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Background: Globorisk is one of the prediction tools for 10-year risk assessment of cardiovascular disease, featuring an office-based (non-laboratory-based) version. This version does not require laboratory tests for determining the CVD risk. The present study aims to determine the 10-year CVD risk using the office-based Globorisk model and factors associated with the 10-year CVD risk. Methods: In this study, baseline data from 6810 individuals participating in the Fasa cohort study, with no history of CVD or stroke, were utilized. The risk equation of the office-based Globorisk model incorporates age, sex, systolic blood pressure (SBP), body mass index (BMI), and smoking status. The Globorisk model categorizes the risk into three groups: low risk (< 10%), moderate risk (10% to < 20%), and high risk (≥ 20%). To identify factors associated with the 10-year CVD risk, the predicted risk was categorized into two groups: <10% and ≥ 10%. Multivariable logistic regression analysis was employed to determine factors associated with an increased CVD risk. Results: According to the 10-year CVD risk categorization, 78.3%, 16.4%, and 5.3% of men were in the low, moderate, and high risk groups, respectively, while 85.8%, 10.0%, and 4.2%, of women were in the respective risk groups. Multivariable logistic regression results indicated that in men, the 10-year CVD risk decreases with being an opium user, and increases with being illiterate, having abdominal obesity, and low or moderate physical activity compared to high physical activity. In women, being married, and higher fiber consumption decrease the 10-year CVD risk, while being illiterate, low or moderate physical activity compared to high physical activity, having abdominal obesity, opium use, and being in wealth quintiles 1 to 4 compared to quintile 5 increase the risk. Conclusions: Considering the factors associated with increased CVD risk, there is a need to enhance awareness and modify lifestyle to mitigate and reduce the risk of CVD. Additionally, early identification of individuals at moderate to high risk is essential for preventing disease progression. The use of the office-based Globorisk model can be beneficial in settings where resources are limited for determining the 10-year CVD risk. [ABSTRACT FROM AUTHOR]

Purpose: Whether youth who follow plant-based diets in Nordic countries meet their dietary needs for micronutrients remains unclear. This study aims to evaluate micronutrient intake and status in Norwegian youth following vegan, lacto-ovo-vegetarian, pescatarian, flexitarian and omnivore diets. Methods: Cross-sectional design, with healthy 16-to-24-year-olds (n = 165). Participants were asked to complete a questionnaire and four 24-hour dietary recalls. Dried blood spots (DBS) and spot-urine samples were collected for analysis of methyl malonic acid (MMA) (n = 65), haemoglobin (Hb) (n = 164) and urinary iodine concentration (UIC) (n = 163). Results: Vegans reported highest habitual supplement usage of multivitamin (58%), B12 (90%) and macroalgae consumption (32%), while flexitarians reported highest habitual usage of omega-3 supplements (56%). For daily supplement usage, vegans reported highest use of multivitamins (42%), B12 (79%), iodine (37%) and iron (63%). Increased risk of inadequate intake (energy-adjusted) were found for vitamin D (60% within lacto-ovo-vegetarians), selenium (70% within lacto-ovo-vegetarians, 65% within omnivores), and iodine (63% within vegans). Median MMA levels suggest low risk of insufficient B12 status across all groups (MMA 0.04‒0.37µmol/l) and 2% had MMA levels indicating possible B12 deficiency and 8% had elevated levels. Median Hb levels indicated low risk of anemia across all groups (≥ 12.0 females, ≥ 13.0 g/dl males), though 7% had Hb values indicating risk of mild anemia and 4% risk of moderate anemia. The median UIC indicates mild iodine deficiency in all groups (UIC < 100 µg/l), except vegans, who were moderately iodine deficient (UIC < 50 µg/l). Conclusions: Our study indicated that the participating youth had low risk of inadequate intake of most micronutrients, partly due to high supplement usage. However, for iodine, vitamin D, and selenium higher risk of inadequate intake was found. UIC corroborated the low iodine intake among vegans. Thus, we suggest iodine status of youth in Norway should be monitored, especially among young fertile women who omits dietary iodine sources, until a mandatory iodine fortification program is implemented. Furthermore, we suggest that food education on how to secure sufficient nutrients from food in general should be provided to the Norwegian youth population, especially how to secure adequate intake of vitamin D, selenium and iodine. [ABSTRACT FROM AUTHOR]

Scandinavian electronic health-care registers provide a unique setting to investigate potential unidentified side effects of drugs. We analysed the association between prescription drugs dispensed in Norway and Sweden and the short-term risk of developing pulmonary embolism. A total of 12,104 pulmonary embolism cases were identified from patient- and cause-of-death registries in Norway (2004–2014) and 36,088 in Sweden (2005–2014). A case-crossover design was used to compare individual drugs dispensed 1–30 days before the date of pulmonary embolism diagnosis with dispensation in a 61–90 day time-window, while controlling for the receipt of other drugs. A BOLASSO approach was used to select drugs that were associated with short-term risk of pulmonary embolism. Thirty-eight drugs were associated with pulmonary embolism in the combined analysis of the Norwegian and Swedish data. Drugs associated with increased risk of pulmonary embolism included certain proton-pump inhibitors, antibiotics, antithrombotics, vasodilators, furosemide, anti-varicose medications, corticosteroids, immunostimulants (pegfilgrastim), opioids, analgesics, anxiolytics, antidepressants, antiprotozoals, and drugs for cough and colds. Mineral supplements, hydrochlorothiazide and potassium-sparing agents, beta-blockers, angiotensin 2 receptor blockers, statins, and methotrexate were associated with lower risk. Most associations persisted, and several additional drugs were associated, with pulmonary embolism when using a longer time window of 90 days instead of 30 days. These results provide exploratory, pharmacopeia-wide evidence of medications that may increase or decrease the risk of pulmonary embolism. Some of these findings were expected based on the drugs' indications, while others are novel and require further study as potentially modifiable precipitants of pulmonary embolism. [ABSTRACT FROM AUTHOR]

Hypertension is a very common comorbidity in type 2 diabetes patients, which leads to important health and treatment challenges. The present study was conducted with the aim of determining the prevalence of hypertension and its risk factors in type 2 diabetes patients. This study was conducted using cross-sectional data from 1245 participants aged between 35 and 70 years and diagnosed with type 2 diabetes at baseline in the Fasa cohort study. The prevalence hypertension was determined and multivariate logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for the association between various risk factors and hypertension prevalence. The average age of the participants was 53.5 ± 8.7 years and 71.7% (n = 893) were female and 28.3% (n = 352) were male. The prevalence of hypertension in people with type 2 diabetes was 45.5% (n = 566). Higher age (AOR, 95% CI: 8.1, 4.6–14.3), female gender (OR, 95% CI: 1.8, 1.2–2.5), Fars (AOR, 95% CI: 1.6, 1.1–2.4) and Turk (AOR, 95% CI: 1.6, 1.1–2.5) vs. other ethnicity, and overweight (AOR, 95% CI: 1.8, 1.38–2.38) and obesity (AOR, 95% CI: 2.7, 2.0–3.8) vs. BMI < 25 was associated with a higher prevalence of hypertension, while higher physical activity (AOR, 95% CI: 0.57, 0.42–0.78) was associated with lower prevalence of hypertension in the multivariable model. The prevalence of hypertension in persons with type 2 diabetes was high and increased with greater age, in some ethnic groups, and with higher BMI and low physical activity. Further prospective studies are needed to investigate these associations in this population. [ABSTRACT FROM AUTHOR]

Background: The allometric body shape index (ABSI) and hip index (HI), as well as multi-trait body shape phenotypes, have not yet been compared in their associations with inflammatory markers. The aim of this study was to examine the relationship between novel and traditional anthropometric indexes with inflammation using data from the European Prospective Investigation into Cancer and Nutrition (EPIC) and UK Biobank cohorts. Methods: Participants from EPIC (n = 17,943, 69.1% women) and UK Biobank (n = 426,223, 53.2% women) with data on anthropometric indexes and C-reactive protein (CRP) were included in this cross-sectional analysis. A subset of women in EPIC also had at least one measurement for interleukins, tumour necrosis factor alpha, interferon gamma, leptin, and adiponectin. Four distinct body shape phenotypes were derived by a principal component (PC) analysis on height, weight, body mass index (BMI), waist (WC) and hip circumferences (HC), and waist-to-hip ratio (WHR). PC1 described overall adiposity, PC2 tall with low WHR, PC3 tall and centrally obese, and PC4 high BMI and weight with low WC and HC, suggesting an athletic phenotype. ABSI, HI, waist-to-height ratio and waist-to-hip index (WHI) were also calculated. Linear regression models were carried out separately in EPIC and UK Biobank stratified by sex and adjusted for age, smoking status, education, and physical activity. Results were additionally combined in a random-effects meta-analysis. Results: Traditional anthropometric indexes, particularly BMI, WC, and weight were positively associated with CRP levels, in men and women. Body shape phenotypes also showed distinct associations with CRP. Specifically, PC2 showed inverse associations with CRP in EPIC and UK Biobank in both sexes, similarly to height. PC3 was inversely associated with CRP among women, whereas positive associations were observed among men. Conclusions: Specific indexes of body size and body fat distribution showed differential associations with inflammation in adults. Notably, our results suggest that in women, height may mitigate the impact of a higher WC and HC on inflammation. This suggests that subtypes of adiposity exhibit substantial variation in their inflammatory potential, which may have implications for inflammation-related chronic diseases. [ABSTRACT FROM AUTHOR]

