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Background Recent operational definitions of sarcopenia have not been replicated and compared in Australia and New Zealand (ANZ) populations. We aimed to identify sarcopenia measures that discriminate ANZ adults with slow walking speed (<0.8 m/s) and determine the agreement between the Sarcopenia Definitions and Outcomes Consortium (SDOC) and revised European Working Group for Sarcopenia in Older People (EWGSOP2) operational definitions of sarcopenia. Methods Eight studies comprising 8 100 ANZ community-dwelling adults (mean age ± standard deviation, 62.0 ± 14.4 years) with walking speed, grip strength (GR), and lean mass data were combined. Replicating the SDOC methodology, 15 candidate variables were included in sex-stratified classification and regression tree models and receiver operating characteristic curves on a pooled cohort with complete data to identify variables and cut points discriminating slow walking speed (<0.8 m/s). Agreement and prevalence estimates were compared using Cohen's Kappa (CK). Results Receiver operating characteristic curves identified GR as the strongest variable for discriminating slow from normal walking speed in women (GR <20.50 kg, area under curve [AUC] = 0.68) and men (GR <31.05 kg, AUC = 0.64). Near-perfect agreement was found between the derived ANZ cut points and SDOC cut points (CK 0.8–1.0). Sarcopenia prevalence ranged from 1.5% (EWGSOP2) to 37.2% (SDOC) in women and 1.0% (EWGSOP2) to 9.1% (SDOC) in men, with no agreement (CK <0.2) between EWGSOP2 and SDOC. Conclusions Grip strength is the primary discriminating characteristic for slow walking speed in ANZ women and men, consistent with findings from the SDOC. Sarcopenia Definitions and Outcomes Consortium and EWGSOP2 definitions showed no agreement suggesting these proposed definitions measure different characteristics and identify people with sarcopenia differently. [ABSTRACT FROM AUTHOR]

Background: Knowledge of preventable disease and differences in disease burden can inform public health action to improve health and health equity. We quantified the future lung cancer burden preventable by behavioural modifications across Australia.Methods: We pooled seven Australian cohort studies (n = 367 058) and linked them to national registries to identify lung cancers and deaths. We estimated population attributable fractions and their 95% confidence intervals (CIs) for modifiable risk factors, using risk estimates from the cohort data and risk factor exposure distribution from contemporary national health surveys.Results: During the first 10-year follow-up, there were 2025 incident lung cancers and 20 349 deaths. Stopping current smoking could prevent 53.7% (95% CI, 50.0-57.2%) of lung cancers over 40 years and 18.3% (11.0-25.1%) in 10 years. The smoking-attributable burden is highest in males, those who smoke <20 cigarettes per day, are <75 years of age, unmarried, of lower educational attainment, live in remote areas or are healthy weight. Increasing physical activity and fruit consumption, if causal, could prevent 15.6% (6.9-23.4%) and 7.5% (1.3-13.3%) of the lung cancer burden, respectively. Jointly, the three behaviour modifications could prevent up to 63.0% (58.0-67.5%) of lung cancers in 40 years, and 31.2% (20.9-40.1%) or 43 300 cancers in 10 years. The preventable burden is highest among those with multiple risk factors.Conclusions: Smoking remains responsible for the highest burden of lung cancer in Australia. The uneven burden distribution distinguishes subgroups that could benefit the most from activities to control the world's deadliest cancer. [ABSTRACT FROM AUTHOR]

Background Previous estimates of the colorectal cancer (CRC) burden attributed to behaviors have not considered joint effects, competing risk, or population subgroup differences. Methods We pooled data from seven prospective Australian cohort studies (n = 367 058) and linked them to national registries to identify CRCs and deaths. We estimated the strength of the associations between behaviors and CRC risk using a parametric piecewise constant hazards model, adjusting for age, sex, study, and other behaviors. Exposure prevalence was estimated from contemporary National Health Surveys. We calculated population attributable fractions for CRC preventable by changes to current behaviors, accounting for competing risk of death and risk factor interdependence. Statistical tests were two-sided. Results During the first 10 years of follow-up, there were 3471 incident CRCs. Overweight or obesity explained 11.1%, ever smoking explained 10.7% (current smoking 3.9%), and drinking more than two compared with two or fewer alcoholic drinks per day explained 5.8% of the CRC burden. Jointly, these factors were responsible for 24.9% (95% confidence interval [CI] = 19.7% to 29.9%) of the burden, higher for men (36.7%) than women (13.2%, P difference <.001). The burden attributed to these factors was also higher for those born in Australia (28.7%) than elsewhere (16.8%, P difference =.047). We observed modification of the smoking-attributable burden by alcohol consumption and educational attainment, and modification of the obesity-attributable burden by age group and birthplace. Conclusions We produced up-to-date estimates of the future CRC burden attributed to modifiable behaviors. We revealed novel differences between men and women, and other high–CRC burden subgroups that could potentially benefit most from programs that support behavioral change and early detection. [ABSTRACT FROM AUTHOR]

