Archive for December, 2009

Autism, Testosterone and Maturation

Thursday, December 31st, 2009

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.


Varying Percentages

Tuesday, December 29th, 2009

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?


Autism and Genetics

Monday, December 28th, 2009

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.


Ritualistic or Compulsive Behaviors

Wednesday, December 23rd, 2009

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?


Associated Conditions

Tuesday, December 22nd, 2009

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.


Autism in the Third

Monday, December 21st, 2009

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?


New Study and Increased Rates

Saturday, December 19th, 2009

A study just released, Prevalence of Autism Spectrum Disorders — Autism and Developmental Disabilities Monitoring Network, United States, 2006, describes an increase in autism in the United States among 8 year olds in 2006. An interesting aspect of the study is the higher incidence of the condition among whites vs. blacks and Hispanic children.

ASD prevalence also varied by race and ethnicity (Table 2). Combining data from all sites, the average prevalence among non-Hispanic white children (9.9; CI = 9.4–10.4) was significantly greater than that among non-Hispanic black children (7.2; CI = 6.6–7.8) and Hispanic children (5.9; CI = 5.3–6.6) (Table 2) (p<0.001). For five (Florida, Georgia, Missouri, North Carolina, and Wisconsin) of the 11 ADDM sites, ASD prevalence was significantly higher among non-Hispanic white children than among non-Hispanic black children (p<0.05). ASD prevalence was significantly lower among Hispanic children than among non-Hispanic white children in six sites (Alabama, Arizona, Georgia, Missouri, North Carolina, and Wisconsin), and was significantly lower than prevalence among non-Hispanic black children in four sites (Alabama, Arizona, Colorado, and Georgia).

My works hypothesizes that if autism is an evolutionary condition with testosterone compelling return to forebear neurologies when equatorial peoples are moved to Northern climes, then blacks and Hispanics should evidence autism more frequently in the Northern U.S..

The male/female ratio varied dramatically depending on where you were in the country. I don’t know how to interpret that.


Geschwind, Galaburda and Autism

Thursday, December 17th, 2009

The literature on stuttering repeatedly refers to allergies (Diehl 1958; Szondi 1932); pediatric neurologists have repeatedly told us of the high frequency of migraine in dyslexics; Coleman (1976) discussed the high rate of a gut-related disorder in autism (p. 92). (Geschwind, N. & Galaburda, A.M. (1987). Cerebral Lateralization. Cambridge:  MIT Press.)

Geschwind and Galaburda’s Cerebral Lateralization was very influential for a short period of time. Supporting studies were often contrasted with studies that supported competing theories. Nevertheless, sense has been emerging from the conflicting studies. Baron-Cohen’s work represents much of that sense.

Perhaps by offering additional attention to the influence of the sexual hormones upon both specific symptoms (such as migraine) and conditions that exhibit maturational delay or acceleration (such as autism and stuttering) we can understand the connection between maturity and physical disorders.


Allergies and Autism

Wednesday, December 16th, 2009

In addition to the reports mentioned earlier of increased frequency of allergies among stutters, celiac disease among autistic children and autoimmune thyroid disorders in their parents, and migraine among childhood dyslexics, a high frequency of food allergies (Tryphonas and Trites 1979) and atopic disorders (Geschwind and Behan 1984) have been reported among hyperactive children (p. 94). (Geschwind, N. & Galaburda, A. M. (1987). Cerebral Lateralization. Cambridge: MIT Press.)

Geschwind and Galaburda’s Cerebral Lateralization is crammed with information that suggests an etiology for autism. It is the first place that I know of that associated autism with a mother’s testosterone levels. When the book discusses allergies and autism, I am reminded that perhaps a mother’s allergies influence her testosterone, or even estrogen levels, and that those changing levels increase chances for conditions featuring maturational delay. I’ve wondered if the recorded season of birth effects associated with autism are related to when a mother’s allergies correlate with certain points in pregnancy when maturation rates are established.


Autism and Evolutionary Precursors

Tuesday, December 15th, 2009

OBJECTIVE: Several studies report a greater than expected concurrence for Tourette’s syndrome (TS) with autistic disorder (AD). TS and bipolar disorder (BD) also may co-occur at a greater than expected rate. The authors assess whether there is a greater than expected concurrence for TS+AD+BD. METHOD: Four patients who had at some time in their lives diagnoses of TS, AD, and BD were identified. Three of these had concurrent TS+AD+BD. Diagnoses were made according to DSM-III-R criteria. Each of these patients was living in North Dakota and was in the authors’ care at the time of this study. RESULTS: The point prevalence (risk) for concurrent TS+AD+BD in North Dakota is not less than 4.6 x10(-6). The developmental sequence of syndromes in these four patients was AD, then TS and then BD. Data from the authors’ previously published, population-based prevalence studies indicate that TS+AD+BD co-occur at a greater than chance expectation. CONCLUSIONS: Common etiological factors may be involved in the greater than chance concurrence of TS+AD+BD. (Kerbeshian, J. & Burd, L. (1996). Case study: Comorbidity among Tourette’s syndrome, autistic disorder, and bipolar disorder. Journal of the American Academy of Child Adolescent Psychiatry, 35(5), 681-5)

A question that often crosses my mind is if autism and Tourette’s are both conditions with evolution origins, is Tourette’s a precursor to autism? Or, do they represent two different forebear evolutionary branches.

