Validation of a food-frequency questionnaire for the assessment of calcium intake in schoolchildren aged 9-10 years.

Bone mass increases steadily until age 20-30 years, when peak bone mass (PBM) is acquired. Nutrition plays a critical role in achievement of the optimal genetically programmed PBM, with reduction in the risk of osteoporosis later in life. Intake of nutrients can be estimated through the use of various tools; typically, food-frequency questionnaires (FFQs) are used in epidemiologic studies. The aim of this study was to validate a 21-item, semiquantitative FFQ to assess important nutrient intakes for bone health in Italian schoolchildren 9-10 years of age. Relative validation was accomplished through comparison of the 7-days weighed food record (7D records) with an FFQ developed ad hoc, completed by a group of 75 Italian schoolchildren (36 females, 39 males). Agreement between the two methods was evaluated by Spearman's correlation test and Bland-Altman analysis applied on the data on intake of energy, macronutrients, and micronutrients. Particular attention was devoted to nutrients relevant for bone health. Good correlations between the two methods (FFQ and 7D records) were observed for all nutrients. In particular, mean dietary calcium intakes were 725.6 mg/day (95 % CI 683.2-768.1) from 7D records and 892.4 mg/day (95 % CI 844.6-940.2) from the FFQ. These results indicate that our FFQ for schoolchildren aged 9-10 years is highly acceptable as it is an accurate method that can be used in large-scale or epidemiological studies for the evaluation of nutrient intakes important for the prevention of osteoporosis in a similar population.

Genistein affects adipose tissue deposition in a dose-dependent and gender-specific manner.

The soy isoflavone genistein targets adipose tissue and elicits physiological effects that may vary based on dietary intake. We hypothesized that the adipose effects of genistein are dose and gender dependent. Four-week-old C57BL/6 male and female mice received daily oral doses of genistein (50-200,000 microg/kg.d) or 17beta-estradiol (E2) (5 microg/kg.d) for 15 d or a diet containing 800 ppm genistein. Genistein increased epididymal and renal fat pad and adipocyte size at doses up to 50,000 microg/kg.d or at 800 ppm in the diet in males but not in females. The alteration in adipocity correlated with changes in peripheral insulin resistance. These treatments increased genistein serum concentrations from 35+/-6 to 103+/-26 nM 12 h after treatment and lowered plasma triglycerides and cholesterol levels. The 200,000 microg/kg.d genistein dose decreased adipose tissue weight similarly to E2. This genistein dose down-regulated estrogen receptor (beta more than alpha) and progesterone receptor expression and induced estrogen-dependent adipose differentiation factors; it did not change expression of the minimal consensus estrogen-responsive element in ERE-tK-LUC mice, which was positively modulated in other tissues (e.g. the lung). E2 down-regulated almost all examined adipogenic factors. Gene microarray analysis identified factors in fat metabolism and obesity-related phenotypes differentially regulated by low and high doses of genistein, uncovering its adipogenic and antiadipogenic actions. The lower dose induced the phospholipase A2 group 7 and the phospholipid transfer protein genes; the 200,000 microg/kg.d dose inhibited them. The antiadipogenic action of genistein and down-regulation of adipogenic genes required the expression of ERbeta. In conclusion, nutritional doses of genistein are adipogenic in a gender-specific manner, whereas pharmacological doses inhibited adipose deposition.