What is SIDS? An overview for the science-minded parent

© 2009 -2014, Gwen Dewar, Ph.D., all rights reserved

What is SIDS? Scientists can offer only partial answers. But we know this much:

SIDS, or sudden infant death syndrome, seems to involve a failure to arouse from sleep during a life-threatening event–like a severe episode of sleep apnea or esophageal reflux (Franco et al 2004).

Why do babies fail to arouse?

That’s not entirely clear. As I note below, some babies seem to suffer from abnormalities of the brain stem and the serotonin system. These babies show alterations in the brain cells that are sensitive to serotonin, a neurotransmitter that regulates both sleep and our ability to gasp in response to asphyxiation (Audero et al 2008; Garcia et al 2013).

But even if we don’t understand everything about the causes of SIDS, we know quite a bit about lowering the risk of SIDS.

Case studies suggest that SIDS deaths occur when vulnerable babies are exposed to one or more environmental risk factors, like second-hand smoke or prone sleeping. To the degree that we can control these SIDS risk factors, we may be able to reduce the number of babies that die each year.

For example, SIDS rates in the United States have declined since medical workers began promoting the supine position for sleep (i.e., putting infants on their backs). In 1992, the United States SIDS rate was 1.2 deaths per 1000 live births. Ten years later, the rate had fallen to 0.57 deaths per 1000 live births (American Academy of Pediatrics Task Force on SIDS 2005).

So here is an overview of the science of SIDS: what researchers mean by “SIDS;” the likely causes of SIDS; and what environmental risk factors may contribute to SIDS.

For a checklist of SIDS prevention tips, see this article on specific ways that you can reduce the risk of SIDS.

What SIDS is not

The term “SIDS” does not apply to all cases of sudden infant death. The terminology “sudden infant death syndrome” was coined in 1960s to describe sudden, unexpected mortalities that couldn’t be ascribed to any known causes (Bergman et al 1969).

So, by definition, “SIDS” excludes deaths caused by known diseases, child abuse, or accidents (including accidental suffocation or strangulation).

In this sense, “SIDS” began as a label for any deaths that couldn’t be explained.

But—and here’s the big “but”—the reason why SIDS was recognized as a syndromewas that researchers noticed certain recurrent features associated with sudden infant death (Krous et al 2004):

  • SIDS appears to strike when babies are asleep.
  • SIDS is associated with a specific age range: Babies older than 21 days and younger than 9 months. SIDS risk peaks around 2 to 3 months of age.

This pattern led researchers to speculate that SIDS wasn’t merely a collection of different diseases and accidents. SIDS was suspected of being a new, if poorly-understood, medical condition.

The problem was: What exactly was this condition?

What is SIDS?

An impaired ability to arouse from sleep

Decades later, SIDS is still not fully understood. But researchers are piecing together the puzzle. The general idea is that SIDS victims fail to awaken when something potentially life-threatening happens during sleep—like a severe episode of sleep apnea, or esophageal reflux, or a pillow pressed up against the face (Franco et al 2004; Garcia et al 2013).

Under normal circumstances, these events don’t lead to death. That’s because the infant’s brain stem detects a drop in oxygen levels and wakes the baby up. She wiggles, she cries. Her heart rate and blood pressure increases, her breathing normalizes, and all is well.

But in the SIDS victim, something goes wrong. Why?

Biological causes of SIDS

Brain stem abnormalities

Postmortem analysis suggests that SIDS victims may suffer from abnormalities of the brain stem, the part of the brain that regulates breathing and sleep (Mitchell 2009; Randall et al 2013).

For instance, studies have reported that victims of SIDS had more abnormalities in the serotonin pathways of the medulla, the lower portion of the brain stem (Paterson et al 2006; Randall et al 2013). Serotonin is a neurotransmitter that directs all sorts of basic functions, including heart rate, breathing, gasping, appetite, body temperature, and vomiting. Researchers speculate that an abnormal serotonin system prevents some babies from awakening when their breathing is obstructed. It may also interfere with the effectiveness of the gasp reflex (Garcia et al 2013).

Re-breathing asphyxia.

A second hypothesis–not incompatible with the brain stem hypothesis–is that a fatal SIDS event can be triggered by “re-breathing asphyxia,” which is what happens when a baby keeps re-breathing the carbon dioxide that he exhales (Paluszynska et al 2004).

Re-breathing asphyxia would be a risk whenever babies sleep on their stomachs—and particularly when babies are sleeping on soft bedding that can trap gases. Re-breathing asphyxia might also occur if the baby’s face is covered or pressed up against a pillow, duvet, or heavy blanket.

