Possible Explanation of "Failure to Thrive"
Infants May Have a Reduced "Melatonin -- DHEA Cycle" ...a basis of the “placebo effect.”

Copyright © 2002, James Michael Howard, Fayetteville, Arkansas, U.S.A.

It is my hypothesis that melatonin and dehydroepiandrosterone (DHEA) were involved in evolution of mammals (Rivista di Biologia / Biology Forum 2001; 94: 177-184) and humans (Rivista di Biologia / Biology Forum 2001; 94: 345-362). This is derived from my principal hypothesis that DHEA optimizes transcription and replication of DNA and, therefore, DHEA may have been involved in evolution of eukaryotes. It is my opinion that melatonin and DHEA directly affect each others’ production and release and this cycle determine our circadian rhythms (the melatonin ­ DHEA cycle, 1997). DHEA and melatonin are directly involved in the growth and development and maintenance of all tissues. Therefore, I suggest the syndrome of poor growth and development of infants called "failure to thrive" may result from disruption of this cycle. The fact that attention and contact ameliorates "failure to thrive" infants may be due to promotion of the melatonin ­ DHEA cycle.

Studies link melatonin with infant growth and development. "6-sulfatoxymelatonin [the melatonin metabolite excreted in urine] levels at 16 weeks of age were significantly lower in infants with abnormal vs. normal development at 3 months of age (7.27 + 1.44 vs. 7.97 + 1.06, p = 0.05) as well as at 6 months of age (7.15 + 1.29 vs. 7.95 + 1.10, p = 0.04). no other significant relation was evident among growth, perinatal complications, medical problems, and 6-sulfatoxymelatonin excretion at 8 weeks of age and at 16 weeks of age. low melatonin excretion in the first weeks of life correlates with delayed psychomotor achievements at 3 and 6 months of age. this association suggests a causal or predictive link between melatonin and neurodevelopment in infants." (Pediatr Neurol 2002 May; 26(5): 379-82). "Massage therapy" by mothers of normal infants significantly increased melatonin production. "At 12 weeks, nocturnal 6-sulphatoxymelatonin excretions were significantly higher in the treated infants (1346.38 +/- 209.40 µg/night vs 823.25 +/- 121.25 µg/night, respectively; <0.05). (J Dev Behav Pediatr 2002 Dec; 23(6): 410-415). It is known that maternal touch is lacking in "failure to thrive" infants" (J Am Acad Child Adolesc Psychiatry 1994 Oct; 33(8): 1098-105). I suggest melatonin is directly involved in normal development of infants and may be part of the mechanism that is lacking in reduced maternal touching in "failure to thrive infants"

It has been determined that DHEA-sulfate (DHEAS), the large, background supply of DHEA, increases production of melatonin by rat pineal glands (Steroids 2000 Sep; 65(9): 491-6) and that melatonin treatment increases DHEAS (Neuroendocrinol Lett 2002 Apr; 23 Suppl 1: 17-9). This supports the "melatonin ­ DHEA cycle," which I suggest may be involved in growth and development. DHEA is a mild androgenic, steroid hormone which produces positive effects on many tissues. I suggest the positive effects of touch on "failure to thrive" infants results from stimulation of the melatonin ­ DHEA cycle.

I suggest the “placebo effect” is the result of mentally- or physically-stimulated DHEA production.