THE ROLE OF GENERAL FAMILY ENVIRONMENT AND SEXUAL AND PHYSICAL ABUSE IN THE ORIGINS OF EATING DISORDERS

This paper reviews the role of childhood family functioning and of sex ual and physical abuse in eating disorders. Bearing in mind the huge m ethodological differences across studies the following tentative concl usions can be reached: there is evidence of more family pathology in e ating disorder families than in normal control families. Those with bu limic disorders seem to have poorer family functioning than restrictor s. Different eating disorder subgroups show less or comparable levels of family pathology compared to psychiatric or other medical controls depending on the comparison group. In bulimia nervosa high levels of f amily disturbance seem to be associated with greater severity and chro nicity of bulimic symptomatology. There is some suggestion that family functioning may have more of an effect on Axis II than on Axis I diso rders. Rates of sexual abuse appear to be higher in bulimia nervosa th an in normal controls. Depending on which psychiatric control groups a re chosen, eating disorder patients may have similar, higher or lower rates of contact sexual abuse. The majority of studies fails to find d ifferences between eating disorder subtypes in terms of rates of sexua l abuse. The evidence on whether there is any link between abuse chara cteristics and the severity of eating disorder is inconclusive. On bal ance, childhood sexual abuse does not seem to be a specific risk facto r for eating disorders. Physical abuse is more common in bulimic than in restricting disorders and usually occurs in the context of a distur bed family environment. The clinical implications of these findings ar e discussed. Future research in the area of family factors or childhoo d trauma in eating disorders needs to get away from mere 'head counts' and needs to focus more strongly on the mediators between abuse and n eglect and the development of eating disorders and also on the relativ e importance of family factors compared with other aetiological factor s. (C) 1997 John Wiley & Sons, Ltd and Eating Disorders Association.