Open AccessSerum phytanic and pristanic acid levels and prostate cancer risk in Finnish smokers
Author(s) -
Wright Margaret E.,
Albanes Demetrius,
Moser Ann B.,
Weinstein Stephanie J.,
Snyder Kirk,
Männistö Satu,
Gann Peter H.
Publication year - 2014
Publication title -
cancer medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.403
H-Index - 53
ISSN - 2045-7634
DOI - 10.1002/cam4.319
Subject(s) - phytanic acid , prostate cancer , medicine , endocrinology , cancer , peroxisome , receptor
Phytanic acid is a saturated branched‐chain fatty acid found predominantly in red meat and dairy products, and may contribute to the elevated risks of prostate cancer associated with higher consumption of these foods. Pristanic acid is formed during peroxisomal oxidation of phytanic acid, and is the direct substrate of α ‐Methyl‐CoA‐Racemase ( AMACR )—an enzyme that is consistently overexpressed in prostate tumors relative to benign tissue. We measured phytanic and pristanic acids as percentages of total fatty acids by gas chromatography‐mass spectrometry in prediagnostic blood samples from 300 prostate cancer cases and 300 matched controls, all of whom were participants in the Alpha‐Tocopherol, Beta‐Carotene Cancer Prevention (ATBC) Study supplementation trial and follow‐up cohort. In addition to providing a fasting blood sample at baseline, all men completed extensive diet, lifestyle, and medical history questionnaires. Among controls, the strongest dietary correlates of serum phytanic and pristanic acids were saturated fat, dairy fat, and butter ( r = 0.50 and 0.40, 0.46 and 0.38, and 0.40 and 0.37, respectively; all P ‐values <0.001). There was no association between serum phytanic acid and risk of total or aggressive prostate cancer in multivariate logistic regression models (for increasing quartiles, odds ratios (OR) and 95% confidence intervals (CI) for aggressive cancer were 1.0 (referent), 1.62 (0.97–2.68), 1.12 (0.66–1.90), and 1.14 (0.67–1.94), P trend = 0.87). Pristanic acid was strongly correlated with phytanic acid levels ( r = 0.73, P < 0.0001), and was similarly unrelated to prostate cancer risk. Significant interactions between phytanic and pristanic acids and baseline circulating β ‐carotene concentrations were noted in relation to total and aggressive disease among participants who did not receive β ‐carotene supplements as part of the original ATBC intervention trial. In summary, we observed no overall association between serum phytanic and pristanic acid levels and prostate cancer risk. Findings indicating that the direction and magnitude of these associations depended upon serum levels of the antioxidant β ‐carotene among men not taking β ‐carotene supplements should be interpreted cautiously, as they are likely due to chance.