Acta Pdiatrica ISSN 08035253

REVIEW ARTICLE

SIDS: past, present and future

Edwin A Mitchell (e.mitchell@auckland.ac.nz)
Department of Paediatrics, University of Auckland, Auckland, New Zealand

Medal issued by the Swedish Paediatric

Society and awarded every five years in
memory of the Father of Paediatrics Nils
Rosen von Rosenstein. Sporrongs engraving by sculptor Ake Hammarberg
19001974.

Keywords
Bed sharing, Prevention, risk- and protective
factors, Sudden infant death syndrome
Correspondence
Edwin Mitchell, Professor of Child Health Research,
Department of Paediatrics, University of Auckland,
Private Bag 92019, Auckland, New Zealand.
Tel: +(64 9) 3737599 |
Fax: +(64 9) 3737486 |
Email: e.mitchell@auckland.ac.nz

Abstract
Despite the large reduction in SIDS mortality, which occurred in the early 1990s following the Back to
Sleep campaigns, SIDS remains the leading cause of death in the postneonatal age group. This paper
describes the position in the 1980s, the contribution of the New Zealand Cot Death Study, what should
be recommended and the current research priorities.
Conclusion: SIDS is preventable. Application of what we currently know could eliminate SIDS. The challenge
is to find ways of implementing our knowledge.

Received
20 May 2009; revised 27 July 2009;
accepted 13 August 2009.
DOI:10.1111/j.1651-2227.2009.01503.x

Sudden infant death syndrome (SIDS) has been present

since antiquity. Indeed it is described in the Old Testament
of the Bible: 1 Kings 3:19 And this womans child died in
the night. It was not until 1965 that a specific International
Classification of Diseases (ICD) code was allocated for
SIDS (ICD-8 795). The prevalence of SIDS increased
largely because of diagnostic transfer, predominantly from
respiratory infections, which were often minor. By the
1980s, SIDS mortality was very high in many developed
countries. SIDS was described as unpredictable and unpreventable. Indeed even today many reputable organizations
subscribe to this view (1). Although SIDS cannot be
predicted, I would like to challenge the contention that it
cannot be prevented.
This study will describe where we were in the 1980s, the
New Zealand Cot Death Study, what should be recommended in 2009, postulated mechanisms and what needs to
be done in the future.

1712

SIDS IN 1980S
In the 1980s, there was considerable concern about SIDS
mortality in New Zealand (2). The SIDS mortality rate was
higher than that in other countries, furthermore, total postneonatal mortality was higher (3), thus the high rate could
not be explained by diagnostic transfer. The non-SIDS mortality rate was similar to other comparable countries, indicating that differences in health care services were unlikely
to explain these differences.
Examination of SIDS mortality data showed that there
was a male excess, the risk was higher in infants born
with low birth weight or preterm, those coming from
disadvantaged communities e.g. Maori, and those born
to young mothers. Deaths varied by latitude (more prevalent in the higher latitudes), and were more frequent
in winter. Furthermore, there was a characteristic age
distribution, with few deaths in the first month of life,
mortality rates peaking at 24 months then becoming

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Mitchell

increasingly uncommon (2). These characteristics were

similar in all countries.
The apnoea hypothesis was the dominant theory for the
mechanism of SIDS in the 1970s and 1980s (4). Infants
who subsequently died of SIDS were found to have significantly fewer apneic pauses than age-matched control
infants, which is in the opposite direction predicted by the
apnoea hypothesis (5). Furthermore, the small differences
are unable to distinguish those infants who are at risk of
SIDS and those who are not. Documented monitoring of
cardiorespiratory patterns of infants dying of SIDS is also
not consistent with the apnoea hypothesis (6,7). Despite
apnoea monitoring programmes, SIDS rates did not
decrease. This hypothesis fell into disrepute following the
murder conviction (in 1993) of the mother of the multiple
cases of SIDS in one family in the original case report (8).
In the mid 1980s, the New Zealand Department of
Health, now Ministry of Health, established postneonatal
mortality review committees. The aims were to (i) identify
preventable deaths, and (ii) develop and recommend prevention strategies, thus reducing infant mortality at a local
level. I established and chaired the first committee, which
covered the Auckland region. After 2 years, we reviewed
the findings (9). We concluded that potentially preventable
deaths were infrequent (10%). There were 80 cases of SIDS,
and notable factors were identified, for example co-sleeping and changes in routine and environment, but we could
not interpret their importance as we did not know how prevalent these factors were in infants who did not die.
The lack of control data led to the development of the New
Zealand Cot Death Study.