Other biological risk factors:

  • Prenatal exposure to smoke and/or alcohol. Babies whose mothers smoked or drank alcohol during pregnancy are more likely to suffer from abnormalities in the serotonin system. They also have higher SIDS rates (Fifer et al 2009).
  • Infection. SIDS rates are higher among babies recovering from a respiratory or intestinal infection (Horne et al 2002; Platt et al 2000).
  • Sleep deprivation. Experiments have shown that babies exposed to short-term sleep deprivation experience more sleep apnea and are harder to arouse from sleep (Franco et al 2004). This suggests that sleep deprivation might trigger SIDS, an idea that is consistent with studies showing that SIDS victims sleep significantly less in the 24 hours preceding death than do controls (Blair et al 2000).
  • Preterm birth. Premies and low-birth weight babies are at higher risk of SIDS than are full-term babies. This may reflect the fact that premies have more trouble arousing from quiet sleep, the infant equivalent of adult “deep” sleep (Horne 2006).
  • Sex. Boys are more likely to die of SIDS than are girls (American Academy of Pediatrics Task Force on Sudden Infant Death Syndrome 2005). Possibly, this reflects sex differences in the frequency of brain stem abnormalities (Paterson et al 2006) or the effects of testosterone on the immune system (Moscovis et al 2014).
  • Genes. Perhaps some genotypes make babies more vulnerable to SIDS (Nonnis Marzano et al 2008). This seems plausible, but the research has only just begun, and the genetic contributions to SIDS risk are not yet understood.

For example, the Serotonin System FEV Gene affects the serotonin pathways of the brain.

One study showed that victims of SIDS were more likely to carry a mutation in this gene than were controls (Rand et al 2007). However, these correlations held for African Americans only. Among Caucasians, there was no link between SIDS and the FEV gene. 

Understanding environmental factors that affect arousal—and the risk of SIDS

Studies have identified several environmental risks factors for SIDS. Here’s what we know about the most important of them.

Smoking and alcohol

As noted above, parental smoking and maternal alcohol consumption are important environmental risk factors for SIDS.

For example, prenatal exposure to cigarettes and alcohol increases the risk of SIDS, perhaps because such exposure alters the development of the serotonin system (Kinney et al 2003; Duncan et al 2008) and causes defects in the lungs and nervous system (Lavezzi et al 2014).

Postnatal smoke exposure is also associated with higher SIDS rates. Babies exposed to second hand smoke are harder to arouse from sleep, and they experience fewer spontaneous arousals (Horne et al 2004; Richardson et al 2009).

The smoking-related risk of SIDS appears to be magnified for babies born preterm (Schneider et al 2008) and for babies who share beds with smokers (Horsley et al 2007).

Prone Sleep

SIDS rates are higher among babies who sleep on their stomachs. Why might the prone sleep position contribute to SIDS? Experimental research suggests that prone sleep can trigger several problems, including an impaired ability to arouse from sleep (Horne et al 2001), rebreathing asphyxia (Paluszynska et al 2004), and a fall in blood pressure (Yiallourou et al 2008).

Overheating

SIDS case studies have revealed that sleeping prone is riskier in colder latitudes, higher altitudes, and during the winter. The prone position is also riskier when an infant is over-bundled and/or sweating (Mitchell 2009). Such findings suggest that overheating plays a role in SIDS.

Why would high temperatures matter? Perhaps the brain has more trouble awakening when it’s overly warm. A study of young mice revealed that overheating, when combined with reduced oxygen levels, could interfere with an individual’s ability to resuscitate himself (Kahraman and Thach 2004).

In addition, an experiment on human babies found that room temperatures of 82 degrees Farenheit / 28 degrees Celsius were associated with fewer arousals than were temperatures of 75F/24C (Franco et al 2001).

Covered heads or faces

In a recent analysis of published SIDS studies, Peter Blair and colleagues found that head covering is a major SIDS risk factor (Blair et al 2008). Indeed, these studies suggest that if we can prevent head covering, we might reduce the risk of SIDS by over 25%. Why?

Covers may make babies hot. They may also trap exhaled gases, putting the baby at risk for rebreathing asphyxia. In addition, covers seem to affect the way baby’s sleep. When something covers a baby’s face—even something as sheer as a bed sheet—the baby is less likely to arouse from sleep in response to noise (Franco et al 2002).

Dangerous sleep surfaces

SIDS case studies suggest that sofas, armschairs, and waterbeds are particularly dangerous places for babies to sleep (e.g., Tappin et al 2005).

Soft mattresses are also considered hazardous. If a baby sleeps with his face turned against a soft mattress, his exhalations could create a dangerous accumulation of CO2, triggering rebreathing asphixia and possibly SIDS (Colditz et al 2002).

