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* [http://www.sidsitalia.it Seeds for SIDS] (Italian support group)
* [http://www.sidsitalia.it Seeds for SIDS] (Italian support group)
* [http://www.sidsandkids.org SIDS and Kids] (Australian support group)
* [http://www.sidsandkids.org SIDS and Kids] (Australian support group)
* [http://www.maxwellsmakerr.org Maxwell's Makerr] (Raises awareness, SIDS prevention, and funds research)


===Related websites===
===Related websites===

Revision as of 05:11, 13 August 2010

SIDS

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.

Definition

Typically the infant is found dead after having been put to bed, and exhibits no signs of having suffered.[1]

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:

  1. an autopsy;
  2. investigation of the scene and circumstances of the death;
  3. exploration of the medical history of the infant and family.

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.[2]

Risk factors

The cause of SIDS is unknown. 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 potential 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 on November 1, 2006 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.[3]

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 a risk factor in some cases of SIDS. Both bacteria were present at greater than usual concentrations in infants who died from SIDS.[4] 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 risk factors associated with increased probability of the syndrome based on information available prior to this recent study.

Prenatal risks

Post-natal risks

  • mold (can cause bleeding lungs plus a variety of other uncommon conditions leading to a misdiagnosis and death). It is often misdiagnosed as a virus, flu, and/or asthma-like conditions.[16]
  • low birth weight (in the U.S. from 1995-1998 the rate for 1000-1499 g was 2.89/1000 and for 3500-3999 g it was 0.51/1000)[17][18]
  • exposure to tobacco smoke[19]
  • prone sleep position (lying on the stomach, see sleep positioning below)[20]
  • not breastfeeding[21]
  • elevated or reduced room temperature[22]
  • excess bedding, clothing, soft sleep surface and stuffed animals[23]
  • co-sleeping with parents or other siblings may increase risk for SIDS, but the mechanism remains unclear[24]
  • infant's age (incidence rises from zero at birth, is highest from two to four months, and declines towards zero at one year)[25]
  • premature birth (increases risk of SIDS death by about 4 times.[17] 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)
  • anemia[26]

Hypotheses

Mattress bugs

A 2004 study hypothesized that insects (called "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.[27]

Brain disorder

A recently published research article[3] 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 greater for premature infants. Males have fewer serotonin receptors than females, perhaps contributing to the increased incidence of SIDS in the demographic. [28]

A 2010 study suggests Interleukin-2, a neuromodulator, as the potential mechanism. They found intense neuronal IL-2 immune-reactivity in the SIDS brainstem, which could be responsible for decreased cardiorespiratory and arousal responses. [29]

In addition, a study done in 2006 showed that a possible cause of SIDS is because parents leave their infants in a position known as the Trendelenburg position.[30] This position can cause the brain stem to fall, and in a result, the brain becomes "crushed". The proper position for an infant is either Fowler's position or Sims'.[citation needed]

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.[31] 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."[32]

However, Dr. John Olssen at East Carolina University has pointed out that this study had a number of methodological flaws, such selection and recall bias, low enrollment numbers, and dissimilar study groups. Olssen argues that although fan use is probably not harmful, it should not be recommended as a means to reduce the risk of SIDS.[33]

Vitamin C

In the 1970s, high doses of vitamin C were touted as a preventive measure for SIDS,[34] although the claim was controversial even then.[35][36] Subsequent studies failed to support a preventive role for vitamin C in SIDS.[37] To the contrary, a 2009 study found that high levels of vitamin C were strongly associated with SIDS, possibly through a pro-oxidant interaction with iron.[38]

Co-sleeping

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.[39] One article reports that co-sleeping infants have a greater risk of airway covering than when the same infant sleeps alone in a cot.[40]

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.[citation needed]

Support for this hypothesis was based on the observation that the risk of cot death rises from one sibling to the next.[citation needed] Richardson claimed 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[41] 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.

Dr. Jim Sprott recommends new parents either buy bedding free of the toxic compounds or to wrap the mattresses in a barrier film to prevent the escape of the gases. Sprott claims that no case of cot death has ever been traced back to a properly manufactured or wrapped mattress.[42]

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."[43] 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."

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.[44]

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.[45]

Cervical spinal injury from 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.[46] 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.

