DESIGN: Use of the International Tobacco Control Policy Evaluation Project surveys of smokers, using the 2007 survey wave (or later, where necessary).
SETTINGS: Australia, Canada, China, France, Germany, Ireland, Malaysia, Mexico, the Netherlands, New Zealand, South Korea, Thailand, United Kingdom, Uruguay and United States.
PARTICIPANTS: Samples of smokers from 15 countries.
MEASUREMENTS: Self-report on use of cessation aids and on visits to health professionals and provision of cessation advice during the visits.
FINDINGS: Prevalence of quit attempts in the last year varied from less than 20% to more than 50% across countries. Similarly, smokers varied greatly in reporting visiting health professionals in the last year (<20% to over 70%), and among those who did, provision of advice to quit also varied greatly. There was also marked variability in the levels and types of help reported. Use of medication was generally more common than use of behavioural support, except where medications are not readily available.
CONCLUSIONS: There is wide variation across countries in rates of attempts to stop smoking and use of assistance with higher overall use of medication than behavioural support. There is also wide variation in the provision of brief advice to stop by health professionals.
OBJECTIVE: Given this information, this study systematically explores what risk factors may be associated with ADRD in Indigenous populations.
METHODS: A search of all published literature was conducted in October 2016, March 2018, and July 2019 using Medline, Embase, and PsychINFO. Subject headings explored were inclusive of all terms related to Indigenous persons, dementia, and risk. All relevant words, phrases, and combinations were used. To be included in this systematic review, articles had to display an association of a risk factor and ADRD. Only studies that reported a quantifiable measure of risk, involved human subjects, and were published in English were included.
RESULTS: Of 237 articles originally identified through database searches, 45 were duplicates and 179 did not meet a priori inclusion criteria, resulting in 13 studies eligible for inclusion in this systematic review.
CONCLUSION: The large number of potentially modifiable risk factors reported relative to non-modifiable risk factors illustrates the importance of socioeconomic context in the pathogenesis of ADRD in Indigenous populations. The tendency to prioritize genetic over social explanations when encountering disproportionately high disease rates in Indigenous populations can distract from modifiable proximal, intermediate, and distal determinants of health.
METHODS: Unmatched case control and comparative studies were carried out among fertilizer factory workers in Sarawak with the aim of determining contributing factors for hearing impairment. Respondents consisted of 49 cases that were diagnosed from 2005 to 2008 with 98 controls from the same work places. Chi-square test and Mann-Whitney test were used in a univariate analysis to determine the association between hearing impairment and the contributing risks being studied.
RESULTS: The results of the univariate analysis showed that hearing impairment was significantly (p<0.05) associated with older age, lower education level, high smoking dose, high occupational daily noise dose, longer duration of service, infrequent used of hearing protection device (HPD), and low perception of sound on HPD usage. Multivariate logistic regression of hearing impairment after controlling for age found the following five variables: occupational daily noise dose ≥50% (OR 3.48, 95% CI 1.36-8.89), ≥15 years of services (OR 2.92, 95% CI 1.16-7.33), infrequent use of HPD (OR 2.79, 95% CI 1.15-6.77), low perception of sound on HPD (POR 2.77, 95% CI 1.09-6.97), and smoking more than 20 packs per year (OR 4.71, 95% CI 1.13-19.68).
DISCUSSION: In conclusion, high occupational noise exposure level, longer duration of service, low perception of sound on HPD, infrequent used of HPD, and smoking more than 20 packs per year were the contributing factors to hearing impairment, and appropriate intervention measures should be proposed and taken into considerations.
METHODS: A case-control study was conducted involving 600 people with type 2 diabetes (300 chronic kidney disease cases, 300 controls) who participated in The Malaysian Cohort project. Retrospective subanalysis was performed on the chronic kidney disease cases to assess chronic kidney disease progression from the recruitment phase. We genotyped 32 single nucleotide polymorphisms using mass spectrometry. The probability of chronic kidney disease and predicted rate of newly detected chronic kidney disease progression were estimated from the significant gene-environment interaction analyses.
RESULTS: Four single nucleotide polymorphisms (eNOS rs2070744, PPARGC1A rs8192678, KCNQ1 rs2237895 and KCNQ1 rs2283228) and five environmental factors (age, sex, smoking, waist circumference and HDL) were significantly associated with chronic kidney disease. Gene-environment interaction analyses revealed significant probabilities of chronic kidney disease for sex (PPARGC1A rs8192678), smoking (eNOS rs2070744, PPARGC1A rs8192678 and KCNQ1 rs2237895), waist circumference (eNOS rs2070744, PPARGC1A rs8192678, KCNQ1 rs2237895 and KCNQ1 rs2283228) and HDL (eNOS rs2070744 and PPARGC1A rs8192678). Subanalysis indicated that the rate of newly detected chronic kidney disease progression was 133 cases per 1000 person-years (95% CI: 115, 153), with a mean follow-up period of 4.78 (SD 0.73) years. There was a significant predicted rate of newly detected chronic kidney disease progression in gene-environment interactions between KCNQ1 rs2283228 and two environmental factors (sex and BMI).
CONCLUSIONS: Our findings suggest that the gene-environment interactions of eNOS rs2070744, PPARGC1A rs8192678, KCNQ1 rs2237895 and KCNQ1 rs2283228 with specific environmental factors could modify the probability for chronic kidney disease.
METHODS: This was a cross-sectional study of 22,210 adult men and women who underwent a comprehensive health screening examination between 2011 and 2013 (median age 40 years). Sugar-sweetened carbonated beverage consumption was assessed using a validated food frequency questionnaire, and CAC was measured by cardiac computed tomography. Multivariable-adjusted CAC score ratios and 95% CIs were estimated from robust Tobit regression models for the natural logarithm (CAC score +1).
RESULTS: The prevalence of detectable CAC (CAC score >0) was 11.7% (n = 2,604). After adjustment for age; sex; center; year of screening examination; education level; physical activity; smoking; alcohol intake; family history of cardiovascular disease; history of hypertension; history of hypercholesterolemia; and intake of total energy, fruits, vegetables, and red and processed meats, only the highest category of sugar-sweetened carbonated beverage consumption was associated with an increased CAC score compared with the lowest consumption category. The multivariable-adjusted CAC ratio comparing participants who consumed ≥5 sugar-sweetened carbonated beverages per week with nondrinkers was 1.70 (95% CI, 1.03-2.81). This association did not differ by clinical subgroup, including participants at low cardiovascular risk.
CONCLUSION: Our findings suggest that high levels of sugar-sweetened carbonated beverage consumption are associated with a higher prevalence and degree of CAC in asymptomatic adults without a history of cardiovascular disease, cancer, or diabetes.