The origins of autism have been hypothesized to be genetic in nature, environmental or a combination of the two. This website proposes and discusses a specific theory of the origins of autism that stems from an expanded theory of human evolution that places a heavy emphasis on sexual selection, social structure, neoteny, and uterine testosterone and estrogen levels in human development. By understanding how humans evolved, we can gain insight into autism as a condition with roots in our evolutionary past. To understand the cause of autism we have to explore the origin of our species.

This blog also discusses other theories on the cause of autism addressing current developments in a casual format. See neoteny.org for several dozen short essays on autism and related subjects. Visit sexualselection.org for a more extended treatment of how autism and evolution interact.

The paper, Independent and dependent contributions of advanced maternal and paternal ages to autism risk by Shelton, Tancredi and Hertz-Picciotto released two weeks ago. It describes how older mothers are far more likely to have an autistic child.

Based on the first examination of heterogeneity in parental age effects, it appears that women’s risk for delivering a child who develops autism increases throughout their reproductive years whereas father’s age confers increased risk for autism when mothers are <30, but has little effect when mothers are past age 30. We also calculated that the recent trend towards delayed childbearing contributed approximately a 4.6% increase in autism diagnoses in California over the decade.

In 1998 I posted at sexualselection.org the hypothesis that older mothers will be discovered to be more likely to have autistic children because their testosterone levels are significantly higher. Simon Baron-Cohen conducted a number of studies that concluded that testosterone level in the mothers are directly connected to autistic tendencies. This study by Shelton, Tancredi and Hertz-Picciotto makes perfect sense in the context of mother’s testosterone levels impacting maturation rates, causing autism.

OBJECTIVE: Autism is referred to as cerebral lateralization abnormality. In this study, the possible relationships among handedness, eyedness and nasal cycle in autism have been investigated. MATERIALS AND METHODS: Thirty-seven children with autism and 20 controls were included in the study. The patient group included 27 boys and 10 girls who ranged in age from 5 to 20 years. For hand preference, hand used to write and throw a ball was accepted as dominant hand. For eye preference or dominance, eye used to look through keyhole of a door was accepted as dominant eye. Nasal dominance was assessed by a method of measuring the nasal airflow. RESULTS: The rates of left-handedness and left-eyedness were higher in children with autism compared to normal populations. A majority of children with autism had left nasal dominance. CONCLUSION: Autism and early language impairment may be associated with left handedness, eyedness and nasal dominance. (Dane, S. & Balci, N.(2007). Handedness, eyedness and nasal cycle in children with autism. International Journal of Developmental Neuroscience, 25(4), 223-6.)

Central to my understanding of handedness is Marion Annett’s theory that the left handed are really random handed, along with almost 10% of the right handers in society. What keeps coming to my mind is, if autism is increasing, and those increases are accompanied by estimations that it is just diagnosis that is more universal, then tell me if there are increases in left handedness. If there are increases in the left handed in this society, that suggests that there are increases in random handedness with is very likely the same as saying there are increases in male maturational delay.

If there are increases in both left handedness and autism, perhaps theorists can start offering attention to theories of autism that have to do with our evolutionary origins.

The present study reports preliminary data from two unselected samples of carefully diagnosed autistic subjects (children and adults) and an assessment procedure that includes a large sample of items, appropriate for lower-functioning autistic subjects, with multiple presentations within and between sessions 1 week apart. The study seeks to determine (1) whether a raised incidence of non-right-handedness exists in these samples (2) if so, what constructs best represent this shift in the handedness distribution (i.e., phenotype and CNS substrate) and (3) whether these handedness phenotypes are associated with different levels of cognitive functioning. The results reveal a dramatic shift away from right-handedness in both autistic samples, due to a raised incidence of two phenotypes, manifest left-handedness and ambiguous handedness. The ambiguously handed, who were postulated to represent substantial bilateral CNS pathology due to early brain injury, were found to have much lower intellectual scores in one of the study samples. (Soper, H., Satz, P., Orsini, D. Henry, R. Zvi, J. & Schulman, M. (1986). Handedness patterns in autism suggest subtypes. Journal of Autism and Developmental Disorders, 16, 155-67.)

Uncovering the differences between brain injury autistics and those that are autistic because of combinations of genetic inclinations (random handed with little cerebral lateralization), environmental effects impacting testosterone and estrogen levels of mother and self, and conventional child rearing practices seem vital to coming to understandings. In other words, how does autism created by brain injury differ from autism created by genetics/environment? Are there studies out there experimenting with potential differences? How would you conclude a child is one but not the other? It’s near impossible until we prove how one of the two causes (brain injury vs genetics/environment can be proved.

