Hypovitaminosis A: A model for sudden infant death syndrome

Abstract

The cause of sudden infant death syndrome (SIDS) is unknown. It is the leading cause of death from age one month to one year in North America. The purpose of this essay is to generate some testable hypotheses as to the cause of SIDS by drawing attention to distinct epidemiological parallels between SIDS and a newly recognized form of enamel hypoplasia, termed localized hypoplasia of the primary canine tooth (LHPC), which has been attributed to vitamin A deficiency. LHPC and SIDS share a common epidemiological profile: winter seasonality, occurrence at 3-5 months, and affecting apparently healthy children, but with increased incidence in socio economically disadvantaged families particularly racial/ethnic minorities (except Hispanics who show a reduced incidence), previously compromised infant health, less prenatal counselling, and less breastfeeding. Vitamin A has pervasive functions throughout the body including bone growth and maintenance of epithelial membranes. It is proposed that SIDS is due in part to hypovitaminosis A through one of several mechanisms: imbalanced basicranial growth producing mechanical constriction on the respiratory nerves passing through the jugular foramen; or through compromised myelination and/or maturation of the brain stem and cranial nerves involved in respiration; or through pharyngeal collapse due to mandibular undergrowth; or dysfunction of hypoxia-sensitive epithelial cells in the trachea. It is recommended that assay of hypoxia-sensitive epithelial cells in the trachea. It is recommended that assay of the retinyl ester content of the liver of SIDS victims be included in autopsy protocol. © 1995 Wiley-Liss, Inc.

Phenotypes and pathways: Working toward an integrated skeletal biology in biological anthropology

“…The number of category 3 articles nearly doubled between 2011 and 2019 and represents a growing emphasis on skeletal integration and the skeleton's dynamic ability to respond to myriad biocultural cues. Researchers have investigated interactions between the skeletal system and other physiological systems during the regulation of energy and vitamin homeostasis (Devlin, 2011; González‐García, Kullo, Coletta, Mandarino, & Shaibi, 2015; Lucock et al, 2019; Mueller et al, 2013; Skinner, 1995), as well as the relationship between bone and reproduction (Madimenos, Snodgrass, Liebert, Cepon, & Sugiyama, 2012) and immune function (Larijani et al, 2004; Zemel, 2017). Other articles emphasize skeletal responses to external cues by focusing on the association between skeletal phenotypes and cultural factors (Bailey et al, 2007; Dent, 2017; Lukacs, Walimbe, & Floyd, 2001; Martin & Danforth, 2009; Reitsema, 2013).…”

Markers of physiological stress in juvenile bonobos (Pan paniscus): Are enamel hypoplasia, skeletal development and tooth size interrelated?

“…The proposed pathway leading to fenestration is multistaged and may begin with a diet insufficient in Vitamin A. Retinol, the active metabolite of Vitamin A, plays an important role in regulating bone growth; however, the effect of hypovitaminosis A on bone growth in humans is not well documented. The idea that diets low in Vitamin A may lead to craniofacial osteopenia in infants and ultimately predispose primary canine teeth to labial enamel hypoplasia is based largely on evidence from experimental studies on nonhuman species (Skinner, 1995(Skinner, , 2002Skinner and Newell, 2003). The effects of hypovitaminosis A on bone formation are variable depending on dos- Means computed from maximum dimension-right or left side.…”

“…Asterisks indicate significant differences (P < 0.05) for primary canine teeth, mean differences in tooth size of incisor and molar teeth are not significant. age, duration, species, and timing, yet disrupted bone modeling and remodeling are commonly reported (Skinner, 1995). The bioavailability of Vitamin A to neonates is a function of multiple sources and regulating influences, and mother's dietary fat may be a primary factor limiting Vitamin A availability in breast milk (Skinner and Newell, 2000).…”