1145 A.F.P.
levels IN INDIAN CHILDHOOD CIRRHOSIS AND OTHER DISORDERS
quate for a test of the hypothesis that nutritional intervention can accelerate fetal growth. Division of Epidemiology, School of Public Health, Columbia University, 600 West 168th Street, New York, N.Y. 10032, U.S.A.
abnormal A.F.P. levels. A basic defect in thus seems unlikely in i.c.c.
MERVYN SUSSER ZENA A. STEIN
hepatocyte maturation p. 815), by failing to my criticisms and by raising irrelevant issues, has supported the contentions I made (Oct. 11, p. 704). He omitted discussion of the fatal flaw in Susser and Stein’s Dutch-famine
SIR,-Professor Thomson (Oct. 25,
answer
Institute of Postgraduate Medical Education and Research,
Punjab University Chandigarh, India.
S. SEHGAL B. N. S. WALIA
MATERNAL NUTRITION AND LOW BIRTH-WEIGHT
SIR,-Your editorial on maternal nutrition (Sept. 6, p. 445) evoked a response (Oct. 11, p. 704) from our respected friend and colleague, Benjamin Pasamanick, whose work provided an early stimulus for recent developments in prenatal epidemiology, including the area of nutrition. Please allow us to comment once more, for Dr Pasamamck appears to have nnsread our findings and our interpretations of the effects of the Dutch famine. Our letter of Oct. 4, (p. 664) must have indicated that we did not conclude, as to his distress he thinks we did, that maternal starvation during the famine was trivial or had trivial effects. On the contrary, we believe that nowhere is stronger evidence to be found in humans of the profound effects of severe prenatal nutritional deprivation on fetal growth and survival. In our cohort analysis of mortality, in particular, the effects of prenatal experience, some nutritional and some unspecified, were of a magnitude and extent that have not previously been shown. Dr Pasamanick says that the uneven availability of food to different social classes invalidates our study (and C. A. Smith’s study) of the famine. If this is so, it undermines much of the direct available evidence in favour of his view that maternal malnutrition has ill effects on birth outcome. We do not agree, however, that food availability affected the validity of the results of our study of the famine. Indeed, we did not simply "acknowledge" the maldistribution but took pains to try and demonstrate it. Our pre-existing suspicion that food was unevenly available was reinforced when we found that the survivors of cohorts conceived at the height of the famine had higher i.Q. scores than the survivors of other cohorts. This advantage could be accounted for, we were able to show, by a decline in fertility during the famine that was greater in the lower classes than in the higher, and by the consequent change in the social-class composition of the survivors in the affected cohorts. Naturally, in subsequent analyses we controlled for these differences wherever indicated. The results of the Dutch famine study lead us to the conclusion that in previously well-nourished women the effects of maternal nutritional deprivation on fetal growth are appreciable, but only below a critical level of nutrient intake. Other studies now in progress in Harlem, New York City,’ and in Guatemala,2in our view, are tending to support a corollarythat is, prenatal nutritional supplementation promotes fetal growth only under specifiable conditions, most of which can be related to poor nutritional state of the mother. Within a year or two, further results from a study in Bogota will become available to test this position. The study in Taiwan of the late Bacon Chow, referred to by Dr Pasamanick, perhaps also may help to clarify the issues when fully analysed, but this is anlikely because the numbers in that study are probably not adeRush, D., Stein, Z., Christakis, G., Susser, M. in Nutrition and Fetal Development (edited by M. Winick); vol. 2, p. 95. New York, 1974. 2. Habicht, J. P., Yarbrough, C., Lechtig, A., Klein, R. E. ibid. p. 127. 1.
study-i.e., the food consumed in the "famine areas" was not randomly distributed. The most parsimonious explanation for the lowest mean birth-weights of 3000 g is that the upper strata, the Nazi collaborators, and others secured sufficient food to conceive, maintain pregnancies, and obtain live births. Since this criticism was not answered, presumably Professor Thomson now agrees that the entire study is a failure. However, he goes on to make the point that "famine" and control areas had been equally affected as far as perinatal mortality was concerned. Since I stated that the "control" areas had also been starved (the mean calorific intake fell to below 1300 calories), this is just what would have been predicted. As for Professor Thomson’s study in Aberdeen, he does not reply to the criticism that his sample was above the malnourishment threshold. The lowest occupational group had a mean intake above 70 g and this was approximately only 10 g below the highest group. Again, he did not reply and thus apparently accepts the validity of this point. He merely indicates that the source of the protein was not fish. Since I was not able to ascertain from the pertinent paper what the source was, we remain in the dark because Professor Thomson has failed to indicate the content of the only remaining fact which deserves discussion. State of New York
Department of Mental Hygiene, Division of Mental Retardation and Children’s Services, 44 Holland Avenue, Albany, N.Y. 12229, U.S.A.
