Sudden infant death syndrome (SIDS) or crib death is a syndrome marked by the sudden death of an infant that is unexpected by history and remains unexplained after a thorough forensic autopsy and a detailed death scene investigation. The term cot death is often used in the United Kingdom, Ireland, Australia, India, South Africa and New Zealand.
2 SIDS Back To Sleep Campaign: History and Theory
3 Undiagnosed conditions
4 Risk factors
4.1 Prenatal risks
4.2 Post-natal risks
5 Risk reduction for SIDS
5.1.1 Sleep positioning
5.1.4 Secondhand smoke reduction
5.2 Sleeping area
5.2.2 Sleep sacks
5.2.4 Air circulation with fan use
5.2.5 Bumper pads
6 Speculated associations
6.2 Mattress bugs
6.3 Brain disorder
6.4 Vitamin C
6.5 Toxic gases
6.6 Central Respiratory Pattern Deficiency
6.7 Upper cervical spinal cord injury as a result of birth trauma
6.9 Child abuse
6.10 Nitrogen dioxide
6.12 Inner ear damage
7 Side effects of SIDS risk reduction recommendations
8 Further reading
10 External links
10.2 Related websites
10.3 Media articles
10.4 Other articles
Typically the infant is found dead after having been put to bed, and exhibits no signs of having suffered.
SIDS is a diagnosis of exclusion. It should only be applied to an infant whose death is sudden and unexpected, and remains unexplained after the performance of an adequate postmortem investigation including
investigation of the scene and circumstances of the death;
exploration of the medical history of the infant and family.
SIDS was responsible for 0.543 deaths per 1,000 live births in the U.S. in 2005 (wonder.cdc.gov). It is responsible for far fewer deaths than congenital disorders and disorders related to short gestation, though it is the leading cause of death in healthy infants after one month of age.
SIDS deaths in the U.S. decreased from 4,895 in 1992 to 2,247 in 2004. But, during a similar time period, 1989 to 2004, SIDS being listed as the cause of death for sudden infant death (SID) decreased from 80% to 55%. According to Dr. John Kattwinkel, chairman of the Center for Disease Control (CDC) Special Task Force on SIDS “A lot of us are concerned that the rate (of SIDS) isn’t decreasing significantly, but that a lot of it is just code shifting”.
Australia and New Zealand are shifting to the term Sudden Unexplained Death in Infancy (SUDI) for professional, scientific and coronial clarity.
The term SUDI is now often used instead of Sudden Infant Death Syndrome (SIDS) because some coroners prefer to use the term ‘undetermined’ for a death previously considered to be SIDS. This change is causing diagnostic shift in the mortality data.
 SIDS Back To Sleep Campaign: History and Theory
In 1985 Davies reported that in Hong Kong, where Chinese custom called for supine infant sleep position, SIDS was a rare problem. In 1987 the Netherlands started a campaign advising parents to place their newborn infants to sleep on their backs (supine position) instead of their stomachs (prone position). This was followed by infant supine sleep position campaigns in the United Kingdom, New Zealand, and Australia in 1991, the U.S. and Sweden in 1992, and Canada in 1993.
This advice was based on the epidemiology of SIDS and physiological evidence which shows that infants who sleep on their back have lower arousal thresholds and less Slow-Wave Sleep (SWS) compared to infants who sleep on their stomachs. In human infants sleep develops rapidly during early development. This development includes an increase in non-rapid eye movement sleep (NREM sleep) which is also called Quiet Sleep (QS) during the first 12 months of life in association with a decrease in rapid eye movement sleep (REM sleep) which is also known as Active Sleep (AS). In addition, slow wave sleep (SWS) which consists of Stage 3 and Stage 4 NREM sleep appears at 2 months of age. and it is theorized that some infants have a brain-stem defect which increases their risk of being unable to arouse from SWS (also called Deep Sleep) and therefore have an increased risk of SIDS due to their increased inability to arouse from SWS.
Studies have shown that preterm infants, full-term infants, and older infants  have greater time periods of quiet sleep and also decreased time awake when they are positioned to sleep on their stomachs. In both human infants and rats, arousal thresholds have been shown to be at higher levels in the Electroencephalography (EEG) during Slow-wave sleep.
In 1992, a SIDS risk reduction strategy based upon lowering arousal thresholds during SWS was implemented by the American Academy of Pediatrics (AAP) which began recommending that healthy infants be positioned to sleep on their back (supine position) or side (lateral position), instead of their stomach (prone position), when being placed down for sleep. In 1994, a number of organizations in the United States combined to further communicate these non-prone sleep position recommendations and this became formally known as the “Back To Sleep” campaign. In 1996, the AAP further refined its sleep position recommendation by stating that infants should only be placed to sleep in the supine position and not in the prone or lateral positions.
In 1992, the first National Infant Sleep Position (NISP) Household Survey was conducted to determine the usual position in which U.S. mothers placed their babies to sleep: (1) Lateral (side); (2) Prone (stomach); (3) Supine (back); (4) Other; (5) No Usual Position. According to the 1992 NISP survey, 13.0% of U.S. infants were positioned in the supine position for sleep. According to the 2006 NISP survey 75.7% of infants were positioned in the supine position to sleep.
Since 1998 there have been several studies published which report that infants placed to sleep in the supine position lag in motor skills, social skills, and cognitive ability development when compared to infants who sleep in the prone position. In the 1998 article entitled “Effects of Sleep Position on Infant Motor Development.”  by Davis, Moon, Sachs, and Ottolini, the authors state “We found that sleep position significantly impacts early motor development.” The prone (stomach) sleeping infants in this study slept an average of 225.2 hours (8.3%) more in their first 6 months of life than the supine (back) sleeping infants.
In the 1998 article entitled “Does the Supine Sleeping Position Have Any Adverse Effects on the Child? II. Development in the First 18 Months” by Dewey, Fleming, Golding, and the ALSPAC Study Team the objective of the study was “To assess whether the recommendations that infants sleep supine could have adverse consequences on their motor and mental development.” They used the Denver Developmental Screening Test (DDST) and studied infants at 6 and 18 months. According to the study, at 6 months of age, the infants who were placed to sleep in the prone position had statistically significant higher social skills scores, gross motor scores, and total development scores than those infants who were put to sleep in the supine position. In the 2005 article entitled “Influence of supine sleep positioning on early motor milestone acquisition” by Majnemer and Barr they used the Alberta Infant Motor Scale Scores (AIMS Scores) to analyze the impact of infant sleep position. They reported that “Typically developing infants who were sleep-positioned in supine had delayed motor development by age 6 months, and this was significantly associated with limited exposure to awake prone positioning.” But, the authors also note that awake prone (stomach) positioning is associated with prone (stomach) sleeping. No studies have been conducted which compare supine sleeping infants who have regular awake prone positioning (tummy time) to prone sleeping infants who have regular awake prone positioning (tummy time).
Placing infants on their stomachs while they are awake (tummy time) has been recommended to offset the motor skills delays associated with the back sleep position but positioning the infant on their stomach while awake will not impact the amount of slow wave sleep since tummy time only occurs when an infant is awake.
 Undiagnosed conditions
Some conditions that may be undiagnosed and thus result in a diagnosis of SIDS include
medium-chain acyl-coenzyme A dehydrogenase deficiency (MCAD deficiency), ;
infant botulism ;
long QT syndrome;
infections with the bacterium Helicobacter pylori;
shaken baby syndrome and other forms of child abuse.
