Eating and Growth Disorders in Infants and Children

Joseph L. Woolston

Sharon M. Hasbani

Although eating disorders are frequently assumed to be synonymous with adolescent-onset anorexia and bulimia nervosa, a panoply of eating and growth disorders occurs earlier in life. This clinical myopia is reflected in DSM-IV (1), which recognizes only three eating disorders of early childhood: pica, rumination, and feeding disorder of infancy or early childhood. The lack of official diagnostic recognition of many eating disorders is reflective of their extraordinary complexity and resulting problems in nosological definition. Eating and growth disorders are unique in medicine and psychiatry in their position at the dynamic interface of the somatopsychic boundary of developmental neuropsychiatric disorders, emotional/behavioral disturbances, and physical changes, all of which interact in a complex fashion over time. Unfortunately, this complex interaction has not been sufficiently recognized. For example, the two most common eating and growth disorders of infancy and childhood, failure to thrive syndrome (FTT) and obesity, are both currently categorized as medical conditions in DSM-IV and ICD-10 (2). The rationale for this approach is that both syndromes are defined by caloric nutritional status regardless of etiology. Therefore, some infants and children may have failure to thrive or obesity but not actually have an eating disorder.

Until recently understanding, and even categorization, of such disorders has been hampered by a reductionistic approach relying on deterministic, linear causality (3) in which each disorder or developmental disturbance was viewed as having a single cause. This approach has gradually been replaced by the concept of a multifactorial, transactional model of development (4,5,6). Despite this more sophisticated theoretical approach of developmental psychopathology, advancement in the understanding of early growth disorders has been hampered by a variety of controversies that actually arise from the complexity of the phenomena. Two such controversies are in phenomenology and etiology. The phenomenology of eating disorders has been plagued by a paucity of data and by persistent diagnostic confusion. For example, FTT and psychosocial dwarfism are frequently used synonymously (7); the distinctions among rumination, gastroesophageal reflux, and psychophysiological vomiting are rarely delineated; and subtypes of such disorders as FTT (8,9), obesity (10), and rumination (11) have proliferated. Furthermore, controversy about etiology has frequently focused upon a rigid dichotomy between an intrinsic, organic cause (“sick baby”) versus an external, environmental disturbance (“bad mother”) (12). The counterproductive effect of such a dichotomous approach has been best demonstrated by research in FTT, in which the organic/nonorganic differentiation has not held up to scrutiny (13,14).

A fundamental obstacle to progress in the understanding and treatment of eating and growth disorders is lack of understanding of the basic mechanisms of hunger and satiety.
The first major advancement in this field occurred with the identification and coding of the ob gene, as well as its protein product, leptin (15,16,17). Experimental evidence suggests that leptin, produced in adipocytes, acts as a hormonal feedback signal to regulate fat cell size through hypothalamic mechanisms controlling food intake and metabolic rate (18,19,20). Leptin levels are highly correlated with body mass index in normal children, but not in children with eating disorders resulting in a significantly elevated or reduced body mass index (21). These findings provide the first steps in elucidating the physiological mechanisms of hunger and satiety. Other mechanisms involved in the control of hunger and satiety, both normal and derailed, are covered in detail in the adjacent chapter on obesity (Chapter 5.7.3).

PICA

Definition and Clinical Description

Pica would appear to be without the nosological problems that beset other eating and growth disorders of infants and children. In fact DSM-IV, which lists pica as the first feeding/eating disorder, defines it as the persistent eating of nonnutritive substances for at least 1 month in such a fashion that such eating is inappropriate to developmental level and is not part of culturally sanctioned practice. The two dependent clauses in this definition disqualify the two largest populations described in the centuries-old literature about pica: toddlers who ingest paint chips and young pregnant women who eat starch and clay (22). This artificial clarity in definition attempts to solve the confusion that bedevils all aspects of the understanding of this disorder. Rather than being a narrowly homogenous phenomenon, pica represents an eating disorder of enormously differing populations, including normally developing toddlers mouthing lead paint chips, rural pregnant women eating clay or starch, severely retarded adults eating feces, and normally developed adults chewing pencil erasers, fingernails, and ice. As if to create an aura of scientific understanding, pica as defined in the literature before DSM-IV was subtyped according to the substance ingested. These terms include geophagia (eating clay), pagophagia (eating ice), plambophagia (eating lead), amylophagia (eating starch), coprophagia (eating feces), cautopyreiophagia (eating burnt matches), tricophagia (eating hair), lithophagia (eating stones), geomelophagia (eating raw potatoes). Aside from a review of Greek root words, such subtyping is most useful at documenting the extraordinary range of substances that people may ingest.

In many ways, the heterogeneity of pica precludes a coherent statement about age of onset, developmental outcome, etiology, or treatment. Because the pediatric literature has paid great attention to the phenomenology of lead poisoning, pica has become synonymous with children eating paint chips. For these children, pica has been reported to be more common in situations of relative environmental deprivation (23) or parental psychopathology. In this population, pica begins in the second or third year of life and may continue into childhood. In a second population, young pregnant women, the onset of pica begins with the first pregnancy in late adolescence or early adulthood and may continue intermittently for several decades. Pica in mentally retarded individuals begins in childhood and may diminish after middle age (24

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