Soft bedding and toys

SIDS research suggests that soft bedding—including pillows, bed sheets, towels, blankets, and duvets—can cause asphyxiation and/or overheating (e.g., Hauck et al 2003; Kanetake et al 2003). As noted above, they might also interfere with a baby’s ability to arouse from sleep.

Bed sharing with young infants

Some studies of SIDS deaths in Western countries have reported a correlation between SIDS and bed sharing in babies under 20 weeks old (Tappin et al 2005; Carpenter et al 2004; McGarvey et al 2006). In response, several agencies have issued general recommendations against bed sharing for young infants (e.g., Task Force on Sudden Infant Death Syndrome 2011).

However, it’s not clear why bed sharing per se–as opposed to specific bed sharing practices–would increase the risk of SIDS.

Because babies experience more spontaneous arousals when they sleep with their mothers, there is reason to suspect that bed sharing–practiced with safeguards by sober, nonsmoking parents–could help protect babies from SIDS (Mosko et al 1997; Mao et al 2004).

For babies in the Western studies, it seems this protective effect was counteracted by other risk factors.

What is very clear is that babies who bed-share are at a much greater risk of SIDS when they are exposed to second-hand smoke.

In addition, common sense suggests that bed sharing is dangerous when the sleeping environment includes known hazards, like soft mattresses or loose bedding.

Research also indicates that SIDS risk is increased when babies share a bed with

  • someone who smokes, drinks, or who is impaired by illness or drugs (Horsley et al 2007)
  • more than one other person, and/or with a non-parent (Hauck et al 2003)
  • someone who is very tired (as when the infant’s longest sleep bout in the last 24 hours was 4 hours or less-—Blair et al 1999)

Tiredness can pose other hazards, too–as when an exhausted caregiver falls asleep on a sofa or armchair while holding an infant.

Such shared sleep surfaces are very dangerous indeed. In one study, the risk of mortality increased 60-fold for babies cosleeping on sofas (Tappin et al 2005).

For more information, see this article bed sharing and safety.

Protective factors

Research has identified a number of things to avoid. Are there any positive steps we can take to reduce the risk? Perhaps. Studies suggest that several practices–including breastfeeding, proximal sleeping, pacifiers, and even electric fan use—might have a protective effect. For more information, see this evidence-based article on lowering SIDS risk.


References: What is SIDS?

American Academy of Pediatrics Task Force on Sudden Infant Death Syndrome. 2005. The Changing Concept of Sudden Infant Death Syndrome: Diagnostic Coding Shifts, Controversies Regarding the Sleeping Environment, and New Variables to Consider in Reducing Risk. Pediatrics 116(5):1245-1255.

Audero, E., Coppi, E., Mlinar, B., Rossetti, T., Caprioli, A., Banchaabouchi, M.A., Corradetti, R. & Gross, C. 2008. Sporadic autonomic dysregulation and death associated with excessive serotonin autoinhibition. Science. 321(5885):130-3.

Bergman AB, Pomeroy MA, and Beckwith JB. 1969. The psychiatric toll of the sudden infant death syndrome. GP. 40(6):99-105.

Blair PS, Mitchell EA, Heckstall-Smith EM, and Fleming PJ 2008. Head Covering – A major modifiable risk factor for Sudden Infant Death Syndrome: A systematic review. Arch Dis Child. 2008 May 1. [Epub ahead of print]

Carpenter RG, Irgens LM, Blair PS, England PD, Fleming P, Huber J, Jorch G, and Schreuder P. 2004. Sudden unexplained infant death in 20 regions in Europe: case control study. Lancet 363(9404): 185-191.

Colditz PB, Joy GJ, and Dunster KR. 2002. Rebreathing potential of infant mattresses and bedcovers. J Paediatr Child Health. 38(2):192-5.

Coleman-Phox K, Odouli R, and Li DK. 2008. Use of a fan during sleep and the risk of sudden infant death syndrome. Arch Pediatr Adolesc Med. 162(10):963-8.

Duncan JR, Paterson DS, Kinney HC. 2008. The development of nicotinic receptors in the human medulla oblongata: inter-relationship with the serotonergic system. Auton Neurosci. 15;144(1-2):61-75.

Franco P, Lipshultz W, Valente F, Adams S, Scaillet S, and Kahn A. 2002. Decreased arousals in infants who sleep with the face covered by bedclothes. Pediatrics 109: 1112-1117.

Franco P, Scaillet S, Valente F, Chabanski S, Groswasser J, Kahn A. 2001. Ambient temperature is associated with changes in infants’ arousability from sleep. Sleep 24(3): 325-329.

