some science today - autism

from FEAT:

Testosterone Levels May Cause Autism

Research links social skills to hormones in the womb
[By Robin McKie and Karen Gold in The Observer.]
http://click.topica.com/maaanxsaaSjcka4vAXvb/

Excess amounts of testosterone in mothers’ wombs may cause their babies to suffer autism in later life. This startling theory has been put forward by Cambridge scientists who have discovered that the hormone - which is primarily found in men, but also in low levels in women - is linked to children’s abilities to communicate and empathise with others.

As a result, scientists at the Cambridge Autism Research Centre are now preparing to launch a major study involving more than 3,000 children to establish testosterone’s links to autism or, in less extreme cases, to inabilities to socialise.

Their results may also provide crucial insights into the causes of autism’s recent dramatic rise in Britain. ‘The condition may simply be one end of a continuum,’ said project leader Professor Simon Baron-Cohen. ‘In other words, social skills may be like height. Some people are smaller than others. Then you get a cut-off point where you start to talk about dwarfism. The same may true of autism.’

If this is true, autism may represent one end of a continuum that separates different people’s ability to socialise, and that these differences are influenced by amounts of testosterone in their mothers’ wombs. The theory would also explain why boys tend to be worse than girls at socialising and why males are more than twice as likely as females to suffer from autism.

Around one child in 200 is now thought to be affected by the condition or a milder version known as Asperger’s syndrome. Victims have difficulties communicating ideas, in socialising, and with controlling their imaginations. As part of their investigation of the condition’s roots, the scientists - Baron-Cohen and Dr Svetlanka Lutchmaya, of the autism centre, and Dr Peter Raggatt, of Addenbrookes Hospital, Cambridge – used sophisticated new techniques to measure testosterone in samples of amniotic fluid taken from mothers during standard prenatal tests of babies.

‘All foetuses produce a surge of testosterone around eight weeks after conception,’ said Raggatt. ‘Much more is produced in boys, and this triggers the development of male sexual organs. However, some testosterone is also produced in female foetuses.’

In fact, the team found that some boy babies have relatively low levels of testosterone - below the average for girls - while some girl babies have relatively high levels, around average for boys. But what effects did these differences have later in life? To find out, the team tested each child using a series of different psychological tests - and discovered that a baby’s ability to maintain eye contact with a parent was linked to testosterone. Those who had experienced high testosterone in the womb tended to be poor at maintaining eye contact, a failing that typifies poor socialisers and communicators, and in severe cases, sufferers of autism.

In addition, the team found that elevated testosterone tended to produce children with the smallest vocabularies. By contrast, low testosterone babies were those who knew the greatest number of words. In between these extremes, there was a steady gradient in ability: as testosterone fell, social and communication skills increased.

Papers on their findings are to be published shortly in the Journal of Infant Behaviour. The Cambridge team point out that the hormone is known to stimulate the growth of the right-hand side of the brain. This may occur, they argue, at the expense of growth of the left-hand side - the brain hemisphere in which most of our language and social skills are thought to be stored.

Establishing such a connection will need further research, however, and the team is preparing to study a far larger sample of children: 3,000 as opposed to the 80 that have taken part in their studies so far. ‘I don’t think high testosterone on its own is the cause of autism,’ said Raggatt. ‘Other factors must be involved, otherwise virtually every male would suffer from the condition. ‘However, once we understand the hormone’s involvement, we will bE able to unravel the other causes, and discover which of those may be responsible for the condition’s increasing prevalence. Then we will be able to think about ways of alleviating the lives of sufferers.’

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Autism and Gastrointestinal Symptoms
Curr Gastroenterol Rep 2002 Jun;4(3):251-8
Horvath K, Perman JA.
Department of Pediatrics, University of Maryland School of Medicine,
22South Greene Street, N5W70, Box 140,
Baltimore, MD 21201-1595, USA.
E-mail:[email protected]

Autism is a collection of behavioral symptoms characterized by dysfunction in social interaction and communication in affected children. It is typically associated with restrictive, repetitive, and stereotypic behavior and manifests within the first 3 years of life. The cause of this disorder is not known.

Over the past decade, a significant upswing in research has occurred to examine the biologic basis of autism. Recent clinical studies have revealed a high prevalence of gastrointestinal symptoms, inflammation, and dysfunction in children with autism. Mild to moderate degrees of inflammation were found in both the upper and lower intestinal tract.