Developmental coordination disorder affects 5% to 8% of the general population, and about 50% to 60% of these children have a comorbid attention-deficit disorder with hyperactivity and learning disorders. Left-handedness is relatively common among children with dyslexia, learning disabilities, and autism; however, its frequency in children with developmental coordination disorder is less clear. The present study investigated the distribution of hand dominance in 98 children (age range, 5.5-17 years) with developmental coordination disorder compared with their parents or siblings. Thirty children (30.6%) were left-handed and 13 (13.3%) were ambidextrous. The prevalence of left-handedness among their parents and siblings was similar to that of the general population. The results suggest that children with developmental coordination disorder, like children with learning disorders and deficit disorder with hyperactivity, present with higher frequency of left-hand dominance compared with the general population. (Goez, H. & Zelnik, N. (2008). Handedness in patients with developmental coordination disorder. Journal of Child Neurology, 23(2), 151-4.)

Until recently I hypothesized that the relatively common appearance of autism in first born children was that perhaps first borns had more stressful births than later borns, and that this might be a different kind of autism than that which features maturational delay. I estimated one way to tell the difference was if digital abilities in autistic newborns was inhibited suggesting a cerebral palsy like infirmity. This would be different than the kind of autism that comes to women giving birth to children at the end of the ability to get pregnant.

There might be some truth in this, but recent work by Sarah Blaffer Hrdy suggests that new borns, with no older siblings, raised in Western households with often only mothers as an integral other, don’t as easily develop theory of mind.

As regards the theory above, perhaps autism that emerges from different causes could be parsed out by differences in digital facility. Perhaps those traumatized exhibit a different effortless use of fingers and limbs than those without an environment that encourages theory of mind.

Hand preference and hand skill were assessed in 20 children with autism, 20 normal controls and 12 children with mental retardation. 90% of the normal controls and 92% of the children with mental retardation showed concordance for hand preference and hand skill (i.e. the preferred hand was also the more skillful), whereas only 50% of the children with autism showed concordance of preference and skill, the remaining 50% preferring to use the hand which was less skillful. Children with autism also showed a lesser degree of handedness and a lesser degree of consistency than the other groups, although this was unrelated to the discordance of skill and asymmetry. A developmental model of handedness is proposed in which the development of handedness as preference is ontogenetically prior to the development of handedness as skill asymmetry, such that in normal children the development of skill asymmetry occurs as a secondary consequence of the establishment of preference. The causal sequence is disrupted in autism, so that although preference is established, it does not subsequently result in concordant skill asymmetry. (McManus, I. C., Murray, B., Doyle, K. & Baron-Cohen, S. (1992). Handedness in childhood autism shows a dissociation of skill and preference. Cortex, 28(3), 373-81.)

There are differences in handedness amoung varying cultures around the world. Asian societies display around 2%. It is not clear how much of this is due to its being discouraged. Some American Aboriginal populations show 12% left handedness (Canadian Northwest populations).

What’s at issue here is the relationship between handedness, maturational delay, and autism. If there are variations among the autistic between those that use a hand that is more adept and those that do not, with more autistics using the left hand than the general population, then perhaps the autistic are more guided by Annett’s right shift theory with their being random handed to such a degree that choosing a less adept hand is not inhibited.

A question would be, among those NW Indian tribes, do they also often choose to emphasize a hand that is less adept?

If the results from these three studies are combined, the overall proportion of left-handers is 13.3 per cent for autistic children and 8.3 per cent for matched controls, not a significant difference.  However, if left- and mixed-handers are summed, then the frequency of non-right-handedness among autistic children is considerably higher than that found in age-matched normally developing children, although it is similar to that found in other children of the same intellectual ability  (Bishop, D. V. M. (1990). Handedness and developmental disorder. London: Mac Keith Press.  p. 111)

There is a close associated between handedness and maturational delay. There is a close association between autism and handedness. There is a close association between maturational delay and autism. There is a close association between a mother’s testosteone levels and her children’s handedness and autism.

Seems pretty clear that a mother’s testosterone levels are closely associated with maturation rate.  There is a whole science devoted to maturation rates as those rates relate to evolution. That science is called heterochrony. Consider that autism is an evolutionary condition.

