Variation in season of birth in singleton and multiple births concordant for autism spectrum disorder
Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, MD 21205, USA. Paediatric and Perinatal Epidemiology
(Impact Factor: 3.13).
04/2008; 22(2):172-9. DOI: 10.1111/j.1365-3016.2007.00919.x
Patterns of seasonal variation in births in some neuropsychiatric conditions have been found in previous research; however, no study to date has examined these disorders for seasonal variation in singletons and multiple births separately. This study aimed to determine whether the birth date distribution for individuals with autism spectrum disorders (ASD), including singletons and multiple births, differed from the general population. Two ASD case groups were studied: 907 singletons and 161 multiple births concordant for ASD. Two control groups were obtained from registered births of singletons and multiples.
Results of the non-parametric time-series analyses, where day of birth was used, suggested there were three peaks in ASD singletons and ASD concordant multiple births. Roughly, the peaks were in April, June and October for singletons and about 2–4 weeks earlier in multiples. Results from multivariable Poisson regression, where month of birth was used, indicated that ASD concordant multiple births in males tended to be higher than expected in March, May and September (with borderline statistical significance), but were 87% less in December (P < 0.05), as compared with January. Overall, the patterns of relative risk estimates from Poisson regression are similar to findings from the non-parametric time-series approach, but are not exactly congruent. It is important to note that indications of seasonality may be sensitive to the selection of time cut-points and therefore an arbitrary binning of time can either mask existing trends or falsely indicate the presence of a trend. The presence of seasonal trends in ASD singletons and concordant multiple births suggests a role for non-heritable factors operating during the pre- or perinatal period, even among cases with a genetic susceptibility.
Figures in this publication
Available from: Robert John Leeming
- ", supported by others showing seasonality as a driver of autism  , although not all reports agree  Possible effects discussed below Possible mechanisms discussed below, but an important point in these constructs is that native folates are UV-A labile and easily oxidised , while vitamin D requires UV radiation for its synthesis and both are linked to autism risk "
[Show abstract] [Hide abstract]
ABSTRACT: An argument is put forward for environmental modulators of photolabile or photosynthetic vitamins mediating autism risk via a complex downstream interaction of genetic/epigenetic phenomena that provide an explanation for seasonality in this and other developmentally originated disorders.
Medical Hypotheses 04/2013; 80(6). DOI:10.1016/j.mehy.2013.03.003 · 1.07 Impact Factor
Available from: adhdnet.com
- "This having been said, research suggests that maternal, placental, and child serotonin may all interact with environmental variables to influence brain development (Bonnin et al., 2011; Zhang et al., 2010). In the case of ASD, the replicated finding of seasonal fluctuations in brain 5-HTT binding (Willeit and Praschak-Rieder, 2010) and autism births (Gadow and DeVincent, 2012; Lee et al., 2008), the effects of seasonal light cycles on serotonin signaling in the brain mediated by the circadian system (Ciarlegio et al., 2011), and possible involvement of circadian system regulatory genes in autism (Hu et al., 2009) all suggest multiple avenues of inquiry. Alternatively, our finding that the high expressing L A /L A genotype was associated with more severe ASD social deficits combined with research indicating (a) lower levels of brain 5-HTT binding in adults with ASD and correlation with social cognition deficits (Nakamura et al., 2010), (b) reduction in cortical serotonin 2A receptors in adults with Asperger syndrome and association with social communication deficits (Murphy et al., 2006), but (c) higher 5-HTT levels in non-ASD adults with the L A /L A genotype (Willeit and Praschak-Rieder, 2010) suggest possible disruption of neuronal homeostatic mechanisms (Ramocki and Zoghbi, 2008); nevertheless, divergent hypotheses based on results from neurodevelopmental, animal, and human cell line studies are also plausible (Azmitia et al., 2011). "
[Show abstract] [Hide abstract]
The aims of the present study were to examine the association between a common serotonin transporter gene (SLC6A4) polymorphism 5-HTTLPR/rs25531 with severity of attention-deficit hyperactivity disorder (ADHD) and autism spectrum disorder (ASD) symptoms.
Mothers and teachers completed a validated DSM-IV-referenced rating scale for ADHD and ASD symptoms in 118 children with ASD.
Analyses indicated that children with at least one copy of the S or L(G) allele obtained significantly more severe maternal ratings of hyperactivity (p=0.001; ηp(2)=0.097) and impulsivity (p=0.027; ηp(2)=0.044) but not inattention (p=0.061; ηp(2)=0.032), controlling for ASD severity, than children homozygous for the L(A) allele. Conversely, mothers' ratings indicated that children with L(A)/L(A) genotype had more severe ASD social deficits than S or L(G) allele carriers (p=0.003; ηp(2)=0.081), controlling for ADHD symptom severity. Teachers' ratings though consistent with mothers' ratings of hyperactivity and social deficits were marginally significant (p=0.07/p=0.09). There was some evidence that the magnitude of parent-teacher agreement regarding symptom severity varied as a function of the child's genotype.
The 5-HTTLPR/rs25531 polymorphism or its correlates may modulate severity of ADHD and ASD symptoms in children with ASD, but in different ways. These tentative, hypothesis-generating findings require replication with larger independent samples.
Progress in Neuro-Psychopharmacology and Biological Psychiatry 10/2012; 40(1). DOI:10.1016/j.pnpbp.2012.10.019 · 3.69 Impact Factor
Available from: kacst.edu.sa
- "Although the data suggest that reading disorders may be caused by high testosterone levels, the data on autism were not significant. Other investigators  studied whether births at certain months of the year were associated with autism. They reported peaks of autism in April, June, and October for single births and 1 month earlier in March, May, and September for multiple births in males. "
[Show abstract] [Hide abstract]
ABSTRACT: This publication, by reviewing 1300 studies published on autism in 2008, represents an update on this topic. Results include possible parental influences, maternal conditions, and studies on genes and chromosomes. Possible etiological factors involve the “extreme male brain,” defects in the mirror neuron system, vaccines, underconnectivity, disorders of central coherence, and many other more specific etiologies. Assessments or tests for autism are also reviewed. Characteristics of autistic individuals include repetitive behavior, language disorders, sleep disturbances, social problems, joint attention disorders, seizures, allergic reactions, and various behavioral changes. Cognitive changes involve IQ, reasoning, and verbal and language disorders. The savant syndrome is a fascinating phenomenon, at times seen in autistic individuals. Neurophysiological and neuroanatomical changes are also reviewed, as are comorbid conditions. Finally, treatment involves various medications including risperidone, ziprasidone, and antipsychotic drugs, as well as different procedures such as magnetic stimulation, acupuncture, and hyperbaric oxygen therapy. As mentioned in the 2007 survey, nearly every conceivable problem that a child can have may be found in these unfortunate children and nearly every conceivable etiology has been mentioned to account for this serious disorder.
Epilepsy & Behavior 12/2009; 16(4-16):569-589. DOI:10.1016/j.yebeh.2009.09.023 · 2.26 Impact Factor
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.