A piece appeared today describing new clinical trials.

CAMBRIDGE, Mass., Nov. 5 (UPI) — U.S. scientists say they are starting a trial of a medication designed to treat the neurochemical defect underlying Fragile X syndrome.

I’ve wondered about how suggestive Fragile X features are of the origin of autism. In 1998, I predicted that a language challenged group of individuals should feature larger brains. I discovered a large percentage of autistics do. Later I estimated that autistic males, if indeed they represent an ancient matrifocal protype, should have larger testicles. (Primates matrifocal promiscious social structures reveal males with large testes.)

I could find no evidence that studies had been conducted on autistic males to determine testicle size, except for Fragile X. Fragile X males display unusually large genitals.

I have no idea how this would relate to the medication intervention in clinical trials. Perhaps there is an gonadal hormone system component.

Family history data on 99 autistic and 36 Down’s syndrome probands are reported. They confirmed a raised familial loading for both autism and more broadly defined pervasive developmental disorders in siblings (2.9% and 2.9%, respectively, vs 0% in the Down’s group) and also evidence for the familial aggregation of a lesser variant of autism, comprising more subtle communication/social impairments or stereotypic behaviours, but not mental retardation alone. Between 12.4 and 20.4% of the autism siblings and 1.6% and 3.2% of the Down’s siblings exhibited this lesser variant, depending on the stringency of its definition. Amongst autistic probands with speech, various features of their disorder (increased number of autistic symptoms; reduced verbal and performance ability) as well as a history of obstetric complications, indexed an elevation in familial loading. No such association was seen in the probands without speech, even though familial loading for the lesser variant in this subgroup, was significantly higher than in the Down’s controls. The findings suggest that the autism phenotype extends beyond autism as traditionally diagnosed; that aetiology involves several genes; that autism is genetically heterogeneous; and that obstetric abnormalities in autistic subjects may derive from abnormality in the foetus. Bolton, P., MacDonald, H., Pickles, A., Rios, P., Goode, S., Crowson, M., Bailey, A. & Rutter, M. (1994). A case-control family history study of autism. Journal of Child Psychology and Psychiatry, and Allied Disciplines, 35(5), 977-900.

Downs Syndrome exhibits powerful suggestions of neoteny with some studies calling attention to the correlations. I’ve hypotheized and discussed in detail the influence of neoteny on autism. Downs is a chromosonal condition. Autism is far more subtle. Do any of the my hypothetical causes of autism also apply to Downs? For example, are there higher rates of Downs among Minnesota Somalis?

The raised incidences of strong left-handedness and of mixed-handedness in homosexual men, as in dyslexics, are mutually consistent under the normal distribution function, as expected by the right shift theory of handedness. It is argued that atypical laterality in these groups is better described as a “reduction of right shift” than as a “left shift”. Annett, M. (1988). Comments on Lindesay: Laterality shift in homosexual men. Neuropsychologia, 26(2), 341-3.

Surveying several studies on gay and lesbian neurological and endocrine system features I am struck by the male maturational delay, female maturational acceleration paradigm. This is what I hypothesize for autism and Aspergers.

McCormick and Witelson (1991) noted specific neurological differences between heterosexuals and homosexuals with McCormick, Witelson and Kingston (1990) observing greater numbers of lefthanders among both lesbians and gays. Stress increases testosterone levels in woman. Dorner, Schenk, Schmiedel, and Ahrens (1983) observed that increased stress in a pregnant woman increases the chance of a homosexual son. Annett (1988) notes the higher percentages of left handedness among gays, compared that to dyslexics and suggested that this increased the likelihood of anomalous dominance or two cerebral hemispheres the same size.

Understanding autism involves exploring similar patterns in other conditions exhibiting maturational delay and acceleration.

Blogs and news stories often note the recent study that concluded that autism rates are dramatically increasing. One in sixty males are now estimated to have autism or Aspergers.

An issue that keeps coming to mind is whether left lefthandedness or ambidexterity is on the rise. This would be a dramatic indicator of the cause of autism. There have been no resent such studies that I am aware of. Left handedness and ambidextrousness or both indicators of “random handedness” or those without a genetic predisposition toward right handedness, people with right cerebral hemispheres that did not experience the degree of cerebral synapse pruning that normal right handers did. These are people with bigger brains. The autistic often have bigger brains.