Genetics

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.[47][48] 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 hypothesis 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 1⁄3 that is protective of transient cerebral anoxia. An unprotected XY male would occur with a frequency of 2⁄3 and an unprotected XX female would occur with a frequency of 4⁄9. The ratio of 2⁄3 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.[49]

The JAMA 2006 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",[3] but the authors could not reproduce it in their 2010 paper.[50] However, such neurological prematurity decreases with age, but the male fraction of approximately 0.61 persists each month throughout the first year of life.[51] 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.[17]

Child abuse

Several instances of infanticide have been uncovered where the diagnosis was originally SIDS.[52][53] This has led some researchers to estimate that 5% to 20% of SIDS deaths are infanticides.[54][55][56][57] 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.[58]

A former pediatrician, Roy Meadow, from the UK 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).[59] 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. Meadow was struck off in 2005.[60]

The Royal Statistical Society issued a media release refuting the expert testimony in one UK case in which the conviction was subsequently overturned.[61]

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."[62] 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

According to the U.S. Centers for Disease Control and Prevention, several studies have failed to provide sufficient evidence of a causal link between vaccinations and SIDS. They state:

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.[63]

Inner ear damage

Records of hearing tests (oto-acoustic emissions, OAEs) administered to certain infants show that those who later died of SIDS had differences in the pattern of these tests compared with normal babies. To be specific the OAE signal to noise ratio was reduced in the right ear in the SIDS babies (Rubens DD et al. Early Human Development 84, 225-9 (2008)).[64] It should be noted this was a small study (n=31 cases and 31 controls), had serious limitations (several significant factors were not controlled), and has been criticised from various perspectives.[65] The authors' suggestion for the cause of SIDS is that the deaths are caused by disturbances in respiratory control (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.[66]

Differential diagnosis

Some conditions that may be undiagnosed and thus could be alternative diagnoses to SIDS include:

For example an infant with MCAD deficiency could have died by "classical SIDS" if found swaddled and prone with head covered in an overheated room where parents were smoking. Genes of susceptibility to MCAD and Long QT syndrome do not protect an infant from dying of classical SIDS. Therefore presence of a susceptibility gene, such as for MCAD, means the infant may have died either from SIDS or from MCAD deficiency. It is impossible for the pathologist to distinguish between them.

Prevention

Sleep positioning

Main article: Back to sleep
A plot of SIDS rate from 1988 to 2003

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 U.S. and New Zealand.[74] However, the absolute incidence of SIDS prior to the Back to Sleep Campaign was already dropping in the U.S., from 1.511 per 1000 in 1979 to 1.301 per 1000 in 1991.[17]

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[75] 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.

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.[76]

Breastfeeding

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."[77] However, a more recent study shows that breast feeding reduces the risk of SIDS by approximately 50% at all infant ages.[78]

Secondhand smoke reduction

According to the U.S. Surgeon General's Report, secondhand smoke is connected to SIDS.[79] Infants who die from SIDS tend to have higher concentrations of nicotine and cotinine (a biological marker for secondhand smoke exposure) in their body fluids than those who die from other causes.[80] 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.[81]

Bedding

Product safety experts advise against using pillows, sleep positioners, bumper pads, stuffed animals, or fluffy bedding in the crib and recommend instead dressing the child warmly and keeping the crib "naked."[82][83]

Blankets should not be placed over an infant's head.[84] It has been recommended that infants should be covered only up to their chest with their arms exposed. This reduces the chance of the infant shifting the blanket over his or her 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[85] 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.[86] The use of swaddling clothes, a traditional form of infant restraint which leaves only the head uncovered, is controversial.[87][88][89][90]

Pacifiers

According to a 2005 meta-analysis, most studies favor pacifier use.[91] 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.[92] SIDS experts and policy makers haven't recommended the use of pacifiers to reduce the risk of SIDS because of several problems associated with pacifier use, like increased risk of otitis, gastrointestinal infections and oral colonization with Candida species.[92] 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 ambient factors, and it reduced the effect of other risk factors.[93] 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.

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[94] 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.

Concerns regarding 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.[95]

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.[96] 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.[97]

Other side effects of the back sleeping position include increased rates of shoulder retraction, positional plagiocephaly, and positional torticollis.[98] 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."[99] 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.[100]

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.[101]

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.[98] 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.[102][103] 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.[104] 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.[105] Supine sleeping infants cannot self-treat their own torticollis.

