What is SIDS?
An overview for the science-minded parent
© 2009 Gwen Dewar, Ph.D., all rights reserved
What is SIDS? After years of research, scientists can offer only partial answers.
What we do know is this:
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 some 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 sleep (Audero et al 2008).
But even if we don’t understand everything about the causes of SIDS, we know quite a bit about preventing 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,” what are 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 syndrome was 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 it?
What is SIDS?
An impaired ability to arouse from sleep
Four 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).
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 cause 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). In one study, victims of SIDS had more abnormalities in the serotonin pathways of the medulla, the lower portion of the brain stem (Paterson et al 2006). Serotonin is a neurotransmitter that directs all sorts of basic functions, including heart rate, breathing, appetite, body temperature, and vomiting. Researchers speculate that an abnormal serotonin system prevents some babies from awakening when their breathing is obstructed.
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).
• 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
Parental smoking and maternal alcohol consumption are important environmental risk factors for SIDS. As noted above, babies whose mothers smoked and/or consumed alcohol during pregnancy are at greater risk of SIDS. Prenatal exposure to cigarettes and alcohol may affect the development of the serotonin system (Kinney et al 2003; Duncan et al 2008).
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).
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).
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.
However, it’s not clear why bed sharing per se--as opposed to specific bed sharing practices--would increase the risk of SIDS. In fact, because babies experience more spontaneous arousals when they sleep with their mothers, there is reason to suspect that bed sharing--practiced safely by sober, nonsmoking parents--could help protect babies from SIDS (Mosko et al 1997; Mao et al 2004).
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 safety.
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 SIDS prevention.
References: What is SIDS?
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