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Prospective association between alcohol intake and hormone-dependent cancer risk: modulation by dietary fiber intake.
Chhim, AS, Fassier, P, Latino-Martel, P, Druesne-Pecollo, N, Zelek, L, Duverger, L, Hercberg, S, Galan, P, Deschasaux, M, Touvier, M
The American journal of clinical nutrition. 2015;(1):182-9
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Abstract
BACKGROUND Alcohol intake is associated with increased circulating concentrations of sex hormones, which in turn may increase hormone-dependent cancer risk. This association may be modulated by dietary fiber intake, which has been shown to decrease steroid hormone bioavailability (decreased blood concentration and increased sex hormone-binding globulin concentration). However, this potential modulation has not been investigated in any prospective cohort. OBJECTIVES Our objectives were to study the relation between alcohol intake and the risk of hormone-dependent cancers (breast, prostate, ovarian, endometrial, and testicular) and to investigate whether dietary fiber intake modulated these associations. DESIGN This prospective observational analysis included 3771 women and 2771 men who participated in the Supplémentation en Vitamines et Minéraux Antioxydants study (1994-2007) and completed at least 6 valid 24-h dietary records during the first 2 y of follow-up. After a median follow-up of 12.1 y, 297 incident hormone-dependent cancer cases, including 158 breast and 123 prostate cancers, were diagnosed. Associations were tested via multivariate Cox proportional hazards models. RESULTS Overall, alcohol intake was directly associated with the risk of hormone-dependent cancers (tertile 3 vs. tertile 1: HR: 1.36; 95% CI: 1.00, 1.84; P-trend = 0.02) and breast cancer (HR: 1.70; 95% CI: 1.11, 2.61; P-trend = 0.04) but not prostate cancer (P-trend = 0.3). In stratified analyses (by sex-specific median of dietary fiber intake), alcohol intake was directly associated with hormone-dependent cancer (tertile 3 vs. tertile 1: HR: 1.76; 95% CI: 1.10, 2.82; P-trend = 0.002), breast cancer (HR: 2.53; 95% CI: 1.30, 4.95; P-trend = 0.02), and prostate cancer (HR: 1.37; 95% CI: 0.65, 2.89; P-trend = 0.02) risk among individuals with low dietary fiber intake but not among their counterparts with higher dietary fiber intake (P-trend = 0.9, 0.8, and 0.6, respectively). The P-interaction between alcohol and dietary fiber intake was statistically significant for prostate cancer (P = 0.01) but not for overall hormone-dependent (P = 0.2) or breast (P = 0.9) cancer. CONCLUSION In line with mechanistic hypotheses and experimental data, this prospective study suggested that dietary fiber intake might modulate the association between alcohol intake and risk of hormone-dependent cancer. This trial was registered at clinicaltrials.gov as NCT00272428.
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Dual association between polyphenol intake and breast cancer risk according to alcohol consumption level: a prospective cohort study.
Touvier, M, Druesne-Pecollo, N, Kesse-Guyot, E, Andreeva, VA, Fezeu, L, Galan, P, Hercberg, S, Latino-Martel, P
Breast cancer research and treatment. 2013;(1):225-36
Abstract
Studies of the association between polyphenols dietary intake and breast cancer risk have been limited due to the lack of detailed food composition tables. In addition, none has examined this association according to alcohol intake, despite the facts that alcohol is an established risk factor for breast cancer and that the contribution of alcoholic beverages to polyphenol intake varies according to the level of alcohol consumption. Our objectives were (1) to estimate the associations between breast cancer risk and a wide range of dietary polyphenols using the recently published Phenol-Explorer database; and (2) to evaluate if/how alcohol intake modulates these relationships. 4,141 women from the SU.VI.MAX prospective cohort were followed from 1994 to 2007 (median followup: 12.6 years); 152 developed a first incident invasive primary breast cancer. Dietary intakes were assessed by repeated 24-h records. The Phenol-Explorer database was used to estimate polyphenol intake. Multivariable Cox proportional hazards models were used to calculate hazard ratios (HRs) and 95 % confidence intervals (CIs) for quartiles of polyphenol intake. Analyses were stratified by median alcohol intake (< vs. ≥ 6.5 g/d). In non-to-low alcohol drinkers, intakes of some classes of polyphenols were associated with decreased breast cancer risk: hydroxybenzoic acids (HR(Q4vsQ1) = 0.38, 95 % CI: 0.17-0.86, P (trend) = 0.005), flavonoids (0.35, 0.17-0.75, P (trend) = 0.02), flavonols (0.36, 0.18-0.74, P (trend) = 0.002), catechins (0.48, 0.22-1.05, P (trend) = 0.02), theaflavins (0.42, 0.19-0.93, P (trend) = 0.02), and proanthocyanidins (0.39, 0.18-0.84, P (trend) = 0.02). In contrast, in women with higher alcohol use, intakes of hydroxybenzoic acids (2.28, 1.16-4.49, P (trend) = 0.04), flavonoids (2.46, 1.23-4.92, P (trend) = 0.01), anthocyanins (2.94, 1.32-6.53, P (trend) = 0.01), catechins (2.28, 1.19-4.36, P (trend) = 0.02), and proanthocyanidins (2.98, 1.40-6.33, P (trend) = 0.006) were associated with increased breast cancer risk. In conclusion, this prospective study suggests that several classes of polyphenols could potentially contribute to breast cancer prevention among non-to-low alcohol drinkers, but some may increase breast cancer risk among women with higher alcohol intake.
