Since we were established in 1985, The Scottish Cot Death Trust has invested more than £3.2 million in research projects locally, nationally and internationally. We have contributed to global understanding of the pathology and risk factors of sudden unexpected death in infancy.

If you are interested in submitting an Initial Proposal for research, please see the Applying for a grant page. Alternatively, call on 0141 357 3946 to discuss the application process.

Research Investment Strategy

Research funded by the Trust must be of the highest scientific merit, in terms of the importance of the investigation, excellence of the study, ability of the research team, and probability of success. Research proposals must demonstrate clear relevance to the issue of cot death and have potential for prevention or other clinical or public health benefit.

Research applications are assessed through a stringent, highly competitive peer review process.

The charity has limited funds with which to fund research grants. As a guideline, the majority of grants awarded in the past are in the region of £30,000 – £80,000 per project for up to three years, with a number of small grants of up to £5,000 per year also meeting success.

We are keen to support pilot studies, and to work in partnership with other research funders and/or professional associations but providing sole funding for large-scale projects is usually beyond our means.

The Trust is favourably disposed towards partnership funding generally within the requirements of a rigorous peer review process. The charity also encourages co-operative and collaborative research as a means of accelerating progress towards new knowledge and understanding of cot deaths.

All applications for funding undergo a rigorous peer review selection procedure, by the Trust’s Scientific Advisory Committee (SAC). Final decisions are made by the trustees on recommendation by the SAC.

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Genetics

Apolipoprotein E Genotype : A comparative study of infants that died from SIDS and infants that died from known causes of death.

Grantholders: Professor Neil McIntosh, Professor Jeanne Bell, Dr Jean Keeling and Dr Julie Clare Becher
University of Edinburgh
Awarded £118, 738 over 3 years

Poor control of breathing or subtle heart abnormalities are two theories about the causes of SIDS. Another theory is that babies who die from SIDS are unusually susceptible to minor infections or other environmental problems, which normal babies are able to survive but which overwhelm the defences of SIDS infants. This variation between babies with SIDS and other babies may well be controlled by babies’ genes.

For several years, this research team has been investigating the possible causes of brain damage in babies who die in infancy. They identified the Apolipoprotein E (ApoeE) gene as potentially relevant to SIDS. This gene is concerned with the transport and maintenance of fatty substances in the body; it also has a role in controlling the response to infection.

The gene exists naturally in three different forms: ApoE e2, ApoE e3 and ApoE e4. These forms vary in their ability to maintain normal fats and proteins. Variations in the gene have been clearly linked to the response of the brain to ageing and to other harmful circumstances, such as stroke and head injury. An example is that ApoE 4 is more common in Alzheimer’s disease.

The researchers wished to establish whether the unusual forms of the ApoE gene (ApoE 4 and ApoE 2) were more common in babies who died of SIDS than in babies who died of known disorders at the same age.

They investigated 296 babies. 170 of these were babies who died of SIDS; 126 were babies who died of other causes. They compared their findings with what they knew about healthy, living babies and adults.

The researchers found that slightly more SIDS babies possessed the ApoE gene than non-SIDS babies. However, this difference was not significant enough to convince them that the ApoE gene was a major influence in causing SIDS.

They are undertaking further research to see if there are differences between the babies who have different ApoE genes. These differences are likely to be subtle. Meanwhile, there are other genes which are likely to influence a baby’s ability to survive and future research will certainly move in this direction.

Multiple Serotonergic Brainstem Abnormalities in SIDS

Grantholder: Dr David Paterson and colleagues
Boston Children’s Hospital

Awarded £12,582

This research was partly funded by the Trust, and we are delighted to be included in the positive outcomes. SIDs is the leading cause of postneonatal infant death in the United States, as well as in Scotland. While the cause remains unknown, previous research has suggested that abnormalities in the area of the brainstem that regulates breathing may play a role in SIDS.

The researchers analysed frozen samples of the medulla from 31 infants who died from SIDS and from 10 infants who died from causes other than SIDS. These samples were compared, and it was found that the abnormalities in SIDS infants were more extensive than previously suggested.

This study strengthens the hypothesis that brainstem dysfunction is associated with SIDS, and may lead to death by a failure of respiratory responses.

