CHAPTER 2 - BIOLOGICAL BASIS FOR INTERPRETATION

To provide a frame of reference for subsequent discussions, Figures 1 and 2 summarize the essential features of human growth and development relevant to the present report. These Figures provide the basis for definitions used in the report and for establishing areas of agreement and areas where further clarification is needed.

Figure 1. Influence of diet and other environmental factors (outside box) on physiological processes in children (inside box) and outcomes (on right, outside box, underlined).

Figure 1 shows certain physiological processes during growth and development, and ways in which a constraining environment affects these. First, inadequacy of dietary supply can reduce nutrient availability to cells, and impair cellular function, thus affecting susceptibility and response to infection, and reducing growth. However, cell function is also regulated internally, under the influence of both genetic factors and previous environmental influences - the latter for example through altered patterns of tissue development. Further, while susceptibility to infection and response to it are influenced by the competence of the body's immune system (a function of tissue activities) one of the responses to infection is itself an effect on the regulation of cellular activity. Thus, for example, the formation of new tissue (hence growth) might be reduced by: (a) an inadequacy of dietary intake, or (b) by an inhibition of cellular processes responsible for growth, secondary to an infectious process, or (c) by other regulatory influence, or (d) a combination of these.

The Figures suggest also that the observed variation in growth rates of young children, or of achieved size in older children, will be derived from the interaction of genetic and environmental factors. Importantly, current environmental effects become a part of the regulatory memory of the body. Consequently, failure to grow at normal stages of development may represent a missed opportunity with a lasting effect observed as stunting at older ages.

Figure 1 portrays a postulated effect of an unfavorable environment upon psychological development While it is not intended to imply a complete absence of effects mediated through tissue growth mechanisms (e.g. brain development), the figure emphasizes the fact that development of brain function involves interactions with the social environment of the child. These interactions may be influenced by the adequacy of energy intake and utilization for physical activity, such as for play, as well as household effects on child care and other family functions. While both growth failure and impaired psychological development may originate from the same constrained environment, they may have unrelated causal pathways. Thus achieved size would be seen as a marker of the environment that produced both growth failure and impaired psychological development. But small size itself would not be seen as a cause of impaired psychological development; and the two would not necessarily move together as the child matured (McGuire and Austin, 1987).

In considering 'underweight' and 'overweight' (as indexed by measures such as weight-for-length or arm circumference), the considerations differ somewhat from those of achieved body size (indexed by achieved length). Body weight is subject to genetic influences and in that sense fits the schema of Figure 1. However, it is also influenced by past and current energy balance - the balance between energy intake and energy expenditure, as displayed in Figure 2. Fatness and thinness (e.g. as indexed by weight-for-length in Fig. 2) reflect the magnitude of body energy stores or reserves. These may increase or decrease as a result of unbalanced changes in either energy intake or energy expenditure. Both intake and expenditure may be seen as influenced by both internal factors (e.g. regulation of intake, regulation of tissue metabolism) and environmental factors (e.g. food available for consumption by the individual, mandatory physical activity, socially desired physical activity, infection as a cause of anorexia, and infection (fever) as a cause of increased energy expenditure). Weight-for-length is generally seen as a measure of current influences on the state of the body, as contrasted to achieved size which is seen as a measure of past influences, or in the young actively growing child, of the combination of past and current influences.

Both Figures 1 & 2 emphasize the fact that neither achieved size nor weight-for-length is specific in relation to causation. While anthropometry is extremely useful, it must be interpreted with care.

One point regarding interpretation and use of anthropometry is now being re-emphasized: the importance of taking account of age (Martorell, 1989; Martorell and Habicht, 1986; Lutter et al., 1990). This is because causes of growth failure are generally age-specific; and the required interventions often depend on age. Different factors affecting infant and child growth need to be borne in mind. At birth, infant weight and length are determined by maternal factors - including nutrition - and gestational age, i.e. whether the infant is full term. Interpretation of birth weight must take these into account. During the first 4 to 6 months, infant feeding practices and maternal health (and ability to take care of the baby) are the main influences on growth; growth failure at this early stage, less common than later, must be interpreted in this light. From about 4-6 months through two years of age, weaning practices and exposure to infectious disease have a major effect. As the age of the child increases, household access to food may have more importance.

Figure 2. A portrayal of the association between weight-for-length and the processes underlying energy balance.

