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M C Pike

Publications and source records attributed to M C Pike.

At least 19 recordsLinked to original sources

Body fatness and physical activity at young ages and the risk of breast cancer in premenopausal women.

We examined the relationship between body fatness, sports participation and breast cancer risk in 1560 premenopausal cases and 1548 controls, from three related population-based case-control studies in the UK. Half of the women with breast cancer were aged less than 36 years at diagnosis. Women who perceived themselves as plump at age 10 years had a relative risk of 0.83 (95% confidence interval 0.69-0.99, P = 0.03) as compared with those who perceived themselves as thin. Self-reported obesity compared with leanness at diagnosis was associated with a relative risk of 0.78 (95% confidence interval 0.56-1.06, P = 0.11). Women who reported having been plump at age 10 years and overweight or obese at diagnosis had a relative risk of 0.75 (95% confidence interval 0.56-1.01, P = 0.06) as compared with those who reported being thin at age 10 years and at diagnosis. Findings for three related measures of body fatness suggested that obesity is associated with a reduced risk of premenopausal breast cancer. There was no association between sports participation and breast cancer risk in these premenopausal women. The relative risk for spending an average of more than 1 h per week in sports compared with less from ages 12 to 30 years was 1.00 (95% CI 0.86-1.16, P = 0.98).

Adipose Tissue↗

An overview of menopausal oestrogen-progestin hormone therapy and breast cancer risk.

Results from the Women's Health Initiative (WHI) trial support findings from observational studies that oestrogen-progestin therapy (EPT) use is associated with an increase in breast cancer risk. We conducted a meta-analysis using EPT-specific results from the Collaborative Group on Hormonal Factors in Breast Cancer (CGHFBC) pooled analysis and studies published since that report to obtain an overview of EPT use and breast cancer risk. We also assessed risk by histologic subtype of breast cancer, by schedule of the progestin component of EPT, and by recency of use. We estimate that overall, EPT results in a 7.6% increase in breast cancer risk per year of use. The risk was statistically significantly lower in US studies than in European studies - 5.2 vs 7.9%. There was a significantly higher risk for continuous-combined than for sequential EPT use in Scandinavian studies where much higher total doses of progestin were used in continuous-combined than in sequential EPT. We observed no overall difference in risk for lobular vs ductal carcinoma but did observe a slightly higher risk for current vs past EPT use.

Aged↗

A candidate gene approach to searching for low-penetrance breast and prostate cancer genes.

Most cases of breast and prostate cancer are not associated with mutations in known high-penetrance genes, indicating the involvement of multiple low-penetrance risk alleles. Studies that have attempted to identify these genes have met with limited success. The National Cancer Institute Breast and Prostate Cancer Cohort Consortium--a pooled analysis of multiple large cohort studies with a total of more than 5,000 cases of breast cancer and 8,000 cases of prostate cancer--was therefore initiated. The goal of this consortium is to characterize variations in approximately 50 genes that mediate two pathways that are associated with these cancers--the steroid-hormone metabolism pathway and the insulin-like growth factor signalling pathway--and to associate these variations with cancer risk.

Breast Neoplasms↗

Does place of birth influence endogenous hormone levels in Asian-American women?

In 1983-87, we conducted a population-based case-control study of breast cancer in Asian women living in California and Hawaii, in which migration history (a composite of the subject's place of birth, usual residence in Asia (urban/rural), length of time living in the West, and grandparents' place of birth) was associated with a six-fold risk gradient that paralleled the historical differences in incidence rates between the US and Asian countries. This provided the opportunity to determine whether endogenous hormones vary with migration history in Asian-American women. Plasma obtained from 316 premenopausal and 177 naturally premenopausal study controls was measured for levels of estrone (E1), estradiol (E2), estrone sulphate (E1S), androstenedione (A), testosterone (T), dehydroepiandrosterone (DHEA), dehydroepiandrosterone sulphate (DHEAS), progesterone (PROG) and sex hormone-binding globulin (SHBG). Levels of the oestrogens and sex hormone-binding globulin did not differ significantly between Asian- and Western-born women, although among premenopausal women, those least westernised had the lowest levels of E1, E2, and E1S. Androgen levels, particularly DHEA, were lower in women born in the West. Among premenopausal women, age-adjusted geometric mean levels of DHEA were 16.5 and 13.8 nmol l(-1) in Asian- and Western-born women respectively; in postmenopausal women these values were 11.8 and 9.2 nmol l(-1), (P<0.001) respectively. Among postmenopausal women, androgens tended to be highest among the least westernised women and declined as the degree of westernisation increased. Our findings suggest that aspects of hormone metabolism play a role in population differences in breast cancer incidence.

