Cover Image
close this bookCauses and Mechanisms of Linear Growth Retardation (International Dietary Energy Consultative Group - IDECG, 1993, 216 pages)
close this folderPsychosocial adversity and growth during infancy
View the document(introductory text...)
View the document1. Introduction
View the document2. Study design and methods
View the document3. Factors determining early and late faltering
View the document4. Conclusions
View the documentReferences
View the documentDiscussion
View the documentReference

(introductory text...)

D. Skuse, S. Reilly and D. Wolke

Behavioural Sciences Unit, Institute of Child Health, 30 Guilford Street, London WC1N 1EH, UK

Correspondence to: D. Skuse.

1. Introduction

For many years it has been widely accepted that an adverse family and social environment can retard physical growth (Department of Health and Social Security, 1976), but there has been relatively little discussion of the mechanisms by which this happens. What are the processes by which social disadvantage results in stunted children in relatively prosperous societies such as our own? Such knowledge is essential if assistance is to be provided for those in the community whose children are at risk. What forms of intervention are likely to be effective in ameliorating the consequences of such social deprivation (Skuse, 1989)? During the 1940s there were reports that emotional deprivation, as such, could influence growth, linked to claims that deprivation during the preschool years usually led to irreversible effects upon psychosocial functioning in later childhood and even adult life. Spitz (1945) described the growth of infants in a foundling home where they had received 'excellent food' yet little individual attention outside feeding times. Growth in both weight and length were severely retarded and Spitz reports that "The physical picture of these children (when 2-4 years of age) impresses the casual observer as that of children half their age". Talbot et al. (1947) described a series of 51 children (aged 2½-15 years) referred to Massachusetts General Hospital who had stunting "with a height age no more than 80% of the actual age". A subsample of 29 children were studied in more detail, from the point of view of their dietary intakes. The nutritional histories of the majority indicated that they had major feeding difficulties which persisted for most of their lives, in many cases since infancy. These were associated, in 60% of the children, with some degree of socioemotional adversity within their families. Attempts to improve the diets of the 66% of the subjects who were underweight for their height met with little success because the children could not be induced to become interested in the idea of eating more food; however, the investigators entertained the hypothesis that nevertheless a number of them had been chronically undernourished. Following 'psychiatric therapy', three subjects showed an improved appetite and, following that change in appetite, demonstrated catch-up growth. An example is given of such catch-up growth commencing between 7 and 8 years of age. Although it was not possible at the time to test the hypothesis, the investigators proposed that the ultimate cause of the children's abnormally slow growth had been a deficiency of growth hormone and that they had tended to adapt themselves to nutritional privation in early life by becoming 'relatively hypopituitary', but the hypopituitarism did not usually reverse when energy intakes were improved. It is of interest to note that 24% of this subsample were considered to have been emotionally rejected by their mothers.

A third account, from the same period, on the growth of children in conditions of psychosocial deprivation or adversity was that of Widdowson (1951). The story of her serendipitous observations is well known. In 1948 she was stationed with an army medical unit in a town in the British zone of occupation in Germany where two small municipal orphanages were located. Each housed around 50 boys and girls between 4-14 years. The children had nothing except rations to eat and they were well below normal in both height and weight. The medical unit instituted a programme of physical examinations of the orphans every two weeks and continued these observations for 12 months. During the first six months the orphans received only the official rations. During the last six months the children in orphanage A received in addition unlimited amounts of bread, an extra ration of jam and a supply of concentrated orange juice. The matron of orphanage A at the start of the study was a cheerful young woman who was fond of the children in her care. In contrast, the matron in charge of orphanage B was older, stern and a strict disciplinarian towards all the children in her care except for a small group of favourites. It so happened that, at the end of the first six months, the cheerful matron left orphanage A for other employment, and the disciplinarian was transferred from orphanage B to orphanage A, bringing her eight favourites with her.

The physical examinations of the children's growth revealed that, during the first six months, the weight gain by the children in orphanage A was substantially more than the weight gain by the children in orphanage B, although the strict matron's favourites did much better than the rest of the children. The shift in matrons then occurred, and this coincided with the provision of extra food for orphanage A. During the next six months the children of orphanage B, whose food supply had not increased but who no longer had the strict disciplinarian in charge of them, showed a rapid rise in weight. Yet, in spite of their improved nutrition, those children who were now subject to the regime of the disciplinarian matron in orphanage A continued to gain weight at about the same rate as before. Trends in weight and height were very similar; the matron's favourites exceeded all others in terms of their rate of growth.

The prevailing view then, during the 1950s and 1960s, was that socioemotional deprivation could indeed be the cause of some cases of abnormally short stature, and that the most likely aetiology was 'deprivation' (or the lack of mothering in a broader sense) (Elmer, 1960; Patton & Gardner, 1962; Coleman & Provence, 1957) and that the failure to thrive was mediated either through diminished intestinal absorption, inefficient utilisation of energy, or possibly some abnormality of endocrine function (Coleman & Provence, 1957; Blodgett, 1963; Leonard, Rhymes & Solnit, 1966).

Then, in 1969, Whitten and colleagues (1969) set out to test the hypothesis that, rather than some subtle influence of deprivation or neglect upon metabolic functioning, the ultimate aetiology of children's growth failure in conditions of socioemotional adversity was simply an inadequate energy intake. Whitten observed that former researchers had all assumed, but not determined, the adequacy of the children's energy intakes during the period when "unfavourable emotional forces were operative". The study was of a series of 16 infants aged between 3-23 months, who were seriously failing to thrive. Their mean length at the time of being taken into the study was -3.06 Z (±1.25 SD) and their mean weight was -3.26 Z (±0.9 SD). By means of an ingenious design they showed, reasonably convincingly, that despite the protestations of the mothers that they had been feeding the children sufficiently, if they were indeed fed 'adequate energy', either during a hospital admission or at home (before or after the hospital admission) they did gain weight, whether or not they received additional stimulation or maternal attention. The authors conclude that "maternally deprived infants are underweight because of undereating, which is secondary to not being offered adequate food or to not accepting it, and not because of some psychologically induced defect in absorption or metabolism". However, they concede that "our evidence that underfeeding is the aetiologic factor in the growth failure of maternally deprived infants is based entirely upon weight gain". In fact the children's average weight for length at the time of admission to the study was -1.8 Z (±0.92 SD); they were clearly not simply stunted and the great majority (88%) were seriously underweight for their length.

The findings of Whitten et al.'s study had the effect of changing the emphasis of research on the association between growth impairment and emotional deprivation and abuse, to focus upon nutritional influences. Now it was reckoned that mothers' accounts of what they fed children who were suspected cases of deprivation could not be true, and that such children were probably being starved. Reviewing the current state of knowledge on the effects of emotional disturbance and deprivation on somatic growth MacCarthy (1974) concludes "hormonal dysfunction appears to be minimal... if there is an explanation, it is probably more in terms of nutrition than of endocrine disturbance".

Krieger (1974) also wrote that maternal rejection could cause a 'psychosocial deprivation syndrome' in which linear growth failure and retarded bone age were associated with persistent restriction of food by mothers who abused their children physically and who had characteristic personality traits. MacCarthy (1981) stated that 'deprivation dwarfism' caused by malnutrition in early childhood, particularly in the first two years of life, was likely to be due to undernutrition", adding "there are strong indicators, short of absolute proof, that this undereating is due to 'under-giving' by the mother and the additional element is the child, who being underfed, becomes undemanding". A reasonable consensus, then, existed in the 1970s that failure to thrive in the early preschool years was due to chronic undernutrition, although there was some perplexity about the child's role. As MacCarthy (1981) put it "why did not these babies cry in hunger, or if they did why were their cries ignored?".

