Re: Oxalates

September 20, 2010

Low oxalate diettake calcium OR magnesium prior to mealtimes (this is not to be considered your supplement, it is being used to bind to oxalate; your supplement, be it mag or cal, should be taken away from mealtime for the actual supplementation/absorption), consume higher dose biotin, use VSL#3 if you can (it contains strept strain and milk I believe) I purchased Custom Probiotics 11 strain b/c it does not contain strept but most of the same probiotics as VSL#3 (VSL#3 has been laboratory proven to degrade oxalate) --- ToniTo: mb12 valtrex Sent: Mon, September 20, 2010 7:53:13 AMSubject: Oxalates

What's is the best way to decrease oxalates and oxaditative stress

Sent from my iPod

September 20, 2010

Rhonda,

Oxalates themselves cause an enormous amount of oxidative stress and lipid

peroxidation, depleting glutathione, and shutting down the energy metabolism in

cells where oxalate gets into the mitochondrion. For more info on this, see the

studies I've put below on oxalate's effects on red blood cells and the

mitochondrion and the kidney.

I've recently gone to the primary hyperoxaluria conference in NYC where they

discussed the genetic condition where an enzyme defect makes their liver churn

out high levels of excess oxalate and there, I found autism.

The field is RUN by kidney doctors who only start treating these patients after

they get in kidney failure, but they have failed to recognize other things that

happen in these patients earlier. Included there would be horrible GI problems

and GI pain, bone pain, and according to one doctor I talked to from Canada, a

list of the same conditions we see getting better on the low oxalate diet

outside autism, like fibromyalgia, interstitial cystitis, and vulvodynia.

They had a mixer where the people at the patient conference could mingle with

the scientists who attended the scientific conference, so in talking to the

families and to the only person who has done a clinical study on a large group

of these patients, I learned about undocumented autism that seems it could be

common in this genetic disease. (There are only about 500 cases of primary

hyperoxaluria that have been identified in the whole world. Because of their

gene defect oxalate levels in blood and urine and tissues soar.)

The first family I met had a son with primary oxaluria who had OCD and

Aspergers. The next family with a toddler had an uncle with autism and the

mother had hydrocephalus. That was striking to me because one of the most

dramatic improvements on the diet has been a child with autism who had failed to

develop past infancy and had hydrocephalus and was given a shunt, but his

development arrested there. He only began " infant " development at age five once

he was on the diet.

A fifteen or so year old boy sat by himself at my table and never looked up as I

got up, sat down, got up over and over again, but he was immersed in a game toy

he was playing with during the whole hour and a half of the party. That seemed

" spectrumish " to me, although I didn't talk to him since I never got eye

contact.

Later, I had lunch with a scientist who is developing the orphan drug probiotic

oxalobacter formigenes. She has been doing Phase II and III drug trials on this

product which is the only treatment study that has ever been done in primary

hyperoxaluria aimed at reducing oxalate. When I told her all the families I had

met that seemed to have autism in the family, she said, " Oh yes. They are not

normal. " (She's a microbiologist...so you wouldn't expect her to be able to

diagnose autism, but what she said told me that the kidney doctors also had been

ignoring this issue, just like doctors and psychiatrists for so many years

ignored the GI issues in autism.)

Rhonda, our listserve has had people with other genetic diseases comorbid with

autism that have genetic reasons for gut permeability and their autism symptoms

have improved on the diet just like the " regular " autism kids.

There may be polymorphisms for oxalate issues that increase risks of not being

able to " handle " oxalate. A study in France found that most patients given a

drug that contains large amounts of oxalate developed neurotoxicity, but the

level of neurotoxicity appeared to be determined by the presence or absence of a

polymorphism in the AGT gene, which is the B6 dependent gene that causes primary

hyperoxaluria. I hope we can do a genetic study like theirs in the autism

population.

Why was the autism and why have their GI issues and metabolic issues been

ignored in primary hyperoxaluria?