Background Diet and sleep are strongly and bidirectionally linked. This study aims to assess the association between dietary inflammatory index (DII) and sleep duration using the National Health and Nutrition Survey (NHANS) of the United States. Methods A total of 27,999 (median age 47 years, 48.6% male) participants were included. Dietary data were collected using 24-hour recall method and DII was calculated using 27 nutrients. Quantiles of DII were constructed (quantile 1, least inflammatory; quantile 5, most inflammatory). Self-reported habitual sleep duration was categorized as ≤ 6 hr (short sleep), ≥7 hr (normal/long sleep). We used log-binomial and multinomial logistic regression, adjusted for potential confounders, to examine the association between DII and short sleep duration. Sensitivity analysis was performed by excluding common chronic diseases. The analyses were adjusted using NHANES sampling weights. Results In the fully adjusted model, higher DII score was associated with shorter sleep duration [odds ratio (OR)quartile2vs1=1.04; 95% confidence interval (CI): 0.84-1.29; ORquartile3vs1=1.27; 95% CI: 1.06, 1.52; ORquartile4vs1=95% CI: 1.47; 95 CI: 1.25, 1.74; ORquartile5vs1=1.62; 95% CI: 1.33, 1.97; P for trend<0.0001]. A similar trend of association was observed with long sleep duration and in both male and female participants. Participants in the fifth quantile, compared to those in the first, on average had 6 minutes (95% CI: 1, 11) less sleep. Conclusions Pro-inflammatory diet was positively associated with increased odds of short sleep duration. Key messages Patients with short sleep duration may benefit from avoiding pro-inflammatory foods. The association between DII and sleep duration could be bidirectional. [ABSTRACT FROM AUTHOR]

Background Systemic inflammation is a precursor of many chronic diseases that contributes to morbidity and mortality. In this study, we examined the joint association of systemic inflammation and diet quality with all-cause mortality. Methods A total of 27,305 adults (mean age = 50 years, male: 50.6%) from the National Health and Nutrition Examination Survey (1999-2010 and 2015-2018) were included in the study. A serum inflammatory marker, C-reactive protein (CRP), was measured. The Healthy Eating Index-2015 (HEI-15) was computed. Multivariable logistic regression analysis was used to determine the cross-sectional association between HEI-15 and inflammation. Multivariable Cox proportional hazard models were performed to assess the risk of all-cause mortality associated with the joint classification of inflammation and diet quality. Results In the cross-sectional study, a higher tertile of HEI-15 was associated with reduced odds of inflammation (OR = 0.85, 95% CI: 0.78-0.93) in all participants. Similar results were observed in obese and non-obese groups. In the prospective study (median follow-up = 9.4 years), a higher adherence to HEI-15 was associated with a reduced risk of mortality. Compared to non-obese group, obese participants with high levels of inflammation had a higher risk of all-cause mortality (HR = 1.26, 95% CI: 1.08-1.47; HR = 1.60, 95% CI: 1.19-2.17, respectively). Conclusions A higher adherence to HEI-15 was associated with reduced inflammation. Higher diet quality may reduce mortality risks associated with inflammation, particularly in non-obese groups and obese participants with moderate inflammation. Key messages Adhering to a high quality diet may mitigate the mortality risk associated with increased inflammation. [ABSTRACT FROM AUTHOR]