This paper is concerned with what abnormal handedness in Pervasive Developmental Disorders (PDD) reveals about the presence, lateralization, and severity of cerebral dysfunction in this population. From previous work, it was predicted that left-handedness would be elevated in the sample and that mixed-handedness subjects should be more impaired than those with established hand dominance. A battery of cognitive and motor tests were administered to a group of PDD children with autistic symptoms, and performance was compared for the left-handed, right-handed, and mixed-preference children. It was found that left-handers tended to do better than right-handers on all cognitive measures, while the mixed-preference children tended to be the lowest on all cognitive measures. No differences were found on motor measures. An extension of the Satz (1972) model, assuming early brain damage, was developed to explain the superiority of the left-handed children; an alternative explanation assuming anomalous lateralization patterns in the natural left-handers was also suggested. (Fein, D., Waterhouse, L. Lucci, D., Pennington, B. & Humes, M. (1985). Handedness and cognitive functions in pervasive developmental disorders. Journal of Autism and Developmental Disorders, 15, 323-33.)

Interesting that mixed handedness performs lower than the left or right handedness. Other studies have concluded that many mixed handers excel in sports such as tennis. Perhaps mixed handedness mixes extremely adept with extremely impaired. Of course, it is also interesting that left handers exceed right handers in dexterity.

Exploring this evolutionarily in the context of cerebral laterailization and Annett’s right shift theory that left handers are random handed, the study above might suggest that lefties are our evolutionary forebears (less cerebral lateralization) and mixed handers are those having trouble making the transition to current right handed neurologies. A problem with this is that Annett suggests both left handers and right handers are random handed, trending toward having no gene for handedness. Why would only mixed handers reveal problems?

BACKGROUND: Sex-differences exist in some areas of human social behaviour. In animals, foetal testosterone (fT) plays a central role in organising the brain and in later social behaviour. fT has also been implicated in language development, eye-contact, and spatial ability in humans. METHODS: Fifty-eight children (35 male and 23 female), whose fT was analysed in amniotic fluid, were followed up at age 4. Their mothers completed the Children’s Communication Checklist, a questionnaire assessing language, quality of social relationships and restricted interests. RESULTS: fT was negatively correlated to quality of social relationships, taking sex-differences into account. fT was also positively correlated with restricted interests in boys. CONCLUSIONS: These findings implicate fT in both social development and attentional focus. They may also have implications for understanding the sex ratio in autism. (Knickmeyer, R., Baron-Cohen, S., Raggatt, P. & Taylor K. (2005). Journal of Child Psychology and Psychiatry, and Allied Disciplines, 46(2), 198-210.)

I keep thinking that estrogen may be integral to understanding the timing of maturation in addition to testosterone influencing the rate of maturation. The rate of maturation seems central to the kinds of discoveries above. Click here for an exploration of the possible effects of estrogen.

Empathy involves an understanding of what others are thinking and feeling, and enables us to interact in the social world. According to the Empathizing-Systemizing (E-S) theory, females on average have a stronger drive to empathize than males. This sex difference may in part reflect developmental differences in brain structure and function, which are themselves under the influence of fetal testosterone (fT). Previous studies have found that fT is inversely correlated with social behaviors such as eye contact in infancy, peer relationships in preschoolers, and mentalistic interpretation of animate motion. Male fetuses are exposed to higher levels of testosterone than are female fetuses. The present study investigates empathizing in children, as a function of amniotic measures of fT. One hundred ninety-three mothers of children (100 males, 93 females) aged 6-8 years of age completed children’s versions of the Empathy Quotient (EQ-C), and the children themselves were tested on “Reading the Mind in the Eyes” Task (Eyes-C). All mothers had had amniocentesis during the 2nd trimester of pregnancy. There was a significant negative correlation between fT and scores on both measures. While empathy may be influenced by post-natal experience, these results suggest that pre-natal biology also plays an important role, mediated by androgen effects in the brain. These results also have implications for the causes of disabilities involving empathy, such as autism spectrum conditions, and may explain the increased rate of such conditions among males. (Chapman, E., Baron-Cohen, S., Auyeung, B., Knickmeyer, R., Taylor, K. & Hackett, G. (2006). Fetal testosterone and empathy: Evidence from the empathy quotient (EQ) and the “reading the mind in the eyes” test. Social Neuroscience, 1(2), 135-48.)

