A few months ago, I was visiting an autism clinic in Albania, one of the underserved countries where Autism Speaks is making a difference through our Global Autism Public Health Initiative. There I met a three-year-old girl receiving a diagnostic assessment for autism. Clearly, she wanted her parents to stop talking to us and take her outside. She kicked her father and bit his hand and then began slapping her own head. This young girl was trying to make her preferences known but lacked speech. Aggression was her way of communicating her needs.
Whatever their age, some individuals on the autism spectrum act out aggressively, and clearly, this can be distressing for everyone involved. In fact, aggression is among the most common challenges reported by parents of children and adolescents with autism.
What can help? I suggest working with your child’s physician and therapists on a four-stage approach to tackling this and other problem behaviors. The four steps are identification, understanding, management, and prevention.
By identification, we mean characterizing the problem behavior. As parents, you can write down the type of aggression your child demonstrates along with the time and setting of when the behavior occurs.
Next comes understanding. Specialists often use tools such as the Functional Behavioral Assessment decipher why a person with autism is behaving a certain way. In other words, what is the function of a given behavior for the person with autism? Is she telling you she doesn’t like what you’re doing? Is he telling his teacher that the school work is too complex? Does she want something she cannot have? Identifying the “communication” behind the behavior is the first step to teaching appropriate behaviors that can convey the person’s needs and desires.
In addition, underlying problems can trigger aggression. Among those with autism, common triggers include disturbing breaks in routine, lack of sleep, jarring “sensory stimuli” (noises, lights, or smells) or even undiagnosed mental health problems. Clearly, it’s important to look beyond the behavior itself to identify the underlying cause.
When it comes to managing aggression, there are many options. The information you gathered in identifying and understanding your child’s behavior may guide you and your child’s healthcare providers in developing a plan.
An abundance of research supports the effectiveness of Applied Behavior Analysis (ABA) in helping children with autism learn new and effective behaviors—so that aggression is no longer needed to communicate wants and needs. Research as shown that, in many cases, ABA alone is effective in reducing aggressive behaviors.
When ABA is not effective, it is important to consider the possibility of an underlying medical condition. For example, we know that autism is frequently associated with sleep disturbances and gastrointestinal distress. Disrupted sleep is likewise associated with uncontrolled seizures. Addressing these medical conditions can make a difference in reducing aggressive outbursts. Also remember that the sudden onset of aggression may signal that your child is in pain, ill, or simply exhausted.
Medication has been used successfully to reduce aggression and self-injury in both children and adults with autism. Risperidone, in particular, has gone through extensive testing in this regard. Both risperidone (Risperdal) and aripiprazole (Abilify) are approved by the U.S. Food and Drug Administration (FDA) for treating autism-related irritability, which includes aggression, tantrums, and self-injury. A recent study demonstrated that a combination of parent training (in behavior intervention) and risperidone reduced tantrums and other problematic behaviors in children with autism to a greater degree than did medication alone.
However, the decision whether or not to use behavior modifying medication is can be difficult. Autism Speaks has developed a medication decision aid to help you work with your child’s physician to determine whether this option fits your family’s goals and values. (Available for free download on our Tools You can Use Page.)
Finally we have prevention. Strategies to prevent aggression include working with your child’s therapists and teachers to create calming, predictable, and rewarding environments. Other helpful approaches include visual timetables and structured schedules—both of which can help smooth transitions between activities. Rewarding positive behavior and providing communication tools are additional strategies that many families find helpful.
I hope some of these suggestions help your child and family. And readers, I’d love you to use the comment section to share resources and ideas you’ve found useful.
Environmental Epigenomics and Susceptibility for Developmental Disorders: Findings from the Keystone Symposium
By Guest Blogger, Jennifer T. Wolstenholme, PhD, Postdoctoral Fellow at the University of Virginia, Charlottesville, VA, working with two Autism Speaks-funded researchers, Emile Rissman, Ph.D. and Jennifer Connelly, Ph.D.
