Bedsharing, roomsharing, and sudden infant death syndrome in Scotland: a case-control study

OBJECTIVE: To examine the hypothesis that bedsharing with an infant is associated with an increased risk of sudden infant death syndrome (SIDS). STUDY DESIGN: A 1:2, case:control study in Scotland UK, population 5.1 million, including 123 infants who died of SIDS between January 1, 1996 and May 31, 2000, and 263 controls. The main outcome measure was sharing a sleep surface during last sleep. RESULTS: Sharing a sleep surface was associated with SIDS (multivariate OR 2.89, 95% CI 1.40, 5.97). The largest risk was associated with couch sharing (OR 66.9, 95% CI 2.8, 1597). Of 46 SIDS infants who bedshared during their last sleep, 40 (87%) were found in the parents' bed. Sharing a bed when <11 weeks (OR 10.20, 95% CI 2.99, 34.8) was associated with a greater risk, P = .010, compared with sharing when older (OR 1.07, 95% CI 0.32, 3.56). The association remained if mother did not smoke (OR 8.01, 95% CI 1.20, 53.3) or the infant was breastfed (OR 13.10, 95% CI 1.29, 133). CONCLUSIONS: Bedsharing is associated with an increased risk of SIDS for infants <11 weeks of age. Sharing a couch for sleep should be strongly discouraged at any age.     

Modifiable risk factors, sleep environment, developmental physiology and common polymorphisms: understanding and preventing sudden infant deaths

Unexpected death in infancy may be a consequence of recognisable pathophysiological processes, or may remain unexplained after thorough investigation. We review the appropriate investigations that should be performed after unexpected infant deaths, and the recent changes to UK law that will make such investigations mandatory from 2008. Current knowledge of the epidemiology and pathophysiology of unexpected infant deaths, together with knowledge of infant developmental physiology leads to an emphasis on the importance of a range of potential gene-environment interactions occurring in vulnerable infants at vulnerable stages of their development.     

Study of the conduction system in a population of patients with sudden infant death syndrome

Summary The conduction system of 23 infant hearts, 15 of sudden infant death syndrome (SIDS) and eight of those dying from known cause, was serially sectioned. A left-sided His bundle was found more commonly in (SIDS) (eight of 15) than in the controls (two of eight). Taking into account a previous study in which a left-sided His bundle was found in only four of 32 hearts from all age groups, this is statistically significant and may be a factor promoting SIDS.This research was aided by grant HL-30558-02 from the National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, Maryland.     

Maternal cannabis use in the sudden death syndrome

The smoking of cannabis and tobacco is common in many countries. In contrast to tobacco, which is an established risk factor for the sudden infant death syndrome (SIDS), nothing is known about cannabis and its effects on SIDS risk. We analysed data collected in a nation-wide case control study in New Zealand (393 cases, 1592 controls) to determine if there is any association between maternal cannabis use and SIDS risk. Adjusting for ethnicity and maternal tobacco use, the SIDS odds ratio for >weekly maternal cannabis use since the infant's birth was 2.23 (95% CI = 1.39, 3.57) compared to non-users; and the multivariate odds ratio was 1.55 (95% CI = 0.87, 2.75). We conclude that frequent maternal cannabis use may be a weak risk factor for SIDS, but this finding requires further research.     

Brainstem auditory evoked responses in infants at risk of sudden infant death

Brainstem auditory evoked responses (BAERs) were recorded from 63 near-miss Sudden Infant Death Syndrome (NMSIDS) infants, 26 siblings of SIDS (SSIBS) infants and 67 control infants between 0 and 30 weeks post-term. The majority of BAERs recorded from the NMSIDS and SSIBS infants had normal form and interpeak intervals (V-I and V-IIn) within normal limits for their age. However, 15% of these infants had interpeak intervals outside the normal range, suggesting abnormal neural function in these cases. The distributions of interpeak intervals for all NMSIDS and SSIBS infants were skewed towards longer times compared to control infants. The distributions of V-IIn intervals for both groups of at risk infants were significantly different to that of control infants. While the observations confirm that the recording of BAERs is not suitable for identifying infants at risk of SIDS, they suggest, however, that maturation of neural processing in the brainstem of these infants may be delayed.     

