Hi CBS....Thanks for posting this interesting information about toxoplasmosis
I therefore thought that it would be interesting to add this review by Prandota who states that autism may be due to cerebral toxoplasmosis
Autism spectrum disorders may be due to cerebral toxoplasmosis associated with chronic neuroinflammation causing persistent hypercytokinemia that resulted in an increased lipid peroxidation, oxidative stress, and depressed metabolism of endogenous and exogenous substances
Joseph Prandota, a,
aDepartment of Social Pediatrics, Faculty of Health Sciences, University Medical School, 5 Bartla Street, 51-618 Wroclaw, Poland
Received 2 September 2009; accepted 15 September 2009. Available online 5 November 2009.
Worldwide, approximately 2 billion people are chronically infected with Toxoplasma gondii with largely yet unknown consequences. Patients with autism spectrum disorders (ASD) similarly as mice with chronic toxoplasmosis have persistent neuroinflammation, hypercytokinemia with hypermetabolism associated with enhanced lipid peroxidation, and extreme changes in the weight resulting in obesity or wasting. Data presented in this review suggest that environmental triggering factors such as pregnancy, viral/bacterial infections, vaccinations, medications, and other substances caused reactivation of latent cerebral toxoplasmosis because of changes in intensity of latent central nervous system T. gondii infection/inflammation and finally resulted in development of ASD. Examples of such environmental factors together with their respective biomarker abnormalities are: pregnancy (increased NO, IL-1, TNF-, IL-6, IL-10, prolactin; decreased IFN-, IL-12), neuroborreliosis (increased IL-1, sIL-1R2, TNF-, IFN-, IL-6, IL-10, IL-12, IL-18, transforming growth factor-1 (TGF-1)), viral infections (increased IL-1, IL-6, IL-8, TNF-, IFN-//, TGF-1), thimerosal (increased IL-5, IL-13; decreased IFN-, TNF-, IL-6, IL-12p70, NOS), and valproic acid (increased NO, reactive oxygen species; decreased TNF-, IL-6, IFN-). The imbalances in pro- and antiinflammatory processes could markedly hinder host defense mechanisms important for immune control of the parasite, such as the production of NO, cytokines, and reactive oxygen/nitrogen species, tryptophan degradation by indoleamine 2,3-dioxygenase and/or tryptophan 2,3-dioxygenase, limitation of the availability of intracellular iron to T. gondii, and the mechanisms mediated by an IFN- responsive gene family. These fluctuations could result in a recurrent profuse multiplication of T. gondii in the brain associated with persistent neuroinflammation, chronic overproduction of pro- and antiinflammatory cytokines, and NO causing increased oxidative stress, and significantly depressed activity of several enzymes including cytochrome P450 monooxygenase family responsible for metabolism of physiological substrates and xenobiotics, such as steroids, fatty acids, prostaglandins, drugs, pollutants, and carcinogens, finally leading to development of ASD. This reasoning may be supported by such abnormal metabolic events as: (1) patients with ASD have significantly decreased melatonin levels caused by marked deficit in acetylserotonin methyltransferase activity, possibly resulting from maternal and/or fetal/postnatal overproduction of NO, characteristic for this clinical entity; (2) thimerosal inhibited both insulin-like growth factor-1- and dopamine-stimulated methylation reactions, and depressed methionine synthase activity, the metabolic events important for promoting normal neurodevelopment; (3) valproic acid, a strong histone deacetylase inhibitor, have potent anti-T. gondii activity. Thus, patients with ASD should be tested for T. gondii infection.
Keywords: Autistic spectrum disorders; Cerebral toxoplasmosis; Immune irregularities; Hypercytokinemia; Nitric oxide; Oxidative stress; Hypermetabolic state; Depressed enzyme activities
Article Outline continued @
I am starting this thread on toxoplasmosis
in the "General Treatment Section" because there does not appear to be a section on "infections," "co-infections," etc. I guess this could go under symptoms but what I want to talk about are verified (and suspected) cases of 'Toxo' infection.
Toxo infection is not uncommon but mine went out of control. Not sure why. Most likely immune suppression.
I don't know if it is reasonable to start a new section on infections but it doesn't seem crazy to do so if we have sections on all sorts of treatments (for what?). Cort?
So, back to Toxoplasmosis, the disease state caused by the parasite, toxoplasma gondii. This was the little bugger that supposedly kickoff the last 16 glorious years of CFS for me. Here's a link to the wikipedia entry on 'Toxo.'
And for those of you who find interesting and thoughtful scientists really interesting, here is a link to a fantastic discussion with Dr. Robert Sapolski (Stanford - Go Trees!) on parasitic (toxo) control of the hosts behavior and neurobiology: http://www.edge.org/3rd_culture/sapolsky09/sapolsky09_index.html
(also author of Why Zebras Don't Get Ulcers ) .
There is another video which has most of the same info but has pictures and is a bit easier for the not scientific community. I'll keep looking for it.
For those of you who are interested in all things amygdala, a lot of this is about toxo and it's fondness for the amygdala.
That said, I am hoping that we can keep this conversation focus on Toxo (and when appropriate, how Toxo relates to inhibition - the amygdala).
And if you watch the video, yes, I do find myself oddly attracted to cats!
I'll post my experience soon.
I'm also interested in the amygdala and you mention toxo and it's fondness for the amygdala which is also very interesting because the amygdala in toddlers with autism is 13 percent larger than unaffected kids
CNN) -- The size of a specific part of the brain may help experts pinpoint when autism could first develop, University of North Carolina researchers report.
The amygdala helps individuals process faces and emotions.
Using MRI brain scans, researchers found that the area of the brain called the amygdala was, on average, 13 percent larger in young children with autism, compared with control group of children without autism. In the study, published in the latest Archives of General Psychiatry, researchers scanned 50 toddlers with autism and 33 children without autism at age 2 and again at age 4. The study adjusted for age, sex and IQ.
"We believe that children with autism have normal-sized brains at birth but at some point, in the latter part of the first year of life, it [the amygdala] begins to grow in kids with autism. And this study gives us insight inside the underlying brain mechanism so we can design more rational interventions," said lead study author Dr. Joseph Piven.
"Many studies have observed the brain grows too big in kids with autism, but this study finds that by age 2, the amygdala is already bigger and stops growing," said Kosofsky. "So it tells us the critical difference has already developed. It now poses the question: Are children born with autism or does it develop in the first two years of life?"