However, another condition was also causing perplexity, for some older children who had excessively short stature and came from homes where it was thought that they were being neglected or abused were reported by their caretakers to have huge appetites, eating far more than their siblings, yet they failed to grow (Powell, Hopwood & Barratt, 1973). This condition has been termed 'psychosocial dwarfism' (Money, 1992), but it is not found as a diagnostic category within ICD-10 (World Health Organization, 1992) or DSM IV (American Psychiatric Association, 1993). The diagnostic criteria for that condition have been summarised by Green (Green, Campbell & David, 1984; Green, Deutsch & Campbell, 1987). The diagnosis has rarely been made before the age of 2 years. In virtually all cases there is said to be a severely disturbed relationship between the primary caretaker and the child, which is the main cause. The most typical behavioural symptoms are bizarre patterns of eating and drinking, with gorging and vomiting, polyphagia and polydipsia. Growth failure usually begins in infancy, but in some cases growth retardation is said to have commenced as late as 6 or 7 years (Ferholt et al., 1985). The children are stunted with a near-normal weight for height. Body proportions are allegedly immature (MacCarthy, 1981) and often there is microcephaly (Marks et al., 1978). Symptoms can be considered under four broad headings: disorders of biological rhythms, of self-regulation, of mood, and of social relationships (Skuse, 1993a). Relevant biological rhythms include sleep, appetite and growth hormone release. Sleep is disrupted, with frequent wakings and night wanderings, often in search of food. Active REM sleep may be increased and stage 3 and 4 NREM sleep decreased (Taylor & Brook, 1986). Appetite is disturbed, normal hunger and satiety rhythms are lost, and there is an apparent inability to achieve satiation. Consequently, these children habitually take food which they have been forbidden, steal food from their peers and-given the opportunity gorge themselves until they vomit. Growth hormone release shows a diminished pulse amplitude (Stanhope et al., 1988), meaning that the cumulated 24 hour circulating levels of the hormone are severely curtailed. Disordered self-regulation means deviant patterns of defecation, urination and attention. It is not uncommon to encounter a history which goes far beyond simple encopresis and enuresis to encompass features in which those bodily functions have acquired the quality of aggressive acts. Deliberate urination over others' belongings, and the concealment of faeces or soiled clothes in public places are typical. Attention span is almost invariably brief. Receptive and expressive language skills are impaired; the children also have poor non-verbal skills and poor practical reasoning abilities (Skuse, 1993b). At school they underfunction, and may require special education for moderate learning difficulties. Mood is almost invariably characterised by depression and poor self-esteem. Social relationships are always severely impaired; these children are disliked by virtually everybody with whom they come into contact including siblings, peers, and schoolteachers as well as their parents. External validation for the condition comes from a fairly well recognised aetiology, primarily emotional abuse (which may be a necessary criterion) but the condition is often associated with physical abuse and sexual abuse too. The natural history is less well documented. A cardinal feature is the potential for reversibility of all symptoms when the child is removed from the abusing environment (Skuse, 1993a; Money, Annecillo & Kelley, 1983; Skuse, 1992; Albanese et al., 1993). The rate of change in mental growth seems to run parallel to that of physical development, and is reflected by a progressive increase in intelligence. The bizarre behavioural features are usually lost within a few weeks of the child being taken into a caring and nurturing family, but if they persist for months or years the possibility that the abuse is also persisting should be considered. The increase in height velocity is often dramatic, and pathognomonic. Children's stature 'catches up' to a trajectory far closer to their genetic potential.

Accordingly, over the past few decades two main subgroups of children with short stature associated with socioemotional deprivation or adversity have been identified. It has come to be appreciated that there could be several quite different ways, involving contrasting mechanisms, in which early experiences can have enduring effects upon linear growth. At one extreme there is growth failure of very early onset, certainly within the first two years of life, in which the aetiology is thought to be undernutrition. The infants with this condition tend not to complain that they are being undernourished, but it has been suggested that the reason they do not complain is that their malnourishment has rendered them apathetic (e.g. Graves, 1976). Such children are said to show reduced activity levels which could be construed as a reductive adaptation to their nutritionally depriving environment (Waterlow, 1984). Once stunting is established within the first three years, so it is hypothesised, the children are unlikely to increase their intake even if offered more food at a later age (Martorell, 1985).

On the other hand, a further subgroup of stunted children from home environments which lack emotional nurture display a very different range of symptoms (Green, Campbell & David, 1984; Green, Deutsch & Campbell, 1987). The children show voracious and bizarre appetites, polyphagia, polydipsia and a variety of other odd behavioural features. Whilst it used to be thought that food restriction was the cause of their obsession with eating (Krieger, 1974), in recent years the view has been expressed that the condition has little to do with malnutrition; although the two disorders may co-exist in the same child, the primary aetiology is a disturbance in growth hormone dynamics (Albanese et al., 1993; Skuse et al., 1993).

The research to be presented comprises part of a series of epidemiological studies on the subject of individual and environmental variables associated with failure to thrive. We are not concerned here with 'psychosocial dwarfism', a far rarer condition, the clinical features of which become manifest in later childhood and, as discussed above, are quite unique. Previous work has demonstrated that stunting in the preschool period usually begins as growth faltering in infancy; persistent growth failure from infancy to 4 years of age is associated with a very poor outcome in terms of cognitive and behavioural development (Dowdney et al., 1987; Skuse, Wolke & Reilly, 1992). Data will be presented to show that infants whose growth falters early on in postnatal life, who live within a socioeconomically disadvantaged area and who are at relatively high risk of inadequate parenting, have contrasting outcomes depending upon whether that growth failure begins immediately after birth or later. We will present data to show that each broad trajectory of growth in the first year, measured in terms of weight gain, is associated with contrasting family circumstances and degree of psychosocial disadvantage. Those with the later onset of failure to thrive, after six months or so of age, had mothers who were subject to greater social and psychological adversity, and who, for a variety of reasons, might have been expected to provide a poorer quality of parenting experience. Yet developmentally these very same children had a better outcome in the second postnatal year than the 'early' failure to thrive group.

2. Study design and methods

The investigation was a prospective longitudinal survey of virtually all infants born during one calendar year within an inner city health district in London, England. The district has an ethnically diverse population (140,000), which in socioeconomic terms is relatively homogeneous and quite severely disadvantaged (South East Thames Regional Health Authority, 1984).

The sampling frame comprised all 2510 births that were registered with participating child health clinics or family doctor practices in 1986. The planning and execution of the survey was facilitated by the good relationship built up between the research team and the local community paediatric services in the course of previous research there (e.g. Dowdney et al., 1987).

The selection of subjects who had growth faltering was made from all children who continued to live in the district until 12 months of age, and who were weighed on at least one occasion. During this period 14.4% of the population moved out of the area. There were also missing data on a small minority of subjects (1.2%) who were known to health visitors but were seen only at home. Other families were untraceable (3.3%). A small proportion of infants (0.8%) are known to have died.

Growth trajectories were computed from weight data recorded at clinic visits and expressed as Z scores (Hamill et al., 1979; Jordan, 1986). Scores have been interpolated to target ages 4 weeks, 6 weeks, 3 months, 6 months, 9 months, 12 months and 15 months. In virtually all cases the interpolations were made where at least one of the data points was within 1 month of the target age. Quadratic (three point) interpolation was undertaken by means of the NEWLONG program developed by Carter (1985).

2.1. Definition of growth faltering

Potential cases were limited to singleton deliveries at term, i.e. between 38 and 41 completed weeks gestation. Preterm infants (gestation 37 weeks 6 days or less) were excluded because of the known association with below average growth in the early postnatal period (Brandt, 1986; Ounsted, Moar & Scott, 1982). Also excluded were infants with severe intra-uterine growth retardation (i.e. birthweights at or below the 3rd centile, on charts standardised for gestation, sex, ordinal position, maternal height and mid-pregnancy weight; Tanner & Thomson, 1970). Confirmed cases of growth faltering had to have a weight for age Z score (WAZ) below -1.88 (corresponding approximately to the 3rd centile). This trajectory relative to population norms had to be attained by 12 months of age, and sustained for three months or more. All children with a suspicious weight gain trajectory, on the basis of clinic data, were traced and visited at home for confirmatory anthropometry.

There were 1554 potential subjects remaining after exclusion criteria had been implemented. Of those, 52 (3.3%) were confirmed cases of growth faltering at 12 months of age. Three of these were excluded because of an overt organic disorder that was considered to be making a major contribution to the infant's poor rate of growth. Further information about the study design and outcome can be found in Skuse, Wolke & Reilly (1992).

2.2. Pattern of growth in first year

Preliminary exploration of the data led to the conclusion that the children could be approximately divided into two subgroups, those in whom the onset of growth failure was before 6 months of age, and those in whom it was later.

This was done according to whether the difference in weight between birth and 6 months was greater than or less than half the difference between birth and one year. The former suggests that the greater part of the faltering had occurred in the first 6 months and the child was classified as early faltering (early failure to thrive; FTT) (Fig. 1); the latter implied that it had occurred in the second 6 months, and the child was classified as late faltering (late failure to thrive; FTT) (Fig. 2). When the mean values for those trajectories were plotted (see Fig. 3) significant differences in standardised weight were found at 3, 6 and 9 months. The early FTT infants actually had higher birthweights than the others.

