Validation studies of food frequency questionnaires (FFQs) describe the extent to which the FFQ reflects true diet and the relation between measured and true diet (calibration). Calibration data can be used to estimate the relation between disease and diet that would have been observed in the absence of error due to the FFQ. In this paper, the authors consider the optimal design of a validation study when the goal is precise calibration of an FFQ. The authors posed the following question: Under the constraint of a fixed total cost for a validation study, what is the optimal choice of number of subjects (n) and number of days (m) of diet records (or 24-hour recalls) per subject? The optimal n and m were found to depend upon 1) the ratio between the costs of the initial and subsequent 1-day diet records and 2) the ratio of the variance in day-to-day nutrient intake to the variance in true diet for a fixed FFQ value. Data for the two ratios and optimal values of n and m are given under a variety of realistic scenarios. The authors conclude that in most settings the optimal study design will rarely require more than four or five 1-day diet records per subject.

Preliminary studies suggest that moderate physical activity may reduce both premenstrual distress (PD) and the ovarian steroid hormones, progesterone and estradiol, which have been implicated in PD. We attempted to replicate these findings, while exploring possible relationships between hormone levels and PD. In a cross-sectional study, 20 moderate exercisers and 34 sedentary women completed PD symptom questionnaires and collected urine samples, daily, throughout a complete menstrual cycle. PD was calculated as the difference in symptom scores reported during the average of the 4 days prior to menses and the average of the 4 days closest to mid-cycle. Urine samples taken from the last quarter of the menstrual cycle were analyzed for urinary estrone glucoronide (E1G) and pregnanediol glucoronide. In a prospective study the same measures were used with 14 sedentary women before and after a 24-week moderate exercise-training program. In the cross-sectional study, exercising women reported lower Pain symptoms, and had lower peak E1G levels than did sedentary women. The baseline PD symptoms loneliness, crying, and skin blemishes with were statistically significantly and positively correlated with pregnanediol glucoronide levels in the cross-sectional study. In the prospective study, exercise reduced the global PD symptom score, including the Water Retention and Pain scales, and reduced pregnanediol glucoronide and peak E1G levels. Moderate aerobic exercise may lessen both PD symptoms and late luteal phase ovarian hormone levels. An exercise program may benefit women with progesterone-related premenstrual affect disturbance.

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. British Journal of Cancer (2002) (Gray et al, 1980;Parkin et al, 1997;SEER Program, 2001). The reasons for this are not clear, however they may be due to ethnic differences in circulating oestradiol (E 2 ) and progesterone (P 4 ) levels. Oestradiol is an established breast-cell mitogen, and considerable epidemiological and experimental evidence indicates that women with higher circulating levels are at greater risk of developing breast cancer (Bernstein and Ross, 1993; Pike et al, 1993;Thomas et al, 1997;Hankinson et al, 1998). Considerable evidence also exists indicating that progestins play an important role in breast carcinogenesis. Recent epidemiological studies have shown that postmenopausal hormone replacement therapy in the form of estrogen -progestin replacement therapy (EPRT) increases breast cancer risk to a much greater extent than estrogen (alone) replacement therapy (ERT; Magnusson et al, 1999;Ross et al, 2000;Schairer et al, 2000). These results are supported by the finding that mammographic densities are increased much more by EPRT than ERT (Greendale et al, 1999), and so is breast-cell proliferation (Hofseth et al, 1999).In the present study, we evaluated differences in ovarian function in African-American, Latina and non-Latina White young women in Los Angeles who were recruited as part of a crosssectional investigation of the frequency of anovulatio...

The effect of opiate receptor blockade on the plasma catecholamine response to hypoxemia was studied in seven chronically catheterized fetal lambs in utero. All animals underwent treatment with hypoxia alone, naloxone infusion alone (2 mg/kg) and hypoxia with naloxone at four different dosages (0.1, 0.5, 1.0, and 2.0 mg/kg). Maternal and fetal hypoxia was maintained for 20 min. There were no differences noted in the degree of hypoxemia or acidemia between the different hypoxia treatment groups. Hypoxia increased both norepinephrine and epinephrine plasma levels in all fetal sheep studied. We found a dose-dependent increase in plasma epinephrine levels in response to naloxone infusion during hypoxia. Plasma epinephrine level by 20 min of hypoxia with the 0.1 mg/kg naloxone dose (geometric mean 5366 pg/ml) was significantly more than with hypoxia alone (997 pg/ml). Naloxone at the other doses did not alter the epinephrine responses. There was no augmentation of plasma norepinephrine levels by naloxone at any dose studied. Thus, naloxone augmented the plasma epinephrine response to hypoxia in fetal sheep suggesting that the opiate peptides act as modulators of the sympathoadrenal system. The naloxone dose response differences observed in this study suggest this modulation is largely by antagonism of mu-receptors.