Additional Adjustment For Smoking Research Articles

Association of blood cell-based inflammatory markers with gut microbiota and cancer incidence in the Rotterdam study.

The immune response-gut microbiota interaction is implicated in various human diseases, including cancer. Identifying the link between the gut microbiota and systemic inflammatory markers and their association with cancer will be important for our understanding of cancer etiology. The current study was performed on 8090 participants from the population-based Rotterdam study. We found a significant association (false discovery rate [FDR] ≤0.05) between lymphocytes and three gut microbial taxa, namely the family Streptococcaceae, genus Streptococcus, and order Lactobacillales. In addition, we identified 95 gut microbial taxa that were associated with inflammatory markers (p < 0.05). Analyzing the cancer data, we observed a significant association between higher systemic immune-inflammation index (SII) levels at baseline (hazard ratio (HR): 1.65 [95% confidence interval (CI); 1.10-2.46, p ≤ 0.05]) and a higher count of lymphocytes (HR: 1.38 [95% CI: 1.15-1.65, p ≤ 0.05]) and granulocytes (HR: 1.69 [95% CI: 1.40-2.03, p ≤ 0.05]) with increased risk of lung cancer after adjusting for age, sex, body mass index (BMI), and study cohort. This association was lost for SII and lymphocytes after additional adjustment for smoking (SII = HR:1.46 [95% CI: 0.96-2.22, p = 0.07] and lymphocytes = HR: 1.19 [95% CI: 0.97-1.46, p = 0.08]). In the stratified analysis, higher count of lymphocyte and granulocytes at baseline were associated with an increased risk of lung cancer in smokers after adjusting for age, sex, BMI, and study cohort (HR: 1.33 [95% CI: 1.09-1.62, p ≤0.05] and HR: 1.57 [95% CI: 1.28-1.92, p ≤0.05], respectively). Our study revealed a positive association between gut microbiota, higher SII levels, and higher lymphocyte and granulocyte counts, with an increased risk of developing lung cancer.

Association between ischemic heart disease and dietary intake of lycopene: a case-control study.

The effect of dietary lycopene on ischemic heart disease (IHD) is not clear. Hence, this study aimed to determine the association between dietary lycopene and IHD. This case-control study was conducted on 443 patients with physician confirmed diagnosis of IHD as the case group and 443 healthy individuals as the control group. Data on demographic, medical history, anthropometric, and physical activity of the participants were collected. Food intake was evaluated using a 237-item semi-quantitative food frequency questionnaire (FFQ). The dietary intake of lycopene was assessed using Nutritionist IV software. A negative association was found between IHD and lycopene (OR: 0.98, CI 95%: 0.963-0.996, p = 0.02). The results remained significant after adjustment for age and sex, additional adjustment for dietary intake of calorie and fat, further adjustments for BMI, and additional adjustment for smoking, drinking alcohol, and physical activity. The risk of IHD in people with the highest quartile of dietary intake of lycopene was significantly lower than those with the lowest quartile (OR = 0.67, CI 95%: 0.46-0.97, p = 0.036). There was a significant inverse relationship between intake of lycopene and IHD. Further prospective studies in different populations are required to elucidate the roles of lycopene against IHD.

Abstract P424: Associations of Taste-Related Genes With Empirical Dietary Patterns Among Community-Dwelling Adults - The Framingham Heart Study