3. Factors determining early and late faltering

3.1. Differences at birth

3.1.1. Perinatal complications It has been proposed by a number of workers (e.g. Mitchell, Gorrell & Greenburg, 1980) that full-term infants who subsequently fail to thrive have an excess of perinatal complications. Table I shows examples of the key variables that were analysed. There were few differences between the groups, and the overall mean scores were similar. The main contribution to the high proportion with some degree of fetal distress was a transient bradycardia (< 120) at some point during delivery.


Fig. 1. Weight gain trajectory from birth to 15 months of child with 'early' growth faltering.


Fig. 2. Weight gain trajectory from birth to 15 months of child with 'late' growth faltering.


Fig. 3. Weight gain trajectories of early and late growth faltering infants from 4 weeks to 15 months of age. 95% confidence intervals are shown.

3.1.2. Anthropometry at birth Virtually all subjects had been born in a teaching hospital where it was a routine procedure to record birth weight, length and occipito-frontal head circumference. Data were available on all subjects for birthweight, on 83% for length' and 96% for head circumference at birth. It was possible to standardise birthweights for maternal stature, mid-pregnancy weight, gestation, ordinal position of the child (first or other born) and gender according to the method of Tanner & Thomson (1970). These corrected birthweights have been converted into standard deviation scores. A ponderal index was computed according to the method of Miller & Hassanein (1971), based on the formula: [birthweight in g/(crown-heel length cm)3] x 100. Values were then corrected for gestational age. Birth length standards from Kitchen et al. (1981) and head circumference from Yudkin et al. (1987) were also corrected for gender and gestational age and both were converted into standard scores.

Table 1. Examples of individual risk factors used to compute total antenatal and perinatal risk score for mothers of 'early' and 'late' growth faltering subjects

Antenatal or perinatal risk factor*

'Early' FTT

'Late' FTT

Vaginal bleeding during pregnancy

14

9

Severe infection during pregnancy (e.g., Rubella, Herpes)

0

9

Albuminuria with high BP (i.e., systolic >140, diastolic >90)

9

4

Diabetes

5

0

Epilepsy

0

0

Fetal distress

55

32

Meconium staining of amniotic fluid

14

4

Placental weight outside normal range (342-530 gm)

0

4

Apgar score < 8 at 1 min

32

28

<8 at 5 min

5

0

<8 at 10 min

5

0

Total scores

mean 6.18 SD 2.8

mean 6.04 SD 3.6

* There are no significant differences between the subgroups on any of the above variables.

The possibility of differences between the groups in the mean values of these three variables was investigated by one-way ANOVA, with gestation as a control variable where appropriate. No significant differences were found.

However, a different picture emerged when we came to compare the groups in terms of standardised birthweights (corrected according to the method of Tanner & Thomson (1970)). The mean values for the early and late FTT children were -0.42 ±0.78 and -1.05 ±0.5 (P = 0.002). A test for the non-normality of both distributions did not reach conventional levels of significance. No child had a standardised birthweight which was more than 2 SD below the population mean (Tanner & Thomson, 1970).

3.1.3. Socioeconomic status A wide range of variables measuring aspects of families' socioeconomic status was obtained based upon the factors used by Osborn (1987) to compute his composite social index (Osborn & Morris, 1979).

There were no differences between early and late FTT in the father's occupation and educational status; in the proportion of single parent households; in the type of accommodation or number of people per room; in parental height and weight (as far as the evidence went), or in distribution between different ethnic groups.

However, there was a highly significant difference in responses to the question "How many times in the past year have you had no money in the house?". Despite similar levels of mean weekly income, 64% of families with late growth faltering infants said this had happened to them at least once, whereas this was true for only 27% of 'early FTT' families. Similar proportions of families in both groups (82% and 83% respectively) said their first spending priority was food.

3.1.4. Mothers' cognitive abilities It is unusual for studies that are examining patterns of growth faltering in infancy to have reliable measures of the cognitive abilities of the mothers. All mothers of children in this investigation were tested with the Wechsler Scales of Adult Intelligence (WAIS-R, Wechsler, 1974). All the measures were made by a senior psychologist who was blind to case-comparison group status. Proration of the scores on block design and picture completion yielded a nonverbal performance score; vocabulary and information a verbal score. Proration is a procedure by which a full scale IQ score can be approximated by computation from a subset of all the subscales which would normally be administered, thereby reducing the time necessary to give the test. Where the native language of the mother was not English, and she was not fluent in the language, no verbal score was computed. Substantial differences were found between the early and late growth faltering infants' mothers, with those in the latter subgroup having lower IQs by a margin that amounted to about 0.75 SD (Table 2).

3.1.5. Mothers' mental state In order to investigate the mental state of the mothers they were asked to fill in a variety of questionnaires. Where the mother's first language was not English, a professional translator assisted her. All instruments were rated during the course of the home visit and were taken away for subsequent scoring. They included a 28-item version of the General Health Questionnaire (GHQ) (Goldberg & Hillier, 1979) which is a scaled version of the parent instrument, with four subscales derived by factor analysis. These include 'somatic symptoms', 'anxiety and insomnia', 'social dysfunction' and 'severe depression'. The validity of the subscales is discussed in Goldberg & Williams (1988, p. 39). These subscales represent dimensions of symptomatology, more symptoms resulting in a higher score, and do not necessarily correspond to any psychiatric diagnosis. There is no absolute consensus about what 'threshold' score best discriminates between cases of probable psychiatric disorder and others, but the modal value has been 4/5 out of a total possible score of 28 (Goldberg & Williams, 1988, p. 64). At this level, the positive predictive value of a high score (i.e. 5 or more), where there is a prevalence of 30% of 'true' disorders in the population being tested, is 0.67.

Table 2. The cognitive abilities of mothers of 'early' and 'late' growth faltering subjects, measured by the Wechsler Adult Intelligence Scales (WAIS)

WAIS scores

'Early' FIT

'Late' FTT

p

Verbal

91 ±20.5 (22)

79.3 ±3.2 (22)

0.03

Performance

92 ±18.5 (22)

81.1 ±14.6 (25)

0.03

Full scale

89.9 ±19.6 (22)

77.8 ±12.4 (25)

0.02

Both the overall scores on the GHQ -28 and the scores on certain of the subscales distinguished between the mental state of the mothers of early and late growth faltering infants. The overall mean scores of the late growth faltering mothers were significantly higher than those in the early growth faltering group (5.8 ±5.6 and 2.9 ±3.9 respectively; P = 0.039). Taking the cut-off point of 4/5 - as recommended - the proportions of mothers who were 'probable cases' of psychiatric disorder (i.e. had scores of ³ 5) in the two groups differed substantially (56% and 27% respectively), but the magnitude of differences did not reach a conventional level of statistical significance, once a continuity correction had been applied (P = 0.09).

On an alternative measure of anxiety (the Multiple Affect Adjective Checklist; Zuckerman & Lubin, 1965) the mothers of later growth faltering children obtained higher scores (3.8 ±3.2 vs 1.6 ±1.7; P = 0.007). They were also more disturbed in terms of social dysfunction (a GHQ -28 subscale that asks about everyday activities) (mean scores 7.8 ±2.9 and 5.8 ±2.8; P = 0.02). However, their most striking form of psychiatric disturbance was on the GHQ -28 subscale for severe depression (2.7 ±2.5; 0.9 ±1.2; P = 0.003).

The broader question of how our findings for the mental health of these mothers compares with other inner city surveys is hard to answer, for none of the mental health scales we used has published norms for a general population sample in this country which is exactly comparable to the subjects of our survey. Perhaps the closest set of comparison data is from Brooke et al. (1989), who studied a consecutive series of 1860 white women booking for delivery at a district general hospital in inner London. The 28-item version of the General Health Questionnaire, administered at 17 weeks gestation, gave the following results (see Table 3). It is clear that the mothers of early growth faltering infants were comparable in their depression scores to those in this pregnant sample, but the scores of the mothers of late growth faltering infants were rather higher, implying more of them were suffering from some depressive symptoms.