This study also found reduced receptor binding in male SIDS cases, as compared with female SIDS cases. This observation may help explain why males are more vulnerable to SIDS.

This study took place at a time when safe sleeping messages were well promoted and publicised, including messages about placing a baby on its back to sleep. Despite this, the majority (65 percent) of the SIDS cases in this data set were sleeping on their fronts or sides at the time of death, indicating the need for continued public health messages on safe sleeping practices. The researchers speculate that the increased risk of SIDS in the prone or face-down position may reflect the infants’ inability to respond to the challenge to breathe in the face-down position.

Published Nov 2006 Journal of the American Medical Association

JAMA. 2006 Nov 1;296(17):2124-32.

10.1001/jama.296.17.2124

The Distribution of B-APP immunoreactivity

Grantholder: Dr Colin Smith

University of Edinburgh

Awarded £34,115

The neuropathologist involved in forensic work is not uncommonly confronted with a case in which there is no or only a limited history or, if available, the information is uncertain or is often conflicting. In recent years the immunohistochemical stain β‐amyloid precursor protein (β‐APP) has been used to assess the extent of axonal injury in a variety of pathological processes but in forensic practice is of greatest utility in the assessment of traumatic brain injury. Diffuse traumatic axonal injury (TAI) in humans has been demonstrated by β‐APP immunoreactivity in patients surviving at least 2 h after head injury. However, many of these patients also have an associated ischaemic injury, either focal or diffuse, which may make the interpretation of β‐APP immunoreactivity difficult. The present study was designed to evaluate if the published descriptions of the different morphological patterns and distributions of β‐APP immunoreactive axons could be used to microscopically distinguish axonal injury attributed to trauma from other causes. To test this hypothesis a total of 73 cases were reviewed. The cases were selected from six different groups based on clinical information.

Published January 2005 Neuropathology and Applied Neuroboilogy

https://doi.org/10.1111/j.1365-2990.2005.00645.x

Sudden Infant Death Syndrome (SIDS) and Seratonin: The Genetic Segue

Grantholder: Professor Debra E. Weese-Mayer
Children’s Memorial Hospital, Chicago

Awarded £85,500 over 2 years, 2007

The aim of this research is to identify variations in genes that may contribute to the risk of SIDS. Identification of these genes may further define the genetic profile of infants at risk of SIDS; explain underlying mechanisms for SIDS; and ideally allow for the implementation of mechanism specific treatment of the “at risk” infant.

Serotonin may provide the genetic segue to SIDS, but it may not be the final chapter in the yet untold story of the genetic basis of SIDS. Until the genetic basis for SIDS is determined it remains the responsibility of medical personnel to teach and model optimal SIDS risk factor compliance, and parents and caregivers to practice SIDS risk factor compliance, thereby minimizing the role of environmental co‐factors in the demise of the at‐risk for SIDS infants.

First published: 02 June 2008 Acta Pediatrica Volume 97, Issue 7 Pages 846-847

https://doi.org/10.1111/j.1651-2227.2008.00860.x

 

Genetic control of inflammatory responses in relation to SIDS

Grantholder: Professor Caroline Blackwell

University of Edinburgh
Awarded £75, 380  over 2 years

Studies by this group include research into risk factors for sudden infant death syndrome (SIDS) known to parallel those for respiratory tract infections. However, infectious agents suggested to be involved in SIDS do not fulfil certain criteria. No single agent has been identified in all cases and there is no suitable animal model for SIDS which could be used to test the candidate organisms. Based on epidemiological and experimental work by our group and others, we suggested some SIDS deaths are due to pathophysiological responses elicited by combinations of microbial products and/or cigarette smoke during a developmental stage when infants’ endocrine responses are less able to “damp down” the effects of inflammatory mediators.

Published 1999

APMIS. 1999 May;107(5):455-73.

 

Possible  involvement of Melatonin in SIDS

Grantholders: Dr Lynda Williams, Dr David Abramovich & Dr Elizabeth Gray,

Rowett Research Institute, Aberdeen, Aberdeen Maternity Hospital & Aberdeen Royal Infirmary.