Adult↗

Ethnic differences in ovulatory function in nulliparous women.

African-American women have a long-standing approximately 20% higher breast cancer incidence rate than USA White women under age 40 while rates among Latinas are lower than those of Whites. The reasons for this are not clear, however they may be due to ethnic differences in circulating oestradiol and progesterone levels. In a cross-sectional study, we investigated whether anovulation frequency and circulating serum oestradiol and/or progesterone levels vary among normally cycling nulliparous African-American (n=60), Latina (n=112) and non-Latina White (n=69) women. Blood and urine specimens were collected over two menstrual cycles among healthy 17- to 34-year-old women. Frequency of anovulation was greater among White women (nine out of 63, 14.3%) than African-American women (four out of 56, 7.1%) or Latina women (seven out of 102, 6.9%), although these differences were not statistically significant. African-American women had 9.9% (P=0.26) higher follicular phase oestradiol concentrations than Latina women and 17.4% (P=0.13) higher levels than White women. African-American women also had considerably higher levels of luteal phase oestradiol (vs Latinas, +9.4%, P=0.14; vs Whites, +25.3%, P=0.003) and progesterone (vs Latinas, +15.4%, P=0.07; vs Whites, +36.4%, P=0.002). Latina women were also observed to have higher follicular oestradiol, and luteal oestradiol and progesterone levels than White women (follicular oestradiol: +6.8%, P=0.48; luteal oestradiol: +14.6%, P=0.04; luteal progesterone: +18.2%, P=0.06). These results suggest that exposure to endogenous steroid hormones may be greater for young African-American and Latina women than for Whites.

Adult↗

Germ-line HER-2 variant and breast cancer risk by stage of disease.

HER-2 gene amplification and protein overexpression has been associated with increased risk of advanced-stage breast cancer and poor prognosis. Recently, a single missense point mutation (Ile(655)Val) in the transmembrane domain of the HER-2 gene was associated with a 40% increase in breast cancer risk among women 45 years of age and younger. In this analysis, we measured the association between the Ile(655)Val variant and postmenopausal breast cancer among women participating in the Hawaii and Los Angeles Multiethnic Cohort. Risk of localized breast cancer was significantly elevated among women with the HER-2 variant, but not among women with regional or metastatic disease. Women with at least one copy of the Valine variant were approximately one-half as likely to have high-stage as low-stage breast cancer (P =.02), and this effect was present across racial/ethnic groups.

Aged↗

Risk of endometrial cancer and estrogen replacement therapy history by CYP17 genotype.

Common variants among genes coding for enzymes in sex steroid biosynthetic pathways may influence the risk of endometrial cancer. We examined the association between endometrial cancer risk and estrogen replacement therapy (ERT) by CYP17 genotype using 51 incident cases and 391 randomly selected controls from a multiethnic cohort in Hawaii and Los Angeles, California. The relative risk of endometrial cancer was calculated for ever use versus never use of ERT by CYP17 genotype (TT, TC, and CC). We found that women who reported ever taking ERT were more than twice as likely to develop endometrial cancer as women who never took ERT [odds ratio (OR), 2.24; 95% confidence interval (CI), 1.19-4.23]. Among these women, the risk of endometrial cancer was higher for women homozygous for the CYP17 T allele (OR, 4.10; 95% CI, 1.64-10.3), but not for women with the C allele (OR, 1.31; 95% CI, 0.53-3.21). These preliminary findings suggest that CYP17 or other variants in estrogen biosynthesis or metabolism pathways may be potential markers of endometrial cancer susceptibility due to ERT.

Aged↗

Mammographic density changes during the menstrual cycle.

The ability to detect small tumors is impaired in dense mammograms. It has been suggested that the sensitivity of mammograms could be lower in mammograms obtained during the luteal phase of the menstrual cycle. We examined the change in mammographic density from the follicular to the luteal phase of the menstrual cycle in 11 women. Although the average increase in densities was quite small (1.2%; P = 0.08), six women had clinically significant increases (1.4-7.8%), suggesting that premenopausal women should undergo mammographic examinations in the follicular part of the menstrual cycle.

