Body Mass Index and Risk of Breast Cancer: A Nonlinear Dose-Response Meta-Analysis of Prospective Studies

Xia, Xiaoping; Chen, Wei; Li, Jiaoyuan; Chen, Xueqin; Rui, Rui; Liu, Cheng; Sun, Yu; Liu, Li; Gong, Jing; Yuan, Peng

doi:10.1038/srep07480

Cited by 72 publications

(61 citation statements)

References 51 publications

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“…As mentioned earlier, obesity has been shown to be an important risk factor for certain types of cancer [2][3][4][5][6][7]. However, most researchers put more effort to examine the role of general obesity in the etiologies of these malignancies, while paying less attention to the potential detrimental effect of abdominal obesity.…”

Section: Discussionmentioning

confidence: 99%

“…There is mounting evidence that obesity increases the risk of certain types of cancers, including post-menopausal breast cancer, colorectal, endometrial, kidney, and pancreatic cancers [2][3][4][5][6][7]. Obesity may have also contributed to the recent rise in gastric cardia carcinoma and esophageal adenocarcinoma (EAC) incidence over the past decades because the prevalence of obesity has increased dramatically at an accelerating and alarming rate during approximately the same time period [8,9].…”

Section: Introductionmentioning

confidence: 99%

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Abdominal Obesity and Gastroesophageal Cancer Risk: Systematic Review and Meta-Analysis of Prospective Studies

Hidayat¹,

Du²,

Shi³

2016

Preprint

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Correspondence: To systematically and quantitatively review the relation of abdominal obesity, as measured by waist circumference (WC) and waist to hip ratio (WHR), to total gastroesophageal cancer, gastric cancer (GC), and esophageal cancer. PubMed and Web of Science databases were searched for studies assessing the association between abdominal obesity and gastroesophageal cancer (GC and/or esophageal cancer) up to August 2016. A random-effect model was used to calculate the summary relative risks (RRs) and 95% confidence intervals (CIs). Seven prospective cohort studies -one publication included two separate cohorts -from six publications were included in the final analysis. A total of 2130 gastroesophageal cancer cases diagnosed amongst 913182 participants. Higher WC and WHR were significantly associated with increased risk of total gastroesophageal cancer (WC: RR 1.68, 95% CI: 1.38, 2.04; WHR: RR 1.49, 95% CI: 1.19, 1.88), GC (WC: RR 1.48, 95% CI: 1.24, 1.78; WHR: 1.33, 95% CI: 1.04, 1.70), and esophageal cancer (WC: RR 2.06, 95% CI: 1.30, 3.24; WHR: RR 1.99, 95% CI: 1.05, 3.75).Findings from our subgroup analyses showed non-significant positive associations between gastric non-cardia adenocarcinoma (GNCA) and both measures of abdominal adiposity, while gastric cardia adenocarcinoma (GCA) was positively associated with WC but not with WHR. On analysis restricted to studies that adjusted for body mass index (BMI), WC was positively associated with GC and esophageal cancer, whereas WHR was positively associated with risk of GC only. Although limited, the findings from our meta-analysis suggest the potential role of abdominal obesity in the etiology of gastric and esophageal cancers.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Abdominal Obesity and Gastroesophageal Cancer Risk: Systematic Review and Meta-Analysis of Prospective Studies

Hidayat¹,

Du²,

Shi³

2016

Preprint

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“…El crecimiento de células cancerosas está regulado por varias señales celulares (STAT3, AP-1, MAPK, ERKs) moduladas por la leptina e IL-6, las cuales incrementan la aromatasa, la síntesis de estrógenos y la activación de receptores alfa en las células malignas, llevando a estas células a una mayor proliferación (37) . El incremento del riesgo de cáncer de mama con la obesidad se observa solo en las mujeres posmenopáusicas, encontrándose un RR de 1,12 (IC 95% 1,01 a 1,24) y 1,26 (IC 95% 1,07 a 1,50) cuando el IMC es de 30 y 35 kg/m2, respectivamente (38) . La obesidad también aumenta el riesgo de cáncer de endometrio, riñón, colon y vesícula en mujeres posmenopáusicas.…”

Section: Cáncerunclassified

Terapia hormonal de la menopausia, ¿por qué prescribirla?

Maldonado

2018

Rev peru ginecol obstet.

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Financiamiento: Autofinanciado Conflicto de interés:La autora declara no tener algún conflicto de interés RESUMENDurante el climaterio, la mayoría de las mujeres presenta muchos síntomas que afectan su calidad de vida. Estos síntomas han sido vinculados con trastornos de la neuroquímica provocados por la carencia de estrógenos. El sistema nervioso central-SNC también está involucrado en los cambios de la composición corporal y en el aumento de tejido adiposo que se produce durante el climaterio. El adipocito del obeso produce adipocitoquinas que llevan a un estado inflamatorio crónico con incremento del riesgo de diabetes, hipertensión e hipercoagulabilidad, aumentando el riesgo cardiovascular. El déficit de estrógenos también modula señales celulares (RANKL, NPY) que favorecen la reabsorción ósea y el riesgo de osteoporosis. La obesidad asociada al climaterio incrementa además el riesgo de cáncer de mama, endometrio, colon y vesícula al aumentar la leptina e interleucina 6. Estas adipocitoquinas modulan una serie señales celulares (STAT3, AP-1, MAPK, ERKs) que a su vez aumentan la aromatasa, la síntesis de estrógenos y la activación de receptores alfa en las células malignas, estimulando la proliferación celular. También, algunos estudios experimentales sugieren una acción anti-Alzheimer de los esteroides ováricos. Palabras clave. Terapia hormonal, Menopausia, Calidad de vida, Enfermedades crónicas. ABSTRACTDuring the climacteric, most women have many symptoms that affect their quality of life. These symptoms have been linked to neurochemical disorders caused by the lack of estrogen. The CNS is also involved in changes in body composition and in the gain in adipose tissue that occurs during the climacteric. Obese adipocytes produce adipocytokines that lead to a chronic inflammatory status with a higher risk for diabetes, hypertension and hypercoagulability; all these increase the cardiovascular risk. Estrogen deficiency also modulates cellular signals (RANKL, NPY) that favor bone resorption and osteoporosis risk. Obesity associated with menopause also increases the risk of breast, endometrial, colon and bladder cancer by raising the levels of leptin and interleukin 6. These adipocytokines modulate a series of cellular signals (STAT3, AP-1, MAPK, ERKs) series which in turn increase aromatase, the synthesis of estrogens and the activation of alpha receptors in malignant cells, stimulating cell proliferation. Also, some experimental studies suggest an anti-Alzheimer action of ovarian steroids.

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“…Weight gain is considered to be associated with the risk of breast cancer; however, studies have shown a higher incidence of proliferative lesions in overweight postmenopausal women. A metaanalysis of prospective studies showed that postmenopausal women with a BMI of 25, 30 and 35 kg/m 2 have a relative risk of breast cancer of RR = 1.02 (95% CI: 0.98; 1.06), RR = 1.12 (95% CI: 1.01; 1.24), and RR = 1.26 (95% CI: 1.07; 1.50), respectively, compared with women of normal body weight [62]. There is, however, no similar relationship for premenopausal women.…”

Section: Obesity and Cancermentioning

confidence: 99%