In recent work in our lab, we have established a mouse model for gestational exposure to an endocrine disrupting compound, bisphenol A (BPA), at human physiological levels. We asked if a low BPA dose ingested during pregnancy (20 ug BPA/kg body weight/day) would affect the social behaviors of the juvenile offspring mice. In addition, we continued to breed the mice from these litters to ask if these effects could be transmitted to future generations that were not directly exposed to dietary BPA. We also examined a handful of genes known to be affected by BPA or involved in social behaviors to determine if BPA also changed the expression of these genes in the brain during embryogenesis. The take home message is this: we do not know if exposure to endocrine disrupting chemicals causes any neurobiological disorders, including autism spectrum disorders (ASD). However, the data are interesting enough to cause us and others to continue to test the hypothesis that exposure to BPA during gestation may result in modified social behaviors in juvenile mice.
Bisphenol A (BPA) is a man-made compound used to make polycarbonate plastics (i.e. food and water containers), epoxy resins (i.e. canned food linings) and thermal register receipts. Human exposure to this chemical is wide spread and nearly unavoidable as it has been detected in urine in 90% of all humans sampled [1, 2]. Public health concerns have been fueled by findings that BPA exposure can reduce sex differences both behaviorally and in the brain. In rats and mice, perinatal exposure to BPA is associated with aggressive behavior, cognitive impairments, increased novelty seeking and impulsivity [3-5]. BPA can also influence social interactions and anxiety in rodents [6-10]. This list of associations have suggested to some that BPA may be somehow related to human neurological disorders, such as ASD. However, such a conclusion at this time is premature.
Many laboratories have suggested that BPA exposure disrupts normal brain development and behaviors through its actions on the steroid receptors [18, 19]. BPA acts as an analog of steroid hormones. Steroid hormones organize the brain during neonatal development [11-13]. BPA has steroid-like properties and binds estrogen receptors, (ERa, ERb ), as well as androgen and thyroid receptors [15-17].
In addition to steroid-related effects, BPA may have even more global actions as it can alter DNA methylation . Dysregulation of DNA methylation during critical developmental windows could disrupt the normal progression of brain and endocrine system development causing robust changes in the developing embryo that can persist into adulthood or even beyond if effects extend to germ cells that later serve reproduction as sperm or egg cells. Embryonic development is a particularly sensitive period, specifically when the body’s germ line cells undergo epigenetic programming and experience a wave of DNA de-methylation and re-methylation.
Skinner et al. have shown trans-generational effects for several endocrine disrupting compounds, but at much higher doses than humans are typically exposed [21, 22]. Specifically, endocrine disruptors found in plastics, pesticides, hydrocarbons and herbicides can affect embryonic testes development and lead to deficits in sperm production in adulthood. These effects are trans-generational in rodents directly exposed to these chemicals during gestation (F1 generation) and through to the great, great grandchildren (F2, F3 and F4 generations).
We use a paradigm in which inbred female mice are placed on control diet free of any phytoestrogens, or control diet with BPA (5mg BPA per kg diet). This diet produced BPA blood levels equivalent to those reported in humans. A week after the start of the diet females were mated. At birth, pups were fostered to control dams to limit BPA’s effect only to gestation. Three generations of offspring were tested for social behaviors at 21 days after birth.
BPA exposure had effects on several social and non-social behaviors and some of these differences between mice on control and BPA-containing diets persisted over generations. The great, great grandchildren of the BPA lineage (the F4 generation) were never directly exposed to dietary sources of BPA, yet social interactions resembled those of mice exposed during gestation. Some of these behavioral effects are correlated with different levels of gene expression in the brains of mice directly exposed to BPA compared to mice that were never exposed to dietary BPA. More work needs to be done to discover if the relationships between the affected genes and the behavioral changes are causal. Since exposure to BPA appears to alter social interactions in young mice, this compound may contribute to the risk of developing neurological disorders such as autism spectrum disorders, but further studies, especially in humans are needed to show a causal relationship.
1. Fujimaki, K., et al., [Estimation of intake level of bisphenol A in Japanese pregnant women based on measurement of urinary excretion level of the metabolite]. Nippon Eiseigaku Zasshi, 2004. 59(4): p. 403-8.
2. vom Saal, F.S., et al., Chapel Hill bisphenol A expert panel consensus statement: integration of mechanisms, effects in animals and potential to impact human health at current levels of exposure. Reprod Toxicol, 2007. 24(2): p. 131-8.
3. Kawai, K., et al., Aggressive behavior and serum testosterone concentration during the maturation process of male mice: the effects of fetal exposure to bisphenol A. Environ Health Perspect, 2003. 111(2): p. 175-8.