If autism is on the rise and random handedness is increasing that means maturational delay is increasing. This would be useful information.

I’m still wresting with a number of themes suggested by the Science News article released last week. I study autism and Aspergers as conditions evidencing information and orientations that may throw light upon how humans evolved. I ended up in this area of study after hypothesizing that if we evolved from larger brained, primary process (one time, one place, no opposites), matrifocal, dance driven societies then the reasons brains may have started growing smaller 25,000 years ago was because we were shifting from primary process to split conscious (smaller) brain structures, patrifocal societies, evidencing speech arts more than dance.

Looking for larger brained, speech impaired, primary process inclined contemporaries, the autistic fit the paradigm to a “t”.

The recent science article noted a study alluding to another study that I was not aware of, one that said about 25% of the autistic have larger brains. I thought it was a larger percentage. I can’t find the study alluded to in the article.

So, I am now particularly interested in what studies state what percentages of the autistic (and Aspergers) have larger brains. I’m particularly interested in how the larger brained autistic spectrum individuals are different than those with normal sized brains. In addition, how much of the larger brain size is due to a left hemisphere that did not experience infant and childhood synapse pruning? Do the autistic with normal brain size have their left hemispheres pruned or not pruned?

Brain size is one of the anomalies of being autistic. It would be also useful to know whether in the increases of autism in the last twenty years if the increases are more or less those with larger brains.

If we are to understand varying etiologies of autism, it is necessary we be able to assign features of the condition to the various ways that autism is neurologically displayed.

Something that the psychologist Laurent Mottron of Hôpital Rivière-des-Prairies in Montreal said in a recent article in Science News struck me as unusual and good. Bruce Bower, author of the article noted, “Mottron regards autism as a variant of healthy brain development and prefers the term ‘autistic’ to ‘person with autism.’”

This seems a particularly useful way of approaching explorations of autism and aspergers, treating those with this unique cluster of characteristics as normal in the context of their unique organizational structures. The word “healthy” seems rarely assigned to Aspergers and autism as parents and practitioners wrestle with its confounding aspects. Not understanding their etiology at the same time that so many feel helpless to address the condition’s debilitations places people in a position of assigning Aspergers and autism a label suggesting defect.

We need more people with Aspergers and autism to write and talk about their experience providing windows into their unique world view. Humanizing the condition perhaps will strip of people’s tendencies to make it something wrong.

Psychologist Laurent Mottron of Hôpital Rivière-des-Prairies in Montreal is quoted in a recent Science News article on a coming paper on analogic thinking autistic children. He notes studies that the autistic display intuition regarding geometric pattern rules. This is important in the context of the autistic often displaying difficulties with sociality (theory of mind), compulsive behavior and commitment to routine, and difficulties thinking symbolically or using analogy.

Mottron notes circumstances where the autistic do seem capable of parsing out relationships displaying an understanding of how one thing can represent another.

Thinking evolutionarily, consider our species just before, during and after the transition to spoken language from non speech communication, and consider each individual wrestling with the an ability to think in a fashion that suggests being two places at once, two times at once, with an ability to think of something’s opposite. This is an ability to exercise a “conscious” mind contrasted with thinking like an “unconscious” mind. One time, one place, no opposites is Freud’s definition of primary process or the way that a small child, an unconscious, a dreaming conscious, or an animal thinks.

Mottron may be teasing out the capabilities of the autistic to think is fashions familiar to most of us. The autistic may not be impaired as much as they are anachronistic, neurologies appearing in an unfamiliar time. Time will tell.

An article in Science News yesterday that described work by two different studies that offered new information about autism.

Kinga Morsanyi of the UK and Keith Holyoak of L.A. report in a not yet published paper in Developmental Science that autistic children can think analogically, able to compare and recognize relationships when presented in a visual format.

“Our findings indicate that the basic ability to reason analogically is intact in autism,” notes Morsanyi

The article notes that in this study of 23 children with autism none had larger than normal brains. Psychologist Uta Frith, noting that approximately one fourth of autistic children have large brains, suggests that among this group a compulsive attention to detail makes for compromised analogic thinking, visual or verbal.

