Blood Isoflavone Levels during Intake of a Controlled Hospital Diet

Takashima, Naomi; Miyanaga, Naoto; Komiya, K; Mori, Mitsuru; Akaza, Hideyuki

doi:10.3177/jnsv.50.246

Cited by 5 publications

(5 citation statements)

References 19 publications

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“…Consequently, in response to soy food intake, even in equol producers, circulating levels of genistein (and to a lesser extent daidzein) far exceed equol levels (131). Thus, there is little justification for extrapolating results from rodents given daidzein to humans given soy foods or mixed isoflavones.…”

Section: Erectile Dysfunctionmentioning

confidence: 98%

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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Section: Erectile Dysfunctionmentioning

confidence: 98%

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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“…Genistein, which is the main circulating and best-studied isoflavone, transactivates ERα and induces estrogenic effects with ~10 3 -10 4 less potency than E2 [ 7 , 8 ]. However, serum isoflavone concentrations after a high-soy meal can reach low micromolar levels [ 36 , 37 ], thereby exceeding postmenopausal total estrogen concentrations by ~10 3 [ 38 ]. This evidence has contributed to the idea that isoflavones may potentially elicit estrogen-like effects and thus serve as a natural alternative to ET in postmenopausal women.…”

Section: Introductionmentioning

confidence: 99%

Soy isoflavones, estrogen therapy, and breast cancer risk: analysis and commentary

Messina

Wood

2008

Nutr J

158

104

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There has been considerable investigation of the potential for soyfoods to reduce risk of cancer, and in particular cancer of the breast. Most interest in this relationship is because soyfoods are essentially a unique dietary source of isoflavones, compounds which bind to estrogen receptors and exhibit weak estrogen-like effects under certain experimental conditions. In recent years the relationship between soyfoods and breast cancer has become controversial because of concernsbased mostly on in vitro and rodent data -that isoflavones may stimulate the growth of existing estrogen-sensitive breast tumors. This controversy carries considerable public health significance because of the increasing popularity of soyfoods and the commercial availability of isoflavone supplements. In this analysis and commentary we attempt to outline current concerns regarding the estrogen-like effects of isoflavones in the breast focusing primarily on the clinical trial data and place these concerns in the context of recent evidence regarding estrogen therapy use in postmenopausal women. Overall, there is little clinical evidence to suggest that isoflavones will increase breast cancer risk in healthy women or worsen the prognosis of breast cancer patients. Although relatively limited research has been conducted, and the clinical trials often involved small numbers of subjects, there is no evidence that isoflavone intake increases breast tissue density in pre-or postmenopausal women or increases breast cell proliferation in postmenopausal women with or without a history of breast cancer. The epidemiologic data are generally consistent with the clinical data, showing no indication of increased risk. Furthermore, these clinical and epidemiologic data are consistent with what appears to be a low overall breast cancer risk associated with pharmacologic unopposed estrogen exposure in postmenopausal women. While more research is required to definitively allay concerns, the existing data should provide some degree of assurance that isoflavone exposure at levels consistent with historical Asian soyfood intake does not result in adverse stimulatory effects on breast tissue.

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“…These studies measured both the aglycone and the conjugate. Eight studies provided data for total GEN in plasma (Arai et al, 2000;Grace et al, 2004;Heald et al, 2006;Iwasaki et al, 2008;Ritchie et al, 2004;Setchell et al, 2003;Shimazu et al, 2011;Takashima et al, 2004). The free GEN was estimated by multiplying the total GEN value by 0.3%.…”

Section: Derivation Of Steady State Concentrations Of Gen In Human Serummentioning

confidence: 99%

“…For GEN, steady state blood concentrations of the active unconjugated compound were developed from measurements reported in the literature (Arai et al, 2000;Busby et al, 2002;Cimino et al, 1999;Grace et al, 2003Grace et al, , 2004Liu et al, 2013;Richelle et al, 2002;Setchell et al, 2003Setchell et al, , 2011Shelnutt et al, 2000Shelnutt et al, , 2002Shimazu et al, 2011;Takashima et al, 2004;Teeguarden et al, 2011;Völkel et al, 2002;Yuan et al, 2012;Zhang et al, 2003). To obtain the EAR value for GEN, the estimated steady state plasma concentration GEN in human serum (see below) was divided by the AC50 value from each of the assays considered.…”

Section: Ear ðUnitlessþ ¼mentioning

confidence: 99%

An exposure:activity profiling method for interpreting high-throughput screening data for estrogenic activity—Proof of concept

Becker

Friedman

Simon³

et al. 2015

Regulatory Toxicology and Pharmacology

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Rapid high throughput in vitro screening (HTS) assays are now available for characterizing dose-responses in assays that have been selected for their sensitivity in detecting estrogen-related endpoints. For example, EPA's ToxCast™ program recently released endocrine assay results for more than 1800 substances and the interagency Tox21 consortium is in the process of releasing data for approximately 10,000 chemicals. But such activity measurements alone fall short for the purposes of priority setting or screening because the relevant exposure context is not considered. Here, we extend the method of exposure:activity profiling by calculating the exposure:activity ratios (EARs) using human exposure estimates and AC50 values for a range of chemicals tested in a suite of seven estrogenic assays in ToxCast™ and Tox21. To provide additional context, relative estrogenic exposure:activity quotients (REEAQ) were derived by comparing chemical-specific EARs to the EAR of the ubiquitous dietary phytoestrogen, genistein (GEN). Although the activity of a substance in HTS-endocrine assays is not a measure of health hazard or risk, understanding how such a dose compares to human exposures provides a valuable additional metric that can be used in decision-making; substances with small EARs and REEAQs would indicate low priority for further endocrine screening or testing.

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Blood Isoflavone Levels during Intake of a Controlled Hospital Diet

Cited by 5 publications

References 19 publications

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

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

Soy isoflavones, estrogen therapy, and breast cancer risk: analysis and commentary

An exposure:activity profiling method for interpreting high-throughput screening data for estrogenic activity—Proof of concept

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