 Risk factors
Very little is certain about the possible causes of SIDS, and there is no proven method for prevention. Although studies have identified risk factors for SIDS, such as putting infants to bed on their stomachs, there has been little understanding of the syndrome’s biological cause or causes. The frequency of SIDS appears to be a strong function of the infant’s sex, age and ethnicity, and the education and socio-economic-status of the infant’s parents.
According to a study published in October 2007 in the Journal of the American Medical Association, babies who die of SIDS have abnormalities in the brain stem (the medulla oblongata), which helps control functions like breathing, blood pressure and arousal, and abnormalities in serotonin signaling. According to the National Institutes of Health, which funded the study, this finding is the strongest evidence to date that structural differences in a specific part of the brain may contribute to the risk of SIDS.
In a British study released May 29, 2008 researchers discovered that the common bacterial infections Staphylococcus aureus (staph) and Escherichia coli (E. coli) appear to be the cause of some cases of Sudden Infant Death Syndrome. Both bacteria were present at greater than usual concentrations in infants who died from SIDS. SIDS cases peak between eight and ten weeks after birth, which is also the time frame in which the antibodies that were passed along from mother to child are starting to disappear and babies have not yet made their own antibodies.
Listed below are several factors associated with increased probability of the syndrome based on information available prior to this recent study.
 Prenatal risks
maternal nicotine use (tobacco or nicotine patch)
inadequate prenatal care 
inadequate prenatal nutrition
use of heroin
subsequent births less than one year apart
alcohol use 
infant being overweight 
mother being overweight 
Teen pregnancy (if the baby has a teen mother, it has a greater risk) 
infant’s sex (60% of SIDS cases occur in males)
 Post-natal risks
mold (can cause bleeding lungs plus a variety of other uncommon conditions leading to a misdiagnoses and death). It is often misdiagnosed as a virus, rlu, and/or asthma-like conditions. 
low birth weight (wonder.cdc.gov reports in the U.S. from 1995-1998 that the rate for 1000-1499 g was 2.89/1000 and for 3500-3999 g it was 0.51/1000)
exposure to tobacco smoke
prone sleep position (lying on the stomach, see sleep positioning below)
elevated room temperature
excess bedding, clothing, soft sleep surface and stuffed animals
infant’s age (incidence rises from zero at birth, is highest from two to four months, and declines towards zero at one year)
premature birth (increases risk of SIDS death by about 4 times. See wonder.cdc.gov. In 1995-1998 the U.S.SIDS rate for 37–39 weeks of gestation was 0.73/1000; The SIDS rate for 28–31 weeks of gestation was 2.39/1000)
 Risk reduction for SIDS
Though SIDS cannot be prevented, parents of infants are encouraged to take several precautions in order to reduce the likelihood of SIDS.
 Sleep positioning
Sleeping on the back has been recommended by (among others) the American Academy of Pediatrics (starting in 1992) to avoid SIDS, with the catchphrases “Back To Bed” and “Back to Sleep.” The incidence of SIDS has fallen sharply in a number of countries in which the back to bed recommendation has been widely adopted, such as the US and New Zealand. However, the absolute incidence of SIDS prior to the Back to Sleep Campaign was already dropping in the US, from 1.511 per 1000 in 1979 to 1.301 per 1000 in 1991 (wonder,cdc,gov).
Among the theories supporting the Back to Sleep recommendation is the idea that small infants with little or no control of their heads may, while face down, inhale their exhaled breath (high in carbon dioxide) or smother themselves on their bedding—the brain-stem anomaly research (above) suggests that babies with that particular genetic makeup do not react “normally” by moving away from the pooled CO2, and thus smother. Another theory is that babies sleep more soundly when placed on their stomachs, and are unable to rouse themselves when they have an incidence of sleep apnea, which is thought to be common in infants.
Arguments against infant back-sleeping include concerns that an infant could choke on fluids it brings up. Hospital neonatal-intensive-care-unit (NICU) staff commonly place preterm newborns on their stomach, although they advise parents to place their infants on their backs after going home from the hospital. 
Other concerns raised about the Back to Sleep Campaign have included the possible increased risk of positional facial and head deformities (see positional plagiocephaly), possible interference with development of good sleep habits (which in turn may have other bad effects), and possible interference with motor skills development (as infants delay attempts to lift their heads, crawl, etc.).
A 2003 study published in Pediatrics, which investigated racial disparities in infant mortality in Chicago, found that previously or currently breastfeeding infants in the study had 1/5 the rate of SIDS compared with non-breastfed infants, but that “it became nonsignificant in the multivariate model that included the other environmental factors”. These results are consistent with most published reports and suggest that other factors associated with breastfeeding, rather than breastfeeding itself, are protective.” However, a more recent study shows that breast feeding reduces the risk of SIDS by approximately 50% at all infant ages .
Select studies suggest that limiting the amount of co-sleeping could lower a child’s risk of SIDS. A 2005 policy statement by the American Academy of Pediatrics on sleep environment and the risk of SIDS deemed co-sleeping and bed sharing unsafe. One article reports that co-sleeping infants have a greater risk of airway covering than when the same infant sleeps alone in a cot.
Some data has suggested that almost all SIDS deaths in adult beds would be occurring when other prevention methods, such as placing infants on their backs, are not used. Co-sleeping studied in the West has been present mostly in poorer families where other risk factors are present. while co-sleeping in other cultures such as in China is more prevalent and is done in combination with practices such as sleeping children on their back, correlating with a significantly lower rate of SIDS than the West. There are also evolutionary theories as to why co-sleeping would be healthier for infants than sleeping alone. Further studies have suggested that factors associated with safe co-sleeping such as enhanced infant arousals are responsible for a positive contribution to SIDS prevention.
Depending on the child, co-sleeping may be made safer through the use of a bedside “co-sleeper”. Unattended adult beds are unsafe for infants, as are adult beds with excess bedding, intoxicated guardians, or those who smoke. Co-sleeping in couches is also very hazardous. Available evidence indicates that the safest place for infants to sleep is a crib in the parent’s room.
 Secondhand smoke reduction
According to the U.S. Surgeon General’s Report, secondhand smoke is connected to SIDS. Infants who die from SIDS tend to have higher concentrations of nicotine and cotinine (a biological marker for secondhand smoke exposure) in their lungs than those who die from other causes. Infants exposed to secondhand smoke after birth are also at a greater risk of SIDS. Parents who smoke can significantly reduce their children’s risk of SIDS by either quitting or smoking only outside and leaving their house completely smoke-free.
The maternal pregnancy smoking rate decreased by 38% between 1990 and 2002.
 Sleeping area
To prevent SIDS, product safety experts advise against using pillows, stuffed animals, or fluffy bedding in the crib and recommend instead dressing the child warmly and keeping the crib “naked.” 
Infants’ blankets should also not be placed over their heads. It has been recommended that infants should be covered only up to their chest with their arms exposed. This helps eliminate the chances of the infant shifting the blanket over his head.