This single article suggests several issues. First, are analogical proclivities related to brain size? Second, to what degree is symbolic thinking among the autistic inhibited in the areas that information is perceived, processed or communicated? Perhaps the autistic are mostly compromised by a auditory or language derived information, than content that is visually provided. Third, if larger brained autistic can be clearly defined by features different that non larger brained autistic, maybe different etiologies can be teased out by the different assortment of clues.

I post every week day at neoteny.org, about three months after the composition of a piece. Everything goes through an editor first, unlike what appears here.

I am excited. I typed words yesterday which felt significant…

If heterochrony is the study of the rates and timing of maturation with testosterone levels impacting rate and estrogen levels controlling timing, then those environmental or social structure adjustments that influence levels of testosterone and estrogen determine the speed, timing, features and direction of evolution.

This feels integral to understanding autism. It seems possible that by exploring both testosterone and estrogen levels, we may uncover the key to how autism emerges in many individuals.

Today I saw a report describing a new study to release that focuses on 27 genes possibly contributing to autism. Sex steroid hormones are part of the focus of the study. Bhismadev Chakrabarti and Simon Baron-Cohen are two of the authors of the study.

“The team carried out 2 experiments. First they looked at these genes in 349 adults in the general population, all of whom had filled in the Autism Spectrum Quotient (AQ) as a measure of autistic traits, and the Empathy Quotient (EQ) as a measure of empathy. Secondly, they looked at 174 adults with a formal diagnosis of AS, and compared them to controls.” The Medical News reports.

I don’t often see estrogen emerge as a contender for contributors to autism. I’m not absolutely that is the case here, but there is that potential. But, as noted here and here, I’m playing with that notion.

The question is, if testosterone controls the rate of maturation, does estrogen manage the timing. If so, might autism be some explained?

Releasing today are articles focusing on a new study that supports the hypothesis that children of a mother with diabetes 1, rheumatoid arthritis or celiac disease are three times more likely to have autism.

These conjectures first emerged in Norman Geschwind and Albert Galaburda’s Cerebral Lateralization in 1987, and papers published earlier that decade. A number of studies have been published since, some supporting, some not supporting their hypothesis that there is a connection between cerebral lateralization, testosterone levels, and specific diseases and conditions.

What strikes me is the connection between this work and the recent conclusions formed by C. W. Kuzawa at Northwestern. The connection is, ontogeny is influenced by the environment. The mother predisposed to particular hormonal states by autoimmune diseases are vulnerable to specific environmental inflences.

The missing piece is what the nineteenth century evolutionary theorists called orthogenesis, or the particular ontogenetic evolutionary trajectories that might follow these kinds of hereditary plus environmental effects. Consider that autism is an evolutionary condition. Consider what might propel such changes, dynamics other than natural selection.

An article came out yesterday that described a study that concluded that autism has one vs. two neurotypical kinds of laughter. In an April posting I was exploring potential differences between autistic vs. non autistic humor. The article that came out yesterday concluded that the autistic engage in only voiced, but not non voiced laughter.

Voiced vs. non voiced consonants are a central focus of linguistics. Chomsky inspired perspectives, currently supported by such writers as Steven Pinker, conclude that language shows no sighs of evolving from society to society insofar as language reflects a change in theory of mind or evolution of mind. Chomsky’s theory of generative grammar posits that we are hard wired or genetically predisposed to learn and use language in the way that we do.

In other pieces I suggest that we might be able to trace a portion of our evolutionary journey by exploring differences in the language structure of aboriginal matrifocal vs. modern langauge groups. The same might apply to exploring the specific differences in the autistic laugh. Perhaps voiced vs. non voiced language use is a signal that correlates with particularly ancient vs non ancient language structures. Are there more used of voiced consonants in aboriginal matrifocal societies?

I saw an article this morning referring to a study that suggests those with autism are faster at some forms of problem solving.

It would be interesting now if people with larger corpus callosums with a right cerebral hemisphere that had not been pruned in early childhood (with both hemispheres the same size) perform similarly to the people that are autistic in this study.

This reminds me of the studies regarding Tourette’s syndrome that note an often astonishing speed of reflex for people with that condition.

Posted a piece today, Estrogen, Puberty and Autism, that explores estrogen as a possible influence on the timing of maturation complementing testosterone which may control the rate. The implication is that estrogen levels may influence the emergence of autism, if estrogen effects the timing of testosterone surges resulting in the pruning of cerebral synapses.

Visit this piece for details.