Adult↗

Reversal of gonadotropin-releasing hormone agonist induced reductions in mammographic densities on stopping treatment.

Previously, we described the reduction in mammographic densities that occurred in premenopausal women after 12 months on a hormonal regimen designed to be chemopreventive for breast (and ovarian) cancer consisting of a gonadotropin-releasing hormone agonist (GnRHA) plus low-dose add-back estrogen-progestin. We sought to determine whether the density reduction persisted with continuation of the regimen for 24 months, and, if so, whether the densities would return to baseline after the regimen was discontinued. Twenty-one women, 27-40 years of age, with a 5-fold greater than normal risk of breast cancer, were randomly assigned in a 2:1 ratio to the treatment group (14 women) and to a control group (7 women). The percentage of mammographic densities, calculated as the proportion of the breast area on the mammogram containing densities, were assessed blindly using a computer-based threshold method at baseline, after 12 and 24 months of treatment, and at between 6 and 12 months after treatment was stopped. The previously described percentage of mammographic density reductions of 9.7% (P = 0.012) after 12 months of treatment were increased slightly to 11.4% (P = 0.010) after 24 months of treatment, but the additional change was not statistically significant. Ten of 11 treated women assessed at 24 months had reduced percentages of mammographic densities compared with baseline. Six to 12 months after completion of treatment, the mean percentage of mammographic density in the treated group was no different from that at baseline (mean decline of 2.0%; P = 0.73). The women in the control group had no statistically significant changes in densities over the period of the study. Reductions in mammographic densities engendered by the GnRHA plus a low-dose add-back estrogen-progestin regimen persist as long as the women receive treatment. The densities return to baseline when the women resume normal menstrual cycles. These results confirm that mammographic densities are influenced by ovarian function. Improved efficacy of mammographic screening is to be expected as long as a woman continues on such a regimen. Whether such a regimen is chemopreventive for breast cancer remains to be established, but the recent report on a randomized trial of use of GnRHA alone in premenopausal breast cancer cases showing a marked reduction in incidence of contralateral disease provides strong support for the hypothesis.

Adult↗

Future possibilities in the prevention of breast cancer: luteinizing hormone-releasing hormone agonists.

The cyclic production of estrogen and progesterone by the premenopausal ovary accounts for the steep rise in breast cancer risk in premenopausal women. These hormones are breast cell mitogens. By reducing exposure to these ovarian hormones, agonists of luteinizing hormone-releasing hormone (LHRH) given to suppress ovarian function may prove useful in cancer prevention. To prevent deleterious effects of hypoestrogenemia, the addition of low-dose hormone replacement to the LHRH agonist appears necessary. Pilot data with such an approach indicates it is feasible and reduces mammographic densities.

Breast↗

Effect of hormone replacement therapy on breast cancer risk: estrogen versus estrogen plus progestin.

BACKGROUND: Hormone replacement therapy (HRT) given as unopposed estrogen replacement therapy (ERT) gained widespread popularity in the United States in the 1960s and 1970s. Recent prescribing practices have favored combination HRT (CHRT), i.e., adding a progestin to estrogen for the entire monthly cycle (continuous combined replacement therapy [CCRT]) or a part of the cycle (sequential estrogen plus progestin therapy [SEPRT]). Few data exist on the association between CHRT and breast cancer risk. We determined the effects of CHRT on a woman's risk of developing breast cancer in a population-based, case-control study. METHODS: Case subjects included those with incident breast cancers diagnosed over 4(1/2) years in Los Angeles County, CA, in the late 1980s and 1990s. Control subjects were neighborhood residents who were individually matched to case subjects on age and race. Case subjects and control subjects were interviewed in person to collect information on known breast cancer risk factors as well as on HRT use. Information on 1897 postmenopausal case subjects and on 1637 postmenopausal control subjects aged 55-72 years who had not undergone a simple hysterectomy was analyzed. Breast cancer risks associated with the various types of HRT were estimated as odds ratios (ORs) after adjusting simultaneously for the different forms of HRT and for known risk factors of breast cancer. All P values are two-sided. RESULTS: HRT was associated with a 10% higher breast cancer risk for each 5 years of use (OR(5) = 1.10; 95% confidence interval [CI] = 1.02-1.18). Risk was substantially higher for CHRT use (OR(5) = 1.24; 95% CI = 1.07-1.45) than for ERT use (OR(5) = 1. 06; 95% CI = 0.97-1.15). Risk estimates were higher for SEPRT (OR(5) = 1.38; 95% CI = 1.13-1.68) than for CCRT (OR(5) = 1.09; 95% CI = 0. 88-1.35), but this difference was not statistically significant. CONCLUSIONS: This study provides strong evidence that the addition of a progestin to HRT enhances markedly the risk of breast cancer relative to estrogen use alone. These findings have important implications for the risk-benefit equation for HRT in women using CHRT.

