Objective To determine the association of different types of meat intake and meat associated compounds with overall and cause specific mortality.Design Population based cohort study.Setting Baseline ...dietary data of the NIH-AARP Diet and Health Study (prospective cohort of the general population from six states and two metropolitan areas in the US) and 16 year follow-up data until 31 December 2011.Participants 536 969 AARP members aged 50-71 at baseline.Exposures Intake of total meat, processed and unprocessed red meat (beef, lamb, and pork) and white meat (poultry and fish), heme iron, and nitrate/nitrite from processed meat based on dietary questionnaire. Adjusted Cox proportional hazards regression models were used with the lowest fifth of calorie adjusted intakes as reference categories.Main outcome measure Mortality from any cause during follow-up.Results An increased risk of all cause mortality (hazard ratio for highest versus lowest fifth 1.26, 95% confidence interval 1.23 to 1.29) and death due to nine different causes associated with red meat intake was observed. Both processed and unprocessed red meat intakes were associated with all cause and cause specific mortality. Heme iron and processed meat nitrate/nitrite were independently associated with increased risk of all cause and cause specific mortality. Mediation models estimated that the increased mortality associated with processed red meat was influenced by nitrate intake (37.0-72.0%) and to a lesser degree by heme iron (20.9-24.1%). When the total meat intake was constant, the highest fifth of white meat intake was associated with a 25% reduction in risk of all cause mortality compared with the lowest intake level. Almost all causes of death showed an inverse association with white meat intake.Conclusions The results show increased risks of all cause mortality and death due to nine different causes associated with both processed and unprocessed red meat, accounted for, in part, by heme iron and nitrate/nitrite from processed meat. They also show reduced risks associated with substituting white meat, particularly unprocessed white meat.
Background
Cancer incidence is higher in men than in women at most shared anatomic sites for currently unknown reasons. The authors quantified the extent to which behaviors (smoking and alcohol use), ...anthropometrics (body mass index and height), lifestyles (physical activity, diet, medications), and medical history collectively explain the male predominance of risk at 21 shared cancer sites.
Methods
Prospective cohort analyses (n = 171,274 male and n = 122,826 female participants; age range, 50–71 years) in the National Institutes of Health‐AARP Diet and Health Study (1995–2011). Cancer‐specific Cox regression models were used to estimate male‐to‐female hazard ratios (HRs). The degree to which risk factors explained the observed male–female risk disparity was quantified using the Peters–Belson method.
Results
There were 26,693 incident cancers (17,951 in men and 8742 in women). Incidence was significantly lower in men than in women only for thyroid and gallbladder cancers. At most other anatomic sites, the risks were higher in men than in women (adjusted HR range, 1.3–10.8), with the strongest increases for bladder cancer (HR, 3.33; 95% confidence interval CI, 2.93–3.79), gastric cardia cancer (HR, 3.49; 95% CI, 2.26–5.37), larynx cancer (HR, 3.53; 95% CI, 2.46–5.06), and esophageal adenocarcinoma (HR, 10.80; 95% CI, 7.33–15.90). Risk factors explained a statistically significant (nonzero) proportion of the observed male excess for esophageal adenocarcinoma and cancers of liver, other biliary tract, bladder, skin, colon, rectum, and lung. However, only a modest proportion of the male excess was explained by risk factors (ranging from 50% for lung cancer to 11% for esophageal adenocarcinoma).
Conclusions
Men have a higher risk of cancer than women at most shared anatomic sites. Such male predominance is largely unexplained by risk factors, underscoring a role for sex‐related biologic factors.
The male predominance of many nonsex‐specific cancers has been explained by differences in exposure prevalence between sexes, but cancer incidence in this study remained significantly higher among men for most sites after a comprehensive adjustment for carcinogenic exposures. These findings suggest a role of sex‐related biologic mechanisms as the major determinants of sex differences in cancer risk.
In the United States, lung cancer death rates have been declining for decades, primarily as a result of pronounced decreases in cigarette smoking. It is unclear, however, whether there have been ...similar declines in mortality rates of lung cancer unrelated to smoking. We estimated trends in US lung cancer death rates attributable and not attributable to smoking from 1991 to 2018.
The study included 30- to 79-year-olds in the National Health Interview Survey who were linked to the National Death Index, 1991-2014. Adjusted hazard ratios for smoking status and lung cancer death were estimated, and age-specific population attributable fractions were calculated. Annual population attributable fractions were multiplied by annual US national lung cancer mortality, partitioning rates into smoking-attributable and smoking-unrelated lung cancer deaths. All statistical tests were 2-sided.
