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Autism and retroviruses...

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Autism has recently been associated with a virus, which brings to mind the somewhat frightening possibility that there are some researchers already working on a vaccine to prevent ... autism.

Cal Crilly isn't agreeing that XMRV is a causative agent for autism, any more than HIV has been shown to cause Aids. But then what is autism caused by. Cal has written up some more of his research ... as usual dense with relevant links. Let's follow him down the rabbit hole ...

Autism and retroviruses...

Well I wrote The Castle Wall Theory of Disease as it happened in my head knowing my net access was going to go at work and the computer at home died within the month.... And I've been too broke to afford a net cafe until now.

In the meantime I did the usual Cal Crilly search this week to see if I was getting abused by people like Todd Deshong and found that on the Age of Autism site someone read the Castle Wall Theory and made some sense of it.
The Whittemore-Peterson Institute - A Light in the Darkness (XMRV Update!!!)

So I will talk about XMRV and why it is like HIV and AIDS as in "NOT THE CAUSE" .....and is only a small part of the picture in Autism.

- - -

In the first place my ideas on methylation were originally learnt from Jill James who does fantastic work on why Mercury in vaccines causes hypomethylation and nerve degeneration etc.
Abnormal transmethylation/transsulfuration metabolism and DNA hypomethylation among parents of children with autism

Thimerosal neurotoxicity is associated with glutathione depletion: protection with glutathione precursors

Which is why a test of hers to measure Methylation gets a mention in my innovation patent.

The XMRV retrovirus turns up in epithelial cells which are cells that help to hold our inner organs in place.

XMRV is present in malignant prostatic epithelium and is associated with prostate cancer, especially high-grade tumors. Or in chronic fatigue patients who often have Fibromyalgia which is pain in muscles and connective tissue.

The human retrovirus XMRV in prostate cancer and chronic fatigue syndrome

So if connective tissue is being degraded what happens to the epithelial cells?

"Epithelium is a tissue composed of cells that line the cavities and surfaces of structures throughout the body. Many glands are also formed from epithelial tissue. It lies on top of connective tissue, and the two layers are separated by a basement membrane."

Because in Autism there are gut pathologies, in that the gut often has lesions and the gut has Epithelial cells which absorb nutrients.

"Absorption: Certain epithelial cells lining the small intestine absorb nutrients from the digestion of food."

"A primary intestinal lesion may occur as part of the broad spectrum of immunological disorders to which autistic children are prone. This could result in increased intestinal permeability to peptides of dietary origin which may then lead to disruption of neuroregulatory mechanisms required for normal brain development."

The intestinal lesion of autistic spectrum disorder

"Recent research has uncovered pathology in the gastrointestinal tract of autistic children. The pathology, reported to extend from the esophagus to the colon, is described here along with other studies pointing to a connection between diet and the severity of symptoms expressed in autism. The evidence that there is impaired intestinal permeability in autism is reviewed, and various theories are discussed by which a leaky gut could develop. Lastly, some possible ways in which impaired gastrointestinal function might influence brain function are discussed."

Intestinal Pathophysiology in Autism

Well if there are holes in the lining of the gut then there will be retroviruses present because the cell walls are crumbling and they are coming out. The XMRV retrovirus is more likely to be a side effect of cell damage.

The way I've started thinking about why retroviruses appear in certain cells is this: Upon cell death caused by DNA Hypomethylation, retroviruses come out and dismantle the dying cells. As there is an interplay normally between retroviruses and apoptotic dying cells when lab scientists expose healthy cells to retroviruses without the normal protections the cells take this as a signal to shut up shop. But the retroviruses also signal to cytokines which are growth hormones, to start regrowth. And retroviruses are also kicked into action by estrogen so why on earth would growth hormones make them transcribe? Because retroviruses are part and parcel of cell growth.

I'll use HERV-W as it's my favourite retrovirus as the example.

HERV-W is a retrovirus that appears at the interface of trophoblasts as they tunnel new arteries for the fetus to get blood supply. It appears with demethylation of placental tissue and then disappears with methylation.

If it's not working the blood supply doesn't get to the fetus and it doesn't happen.

