Concept: Sudden infant death syndrome
To investigate practices, knowledge, attitudes, and beliefs regarding infant sleep among adolescent mothers, a demographic at high risk for sudden unexpected infant death, and to identify novel public health interventions targeting the particular reasons of this population.
IMPORTANCE A strong association between infant bed sharing and sudden infant death syndrome or unintentional sleep-related death in infants has been established. Occurrences of unintentional sleep-related deaths among infants appear to be increasing. OBJECTIVES To determine the trends and factors associated with infant bed sharing from 1993 through 2010, including the association of physician advice on bed sharing. DESIGN National Infant Sleep Position study conducted with annual telephone surveys. SETTING The 48 contiguous states. PARTICIPANTS Nighttime caregivers of infants born within 7 months of each survey administration. Approximately 1000 interviews were completed annually. MAIN OUTCOMES AND MEASURES Infant bed sharing as a usual practice. RESULTS Of 18 986 participants, 11.2% reported an infant sharing a bed as a usual practice. Bed sharing increased from 1993 (6.5%) to 2010 (13.5%). Although bed sharing increased significantly among white respondents from 1993 to 2000 (P < .001), the increase from 2001 to 2010 was not significant (P = .48). Black and Hispanic respondents reported an increase in bed sharing throughout the study period, with no difference between the earlier and later periods (P = .63 and P = .77, respectively). After accounting for the study year, factors associated with increase in infant bed sharing as a usual practice included maternal educational level of less than high school compared with college or greater (adjusted odds ratio, 1.42 [95% CI, 1.12-1.79]); black (3.47 [2.97-4.05]), Hispanic (1.33 [1.10-1.61]), and other (2.46 [2.03-2.97]) maternal race or ethnicity compared with white race; household income of less than $20 000 (1.69 [1.44-1.99]) and $20 000 to $50 000 (1.29 [1.14-1.45]) compared with greater than $50 000; living in the West (1.61 [1.38-1.88]) or the South (1.47 [1.30-1.66]) compared with the Midwest; infants younger than 8 weeks (1.45 [1.21-1.73]) or ages 8 to 15 weeks (1.31 [1.17-1.45]) compared with 16 weeks or older; and being born prematurely compared with full-term (1.41 [1.22-1.62]). Almost 46% of the participants reported talking to a physician about bed sharing. Compared with those who did not receive advice from a physician, those who reported their physicians had a negative attitude were less likely to have the infant share a bed (adjusted odds ratio, 0.66 [95% CI, 0.53-0.82]), whereas a neutral attitude was associated with increased bed sharing (1.38 [1.05-1.80]). CONCLUSIONS AND RELEVANCE Our finding of a continual increase in bed sharing throughout the study period among black and Hispanic infants suggests that the current American Academy of Pediatrics recommendation about bed sharing is not universally followed. The factors associated with infant bed sharing may be useful in evaluating the impact of a broad intervention to change behavior.
The laryngeal chemoreflex (LCR), an airway protective reflex that causes apnea and bradycardia, has long been suspected as an initiating event in the sudden infant death syndrome (SIDS). Serotonin (5-HT) and 5-HT receptors may be deficient in the brainstems of babies who die of SIDS, and 5-HT seems to be important in terminating apneas directly or in causing arousals or as part of the process of autoresuscitation. We hypothesized that 5-HT in the brainstem would limit the duration of the LCR. We studied anesthetized rat pups between 7 and 21 days of age and made microinjections into the cisterna magna or into the nucleus of the solitary tract (NTS). Focal, bilateral microinjections of 5-HT into the caudal NTS significantly shortened the LCR. The 5-HT 1a receptor antagonist, WAY 100635, did not affect the LCR consistently, nor did a 5-HT2 receptor antagonist, ketanserin, alter the duration of the LCR. The 5-HT3 specific agonist, 1-(3-chlorophenyl)-biguanide, microinjected bilaterally into the caudal NTS significantly shortened the LCR. Thus, endogenous 5-HT released within the NTS may curtail the respiratory depression that is part of the LCR, and serotonergic shortening of the LCR may be attributed to activation of 5-HT3 receptors within the NTS. 5-HT3 receptors are expressed presynaptically on C-fiber afferents of the superior laryngeal nerve, and serotonergic shortening of the LCR may be mediated presynaptically by enhanced activation of inhibitory interneurons within the NTS that terminate during the LCR. This article is protected by copyright. All rights reserved.