Table 3. The mental state (severe depression) of mothers of 'early' and 'late' growth faltering subjects, compared with population sample

Depression scale score a

'Early' FTT mothers %

'Late' FTT mothers %

Brooke et al., 1989* %

0

54.5

24

63.8

1

22.7

16

10.6

2-3

13.6

28

10.6

> 4

9.1

32

14.9

* Pregnant women, 17 weeks gestation, inner London population.
a 'Severe depression' subscale of GHQ (Goldberg & Hillier, 1979).

3.1.6. Mothers' social support It has been suggested that mothers of failing to thrive infants are exceptionally socially isolated (e.g. Kotelchuck, 1980) and that they lack social support (Bithoney & Rathbun, 1983; Kotelchuck & Newberger, 1983). This issue was addressed with the aid of a scale devised specifically for the purpose of our own investigation, based upon the work of Tietjen & Bradley (1985). The scale was filled in by the mother, with guidance from the research worker if necessary. Typical questions ask about whether there is anybody to whom the mother could turn in an emergency, or if she had a personal problem, how often there is no-one willing to talk to her, how satisfied she is with her neighbourhood, and so on.

Significant differences were found, with the mothers of the early failing to thrive babies having a higher social support score, on average, than mothers in the late failure to thrive group (31.0 ±5.1 vs 25.7 ±5.4; P = 0.001).

3.1. 7. Marital relationship Disharmony in the intimate relationships of the mothers we surveyed may have contributed to parenting difficulties. Whilst this is true for parenting in general (Rutter, 1985), it has been argued specifically that the quality of a father's relationship with his spouse and his family may have an important longer term influence upon the mental health outcome of failing to thrive children (e.g. Drotar, 1985).

Mothers' relationship with their spouses were assessed with the Dyadic Adjustment Scale (Spanier, 1976; Spanier & Thompson, 1982; Antill & Cotton, 1982). Only the Dyadic Satisfaction subscale was rated. There was only a small and non-significant difference between the reports of mothers of early growth faltering infants (mean 39.2 ±5.5) and others (mean 35.7 ±8.8). Both scores were similar to the values for a wider sample of women (mean 38.7 ±6.1) given by Antill & Cotton (1982).

3.1.8. Familial patterns of growth failure The distinct psychosocial characteristics of families whose children had early or late growth faltering led to the hypothesis that similar patterns of growth would tend to be found in the siblings of affected individuals; if the mechanisms producing the growth trajectories were different in the groups there might be a tendency for affected siblings to have similar profiles of growth faltering in the first year. Accordingly, a search was made for data on sibling growth patterns in infancy. All information came from child health or 'well baby' clinics, not from paediatricians or other hospital records.

In the group with early failure to thrive just 35% of siblings could be said with certainty to have grown normally in the first year. Thirty percent had a similar pattern of 'early' growth failure but this was not necessarily sustained for as long a period; however, these siblings did have weights for age which fell clearly below the 3rd population centile at some point in the first six postnatal months. Just one of the 20 siblings had growth faltering after six months. An additional 30% had some degree of growth faltering at some point in the first year; in a few cases this was severe but the onset was uncertain. In others it was not sufficiently severe (i.e. weight for age fell to below the 10th but not the 3rd population centile) to meet diagnostic criteria.

In the group with late growth faltering 57% of the siblings grew normally through the first year. Surprisingly just 10% had a pattern of failure to thrive which commenced in the latter part of that year, and in 20% the onset was 'early', in the first six months. There were an additional 14% of siblings whose degree of growth faltering did not quite meet criteria, or for whom the onset was uncertain.

Cross tabulating growth trajectory by the timing of the growth failure onset among siblings revealed no significant differences between the groups. However, it is important to note that overall 54% of the siblings of our subjects had had some degree of growth faltering within the first postnatal year, and in 32% it was relatively severe although not necessarily sustained for as long a period as in the probands.

3.2. Differences during the first year

3.2.1. Medical history Children with serious medical illness, which might have caused growth faltering, were excluded from the samples of infants discussed here. There were reports of only relatively minor illnesses during the first year of life, such as episodes of upper respiratory tract infection, diarrhoea and otitis media. A weighted score was computed for 17 such variables, which took a maximum value of 25. Neither individual indices of risk nor the total score distinguished the early from the late growth falterers (the mean value being 8.5 ±3.7 and 8.0 ±3.4, respectively), suggesting that the frequency of illness was not a relevant factor in causing their disorder. However, because the data were collected retrospectively it was not possible to specify the timing of most of their illnesses within the first year; the data would have been too unreliable.

3.2.2. Feeding histories Histories of how the children were fed as infants were obtained from mothers by interview at follow-up, when the infants were about 15 months of age. The information was therefore retrospective and for that reason cannot be regarded as wholly reliable. Twenty percent of the 'early FTT' group and 13.6% of the 'late FTT' group were exclusively breast fed. Twenty-four percent of the 'early' and 32% of the 'late' group were exclusively bottle fed; the corresponding figure for those given a mixture of breast and bottle was 56% and 54.5%. None of these differences reached statistical significance. The mean age at which solids were introduced was virtually identical in the 'early' and 'late' groups too, being 17 + 6.7 and 17 + 6 weeks respectively. There did not seem to be any major feature of their early feeding histories which distinguished the groups, although it might have been expected that the 'later' FTT group began to show growth faltering around the time of weaning, possibly because of difficulties in getting the children to accept solid foods. We did attempt to 'map onto' standardised charts of the children's growth trajectories the times at which weaning occurred for individual subjects, according to mothers' reports, but the findings were inconclusive.

A substantial proportion of the infants in both groups were reported as having slept through feeds at some time in the first year. That is to say, when it was time for the infant to have a meal the child was asleep, or alternatively fell asleep during a feed. This was the case for 68% of infants with early growth faltering and 64% of the infants with growth faltering after six months. Although we attempted to discover whether there were systematic differences between the groups according to the timing and the duration of this behaviour, no differences could be detected.

It is, of course, of great interest to know how mothers responded to this pattern of behaviour. Of those who slept through feeds at some time, in the 'early FTT' group 40% were woken by their mother, according to their retrospective reports. In the 'late FTT' group 62% were woken by their mother. Although these differences are relatively small, they are at least suggestive that perhaps infants who were sleeping through feeds at a time when their growth rate was at its most rapid, and who were not yet weaned, were being chronically undernourished because of missed meals. The interview material certainly raised the suspicion that overnight feeds were frequently missed in the early days if the infant was a 'good' baby and slept through the night without demanding to be fed.

However, similar proportions of infants in both groups were said to sleep through the night before 6 weeks of age, 'early' 24%; 'late' 25%.

3.2.3. Growth of sleepy infants If these mothers' reports of their babies lack of demandingness were correct, and they were indeed missing feeds because they were asleep, one would expect this to be reflected in their growth trajectories-although it could not of course explain the difference in the growth trajectories of the 'early' and 'late' groups. Accordingly, the groups were combined and then categorised according to whether their mothers reported them as having ever slept through feeds, or not. Remarkably, the weight gain trajectories of those who were in the 'sleepy baby' group fell below the remainder, and a significant discrepancy persisted from 4 weeks (the earliest standardised measurement) right up until 12 months of age (Fig. 4).

Their birthweights were not significantly different from one another, whether measured in absolute terms (sleepy infants mean 2938 ±344, others mean 3150 ±380) or in standard deviation scores (Tanner & Thomson, 1970). Nor were their ponderal indices or occipito-frontal circumferences, but the sleepy infants were shorter (mean 49.6 cm SD 12.5 vs mean 51.3 cm SD 2.7; P = 0.06). Where the birth length was standardised for gestation and gender a much greater magnitude of differences emerged (-0.31 ±1.1 vs 0.66 ±1.1; P = 0.01). It is worth noting that, despite a difference in standardised length of about 1 SD, both mean values are well within the normal range.

In order to explore this matter further, a series of analyses of variance was undertaken with weights (standardised) at 4 weeks, 6 weeks, 3 months, 6 months, 9 months and 12 months as the dependent variables, and a set of predictor variables which included whether the child had ever slept through feeds, whether mother reported that she regularly woke the baby for feeds or not, whether the child was breast, bottle or combination fed, and the gender and ordinal position of the child. Other potential explanatory variables included mother's IQ, various measures of her mental state and the summary score for the child's oral motor difficulties. Potential interactions between these variables were investigated but none of any significance was found. A series of multiple regression equations was then calculated for each of the above mentioned ages, in which only those predictor variables that had been found to be of relevance in the former exploratory analyses were entered. The results are shown in Table 4.


Fig. 4. Weight gain trajectories of growth faltering infants, according to whether they 'slept' through feeds. 95% confidence intervals are shown.

