Based on the available evidence, a tax on SSB will deliver similar population weight benefits across socio-economic strata or greater benefits for lower SEP groups. An SSB tax is shown to be consistently financially regressive, but to a small degree.

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BackgroundCirculating osteoprotegerin (OPG), a member of the receptor activator of nuclear factor kappa-B (RANK) axis, may influence breast cancer risk via its role as the decoy receptor for both the RANK ligand (RANKL) and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL). Circulating OPG and breast cancer risk has been examined in only one prior study.MethodsA case-control study was nested in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. A total of 2008 incident invasive breast cancer cases (estrogen receptor (ER)+, n = 1622; ER–, n = 386), matched 1:1 to controls, were included in the analysis. Women were predominantly postmenopausal at blood collection (77%); postmenopausal women included users and non-users of postmenopausal hormone therapy (HT). Serum OPG was quantified with an electrochemiluminescence assay. Relative risks (RRs) and 95% confidence intervals (CIs) were calculated using conditional logistic regression.ResultsThe associations between OPG and ER+ and ER– breast cancer differed significantly. Higher concentrations of OPG were associated with increased risk of ER– breast cancer (top vs. bottom tertile RR = 1.93 [95% CI 1.24–3.02]; p trend = 0.03). We observed a suggestive inverse association for ER+ disease overall and among women premenopausal at blood collection. Results for ER– disease did not differ by menopausal status at blood collection (p het = 0.97), and we observed no heterogeneity by HT use at blood collection (p het ≥ 0.43) or age at breast cancer diagnosis (p het ≥ 0.30).ConclusionsThis study provides the first prospective data on OPG and breast cancer risk by hormone receptor subtype. High circulating OPG may represent a novel risk factor for ER– breast cancer.Electronic supplementary materialThe online version of this article (doi:10.1186/s12916-017-0786-8) contains supplementary material, which is available to authorized users.

Receptor activator of nuclear factor kappa-B (RANK)-RANK ligand (RANKL) signaling promotes mammary tumor development in experimental models. Circulating concentrations of soluble RANKL (sRANKL) may influence breast cancer risk via activation of RANK signaling; this may be modulated by osteoprotegerin (OPG), the decoy receptor for RANKL. sRANKL and breast cancer risk by hormone receptor subtype has not previously been investigated.A case-control study was nested in the European Prospective Investigation into Cancer and Nutrition (EPIC) cohort. This study included 1976 incident invasive breast cancer cases (estrogen receptor positive (ER+), n=1598), matched 1:1 to controls. Women were pre-or postmenopausal at blood collection. Serum sRANKL was quantified using an enzyme-linked immunosorbent assay, serum OPG using an electrochemiluminescent assay. Risk ratios (RRs) and 95% confidence intervals (95%CIs) were calculated using conditional logistic regression.Associations between sRANKL and breast cancer risk differed by tumor hormone receptor status (p het 0.05). Higher concentrations of sRANKL were positively associated with risk of ER+ breast cancer (5th vs. 1st quintile RR 1.28 [95%CI 1.01-1.63]; p trend 0.20), but not ER-disease. For both ER+ and estrogen and progesterone receptor positive (ER+PR+) breast cancer, results considering the sRANKL/OPG ratio were similar to those for sRANKL; we observed a suggestive inverse association between the ratio and ER-PR-disease (5 th vs. 1 st quintile RR 0.60 [0.31-1.14]; p trend 0.03).This study provides the first large-scale prospective data on circulating sRANKL and breast cancer. We observed limited evidence for an association between sRANKL and breast cancer risk. Sarink et al.