Sarah Blaffer Hrdy’s Mothers and Others describes the intensity with which aboriginal hunter gatherer societies teach egalitarian principles that include sharing and thinking of others. Many of these societies are matrilocal with males compelled to travel to find a wife. I’ve hypothesized that our matrifocal hunter gatherer forebears feature high testosterone females and low testosterone males. What if it is necessary the compassion or empathy be a taught experience in societies where women have high testosterone? High testosterone wombs are associated with children exhibiting autism.

What I’m getting at here is perhaps we evolved with societal structures that prevented autism or difficulties developing theory of mind by intensely teaching to think of others. High testosterone women may less reflexively exhibit compassion requiring a social intervention to make it intuitive.

Empathy involves an understanding of what others are thinking and feeling, and enables us to interact in the social world. According to the Empathizing-Systemizing (E-S) theory, females on average have a stronger drive to empathize than males. This sex difference may in part reflect developmental differences in brain structure and function, which are themselves under the influence of fetal testosterone (fT). Previous studies have found that fT is inversely correlated with social behaviors such as eye contact in infancy, peer relationships in preschoolers, and mentalistic interpretation of animate motion. Male fetuses are exposed to higher levels of testosterone than are female fetuses. The present study investigates empathizing in children, as a function of amniotic measures of fT. One hundred ninety-three mothers of children (100 males, 93 females) aged 6-8 years of age completed children’s versions of the Empathy Quotient (EQ-C), and the children themselves were tested on “Reading the Mind in the Eyes” Task (Eyes-C). All mothers had had amniocentesis during the 2nd trimester of pregnancy. There was a significant negative correlation between fT and scores on both measures. While empathy may be influenced by post-natal experience, these results suggest that pre-natal biology also plays an important role, mediated by androgen effects in the brain. These results also have implications for the causes of disabilities involving empathy, such as autism spectrum conditions, and may explain the increased rate of such conditions among males. (Chapman, E., Baron-Cohen, S., Auyeung, B., Knickmeyer, R., Taylor, K. & Hackett, G. (2006). Fetal testosterone and empathy: Evidence from the empathy quotient (EQ) and the “reading the mind in the eyes” test. Social Neuroscience, 1(2), 135-48.)

Several studies have noted that adult male testosterone levels drop when integrated into a family or when spending sizable amounts of time with children. Other studies have shown that in hunter gatherer societies males spend more time with children than in agricultural or industrial societies. Sarah Blaffer Hrdy hypothesizes that humans evolved in matrilineal/matrilocal societies featuring mothers and daughters spending lifetimes together or in close proximity, dramatically increasing the chances children will reach adulthood.

If higher mother testosterone levels increase the chances of autism, and we evolved in societies with higher female testosterone (matrilineal/matrilocal societies revealing more female authority) with males with lower testosterone (males spending far more time around children) then perhaps high testosterone mothers giving birth to autistic children are creating children designed to operate in a matrilineal/matrilocal society.

If so, do the children of high testosterone women require the constant multi adult female encouragement (alloparent paradigm) that children display compassion, sharing, consideration of others, all the features of theory of mind?

It is widely accepted that genes play a role in the etiology of autism. Evidence for this derives, in part, from twin data. However, despite converging evidence from gene-mapping studies, aspects of the genetic contribution remain obscure. In a sample of families selected because each had exactly two affected sibs, we observed a remarkably high proportion of affected twin pairs, both MZ and DZ. Of 166 affected sib pairs, 30 (12 MZ, 17 DZ, and 1 of unknown zygosity) were twin pairs. Deviation from expected values was statistically significant (P<10(-6) for all twins); in a similarly ascertained sample of individuals with type I diabetes, there was no deviation from expected values. We demonstrate that to ascribe the excess of twins with autism solely to ascertainment bias would require very large ascertainment factors; for example, affected twin pairs would need to be, on average, approximately 10 times more likely to be ascertained than affected non-twin sib pairs (or 7 times more likely if “stoppage” plays a role). Either risk factors (related to twinning or to fetal development) or other factors (genetic or nongenetic) in the parents may contribute to autism. (Greenberg, D. A., Hodge, S. E., Sowinski, J. & Nicoll, D. (2001). Excess of twins among affected sibling pairs with autism: Implications for the etiology of autism. American Journal of Human Genetics, 69(5), 1062-7.)

Twins and handedness are related, with lefthandedness being more common among twins than non twins, particularly identical twins. (I’m not sure of this, I’m going my memory.)