"Development of placentation and successful pregnancy depend on co-ordinated interactions between the maternal decidua and myometrium, and the invasive properties of the fetal trophoblast. Syncytin, a protein encoded by the envelope gene of a recently identified human endogenous defective retrovirus, HERV-W, is highly expressed in placental tissue. Previously, we have shown that the major site of syncytin expression is the placental syncytiotrophoblast, a fused multinuclear syncytium originating from cytotrophoblast cells. Here we present the first evidence that in pre-eclampsia, syncytin gene expression levels are dramatically reduced."

Downregulation of Placental Syncytin Expression and Abnormal Protein Localization in Pre-eclampsia

Which is why antiretroviral AIDS drugs cause Preeclampsia.

Increased risk of pre-eclampsia and fetal death in HIV-infected pregnant women receiving highly active antiretroviral therapy

So women who are HIV positive and don't take drugs are likely to be healthier....
Someone out there is asking this question..

"There is uncertainty as to whether HIV lowers the rate of pre-eclampsia"

Is pre-eclampsia less common in patients with HIV/AIDS?

Therefore HERV-W is needed for fetal growth. But in Multiple Sclerosis it gets blamed for causing cytokines to gather and kill brain and nerve cells.

Brains and peripheral blood mononuclear cells of multiple sclerosis (MS) patients hyperexpress MS-associated retrovirus/HERV-W endogenous retrovirus, but not Human herpesvirus 6

Correlation between disease severity and in vitro cytokine production mediated by MSRV (Multiple Sclerosis associated RetroViral element) envelope protein in patients with multiple sclerosis

But HERV-W also signals a cytokine called Brain Derived Neurotrophic Factor which is needed for new cell growth....

"BDNF promoter reporter gene assays showed that the HERV-W env triggers BDNF"

Implication of the env Gene of the Human Endogenous Retrovirus W Family in the Expression of BDNF and DRD3 and Development of Recent-Onset Schizophrenia

"Brain-derived neurotrophic factor (BDNF) promotes neuronal survival and protection against neuronal damage."

And also appears in the placenta...

Brain-Derived Neurotrophic Factor Promotes Implantation and Subsequent Placental Development by Stimulating Trophoblast Cell Growth and Survival

So which comes first? The retroviruses or the cytokines which encourage growth. I don't have a lab and I wonder who's checking?

So in the case of autism do you now think XMRV is the cause or just an effect of epithelial cells getting damaged?

What can cause the damage?

Well I blame metals, mercury, cadmium and lead which are the usual culprits as they knock holes in our cell walls and then cells die and retroviruses come out.

The role of mercury and cadmium heavy metals in vascular disease, hypertension, coronary heart disease, and myocardial infarction

Cadmium and mercury toxicity in a human fetal hepatic cell line

And Iron is the other metal since there are gut pathologies, too much Iron is the main cause of infections in people.

"Iron is an oxidant as well as a nutrient for invading microbial and neoplastic cells. Excessive iron in specific tissues and cells (iron loading) promotes development of infection, neoplasia, cardiomyopathy, arthropathy, and various endocrine and possibly neurodegenerative disorders. To contain and detoxify the metal, hosts have evolved an iron withholding defense system, but the system can be compromised by numerous factors."

Iron Loading and Disease Surveillance

Which is also why someone said this.....

"Autism is a profoundly and poorly understood developmental disorder that impairs a person's social and communication abilities. I propose a hypothesis that the excessive dietary iron consumed by today's infants is the root cause of increased cases of Autism, allergies and other childhood diseases. Iron is a powerful immune system modulator. Excess iron causes hyperactive immune system. This hyperactive immune system attacks undigested food peptides. The chemicals released during these intense allergic reactions can damage surrounding tissue. Neurodegeneration is caused by combination of, oxidative stress induced by free iron radicals and intense immune reactions."

Excess dietary iron is the root cause for increase in childhood autism and allergies

What can cause the Iron to accumulate?

There are two factors I see, one is a missing methylation gene which brings us back to Jill James and her studies.

I'll thank Fred Greenwood for educating me on the issue this year, he's a 70 year old HIV+ who is missing the MTHFR1 gene which is needed to process folic acid. He tells me that the forms of Folic acid we take are unmethylated and possibly dangerous in that they can accelerate cancer growth. The gene is apparently missing in up to 20% of caucasians. And there's another called MTHFD1 which if not working means there's too much hypomethylation going on due to Folate and B12 loss.

