Crisp, Arthur, Gowers, Simon, Joughin, Neil, McClelland, Lisa, Rooney, Barbara, Nielsen, Soren, Bowyer, Carol, Halek, Chris, and Hartman, David (2006) Vulnerability to anorexia nervosa: constitutional markers. European Eating Disorders Review, 14 (3). pp. 176-182.

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Abstract

INTRODUCTION The search for constitutional markers for anorexia nervosa, mainly within the realm of psychopathology, goes back many years. Claims for constitutional associations with schizophrenia (e.g. Brill, 1939; Nicolle, 1939), depressive disorders (e.g. Cobb, 1943; Meyer & Weinroth, 1957; Nemiah, 1950), and obsessive compulsive disorders (e.g. Dubois, 1949; Palmer & Jones, 1939; Rahman, Richardson, & Ripley, 1939) were rife 50 years or more ago. Earlier still, and searching for constitutional psychodynamic mechanisms, writers such as Laseque (1873), La Tourette (1895), Waller, Kaufman, & Deutsch (1940), postulated a conversion hysteria process at work, whilst others construed the condition as a form of suicide (Strauss, 1956) or, more cogently, ‘a compromise with suicide’ (Crichton-Miller, 1938). Thus, there has long been an urge to fit the disorder into the existing diagnostic frameworks available to psychiatry (Crisp, 1967). In the 1960s the first author began to wonder whether there might be some growth markers for the condition. He investigated and reported on birth weights, patterns of breastfeeding, growth rates and maximum premorbid weights (e.g. Crisp, 1970). Such reports, especially from patients with eating disorders and perhaps also their families, are liable to distortion and it was crucial to pursue accuracy as much as possible. There was the usual diversity within all these measures but, overall, there was a tendency to higher birth weights, growth rates and premorbid weights. In particular, during a study of weights at onset of amenorrhoea (Crisp&Stonehill, 1971) within which we gained information from sources other than the patient (who fearfully tends to deny or conceal from others, such personally distressing memories), we found that the patients, as a group, had been heavier than normal, preceding illness onset. Subsequent studies by others, drawing simply on case-note records reflecting data provided mainly by patients themselves, did not always support these findings. However, the notion that premorbid overweight (associated with greater ‘plumpness’) occurs significantly often, though obviously not a necessary feature of anorexia nervosa, subsequently gained some support from a study by Nielsen (1985) and has also recently been confirmed in a thorough Swedish prospective study based on serially measured body weights (Swenne, 2001). We also know that those relatively obese in childhood grow more quickly than others and reach puberty and its related impulsivity earlier (Crisp, Douglas, Ross, & Stonehill, 1970). I mention these findings because they may have relevance to biological markers of a metabolic kind sometimes found amongst ‘recovered’ anorectics. Meanwhile, our combined study with the Maudsley of twin sets where one or both of them had presented with anorexia nervosa, and wherein 55% of the variance in the expression of the condition seemed possibly attributable to genetic factors, again prompted the suggestion that a variety of genetic factors could often be operating. It was suggested that this might include those governing growth characteristics, unidimensional cognitive structure and the potential for avoidance behaviour (in this case, the harnessing of calorie restriction and its selective reversal of the pubertal process) in the face of conflict and panic (Crisp, Hall, & Holland, 1985).

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