During 1991-2018, the proportion of never smokers increased among both men (35.1%-54.6%) and women (54.0%-65.4%). Compared with those who had ever smoked, those who had never smoked had 86% lower risk (hazard ratio = 0.14; 95% confidence interval CI = 0.12 to 0.16) of lung cancer death. The fraction of lung cancer deaths attributable to smoking decreased from 81.4% (95% CI = 78.9 to 81.4) to 74.7% (95% CI = 78.1 to 71.4). Smoking-attributable lung cancer death rates declined 2.7% per year (95% CI = ‒2.9% to ‒2.5%) and smoking-unrelated lung cancer death rates declined 1.8% per year (95% CI = ‒2.0% to ‒1.5%); these declines have accelerated in recent years.
An increasing proportion of lung cancer deaths are unrelated to smoking based on declines in smoking prevalence. Smoking-unrelated lung cancer death rates have declined, however, perhaps because of decreases in secondhand smoke and air pollution exposure as well as treatment improvements.
15% of US adults have gallstones, most of which are clinically "silent". Several studies show that menopausal hormone therapy (MHT) increases symptomatic gallstones and cholecystectomy risk. MHT use ...may be contraindicated in women with gallstones and population studies may be biased by "confounding by contraindication" while the true association between MHT and gallstones remains underestimated. We sought to examine whether MHT use was associated with asymptomatic gallstones using instrumental variable (IV) analysis to account for confounding by contraindication. We used 2018 postmenopausal women from the Third National Health and Nutrition Examination Survey to estimate associations of MHT use with asymptomatic gallstones. A traditional logistic regression analysis was compared to instrumental variable (IV) analysis to account for confounding by contraindication. 12% of women with asymptomatic gallstones and 25% of women without gallstones were current MHT users (P < 0.001). The traditional analysis suggested a decreased odds of asymptomatic gallstones in current versus never users (OR 0.58, 95% CI 0.37, 0.89), but increased odds (OR 1.51, 95% CI 0.44, 5.16) in the IV analysis. The traditional analysis consistently underestimated the odds of asymptomatic gallstones with MHT use compared to the IV analysis. Accounting for confounding by contraindication, we found a suggestive, though imprecise, positive association between MHT use and asymptomatic gallstones among postmenopausal women. Failure to consider contraindication can produce incorrect results.
Background and Aims
HCC is characterized by racial/ethnic disparities in rates. Recent USA reports suggest that incidence has begun to decline, but it is not clear whether the declines have occurred ...among all groups, nor whether mortality has declined. Thus, the current study examined USA incidence and mortality between 1992 and 2018.
Approach & Results
HCC incidence and incidence‐based mortality data from the Surveillance, Epidemiology, and End Results program were used to calculate age‐standardized rates by race/ethnicity, sex, and age. Trends were analyzed using joinpoint regression to estimate annual percent change (APC). Age‐period‐cohort models assessed the effects on trends of age, calendar period, and birth cohort. Overall, HCC incidence significantly declined between 2015 and 2018 (APC, −5.6%). Whereas most groups experienced incidence declines, the trends were most evident among Asians/Pacific Islanders, women, and persons <50 years old. Exceptions were the rates among non‐Hispanic Black persons, which did not significantly decline (APC, −0.7), and among American Indians/Alaska Natives, which significantly increased (APC, +4.3%). Age‐period‐cohort modeling found that birth cohort had a greater effect on rates than calendar period. Among the baby boom cohorts, the 1950–1954 cohort had the highest rates. Similar to the overall incidence decline, HCC mortality rates declined between 2013 and 2018 (APC, −2.2%).
Conclusions
HCC incidence and mortality rates began to decline for most groups in 2015, but persistent differences in rates continued to exist. Rates among non‐Hispanic Black persons did not decline significantly, and rates among American Indians/Alaska Natives significantly increased, suggesting that greater effort is needed to reduce the HCC burden among these vulnerable groups.
Age‐adjusted rates per 100,000 person‐years overall and by race/ethnicity of HCC incidence (left) and mortality (right) in the USA, 1992‐2018. AIAN, American Indian/Alaska Native; API, Asian/Pacific Islander; NHB, non‐Hispanic Black; NHW, non‐Hispanic White.