An example of why proper methylation is needed in pregnancy...

A polymorphism in the MTHFD1 gene increases a mother's risk of having an unexplained second trimester pregnancy loss

So in the population of children without this gene any extra Iron can't be absorbed properly and it burns holes in the stomach and also causes the infections.

"New evidence suggests that autism may be associated with (a) varied behavioral responses to folate therapy and (b) metabolic anomalies, including those in folate metabolism, that contribute to hypomethylation of DNA."

The MTHFR 677C-->T polymorphism and behaviors in children with autism: exploratory genotype-phenotype correlations

Association of MTHFR Gene Variants with Autism

The other factor is gluten allergies. Gluten binds to people with HLA-DQ genes. When this happens they can react and the immune system then inflames gut tissue and the end result is malabsorption.

"Fifty-eight percent of the examined children with autism suffered from chronic diarrhea caused by malabsorption of carbohydrates."


Diarrhea by the way when I see it indicates high Iron feeding bacteria and not enough copper being absorbed to make cerulosplasmin. Which is why we see this happen in autism.

"Lipid peroxidation was found to be elevated in autism indicating that oxidative stress is increased in this disease. Levels of major antioxidant proteins namely, transferrin (iron-binding protein) and ceruloplasmin (copper-binding protein) in the serum, were significantly reduced in autistic children as compared to their developmentally normal non-autistic siblings. A striking correlation was observed between reduced levels of these proteins and loss of previously acquired language skills in children with autism. These results indicate altered regulation of transferrin and ceruloplasmin in autistic children who lose acquired language skills. It is suggested that such changes may lead to abnormal iron and copper metabolism in autism, and that increased oxidative stress may have pathological role in autism."

Oxidative stress in autism: increased lipid peroxidation and reduced serum levels of ceruloplasmin and transferrin--the antioxidant proteins

Which I would fix by making sure Folic acid, B12, and B6 with copper are available in foods with enough Vitamin C. I use Chlorella for the Folic and B12 as it's such a highly methylated food but also because it supplies bioavailable Iron with magnesium and also removes Mercury, Lead and Cadmium.

B6 or Pyridoxine should be given as a supplement at night to enable methylation.

Cashews can stop diarrhea simply due to their copper content. Very useful.

Cod Liver Oil is already being used in autistic children, the reason it may help is due to both Vit A which is needed for neuronal cell differentiation and the Vitamin D content.

Vitamin A or Retinoic Acid though is a natural hypomethylating agent and encourages retroviruses so I see it as vital for proper retroviral functioning and cell growth.

I also think Sialic acid may be needed to encourage nerve growth, it's a thing I tell people to avoid in cancer as it encourages growth.

If Gluten sensitivity is the cause of nutritional deficiencies and gut inflammation Bromelain can be used as it breaks down Gluten and stops cytokines attacking the gut. Bromelain also a nuclease inhibitor and is therefore an antiviral and antiretroviral if you are worried about retroviruses.

I know there is a huge movement of well educated mothers of autistic children who are already working these things out. Blaming the XMRV virus I think just clouds the issue.

.....But the Attenuated Measles Virus from the vaccine is still a prime candidate for causing autism.

Attenuated viruses are only attenuated in highly methylated tissue, if you add them to tissue that is hypomethylated they will start expressing again. Which involves autistic children.

Metabolic biomarkers of increased oxidative stress and impaired methylation capacity in children with autism

....And even normal children are likely to have hypomethylating tissue because they still are growing, this is why fetuses have a heap of retroviruses and why mothers at the end of pregnancy express the highest levels of abzymes in people.
In post pregnancy a women is shutting down their retroviruses.

"Blood of healthy male and female volunteers lacked catalytically active antibodies, whereas antibodies from blood of pregnant women hydrolyzed DNA and RNA and their relative activity varied over a wide range. Relative blood abzyme activities significantly increased after delivery and at the beginning of lactation. The highest abzyme activity was observed in blood of parturient women. Although the dynamics of changes in antibody DNase activity during pregnancy was rather individual for each woman, there was a common trend in the increase in antibody activity in the first and/or third trimester of the pregnancy. The DNase activity of IgG and IgM from blood of healthy pregnant women was 4-5 times less than that from pregnant women with pronounced autoimmune thyroiditis."

