In vitro vascular ring and isolated heart experiments were performed to measure vascular reactivity and cardiac function. Blood from control and smoking mice was studied for the nitric oxide (NO) decay rate and reactive oxygen species (ROS) generation. With 32 wk of CS exposure, mice had significantly less body weight gain and markedly higher blood pressure. At 32 wk of CS exposure, ACh-induced vasorelaxation was significantly shifted to the right and downward, left ventricular mass was significantly larger along with an increased heart-to-body weight ratio, in vitro cardiac function tended to be impaired with high afterload, white blood cells had significantly higher ROS generation, and the blood NO decay rate was significantly faster. Thus, smoking led to blunted weight gain, hypertension, endothelial dysfunction, leukocyte activation with ROS generation, decreased NO bioavailability, and mild cardiac hypertrophy in mice that were not otherwise predisposed to disease. This mouse model is a useful tool to enable further elucidation of the molecular and cellular mechanisms of smoking-induced cardiovascular diseases.
Article
A short-term increase in fine particulate matter air pollution (PM(2.5)) concentration increases the risk for myocardial infarctions, strokes, and heart failure exacerbations. An important mechanism likely contributing to these associations is an elevation in arterial blood pressure (BP). Exposure to ambient PM(2.5) even at present-day concentrations can increase BP within a period of a few days while long-term exposure might also promote the development of chronic hypertension. Controlled human and animal experiments have corroborated the veracity of these findings and elucidated plausible biological mechanisms. PM(2.5) deposition within the pulmonary tree is capable of rapidly triggering autonomic nervous system imbalance, thereby increasing BP within minutes of inhalation. In addition, fine particles can instigate a systemic pro-inflammatory response over a more prolonged period of exposure. Higher circulating levels of activated immune cells and inflammatory cytokines could consequently cause vascular endothelial dysfunction leading to an imbalance in vascular homeostatic responses. Indeed, chronic PM(2.5) exposure augments pro-vasoconstrictive pathways while blunting vasodilator capacity. Finally, certain particle constituents (e.g., metals, organic compounds, and ultra-fine particles) might also be capable of reaching the systemic circulation upon inhalation and thereafter directly impair vascular function. At the molecular level, the generation of oxidative stress with the consequent up-regulation of redox sensitive pathways appears to be a common and fundamental mechanism involved in the instigation of these pro-hypertensive responses. Due to the ubiquitous, continuous and often involuntary nature of exposure, PM(2.5) may be an important and under-appreciated worldwide environmental risk factor for increased arterial BP.
Article
Elevated resting heart rate (RHR) is known to be associated with reduced survival but inconsistencies remain, including lack of significance in most studies of healthy women, lack of independence from systolic blood pressure (SBP) in some, and the suggestion that RHR is merely functioning as a marker of physical inactivity or other comorbidities. We aimed to clarify these inconsistencies. We analyzed the effect of RHR on end points in the National FINRISK Study; a representative, prospective study using Cox proportional hazards model. Ten-thousand five-hundred nineteen men and 11,334 women were included, excluding those with preexisting coronary heart disease, angina, heart failure, or on antihypertensive therapy. The hazard ratios for cardiovascular disease (CVD) mortality for each 15 beats/min increase in RHR were 1.24 (1.11-1.40) in men and 1.32 (1.08-1.60) in women, adjusted for age, gender, total cholesterol, physical activity (categorical), SBP, body mass index, and high-density lipoprotein cholesterol. This relationship remained significant after exclusion of those with comorbidities and events occurring within first 2 years of observation. Relationship with coronary mortality was stronger and with total mortality was slightly weaker. Inclusion of nonfatal end points weakened the relationship. A strong, graded, independent relationship between RHR and incident CVD was demonstrated. This was consistent in healthy men and women. We have clarified that the relationship is independent of SBP and that the temporal sequence would be compatible with a causal relationship. New findings include independence from both a validated measure of physical activity and comorbidities and the demonstration of a stronger effect for fatal than nonfatal events, supporting increased arrhythmogenicity of one of the mechanisms.
