Philip S. Spiers

Thermal Stress in Sudden Infant Death: Is There an Ambiguity With the Rebreathing Hypothesis?

Objective. To assess the role of thermal stress in the cause of sudden infant death syndrome (SIDS), and to compare risk factors with those of rebreathing. Methodology. Analysis of publications concerning the epidemiology and physiology of thermal stress in SIDS. Results. A strong association between thermal regulation and ventilatory control was found, specifically for prolonged apnea. Infections, excessive room heat and insulation, and prone sleeping produce significantly increased odds ratios for SIDS. Although some of the risk factors for rebreathing could be explained by the effects of thermal stress, several factors for thermal stress could not reasonably be explained by the rebreathing hypothesis. Conclusions. Although the risk of thermal stress is widely accepted abroad, it has received relatively little attention in the United States. The incidence of SIDS in the United States can likely be further reduced by educating the public against the dangers of overheating, as an integral part of the back-to-sleep campaign.

Prolongation of the QT interval and the sudden infant death syndrome

* Abbreviations: SIDS = : sudden infant death syndrome • ECG = : electrocardiogram • LQTS = : long QT syndrome A recent article by Peter Schwartz and his colleagues1 in Italy in the New England Journal of Medicine implicated prolongation of the QT interval in the sudden infant death syndrome (SIDS), and made recommendations for electrocardiographic (ECG) screening in normal infants at the third or fourth day of life. The cumulative expense to parents, both financial and emotional, would be staggering, and careful scrutiny of the data and its interpretation is required. The long QT syndrome (LQTS) is a rare and frightening genetic disorder that leads to ventricular arrhythmias, typically torsade de pointe , manifested by repeated syncope and … Address correspondence to Warren G. Guntheroth, MD, University of Washington School of Medicine, Department of Pediatrics, 1959 NE Pacific St, Box 356320, Seattle, WA 98195-6320.

The black infant's susceptibility to sudden infant death syndrome and respiratory infection in late infancy.

Between 2 and 11 months of age, the risk of sudden infant death syndrome (SIDS) declines more slowly in black infants than in infants of other races. This phenomenon might also be a feature of certain non-SIDS causes of death. Identifying these causes may through analogy provide support for the theory that SIDS is a disease of the central nervous system, an unusual consequence of respiratory infection, or a form of suffocation. We used logistic regression analysis on details of infant deaths in the United States, 1985–1991, to examine the difference between the rates of decline with increasing age in the mortality rates of black infants and infants of other races. We defined slower rate of decline in black infants as a positive difference. The magnitude and direction (positive) of the difference for deaths due to respiratory infection were similar to those for SIDS. It is unlikely that this difference in the rates of decline for respiratory infection can be explained by diagnostic cross-misclassification between respiratory infection and SIDS. SIDS appears to be a disease of the respiratory system caused by infection that affects that system’s control centers.

Sex ratio by age in childhood malignancies

Abstract Mortality data from both the United States and England and Wales indicates that the sex ratio (male/female mortality rate) decreases by age at death for tumors of the genito-urinary system, but increases for other malignancies of childhood. Although interpretation of these findings must be somewhat speculative, it is postulated, on the basis of supportive evidence, that they can be explained by the differential effect of age and sex upon the hosts susceptibility to some carcinogenic agents or agents.

Should Officers of the US Department of Health and Human Services Advocate Pet Theories of Sudden Infant Death Syndrome

In late December 2004, the publication “What Is SIDS?” was sent out by the US Department of Health and Human Services.1 It begins with a definition of sudden infant death syndrome (SIDS) by Willinger et al2 that requires examination of the death scene before that diagnosis can be made. Although that requirement has achieved some support, it has not been accepted universally because of limited resources in many regions. It is even more critical to note that Haas et al3 found that only 45% of the cases in King County, Washington, had an intact death scene because of the urgent removal of the body to a hospital emergency department. Enforcing this definitional requirement would thus diminish by one half the true population base for SIDS. The original definition by Beckwith4 was not mentioned in this publication, although it includes 24 references (of those 24 references, 11 were by personnel from federal agencies). The publication gives a brief half page of sound recommendations for prevention of SIDS, but only a single causal theory, the “triple-risk hypothesis,” is favorably reviewed in a longer section on causation.1 This theory was proposed by researchers supported by grants from the National Institute of Child Health and Human Development. However, no article critical of this theory, or any other theory, are mentioned or cited in this publication despite their appearance in recent peer-reviewed pediatric journals. There is a conflict of interest when the agency that funds almost all grants for research on SIDS vigorously advocates selected theories; it requires a brave or imprudent researcher in this field to oppose them. The public good, and good science, are not well served by funding agencies advocating pet theories.