Dynamics of Antibody Nuclease Activity in Blood of Women during Pregnancy and Lactation

So here is an example of attenuation in one type of cell and expression in another

"Baby hamster kidney cells (BHK), a well-characterized, easily maintained cell line, supported MVA growth and as proficient expression of the E. coli lacZ reporter gene as the highly efficient CEF, whereas other cell lines were non-permissive or allowed only very limited MVA replication. Importantly, no virus production occurred in patient-derived infected primary human cells."

Highly attenuated modified vaccinia virus Ankara replicates in baby hamster kidney cells, a potential host for virus propagation, but not in various human transformed and primary cells

Baby cells are hypomethylated so the virus replicates, normal adult kidney cells don't produce the virus.

Another example.

"Measles virus (MV) isolated in B95a cells, a marmoset B-cell line, retains full pathogenicity for cynomolgus monkeys, while its derivative obtained by adaptation to the growth in Vero cells, a monkey kidney cell line, loses the pathogenic potential. Here, we show with a pair of strains, a fresh isolate (9301B) in B95a cells and its Vero cell-adapted form (9301V), that the in vivo attenuation parallels the decrease of replication and syncytium-inducing capabilities in the original B95a cells and that these in vitro phenotypes are attributable to impediment of transcription, which is already obvious at the level of primary transcription catalyzed by the virion-associated RNA polymerase. On the other hand, cell fusion assays detected no functional difference between the glycoproteins of the two viruses."

Measles Virus Attenuation Associated with Transcriptional Impediment and a Few Amino Acid Changes in the Polymerase and Accessory Proteins

This is why measles and cytomegalovirus appear in infancy, I think it has more to do with reproduction than infections. And using B95a cells which are monkey lymphoblastoid cells is a way to use hypomethylated cells to grow a virus. Vero kidney cells have already grown and are methylated. The concept really should put a stop to all attenuated viral vaccines in children.

This is why they say things like this....

"The modes of transmission of Cytomegalovirus from person to person are not completely understood."

The cytomegalovirus comes out of our reproductive tissue.

So the attenuated measles will become wild type and cause immense internal damage to children with low methylation nutrients before any antibodies can be formed.

This is why you get these sorts of effects...

"Several of these studies that used high-dose (4.84 In TCID50) EZ measles vaccine found increased mortality predominantly or exclusively among African female infants immunized with high-dose EZ measles vaccine. In these cases, death occurred approximately one year after vaccination."


In African children the lack of methylation nutrients leaves them wide open to RNA from 'attenuated' measles dismantling and damaging internal organs. I suspect that in areas too with very low Selenium soil levels will allow virus replication to go unchecked in people who don't get Selenium in their diet.

What they are in effect doing is giving measles to children to create antibodies. It would make far more sense to give children adequate Methylation nutrients to stop measles from causing damage anyway. As in children with proper methylation will not get the same symptoms.

This is why there will always be measles outbreaks whether vaccinated or not. You know the usual propaganda....

"The cause of a measles outbreak sweeping South Africa has not as yet been determined, but initial suspicions point to religious objections and unfounded fears that immunizations against the disease increase the risk of autism in children."

SOUTH AFRICA: Measles outbreak spreading

What I believe is that measles affects endothelial cells as normally happens and the symptoms of wild type infection can be seen externally. With the use of vaccine-delivered attenuated measles it infects epithelial cells internally and causes damage before antibodies are produced and it becomes inactivated. But they don't see these symptoms and so declare they've stopped an epidemic.

Of course I'm a tad more radical and suspect these viruses appear during pregnancy... hence the unknown source of cytomegalovirus and the mother's milk normally passes on abzymes to the infants which then provides a way of nicking and stopping any viral replication continuing in the child.

My thoughts.

"The Empire apple crumbles"

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Thanks, what Peter Tocci says about probiotic gut bacteria is spot on.

"A medical study on probiotics for autism has proven so successful that the study ‘failed’, according to a New Scientist report on September 9, 2006."

"The results were too obvious. Parents whose autistic children were taking the actual probiotics saw such great improvements in their children's behaviour that they knew their children were taking the real thing.