THE NEW ZEALAND COT DEATH STUDY

This was a large nationwide casecontrol study (10,11). The
specific aim was to identify risk factors for SIDS, with a
particular emphasis on infant care practices. This research
project commenced on 1 November 1987 under my
directorship and collected comprehensive information on
infants dying from SIDS in the postneonatal age groups in
most main centres in New Zealand (covering about 80% of
all live births in New Zealand). This study examined 485
SIDS cases and 1800 controls. Very satisfactory completion
rates were achieved; obstetric records were examined and
parental interviews were completed in 97.5% and 86.9% of
subjects respectively. This major study would not have been
possible without the skills and enthusiasm of Drs Scragg
(epidemiologist), Becroft (pathologist), Taylor, Hassall,
Barry, Allen, Roberts and Ford (paediatricians) and Mr
Stewart (biostatistician) and the co-operation of the Department of Health Statistics Services.
Because of public and health professional concern about
SIDS, we analysed some of the data from the first year of
the study (10). As expected many risk factors for SIDS were
confirmed including:
Socioeconomic factors: (unmarried, manual occupation and younger age mother left school),

SIDS: Past, present and future

Pregnancy (younger age of mother at first pregnancy,

younger age of mother at infants birth, more than
4 months pregnant when first attended antenatal
clinic, non-attendance at antenatal education classes
and increasing number of previous pregnancies),
Infant: (Maori ethnicity, male, low birth weight and
preterm birth) and
Postnatal factors: (age of infant, time of day, season,
region and infant admission to a neonatal unit).
In addition, however, we identified risk factors, which
were potentially amenable to modification. These were:
prone sleeping position of baby,
maternal smoking and
not breastfeeding.
After controlling for all the above variables, the relative
risks associated with prone sleeping position, maternal
smoking and not breast feeding were still statistically significant. Population attributable risk calculations suggested
that these three risk factors accounted for 79% of deaths
from SIDS in New Zealand. The SIDS rate could theoretically be reduced from 4 1000 live births to 1 1000 live
births if infants were not placed prone to sleep, mothers did
not smoke and babies were breastfed.
At my instigation a group comprising of the Plunket
Society, Department of Health, New Zealand Cot Death
Association, Area Health Boards, Maori representatives, the
Commissioner for Children and the research group met to
devise strategies to produce these changes in infant care
practices. The New Zealand Cot Death Prevention Programme was launched on 27 February 1991 (11), although
the prevalence of prone sleeping position was decreasing
before the launch (12). Figure 1 shows the first poster used
in the national prevention campaign in 1991. Note at this
time, the message was side or back sleeping position, as the
increased risk with side sleeping was not firmly established.
This subsequently was changed to back or side, then back
only.

Figure 1 The first poster in the New Zealand Cot Death Prevention Campaign
in 1991.

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SIDS: Past, present and future

Mitchell

Sleep position
The risk of SIDS with prone sleeping position is well established (28) and has been largely eliminated and thus will
not be discussed further. We were the first group to report
an increased risk of SIDS with the side sleeping position
(10,13). A meta-analysis of 10 studies examining side sleeping position reported a pooled odds ratio (OR) of 2.0 [95%
confidence interval (CI) = 1.72.4] (29). Infants placed
supine (back) to sleep are at the lowest risk of SIDS, which
supports the recommendation that this is the preferred
sleeping position of healthy infants. The prevalence of side
sleeping position is declining but in New Zealand is still
about 26.3% (30).

