Single body mass index (BMI) measurements have been associated with increased risk of 13 cancers. Whether life course adiposity-related exposures are more relevant cancer risk factors than baseline BMI (ie, at start of follow-up for disease outcome) remains unclear. We conducted a cohort study from 2009 until 2018 with population-based electronic health records in Catalonia, Spain. We included 2,645,885 individuals aged >/=40 years and free of cancer in 2009. After 9 years of follow-up, 225,396 participants were diagnosed with cancer. This study shows that longer duration, greater degree, and younger age of onset of overweight and obesity during early adulthood are positively associated with risk of 18 cancers, including leukemia, non-Hodgkin lymphoma, and among never-smokers, head and neck, and bladder cancers which are not yet considered as obesity-related cancers in the literature. Our findings support public health strategies for cancer prevention focussing on preventing and reducing early overweight and obesity.
The implementation of primary and secondary preventive strategies is based on the evidence generated by cancer epidemiology, where the identification of risk factors and the description of their prevalence are fundamental to derive estimates on the burden of cancer from different etiologies, typically expressed as the population attributable fraction, which corresponds to the proportion of a cancer that may be prevented by controlling a given risk factor. However, even when cancer finds its etiology in modifiable factors, its prevention through the control of those factors is not always feasible, or it remains suboptimal despite the possibility of reducing the burden. We reviewed selected associations between modifiable risk factors and cancer, including tobacco smoking, occupational exposures, infections, air pollution, alcohol, and diet and obesity, and illustrated examples of both successes and failures in cancer control, underlying how current understanding of the avoidable causes of cancer is incomplete.
BACKGROUND: Multiple development of esophageal squamous-cell carcinoma is explained by field cancerization and is associated with alcohol consumption and smoking. We investigated the association between the development of second primary esophageal squamous-cell carcinoma after endoscopic resection for esophageal squamous-cell carcinoma and genetic polymorphisms related to alcohol and nicotine metabolism.
METHODS: The study group comprised 56 patients with esophageal squamous-cell carcinoma after endoscopic resection. The main variables were the following: (i) cumulative incidence and total number of second primary esophageal squamous-cell carcinoma according to genetic polymorphisms in alcohol dehydrogenase 1B, aldehyde dehydrogenase 2 and cytochrome P450 2A6; and (ii) risk factors of second primary esophageal squamous-cell carcinoma identified using a multivariate Cox proportional-hazards model. The frequencies of alcohol dehydrogenase 1B, aldehyde dehydrogenase 2 and cytochrome P450 2A6 genetic polymorphisms in the buccal mucosa were analyzed.
RESULTS: The median follow-up was 92.8 months (range: 2.7-134.2). Slow-metabolizing alcohol dehydrogenase 1B was associated with a higher 7-year cumulative incidence of second primary esophageal squamous-cell carcinoma (fast-metabolizing alcohol dehydrogenase 1B vs slow-metabolizing alcohol dehydrogenase 1B: 20.5% vs 71.4%, P = 0.006). Slow-metabolizing alcohol dehydrogenase 1B (relative risk [95% confidence interval]: 3.17 [1.49-6.73]), inactive aldehyde dehydrogenase 2 (2.17 [1.01-4.63]) and poorly-metabolizing cytochrome P450 2A6 (4.63 [1.74-12.33]) had a significantly higher total number of second primary esophageal squamous-cell carcinoma per 100 person-years. In the multivariate Cox proportional-hazards model, slow-metabolizing alcohol dehydrogenase 1B was a significant risk factor of the development of second primary esophageal squamous-cell carcinoma (hazard ratio 9.92, 95% confidence interval: 2.35-41.98, P = 0.0018).
CONCLUSIONS: Slow-metabolizing alcohol dehydrogenase 1B may be a significant risk factor for the development of second primary esophageal squamous-cell carcinoma. In addition, inactive aldehyde dehydrogenase 2 and poorly-metabolizing cytochrome P450 2A6 may be important factors.
Polyphenols are secondary plant metabolites synthesized during the development of the grape berry as a response to stress conditions. They are important constituents in red wines that contribute to the sensory properties and antioxidant activity of wines. Due to the development of highly sophisticated analytical devices, it is now possible to characterize the structure of highly polymerized polyphenols and obtain a full polyphenol profile of red wines. Red wine polyphenols include the ones present in grapes as well as new polyphenol products formed during the winemaking process.
Among them, the most important groups and their representatives are flavanols (catechin), stilbenes (trans-resveratrol), flavonols (quercetin) and hydroxybenzoic acids (gallic acid). It is known that polyphenols exhibit beneficial effects on human health, such as anti-inflammatory, anticarcinogenic and cardio-protective effects. Many studies have been conducted on the health effects of red wine polyphenols in cancer chemopreventive activities, neuroprotective effects and impact on cardiovascular diseases, gut microbiota in humans, etc. This review will provide major scientific findings on the impact of red wine polyphenols on human health as well as a review of polyphenols present in red wines and their main features.