Awarded £22,195 over 1 year, 1997

Studies have shown SIDS occurs most often during the winter months and at night, implicating the “darkness hormone”, melatonin, as a possible influencing factor. Melatonin is best known for its actions on seasonal and daily rhythmicity in animals. The role of melatonin in the human is less clearly defined, but in the adult appears to influence activity rhythms and the induction of sleep, both of which may be related to changes in core body temperature. This study aims to assess the sensitivity of both SIDS and non-SIDS neonates to melatonin by studying specific receptors for melatonin using receptor binding studies and molecular biology techniques.

 

Human heat shock protein gene polymorphisms and sudden infant death syndrome

Grantholder: Rahim RA¹, Boyd PA, Ainslie Patrick WJ, Burdon RH.

1Department of Bioscience and Biotechnology, Todd Centre, University of Strathclyde, Glasgow.

Published 1996

Arch Dis Child. 1996 Nov;75(5):451-2.

Abstract

Comparison of the frequency of occurrence of restriction fragment length polymorphisms in control human DNAs and DNAs from infants dying from sudden infant death syndrome has indicated no significant difference in the case of restriction fragment length polymorphisms associated with the heat shock protein genes hsp70 and hsp90. A highly significant difference was detected, however, in the case of the specific restriction fragment length polymorphisms detected by an hsp60 gene probe in MspI digests.

 

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Physiological Development

Understanding why preterm babies are at increased risk for SUDI

Project Abstract: Infants born preterm are at three times the risk of Sudden Unexpected Death in Infancy (SUDI) compared to infants born at term. SUDI occurs during sleep and it is thought to result from impaired control of heart rate and blood pressure with a failure to arouse from sleep in response to a life threatening event. Apnoea, or a pause in breathing and periodic breathing (more than 3 short apnoeas in a row) are very common in preterm infants, and are often not detected clinically and are not screened for before hospital discharge. We have shown that short apnoeas and periodic breathing are associated with significant hypoxia and reduced cerebral oxygenation and have the potential to influence long term cardiovascular control and arousal responses. There is a large and growing number of children born preterm consequently displaying a high frequency of apnoea and periodic breathing. Thus, understanding the role of respiratory instability on cardiovascular control and arousal responses over the first 6 months after term equivalent age when the risk of SUDI is highest will have important implications for preventing SUDI in infants born preterm. We will also identify factors which increase
the risk of persistent apnoea and periodic breathing.

Grantholder: Professor Rosemary Horne

Melbourne, Australia

Awarded £42,117 in 2018 for 2 years

Published 2021 – 2023

Journal of Pediatrics

DOI: 10.1038/s41390-021-01816-9

DOI: 10.1016/j.jpeds.2022.10.035

Journal of Pediatric Pulmonology

DOI: 10.1002/ppul.26273

Journal of Perinatology

DOI: 10.1038/s41372-023-01748-8

Acta Paediatrica

DOI: 10.1111/apa.16955

Is sleeping preterm infants prone in the NICU really good for their brains

Grantholder: Professor Rosemary Horne
Melbourne, Australia

Awarded 2013 for 2 years

Published 2019

Journal of Pediatrics

DOI: 10.1016/j.jpeds.2018.08.076

The effects of family stress on the physiological  development of babies

Grantholders: Dr Michael Wailoo, Dr Stewart Petersen and Dr Elizabeth Anderson

University of Leicester

Awarded £39,145 over 2 years

Deprivation is widely recognised as a risk factor for SIDS. This project will study the physiological effects on babies of stressful home circumstances in order to examine the hypothesis that the endocrine and other effects of stress may increase vulnerability by modifying the babies’ responses to minor illness and other challenges.

Disruptions in the balance between Placental Villous Trophoblast Proliferation and Apoptosis

Grantholder: Dr Tahera Ansari, NPIMR

Awarded £80,194.80 over 3 years, 2006

There has been a considerable reduction in the number of infants dying from Sudden Infant Death Syndrome (SIDS) over the past decade. World wide scientific research on SIDS has highlighted a number of specific risk factors and has also pointed towards an infant born with hidden developmental vulnerability.
Disruptions in the balance between Placental Villous Trophoblast Proliferation and Apoptosis in IUGR and SIDS, and the consequences for foetal growth.

