22 February 2019 In Cancer

BACKGROUND: We aimed to understand the factors shaping alcohol consumption patterns in middle-aged women (45-64), and to identify participant-driven population- and policy-level strategies that may be used to addresses alcohol consumption and reduce breast cancer risk.

METHODS: Semi-structured interviews (n = 35) were conducted with 'middle-aged' women conversant in English and living in South Australia with no history of breast cancer diagnosis. Data were deductively coded using a co-developed framework including variables relevant to our study objectives. Women were asked about their current level of awareness of the association between alcohol and breast cancer risk, and their personal recommendations for how to decrease consumption in middle-aged Australian women.

RESULTS: Women discussed their previous efforts to decrease consumption, which we drew on to identify preliminary recommendations for consumption reduction. We identified a low level of awareness of alcohol and breast cancer risk, and confusion related to alcohol as a risk for breast cancer, but not always causing breast cancer. Participants suggested that education and awareness, through various means, may help to reduce consumption.

CONCLUSIONS: Participants' description of strategies used to reduce their own consumption lead us to suggest that campaigns might focus on the more salient and immediate effects of alcohol (e.g. on physical appearance and mental health) rather than longer-term consequences. Critical considerations for messaging include addressing the personal, physical and social pleasures that alcohol provides, and how these may differ across socio-demographics.

05 December 2018 In Cancer

Alcohol has consistently been shown to increase breast cancer (BC) risk. This association may be modified by single nucleotide polymorphisms in alcohol dehydrogenase isoenzymes ADH1B and ADH1C. The Netherlands Cohort Study comprises 62 573 women, aged 55-69 years at baseline (1986). Follow-up for postmenopausal BC for 20.3 years was available. Genotyping of 6 tag SNPs in ADH1B and ADH1C, respectively, was performed on DNA from toenails. A case-cohort approach was used for analysis (complete data available for: nsubcohort= 1301; ncases= 1630). Cox regression models for postmenopausal BC were applied to determine marginal effects of alcohol intake and SNPs using a dominant genetic model, as well as multiplicative interaction of the two. Results were also obtained for subtypes by estrogen (ER) and progesterone receptor (PR) status. Multiple testing was adjusted for by applying the false discovery rate (FDR). Alcohol intake (categorical) increased the risk of postmenopausal BC (ptrend=0.031). Trends for ER and PR subgroups followed a similar pattern. Continuous modelling of alcohol resulted in a hazard rate ratio (HR) for overall postmenopausal BC of 1.09 (95% CI: 1.01 - 1.19) per 10g/d of alcohol. SNPs were not associated with BC risk. No effect modification of the alcohol-BC association by SNP genotype was seen after FDR-correction in overall BC and ER/PR subgroups. In conclusion, alcohol was shown to increase the risk of postmenopausal BC. This association was not significantly modified by common ADH1B and ADH1C SNPs, neither in overall BC nor in hormone receptor defined subtypes.

29 October 2018 In Cancer

Epidemiological studies have been used to show associations between modifiable lifestyle habits and the incidence of breast cancer. Among such factors, a history of alcohol use has been reported in multiple studies and meta-analyses over the past decades. However, associative epidemiological studies that were interpreted as evidence that even moderate alcohol consumption increases breast cancer incidence have been controversial. In this review, we consider the literature on the relationship between moderate or heavy alcohol use, both in possible biological mechanisms and in variations in susceptibility due to genetic or epigenetic factors. We argue that there is a need to incorporate additional approaches to move beyond the associations that are reported in traditional epidemiological analyses and incorporate information on molecular pathologic signatures as a requirement to posit causal inferences. In particular, we point to the efforts of the transdisciplinary field of molecular pathological epidemiology (MPE) to evaluate possible causal relationships, if any, of alcohol consumption and breast cancer. A wider application of the principles of MPE to this field would constitute a giant step that could enhance our understanding of breast cancer and multiple modifiable risk factors, a step that would be particularly suited to the era of "personalized medicine".

03 May 2018 In Cancer
BACKGROUND: Racial disparities in the incidence of major cancers may be attributed to differences in the prevalence of established, modifiable risk factors such as obesity, smoking, physical activity and diet. METHODS: Data from a prospective cohort of 566,398 adults aged 50-71 years, 19,677 African-American and 450,623 Whites, was analyzed. Baseline data on cancer-related risk factors such as smoking, alcohol, physical activity and dietary patterns were used to create an individual adherence score. Differences in adherence by race, gender and geographic region were assessed using descriptive statistics, and Cox proportional hazards models were used to determine the association between adherence and cancer incidence. RESULTS: Only 1.5% of study participants were adherent to all five cancer-related risk factor guidelines, with marked race-, gender- and regional differences in adherence overall. Compared with participants who were fully adherent to all five cancer risk factor criteria, those adherent to one or less had a 76% increased risk of any cancer incidence (HR: 1.76, 95% CI: 1.70 - 1.82), 38% increased risk of breast cancer (HR: 1.38, 95% CI: 1.25 - 1.52), and doubled the risk of colorectal cancer (HR: 2.06, 95% CI: 1.84 - 2.29). However, risk of prostate cancer was lower among participants adherent to one or less compared with those who were fully adherent (HR: 0.79, 95% CI: 0.75 - 0.85). The proportion of cancer incident cases attributable to low adherence was higher among African-Americans compared with Whites for all cancers (21% vs. 19%), and highest for colorectal cancer (25%) regardless of race. CONCLUSION: Racial differences in the proportion of cancer incidence attributable to low adherence suggests unique opportunities for targeted cancer prevention strategies that may help eliminate racial disparities in cancer burden among older US adults
Page 2 of 32

Disclaimer

The authors have taken reasonable care in ensuring the accuracy of the information herein at the time of publication and are not responsible for any errors or omissions. Read more on our disclaimer and Privacy Policy.