Betreff: Autism/em bits
Von: Mobile phone mast network
Datum: Sat, 27 May 2006 00:21:45 +0100

For more avid readers: not answers so much as pointers that are all part of the big picture. If the indications are right that EMFs disrupt nitric oxide synthase, then it does help explain the rise in such disorders as autism.
from Andy
Lots about autism, some EMR but not directly NO or oxytocin.
Med Hypotheses. 2006 Mar 9; [Epub ahead of print]

Out of time: A possible link between mirror neurons, autism and electromagnetic radiation.

Thornton IM.

Psychology Department, University of Wales Swansea, Singleton Park, Swansea SA2 8PP, Wales, UK.

Recent evidence suggests a link between autism and the human mirror neuron system. In this paper, I argue that temporal disruption from the environment may play an important role in the observed mirror neuron dysfunction, leading in turn to the pattern of deficits associated with autism. I suggest that the developing nervous system of an infant may be particularly prone to temporal noise that can interfere with the initial calibration of brain networks such as the mirror neuron system. The most likely source of temporal noise in the environment is artificially generated electromagnetic radiation. To date, there has been little evidence that electromagnetic radiation poses a direct biological hazard. It is clear, however, that time-varying electromagnetic waves have the potential to temporally modulate the nervous system, particularly when populations of neurons are required to act together. This modulation may be completely harmless for the fully developed nervous system of an adult. For an infant, this same temporal disruption might act to severely delay or disrupt vital calibration processes.
(and select the link for related articles as well)

Research report  / 1999:20

Deficient Synthesis of Nitric Oxide - a Candidate for an Etiology for Autism

FöRFATTARE: Gustafsson, Lennart

DATUM: 1999-11-01

INSTITUTION: Systemteknik / Industriell elektronik


It is commonly accepted that the autistic syndromes are caused by neurological dysfunctions. Hermelin's observations of information processing dysfunctions in autism and Frith's theory of a lack of drive for central coherence delineate essential cognitive characteristics in autism. Inadequate cortical feature maps has been proposed as a neural-level theory of autism. The consequences of this theory are in agreement with Hermelin's observations and Frith's theory. In this paper it is argued that deficient synthesis of nitric oxide will cause inadequate cortical feature maps and also will result in impaired learning in cerebellum and hippocampus. Deficient synthesis of nitric oxide will also cause some specific characteristics, observed in autism. It is proposed that deficient synthesis from neuronal Nitric Oxide Synthase is most likely involved.

ISSN 1402-1528 / ISRN LTU-FR--99/20--SE / NR 1999:20

Clin Chim Acta. 2003 May;331(1-2):111-7.

Changes in nitric oxide levels and antioxidant enzyme activities may have a role in the pathophysiological mechanisms involved in autism.

Sogut S, Zoroglu SS, Ozyurt H, Yilmaz HR, Ozugurlu F, Sivasli E, Yetkin O, Yanik M, Tutkun H, Savas HA, Tarakcioglu M, Akyol O.

Department of Biochemistry, Faculty of Medicine, Inonu University, Pasakosku Mahallesi 11, Sok. Ozkaracalar Apt. No: 42/4, Malatya 44200, Turkey.

BACKGROUND: There is evidence that oxygen free radicals play an important role in the pathophysiology of many neuropsychiatric disorders. Although it has not been investigated yet, several recent studies proposed that nitric oxide (NO) and other parameters related to oxidative stress may have a pathophysiological role in autism. METHODS: We assessed the changes in superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) activities and thiobarbituric acid-reactive substances (TBARS) levels in plasma as well as NO levels in red blood cells (RBC) in patients with autism (n=27) compared to age- and sex-matched normal controls (n=30). RESULTS: In the autistic group, increased RBC NO levels (p<0.0001) and plasma GSH-Px activity (p<0.0001) and unchanged plasma TBARS levels and SOD activity were detected. CONCLUSIONS: These findings indicate a possible role of increased oxidative stress and altered enzymatic antioxidants, both of which may be relevant to the pathophysiology of autism.

Cell Biochem Funct. 2003 Mar;21(1):55-60

Pathophysiological role of nitric oxide and adrenomedullin in autism.

Zoroglu SS, Yurekli M, Meram I, Sogut S, Tutkun H, Yetkin O, Sivasli E, Savas HA, Yanik M, Herken H, Akyol O.

Department of Child and Adolescent Psychiatry, Gaziantep University Medical School, Gaziantep, Turkey.