Background: Understanding the genetic contribution to food choices and intake is critical for the development of effective precision nutrition guidance. Recent findings by our lab suggest that genetic variants (SNPs) related to bitter and umami taste perception are differentially associated with food group intakes. The aim of this study was to examine the associations of bitter- and umami-related SNPs, combined as polygenic taste scores, with overall dietary patterns. Methods: Cross-sectional analyses were conducted in 5,817 Framingham Heart Study Offspring (1998-2001) and Third Generation (2002-05) participants (mean age ± SD: 50 ± 14 years; 54% female). Weighed polygenic taste scores were derived using SNPs identified from prior genome-wide association studies for taste perception (11 SNPs: 9 bitter and 2 umami). Higher scores indicated more alleles for higher taste perception. Empirical dietary patterns were derived using Principal Component (PC) analysis with food groups tabulated from food frequency questionnaires. Associations were assessed using linear mixed effects models with FDR adjustment. Results: Three dietary patterns were identified, explaining 32% of total variance in dietary intake: a vegetables, fruits, legumes, and fish pattern (Prudent); a refined grains, sweets, salty foods, and pizza pattern (Western); and a liquor, beer, and wine pattern (Alcohol). On average, after adjusting for age, sex, genetic PCs and energy intake, higher umami polygenic taste scores were associated with lower adherence to the Prudent dietary pattern (OR [95% CI] for upper vs. lower tertial of dietary pattern adherence scores per additional allele for higher umami perception: 0.87 [0.79, 0.97]; P = 0.01). Subsequent analysis at the SNP-level identified one umami-related SNP (rs7691456_T) independently associated with lower Prudent dietary pattern adherence ( P = 0.009), potentially driving the observed association. Both associations remained significant after additional adjustment for smoking, physical activity, and BMI. No significant associations were identified for bitter-related genes and dietary patterns. Conclusions: Among community dwelling adults, higher genetic predisposition to perceive umami was associated with lower adherence to a Prudent dietary pattern, suggesting the potential benefit of leveraging knowledge of taste-related genes in precision nutrition.

Association between periodontitis and metabolic syndrome in the Hamburg City Health Study.

Previous studies demonstrated an association between severe chronic periodontitis (CP) and metabolic syndrome (MetS). However, these studies mostly used the outdated National Cholesterol Education Program-Adult Treatment Panel (NCEP-ATP) III case definition of MetS. Additionally, CP was rarely diagnosed based on a full-mouth examination. Thus, the aim of the current study was to re-evaluate the potential association between CP and MetS in the Hamburg City Health Study (HCHS), a large population-based survey of middle-aged and elderly men and women in Germany, in view of more current definitions of MetS and CP. A cross-sectional study was performed with baseline-data from participants of the HCHS. Periodontitis severity grades were determined in a random sample of 6,209 participants of which 5,456 had sufficient data to call absence or presence of MetS. Variables defining MetS according to the currently valid harmonized definition were determined and a full-mouth examination was performed, including determination of the clinical attachment loss, bleeding on probing, and dental plaque index. CP was classified in three grades of severity (none/mild, moderate, and severe). The Kruskal-Wallis test or the Chi-squared test were used for descriptive statistics and multivariate logistic regression models with and without adjustments for potential confounders (age, sex, smoking, high-sensitivity C-reactive protein [hsCRP], energy intake, and physical activity) were used to test for associations. The prevalence of MetS (39.0%) increased according to the severity grades of periodontitis (none/mild: 33.6%; moderate: 38.7%, and severe: 46.8%). Multivariate logistic regression analyses demonstrated that severe but not moderate CP was associated with MetS after adjusting for age and sex (odds ratio [OR], 1.24; 95% confidence interval [CI], 1.03 to 1.48; P=0.02). However, the association was attenuated after additional adjustment for smoking (OR, 1.19; 95% CI, 0.99 to 1.43; P=0.058) and hsCRP, energy intake, and physical activity (OR, 1.11; 95% CI, 0.91 to 1.36; P=0.294). The use of the more current definitions for MetS and CP confirmed previous observations of an age- and sex-adjusted association between severe CP and MetS. Smoking, high-energy intake, and low physical activity were identified as important lifestyle-related confounders. Abdominal obesity, as indicated by elevated waist circumference, was determined as the most important component of MetS in relationship to CP.

Identifying Potential Therapeutic Applications and Diagnostic Harms of Increased Bilirubin Concentrations: A Clinical and Genetic Approach.

Bilirubin has antioxidant and anti-inflammatory properties in vitro and in animal studies and protects against inflammatory, cardiovascular, and other diseases in observational studies; therefore, bilirubin has potential as a therapeutic agent. However, observational studies could be confounded by many factors. We used a genetic (n=61,281) and clinical (n=234,670) approach to define the association between bilirubin and 19 conditions with a putative protective signal in observational studies. We also tested if individuals with genetically higher bilirubin levels underwent more diagnostic tests. We used a common variant in UGT1A1 (rs6742078) associated with an 26% increase in bilirubin levels in the genetic studies. Carriers of the variant had higher bilirubin levels (P=2.2×10-16 ) but there was no significant association with any of the 19 conditions. In a phenome-wide association study (pheWAS) to seek undiscovered genetic associations, the only significant finding was increased risk of "jaundice-not of newborn." Carriers of the variant allele were more likely to undergo an abdominal ultrasound (odds ratio=1.04, [1.00-1.08], P=0.03). In contrast, clinically measured bilirubin levels were significantly associated with 15 of the 19 conditions (P<0.003) and with 431 clinical diagnoses in the pheWAS (P<1×10-5 adjusted for sex, age, and follow-up). With additional adjustment for smoking and body mass index, 7 of 19 conditions and 260 pheWAS diagnoses remained significantly associated with bilirubin levels. In conclusion, bilirubin does not protect against inflammatory or other diseases using a genetic approach; the many putative beneficial associations reported clinically are likely due to confounding.

