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7. Two-year follow-up study

Diet: Few changes were found in the frequency of consumption of foods typical of the macrobiotic diet, but there were some changes in the consumption of animal products, especially dairy products and fish, as well as vegetable oil and vitamin D supplements (see Table 3). However, only 6% of those regularly consuming fish had adopted the advice of eating fatty fish (Smeets et al., 1992).

Growth: Growth velocity, expressed as change in SDS (calculated from the P50 and SD of the cross-sectional Dutch reference curve) of the macrobiotic children in various age groups is presented in Table 4. A marked growth depression for height was observed in the children who at the time of follow-up were 2 years old. For children 3-5 years of age, a slight but significant positive change in SDS had occurred for both weight and height. In children 6-9 years of age, no changes in SDS occurred except a slight but significant positive trend towards the P50 for height in girls. Thus, these data confirm our earlier observations concerning linear growth retardation during the first two years of life and only partial catch-up (for weight and arm circumference) during the following years.

Relation to diet: The frequency of consumption of animal products (i.e. fish and dairy products) was positively associated with height (P < 0.05) (cross-sectional analysis). In those children whose consumption of fish and dairy products had increased since 1985, linear growth was significantly faster (P < 0.05) than in other macrobiotic children (longitudinal analysis) (Smeets et al., 1992). A marked example of catch-up growth in weight and height after the introduction of dairy products and fatty fish in three macrobiotic siblings aged 3, 5 and 8 years is shown in Figs 3a - c.

Table 3. Consumption frequency of selected foods by children in macrobiotic families in 1985 (n = 173) and in 1987 (n = 152)

Table 4. Change in SDS per year of macrobiotic children in different age groups

Significance of changes (paired t-test):
^a P < 0.01;
^b P< 0.001;
^c P < 0.05.

8. Discussion

The results of these studies on growth of children on macrobiotic diets have provided the following answers to our research questions:

1. Timing of growth faltering in children fed macrobiotic diets: A small but significant intrauterine growth retardation was indicated by a lower birth weight of macrobiotic children. Growth velocities in height and weight were most depressed between 8 and 14 months of age. Between 14 and 18 months of age, growth stabilized parallel to the 10th centile of the Dutch references, after which some, but incomplete catch-up growth was observed for weight and arm circumference. No catch-up growth was observed for height.

2. Nutritional factors associated with deviations in growth in children on macrobiotic diets: Low birth weight was associated with a low frequency of consumption of fish and dairy products by the mother. SDS of weight, height and arm circumference were significantly higher in children from families consuming dairy products regularly compared to children from families which rarely used dairy products. The increase in weight and arm circumference between 4 and 18 months of age was associated with both the energy intake and protein content of the diet. Growth in length was only associated with the protein content of the diet.

3. Effect of modification of the macrobiotic diet on growth: Catch-up growth in height and weight occurred after increased consumption of fish and dairy products. Our findings demonstrate that, provided unfavourable nutritional circumstances change, catch-up growth in height is still possible even at the age of 8 years, even though the original growth channel may not be attained.

Our data demonstrate that the observed linear growth retardation in children on macrobiotic diets is caused by nutritional deficiencies alone. By using a matched control group in the mixed-longitudinal study, confounding factors as sex, parity, socio-economic level and region of residence were excluded. The educational level of the parents was high, and 92% of macrobiotic infants grew up in a two-parent family (control group: 100%). No indications of any other adverse circumstances such as prevalence of infectious diseases were observed.

Fig. 3. Growth in weight and height of three macrobiotic siblings in the Netherlands before and after the modification of the macrobiotic diet by introducing dairy products and fatty fish (shown as 'A').

The associations observed in this study of linear growth with consumption of dairy products and fish suggest the importance of protein, and particularly animal protein in the diet. It has been suggested that height is affected most by protein deficiency (Ashworth & Millward, 1986; Malcolm, 1978) whereas weight is more sensitive to a low energy intake (Malcolm, 1978; Waterlow, 1978). Our data seem to support this hypothesis. However, although we can analyse the separate effects of various nutrients in a regression analysis, in real life we cannot disentangle the influence of the protein content of dairy products and fish from the influence of the extra energy, calcium, zinc, or changing bioavailability of iron and other nutrients, which are supplied simultaneously with the consumption of these products. Furthermore, a low utilization of the protein in the macrobiotic diet, due to its low energy and high fibre content, might have played a role in limiting linear growth. Finally, our data also support the notion that linear growth retardation is related to inadequate weight gain (Waterlow, 1991): growth velocity in height was lower for the wasted macrobiotic infants compared to the non-wasted macrobiotic infants in the mixed-longitudinal study. Thus, this suggests that sufficient energy is also needed for normal linear growth.