 Sleep sacks
In colder environments where bedding is required to maintain a baby’s body temperature, the use of a “baby sleep bag” or “sleep sack” is becoming more popular. This is a soft bag with holes for the baby’s arms and head. A zipper allows the bag to be closed around the baby. A study published in the European Journal of Pediatrics in August 1998 has shown the protective effects of a sleep sack as reducing the incidence of turning from back to front during sleep, reinforcing putting a baby to sleep on its back for placement into the sleep sack and preventing bedding from coming up over the face which leads to increased temperature and carbon dioxide rebreathing. They conclude in their study “The use of a sleeping-sack should be particularly promoted for infants with a low birth weight.” The American Academy of Pediatrics also recommends them as a type of bedding that warms the baby without covering its head.
According to a 2005 meta-analysis, most studies favor pacifier use. According to the American Academy of Pediatrics, pacifier use seems to reduce the risk of SIDS, although the mechanism by which this happens is unclear. SIDS experts and policy makers haven’t recommended the use of pacifiers to reduce the risk of SIDS because of several problems associated to pacifier use, like increased risk of otitis, gastrointestinal infections and oral colonization with Candida species.. A recent study shows that pacifier use by breastfed infants does not reduce the rate of breastfeeding.
A 2005 study indicated that use of a pacifier is associated with up to a 90% reduction in the risk of SIDS depending on the ambiental factors, and it reduced the effect of other risk factors. It has been speculated that the raised surface of the pacifier holds the infant’s face away from the mattress, reducing the risk of suffocation. If a postmortem investigation does not occur or is insufficient, a suffocated baby may be misdiagnosed with SIDS.
 Air circulation with fan use
According to a study of nearly 500 babies published the October 2008 Archives of Pediatrics & Adolescent Medicine, using a fan to circulate air correlates with a lower risk of sudden infant death syndrome. Researchers took into account other risk factors and found that fan use was associated with a 72% lower risk of SIDS. Only 3% of the babies who died had a fan on in the room during their last sleep, the mothers reported. That compared to 12% of the babies who lived. Using a fan reduced risk most for babies in poor sleeping environments. Author De-Kun li said that “the baby’s sleeping environment really matters” and that “this seems to suggest that by improving room ventilation we can further reduce risk.”
 Bumper pads
Bumper pads may be a contributing factor in SIDS deaths and should be removed. Health Canada, the Canadian government’s health department, issued an advisory recommending against the use of bumper pads, stating:
The presence of bumper pads in a crib may also be a contributing factor for Sudden Infant Death Syndrome (SIDS). These products may reduce the flow of oxygen rich air to the infant in the crib. Furthermore, proposed theories indicate that the rebreathing of carbon dioxide plays a role in the occurrence of SIDS.
 Speculated associations
A number of theoretical causes have been proposed as a trigger for SIDS, but many of them are unproven or have not been thoroughly studied and peer-reviewed. As of June 2009 there were 113 such articles found in Medical Hypotheses as cited in PubMed.
Anemia is not a documented SIDS risk factor per se because at the moment of death the blood hemoglobin begins to degrade. . This degradation can be slow or rapid and it shows up as livor mortis, the mottled and reddened coloring that can develop within 30 minutes of death. Because SIDS usually occurs during sleep and is unnoticed, the time interval between moment of death and autopsy is unknown so no correction can be made to the hemoglobin value measured postmortem to estimate the antemortem value immediately before death. However anemia is a risk factor for apparent-life-threatening-events (ALTE) as described by Poets et al. (1992) referred to above where anemia is listed as a postnatal risk factor.
 Mattress bugs
A 2004 study hypothesized that bugs feeding on baby vomit and dust could be fatal for small children, creating ‘supertoxins’ which spur the baby’s body into overreacting, leading to anaphylactic shock. 
 Brain disorder
A recently published research article  showed evidence that cells in the brainstem fail to develop receptors for serotonin in the womb. This abnormality can continue postpartum until the end of the first year. This would account for there being few to no SIDS deaths after the first year of infancy and the reason the risk is more for premature infants.
 Vitamin C
According to a 1993 article in Journal of Orthomolecular Medicine, Australian medical doctor Archie Kalokerinos performed research showing that high doses of vitamin C eliminates SIDS. As of May 2009, the Journal of Orthomolecular Medicine was not included among journals selected by the U.S. National Library of Medicine for inclusion in their Medline database. A later article does not support this hypothesis. 
 Toxic gases
In 1989, a controversial piece of research by UK Scientist Barry Richardson claimed that all cot deaths were the result of toxic nerve gases being produced through the action of fungus in mattresses on compounds of phosphorus, arsenic and antimony. These chemicals are frequently used to make mattresses fire-retardant.
A major plank in this explanation is the widely-observed phenomenon that the risk of cot death rises from one sibling to the next. Richardson claims that the cause is that parents are more likely to buy new bedding for their first child, and to re-use that bedding for later children. The more frequently used the bedding is, the more chance there will be that fungus has become resident in the material; thus, a higher chance of cot death. A paper by Peter Fleming and Peter Blair references evidence from other studies that both supports and refutes the increasing occurrence of SIDS with mattress sharing and suggests that this is still inconclusive.
In 1994, the New Zealand government, under the advice of Dr. Jim Sprott, issued advice recommending new parents to either buy bedding free of the toxic compounds or to wrap the mattresses in a barrier film to prevent the escape of the gases. Dr. Sprott claims that no case of cot death has ever been traced back to a properly manufactured or wrapped mattress.
However, a final report of The Expert Group to Investigate Cot Death Theories: Toxic Gas Hypothesis, published in May 1998, concluded that “there was no evidence to substantiate the toxic gas hypothesis that antimony- and phosphorus-containing compounds used as fire retardants in PVC and other cot mattress materials are a cause of SIDS. Neither was there any evidence to believe that these chemicals could pose any other health risk to infants.” The report also states that “in normal cot-like conditions it is not possible to generate toxic gas from antimony in mattresses” and “babies have also been found to die on wrapped mattresses.” Dr. Sprott’s website, however, claims that the study does not actually refute his theory:
Contrary to media publicity, the 1998 UK Limerick Report did not disprove the toxic gas theory—as a highly qualified environmental scientist has stated in the New Zealand Medical Journal. In fact, the Limerick Committee’s experiments proved the fungal generation of toxic gases (forms of stibine and arsine) from cot mattress materials.
According to Dr. Sprott, as of 2006, the New Zealand government has not reported any SIDS deaths when babies have slept on mattresses wrapped according to his method. While the Limerick report claims that babies have been found to die on wrapped mattresses, Dr. Sprott argues that a chemical analysis of the bedding should be performed. He additionally claims that this part of the report was flawed:
In February 2000 Dr Peter Fleming (a co-author of the Limerick Report and principal author of the UK CESDI Report) conceded that the claim that three babies in the United Kingdom had died of cot death on polythene-covered mattresses could not be substantiated.
 Central Respiratory Pattern Deficiency
There is ongoing research in the pediatric/neonatal community that has begun to associate apnea-like breathing cessations in animal models with unusual neural architecture or signal transduction in central pattern generator circuits including the pre-Bötzinger complex. It is possible that irregularities in neurotransmitter release (such as GABA, adenosine, and NMDA) or deficiencies in their associated receptors (including both GABAA, GABAB subtypes and NMDA-glutamate receptors) are linked to incomplete prenatal development as is evident in pre-term infants.
 Upper cervical spinal cord injury as a result of birth trauma
During birth, if the infant’s head is traumatically turned side to side, upper cervical spinal injury can result. Difficulty breathing is a classic sign of upper spinal cord and brain-stem injury. When infants with undiagnosed upper cervical spinal cord injury are continually placed on their stomach for sleep, they are forced to turn their head to the side to breathe. This is hypothesised to aggravate and prolong the spinal cord injury sustained during birth, preventing proper healing and ultimately leading to fatal breathing difficulty.