Psychological Distress and Alzheimer's Disease Mortality in the United States: Results from the 1997-2014 National Health Interview Survey-National Death Index Record Linkage Study.

Objective: This study examines the association between psychological distress and Alzheimer's disease mortality among US adults aged ≥45. Methods: We analyzed the Kessler 6-item psychological distress scale as a risk factor for Alzheimer's mortality using the pooled 1997-2014 National Health Interview Survey (NHIS)- National Death Index (NDI) database (N = 265,089). Cox regression was used to model mortality as a function of psychological distress and sociodemographic and behavioral covariates. Results: The Alzheimer's mortality risk was 97% higher (HR = 1.97; 95% confidence interval [CI] = 1.37, 2.84) in adults with serious psychological distress compared with those without psychological distress, controlling for sociodemographic covariates. The relative mortality risk remained statistically significant (HR = 1.49; 95% CI = 1.04, 2.13) after additional adjustment for smoking, alcohol consumption, health status, activity limitation, and body mass index. Discussion: US adults had significantly higher risks of Alzheimer's disease mortality at higher psychological distress levels. These findings underscore the significance of addressing psychological well-being as a strategy for reducing Alzheimer's disease mortality.

Corrigendum to: Is mode of transport to work associated with mortality in the working-age population? Repeated census-cohort studies in New Zealand, 1996, 2001 and 2006.

BACKGROUND Increasing active transport is proposed as a means to address both health and environmental issues. However, the associations between specific modes, such as cycling, walking and public transport, and health outcomes remain unclear. We examined the association between mode of travel to work and mortality. METHODS Cohort studies of the entire New Zealand working population were created using 1996, 2001 and 2006 censuses linked to mortality data. Mode of travel to work was that reported on census day, and causes of death examined were ischaemic heart disease and injury. Main analyses were Poisson regression models adjusted for socio-demographics. Sensitivity analyses included: additional adjustment for smoking in the 1996 and 2006 cohorts, and bias analysis about non-differential misclassification of cycling vs car use. RESULTS Walking (5%) and cycling (3%) to work were uncommon. Compared with people reporting using motor vehicles to travel to work, those cycling had a reduced all-cause mortality (ACM) in the socio-demographic adjusted models RR 0.87 (0.77-0.98). Those walking (0.97, 0.90-1.04) and taking public transport (0.96, 0.88-1.05) had no substantive difference in ACM. No mode of transport was associated with detectable statistically significant reductions in cause-specific mortality. Sensitivity analyses found weaker associations when adjusting for smoking and stronger associations correcting for likely non-differential misclassification of cycling. CONCLUSIONS This large cohort study supports an association between cycling to work and reduced ACM, but found no association for walking or public-transport use and imprecise cause-specific mortality patterns.

Is mode of transport to work associated with mortality in the working-age population? Repeated census-cohort studies in New Zealand, 1996, 2001 and 2006.

Increasing active transport is proposed as a means to address both health and environmental issues. However, the associations between specific modes, such as cycling, walking and public transport, and health outcomes remain unclear. We examined the association between mode of travel to work and mortality. Cohort studies of the entire New Zealand working population were created using 1996, 2001 and 2006 censuses linked to mortality data. Mode of travel to work was that reported on census day, and causes of death examined were ischaemic heart disease and injury. Main analyses were Poisson regression models adjusted for socio-demographics. Sensitivity analyses included: additional adjustment for smoking in the 1996 and 2006 cohorts, and bias analysis about non-differential misclassification of cycling vs car use. Walking (5%) and cycling (3%) to work were uncommon. Compared with people reporting using motor vehicles to travel to work, those cycling had a reduced all-cause mortality (ACM) in the socio-demographic adjusted models RR 0.87 (0.77-0.98). Those walking (0.97, 0.90-1.04) and taking public transport (0.96, 0.88-1.05) had no substantive difference in ACM. No mode of transport was associated with detectable statistically significant reductions in cause-specific mortality. Sensitivity analyses found weaker associations when adjusting for smoking and stronger associations correcting for likely non-differential misclassification of cycling. This large cohort study supports an association between cycling to work and reduced ACM, but found no association for walking or public-transport use and imprecise cause-specific mortality patterns.