8.0

Mortality per 1000 live births

7.0
6.0
5.0
4.0
3.0
2.0
1.0

02

00

04
20

20

98

20

94

96

19

19

90

88

92

19

19

19

19

84

86
19

19

19

82

0.0

Figure 2 New Zealand postneonatal (thin line) and SIDS (thick line) mortality
(per 1000 live births), 19822005 (2005 is provisional data).

A fourth risk factor, namely infants sharing a bed with

another person, was added to the prevention programme in
1992 (13). The prevention programme has been spectacularly successful (Fig. 2).
The New Zealand Cot Death Study has identified many
new risk factors, including smoking by the father (14), postnatal depression (15), interaction between smoking and bed
sharing (16), the protective effect of pacifiers (17) and the
protective effect of sleeping in the same bedroom as the parents (18). We also showed that the increased risk in Maori
was explained by higher prevalence of maternal smoking
and co-sleeping with infant (19). The data have confirmed
the importance of thermal insulation (20), duration and
degree of breastfeeding (21) and symptoms of illness (22). It
has excluded a causal relationship between SIDS and
immunizations (23), types of nappies and how they are
cleaned (24) and travel and changes in routine in the preceding 2 days (25). We also described the epidemiology of
intrathoracic petechial haemorrhages and intrapulmonary
haemorrhage in SIDS for the first time (26,27).

WHAT SHOULD BE RECOMMENDED?

Table 1 summarizes the major modifiable risk and protective factors for SIDS.

Table 1 Major modifiable risk and protective factors for SIDS

Risk factors
Prone and side sleeping position
Maternal smoking in pregnancy
Bed sharing for infants of mothers who smoked
Head covering
Protective factors
Sleeping in the parental bedroom
Breastfeeding
Pacifier use

1714

Smoking
There were 52 studies before the Back to Sleep campaigns
and these showed an increased risk of SIDS with maternal
smoking [pooled OR = 2.9 (2.83.0)] (31). Since the Back
to Sleep campaign, there have been at least 17 studies. All
showed an increased risk [pooled OR = 3.9 (3.84.1)].
However, it is difficult to disentangle the effect of maternal
smoking in pregnancy from smoking by the mother after the
birth, as few mothers change their smoking behaviour in
such a short period of time. One way of establishing the
importance of environmental tobacco smoking is to examine the risk of SIDS with smoking by the father where the
mother is a non-smoker. There have been seven such studies [pooled OR = 1.5 (95% CI = 1.21.8)]. Although this is
statistically significant, the effect of environmental tobacco
smoking is small. We have argued that the relationship
between maternal smoking in pregnancy and SIDS is causal. From a biological perspective, it is likely that the
predominant effect from maternal smoking is likely to be
in utero exposure of the foetus (31).
Bed sharing
In 1992, we reported the association of bed sharing with
SIDS (11). The following year my colleague Dr Robert
Scragg showed that the association was predominantly
among infants of mothers who smoked (16). This has been
confirmed in many studies (3234). We showed that duration of bed sharing was important, with infants spending the
whole night in bed with their parents being at higher risk of
SIDS than those spending less than 2 h (16). Bed sharing
infants who are placed back in their own beds are not at
increased risk (33). However, mothers may intend to place
their infant back in their own cot, but fall asleep. This may
account for why tired mothers and SIDS cases unaccustomed to bed sharing appear to be at higher risk. This provides strong evidence that bed sharing is the problem, and
not just the characteristics of the families that bed share.
The risk of SIDS with bed sharing is higher in younger
infants. Carpenter et al. showed that even in infants whose
mothers did not smoke there is an increased risk of SIDS in
infants up to 3 months of age (32,35). Co-sleeping on a sofa
or couch has been identified as a risk for SIDS (33,36).
Infants sharing a bed with older siblings are at increased
risk (16,37), although there are no data to state whether

