Childhood obesity rates have incrementally increased since the 1980s, sparking calls for initiatives focused on addressing this public health concern. In response, the family medicine residency clinic profiled in this research designed, executed, and evaluated a practice improvement initiative focused on physician communication behaviors and clinic processes that impact the management of unhealthy pediatric weight. The results of the evaluation effort demonstrated increased physician knowledge of communication principles, improvements in weight management counseling rates, and opportunities for health delivery system changes to promote the effective clinical management of unhealthy pediatric weight.
Our findings suggest that rapid weight gain in Chinese-American infants in the first 6 months after birth can be expected, and may then lessen. By the first year, on average, these infants' weights will be < 50th percentile using the American National Center for Health Statistics growth standard. These findings can reassure health providers and help them to provide sound nutritional recommendations and counselling to parents.
who published the first account of Prader-Willi syndrome (PWS) in 1956 (Greenswag & Alexander, 1995), the syndrome is characterized by hyperphagia (a compulsion to overeat that is never satisfied), congenital hypotonia (less than normal muscle tone), and mental retardation. PWS has a n estimated prevalence of 1 in 15,000 to 1 in 30,000, is lifelong and life-threatening, and affects all races and both sexes (McKusick, 1992; Prader-Willi Syndrome Association [PWSA], 1994; Thoene & Coker, 1995). When the development of diabetes mellitus occurs with the other symptoms, the condition is called Royer's syndrome. Although PWS has been recognized for 40 years, it frequently goes undiagnosed because of its obscurity. The etiology of this multisystem disorder remains unclear (Greenswag & Alexander, 1995). Many (e.g., McKusick, 1992) have argued for an autosomal recessive etiology because 50-60% of patients diagnosed with PWS have a deletion on the upper arm of the number 15 chromosome contributed by the father. No clinical difference is evident between those with and without the chromosome abnormality, however, suggesting that other factors contribute to the syndrome (Lai, Erickson, & Cassidy, 1993; PWSA, 1994). Of those without the deletion, 20% have been found to have both number 15 chromosomes from their mother instead of the usual case where each parent contributes one chromosome (Thoene & Coker, 1995).The recurrence rate of PWS in a family with one affected offspring is less than 1 in 1,000 (Thoene & Coker, 1995). Given this low recurrence rate and the observation that some fathers of offspring with PWS have normal number 15 chromosomes, many researchers argue that the deletion associated with PWS may be a random mutation rather than an inherited abnormality (McKusick, 1992;Thoene & Coker, 1995). Inheritance of the syndrome cannot be investigated through chromosomal analysis of offspring, because individuals with PWS are infertile (PWSA, 1994).Focusing on the distinctive hyperphagia and other regulatory deficits found in PWS, many researchers have attributed the syndrome to a metabolic-hypothalamic dysfunction (McKusick, 1992). Specifically, the 534
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