Polysomnographic studies and home monitoring of siblings of SIDS victims and of infants with no family history of sudden infant death

We report preliminary results of a prospective study conducted to prevent sudden death in asymptomatic infants. From 1977–1984, 3658 infants were studied polygraphically. There were 923 siblings of SIDS victims and 2735 infants with no personal of family history of SIDS. The infants were studied at 8 weeks of age. Polygraphic risk factors were defined by central apnoeas longer than 15s; periodic breathing above 5% sleep time; or obstructive apnoeas above 3s. In 937 infants risk factors were seen and a second study was requested 4 weeks later. Out of 891 infants re-studied at 12 weeks, 153 still presented some risk factors and were selected for a home monitoring programme; 150 families agreed to monitor their infants at home with a cardiorespiratory monitor with the alarms set at 20s apnoea, and 50 beats per min bradycardia. Repeated alarms were reported for 97/150 (65%) infants; 48/150 (32%) infants were stimulated and 8/150 (5.3%) were resuscitated on at least one occasion. No death occurred during monitoring, which could be interrupted before the end of the first year of life in all infants. In the group of 3459 infants with normal results and not monitored, three siblings (0.35%) and one infant without history (0.04%) died of SIDS. Of the infants with abnormal polygraphic results, one sibling not returned for the second recording, and two out of three infants for whom the parents refused monitoring, died of SIDS. It is concluded that the programme, may prevent the death of some infants, but that the outcome of a child with normal results cannot be foreseen.Abbreviation SIDS sudden infant death syndrome     

Breast feeding and the sudden infant death syndrome in Scandinavia, 1992-95

Aims: To assess the effects of breast feeding habits on sudden infant death syndrome (SIDS). Methods: The analyses are based on data from the Nordic Epidemiological SIDS Study, a case–control study in which parents of SIDS victims in the Scandinavian countries between 1 September 1992 and 31 August 1995 were invited to participate, each with parents of four matched controls. The odds ratios presented were computed by conditional logistic regression analysis. Results: After adjustment for smoking during pregnancy, paternal employment, sleeping position, and age of the infant, the adjusted odds ratio (95% CI) was 5.1 (2.3 to 11.2) if the infant was exclusively breast fed for less than four weeks, 3.7 (1.6 to 8.4) for 4–7 weeks, 1.6 (0.7 to 3.6) for 8–11 weeks, and 2.8 (1.2 to 6.8) for 12–15 weeks, with exclusive breast feeding over 16 weeks as the reference. Mixed feeding in the first week post partum did not increase the risk. Conclusions: The study is supportive of a weak relation between breast feeding and SIDS reduction.     

Serum testosterone and estradiol in sudden infant death

OBJECTIVE: To test the hypothesis that among infants who die unexpectedly, testosterone and/or estradiol levels are elevated in those diagnosed with SIDS versus those with known causes of death (controls). STUDY DESIGN: Postmortem blood was collected and coded from infant autopsies, and serum was prepared and frozen until assayed for total testosterone and estradiol by fluoroimmunoassay. Subject information was then collected from the medical examiner's report. RESULTS: Testosterone, but not estradiol, was significantly higher in 127 SIDS cases versus 42 controls for both males (4.8 +/- 0.4 vs 2.2 +/- 0.4 nmol, respectively; P < .005) and females (2.4 +/- 0.2 vs 1.6 +/- 0.2 nmol, respectively; P < 0.03). CONCLUSIONS: Higher testosterone levels in infant victims of unexpected, unexplained death may indicate a role for testosterone or related steroids in SIDS. Further research is needed to understand the potential utility of testosterone as an indicator of SIDS risk.     

Breast feeding and the sudden infant death syndrome in Scandinavia, 1992-95.