Catch-up growth is a self-correcting response which occurs as soon as an adequate diet is provided (Ashworth & Millward, 1986). Thus, catch-up growth may serve as a retrospective diagnostic tool (Bergmann & Bergmann, 1978). The catch-up growth in height in children whose diet has been extended with dairy products and fish suggests that before modification the diet was nutritionally inadequate. As discussed above, we cannot tell which nutrients, or combinations of nutrients and absorption enhancing factors were responsible for the linear catch-up growth after extension of the diet with dairy products and fish. The influences of separate nutrients can only be studied by intervention. The fact that catch-up growth in height even occurred in macrobiotic children of 8 years of age indicates that also for older children the macrobiotic diet continues to be nutritionally inadequate.

The importance of dairy products is also illustrated by comparison of anthropometric data of children on facto-vegetarian diets and children on macrobiotic diets. In macrobiotic children, whose diet lacks dairy products, stunting is combined with a normal weight for height, whereas children on facto-vegetarian diets, who receive dairy products, show some degree of wasting but virtually no stunting (Van Staveren et al., 1985; Dwyer et al., 1980).

References

Ashworth A & Millward DJ (1986): Catch-up growth in children. Nutr. Rev. 44,157-163.

Bergmann RL & Bergmann KE (1978): Nutrition and growth in infancy. In Human growth, Vol. 3. Neurobiology and nutrition, eds F Falkner & JM Tanner, pp. 331-360. New York/London: Plenum Press.

Central Bureau of statistics (1983): Gegevens over bevolking en beroepsbevolking van 15-64 jaar naar geslacht, leeftijd, burgerlijke stoat en niveau van het hoogst behaalde onderwijsdiploma. The Hague, The Netherlands: Arbeidstelling. Central Bureau of statistics.

Dagnelie PC, van Staveren WA, van Klaveren JD & Burema J (1988): Do children on macrobiotic diets show catch-up growth? A population-based cross-sectional study in children aged 0-8 years. Eur. J. Clin. Nutr. 42, 1007-1016.

Dagnelie PC, van Staveren WA, Verschuren SAJM & Hautvast JGAJ (1989a): Nutritional status of infants aged 4 to 18 months on macrobiotic diets and matched omnivorous control infants: a population-based mixed longitudinal study. L weaning pattern, energy and nutrient intake. Eur. J. Clin. Nutr. 43, 311-323.

Dagnelie PC, van Staveren WA, Vergote FJVRA et al. (1989b): Nutritional status of infants aged 4 to 18 months on macrobiotic diets and matched omnivorous control infants: a population-based mixed-longitudinal study. II. Growth and psychomotor development. Eur. J. Clin. Nutr. 43, 325-338.

Dagnelie PC, van Staveren WA, Vergote FJVRA, Dingjan PG, van den Berg H & Hautvast JGAJ (1989c): Increased risk of vitamin B-12 and iron deficiency in infants on macrobiotic diets. Am. J. Clin. Nutr. 50, 818-824.

Dagnelie PC, Vergote JVRA, van Staveren WA et al. (1990): High prevalence of rickets in infants on macrobiotic diets. Am. J. Clin. Nutr. 51, 201-208.

Dwyer JT, Andrew EM, Valadian I & Reed RB (1980): Size, obesity, and leanness in vegetarian preschool children. J. Am. Diet. Assoc. 77, 434-439.

Gerver WJM (1988): Measurement of the body proportions in children: the Oosterwolde study. Dissertation. Groningen: State University, Department of Medicine.

Kushi M (1987): The book of macrobiotics, the universal way of health, happiness and peace. Tokyo/New York: Japan Publications.

Malcolm L (1978): Protein energy malnutrition and growth. In Human growth, vol. 3. Neurobiology and nutrition, eds F Falkner & JM Tanner, pp. 361-371. New York/London: Plenum Press.

Netherlands Nutrition Council (1981). Nederlandse voedingsmiddelentabel, aanbevolen hoeveelheden energie en voedingsstoffen. The Hague, The Netherlands: Voorlichtingsbureau voor de Voeding.

Roede MJ & Van Wieringen JC (1985): Growth diagrams 1980. Netherlands third nation-wide survey. Tijdschr. Sociale Gezondheidszorg 63, Suppl., 1-34.

Schürch B & Scrimshaw NS (eds) (1987): Chronic energy deficiency: consequences and related issues. Lausanne, Switzerland: IDECG.

Shull MW, Reed RB, Valadian I, Palombo R, Thorne H & Dwyer JT (1977): Velocities of growth in vegetarian preschool children. Pediatrics 60, 410-417.

Smeets FWM, Dagnelie PC, Van Staveren WA, Van Kuik MJJA, Matze M & Schlatmann AM (1992): Acceptatie van voedingsadviezen door Nederlandse macrobiotische gezinnen en groeisnelheid van macrobiotisch gevoede kinderen tot en met 9 jaar. Tijdschr. Sociale Geneeskd. 70, 227-233.

Stichting NEVO (1986). Nederlands voedingsstoffenbestand 1986-1987 The Hague, The Netherlands: Voorlichtingsbureau voor de Voeding.

Van Staveren WA, Dhuyvetter JHM, Bons A, Zeelen M & Hautvast JGAJ (1985): Food consumption and height/weight status of Dutch preschool children on alternative diets. J. Am. Diet. Assoc. 85, 1579-1584.

