Tag Archives: Research

Extreme Male Theory of Autism #AtoZChallenge

Welcome to day 24 in the A to Z Challenge on autism. Today, I have cheated a little because my word for the X post doesn’t really start with an X. Then again, many bloggers participating in the challenge choose words for their X posts that start with “ex”. Today’s topic is the extreme male theory of autism. I might even try to find something on genetics so that the X and Y chromosomes, which determine a person’s sex, will be involved.

As I said yesterday, autism spectrum disorders are thought to be more common in boys and men than women and girls. Leo Kanner concluded this already in his initial study of autism in 1943, and Hans Asperger initially thought that the condition he described only affects males.

Not only is autism, and particularly Asperger’s Syndrome, still thought to occur more commonly in males than females, but researchers also believe that there is something “male ad then some” about autism. Asperger himself wrote that the boys he described might display something that is akin to a more extreme variant of male intelligence. Simon Baron-Cohen, an autism researcher in Cambridge, has therefore developed a theory by which autism is described as an “extreme male brain”.

Compared to females, even typically developing males have strengths in mathematical and spatial reasoning and weaknesses in social judgment, empaty and imaginiative play. They are also at a higher risk for delayed language development.

Baron-Cohen and his colleagues have developed a model to test their theory which divides the way the brain operates into two major areas: systemizing and empathizing. Systemizing refers to the drive to analyze or construct systems, whereas empathizing refers to the drive to understand other people’s emotions and thoughts.

The extreme male theory of autism views people with autism spectrum disorders ans hyper-systemizers. They are very much interested in non-human, rule-bound systems. This might seem like an idea that only applies to higher-functioning autistics, but it is thougth that in lower-functioning autisticcs, hypersystemizing might show itself in for example collecting and organizing buttons or suchlike.

On the other hand, autistic people would show weaknesses in social judgment, such as figuring out social cues, understanding what another person is feeling and grasping social hierarchies.

There is a theory that says that higher testosterone (male sex hormone) levels while in the womb lead to a more male-like profile on the systemizing-empathizing dichotomy, ie. higher systemizing scores and lower empathizing scores. Lower testosterone levels in the womb are thought to lead to a more empathizing-oriented brain style. This however has not been proven to explain autism. Further research in this area is needed.

Do you want to know whether you’re more of an empathizer or a systemizer? There is a test which gives you a score on both of these scales. My own empathizing score was 20 while my systemizing score was 30. Both are below-average.

Vaccines and Autism: Stop Beating a Dead Horse #AtoZChallenge

Welcome to day 22 in the A to Z Challenge on autism. Today, I focus on a very controversial subjects: do vaccines cause autism?

The answer to this question could be very short: no. The Autism Science Foundation has compiled an exhaustive list of studies on the subject, which investigate pretty much every aspect of vaccines that the anti-vaccine community has blamed for autism, including whether vaccinated children are generally more likely to be autistic than non-vaccinated children. The anti-vaccine crowd have consistently demanded such a population-based study, but several were published and they still believe vaccines cause autism.

The problem is a little more complicated in one tiny aspect, and this is the fact that the general autism community believes that autism is purely genetic. This has not been proven, and the anti-vaccine community has a point to suggest environmental factors in general could be risk factors for autism.

What if avoidable environmental factors, such as vaccines, did cause autism in genetically vulnerable children? After all, we know that vaccines and other environmental factors carry risks. It is easy to say that no more vaccinated children are autistic than non-vaccinated children, for example, but what if a multitude of environmental factors, including vaccines, could contribute to autism? As a parent, after all, you’re not dealing with a population of vaccinated and unvaccinated children; you are dealing with your own child.

You have to weigh risks. With vaccines, however, the problem is you run the risk of losing herd immunity if you and a lot of parents are not vaccinating. Herd immunity is the condition in which a disease has been extinguished due to a large part of the population being immunized to it. This is tough, because you are not dealing with the entire population as I said; you are dealing with your child. It is not like, if you don’t vaccinate, they are guaranteed to die of the disease the vaccine protects against, but another child just might. In this sense, while I advocate parents’ right to make decisions about their children’s health, I urge parents to be responsible.

Another problem is that the vaccine controversy hinders research into other environmental and genetic factors that might cause autism. For example, many people using biomedical interventions for autism find that their child has (or is thought to have) a lot of things wrong with them, including for example food intolerances. What if the key to finding the cause of autism lay in fact with such other, often trivialized, biological factors? It is understandable that parents who are part of the pro-biomed community are discredited, because they keep insisting vaccines cause autism in spite of overwheming evidence to the contrary.