Our research has centred on events prior to birth, whilst the baby is still growing and developing inside the mother. The organ that plays the greatest role whilst a baby is developing is the placenta. This organ is responsible for the transfer of nutrients and oxygen to the baby and for the removal of waste products. Any abnormality within the placenta has the potential to adversely affect the way the baby develops.

The placenta has a unique group of cells which make up a membrane responsible for the transfer of oxygen and nutrients to the baby from the mother. The way this placental membrane develops is crucial for the healthy growth of both the placenta and the baby. Our investigation will look at how this membrane renews itself. We will analyse the balance between cells dying and reproducing in placentae from healthy infants and compare the data with data from placentae from SIDS infants. The information obtained will help us understand why SIDS infants show altered patterns of growth and development whilst inside the womb.

The molecular basis of intrauterine growth retardation in cases of SIDS

Grantholders: Dr Anne Burchell, Professor Robert Hume (University of Dundee), Dr Fiona Drimmie (Tayside University Hospitals NHS Trust), Dr Allan Howatson
Royal Hospital for Sick Children, Glasgow
(2000: £43,300 over 2 years)

Glucose is the primary source of energy for the brain. The brain cannot make sufficient glucose for its needs by itself, so it must obtain glucose from the blood. It is therefore vital that blood glucose concentrations are maintained within a restricted range – neither too high or too low. Episodes of low blood glucose can lead to brain damage and, in extreme cases, even to death.

Low birth weight infants are particularly vulnerable to low blood glucose levels; low birth weight is also a risk factor for SIDS. Research has previously shown that some infants dying suddenly and unexpectedly have defects in liver glucose production, which could lead to low blood glucose at times of stress or reduced milk intake.

The researchers in Dundee believe that many of these defects in liver glucose production result from failures to regulate this system at birth. They have investigated the molecular nature of this regulation, and have shown that subtle alteration in the structure of regulatory regions of genes that control glucose levels occur in some infants.

The next phase of this work is to identify these changes in genes at the time of birth, to determine which infants are at greatest risk at times of stress. Once we have the knowledge of which infants are at risk, then simple preventative measures (such as changes in feeding patterns, combined with emergency action plans to deal with the normal minor ailments of infancy) will lower the risks.

 

Sleep Apnoea/ Hypopnoea Syndrome and SIDS

Grantholders: Professor Neil Douglas & Dr Karen Rees

University of Edinburgh,

Awarded £66, 703 over 3 years 1998

There is an increased frequency of SIDS in families of sleep apnoea patients. Sleep apnoea is familial and, like SIDS, is associated with small upper airways. The study will investigate the frequency of irregular breathing during sleep and possible associated abnormalities of facial structure in relatives of SIDS victims compared with controls.

 

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Pathology

Pathological defects in placentas from women whose newborn babies have suffered intra-uterine growth retardation and/or sudden infant death syndrome

Grantholders: Professor Colin Green and Dr Paul Sibbons

Northwick Park Institute for Medical Research and Dr John Gillan, The Rotunda Hospital and University College, Dublin.

Awarded £4,500 over 6 months. 2000

 

Detection of Respiratory Syncytial Virus Nucleic Acid in Archival Postmorterm Tissue from Infants

Grantholders: Cubie HA, Duncan LA, Marshall LA, Smith NM.

Regional Virus Laboratory, City Hospital, Edinburgh, United Kingdom.

Published 1997

https://www.ncbi.nlm.nih.gov/pubmed/9353832

Abstract

Archival lung tissue from 99 cases of sudden infant death syndrome (SIDS) and from 58 matched comparison cases with known causes of death was studied. Sections were examined by in situ hybridization (ISH) using a cocktail of three synthetic oligonucleotides with sequences chosen from the published sequence of the nucleoprotein gene of respiratory syncytial virus (RS virus). The oligonucleotides were end-labelled with dinitrophenyl (DNP) or digoxigenin (DIG) and hybrids were detected immunocytochemically. RS virus nucleic acid was detected in 24 cases of SIDS (24%) and in 11 (19%) of the comparison group. Specificity was confirmed using a DIG-labeled cloned probe covering the whole of the nucleoprotein gene sequence. With one exception, the same results were obtained. Reverse transcriptase-polymerase chain reaction (RT-PCR) was used to confirm the specificity of these results. When matched for age and month and year of death, 76 SIDS cases and 38 controls could be compared. Twenty-one SIDS cases (27.6%) and seven comparison cases (18.4%) contained detectable RS virus sequences by ISH, with a higher detection rate in winter in both groups. The differences were not significant and reflected the seasonal pattern of RS virus infection in the community rather than a causal relationship of RS virus with SIDS. Detection of RS viral mRNA through the summer months suggests that persistence is possible

