Is excess male infant mortality from sudden infant death syndrome and other respiratory diseases X‐linked?

Mage, David T.; Donner, E. Maria

doi:10.1111/apa.12482

Cited by 28 publications

(25 citation statements)

References 19 publications

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“…As described above, all infant mortality from respiratory causes has an apparent 50% X-linkage male excess rate for equal numbers of XY males and XX females at risk (we neglect chromosomal abnormalities, such as XXY male and XXX female, and assume no infanticides). As also shown, there is no male excess (0%) for cardiac failures, which include congenital anomalies related to genetic variants on the 22 autosomes, which males and females have with equal probabilities, assuming HWE (40, 41). That is, for every two females dying from respiratory causes, three males will die, and for every two females dying of cardiac causes, two males will die.…”

Section: Prediction Of Male Fraction Of All Total Infant Mortality Frmentioning

confidence: 90%

An Acute Respiratory Infection of a Physiologically Anemic Infant is a More Likely Cause of SIDS than Neurological Prematurity

Mage¹,

Latorre²,

Jeník

et al. 2016

Front. Neurol.

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introduction: The cause of the sudden infant death syndrome (SIDS) is perhaps the oldest of unsolved mysteries of medicine, possibly dating back to Exodus in Biblical times when Egyptian children died in their sleep as if from a plague. It occurs when infants die unexpectedly with no sufficient cause of death found in a forensic autopsy, including death scene investigation and review of medical history. That SIDS is an X-linked recessive death from infectious respiratory disease of a physiologically anemic infant and not a simple anomalous cardiac or neurological condition is an extraordinary claim that requires extraordinary evidence. If it were by a simple cause, it would have already been solved, with over 11,000 papers on SIDS listed now in PubMed. Our aim is to use mathematical models of SIDS to explain: (1) its 50% excess male death rate; (2) its 4-parameter lognormal distribution of ages at death; (3) its winter maxima and summer minima; and (4) its increasing rate with live-birth order.Methods: From extensive SIDS vital statistics data and published epidemiologic studies, we developed probability models to explain the mathematical behavior of SIDS meeting the four constraints mentioned above. We, then, compare these SIDS properties to infant death from acute respiratory infection (ARI), and infant death from encephalopathy, unspecified (EU).results: Comparisons show that SIDS are congruent with ARI and are not consistent with EU and that these probability models not only fit the SIDS data but they also predict and fit the male fraction of all infant and child mortality from birth through the first 5 years of their life.conclusion: SIDS are not rejected as an X-linked disease involving ARI and are not explained by a triple risk model that has been commonly accepted by the SIDS medical community, as implicating a neurological causation process in a subset of SIDS.

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Section: Prediction Of Male Fraction Of All Total Infant Mortality Frmentioning

confidence: 90%

An Acute Respiratory Infection of a Physiologically Anemic Infant is a More Likely Cause of SIDS than Neurological Prematurity

Mage¹,

Latorre²,

Jeník

et al. 2016

Front. Neurol.

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“…Approximately one-half of SIDS victims have a slight upper airway infection before death (124) with males reported to have an excess of infant mortality from respiratory deaths as well as SIDS (125). The risk of SIDS also increases with the number of siblings, otherwise known as “birth order” (124), another known SIDS risk factor.…”

Section: Introductionmentioning

confidence: 99%

A “Wear and Tear” Hypothesis to Explain Sudden Infant Death Syndrome

Elhaik

2016

Front. Neurol.

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Sudden infant death syndrome (SIDS) is the leading cause of death among USA infants under 1 year of age accounting for ~2,700 deaths per year. Although formally SIDS dates back at least 2,000 years and was even mentioned in the Hebrew Bible (Kings 3:19), its etiology remains unexplained prompting the CDC to initiate a sudden unexpected infant death case registry in 2010. Due to their total dependence, the ability of the infant to allostatically regulate stressors and stress responses shaped by genetic and environmental factors is severely constrained. We propose that SIDS is the result of cumulative painful, stressful, or traumatic exposures that begin in utero and tax neonatal regulatory systems incompatible with allostasis. We also identify several putative biochemical mechanisms involved in SIDS. We argue that the important characteristics of SIDS, namely male predominance (60:40), the significantly different SIDS rate among USA Hispanics (80% lower) compared to whites, 50% of cases occurring between 7.6 and 17.6 weeks after birth with only 10% after 24.7 weeks, and seasonal variation with most cases occurring during winter, are all associated with common environmental stressors, such as neonatal circumcision and seasonal illnesses. We predict that neonatal circumcision is associated with hypersensitivity to pain and decreased heart rate variability, which increase the risk for SIDS. We also predict that neonatal male circumcision will account for the SIDS gender bias and that groups that practice high male circumcision rates, such as USA whites, will have higher SIDS rates compared to groups with lower circumcision rates. SIDS rates will also be higher in USA states where Medicaid covers circumcision and lower among people that do not practice neonatal circumcision and/or cannot afford to pay for circumcision. We last predict that winter-born premature infants who are circumcised will be at higher risk of SIDS compared to infants who experienced fewer nociceptive exposures. All these predictions are testable experimentally using animal models or cohort studies in humans. Our hypothesis provides new insights into novel risk factors for SIDS that can reduce its risk by modifying current infant care practices to reduce nociceptive exposures.