BENJAMIN PASAMANICK
INTRAUTERINE NUTRITION AND BABIES’ HAIR SIR,-Professor Bradfield has developed a simple method’I for using hair-root morphology as an indicator of malnutrition in pre-school children and adults. He and his colleagues suggest (Nov. 8, p. 928) that the technique might also be applied to the antenatal period in that the morphology of maternal hair could be used to predict the risk of a low-birth-weight delivery. We have used their technique in the perinatal period to study the effects of intrauterine nutrition on the hair of babies. We found that at term the hair-roots of the boys were often in a resting (telogen) phase even when they appeared well nourished. We were, therefore, able to compare the effect of "intrauterine malnutrition" in girls only. The hair-root morphology was studied of 13 girls born at term of birth-weight appropriate for their gestational age (weight >3-0 kg, gestation 37-41 completed weeks) and 14 light-for-dates (weight < 2.5 kg) term girls. In the hair sample which was taken in the first 24 hours after birth there was no significant difference between the percentage of growing roots (anagen) in the two groups of babies. However, there was a highly significant difference (p < 0-001) between the hair-root diameter of the light-for-dates babies (8-22 +_ 3.1xx 10-zmm) and the appropriate-for-dates babies (13-8+3-7x10’mm). This difference remained significant (P < 0 - 01) when the babies were further subdivided into Caucasian and Asian groups. It appears, at least in girls, that hair-root morphology is a sensitive indicator of intrauterine nutrition and we wonder 1.
Bradfield,
R. B.
Am. J.
clin. Nutr.
1972, 25, 720.
levels IN INDIAN CHILDHOOD CIRRHOSIS AND OTHER DISORDERS
quate for a test of the hypothesis that nutritional intervention can accelerate fetal growth. Division of Epidemiology, School of Public Health, Columbia University, 600 West 168th Street, New York, N.Y. 10032, U.S.A.
abnormal A.F.P. levels. A basic defect in thus seems unlikely in i.c.c.
MERVYN SUSSER ZENA A. STEIN
hepatocyte maturation p. 815), by failing to my criticisms and by raising irrelevant issues, has supported the contentions I made (Oct. 11, p. 704). He omitted discussion of the fatal flaw in Susser and Stein’s Dutch-famine
SIR,-Professor Thomson (Oct. 25,
answer
Institute of Postgraduate Medical Education and Research,
Punjab University Chandigarh, India.
S. SEHGAL B. N. S. WALIA
MATERNAL NUTRITION AND LOW BIRTH-WEIGHT
SIR,-Your editorial on maternal nutrition (Sept. 6, p. 445) evoked a response (Oct. 11, p. 704) from our respected friend and colleague, Benjamin Pasamanick, whose work provided an early stimulus for recent developments in prenatal epidemiology, including the area of nutrition. Please allow us to comment once more, for Dr Pasamamck appears to have nnsread our findings and our interpretations of the effects of the Dutch famine. Our letter of Oct. 4, (p. 664) must have indicated that we did not conclude, as to his distress he thinks we did, that maternal starvation during the famine was trivial or had trivial effects. On the contrary, we believe that nowhere is stronger evidence to be found in humans of the profound effects of severe prenatal nutritional deprivation on fetal growth and survival. In our cohort analysis of mortality, in particular, the effects of prenatal experience, some nutritional and some unspecified, were of a magnitude and extent that have not previously been shown. Dr Pasamanick says that the uneven availability of food to different social classes invalidates our study (and C. A. Smith’s study) of the famine. If this is so, it undermines much of the direct available evidence in favour of his view that maternal malnutrition has ill effects on birth outcome. We do not agree, however, that food availability affected the validity of the results of our study of the famine. Indeed, we did not simply "acknowledge" the maldistribution but took pains to try and demonstrate it. Our pre-existing suspicion that food was unevenly available was reinforced when we found that the survivors of cohorts conceived at the height of the famine had higher i.Q. scores than the survivors of other cohorts. This advantage could be accounted for, we were able to show, by a decline in fertility during the famine that was greater in the lower classes than in the higher, and by the consequent change