Differences between groups at 4 weeks 3 months 6 months 12 months c 0.01 and at 6 weeks 9 months < 0.02. No significant differences at birth or 15 months

As can be seen, the variable 'slept through feeds' was significant at every age, and children who did so had lower weights for age. Interestingly, the variable 'mother woke baby' had no significant effect and was not included in the final models. Neither did mother's mental state, even when this was entered as a variable relating to the duration of postnatal depression. The ordinal position of the child had no significant influence once the other variables had been entered. Mother's IQ had a substantial impact on the child's weight at 12 months only, children of mothers with higher IQs having a greater weight for age, presumably reflecting their better feeding practices.

3.3. Differences at outcome

3.3.1. Anthropometry The children were examined as close to 15 months of age as possible. A variety of anthropometric indices are presented in Table 5. The computation of the anthropometric indices for arm muscle and fat areas are from Sann et al. (1980). Norms for mid and upper arm circumference are available from Rees et al. (1987). There are no significant differences in any of the indices, whether the groups are compared on the basis of mean values or on the basis of their centile distributions, suggesting that by the age of 15 months or so, despite contrasting trajectories of early growth, on average their anthropometric outcome is identical.

Mean values of weight for length are given in Table 5. All infants, in both groups, were to some degree underweight for their length. Nearly half (45%) of those with early growth faltering were at or below the 3rd population centile; the figure was similar for the late growth faltering infants (40%).

Case criteria demanded a substantial fall in weight, relative to population norms, over the first postnatal year. Overall, the mean decrement in standardised weight for age was -1.33 (±0.81). This was associated with an equivalent fall in length (-1.33 ±1.3), suggesting that the children were becoming stunted. However, taking 90% of NCHS median lengths as the cutoff point for a child to be classified as stunted, at the time of follow-up only 13% of our sample met this criterion. We do not have serial measures of length through the first postnatal year as these are not routinely measured in child health clinics, so it has not been possible to look at changes in length velocity in any meaningful way. Head circumference was below norms for gender and gestation at birth for 89% of the sample. There was a small degree of catch-up in this variable for two out of five subjects, such that at follow-up 28% had values at or above the 50th population centile.

Table 4. Multiple regression of postnatal standardised weights on explanatory variables

Dependent variable: standardised weight at

Explanatory variables

F ratio for R2

Change in adjusted R2

Standardised regression coefficient





DF

F

Significance



t

p

4 weeks

1. Exclusively breast-fed




0.17

0.36

2.8

0.008


2. Slept through feeds




0.10

-0.33

-2.5

0.016


Total explained

2,44

8.3

0.0009

0.27




6 weeks

1. Exclusively breast-fed




0.18

0.38

2.9

0.006


2. Slept through feeds




0.08

-0.29

-2.18

0.035


Total explained

2,44

7.8

0.0013

0.26




3 months

1. Exclusively breast-fed




0.19

0.40

3.10

0.003


2. Slept through feeds




0.10

-0.33

-2.6

0.01


Total explained

2,44

9.6

0.0004

0.30




6 months

1. Slept through feeds




0.11

-0.34

-2.42

0.02


Total explained

1,45

5.9

0.02





9 months

1. Slept through feeds




0.09

-0.3

-2.1

0.04


Total explained

1,45

4.5

0.04





12 months

1. Solids




0.16

-0.3

-2.3

0.02


2. Slept through feeds




0.11

-0.27

-2.1

0.04


3. Gender (male = 1, female = 2)




0.05

0.22

1.7

0.09


4. Mother's IQ




0.06

0.22

1.7

0.05


Total explained

4,42

6.55

0.0003

0.33




Table 5. Anthropometry of 'Early' and 'Late' growth faltering infants

Variable

'Early' FTT

'Late' FTT

At birth (n = 47)

Weight

-0.42 ±0.78

-1.05 ±0.5**

Head circumference (n = 46)

-0.96 ±0.9

-1.36 ±1.1

Length (n = 42)

0.11 ±1.1

-0.02 ±1.25

At outcome (n = 47)

Weight (SDS)

-2.07 ±0.54

-2.07 ±033

Length (SDS)

-1.31 ±0.84

-1.22 ±1.04

Weight for length (SDS)

-1.63 ±0.6

-1.71 ±0.68

Head circumference (SDS)

-0.96 ±0.9

-0.81 ±1.08

Mid-upper arm circumference (cm)

13.7 ±0.7

13.5 ±0.76

Arm muscle circumference (cm)

11.05 ±0.54

11.03 ±0.67

Arm fat area (mm2)

15.9 ±1.8

15.5 ±1.7

Velocity of head circumference growth since birth (cm/yr) (n = 46)

9.86 ±1.3

10.44 ±1.8

Change from birth to outcome (n = 47)

Weight

-1.66 ±0.9

-1.05 ±0.6**

Head circumference (n = 46)

0.01 ±1.2

0.57 ±1.1

Length (n = 42)

-1.43 ±1.2

-1.25 ±1.3

Values are given as mean Z scores ±1 standard deviation. There are no significant differences between groups on any variables, except where indicated.

3.3.2. Blood tests A 1 ml (minimum) sample of capillary blood was taken at 15 months from all subjects for a full blood count, haemoglobin electrophoresis and ferritin estimation. Analyses were also made for red blood cell folate and serum B12 The mean haemoglobin levels of late faltering subjects were significantly lower than those of early faltering subjects (11.46 ±1.13; 12.11 ±0.92; P = 0.03). Taking the WHO (1972) recommended cut-off of 11 g/dl between 6 months and 6 years as an indicator of anaemia, we found 14% of the early FTT group and 36% of the later FTT group had haemoglobin at or below this level, but the difference failed to reach statistical significance. Both mean corpuscular haemoglobin (26.0 ±1.8; 24.8 ±2.4) and mean corpuscular volume (80.1 ±3.2; 76.9 ±6.4) were significantly lower in the 'late' failure to thrive children (P < 0.05) suggesting that the anaemia was for the most part a hypochromic microcytic one and that iron deficiency was most likely to have been responsible. We had screened for possible inherited anaemias such as thalassaemia or sickle cell anaemia but none of the children was found to be suffering from these conditions. Serum ferritin levels were very similar in the two groups: the mean values for early FTT were 20.3 ±15.5 ng/ml; for late FTT 19.3 ±13.1 ng/ml and the proportions with values < 7 ng/ml (Slimes, Addiego & Dallman, 1974) were 14% and 24% respectively. Values of serum B12 and red cell folate were all within the normal range for infancy.

3.3.3. Neurodevelopmental attainments There is a risk that children with early severe growth faltering may suffer detriment to their neurological development. Studies of children who have been hospitalised with failure to thrive are reported to show a wide range of 'neurodevelopmental deficits', including low scores on standardised developmental assessments (Leonard, Rhymes & Solnit, 1966; Ramey et al., 1975, Field, 1984; Singer & Fagan III, 1984; Powell & Low, 1983). However, the relationship between early growth faltering and persistent developmental impairment is complicated by the fact that nutritional deprivation is usually accompanied by other forms of socioeconomic deprivation too (e.g. Casey, Bradley & Wortham, 1984) which can independently influence attainments.

Frank (1985) discussed the possibility that early malnutrition during a critical period of brain growth (Dobbing, 1990) may produce structural deficits which have functional consequences. There is evidence from studies in animals that the cerebellum, which contains large populations of microneurons, might be especially vulnerable to early undernutrition (e.g. Rodier, 1980). However, it is difficult to distinguish cause and effect here. Children born with subtle neurodevelopmental problems may themselves be at risk of undernourishment (for example, because of poor oral-motor skills; see Mathisen et al., 1989), and consequently of a suboptimal rate of growth. Subsequently, persistent malnutrition could of course independently contribute to neurodevelopmental disorders (see for example, Reyes et al., 1990).

The role of congenital determinants of behaviour and cognition is relatively easily demonstrated in clearly recognised medical syndromes such as the Down or Prader Willi syndromes. Nevertheless, a wide variety of minor physical stigmata is found within populations of children with no recognised medical disorder. Waldrop, Pederson & Bell (1968) have suggested that an inverse relationship exists between intellectual functioning and the number of anomalies in young children. Accordingly, physical anomalies that could be entered into the computation of a congenital anomalies score were sought in the course of physical examinations. The total possible anomaly score was 24. The mean scores for the two groups were very similar: early FTT children 1.8 ±1.8 and late FTT children 2.2 ±2.9. There was a highly significant correlation with head circumference at birth, standardised for gestation and gender (-0.42; P = 0.002).

