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close this bookChronic Energy Deficiency : Consequences and Related Issues (International Dietary Energy Consultative Group - IDECG, 1987, 201 pages)
close this folderA critical view of three decades of research on the effects of chronic energy malnutrition on behavioral development
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View the document1. Background
View the document2. The main-effect model
Open this folder and view contents3. Deficiencies of the main-effect model
View the document4. Suggestions for future research
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2. The main-effect model

Early studies of the effects of prenatal and early postnatal undernutrition on behavioral development were guided by a static main-effect model, which has its roots in the biomedical model of disease causation. In its simplest form the biomedical model is a reductionistic approach in which agent and disease are conceptualized as causally and linearly related (ENGEL, 1979). A simple version of this model in relation to the hypothesis of an adverse effect of early protein energy malnutrition on mental development is represented in the following bivariate equation:

BD = f (NR)

where BD = behavioral deviation and NR = nutritional risk factor (e.g., wasting during the second six months of life). That is, the probabilities of a delay in behavioral development will vary as a function of severity and timing of the nutritional disorder.

This main-effect model can be traced in the developmental literature to the early-trauma, later-deficit hypothesis, which goes back to the mid-19th century (LITTLE, 1982). A basic assumption is that exposure to biological risk factors2 during critical periods of brain growth results in structural lesions in the brain, which in turn leave sequelae such as mental retardation. The emphasis is on the measurement of an input (e.g., chronic fetal hypoxia) and an output (e.g., IQ; see, for example NAEYE, 1987). Besides epidemiological studies using large sample sizes and establishing bivariate correlations, clinical trials and the measurement of a dose-response are sharp expressions of this conceptual and methodological approach.

2 In the present context risk is defined as the probability of an individual's developing a given disease or experiencing a health-status change over a specified period of time (KLEINBAUM, KUPPER and MORGENSTERN, 1982). Biological risk factors are adverse environmental circumstances or events that occur in pregnancy (e.g., intra-uterine growth retardation), at birth (e.g., hypoxia), during lactation, or during the preschool period (e.g., lead intoxication) and increase the probability of diverting a child's growth and developmental trajectory from a course typically followed when physiological and emotional needs are adequately met.

The main-effect model does not account for either the social context in which development occurs, for the previous and subsequent health history of an individual, or for the interactions3. Most importantly, the model, within the context of developmental research, has failed to incorporate two critical developmental characteristics: plasticity and canalization (MCCALL, 1981). Plasticity refers to the notion that, within the limits of individual differences and structural functional capacities, the organism has the elasticity or flexibility to be influenced by, and adapt to, new environmental contingencies (KUO, 1967; GOLLIN, 1981). Canalization refers to the organism's characteristic of following a species-specific developmental path that allows it to withstand a great amount of environmental stress before any significant deviation is observed4.

3 There are, among others, two categories of interactions that have been identified in human developmental research (RUTTER, 1983). One refers to the interactions (synergistic or antagonistic) between variables outside the organism that affect developmental outcome. The other (ordinal interactions) refers to interactions between an environmental variable and an organismic variable that determine different effects from similar experiences in different people, or from similar experiences in the same people at different ages.

4 At least three different definitions of canalization have been advanced (see GOTTLIEB, 1983). In the present context reference is made to canalization as defined by the developmental geneticist WADDINGTON (1971).

The main-effect model guided correlational and experimental (or quasi-experimental) research in the field and in the laboratory. Correlational studies measured the associations between retardation in physical growth and delays in mental development (i.e., DQ or IQ; KLEIN et al., 1972) or in tests of specific cognitive function (CRAVIOTO, DELICARDIE and BIRCH, 1966). Height-forage, weight-for-age or weight-for-height were taken as indicators of present nutritional status or of nutritional history. Statistically significant correlations between, for example, height-for-age and low intelligence test performance were interpreted to mean that exposure to undernutrition increased the probabilities of developmental risk. Experimental studies of nutrition supplementation measured the variance in developmental outcome accounted for by the variance in dietary intake (Jogs and POLLITT, 1984).

A striking illustration of the influence of the main-effect model on the conduct and interpretation of research on undernutrition and behavior was the calculation of regression coefficients to measure the changes in protein intake presumably required for a given change in an intelligence quotient (TAYLOR and SELOWSKY, 1973). This econometric analysis might not be representative, but it does convey the flavor of the conceptual approach that dominated the field.

Animal and basic research, and influential theoretical concepts such as the critical period of behavioral development (SCOTT, 1962) 5, strengthened the face validity 6 of the main-effect model. The critical period hypothesis in connection with a nutritional insult predicted that protein and energy malnutrition during a time of accelerated brain growth (i.e., the first 24 months of life) resulted in a deviation from the normal trajectory of central nervous system development (DOBBING and SANDS, 1979). Implicit in this definition is the idea that past a certain "critical point" (duo, 1967), there is little chance for rehabilitation from the insult produced by undernutrition. A corollary is that past such critical point of brain growth the presence of undernutrition would not have severe developmental consequences.

5 A critical period is defined as a limited period during development in which a particular stimulus will have a profound effect upon the organism. The same stimulation before or after this interval will have little or no effect upon the organism.

6 Face validity is a subjective evaluation by judges as to what a measuring device appears to measure.

Experimental and basic research data in part supported the main-effect model and fed into the critical period hypothesis. Experimentally-induced malnutrition in early life on laboratory rodents (BARNES et al., 1966; FRANKOVA and BARNES, 1968) and pigs (BARNES, MOORE and POND, 1970) adversely affected learning in later development. Early undernutrition in rats retarded the division process of every type of proliferating brain cell and delayed migration of cells and myelination (WINICK and NOBLE, 1966). Curtailment of brain cell division was also documented in infants who died of severe undernutrition (WINICK and ROSSO, 1969).