Background The link between diet, inflammation and depressive symptoms (DepS) are of increasing interest. The study aims to assess the association between the dietary inflammatory index (DII®) and DepS using the North-West Adelaide Health Study (NWAHS) cohort and update the previous meta-analysis. Methods A total of 1743 (mean□SD age 56.6±13.6 years, 51% female) and 859 (mean□SD age 58.4±12.1 years, 52.6% female) of NWAHS participants were included for cross-sectional and longitudinal analysis respectively. DII was determined using food frequency questionnaires, and the Center for Epidemiologic Studies Depression Scale (CES-D) assessed DepS. Log- and negative binomial regression were used to assess the association between quartiles of DII and DepS. Results In a fully adjusted model, higher DII score (i.e. pro-inflammatory diet) was associated with 79% increase in odds of reporting DepS (ORQuartile4vs1:1.79; 95% CI: 1.14-2.81; p trend =0.026). Men with higher DII had two-fold higher odds of DepS (ORQuartile4vs1:2.27; 95% CI: 1.02-5.06; p trend =0.089). Women with higher DII had an 81% increase in odds of DepS (ORQuartile4vs1:1.81; 95% CI: 1.01-3.26; p trend =0.068). These associations were consistent in the longitudinal analysis. The meta-analysis (n = 12) showed that a pro-inflammatory diet was associated with a 45% increase in odds of having DepS (ORQuartile4vs1:1.45; 95% CI: 1.20,1.74, p-value<0.01). Conclusions A pro-inflammatory diet was positively associated with increased risk of DepS. Our findings support the current evidence that shows the role of pro-inflammatory diet in DepS. Key messages Increase the consumption of anti-inflammatory diet to reduce depressive symptoms [ABSTRACT FROM AUTHOR]

Background Evidence regarding the association between perinatal smoking and insomnia symptoms in adulthood is limited. Using the UK 1970 Birth Cohort Study, we determined the association of maternal smoking during pregnancy and early-childhood with insomnia symptoms at 42 years. Methods Participants were followed from birth (1970; N = 9020; male, 48%) and age 5 (1975; N = 8050; male, 47.9%) to 42 years (2012). Data on maternal smoking was collected at birth and age 5; difficulties initiating or maintaining sleep (DIMS) and DIMS plus daytime symptoms (tiredness, irritability, depression and nervousness) [DIMS plus] at age 42. We used a direct acyclic graph to select confounders. A log-binomial logistic regression, adjusted for confounders, was used to estimate the association. Missing data were imputed via multiple imputation. Results The prevalence of DIMS and DIMS plus was 32% and 25%, respectively. There was a 25% [odds ratio (OR)=1.25; 95% confidence interval (CI): 1.12-1.38)] and 23% [OR = 1.23; 95% CI: 1.09-1.38] increase in odds of DIMS and DIMS plus among participants whose mothers smoked during pregnancy compared to those whose mother did not. A 24% [OR = 1.24; 95% CI: 1.12-1.37] and 18% [OR = 1.18; 95% CI: 1.05-1.33] increase in odds of DIMS and DIMS plus respectively, was observed among participants who had smoking mothers at age 5. Intensity and duration of smoking had a dose-response relationship with insomnia symptoms. Conclusions Maternal smoking during pregnancy and early-childhood is associated with increased risk of adult insomnia symptoms. Key messages This study suggests that reducing maternal smoking may reduce the risk of adult insomnia. [ABSTRACT FROM AUTHOR]

Background Estimates of the future burden of invasive cancer attributable to current modifiable causal exposures can guide cancer prevention. Methods We linked pooled data from seven Australian cohort studies (N = 367,058) to national cancer and death registries, and estimated exposure-cancer and exposure-death associations using adjusted proportional hazards models. We estimated exposure prevalence from contemporary national health surveys and calculated population attributable fractions (PAFs) and 95% confidence intervals, using advanced methods accounting for competing risk of death. Results Current levels of past and current smoking explain 36.1% (95%CI 33.2%-38.9%), body fatness 13.6% (10.9%-16.2%) and alcohol consumption exceeding two drinks/day 2.3% (1.0%-3.6%) of cancers causally related to these exposures, corresponding to 210,000, 81,300 and 14,800 cancers in Australia in the next 10 years, respectively. Ever smoking is the leading modifiable cause of lung (82.1%), bladder (49.8%), oesophageal (42.8%), liver (39.8%), head and neck (35.6%), and pancreatic (21.3%) cancer burden. Body fatness is the leading modifiable cause of corpus uteri (42.5%), gastric cardia (33.6%), renal cell (29.1%), thyroid (20.1%), colorectal (12.6%) and postmenopausal breast (12.6%) cancer burden. The absolute numbers of cancers in the next 10 years attributable to smoking are highest for lung cancer (114,000). The numbers of cancers attributable to body fatness and alcohol are highest for colorectal cancer (23,000 and 9,900, respectively). Conclusions More reliable advanced methods demonstrate large proportions and numbers of cancers are preventable by modifying behaviours. Key messages Ever smoking and body fatness are the leading causes of preventable future burden of causally related cancers in Australia. [ABSTRACT FROM AUTHOR]