AIMS: To assess the effects of breast feeding habits on sudden infant death syndrome (SIDS). METHODS: The analyses are based on data from the Nordic Epidemiological SIDS Study, a case-control study in which parents of SIDS victims in the Scandinavian countries between 1 September 1992 and 31 August 1995 were invited to participate, each with parents of four matched controls. The odds ratios presented were computed by conditional logistic regression analysis. RESULTS: After adjustment for smoking during pregnancy, paternal employment, sleeping position, and age of the infant, the adjusted odds ratio (95% CI) was 5.1 (2.3 to 11.2) if the infant was exclusively breast fed for less than four weeks, 3.7 (1.6 to 8.4) for 4-7 weeks, 1.6 (0.7 to 3.6) for 8-11 weeks, and 2.8 (1.2 to 6.8) for 12-15 weeks, with exclusive breast feeding over 16 weeks as the reference. Mixed feeding in the first week post partum did not increase the risk. CONCLUSIONS: The study is supportive of a weak relation between breast feeding and SIDS reduction.     

Overview of sudden infant death syndrome in Japan

In spite of rapid medical advancement in the care of infants and children, not only the general public but also many medical personnel have remained unaware of sudden infant death syndrome (SIDS) until very recently in Japan. In 1981, a research project team on SIDS financed by the Ministry of Health and Welfare was founded. Current incidence of SIDS is estimated to be about 0.5 per 1000 live births. The SIDS Family Association was organized in 1993 in Japan and began to publicize the social importance of SIDS and to support SIDS families by training befrienders. A series of articles on current achievements from SIDS research projects and from the SIDS Family Association are submitted to this issue. The present paper summarizes the status of SIDS in Japan by overviewing the activities of the research team and the SIDS Family Association.     

Role of congenital long-QT syndrome in unexplained sudden infant death: proposal for an electrocardiographic screening in relatives

Introduction  Congenital long-QT syndrome (LQTS) is a sporadic or familial inherited arrhythmia. It can lead to sudden death by ventricular fibrillation which occurs at any age but particularly during infancy. Recent studies of postmortem molecular analysis in infants who died of unexplained sudden infant death syndrome (SIDS) showed abnormal mutations to LQTS in 10% to 12%. Current methods of etiologic investigation of sudden infant death syndrome do not allow the diagnosis of LQTS. A targeted anamnesis together with systematic electrocardiograms of first- and second-degree relatives could be an efficient LQTS diagnostic tool. Therefore, we propose to include them in screening procedures for SIDS etiologies. Conclusion  LQTS accounts for a significant number of unexplained SIDS. We suggest adding a systematic familial electrocardiographic screening to the current etiologic investigations in order to track congenital LQTS in relatives.     

Analysis of the mitochondrial genome in sudden infant death syndrome

AIM: To investigate the mitochondrial genome and its association with sudden infant death syndrome (SIDS). METHODS: Twenty SIDS infants were screened for previously reported mitochondrial DNA mutations using direct sequencing. The whole mitochondrial genome was also sequenced for six of the infants. RESULTS: Three substitutions, A11467G, A12308G and G12372A, comprising a haplogroup were present in four infants diagnosed as pure SIDS. This haplogroup was also common in a control group. CONCLUSIONS: No specific mutation or polymorphism was found in association with SIDS.     

Formative evaluation to improve prevention of sudden infant death syndrome (SIDS): a prospective study

Aim: To evaluate formative evaluation, a pedagogic method that sensitizes mothers to sudden infant death syndrome (SIDS), as a new way to improve prevention of SIDS. Methods: Prospective and randomized study. Mothers in a test group (n = 148) received an educative questionnaire about SIDS during maternity stay. Three months later, we evaluated, by a telephonic interview, their scores of knowledge and observance of the recommendations in comparison with a control group (n = 144). Results: Mothers’ scores at the educative questionnaire was 5.12 (1.52) [mean(standard deviation)]. The scores performed 3 months later were better in test group for knowledge [7.64 (1.56) vs. 7.16 (1.61), p < 0.01] and for observance [8.28 (1.51) vs. 7.62 (1.72), p < 0.001]. Logistic regression analysis confirmed the benefits in test group regarding knowledge of SIDS risk factors [ORa = 1.69 (1.02–2.77), p < 0.05], of the advice to avoid overheating infants [ORa = 2.50 (1.43–4.38), p < 0.01] and of the risks of bed sharing [ORa = 2.7 (1.6–4.5), p < 0.001]. There was a significant association between non‐compliance with the sleeping position recommendation and unemployment (p < 0.01) and absence of postsecondary school education (p < 0.01). Conclusion: Formative evaluation using an educative questionnaire could improve maternal awareness on SIDS risk factors and their compliance with recommendations about SIDS prevention.     