Handedness is genetic to a large degree. Individuals with left handed mothers are more likely to be left handed than if they have left handed fathers. If they have one left handed parent they are more likely to be left handed than if they have none.

According to some studies there are those that are autistic that come from older mothers, and those that are first born. I’m suggesting higher testosterone levels compels one, a lack of alloparents and/or older siblings causes the other. A question I have is, do first borns and later borns both exhibit elevated rates of left handedness?  Is there a difference in handedness percentages between first born or later born autistics?

I’m looking for what differences there might be between these two groups of autistics. Is it possible that first born autistics only occur in family with higher rates of left handedness? I assume that a genetic predisposition makes a child more likely to get autism if not provided an environment that encourages theory of mind. What if an environment with few opportunities to develop theory of mind encouraged maturational delay and left handedness? That seems backwards, but interesting.

However, Morley (1972) found that some 26%  sample of 96 children with articulatory difficulties were left-handed and another 14% were poorly lateralized. An increased incidence of handedness, therefore, may be specific to children showing early articulatory problems, rather than being characteristic of all developmental language problems (see Bishop 1990a) (p. 144). (Bryden, M. P., McManus, I. C. & Bulman-Fleming, M. B. (1994). Evaluating the empirical support for the Geschwind-Behan-Balaburda model of cerebral lateralization. Brain and Cognition 26, 50-151.)

Handedness is closely related to cerebral lateralization which is related to uterine testosterone levels. When studies conclude that later born and the first born child are more likely to get autism, looking for what effects lateratlization makes sense.

Children born later in the reproductive live of a mother are emerging from wombs bathed in higher levels of testosteone. That more of these children would be autistic makes sense. What would cause a first born child to exhibit autism?

Are first borns more often left handed? If left handedness is related to testosterone, we would predict that children born from older mothers would be more often left handed. If first born and later borns are both more often left handed, exploring the what causes lefthandedness would be useful.

If Sarah Blaffer Hardy’s conclusion that children with no alloparents and no older siblings exhibit a less robust theory of mind, then might less theory of mind and left handedness be connected?

The implication is that autism, left handedness, mother’s testosterone levels, and a childhood featuring only one motherlike figure may be all related.

Thoughts sometimes emerge here that don’t get fleshed out until they appear on neoteny.org, after they’ve been gone over by an editor. Yesterday, reading Mothers and Others by Sarah Blaffer Hrdy, several poweful thoughts cruised through me.

The more older siblings a child has, engaging (and also perhaps tormenting) her, the better a child does on tests that require her to see the world the way someone else does. On closer examination, however, it turns out that it is not so much the number of siblings that matter as the fact that some are older. (p. 136)

Hrdy discusses the emergence of theory of mind in the context of human evolution driven by compassion with naturally selected communities of hominds displaying females working together to raise the kids. Hydy hypothesizes that far more children survived when caring for them was a community event. Theory of mind resulted from the exercise of compassion.

With her citation of studies that observe that first born children develop a less sophisticated theory of mind, it becomes a possiblity that the reason autistics congregate in the first born and those born to older mothers is because first borns aren’t introduced to a caring environment with multiple principles while later born gestate in higher testosterone wombs.

This feels significant. Autism may be partly a result of children raised in environments not natural to our species, homes with only one principle female. This would suggest that older mothers with only one child should have significantly higher percentages of autism. Recent studies calling attention to wealthier parents having higher percentages of autistic children may acutually be noting the tendency of wealther parents to have only one child when the parents are older.

The androgen theory of autism proposes that autism spectrum conditions (ASC) are in part due to elevated fetal testosterone (FT) levels, which are positively correlated with a number of autistic traits and inversely correlated with social development and empathy. A medical questionnaire was completed by n=54 women with ASC, n=74 mothers of children with ASC, and n=183 mothers of typically developing children to test whether women with ASC have an increased rate of testosterone-related medical conditions, and to see whether mothers of children with ASC show similar abnormalities, as part of the ‘broader autism phenotype’. Compared to controls, significantly more women with ASC reported (a) hirsutism, (b) bisexuality or asexuality, (c) irregular menstrual cycle, (d) dysmenorrhea, (e) polycystic ovary syndrome, (f) severe acne, (g) epilepsy, (h) tomboyism, and (i) family history of ovarian, uterine, and prostate cancers, tumors, or growths. Compared to controls, significantly more mothers of ASC children reported (a) severe acne, (b) breast and uterine cancers, tumors, or growths, and (c) family history of ovarian and uterine cancers, tumors, or growths. These results suggest current hormone abnormalities in women with ASC and their mothers. Direct investigations of serum testosterone levels and genetic susceptibility to high testosterone production or sensitivity in women with ASC would illuminate the origin of these conditions. The relationship between FT and current testosterone levels also needs to be clarified. The present results may be relevant to understanding the increased male risk to developing autism. (Ingudomnukul, E., Baron-Cohen, S., Wheelwright, S. & Knickmeyer, R. (2007). Elevated rates of testosterone-related disorders in women with autism spectrum conditions. Hormones and Behavior, 51(5), 597-604.)