Using nationally representative survey data for external adjustment of unmeasured confounders: An example using the NHANES data.

To evaluate the use of data from population-based surveys such as the National Health and Nutrition Examination Survey (NHANES) for external adjustment for confounders imperfectly measured in health care databases in the United States. Our example study used Medicaid Analytic eXtract (MAX) data to estimate the relative risk (RR) for prenatal serotonin-norepinephrine reuptake inhibitors (SNRIs) exposure and cardiac defects. Smoking and obesity are known confounders poorly captured in databases. NHANES collects information on lifestyle factors, depression, and prescription medications. External adjustment requires information on the prevalence of confounders and their association with SNRI use; which was obtained from the NHANES. It also requires estimates of their association with the outcome, which were based on the literature and allowed us to correct the RR using sensitivity analyses. In MAX, the RR for the association between prenatal SNRI exposure and cardiac defects was 1.51 unadjusted and 1.20 adjusted for measured confounders and restricted to women with depression. In NHANES, among women of childbearing age with depression, the prevalence of smoking was 60.2% (95% Confidence Interval 43.2, 74.3) for SNRI users and 44.1% (39.6, 48.8) for nonusers of antidepressants. The corresponding estimates for obesity were 59.2% (43.2, 74.3) and 40.5% (35.9, 45.0), respectively. If the associations between smoking and obesity with cardiac defects are independent from each other and from other measured confounders, additional adjustment for smoking and obesity would move the RR from 1.20 to around 1.10. National surveys like NHANES are readily available sources of information on potential confounders and they can be used to assess and improve the validity of RR estimates from observational studies missing data on known risk factors.

Comorbid Conditions Explain the Association Between Posttraumatic Stress Disorder and Incident Cardiovascular Disease.

BackgroundPosttraumatic stress disorder (PTSD) is associated with risk of cardiovascular disease (CVD). Biopsychosocial factors associated with PTSD likely account for some or all of this association. We determined whether 1, or a combination of comorbid conditions explained the association between PTSD and incident CVD.Methods and ResultsEligible patients used 1 of 5 Veterans Health Affairs medical centers distributed across the United States. Data were obtained from electronic health records. At index date, 2519 Veterans Health Affairs (VA) patients, 30 to 70 years of age, had PTSD diagnoses and 1659 did not. Patients had no CVD diagnoses for 12 months before index date. Patients could enter the cohort between 2008 and 2012 with follow‐up until 2015. Age‐adjusted Cox proportional hazard models were computed before and after adjusting for comorbidities. Patients were middle aged (mean=50.1 years, SD±11.0), mostly male (87.0%), and 60% were white. The age‐adjusted association between PTSD and incident CVD was significant (hazard ratio=1.41; 95% CI: 1.21–1.63). After adjustment for metabolic conditions, the association between PTSD and incident CVD was attenuated but remained significant (hazard ratio=1.23; 95% CI: 1.06–1.44). After additional adjustment for smoking, sleep disorder, substance use disorder, anxiety disorders, and depression, PTSD was not associated with incident CVD (hazard ratio=0.96; 95% CI: 0.81–1.15).Conclusions PTSD is not an independent risk factor for CVD. Physical and psychiatric conditions and smoking that co‐occur with PTSD explain why this patient population has an increased risk of CVD. Careful monitoring may limit exposure to CVD risk factors and subsequent incident CVD.

Advanced glycation end products and risk of hypertension in Iranian adults: Tehran lipid and glucose study.