There is a consistent 50% male excess in SIDS per 1000 live births of each sex. Given a 5% male excess birth rate (105 male to 100 female live births) there appear to be 3.15 male SIDS per 2 female SIDS for a male fraction of 0.61. This value of 61% in the U.S. is an average of 57% Black male SIDS,62.2% White male SIDS and 59.4% for all other races combined. Note that when multiracial parentage is involved,infant “race” is arbitrarily assigned to one category or the other, most often it is chosen by the mother. The X-linkage hypotheses for SIDS and the male excess in infant mortality have shown that the 50% male excess could be related to a dominant X-linked allele that occurs with a frequency of ⅓ that is protective of transient cerebral anoxia. An unprotected XY male would occur with a frequency of ⅔ and an unprotected XX female would occur with a frequency of 4⁄9. The ratio of ⅔ to 4⁄9 is 1.5 to 1 which matches the observed male 50% excess rate of SIDS.
Although many authors have found autosomal and mitochondrial genetic risk factors for SIDS they cannot explain the male excess because such gene loci have the same frequencies for males and females. Supporting evidence for an X-linkage is found by examination of other causes of infant respiratory death, such as suffocation by inhalation of food and other foreign objects. Although food is prepared identically for male and female infants, there is a similar 50% male excess of death from such causes indicating that males are more susceptible to the cerebral anoxia created by such incidents in exactly the same proportion as found in SIDS. See the data found at http://wonder.cdc.gov for 9ICD 911-912 and 10ICD W79-W80 for death rates from inhalation of food and foreign objects by sex.
The study which indicated that there was a relationship between fewer serotonin binding sites and SIDS noted that the boys “had significantly fewer serotonin binding sites than girls.” However, such neurological prematurity decreases with age, but the male fraction of approximately 0.61 persists each month throughout the first year of life . Furthermore, this cannot explain the identical male fraction of 0.61 in other respiratory mortality causes such as respiratory distress syndrome or suffocation from inhalation of food or foreign objects cited above, that also exists for all ages 1 to 14 years in the U.S. from 1979 to 2005 as reported in wonder.cdc.gov.
 Child abuse
Several instances of infanticide have been uncovered where the diagnosis was originally SIDS. This has led some researchers to estimate that 5% to 20% of SIDS deaths are infanticides. In 1997 The New York Times, covering a book called The Death of Innocents: A True Story of Murder, Medicine and High-Stakes Science, wrote:
The misdiagnosis of infanticide as SIDS “happens all over,” Ms. Talan, a medical reporter at Newsday, said. “A lot of doctors and police don’t know how to handle it. They don’t take it as seriously as they should.” As a result of the book’s revelations, people are starting to scrutinize possible cases of this “perfect crime,” which involves no physical evidence and no witnesses.
British former pediatrician Roy Meadow believes that many cases diagnosed as SIDS are really the result of child abuse on the part of a parent displaying Munchausen Syndrome by Proxy (a condition which he was first to describe, in 1977). During the 1990s and early 2000s, a number of mothers of multiple apparent SIDS victims were convicted of murder, to varying degrees on the basis of Meadow’s opinion. In 2003 a number of high-profile acquittals brought Meadow’s theories into disrepute. Several hundred murder convictions were reviewed, leading to several high-profile cases being re-opened and convictions overturned.
The Royal Statistical Society issued a media release refuting the expert testimony in one UK case in which the conviction was subsequently overturned.
 Nitrogen dioxide
A 2005 study by researchers at the University of California, San Diego found that “SIDS may be related to high levels of acute outdoor NO2 exposure during the last day of life.” While nitrogen dioxide (NO2) exposure may be one of many possible risk factors, it is not considered causal, and the report cautioned that further studies were needed to replicate the result.
Vaccination does not increase the risk of SIDS. According to the US Centers for Disease Control and Prevention:
From 2 to 4 months old, babies begin their primary course of vaccinations. This is also the peak age for sudden infant death syndrome (SIDS). The timing of these two events has led some people to believe they might be related. However, studies have concluded that vaccines are not a risk factor for SIDS.
 Inner ear damage
Records of hearing tests administered to certain infants show that those who later died of SIDS had a unique pattern of partial hearing loss, according to the journal Early Human Development. One suggestion for the cause of SIDS is that the deaths are caused by disturbances in respiratory control (from other than suffocation). The vestibular apparatus of the inner ear has been shown to play an important role in respiratory control during sleep. It is speculated that this inner ear damage could be linked to SIDS. It is speculated that the damage occurs during delivery, particularly when prolonged contractions create greater blood pressure in the placenta. The right ear is directly in the “line of fire” for blood entering the fetus from the placenta, and thus could be most susceptible to damage. If the findings are relevant, it may be possible to take corrective measures. Researchers are beginning animal studies to explore the connection.
 Side effects of SIDS risk reduction recommendations
Dr. Rafael Pelayo from Stanford University and a number of other pediatric sleep researchers in the U.S. have stated that they believe that the American Academy of Pediatrics’ recommendations regarding cosleeping and pacifier use may have unintended consequences. They have stated that the SIDS prevention strategy of the American Academy of Pediatrics which keeps infants at a low arousal threshold and reduces the time in quiet sleep may be unhealthy for children. They state that slow wave sleep is the most restorative form of sleep and limiting this sleep in the first 12 months of life may have unintended consequences to both the sleep and the infant.
According to a 1998 study by British researchers that compared back sleeping infants to stomach sleeping infants there were developmental differences at 6 months of age between the two groups. At 6 months of age the stomach sleeping infants had higher gross motor scores, social skills scores, and total development skills scores than the back sleeping infants. The differences were apparent at the 5% statistical significant level. But, at 18 months the differences were no longer apparent. The researchers deemed the lower development scores of back sleeping infants at 6 months of age to be transient and stated that they do not believe the back sleeping recommendations should be changed. Other scientists have stated that the conclusion that the negative effects of back sleep at 18 months of age is transient is based upon very little evidence and that no long-term randomized trials have been completed.
Other side effects of the back sleeping position include increased rates of shoulder retraction, positional plagiocephaly, and positional torticollis. Some scientists dispute that plagiocephaly is a negative side effect. Dr. Peter Fleming, who is co-author of the study that deemed delays at 6 months of age to be transient, has stated that he does not think plagiocephaly is a negative side effect of back sleep. In an interview with the Guardian Dr. Fleming stated “I do not think it is a medical problem—it is more of a cosmetic one. Mothers may feel it is a syndrome and a problem when it really is nonsense.” A research study on children with plagiocephaly found that 26% had mild to severe psychomotor delay. This study also showed that 10% of infants with plagiocephaly had mild to severe mental development delay.
Because of the delays caused by back sleep some medical professionals have suggested that the “normal” ages at which children had previously attained developmental milestones should be pushed back. This would enable medical professionals to consider “normal” children who previously were considered developmentally delayed.
