Risk Of Overall Cancer Research Articles

Association of hypertension and the risk of cancer: a study based on the UK Biobank

Abstract Introduction With the increasing incidence rate of hypertension and carcinoma, there is a growing interest in investigating the potential link between these two diseases. The subdiscipline of hypertension, Onco-hypertension, has been proposed and attracted much attention. However, there are still few researches on this subdiscipline. Purpose This study aims to investigate the relationship between hypertension and the occurrence of cancer. Additionally, we explore whether anti-hypertensive treatment has any impact on the incidence of cancer. Methods This study involved 244,496 participants recruited between 2006-2010 from the UK Biobank, with 21,765 participants were diagnosed with the hypertension according to the ICD10 coding. The Cox regression was used to analyse the the risk of cancer associated with hypertension. The effect of anti-hypertensive treatment on the occur of cancer was also verified according to the Cox regression and the Drug target Mendelian randomization. Results Compared to those participants without hypertension, those people with hypertension have higher risk of the occur of cancer(adjusted hazard ratio(aHR) 1.35, 95% confidence interval(CI)1.3-1.4), especially in breast cancer(aHR 1.43, 95% CI 1.27-1.61), prostate cancer(aHR 1.85, 95% CI 1.7-2.02), lung cancer(aHR 2.15, 95% CI 1.86-2.48), renal cancer(aHR 1.91, 95% CI 1.46-2.49), pancreas cancer(aHR 1.55, 95% CI 1.2-2). Compared to those people with hypertension but without anti-hypertensive treatment, the anti-hypertensive treatment increase the cancer risk(aHR 1.19, 95% CI 1.06-1.33). However, thiazide diuretic have protect effect for hypertension patients on occur of the prostate cancer (aHR 0.74, 95% CI 0.61-0.89) and beta-receptor blocker have protect effect for hypertension patients on occur of the lung cancer (aHR 0.71, 95% CI 0.54-0.93). The result of Drug target Mendelian randomization shows the anti-hypertensive treatment have no significant effect on the risk of cancer. Conclusion The onset of high blood pressure is linked to an elevated risk of several cancers. However, it cannot be conclusively determined whether the use of medications for high blood pressure increases or decreases the overall risk of cancer. This study provides instructive evidences for the further study of Onco-hypertension.The result of main analyseThe analyse of the antihypertensive drug

Vitamin B12 Intake and Cancer Risk: Findings from a Case-Control Study in Vietnam

There is inconclusive evidence on the role of dietary intake of vitamin B12 in cancer. We evaluated the association between vitamin B12 intake and cancer risk in a hospital-based case-control study, comprising 3,758 cancer cases and 2,995 controls in Vietnam. Vitamin B12 intake was derived from the validated food frequency questionnaire. Unconditional logistic regression model was used to calculate the odds ratios (ORs), and respective 95% confidence intervals (CIs) for the association between vitamin B12 and cancer risk. There was a U-shaped association between vitamin B12 intake and overall risk of cancer. Individuals with intakes lower than the median intake had a 6% (OR = 1.06, 95% CI: 0.86–1.31)-107% (OR = 2.07, 95% CI: 1.58–2.71), increased risk of cancer (Ptrend <0.001), whereas those with higher intakes than the median intake had a 20% (OR = 1.20, 95% CI: 0.97–1.48)-52% (OR = 1.52, 95% CI: 1.22–1.89) increased risk of cancer (Ptrend <0.04). The excess risk of cancer associated with low intakes of vitamin B12 was observed among esophageal, lung, and breast cancer patients, whereas with high intakes of vitamin B12 among gastric cancer patients. In summary, a U-shaped association between vitamin B12 intake and increased cancer risk was observed in the Vietnamese population.

Association between prediabetes and the incidence of gastric cancer: A meta-analysis.