Franco P, Seret N, Van Hees JN, Scaillet S, Vermeulen F, and Groswasser J, and Kahn A. 2004. Decreased arousals among healthy infants after short-term sleep deprivation. Pediatrics 114(2): e192-e197.

Fifer WP, Fingers ST, Youngman M, Gomez-Gribben E, and Myers MM. 2009. Effects of alcohol and smoking during pregnancy on infant autonomic control. Dev Psychobiol. 51(3):234-42.

Garcia AJ 3rd, Koschnitzky JE, and Ramirez JM. 2013. The physiological determinants of Sudden Infant Death Syndrome. Respir Physiol Neurobiol. 189(2):288-300.

Horne RSC, Ferens D, Watts AM, Vitkovic J, Lacey B, Andrew S, Cranage SM, Chau B, and Adamson TM. 2001. The prone sleeping position impairs arousability in term infants. J Pediatrics 138: 811-816.

Horne RSC, Franco P, Adamson TM, Groswasser J, and Kahn A. 2004. Influences of maternal cigarette smoking on infant arousability. Early Human Development 79(1):49-58.

Horne RS, Osborne A, Vitkovic J, Lacey B, Andrew S, Chau B, Cranage SM, and Adamson TM. 2002. Arousal from sleep in infants is impaired following an infection. Early Human Development 66(2):89-100.

Jenkins RO and Sherburn RE. 2008. Used cot mattresses as potential reservoirs of bacterial infection: nutrient availability within polyurethane foam. J Appl Microbiol. 104(2):526-33.

Kahraman L and Thach BT. 2004. Inhibitory effects of hyperthermia on mechanisms involved in autoresuscitation from hypoxic apnea in mice: a model for thermal stress causing SIDS . J Appl Physiol 97: 669-674.

Kanetake J, Aoki Y, and Funayama M. 2003. Evaluation of rebreathing potential on bedding for infant use. Pediatr Int. 45(3):284-9.

Kinney HC, Randall LL, Sleeper LA, Willinger M, Belliveau RA, Zec N, Rava LA, Dominici L, Iyasu S, Randall B, Habbe D, Wilson H, Mandell F, McClain M, Welty TK. 2003. Serotonergic brainstem abnormalities in Northern Plains Indians with the sudden infant death syndrome. J Neuropathol Exp Neurol. 62(11):1178-91.

Krous HF, Beckwith JB, Byard RW, Rognum TO, Bajanowski T, et al. 2004. Sudden infant death syndrome and unclassified sudden infant deaths: A definitional and diagnostic approach. Pediatrics 114(1): 234-238.

Lavezzi AM, Corna MF, Alfonsi G, and Matturri L. 2014. Possible role of the alpha7 nicotinic receptors in mediating nicotine’s effect on developing lung – implications in unexplained human perinatal death. BMC Pulm Med. 14(1):11.

Nelson EA and Chan PH. 1996. Child care practices and cot death in Hong Kong. N Z Med J. 109(1020):144–146.

Mao A, Burnham MM, Goodlin-Jones BL, Gaylor EE, and Anders TF. 2004. A comparison of the sleep-wake patterns of co-sleeping and solitary infants. Child Psychiatry and Human Development 32(2): 95-105.

McGarvey C et al (2006) An 8 year study of risk factors for SIDS: bed-sharing versus non-bed-sharing. Arch Dis Child 91:318-323.

McKenna JJ, Ball HL, and Gettler LT. 2007. Mother-infant cosleeping, breastfeeding and sudden infant death syndrome: what biological anthropology has discovered about normal infant sleep and pediatric sleep medicine. Am J Phys Anthropol. Suppl 45:133-61.

Mitchell EA. 2009. What is the mechanism of SIDS? Clues from epidemiology. Dev Psychobiol. 51(3):215-22.

Mitchell EA, Thompson JM, Becroft DM, Bajanowski T, Brinkmann B, Happe A, Jorch G, Blair PS, Sauerland C, and Vennemann MM. 2008. Head covering and the risk for SIDS: findings from the New Zealand and German SIDS case-control studies. Pediatrics. 121(6):e1478-83.

Moon RY, Horne RS, and Hauck FR. 2007. Sudden infant death syndrome. Lancet 370(9598):1578-87.

Moscovis SM, Hall ST, Burns CJ, Scott RJ, and Blackwell CC. 2014. The male excess in sudden infant deaths. Innate Immun. 20(1):24-9.

Mosko S, Richard C, McKenna J. 1997. Infant arousals during mother-infant bed sharing: implications for infant sleep and sudden infant death syndrome research. Pediatrics. 100(5):841-9.

