title: Binge-eating disorder as a distinct familial phenotype in obese individuals.
abstract: BACKGROUND
  Binge-eating disorder (BED)-a syndrome that only recently has attracted scientific attention-is often seen in obese individuals, especially those with severe obesity. However, it remains unclear whether BED represents an etiologically distinct behavioral phenotype of obesity or simply a nonspecific eating pattern sometimes seen in obese individuals.
  
  
  OBJECTIVE
  To test whether BED aggregates in families independently of obesity, and if so, whether familial factors for BED also independently increase the risk of obesity.
  
  
  METHODS
  Blinded family interview study of overweight or obese probands with (n = 150) and without (n = 150) BED, and their first-degree relatives (n = 888) in a community setting evaluated between October 2002 and July 2004.
  
  
  METHODS
  Lifetime diagnosis of BED; current and highest lifetime body mass index (calculated as the weight in kilograms divided by the square of the height in meters).
  
  
  RESULTS
  Binge-eating disorder aggregated strongly in families independently of obesity (odds ratio, 2.2; 95% confidence interval, 1.4-3.6; P<.001). Furthermore, relatives of probands with BED displayed a markedly higher prevalence of severe obesity in adulthood (body mass index >/=40) than relatives of probands without BED even when controlling for proband body mass index (odds ratio, 2.5; 95% confidence interval, 1.4-4.4; P = .002).
  
  
  CONCLUSIONS
  Binge-eating disorder is a familial disorder caused in part by factors distinct from other familial factors for obesity. Furthermore, these BED-specific familial factors may independently increase the risk of obesity, especially severe obesity. It follows that targeted interventions capable of preventing or treating traits influenced by these BED-specific familial factors could reduce the public health burden of obesity.
authors.affiliation: Department of Psychiatry, Harvard Medical School and McLean Hospital, Belmont, Mass 02478, USA. jhudson@mclean.harvard.edu
authors.forename: James I
authors.initials: JI
authors.lastname: Hudson
authors.forename: Justine K
authors.initials: JK
authors.lastname: Lalonde
authors.forename: Judith M
authors.initials: JM
authors.lastname: Berry
authors.forename: Lindsay J
authors.initials: LJ
authors.lastname: Pindyck
authors.forename: Cynthia M
authors.initials: CM
authors.lastname: Bulik
authors.forename: Scott J
authors.initials: SJ
authors.lastname: Crow
authors.forename: Susan L
authors.initials: SL
authors.lastname: McElroy
authors.forename: Nan M
authors.initials: NM
authors.lastname: Laird
authors.forename: Ming T
authors.initials: MT
authors.lastname: Tsuang
authors.forename: B Timothy
authors.initials: BT
authors.lastname: Walsh
authors.forename: Norman R
authors.initials: NR
authors.lastname: Rosenthal
authors.forename: Harrison G
authors.initials: HG
authors.lastname: Pope
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D015992:Body Mass Index; D052018:Bulimia Nervosa / Q000453:epidemiology* / Q000235:genetics*; D015897:Comorbidity; D017281:Cost of Illness; D005190:Family; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009765:Obesity / Q000453:epidemiology* / Q000235:genetics*; D010375:Pedigree; D010641:Phenotype; D015995:Prevalence; D012307:Risk Factors; D012931:Social Environment