in the social-class composition of the survivors in the affected cohorts. Naturally, in subsequent analyses we controlled for these differences wherever indicated. The results of the Dutch famine study lead us to the conclusion that in previously well-nourished women the effects of maternal nutritional deprivation on fetal growth are appreciable, but only below a critical level of nutrient intake. Other studies now in progress in Harlem, New York City,’ and in Guatemala,2in our view, are tending to support a corollarythat is, prenatal nutritional supplementation promotes fetal growth only under specifiable conditions, most of which can be related to poor nutritional state of the mother. Within a year or two, further results from a study in Bogota will become available to test this position. The study in Taiwan of the late Bacon Chow, referred to by Dr Pasamanick, perhaps also may help to clarify the issues when fully analysed, but this is anlikely because the numbers in that study are probably not adeRush, D., Stein, Z., Christakis, G., Susser, M. in Nutrition and Fetal Development (edited by M. Winick); vol. 2, p. 95. New York, 1974. 2. Habicht, J. P., Yarbrough, C., Lechtig, A., Klein, R. E. ibid. p. 127. 1.
study-i.e., the food consumed in the "famine areas" was not randomly distributed. The most parsimonious explanation for the lowest mean birth-weights of 3000 g is that the upper strata, the Nazi collaborators, and others secured sufficient food to conceive, maintain pregnancies, and obtain live births. Since this criticism was not answered, presumably Professor Thomson now agrees that the entire study is a failure. However, he goes on to make the point that "famine" and control areas had been equally affected as far as perinatal mortality was concerned. Since I stated that the "control" areas had also been starved (the mean calorific intake fell to below 1300 calories), this is just what would have been predicted. As for Professor Thomson’s study in Aberdeen, he does not reply to the criticism that his sample was above the malnourishment threshold. The lowest occupational group had a mean intake above 70 g and this was approximately only 10 g below the highest group. Again, he did not reply and thus apparently accepts the validity of this point. He merely indicates that the source of the protein was not fish. Since I was not able to ascertain from the pertinent paper what the source was, we remain in the dark because Professor Thomson has failed to indicate the content of the only remaining fact which deserves discussion. State of New York
Department of Mental Hygiene, Division of Mental Retardation and Children’s Services, 44 Holland Avenue, Albany, N.Y. 12229, U.S.A.
BENJAMIN PASAMANICK
INTRAUTERINE NUTRITION AND BABIES’ HAIR SIR,-Professor Bradfield has developed a simple method’I for using hair-root morphology as an indicator of malnutrition in pre-school children and adults. He and his colleagues suggest (Nov. 8, p. 928) that the technique might also be applied to the antenatal period in that the morphology of maternal hair could be used to predict the risk of a low-birth-weight delivery. We have used their technique in the perinatal period to study the effects of intrauterine nutrition on the hair of babies. We found that at term the hair-roots of the boys were often in a resting (telogen) phase even when they appeared well nourished. We were, therefore, able to compare the effect of "intrauterine malnutrition" in girls only. The hair-root morphology was studied of 13 girls born at term of birth-weight appropriate for their gestational age (weight >3-0 kg, gestation 37-41 completed weeks) and 14 light-for-dates (weight < 2.5 kg) term girls. In the hair sample which was taken in the first 24 hours after birth there was no significant difference between the percentage of growing roots (anagen) in the two groups of babies. However, there was a highly significant difference (p < 0-001) between the hair-root diameter of the light-for-dates babies (8-22 +_ 3.1xx 10-zmm) and the appropriate-for-dates babies (13-8+3-7x10’mm). This difference remained significant (P < 0 - 01) when the babies were further subdivided into Caucasian and Asian groups. It appears, at least in girls, that hair-root morphology is a sensitive indicator of intrauterine nutrition and we wonder 1.
Bradfield,
R. B.
Am. J.
clin. Nutr.
1972, 25, 720.