Low physical activity and high sedentary behaviour have been clearly linked with colorectal cancer development, yet data on their potential role in colorectal cancer survival is limited. Better characterisation of these relationships is needed for the development of post‐diagnosis physical activity and sedentary behaviour guidance for colorectal cancer survivors. We searched PubMed and Embase through 28 February 2022 for studies assessing post‐diagnosis physical activity, and/or sedentary behaviour in relation to all‐cause and cause‐specific mortality and recurrence after colorectal cancer diagnosis. Total and recreational physical activity were assessed overall and by frequency, duration, intensity, and volume using categorical, linear, and non‐linear dose–response random‐effects meta‐analyses. The Global Cancer Update Programme (CUP Global) independent Expert Committee on Cancer Survivorship and Expert Panel interpreted and graded the likelihood of causality. We identified 16 observational studies on 82,220 non‐overlapping patients from six countries. Physical activity was consistently inversely associated with colorectal cancer morbidity and mortality outcomes, with 13%–60% estimated reductions in risk. Sedentary behaviour was positively associated with all‐cause mortality. The evidence had methodological limitations including potential confounding, selection bias and reverse causation, coupled with a limited number of studies for most associations. The CUP Global Expert panel concluded limited‐suggestive evidence for recreational physical activity with all‐cause mortality and cancer recurrence. Total physical activity and its specific domains and dimensions, and sedentary behaviour were all graded as limited‐no conclusion for all outcomes. Future research should focus on randomised trials, while observational studies should obtain objective and repeated physical activity measures and better adjustment for confounders. [ABSTRACT FROM AUTHOR]

Based on the World Cancer Research Fund Global Cancer Update Programme, we performed systematic reviews and meta‐analyses to investigate the association of post‐diagnosis adiposity, physical activity, sedentary behaviour, and dietary factors with colorectal cancer prognosis. We searched PubMed and Embase until 28th February, 2022. An independent expert committee and expert panel graded the quality of evidence. A total of 167 unique publications were reviewed, and all but five were observational studies. The quality of the evidence was graded conservatively due to the high risk of several biases. There was evidence of non‐linearity in the associations between body mass index and colorectal cancer prognosis. The associations appeared reverse J‐shaped, and the quality of this evidence was graded as limited (likelihood of causality: limited‐no conclusion). The evidence on recreational physical activity and lower risk of all‐cause mortality (relative risk [RR] highest vs. lowest: 0.69, 95% confidence interval [CI]: 0.62–0.77) and recurrence/disease‐free survival (RR: 0.80, 95% CI: 0.70–0.92) was graded as limited‐suggestive. There was limited‐suggestive evidence for the associations between healthy dietary and/or lifestyle patterns (including diets that comprised plant‐based foods), intake of whole grains and coffee with lower risk of all‐cause mortality, and between unhealthy dietary patterns and intake of sugary drinks with higher risk of all‐cause mortality. The evidence for other exposures on colorectal cancer outcomes was sparse and graded as limited‐no conclusion. Analyses were conducted excluding cancer patients with metastases without substantial changes in the findings. Well‐designed intervention and cohort studies are needed to support the development of lifestyle recommendations for colorectal cancer patients. [ABSTRACT FROM AUTHOR]

The adiposity influence on colorectal cancer prognosis remains poorly characterised. We performed a systematic review and meta‐analysis on post‐diagnosis adiposity measures (body mass index [BMI], waist circumference, waist‐to‐hip ratio, weight) or their changes and colorectal cancer outcomes. PubMed and Embase were searched through 28 February 2022. Random‐effects meta‐analyses were conducted when at least three studies had sufficient information. The quality of evidence was interpreted and graded by the Global Cancer Update Programme (CUP Global) independent Expert Committee on Cancer Survivorship and Expert Panel. We reviewed 124 observational studies (85 publications). Meta‐analyses were possible for BMI and all‐cause mortality, colorectal cancer‐specific mortality, and cancer recurrence/disease‐free survival. Non‐linear meta‐analysis indicated a reverse J‐shaped association between BMI and colorectal cancer outcomes (nadir at BMI 28 kg/m2). The highest risk, relative to the nadir, was observed at both ends of the BMI distribution (18 and 38 kg/m2), namely 60% and 23% higher risk for all‐cause mortality; 95% and 26% for colorectal cancer‐specific mortality; and 37% and 24% for cancer recurrence/disease‐free survival, respectively. The higher risk with low BMI was attenuated in secondary analyses of RCTs (compared to cohort studies), among studies with longer follow‐up, and in women suggesting potential methodological limitations and/or altered physiological state. Descriptively synthesised studies on other adiposity‐outcome associations of interest were limited in number and methodological quality. All the associations were graded as limited (likelihood of causality: no conclusion) due to potential methodological limitations (reverse causation, confounding, selection bias). Additional well‐designed observational studies and interventional trials are needed to provide further clarification. [ABSTRACT FROM AUTHOR]

The role of diet in colorectal cancer prognosis is not well understood and specific lifestyle recommendations are lacking. We searched for randomised controlled trials (RCTs) and longitudinal observational studies on post‐diagnosis dietary factors, supplement use and colorectal cancer survival outcomes in PubMed and Embase from inception until 28th February 2022. Random‐effects dose–response meta‐analyses were conducted when at least three studies had sufficient information. The evidence was interpreted and graded by the CUP Global independent Expert Committee on Cancer Survivorship and Expert Panel. Five RCTs and 35 observational studies were included (30,242 cases, over 8700 all‐cause and 2100 colorectal cancer deaths, 3700 progression, recurrence, or disease‐free events). Meta‐analyses, including 3–10 observational studies each, were conducted for: whole grains, nuts/peanuts, red and processed meat, dairy products, sugary drinks, artificially sweetened beverages, coffee, alcohol, dietary glycaemic load/index, insulin load/index, marine omega‐3 polyunsaturated fatty acids, supplemental calcium, circulating 25‐hydroxyvitamin D (25[OH]D) and all‐cause mortality; for alcohol, supplemental calcium, circulating 25(OH)D and colorectal cancer‐specific mortality; and for circulating 25(OH)D and recurrence/disease‐free survival. The overall evidence was graded as 'limited'. The inverse associations between healthy dietary and/or lifestyle patterns (including diets that comprised plant‐based foods), whole grains, total, caffeinated, or decaffeinated coffee and all‐cause mortality and the positive associations between unhealthy dietary patterns, sugary drinks and all‐cause mortality provided 'limited—suggestive' evidence. All other exposure‐outcome associations provided 'limited—no conclusion' evidence. Additional, well‐conducted cohort studies and carefully designed RCTs are needed to develop specific lifestyle recommendations for colorectal cancer survivors. [ABSTRACT FROM AUTHOR]

Background: Metabolic syndrome (MetS) is a cluster of risk factors and the Framingham risk score (FRS) is a useful metric for measuring the 10-year cardiovascular disease (CVD) risk of the population. The present study aimed to determine the 10-year risk of cardiovascular disease using the Framingham risk score in people with and without MetS in a large Iranian cohort study. Methods: This cross-sectional study was done using the Fasa cohort. Participants aged ≥ 35 years old were recruited to the study from 2015 to 2016. The FRS was calculated using age, sex, current smoking, diabetes, systolic blood pressure (SBP), total cholesterol, and high-density lipoprotein (HDL) cholesterol. MetS was defined as the presence of three or more of the MetS risk factors including triglyceride (TG) level ≥ 150 mg dl− 1, HDL level < 40 mg dl− 1 in men and < 50 mg dl− 1 in women, systolic/diastolic blood pressure ≥ 130/≥85 mmHg or using medicine for hypertension, fasting blood sugar (FBS) level ≥ 100 mg dl− 1 or using diabetes medication and abdominal obesity considered as waist circumference (WC) ≥ 88 cm for women and ≥ 102 cm for men. Multiple logistic regressions were applied to estimate the 10- year CVD risk among people with and without MetS. Results: Of 8949 participants, 1928 people (21.6%) had MetS. The mean age of the participants with and without Mets was 50.4 ± 9.2 years and 46.9 ± 9.1 years respectively. In total 15.3% of participants with MetS and 8.0% of participants without MetS were in the high-risk category of 10-year CVD risk. Among participants with MetS gender, TG, SBP, FBS and in people without MetS gender, TG, SBP, FBS, and HDL showed strong associations with the predicted 10-year CVD risk. Conclusion: Male sex and increased SBP, TG, and FBS parameters were strongly associated with increased 10-year risk of CVD in people with and without MetS. In people without MetS, reduced HDL-cholestrol was strongly associated with increased 10-year risk of CVD. The recognition of participant's TG, blood pressure (BP), FBS and planning appropriate lifestyle interventions related to these characteristics is an important step towards prevention of CVD. [ABSTRACT FROM AUTHOR]