Thus, problems arose during the ‘crossover’ point of this probiotics for autism study, where the two groups were supposed to switch medicines. Many of the parents whose children were taking the actual probiotics refused to make the switch as they wanted their autistic children to continue their improvement."

I'm a Bechampist, simply because after having seen my skin get dissolved by my own cytokines years ago I discovered that the brickwork nutrients that hold our body together are also antivirals and antibacterials.

I feel like an engineer telling architects it won't matter what you're theories are and what drugs you design to fit your theories, these folk fall apart because the bricks aren't there.

This applies to all diseases.

Autism and AIDS are multifactorial syndromes, the retroviral explanations are far too narrow minded and send people barking up the wrong trees, they are indicators.

The reason I wrote this piece is because I can see where the "XMRV causes Autism" idea is going.

Once enough fear of this retrovirus has clouded everyone's thinking then some bright spark will suggest antiretrovirals.

"Xenotropic murine leukemia virus related virus (XMRV) has been implicated in prostate cancer and chronic fatigue syndrome (CFS). Because XMRV is a retrovirus, it has been suggested that it might be susceptible to some of the many drugs available for treatment of AIDS. Of ten licensed compounds evaluated for activity against XMRV, just one, AZT (azidothymidine), was found to inhibit viral replication."

"None of the HIV-1 protease inhibitors, NNRTI, or integrase inhibitors blocked XMRV replication. Of the NRTIs, only AZT significantly inhibited viral replication."

AZT inhibits XMRV

Well back in 1989 they tried AZT on HIV tagged children who had encephalopathy and possible autistic symptoms.

The effects of encephalopathy and AZT treatment on the social and emotional behavior of pediatric AIDS patients.

So how could AZT work? And remember this is a stab in the dark study, as in if you keep stabbing with AZT you'll kill the patient.

My first thought was that because AZT causes severe anemia it was removing iron?

Or because AZT causes global hypermethylation it had the effect of stopping hypomethylation?

The doses required to 'stop retroviruses' in the brain are too toxic anyway and AZT can't get into the brain to have that effect.

Then lately I found AZT removes sialic acid?

There is an increase of high sialic acid gangliosides in autism so sialic acid is not being used properly and may be clogging things.

The catch 22 here is that the proper utilization of sialic acid is needed to repair it all and AZT in the long run causes nerve degeneration and mental retardation in children.

AZT also cause mitochondrial dysfunction and anemia which will only make autism worse and over a million people have died on it so it's not an option.

"In particular, AZT-treated K562 cells exhibited a decreased incorporation of sialic acid (86% of control) into protein glycans"

"The ASD group had a significantly higher concentration of ganglioside GM1 compared with the comparison group."

Gangliosides in cerebrospinal fluid in children with autism spectrum disorders.

But Sialic acid is necessary for development.

"ganglioside-bound and protein-bound sialic acid concentrations were 32% and 22% higher, respectively, in the frontal cortex gray matter of breastfed infants than in that of formula-fed infants"

Brain ganglioside and glycoprotein sialic acid in breastfed compared with formula-fed infants

Salla disease which involves inability to absorb sialic acid has many symptoms of autism and some autistic children get this gene loss diagnosis.

Salla disease (SD), also called sialic acid storage disease

That's one angle but all of this keeps returning to high Homocysteine as is seen in many diseases and inability to aborb the methylation nutrients either from Coeliac disease or MTHFR gene problems making Folic acid and B12 unavailable to break down toxic levels of homocysteine or absorb iron.


Anti-ganglioside antibodies in children with coeliac disease: correlation with gluten-free diet and neurological complications

Cerebrospinal fluid antiganglioside antibodies in patients with AIDS

Celiac sprue, hyperhomocysteinemia, and MTHFR gene variants.

I'll use a case study to show the possible effects of losing the MRHFR gene....