I’m a newcomer in that world of people seeking to understand autism. About eleven years ago I tripped into it while exploring the possible repercussions of a theory of human evolution that presupposed we evolved from matrifocal social structures. The theory predicted a group of people with large brains and difficulty speaking. Ever since I’ve been exploring the connections between this alternative theory of evolution and conditions characterized by the possible emergence of features of ancient matrifocal aboriginal societies.

I continue to be astonished by the work of Simon Baron-Cohen. It’s not just his studies that are superb. As an advocate for the autistic, he reveals a deep respect, almost reverence for those whose lives are effected by the condition. It seems rare that a single academic reveals intelligence, compassion and common sense. Jane Goodall and her work comes to mind.

Over and over I read about practitioners and studies that forget that we are the middle of a mystery. Fear and ego seem to drive no small part of the discussion regarding autism and Aspergers. Baron-Cohen’s contribution offers calm.

In the last few days a number of articles and blog postings have been discussing a recent study that provides gene support for why more boys than girls get autism. There are a number of studies being conducted that focus on a genetic cause.

From my perspective, genes are part of the equation of what causes autism. Still, exploring autism’s evolutionary origins seems more on target. At some level there is no difference between the two. The question is which research path offers the most useful interventions.

I posted a piece today titled, Aboriginal Primary Process and Contemporary Autism. The short essay suggests that the Freudian concept of primary process, applied to particular features of aboriginal matrifocal societies, might provide us some understanding of how autism comes about in modern society. There may be a connection. The connection has to do with understanding how society evolves.

Investigating the neurological and hormonal similarities between matrifocal aboriginals and families of autistics would be a place to consider conducting an exploration.

I just noted an article about bad handwriting with autistic spectrum kids. My father is ambidextrous and has terrible hand writing. My handwriting was always the worst thing I got grades in….

…unless I drew my words. If I wrote while thinking I was drawing, my handwriting comes out unique and pretty. In addition, I could write almost as well with my left hand if I was also “drawing” the letters rather than writing them.

I’m not sure what this means as regards autistic spectrum, but perhaps a shift to visual from symbolic provides leverage as regards communication. This may have something to do why gesture is easier and faster to pick up than speech. Then there is the theory that gesture preceded speech, which seems very possible to me.

I noticed a piece appearing yesterday, Autism in California increases twelvefold.

In this short essay I described hypothetical repercussion of a resurgence of matrifocal values. Males formerly shut out of the procreation pool, those with Asperger tendencies and an affiliation with compulsive pattern replication and non conventional social skills become highly valued in a world where computer programming is a highly desired talent and a macho high testosterone mating strategy becomes less important than a man that won’t inhibit a woman’s ambitions.

California seems a window into the future, not unlike Scandinavia. 1960’s waves of hippiedom suggesting that the laid back male was an acceptable mate has evolved into the Sillicon Valley unconventional at-home-with-the-abstract male working overtime to achieve material success.

A question is whether the evident increase in autism in California is a suggestion of things to come across the country.

I seem to often come across references to studies that observe that there is an increase in autism in children that are first born and children born of older mothers.

This leaves me with several questions.

Is there a clear exponential increase in the likelihood of autism in only children born later and later? Many parents would have an autistic child and then hesitate to have another child influencing the numbers.

As far fetched as this sounds, when children are adopted, does this same pattern apply of first born and older mother’s having autistic children? I can’t imagine this to be the case, but an answer might be interesting.

It is possible that there is a different etiology for younger mother’s with first born children having autism and older mothers having autistic children. I would guess that younger mothers might reveal causes related to stress factors or maybe lifestyle impacts that would influence testosterone levels. Do the specific features of an autistic child of a younger mother differ from the specific features of an autistic child born of an older mother? What of a mother who has her first child when she is older?

Opportunities to break out variations in autistic features in association with particular conditions would be useful in hypothesizing autism’s causes.

An Article appeared in Scientific American yesterday that’s been picked up here and here titled, What If Vitamin D Deficiency Is a Cause of Autism?

Consider that the amount of sunlight does influence the emergence of autism. Instead of Vitamin D, which does not influence maturation rates that I am aware of, light influences the pineal gland which moderates melatonin levels influencing testosterone levels that impact maturation rates.

Autism is a condition characterized by variation in maturation rate.