Additional studies have reported that the following negative conditions are associated with the back sleep position: increase in sleep apnea, decrease in sleep duration, strabismus, social skills delays, deformational plagiocephaly, and temporomandibular jaw difficulties. In addition, the following are symptoms that are associated with sleep apnea: growth abnormalities, failure to thrive syndrome in infants, neurocognitive abnormalities, daytime sleepiness, emotional problems, decrease in memory, decrease in learning, and a delay in nonverbal skills. The conditions associated with deformational plagiocephaly include visual impairments, cerebral dysfunction, delays in psychomotor development and decreases in mental functioning. The conditions associated with gross motor milestone delays include speech and language disorders. In addition, it has been hypothesized that delays in motor skills can have a negative impact on the development of social skills. In addition, other studies have reported that the prone position prevents subluxation of the hips, increases psychomotor development, prevents scoliosis, lessens the risk of gastroesophageal reflux, decreases infant screaming periods, causes less fatigue in infants, and increases the relief of infant colic. In addition, prior to the “Back to Sleep” campaign many babies self-treated their own torticollis by turning their heads from one side to the other while sleeping in the prone position. Supine sleeping infants cannot self-treat their own torticollis.
 Further reading
Joan Hodgman; Toke Hoppenbrouwers (2004). SIDS. Calabasas, Calif: Monte Nido Press. ISBN 0-9742663-0-2. 
^ Health Canada SIDS Healthy Babies SIDS Page.
^ a b c Bowman L, Hargrove T. Exposing Sudden Infant Death In America. Scripps Howard News Service. http://dailycamera.com/news/2007/oct/08/saving-babies-exposing-sudden-infant-death-in/
^ http://www.moh.govt.nz/moh.nsf/0/5118C5C5561CEC79CC2573A6000B3BBE NZ Ministry of Health
^ Davies DP. Cot death in Hong Kong: A rare problem? Lancet 2:1346-1349.
^ a b c Högberg U, Bergström E (April 2000). “Suffocated prone: the iatrogenic tragedy of SIDS”. Am J Public Health 90 (4): 527–31. doi:10.2105/AJPH.90.4.527. PMID 10754964. PMC: 1446204. http://www.ajph.org/cgi/pmidlookup?view=long&pmid=10754964.
^ Rusen ID, Liu S, Sauve R, Joseph KS, Kramer MS (2004). “Sudden infant death syndrome in Canada: trends in rates and risk factors, 1985–1998”. Chronic Dis Can 25 (1): 1–6. PMID 15298482.
^ a b Kattwinkel J, Hauck F.R., Moon R.Y., Malloy M and Willinger M Infant Death Syndrome: In Reply, Bed Sharing With Unimpaired Parents Is Not an Important Risk for Sudden\Pediatrics 2006;117;994-996
^ Louis J, Cannard C, Bastuji H, Challamel MJ (May 1997). “Sleep ontogenesis revisited: a longitudinal 24-hour home polygraphic study on 15 normal infants during the first two years of life”. Sleep 20 (5): 323–33. PMID 9381053.
^ Navelet Y, Benoit O, Bouard G (July 1982). “Nocturnal sleep organization during the first months of life”. Electroencephalogr Clin Neurophysiol 54 (1): 71–8. doi:10.1016/0013-4694(82)90233-4. PMID 6177520.
^ Roffwarg HP, Muzio JN, Dement WC (April 1966). “Ontogenetic Development of the Human Sleep-Dream Cycle”. Science (journal) 152 (3722): 604–619. doi:10.1126/science.152.3722.604. PMID 17779492.
^ Anders TF, Keener M (1985). “Developmental course of nighttime sleep-wake patterns in full-term and premature infants during the first year of life. I”. Sleep 8 (3): 173–92. PMID 4048734.
^ Bes F, Schulz H, Navelet Y, Salzarulo P (February 1991). “The distribution of slow-wave sleep across the night: a comparison for infants, children, and adults”. Sleep 14 (1): 5–12. PMID 1811320.
^ Coons S, Guilleminault C (June 1982). “Development of sleep-wake patterns and non-rapid eye movement sleep stages during the first six months of life in normal infants”. Pediatrics 69 (6): 793–8. PMID 7079046.
^ Fagioli I, Salzarulo P (April 1982). “Sleep states development in the first year of life assessed through 24-h recordings”. Early Hum. Dev. 6 (2): 215–28. doi:10.1016/0378-3782(82)90109-8. PMID 7094858.
^ a b Myers MM, Fifer WP, Schaeffer L, et al. (June 1998). “Effects of sleeping position and time after feeding on the organization of sleep/wake states in prematurely born infants”. Sleep 21 (4): 343–9. PMID 9646378.
^ a b Sahni R, Saluja D, Schulze KF, et al. (September 2002). “Quality of diet, body position, and time after feeding influence behavioral states in low birth weight infants”. Pediatr Res. 52 (3): 399–404. PMID 12193675. http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?issn=0031-3998&volume=52&issue=3&spage=399.
^ a b Brackbill Y, Douthitt TC, West H (January 1973). “Psychophysiologic effects in the neonate of prone versus supine placement”. J Pediatr. 82 (1): 82–4. doi:10.1016/S0022-3476(73)80017-4. PMID 4681872.
^ a b Amemiya F, Vos JE, Prechtl HF (May 1991). “Effects of prone and supine position on heart rate, respiratory rate and motor activity in fullterm newborn infants”. Brain Dev. 13 (3): 148–54. PMID 1928606.
^ a b Kahn A, Rebuffat E, Sottiaux M, Dufour D, Cadranel S, Reiterer F (February 1991). “Arousals induced by proximal esophageal reflux in infants”. Sleep 14 (1): 39–42. PMID 1811318.
^ Ashton R (April 1973). “The influence of state and prandial condition upon the reactivity of the newborn to auditory stimulation”. J Exp Child Psychol 15 (2): 315–27. doi:10.1016/0022-0965(73)90152-5. PMID 4735894. http://linkinghub.elsevier.com/retrieve/pii/0022-0965(73)90152-5.
^ Rechtschaffen A, Hauri P, Zeitlin M (June 1966). “Auditory awakening thresholds in REM and NREM sleep stages”. Percept Mot Skills 22 (3): 927–42. PMID 5963124.
^ Neckelmann D, Ursin R (August 1993). “Sleep stages and EEG power spectrum in relation to acoustical stimulus arousal threshold in the rat”. Sleep 16 (5): 467–77. PMID 8378687.
^ “American Academy of Pediatrics AAP Task Force on Infant Positioning and SIDS: Positioning and SIDS”. Pediatrics 89 (6 Pt 1): 1120–6. June 1992. PMID 1503575.
^ U.S. Department of Human Services. “BACK TO SLEEP” CAMPAIGN SEEKS To Reduce Inicidence of SIDS In African American Populations PressRelease. http://www.hhs.gov/news/press/1999pres/991026.html Tuesday, October 26, 1999
^ “Positioning and sudden infant death syndrome (SIDS): update. American Academy of Pediatrics Task Force on Infant Positioning and SIDS”. Pediatrics 98 (6 Pt 1): 1216–8. December 1996. PMID 8951285.
^ a b National Infant Sleep Position Household Survey. Summary Data 1992. http://dccwww.bumc.bu.edu/ChimeNisp/NISP_Data.asp updated: 09/04/07
^ National Infant Sleep Position Household Survey. Summary Data 2006. http://dccwww.bumc.bu.edu/ChimeNisp/NISP_Data.asp updated: 09/04/07
^ a b c Majnemer A, Barr RG (June 2005). “Influence of supine sleep positioning on early motor milestone acquisition”. Dev Med Child Neurol 47 (6): 370–6; discussion 364. doi:10.1017/S0012162205000733. PMID 15934485. http://www3.interscience.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=0012-1622&date=2005&volume=47&issue=6&spage=370.