A not uncommon feature of Tourette’s is obsessive compulsive disorder. A man with Tourette’s I know compulsively self grooms, picking at tiny flecks upon his person. When a woman walks into a room he often emotes unique noises. This man is also brilliant and uncommonly strong.

This particular person was displaying possible features of a human progenitor. If autism and Tourette’s are related, as this study suggests, what features of autism might suggest precursor?


Vitamin D and Autism

Monday, December 14th, 2009

As this post from yesterday’s Autisable notes, Vitamin D has been becoming more accepted as a possible explanation for some forms of autism. I’ve been proposing that light’s effect on the pineal gland has been regulating testosterone levels in directions that can cause autism, predicting in 1998 (sexualselection.org) that equatorial populations moving to northern climes would evidence higher percentages of autism.

Both my pineal theory, based on fluctuating testosterone levels, and the Vitamin D theory suggest that there would be clear season of birth effects with autistic children being conceived in certain times of the year. I’ve not seen studies that support that prediction.


Twins and Autism

Friday, December 11th, 2009

Previous studies have suggested that among affected sib pairs with autism there is an increase in the frequency of twins over what would be expected in comparison to the prevalence of twins in the general population. In this study we sought to determine whether sub-threshold autistic traits were more pronounced in twins than in non-twins. The Social Responsiveness Scale (SRS) was administered in an epidemiologic twin sample (n=802) and in a separate population-based sample of non-twins ascertained from a local school district (n=255). For males (but not females), the mean SRS score was significantly higher among twins than among non-twins. As has been suggested for autism, twin status may incur increased liability to subthreshold autistic symptomatology, particularly in males. (Ho, A., Todd, R. D. & Constantino, J. N. (2005). Brief report: Autistic traits in twins vs. non-twins–a preliminary study. Journal of Autism and Developmental Disorders, 35(1), 129-33.)

Higher incidence of autism among twins, of course, suggests genetic origins, though embronic environmental influences come into play. A couple things come to mind reading this passage.

Studies seeking genetic causes of autism point to twins studies as integral to their conclusion that autism is largely a genetic condition. Nevertheless, the relationship between genetics and environment is still very much in flux. Evolutionary developmental biology is just beginning to open those doors.

Second, is there a smaller percentage of identical female twins with at least one twin exhibiting autism or Aspergers than the normal percentage of females to males? In other words, if it is a 4/1 ration male/female, and the number of males to females that are autistic that are identical twins is different that 4/1, then perhaps the etiology of female autism is significantly different than male autism.


Autism, Brain Size and Maturation

Wednesday, December 9th, 2009

Increased brain size has been observed in individuals with autism with a wide range of cognitive functioning. The purpose of this investigation was to obtain measurements of the brain volume in a sample of nonmentally retarded autistic individuals. Magnetic resonance imaging scans from 16 nonmentally retarded individuals with autism and 19 male volunteer comparison subjects were obtained and the following structures were measured: third, fourth, and lateral ventricles and intracranial and cerebral volumes. Mean cerebral and third ventricle volumes in the autistic subjects were significantly greater than in the controls when adjusted for intracranial volume. No other significant results were found. Our finding of increased brain volume in autism is consistent with previous reports in the literature. Additional longitudinal neuroimaging and, more importantly, neuropathologic studies are warranted to provide a better understanding of the complexities underlying increased brain size in autism. (Harden, A. Y., Minshew, N. J., Mallikarjuhn, M. & Keshavan, M. S. (2001). Brain volume in autism. Journal of Child Neurology, 16(6), 421-4.)

Studies continue to be published that call attention to possible genetic causes of autism. Yet, a larger brain size in many of those that are autistic is not explored in the context of evolutionary changes over time.

Over the last 25 thousand years human brain size has grown smaller. Consider that if autistics have larger brains, they are neurological retreats to a slightly older neurological convention.

Instead of examining genes for autistic tendencies, perhaps we should be exploring the connection between evolution and ontogeny, brain size being related to maturation.


Autism and Handedness

Tuesday, December 8th, 2009

Twenty-six autistic children, constituting a total population sample of children diagnosed in accordance with Rutter’s criteria as suffering from infantile autism, were assessed with regard to handedness and certain associated factors. They were compared with 52 age-, sex-, and IQ-matched controls. Sixty-two percent of the autistic children were non-right-handed compared with 37% of the controls. Left-handedness in autism was associated with an abundance of delayed echolalia. Heredity for left-handedness in some cases, and assumed brain damage and immature patterns of lateralization in others, were considered the cause of non-right-handedness in the autistic children. Computed tomographic (CT) brain scans and other neurobiological examinations did not provide evidence indicating clear-cut unilateral left hemisphere dysfunction in autism. Rather, a slight trend in the opposite direction (i.e., an association with right hemisphere dysfunction) was seen in the left-handed autistic children. The result points toward the need for further studies of handedness in autism. (Gillberg, C. (1983). Autistic children’s hand preferences: Results from an epidemiological study of infantile autism. Psychiatry Research, 10(1), 21-30.)

