No abstract

Scope Sulforaphane (SFN), an isothiocyanate derived from crucifers, has numerous health benefits. SFN bioavailability from dietary sources is a critical determinant of its efficacy in humans. A key factor in SFN absorption is the release of SFN from its glucosinolate precursor, glucoraphanin, by myrosinase. Dietary supplements are used in clinical trials to deliver consistent SFN doses, but myrosinase is often inactivated in available supplements. We evaluated SFN absorption from a myrosinase-treated broccoli sprout extract (BSE) and are the first to report effects of twice daily, oral dosing on SFN exposure in healthy adults. Methods and results Subjects consumed fresh broccoli sprouts or the BSE, each providing 200 μmol SFN daily, as a single dose and as two 100-μmol doses taken 12 h apart. Using HPLC-MS/MS, we detected ~3 x higher SFN metabolite levels in plasma and urine of sprout consumers, indicating enhanced SFN absorption from sprouts. Twelve-hour dosing retained higher plasma SFN metabolite levels at later time points than 24-hour dosing. No dose responses were observed for molecular targets of SFN (i.e. heme oxygenase-1, histone deacetylase activity, p21). Conclusion We conclude that the dietary form and dosing schedule of SFN may impact SFN absorption and efficacy in human trials.

Our results support a protective effect of n-3 fatty acids on breast cancer risk and provide additional evidence for the importance of evaluating the ratio of fatty acids when evaluating diet and breast cancer risk.

Observational studies have shown that 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor (statin) use may be associated with reduced cancer risk. The purpose of this case-control study was to elucidate the association between statin use and prostate cancer risk. Prostate cancer cases (n ¼ 100), recruited upon referral for prostate biopsy, and frequency age-matched, prostate-specific antigen-normal clinic controls (n ¼ 202) were recruited from the Portland, Oregon, Veterans Affairs Medical Center. Information on any use of statins from May 1997 through August 2004 was obtained from an electronic pharmacy database. Days of use, type of statin, dose, and prescription changes were recorded. Duration and intensity were calculated for each statin type on the basis of days of use and prescribed dose. Thirty-six percent of cases and 49 percent of controls had a record of any statin use. Following adjustment for other potential risk factors, statin use was associated with a significant reduction in prostate cancer risk (odds ratio ¼ 0.38, 95% confidence interval: 0.21, 0.69). Furthermore, in analyses stratified by Gleason score, the inverse association with statin use was maintained only among men with Gleason scores of 7 (odds ratio ¼ 0.24, 95% confidence interval: 0.11, 0.53). The results of this case-control study suggest that statins may reduce the risk of total prostate cancer and, specifically, more aggressive prostate cancer.case-control studies; cholesterol; hydroxymethylglutaryl-CoA reductase inhibitors; mevalonic acid; prostatespecific antigen; prostatic neoplasms; veterans Abbreviations: CI, confidence interval; FPP, farnesylpyrophosphate; GGPP, geranylgeranyl pyrophosphate; NSAID, nonsteroidal antiinflammatory drug; OR, odds ratio; p21, M r 21,000 protein (p27 defined similarly); PVAMC, Portland Veterans Affairs Medical Center; VA, Veterans Affairs.One in six men over age 60 years will be diagnosed with prostate cancer (1). Prostate cancer is the second leading cause of cancer deaths among US men (2). Therefore, the need to identify and to develop means to prevent this common malignancy is a high priority. Recent research on the chemopreventive potential of a group of cholesterollowering drugs, 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase inhibitors (statins), has shown intriguing results (3, 4). Statins lower serum cholesterol levels by inhibiting 3-hydroxy-3-methylglutaryl coenzyme A reductase, the rate-determining enzyme in the mevalonate pathway (4). In addition to their cholesterol-lowering ability, statins have been shown to inhibit prostate and breast cancer cell proliferation and to induce tumor-specific apoptosis (4-6) in in vitro studies.While the mechanism remains unclear, clinical trials with cancer as a secondary endpoint have shown a nonsignificant inverse association between statin use and total cancer incidence (7,8). Additionally, Bjerre and LeLorier's metaanalysis (9) of five trials of statins and cardiovascular