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Background Cardiovascular disease (CVD) and cancer frequently co‐occur due to shared risk factors such as obesity, which is linked to CVD and 14 cancer types. This study explores whether CVD pathophysiologies, combined with obesity, increase cancer risk, impacting clinical management. Methods and Results Data from the ARIC (Atherosclerosis Risk in Communities) study, spanning 28 years, were analyzed. The cohort included 5127 participants with incident CVD (myocardial infarction, stroke, heart failure, coronary heart disease), of whom 1511 developed a first primary cancer. Follow‐up began at CVD diagnosis after Visit 1. Obesity was assessed using body mass index, waist circumference, and waist‐to‐hip ratio. Incidence rate differences between obesity groups were adjusted for age, sex, and center, whereas the obesity–cancer association was estimated using Fine‐Gray regression adjusted for shared risk factors including smoking. Cancer incidence in obese individuals with CVD (body mass index: rate differences=226.6/100 000 person‐years) was higher than in those with normal weight. Although obesity was not linked to overall cancer after adjusting for shared risk factors, it was nominally associated with obesity‐related cancers. Specifically, women with CVD and obesity had increased obesity‐related cancer risk (body mass index: hazard ratio, 1.67 [95% CI, 1.17–2.31]). No significant associations were found in men, even after excluding prostate cancer. Conclusions This study suggests that obesity is linked to higher obesity‐related cancer risk in women with incident CVD, independent of shared risk factors. Further research is needed to eliminate residual confounding, understand sex differences, and explore how CVD pathophysiologies and obesity together influence cancer risk.

Abstract Ginger has been associated with a decreased incidence of colorectal cancer (CRC) through reduction in inflammatory pathways and inhibition of tumor growth. Recent pre-clinical models have implicated changes in the gut microbiome as a possible mediator of the ginger effect on CRC. We hypothesized that, in adults previously diagnosed with a colorectal adenoma, ginger supplementation would alter the fecal microbiome in the direction consistent with its CRC-inhibitory effect. Sixty-eight adults were randomized to take either ginger or placebo daily for 6 weeks, with a 6-week washout and longitudinal stool collection throughout. We performed 16S rRNA sequencing and evaluated changes in overall microbial diversity and the relative abundances of pre-specified CRC-associated taxa using mixed-effects logistic regression. Ginger supplementation showed no significant effect on microbial community structure through alpha or beta diversity. Of 10 pre-specified CRC-associated taxa, there were significant decreases in the relative abundances of the genera Akkermansia (p

Factors driving accelerated biological age (BA), an important predictor of chronic diseases, remain poorly understood. This study focuses on the impact of diet and gut microbiome on accelerated BA. Accelerated Klemera–Doubal biological age (KDM-BA) was estimated as the difference between KDM-BA and chronological age. We assessed the cross-sectional association between accelerated KDM-BA and diet/gut microbiome in 117 adult participants from the 10,000 Families Study. 16S rRNA sequencing was used to estimate the abundances of gut bacterial genera. Multivariable linear mixed models evaluated the associations between accelerated KDM-BA and diet/gut microbiome after adjusting for family relatedness, diet, age, sex, smoking status, alcohol intake, and BMI. One standard deviation (SD) increase in processed meat was associated with a 1.91-year increase in accelerated KDM-BA (p = 0.04), while one SD increase in fiber intake was associated with a 0.70-year decrease in accelerated KDM-BA (p = 0.01). Accelerated KDM-BA was positively associated with Streptococcus and negatively associated with Subdoligranulum, unclassified Bacteroidetes, and Burkholderiales. Adjustment for gut microbiome did not change the association between dietary fiber and accelerated KDM-BA, but the association with processed meat intake became nonsignificant. These cross-sectional associations between higher meat intake, lower fiber intake, and accelerated BA need validation in longitudinal studies.

The population of cancer survivors has markedly increased due to the rapid improvements in cancer treatment. However, cancer survivors experience accelerated aging, which leads to chronic diseases and other age-related conditions, such as frailty. Those conditions may persist years after cancer diagnosis and treatment. Cellular senescence, a hallmark of aging, is one of the mechanisms that contribute to accelerated aging in cancer survivors. Several aging measures, including measures based on clinical markers and biomarkers, have been proposed to estimate the aging process, and some of them have shown associations with mortality and frailty in cancer survivors. Several anti-aging interventions, including lifestyle changes and anti-aging drugs, have been proposed. Future research, particularly in large-scale studies, is needed to determine the efficiency of these aging measures and anti-aging interventions before considering their application in clinics. This review focuses on the mechanisms of cellular senescence and accelerated aging in cancer survivors, assessment of the aging process using clinical markers and biomarkers, and the high prevalence of frailty in that population, as well as possible opportunities for anti-aging interventions. A deeper understanding of aging measures and anti-aging interventions in cancer survivors will contribute to the development of effective strategies to mitigate accelerated aging in cancer survivors and improve their quality of life.