"Although the neonatal period and early infancy were normal, at the age of 6 months, she presented with an acute encephalopathy and loss of psychomotor abilities, hypotonia, alternating esotropia, pseudo-ptosis and mental retardation. She later developed a cerebellar syndrome with prominent ataxia and action myoclonus. At 17 months, during gastroenteritis, she had a unilateral status epilepticus and lethargy lasting for 5 days. During infancy, she exhibited PFAPA syndrome (periodic fever, aphthous stomatitis, pharyngitis and adenitis); although these episodes occurred normally without worsening of the neurological problems, during one of them, she had encephalopathic symptoms and became lethargic with increased hypotonia for several days"

"Because of her occasional coagulation problems, bleeding or thrombosis, and the fluctuation of the coagulation parameters throughout development (protein C and protein S deficiency, decreased prothrombin time and coagulation factors), a wide study for ‘increased risk of thrombosis’ was performed. Although homocysteine, vitamin B12 and folic acid levels were normal, a heterozygous C677T mutation in the methylenetetrahydrofolate reductase (MTHFR) gene was found. The factor V Leiden and factor II mutations were absent.

Her father also has a very high level of plasma homocysteine, undetectable vitamin B12 levels, antibodies against intrinsic factor and incipient macrocitic anemia. He was diagnosed with a pernicious anemia. The mother is heterozygous for the C677T mutation in the MTHFR gene."

A new inborn error of glycosylation due to a Cog8 deficiency reveals a critical role for the Cog1–Cog8 interaction in COG complex formation

Scary stuff if it all gets missed and treated randomly with theoretical drug treatments because that's what most drugs are, new and unknown treatments.

I have to mention one more gene which also crosses over into all these diseases, in fact possible every disease, I went looking and found low paraoxonase levels in cancer, AIDS, autism, heart disease, all autoimmune diseases except perhaps psoriasis.

Polymorphism of apoprotein E (APOE), methylenetetrahydrofolate reductase (MTHFR) and paraoxonase (PON1) genes in patients with cerebrovascular disease.

Association of genetic variants in Methylenetetrahydrofolate Reductase and Paraoxonase-1 genes with homocysteine, folate and vitamin B12 in coronary artery disease

Well I've known about paraoxonase for a year or two because of this study in that if you can't make it organophosphates will cause brain damage.

"Organophosphates (OPs) are routinely used as pesticides in agriculture and as insecticides within the household. Our prior work on Reelin and APOE delineated a gene-environment interactive model of autism pathogenesis, whereby genetically vulnerable individuals prenatally exposed to OPs during critical periods in neurodevelopment could undergo altered neuronal migration, resulting in an autistic syndrome. Since household use of OPs is far greater in the USA than in Italy, this model was predicted to hold validity in North America, but not in Europe. Here, we indirectly test this hypothesis by assessing linkage/association between autism and variants of the paraoxonase gene (PON1) encoding paraoxonase, the enzyme responsible for OP detoxification."

with the chilling conclusion...

"These results are consistent with our model and provide further support for the hypothesis that concurrent genetic vulnerability and environmental OP exposure may possibly contribute to autism pathogenesis in a sizable subgroup of North American individuals."

Paraoxonase gene variants are associated with autism in North America, but not in Italy: possible regional specificity in gene-environment interactions.

Paraoxonase 1 activities and polymorphisms in autism spectrum disorders.

So what helps make paraoxonase?

Well homocysteine levels lower it so all the methylation nutrients suggested by people like Jill James work.

"Gene-nutrient interactions, folate and paraoxonase (PON)

Dr. Jakubowski reported recently that the enzyme Hcy thiolactonase, which hydrolyzes Hcy thiolactone to Hcy, could be in fact paraoxonase. If it is so, paraoxonase can hydrolyze Hcy thiolactone back to Hcy and Hcy may be then converted either back to methionine (by reaction which needs folate and vitamin B12 as co-factors), or condensed with serine to form cystathionine in a reaction that is dependent on vitamin B6 (transsulphuration pathway). In light of Dr Jakubowski's study, it is possible that folic acid supplementation or high folate intake decreases plasma tHcy (and plasma Hcy-thiolactone levels) and affects serum PON activity by this mechanism"

Folate and methionine intake, gene-nutrition interactions and homocysteine as CVD risk factor

Remember it has to be a methylated form of folic acid.

High levels of homocysteine and low serum paraoxonase 1 arylesterase activity in children with autism.

"Our results show that paraoxonase and arylesterase activities, which have antiatherogenic capability, are decreased in patients with iron deficiency anemia."

Assessment of paraoxonase and arylesterase activities in patients with iron deficiency anemia.

"Our results showed that significantly fewer biopsies expressed PON1 and PON3 in the duodenum of celiac patients"

Heavy metals deplete paraoxonase and copper is needed to produce it.