Article
As part of a larger study to estimate the global burden of disease and injury attributable to alcohol: to evaluate the evidence for a causal impact of average volume of alcohol consumption and pattern of drinking on diseases and injuries; to quantify relationships identified as causal based on published meta-analyses; to separate the impact on mortality versus morbidity where possible; and to assess the impact of the quality of alcohol on burden of disease. Systematic literature reviews were used to identify alcohol-related diseases, birth complications and injuries using standard epidemiological criteria to determine causality. The extent of the risk relations was taken from meta-analyses. Evidence of a causal impact of average volume of alcohol consumption was found for the following major diseases: tuberculosis, mouth, nasopharynx, other pharynx and oropharynx cancer, oesophageal cancer, colon and rectum cancer, liver cancer, female breast cancer, diabetes mellitus, alcohol use disorders, unipolar depressive disorders, epilepsy, hypertensive heart disease, ischaemic heart disease (IHD), ischaemic and haemorrhagic stroke, conduction disorders and other dysrhythmias, lower respiratory infections (pneumonia), cirrhosis of the liver, preterm birth complications and fetal alcohol syndrome. Dose-response relationships could be quantified for all disease categories except for depressive disorders, with the relative risk increasing with increased level of alcohol consumption for most diseases. Both average volume and drinking pattern were linked causally to IHD, fetal alcohol syndrome and unintentional and intentional injuries. For IHD, ischaemic stroke and diabetes mellitus beneficial effects were observed for patterns of light to moderate drinking without heavy drinking occasions (as defined by 60+ g pure alcohol per day). For several disease and injury categories, the effects were stronger on mortality compared to morbidity. There was insufficient evidence to establish whether quality of alcohol had a major impact on disease burden. Overall, these findings indicate that alcohol impacts many disease outcomes causally, both chronic and acute, and injuries. In addition, a pattern of heavy episodic drinking increases risk for some disease and all injury outcomes. Future studies need to address a number of methodological issues, especially the differential role of average volume versus drinking pattern, in order to obtain more accurate risk estimates and to understand more clearly the nature of alcohol-disease relationships.
Article
Effective tobacco control efforts have resulted in substantial declines in tobacco use and tobacco-related cancer deaths in the United States. Nearly 40% of reductions in male lung cancer deaths between 1991 and 2003 can be attributed to smoking declines in the last half century. Nevertheless, tobacco use still remains the single, largest preventable cause of disease and premature death in the United States. Each year, smoking and exposure to secondhand smoke result in nearly half a million premature deaths of which nearly one-third are due to cancer. In a previous report, we described youth and adult smoking prevalence and patterns and discussed policy measures that had proven effective in comprehensive tobacco control. In this report, we update trends in youth and adult smoking prevalence. We find that while adult smoking prevalence has declined overall, socioeconomic gradients in smoking still persist within race and ethnic subgroups. In addition, we describe the diffusion of tobacco-control strategies at the national, state, and community level. Although recent developments, such as the Food and Drug Administration's (FDA) regulation of tobacco products, hold promise for tobacco control, there continues to be a need for broader dissemination of sustainably funded comprehensive national and state tobacco-control programs.
Article
Cigarette smoking is the major cause of preventable morbidity and mortality in the United States and constitutes a major risk factor for atherosclerotic vascular disease, including coronary artery disease and stroke. Increasing evidence supports the hypothesis that oxidative stress and inflammation provide the pathophysiological link between cigarette smoking and CAD. Previous studies have shown that cigarette smoke activates leukocytes to release reactive oxygen and nitrogen species (ROS/RNS) and secrete pro-inflammatory cytokines, increases the adherence of monocytes to the endothelium and elicits airway inflammation. Here we present an overview of the direct effects of water-soluble cigarette smoke constituents on endothelial function, vascular ROS production and inflammatory gene expression. The potential pathogenetic role of peroxynitrite formation, and downstream mechanisms including poly(ADP-ribose) polymerase (PARP) activation in cardiovascular complications in smokers are also discussed.