Almost all of the growth retardation documented in studies carried out in poor societies has its origins in the first 2 or 3 years of life. Studies in Guatemala (Martorell, Rivera and Kaplowitz, 1990) indicate that growth failure in early childhood is not recuperated through catch-up growth in later childhood and adolescence in males or females. In a similar prospective study from India, catch-up growth was not observed in males (Satyanarayana et al., 1980) but partial catch-up growth was observed in females (Satyanarayana et al., 1981). In both Guatemala and India, growth in length achieved between 5 years of age and adulthood was similar or greater than observed in developed societies. Cross-sectional studies from other areas of the developing world also suggest that growth retardation primarily occurs in early childhood and that catch-up growth does not occurr (Hussain et al., 1985; Billewicz and McGregor, 1982; Hauspie et al., 1980).

Across populations of different socio-economic status the differences in growth velocity and size are above all caused by environmental circumstances and not by ethnic differences in growth potential, at least up to five years of age (Martorell, 1985). This is not incompatible with the fact that within a well-nourished population the sizeable variability in growth and size is indeed genetic. One consequence is that where there are few detrimental influences on growth, small children will be small for genetic reasons and this smallness may have had no deleterious causes or future consequences. In contrast, in the deprived populations of concern to this report, environmental factors are a prime determinant of growth failure. While dietary inadequacy alone is not usually the prime determinant of growth failure, it is often an associated contributing factor along with repeated episodes of infectious disease (Martorell, 1989; Chen, 1983). Where stunting³ is prevalent, the causes are likely to be found in environmental factors characterized by generalized conditions of dietary inadequacies, infectious disease and social deprivation. Where stunting prevalence is low, the causes of smallness may lie in normal genetic variation or in factors operating to the detriment of the individual child (including the effects of malnutrition and infection). It follows that the implications and interpretations of stunting observed in the individual child differ depending upon the circumstances in which it is observed.

³ Stunting is used to denote reduced body length in relation to a reference standard. Usually reduced body weight will also be seen.

The theoretical model represented in Figure 1 is intended to clarify thinking on a number of general issues related to the uses of anthropometry in varied contexts. Essentially, the whole report is concerned with how measures of one outcome - growth - can be used to draw useful conclusions on complex biological processes and their determinants; and how to relate these to decisions on interventions to improve the determinants and outcomes. Moreover, of the various outcomes, growth is not necessarily the most important - it is still an indicator.

In this report, relative risk of an undesirable outcome (e.g. those shown in Figure 1) is regarded as marked by one or more of the anthropometric indices. As the index changes, the risk of undesirable outcome changes. It is not a necessary assumption that the actual index recorded (achieved size, current growth rate or weight-for-length) is on the direct causal pathway of the outcome. Different risks (for instance risk of morbidity, risk of cognitive impairment, risk of mortality or risk of other functional impairment) may be marked by the same index (for example length for age). Two important implications arise: (a) seldom is there a sharp break in the risk curve denoting a change from a 'no risk' to a 'risk' situation (rather the change is likely to be progressive although the slope of the curve may change with the level of the index), and (b) the level of risk associated with a given level of the index will depend upon which risk is being assessed and the circumstances in which it is assessed. As a generalization, the more deviant is the anthropometric measure for an individual, the more likely it is that significant risk (of many outcomes) is present. In some applications discussed in Chapters 4-7, the goal is to assess or monitor population risk. In its simplest form this is done by estimation of the proportion (prevalence) of individuals with index measurements falling below cut-off points accepted as marking a selected level of risk.⁴

⁴ Given that risk is a continuous variable, this is a conceptually limited but practically feasible approach. Preferred approaches include examination of total distributions and their displacement from reference distributions coupled with estimations of risk probability functions (Mora, 1989).

In summary, three biological considerations have major impact upon the use and interpretation of anthropometric indices. The first principle is that interpretation of length varies with age of the subject. In very young children (particularly in the first year but perhaps through the first two years of life) achieved size (length) may reflect a process of failing to grow. After about two years it is likely to reflect a state of having failed to grow. (See Annex A). The state of having failed to grow continues to mark risk of detrimental outcomes (morbidity, mortality, psychological development, etc.) but no longer suggests that interventions will improve growth status. The second principle is that indices of weight in relation to length reflect current under- or over-nutrition (relative thinness or fatness) regardless of age. Major deficits in weight-for-length are suggestive of short-term risk of morbidity or mortality; in this case, the anthropometric index is likely to respond to immediate intervention. The third principle is that achieved size may be seen as a marker of the environment in which growth failure occurred and, as such, a marker of other risks associated with that environment. In this sense, achieved size in an older child might be seen, for example, as a marker of risk for a younger sibling.