Sudden Infant Death Syndrome

The Physicians Committee

Beyond Animal Research

By Jonathan Balcombe, Ph.D.
April 2006

Sudden Infant Death Syndrome

Sudden Infant Death Syndrome (SIDS) is implicated in about 5,000 to 7,000 infant deaths yearly in the United States. It’s a terrible tragedy for parents to suddenly lose an otherwise healthy-looking baby. Not surprisingly, dozens of studies are published each year aimed at trying to solve the SIDS riddle.

A considerable amount of this research is in the clinical setting. Here are a few recent examples:

  • Infant mortality risk markers were identified in a predefined South Dakota population using death certificates, obituaries, and deaths reported by area hospitals and government service units. Each case was reviewed and assigned a cause and manner of death, yielding trends and aiding public education.1
  • A study of 138 SIDS cases included parent interviews and examination of histological sections from the lung periphery for evidence of stomach aspiration. Aspiration was identified in 37 percent of cases, but in no case was it deemed a potential cause of death.2
  • An autopsy performed on a 5-month-old baby who died of SIDS demonstrated an enlarged adrenal gland, which genetic analysis revealed was linked to a mutation. Newborn screening is recommended.3
  • Gastric tissues from 94 SIDS cases were formalin-fixed and paraffin-embedded, then polymerase chain reaction and immunohistochemistry techniques were used to determine that H. pylori (bacterial) infection is very rare in SIDS cases.4

There are also many animal studies, including the following:

  • Thirty-two pregnant rats exposed to magnetic fields produced significantly fewer pups, and sex ratios were affected by magnetic field direction. Authors concluded that magnetic activity can increase the number of nonvital young.5
  • Thirty-nine piglets aged 5 to 7 days were exposed to moderate oxygen deprivation for 24 hours, and/or dosed with a bacterial toxin. Fever reactions were monitored and related to response time to partial airway obstruction during sleep. Authors report having demonstrated an animal model of delayed respiratory responsiveness to airway obstruction during recovery from fever.6
  • When hydrochloric acid was applied to the larynxes of newborn puppies, it usually caused spasms and elevated breathing. Authors suggest that acid-induced, laryngospasm-associated apnea may be a cause of SIDS and urge more puppy studies.7
  • Intestinal sections from rabbits were exposed to several bacterial toxins. Tissue damage was compared with that from 14 human SIDS victims. Authors claim support for the hypothesis that many SIDS cases result from the absorption of toxins from the intestinal tract, initiating a toxic shock reaction.8,9

As these examples show, clinical studies tend to be retrospective, involving such tools as autopsy, tissue and genetic analysis, and interviews, usually to try to uncover some pattern of causation. Animal experimenters tend to start with a known clinical phenomenon (e.g., nicotine exposure), seek to replicate it artificially in the lab using an “animal model,” then speculate on its possible significance to the illness. As usual, the clinical methods cause no harm, but in the animal studies, few if any get out alive.

1. EagleStaff ML, Klug MG, Burd L. Infant mortality reviews in the Aberdeen Area of the Indian Health Service: strategies and outcomes. Public Health Rep. 2006;121:140-148.
2. Alex N, Thompson JM, Becroft DM, Mitchell EA. Pulmonary aspiration of gastric contents and the sudden infant death syndrome.
J Paediatr Child Health. 2005;41:428-431.
3. Gozzi TG, Harris NP, McGown IN, Cowley DM, Cotterill AM, Campbell PE, Anderson PK, Warne GL. Autopsy diagnosis of 21-hydroxylase deficiency CAH in a case of apparent SIDS. Pediatr Dev Pathol. 2005;8:397-401.
4. Loddenkotter B, Becker K, Hohoff C, Brinkmann B, Bajanowski T. Real-time quantitative PCR assay for the detection of Helicobacter pylori: no association with sudden infant death syndrome. Int J Legal Med. 2005;119:202-206.
5. Dupont MJ, Parker G, Persinger MA. Reduced litter sizes following 48-h of prenatal exposure to 5 nT to 10 nT,0.5 Hz magnetic fields: implications for sudden infant deaths. Int J Neurosci. 2005;115:713-15.
6. Voss LJ, Bolton DP, Galland BC, Taylor BJ. Effects of prior hypoxia exposure, endotoxin and sleep state on arousal ability to airway obstruction in piglets: implications for sudden infant death syndrome. Biol Neonate. 2005;88:145-155.
7. Duke SG, Postma GN, McGuirt WF Jr, Ririe D, Averill DB, Koufman JA. Laryngospasm and diaphragmatic arrest in immature dogs after laryngeal acid exposure: a possible model for sudden infant death syndrome. Ann Otol Rhinol Laryngol. 2001;110:729-733.
8. Kamaras J, Murrell WG. The effect of bacterial enterotoxins implicated in SIDS on the rabbit intestine. Pathology. 2001;33:187-196.
9. Kamaras J, Murrell WG. Intestinal epithelial damage in SIDS babies and its similarity to that caused by bacterial toxins in the rabbit. Pathology. 2001;33:197-203.