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Alcohol consumption in midlife and cognitive performance assessed 13 years later in the SU.VI.MAX 2 cohort.
Kesse-Guyot, E, Andreeva, VA, Jeandel, C, Ferry, M, Touvier, M, Hercberg, S, Galan, P
PloS one. 2012;(12):e52311
Abstract
BACKGROUND Associations between alcohol consumption and cognitive function are discordant and data focusing on midlife exposure are scarce. OBJECTIVE To estimate the association between midlife alcohol consumption and cognitive performance assessed 13 y later while accounting for comorbidities and diet. METHODS 3,088 French middle-aged adults included in the SU.VI.MAX (1994) study with available neuropsychological evaluation 13 y later. Data on alcohol consumption were obtained from repeated 24h dietary records collected in 1994-1996. Cognitive performance was assessed in 2007-2009 via a battery of 6 neuropsychological tests. A composite score was built as the mean of the standardized individual test scores (mean=50, SD=10). ANCOVA were performed to estimate mean differences in cognitive performance and 95% confidence intervals (CI). RESULTS In women, abstainers displayed lower cognitive scores than did low-to-moderate alcohol drinkers (1 to 2 drinks/day) (mean difference= -1.77; 95% CI: -3.29, -0.25). In men, heavy drinkers (>3 drinks/day) had higher cognitive scores than did low-to-moderate (1 to 3 drinks/day) (mean difference=1.05; 95% CI: 0.10, 1.99). However, a lower composite cognitive score was detected in male drinkers consuming ≥ 90 g/d (≈8 drinks/d). A higher proportion of alcohol intake from beer was also associated with lower cognitive scores. These associations remained significant after adjustment for diet, comorbidities and sociodemographic factors. CONCLUSION In men, heavy but not extreme drinking was associated with higher global cognitive scores. Given the known harmful effects of alcohol even in low doses regarding risk of cancer, the study does not provide a basis for modifying current public health messages. TRIAL REGISTRATION ClinicalTrials.gov NCT00272428.
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Alcohol and genetic polymorphisms: effect on risk of alcohol-related cancer.
Druesne-Pecollo, N, Tehard, B, Mallet, Y, Gerber, M, Norat, T, Hercberg, S, Latino-Martel, P
The Lancet. Oncology. 2009;(2):173-80
Abstract
Public health guidelines aim to limit the consumption of alcoholic beverages worldwide and the subsequent health burden. In particular, alcohol consumption is an avoidable risk factor for cancer. In human beings, ethanol in alcoholic drinks is mainly oxidised in the liver by alcohol dehydrogenases to acetaldehyde, and is further detoxified to acetate by aldehyde dehydrogenases. Functional variants in genes involved in alcohol metabolism result in differences between individuals in exposure to carcinogenic acetaldehyde, suggesting a possible interaction of genetic susceptibility and alcohol exposure in cancer. We reviewed available studies of the combined effects of alcohol drinking and genetic polymorphisms on alcohol-related cancer risk. Most available data were for polymorphisms in alcohol and folate metabolism. We give an overview of published studies on the combined effects of alcohol drinking and polymorphisms in genes for alcohol dehydrogenase (ADH), aldehyde dehydrogenase (ALDH), cytochrome P450 2E1, and methylene-tetrahydrofolate reductase on the risk of alcohol-related cancer. Current data lend support to a role of polymorphisms ADH1B and ALDH2 combined with alcohol consumption in cancer. Other available data are insufficient or inconclusive, highlighting the need for additional studies.