An assessment of neurological functioning and maturity was also undertaken, based upon the work of Touwen (1976) and Amiel-Tison & Grenier (1986). A composite score of gross motor skills was derived from the ten variables for which there was the least missing data; this allowed the comparison of 18 cases of early FTT and 24 cases of later FTT: Skills such as the ability to walk or sit unsupported, visual following while sitting, optical placing, reaction of hands, were scored according to the weighting system recommended by Touwen (1976).

The total mean scores were very similar in respect of both gross motor skills (20.7 ±4.8 and 21.2 ±4.0) and fine motor skills (6.8 ±2.6 and 7.9 ±1.4) for early FTT and late FTT group respectively. A composite score comprising five variables that related to the appearance of the children-whether skin or nails were clean or dirty, whether burns or scars were visible, and whether extremities were red, puffy or shiny in appearance-did not distinguish between the groups either (0.81 ±1.1 and 0.88 ±1.1).

3.3.4. Cognitive abilities There is ample evidence that children in the developing world who are stunted, on account of chronic undernutrition and related adversities, have impaired mental abilities. This evidence has accumulated over many years (e.g. Hertzig, Birch & Richardson, 1972; Galler, 1987). Developmental undernutrition during early postnatal life may have greater consequences than were it to occur later. Dobbing (1990) has emphasised the importance of taking into account the duration, severity and above all the timing of any such insult when making extrapolation about the likely impact upon development.

Accordingly, it was of considerable interest to see whether the cognitive abilities of the early and late growth faltering infants were significantly different when measured early in the second postnatal year. The instrument used was the Bayley Scales of Mental Development (Bayley, 1969). The mental scale contains language items and many types of problem solving tasks. The psychomotor scale mainly addresses gross motor development. The tests were administered blind to the status of the infants. The results of an ANOVA, with both the psychomotor (PDI) and mental development index (MDI) of the Bayley Scales as dependent variables, and with mother's IQ as a covariate, are shown in Tables 6 and 7.

Table 6. Analysis of variance for effects of postnatal weight gain trajectory on mental development index

Source of variation

Degrees of freedom

Sum of square

Mean square

F

P

Covariate: maternal IQ

1

1325

1325

5.0

0.03

Main effects: trajectory (early/late)


3512

3511

13.22

0.001

Explained

2

4838

2419

9.1

<0.001

Residual

44

11675

265



Total

46

16512

359



Multiple classification analysis

Grand mean 98.2




Variable and category

N

Unadjusted deviation (ETA)

Adjusted for trajectory and maternal IQ

'Late' FTT

25

5.8

8.7

'Early' FTT

22

-6.6

-9.9

Multiple R2



0.29

The data show that the growth trajectory did indeed have a substantial and highly significant influence upon the cognitive and psychomotor abilities of the infants at 15 months, with the early growth faltering children doing much worse than those whose faltering began after 3-6 months of age. Mother's IQ does have a significant influence, but upon the MDI only. Both MDI and PDI are depressed to an equivalent extent by the early growth faltering.

Further analyses of these data have shown that, even when other potentially confounding psychosocial variables, such as the cognitive stimulation the child receives at home, are taken into account a statistical model can be constructed that enables the timing, duration and severity of growth faltering to be used as predictors of mental functioning. Up to 37% of the variance in cognitive and psychomotor outcome at 15 months can be explained by the model. The first six postnatal months appear to constitute a 'sensitive period' for growth and mental development (Skuse et al., 1993).

Table 7. Analysis of variance for effects of postnatal weight gain trajectory on psychomotor development index

Source of variation

Degrees of freedom

Sum of square

Mean square

F

P

Covariate: maternal IQ

1

214

214

0.83

ns

Main effects: trajectory (early/late)


2115

2115

8.2

0.006

Explained

2

2330

1165

4.5

0.017

Residual

44

11397

259



Total

46

13726

298



Multiple classification analysis

Grand mean 96.7




Variable and category

N

Unadjusted deviation (ETA)

Adjusted for trajectory and maternal IQ

'Late' FTT

25

5.2

6.7

'Early' FTT

22

-5.9

-7.7

Multiple R2



0.17

4. Conclusions

We have found, in a community survey of infants who were full term births, with birthweights in the normal range, that about 3.5% have growth faltering in the first postnatal year (Skuse, Wolke & Reilly, 1992). To reach our case criteria the degree of growth failure had to be such as to warrant clinical concern, and is equivalent to that seen in previous investigations of hospitalised infants with the condition (see Skuse, 1993c). Yet at the time of our assessment less than 20% of the cases we identified had been referred to hospital for investigation (Skuse, Wolke & Reilly, 1992). Accordingly, the annual incidence figure we report of 3.5% of full term births is considerably higher than might be expected.

At approximately 15 months of age all case children were found to be underweight for their length to some degree. A variety of anthropometric variables which have been shown, in the developing world, to be weakly associated with poverty and malnutrition (e.g. Martorell, Mendoza & Castillo, 1988) were also obtained. They did not show any significant correlation with measures of psychosocial adversity in the families studied in this survey, but this is not surprising as the sample was relatively small. On a variety of criteria the population studied was socioeconomically disadvantaged and other indices of psychosocial adversity were positive indicating families were at relatively high risk of experiencing parenting difficulties. For example, a high proportion of mothers were depressed or suffering from other minor psychiatric disturbance, were living in unsatisfactory accommodation, had relatively low intellectual abilities and a lack of education.

By means of a simple arithmetical procedure it was possible to partition this sample of growth faltering infants into two subgroups: those in whom the onset of the condition was immediately after birth and those for whom it began three to six months later. Remarkably, the outcome in terms of cognitive and psychomotor development, but not in terms of anthropometric criteria, was much worse for those whose growth failure was early. In fact for those in the later group this outcome was not different from a normal comparison group drawn from the same population and closely matched on a wide range of criteria (see Skuse, Wolke & Reilly, 1992). Yet these children who faltered early came from relatively advantaged homes in which the burden of psychosocial adversity was lower than for the later growth faltering subjects.

In conclusion, serious growth faltering during the first postnatal year is more common among full term, otherwise healthy, infants living in a socioeconomically disadvantaged inner city environment than might be expected from the perspective of hospital practice. Their outcome, in terms of cognitive and psychomotor development in the second year of life, seems to be determined primarily be the timing, duration and onset of that growth failure (Skuse et al., 1993). Sustained failure to thrive through the whole period of early childhood, which leads eventually to stunting, is associated with an exceptionally poor outcome for mental abilities (Dowdney et al., 1987). The aetiology of such growth faltering is not simply a matter of nutrition, nor of poor parenting practices. An adequately broad perspective on the subject must also take into account the interaction between behavioural risk factors, a perspective that points the way towards the imperatives of any programme of preventive intervention.

Acknowledgements - This research was supported by grants from the Wellcome Trust, the Child Growth Foundation and the Newcome Educational Foundation, and the work was carried out at the Behavioural Sciences Unit, Institute of Child Health, London.

We thank the staff of Guy's Hospital Community Paediatric service, the Lewisham and North Southwark Health Authority Priority Care Unit and the local general practitioners who actively cooperated with our investigations. Further invaluable assistance with tracing subjects and records was provided by Mrs. Dorothy Gill and Mrs. Jennifer Smith, administrative assistant, who coordinated data collection and prepared the manuscript.

References

Alabanese A, Hamill G, Jones J, Skuse D, Matthews D & Stanhope R (1993, in press): Reversibility of physiological growth hormone (GH) secretion in children with psychosocial dwarfism. Clinical Endocrinology.

American Psychiatric Association (1993): Diagnostic and statistical manual of mental disorders, 4th ed. Washington, DC: APA.

Amiel-Tison C & Grenier A (1986): Neurological assessment during the first year of life. New York: Oxford University Press.

Antill JK & Cotton S (1982): Spanier's dyadic adjustment scale: Some confirmatory analyses. Aust. Psychol. 17, 181-189.

Bayley N (1969): Bayley Scales of Infant Development. New York: Psychological Corporation.

Bithoney WG & Rathbun J (1983): Failure to thrive. In Developmental behavioral pediatrics, eds M. Levine, W. Carey, A. Crocker et al., pp. 552-557. Philadelphia, PA: W.B. Saunders.