High health literacy (HL) plays a critical role in preventing or delaying the onset of cardiovascular diseases (CVDs) and can improve disease management and control. The present study aims to determine the association between HL and non-laboratory-based (office-based) Framingham 10-year risk score of CVD. This cross-sectional study was conducted on 648 people aged 30–65 in the health centers of Jahrom. The Health Literacy Instrument for Adults (HELIA) was used to assess HL. The non-laboratory-based Framingham risk score (FRS) was utilized to determine the 10-year risk of CVDs. Risk factors such as age, gender, diabetes, current smoking status, systolic blood pressure (SBP), hypertension (HTN) treatment, and body mass index (BMI) were applied in the non-laboratory-based model. The average age of the subjects was 44.7 ± 10.5 years, among which 49.2% were males. The prevalence of diabetes, HTN, and smoking equaled 8.5%, 15.7%, and 10%, respectively. In addition, the average BMI was 26.1 ± 3.6 kg/m2. Based on the non-laboratory-based Framingham 10-year risk score of CVD, 72.5%, 13.9%, and 13.6% of the subjects were in the low, moderate, and high risk groups, respectively. Based on the HL grouping, the levels of insufficient, borderline, sufficient, and excellent HL were 19.3%, 26.4%, 34.6%, and 19.7%, respectively. A significant association was observed between 10-year CVD risk and HL grouping. In addition, a negative correlation was reported at the individual level between HL and non-laboratory-based FRS among the whole population (r = − 0.39, p < 0.001), men (r = − 0.32, p < 0.001), and women (r = − 0.42, p < 0.001). A higher HL score is associated with a lower risk of CVD. In addition, the adjusted logistic regression analysis showed that there was a strong association between elevated CVD risk (≥ 10%) and HL (OR 6.1, 95% CI 2.9–12.6) among inadequate HL participants compared with excellent HL individuals. Thus, designing and implementing training programs to increase HL, especially among those who are at risk of CVDs, should be regarded as an important issue for the prevention of such diseases. [ABSTRACT FROM AUTHOR]

Background and objective: Physical activity has benefits for the cardiovascular system, however, what levels and types of activity provide optimal cardiovascular health is unclear. We aimed to determine the level of physical activity that has the most benefits against cardiovascular diseases (CVD). Methods: PubMed, Scopus, and Web of Science were searched for prospective cohort studies on leisure-time (LTPA) or occupational physical activity (OPA) as the exposure and major types of CVD (total CVD, coronary heart disease [CHD], stroke, and atrial fibrillation [AF]) incidence as the outcome. Risk of bias of studies was evaluated using the ROBINS-I tool. Summary hazard ratios (HR) were calculated using random-effects pairwise model. Results: A total of 103 studies were included in the analysis. The highest versus the lowest LTPA was associated with a lower risk of overall CVD (HR = 0.81; 95% CI: 0.77–0.86), CHD (HR = 0.83; 0.79–0.88), and stroke (HR = 0.83; 0.79–0.88), but not AF (HR = 0.98; 0.92–1.05). Linear dose-response analyses showed a 10%, 12%, 9%, and 8% risk reduction in CVD, CHD, stroke, and AF incidence, respectively, for every 20 MET-hours/week increase in LTPA. In nonlinear dose-response analyses, there were inverse associations up to 20 MET-hours/week with 19% and 20% reduction in CVD and CHD risk, and up to 25 MET-hours/week with 22% reduction in stroke, with no further risk reduction at higher LTPA levels. For AF, there was a U-shaped nonlinear association with the maximum 8% risk reduction at 10 MET-hours/week of LTPA. Higher levels of OPA were not associated with risk of CVD, CHD, stroke, or AF. Conclusions: Overall, results showed an inverse dose-response relationship between LTPA and risk of CVD, CHD, stroke, and AF. Running was the most beneficial LTPA but the risk was similar among various LTPA intensities. OPA showed no benefits in total or any type of CVD. [ABSTRACT FROM AUTHOR]

Background Phytonutrient intakes may improve outcomes following breast cancer, but the impact of postdiagnosis introduction vs established prediagnostic exposure as well as optimum doses has not been established. Evidence from observational studies for key exposures was evaluated, including dosage and intake time frames. Methods MEDLINE, EMBASE, CINAHL, Cochrane Library, ClinicalTrials.gov, and the ISRCTN registry were searched for prospective and retrospective observational studies investigating the impact of soybean, lignans, cruciferous (cabbage-family) vegetables, green tea, or their phytonutrients on breast cancer survival outcomes. A random-effects model was used to calculate summary hazard ratios (HRs) and 95% confidence intervals (CIs). Nonlinear dose-response analyses were conducted using restricted cubic splines. Results Thirty-two articles were included. Soy isoflavones were associated with a 26% reduced risk of recurrence (HR = 0.74, 95% CI = 0.60 to 0.92), particularly among postmenopausal (HR = 0.72, 95% CI = 0.55 to 0.94) and estrogen receptor–positive survivors (HR = 0.82, 95% CI = 0.70 to 0.97), with the greatest risk reduction at 60 mg/day. In mortality outcomes, the reduction was mostly at 20 to 40 mg/day. Soy protein and products were inversely associated with cancer-specific mortality for estrogen receptor–positive disease (HR = 0.75, 95% CI = 0.60 to 0.92). An inverse association was observed for serum or plasma enterolactone, measured prediagnosis and early postdiagnosis, with cancer-specific mortality (HR = 0.72, 95% CI = 0.58 to 0.90) and all-cause mortality (HR = 0.69, 95% CI = 0.57 to 0.83). No effects were observed for cruciferous vegetables. There was a 44% reduced risk of recurrence with prediagnostic green tea for stage I and II breast cancer (HR = 0.56, 95% CI = 0.38 to 0.83). Conclusions Soy, enterolactone, and green tea demonstrated significant risk reductions in outcomes following breast cancer. Evidence is needed regarding the impact of postdiagnostic introduction or substantial increase of these exposures. [ABSTRACT FROM AUTHOR]

Background: Whether cancer risk associated with a higher body mass index (BMI), a surrogate measure of adiposity, differs among adults with and without cardiovascular diseases (CVD) and/or type 2 diabetes (T2D) is unclear. The primary aim of this study was to evaluate separate and joint associations of BMI and CVD/T2D with the risk of cancer. Methods: This is an individual participant data meta-analysis of two prospective cohort studies, the UK Biobank (UKB) and the European Prospective Investigation into Cancer and nutrition (EPIC), with a total of 577,343 adults, free of cancer, T2D, and CVD at recruitment. We used Cox proportional hazard regressions to estimate multivariable-adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) for associations between BMI and incidence of obesity-related cancer and in turn overall cancer with a multiplicative interaction between BMI and the two cardiometabolic diseases (CMD). HRs and 95% CIs for separate and joint associations for categories of overweight/obesity and CMD status were estimated, and additive interaction was quantified through relative excess risk due to interaction (RERI). Results: In the meta-analysis of both cohorts, BMI (per ~ 5 kg/m2) was positively associated with the risk of obesity-related cancer among participants without a CMD (HR: 1.11, 95%CI: 1.07,1.16), among participants with T2D (HR: 1.11, 95% CI: 1.05,1.18), among participants with CVD (HR: 1.17, 95% CI: 1.11,1.24), and suggestively positive among those with both T2D and CVD (HR: 1.09, 95% CI: 0.94,1.25). An additive interaction between obesity (BMI ≥ 30 kg/m2) and CVD with the risk of overall cancer translated into a meta-analytical RERI of 0.28 (95% CI: 0.09–0.47). Conclusions: Irrespective of CMD status, higher BMI increased the risk of obesity-related cancer among European adults. The additive interaction between obesity and CVD suggests that obesity prevention would translate into a greater cancer risk reduction among population groups with CVD than among the general population. [ABSTRACT FROM AUTHOR]

Introduction: Rheumatic heart disease is considered well-controlled in high-income countries; however, its actual trends in mortality remain unclarified. We analyzed trends in mortality from rheumatic heart disease in association with age, period, and birth cohort. Methods: We analyzed the WHO mortality database to determine trends in mortality from rheumatic heart disease in the UK, Germany, France, Italy, Japan, Australia, USA, and Canada from 2000 to 2020. We used age-cohort-period modeling to estimate cohort and period effects. Net drift (overall annual percentage change), local drift (annual percentage change in each age group) and heterogeneity were calculated. Results: In the most recent year, crude mortality rates and age-standardized mortality rates ranged from 1.10 in the USA to 6.17 in Germany, and 0.32 (95% CI 0.31–0.34) in Japan and 1.70 (95% CI 1.65–1.75) in Germany, respectively. During the observation period, while Germany had a constant trend in overall annual percentage change, all the other countries had significant decreasing trends (p < 0.0001, respectively). Annual percent change was not homogeneous across each group in all 8 countries (pheterogeneity < 0.0001), with 2 peaks in the younger and older age categories. In Germany, Italy, Australia, and Canada, we found increasing mortality rates among older patients. Improving period and cohort risks for rheumatic heart disease mortality were generally observed, excluding Germany where the period effect was worsening and the cohort effect was constant. Conclusions: Mortality trends from rheumatic heart disease were decreasing in the study high-income countries except for Germany where higher mortality and two peaks in annual percentage change in younger and older age groups warrant further investigation. [ABSTRACT FROM AUTHOR]