Background:Elevated blood pressure is still one of the major risk factors for diseases and disabilities and also a public health challenge worldwide. In the present longitudinal study, we aimed to evaluate the association between risk of hypertension and dietary advanced glycation end products (AGEs) as a recently discussed potential risk factor.Materials and Methods:Dietary assessment of 1775 participants in the third phase of Tehran lipid and glucose study to obtain dietary intake of AGEs was performed using a validated semi-quantitative food frequency questionnaire, and they were followed up for a mean duration of approximately 6 years. To determine the incidence of hypertension across quartiles of AGEs intake, logistic regression models with adjustment for potential confounding variables were used. All statistical analyses were conducted using SPSS, and P < 0.05 was considered statistically significant.Results:Higher hypertension occurrence risk was generally attributed to higher AGEs intake quartiles after adjusting for age in men (odds ratio [OR] = 1.48, 95% confidence interval [CI] = 1.11–1.52, P = 0.038) and additional adjustment for smoking, drugs, and physical activity in women (OR = 1.38%–95% CI = 1.09–1.42, P = 0.042). Moreover, across the increasing trend of dietary AGEs intake, the percentage of fat intake increased and that of carbohydrate significantly decreased (P < 0.0001).Conclusion:In conclusion, it is highly recommended to limit dietary AGEs consumption to prevent and manage hypertension and its complications.

Family history of cancer and the risk of bladder cancer: A case–control study from Italy

BackgroundA family history of bladder cancer has been associated with the risk of bladder cancer, but quantification of the excess risk in different populations is still a relevant issue. Further, the role of a family history of other cancers on the risk of bladder cancer remains unclear. MethodsWe analyzed data from an Italian case–control study, including 690 bladder cancer cases and 665 hospital controls. Odds ratios (ORs) were estimated through unconditional logistic regression models, adjusted for sex, age, study center, year of interview and further for education, smoking and sibling’s number. ResultsThe OR for family history of bladder cancer was 2.13 (95% confidence intervals (95%CIs) 1.02–4.49) from the model with partial adjustment, and 1.99 (95%CI 0.91–4.32) after additional adjustment for smoking and siblings’ number, based on 23 cases (3.3%) and 11 controls (1.7%) with a family history of bladder cancer. The fully adjusted OR was 3.77 when the relative was diagnosed at age below 65years. Smokers with a family history of bladder cancer had a four-fold increased risk compared to non-smokers without a family history. Bladder cancer risk was significantly increased among subjects with a family history of hemolymphopoietic cancers (OR=2.97, 95%CI 1.35–6.55). Family history of cancer at other sites showed no significant association with bladder cancer risk. ConclusionThis study confirms an approximately two-fold increased risk of bladder cancer for family history of bladder cancer, and indicates a possible familial clustering of bladder cancer with cancers of the hemolymphopoietic system.

Abstract 12: Whole Blood DNA Methylation Signatures of a Mediterranean-style Dietary Pattern

Introduction: Mediterranean-style dietary patterns (MSDPs) have been associated with lower risk of cardiometabolic diseases, but the underlying biological mechanisms are poorly understood. To date, little is known in humans of the relationship between MSDPs and epigenetics. We hypothesized that adherence to a MSDP is associated with DNA methylation, an important epigenetic modification. Methods: We conducted a cross-sectional study of 3,563 Framingham Heart Study participants (median age 59 years, 55% women). We excluded participants with heavy alcohol use. Whole-blood derived DNA methylation of 480,000 cytosine-phosphate-guanine dinucleotides (CpGs) was assessed using the Illumina HumanMethylation450 BeadChip. A MSDP score was created based on nine dietary components, including fruits, vegetables, legumes, nuts, whole grains, fish, red meat, alcohol, and ratio of monounsaturated fatty acids to saturated fatty acids. Food intake was assessed by a validated food frequency questionnaire. Our study sample was randomly split into separate discovery/replication groups (n=1,788 and n=1,775) by pedigrees. We tested the association of CpG methylation with the MSDP score using linear mixed model, adjusted for sex, age, and energy intake (as well as family structure, imputed leukocyte composition, and technical variables). CpGs identified in discovery at FDR&lt;0.05 were taken forward for replication. We then tested the significance (Bonferroni corrected α 0.05) of the identified CpGs after additional adjustment for smoking, physical activity, and BMI in whole study sample. Results: One CpG, cg05575921 in the AHRR gene, was associated with MSDP score in the discovery sample ( P =3.3x10 -10 ) and replicated in the replication sample ( P =3.6x10 -5 ). In whole study sample, higher MSDP score was associated with greater methylation of cg05575921 after adjustment for sex, age, energy intake, smoking, physical activity, and BMI ( P =4.5x10 -3 ). Higher fruit and whole grain intake was also associated with higher methylation level of cg05575921 ( P =3.8x10 -7 and 5.1x10 -8 , respectively) and legume intake was associated with higher methylation level of cg17333223 (annotated to the NSA2 gene, P =1.3x10 -7 ). In contrast, fruit intake was associated with lower methylation of cg07035242 (annotated to the UBIAD1 gene, P =2.0x10 -7 ). These patterns persisted in the replication and in whole study sample. Conclusions: These data demonstrate a unique whole blood DNA methylation signature of a MSDP score and some of its individual components. The differentially methylated genes may represent therapeutic targets for prevention or treatment of cardiometabolic diseases. Future work is needed to explore the underlying mechanisms.

