Abstract
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There is clear and convincing evidence that an enriched environment may increase the release of oxytocin from the hypothalamic nuclei and have a permanent effect on the physiology and behavior of mammalian species. 1 Imaging studies comparing the activation of oxytocin receptors in formula-feeding and breastfeeding mothers were reported by Bartels and Zeki, 2 demonstrating significant enhancement of oxytocin receptor sites in breastfeeding mothers that correlated with greater neural response. Furthermore, Grewen et al. 3 reported a higher concentration of oxytocin in blood and saliva of breastfeeding compared with formula-feeding mothers: 36% in plasma and 23% in saliva, respectively.
There is significant evidence that maternal love and bonding are mediated by oxytocin, 1 and the periaqueductal gray matter, the limbic area, and the lateral orbitofrontal cortex are identified with maternal behavior. 2 Additionally, the oxytocinergic system appears to encompass the sensory, emotional, motivational, and cognitive pathways, which are affected in various degrees in individuals with ASD.
In the past decade there has been credible evidence that ASDs are associated with oxytocin dysfunction. Modahl et al. 4 have reported lower oxytocin levels in children and adults with ASDs. Furthermore, oxytocin infusion or intranasal oxytocin administration to adults with ASD resulted in the reversal of some of their symptoms. Finally, genetic alterations in oxytocin peptide form or the receptor protein are associated with ASDs.
In this communication we hypothesize that breastfeeding and nurturing result in a decrease in the prevalence of ASD diagnosis. In order to validate this hypothesis we conducted a retrospective parents' survey of children with ASD diagnosis and the duration of breastfeeding, feeding with breastmilk, or formula feeding.
One hundred forty-five parents responded to our survey. There were 60 children with ASD diagnosis, and 85 reported no ASD diagnosis. The children were divided into three groups. Those infants who were formula fed from birth were assigned to the formula-fed group. Those infants who were breastfed from birth were placed in the breastfed group, even though many infants were weaned before 2 months of age. The survey results demonstrate that increasing the duration of breastfeeding is associated with a decline in ASD diagnosis as shown in Table 1. The statistical data reveal that children who were breastfed longer than 12 months were 6.53 times more likely to be non-ASD than the children who were breastfed for less than 12 months. Twenty-two of 64 children who were fed breastmilk via a bottle were reported to have ASD, and increasing the duration of breastmilk feeding was not associated with a decline in ASD diagnosis.
ASD, autism spectrum disorder.
In this communication we have reported data that indicate an association between early weaning or breastmilk feeding and higher prevalence of ASDs in “presumed” genetically susceptible individuals. We believe that formula and breastmilk feeding, via a bottle, results in less sensory stimulation than breastfeeding and therefore lower oxytocin release from the hypothalamic nuclei and reduced binding of oxytocin to the oxytocin receptors.
There are numerous hormones and growth factors in the mother's milk that function as signals to regulate metabolic pathways in the newborns. Breastmilk estrogens act as transcriptional promoters for both oxytocin and oxytocin receptor genes. The absence of estrogens in the infant's feeding source or the use of oxytocin receptor blockers results in lower levels of endogenous oxytocin and oxytocin receptors in experimental animals. Oxytocin and estrogens have a regulatory influence on the oxytocinergic system and have the potential to enhance neuroplasticity. Furthermore, oxytocin is a neurotransmitter and neuromodulator and may increase synaptic connections and suppress expression of ASD genes. Other ingredients of breastmilk may function as epigenetic factors through DNA methylation and histone acetylation and may result in gene activation or suppression.
There are several ongoing clinical trials including targeted treatments, specifically the use of γ-aminobutyric acid-B agonists for patients with fragile X syndrome. 4 However, an effective drug therapy for children and adults with ASDs has been elusive. Therefore it is imperative to identify the risk factors and develop strategies for prevention of ASDs, including newborn screening for fragile X syndrome and identification of carriers.
The short- and long-term benefits of breastfeeding for mother and baby have been well documented. This preliminary study demonstrates the mental health benefits of breastfeeding and identifies lack of breastfeeding as the major risk factor for development of ASDs in genetically susceptible children. Further studies on the impact of infants' feeding methods on the prevalence of ASDs, utilizing a prospective longitudinal children's developmental evaluation, are warranted to further validate our findings.