Background: Two versions of Framingham's 10-year risk score are defined for cardiovascular diseases, namely laboratory-based and office-based models. The former is mainly employed in high-income countries, but unfortunately, it is not cost-effective or practical to utilize it in countries with poor facilities. Therefore, the present study aims to identify the agreement and correlation between laboratory-based and office-based Framingham models. Methods: Using laboratory-based and office-based Framingham models, this cross-sectional study used data from 8944 participants without a history of CVDs and stroke at baseline in the Fasa cohort study to predict the 10-year risk of CVDs. The laboratory-based model included age, sex, diabetes, smoking status, systolic blood pressure (SBP), treatment of hypertension, total cholesterol, and high-density lipoprotein (HDL); and the office-based model included age, sex, diabetes, smoking status, SBP, treatment of hypertension, and body mass index (BMI). The agreement between risk categories of laboratory-based and office-based Framingham models (low [< 10%], moderate [from 10 to < 20%], high [≥ 20%]) was assessed by kappa coefficients and percent agreement. Then, the correlation between the risk scores was estimated using correlation coefficients and illustrated using scatter plots. Finally, agreements, correlation coefficient, and scatter plots for laboratory-based and office-based Framingham models were analyzed by stratified Framingham risk score factors including sex, age, BMI categories, hypertension, smoking, and diabetes status. Results: The two models showed substantial agreement at 89.40% with a kappa coefficient of 0.75. The agreement was substantial in all men (kappa = 0.73) and women (kappa = 0.72), people aged < 60 years (kappa = 0.73) and aged ≥ 60 years (kappa = 0.69), smokers (kappa = 0.70) and non-smokers (kappa = 0.75), people with hypertension (kappa = 0.73) and without hypertension (kappa = 0.75), diabetics (kappa = 0.71) and non-diabetics (kappa = 0.75), people with normal BMI (kappa = 0.75) and people with overweight and obesity (kappa = 0.76). There was also a very strong positive correlation (r ≥ 0.92) between laboratory-based and office-based models in terms of age, sex, BMI, hypertension, smoking status and diabetes status. Conclusions: The current study showed that there was a substantial agreement between the office-based and laboratory-based models, and there was a very strong positive correlation between the risk scores in the entire population as well across subgroups. Although differences were observed in some subgroups, these differences were small and not clinically relevant. Therefore, office-based models are suitable in low-middle-income countries (LMICs) with limited laboratory resources and facilities because they are more convenient and accessible. However, the validity of the office-based model must be assessed in longitudinal studies in LMICs. [ABSTRACT FROM AUTHOR]

The Globorisk and WHO cardiovascular risk prediction models are country-specific and region-specific, respectively. The goal of this study was to assess the agreement and correlation between the WHO and Globorisk 10-year cardiovascular disease risk prediction models. The baseline data of 6796 individuals aged 40–74 years who participated in the Fasa cohort study without a history of cardiovascular disease or stroke at baseline were included. In the WHO and Globorisk models scores were calculated using age, sex, systolic blood pressure (SBP), current smoking, diabetes, and total cholesterol for laboratory-based risk and age, sex, SBP, current smoking, and body mass index (BMI) for non-laboratory-based risk (office-based or BMI-based). In Globorisk and WHO risk agreement across risk categories (low, moderate, and high) was examined using the kappa statistic. Also, Pearson correlation coefficients and scatter plots were used to assess the correlation between Globorisk and WHO models. Bland–Altman plots were presented for determination agreement between Globorisk and WHO risk scores in individual's level. In laboratory-based models, agreement across categories was substantial in the overall population (kappa values: 0.75) and also for females (kappa values: 0.74) and males (kappa values: 0.76), when evaluated separately. In non-laboratory-based models, agreement across categories was substantial for the whole population (kappa values: 0.78), and almost perfect for among males (kappa values: 0.82) and substantial for females (kappa values: 0.73). The results showed a very strong positive correlation (r ≥ 0.95) between WHO and Globorisk laboratory-based scores for the whole population, males, and females and also a very strong positive correlation (r > 0.95) between WHO and Globorisk non-laboratory-based scores for the whole population, males, and females. In the laboratory-based models, the limit of agreements was better in males (95%CI 2.1 to − 4.2%) than females (95%CI 4.3 to − 7.3%). Also, in the non-laboratory-based models, the limit of agreements was better in males (95%CI 2.9 to − 4.0%) than females (95%CI 3.2 to − 6.1%). There was a good agreement between both the laboratory-based and the non-laboratory-based WHO models and the Globorisk models. The correlation between two models was very strongly positive. However, in the Globorisk models, more people were in high-risk group than in the WHO models. The scatter plots and Bland–Altman plots showed systematic differences between the two scores that vary according to the level of risk. So, for these models may be necessary to modify the cut points of risk groups. The validity of these models must be determined for this population. [ABSTRACT FROM AUTHOR]

Purpose: A high fruit and vegetable intake has been associated with reduced risk of hypertension; however, results have been inconsistent and it is unclear whether specific types of fruits and vegetables are particularly beneficial. This systematic review and meta-analysis aimed to summarize the published prospective studies on fruit and vegetable consumption and risk of hypertension. Methods: Embase and PubMed databases were searched for relevant prospective studies up to 15th May 2022. Random effects models were used to calculate summary relative risks (RRs) and 95% confidence intervals (CIs) for the association between fruit and vegetable intake and risk of hypertension. Strength of evidence was assessed using World Cancer Research Fund (WCRF) criteria. Results: Eighteen prospective studies (451 291 participants, 145 492 cases) were included. The summary RR (95% CI) of hypertension per 200 g/day was 0.97 (0.95–0.99, I2 = 68%, n = 8) for fruits and vegetables, 0.93 (0.89–0.98, I2 = 77%, n = 10) for fruits, and 1.00 (0.98–1.02, I2 = 38%, n = 10) for vegetables. Reductions in risk were observed up to 800 g/day for fruits and vegetables, and 550 g/day for fruits, and these two associations were considered probably causal using WCRF criteria. Inverse associations were observed for apples or pears, blueberries, raisins or grapes, avocado, broccoli, carrots and lettuce, while positive associations were observed for cantaloupe, Brussels sprouts, cruciferous vegetables, and total and fried potatoes (n = 2–5). Conclusion: A high intake of fruit and vegetables combined, and total fruit was associated with reduced risk of hypertension, while results for fruit and vegetable subtypes were mixed and need further study. [ABSTRACT FROM AUTHOR]

To investigate the longitudinal association of different phenotypes of diabetes and obesity with the incidence of cardiovascular disease (CVD), CVD- and all-cause mortality. A total of 5432 adults, aged ≥ 35 years and free of CVD were included in this cohort study. Diabesity phenotypes were defined in six categories based on the presence of diabetes (normal (NG), prediabetes and diabetes) and obesity (obese, non-obese). Fasting blood sugar, 2-h post prandial glucose, or using anti-diabetic medicines were used to define diabetes, and body mass index and waist circumference were used to define obesity. Cox proportional hazards models were used to estimate hazard ratios (HRs) for incident CVD, CVD- and all-cause mortality across these categories. After a median follow-up of 11.25 years, 819 CVD cases, 181 CVD deaths and 488 all-cause deaths occurred. In multivariable-adjusted models and irrespective of obesity definition, the phenotypes of normal glucose-obese, prediabetes-obese and pre-diabetes-non obese were not associated with CVD incidence in comparison with NG-non obese phenotype, however, the phenotypes of diabesity, either defined by general or abdominal obesity, were associated with increased risk of incident CVD events (HR = 1.42, 95% CI 1.01, 1.99, and HR = 1.46, 95% CI 1.07, 1.98, respectively). These findings were sex-specific and only in men with a phenotype of abdominal obesity-diabetes, a positive link was observed for CVD incidence (HR = 1.60, 95% CI 1.01, 2.52). No significant association was found between diabesity and death from CVD or all causes. Diabesity is a predictor of CVD and stroke incidence, but not CVD or all-cause mortality, among Iranians. This association is more pronounced amongst men than women. [ABSTRACT FROM AUTHOR]

Background: The WHO model has laboratory-based and non-laboratory-based versions for 10-year risk prediction of cardiovascular diseases. Due to the fact that in some settings, there may not be the necessary facilities for risk assessment with a laboratory-based model, the present study aimed to determine the agreement between laboratory-based and non-laboratory-based WHO cardiovascular risk equations. Methods: In this cross-sectional study, we used the baseline data of 6796 individuals without a history of cardiovascular disease and stroke who participated in the Fasa cohort study. The risk factors of the laboratory-based model included age, sex, systolic blood pressure (SBP), diabetes, smoking and total cholesterol, while the non-laboratory-based model included age, sex, SBP, smoking and BMI. Kappa coefficients was used to determine the agreement between the grouped risk and Bland–Altman plots were used to determine the agreement between the scores of the two models. Sensitivity and specificity of non-laboratory-based model were measured at the high-risk threshold. Results: In the whole population, the agreement between the grouped risk of the two models was substantial (percent agreement = 79.0%, kappa = 0.68). The agreement was better in males than in females. A substantial agreement was observed in all males (percent agreement = 79.8%, kappa = 0.70) and males < 60 years old (percent agreement = 79.9%, kappa = 0.67). The agreement in males ≥ 60 years old was moderate (percent agreement = 79.7%, kappa = 0.59). The agreement among females was also substantial (percent agreement = 78.3%, kappa = 0.66). The agreement for females < 60 years old, (percent agreement = 78.8%, kappa = 0.61) was substantial and for females ≥ 60 years old, (percent agreement = 75.8%, kappa = 0.46) was moderate. According to Bland–Altman plots, the limit of agreement was (95%CI: -4.2% to 4.3%) for males and (95%CI: -4.1% to 4.6%) for females. The range of agreement was suitable for both males < 60 years (95%CI: -3.8% to 4.0%) and females < 60 years (95%CI: -3.6% to 3.9%). However, it was not suitable for males ≥ 60 years (95% CI: -5.8% to 5.5%) and females ≥ 60 years (95%CI: -5.7% to 7.4%). At the high-risk threshold of 20% in non-laboratory and laboratory-based models, the sensitivity of the non-laboratory-based model was 25.7%, 70.7%, 35.7%, and 35.4% for males < 60 years, males ≥ 60 years, females < 60 years, and females ≥ 60 years, respectively. At the high-risk threshold of 10% in non-laboratory-based and 20% in laboratory-based models, the non-laboratory model has high sensitivity of 100% for males ≥ 60 years, females < 60 years, females ≥ 60 years, and 91.4% for males < 60 years. Conclusion: A good agreement was observed between laboratory-based and non-laboratory-based versions of the WHO risk model. Also, at the risk threshold of 10% to detect high-risk individuals, the non-laboratory-based model has acceptable sensitivity for practical risk assessment and the screening programs in settings where resources are limited and people do not have access to laboratory tests. [ABSTRACT FROM AUTHOR]