Blodgett FM (1963): Growth retardation related to maternal deprivation. In Modem perspectives in child development, eds J Solnit & SA Provence, pp. 83-93. New York: International University Press Inc.

Brandt I (1986): Growth dynamics of low birthweight infants with emphasis on the perinatal period. In Human growth: A comprehensive treatise, 2nd edn, eds F Faulkner & J Tanner, pp. 415-475. New York: Plenum.

Broman SH, Nichols PL & Kennedy WA (1975): Preschool IQ: prenatal and early developmental correlates. Hillsdale, NJ: Lawrence Erlbaum Associates.

Brooke OG, Anderson HR, Bland JM, Peacock IL Stewart CM (1989): Effects on birth weight of smoking, alcohol, caffeine, socioeconomic factors, and psychosocial stress. Br. Med. J. 298, 795-802.

Cameron N (1984): The measurement of human growth. London: Croom Helm.

Carter B (1985): NEWLONG: a program for manipulation of data in populations of individuals subject to change. Software-practice and experience 15, 369-377.

Casey PH, Bradley R & Wortham B (1984): Social and nonsocial home environments of infants with nonorganic failure to thrive. Pediatrics 73, 348-353.

Coleman RW & Provence S (1957): Environmental retardation (hospitalism) in infants living in families. Pediatrics 19, 285-292.

Department of Health and Social Security (1976): Fit for the future. Report of the Committee on Child Health Services, vol. 1, Chair: Prof. SDM Court, p. 50. London: HMSO.

Dobbing J (1990): Early nutrition and later achievement. Proc. Nutr. Soc. 49, 103-118.

Dobbing J & Smart JL (1974): Vulnerability of developing brain and behaviour. Br. Med. Bull. 30, 164-168.

Dowdney L, Skuse D, Heptinstall E, Puckering C & Zur-Szpiro S (1987): Growth retardation and developmental delay amongst inner-city infants. J. Child Psychol. Psychiatry 28, 529-541.

Drotar D (1985): New directions in failure to thrive. New York: Plenum.

Elmer E (1960): Failure to thrive: Role of the mother. Pediatrics 25, 717-725.

Ferholt JB, Rotnem DL, Genel M, Leonard M, Cary M & Hunter DEK (1985): A psychodynamic study of psychosomatic dwarfism: a syndrome of depression, personality disorder, and impaired growth. J. Am. Acad. Child Adolesc. Psychiatry 24, 49-57.

Field M (1984): Follow-up developmental status of infants hospitalized for nonorganic failure to thrive. J. Pediatr. Psychol. 9, 241-255.

Frank DA (1985): Biologic risks in 'non-organic' failure to thrive: diagnostic and therapeutic implications. In New directions in failure to thrive. Implications for research and practice, ed. D Drotar, pp. 17-26. London: Plenum.

Galler J (1987): Behavioral consequences of malnutrition in early life. In Human nutrition: A comprehensive treatise: Nutrition and behavior, ed. JR Galler, pp. 63-116. New York: Plenum.

Goldberg DP & Hillier VF (1979): A scaled version of the General Health questionnaire. Psychol. Med. 9, 139-145.

Goldberg D & Williams P (1988): A user's guide to the General Health questionnaire. Windsor: NFER-Nelson.

Graves PL (1976): Nutrition, infant behavior, and maternal characteristics: a pilot study in West Bengal, India. Am. J. Clin. Nutr. 29, 305-319.

Green WH, Campbell M & David R (19X4): Psychosocial dwarfism: a critical review of the evidence. J. Am. Acad. Child Adolesc. Psychiatry 23, 39-48.

Green WH, Deutsch SI & Campbell M (1987): Psychosocial dwarfism: psychological and etiological considerations. In Handbook of psychoneuroendocrinology, eds CB Nemeroff & PT Loosen, pp. 109-142. New York: Guilford.

Hamill PVV, Drizd TA, Johnson CL, Reed RB, Roche AF & Moore WM (1979): Physical growth: National Center for Health Statistics percentiles. Am. J. Clin. Nutr. 32, 607-629.

Hertzig ME, Birch HG, Richardson SA & Tizard J (1972): Intellectual measures of school children severely malnourished during the first two years of life. Pediatrics 49, 814-824.

Jordan MD (1986): The CDC anthropometric software package, version 3. Atlanta, GA: Centers for Disease Control.

Kanawati AA & McClaren DS (1970): Assessment of marginal malnutrition. Nature 228, 573-575.

Kitchen WH, Bajuk B, Lissenden JV & Yu VYH (1981): Intra-uterine growth charts from 24-29 weeks gestation. Aust. Paediatr. J. 17, 269-272.

Kotelchuck M (1980): Nonorganic failure to thrive: the status of interactional and environmental etiologic theories, pp. 29-41. Boston, MA: Children's Hospital Medical Centre

Kotelchuck M & Newberger EH (1983): Failure to thrive: a controlled study of familial characteristics. J. Am. Acad. Child Adolesc. Psychiatry 22, 322-328.

Krieger I (1974): Food restriction as a form of child abuse in ten cases of psychosocial deprivation dwarfism. Clin. Pediatr. 13, 127-133.

Leonard MF, Rhymes JP & Solnit AJ (:1966): Failure to thrive in infants: a family problem. Am. J. Dis. Child 111, 600-612.

MacCarthy D (1974): Effects of emotional disturbance and deprivation (maternal rejection) on somatic growth. In Scientific foundations of paediatrics, eds JA Davis & J Dobbing, pp. 56-67. London: Heinemann Medical.

MacCarthy D (1981): The effect of emotional disturbance and deprivation on somatic growth. In Scientific foundations of paediatrics, 2nd edn, eds JA Davis & J Dobbing, pp. 54-73. London: Heinemann Medical.

Marks HG, Borns P, Steg NL, Stine SB, Stroud HH & Vates TS (1978): Catch-up brain growth demonstration by CAT scan. Pediatrics 93, 254-257.

Martorell R (1985): Child growth retardation: a discussion of its causes and its relationship to health. In Nutritional adaptation in man, eds K Blaxter & JC Waterlow, pp. 13-29. London: John Libbey.

Martorell R, Mendoza F & Castillo R (1988): Poverty and stature in children. In Linear growth retardation in less developed countries, ed. J.C. Waterlow, pp. 57-73. Nestle Nutrition Workshop Series, vol. 14. Vevey/New York: Raven Press.

Mathisen B, Skuse D, Wolke D & Reilly S (1989): Oral-motor dysfunction and failure to thrive amongst inner-city children. Dev. Med. Child Neurol. 31, 293-302.

Miller HC & Hassanein K (1971): Diagnosis of impaired fetal growth in newborn infants. Pediatrics 48, 511-521.

Mitchell WG, Gorrell RW & Greenberg RA (1980): Failure-to-thrive: A study in a primary care setting. Epidemiology and follow up. Pediatrics 65, 971-977.

Money J (1992): The Kaspar Hauser syndrome of 'psychosocial dwarfism'. Buffalo, New York: Prometheus Books.

Money J, Annecillo C & Kelley JF (1983): Growth of intelligence: failure and catch-up associated respectively with abuse and rescue in the syndrome of abuse dwarfism. Psychoneuroendocrinology 8, 309-319.

Osborn AF (1987): Assessing the socio-economic status of families. Sociology 21, 429-448.

Osborn A & Morris TC (1979): Rationale for a composite index of social class and its evaluation. Br. J. Sociol. 30, 39-60.

Ounsted M, Moar V & Scott A (1982): Growth in the first year of life: effects of sex and weight for gestational age at birth. Dev. Med. Child Neurol. 24, 356-365.

Patton RG & Gardner LI (1962): Influence of family environment on growth: the syndrome of 'maternal deprivation'. Pediatrics 30, 957-962.

Pollitt E & Leibel RL (1976): Iron deficiency and behaviour. J. Pediatr. 88, 372-381.

Powell GF & Low J (1983): Behaviour in nonorganic failure to thrive. J. Dev. Behav. Pediatr. 4, 26-33.

Powell GF, Hopwood, NJ & Barratt ES (1973): Growth hormone studies before and during catch-up growth in a child with emotional deprivation and short stature. J. Clin. Endocrinol. Metab. 37, 674-679.

Ramey CT, Starr RH, Pallas J, Whitten CF & Reed V (1975): Nutrition, response contingent stimulation, and the maternal deprivation syndrome: results of an early intervention program. Merrill-Palmer Quart. 21, 44-53.