If there is now an intense focus on women with higher testosterone levels birthing chidren with higher chances of autism, and it is concluded that aboriginal matrifocal social structures exhibit woman with higher testosterone levels but the societies have extremely low rates of autism, then maybe we should consider how exactly those children are being raised.

Information is appearing about a new study from UC Davis researchers discussing higher rates of autism in regions of California with higher income, older parents.

Using data on about 2.5 million births in California in a five-year period, researchers identified 10 autism clusters, or geographical areas in which there was a higher than usual incidence of children diagnosed with the neurodevelopmental disability that’s marked by impaired social and communication skills, and repetitive behaviors.

The rate of autism in the clusters was about twice that of the surrounding areas.

Discussions are revolving around wealthier, more educated parents having access to the services and evaluations that suggest autism. Other studies have concluded that older parents are more likely to have autism. It would be interesting to note whether older, wealther, more educated ethnic populations such as African Americans and Latinos show higher rates of autism. Some studies show increases, some decreases of autism among African Americans.

Van Meter said that the increased risk of autism in these areas is roughly a doubling of the incidence of autism over the incidence in the surrounding zone. For example, for the cluster area located in the service zone of the San Diego Regional Center, the autism incidence was 61.2 per 10,000 births and, in the rest of the Regional Center service zone, 27.1 per 10,000 births. For the Harbor Regional Center the incidence was 103.4 and 57.8, respectivel

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Analyses from the ALSPAC cohort also found evidence of a link between antenatal anxiety and neurological development. High maternal anxiety at 18 weeks’ gestation predicted atypical laterality (i.e. mixed handedness) in the child (further details available from the author upon request), independently of maternal and paternal handedness and obstetric and other antenatal risks.  No association was found with postnatal anxiety, indicating that maternal anxiety had qualitatively different effects on child handedness in the antenatal and postnatal periods. An association between antenatal anxiety and mixed handedness in the child was also found in a Danish cohort (C. Obel et al, personal communication, 2002). If antenatal anxiety is causally associated with mixed handedness, then it could have a role in other disorders associated with mixed handedness that have a neurodevelopmental component, such as dyslexia and autism. (Glover, V. & O’Connor, T. G. (2002). Effects of antenatal stress and anxiety. The British Journal of Psychiatry, 180, 389-91.)

There are a number of factors that increase or decrease testosterone levels. One of them is stress. Baron-Cohen’s work has made clear that a mother’s testosterone levels influence possibilities of autism in her children.

This study suggests that at 4.5 months during pregnancy, stress may be a factor, Studies would need to be conducted evaluating fluctuating testosterone levels in a pregnant mother over time to be able to conclude at what point during pregnancy maturation rates, and possibilities of autism, are impacted.

Children with Severe Hyperactive Syndrome had elevated lefthandedness, were largely blond and blue eyed, with cases of autism and dyslexia. (Behan, P. & Geschwind, N. (1985). Dyslexia, congenital anomalies, and immune disorders: The role of the fetal environment.  Annals of the New York Academy of Sciences, 457, 13-18.)

Anthropologist Marvin Harris hypothesized that Scandinavian need for Vitamin A and D propelled lighter skins to absorb light and an ability to process dairy. By acquiring the lighter skin, blue eyes and lactate processing abilities of infants, humans living in far Northern climes could more easily survive.

One could also estimate that there would be a larger percentage of left handers (infants are random handed) among these people. If the autistic are blond haired and blue eyed a higher percentage of the time, exhibiting maturational delay with these infant features, does this suggest that Scandinavian populutions should have higher percentages of autism?

Researchers at the U.C. Davis MIND Institute has discovered regions in the state of California that have notably higher autism incidence. But the story is more complicated, and more sad, than one might think at first. Instead of indications of an “autism epidemic”, these clusters point to the fact that minority and poor children are much less likely to receive autism diagnoses.