Waterlow JC (1978): Observations on the assessment of protein-energy malnutrition with special reference to stunting. Courrier 28, 455-460.

Waterlow JC (1991): Reflections on stunting. Int. Child Health, II (2) 25-35.

Willems MAW, De Graaf TW, Katan MB, Hollman PCH, Van Staveren WA & Van de Bovenkamp P (1987): Voedingsmiddelenanalyses van de Vakgroep Humane Voeding en het Rijks-Kwaliteitsinstituut voor Land - en Tuinbouwprodukten. Deel VIII. Alternatieve voedingsmiddelen. Wageningen: Vakgroep Humane Voeding en RIKILT.

Discussion of papers by Allen, Neumann & Harrison and Dagnelie et al.

The CRSP studies in Mexico and Kenya and that on vegans in Holland suggested a relation between stunting and a diet of poor quality. As a preliminary, technical questions were raised about the nature of the correlations: do they apply across individuals as well as groups? are the dietary intakes normally distributed? would the correlations be improved by log transforms? In the vegan study the comparison was made with matched controls, but it is impossible to match for more than a small number of variables: for example, the macrobiotic children had lower birth weight. Therefore the conclusion can only be a negative one: that the particular variables that were matched did not explain the differences between the groups.

Granted that the correlations are real, the term 'poor quality diet' covers many potential deficiencies. The discussion centered first round the question of animal protein. In Allen's report it was stated that stunting occurred in spite of adequate intakes of protein and amino acids. It was pointed out, however, that adequacy of protein for children has always been calculated on the basis of the amount needed for weight gain. No account has been taken of height gain; in fact, we simply do not know what the requirements are for growth in height. Large numbers of people in the world live on mainly vegetable diets, and it has been argued that it is not necessary to have any animal protein in the diets of children (Town). Again the question arises: necessary for what? Apart from effects on linear growth, it was pointed out that in the CRSP studies measurements of cognitive function repeatedly showed a relation with animal products in the diet (Neumann).

If animal protein is necessary, how much? The Mexican children received only about 80 kcal/d from milk, eggs and meat (Allen). In the vegan children, breast-feeding seemed to delay the onset of stunting. The nutrient content of the mother's milk was the same as that of the controls at 3 months, but it was lower at 1 year (van Dusseldorp). It was when supplementary foods were given that growth began to fall off. Nevertheless, it cannot be assumed that breast-fed children never become stunted; it depends on whether lactation is adequate in undernourished mothers-a subject that is still somewhat controversial.

The discussion moved on to the question of how the requirements for linear growth could be established. As far as concerns protein, the classical nitrogen balance method is clearly not applicable. The only solution would seem to be experimental intervention. Early feeding trials were recalled, going back to those of Corry Mann, Boyd Orr and Aykroyd in the 1930s. All these showed some effect on linear growth of foods containing good quality protein, particularly milk. Indeed, it was these observations that suggested the sulphur amino acid hypothesis referred to in discussion of the paper by Golden. However, except for the study in India by Aykroyd & Krishnan (1939), in which calcium lactate was given, all the trials showing an effect on growth involved foods such as milk or meat, and not single nutrients. Therefore the stimulation of growth could not be attributed unequivocally to good quality protein; it could equally result from the micronutrients associated with protein, such as iron, trace elements and vitamin B₁₂. Moreover, amino acids may enhance the bioavailability of some minerals, and vegetable diets are likely to contain more phytate and fibre which have the opposite effect. For example, the macrobiotic diet provided more iron than the control diet, but a higher proportion of the children were anaemic because they received no haem iron. In Mexico the diet was very high in calcium but probably very little of it was absorbed.

The question of bioavailability was considered to be particularly important in relation to zinc, especially since in the CRSP studies zinc intakes were frequently low. The question was raised, but not resolved, of the possibility of absorption of zinc from the colon. Another point is that zinc plays a special role in the response to infections, and it has often been suggested that infections and infestations are a major factor in the production of stunting. The requirements of nutrients for growth may be different from the requirements for counteracting infection, so it could be dangerous to extrapolate to the Third World estimates of requirements obtained in affluent countries. It was also pointed out that in many experimental studies male animals were found to be more susceptible to zinc deficiency than females (Golden). In the CRSP studies, girls seemed to do better than boys and get fewer infections in the preschool years (Neumann).

Lastly, it was suggested that fat intake, which is low in the vegan and Third World diets, may be important because there is evidence of obligatory fat oxidation in the postabsorptive state (Jéquier).

The conclusion from these three studies, and from earlier intervention trials, is that stunting occurs in children whose diets are low in animal protein and in factors associated with animal protein in foods. This conclusion can best be tested by intervention studies. The question was not discussed, whether there would be any value in setting up studies designed to elucidate which particular nutrients are involved. From a scientific point of view such studies would be very important. From the practical point of view, since people eat foods not nutrients, the lesson would be that there is a need for improving the quality as well as the quantity of the diets of preschool children.

Reference

Aykroyd WR & Krishnan BG (1939): A further experiment on the value of calcium lactate for Indian children. Indian J. Med. Res. 27, 409-412.

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