The Increase in Autism in California (which is also occurring in other areas)

New Support Below (May, 2005); Some new ideas, April, 2010, below.

New: Dendritic Spines, Synapses, and Connectivity

New: Preterm and Reduced Growth and Development

Copyright 2003-2010, James Michael Howard, Fayetteville, Arkansas, U.S.A.

The increase in autism, in California and elsewhere, may be caused by the same mechanism that causes the "secular trend," the increase in size and earlier puberty currently ongoing in the U.S. My work suggests the secular trend is produced by an increase in percentage of individuals of higher testosterone in society. (Some say the secular trend is due to better nutrition; better nutrition simply accelerates the reproductive rate of individuals of higher testosterone.) The increase in percentage of individuals of higher testosterone increases their characteristics in society; as they increase we begin to perceive these characteristics over time. These characteristics include pathologies such as increased breast cancer, obesity, small birth weight, decreased ability to learn English and mathematics, etc. As they increase their percentage, they increase the incidence of these pathologies.

Of interest to you, of course, is the increase in autism. While I contend the characteristics, above and of autism, are due to the effects of increased testosterone reducing the availability of the hormone, dehydroepiandrosterone (DHEA), I need not explain this in detail for you to see the connection of testosterone with autism. Manning, et al., have already suggested that increased testosterone may be involved in autism (Dev Med Child Neurol 2001 Mar; 43(3):160-4). Therefore, I suggest that the increase in testosterone, and the other characteristics listed above, are the result of the increase in individuals of higher testosterone and pathologies associated with this group. (The mechanism is simple. Individuals of higher testosterone are more sexual and aggressive, they reproduce faster. Women of higher testosterone expose their fetuses to higher testosterone levels, which may be the source of these increased pathologies.) A simple, single mechanism may account for all of these problems. This may be why these are occurring simultaneously. Increasing autism may be due to an increase in the percentage of individuals of higher testosterone in our society.

 This was emailed to a researcher who brought this to the attention of the California Legislature October 19, 2002.

How the "Autistic Savant" Syndrome May Occur

Some years ago I developed an explanation of the "Autistic Savant" syndrome. My explanation is that a competition for DHEA exists between all tissues, with the brain able to sequester DHEA better than other tissues. (This competition is explained in "Androgens in Human Evolution.") I think this competition also exists between tissues composing the brain. A defect in growth and development of one part of the brain will affect the availability of DHEA to that part/s and, therefore, other parts. If one part is so underdeveloped that it will not sequester DHEA at a normal rate, this will free available DHEA for other parts and these parts will have access to increased DHEA and develop accordingly. That is, as one part declines, another may accelerate development. This would produce increases in some abilities while others decrease. I think this occurs in all of us and may be manipulated to some degree, probably not much, by the environment. We all have different abilities. In "autistic savants," this may occur to its maximum.

New Support:

Eur Neuropsychopharmacol. 2005 May;15(3):305-9.



Lowered DHEA-S plasma levels in adult individuals with autistic disorder.

Strous RD, Golubchik P, Maayan R, Mozes T, Tuati-Werner D, Weizman A, Spivak B.

Beer Yaakov Mental Health Center, Beer Yaakov, Israel; Sackler Faculty of Medicine, Tel Aviv University, Israel.

The aim of this study was to determine for the first time neurosteroid levels, dehydroepiandrosterone (DHEA) and DHEA-sulfate (DHEA-S) in particular, in a group of adult patients with autistic disorder and compare these levels with normal healthy individuals. Levels of DHEA, DHEA-S and cortisol were compared between 15 adult drug-free patients with autistic disorder and 13 healthy controls. The Ritvo-Freeman Real-Life Rating Scale (RLRS) and the Overt Aggression Scale (OAS) were assessed as a measure of symptom severity. Significant lower DHEA-S levels were observed in the group with autistic disorder as compared to controls (p<0.05). DHEA-S levels appear to be low in patients with autistic disorder and, while speculative, may play a role in the etiopathophysiology of the disorder.