This piece appeared yesterday referring to a new study that is observing differences between poorer and wealthier communities as regards number of children diagnosed with autism or Aspergers. Where there is less money, there are fewer children diagnosed.

Children with autism have a relatively shorter index finger (2D) compared with their ring finger (4D). It is often presumed that the 2D:4D ratio is associated with fetal testosterone levels and that high fetal testosterone levels could play a role in the aetiology of autism. It is unknown whether this effect is specific to autism. In this study, 2D:4D ratios of 144 males aged 6 to 14 years (mean age 9y 1 mo [SD 1y 11 mo]) with psychiatric disorders were compared with those of 96 males aged 6 to 13 years from the general population (mean age 9y 1 mo [SD 1y 10 mo]). Psychiatric disorders were divided into autism/Asperger syndrome (n=24), pervasive developmental disorder-not otherwise specified (PDD-NOS; n=26), attention-deficit-hyperactivity disorder (ADHD)/oppositional defiant disorder (ODD; n=68), and anxiety disorders (n=26). Males with autism/Asperger syndrome (p<0.05) and ADHD/ODD (p<0.05) had significantly lower (though not significantly; p=0.52) ratios than males with an anxiety disorder, and males with autism/Asperger syndrome had lower ratios than those in the comparison group. These results indicated that higher fetal testosterone levels may play a role, not only in the origin of autism, but also in the aetiology of PDD-NOS and of ADHD/ODD. Males with anxiety disorders might have been exposed to lower prenatal testosterone levels. (de Bruin, E. I., Verheij, F., Wiegman, T. & Ferdinand, R. F. (2006). Differences in finger length ratio between males with autism, pervasive developmental disorder-not otherwise specified, ADHD, and anxiety disorders. Developmental Medicine and Child Neurology, 48(12), 962-5.)

I’m not clear why it is the case that testosterone levels are associated with handedness (left handedness correlated with low testosterone in males), left handedness is assocated with maturational delay, but testosterone is rarely approached in the context of maturational delay. It would seem that this would be important in such studies as noted above.

I explore the connection between autism, testosterone levels and maturation rates and timing. If maturation rates and timing are integral to understanding how we evolved (See Gould’s Ontogeny and Phylogeny), then understanding autism, and related conditions, may be central to understanding what being human exactly is.

We investigated the association between selected infant and maternal characteristics and autism risk. Children with autism born in California in 1989-1994 were identified through service agency records and compared with the total population of California live births for selected characteristics recorded on the birth certificate. Multivariate models were used to generate adjusted risk estimates. From a live birth population of more than 3.5 million, 4381 children with autism were identified. Increased risks were observed for males, multiple births, and children born to black mothers. Risk increased as maternal age and maternal education increased. Children born to immigrant mothers had similar or decreased risk compared with California-born mothers. Environmental factors associated with these demographic characteristics may interact with genetic vulnerability to increase the risk of autism. (Croen, L. A., Grether, J. K. & Selvin, S. (2002). Descriptive epidemiology of autism in a California population: Who is at risk? Journal of Autism and Developmental Disorders, 32(3), 217-24.)

The study above shows trends different than studies just released regarding which populations are more vulnerable to autism. African Americans sometimes have increased percentages, sometimes decreased percentages.

I wonder if there are any studies concentrating on how studies are conducted. Are urban populutions approached different than cities, poor from wealthy, school systems with local property taxes providing extra services vs. schools surviving on state and municiple funding?

How closely are autism rates connected to information retrieval protocols?

The UCLA Registry for Genetic Studies in Autism was established in 1980 to test the hypothesis that genetic factors may be etiologically significant in subsets of patients. To date 61 pairs of twins have enrolled and 40 meet research diagnostic criteria for autism. The authors found a concordance for autism in these 40 pairs of 95.7% in the monozygotic twins (22 of 23) and 23.5% in the dizygotic twins (four of 17). (Ritvo, E. R., Freeman, B. J., Mason-Brothers, A., Mo, A. & Ritvo, A. M. (1985). Concordance for the syndrome of autism in 40 pairs of afflicted twins. The American Journal of Psychiatry, 142(1), 74-7.)

It’s been 25 years since the above published study explored genetic factors in autism etiology. New studies asking similar questions emerge several times a year. There is little doubt the genetics are integrally related to how autism emerges, but what we think the genes are, is changing.

