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ADC Fetal and Neonatal Edition Letters and ADC Education and Practice Letters
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James M. Howard, Biologist independent
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jmhoward{at}arkansas.net James M. Howard
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Dear Editor It is my hypothesis (1985) that depression may be caused by low dehydroepiandrosterone (DHEA) and that postpartum depression / psychosis result from very low DHEA in the mother. (Low DHEA in depression has since been demonstrated and maternal DHEA declines following a first birth.) Maternal depression either current or postpartum, therefore, may be due to very low DHEA. It is my hypothesis that "prematurity" or "small for gestational age" results from low maternal DHEA. The mother produces DHEA for herself and her fetus; any shortages of DHEA will adversely affect fetal growth and development. Low maternal DHEA may occur for various reasons, low DHEA, reduced conversion from DHEA sulfate (DHEAS), and/or reduced prolactin, which specifically stimulates DHEA production. Testosterone is known to inhibit conversion from DHEAS to DHEA. Testosterone is also connected with learning disabilities, aka, low intelligence. The connection of low intelligence with malnutrition may be increased maternal testosterone, which I consider to be a primary factor in increased low birth weight. While I cannot find much regarding DHEA in breast milk in the literature, it is clear that prolactin is provided in breast milk. Prolactin has been demonstrated to be a specific stimulator of DHEA. I suggest it is this prolactin in breast milk which is so beneficial to nursing infants. This will hold true except in infants who cannot produce sufficient DHEA for growth and development on their own or stimulated by mother's milk. Increased maternal testosterone may reduce lactation and also reduce prolactin which may stimulate DHEA production in the infant. Reduced DHEA production in the infant may result in the symptoms of malnutrition. I suggest the findings of Anoop et al. may be explained by reduced maternal DHEA and / or increased maternal testosterone which combine to adversely affect the availability of DHEA in the infants. Calorie restriction reduces DHEA levels and low DHEA may produce the symptoms of malnutrition. |
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K.S. Jacob, Professor of Psychiatry Christian Medical College, Vellore 632002 India, B. Saravanan, K.S. Jacob
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ksjacob{at}cmcvellore.ac.in K.S. Jacob, et al.
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Dear Editor We read Dr Howard’s letter [1] about the possible role of increased testosterone and low dehydroepiandrosterone in the production of post partum depression in the mother and malnutrition in the child with interest. We agree that this biological causal explanation seems plausible and needs to be evaluated. However, there is little evidence to support a biological basis to postpartum depression.[1] Despite extensive research, no firm evidence has emerged linking these or other hormones to the development of postnatal depression.[2] The consistent finding of the epidemiological studies that the major factors of etiological importance are largely of a psychosocial nature.[1] Risk factors for postnatal depression are antenatal psychiatric morbidity, economic deprivation, low education and marital disharmony. Education, support from extended family members and employment are protective factors. While most of these risk factors have also been demonstrated in developed countries,[3] studies from the South Asia have also shown the importance of the gender of the newborn infant as a determinant of postnatal depression.[4,5] The preference for male children is deeply rooted in the region. Women are often blamed for the birth of girls, especially in situations where the woman already has a girl child. Such bias and the limited ability of women to control their reproductive health can make pregnancy and the birth of a daughter a very stressful event contributing to the onset of postnatal depression. We feel that single and simple explanations are very unlikely to be true for all people with similar psychiatric syndromes. Post natal depression is a syndrome, which may be caused by diverse etiologies and different mechanisms. This would suggest that specific abnormalities may be present in a sub-group of people with post partum depression. While we agree that biological hypothesis need to be evaluated, we believe that reducing the diverse risk and protective factors to a single abnormality is reductionistic and may not prove useful. References 1. Howard JM. This may be due to increased testosterone and low DHEA [electronic response to Anoop et al. Maternal depression and low maternal intelligence as risk factors for malnutrition in children: a community based case-control study from South India] archdischild.com 2004 http://adc.bmjjournals.com/cgi/eletters/archdischild;89/4/325#785 2. O'Hara MW. The nature of postpartum depressive disorders. In: Murray L, Cooper PJ, eds. Postpartum depression and child development. , New York: Guilford, 1997:3-31. 3. Harris B. A hormonal component to postnatal depression. Br J Psychiatry 1993; 163: 403-405. 4. O'Hara M, Swain A. Rates and risk of postpartum depression-a metaanalysis. International Review of Psychiatry 1996; 8: 37-54. 5. Patel V, Rahman A, Jacob KS, Hughes M. Why maternal mental health matters for infant growth in low income countries: new evidence from South Asia. BMJ 2004 (in press). 6. Chandran M, Tharyan P, Muliyil J, Abraham S. Post-partum depression in a cohort of women from a rural area of Tamil Nadu, India. Incidence and risk factors. British Journal of Psychiatry 2002; 181: 499- 504. |
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