Research is not advanced if people advocating for it keep asking the same questions that have been answered a million times. If you truly want to prevent autism (which I for one don’t, but many parents do), support research into a variety of enviornmental and genetic risk factors and stop beating a dead horse.

Quirkiness: The Broader Autism Phenotype #AtoZChallenge

Welcome to another week and another day in the A to Z Challenge on autism. Today’s post is called “Quirkiness” because I couldn’t think of any other relevant word starting with the letter Q. I bet other people have trouble with this letter too. I will focus on the broader autism phenotype, which basically describes people who are quirky. This post is quite involved, so I hope I have explained things properly.

The broader autism phenotype (BAP) describes people who have similar but milder traits than those found in autism spectrum disorder people, and who are not impaired in their functioning by these traits. The broader autism phenotype is particulalry useful for research into the heritability of autism. It is likely that autism is largely a genetic disorder, and this idea is supported by research into the BAP. Non-autistic parents of autistic children more often than parents of neurotypical children exhibit the broader autism phenotype.

So what is the broader autism phenotype? It describes traits that are related to autism and are more common among family members of autistic people. According to Losh et al. (2008), this includes characteristics such as a socially reticent or aloof personality, untactful behavior and fewer high-quality (ie. emotionally reciprocial) friendships. It also includes a rigid personality, little interest in novelty, difficulty adjusting to change and a perfectionistic or overly conscientious personality. Family members of autistic people also exhibit more fear or neuroticism and are at a higher risk of developing anxiety disorders.

Non-autistic parents’ autistic traits are, for research purposes, commonly measured by the broad autism phenotype questionnaire (BAPQ). The BAPQ focuses on the traits and behaviors I mentioned above.

Only 10% to 20% of cases of autism can be explained by a known biological cause, such as a genetic mutation (Sasson et al, 2013). These are often sporadic mutations, meaning they occur in the autistic person only and not their parents.

With the broad autism phenotype, autism symptoms do carry over from one generation onto the next. A large number of autistic children in a study by Sasson et al. (2013) had one parent who displayed the broad autism phenotype. If both parents displayed the BAP, a child was also more likely to be autistic than not. The presence of the broader autism phenotype was also associated with the severity of autistic symptoms. In other words, if one or both parents had autistic quirks, an autistic child was more likely to be more severely affected. Maxwell et al. (2013) found the same: a higher score on the BAPQ in parents was related to more severe autistic symptoms (as measured by the Social Responsiveness Scale) in their children. The parents’ BAPQ score was not related to the child’s IQ, which is a common measure of functioning level in autistics.


Losh M, Childress D, Lam KSL and Piven J (2008), Defining Key Features of the Broad Autism Phenotype: A Comparison Across Parents of Multiple- and Single-Incidence Autism Families. Am J Med Genet B Neuropsychiatr Genet, 147B(4):424-433. DOI: 10.1002/ajmg.b.30612.

Maxwell CR, Parish-Morris J, Hsin O, Bush JC, and Schultz RT, The Broad Autism Phenotype Predicts Child Functioning in Autism Spectrum Disorders. J Neurodev Disord. 2013; 5(1): 25. DOI: 10.1186/1866-1955-5-25.

Sasson NJ, Lam KS, Parlier M, Daniels JL, Piven J (2013), Autism and the Broad Autism Phenotype: Familial Patterns and Intergenerational Transmission. J Neurodev Disord, 5(1):11. doi: 10.1186/1866-1955-5-11.

Mass Murder and Autism: I’m Not Impressed

Today, I came across a post on why the new DSM-5 definition of autism may actually be good. In it, the author talked about an apparent mass murder and the associated speculation of the killer having Asperger’s Syndrome. I googled, hoping to find out which mass murder she was writing about, but instead came across a Washington Post article which claimed a “significant” link beteeen mass murder and autism. I read the original study (Allely et al., 2014) on which this article was based, and I’m not impressed.

First, the actual question the authors aim to answer, is inverted. They research whether a significant number of mass or serial killers have autism and/or head injury. They found that this is so: roughly ten percent of the mass or serial killers the researchers read about, had suspected or diagnosed ASD, and a similar percentage had a possible or definite head injury. This may be significantly more than the prevalence of autism or head injury in the general population, but so what? The really important question is whether autistics or those who sustained head trauma are more likely to become serial killers. One thing I learned from Ton Dekrsen, author of Lucia de B., a book on the Dutch nurse falsely accused of serial murder on her patients, is that a statistical link that runs in one direction, doesn’t necessarily run in the other as well. Since serial or mass murders are rare, this is especially important.