 

Direct gas chromatographic assay of urinary medium-chain fatty acylcarnitines by their thermal decomposition

Grantholders: Farquharson J, Jamieson EC, Muir J, Cockburn F, Logan RW

Royal Hospital for Sick Children, Glasgow, Scotland, UK.

Published 1992

Clin Chim Acta. 1992 Feb 14;205(3):233-40.

Abstract

We report a gas chromatographic assay for urinary medium-chain acylcarnitines which employs their property of thermal lability, and by circumventing the need for specialised mass spectroscopy is suitable for routine laboratory use. The method produces readily interpreted, uncomplicated chromatograms and has proved to be both sufficiently sensitive and specific to enable detection of octanoylcarnitine in a symptomatic individual with medium-chain CoA dehydrogenase deficiency and in two asymptomatic siblings following administration of a carnitine load.

 

Measurement of urinary medium chain acyl glycines by gas chromatography–negative ion chemical ionization mass spectrometry.

Grantholders: Carter SM¹, Midgley JM, Watson DG, Logan RW.

Department of Pharmacy, University of Strathclyde, Glasgow, UK.

Published 1991

J Pharm Biomed Anal. 1991;9(10-12):969-75.

Abstract

Medium chain acyl-CoA dehydrogenase (MCAD) deficiency is an inborn error of fatty acid metabolism, which is difficult to diagnose, partly because of its unpredictable clinical presentation. A specific diagnostic marker is an increased excretion of certain medium chain acyl glycines. A sensitive and specific method has been developed for the extraction, derivatization, identification and quantitation of urinary medium chain acyl glycines by gas chromatography-negative ion chemical ionization mass spectrometry (GC-NICIMS). The following series of standard acyl glycines has been synthesized and characterized: hexanoyl, octanoyl, 3-phenylpropionyl and suberyl and their respective isotopomers (using 13C2-glycine; for use as internal standards). The range of excretion of these compounds in normal subjects has been established using this method and increased excretion of acyl glycines, particularly hexanoyl, 3-phenylpropionyl and suberyl was successfully demonstrated in three MCAD deficient subjects from one family.

 

Synthetic oligonucleotide cocktails as probes for detection of human parvovirus B19.

Grantholders: Cubie HA¹, Grzybowski J, da Silva C, Duncan L, Brown T, Smith NM.

Regional Virus Laboratory, City Hospital, Edinburgh, Scotland

Published 1995

.J Virol Methods. 1995 May;53(1):91-102

Abstract

A cocktail of 10 oligonucleotides selected at intervals along the length of the genome of human parvovirus B19 was labelled enzymically with digoxigenin and chemically with either digoxigenin (DIG) or dinitrophenyl (DNP). Chemical labelling was easier and more practical for the production of large quantities of probe. Pools labelled with either digoxigenin or DNP could detect 10 fg of B19 DNA in a dot blot reaction using an alkaline phosphatase antibody conjugate and colorimetric detection. Formalin fixed tissue from 11 consecutive cases of fetal hydrops were examined by in situ hybridisation (ISH). Both probe cocktails detected human parvovirus B19 DNA in 3 cases, with positive cells in all tissues examined and with equal sensitivity. The DNP pool is significantly cheaper and simpler to produce and could provide an inexpensive reagent suitable for diagnostic detection of viral nucleic acid in histopathological material.

 

Eight year study of viral isolates from cot deaths in Glasgow

Grantholders: Patrick WJ¹, Carrington D, Armstrong AA, Gibson AA, Urquhart GE.

Department of Perinatal and Paediatric Pathology, Royal Hospital for Sick Children, Glasgow, Scotland.