Association between Dietary Sodium Intake and Cognitive Function in Older Adults.

To examine the association of dietary sodium intake with cognitive function in community-dwelling older adults. Cross-sectional study. Southern California community. White men (n=373) and women (n=552), aged 50-96 years from the Rancho Bernardo Study, a longitudinal study of cardiovascular disease risk factors and healthy aging. During the 1992-1996 research clinic visit, a food frequency questionnaire was used to determine daily sodium intake; cognitive function was assessed with Trails Making Test, part B (Trails B), Mini-Mental State Exam (MMSE), and Verbal Fluency Test (VFT); and medical, clinical and demographic information was obtained. Linear regression was used to assess the association between calorie-adjusted sodium intake and cognitive test scores with adjustment for demographic, behavioral and health measures. Logistic regression examined the odds of having cognitive impairment by sodium intake. Lower sodium intake was associated with poorer performance on Trails B (p=0.008) and MMSE (p=0.003) after controlling for age, sex, and education. Associations did not differ by sex, but there was a significant interaction by age for the Trails B: older (≥80 years), but not younger, adults showed worse performance with lower sodium intake (p=0.03). Associations remained significant after additional adjustment for smoking, alcohol intake, exercise, body weight, cardiovascular risk factors, kidney function, diuretic medication use, and diet quality. Lower daily sodium intake was associated with increased odds of cognitive impairment on the MMSE (score < 26; OR per SD decrease = 1.12, 95% CI 1.08, 1.16). Concluson: Lower sodium intake was associated with worse cognitive function in older community-dwelling adults. For the maintenance of cognitive health, older adults may be advised to avoid very low sodium diets.

Expired-air carbon monoxide as a predictor of 16-year risk of all-cause, cardiovascular and cancer mortality

BackgroundMeasurement of expired-air carbon monoxide (EACO) is commonly used to ascertain non-smoking status, although it can also reflect exposures not related to smoking. Our aim was to assess 16-year mortality according to EACO measured at baseline, in a general population. MethodsOur analysis was based on the Third French MONICA population survey (1994–1997). Causes of death were obtained 16years after inclusion, and assessment of determinants of mortality was based on Cox modeling. ResultsEACO was measured in 2232 apparently healthy participants aged 35-64. During follow-up, 195 deaths occurred (19% were due to cardio-vascular (CV) causes and 49% to cancer). At baseline, the mean EACO was 11.8 (±7.4)ppm, 4.6 (±2.5)ppm, 4.3 (±2.2)ppm for current, former and never smokers, respectively (P<0.001). After adjustment for main mortality risk factors and smoking, the hazard ratio (HR) for total mortality was 1.03[95% confidence interval: 1.01–1.06] per 1-unit increase in EACO, and it was 1.04[1.01–1.07] for cancer mortality. Adjusted HR for CV mortality was 1.05[1.01–1.10] but did not remain significant after additional adjustment for smoking (0.98[0.91–1.04]). Interactions between EACO and smoking were not significant. ConclusionsIn a general population, baseline EACO is an independent predictor of 16-year all-cause and cancer mortality, after adjustment for confounders including smoking. Given that the effect of EACO is similar among smokers and non-smokers, EACO is probably not solely related to smoking but could also be a marker of inhaled ambient carbon monoxide and/or endogenous production. Besides, smoking better predicts CV mortality than EACO.

Adverse Childhood Events are Related to the Prevalence of Asthma and Chronic Obstructive Pulmonary Disorder Among Adult Women in Hawaii.