Also please note that Allely et al. state that, of none of the six murderers (out of 239 total!) with “definite” autism, diagnostic data was available. “Probable” ASD also included a psychiatrist or psychologist having said the murderer had ASD. This raises suspicion, as psychologists and psychiatrists are not immune to media hyping wanting to label every murderer with the mental illness du jour. Dutch readers might remember psychiatrist Menno Oosterhoff accusing Volkert van der Graaf, who murdered politician Pim Fortuyn, of having Asperger’s in 2003. With no diagnostic data on any of the murderers with suspected or “definite” ASD, it is really speculative to even say that there is a one-directional link between mass murder and ASD. And don’t get me talking on the “possible” ASD people, who were simply described as “odd” or “loners” by their family members.

Allely et al. do say in their discussion that speculation about a link between autism and mass murder may lead to negative steretoypes. This of course is not a reason not to document it. If autistics are in fact more likely to be serial or mass murderers, there’s no reason not to write that into a research paper. The thing is, due to the rarity of serial and mass murders, this is unlikely to ever become truly apparent. And even if a definite link could be found, so what? I recently read in another book that, while there is a link between schizophrenia and violence, locking away all schizophrenics in England and Wales for the rest of their lives would save the lives of four potential murder victims each year.


Allely CS, Minnis H, Thompson L, Wilson P, and Gillberg C (2014), Neurodevelopmental and Psychosocial Risk Factors in Serial Killers and Mass Murderers. Aggression and Violent Behavior, 19(3)288-301. DOI: 10.1016/j.avb.2014.04.004.

What’s in a Name: Dual Sensory Impairment, Deafblindness, or What?

It’s always interesting to see how the language surrounding disability evolves over time. In the DSM-IV, for example, “mental retardation” is the accepted term for what is now called intellectual developmental disorder in DSM-5 and intellectual disability by most professionals and the general public. I had to modify a blog post from 2007 when I republished it here, because it had “mental retardation” in it. This term is totally out of use now.

With regards to visual and hearing impairmetns, there are even more varied terms. “Blindness” and “deafness” are the most common, but “hard of hearing”, “hearing impairment”, “visual impairment”, “low vision”, “partially sighted”, etc. are also used. With regards to people who have both a vision and hearing impairment, the question is asked by Wittich et al. (2013) what term should be used for research purposes: deafblindess, dual sensory impairment, or somethign else entirely? The authors reviewed the literature and surveyed a number of professinals and reseachers in the area of deafblindness/dual sensory impairment/whatever. They found that “deafblindness” was more commonly used in journals speciifcally catering towards the vision or hearing field, whereas “dual sensory impairment” was used in more general journals and in journals with a higher impact factor. Similarly, those people surveyed who considered themselves primarily involved with research, preferred “dual sensory impairment”, whereas rehabilitation professionals preferred “deafblindness”. The study authros themselves propose “combined vision and hearing impairment”.

Wittich et al. do not discuss the cultural implications of each term, which were actually what motivated the DSM-5 committee to change the term for intellecutal disability more than did science. Wittich et al. also didn’t survey people with a combined vision and hearing impairment themselves.

Just my thought, but I find “dual sensory impairment” particularly confusing. I also find “combined vision and hearing impairment” really unnecessarily lengthy unless it serves a particular purpose, such as clarifying that hte individual has some vision and/or hearing. It also wouldn’t surprise me if people with acquired vision and hearing loss would prefer “dual sensory impairment” or “combined vision and hearing loss”. After all, people with an acquired disability, in my expeirnece, insist more on “person first” language, whereas those born with their disability prefer to see it as an inherent part of their identity and use language accordingly. I’ll be curious to know how the terminology in this area evolves over the next so many years.


Wittich W, Southall K, Sikora L, Watanabe DH & Gagné JP (2013), What’s in a Name: Dual Sensory Impairment or Deafblindness? British Journal of Visual Impairment, 31(3):198-207. DOI: 10.1177/0264619613490519.

