The effects of diet on circulating sex hormone levels in men

Allen, Naomi E.; Key, Timothy J.

doi:10.1079/095442200108729052

Cited by 47 publications

(39 citation statements)

References 150 publications

(227 reference statements)

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“…There are several reasons why we could have failed to find significant associations between TS levels or E2/TS ratios and the SNPs. It is possible that extrinsic factors, including dietary habit and lifestyle, may affect circulating levels of sex hormones and sex hormone‐binding globulin . Other factors, such as genetic variations in CYP17A1, 17HDS5 , or other genes, age, ethnicity and body mass index, may also have impacts on circulating sex hormone levels .…”

Section: Discussionmentioning

confidence: 99%

Effects of functional genetic polymorphisms in theCYP19A1gene on prostate cancer risk and survival

et al. 2014

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CYP19 catalyzes the conversion of androgens to estrogens and is a critical enzyme affecting the sex hormone milieu. In this study, we investigated the functions of CYP19A1 polymorphisms and their associations with prostate cancer risk and clinical outcome. This case-control study evaluated the effects of three single nucleotide polymorphisms (SNPs) in CYP19A1 on the risk of prostate cancer in 330 prostate cancer patients and 354 normal controls. The associations between each SNP and sex hormone levels were evaluated in 164 healthy male patients. The functions of the SNPs were determined by reporter gene assays in PC3 and DU145 cell lines. Prostate-specific antigen nadir was evaluated in 142 patients with metastatic prostate cancer treated with androgen deprivation therapy. Cancer-specific survival (CSS) was determined in 166 patients with metastatic prostate cancer, to evaluate the influence of the three SNPs. Each variant allele of the three SNPs significantly decreased the risk of prostate cancer. Haplotype analysis showed that the T-A-G haplotype (corresponding to rs2470152-rs10459592-rs4775936) increased the risk of prostate cancer, while the C-C-A haplotype decreased the risk. The estrone/ androstenedione ratio was significantly higher in men with the C allele of rs2470152, the C allele of rs10459592, and the A allele of rs4775936 in a gene-dosage-dependent manner. Patients with the variant allele at rs4775936 had significantly shorter CSS. These results indicate that CYP19A1 polymorphisms may influence prostate cancer risk and survival by modifying promoter activity, with subsequent effects on the sex hormone milieu.Sex hormones, especially androgens, appear to play an important role in the carcinogenesis and progression of prostate cancer. 1,2 Testosterone propionate was shown to induce prostate cancer in an Nb rat model, 3 and the 5-a reductase inhibitor, finasteride, inhibited carcinogenesis in rat prostate cancer induced by testosterone (TS) propionate and the carcinogen, 3,2 0 -dimethyl-4-aminobiphenyl. 4 In the clinical setting, Huggins et al. first reported that androgen deprivation therapy (ADT) caused tumor regression in patients with metastatic prostate cancer, 1 since when endocrine therapies became a key part of the treatment for patients with advanced prostate cancer. Abraterone, which inhibits CYP17 androgen-synthesis enzyme activity, was recently shown to be a powerful drug, even in patients with castration-resistant prostate cancer previously treated with chemotherapy. 5 The importance of androgens in prostate cancer means that the synthetic pathways for these hormones have been targets for intensive study. Androgens are synthesized by many enzymes, primarily in the testes and the adrenal gland, and to a lesser extent in peripheral organs including the prostate and skin. 2 Among the enzymes involved in sex hormone synthesis, CYP19, also known as aromatase and encoded by CYP19A1, catalyzes the conversions of androstenedione

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Section: Discussionmentioning

confidence: 99%

Effects of functional genetic polymorphisms in theCYP19A1gene on prostate cancer risk and survival

et al. 2014

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“…Excessive alcohol intake has been suggested to increase male breast cancer risk because of its influence on hormone levels (33). Several (15,16), although not all (34), studies of chronic alcoholics have noted an increased risk of male breast cancer.…”

Section: Discussionmentioning

confidence: 99%

Etiologic factors for male breast cancer in the U.S. Veterans Affairs medical care system database

Brinton

Carreon

Gierach

et al. 2009

Breast Cancer Res Treat

100

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The etiology of male breast cancer is largely unknown, reflecting its relative rarity. Although a number of previous studies have suggested relationships with a variety of medical conditions, the results have largely derived from case-control studies and may reflect recall biases. Within the large U.S. Veterans Affairs computerized medical care system database, we had the opportunity to access 26 million hospitaldischarge records over the period and to relate various documented medical conditions to the risk of subsequent male breast cancer. This allowed us to calculate relative risks (RR) and 95% confidence intervals (CI) for male breast cancer associated with conditions occurring one or more years after initial hospitalization, adjusted for age, race, calendar year, duration of follow-up, and number of hospital visits. Among 4,501,578 men aged 18-100 years, a total of 642 cases of primary male breast cancer were identified (523 among whites, 119 among blacks). Medical conditions that were significantly related to risk were diabetes (RR=1.30, 95% CI 1.05-1.60), obesity (1.98, 1.55-2.54), orchitis/epididymitis (1.84, 1.10-3.08), Klinefelter syndrome (29.64, 12.26-71.68), and gynecomastia (5.86, 3.74-9.17). Additionally, among black patients, cholelithiasis emerged as a significant risk predictor (3.45, 1.59-7.47). Diseases that have previously been related to male breast cancer risk that were not supported by our study results included thyroid diseases, smoking-related conditions, liver cirrhosis, prostatic hyperplasia, and fractures. After adjustment for obesity, the association with diabetes disappeared, but that with gynecomastia persisted. In multivariate models that simultaneously considered all important medical predictors of risk, significant risks were seen for Klinefelter syndrome (16.83, 6.81-41.62), gynecomastia (5.08, 3.21-8.03), obesity (1.91, 95% CI 1.50-2.44) and orchitis/epididymitis (1.80, 1.08-3.01). These results support previous speculations that male breast cancer is influenced not only by tissue at risk, but also by hormonal and inflammatory factors.

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“…The highest exposure level in any study was 139 mg/d. Because changes in hormone levels respond quickly to a variety of influences including dietary changes, the relatively short duration of several studies would appear not to limit their ability to observe effects (93).…”

Section: Soy Isoflavones and Estrogenmentioning

confidence: 99%

Soybean isoflavone exposure does not have feminizing effects on men: a critical examination of the clinical evidence

Messina

2010

Fertility and Sterility

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The effects of diet on circulating sex hormone levels in men

Cited by 47 publications

References 150 publications

Effects of functional genetic polymorphisms in theCYP19A1gene on prostate cancer risk and survival

Effects of functional genetic polymorphisms in theCYP19A1gene on prostate cancer risk and survival

Etiologic factors for male breast cancer in the U.S. Veterans Affairs medical care system database

Soybean isoflavone exposure does not have feminizing effects on men: a critical examination of the clinical evidence

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