Research on the relationship of meat, fish, and egg consumption and mortality among prostate cancer survivors is limited.
In the Cancer Prevention Study-II Nutrition Cohort, men diagnosed with ...nonmetastatic prostate cancer between baseline in 1992/1993 and 2015 were followed for mortality until 2016. Analyses of pre- and postdiagnosis intakes of red and processed meat, poultry, fish, and eggs included 9,286 and 4,882 survivors, respectively. Multivariable-adjusted RRs and 95% confidence intervals (CI) were estimated using Cox proportional hazards models.
A total of 4,682 and 2,768 deaths occurred during follow-up in pre- and postdiagnosis analyses, respectively. Both pre- and postdiagnosis intakes of total red and processed meat were positively associated with all-cause mortality (quartile 4 vs. 1: RR = 1.13; 95% CI, 1.03-1.25;
= 0.02; RR = 1.22; 95% CI, 1.07-1.39;
= 0.03, respectively), and both pre- and postdiagnosis poultry intakes were inversely associated with all-cause mortality (quartile 4 vs. 1 RR = 0.90; 95% CI, 0.82-0.98;
= 0.04; RR = 0.84; 95% CI, 0.75-0.95;
= 0.01, respectively). No associations were seen for prostate cancer-specific mortality, except that higher postdiagnosis unprocessed red meat intake was associated with lower risk.
Higher red and processed meat, and lower poultry, intakes either before or after prostate cancer diagnosis were associated with higher risk of all-cause mortality.
Our findings provide additional evidence that prostate cancer survivors should follow the nutrition guidelines limiting red and processed meat consumption to improve overall survival. Additional research on the relationship of specific meat types and mortality is needed.
To compare mental health indicators among undergraduates in Fall 2019, before the COVID-19 pandemic, and Fall 2020, when many students returned to campus amidst restrictions on in-person contact.
...Analyses included 26,881 undergraduate students, aged 18-24, from 70 U.S. institutions.
Students completed the National College Health Assessment-III survey in Fall 2019 or Fall 2020.
The prevalences of high stress, loneliness, a low flourishing score, and serious psychological distress increased in 2020 compared to 2019. Serious psychological distress increased substantially in 2020 among students not living with family (adjusted prevalence ratio (aPR)=1.36, 95% CI 1.29-1.45) but not among students living with family (aPR = 1.09, 95% CI 0.95-1.26).
These results suggest prevalences of several indicators of poor mental health were elevated among U.S. undergraduates several months into the pandemic. The pandemic may have had greater impact on mental health among students not living with family.
As online classes became the norm in many countries as a response to the COVID-19 pandemic, the concern for child and adolescent mental health became an issue of concern. This study evaluates the ...differences in the psychosocial status of school children based on engagement in in-person or Emergency Remote Education (ERE) and assessed the prevalence and predictors of symptom-derived risk levels for anxiety, depression, and obsessive-compulsive disorders (OCD). Cross-sectional data were collected from students at a Florida K-12 school and their household members through an online survey conducted in October 2020 (
= 145). No significant difference was found between ERE and in-person learning for risk of anxiety, depression, or OCD. Prevalence of students presenting as at risk for anxiety, depression, and OCD was 42.1%, 44.8%, and 41.4%. Several student factors (e.g., child sex, school level) and parental factors (e.g., parental COVID-19 attitudes) were associated with students presenting as at risk for anxiety, depression, or OCD; child's participation in sports was protective against all three outcomes. Participation in sports was found to be protective against risk of anxiety (aOR = 0.36, CI = 0.14-0.93), depression (aOR = 0.38, CI = 0.15-0.93), and OCD (aOR = 0.31, CI = 0.11-0.85).
Large prospective cohort studies need to confirm the associations between recreational physical activity (PA), including the most common type—walking, and prostate cancer–specific mortality (PCSM) ...among prostate cancer patients.
To investigate the associations of recreational PA, reported before and after diagnosis, with PCSM, overall and by tumor risk category.
In a prospective cohort study conducted in the USA, men diagnosed with nonmetastatic prostate cancer between 1992/1993 and June 2011 were followed for mortality until 2012. Patients were included in pre- (n=7328) and/or postdiagnosis (n=5319) analyses.
Cox proportional hazards models were used to assess PCSM with recreational PA.
A total of 454 and 261 prostate cancer deaths occurred during pre- and postdiagnosis follow-up, respectively. Prior to diagnosis, engaging in ≥17.5 metabolic equivalent hours per week (MET-h/wk) of recreational PA, compared with 3.5–<8.75 MET-h/wk, was associated with a significant 37% lower risk of PCSM (hazard ratio: 0.63, 95% confidence interval: 0.43–0.91, p trend=0.03) only among men with lower-risk tumors (Gleason score 2–7 and T1–T2; p interaction=0.02). A similar result was seen for walking but not for other recreational PA. After diagnosis, the same comparison (≥17.5 vs 3.5–<8.75 MET-h/wk) was associated with a significant 31% lower risk of overall PCSM (hazard ratio: 0.69, 95% confidence interval: 0.49–0.95, p trend=0.006), which did not differ by tumor risk category. Postdiagnosis walking had a suggestive inverse association with PCSM (p trend=0.07). These results were observational and may not be generalized to patients with metastatic prostate cancer. Residual confounding due to a higher screening rate among men with lower-risk tumors cannot be ruled out.