Nonnis Marzano F, Maldini M, Filonzi L, Lavezzi AM, Parmigiani S, Magnani C, Bevilacqua G, and Matturri L. 2008. Genes regulating the serotonin metabolic pathway in the brain stem and their role in the etiopathogenesis of the sudden infant death syndrome. Genomics. 91(6):485-91.

Paterson DS, Trachtenberg FL, Thompson EG, Belliveau RA, Beggs AH, Darnall R, Chadwick AE, Krous HF, and Kinney HC. 2006. Multiple serotonergic brainstem abnormalities in sudden infant death syndrome. JAMA 296(17):2124-32.

Paluszynska DA, Harris KA, and Thach BT. 2004. Influence of sleep position experience on ability of prone-sleeping infants to escape from asphyxiating microenvironments by changing head position. Pediatrics. 114(6):1634-9.

Platt MW, Blair PS, Fleming PJ, Smith IJ, Cole TJ, Leach CE, Berry PJ, and Golding J. 2000. A clinical comparison of SIDS and explained sudden infant deaths: how healthy and how normal? CESDI SUDI Research Group. Confidential Inquiry into Stillbirths and Deaths in Infancy study. Arch Dis Child. 82(2):98-106.

Rand CM, Berry-Kravis EM, Zhou L; Fan W, and Weese-Mayer DE. 2007. Sudden Infant Death Syndrome: Rare mutation in the serotonin system FEV gene. Pediatric Research. 62(2):180-182.

Randall BB, Paterson DS, Haas EA, Broadbelt KG, Duncan JR, Mena OJ, Krous HF, Trachtenberg FL, and Kinney HC. 2013. Potential asphyxia and brainstem abnormalities in sudden and unexpected death in infants. Pediatrics. 132(6):e1616-25.

Richardson HL, Walker AM, and Horne RSC. 2009. Maternal smoking impairs arousal patterns in sleeping infants. Sleep 32 (4): 515-521.

Rognum IJ, Tran H, Haas EA, Hyland K, Paterson DS, Haynes RL, Broadbelt KG, Harty BJ, Mena O, Krous HF, and Kinney HC. 2014. Serotonin metabolites in the cerebrospinal fluid in sudden infant death syndrome. J Neuropathol Exp Neurol. 73(2):115-22.

Sakai J, Kanetake J, Takahashi S, Kanawaku Y, and Funayama M. 2008 Gas dispersal potential of bedding as a cause for sudden infant death. 2008Forensic Sci Int. 180(2-3):93-7.

Scheers NJ, Rutherford GW, and Kemp JS. 2003. Where should infants sleep? A comparison of risk for suffocation of infants sleeping in cribs, adult beds, and other sleeping locations. Pediatrics 112: 883-889.

Schneider J, Mitchell I, Singhal N, Kirk V, and Hasan SU. 2008. Prenatal cigarette smoke exposure attenuates recovery from hypoxemic challenge in preterm infants. Am J Respir Crit Care Med. 178(5):520-6.

Tappin D, Ecob R, and Brooke H. 2005. Bedsharing, roomsharing, and sudden infant death syndrome in Scotland: a case-control study. J Pediatr. 147(1):32-7.

Task Force on Sudden Infant Death Syndrome 2011. SIDS and other sleep-related infant deaths: expansion of recommendations for a safe infant sleeping environment. Pediatrics 128(5):1030-9.

Vennemann M, Bajanowski T, Butterfass-Bahloul T, Sauerland C, Jorch G, Brinkmann B, and Mitchell EA. 2007. Do risk factors differ between explained sudden unexpected death in infancy and sudden infant death syndrome? Arch Dis Child. 92(2):133-6.

Vennemann MM, Höffgen M, Bajanowski T, Hense HW, and Mitchell EA. 2007. Do immunisations reduce the risk for SIDS? A meta-analysis. Vaccine. 25(26):4875-9.

Yiallourou SR, Walker AM, and Horne RS. 2008. Effects of sleeping position on development of infant cardiovascular control. Arch Dis Child. 93(10):868-72.

Zhong CY, Zhou YM, Joad JP, and Pinkerton KE. 2006. Environmental Tobacco Smoke Suppresses Nuclear Factor Kappa B Signaling to Increase Apoptosis in Infant Monkey Lungs. American Journal of Respiratory and Critical Care Medicine 174: 428-436.

Content of “What is SIDS?” last modified 2/14

The owner of this website has made a committment to accessibility and inclusion, please report any problems that you encounter using the contact form on this website. This site uses the WP ADA Compliance Check plugin to enhance accessibility.