Published 1989

Scott Med J. 1989 Jun;34(3):462-4.

Abstract

Over an eight year period 21 different viral strains excluding polioviruses were isolated in 44 (19%) of 237 cot deaths. The percentage of viral positive cases was significantly greater in over 16 week age groups and in cultures obtained less than 24 hours after death.

PMID:2546253

DOI:10.1177/003693308903400306

Risk factors and Environment

A mechanism for the increased risk of the Sudden Infant Death Syndrome in infants sleeping in the prone position

Grantholder: Professor Rosemary Horne
Melbourne, Australia

Awarded 2010 for 1 year

Infants born preterm are at significantly increased risk for a range of neural, cardiovascular and respiratory abnormalities and for death, the most prominent cause being SIDS. As around 10% of all births are preterm and the numbers of surviving preterm infants are increasing, the long-term problems following preterm birth are also increasing. The proposed study will fill key knowledge gaps in the developmental legacies of preterm birth by investigating the progression of arousal responses from subcortical to cortical levels in groups of healthy preterm infants and those with a neonatal history of apnoea of prematurity. By its focus on the natural history of arousal responses during infant development, and on the impact of preterm birth on this development, our project will promote two major advances. First, it will aid innovation of specific diagnostic and therapeutic strategies to improve longer term outcomes for infants born preterm; and secondly it will inform and accelerate progress toward eradicating SIDS deaths which are so prominent in the preterm-born infant group.

Safe Sleeping: Does swaddling improve infant sleep without decreasing arousability?

Grantholder: Professor Rosemary Horne
Melbourne, Australia
£12,900 over 1 year

Swaddling is a method of improving infant sleep in the supine position. However, swaddling may reduce infant arousability. This study will examine the effects of swaddling on infant sleep and arousal. It aims to identify if swaddling can be safely recommended to reduce SIDS.

Carbon monoxide from Smoking: A possible risk factor for SIDS

Grantholder: Professor Allesandro Mugelli and colleagues
University of Florence, Italy
(2001: £22000 over 2 years, 2004: 38000 over 2 years)

Research has shown that parental smoking, particularly maternal smoking during pregnancy, greatly increases the risk of SIDS for a baby. However, the reason for this has never been properly explained.

In newborn babies there is a temporary change in the electro-physiology of the heart. In the vast majority of cases, this change reverts to normal by 6 months of age. If there is a delay in reverting to normal, it may lead to abnormal rhythm of the heart pump and perhaps expose the infant to sudden death.

This research group will examine the possibility that babies exposed to carbon monoxide in the womb (that is, whose mothers smoke) may not make this important move back to normal at the same time as babies whose mothers do not smoke.

A pilot study to establish a randomized trial methodology of a behavioural intervention

Grantholders: Dr David Tappin
University of Glasgow

Funding provided

This pilot study aims to test the efficacy of  midwife home-based motivational interviewing in smoking cessation services during pregnancy.

Published 2000

Health Education Research Vol. 15 no. 4 2000 Pages 491 – 502

Smokechange: Smoking Cessation during Pregnancy
A Randomised Controlled Trial of Home-based Motivational Interviewing

Grantholders: Dr David Tappin, Dr Mary Lumsden, Ms Fiona Crawford, Mr Harper Gilmour, Ms Doreen McIntyre, Professor David Stone and Ms Patricia Meldrum.
University of Glasgow

Awarded £107,311

This study aimed to establish whether the use of motivational counselling during pregnancy would help pregnant women to stop smoking.

All self-reported smokers in two Glasgow maternity hospitals were given routine information about smoking and pregnancy by the study midwives. Half of them were, in addition, offered an extra 2-5 home-based motivational interviewing sessions, lasting about 30 minutes each. Their quit and reduction rate was compared with those offered information only. Self reporting was corroborated by measuring routine blood or saliva cotinine (an alkaloid found in tobacco) at late pregnancy follow-up, as compared with booking.