Cytokine gene polymorphisms and sudden infant death syndrome

Aim: Several studies indicate that the mucosal immune system is stimulated in cases of sudden infant death syndrome (SIDS), and our hypothesis is that this immune reaction is because of an unfavourable combination of functional polymorphisms in the cytokine genes. Methods: Thus, in this study, single nucleotide polymorphisms (SNPs) in the genes encoding IL‐6, IL‐8, IL‐12, IL‐13, IL‐16, IL‐18 and IFNγ were investigated in 148 SIDS cases, 56 borderline SIDS cases, 41 cases of infectious death and 131 controls. Results: Regarding genotype distribution, no differences between the investigated groups were found. However, in the SIDS group, the genotypes IL‐8 ?251AA/AT and IL‐8 ?781CT/TT were significantly more frequent in the SIDS cases found dead in a prone sleeping position, compared with SIDS cases found dead in other sleeping positions. In addition, there was an association between fever prior to death and the genotype IL‐13 +4464GG in the cases of infectious death. Conclusion: This study indicates that specific interleukin genotypes are a part of a genetic make up that make infants sleeping prone at risk for SIDS.     

Mitochondrial tRNA genes and flanking regions in sudden infant death syndrome

AIM: Mitochondrial DNA (mtDNA) mutations have been proposed as a genetic risk factor for sudden infant death syndrome (SIDS). The aim of this study was to further investigate this issue, by sequencing the mitochondrial tRNA genes with flanking regions in SIDS cases and controls. METHOD: The selected genes were investigated in 24 cases of SIDS and 10 controls, the method used were direct sequencing. In addition, the A10398G mutation in the ND3 gene was investigated in 220 SIDS cases, 26 cases of infectious death and 93 controls, using allele-specific PCR. RESULTS: Mutations, recorded as differences from the revised Cambridge sequence, were found in 32 different sites in the coding regions investigated. There was no difference in mutation frequency between SIDS cases and controls, and no single mutation was found associated with SIDS. CONCLUSION: The present study does not indicate an association between a specific mitochondrial tRNA gene mutation and SIDS, nor a higher mtDNA tRNA mutation frequency in SIDS cases than in controls.     

HTR2A variation and sudden infant death syndrome: a case-control analysis

Aim: The serotonergic (5-HT) system functions in central autonomic regulation with homeostatic roles in cardiorespiratory control, thermoregulation, arousal and sleep-wake cycling. Altered function and development of this system in cases of sudden infant death syndrome (SIDS) have been established, but the aetiology of these disturbances remains unclear. The serotonin receptor, HTR2A, functions within this system with roles in the homeostatic response to hypoxia including excitatory effects on respiration, gasping and rhythm generation, all functions potentially compromised in SIDS. The objective of this study was to examine the relationship between SIDS risk and HTR2A variation.
Methods: All coding regions, intron–exon boundaries and the promoter region of HTR2A were PCR amplified and analysed by standard sequencing in 96 SIDS cases and 96 matched controls.
Results: Twenty-one HTR2A variations were identified in this case–control cohort, including four novel variations (c.C-1185A, c.T-923C, c.T-17C and c.C50T). None of the variations identified showed a significant association with SIDS.
Conclusion: This report provides evidence that despite known alterations of the 5-HT system in SIDS, and the logical role for the HTR2A receptor, genetic variation of HTR2A as studied in our cohort is not responsible for these alterations. These results represent a further step in the investigation of the aetiology of the altered serotonin system in SIDS cases.