Medical Hypotheses
Volume 58, Issue 3 , Pages 232-236, March 2002

A serotonin malfunction hypothesis by finding clear mutual relationships between several risk factors and symptoms associated with sudden infant death syndrome

  • N. Okado

      Affiliations

    • Correspondence to: N. Okado, Neurobiology Laboratory, Institute of Basic Medical Sciences, University of Tsukuba, Tsukuba, Ibaraki 305-8577, Japan. Phone: +81 298 53 6961; Fax: +81 298 53 6960; E-mail:nokado@md.tsukuba.ac.jp
  • ,
  • M. Narita
  • ,
  • N. Narita

Neurobiology Laboratory, Institute of Basic Medical Sciences, University of Tsukuba, Tsukuba, Ibaraki, 305-8577, Japan

Received 30 April 2001; accepted 9 July 2001.

Abstract 

In our recent study allele variants in the promoter of serotonin transporter (5-HTT) gene have been shown as a novel risk factor for sudden infant death syndrome (SIDS). L and XL alleles were more frequent and S allele was less frequent in SIDS victims compared to age-matched controls. Serotonin (5-HT) is suggested as a major agent that is closely involved in the etiology of SIDS. Although many risk factors of SIDS looked mutually unrelated each other, we found in literature many of them other than prone position to change 5-HT levels in the brain. Along with the genetic factors, environmental and temporal factors appear additively to lower the excitatory function of 5-HT to the respiratory center, and finally SIDS might occur. Now the pathophysiological mechanisms and symptoms of SIDS are explained by decreased levels of 5-HT.

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PII: S0306-9877(01)91483-5

doi:10.1054/mehy.2001.1483

Medical Hypotheses
Volume 58, Issue 3 , Pages 232-236, March 2002