In addition, decreased sulfation capacity of the liver, pathologic intestinal permeability, increased secretory response to intravenous secretin injection, and decreased digestive enzyme activities were reported in many children with autism.

Treatment of digestive problems appears to have positive effects on autistic behavior. These new observations represent only a piece of the unsolved autism “puzzle” and should stimulate more research into the brain-gut connection.

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Autism and the Human Gut Microflora
[By Max Bingham,
Food Microbial Sciences Unit Science and Technology Centre, Earley Gate,
University of Reading, Whiteknights Road, Reading, Berkshire, UK. RG6 6BZ.]
http://click.topica.com/maaanxsaaSjcla4vAXvb/

Introduction Research to date has suggested that there may be a link between the development of autistic symptoms and an abnormal human gut microflora. It has been shown previously, that autistic subjects tend to exhibit an elevated level of yeasts (particularly Candida spp) (Shaw, Kassen & Chaves,1995) and/or certain gut anaerobes in their lower intestines.

Other reports have suggested that the onset of certain Autistic Spectrum Disorders may be related to the occurrence of otitis media (ear infections) (Kontstantareas &Homatidis, 1987) or maybe other typical childhood illnesses. It is common totreat this sort of infection with some sort of broad-spectrum antibiotic.

Intestinal overgrowth of yeast and certain anaerobic bacteria are a well documented outcome of administration of broad spectrum antibiotics (Kennedy& Volz, 1983; Danna et al, 1991; Ostfield et al, 1977; Kinsman et al, 1989;Van der Waaij, 1987; Samsonis et al, 1993, 1994a,b).

While the onset of otitis media/ other childhood illnesses and the occurrence of a yeast/ selected gut anaerobe overgrowth may not be the cause of autistic symptoms, it appears there may be a link. Products of the human gut microflora in relation to autism and its symptoms appear to have been largely ignored in the past.

However they appear to be relevant certainly in terms of yeast species and certain gut anaerobes. This report will outline the currently available evidence for a possible link between the development of autistic symptoms and abnormal human gut microflora.

It will consider the roles species may take in this development and consider methods currently available that may help treat these abnormalities and as a result help alleviate the severity of some symptoms seen in autism.

Report Continues at: http://click.topica.com/maaanxsaaSjcla4vAXvb/

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Tuberous Sclerosis and Autism

“Neuro-epileptic determinants of autism spectrum disorders in tuberous sclerosis complex.”

http://click.topica.com/maaanxsaaSjcKa4vAXvb/ds=12023313&dopt=Abstract

Bolton PF, Park RJ, Higgins JN, Griffiths PD, Pickles A.
Autism Research Centre, Developmental Psychiatry Section,
Addenbrooke’s Hospital Neuroradiology Department,
University of Cambridge, Section of Academic Radiology,
University of Sheffield and School of Epidemiology and Health Sciences,
University of Manchester, UK.

Tuberous sclerosis is one of the few established medical causes of autism spectrum disorder and is a unique neurogenetic model for testing theories about the brain basis of the syndrome.

We conducted a retrospective case study of the neuro-epileptic risk factors predisposing to autism spectrum disorder in individuals with tuberous sclerosis to test current neurobiological theories of autism spectrum disorder. We found that an autism spectrum disorder diagnosis was associated with the presence of cortical tubers in the temporal but not other lobes of the brain. Indeed, the presence of tubers in the temporal lobes appeared to be a necessary but not sufficient risk factor for the development of an autism spectrum disorder.

However, contrary to the predictions of some theories, the location of tubers in specific regions of the temporal lobe, such as the superior temporal gyrus or the right temporal lobe, did not determine which individuals with temporal lobe tubers developed an autism spectrum disorder. Instead, outcome was associated with various indices of epileptic activity including evidence of temporal lobe epileptiform discharges on EEG, the age to onset of seizures in the first 3 years of life and a history of infantile spasms.

The results indicated that individuals with tuberous sclerosis are at very high risk of developing an autism spectrum disorder when temporal lobe tubers are present and associated with temporal lobe epileptiform discharges and early-onset, persistent spasm-like seizures. These risk markers constitute useful clinical indicators of prognosis, but further research is required to identify the neurobiological mechanisms responsible for their association with outcome.

Most especially, it will be important to test whether, as the findings suggest, there is a critical early stage of brain maturation during which temporal lobe epilepsy perturbs the development of brain systems that underpin ‘social intelligence’ and possibly other cognitive skills, thereby inducing an autism spectrum disorder.

PMID: 12023313 [Pub Med - as supplied by publisher]