Twenty five years ago researchers observed the close connection between autism and handedess. A generation later and the connection between handedness and Marian Annett’s work regarding random handedness as an evolutionary precurser to contemporary right handedness has not been explored as related to autism. If autism is an evolutionary condition, and we understand evolution as a process deeply influenced by social structure and environmental effects, then perhaps we can understand what causes some forms of autism.


Autism and Genetics

Monday, December 7th, 2009

A review of the current literature suggests that genetic factors play an important role in the etiology of autism. It is likely that the etiology of currently idiopathic cases of autism will be shown to be heterogeneous, just as the few known etiologies are both environmental and genetic. Moreover, we would speculate that within the group of cases shown to have genetic etiologies, more than one genetic locus will be found. Some evidence suggests that quite often it is not autism itself that is inherited but rather some genetic abnormality of language or sociability that interacts with other factors to produce autism. (Folstein, S. E. & Rutter, M. L. (1988) Autism: Familial aggregation and genetic implications. Journal of Autism and Developmental Disorders, 18(1), 3-30.0

Google alerts me every day to articles emerging about autism. Many of those articles allude to papers published calling attention to possible genetic causes of autism.

Susan Oyama writes about the challenges our society creates confusing genetic and environment causes, nature and nature, by often really thinking in terms of genetics but stating both are in play. If feels to me that this is often an issue in autism research. We understand so little the impact of ontogeny upon unique conditions that we instead concentrate on genetics which looks like a code to decipher, not a pattern to resolve.

Understanding ontogeny as evolutionary as its foundation, perhaps we can reinterpret autism as an evolutionary condition and then see how genetics are in play.


Autism & Early Intervention

Saturday, December 5th, 2009

A recent article in Science Blog described a study pubished in Pediatrics that discussed the Early Start Denver Model, “which combines applied behavioral analysis (ABA) teaching methods with developmental ‘relationship-based’ approaches.”

“This is the first controlled study of an intensive early intervention that is appropriate for children with autism who are less than 2½ years of age. Given that the American Academy of Pediatrics recommends that all 18- and 24-month-old children be screened for autism, it is crucial that we can offer parents effective therapies for children in this age range,” said Geraldine Dawson, Ph.D., chief science officer of Autism Speaks and the study’s lead author. “By starting as soon as the toddler is diagnosed, we hope to maximize the positive impact of the intervention.”

It comes to mind again the relavance of making ontogenetic interventions (early childhood interventions) without an evolutionary model. How might an understanding of what humans needed several thousand generations ago be connected to what a toddler needs today? This seems particularly important when working on language, socialization, and theory of mind issues.

Consider a model of early childhood delelopment connected to evolutionary development, not unlike the exact paradigm Piaget played with, except one that takes into consideration particularly practices that might be necessary for those having difficulty with the conventional transitions.


Autism and Social Stresses

Thursday, December 3rd, 2009

Reviews research relevant to the questions of whether childhood schizophrenia and infantile autism are evenly distributed across the population of the world or even across a single society, whether social selection or social causation may operate in their occurrence, and whether there is a relationship between social class and infantile autism. Studies examined include early investigations in the US and UK on the possible importance of social background and parental behavior in childhood schizophrenia; studies conducted in continental Europe, Africa, Asia, and Australia; studies of Blacks and Hispanics in the US; and investigations suggesting that parental socioeconomic status (SES) may be more important than ethnicity in the development of childhood psychoses. It is concluded that evidence supports the speculation that problems of modern living, particularly the nuclearization of the family, are likely to increase the stresses experienced by the infant. (Sanua, V. D. (1981). Autism, childhood schizophrenia and culture: A critical review of the literature. Transcultural Psychiatric Research Review, 18, 165-81.)

The question is, what are the nature of these “stresses”. Social structure is rarely examined for the impact that it has upon the hormonal distribution of  populations. If it is true that testosterone and estrogen levels are integral in the etiology of autism and conditions exhibiting maturational delay and acceleration, then perhaps we should explore what influences those hormone levels.


Bernard Crespi and Autism

Tuesday, December 1st, 2009

It was noted yesterday that Bernard Crespi and colleagues have released further findings suggesting a relationship between schizophrenia and autism. At neoteny.org I’ve written about Crespi’s work and where I agree with the direction he is taking.

Crespi and I both believe that how brains lateralize and the width of corpus callosum connections influence the etiology of both conditions. I suggest that the origin of human split consciousness or self awareness is also integrally connected to these issues. We are both approaching this from an evolutionary perspective.

Whereas autism displays features of primary process or humans perhaps 4000 generations ago, I hypothesize that some forms of schizophrenia represents an opposite of primary process or a human so split, so self aware, they can’t easily encourage both sides to work together.

Crespi’s conclusion that autistic brains are larger, schizophrenic’s smaller, support this way of looking at the information.


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