Epidemiology

SIDS was responsible for 0.543 deaths per 1,000 live births in the U.S. in 2005.[17] 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.[106] 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%.[106] 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".[106]

Notes

  1. ^ Health Canada SIDS Healthy Babies SIDS Page.
  2. ^ NZ Ministry of Health
  3. ^ a b c Paterson DS, Trachtenberg FL, Thompson EG; et al. (2006). "Multiple serotonergic brainstem abnormalities in sudden infant death syndrome". JAMA. 296 (17): 2124–32. doi:10.1001/jama.296.17.2124. PMID 17077377. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  4. ^ Attention: This template ({{cite pmid}}) is deprecated. To cite the publication identified by PMID 18514728, please use {{cite journal}} with |pmid=18514728 instead.
  5. ^ Buttigieg J, Brown S, Zhang M, Lowe M, Holloway AC, Nurse CA (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. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link) CS1 maint: unflagged free DOI (link)
  6. ^ Kraus JF, Greenland S, Bulterys M (1989). "Risk factors for sudden infant death syndrome in the US Collaborative Perinatal Project". Int J Epidemiol. 18 (1): 113–20. doi:10.1093/ije/18.1.113. PMID 2722353. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  7. ^ Henriksen T (1999). "Foetal nutrition, foetal growth restriction and health later in life". Acta Paediatr Suppl. 88 (429): 4–8. doi:10.1080/080352599750029862. PMID 10419226. {{cite journal}}: Unknown parameter |month= ignored (help)
  8. ^ Kandall SR, Gaines J, Habel L, Davidson G, Jessop D (1993). "Relationship of maternal substance abuse to subsequent sudden infant death syndrome in offspring". J. Pediatr. 123 (1): 120–6. doi:10.1016/S0022-3476(05)81554-9. PMID 8320605. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  9. ^ Spiers PS, Wang L (1976). "Short pregnancy interval, low birthweight, and the sudden infant death syndrome". Am. J. Epidemiol. 104 (1): 15–21. PMID 937342. {{cite journal}}: Unknown parameter |month= ignored (help)
  10. ^ Zhou FC, Fang Y, Goodlett C (2008). "Peptidergic agonists of activity-dependent neurotrophic factor protect against prenatal alcohol-induced neural tube defects and serotonin neuron loss". Alcohol. Clin. Exp. Res. 32 (8): 1361–71. doi:10.1111/j.1530-0277.2008.00722.x. PMC 2758042. PMID 18565153. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  11. ^ Byard RW (2007). "Marked obesity in infancy and relationship to sudden infant death". J Paediatr Child Health. 43 (9): 649–50. doi:10.1111/j.1440-1754.2007.01179.x. PMID 17688652. {{cite journal}}: Unknown parameter |month= ignored (help)
  12. ^ Carroll-Pankhurst C, Mortimer EA (2001). "Sudden infant death syndrome, bedsharing, parental weight, and age at death". Pediatrics. 107 (3): 530–6. doi:10.1542/peds.107.3.530. PMID 11230594. {{cite journal}}: Unknown parameter |month= ignored (help)
  13. ^ American Sudden Infant Death Syndrome Institute
  14. ^ Mage DT, Donner M (1997). "A genetic basis for the sudden infant death syndrome sex ratio". Med. Hypotheses. 48 (2): 137–42. doi:10.1016/S0306-9877(97)90280-2. PMID 9076695. {{cite journal}}: Unknown parameter |month= ignored (help)
  15. ^ David T. Mage and Maria Donner, "A Unifying Theory for SIDS," International Journal of Pediatrics, vol. 2009, Article ID 368270, 10 pages, 2009. doi:10.1155/2009/368270
  16. ^ Weinberg ED (2000). "Association of primary Pneumocystis carinii infection and sudden infant death syndrome". Clin. Infect. Dis. 30 (6): 991. doi:10.1086/313796. PMID 10880335. {{cite journal}}: Unknown parameter |month= ignored (help)
  17. ^ a b c d e "Cdc Wonder". Wonder.cdc.gov. 2010-02-24. Retrieved 2010-04-17.
  18. ^ Hunt CE (2007). "Small for gestational age infants and sudden infant death syndrome: a confluence of complex conditions". Arch. Dis. Child. Fetal Neonatal Ed. 92 (6): F428–9. doi:10.1136/adc.2006.112243. PMID 17951549. {{cite journal}}: Unknown parameter |month= ignored (help)
  19. ^ Office of the Surgeon General of the United States Report on Involuntary Exposure to Tobacco Smoke (PDF)
  20. ^ Willinger M, Hoffman HJ, Hartford RB (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. {{cite journal}}: Unknown parameter |month= ignored (help)CS1 maint: multiple names: authors list (link)
  21. ^ McKenna JJ, McDade T (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. {{cite journal}}: Unknown parameter |month= ignored (help)
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Further reading

Organizations

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