And also why I consider copper so important as it's needed to stop anemia and also stops bacterial infections if they occur.

"Lead intoxication has many manifestations, lesser-known of which is induction of copper deficiency. Rats deficient in copper have an approximately 28% decrease in paraoxonase activity. These observations are consonant with the decrease in superoxide dismutase (SOD) associated with occupational exposure to lead because this enzyme also depends on adequate copper nutriture for activity. Thus, SOD is an index of copper nutriture in humans.

Li et al. (2006) stated that “the mechanism by which heavy metals inhibit serum PON1 activity is still not clear.”
Copper Deficiency, Lead, and Paraoxonase

I'll put some of the study about the copper protein in to clarify the importance of copper.

"Hephaestin was isolated from mice and named after the Greek god for metal-working, Hephaestus. The protein is produced by the gene Heph, also discovered by the researchers and reported in the Nature paper, and is tethered to the membrane of intestinal cells. The researchers suspect it is a "multi-copper ferroxidase" protein that contains copper and works on iron molecules.
Vulpe led the original study while a postdoctoral fellow in the laboratory of Professor Jane Gitschier of UCSF. Gitschier said in a recent UCSF statement that "more work needs to be done to determine if and how often genetic defects in iron transport occur in humans."

In describing the possible role of the new protein, Vulpe traced the path of iron through the body.

Iron, he said, usually originates in the food supply, either as "heme," a cage of iron that transports oxygen in blood and comes mainly from meats, or as "free" iron from other sources. Both kinds of iron are processed by the gut -- stomach and intestine -- where they are converted by means not well understood to a form of iron readily used by the body. Finally, the iron winds up in the intestinal epithelial cells, ready for export to red blood cells, muscle tissue and organs.

But somehow "it has to get out of the gut and into the bloodstream," said Vulpe.

This is particularly difficult, he said, because the so-called "hydrophobic" intestinal membrane wants to reject the charged iron molecule.

So hephaestin comes into play. Probably acting as a helper molecule forming a complex with a yet unknown transport protein, it allows iron to make its way through the membrane."

Protein Discovery Leads Researchers to New Suspect in Iron Anemia

I should mention that Chlorella doesn't have enough folic acid and I did a typo.
I use it these days to remove lead and god knows what else from years of soldering and being raised for my first 2 years near the Mt Isa lead mines.
Just drink water with it.

Addressing Human Exposure to Environmental Toxins with Chlorella Pyrenoidosa- Medicinal Properties in Whole Foods

Now I've totally opened as many cans as possible so folk know these syndromes have quite a few factors which we often don't think about.

Peter, a friend in the US, has made some comments to this article in an email, which I would like to make available. Here is what he says:

I was going through some pretty old emails that I never had a chance to follow up on, which led me to laleva and to the very scholarly article by Cal Crilly on autism. There are a couple of matters of interest, one a constructive (hopefully) comment.

The first matter is one he indicates with regard to retroviruses, but not with others (which is probably a bit beyond the scope of the article), that viruses are probably not the cause of disease in general (with an exception to be noted). They appear in disease because the body needs them, and since bioscience observes what it presumes to be foreign particles, the pathology is blamed on them. This pathogenesis is 'proven' by the highly questionable practice of injecting 'viruses' into test subjects and observing the result. However, in most such experiments, toxins have likely been introduced as well, since, especially in earlier time, isolating pure virus was technically difficult if not impossible. Nor is injection a 'normal' way of contracting illness. It bypasses the critical immune globulin component, thus creating a faulty situation.

BTW, a great book on the subject of viruses (including HIV and the AIDS scam) and disease, written for the lay reader, is "Fear Of the Invisible," by Janine Roberts. Elsewhere, doubt is now being expressed about the very existence of HIV.