^ a b Davis BE, Moon RY, Sachs HC, Ottolini MC (November 1998). “Effects of sleep position on infant motor development”. Pediatrics 102 (5): 1135–40. doi:10.1542/peds.102.5.1135. PMID 9794945. http://pediatrics.aappublications.org/cgi/pmidlookup?view=long&pmid=9794945.
^ a b Dewey C, Fleming P, Golding J (January 1998). “Does the supine sleeping position have any adverse effects on the child? II. Development in the first 18 months.ALSPAC Study Team”. Pediatrics 101 (1): E5. doi:10.1542/peds.101.1.e5. PMID 9417169. http://pediatrics.aappublications.org/cgi/pmidlookup?view=long&pmid=9417169.
^ Yang Z, Lantz PE, Ibdah JA. Post-mortem analysis for two prevalent beta-oxidation mutations in sudden infant death. Pediatr Int. 2007 Dec;49(6):883-7. PubMed PMID: 18045290.
^ Nevas M, Lindström M, Virtanen A, Hielm S, Kuusi M, Arnon SS, Vuori E, Korkeala H. Infant botulism acquired from household dust presenting as sudden infant death syndrome. J Clin Microbiol. 2005 Jan;43(1):511-3. PubMed PMID: 15635031;
^ Millat G, Kugener B, Chevalier P, Chahine M, Huang H, Malicier D,Rodriguez-Lafrasse C, Rousson R. Contribution of long-QT syndrome genetic variants in sudden infant death syndrome. Pediatr Cardiol. 2009 May;30(4):502-9. Epub 2009 Mar 26. PubMed PMID: 19322600.
^ Stray-Pedersen A, Vege A, Rognum TO. Helicobacter pylori antigen in stool is associated with SIDS and sudden infant deaths due to infectious disease. Pediatr Res. 2008 Oct;64(4):405-10. PubMed PMID: 18535491.
^ Bajanowski T, Vennemann M, Bohnert M, Rauch E, Brinkmann B, Mitchell EA; GeSID Group. Unnatural causes of sudden unexpected deaths initially thought to be sudden infant death syndrome. Int J Legal Med. 2005 Jul;119(4):213-6. Epub 2005 Apr 14. PubMed PMID: 15830244.
^ Du Chesne A, Bajanowski T, Brinkmann B. [Homicides without clues in children]. Arch Kriminol. 1997 Jan-Feb;199(1-2):21-6. German. PubMed PMID: 9157833.
^ Paterson DS, Trachtenberg FL, Thompson EG, et al. (November 2006). “Multiple serotonergic brainstem abnormalities in sudden infant death syndrome”. JAMA 296 (17): 2124–32. doi:10.1001/jama.296.17.2124. PMID 17077377.
^ Buttigieg J, Brown S, Zhang M, Lowe M, Holloway AC, Nurse CA (May 2008). “Chronic nicotine in utero selectively suppresses hypoxic sensitivity in neonatal rat adrenal chromaffin cells”. Faseb J. 22 (5): 1317–26. doi:10.1096/fj.07-9194com. PMID 18070822.
^ Kraus JF, Greenland S, Bulterys M. Risk factors for sudden infant death syndrome in the US Collaborative Perinatal Project. Int J Epidemiol. 1989 Mar;18(1):113-20.
^ Henriksen T. Foetal nutrition, foetal growth restriction and health later in life. Acta Paediatr Suppl. 1999 May;88(429):4-8.
^ Kandall SR, Gaines J, Habel L, Davidson G, Jessop D.J Relationship of maternal substance abuse to subsequent sudden infant death syndrome in offspring. Pediatr. 1993 Jul;123(1):120-6.
^ Spiers PS, Wang L. Short pregnancy interval, low birthweight, and the sudden infant death syndrome. Am J Epidemiol. 1976 Jul;104(1):15-21.
^ Zhou FC, Fang Y, Goodlett C. Peptidergic agonists of activity-dependent neurotrophic factor protect against prenatal alcohol-induced neural tube defects and serotonin neuron loss. Alcohol Clin Exp Res. 2008 Aug;32(8):1361-71. Epub 2008 Jun 28.
^ Byard RW. Marked obesity in infancy and relationship to sudden infant death. J Paediatr Child Health. 2007 Sep;43(9):649-50.
^ Carroll-Pankhurst C, Mortimer EA Jr. Sudden infant death syndrome, bedsharing, parental weight, and age at death. Pediatrics. 2001 Mar;107(3):530-6.
^ American Sudden Infant Death Syndrome Institute
^ Mage DT, A genetic basis for the sudden infant death sex ratio, Medical Hypotheses, February 1997, 48 (2):137-142
^ Weinberg ED. Association of primary Pneumocystis carinii infection and sudden infant death syndrome. Clin Infect Dis. 2000 Jun;30(6):991.
^ Hunt CE. Small for gestational age infants and sudden infant death syndrome: a confluence of complex conditions. Arch Dis Child Fetal Neonatal Ed. 2007 Nov;92(6):F428-9. PubMed PMID: 17951549.
^ Office of the Surgeon General of the United States Report on Involuntary Exposure to Tobacco Smoke (PDF).
^ Willinger M, Hoffman HJ, Hartford RB (May 1994). “Infant sleep position and risk for sudden infant death syndrome: report of meeting held January 13 and 14, 1994, National Institutes of Health, Bethesda, MD”. Pediatrics 93 (5): 814–9. PMID 8165085.
^ McKenna JJ, McDade T (June 2005). “Why babies should never sleep alone: a review of the co-sleeping controversy in relation to SIDS, bedsharing and breast feeding”. Paediatr Respir Rev 6 (2): 134–52. doi:10.1016/j.prrv.2005.03.006. PMID 15911459. http://linkinghub.elsevier.com/retrieve/pii/S1526054205000230.
^ Moon RY, Horne RS, Hauck FR (November 2007). “Sudden infant death syndrome”. Lancet 370 (9598): 1578–87. doi:10.1016/S0140-6736(07)61662-6. PMID 17980736.
^ Fleming PJ, Levine MR, Azaz Y, Wigfield R, Stewart AJ (June 1993). “Interactions between thermoregulation and the control of respiration in infants: possible relationship to sudden infant death”. Acta Paediatr Suppl 82 (Suppl 389): 57–9. doi:10.1111/j.1651-2227.1993.tb12878.x. PMID 8374195.
^ Mage DT. A probability model for the age distribution of SIDS. Journal of Sudden Infant Death Syndrome and Infant Mortality 1996: 1:13-31.
^ Poets CF, Samuels MP, Wardrop CA, Picton-Jones E, Southall DP. Reduced haemoglobin levels in infants presenting with apparent life-threatening events–a retrospective investigation. Acta Paediatr. 1992 Apr;81(4):319-21. PubMed PMID: 1606392.
^ Mitchell EA, Hutchison L, Stewart AW (July 2007). “The continuing decline in SIDS mortality”. Arch Dis Child. 92 (7): 625–6. doi:10.1136/adc.2007.116194. PMID 17405855.
^ a b c d
^ Aris C, Stevens TP, Lemura C, Lipke B, McMullen S, Côté-Arsenault D, Consenstein L. NICU nurses’ knowledge and discharge teaching related to infant sleep position and risk of SIDS. Adv Neonatal Care. 2006 Oct;6(5):281-94. Erratum in: Adv Neonatal Care. 2006 Dec;6(6):340. PubMed PMID: 17045948.