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Mitchell

Table 2 Summary of the risk of sudden unexpected death in infancy and sudden infant death syndrome with bed sharing
The risk of SIDS with bed sharing is high when the mother smokes or smoked
in pregnancy
The risk of SIDS with bed sharing is higher in younger infants
There is a small increased risk with bed sharing when the mother does not
smoke in infants less than 3 months of age
Bed sharing infants placed back in their cot are not at increased risk of SIDS
The longer the infant bed shares during the night the greater the risk of SIDS
The risk of SIDS with bed sharing is higher if the adult has been drinking, taking
drugs or medications that might impair their awareness of the infant or if the
adult is obese or if the baby was preterm or low birth weight
Co-sleeping on a couch or sofa is associated with a high risk of SIDS, although
the number of infants exposed to this risk is small
Infants bed sharing with older siblings are at increased risk, although there are
no data either way for twins sharing (sometimes referred to as co-bedding)
There is no evidence that bed sharing is protective against SIDS in any group

co-bedding of twins is a risk or not. There is no evidence

that bed sharing is protective against SIDS in any group.
The epidemiological evidence is summarized in Table 2.
When an interaction is present, removal of either factor
will achieve the same effect. Although stopping smoking is
desirable, this is difficult to achieve. The emphasis on stopping the co-sleeper from smoking rather than stopping the
smoker from co-sleeping is not addressing the problem.
Bed sharing is fine for cuddles and breastfeeding, but
baby should be in its own bed when parents go to sleep. In
1994, we recommended a cot beside the parent bed for the
first 6 months of life (38). This approach has been followed
by United Kingdom Department of Health (39) and the
American Academy of Pediatrics (40).
What is the down side of advising that infants should not
bed share? The major concern is that this will impact on
breastfeeding (41). Bed sharing increases the frequency and
duration of suckling (42,43). Although bed sharing is associated with a longer duration of breastfeeding, the effect is
quite small. The other concern is that parents will reject this
advice and with it other SIDS prevention messages. I
believe that parents have a right to know what risks they are
exposing their infants to and that health professionals
should advise parents that the safest place for an infant to
sleep is in a cot beside the parental bed in the first 6 months
of life.
Head covering
A recent meta-analysis has been reported (44). There were
10 studies with control data. The prevalence of head covering in SIDS cases was 24.6% vs. 3.2% in controls [pooled
unadjusted OR = 9.6 (95% CI = 7.911.7) and the pooled
adjusted OR = 16.9 (95% CI = 12.622.7)]. Population
attributable risk was 27.1%.
In UK the Feet to foot campaign advised parents to place
the feet of the infant at the foot of the cot to prevent head
covering (45). This advice was endorsed by the American
Academy of Pediatrics (46). Although intuitively sensible,
there is no evidence that it reduces risk of head covering or
lowers risk of SIDS.

SIDS: Past, present and future

Pacifiers
The New Zealand Cot Death Study was the first to examine
the association between pacifier use and a reduced risk of
SIDS (17). There are now seven further studies. Two metaanalyses both concluded that pacifier use was associated
with a reduced risk of SIDS and that the evidence is consistent and moderately strong (47,48). The American Academy
of Pediatrics task force recommended the use of a pacifier
throughout the first year of life according to the following
procedures (40):
The pacifier should be used when placing the infant
down for sleep and not be reinserted once the infant
falls asleep. If the infant refuses the pacifier, he or she
should not be forced to take it.
Pacifiers should not be coated in any sweet solution.
Pacifiers should be cleaned often and replaced regularly.
For breastfed infants, delay pacifier introduction until
1 month of age to ensure that breastfeeding is firmly
established.
However, the potential disadvantages were dismissed,
particularly a reduced duration of breastfeeding (49) and
increase in otitis media (50).
The approach we have taken in New Zealand is that the
possible detrimental effects have to be balanced against the
low risk of SIDS. We recommend that pacifiers should no
longer be discouraged, but not specifically encouraged.
Room sharing
In 1996, our group was first to show the protective effect of
sleeping in the parental bedroom (18). There have been several other studies, which have reported similar findings
(Table 3) (32,33,37,38,51). Room sharing providing the
infant is not bed sharing decreases 3-fold the risk of SIDS.
This supports the recommendation that baby should sleep
in the same room as the parents for the first 6 months of life.
Breastfeeding
Most studies have shown that SIDS is lower in breast fed
infants (52), but as breastfeeding in most developed countries is associated with socioeconomic advantage, adjustment for socioeconomic factors results in a reduced level of
protection. Some studies have concluded there is no
decreased risk from breastfeeding (53,54). However, others,
including us, have argued for a protective effect (21,55,56).
Table 3 Studies showing reduced risk of SIDS with room sharing
Percent
exposed
Author