Prediabetes has been found to be associated with an elevated overall risk of cancer, which may be site-specific. we performed a protocol for systematic review and meta-analysis to investigate the correlation between prediabetes and the incidence of gastric cancer (GC). A thorough review of the literature was conducted in the PubMed, Embase, and Web of Science databases to identify pertinent observational studies with longitudinal follow-up. The random-effects model was employed to consolidate the data, taking into account the potential impact of heterogeneity. A total of 13 datasets from 8 prospective cohort studies were included. The prevalence of prediabetes was 9.6%. During the mean follow-up duration of 7.1 to 12.2 years, 33,135 patients were diagnosed with GC. According to the results of the pooled analysis, prediabetes was associated with a mildly higher incidence of GC over time (risk ratio: 1.07, 95% confidence interval: 1.01-1.13, P = .03; I2 = 44%). Subsequent subgroup analyses indicated that the relationship between prediabetes and the heightened risk of GC may not be substantially influenced by factors such as the country in which the study was conducted, the average age of participants, their gender, the definition of prediabetes used, the prevalence of prediabetes at the beginning of the study, the incidence of GC within the studied population, or the adjustment made for body mass index (P for subgroup difference all >.05). The presence of prediabetes may increase the risk of GC by a mild amount when compared with people with normoglycemia in community-derived adult populations.

Height and cancer risk in East Asians: Evidence from a prospective cohort study and Mendelian randomization analyses

BackgroundHeight is associated with increased cancer risk, but most studies focus on Western populations. We aimed to evaluate this relationship in East Asians. MethodObservational analyses were performed utilizing data from China Kadoorie Biobank (CKB) prospective cohort. Adjusted hazard ratios (HRs) and corresponding 95 % confidence intervals (CIs) were estimated using Cox proportional hazards models. Two-sample Mendelian randomization (MR) analyses explored causal effects between height and cancer using data from Korean Genome and Epidemiology Study (KoGES), Biobank Japan (BBJ), and CKB. ResultsOver a median 10.1-years follow-up, 22,731 incident cancers occurred. In observational analyses, after Bonferroni correction, each 10 cm increase in height was significantly associated with higher risk of overall cancer (HR 1.16, 95 % CI 1.14–1.19, P < 0.001), lung cancer (1.18, 95 % CI 1.12–1.24, P < 0.001), esophageal cancer (1.21, 95 % CI 1.12–1.30, P < 0.001), breast cancer (1.41, 95 % CI 1.31–1.53, P < 0.001), and cervix uteri cancer (1.29, 95 % CI 1.15–1.45, P < 0.001). Each 10 cm increase in height was suggestively associated with increased risk for lymphoma (1.18, 95 % CI 1.04–1.34, P = 0.010), colorectal cancer (1.09, 95 % CI 1.02–1.16, P = 0.010), and stomach cancer (1.07, 95 % CI 1.00–1.14, P = 0.044). In MR analyses, genetically predicted height (per 1 standard deviation increase, 8.07 cm) was suggestively associated with higher risk of lung cancer (odds ratio [OR] 1.17, 95 % confidence interval [CI] 1.02–1.35, P = 0.0244) and gastric cancer (OR 1.14, 95 % CI 1.02–1.29, P = 0.0233). ConclusionsTaller height was significantly related to a higher risk for overall cancer, lung cancer, esophageal cancer, breast cancer, and cervix uteri cancer. Our findings suggest that height may be a potential causal risk factor for lung and gastric cancers among East Asians.

Cardiovascular health, polygenic risk score, and cancer risk: a prospective cohort study

BackgroundCancer and cardiovascular disease share common lifestyle risk factors. However, it remains unclear whether cardiovascular health (CVH) evaluated by Life’s Essential 8 can predict cancer risk, and attenuate the influence of genetic susceptibility on cancer. ObjectivesWe aimed to evaluate independent and joint associations of CVH and polygenic risk score (PRS) with risks of overall and site-specific cancers. MethodsWe undertook a population-based cohort study based on the UK Biobank. The CVH score was constructed by physical activity, body mass index, nicotine exposure, sleep, diet, blood pressure, lipid profile, and blood glucose. PRSs were assessed individually for 18 cancer types by their independent single-nucleotide polymorphisms previously identified in genome-wide association studies. Multivariable Cox proportional-hazards models were applied to explore the independent and joint associations of CVH and PRS with cancer incidence risk. The results were displayed as hazard ratio (HR) and 95% confidence interval (CI). ResultsCompared with low CVH, high CVH was associated with decreased risks of overall cancer and the majority of common cancers, including digestive system [HRs (95% CI): 0.33 (0.23, 0.45)–0.66 (0.58, 0.75)], lung (HR: 0.25; 95% CI: 0.21, 0.31), renal (HR: 0.42; 95% CI: 0.32, 0.56), bladder (HR: 0.55; 95% CI: 0.44, 0.69), breast (HR: 0.83; 95% CI: 0.74, 0.92), and endometrial cancers (HR: 0.39; 95% CI: 0.30, 0.51). For overall cancer in males, there was an interaction between CVH and PRS. Notably, individuals with high CVH across all levels of PRS had lower risks of overall cancer for females and 8 site-specific cancers than those with low CVH and high PRS [HRs (95% CIs): 0.18 (0.12, 0.25)–0.79 (0.71, 0.87)]. ConclusionsHigh CVH was related to decreased risks of overall cancer and multiple cancers regardless of genetic predispositions. Our findings underscored the value of improving CVH for cancer prevention in the general population.