I’m suggesting that to understand autism we have to reappraoch how we understand genetics and what we understand consciousness to be. We reflexively behave as if genes compel individual ontogeny with little reference to the environment. As regards autism, this may be a failure of model making. When approaching an understanding of consciousness, autism is nothing if not alternative consciousness, one committed to primary process: one time, one place, no opposites. Understanding autism is to understand the unconscious, and perhaps how normal waking (non primary process) consciousness evolved.

Although children with Tourette syndrome (TS) only rarely present with a profound failure to develop social relations, they frequently have problems with delayed or defective speech and characteristically show many ritualistic or compulsive behaviors. Autistic and TS patients may have the following symptoms in common (Commings, 1990a): attention deficits, babbling, echolalia, palialia, echopraxia, facial grimacing, hand flicking, hyperactivity, inappropriate anger, obsessive-compulsive behaviors, onset in childhood, panic at minor environmental change, perseveration, poor control of speech volume, sniffing and smelling of objects, stereotyped movements, improvement with haloperidol treatment (Campbell et al., 1982), excerbation with dopamine agonists (Leckman and Cohen, 1983), and an implication of defective control of serotonin and tryptophan levels (Boulin el al., 1982; Hanley el al., 1977; Ritvo et al., 1970, 1971; Schain and Freedman, 1961; Takahashi et al., 1976; McBride et al., 1989; Blum et al., 1990; Comings, 1990a, 1990b) (p. 180). (Comings, D. E. & Comings, B. G. (1991). Clinical and genetic relationships between autism-pervasive developmental disorder and Tourette syndrome: A study of 19 cases. American Journal of Medical Genetics, 39(2), 180-91.)

I focus on possible evolutionary origins of autism. Tourette syndrome often feels closely related. Consider that a major barrier to understanding the relationship between evolution, autism and TS  is our focus on natural selection as being the exclusive cause of human evolution.

Geoffrey Miller hypothesizes that sexual selection created the human species. If ritualistic and compulsive behaviors are signs of human forebear traits, then what might propel those with autism and Tourette syndrome back to when those traits were ubiquitous?

What prevents contemporary clinitians from studying what causes slides backward to pick up forebear features, and why are theorists not related that to TS and autism?

Two recent epidemiological studies based on physician surveys and public anouncements have suggested a frequency in male childen [of TS] of 1 in 1,500  to 1 in 1,000 (Burd et al., 1986; Caine et al., 1988). We felt that the frequency of TS would be more accurately determined by having a trained observer constantly monitor everyone in a defined population. In such a study where students were monitored almost daily for a period of 2 years, we observed a frequency of TS in school boys of 1 in 95, and in school girls of 1 in 759, for a combined frequency of 1 in 169 (Comings et al., 1990a) (p. 189). (Comings, D. E. & Comings, B. G. (1991). Clinical and genetic relationships between autism-pervasive developmental disorder and Tourette syndrome: A study of 19 cases. American Journal of Medical Genetics, 39(2), 180-91.)

A recent study has called attention to dramatic rises in autism. Several conditions associated with maturational delay or acceleration are associated with autism including Tourette’s, stuttering and left handedness. A relevant question would be whether these three conditions are also increasing, and increasing at the same rates.

If autism is part of an associated whole cluster of conditions increasing across the world, perhaps by understanding where exactly those increases are taking place we can narrow the situations that are responsible.

Mentally handicapped children, mostly in institutions, were screened in 5 countries in Africa in order to explore the usefulness of Western criteria for the recognition of childhood autism in developing countries. Approximately 1,300 children were seen, of whom 30 had some autistic-like behavior. Nine were autistic according to Western criteria. Autistic behavior was found in speaking and nonspeaking children of all grades; in sex ratio, occurrence of epilepsy, and social background the African group was broadly comparable to Western groups. Behavioral comparison with a British sample suggests some prominent features of the syndrome are very uncommon in Africa. Implications for recognition and classification are discussed. (Lotter, V. (1978). Childhood autism in Africa. Journal of Child Psychology and Psychiatry, 19(3), 231-44.)

The above is an old study, but it begs questions regarding increases in autism across the world. Which portions of the world are seeing the kinds of increases we’re seeing in the United States? Some sections of West Africa have far higher percentages of left handed children. Do those regions of higher or lower percentages of autism? Because diagnosis protocols differ, are there different rates of autism in African cities vs. African rural areas?