Ref

Country

Univariate Multivariate
OR
Case Control OR

Scragg (1996)
Blair (1999)
Hauck (2003)
Carpenter (2004)
Tappin (2005)

(18)
(33)
(37)
(32)
(51)

New Zealand
England
United States
Europe
Scotland

20.7
25.3
20.8
28.0
35.8

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37.1
39.0
28.1
44.5
63.5

0.44
0.53
0.67
0.49
0.32

0.25
0.51
Not reported
0.32
0.31

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SIDS: Past, present and future

Mitchell

POSTULATED MECHANISMS
A large number of mechanisms for SIDS have been proposed, although most such as poisoning by immunizations
or toxic gases are unsubstantiated.
The triple risk hypothesis has been proposed by a number of authors (5759). This hypothesis proposes that there
is an underlying vulnerability of the infant, an age-related
developmental stage and precipitating factor or stressors
(Fig. 3). Factors producing a vulnerable infant include
genetic, abnormalities of serotonin (5-HT) neurones and
pregnancy related factors. Genetic studies have identified
several ways that SIDS cases differ from healthy infants.
Polymorphisms include cardiac ion channelopathies, serotonin transporter gene, autonomic nervous system development, complement C4 gene and interleukin-10 cytokine
(60,61). 5-HT neurons in the medulla oblongata regulate
multiple aspects of brainstem-mediated control of respiratory and autonomic function (62,63). Failure of protective
reflexes would place the infant at risk for sudden death during normal life stresses that may occur in sleep such as
hypoxia, rebreathing or airway obstruction. Detailed studies
of the brainstem show that some SIDS infants have a developmental abnormality in the medullary network (63). Pregnancy related factors include low birth weight, preterm
birth and maternal smoking. Maternal smoking causes foetal growth retardation (64), reduction in lung growth and
elasticity (65), and alters the neural control of autonomic,
behavioural and homeostatic function (62,66). Maternal
smoking during pregnancy alters cardiovascular function in
the weeks after birth (67). This might lead to failure of the
homeostatic cardiovascular responses resulting in substantial loss of blood pressure, bradycardia and death (68).
Precipitating factors or stressors include sleep position,
bed sharing, thermal stress, head covering, infection, etc.
The risk of SIDS associated with the prone sleeping position
is greater in winter (69), at higher latitudes (70) and altitudes (71), with excess thermal insulation (20,72) and with
illness (22,72). This suggests that the mechanism by which
prone sleeping position causes SIDS is in some way related
Genetic risk factors

Pregnancy related risk factors

(low birthweight, smoking)

Vulnerable infant
(impaired autonomic regulation)

At risk age group

Environmental risk factors

(sleep position, bed sharing, thermal stress, head covering, etc)

SIDS
Figure 3 Schematic representation of how genetic and environmental risk factors might interact.

1716

to temperature (73). Bed sharing and head covering might

cause thermal stress, airway obstruction or rebreathing of
expired gases.
Parents frequently report that their babies had minor
symptoms of infection, especially respiratory tract symptoms, in the days immediately before the death (22,74).
These infections are not thought to cause the death. Immunoglobulin levels (IgG) in the first year of life are high in the
first month of life due to passive transfer from the mother
in utero. The levels then decrease and are lowest at 2
4 months of age, but then gradually increase as the infants
produce their own IgG. The levels are a mirror image of the
age distribution of SIDS cases. Blackwell et al. have postulated that some SIDS deaths are caused by uncontrollable
inflammatory reaction to infectious agents (especially pyrogenic toxins of Staphylococcus aureus) (75,76). The proinflammatory cytokines induced by the infections can cause
respiratory and cardiac dysfunction, pyrexia, shock and
arousal defects. Prone sleeping position increases pooling of
nasal secretions resulting in an increase in bacterial colonization (77). Staphylococcus aureus may produce pyrogenic
toxins, but only when the temperature is between 37 and
40C (76). The nasopharynx is usually below this, but prone
position and a viral infection may increase the temperature
in the nasopharynx (78).