Exploring the association between metabolic syndrome, its components and subsequent cancer incidence: A cohort study in Catalonia.

Metabolic syndrome (MS) has emerged as a significant global health concern. The relationship between MS and the risk of cancer doesn't seem clear, whether examining by components or in combination. The objective of this study is to examine the relationship between MS, its components, and the overall risk of cancer, including the risk of 13 specific cancer types. We included 3,918,781 individuals aged 40 years or older sourced from the SIDIAP database between 2008 and 2017. Cox models were employed with MS components and their combinations. A subsample was created using a matched cohort (by age and sex). Incidence curves were computed to determine the time elapsed between the date of having 1-5 MS components and cancer incidence, compared to matched participants with no MS components, which showed that individuals who had one MS component experienced a greater incidence of cancer over 5 and 10 years than individuals with no MS, and the incidence rose with an increase in the number of MS components. Individuals exposed to MS components were diagnosed with cancer earlier than those who were not exposed to them. In the Cox model, HDL (HR 1.46, 95% CI: 1.41-1.52) and Glycemia (HR 1.40, 95% CI: 1.37-1.44) were the individual combinations with the highest risk of overall cancer. In combinations with two components, the highest HR was HDL+Glycemia (HR 1.52, 95% CI: 1.45-1.59) and Glycemia+HBP (HR 1.48, 95% CI: 1.45-1.50). In combinations with three components, the highest HR was HDL+Glycemia+HBP (HR 1.58, 95% CI: 1.55-1.62). In summary, having one or more MS components raises the risk of developing at least 11 cancer types and these risk differ according to type of component included. Some sex differences are also observed. Our findings suggest that implementing prevention measures aimed at specific MS components may lower the risk of various cancer types.

Benign and Malignant Outcomes in the Offspring of Females Exposed In Utero to Diethylstilbestrol (DES): An Update from the NCI Third Generation Study.

Females exposed prenatally to diethylstilbestrol (DES) have an elevated risk of cervical dysplasia, breast cancer, and clear cell adenocarcinoma (CCA) of the cervix/vagina. Testicular cancer risk is increased in prenatally exposed males. Epigenetic changes may mediate the transmission of DES effects to the next ("third") generation of offspring. Using data self-reported by third-generation females, we assessed DES in relation to the risk of cancer and benign breast and reproductive tract conditions. Using data from prenatally DES-exposed and unexposed mothers, we assessed DES in relation to cancer risk in their female and male offspring. Cancer risk was assessed by standardized incidence ratios (SIR) and 95% confidence intervals (CI); the risks of benign and malignant diagnoses were assessed by hazard ratios (HR) and 95% CI. In self-reported data, DES exposure was not associated with an increased risk of overall cancer (HR 0.83; CI 0.36-1.90), breast cancer, or severe cervical dysplasia. No females reported CCA. The risk of borderline ovarian cancer appeared elevated, but the HR was imprecise (3.46; CI 0.37-32.42). Based on mothers' reports, DES exposure did not increase the risk of overall cancer (HR 0.80; CI 0.49-1.32) or of other cancers in third-generation females. Overall cancer risk in exposed males appeared elevated (HR 1.41; CI 0.70-2.86), but the CI was wide. The risk of testicular cancer was not elevated in exposed males; no cases of prostate cancer were reported. To date, there is little evidence that DES is associated with cancer risk in third-generation females or males, but these individuals are relatively young, and further follow-up is needed.