In responding to an e-mail inquiry from Somers in October 2012, we explained that we do not have specific data on crib mattress firmness in the National Child Death Review-Case Reporting System data used in our analysis of Sudden Unexpected Deaths (SUID). We do not, however, interpret our findings as conflicting with what is an increasing body of evidence that soft sleep surfaces and presence of other hazards in the sleep environment may increase the risk of suffocation in infants. Quite the contrary; as we point out, our findings were largely consistent with other research that has described the characteristics of SUID using child death review or medical examiner data in the United States(1-4) and consistent with research focused specifically on deaths from Sudden Infant Death Syndrome (SIDS) that report characteristics of the sleep environment.(2,5-7) (Am J Public Health. Published online ahead of print March 14, 2013: e1. doi:10.2105/AJPH.2013.301244).
BACKGROUND: Sudden infant death syndrome (SIDS) is the leading cause of death in the first 6 months after birth in the industrialized world. The genetic contribution to SIDS has been investigated intensively and to date, 14 cardiac channelopathy genes have been associated with SIDS. Newly published data from National Heart, Lung, and Blood Institute Grand Opportunity (NHLBI GO) Exome Sequencing Project (ESP) provided important knowledge on genetic variation in the background population. Our aim was to identify all variants previously associated with SIDS in ESP to improve the discrimination between plausible disease-causing mutations and variants most likely to be false-positive. METHODS: The PubMed database was searched to identify SIDS-associated channelopathy variants and the prevalence of these in the ESP population (6500 individuals) were obtained. In silico prediction tools were applied to variants present in ESP and 6 SIDS-associated variants (CAV3 p.C72W, p.T78M; KCNH2 p.R148W, and SCN5A p.S216L, p.V1951L, p.F2004L) were genotyped in our own control population. RESULTS: Nineteen different missense variants previously associated with SIDS were identified in ESP affecting 225 of 6424 alleles. This corresponds to 1:29 individuals in the ESP population being carriers of a SIDS-associated variant. Genotyping of 6 SIDS-associated variants in our own controls revealed frequencies comparable with those found in ESP. CONCLUSIONS: A very high prevalence of previously SIDS-associated variants was identified in exome data from population studies. Our findings indicate that the suggested disease-causing role of some of these variants is questionable. A cautious interpretation of these variants must be made when found in SIDS victims.
OBJECTIVES: To test the hypothesis that there is a significant association between functionally relevant allelic variants of the monoamine oxidase A (MAO-A) polymorphism and sudden infant death syndrome (SIDS). STUDY DESIGN: In a case-control study of 142 cases of SIDS and 280 sex-matched control cases, the distribution of allelic and genotype variants of a promoter polymorphism of the MAO-A gene was examined using polymerase chain reaction locus amplification and fluorescence based fragment length analysis. RESULTS: There was a significantly differential distribution of allelic and genotype variants between females with SIDS and controls. Moreover, there was a significant association between SIDS in females and allelic and genotype variants, each related to a higher transcriptional activity at the MAO-A locus. CONCLUSIONS: Our results suggest a role of MAO-A in female SIDS pathogenesis exerted by functionally relevant allelic and genotype variants of the MAO-A polymorphism. However, with the complex and inconsistent evidence available to date, the impact of the MAO-A promoter polymorphism on SIDS etiology remains unclear.
Sudden infant death syndrome (SIDS) is a leading cause of postneonatal infant mortality. Our previous meta-analyses showed that any breastfeeding is protective against SIDS with exclusive breastfeeding conferring a stronger effect.The duration of breastfeeding required to confer a protective effect is unknown.
Our group and others have reported a high rate of vitamin D deficiency in obstructive sleep apnoea syndrome (OSAS), where vitamin D levels (25(OH)D) correlate negatively with OSAS severity and some of its associated metabolic alterations. Data regarding vitamin D supplementation in OSAS are lacking. We wanted to evaluate the effect of vitamin D3 supplementation on OSAS symptoms and metabolic parameters.
In industrialized countries, sudden infant death is the most common cause of death in young children. Although prone sleeping position is a well-known risk factor, hyperthermia might also be important. Pathognomonic findings of premortem hyperthermia do not exist. During stress, including thermal effects, heat-shock protein (HSP) expression increases. This study investigated hyperthermia as a contributing or pathogenic factor for sudden infant death syndrome (SIDS).
Air pollution has been associated with increased mortality and morbidity in several studies with indications that its effect could be more severe in children. This study examined the relationship between short-term variations in criteria air pollutants and occurrence of sudden infant death syndrome (SIDS).