SIDS, prone sleep position and infection: An overlooked epidemiological link in current SIDS research? Key evidence for the “Infection Hypothesis”

Abstract

Mainstream researchers explain the etiology of SIDS with the cardiorespiratory paradigm. This has been the focus of intense study for many decades without providing consistent supporting data to link CNS findings to epidemiological risk factors or to the usual clinicopathological findings. Despite this, and the apparent oversight of the link between prone sleep position and respiratory infection, papers citing CNS, cardiac and sleep arousal findings continue to be published. Discovery of the prone sleep position risk factor provided tangential support for the cardiorespiratory control hypothesis which defines the mainstream approach. Despite many decades of research and huge expenditure, no aetiological answer has been forthcoming. In asking why?This paper exposes some of the shortcomings regarding this apparent oversight by mainstream SIDS researchers and examines the role of respiratory infection and puts the case for the “Infection Hypothesis.” In addition, the paper provides encouragement to neuropathologists to examine the potential link between CNS findings and cardiac function (as opposed to respiratory function) in relation to infection and to examine possible correlates between CNS findings and established risk factors such as recent infection, contaminated sleeping surfaces, maternal/obstetric/higher birth, ethnicity, non-breast-feeding, male gender, etc. or with the usual gross pathological findings of SIDS (intrathoracic petechial hemorrhages, liquid blood, congested lungs). The shortcomings exposed through this review invite questions over current research directions and hopefully encourage research into other more plausible hypotheses, such as the infection paradigm. Mainstream SIDS researchers appear to have overlooked the key relationship between prone sleep position and infection. This omission has major implications for current and future SIDS research.

The Genetics of Sudden Infant Death Syndrome—Towards a Gene Reference Resource

“…By contrast, Elhaik [ 18 ] showed that gender bias varies widely between population groups and states and that male neonatal circumcision (MNC) explains 16% of the variability in male SIDS deaths in the US. This finding supported the “wear and tear” hypothesis for SIDS [ 17 ], which explains the main characteristics of SIDS, namely male predominance (60:40) by MNC, the significantly different SIDS rate among USA Hispanics (80% lower) compared to whites by the different circumcision practices of these populations, the 50% of cases occurring between 7.6 and 17.6 weeks after birth, with only 10% after 24.7 weeks by the weaning from the maternally acquired antibodies that protect from infections, and the seasonal variation with most cases occurring during winter by the rise of infections (see the “Infection Hypothesis” [ 90 ]) that increase the allostatic load [ 17 ] (summarized in Table 1 [ 17 ]).…”

Infection, Celestial Influences, and Sudden Infant Death Syndrome: A New Paradigm

“…Despite decades of research, mainstream researchers have not been able to establish a connection between SIDS and reproducible and broad-sweeping neuropathological findings [ 40 , 41 ]. The only remarkably consistent gross pathological findings in SIDS are heavy fluid-laden lungs, intrathoracic petechial hemorrhages, and liquid (unclotted) blood, as described previously.…”

“…The important role of infection in SIDS has been described previously [ 40 ] and cannot be overstated [ 41 ]. A plausible mechanism would be an abnormal response to viral respiratory infection when the infant is challenged by a bacterial toxin.…”

“…A Nordic study showed a 29-fold increase in risk due to prone plus infection [ 38 , 39 ]. Moreover, the infection paradigm is supported by and is congruent with all epidemiological SIDS risk factors [ 40 , 41 ]. It remains unclear as to why the infection hypothesis has not achieved greater prominence.…”

Feasibility and Acceptability of a Tailored Infant Safe Sleep Coaching Intervention for African American Families

“…African American infants in the U.S. experience Sudden Unexpected Infant Deaths at twice the rate of white infants (at 186.9 infant deaths per 100,000 live births and 84.9, respectively) [ 1 ]. Risk for Sudden Unexpected Infant Death and SIDS has been suggested using, for example, the infection hypothesis [ 2 ] and the triple risk hypothesis [ 3 , 4 ], which suggest potential underlying vulnerability that may be exacerbated by modifiable behaviors such as maternal smoking, lack of breast feeding, unsafe sleep surfaces, and prone sleeping. Most sleep-related infant deaths occur in environments that have at least one modifiable behavioral risk factor [ 5 , 6 , 7 ].…”