THE FUTURE
SIDS can be prevented and the application of what we
already know has the potential to further reduce SIDS. The
evidence supporting these risk and protective factors is
strong, as I have described, and should be included in SIDS
prevention campaigns. Antenatal and neonatal services
have an important role. Nursing care plans should be developed to establish these infant care practices as the norm.
The biggest influence is what is performed on the postnatal
wards in the first few days of life. If a midwife nurse places
a baby on the back to sleep, then this sleeping position will
be continued by the mother following discharge home. Neonatal Intensive Care Unit graduates should be placed supine
prior to discharge home. The UNICEF WHO Baby
Friendly Hospital Initiative is applicable to developed as
well as developing countries (79).
In New Zealand in 2004, there were 45 SIDS cases
(ICD-10 R95); many were described as being in an unsafe
sleeping environment (80). In addition, there were eight
deaths certified as other ill defined (ICD-10 R99), which
include unascertained. In many of these cases the coroner
was unable to determine whether the death was due to SIDS
or accidental suffocation in bed. Worryingly, there were 16
deaths resulting from accidental suffocation and strangulation in bed (W75). In Wellington, New Zealand over a 10year period 54% of sudden unexpected deaths in infancy
occurred while co-sleeping (81). Thus the biggest gain in
New Zealand would come from stopping bed sharing.
There are two innovative interventions Cribs for Kids
(82), which is a cradle loan scheme, and the wahakura safe
bed-sharing project, which is a Maori initiative in New

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SIDS: Past, present and future

DEDICATION
This study is dedicated to the parents of both cases and
controls who so willingly shared information with our
research team. Without their contribution we would not
have made the advances that have resulted in a reduction of infant mortality in New Zealand and many other
countries.

References

Figure 4 The Wahakura.

Zealand (83). Wahakura is a flax woven basket in which

baby sleeps and the basket can be taken into the parental
bed (Fig. 4). The families are also taught about the dangers
of bed sharing with their infant. Although these interventions have yet to be evaluated, it is pleasing to see new
approaches to establishing a safe sleeping environment for
infants.
The major research need is educational research, in particular how to produce behavioural change. The major
questions are how to avoid head covering and how to bed
share safely, as we know that some parents will choose to
continue bed sharing despite the evidence of the risk.
Until we understand the mechanism of SIDS, there will
always be concerns that the risk factors are associations
and not part of the causal mechanisms. Genetic studies
offer a way forward, and I expect that in the next decade
there will be considerable advances in this area. It is
likely that the list of polymorphisms will expand rapidly
once genome wide association studies for SIDS are
reported. The next major advance will come from studies
examining the interaction between genetic and environmental risk factors.

CONCLUSIONS
SIDS is preventable. Application of what we currently know
could eliminate SIDS. The challenge is to find ways of
implementing our knowledge.

ACKNOWLEDGEMENTS
This paper is based on the Nils Rosen von Rosenstein
Award Lecture given on 24 April 2009 in Uppsala, Sweden.
The award honours the recipient and all members of the
New Zealand Cot Death Study Group, which comprised
Robert Scragg, David Becroft, Alistair Stewart, Carol Everard, John Thompson, Liz Allen, David Barry, Ian Hassall, Alison Roberts, Rodney Ford, Barry Taylor and Sheila
Williams. The New Zealand Cot Death Study was funded
by the Medical Research Council of New Zealand and
Hawkes Bay Medical Research Foundation. Ed Mitchell is
supported by the Child Health Research Foundation.

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