In the stories I’ve read so far regarding Vitamin D as a cause of Somali autism, there has been no attention to season of birth effects. Clearly, the births of autistic children should be congregating in certain months if the Vitamin D or pineal/melatonin conjectures are potentially useful.

In addition, the diet of Minnesota and Swedish Somalis may be radically shifting a mother’s hormonal levels with increases of both testosterone and estrogen if she puts on weight. This could influence the rate and timing of the maturation of her children.

Perhaps Somali and Swedish autism is caused by a combination of fluctuations in light and radical changes in diet.

Complicating discussions of autism is controversy around the number of children that are subject to this condition. (Click here) It is not clear how fast autism and related conditions are growing with some professionals stating that better diagnosis is increasing numbers vs. others that show autism is growing fast.

There also seems to be regional variations, differences among ethnicities and different percentages in different societies.

Autism does not seem to have just one cause or etiology. Still, issues associated with maturational delay and acceleration seems to be closely connected to the condition. Maybe it is not by chance that there also seems to be an increase in left handedness over the last few decades, though this also is a feature influenced by how the condition is measured. Left handedness is closely associated with issues around maturation.

Perhaps we can understand autism better if we pay closer attention to the conditions that encourage changes in maturation rate. This would include handedness, pubertal onset, the timing of infant and toddler synapse pruning and the influences of mothers uterine testosterone and estrogen levels on the rate and timing of maturation.

In other words, changes in the numbers of children diagnosed with autism might be usefully informed by an exploration of related conditions and what might contribute to changes in maturation rates and timing.

In late January, I noted comments popping up around the web regarding a study that had just come out…

“Positive Screening on the Modified Checklist for Autism in Toddlers (M-CHAT) in Extremely Low Gestational Age Newborns” by Karl C. K. Kuban, MD, SM, Epi, T. Michael O’Shea, MD, MPH, Elizabeth N. Alfred, MS, Helen Tager-Flusberg, PhD, Donald J. Goldstein, PhD, Alan Leviton, M, DOI: 10.1016/j.jpeds.2008.10.011.

…that concluded that very premature infants showed increased likelihood for becoming autistic. If maturation rates are set by a mother’s testosterone levels around six weeks before birth, and a child emerges before that crucial ontological epigenetic day, then it seems to me that the child will likely emerge with radical maturation rate repercussions.

I would want to know what other conditions besides autism those children might exhibit, and what diseases they are likely to contract. Do some of the children emerge maturational accelerated? Are there cerebral lateralization repercussions? Using Annett’s peg tests, do the children born that premature show signs of both extreme left-handedness and extreme right-handedness?

If, indeed, these children tend to polarize, does it seem like they do so randomly or are there perhaps other factors that emerge, influencing their rates of maturation when the primary trigger is absent?

Then there are the issues that revolve around estrogen. There have not been studies conducted to determine if estrogen levels are also established by a mother’s uterine estrogen levels. If so, do extremely premature infants exhibit estrogen-related maladies such as breast cancer in higher proportion? Hypothesizing personality markers for extremely high and low estrogen in males and females, what might be the evidence that these extremely premature individuals are experiencing the estrogen equivalent of testosterone influencing maturational delay and acceleration?

It seems to me that detailed studies exploring the diseases, conditions, personalities, handedness propensities, cerebral lateralization, talents and skills of people born very premature might shed light on the influence of testosterone and estrogen, using an epigenetic model.

It would also be interesting to see if these features carry forward to future generations.

Politics and Science ally themselves in ways that are not useful to those seeking an answer to the causes of autism. Darwin wrote three books proposing three different theories of evolution. Darwin’s theory of natural selection we know best. Sexual selection is growing in influence. Pangenesis has been disappeared.

 Pangenesis was Darwin’s attempt to understand how he observed the environment to influence evolution in a single generation. Jean-Baptiste Lamarck was a French evolutionary theorist from earlier in Darwin’s century that pioneered the premise that the engine of evolution was the use and disuse of particular organs or features, and that the environment could influence changes. By late in Darwin’s life, evolutionary theory had polarized such that Larmarckian and natural selection paradigms were considered opponent frames of reference. Darwin, when describing his “Larmarckian” ideas when discussing pangenesis did not use Lamarck’s names or cite Lamarck’s followers.