Aged↗

A multiethnic cohort in Hawaii and Los Angeles: baseline characteristics.

The authors describe the design and implementation of a large multiethnic cohort established to study diet and cancer in the United States. They detail the source of the subjects, sample size, questionnaire development, pilot work, and approaches to future analyses. The cohort consists of 215,251 adult men and women (age 45-75 years at baseline) living in Hawaii and in California (primarily Los Angeles County) with the following ethnic distribution: African-American (16.3%), Latino (22.0%), Japanese-American (26.4%), Native Hawaiian (6.5%), White (22.9%), and other ancestry (5.8%). From 1993 to 1996, participants entered the cohort by completing a 26-page, self-administered mail questionnaire that elicited a quantitative food frequency history, along with demographic and other information. Response rates ranged from 20% in Latinos to 49% in Japanese-Americans. As expected, both within and among ethnic groups, the questionnaire data show substantial variations in dietary intakes (nutrients as well as foods) and in the distributions of non-dietary risk factors (including smoking, alcohol consumption, obesity, and physical activity). When compared with corresponding ethnic-specific cancer incidence rates, the findings provide tentative support for several current dietary hypotheses. As sufficient numbers of cancer cases are identified through surveillance of the cohort, dietary and other hypotheses will be tested in prospective analyses.

Black or African American↗

Calibration of the dietary questionnaire for a multiethnic cohort in Hawaii and Los Angeles.

The performance of the dietary questionnaire used in a multiethnic cohort study in Hawaii and Los Angeles was assessed in a calibration substudy that compared diet reported from the questionnaire with three 24-hour dietary recalls. For the calibration substudy, subjects from each of eight subgroups defined by sex and ethnic group (African-American, Japanese-American, Latino, and White) were chosen randomly from among the cohort members, and each participant's previous day's diet was assessed by telephone recall on three occasions over approximately 2 months. After completing the three 24-hour recalls, each calibration subject was sent a second questionnaire; 1,606 persons completed three recalls and a second questionnaire (127 to 267 per ethnic-sex group). This report describes correlation coefficients and calibration slopes for the relation between the 24-hour recalls and second questionnaire values for a selected set of macro- and micronutrients, as absolute intakes, nutrient densities, and calorie-adjusted nutrients. In all subgroups, estimates of the correlation between the questionnaire and 24-hour recalls were greater after energy adjustment (average correlations ranged from 0.57-0.74 for nutrient densities and from 0.55-0.74 for calorie-adjusted nutrients) than when absolute nutrient values were used (average range 0.26-0.57). For absolute nutrient intakes, the correlations were greatest for Whites, somewhat lower for Japanese-Americans and Latinos, and lowest for African-Americans. After energy adjustment, the difference between subgroups were diminished, and the correlations were generally highly satisfactory.

Black or African American↗

Ovarian epithelial tumor growth promotion by follicle-stimulating hormone and inhibition of the effect by luteinizing hormone.