Comparing Cancer Risks and Mortality between Phytopharmaceuticals and Estrogen-Progestogen Medications for Menopausal Women: A Population-Based Cohort Study.

We evaluated the long-term risks of overall cancer and all-cause mortality associated with five types of phytopharmaceuticals and the most commonly used estrogen-progestogen medications for the treatment of postmenopausal syndrome in women. Using data from Taiwan's National Health Insurance Research Database (NHIRD) from 1 January 2000 to 31 December 2018, we conducted a 1:2 matched cohort study with 12,087 eligible patients. We compared phytopharmaceuticals -only users (n = 4029, phytopharmaceuticals group) with HRT-only users (n = 8058, HRT group) with a washout period of ≥6 months. The phytopharmaceuticals group had significantly lower risks of overall cancer and all-cause mortality than the HRT group (adjusted hazard ratio [95% confidence interval]: 0.60 [0.40-0.9] and 0.40 [0.16-0.99], respectively) after over 180 days of use. Bupleurum and Peony Formula were associated with lower risks of overall cancer and all-cause mortality (aHR: 0.57 [0.36-0.92] and 0.33 [0.11-1.05], respectively). In conclusion, phytopharmaceuticals may serve as an alternative therapy to HRT for alleviating menopausal symptoms and reducing health risks, leading to more favorable long-term health outcomes. Further randomized control trials are necessary to validate the findings of this study.

Relationship between carrot intake, dietary/circulating α-carotene and cancer risk: A systematic review and meta-analysis of prospective observational studies

Carrot consumption reduces tumour development in several animal models. The constituent alpha- carotene has not by itself shown anti-cancer properties, however carrots typically provide &gt;85% of alpha-carotene dietary intake(1-3), justifying its use as an indicator of carrot intake(3). We conducted a meta-analysis to investigate inverse associations of carrot/dietary α-carotene intakes and cancer risk, and to quantify potential dose–response relationships.PubMed, Cochrane Library, Web of Science, Scopus, EBSCO, and JSTOR were searched (from database inception to August 2021) for studies reporting risk estimates with 95% CIs for the relationship between carrot intake or α-carotene and cancer risk. Meta-analyses were conducted using a random-effects model comparing highest and lowest intakes to estimate summary risk estimates (RRs).Of 80 prospective studies included, 15 (with 25738 cases) reported data on carrot intake, 35 (26262 cases) on dietary α-carotene intake and 30 (9331 cases) on plasma α-carotene levels. A significantly (P&lt;0.01) decreased risk of overall cancer was associated with carrot intake (RR = 0·90), dietary α- carotene intake (RR = 0·90) and plasma α-carotene (RR = 0·80). In addition, both carrot intake and plasma α-carotene level manifested linear dose-response relationships with cancer risk, with increasing carrot intake reaching 20% risk reduction at 5 servings (400g) per week (p &lt; 0·0001),and successive 50μg/L increments in plasma α-carotene associated with 11% risk reduction (p &lt; 0·0058).Carrot consumption is robustly associated with decreased cancer risk. Carrot consumption should be encouraged, and the causal mechanisms further investigated.

The association between being breastfed in infancy and risks of cancer in adulthood—a UK Biobank study

BackgroundBeing breastfed has established benefits for infant health, but its long-term effects on adult diseases, including cancer, remain underexplored. We examined associations between being breastfed in infancy and the risks of common cancers.MethodsData from 339,115 participants (191,117 women) enrolled in the UK Biobank with self-reported breastfeeding data were linked to national cancer registries. Cox models estimated sex-specific hazard ratios (HR) and 95% confidence intervals (CI) for the associations between being breastfed (ever/never) and risks of overall cancer as well as common cancer sites.ResultsIn total, 34,392 incident cancers (17,895 in women) were registered. The HR of overall cancer associated with being breastfed was 1.05 (95% CI 1.01–1.09) in women and 1.00 (95% CI 0.96–1-04) in men. In site-specific analysis being breastfed was associated with an increased risk of breast and ovarian cancer in women and a reduced risk of oesophageal cancer in men.DiscussionWe found that having been breastfed was associated with a marginally increased risk of adult cancer in women, but we found no evidence of an association in men. These findings should be viewed within the study limitations, and do not outweigh the many benefits that breastfeeding provides.