A diagnosis of diabetes mellitus and prediabetes has been associated with increased risk of Parkinson's disease (PD) in several studies, but results have not been entirely consistent. We conducted a systematic review and meta-analysis of cohort studies on diabetes mellitus, prediabetes and the risk of PD to provide an up-to-date assessment of the evidence. PubMed and Embase databases were searched for relevant studies up to 6th of February 2022. Cohort studies reporting adjusted relative risk (RR) estimates and 95% confidence intervals (CIs) for the association between diabetes, prediabetes and Parkinson's disease were included. Summary RRs (95% CIs) were calculated using a random effects model. Fifteen cohort studies (29.9 million participants, 86,345 cases) were included in the meta-analysis. The summary RR (95% CI) of PD for persons with diabetes compared to persons without diabetes was 1.27 (1.20–1.35, I2 = 82%). There was no indication of publication bias, based on Egger's test (p = 0.41), Begg's test (p = 0.99), and inspection of the funnel plot. The association was consistent across geographic regions, by sex, and across several other subgroup and sensitivity analyses. There was some suggestion of a stronger association for diabetes patients reporting diabetes complications than for diabetes patients without complications (RR = 1.54, 1.32–1.80 [n = 3] vs. 1.26, 1.16–1.38 [n = 3]), vs. those without diabetes (pheterogeneity=0.18). The summary RR for prediabetes was 1.04 (95% CI: 1.02–1.07, I2 = 0%, n = 2). Our results suggest that patients with diabetes have a 27% increased relative risk of developing PD compared to persons without diabetes, and persons with prediabetes have a 4% increase in RR compared to persons with normal blood glucose. Further studies are warranted to clarify the specific role age of onset or duration of diabetes, diabetic complications, glycaemic level and its long-term variability and management may play in relation to PD risk. [ABSTRACT FROM AUTHOR]

Obesity has been associated with increased risk of adult asthma, however, not all studies have found a clear association between overweight and the incidence of asthma, and data on other adiposity measures have been limited. Hence, we aimed to summarize evidence on association between adiposity and adult asthma. Relevant studies were retrieved through searches conducted in PubMed, and EMBASE up to March 2021. A total of sixteen studies (63,952 cases and 1,161,169 participants) were included in the quantitative synthesis. The summary RR was 1.32 (95% CI 1.21–1.44, I2 = 94.6%, pheterogeneity < 0.0001, n = 13) per 5 kg/m2 increase in BMI, 1.26 (95% CI 1.09–1.46, I2 = 88.6%, pheterogeneity < 0.0001, n = 5) per 10 cm increase in waist circumference and 1.33 (95% CI 1.22–1.44, I2 = 62.3%, pheterogeneity= 0.05, n = 4) per 10 kg increase in weight gain. Although the test for nonlinearity was significant for BMI (pnonlinearity < 0.00001), weight change (pnonlinearity = 0.002), and waist circumference (pnonlinearity = 0.02), there was a clear dose-response relationship between higher levels of adiposity and asthma risk. The magnitude of the associations and the consistency of the results across studies and adiposity measures provide strong evidence that overweight and obesity, waist circumference and weight gain increases asthma risk. These findings support policies to curb the global epidemic of overweight and obesity. [ABSTRACT FROM AUTHOR]

Aims: To investigate the association between circulating lipoprotein(a) (Lp(a)) and risk of all-cause and cause-specific mortality in the general population and in patients with chronic diseases, and to elucidate the dose-response relations. Methods and results: We searched literature to find prospective studies reporting adjusted risk estimates on the association of Lp(a) and mortality outcomes. Forty-three publications, reporting on 75 studies (957,253 participants), were included. The hazard ratios (HRs) and 95% confidence intervals (95%CI) for the top versus bottom tertile of Lp(a) levels and risk of all-cause mortality were 1.09 (95%CI: 1.01–1.18, I2: 75.34%, n = 19) in the general population and 1.18 (95%CI: 1.04–1.34, I2: 52.5%, n = 12) in patients with cardiovascular diseases (CVD). The HRs for CVD mortality were 1.33 (95%CI: 1.11–1.58, I2: 82.8%, n = 31) in the general population, 1.25 (95%CI: 1.10–1.43, I2: 54.3%, n = 17) in patients with CVD and 2.53 (95%CI: 1.13–5.64, I2: 66%, n = 4) in patients with diabetes mellitus. Linear dose-response analyses revealed that each 50 mg/dL increase in Lp(a) levels was associated with 31% and 15% greater risk of CVD death in the general population and in patients with CVD. No non-linear dose-response association was observed between Lp(a) levels and risk of all-cause or CVD mortality in the general population or in patients with CVD (Pnonlinearity > 0.05). Conclusion: This study provides further evidence that higher Lp(a) levels are associated with higher risk of all-cause mortality and CVD-death in the general population and in patients with CVD. These findings support the ESC/EAS Guidelines that recommend Lp(a) should be measured at least once in each adult person's lifetime, since our study suggests those with higher Lp(a) might also have higher risk of mortality. [ABSTRACT FROM AUTHOR]

Dried fruits and nuts contain high amounts of nutrients and phytochemicals—all of which may have anticarcinogenic, anti-inflammatory, and antioxidant properties. This narrative review summarizes the evidence for dried fruits and nuts and cancer incidence, mortality, and survival and their potential anticancer properties. The evidence for dried fruits in cancer outcomes is limited, but existing studies have suggested an inverse relationship between total dried fruit consumption and cancer risk. A higher consumption of nuts has been associated with a reduced risk of several site-specific cancers in prospective cohort studies, including cancers of the colon, lung, and pancreas, with relative risks per 5 g/day increment equal to 0.75 (95% CI 0.60, 0.94), 0.97 (95% CI 0.95, 0.98), and 0.94 (95% CI 0.89, 0.99), respectively. A daily intake of total nuts of 28 g/day has also been associated with a 21% reduction in the rate of cancer mortality. There is also some evidence that frequent nut consumption is associated with improved survival outcomes among patients with colorectal, breast, and prostate cancer; however, further studies are needed. Future research directions include the investigation of additional cancer types, including rare types of cancer. For cancer prognosis, additional studies with pre- and postdiagnosis dietary assessment are warranted. [ABSTRACT FROM AUTHOR]

Background: Higher BMI in middle age is associated with ischemic stroke, but little is known about BMI over adulthood, and the risk for ischemic stroke as most studies relied on a single measurement of BMI. Methods: BMI was measured four times over a period of 42 years. We calculated average BMI values and group-based trajectory models and related these to the prospective risk of ischemic stroke after the last examination in Cox models with a follow-up time of 12 years. Results: A total of 14,139 participants, with a mean age of 65.2 years and 55.4% women, had information on BMI from all four examinations, and we observed 856 ischemic strokes. People with overweight and obesity over adulthood had a higher risk for ischemic stroke with a multivariable-adjusted hazard ratio of 1.29 (95% CI 1.11−1.48) and 1.27 (95% CI 0.96−1.67), respectively, when compared to normal weight participants. Excess weight tended to have stronger effects earlier than later in life. A trajectory of developing obesity throughout life was associated with higher risk than other trajectories. Conclusions: High average BMI, especially at an early age, is a risk factor for ischemic stroke. Early weight control and long-term weight reduction for those with high BMI may decrease the later occurrence of ischemic stroke. [ABSTRACT FROM AUTHOR]

Nuts are nutrient-rich foods that contain many bioactive compounds that are beneficial for cardiovascular health. Higher consumption of nuts has been associated with a reduced risk of several cardiovascular diseases (CVD) in prospective cohort studies, including a 19% and 25% lower risk of CVD incidence and mortality, respectively, and a 24% and 27% lower risk of coronary heart disease incidence and mortality, respectively. An 18% lower risk of stroke mortality, a 15% lower risk of atrial fibrillation, and a 19% lower risk of total mortality have also been observed. The role of nuts in stroke incidence, stroke subtypes, peripheral arterial disease and heart failure has been less consistent. This narrative review summarizes recommendations for nuts by clinical practice guidelines and governmental organizations, epidemiological evidence for nuts and CVD outcomes, nut-containing dietary patterns, potential mechanisms of nuts and CVD risk reduction, and future research directions, such as the use of biomarkers to help better assess nut intake. Although there are still some uncertainties around nuts and CVD prevention which require further research, as summarized in this review, there is a substantial amount of evidence that supports that consuming nuts will have a positive impact on primary and secondary prevention of CVD. [ABSTRACT FROM AUTHOR]