The findings provide additional evidence for prostate cancer survivors to adhere to PA recommendations, and support clinical trials of exercise among prostate cancer survivors with progression or mortality as outcomes.
In a large follow-up study of men diagnosed with nonmetastatic prostate cancer, those who exercise more after diagnosis had a lower risk of dying from prostate cancer.
In this large follow-up study of men diagnosed with nonmetastatic prostate cancer, engaging in at least 17.5 metabolic equivalent hours or 5h of moderate-intensity activity per week may improve prostate cancer–specific survival and overall survival.
The presence of circulating antibodies to the p53 tumor suppressor protein is a potential early detection colorectal cancer biomarker. However, studies of prediagnostic measures of p53 seropositivity ...in relation to colorectal cancer risk are limited.
We conducted a nested case-control study of serum p53 autoantibodies and risk of colorectal cancer within the Cancer Prevention Study-II Nutrition Cohort. Among cohort participants who were cancer free at the time of blood collection, 392 were subsequently diagnosed with colorectal cancer over 11 years of follow-up. Two controls were matched to each case on birth date, blood draw date, race, and sex. Autoantibodies to p53 were detected in 41 of the 392 cases (10.5%) and 49 of the 774 controls (6.3%).
Participants who were seropositive for p53 antibodies before diagnosis were more likely to be subsequently diagnosed with colorectal cancer RR = 1.77; 95% confidence interval (CI), 1.12-2.78. This association was strongest within 3 years of diagnosis (RR = 2.26; 95% CI, 1.06-4.83). An association was also suggested when colorectal cancer was diagnosed 4 to <6 years after p53 measurement (RR = 1.84; 95% CI, 0.89-3.79), but not 6 or more years later (RR = 1.15; 95% CI, 0.44-2.99).
If these results are confirmed, serum p53 antibodies may be useful on a panel of early detection markers for colorectal cancer.
Individuals who were seropositive for p53 antibodies were twice as likely to develop colorectal cancer within the next 3 years compared with those who were seronegative. This marker is a good candidate for inclusion on an early detection marker panel for colorectal cancer.
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Background
In the era of widespread prostate-specific antigen testing, it is important to focus etiologic research on the outcome of aggressive prostate cancer, but studies have defined this outcome ...differently. We aimed to develop an evidence-based consensus definition of aggressive prostate cancer using clinical features at diagnosis for etiologic epidemiologic research.
Methods
Among prostate cancer cases diagnosed in 2007 in the National Cancer Institute’s Surveillance, Epidemiology, and End Results-18 database with follow-up through 2017, we compared the performance of categorizations of aggressive prostate cancer in discriminating fatal prostate cancer within 10 years of diagnosis, placing the most emphasis on sensitivity and positive predictive value (PPV).
Results
In our case population (n = 55 900), 3073 men died of prostate cancer within 10 years. Among 12 definitions that included TNM staging and Gleason score, sensitivities ranged from 0.64 to 0.89 and PPVs ranged from 0.09 to 0.23. We propose defining aggressive prostate cancer as diagnosis of category T4 or N1 or M1 or Gleason score of 8 or greater prostate cancer, because this definition had one of the higher PPVs (0.23, 95% confidence interval = 0.22 to 0.24) and reasonable sensitivity (0.66, 95% confidence interval = 0.64 to 0.67) for prostate cancer death within 10 years. Results were similar across sensitivity analyses.
Conclusions
We recommend that etiologic epidemiologic studies of prostate cancer report results for this definition of aggressive prostate cancer. We also recommend that studies separately report results for advanced category (T4 or N1 or M1), high-grade (Gleason score ≥8), and fatal prostate cancer. Use of this comprehensive set of endpoints will facilitate comparison of results from different studies and help elucidate prostate cancer etiology.
Abstract Purpose The proportion of cancer deaths in the contemporary United States caused by cigarette smoking (the population attributable fraction PAF) is not well documented. Methods The PAF of ...all cancer deaths due to active cigarette smoking among adults 35 years and older in the United States in 2010 was calculated using age- and sex-specific smoking prevalence from the National Health Interview Survey (NHIS) and age- and sex-specific relative risks from the Cancer Prevention Study-II (for ages 35–54 years) and from the Pooled Contemporary Cohort data set (for ages 55 years and older). Results The PAF for active cigarette smoking was 28.7% when estimated conservatively, including only deaths from the 12 cancers currently formally established as caused by smoking by the US Surgeon General. The PAF was 31.7% when estimated more comprehensively, including excess deaths from all cancers. These estimates do not include additional potential cancer deaths from environmental tobacco smoke or other type of tobacco use such as cigars, pipes, or smokeless tobacco. Conclusions Cigarette smoking causes a large proportion of cancer deaths in the contemporary United States. Reducing smoking prevalence as rapidly as possible should be a top priority for the US public health efforts to prevent cancer deaths.