In the US, women surpass men in the prevalence of lung diseases. Limited studies exist on the association of adverse childhood events (ACEs) to asthma and chronic obstructive pulmonary disorder (COPD) particularly among women and cohorts of understudied populations (e.g., Pacific Islanders). This study evaluated the ACEs-asthma and ACEs-COPD relationships among women in Hawaii and the contribution of poor health factors (smoking, binge drinking, and obesity) in these associations. Using data from 3363 women in the Behavioral Risk Factor Surveillance System-Hawaii, we assessed how self-reported ACEs [count and type (household dysfunction, and physical, verbal and sexual abuse)] relate to asthma and COPD. Multivariable log-binomial regression, accounting for the sampling design, and model adjustments for socio-demographics, healthcare access, emotional support, current smoking, binge drinking, and BMI status were used to generate prevalence ratios. For every increase in ACE count, the likelihood for asthma increased by 7 % (CI = 1.02-1.13), and for COPD, by 21 % (CI = 1.12-1.31) accounting for socio-demographics, healthcare access, and emotional support. Verbal abuse was also associated with greater likelihood for asthma independent of these covariates (PR = 1.43, CI = 1.14-1.79). Household dysfunction (PR = 1.82, CI = 1.15-2.82) and physical (PR = 2.01, CI = 1.20-3.37), verbal (PR = 2.24, CI = 1.38-3.65) and sexual (PR = 1.81, CI = 1.10-2.97) abuse were all associated with COPD using similar adjustments. Additional adjustment for smoking, binge drinking, and BMI status did not impact the ACE-asthma associations and only modestly attenuated the ACE-COPD relationships. Primary and secondary prevention of ACEs may optimize the health of young girls in Hawaii, and reduce the burden of asthma and COPD among women in the state.

Contribution of demographic and behavioral factors on the changing incidence rates of oropharyngeal and oral cavity cancers in northern California.

It is unknown to what extent patient demographics, smoking, and alcohol use have contributed to changes in oropharyngeal and oral cavity cancer incidence rates. We performed a cohort study of Kaiser Permanente health plan members, ages 20 to 89, for years 1995-2010 (n = 2.2 million annual members). Poisson Regression models estimated calendar trends in cancer rates both adjusted for and stratified by age, sex, smoking, and alcohol abuse history. We identified 1,383 human papillomavirus (HPV)-related and 1,344 HPV-unrelated oral cavity and oropharyngeal cancer cases. With adjustment for age and sex, HPV-related cancer incidence rates increased 3.8% per year (P < 0.001) between 1995 and 2010, whereas rates for HPV-unrelated cancers decreased 2.4% per year (P < 0.001). For years 2007 to 2010, with additional adjustment for smoking and alcohol abuse, results were nonsignificant, but similar in magnitude. The increasing rates for HPV-related cancers were more prominent among nonsmokers (+14.5%) compared with smokers (-2.5%; P-interaction = 0.058). The decreased rates for HPV-unrelated sites were more prominent among those ≥ 60 years (-11.0%) compared with those <60 years (+16.8%; P-interaction = 0.006), among smokers (-9.7%) compared with nonsmokers (+8.4%; P-interaction = 0.055), and among those with an alcohol abuse history (-20.4%) compared with those without a history (+5.8%; P-interaction = 0.009). The observed increasing HPV-related cancer rates are most evident among nonsmokers, whereas the decreasing HPV-unrelated cancer rates are least evident among younger individuals, nonsmokers, and those without an alcohol abuse history. Continued vigilance for oropharyngeal and oral cavity cancer is warranted, including among those without traditional risk factors such as smoking and alcohol abuse.

Snus use and cardiovascular risk factors in the general population: the HUNT3 study

Snus, a form of smokeless tobacco, is increasingly popular in its traditional Nordic markets, and was recently launched commercially in the United States. We examined the cross-sectional associations between snus use and cardiovascular risk factors, and compared them with the corresponding associations of smoking. Cross-sectional study. The HUNT3 general population survey, Nord-Trøndelag, Norway (2006-08). A general population sample of n = 25 163. Measured triglyceride,- glucose- and high-density lipoprotein (HDL)-cholesterol levels, blood pressure and waist circumference, registry information on gender, age and education level, self-reported snus use, smoking, physical exercise and alcohol use. In age- and gender-adjusted linear regression analyses, extensive snus use was associated with larger waist circumference (b = 1.65, 95% CI = 0.86, 2.43) and higher systolic blood pressure (b = 2.58, 95% CI = 1.48, 3.68), but with higher rather than lower levels of HDL-cholesterol (b = 1.66, 95% CI = 0.79, 2.53). These three differences remained significant after additional adjustment for smoking, education level, physical exercise and alcohol use. Smokers had higher triglyceride and lower HDL-cholesterol than snus users, but lower systolic blood pressure. After adjusting statistically for major confounding variables, Norwegians who use snus extensively have a mixed profile in terms of cardiovascular risk: slightly higher waist circumference and systolic blood pressure but also higher high-density lipoprotein-cholesterol.