^ Hauck FR, Herman SM, Donovan M, Iyasu S, Merrick Moore C, Donoghue E, Kirschner RH, Willinger M (2003). “Sleep environment and the risk of sudden infant death syndrome in an urban population: the Chicago Infant Mortality Study”. Pediatrics 111: 1207–14. doi:10.1542/peds.111.5.S1.1207 (inactive 2008-06-25). PMID 12728140. http://pediatrics.aappublications.org/cgi/content/abstract/111/5/S1/1207. .
^ Vennemann MM, Bajanowski T, Brinkmann B, Jorch G, Yücesan K, Sauerland C, Mitchell EA; GeSID Study Group. Does breastfeeding reduce the risk of sudden infant death syndrome? Pediatrics. 2009 Mar;123(3):e406-10. PubMed PMID:19254976.
^ “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): 1245–55. November 2005. doi:10.1542/peds.2005-1499. PMID 16216901.
^ Ball H, Airway covering during bed-sharing Child Care Health Dev. 2009 Jun 15. [Epub ahead of print]
^ a b Wenda Trevathan, Euclid O. Smith, James Joseph McKenna (1999). Evolutionary Medicine. Oxford University Press US. pp. 55–9. ISBN 0195103556.
^ McKenna, James J. (1996), “SUDDEN INFANT DEATH SYNDROME IN CROSS-CULTURAL PERSPECTIVE: is Infant-Parent Cosleeping Protective?”, Annual Review of Anthropology 25: 201–16, doi:10.1146/annurev.anthro.25.1.201, http://arjournals.annualreviews.org/doi/abs/10.1146/annurev.anthro.25.1.201
^ Sarah Mosko, James Mckenna; Hunt, Lynn (2004), “Parent-infant cosleeping: the appropriate context for the study of infant sleep and implications for sudden infant death syndrome (SIDS) research”, Journal of Behavioral Medicine 16 (6): 589–610, doi:10.1007/BF00844721, http://www.springerlink.com/content/l44150210255t523/
^ Pasquale-Styles MA, Tackitt PL, Schmidt CJ. Infant death scene investigation and the assessment of potential risk factors for asphyxia: a review of 209 sudden unexpected infant deaths. J Forensic Sci. 2007 Jul;52(4):924-9. Epub 2007 Jun 6. PubMed PMID: 17553088.
^ “The Changing Concept of Sudden Infant Death Syndrome: Diagnostic Coding Shifts, Controversies Regarding the Sleeping Environment, and New Variables to Consider in Reducing Risk. ‘Bed Sharing’ section”. American Academy of Pediatrics. http://pediatrics.aappublications.org/cgi/content/full/116/5/1245#SEC4. Retrieved 2008-11-06.
^ Chapter 5; pages 180–194, secondhand smoke is connected to SIDS.
^ “Smoking during pregnancy—United States, 1990–2002”. MMWR Morb Mortal Wkly Rep. 53 (39): 911–5. October 2004. PMID 15470322. http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5339a1.htm.
^ Smartmoney.com on bedding.
^ L’Hoir MP, Engelberts AC, van Well GT, et al. (1998). “Risk and preventive factors for cot death in The Netherlands, a low-incidence country”. Eur. J. Pediatr. 157 (8): 681–8. doi:10.1007/s004310050911. PMID 9727856.
^ “The Changing Concept of Sudden Infant Death Syndrome: Diagnostic Coding Shifts, Controversies Regarding the Sleeping Environment, and New Variables to Consider in Reducing Risk”. American Academy of Pediatrics. http://aappolicy.aappublications.org/cgi/content/full/pediatrics;116/5/1245#SEC15. Retrieved 2008-11-06.
^ “Fig 4. Meta-analysis of studies examining the relationship of a pacifier used during the last sleep in SIDS victims versus controls”. American Academy of Pediatrics. http://aappolicy.aappublications.org/cgi/content/full/pediatrics;116/5/1245/F4. Retrieved 2008-11-06.
^ a b “The Changing Concept of Sudden Infant Death Syndrome: Diagnostic Coding Shifts, Controversies Regarding the Sleeping Environment, and New Variables to Consider in Reducing Risk”. American Academy of Pediatrics. http://aappolicy.aappublications.org/cgi/content/full/pediatrics;116/5/1245#SEC6. Retrieved 2008-11-06.
^ Jenik AG, Vain NE, Gorestein AN, Jacobi NE; for the Pacifier and Breastfeeding Trial Group. Does the Recommendation to Use a Pacifier Influence the Prevalence of Breastfeeding? J Pediatr. 2009 May 20. [Epub ahead of print] PubMed PMID:19464025.
^ Li DK, Willinger M, Petitti DB, Odouli R, Liu L, Hoffman HJ (2006). “Use of a dummy (pacifier) during sleep and risk of sudden infant death syndrome (SIDS): population based case-control study”. BMJ 332 (7532): 18–22. doi:10.1136/bmj.38671.640475.55. PMID 16339767.
^ Coleman-Phox K, Odouli R, Li DK (October 2008). “Use of a fan during sleep and the risk of sudden infant death syndrome”. Arch Pediatr Adolesc Med 162 (10): 963–8. doi:10.1001/archpedi.162.10.963. PMID 18838649. http://archpedi.ama-assn.org/cgi/content/abstract/162/10/963.
^ Carla K. Johnson (Associated Press writer) (2008-09-08). “Fan use linked to lower risk of sudden baby death”. Toronto Star. http://www.parentcentral.ca/parent/article/513143. Retrieved 2008-11-09. , also in Live Science 
^ “Policy Statement for Bumper Pads in Cribs – Consumer Product Safety”. http://www.hc-sc.gc.ca/cps-spc/legislation/pol/bumper-bordure_e.html. Retrieved 2007-06-27.
^ Gizela BA (2001). Postmortem hemoglobin concentration changing in Sprague-Dawley white mouse. Berkala Ilmu Kedokteran 33:207-210 (Indonesian, English Abstract
^ Sherburn RE, Jenkins RO. Cot mattresses as reservoirs of potentially harmful bacteria and the sudden infant death syndrome. FEMS Immunol Med Microbiol. 2004 Sep 1;42(1):76-84. PubMed PMID: 15325400.
^ Paterson DS, Trachtenberg FL, Thompson EG, Belliveau RA, Beggs AH, Darnall R, Chadwick AE, Krous HF, Kinney HC. Multiple serotonergic brainstem abnormalities in sudden infant death syndrome. JAMA. 2006 Nov 1;296(17):2124-32.
^ Hattersley JG. “The answer to crib death: ‘Sudden Infant Death Syndrome’ (SIDS)”. Journal of Orthomolecular Medicine 8 (4). http://www.orthomolecular.org/library/jom/1993/pdf/1993-v08n04-p229.pdf.
^ (January 2007.) “List of journals indexed for Medline, 2007.” (Website). U.S. National Library of Medicine, National Institutes of Health. Retrieved on 2007-09-22.
^ “Fact sheet: Medline journal section.”. (Website.) U.S. National Library of Medicine, National Institutes of Health. Retrieved on 2007-09-22.
^ Cheraskin E. Vitamin C, smoking and SIDS. J R Soc Health. 1995 Oct;115(5):332.