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“…For proof of its causation, the predicted missing X-linked p = 1/3 dominant allele that is protective of neuronal cell death by acute anoxic encephalopathy by enabling the infant to shift from aerobic to anaerobic oxidation must be identified [3,14]. This may be difficult because of the likely presence of false positive SIDS in the study cohorts, where a non-SIDS cardiac cause of death or a case of infanticide may have been missed.…”

Section: Scandinavian Journal Ofmentioning

confidence: 99%

“…We have shown previously that: 1) SIDS cannot be a cardiac death, because SIDS has a constant 50% male excess and cardiac infant deaths have a 0% male excess [1][2][3]; 2) SIDS is not likely to be caused by a brainstem-abnormality because SIDS ages have a lognormal age distribution, sparing infants at or shortly after birth, whereas infants born with fatal neurological defects have maximum mortality shortly after birth [4][5][6]. Rather, we show that SIDS have the same gender distribution (50% excess male rate) as infant deaths from respiratory infection [5,7] and a similar 4-parameter lognormal age distribution as with hospital admissions for bronchiolitis [7].…”

Section: Introductionmentioning

confidence: 99%

The Role of Respiratory Infection in Sudden Infant Death Syndrome (SIDS)

Mage¹,

Latorre²,

Jeník³

et al. 2016

Scandinavian Journal of Forensic Science

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Abstract:Introduction: The Sudden Infant Death Syndrome (SIDS) is not likely to be explained by a currently measureable presence in all cases and absence in controls, as otherwise it would have been solved already. Indeed, any proposed physiological model for SIDS causation must explain the constant mathematical and statistical properties of SIDS age and gender. We have shown previously that SIDS are characterized by a common 4-parameter lognormal age distribution sparing neonatal infants, by a nominal 50% male excess, and by a higher rate in winter than summer. We test now whether SIDS is closely related to a fulminating prodromal Acute Respiratory Infection (ARI) by a common increasing rate with the infants increasing Live Birth Order (LBO), all remaining the same, independent of the change in preferred sleeping positions of the infants, prone or supine. Methods: We use U.S. published infant mortality data from wonder.cdc.gov and other countries (Colombia, U.K., Europe, Australasia) to make comparisons between the two causes of death (ARI and SIDS) to evaluate how closely ARI resembles the characteristics of SIDS. Results: Gender: SIDS male excess 50%, ARI male excess 50%; Ages: SIDS 90% post-neonatal, ARI 96% post-neonatal; Seasonality: SIDS and ARI are higher in winter than summer; Live birth order: SIDS and ARI rates increase with increasing LBO with similar mathematical relationship. Conclusion: Our results show that all SIDS are very likely relatable to a single cause tied to a fulminating prodromal ARI in a physiologically anemic infant who is genetically (X-link recessive) susceptible to cerebral anoxia. An alternative cause of all SIDS death by a collection of subsets of different causes, such as brainstem-related respiratory abnormalities and cardiac QT abnormalities, is not supported because they cannot all have the same age-gender-seasonal-familial-distributions of SIDS, required by Cramér's Theorem.

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Is excess male infant mortality from sudden infant death syndrome and other respiratory diseases X‐linked?

Cited by 28 publications

References 19 publications

An Acute Respiratory Infection of a Physiologically Anemic Infant is a More Likely Cause of SIDS than Neurological Prematurity

An Acute Respiratory Infection of a Physiologically Anemic Infant is a More Likely Cause of SIDS than Neurological Prematurity

A “Wear and Tear” Hypothesis to Explain Sudden Infant Death Syndrome

The Role of Respiratory Infection in Sudden Infant Death Syndrome (SIDS)

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