The fifty percent male excess of infant respiratory mortality

Abstract

Aim: To test whether infant mortality from clearly respiratory causes has a consistent male excess that is different from the male excess in most cardiac conditions. Methods: Analysis of male excess in infant mortality data from the United States and from north European countries. Data are analyzed for the period 1979–2002 in autopsied and unautopsied cohorts. Results: Several modes of respiratory death in infancy are characterized by an approximate 50% male excess. This common excess is demonstrated in vital statistics for infant respiratory distress syndrome, sudden infant death syndrome, inhalation of food and other objects causing obstruction of respiratory tract or suffocation, congenital pneumonia, viral pneumonia, bronchiolitis and bronchitis, and accidental drowning. Results are presented for these and other respiratory causes of mortality in all United States infant deaths from 1979–1998 and for sudden infant death syndrome from the United Kingdom and Scandinavia. In sudden infant death syndrome, the common male excess appears to exist only for the autopsied post‐neonatal cases. Comparisons are made to the male excess mortality from congenital cardiac anomalies showing a similarly large male excess for those conditions resulting in severe hypoxic and ischemic hypoxia. Conclusion: Because these respiratory disease conditions are quite different, it is proposed that their common ∼50% male excess implies a common terminal hypoxic condition and mechanism of death reached via the different pathways. We hypothesize that an unknown X‐linkage may be responsible for this consistent male excess in infant mortality.

Do Infants Die of Sudden Infant Death Syndrome (SIDS) With Long QT Syndrome (LQTS) or From LQTS?

“…Thus, if a genetic marker is present, there is no way to discern whether the infant died of SIDS with LQTS susceptibility or from SCD by LQTS. (2) Universally, SIDS has approximately a 50 % male excess corresponding to a male fraction of about 0.60 for all races combined [2]. However, Stramba-Badiale et al [3] have shown ''that gender-related differences in QTc observed in the adult population are not present at birth''.…”

The rise and fall of excess male infant mortality

“…The decline in deaths from infection is likely to affect males and females differently. Because females have more vigorous immune responses and greater resistance to infection (11), female infants have lower mortality from infections (12) and respiratory ailments (13). The male disadvantage begins in utero (14), when gonadal steroid production already differs strongly by sex.…”

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

“…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].…”