Several studies indicate that nitric oxide (NO) is involved in the aetiopathogenesis of many neuropsychiatric disorders such as schizophrenia, bipolar disorder, depression, Alzheimer's disease, Hungtington disease and stroke. Although it has not been investigated yet, several recent studies proposed that NO may have a pathophysiological role in autism. Adrenomedullin (AM), a recently discovered 52-amino acid peptide hormone, induces vasorelaxation by activating adenylate cyclase and also by stimulating NO release. AM immune reactivity is present in the brain consistent with a role as a neurotransmitter. It has been stated that NO and AM do function in the regulation of many neurodevelopmental processes. We hypothesized that NO and AM activities have been affected in autistic patients and aimed to examine these molecules. Twenty-six autistic patients and 22 healthy control subjects were included in this study. AM and total nitrite (a metabolite of NO) levels have been measured in plasma. The mean values of plasma total nitrite and AM levels in the autistic group were significantly higher than control values, respectively (p < 0.001, p = 0.028). There is no correlation between total nitrite and AM levels (r = 0.11, p = 0.31). Certainly, this subject needs much further research investigating autistic patients in earlier periods of life and with subtypes of the disorder.


Remember the fuss over autism and the MMR vaccine? Some put it down to mercury as a preservative.

H2 Oxidation of Proteins

Oral: July 4 2005 15:30-18:30, Room 2a and optionally Room 2b

Poster: July 4 13:30-15:30, Building-A, Section-5

H2-017P - Poster presentation

L-Glutamine effect on liver citrulline level

J. I. Nikolic1, D. T. Sokolovic1 and B. J. Djindjic2

1Department of Biochemistry, University of Nis, Nis, Serbia and Montenegro, 2Department of Pathological Physiology, University of Nis, Nis, Serbia and Montenegro. E-mail:

Trauma, systemic inflamation, sepsis or toxins can modulate tissue functions. Glutamine has been shown to have beneficial effects in sepsis, trauma, infections, chemotherapy etc. The aim of this study was to investigate the possible beneficial effect of L-glutamine on acute hepatotoxicity induced by mercury chloride (HgCl2). To study possible role of nitric oxide in mechanisms toxicity of mercury chloride we have study interaction between L-Glutamine and nitric oxide synthesis in tissue metabolism. Male Spraque Dawley rats weighing about 200 g. were used in the experiment. Acute toxicity was induced by i.p administration of mercury chloride in a dose of 3mg/kg. One group of animals was pretreated with L-glutamine (200 mg/kg) 1 hour before mercury chloride administration. Control group of animals was treated with equal volume of saline. The animals were killed 24 hours after HgCl2 administration. The level of citrulline, by product in nitric oxide synthesis, was measured by diacetylmonoxime reaction. Results of the study show that acute toxicity of mercury chloride leads to elevation of tissue level of citrulline compared to control group (p<0.01). Administration of glutamine to control rats decreases slowly citrulline level compared to control, while pretreatment of animals with Glutamine before mercury chloride administration leads to the most greater decreases in citrulline level (p< 0.01). Bearing in mind that overproduction of nitric oxide has cytotoxic effects administration of L-Glutamine may be beneficial in mercury toxicity through decreasing nitric oxide level.


NO plays a role in brain neurogenesis too:

PNAS | August 5, 2003 | vol. 100 | no. 16 | 9566-9571


Nitric oxide negatively regulates mammalian adult neurogenesis

Yes, there is a role for oxytoicin in autism:
(never realised the role of oxytocin! :
but note also that the role is co-related with vasopressin, which takes us back to NO as a mediator with this in vasodilation (about which there is much).
so here:
 Neuroreport. 2005 Mar 15;16(4):413-7.
Effects of nitric oxide synthase isoform deletion on oxytocin and vasopressin messenger RNA in mouse hypothalamus.

Nomura M, Tsutsui M, Shimokawa H, Fujimoto N, Ueta Y, Morishita T, Yanagihara N, Matsumoto T.

Department of Urology, School of Medicine, University of Occupational and Environmental Health, Kitakyushu 807-8555, Japan.

The effects of neuronal, endothelial, or inducible nitric oxide synthase gene disruption on the expression of oxytocin and vasopressin gene were examined in the hypothalamus (paraventricular, supraoptic, suprachiasmatic, and anterior commissural nuclei) and extrahypothalamus (bed nucleus of the stria terminalis). The oxytocin messenger RNA levels in the anterior commissural nucleus of neuronal nitric oxide synthase knockout mice were significantly higher than in control mice, but not in endothelial or inducible nitric oxide synthase knockout mice. In contrast, no significant effects of neuronal, endothelial, or inducible nitric oxide synthase gene disruption on oxytocin and vasopressin messenger RNA levels in the other hypothalamic and extrahypothalamic nuclei were observed. These results suggest that neuronal nitric-oxide-synthase-derived nitric oxide may be involved in the regulation of oxytocin gene expression in the anterior commissural nucleus.
----- Original Message -----
From: Mobile phone mast network
Sent: Friday, May 26, 2006 8:49 PM
Subject: [Masts] autism/em bits

Medical hypothesis -
A possible link between mirror neurons, autism and electromagnetic radiation
Possible assoc. between autism and foetal/neo-natal exposure to em fields (Kane)  -
Firstenberg & Molloy on ES - autism incidence  -
Also -
from Catherine  (via artjar)