4. Miyagawa, K., et al., Memory impairment associated with a dysfunction of the hippocampal cholinergic system induced by prenatal and neonatal exposures to bisphenol-A. Neurosci Lett, 2007. 418(3): p. 236-41.
5. Tian, Y.H., et al., Prenatal and postnatal exposure to bisphenol a induces anxiolytic behaviors and cognitive deficits in mice. Synapse, 2010. 64(6): p. 432-9.
6. Dessi-Fulgheri, F., S. Porrini, and F. Farabollini, Effects of perinatal exposure to bisphenol A on play behavior of female and male juvenile rats. Environ Health Perspect, 2002. 110 Suppl 3: p. 403-7.
7. Negishi, T., et al., Behavioral alterations in response to fear-provoking stimuli and tranylcypromine induced by perinatal exposure to bisphenol A and nonylphenol in male rats. Environ Health Perspect, 2004. 112(11): p. 1159-64.
8. Ryan, B.C. and J.G. Vandenbergh, Developmental exposure to environmental estrogens alters anxiety and spatial memory in female mice. Horm Behav, 2006. 50(1): p. 85-93.
9. Cox, K., et al., Gestational exposure to bisphenol A and cross-fostering affect behaviors in juvenile mice. Horm Behav, 2010. 58(5): p. 754-61.
10. Porrini, S., et al., Early exposure to a low dose of bisphenol A affects socio-sexual behavior of juvenile female rats. Brain Res Bull, 2005. 65(3): p. 261-6.
11. McEwen, B.S. and S.E. Alves, Estrogen actions in the central nervous system. Endocr Rev, 1999. 20(3): p. 279-307.
12. Phoenix, C.H., et al., Organizing action of prenatally administered testosterone propionate on the tissues mediating mating behavior in the female guinea pig. Endocrinology, 1959. 65: p. 369-82.
13. Negri-Cesi, P., et al., Sexual differentiation of the brain: role of testosterone and its active metabolites. J Endocrinol Invest, 2004. 27(6 Suppl): p. 120-7.
14. Kuiper, G.G., et al., Interaction of estrogenic chemicals and phytoestrogens with estrogen receptor beta. Endocrinology, 1998. 139(10): p. 4252-63.
15. Sohoni, P. and J.P. Sumpter, Several environmental oestrogens are also anti-androgens. J Endocrinol, 1998. 158(3): p. 327-39.
16. Xu, L.C., et al., Evaluation of androgen receptor transcriptional activities of bisphenol A, octylphenol and nonylphenol in vitro. Toxicology, 2005. 216(2-3): p. 197-203.
17. Bonefeld-Jorgensen, E.C., et al., Endocrine-disrupting potential of bisphenol A, bisphenol A dimethacrylate, 4-n-nonylphenol, and 4-n-octylphenol in vitro: new data and a brief review. Environ Health Perspect, 2007. 115 Suppl 1: p. 69-76.
18. Fujimoto, T., K. Kubo, and S. Aou, Prenatal exposure to bisphenol A impairs sexual differentiation of exploratory behavior and increases depression-like behavior in rats. Brain Res, 2006. 1068(1): p. 49-55.
19. Rubin, B.S., et al., Evidence of altered brain sexual differentiation in mice exposed perinatally to low, environmentally relevant levels of bisphenol A. Endocrinology, 2006. 147(8): p. 3681-91.
20. Dolinoy, D.C., D. Huang, and R.L. Jirtle, Maternal nutrient supplementation counteracts bisphenol A-induced DNA hypomethylation in early development. Proc Natl Acad Sci U S A, 2007. 104(32): p. 13056-61.
21. Anway, M.D., et al., Epigenetic transgenerational actions of endocrine disruptors and male fertility. Science, 2005. 308(5727): p. 1466-9.
22. Chang, H.S., et al., Transgenerational epigenetic imprinting of the male germline by endocrine disruptor exposure during gonadal sex determination. Endocrinology, 2006. 147(12): p. 5524-41.
23. Patisaul, H.B. and H.L. Bateman, Neonatal exposure to endocrine active compounds or an ERbeta agonist increases adult anxiety and aggression in gonadally intact male rats. Horm Behav, 2008. 53(4): p. 580-8.
24. Farabollini, F., et al., Effects of perinatal exposure to bisphenol A on sociosexual behavior of female and male rats. Environ Health Perspect, 2002. 110 Suppl 3: p. 409-14.
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