BUILDING BETTER BONES IN CHILDREN

增加钙的摄入量已被证明在增加儿童骨密度方面是有效的，但当停止补钙时，这种作用就消失了。日常饮食和其他食物来源的钙增加对骨密度的影响可能比补钙更大，但从食物来源获得的钙的持续增加还没有得到证明。此外，钙摄入量的基线特征、骨密度和青春期状态的影响可能会影响对干预的反应。这项研究将制定和实施旨在增加膳食钙的行为调整-营养教育(BM-NE)干预计划，将随机分配年龄为7-10岁(Tanner阶段I或II)的男性和女性受试者(n=154)参加强化BM-NE干预组，以将摄入量增加到1500 mg/d，或将接受常规护理(UC)作为骨健康咨询的组。BM-NE计划将包括五个单独的小组会议，为父母和孩子在五到六周的时间里，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：一组是没有已知危险因素的健康儿童(即没有已知的慢性病或既往接触过类固醇)，另一组是有低骨密度潜在危险因素的健康儿童(既往因童年日常活动而骨折、日常拒绝或乳糖不耐受、骨质疏松症家族史)。这两个小组在分配给BM-NE和UC小组时将有同等的代表。后一种策略将用于确定风险因素的存在是否影响参与者对计划的遵从性。我们假设：(A)在36个月末，与接受UC的患者相比，无风险BM-NE组的饮食钙至少增加了300 mg/d，(B)基线钙摄入量和存在的危险因素将与研究过程中钙摄入量的变化有关，(C)在控制了重要的协变量，如身体尺寸和性成熟和骨骼成熟后，骨密度的变化将与钙摄入量和体力活动相关。这些发现将有助于确定重要的行为策略，以增加峰值骨量和预防晚年的骨质疏松症，这些策略可以在短期内实施，并产生长期影响。此外，它还将有助于量化膳食钙增加对生长和发育期间骨密度的影响，并可能确定最需要这种治疗并对其做出反应的儿童的特征。

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.