BUILDING BETTER BONES IN CHILDREN

增加钙的摄入已被证明对提高儿童的骨密度是有效的，但是当钙补充剂停止时，这种效果就消失了。从日常饮食和其他食物中增加钙可能比补钙对骨密度的影响更大，但从食物中持续增加钙的效果尚未得到证实。此外，钙摄入量和骨密度的基线特征以及青春期状态的影响可能会影响对干预的反应。本研究将制定并实施一项旨在增加膳食钙的行为改变-营养教育（BM-NE）干预计划，年龄在7-10岁的男性和女性受试者（n=154） （Tanner阶段I或II）将被随机分配参加强化BM-NE干预组，将摄入量增加到1500毫克/天，或一组将接受常规护理（UC）作为骨骼健康咨询。BM-NE计划将包括5个单独的小组会议，家长和孩子在5到6周的时间内，并使用个性化的计划来增加钙的摄入量。参与者将被招募为两组：一组健康儿童（即，没有已知的慢性疾病或口服类固醇暴露），没有已知的危险因素；另一组健康儿童有潜在的低骨密度危险因素（以前的儿童常规活动导致骨折，日常拒绝，或乳糖不耐受，骨质疏松家族史）。这两个小组在分配给BM-NE和UC小组时将有相同的代表。后一种策略将用于确定风险因素的存在是否会影响参与者对项目的依从性。我们假设(a)在36个月结束时，与接受UC治疗的患者相比，BM-NE组的饮食钙摄入量将增加至少300毫克/天；(b)基线钙摄入量和风险因素的存在将与研究过程中钙摄入量的变化有关；(c)在控制了重要的共变量（如体型增加、性和骨骼成熟）之后，骨密度的变化与钙的摄入和身体活动有关。这些发现将有助于确定重要的行为策略，以增加骨量峰值和预防晚年的骨质疏松症，这些策略可以在短时间内实施，并产生持久的效果。此外，它将有助于量化在生长发育过程中增加膳食钙对骨密度的影响，并可能确定最需要这种治疗并对这种治疗有反应的儿童的特征。

Increased calcium intake has proven effective in increasing bone mineral density in children, but the effect disappears when calcium supplements are discontinued. Increased dietary calcium from daily and other food sources may have an even greater impact on bone density than that achieved by calcium supplements, but achieving sustained increased calcium from food sources has not been demonstrated. In addition, the effects of baseline characteristics of calcium intake and bone density and puberty status may influence the response to intervention. This study will develop and implement a Behavioral Modification-Nutrition Education (BM-NE) Intervention Program aimed at increasing dietary calcium Male and female subjects (n=154), ages 7-10 years (Tanner stage I or II), will be randomly assigned to participate in an intensive BM-NE intervention group to increase intake to 1500 mg/d or a group that will receive usual care (UC) as counseling on bone health. The BM-NE Program will consist of five separate group sessions for parents and children over a five to six week period, and use individualized plans to increase calcium intake. Participants will be recruited into two groups: a group of healthy children (i.e.,no known chronic disease or previous oral steroid exposure) with no known risk factors, and a group of healthy children with potential risk factors for low bone density (previous fracture from usual childhood activities, daily refusal, or lactose intolerance, family history of osteoporosis). These two groups will be equally represented in their assignment to BM-NE and UC groups. This latter strategy will be used to determine whether the presence of risk factors influences participant compliance with the programs. We hypothesize that (a) at the end of 36 months the BM-NE group will have increased dietary calcium of at least 300 mg/d in the no-risk BM-NE group compared to those receiving UC, (b) baseline calcium intake and presence of risk factors will be associated with changes in calcium intake over the course of the study, and (c) after controlling for important co-variates such as increases in body size and sexual and skeletal maturation, changes in BMD will be associated with calcium intake and physical activity. These findings will help define important behavioral strategies for increasing peak bone mass and prevention of osteoporosis later in life that can be implemented in a short period of time with long-lasting effects. Furthermore, it will help quantify the impact of increased dietary calcium on bone density during growth and development with possible identification of the characteristics of children most in need of and responsive to this treatment.