Based on the Global Cancer Update Programme, formally known as the World Cancer Research Fund/American Institute for Cancer Research Continuous Update Project, we performed systematic reviews and meta‐analyses to investigate the association of postdiagnosis body fatness, physical activity and dietary factors with breast cancer prognosis. We searched PubMed and Embase for randomised controlled trials and longitudinal observational studies from inception to 31 October 2021. We calculated summary relative risks (RRs) and 95% confidence intervals (CIs) using random‐effects meta‐analyses. An independent Expert Panel graded the quality of evidence according to predefined criteria. The evidence on postdiagnosis body fatness and higher all‐cause mortality (RR per 5 kg/m2 in body mass index: 1.07, 95% CI: 1.05‐1.10), breast cancer‐specific mortality (RR: 1.10, 95% CI: 1.06‐1.14) and second primary breast cancer (RR: 1.14, 95% CI: 1.04‐1.26) was graded as strong (likelihood of causality: probable). The evidence for body fatness and breast cancer recurrence and other nonbreast cancer‐related mortality was graded as limited (likelihood of causality: limited‐suggestive). The evidence on recreational physical activity and lower risk of all‐cause (RR per 10 metabolic equivalent of task‐hour/week: 0.85, 95% CI: 0.78‐0.92) and breast cancer‐specific mortality (RR: 0.86, 95% CI: 0.77‐0.96) was judged as limited‐suggestive. Data on dietary factors was limited, and no conclusions could be reached except for healthy dietary patterns, isoflavone and dietary fibre intake and serum 25(OH)D concentrations that were graded with limited‐suggestive evidence for lower risk of the examined outcomes. Our results encourage the development of lifestyle recommendations for breast cancer patients to avoid obesity and be physically active. [ABSTRACT FROM AUTHOR]

It is important to clarify the associations between modifiable lifestyle factors such as physical activity and breast cancer prognosis to enable the development of evidence‐based survivorship recommendations. We performed a systematic review and meta‐analyses to summarise the evidence on the relationship between postbreast cancer diagnosis physical activity and mortality, recurrence and second primary cancers. We searched PubMed and Embase through 31st October 2021 and included 20 observational studies and three follow‐up observational analyses of patients enrolled in clinical trials. In linear dose‐response meta‐analysis of the observational studies, each 10‐unit increase in metabolic equivalent of task (MET)‐h/week higher recreational physical activity was associated with 15% and 14% lower risk of all‐cause (95% confidence interval [CI]: 8%‐22%, studies = 12, deaths = 3670) and breast cancer‐specific mortality (95% CI: 4%‐23%, studies = 11, deaths = 1632), respectively. Recreational physical activity was not associated with breast cancer recurrence (HR = 0.97, 95% CI: 0.91‐1.05, studies = 6, deaths = 1705). Nonlinear dose‐response meta‐analyses indicated 48% lower all‐cause and 38% lower breast cancer‐specific mortality with increasing recreational physical activity up to 20 MET‐h/week, but little further reduction in risk at higher levels. Predefined subgroup analyses across strata of body mass index, hormone receptors, adjustment for confounders, number of deaths, menopause and physical activity intensities were consistent in direction and magnitude to the main analyses. Considering the methodological limitations of the included studies, the independent Expert Panel concluded 'limited‐suggestive' likelihood of causality for an association between recreational physical activity and lower risk of all‐cause and breast cancer‐specific mortality. [ABSTRACT FROM AUTHOR]

Previous evidence on postdiagnosis body fatness and mortality after breast cancer was graded as limited‐suggestive. To evaluate the evidence on body mass index (BMI), waist circumference, waist‐hip‐ratio and weight change in relation to breast cancer prognosis, an updated systematic review was conducted. PubMed and Embase were searched for relevant studies published up to 31 October, 2021. Random‐effects meta‐analyses were conducted to estimate summary relative risks (RRs). The evidence was judged by an independent Expert Panel using pre‐defined grading criteria. One randomized controlled trial and 225 observational studies were reviewed (220 publications). There was strong evidence (likelihood of causality: probable) that higher postdiagnosis BMI was associated with increased all‐cause mortality (64 studies, 32 507 deaths), breast cancer‐specific mortality (39 studies, 14 106 deaths) and second primary breast cancer (11 studies, 5248 events). The respective summary RRs and 95% confidence intervals per 5 kg/m2 BMI were 1.07 (1.05‐1.10), 1.10 (1.06‐1.14) and 1.14 (1.04‐1.26), with high between‐study heterogeneity (I2 = 56%, 60%, 66%), but generally consistent positive associations. Positive associations were also observed for waist circumference, waist‐hip‐ratio and all‐cause and breast cancer‐specific mortality. There was limited‐suggestive evidence that postdiagnosis BMI was associated with higher risk of recurrence, nonbreast cancer deaths and cardiovascular deaths. The evidence for postdiagnosis (unexplained) weight or BMI change and all outcomes was graded as limited‐no conclusion. The RCT showed potential beneficial effect of intentional weight loss on disease‐free‐survival, but more intervention trials and well‐designed observational studies in diverse populations are needed to elucidate the impact of body composition and their changes on breast cancer outcomes. [ABSTRACT FROM AUTHOR]

Little is known about how diet might influence breast cancer prognosis. The current systematic reviews and meta‐analyses summarise the evidence on postdiagnosis dietary factors and breast cancer outcomes from randomised controlled trials and longitudinal observational studies. PubMed and Embase were searched through 31st October 2021. Random‐effects linear dose‐response meta‐analysis was conducted when at least three studies with sufficient information were available. The quality of the evidence was evaluated by an independent Expert Panel. We identified 108 publications. No meta‐analysis was conducted for dietary patterns, vegetables, wholegrains, fish, meat, and supplements due to few studies, often with insufficient data. Meta‐analysis was only possible for all‐cause mortality with dairy, isoflavone, carbohydrate, dietary fibre, alcohol intake and serum 25‐hydroxyvitamin D (25(OH)D), and for breast cancer‐specific mortality with fruit, dairy, carbohydrate, protein, dietary fat, fibre, alcohol intake and serum 25(OH)D. The results, with few exceptions, were generally null. There was limited‐suggestive evidence that predefined dietary patterns may reduce the risk of all‐cause and other causes of death; that isoflavone intake reduces the risk of all‐cause mortality (relative risk (RR) per 2 mg/day: 0.96, 95% confidence interval (CI): 0.92‐1.02), breast cancer‐specific mortality (RR for high vs low: 0.83, 95% CI: 0.64‐1.07), and recurrence (RR for high vs low: 0.75, 95% CI: 0.61‐0.92); that dietary fibre intake decreases all‐cause mortality (RR per 10 g/day: 0.87, 95% CI: 0.80‐0.94); and that serum 25(OH)D is inversely associated with all‐cause and breast cancer‐specific mortality (RR per 10 nmol/L: 0.93, 95% CI: 0.89‐0.97 and 0.94, 95% CI: 0.90‐0.99, respectively). The remaining associations were graded as limited‐no conclusion. [ABSTRACT FROM AUTHOR]

Purpose: Vegetarian diets have been associated with reduced risk of ischemic heart disease (IHD). However, results regarding cardiovascular disease (CVD) overall and stroke are less clear. We conducted a systematic review and meta-analysis of prospective cohort studies on CVD, IHD and stroke risk among vegetarians or vegans versus nonvegetarians to clarify these associations. Methods: PubMed and Ovid Embase databases were searched through August 12, 2021. Prospective cohort studies reporting adjusted relative risk (RR) estimates and 95% confidence intervals (CIs) for incidence or mortality from CVD, IHD and stroke, comparing vegetarians and vegans to nonvegetarians were included. Risk of bias (RoB) was assessed using ROBINS-I and the strength of evidence was assessed using World Cancer Research Fund (WCRF) criteria. Summary RRs (95% CIs) were estimated using a random effects model. Results: Thirteen cohort studies (844,175 participants, 115,392 CVD, 30,377 IHD, and 14,419 stroke cases) were included. The summary RR for vegetarians vs. nonvegetarians was 0.85 (95% CI: 0.79–0.92, I2 = 68%, n = 8) for CVD, 0.79 (95% CI: 0.71–0.88, I2 = 67%, n = 8) for IHD, 0.90 (95% CI: 0.77–1.05, I2 = 61%, n = 12) for total stroke, and for vegans vs. nonvegetarians was 0.82 (95% CI: 0.68–1.00, I2 = 0%, n = 6) for IHD. RoB was moderate (n = 8) to serious (n = 5). The associations between vegetarian diets and CVD and IHD were considered probably causal using WCRF criteria. Conclusions: Vegetarian diets are associated with reduced risk of CVD and IHD, but not stroke, but further studies are needed on stroke. These findings should be considered in dietary guidelines. Review registration: No review protocol registered. [ABSTRACT FROM AUTHOR]