Rees DG, Henry CJK, Diskett P & Shears P (1987): Measures of nutritional status. Lancet i, 87-89.

Reyes MR, Valdecanas CM, Reyes OL & Reyes TM (1990): The effects of malnutrition on the motor, perceptual and cognitive functioning of Filippino children. Int. Disabil. Stud. 12, 131-136.

Rodier PM (1980): Chronology of neuro-development: animal studies and their clinical implications. Dev. Med. Child Neurol. 22, 525-545.

Rona RJ, Chinn S & Manning R (1989): The validity of reported parental height in inner city areas in England. Ann. Hum. Biol. 16, 41-44.

Rutter M (1985): Family and school influences on behavioural development. J. Child Psychol. Psychiatry 26, 349-368.

Sann L, Durand M, Picard J, Lasne Y & Bethenod M (1980): Arm fat and muscle areas in infancy. Arch. Dis. Child. 63, 256-260.

Siimes MA, Addiego JE & Dallman PR (1974): Ferritin in serum: diagnosis of iron deficiency and iron overload in infants and children. Blood 4, 581-590.

Singer LT & Fagan III JF (1984): Cognitive development in the failure-to-thrive infant: A three year longitudinal study. J. Pediatr. Psychol. 9, 363-383.

Skuse D (1989): Psychosocial adversity and impaired growth: in search of causal mechanisms. In The scope of epidemiological psychiatry. Essays in honour of Michael Shepherd, eds P Williams, G Wilkinson & K Rawnsley, pp. 240-263. London: Routledge.

Skuse D (1992): The relationship between deprivation, physical growth and the impaired development of language. In Specific speech and language disorders in children. Correlates, characteristics and outcome, eds P Fletcher & D Hall, pp. 29-50. London: Whurr.

Skuse D (1993a): Abuse and short stature. In ABC of child abuse, 3rd edn, ed. R Meadow, pp. 31-34. London: British Medical Association.

Skuse D (1993b): Emotional abuse and neglect. In ABC of child abuse, 3rd edn, ed. R Meadow, pp. 28-30. London: British Medical Association.

Skuse D (1993c): Epidemiological and definitional issues in failure to thrive. In Child and adolescent psychiatric clinics of North America, ed. J. Woolston, 2(1), 37-59. Philadelphia, PA: Saunders.

Skuse D, Wolke D & Reilly S (1992): Failure to thrive. Clinical and developmental aspects. In Child and youth psychiatry. European perspectives, vol. 2 Developmental psychopathology, eds H Remschmidt & M Schmidt, pp. 46-71. Gottingen: Hogrefe and Huber.

Skuse D, Chan S, Holder S, Stanhope R & Voss L (1993): Diagnostic criteria for 'psychosocial short stature': deriving and validating a diagnostic algorithm.

Skuse D, Pickles A, Wolke D & Reilly S (1993): Postnatal growth and mental development: evidence for a 'sensitive period'. J. Child Psychol. Psychiatr.

South East Thames Regional Health Authority (1984): Statistical and Operational Research Department. District Health Authority ACORN populations.

Spanier GB (1976): Measuring dyadic adjustment: New scales for assessing the quality of marriage and similar dyads. J. Marr. Fam. 38,15-38.

Spanier GB & Thompson L (1982): A confirmatory analysis of the dyadic adjustment scald. J. Marr. Fam. 44, 731-738.

Spitz RA (1945): Hospitalism: an inquiry into the genesis of psychiatric conditions in early childhood. Psychoanal. Study Child 1, 55-74.

Stanhope R, Adlard P, Hamill G, Amos J, Jones J, Skuse D & Preece M (1987): Physiological growth hormone (GH) secretion during recovery from psychosocial dwarfism. J. Endocrinol. 115, Suppl. 21.

Stanhope R, Adlard P, Hamill G, Jones J, Skuse D & Preece MA (1988): Physiological growth hormone (GH) secretion during the recovery from psychosocial dwarfism: a case report. Clin. Endocrinol. 28, 335-339.

Stewart AW, Jackson RT, Ford MA & Beaglehole R (1987): Underestimation of relative weight by use of self-reported height and weight. Am. J. Epidemiol. 125, 122-127.

Talbot NB, Sobel EH, Burke BS, Lindemann E & Kaufman SB (1947): Dwarfism in healthy children: its possible relation to emotional, nutritional and endocrine disturbances. N. Engl. J. Med. 236, 783-793.

Tanner JM & Thomson AM (1970): Standards for birthweight at gestation periods from 32 to 42 weeks allowing for maternal height and weight. Arch. Dis. Child 45, 566-569.

Taylor BJ & Brook CGD (1986): Sleep EEG in growth disorders. Arch. Dis. Child 61, 754-760.

Tietjen AM & Bradley CF (1985): The social networks and social support of married and single mothers in Sweden. J. Marr. Fam. 46, 489-496.

Touwen B (1976): Neurological development in infancy, pp. 1-143. London/Philadelphia: William Heinemann Medical Books Ltd.

Vietze P, Falsey S, O'Connor S, Sandler H, Sherrod K & Altemeier WA (1980): Newborn behavioural and interactional characteristics of nonorganic failure to thrive infants. In High risk infants and children. Adult and peer interactions, ed. T Field, pp. 5-23. New York: Academic Press.

Waldrop MF, Pedersen FA & Bell RQ (1968): Minor physical anomalies and behavior in preschool children. Child Dev. 39, 391-400.

Waldrop MF & Halferson CF (1971): Minor physical anomalies and hyperactive behaviour in young children. In The exceptional infant, vol. 2, ed. J Hellmuth. New York: Brunner/Mazel.

Waterlow J (1984): Current issues in nutritional assessment by anthropometry. In Malnutrition and behavior: Critical assessment of key issues, eds J Brozek & B Schürch pp. 77-90. Lausanne, Switzerland: Nestle Foundation.

Wechsler D (1974): Wechsler Adult Intelligence Scale revised. New York: Psychological Corporation.

Whitten CF, Pettit MG & Fischhoff J (1969): Evidence that growth failure from maternal deprivation is secondary to undereating. J. Am. Med. Wom. Assoc. 209, 1675-1682.

Widdowson EM (1951): Mental contentment and physical growth. Lancet i, 1316-1318.

Wolke D, Skuse D & Mathisen B (1990): Behavioral style in failure to thrive infants: a preliminary communication. J. Pediatr. Psychol. 15, 237-254.

World Health Organization (1972): Nutritional anaemias. Techn. Rep. Series, 503.

World Health Organization (1992): The ICD-10 classification of mental and behavioural disorders. Geneva: World Health Organization.

Yudkin PL, Aboualfa M, Eyre JA, Redman CW & Wilkinson AR (1987): New birthweight and head circumference centiles for gestation ages 24 to 42 weeks. Early Hum. Dev. 15, 45-52.

Zuckerman M & Lubin B (1965): Manual for the MAACL San Diego, CA: Educational and Industrial Testing Service.

Discussion

The aim of most questions was to obtain further information on Skuse et al.'s study. James wondered if an important cause of growth faltering could have been that the mothers of stunted infants introduced inappropriate foods too early, which could have led to metabolic disturbances. Skuse replied that he and his colleagues had studied dietary intakes in all infants, but that they had found no evidence in support of this hypothesis. On the whole, slightly more of the case infants were breastfed (75% vs 60%) and on average for a longer period (5 vs 3 months) than infants without growth faltering. No important differences in dietary intakes could be found between early and late faltering infants.

There was a negative correlation between a score for minor congenital malformations and the Bayley Mental Development Index, it accounted for about 10% of the variance, but did not distinguish the groups.

The population of South London, where this study was undertaken, is composed of groups of different ethnic backgrounds. Growth faltering was more common in infants from the Indian Subcontinent than among infants of African origin. Asking the parents whether they had wanted another child or not, did not result in different answers for different groups of children.

Waterlow asked Skuse what he thought of MacCarthy's (1981) idea that the hypothalamus and pituitary of neglected and malnourished infants was affected and that this led to stunting via a secondary growth hormone deficiency. According to Skuse, this could be so in cases of psychosocial dwarfism, but these are very rare.

Reference

MacCarthy D (1981): The effect of emotional disturbance and deprivation on somatic growth. In Scientific foundations of paediatrics, 2nd edn, eds JA Davis & J Dobbing, pp. 54-73. London: Heinemann Medical.