Research Recommendations for Improving Treatment for People with Personality Disorders

Two studies in nursing journals that I read recently examine good practice for personality disorder treatment. Bowen (2013) specifically studied ideas for intervention with borderline personality disorder patients, whereas Fanaian, Lewis & Grenyer (2013) studied more general ideas for implementing personality disorder services. Bowen also emphasized direct intervention strategies, whereas Fanaian et al.’s study more focused on organizational structure. Bowen (2013) interviewed nine mental health professionals, four of whom were nurses, working at a specialist unit for patients with BPD. Key apsects of good practice mentioned by interviewees were:

  • Shared decison making: for example, service users and staff should meet in community meetings to discuss and think through decisions that a service user might otherwise make impulsively. This thinking thorugh also counters black-and-white thinking.
  • Rules should be actively recreated, rather than being strictly enforced or being abandoned. This is an offshoot from the shared decision making in the above bullet.
  • Patients should have social roles, such as jobs on the unit nd group therapy with a pratical focus. This is a way of bringing into the open and then challenging interpersonal difficulties that are so typical of BPD.
  • Social disturubances must not just be prevented, but also be used as an opportunity for learning.
  • Peer support, including feedback on behaviors, but also including compassion. One interviewee also commented that peer support can enhance the patients’ looking inward for the resources to help themselves, rather than viewing the staff as sole bearers of wisdom.
  • Open communication. For example, this unit had a structure whereby three service users were elected to discuss issues happening on the unit with the staff as a means of liaison.
  • Involvement with the person as a whole, seeing them as more than their BPD symptoms.
Bowen (2013) does highlight that not all of these aspects of good practice can be generalized. After all, this unit was a specialist unit for treating BPD and had its structure built so that these aspects of good practice could be met. For example, there were daily meetings, group therapy, and patients had jobs on the ward.

It was found that mental health workers on this unit had a pretty optimistic outlook on recovery from BPD. This is in contrast to research which shows that mental nurses have negative attitudes about BPD patients. Fanaian et al. (2013) emphasize this negative attitude towards people with personaltiy disorders as a major barrier to appropriate care.

Fanaian et al. (2013) had about 60 experienced clinicians in personality disorder treatment, including psychiatrists, psychologists, social workers, a nurse and a counselor sit in groups of four and brainstorm on topics relevant to personality disorder treamment. They overwhelmingly found that current practice in mainstream mental health settings is both poor and inaccurate. Ways to improve practice included:

  • More education and training on the subject. Some groups also recommended that workers in non-psychiatric settings who have frequent contact with personality disorered people, such as social services staff, be trained in personality disorders. Carers, such as family and friends, also were said to need education and training.
  • More support through supervision and leadership. For example, there should be more supportive and regular treatment team meetings. Clinicians also mentioned better access to Internet resources on treatmetn and assessment for mainstream mental health staff. There also should be greater support for staff approaching burn-out, as it was felt that staff working with personality disordered people have a high risk of burn-out and work-related stress.
  • A shift from risk management to recovery-focused treatment and case management. Acute hospitalization should be avoided when possible. Rather, patients with personality disordeers need intensive, multidiscipinary case management.
  • Clearer guidelines and protocols. Many groups of clinicians emphasized a consistent approach across teams, particularly when managing crises.
  • An attitude shift to decrease stigma. Some groups emphasized the fact that many health professionals have a negative attitude about personalityy disorder patietns, and this is a barrier to effective treatment.
Fanaian et al.’s (2013) study, like all studies, has its limitations. The clinicians participating in the study were invited to a personality disorders meeting based on expertise and experience. Therefore, it is not known whether these findings generalize well into mainstream mental health provision.


Bowen M (2013), Borderline Personality Disorder: Clinicians’ Accounts of Good Practice. Journal of Psychiatric and Mental Health nursing, 20(6):491-498. DOI: 10.1111/j.1365-2850.2012.01943.x

Fanaian M, Lewis KL, & Grenyer BFS (2013), Improving Services for People with Personality Disorders: Views of Experienced Clinicians. International Journal of Mental Health Nursing, 22(5):465-471. DOI: 10.1111/inm.12009.

Medication Treatment of ADHD Symptoms in Autistic Children

Autistics often have symptoms of ADHD. These symptoms are often treated with medication. About 15% of autistic children take psychostimulants or atomoxetine (Rosenberg et al, 2010). Stimulants are proven to be effective for ADHD in non-autistic children. Whether the same holds true for autistics, however, had not been systematically researched until now. Reichow, Volkmar & Bloch (2013) examined seven randomized, double=blind, placebo-controlled studies comparing methylphenidate, clonidine or atomoxetine to placebo in children with autism spectrum disorders and ADHD symptoms. Four trials were found for methylphenidate, two for atomoxetine and one for clonidine.