Elevated blood pressure and hypertension have been associated with increased risk of atrial fibrillation in a number of epidemiological studies, however, the strength of the association has differed between studies. We conducted a systematic review and meta-analysis of the association between blood pressure and hypertension and atrial fibrillation. PubMed and Embase databases were searched for studies of hypertension and blood pressure and atrial fibrillation up to June 6th 2022. Cohort studies reporting adjusted relative risk (RR) estimates and 95% confidence intervals (CIs) of atrial fibrillation associated with hypertension or blood pressure were included. A random effects model was used to estimate summary RRs. Sixty eight cohort studies were included in the meta-analysis. The summary RR was 1.50 (95% CI: 1.42–1.58, I2 = 98.1%, n = 56 studies) for people with hypertension compared to those without hypertension (1,080,611 cases, 30,539,230 participants), 1.18 (95% CI: 1.16–1.21, I2 = 65.9%, n = 37 studies) per 20 mmHg increase in systolic blood pressure (346,471 cases, 14,569,396 participants), and 1.07 (95% CI: 1.03–1.11, I2 = 91.5%, n = 22 studies) per 10 mmHg increase in diastolic blood pressure (332,867 cases, 14,354,980 participants). There was evidence of a nonlinear association between diastolic blood pressure and atrial fibrillation with a steeper increase in risk at lower levels of diastolic blood pressure, but for systolic blood pressure the association appeared to be linear. For both systolic and diastolic blood pressure, the risk increased even within the normal range of blood pressure and persons at the high end of systolic and diastolic blood pressure around 180/110 mmHg had a 1.8–2.3 fold higher risk of atrial fibrillation compared to those with a blood pressure of 90/60 mmHg. These results suggest that elevated blood pressure and hypertension increases the risk of atrial fibrillation and there is some increase in risk even within the normal range of systolic and diastolic blood pressure. [ABSTRACT FROM AUTHOR]

Background Physical activity (PA) is associated with improved health-related quality of life (HRQoL) among women with breast cancer; however, uncertainty remains regarding PA types and dose (frequency, duration, intensity) and various HRQoL measures. A systematic review and meta-analysis of randomized controlled trials was conducted to clarify whether specific types and doses of physical activity was related to global and specific domains of HRQoL, as part of the Global Cancer Update Programme, formerly known as the World Cancer Research Fund–American Institute for Cancer Research Continuous Update Project. Methods PubMed and CENTRAL databases were searched up to August 31, 2019. Weighted mean differences (WMDs) in HRQoL scores were estimated using random effects models. An independent expert panel graded the evidence. Results A total of 79 randomized controlled trials (14 554 breast cancer patients) were included. PA interventions resulted in higher global HRQoL as measured by the Functional Assessment of Cancer Therapy–Breast (WMD = 5.94, 95% confidence intervals [CI] = 2.64 to 9.24; I 2 = 59%, n = 12), Functional Assessment of Cancer Therapy–General (WMD = 4.53, 95% CI = 1.94 to 7.13; I 2 = 72%, n = 18), and European Organization for Research and Treatment of Cancer Quality of Life Questionnaire–C30 (WMD = 6.78, 95% CI = 2.61 to 10.95; I 2 = 76.3%, n = 17). The likelihood of causality was considered probable that PA improves HRQoL in breast cancer survivors. Effects were weaker for physical function and mental and emotional health. Evidence regarding dose and type of PA remains insufficient for firm conclusions. Conclusion PA results in improved global HRQoL in breast cancer survivors with weaker effects observed for physical function and mental and emotional health. Additional research is needed to define the impact of types and doses of activity on various domains of HRQoL. [ABSTRACT FROM AUTHOR]

Background: Globorisk is a novel risk prediction model for predicting cardiovascular disease (CVD). Globorisk is a country-specific risk prediction model that determines CVD risk for all countries. This model has two versions; laboratory-based and office-based. This study aimed to determine the agreement between laboratory-based and office-based models in a large sample of the general population.Methods: Baseline data from the Fasa cohort study was used for the current study. In total, 6810 participants ≥ 40 years without any history of cardiovascular disease or stroke were included in the study. To determine the laboratory-based risk model, factors include age, sex, current smoking status, history of diabetes, systolic blood pressure (SBP), and total cholesterol. To estimate the office-based risk model, factors were age, sex, current smoking status, SBP, and body mass index (BMI). Kappa statistics was used to distinguish the agreement between grouped scores in these two models. Additionally, correlation coefficients and scatter plots were used to determine the linear correlation between the two models.Results: In this study 46.53% of the participants were men. The mean age (SD) of participants was 51.08 (7.88) years. Agreements between the two models were moderate and substantial in all women and all men, respectively. The agreement between the two CVD risk groups was 90.15% (kappa = 0.717) in all men, 92.94% (kappa = 0.571) among men aged < 60 years and 77.60% (kappa = 0.645) in men aged ≥ 60 years. The agreement between the two CVD risk groups was 86.68% (kappa = 0.572) among all women, 93.96% (kappa = 0.274) among women aged < 60 years and 62.46% (kappa = 0.422) among women aged ≥ 60 years. A very strong positive correlation (r = 0.94) was found between the two risk scores in all men, and it was similar among men aged < 60 years (r = 0.84) and men aged > 60 years (r = 0.94). Among all women, there was a very strong positive correlation (r = 0.87), and the strong positive correlation remained among < 60 years old (r = 0.76) and women > 60 years old (r = 0.76).Conclusion: The Globorisk office-based model which is easier to use as it does not require blood testing can determine the risk groups in this population. The Globorisk office-based model may be used for CVD risk screening in low-middle income countries where resources are limited. [ABSTRACT FROM AUTHOR]

Purpose: There is existing evidence on the potential role of chronic inflammation in the pathogenesis of pancreatic cancer (PC) and on how risk may be modulated by dietary factors. Pro-inflammatory diets are suggested to be associated with increased risk of PC but, so far, evidence remains not conclusive. We examined the association between the dietary inflammatory potential and PC risk within the European Prospective Investigation into Cancer and Nutrition (EPIC) study, which includes 450,112 participants. Methods: After a 14-year follow-up, a total of 1239 incident PC cases were included in this study. The inflammatory potential of the diet was estimated using an Inflammatory Score of the Diet (ISD). Hazard ratios (HRs) and 95% confidence intervals (CIs) for the association between the ISD and PC were estimated using multivariable Cox regression models, adjusted for known risk factors for PC. Results: Participants with higher ISDs had a higher risk of developing PCs. In the fully adjusted multivariate model, the risk of PC increased by 11% (HR 1.11, 95% CI 1.02–1.22) for 1 point each standard deviation increase in the ISD score. Neither obesity nor any other known risk factor for PC showed statistically significant interactions. Conclusion: To the best of our knowledge, this is the first prospective study reporting a positive relationship between the inflammatory potential of diet and PC. Since early diagnosis and treatment of pancreatic cancer might be challenging, prevention remains the major hope for reducing the burden of this disease. [ABSTRACT FROM AUTHOR]

Epidemiologic studies have indicated that cruciferous vegetables can influence the cancer risk; therefore, we examined with a cross-sectional approach the correlation between the frequent consumption of the total cruciferous vegetables and the formation of bulky DNA damage, a biomarker of carcinogen exposure and cancer risk, in the Gen-Air study within the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. DNA damage measurements were performed in the peripheral blood of 696 of those apparently healthy without cancer controls, including 379 never-smokers and 317 former smokers from seven European countries by the 32P-postlabeling assay. In the Gen-Air controls, the median intake of cruciferous vegetables was 6.16 (IQR 1.16–13.66) g/day, ranging from 0.37 (IQR 0–6.00) g/day in Spain to 11.34 (IQR 6.02–16.07) g/day in the UK. Based on this information, participants were grouped into: (a) high consumers (>20 g/day), (b) medium consumers (3–20 g/day) and (c) low consumers (<3.0 g/day). Overall, low cruciferous vegetable intake was correlated with a greater frequency of bulky DNA lesions, including benzo(a)pyrene, lactone and quinone-adducts and bulky oxidative lesions, in the adjusted models. Conversely, a high versus low intake of cruciferous vegetables was associated with a reduction in DNA damage (up to a 23% change, p = 0.032); this was particularly evident in former smokers (up to a 40% change, p = 0.008). The Generalized Linear Regression models indicated an overall Mean Ratio between the high and the low consumers of 0.78 (95% confidence interval, 0.64–0.97). The current study suggests that a higher intake of cruciferous vegetables is associated with a lower level of bulky DNA adducts and supports the potential for cancer prevention strategies through dietary habit changes aimed at increasing the consumption of cruciferous vegetables. [ABSTRACT FROM AUTHOR]

Delirium is a neuropsychiatric syndrome represented by an acute disturbance in attention, awareness and cognition, highly prevalent in older, and critically ill patients, and associated with poor outcomes. This review synthesized existing evidence on the effectiveness of music interventions on delirium in adults, and music interventions (MIs), psychometric assessments and outcome measures used. We searched MEDLINE, PsychINFO, SCOPUS, Clinical Trials and CENTRAL for quantitative designs comparing any MIs to standard care or another intervention. From 1150 studies 12 met the inclusion criteria, and 6 were included in the meta-analysis. Narrative synthesis showed that most studies focused on prevention, few assessed delirium severity, with the majority of studies reporting beneficial effects. The summary relative risk for incident delirium comparing music vs. no music in postsurgical and critically ill older patients was 0.52 (95% confidential interval (CI): 0.20–1.35, I2 = 79.1%, heterogeneity <0.0001) for the random effects model and 0.47 (95% CI: 0.34–0.66) using the fixed effects model. Music listening interventions were more commonly applied than music therapy delivered by credentialed music therapists, and delirium assessments methods were heterogeneous, including both standardized tools and systematic observations. Better designed studies are needed addressing effectiveness of MIs in specific patient subgroups, exploring the correlations between intervention-types/dosages and delirium symptoms. [ABSTRACT FROM AUTHOR]