Body mass index (BMI), waist circumference (WC), and the waist-stature ratio (WSR) are considered to be possible proxies for adiposity.
The objective was to investigate the relations between BMI, WC, ...WSR, and percentage body fat (measured by dual-energy X-ray absorptiometry) in adults in a large nationally representative US population sample from the National Health and Nutrition Examination Survey (NHANES).
BMI, WC, and WSR were compared with percentage body fat in a sample of 12,901 adults.
WC, WSR, and BMI were significantly more correlated with each other than with percentage body fat (P < 0.0001 for all sex-age groups). Percentage body fat tended to be significantly more correlated with WC than with BMI in men but significantly more correlated with BMI than with WC in women (P < 0.0001 except in the oldest age group). WSR tended to be slightly more correlated with percentage body fat than was WC. Percentile values of BMI, WC, and WSR are shown that correspond to percentiles of percentage body fat increments of 5 percentage points. More than 90% of the sample could be categorized to within one category of percentage body fat by each measure.
BMI, WC, and WSR perform similarly as indicators of body fatness and are more closely related to each other than with percentage body fat. These variables may be an inaccurate measure of percentage body fat for an individual, but they correspond fairly well overall with percentage body fat within sex-age groups and distinguish categories of percentage body fat.
Restaurant prepared foods are known to be energy-dense and high in fat and sodium, but lower in protective nutrients. There is evidence of higher risk of adiposity, type II diabetes, and heart ...disease in frequent consumers of restaurant meals. However, the risk of mortality as a long-term health consequence of frequent consumption of restaurant meals has not been examined. We examined the prospective risk of all-cause and coronary heart disease, cerebrovascular disease and diabetes (cardiometabolic) mortality in relation to frequency of eating restaurant prepared meals in a national cohort. We used frequency of eating restaurant prepared meals information collected in the National Health and Nutrition Examination Surveys, conducted from 1999-2004, with mortality follow-up completed through Dec. 31, 2011 (baseline age ≥ 40y; n = 9107). We estimated the relative hazard of all-cause and cardiometabolic mortality associated with weekly frequency of eating restaurant meals using Cox-proportional hazards regression methods to adjust for multiple covariates. All analyses accounted for complex survey design and included sample weights. Over 33% of all respondents reported eating ≥3 restaurant prepared meals/week. In this cohort, 2200 deaths due to all causes and 665 cardiometabolic deaths occurred over a median follow-up of 9 years. The covariate-adjusted hazard ratio of all cause or cardiometabolic mortality in men and women reporters of <1 or 1-2 restaurant prepared meals did not differ from those reporting ≥3 meals/week (P>0.05). The results were robust to effect modification by baseline BMI, years of education, and baseline morbidity. Expectedly, the 24-h dietary intakes of whole grains, fruits, dietary fiber, folate, vitamin C, potassium and magnesium at baseline were lower, but energy, energy density, and energy from fat were higher in more frequent restaurant meal reporters (P<0.05). Baseline serum HDL cholesterol, folate, and some carotenoids were inversely associated with the frequency of eating restaurant prepared meals (P<0.05); however, serum concentrations of total cholesterol, triglycerides, fasting glucose, insulin, glycated hemoglobin, and c-reactive protein were unrelated (P<0.05). The weekly frequency of eating restaurant prepared meals and prospective risk of mortality after 9 years were not related in this cohort.
Celotno besedilo
Dostopno za:
DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
The World Health Organization (Geneva, Switzerland) and the National Heart, Lung, and Blood Institute (Bethesda, Maryland) have developed standard categories of body mass index (BMI) (calculated as ...weight (kg)/height (m)(2)) of less than 18.5 (underweight), 18.5-24.9 (normal weight), 25.0-29.9 (overweight), and 30.0 or more (obesity). Nevertheless, studies of BMI and the risk of death sometimes use nonstandard BMI categories that vary across studies. In a meta-analysis of 8 large studies that used nonstandard BMI categories and were published between 1999 and 2014 and included 5.8 million participants, hazard ratios tended to be small throughout the range of overweight and normal weight. Risks were similar between subjects of high-normal weight (BMI of approximately 23.0-24.9) and those of low overweight (BMI of approximately 25.0-27.4). In an example using national survey data, minor variations in the reference category affected hazard ratios. For example, choosing high-normal weight (BMI of 23.0-24.9) instead of standard normal weight (BMI of 18.5-24.9) as the reference category produced higher nonsignificant hazard ratios (1.05 vs. 0.97 for men and 1.06 vs. 1.02 for women) for the standard overweight category (BMI of 25.0-29.9). Use of the standard BMI groupings avoids problems of ad hoc and post hoc category selection and facilitates between-study comparisons. The ways in which BMI data are categorized and reported may shape inferences about the degree of risk for various BMI categories.