The researchers concluded that, even with dedicated, well-trained midwives, the offer of motivational counselling on its own did not decrease the habits of pregnant smokers

Publications in 2005

2005 BMJ 2005; 331 doi: https://doi.org/10.1136/bmj.331.7513.373

The effect of developmental stage and environmental risk factors for SIDS on the nasopharyngeal flora of different ethnic groups

Grantholder: Professor Caroline Blackwell

University of Edinburgh

Awarded £118,738 over 3 years, 2000

 

Measurement of nasopharyngeal  temperature in infants and newborns

Grantholder: Dr Neil Molony

Royal Hospital for Sick Children, Edinburgh

Awarded £1,200 for 1 year 1998

Previous work in Edinburgh, also funded by the Scottish Cot Death Trust, has suggested that some SIDS deaths may be triggered by toxins produced by bacteria growing in an infant’s upper airway. These toxins, however, are only produced at temperatures of 37⁰C and above. Dr Molony aims to measure temperature in the airways of infants to assess whether under certain circumstances this could rise to 37⁰C. This study follows a previous study which found nasopharyngeal temperature in children aged 4 – 10 years to be approximately 35.5⁰C, significantly warmer than adults.

 

Anoxia and  hair shaft  defects: A useful  indicator of children at risk of SIDS?

Grantholder: Dr Robin Dover

Hammersmith Hospital, London

Awarded £3,245 1998

Scalp hairs of SIDS victims often show shaft narrowing. Such narrowing are found in those exposed to high altitudes. Thus it is possible that mild hypoxia may result in measurable changes in the hair shaft and that these might be a useful marker of infants at risk.

 

Risks to infants of sharing the parental bed: A physiological and behavioural study

Grantholder: Professor Helen L Ball

Durham University, UK

Awarded £64.607 in 1999

 

Protective effect of immunisation against Diptheria, Pertussis and Tetanus (DPT) in relation to SIDS

Grantholder: Professor Caroline Blackwell

University of Edinburgh

Awarded £64,998 over 2 years, 1998

Epidemiological evidence indicates infants immunised against diphtheria, pertussis and tetanus (DPT) are at decreased risk of sudden infant death syndrome (SIDS). Asymptomatic whooping cough and pyrogenic toxins of Staphylococcus aureus have been implicated in the aetiology of SIDS. The objectives of the present study were: (1) to determine if the DPT vaccine induced antibodies cross-reactive with the staphylococcal toxins; (2) to determine if antibodies to the pertussis toxin (PT) and the staphylococcal toxins were present in the sera of women during late pregnancy; (3) to examine the effects of infant immunisation on levels of antibodies to PT and the staphylococcal toxins; (4) to assess the effects of changes in immunisation schedules in the UK on the incidence and age distribution of SIDS

Published 1999

FEMS Immunol Med Microbiol. 1999 Aug 1;25(1-2):183-92.

DOI:10.1111/j.1574-695X.1999.tb01342.x

Determinants of seasonality of SIDS

Grantholder: Professor Peter Helms

Department of Medicine & Therapeutics, University of Aberdeen.

Awarded £45,613 over 3 years

This study aimed to clarify the optimal birth month for avoidance of SIDS and the seasonal characteristic of each birth-month cohort. The statistical method  there is a known seasonal variation is the incidence of death by birth month.

Published in 1996

Scott Med J. 1996 Apr;41(2):39-43.

DOI:10.1177/003693309604100203

 

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Products

An Evaluation of Cot Mattresses and their Covers as Reservoirs of Toxigenic Bacteria

Dr Richard Jenkins, Professor Peter Craig and Dr Tania Webb
De Montfort University, Leicester

Awarded £58,425 over 2 years, 2000

The purpose of this research was to investigate the possibility that potentially harmful bacteria might become established in cot mattress foams and/or their covers, giving rise to sources of possible infection that may invade the upper respiratory tract of infants.

The methodology involved bacteriological testing of currently used polyurethane foam cot mattresses donated by the public. Information on the history of use of the cot mattresses was obtained via a mattress donor questionnaire.

The study found that the bacteria in cot mattresses was influenced by the sleeping position of the infant. Movement on a cot mattress promoted aerial release of bacteria from polyurethane foam. Use of a non-integral (not completely covered in plastic) cot mattress was associated with increased levels of bacterial contamination within the exposed polyurethane foam. Previous use by another child of a non-integral mattress was associated with significantly increased levels of Staphylococcus aureus within cot mattress polyurethane foams. This is a bacterium which is found more frequently in infants who have died suddenly and unexpectedly than in infants who have died from known causes.