Background: A diagnosis of chronic kidney disease has been strongly associated with cardiovascular disease and mortality in a number of studies, but the association with specific causes of death has not been assessed in detail. We analysed the association between chronic kidney disease and all-cause mortality and 54 causes of death in the National Health Interview Survey, a prospective study of 210,748 US adults.Methods: We used multivariable Cox regression models to estimate hazard ratios (HRs) and 95% confidence intervals (CIs) for all-cause and cause-specific mortality associated with self-reported chronic kidney disease. Men and women aged 18-84 years were recruited between 1997 and 2004 and followed up for mortality through December 31, 2006.Results: During an average of 6 years follow-up, 9564 deaths occurred. A history of chronic kidney disease vs. no chronic kidney disease was associated with increased risk of all-cause mortality (HR = 2.69, 95% CI: 2.38-3.04), and mortality from septicemia (5.65, 2.84-11.25), viral hepatitis (10.67, 2.43-46.95), other infectious parasitic diseases (10.58, 3.59-31.21), total cancer (1.48, 1.05-2.09), lung cancer (1.94, 1.10-3.44), kidney cancer (4.74, 1.81-12.41), diabetes mellitus (8.57, 5.60-13.11), circulatory disease overall (3.36, 2.70-4.18) and 11 specific circulatory diseases with the strongest associations observed for primary hypertension/renal disease (13.60, 6.42-28.84), hypertensive heart/renal disease (10.72, 2.47-46.49), and other diseases of circulatory system (7.36, 3.22-16.81). Elevated risk was also observed for alcoholic liver disease (5.63, 1.90-16.66), other chronic liver disease (4.41, 1.74-11.17), kidney failure (13.07, 8.23-20.77), and five other causes of death.Conclusions: A history of chronic kidney disease was associated with increased risk of all-cause mortality and 27 out of 54 causes of death. Further studies are needed to clarify associations with less common causes of death. [ABSTRACT FROM AUTHOR]

Background: Findings and limitations of previous studies on persistent organic pollutants (POPs) and pancreatic cancer risk support conducting further research in prospective cohorts.Methods: We conducted a prospective case-control study nested within the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. Participants were 513 pancreatic cancer cases and 1020 matched controls. Concentrations of 22 POPs were measured in plasma collected at baseline.Results: Some associations were observed at higher concentrations of p, p'-DDT, trans-nonachlor, β-hexachlorocyclohexane and the sum of six organochlorine pesticides and of 16 POPs. The odds ratio (OR) for the upper quartile of trans-nonachlor was 1.55 (95% confidence interval 1.06-2.26; P for trend = 0.025). Associations were stronger in the groups predefined as most valid (participants having fasted >6 h, with microscopic diagnostic confirmation, normal weight, and never smokers), and as most relevant (follow-up ≥10 years). Among participants having fasted >6 h, the ORs were relevant for 10 of 11 exposures. Higher ORs were also observed among cases with microscopic confirmation than in cases with a clinical diagnosis, and among normal-weight participants than in the rest of participants. Among participants with a follow-up ≥10 years, estimates were higher than in participants with a shorter follow-up (for trans-nonachlor: OR = 2.14, 1.01 to 4.53, P for trend = 0.035). Overall, trans-nonachlor, three PCBs and the two sums of POPs were the exposures most clearly associated with pancreatic cancer risk.Conclusions: Individually or in combination, most of the 22 POPs analysed did not or only moderately increased the risk of pancreatic cancer. [ABSTRACT FROM AUTHOR]

Purpose: The risk psychological distress (PD) confers on mortality due to specific chronic diseases compared to suicide is unclear. Using the National Health Interview Survey (NHIS), we investigated the association between PD levels and risk of all-cause and chronic disease-specific mortality and compared the contribution of chronic disease-related mortality to that of suicide. Methods: Data from 195, 531 adults, who participated in the NHIS between 1997 and 2004, were linked to the National Death Index records through to 2006. Multivariable Cox regression models were used to estimate hazard ratios (HRs) and their 95% confidence intervals (CIs) across four levels of PD, measured using the Kessler-6 scale. Outcomes included all-cause mortality, and mortality due to all CVDs and subtypes, all cancers and subtypes, diabetes mellitus, alcoholic liver disease and suicide. Results: During a mean follow-up time of 5.9 years, 7665 deaths occurred. We found a dose–response association between levels of PD and all-cause mortality, with the adjusted HRs (95% CI) elevated for all levels of PD, when compared to asymptomatic levels: subclinical 1.10 (1.03–1.16), symptomatic 1.36 (1.26–1.46) and highly symptomatic 1.57 (1.37–1.81). A similar association was found for all CVDs and certain CVD subtypes, but not for cancers, cerebrovascular diseases diabetes mellitus. Excess mortality attributable to suicide and alcoholic liver disease was evident among those with levels of PD only. Conclusion: PD symptoms, of all levels, were associated with an increased risk of all-cause and CVD-specific mortality while higher PD only was associated with suicide. These findings emphasise the need for lifestyle interventions targeted towards improving physical health disparities among those with PD. [ABSTRACT FROM AUTHOR]

Background: Lifestyle risk factors have been associated with increased all-cause and cause-specific mortality, but the influence of reverse causation has been underappreciated as a limitation in epidemiological studies. Methods: Prospective cohort study including 457,021 US adults from the National Health Interview Survey 1997–2013 linked to the National Death Index records through December 31, 2015. Multivariable Cox models were performed to examine the association of lifestyle risk factors with all-cause and cause-specific mortality. Participants with prevalent diseases and the first 2, 5, 10, and 15 years of follow-up were excluded to account for reverse causation. Results: During 4,441,609 person-years, we identified 60,323 total deaths. Heavy alcohol drinking (HR 1.12; 95% CI 1.08 to 1.16), smoking (HR 1.78; 95% CI 1.74 to 1.83) and lack of physical activity (HR 1.51; 95% CI 1.47 to 1.54) were associated with increased all-cause mortality. Overweight was associated with lower all-cause mortality (HR 0.88; 95% CI 0.86 to 0.90). After exclusion of participants with diseases and first 10 years of follow-up, associations changed to: heavy alcohol drinking (HR 1.31; 95% CI 1.20 to 1.43), smoking (HR 1.99; 95% CI 1.87 to 2.11), lack of physical activity (HR 1.21; 95% CI 1.15 to 1.27), and overweight (HR 1.05; 95% CI 1.00 to 1.10). Conclusions: Methods to account for reverse causation suggest different effects of reverse causation on the associations between lifestyle risk factors and mortality. Exclusion of participants with diseases at baseline, and exclusion of 5–10 years of follow-up may be necessary to mitigate reverse causation. [ABSTRACT FROM AUTHOR]

Background Observational studies have consistently reported that postmenopausal hormone therapy use is associated with lower colon cancer risk, but epidemiologic studies examining the associations between circulating concentrations of endogenous estrogens and colorectal cancer have reported inconsistent results. Methods We investigated the associations between circulating concentrations of estrone, estradiol, free estradiol, testosterone, free testosterone, androstenedione, dehydroepiandrosterone (DHEA), progesterone, and sex hormone–binding globulin (SHBG) with colon cancer risk in a nested case-control study of 1028 postmenopausal European women (512 colon cancer cases, 516 matched controls) who were noncurrent users of exogenous hormones at blood collection. Multivariable conditional logistic regression models were used to compute odds ratios and 95% confidence intervals to evaluate the association between circulating sex hormones and colon cancer risk. We also conducted a dose-response meta-analysis of prospective studies of circulating estrone and estradiol with colorectal, colon, and rectal cancer risk in postmenopausal women. All statistical tests were 2-sided. Results In the multivariable model, a nonstatistically significantly positive relationship was found between circulating estrone and colon cancer risk (odds ratio per log2 1-unit increment   =   1.17 [95% confidence interval   =   1.00 to 1.38]; odds ratioquartile4-quartile1   =   1.33 [95% confidence interval   =   0.89 to 1.97], P trend   =  .20). Circulating concentrations of estradiol, free estradiol, testosterone, free testosterone, androstenedione, DHEA, progesterone, and SHBG were not associated with colon cancer risk. In the dose-response meta-analysis, no clear evidence of associations were found between circulating estradiol and estrone concentrations with colorectal, colon, and rectal cancer risk. Conclusion Our observational and meta-analysis results do not support an association between circulating concentrations of endogenous sex hormones and colon or rectal cancer in postmenopausal women. [ABSTRACT FROM AUTHOR]

Background: Physical activity has been hypothesized to reduce the risk of gallbladder disease (gallstones, cholecystitis, cholecystectomy); however, results from epidemiological studies have not always shown statistically significant associations. We conducted a systematic review and meta-analysis to clarify the presence and strength of an association between physical activity and gallbladder disease risk. Methods: PubMed and Embase databases were searched for studies of physical activity and gallbladder disease up to 9th of January 2015. Prospective studies reporting relative risk (RR) estimates and 95% confidence intervals (CIs) of gallbladder disease associated with physical activity were included. Summary RRs were estimated using a random effects model. Results: Eight studies including 6958 cases and 218,204 participants were included. The summary RR for the highest versus the lowest level of physical activity was 0.75 (95% CI: 0.69-0.81, n = 8) and there was no evidence of heterogeneity, I2 = 0%). In the dose-response analysis the summary relative risk per 20 MET-hours of activity was 0.85 (95% CI: 0.80-0.90, I2 = 0%, n = 2) for leisure-time physical activity, 0.83 (95% CI: 0.76-0.90, I2 = 0%, n = 2) for vigorous physical activity, and 0.86 (95% CI: 0.76-0.98, I2 = 0%, n = 2) for nonvigorous physical activity. Conclusion: Our analysis confirms a protective effect of physical activity on risk of gallbladder disease. [ABSTRACT FROM AUTHOR]