Association between walking pace and risks of major chronic diseases in individuals with hypertension based on a prospective study in UK Biobank: Involvement of inflammation

ObjectiveWalking pace is associated with risks of major chronic diseases including cancer, cardiovascular disease (CVD) and diabetes mellitus type 2 (T2DM) in the general population. However, whether increasing walking pace could reduce risks of major chronic diseases in individuals with hypertension remains to be explored, and the underlying mechanism potentially mediated by low-grade inflammation is also unclear. MethodsA total of 160,470 participants with hypertension were included based on the UK Biobank. The relationships of the walking pace and low-grade inflammation with risks of major chronic diseases in individuals with hypertension were assessed by the Cox proportional hazards model. Mediation analyses were performed to investigate the contribution of low-grade inflammation to the association between walking pace and risks of major chronic diseases. ResultsIndividuals with hypertension at the brisk walking pace had decreased risks of overall cancer and site-specific cancers (liver, lung, and endometrial cancers), all CVD events (angina, atrial fibrillation, heart failure, myocardial infarction, peripheral vascular disease and stroke), and T2DM (hazard ratios: 0.42–0.91). Increasing low-grade inflammation was associated with higher risks of aforementioned diseases except liver cancer and atrial fibrillation. Furthermore, low-grade inflammation partially mediated associations of the walking pace with risks of lung cancer, T2DM, and all CVD events (except atrial fibrillation), with mediation proportion of 2.0%–9.8%. ConclusionsBrisk walking pace was linked to reduced risks of major chronic diseases in individuals with hypertension, partially mediated by low-grade inflammation. Improving walking pace may be beneficial for health in individuals with hypertension.

Medically Assisted Reproduction and Risk of Cancer Among Offspring

Cancer is a leading cause of death among children worldwide. Treatments used for medically assisted reproduction (MAR) are suspected risk factors because of their potential for epigenetic disturbance and associated congenital malformations. To assess the risk of cancer, overall and by cancer type, among children born after MAR compared with children conceived naturally. For this cohort study, the French National Mother-Child Register (EPI-MERES) was searched for all live births that occurred in France between January 1, 2010, and December 31, 2021 (and followed up until June 30, 2022). The EPI-MERES was built from comprehensive data of the French National Health Data System. Data analysis was performed from December 1, 2021, to June 30, 2023. Use of assisted reproduction technologies (ART), such as fresh embryo transfer (ET) or frozen ET (FET), and artificial insemination (AI). The risk of cancer was compared, overall and by cancer type, among children born after fresh ET, FET, or AI and children conceived naturally, using Cox proportional hazards regression models adjusted for maternal and child characteristics at birth. This study included 8 526 306 children with a mean (SD) age of 6.4 (3.4) years; 51.2% were boys, 96.4% were singletons, 12.1% were small for gestational age at birth, and 3.1% had a congenital malformation. There were 260 236 children (3.1%) born after MAR, including 133 965 (1.6%) after fresh ET, 66 165 (0.8%) after FET, and 60 106 (0.7%) after AI. A total of 9256 case patients with cancer were identified over a median follow-up of 6.7 (IQR, 3.7-9.6) years; 165, 57, and 70 were born after fresh ET, FET, and AI, respectively. The overall risk of cancer did not differ between children conceived naturally and those born after fresh ET (hazard ratio [HR], 1.12 [95% CI, 0.96 to 1.31]), FET (HR, 1.02 [95% CI, 0.78 to 1.32]), or AI (HR, 1.09 [95% CI, 0.86 to 1.38]). However, the risk of acute lymphoblastic leukemia was higher among children born after FET (20 case patients; HR 1.61 [95% CI, 1.04 to 2.50]; risk difference [RD], 23.2 [95% CI, 1.5 to 57.0] per million person-years) compared with children conceived naturally. Moreover, among children born between 2010 and 2015, the risk of leukemia was higher among children born after fresh ET (45 case patients; HR, 1.42 [95% CI, 1.06 to 1.92]; adjusted RD, 19.7 [95% CI, 2.8 to 43.2] per million person-years). The findings of this cohort study suggest that children born after FET or fresh ET had an increased risk of leukemia compared with children conceived naturally. This risk, although resulting in a limited number of cases, needs to be monitored in view of the continuous increase in the use of ART.