Weekend–weekday differences in time of ingestive events may be implicated in adverse metabolic and health outcomes. However, little is known about the nature of weekend–weekday differences in ...temporal eating behaviors of the US adult population.
The study aimed to examine weekend–weekday differences in temporal and energy characteristics of ingestive events self-reported by American adults.
Observational; within-person comparative.
The data were from the National Health and Nutrition Examination Surveys (NHANES) 2015–March 2020 (pre-pandemic) for ≥20-year-old adults who provided 1 weekday (M–Th) and 1 weekend (F, S, Su) 24-h dietary recall (n = 3564 men and 3823 women).
Prespecified primary temporal outcomes were recalled: time of ingestive events, and the duration of ingestive and fasting windows. Secondary outcomes included frequency and energy characteristics of ingestive events.
Gender-specific, survey-weighted, multiple linear regression models that accounted for complex survey design with dummy covariates for weekend/weekday, mode of recall administration (in-person on day 1 and telephone on day 2), and a respondent-specific fixed intercept.
In both men and women, the weekend recalled time of first ingestive event, breakfast, and lunch were later than weekday (P ≤ .0008); however, no statistically significant differences were observed in time of dinner and the last eating episode. The mean weekend ingestive window (interval between the time of first and last eating events of the day) was shorter by 24 minutes (95% confidence interval CI, –32, –11) in men and 18 minutes (95% CI, –20, –15) in women, and the mean overnight fasting window was correspondingly longer (P ≤ .0001). No statistically significant differences were observed between weekend and weekday frequency of ingestive events. Energy density of weekend food selections reported by women, and of beverages by men, was found to be higher than weekday (P ≤ .002).
Weekend ingestive patterns were characterized by later time of first ingestive event, breakfast, and lunch, and selection of higher-energy-density foods and beverages.
We evaluated proof of principle for resource-efficient, risk-based screening through reanalysis of the Kerala Oral Cancer Screening Trial.
The cluster-randomized trial included three triennial rounds ...of visual inspection (seven clusters, n = 96,516) versus standard of care (six clusters, n = 95,354) and up to 9 years of follow-up. We developed a Cox regression-based risk prediction model for oral cancer incidence. Using this risk prediction model to adjust for the oral cancer risk imbalance between arms, through intention-to-treat (ITT) analyses that accounted for cluster randomization, we calculated the relative (hazard ratios HRs) and absolute (rate differences RDs) screening efficacy on oral cancer mortality and compared screening efficiency across risk thresholds.
Oral cancer mortality was reduced by 27% in the screening versus control arms (HR = 0.73; 95% CI, 0.54 to 0.98), including a 29% reduction in ever-tobacco and/or ever-alcohol users (HR = 0.71; 95% CI, 0.51 to 0.99). This relative efficacy was similar across oral cancer risk quartiles (
interaction = .59); consequently, the absolute efficacy increased with increasing model-predicted risk-overall trial: RD in the lowest risk quartile (Q1) = 0.5/100,000 versus 13.4/100,000 in the highest quartile (Q4),
trend = .059 and ever-tobacco and/or ever-alcohol users: Q1 RD = 1.0/100,000 versus Q4 = 22.5/100,000;
trend = .026. In a population akin to the Kerala trial, screening of 100% of individuals would provide 27.1% oral cancer mortality reduction at number needed to screen (NNS) = 2,043. Restriction of screening to ever-tobacco and/or ever-alcohol users with no additional risk stratification would substantially enhance efficiency (43.4% screened for 23.3% oral cancer mortality reduction at NNS = 1,029), whereas risk prediction model-based screening of 50% of ever-tobacco and/or ever-alcohol users at highest risk would further enhance efficiency with little loss in program sensitivity (21.7% screened for 19.7% oral cancer mortality reduction at NNS = 610).
In the Kerala trial, the efficacy of oral cancer screening was greatest in individuals at highest oral cancer risk. These results provide proof of principle that risk-based oral cancer screening could substantially enhance the efficiency of screening programs.
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