^ Fleming PJ, Blair PS, Mitchell EA (November 2002). “Mattresses, microenvironments, and multivariate analyses”. BMJ 325 (7371): 981–2. doi:10.1136/bmj.325.7371.981. PMID 12411332. PMC: 1124537. http://bmj.com/cgi/pmidlookup?view=long&pmid=12411332.
^ See FSID Press release.
^ cotlife2000.co.nz Errors and fallacies in the UK Limerick Report: an overview, Cot Life 2000
^ Katz DM (2005). “Regulation of respiratory neuron development by neurotrophic and transcriptional signaling mechanisms”. Respiratory physiology & neurobiology 149 (1-3): 99–109. doi:10.1016/j.resp.2005.02.007. PMID 16203214.
^ ICPA – SIDS Research
^ See http://wonder.cdc.gov and http://www3.who.int/whosis/menu.cfm?path=whosis,inds,mort&language=english for data on SIDS by gender in the U.S. and throughout the world.
^ Mage DT, Donner EM (September 2004). “The fifty percent male excess of infant respiratory mortality”. Acta Paediatr. 93 (9): 1210–5. doi:10.1080/08035250410031305. PMID 15384886. http://www3.interscience.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=0803-5253&date=2004&volume=93&issue=9&spage=1210.
^ Osmond C, Murphy M. Seasonality in the sudden infant death syndrome. Paediatr Perinat Epidemiol. 1988 Oct;2(4):337-45.
^ Glatt, John (2000). Cradle of Death: A Shocking True Story of a Mother, Multiple Murder, and SIDS. Macmillan. ISBN 0312973020.
^ Havill, Adrian (2002). While Innocents Slept: A Story of Revenge, Murder, and SIDS. Macmillan. ISBN 0312975171,.
^ Spinelli, Margaret (2003). Infanticide: Psychosocial and Legal Perspectives on Mothers Who Kill. American Psychiatric Pub. pp. 27. ISBN 1585620971,.
^ Stanton J, Simpson A (December 2001). “Murder misdiagnosed as SIDS: a perpetrator’s perspective”. Arch Dis Child. 85 (6): 454–9. doi:10.1136/adc.85.6.454. PMID 11719326. PMC: 1719021. http://adc.bmj.com/cgi/pmidlookup?view=long&pmid=11719326.
^ Emery JL (October 1993). “Child abuse, sudden infant death syndrome, and unexpected infant death”. Am J Dis Child. 147 (10): 1097–100. PMID 8213682.
^ “Investigation of SIDS”. N Engl J Med. 315 (26): 1675–7. December 1986. PMID 3785340.
^ Carol Strickland (1997-10-19). “Investigating a Rash of SIDS Deaths, Exposing Infanticide”. The New York Times. http://query.nytimes.com/gst/fullpage.html?sec=health&res=9A06EED9163FF93AA25753C1A961958260. Retrieved 2008-04-20.
^ “About Statistics and the Law” (Website). Royal Statistical Society. (2001-10-23) Retrieved on 2007-09-22
^ Klonoff-Cohen H, Lam PK, Lewis A (July 2005). “Outdoor carbon monoxide, nitrogen dioxide, and sudden infant death syndrome”. Arch Dis Child. 90 (7): 750–3. doi:10.1136/adc.2004.057091. PMID 15970620.
^ Sudden Infant Death Syndrome (SIDS) and Vaccines http://www.cdc.gov/vaccinesafety/concerns/sids_faq.htm
^ Thomas H. Maugh II (2007) ([dead link] – Scholar search). Hearing loss may foretell SIDS risk. http://www.latimes.com/news/science/la-sci-sids28jul28,1,2214491.story?track=rss.
^ Alastruey J, Sherwin SJ, Parker KH, Rubens DD. Placental transfusion insult in the predisposition for SIDS: A mathematical study. Early Hum Dev. 2009 May 13. [Epub ahead of print]
^ Pelayo R, Owens J, Mindell J, Sheldon S (March 2006). “Bed sharing with unimpaired parents is not an important risk for sudden infant death syndrome: to the editor”. Pediatrics 117 (3): 993–4; author reply 994–6. doi:10.1542/peds.2005-2748. PMID 16510694. http://pediatrics.aappublications.org/cgi/reprint/117/3/993.pdf.
^ Pelligra R, Doman G, Leisman G (July 2005). “A reassessment of the SIDS Back to Sleep Campaign”. Scientific World Journal 5: 550–7. doi:10.1100/tsw.2005.71. PMID 16075152. http://cgi.thescientificworld.co.uk/cgi-bin/processHtml.pl?Id=2005.03.71.html&format=Dreamweaver.
^ a b Jones MW (2004). “Supine and Prone Infant Positioning: A Winning Combination”. J Perinat Educ 13 (1): 10–20. doi:10.1624/105812404X109357. PMID 17273371.
^ Carter H, “Flat Out” – The Guardian: Tuesday July 8, 2003.
^ Kordestani RK, Patel S, Bard DE, Gurwitch R, Panchal J (January 2006). “Neurodevelopmental delays in children with deformational plagiocephaly”. Plast Reconstr Surg. 117 (1): 207–18; discussion 219–20. doi:10.1097/01.prs.0000185604.15606.e5. PMID 16404269. http://meta.wkhealth.com/pt/pt-core/template-journal/lwwgateway/media/landingpage.htm?an=00006534-200601000-00032.
^ Stevens P, “The Flip Side of Back to Sleep”, The O&P Edge.
^ Hofsten C. An action perspective on motor development. Trends Cogn Sci. 2004;Jun;8(6):266-272
^ Sigmundsson H, Haga M. Children and motor competence Tidsskr Nor Laegeforen. 2000;120(25):3048-50
^ Graham J, Gomez M, Halberg A, Earl D, Kreuzman J, Cui J, Guo X. Management of Deformational Plagiocephaly: Repositioning Versus Orthotic Therapy. The Journal of Pediatrics. 2005;10.016:258-22
^ Lewak N. “Book Review: SIDS”. Arch Pediatr Adolesc Med 158 (4): 405. http://archpedi.highwire.org/cgi/content/full/158/4/405.
1989 “Sleep and Arousal Synchrony of Co-Sleeping Human Mother-Infant Pairs: Implications for the Study of SIDS.” Fourth World Congress of Infant Psychiatry and Allied Disciplines (poster session). Lugano, Switzerland. Presented also at 58th Annual Meeting, American Association of Physical Anthropologists.
1989 “Why Anthropologists Should Study SIDS.” Annual Meeting of the Southwest Anthropological Society. Riverside, California, April.
1988 “Sleep and Breathing Patterns of Co-Sleeping Mothers and Infants.” Eighty-seventh Meeting of the American Anthropological Association. Chicago, Illinois, November 19-23.
1986 “Can Parents Drive the Breathing of Their Infants? Evolutionary and Developmental Hypotheses on Contributing Environmental Factors in Sudden Infant Death.” Third World Congress on Infant Psychiatry and Allied Disciplines. Stockholm, Sweden, August 3-7.
Heaton PA, Sage MD (February 1995). “Fatal smothering by a domestic cat”. N Z Med J. 108 (994): 62–3. PMID 7885652.
Kearney MS, Dahl LB, Stalsberg H (September 1982). “Can a cat smother and kill a baby?”. Br Med J (Clin Res Ed) 285 (6344): 777. PMID 6810995.