Associations of combined phenotypic aging and genetic risk with incident cancer: A prospective cohort study.

Age is the most important risk factor for cancer, but aging rates are heterogeneous across individuals. We explored a new measure of aging-Phenotypic Age (PhenoAge)-in the risk prediction of site-specific and overall cancer. Using Cox regression models, we examined the association of Phenotypic Age Acceleration (PhenoAgeAccel) with cancer incidence by genetic risk group among 374,463 participants from the UK Biobank. We generated PhenoAge using chronological age and nine biomarkers, PhenoAgeAccel after subtracting the effect of chronological age by regression residual, and an incidence-weighted overall cancer polygenic risk score (CPRS) based on 20 cancer site-specific polygenic risk scores (PRSs). Compared with biologically younger participants, those older had a significantly higher risk of overall cancer, with hazard ratios (HRs) of 1.22 (95% confidence interval, 1.18-1.27) in men, and 1.26 (1.22-1.31) in women, respectively. A joint effect of genetic risk and PhenoAgeAccel was observed on overall cancer risk, with HRs of 2.29 (2.10-2.51) for men and 1.94 (1.78-2.11) for women with high genetic risk and older PhenoAge compared with those with low genetic risk and younger PhenoAge. PhenoAgeAccel was negatively associated with the number of healthy lifestyle factors (Beta = -1.01 in men, p<0.001; Beta = -0.98 in women, p<0.001). Within and across genetic risk groups, older PhenoAge was consistently related to an increased risk of incident cancer with adjustment for chronological age and the aging process could be retarded by adherence to a healthy lifestyle. This work was supported by the National Natural Science Foundation of China (82230110, 82125033, 82388102 to GJ; 82273714 to MZ); and the Excellent Youth Foundation of Jiangsu Province (BK20220100 to MZ).

Associations of combined phenotypic aging and genetic risk with incident cancer: A prospective cohort study

Background:Age is the most important risk factor for cancer, but aging rates are heterogeneous across individuals. We explored a new measure of aging-Phenotypic Age (PhenoAge)-in the risk prediction of site-specific and overall cancer.Methods:Using Cox regression models, we examined the association of Phenotypic Age Acceleration (PhenoAgeAccel) with cancer incidence by genetic risk group among 374,463 participants from the UK Biobank. We generated PhenoAge using chronological age and nine biomarkers, PhenoAgeAccel after subtracting the effect of chronological age by regression residual, and an incidence-weighted overall cancer polygenic risk score (CPRS) based on 20 cancer site-specific polygenic risk scores (PRSs).Results:Compared with biologically younger participants, those older had a significantly higher risk of overall cancer, with hazard ratios (HRs) of 1.22 (95% confidence interval, 1.18–1.27) in men, and 1.26 (1.22–1.31) in women, respectively. A joint effect of genetic risk and PhenoAgeAccel was observed on overall cancer risk, with HRs of 2.29 (2.10–2.51) for men and 1.94 (1.78–2.11) for women with high genetic risk and older PhenoAge compared with those with low genetic risk and younger PhenoAge. PhenoAgeAccel was negatively associated with the number of healthy lifestyle factors (Beta = –1.01 in men, p&lt;0.001; Beta = –0.98 in women, p&lt;0.001).Conclusions:Within and across genetic risk groups, older PhenoAge was consistently related to an increased risk of incident cancer with adjustment for chronological age and the aging process could be retarded by adherence to a healthy lifestyle.Funding:This work was supported by the National Natural Science Foundation of China (82230110, 82125033, 82388102 to GJ; 82273714 to MZ); and the Excellent Youth Foundation of Jiangsu Province (BK20220100 to MZ).

