BackgroundWhile many studies have examined environmental risk factors for autism spectrum disorder (ASD), much of the research focus has been on prenatal or perinatal factors. Yet, the postnatal environment may affect the risk of ASD as well.ObjectiveTo determine whether a set of five postnatal variables are associated with ASD. These variables are: acetaminophen exposure, antibiotic exposure, incidence of ear infection, decreased duration of breastfeeding, and decreased consumption of oral vitamin D drops.Materials and methodsAn Internet-based survey was conducted. Participants were parents living in the USA with at least one biological child between 3 and 12 years of age. Potential participants were informed about the survey via postings on social media, websites, and listservs and were offered an opportunity to participate in a raffle as well. Participants were also recruited through the Interactive Autism Network.ResultsThere were 1,741 completed survey responses. After exclusions, there remained 1,001 responses associated with children with ASD (cases) and 514 responses associated with children who do not have ASD (controls). In this data set, doses of postnatal acetaminophen (adjusted odds ratio [aOR] 1.016, CI: 1.003–1.032, p=0.026), courses of postnatal antibiotics (aOR 1.103, CI: 1.046–1.168, p<0.001), incidence of postnatal ear infection (aOR 1.137, CI: 1.046–1.236, p=0.003), and decreased duration of breastfeeding (aOR 0.948, CI: 0.932–0.965, p<0.001) are all associated with ASD when adjusted for eight demographic variables. A weak association between oral vitamin D drop exposure and ASD was also found when adjusted for breastfeeding and demographics (aOR 1.025, CI: 0.995–1.056, p=0.102).ConclusionThis study adds to evidence that postnatal acetaminophen use, postnatal antibiotic use, incidence of ear infection, and early weaning are associated with an increased risk of ASD. It also finds that postnatal oral vitamin D drops are weakly associated with ASD when adjusted for breastfeeding and demographics.
Background: Celiac disease (CD) prevalence has increased significantly in recent decades in some developed countries. Yet the environmental factors in the existing literature do not appear to provide a satisfactory explanation for this increase. Objective: To determine whether nine variables are associated with CD in children. These variables are: incidence of ear infection before 2 years old, courses of antibiotics before 2 years old, duration of breastfeeding, vitamin D drop exposure in infancy, vitamin D supplement exposure between 2–3 years old, age at gluten introduction into the diet, fat content of cow’s milk consumed between 2–3 years old, quantity of cow’s milk consumed between 2–3 years old, and type of water consumed at 2 years old. Methods: An Internet-based survey was conducted among parents living in the US with at least one biological child between 3 and 12 years old. Potential participants were informed about the survey through social media, websites, electronic newsletters, and advertisements. Results: After exclusions, there remained 332 responses associated with children with CD (cases), and 241 responses associated with children who do not have CD (controls). In this data set, skim milk as the primary form of liquid cow’s milk consumed between 2–3 years old (adjusted odds ratio [aOR]=3.556, CI=1.430–10.22, P =0.010), vitamin D drops administered for more than 3 months (aOR=1.749, CI=1.079–2.872, P =0.025), courses of antibiotics (aOR=1.133, CI=1.037–1.244, P =0.007), and incidence of ear infection (aOR=1.183, CI=1.041–1.348, P =0.010) are all associated with CD in children. Conclusions: This study is the first to find an association between skim milk consumption and CD and vitamin D drop use for greater than 3 months and CD. It also adds to evidence that early life exposure to antibiotics and early life infection, specifically ear infection, are associated with CD.
The prevalence of celiac disease (CD) has increased significantly in some developed countries in recent decades. Potential risk factors that have been considered in the literature do not appear to provide a convincing explanation for this increase. This has led some researchers to hypothesize that there is a "missing environmental factor" that increases the risk of CD. Based on evidence from the literature, the author proposes that elevation in plasma levels of 1,25-dihydroxyvitamin D [1,25(OH) 2 D] is a missing risk factor for CD, and relatedly that significant oral vitamin D exposure is a "missing environmental factor" for CD. First, elevated plasma levels of 1,25(OH) 2 D are common in CD, especially in the newly diagnosed. Second, nine distinct conditions that increase plasma levels of 1,25(OH) 2 D are either associated with CD or have indications of such an association in the literature. Third, a retrospective study shows that sustained oral vitamin D supplementation in infancy is associated with increased CD risk, and other studies on comorbid conditions support this association. Fourth, large doses of oral vitamin D upregulate many of the same cytokines, chemokines, and toll-like receptors that are upregulated in CD. Fifth, epidemiological evidence, such as the timing of the inception of a CD "epidemic" in Sweden, the increased prevalence of CD in Finland and the United States in recent decades, the unusually low prevalence of CD in Germany, and the differential in prevalence between Finnish Karelians and Russian Karelians, may all be explained by oral vitamin D exposure increasing CD risk. The same is true of some seemingly contradictory results in the literature on the effects of breastfeeding on CD risk. If future research validates this hypothesis, adjustments to oral vitamin D consumption among those who have genetic susceptibility may decrease the risk of CD in these individuals.
Some evidence from the literature suggests that postnatal acetaminophen exposure may be associated with increased risk of autism spectrum disorder (ASD). Using a data set obtained from a previous study that was derived from an Internet-based survey among parents on 1515 children from the US, an adjusted odds ratio (aOR) and gender-specific aORs for doses of postnatal acetaminophen provided before age two were calculated against the outcome of ASD. Separately, parental uncertainty on the number of doses of acetaminophen provided was analyzed. A population attributable fraction (PAF) associated with postnatal acetaminophen exposure before age two for ASD among males was also estimated. Postnatal acetaminophen exposure, measured in doses before age two, was found to be associated with ASD among male children (aOR 1.023, CI 1.005–1.043, p = 0.020*), and parental uncertainty on the number of doses of acetaminophen provided before age two was also found to be associated with ASD. Using this data set, the PAF associated with postnatal acetaminophen was estimated to be about 40% of the risk of ASD among male children in the US. These results suggest the possibility that postnatal acetaminophen may be a significant contributor to the risk of ASD among males in the US.
Celiac disease is an autoimmune disease initiated by an allergic reaction to gliadin a component of the protein gluten that is found in wheat and other grains.
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