According to Reichow et al. (2013), methylphenidate was found to be effective for ADHD symptoms in autistic children. The effectiveness was slightly lower than it is for typically developing children with ADHD but still statistically significant. There was a greater risk of side effects in autistics, particularly for irritability, depression and withdrawal. The risk for common side effects such as insomnia and decreased appetite was similar to that found in typically developing children. One of the studies involved preschool children, and it was recommended by Reichow et al. after reviewing this study that methylphenidate-taking preschoolers with autis be closely monitored due to increased adverse events.

Clonidine and atomoxetine both showed moderate but not statistically significant effectiveness in autistic children (Reichow et al., 2013). These medications warrant further study, also given the fact that only one or two studies were found that met the inclusion criteria for a systematic review.


Reichow B, Volkmar FR, & Bloch MH (2013), Systematic Review and Meta-analysis of Pharmacological Treatment of the Symptoms of Attention-Deficit/Hyperactivity Disorder in Children with Pervasive Developmenetal Disorders. Journal of Autism and Developmental Disorders, 43(10):2435-2441. DOI: 10.1007/s10803-013-1793-z.

Rosenberg R, Mandell BS, Farmer JE, Law JK, Marvin AR, & Law PA (2010). Psychotropic Medication Use among Children with Autism Spectrum Disorders Enrolled in a National Registry, 2007-2008. Journal of Autism and Developmental Disorders, 40(3):342-351. DOI: 10.1007/s10803-009-0878-1.

The Childhood Bipolar Controversy Reviewed

Bipolar disorder in children is controversial. It didn’t use to be diagnosed as often as it is now, especially in the U.S., and more atypical symptosm are suggested to be bipolar. In the journal Child and Adolescent Mental Health, Boris Birmaher reviewed the literature surrounding this controversy. It’s an interesting article, viewing the controversy from all sides.

Birmaher starts by describing the diffiuclties diagnosing manic, hypomanic and depressive episodes in children and adolescents. Particularly, it is hard to distinguish symptoms of (hypo)mania from normal episodes of increased activity or from ADHD. Depressed symptoms are also hard to diagnose because children do not always feel or look depressed all the time. Adolescents experiece more atypical symptoms (increased sleep and appetite and weight gain) than adults do. Birmaher discusses whether onepisodic mania can be seen as bipolar.

He fortunately also shreds the idea that irritability only is bipolar. It isn’t. In fact, it is not severe mood dysregulation (also known as disruptive mood dysregulation disorder) eitehr, which surprised me. Irritability only is more indicative of ADHD or disruptive behavior disorders than of bipolar or SMD. Elation only, also, is not common in childhood or adolescent bipolar. More likely, patients experience both irritability and mood elation.

Birmaher is quite clear that pediatric bipolar disorder exists. The prevalence is around 2%, with just over 1% of children and adolescents presenting with bipolar I. For some perspective, Levorich et al. (2007) show that as many as half of adult bipolar patients in their study reported onset in childhood (14%) or adolescence (36%).

Birmaher is not a bipolar proponent, in the sense that he thinks atypical symptoms warrant a diagnosis of BP. He makes it quite clear that more research is needed into the risk factors for converting from atypical or subsyndromal bipolar-like symptoms into full-blown bipolar in children and adolescents. It looks like family history of bipolar is one such factor. Levorich et al (2007) found that, the earlier the onset of bipolar disorder, the more likely the patients were to have a parental history of bipolar or depressive disorders.

Levorich et al. (2007) particularly studied prognosis in adults with bipolar disorder, comparing those with (retrospectively reported) childhood or adolescent onset bipolar to those with onset in adulthood. They found that, the earlier the onset of the disorder, the more likely patients were to suffer from dysphoric (irritable) rather than euphoric mania and the more likely they were to have comorbid anxiety and drug abuse. In addition, the researchers tracked all participants’ mood over a year’s period. This showed that those with early onset bipolar had more depressed episodes, more severe manic and depressive symptoms and fewer good days in a year than those whose bipolar started in adulthood. For these and other reasons, Levorich et al. advocate an active ruling in or outo f bipolar d isorder in children and adolescents, rather than it being considered a last resort diagnosis.


Birmaher B (2013), Bipolar Disorder in Children and Adolescents. Child and Adolescent Mental Health, 18: 140-148. DOI: 10.1111/camh.12021.

Levorich GS, Post RM, Keck PE, Altshuler LL, Frye MA, Kupka RW, Nolen WA, Suppes T, McElroy SL, Grunze H, Denicoff K, Moravec MKM, & Luckenbaugh D (2007), The Poor Prognosis of Childhood-Onset Bipolar Disorder. Journal of Pediatrics, the, 150(5):485-490. DOI: 10.1016/j.jpeds.2006.10.070.