Some new thoughts, April, 2010.


The brains and bodies of individuals with autism are bigger and, in the more severe cases of autism, “pruning” does not occur.  I have written an explanation of pruning in which I contend that pruning occurs as a result of competition for DHEA.  I think this is why there is a “dip” in the “life span levels of DHEA,” seen as “B” in this chart(Note that autism most often begins at the end of “A” at the beginning of “B.”  This is also the time of most SIDS deaths.)



It is part of my explanation of autism that increased maternal testosterone increases androgen receptors in the fetus.  Increased androgen receptors will absorb increased DHEA in the brain and body.  Androgen receptors are high in the brain and cause the increase in brain size at the expense (competition) of the body in humans.  This causes the characteristic increased brain size and reduced body “robustness” in humans, the basis of my explanation of human evolution, published in 2001.  (Examinations regarding androgen receptors in autism are not new with me; my explanation of how they may cause autism is new.)


I suggest autism may be caused by increased available DHEA that is available for androgen receptors.  (I know, I talk about low DHEA, above, but I will explain this in terms of this explanation of autism.)  If so much DHEA is available for brain and body androgen receptors, then the brain and the body will both grow bigger than usual.  That is, the brain will not exhibit competition between its structures, hence no pruning, and the body will not exhibit the reduction in robustness caused by the brain’s use of available DHEA.  The brains and bodies of autistics are bigger.


Here is the irony; if DHEA is increased and it is used by the brain and the body for increased growth, then measurable DHEA in autistics will be low.  It will be low because of use by the brain and the body.  Since I think “low DHEA” causes the lack of proper brain function in autism, the low DHEA that results from brain and body use will, therefore, reduce brain function in autism. 


There is suport for my hypothesis: “Results showed that head circumference and weight growth were significantly greater in both autism spectrum disorder groups compared with controls, with no significant differences between autism spectrum disorder groups. However, when length and weight were controlled for, accelerated head growth remained significant in the children who lost their diagnoses. Findings suggest that children who lose their autism spectrum disorder diagnoses and children who maintain their diagnoses show similar head circumference, length, and weight growth trajectories during infancy, although subtle differences in body growth between groups may exist.” (J Child Neurol 2009; 24: 833-45, Mraz, et al.).  I suggest the new borns who develop autism, according to my current explanation, are born with a high level of DHEA as period A begins.  A study in China has found that mothers of autistic children exhibit factors which my other work indicates will reduce maternal DHEA for their fetuses (J Autism Dev Disord 2010: Zhang, et al., “Prenatal and Perinatal Risk Factors for Autism in China.”  The high period A is a response at birth of the newborns to low DHEA in utero.  Marz point out that those children who retained significant head growth “lost their diagnoses.”  I suggest this indicates that they continued to produce sufficient levels of DHEA that enabled them to maintain brain growth.  In those children whose brains did not maintain accelerated head growth, I suggest their DHEA declined too much at the end of period A to maintain their increased growth and thus not enough DHEA to maintain brain function.  For sake of support, and since I have suggested the same / very similar etiology of SIDS, link above as “SIDS deaths,” a common risk factor found with SIDS is prenatal smoking (Early Hum Dev. 2007 Nov;83(11):713-20) and “we noticed that the weights of the brains of infants who died from sudden infant death syndrome (n = 97) were invariably heavier in comparison with those of a group of age-matched controls (n = 23) issuing from the same local population. Brain edema was not a major element, and there were no significant microscopic or macroscopic cerebral anomalies in the brains from either of the study groups. Head circumference did not show a parallel increase in infants with sudden infant death syndrome.” (J Child Neurol. 2005 Mar;20(3):244-6).  In the case of SIDS, which also occurs at the end of period A, the DHEA would reach such low levels at night that brainstem function ceases.


The brain differs in autistics and it is supplied with low DHEA, which I think causes many brain problems.