Anti-müllerian hormone is not associated with cardiometabolic risk factors in adolescent females.

ObjectivesEpidemiological evidence for associations of Anti-Müllerian hormone (AMH) with cardiometabolic risk factors is lacking. Existing evidence comes from small studies in select adult populations, and findings are conflicting. We aimed to assess whether AMH is associated with cardiometabolic risk factors in a general population of adolescent females.MethodsAMH, fasting insulin, glucose, HDLc, LDLc, triglycerides and C-reactive protein (CRP) were measured at a mean age 15.5 years in 1,308 female participants in the Avon Longitudinal Study of Parents and Children (ALSPAC). Multivariable linear regression was used to examine associations of AMH with these cardiometabolic outcomes.ResultsAMH values ranged from 0.16–35.84 ng/ml and median AMH was 3.57 ng/ml (IQR: 2.41, 5.49). For females classified as post-pubertal (n = 848) at the time of assessment median (IQR) AMH was 3.81 ng/ml (2.55, 5.82) compared with 3.25 ng/ml (2.23, 5.05) in those classed as early pubertal (n = 460, P≤0.001). After adjusting for birth weight, gestational age, pubertal stage, age, ethnicity, socioeconomic position, adiposity and use of hormonal contraceptives, there were no associations with any of the cardiometabolic outcomes. For example fasting insulin changed by 0% per doubling of AMH (95%CI: −3%,+2%) p = 0.70, with identical results if HOMA-IR was used. Results were similar after additional adjustment for smoking, physical activity and age at menarche, after exclusion of 3% of females with the highest AMH values, after excluding those that had not started menarche and after excluding those using hormonal contraceptives.ConclusionOur results suggest that in healthy adolescent females, AMH is not associated with cardiometabolic risk factors.

The plasma leptin/adiponectin ratio predicts first cardiovascular event in men: A prospective nested case–control study

ObjectiveThe plasma leptin/adiponectin (L/A) ratio has been proposed as a preferential marker of atherosclerosis susceptibility compared to leptin and adiponectin alone. We determined the extent to which the L/A ratio predicts incident cardiovascular disease (CVD) taking account of clinical risk factors, microalbuminuria, the total cholesterol/HDL cholesterol (TC/HDL-C ratio), triglycerides, high sensitive C-reactive protein (hs-CRP) and insulin sensitivity (homeostasis model assessment (HOMAir)). MethodsA community-based prospective nested case–control study was carried out in 103 non-diabetic men who developed a first cardiovascular event (cases) and 106 male control subjects (no clinically manifest CVD and no lipid lowering drug use at baseline; median follow-up of 3.0 and 10.5years, respectively). Plasma leptin, adiponectin, the leptin/adipnectin (L/A) ratio, as well as hs-CRP, HOMAir and the TC/HDL-C ratio were determined at baseline. ResultsPlasma leptin levels and the L/A ratio were higher in cases vs. controls (p=0.002 for both), but the difference in adiponectin was not significant (p=0.10). Age-adjusted incident CVD was associated with plasma leptin, adiponectin and the L/A ratio (p=0.045 to p=0.001). The relationships of incident CVD with plasma leptin (p=0.19) and adiponectin (p=0.073) lost statistical significance after additional adjustment for smoking, waist circumference, hypertension, microalbuminuria, the TC/HDL-C ratio, hs-CRP and HOMAir. In this fully adjusted analysis, the L/A ratio remained predictive of incident CVD (hazard ratio: 1.40 (95% CI 1.05–1.87), p=0.024). ConclusionThis study suggests that the L/A ratio may be a preferential marker of a first cardiovascular event in men compared to plasma leptin and adiponectin levels alone.