The association of the dietary inflammatory potential with risk of overall and site-specific cancers: A community-based longitudinal study in the UK Biobank

ObjectivesThe association of the dietary inflammatory potential with cancer risk remains uncertain. We examined the relationship of the dietary inflammatory potential with risk of overall and site-specific cancers and explored its sex and age differences. DesignA community-based longitudinal study. SettingParticipants from the UK Biobank completed baseline surveys during 2006–2010 and were followed for up to 15 years to detect incident cancer. Participants170,899 cancer-free participants with dietary data available (mean age: 55.73 ± 7.95, 54.10% female). MeasurementsAt baseline, dietary intake was assessed with a 24-h dietary record for up to 5 times. The inflammatory diet index (IDI) was calculated to assess the dietary inflammatory potential as a weighted sum of 31 food groups (including 14 anti-inflammatory and 17 pro-inflammatory) based on plasma high-sensitivity C-reactive protein (hsCRP) levels, and tertiled as low (indicating low-inflammatory diet), moderate, and high IDI (as reference). Overall and site-specific cancers were ascertained via linkage to routine hospital admission, cancer registry, and death certificate data. Data were analyzed using Cox regression and Laplace regression. ResultsDuring the follow-up (median 10.32 years, interquartile range: 9.95–11.14 years), 18,884 (11.05%) participants developed cancer. In multi-adjusted Cox regression, low IDI scores were associated with decreased risk of rectal cancer (hazard ratio [95% confidence interval, CI] 0.76 [0.61, 0.94]), thyroid cancer [0.45 (0.27, 0.74)], lung cancer [0.73 (0.61, 0.88)]. However, the association between IDI score and the risk of overall cancer was not significant. Laplace regression analysis showed that 10th percentile differences (95% CIs) of cancer onset time for participants with low IDI scores was prolonged by 1.29 (0.32, 2.27), 1.44 (0.58, 2.30), and 2.62 (0.98, 4.27) years for rectal cancer, thyroid cancer, and lung cancer, respectively, compared to those with high IDI scores. Stratified analysis revealed that low IDI scores were associated with a lower risk of rectal cancer (p interaction between IDI score and sex = 0.035) and lung cancer in males, but not in females, and with a reduced risk of thyroid cancer in females, but not in males. Moreover, low IDI scores were associated with a reduced risk of rectal cancer and lung cancer in the participants aged ≥60 years, but not in those <60 years, and with a reduced risk of thyroid cancer in those aged ≥60 years and <60 years. ConclusionsA low-inflammatory diet is associated with decreased risk and prolonged onset time of rectal cancer and lung cancer, especially among males and individuals aged ≥60 years, and thyroid cancer among females.

Risk of cancer in patients with bile acid diarrhoea: a Danish nationwide matched cohort study

ObjectiveBile acid diarrhoea is a common cause of chronic diarrhoea. Increased levels of potentially carcinogenic bile acids in faeces, theoretically, may increase the risk of colorectal cancer in particular, but...

Joint association of biological aging and lifestyle with risks of cancer incidence and mortality: A cohort study in the UK Biobank

BackgroundAging is a risk factor for cancer incidence and mortality. Biological aging can reflect the aging degree of the body better than chronological age and can be aggravated by unhealthy lifestyle factors. We aimed to assess the joint effect of biological aging and lifestyle with risks of cancer incidence and mortality. MethodsThis study included a total of 281,889 participants aged 37 to 73 from the UK Biobank database. Biological age was derived from chronological age and 9 clinical blood indicators, and lifestyle score was constructed by body mass index, smoking status, alcohol consumption, physical activity, and diet. Multivariate Cox hazard proportional regression model was used to analyze the independent and joint association of biological aging and lifestyle with risks of cancer incidence and mortality, respectively. ResultsOver a median follow-up period of 12.3 years, we found that older biological age was associated with increased risks of overall cancer, digestive system cancers, lung, breast and renal cancers incidence and mortality (HRs: 1.12–2.25). In the joint analysis of biological aging and lifestyle with risks of cancer incidence and mortality, compared with unhealthy lifestyle and younger biological age, individuals with healthy lifestyle and older biological age had decreased risks of incidence (8% ∼ 60%) and mortality (20% ∼ 63%) for overall, esophageal, colorectal, pancreatic and lung cancers. ConclusionsBiological aging may be an important risk factor for cancer morbidity and mortality. A healthier lifestyle is more likely to mitigate the adverse effects of biological aging on overall cancer and some site-specific cancers.