OBJECTIVES: The role of gonadotropins in ovarian epithelial cancer development is still controversial. Follicle-stimulating hormone receptor (FSHR) status in ovarian epithelial tumors (OETs) and their presumed precursor lesions has never been studied in detail. The objective of this study was to examine whether FSHR is expressed in OETs and to investigate the possible different roles of the gonadotropins in ovarian cancer development. METHODS: Twenty ovarian epithelial inclusions (entrapments or invaginations of ovarian surface epithelium) from benign ovaries and 60 OETs including 12 cystadenomas, 18 borderline tumors, and 30 carcinomas were examined for FSHR expression by using reverse transcription polymerase chain reaction (RT-PCR), in situ hybridization (ISH), and immunohistochemistry (IHC). We also studied the mitogenic activity of FSH on two FSH and luteinizing hormone (LH) receptor-positive ovarian epithelial carcinoma cell lines (AO and 3AO) and on the modifying effect of LH on this activity. Growth-stimulating effects of the gonadotropins were tested in vitro with measurement of cell numbers, S-phase by flow cytometry, and changes in the cellular proliferative marker Ki-67. RESULTS: Positive FSHR mRNA expression by RT-PCR (the most sensitive method) was found in 100% of epithelial inclusions, 100% of cystadenomas, 94% of borderline tumors, and 60% of carcinomas. There was a nonstatistically significant trend of decreasing positivity with increasing carcinoma grade. ISH and IHC gave similar, but somewhat less sensitive, results. A dose-response effect was seen with FSH, with a 1.6-fold increase in cell numbers with a maximally stimulating FSH concentration of 40 IU/L for a period of 48 h. These proliferative cellular effects were not observed when the cells were stimulated by LH in the range 1 to 100 IU/L. Most significantly, the growth stimulating effects of FSH could be blocked by the simultaneous administration of LH. CONCLUSIONS: FSHR is present in the majority of ovarian epithelial inclusions and OETs. The steady decline of FSHR expression from benign cystadenoma to borderline tumor to carcinoma suggests that FSH may be needed in early ovarian cancer development. Gonadotropins, FSH and LH, may have different roles in ovarian cancer cell proliferation. FSH, not LH, may be an important ovarian epithelial cell growth-promoting factor. The "opposing" effect of LH on FSH stimulation may explain why high FSH levels at postmenopausal ages are not associated with great increases in ovarian cancer risk.

Adult↗

Reduction of BRCA1 expression in sporadic ovarian cancer.

OBJECTIVE: The purpose of this study was to examine BRCA1 expression and its relationship to cell proliferation in sporadic ovarian epithelial tumors (OETs). METHODS: We investigated BRCA1 expression and cell proliferative activity in 72 unselected OETs. They comprised 16 benign cystadenomas, 18 borderline (low malignant potential) tumors, and 38 carcinomas (OECs). These patients had no known family history of breast and/or ovarian cancer. BRCA1 and the cell proliferation marker, MIB-1, expressions in fixed tissue were investigated in all 72 cases by immunohistochemistry (IHC). BRCA1 mRNA in fresh frozen tissue samples from 20 of these cases was measured by a semi-quantitative reverse transcription-polymerase chain reaction (RT-PCR) method. RESULTS: The average percentage of BRCA1-positive cells was 5.6% in cystadenomas, 29.7% in borderline tumors, and 6.6% in OECs. The average decreased steadily with increasing grade of OECs: grade 1 (21.4%), grade 2 (1.1%), and grade 3 (0%). The average percentage of MIB-1-positive cells increased steadily from cystadenomas (7.5%) to borderline tumors (22.6%) to carcinomas (41.2%). BRCA1 expression was highly correlated with MIB-1 expression in cystadenomas and borderline tumors. Six of seven OECs negative for BRCA1 by IHC showed low levels of BRCA1 mRNA by RT-PCR. CONCLUSIONS: BRCA1 expression paralleled cell proliferation in benign and borderline OETs, but not in OECs. Sporadic OECs showed significantly reduced levels, rather than complete loss, of BRCA1 expression. The reduction was closely related to tumor grade. Reduction of BRCA1 expression may be of etiologic significance in the occurrence and progression of sporadic ovarian cancer.

Antigens, Nuclear↗

Decreased luteinizing hormone receptor mRNA expression in human ovarian epithelial cancer.