American chestnut (Castanea dentata) was functionally extirpated from eastern US forests by chestnut blight, caused by a fungus from Asia. As efforts to produce blight‐resistant American chestnut ...germplasm advance, approaches to reintroduce chestnut throughout its former range are being developed. However, chestnut is also quite susceptible to a root disease in the southern half of its former range, and the pathogen that causes the disease (Phytophthora cinnamomi) is expected to move northward as climate warms. Genetic resistance to root rot appears to vary among individual chestnut trees, and the prevalence of resistance is highly uncertain. Because restoration of a self‐sustaining chestnut population is ultimately a landscape‐scale problem, we used a process‐based forest landscape model (LANDIS‐II) to conduct experiments to quantify the effects of root rot on the effectiveness of chestnut population restoration efforts in the center of the former range of chestnut under various climate scenarios. We developed a new LANDIS‐II extension to simulate root rot‐induced tree mortality as a function of temperature and soil moisture. We conducted a factorial simulation experiment with climate and resistance to root rot as factors and found that root rot greatly reduced chestnut biomass on the landscape, even when resistance to root rot infection was at the highest levels currently observed in published studies. Warming climate enhanced the virulence of the pathogen and resulted in a greater reduction in chestnut biomass. Results indicate that root rot has the potential to seriously hamper chestnut restoration efforts if resistance of chestnut is not enhanced through breeding and biotechnology, suggesting restoration efforts will be more successful if targeted to latitudes, elevations, and site conditions where root rot is not expected to be present well into the future, including areas north of the historical chestnut range (Canada). These results demonstrate the vital importance of incorporating root rot resistance into the larger blight resistance breeding program.
Purpose
Prospective cohort studies suggest that red and processed meat consumption is associated with increased risk of pancreatic cancer among men, but not women. However, evidence is limited, and ...less evidence exists for other types of meat.
Methods
Cox proportional hazards regression was used to estimate multivariable-adjusted hazard ratios (HR) for the association of meat consumption, by type, with pancreatic cancer risk among 138,266 men and women in the Cancer Prevention Study-II Nutrition Cohort. Diet was assessed at baseline in 1992, and 10 years earlier, at enrollment into the parent CPS-II mortality cohort. 1,156 pancreatic cancers were verified through 2013.
Results
Red meat, processed meat, and fish intake at baseline were not associated with pancreatic cancer risk. However, for long-term red and processed meat consumption (highest quartiles in 1982 and 1992, vs. lowest quartiles), risk appeared different in men hazard ratio (HR) 1.32, 95% confidence interval (CI) 0.90, 1.95 and women (HR 0.72, 95% CI 0.47, 1.10,
p
heterogeneity by sex = 0.05). Poultry consumption in 1992 was associated with increased pancreatic cancer risk (HR 1.27, 95% CI 1.04, 1.55,
p
trend = 0.01, top vs. bottom quintile).
Conclusions
The associations of meat consumption with pancreatic cancer risk remain unclear and further research, particularly of long-term intake, is warranted.
Germline variation and smoking are independently associated with pancreatic ductal adenocarcinoma (PDAC). We conducted genome-wide smoking interaction analysis of PDAC using genotype data from four ...previous genome-wide association studies in individuals of European ancestry (7,937 cases and 11,774 controls). Examination of expression quantitative trait loci data from the Genotype-Tissue Expression Project followed by colocalization analysis was conducted to determine whether there was support for common SNP(s) underlying the observed associations. Statistical tests were two sided and
< 5 × 10
was considered statistically significant. Genome-wide significant evidence of qualitative interaction was identified on chr2q21.3 in intron 5 of the transmembrane protein 163 (TMEM163) and upstream of the cyclin T2 (CCNT2). The most significant SNP using the Empirical Bayes method, in this region that included 45 significantly associated SNPs, was rs1818613 per allele OR in never smokers 0.87, 95% confidence interval (CI), 0.82-0.93; former smokers 1.00, 95% CI, 0.91-1.07; current smokers 1.25, 95% CI 1.12-1.40,
= 3.08 × 10
). Examination of the Genotype-Tissue Expression Project data demonstrated an expression quantitative trait locus in this region for TMEM163 and CCNT2 in several tissue types. Colocalization analysis supported a shared SNP, rs842357, in high linkage disequilibrium with rs1818613 (
= 0. 94) driving both the observed interaction and the expression quantitative trait loci signals. Future studies are needed to confirm and understand the differential biologic mechanisms by smoking status that contribute to our PDAC findings. SIGNIFICANCE: This large genome-wide interaction study identifies a susceptibility locus on 2q21.3 that significantly modified PDAC risk by smoking status, providing insight into smoking-associated PDAC, with implications for prevention.
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