The findings could provide a plausible explanation for recently identified possible risk factors for SIDS, i.e. sleeping at night on mattresses used previously by another child and use of mattresses not entirely covered with a waterproof cover. Data obtained on soluble protein and dust-mite allergen levels within polyurethane foams corroborate these findings. The fact that bacterial growth/survival is encouraged by organic matter contamination, such as urine, breast or formula milk, or by high relative humidity, indicates that maintenance of a clean and dry cot environment would help to minimise development of reservoirs of bacteria within cot mattress materials. Staphylococcus aureus was shown to have good survival capability on polyurethane foam even at low relative humidity and to be capable of breakdown of polyurethane.

This study shows that it is important to keep your cot dry and clean, to use a mattress that is completely covered with plastic, and to use a new mattress for each baby if you can.

 

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SCDT Research

In addition to funding research, the Scottish Cot Death Trust assists groups who are conducting research and require the expertise of the charity. Some research projects are also conducted by staff and Trustees. Where studies are using charitable resources, the lead contact is required to submit an application to the SAC to seek backfill of funds.

National Post-Perinatal Infant Mortality and Cot Death Study, Scotland 1981-82.

Grantholders: Arneil GC, Brooke H, Gibson AA, Harvie A, McIntosh H, Patrick WJ.

Published 1985

Lancet. 1985 Mar 30;1(8431):740-3.

Abstract

Throughout 1981 and 1982 all deaths of infants aged 8-365 days (post-perinatal infant mortality, PPIM) in Scotland were studied. During this period there were 135 250 live births and 1533 infant deaths (infant mortality rate 11.3), including 763 PPIM deaths (5.6 per 1000 live births). These 763 deaths fell into three main categories: birth-determined (329), accident or acquired disease (65), and cot deaths (369). Birth-determined deaths included 109 preterm, 199 congenital disorders, and 21 miscellaneous deaths. 61 of the cot deaths were fully explained on necropsy, in 141 an associated finding which might or might not be relevant was found, and in the remaining 167 no explanation was found. The cot death rate was 2.7 per 1000 live births overall (3.3 for boys, 2.1 for girls), and more second-born than first-born children died (approximately 3:2). Excluding “explained” cot deaths the rate was 2.3 per 1000 live births

RESULTS:

Sleeping prone (odds ratio 6.96 (95% confidence interval 1.51 to 31.97) and drug treatment in the previous week (odds ratio 2.33 (1.10 to 4.94)) were more common in the cases than controls on multivariate analysis. Smoking was confirmed as a significant risk factor (odds ratio for mother and father both smoking 5.19 (2.26 to 11.91)). The risk increased with the number of parents smoking (P < 0.0001), with the number of cigarettes smoked by mother or father (P = 0.0001), and with bed sharing (P < 0.005). A new finding was an increased risk of dying of the syndrome for infants who slept at night on a mattress previously used by another infant or adult (odds ratio 2.51 (1.39 to 4.52)). However, this increased risk was not established for mattresses totally covered by polyvinyl chloride.

CONCLUSIONS:

Sleeping prone and parental smoking are confirmed as modifiable risk factors for the sudden infant death syndrome. Sleeping on an old mattress may be important but needs confirmation before recommendations can be made.

Case-control study of sudden infant death syndrome in Scotland, 1992-5

Brooke H¹, Gibson A, Tappin D, Brown H.

1Scottish Cot Death Trust, Royal Hospital for Sick Children, Glasgow.

BMJ. 1997 May 24;314(7093):1516-20.

Abstract

OBJECTIVE:

To investigate the relation between routine infant care practices and the sudden infant death syndrome in Scotland.

METHODS:

National study of 201 infants dying of the sudden infant death syndrome (cases) and 276 controls by means of home interviews comparing methods of infant care and socioeconomic factors.

Case Review of Sudden Unexpected Deaths in Infancy (SUDI) in Scotland

A report from SUDI Case review in Scotland from 2001 – 2004 was published in 2007. You can read the report here:

http://www.healthcareimprovementscotland.org/previous_resources/performance_review/sudi_case_review.aspx