The exception mentioned is that viral material foreign to the host (from other species), especially that introduced by injection, could result in disease. Such 'nonscience' has long been part and parcel of vaccination. As you probably know, the great19th century scientist Antoine Bechamp warned against injecting material, especially morbidly evolved, from one individual into another of even the same species. One thing old Antoine said of the Germ Theory even back then was that it was all the more dangerous because it could be proven scientifically :-)

The second matter concerns the gut issues. Although overall the subjects of the cited research are interesting, the status and effect of the population of probiotic gut bacteria seems to be missing in all the research, as it applies to autism and is used to support Mr Crilly's hypothesis. I confess I haven't perused the associated links, so this is based on the absence of the subject in Mr. Crilly's text. The probiotic population is so fundamental to health, that research which ignores it can be seen as flawed or even irrelevant. It would seem that science needs to know this status in autism cases--in a wide range of health research, actually--and verify or refute cause and effect?

For example, Crilly says:

Oxidative stress in autism: increased lipid peroxidation and reduced serum levels of ceruloplasmin and transferrin--the antioxidant proteins

Which I would fix by making sure Folic acid, B12, and B6 with copper are available in foods with enough Vitamin C. I use Chlorella for the Folic and B12 as it's such a highly methylated food but also because it supplies bioavailable Iron with magnesium and also removes Mercury, Lead and Cadmium.
B6 or Pyridoxine should be given as a supplement at night to enable methylation.

and elsewhere, gut permeability is mentioned.

Gut bacteria are not only the best protection against permeability, as they maintain the integrity of the lining, but probiotics are also central to digestion--that is, to breaking food down for absorption. More to the point, they manufacture all the B vitamins and feed them to the host. While it may be true that in pathology such supplementation might be necessary even with a full complement of gut bacteria, the chances of becoming ill in the first place under that condition (provided there are not other serious imbalances) is very small. Another quick example--what is the relationship between gut dysbiosis and gluten sensitivity if any? It would seem we need to know?

Of course, toxins mentioned in the text are serious imbalances, and heavy metals and such (among a host of other negative influences) do have a deleterious effect on gut populations. So it seems possible that such toxins could have both a direct and indirect effect in autism.

There are quite astonishing similarities between AIDS and Autism.
if you step back from the retroviruses you find all sorts of blood problems in both with either anemia or iron overload and you'll find studies that say an anemia and iron overload are predictors of mortality in AIDS.
There is often hypothyroid in both syndromes and hypoxia or low oxygen reaching cells.
This is why the example of kaposi's sarcoma in gays who use poppers or sardinian men drinking super red wine is so important.
Low oxygen causes nitric oxide release which can cook cells if you don't have enough antoxidants.
Both poppers and the high polyphenol red wines cause nitric oxide release.
You'll find high nitric oxide production happens in autism.
I think in the long run all of this will have more to do with anemia, iron overload and blood poisoning than retroviruses.
See [if posting] off this phone works.....

Cal added some suggestions on foods that may be used in case of 'infections'...

'oh lol, I'm not sure I wanted to tell that ebola anomaly as people would freak out. I'd really like people who get viral outbreaks to calm down and use things that work.

A good example is Aids, for a quarter of a century patients have been dying from herpes and cancers and barely anyone has been taking lysine which is vital to treat all viral outbreaks including ebola and all cancers.

Likewise selenium, there are good reasons why garlic has been used for flu forever, it has selenium and germanium, both antiviral. It's why I recommend Brazil nuts for selenium at 4 a day if you have any viral event.

The study to make people stop freaking out about viruses is 'Theoretical evidence that the ebola virus may be selenium dependent, a factor in pathogenesis and viral outbreaks'. And this article gives examples of all viruses being selenium dependent including hiv, whatever that is.

Along with plain old lemons which are better than synthetic vitamin C, selenium foods and lysine are the antivirals and avoiding arginine foods while having an outbreak is necessary or you feed the 'infection'.

I would suggest trying bromelain too, if you haven't before, it's the most effective non toxic antiviral in my cupboard.

I need to mention that copper foods are antibacterial as well and without copper you get anemia which then allows iron to be used by bacteria instead of being absorbed into our blood.
Protein discovery leads researchers to new suspect in iron anemia.

A comment by Cal arrived on another line...

"I didn't mention that if you google ebola outbreaks and copy the towns where they occur into a google with 'measles campaign' they always occur a year after the vaccine campaign.
The only way to explain this is by realising measles mutates into ebola in populations with no food and low selenium, soil etc."


" you also know kaposi's scarcoma happens in italian old men because myrtle wine has too much polyphenols which then pops endothelial cells after years of drinking it.
Just like poppers do.
Mad hey?"

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