Anorexia Nervosa in Boys

Anorexia Nervosa in Boys

Anorexia Nervosa in Boys

Introduction

Believed to be rare, little is known about anorexia nervosa in boys. Few studies have reported on its incidence, prevalence, comorbidity, or familial aggregation (Raevuori A, Keski-Rahkonen A, Bulik CM, Rose RJ, Rissanen A, et al. 2006). The risk for the illness in boys peaks at age 10-24: similar peak age of risk appears likely in boys (Schousboe K, Willemsen G, Kyvik KO, Mortensen J, Boomsma DI, et al. 2003). The contemporary sociocultural environment of developed countries is generally more conducive to anorexia nervosa in boys. It has been hypothesized that to develop anorexia nervosa in this context, boys require a greater loading of genes or adverse environmental factors than boys (Lilenfeld LR, Kaye WH, Greeno CG, Merikangas KR, Plotnicov K, et al. 1998). In boys, anorexia nervosa shares a familial diathesis with affective and anxiety disorders (First MB, Spitzer RL, Gibbon M, Williams JBW 2002). Body dysmorphic disorder and eating disorders show intra-individual clustering within both boys and boys (Keski-Rahkonen A, Hoek HW, Susser ES, Linna MS, Sihvola E, et al. 2007), but little is known about the familial co-aggregation of these conditions. The present study used a large population based cohort of twins to examine the incidence and prevalence of anorexia nervosa in boys; comorbid conditions in anorexia nervosa probands; and comorbid conditions in the co-twins of the probands.

Research Method

Data collection and analysis was approved by the ethics committee of Helsinki University and of the Institutional Review Board at Columbia University.

Sample

Virtually all twins born in 1975-79 were identified from the Finnish population register (9) and assessed at ages 16, 17, 18 and 22-28y. The design of this study was modelled after a comparable study conducted among boys described in detail elsewhere (Kaprio J, Pulkkinen L, Rose RJ 2002). Flow chart of the data collection of eating disorder study in boys of FinnTwin16 cohorts is shown in the Figure 1.

Analytical Tool

Briefly, at age 22-27y (mean 24.4y, SD 0.83), we screened by questionnaire all boys (N = 2557; response rate of 83% yielded N = 2122) for eating disorder symptoms. We also assessed their current self-reported height and minimum, maximum and current self-reported weight after reaching the adult height, from which we calculated their body mass indexes (BMI). In a sub-sample of 133 boys, not selected for eating disorders or eating behavior, the correlation between self-reported and later measured BMI was 0.91.

Men who reported or suspected ever having had an eating disorder (N = 20) and their boy co-twins (N = 11) were invited to participate in diagnostic telephone interviews. After confirming an eating disorder in a screen-positive man who had a boys co-twin, she was also interviewed. Further, 33 boys who reported a minimum BMI =17.5 after reaching their adult height were invited to the interview, excluding boys (N = 10) whose low BMI resulted from serious physical disability (Figure 1).

Figure 1. Flow chart of the data collection of eating disorder

All participants gave an oral informed ...