Tobacco smoking patterns and differential food effects on prostate and breast cancers among smokers and nonsmokers in Córdoba, Argentina

Abstract

The aim of this study was to estimate the effect of diet on prostate and breast cancer (PC and BC) risks in smokers and nonsmokers and to explore the effect modification between smoking and dietary patterns. PC or BC incidence rates were assessed spatially according to tobacco exposure, age-adjusted standardization using lung cancer mortality as a proxy. Two case-control studies were carried out in Argentina (2008-2012). Participants were interviewed about their diet, smoking habits, and other lifestyle factors. Multilevel models were fitted including family history of cancer as the random intercept for the second level, and diet and lifestyle variables as covariates. Tobacco exposure was aggregated spatially. Family history of cancer significantly accounts for PC and BC. In smokers, high intake of fat meat increased PC and BC risks [odds ratio (OR) 1.56, 95% confidence interval (CI) 0.81-3.05 and OR 6.01, 95% CI 1.99-8.19, respectively]. PC and BC risks were also greater in smokers with high intakes of fatty foods (OR 1.95, 95% CI 1.09-3.50 and OR 24.2, 95% CI 0.82-7.21, respectively). Moderate intake of nonstarchy vegetables and risk of PC were inversely associated in nonsmokers (OR 0.55, 95% CI 0.20-1.48). In smoker women, BC risk was associated with sweet drink consumption (OR 2.96, 95% CI 1.10-7.92) and ethanol intake (OR 5.15, 95% CI 1.88-14.16). Spatial distributions of cancer incidence rates match those of tobacco exposure. Differential effects of diet on PC and BC risks were found in smokers and nonsmokers.

Long-Term Administration of Prolactin or Testosterone Induced Similar Precancerous Prostate Lesions in Rats

“…Every year, hundreds of thousands of new cases of CaP are detected and up to 6.6% of them result in death [1]. The etiology of the disease is diverse, and may include family history, age (> 65) [2], race (> african-ancestry) [3], diet (> high-fat products) [4], obesity (body mass index (BMI) > 25) [5], and bad habits, such as smoking [6]. For that reason, treatments are also diverse and may include surgery, radiation, chemotherapy, vaccines, or hormone treatments.…”

Efecto del estrés agudo prepuberal sobre la próstata: Histología y expresión de OB-R, PRL-R, IL-6 y NFkB en la rata

“…Por ejemplo, se sabe que existe mayor susceptibilidad en aquellos individuos que presentan alguno de los siguientes factores: ser mayores de 65 años, 5 tener ascendencia Africana, 6 consumir dietas altas en grasas de origen animal, 7 tener obesidad, 8 o con ciertas adicciones como al tabaco. 9 Sin embargo, las alteraciones hormonales parecen representar el factor principal, tanto para el desarrollo de CaP como para su tratamiento. 10 Esto sugiere que aquellas condiciones que modifiquen los niveles sistémicos de hormonas o sus receptores en la próstata pudieran ser exploradas como factores de riesgo.…”

Prepuberal stress and obesity: effects on serum corticosterone, prolactin, testosterone and precancerous prostate lesions in adult rats

“…can be found in individuals with a previous history of chronic prostatitis due to infections [4]. However, the development of CaP is mainly linked to chronic high levels of hormones that facilitate cell proliferation like testosterone [5,6] or prolactin [7][8][9]; and it is also linked to factors such as older age [10], africanancestry [11], and smoking [12]. Inte restingly, other factors such as the consumption of high-fat products [13], obesity [14] and stress [15] appear to play an important role in the risk for developing CaP or precancerous prostate lesions, which represent the anteroom for CaP.…”