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Elevated urine levels of bufotenine in patients with autistic spectrum disorders

and schizophrenia.

Emanuele E, Colombo R, elli V, Brondino N, Marini M, Boso M, Barale F,

Politi P.

Department of Health Sciences, Section of Psychiatry, University of Pavia,

Pavia, Italy. enzo.em@...

Abstract

OBJECTIVE: Previous studies have suggested that the endogeneous psychotomimetic

molecule bufotenine (N-N-dimethyl-5-idroxytryptamine) may play a role in the

pathogenesis of severe mental disorders. The potential association of bufotenine

with the clinical features of autism and schizophrenia is not entirely

understood. In this study, we measured urinary levels of bufotenine in subjects

with autistic spectrum disorder (ASD), schizophrenia and healthy comparison

subjects free of psychiatric symptoms. We also sought to assess whether urine

concentrations of this molecule may be associated with the clinical

characteristics of psychiatric patients.

DESIGN: Urine bufotenine levels were measured using a high-performance liquid

chromatography-mass spectrometry (HPLC-MS) assay in young adults with severe ASD

(n=15), patients with schizophrenia (n=15), and healthy control subjects (n=18).

The Vineland Adaptive Behavior Scale was used to measure adaptive behaviors in

ASD individuals. The Brief Psychiatric Rating Scale (BPRS) was used for patients

with schizophrenia.

RESULTS: Urine bufotenine levels were significantly higher in ASD subjects (3.30

+/- 0.49 microg/L, p<0.05) and patients with schizophrenia (4.39 +/- 0.43

microg/L, p<0.001) compared with controls (1.53 +/- 0.30 microg/L). Among

patients with ASD, there was a significant positive correlation between urine

bufotenine and hyperactivity scores on the Vineland Adaptive Behavior Scale

(r=0.479, p<0.05). No other associations were detected.

CONCLUSIONS: Our results indicate that elevated urine levels of the endogeneous

psychotomimetic molecule bufotenine may play a role in ASD and schizophrenia,

and can be correlated with hyperactivity scores in autism.

PMID: 20150873 [PubMed - indexed for MEDLINE]

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>

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http://www.thepsychologist.org.uk/archive/archive_home.cfm?volumeID=22 & editionID\

=171 & ArticleID=1452

>

> By Selwyn, Tooting London

> 'The Psychologist' 2009

>

> The autism `trip' – a lifetime of altered perception?

> Following my son's diagnosis of autism some years ago, I have developed a

theory that I would like to share with readers and ask whether anyone has any

related evidence or would like to seek some.

>

> I published a paper on my theory with the National Autistic Society, and

delivered it at the NHS research conference Experimental Biology and the

Autistic Syndromes at Sunderland University.

>

> Many behavioural characteristics typical of autism closely parallel the

effects of psychoactive compounds such as LSD and mescaline. I believe that if

one were to be in a permanent state of altered perception, such as would be the

case if the brain was spontaneously producing an endogenous psychoactive

compound, you would effectively get the autistic state, which was why I called

the paper `The Trip of a Lifetime'.

>

> One of the most common findings in the biochemical makeup of autistic children

is the presence of high levels of bufotenin. Bufotenin is a minor metabolite of

tryptophan, the amino acid precursor of the neurotransmitter serotonin. Another

reason to suspect bufotenin is that the tryptophan molecule's structure is

`indole'; it is the only amino acid in the body to be so and shares this

characteristic with psychoactive compounds such as LSD and mescaline. It is, if

you like, the common `link' between the two states.

>

> Bufotenin levels are normally held in balance by monoamine oxidase (MAO). If,

however, MAO was inhibited, bufotenin levels could rise to a point where

concentrations become such that behaviour is affected and the subject

effectively begins to `trip'.

>

> This idea seems to be supported by recent research, published in New

Scientist, carried out by Dr Ira Cohen, a psychologist at New York's State

Institute for Basic Research in New York. Dr Cohen's research team has

identified a relationship between the more severely affected autistic boys in

their control group and a variation in the length of a control region at the

start of the MAO gene. The variation determines how much of the enzyme is

produced. Dr Cohen's work also seems to support the prevalence of autism in

males, inasmuch as boys have only one copy of the gene, because it is only found

on the X chromosome, while females of course have two.

>

> In summary I believe that we should be doing studies to confirm the presence

of bufotenin in both the autistic child and in their parents – this would be

relatively simple because it's detectable in urine – and then perhaps developing

a drug to block bufotenin receptor sites in the brain.

> Selwyn

> Tooting

> London

> SW17

>

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