 Natural selection won the debate. Mendelian genetics in combination with a deep respect for the elegance of the natural selection solution suggested the Lamarckian solution was an unnecessary embellishment to an explanation of how evolution unfolds. The Lamarckian theories were never disproved. They just seemed unnecessary. It is rare you find Darwin’s Lamarckism discussed when his theories are reviewed.

 What does this have to do with autism?

 Darwin’s theory of natural selection is a theory that reflects a “might makes right” patrifocal societal interpretation of how human society unfolds. Natural selection supports a highly stratified view of how society most efficiently operates. In the West, it is believed by many that by encouraging “the survival of the fittest” a society stokes innovation with wealth tricking down to those with less useful gifts. We believe the horizontal cooperative interconnection between individuals and the influence of the environment are far less important regarding evolutionary processes than what it takes to reach procreation age and have progeny.

 The Variation of Animals and Plants Under Domestication is Darwin’s work exploring how he believes the environment influences evolution in a single generation. It is a work that suggests how autism can be explained.

 All that’s stopping us from making the connection is the political allegiance to the concept that societal success is a function of individual survival. We in the West adore this myth. It obfuscates our ability to see autism as an evolutionary condition. Autism is not about natural selection.

 I saw an article yesterday in The Canary Report that connects autism to environmental pollution. Several studies have been released lately connecting autism to various environmental effects including linoleum floors, rainy climes and cooler climates. The environment is being considered closely as effecting the autism. Only, we have no explanatory paradigm to evolutionarily connect the dots.

 We might begin with how our beliefs influence what we can know. Our politics are dedicated to the drama of resource control with the savvy few controlling the less lucky many. Our science reflects this story line when it embraces theories that emphase struggle over cooperation. If autism is revealed to emerge as a result of both environmental and heredity factors, then perhaps we should explore the stories we tell ourselves that makes it so difficult to see how genes and the environment cooperate to achieve what we become.

 Evolutionary developmental biology offers an epigenetic or heredity plus environment point of view. Recent discoveries in neuropsychology suggest that the environment influences hormone levels that in turn influence the rate and timing of maturational delay.

 Autism is all about the rate and timing of maturational delay.

 Maybe with a different way of looking at how society unfolds we’ll be able to interpret information that suggests that evolution and autism have little to do with stories and theories of competition.

Sometimes theories or cuisines go out of style. It is not because they failed or tasted bad. They just didn’t fit the contemporary trends.

 A story in the NY Times today (click here) describes the difficulty researchers and theorists are having finding cures to diseases with a genetic component. It was more complicated than they thought.

 A blog post today (click here) notes evident increases in autism when there are toxins, such as toxic waste dumps, close to where children live.

 When the mid twentieth century Darwinian synthesis occurred several other theories of evolution were moved to the back burner or removed from the kitchen altogether. Sexual selection has seen a resurgence over the last generations. Evolutionary developmental biology has offered insights into the effects of the environment upon our genetics, a concept even Darwin embraced when he discussed the theory he called pangenesis.

 The answer to what causes autism may have much to do with theories of evolution that were rejected when we worshiped Occam’s razor and selected a theory that fit the criteria of least complicated to achieve a desired goal. Yet, as we’re discovering now, it’s complicated. Perhaps a theory, the theory of natural selection, that appeals to our reductionist compulsions is not the right theory.

 Particularly when it comes to autism.

 Consider a theory, heterochronic theory, that specializes in what causes maturational delay. Autism is a condition the revolves around changes in the rate and timing of maturation. Let’s bring heterochronic theory back into the kitchen and start cooking with spices not tasted since the 1800’s. 

Autism being the name for the way a condition looks and behaves, not its cause, creates numerous communication problems and misunderstandings.

First, when discussing the condition, it is often not said that any given discussion is in a context of their being several causes. This creates miscommunications. Language tends to make fundamentalists of users when one word is all we have for several things. Autism is a pluralist’s condition.

Second, in those cases where environmental effects contribute to its manifestation, there may be several different environmental effects. A relatively obscure possible cause, such as vaccines, may be a cause in relatively rare situations. It’s difficult to rule causes out when you don’t know the etiology. This is particularly true with a multi-cause condition. This ambiguity polarizes proponents of particular theories.

I guess a question I have is, which particular hypothesized causes of autism influence a mother’s uterine testosterone and estrogen levels, or the hormone levels of the young children that shows symptoms?