OBJECTIVES: The objective of this study was to examine the distribution and cellular localization of luteinizing hormone receptor (LHR) in ovarian epithelial tumors (OETs) and their presumed precursor lesions-ovarian epithelial inclusions (OEIs). The clinicopathologic correlation of the receptor expression in OET was also examined. METHODS: Fifteen microdissected samples of ovarian surface epithelium (OSE), 20 OEIs from benign ovaries, and 141 OETs, including 48 cystadenomas, 33 borderline tumors, 60 carcinomas, and 5 metastatic cancers, were examined for LHR expression by using reverse transcription polymerase chain reaction and in situ hybridization. LHR expression in tumor epithelium and tumor stroma was analyzed separately. The clinicopathologic correlation data were analyzed by standard analysis of variance and contingency table methods. RESULTS: LHR expression was identified in the majority of OSE and OEI samples. In OETs, LHR positivity was found in the epithelial cells in 27% of cases and in the stromal compartment in 37% of cases. LHR-positive stromal cells were mainly luteinized cells. Within the tumor epithelium, LHR expression was detected in 42% of benign, 24% of borderline, and 17% of malignant OETs. LHR expression in tumor stroma showed a similar trend of reduction from benign to malignant OETs. Within the 17 carcinomas, LHR was expressed in the epithelium in 47% of grade 1, 12% of grade 2, and only 5% of grade 3 cancers. The mean age of the LHR-positive group was younger than that of the receptor-negative patients. Compared with mucinous and other types of OETs, serous OETs showed higher LHR expression in the epithelium. Compared with the OETs removed in the different menstrual phases, OETs in the secretory phase showed higher LHR in the tumor stroma than in the proliferative phase. No receptor mRNA was detected in the epithelium of five carcinomas metastatic to the ovary. LHR transcription splicing variants from a single previous report were confirmed in this study. CONCLUSIONS: Malignant OETs have significant reduction of LHR expression compared with precursor lesions and benign and borderline OETs. LHR expression shows a steady decline from low-grade to high-grade ovarian cancer. The presence of LHR receptor in tumor epithelium suggests that luteinizing hormone in serum may have direct influence on tumor growth, whereas the receptor in tumor stroma may be indicative of a paracrine function of LH in the development of OETs.

Adolescent↗

Ethnic differences in post-menopausal plasma oestrogen levels: high oestrone levels in Japanese-American women despite low weight.

Breast cancer incidence in Japanese-American women is approaching that of US Whites. We investigated whether this shift is paralleled by similar post-menopausal plasma hormone levels in the two ethnic groups. We also included African-American and Latina women to further our understanding of possible ethnic differences in oestrogen metabolism. We measured androstenedione (A), oestrone (E1) and oestradiol (E2) in 30 Japanese-American, 39 non-Latina White ('White'), 66 African-American and 58 Latina women. The (age-adjusted) geometric mean E1 levels were 34 pg ml(-1) in Japanese-Americans, 28 pg ml(-1) in Whites, 35 pg ml(-1) in African-Americans and 31 pg ml(-1) in Latinas. After adjustment for body mass index, Japanese-Americans had the highest mean E1 value of all groups and this was statistically significantly greater than the value for Whites (P(t-test) = 0.05). The geometric mean A concentrations were also highest in Japanese-Americans. There was little ethnic difference in E2 levels. In conclusion, post-menopausal plasma oestrogen levels in Japanese-American women are at least as high as those in Whites.

Aged↗

Effects of soy foods on ovarian function in premenopausal women.

It has been proposed that the high intake of soy foods among Asians may partly explain their lower rates of breast cancer, perhaps by lowering endogenous oestrogen levels, although this has been inadequately studied. Twenty healthy cycling premenopausal women (ten Asians and ten non-Asians) participated in a 7-month soy intervention study which was designed to investigate the effect of supplementation on ovarian function. Asian soy foods (tofu, soymilk, green soybean peas) in the amount of approximately 32 mg of isoflavones per day were added to the women's diets for three menstrual cycles. The women's baseline (two cycles) serum hormone levels were compared to levels during soy intervention (three cycles) and levels after intervention (two cycles). During the entire study period, subjects provided almost daily overnight urine samples and blood specimens during specified days of their menstrual cycles. The day of urinary luteinizing hormone (LH) peak was used as a marker for the day of ovulation. Knowledge of day of ovulation allowed comparison of hormone measurements at baseline to those obtained during intervention and recovery cycles with standardization of day of cycle. Soy intervention was associated with a statistically significant reduction in serum luteal oestradiol level (-9.3%, P < 0.05), but there were no significant changes in follicular phase oestradiol, follicular or luteal phase progesterone, sex hormone-binding globulin or menstrual cycle length. This significant reduction in luteal phase oestradiol was, however, observed only among Asian (-17.4%) but not among non-Asian (-1.2%) participants; urinary excretion of isoflavones was higher among Asians than non-Asians (29.2 vs 17.1 micromol day(-1), P= 0.16) during the intervention period. Thus, supplementation using traditional soy foods reduced serum oestradiol levels among Asian participants in this study. Differences in the type of soy products (i.e. traditional soy foods versus soy protein products), amount of isoflavones, and race/ethnicity of participants may have contributed to the divergent results. Larger soy intervention studies designed specifically to include participants of different race/ethnicities and using both traditional soy foods and soy protein products providing comparable doses of isoflavones are needed to definitively determine the effect of soy on ovarian function.

Adult↗