Metabolomic landscape of overall and common cancers in the UK Biobank: A prospective cohort study.

Information about the NMR metabolomics landscape of overall, and common cancers is still limited. Based on a cohort of 83,290 participants from the UK Biobank, we used multivariate Cox regression to assess the associations between each of the 168 metabolites with the risks of overall cancer and 20 specific types of cancer.Then, we applied LASSO to identify important metabolites for overall cancer risk and obtained their associations using multivariate cox regression. We further conducted mediation analysis to evaluate the mediated role of metabolites in the effects of traditional factors on overall cancer risk. Finally, we included the 13 identified metabolites as predictors in prediction models, and compared the accuracies of our traditional models. We found that there were commonalities among the metabolic profiles of overall and specific types of cancer: the top 20 frequently identified metabolites for 20 specific types of cancer were all associated with overall cancer; most of the specific types of cancer had common identified metabolites. Meanwhile, the associations between the same metabolite with different types of cancer can vary based on the site of origin. We identified 13 metabolic biomarkers associated with overall cancer, and found that they mediated the effects of traditional factors. The accuracies of prediction models improved when we added 13 identified metabolites in models. This study is helpful to understand the metabolic mechanisms of overall and a wide range of cancers, and our results also indicate that NMR metabolites are potential biomarkers in cancer diagnosis and prevention.

The intersection of heart failure and cancer in women: a review.

Cancer and cardiovascular disease represent the two leading causes of morbidity and mortality worldwide. Women continue to enjoy a greater life expectancy than men. However, this comes at a cost with more women developing diabetes, hypertension and coronary artery disease as they age. These traditional cardiovascular risk factors not only increase their lifetime risk of heart failure but also their overall risk of cancer. In addition to this, many of the cancers with female preponderance are treated with potentially cardiotoxic therapies, adding to their increased risk of developing heart failure. As a result, we are faced with a higher risk population, potentially suffering from both cancer and heart failure simultaneously. This is of particular concern given the coexistence of heart failure and cancer can confer a worse prognosis than either a single diagnosis of heart failure or cancer alone. This review article explores the intersection of heart failure and cancer in women at multiple levels, including traditional cardiovascular risk factors, cardiovascular toxicity derived from antineoplastic and radiation therapy, shared pathophysiology and HF as an oncogenic process. This article further identifies opportunities and strategies for intervention and optimisation, whilst highlighting the need for contemporary guidelines to better inform clinical practice.

Temporal relationship between inflammation and metabolic disorders and their impact on cancer risk.

Inflammation and metabolic disorders are closely associated with cancer. Whether inflammation leads to metabolic disorders or vice versa during cancer initiation remains unclear. In this study, we explored this temporal relationship and the co-exposure effect on cancer risk. This prospective study had two phases. Initially, we examined the temporal relationship between inflammation (high-sensitivity C-reactive protein (CRP)) and metabolic disorders (metabolic syndrome severity Z-score (MetS-Z)) using a 3.98-year survey and cross-lagged analysis. Subsequently, we assessed the connection of co-exposure to inflammation and metabolic disorders, and the risks of overall cancer, as well as specific obesity-related, non-obesity-related, digestive system, lung, and other cancers using an 11.04-year survey and Cox proportional hazard models. The cross-lagged analysis revealed that the path coefficient from baseline CRP to follow-up MetS-Z (β2 = 0.032; 95% confidence interval (CI) = 0.026, 0.046) was more significant than the path coefficient from baseline MetS-Z to follow-up CRP (β1 = 0.009; 95% CI = -0.001, 0.019). During the follow-up, 2304 cases of cancer occurred. Compared with the risk of cancer of patients with low average cumulative CRP and MetS-Z, patients with high value had a significantly increased risk (hazard ratio = 1.54, 95% CI = 1.30, 1.83). The mediation analysis showed that MetS-Z mediated the association between CRP levels and overall cancer (12.67%), digestive system cancer (10.16%), and obesity-related cancer risk (13.87%). Inflammation had a greater impact on metabolic disorders than vice versa. Co-exposure to inflammation and metabolic disorders significantly increased the risk of cancer, particularly digestive system and obesity-related cancers. Chinese Clinical Trial Registry: ChiCTR-TNRC-11001489.