There was a complaint at the conference from a scientist who had done mouse

studies that the " field " was ignoring the rest of the body and especially the

blow that oxalate makes on the general metabolism, and the lack of treatments

beyond liver transplants. I talked to him and gave him the good news that the

Autism Oxalate Project at ARI HAS developed treatments that aide in the

detoxification of oxalate.

It is when detoxing oxalate that you see the worst symptoms, both in autism and

in primary hyperoxaluria after they have a transplant.

The detox process occurs in the body in earnest ONLY AFTER the sources of excess

oxalate have been reduced...such as diet, and correcting vitamin deficiencies

that lead to our cells making oxalate.

The biggest issue on the vitamin front is pyridoxine (vitamin B6).

Bernie Rimland studied B6 and magnesium therapy in autism for decades but he

didn't know that these nutrients are critical to keep people from making oxalate

metabolically. Enzymes that handle oxalate function in an organelle called the

peroxisome, but until that enzyme binds B6, it cannot be imported into the

peroxisome, so it cannot work properly. A scientist at the conference reported

there is one mutation in primary hyperoxaluria where they found giving 400-600

mgs of pyridoxine a day pretty much solved the oxalate problem in that group!

That's higher amount of B6 than anyone has gone for studying its effects in

autism.

So Rhonda, you asked a simple question, but the answer involves much more than

Toni offered, though what she said was good. What Toni mentioned will help in

reducing how much oxalate you absorb, but on our listserve I get into the

particulars of which supplements have been documented as reducing the oxidative

stress that comes from oxalate's effects on cells. There was lots in the

literature to help us and it is incorporated into the recommendations I make on

the listserve.

Oxalate knocks out every important complex in the electron transport chain, at

the same time as compromising glycolysis, gluconeogenesis, and the TCA cycle

because of other enzymes it knocks out. Mitochondrial scientists do not know

this literature as I learned while attending the United Mitochondrial Disease

Foundation meeting this summer.

Oxalate knocks out the enzyme that uses pyruvate to make citrate at the entrance

into the Krebs cycle. People with high oxalate tend to be low citrate, and

correcting the citrate will help reduce oxidative stress as the article below

states! This is why the preferred form of calcium used is calcium citrate.

If you want to know more, join our listserve where we discuss all this and have

great helps for " newbies " .

I do not recommend people reducing oxalate without getting the benefit of the

discussions on our listserve where you get the latest science as it happens.

I cannot tell you how many people come to our listserve saying they've been LOD,

but they were not getting the information they needed to get the results that

they did get once they joined. This has happened because DAN! has not provided

access for me to train ANY of the nutritionists/dieticians in Defeat Autism Now!

that are trying to train others or advice patients on how to use the diet.

Unfortunately, the ones who are giving out advice on LOD don't know what they

don't know!

Hum Exp Toxicol. 2009 Apr;28(4):245-51.

Oxalate-mediated oxidant-antioxidant imbalance in erythrocytes: role of

N-acetylcysteine.

Bijarnia RK, Kaur T, Singla SK, Tandon C.

Department of Biotechnology and Bioinformatics, Jaypee University of Information

Technology, Waknaghat, India.

Abstract

The present in-vivo study was to observe the effect of N-acetylcysteine (NAC) on

oxalate-induced oxidative stress on rat erythrocytes. A total of 15 Wistar rats

were divided into three groups. The control group received normal saline by

single intraperitoneal injection. Hyperoxaluria was induced by single

intraperitoneal (i.p.) dose of sodium oxalate (70 mg/kg body weight in 0.5 mL

saline) to a second group. The third group was administered single i.p. dose of

NAC according to 200 mg/kg body weight dissolved in 0.5 mL saline, half an hour

after oxalate dose. NAC administration normalized antioxidant enzyme activities

(superoxide dismutase and catalase) and reduced malondialdehyde content

(indicator of lipid peroxidation) in hyperoxaluric rat's red blood cell (RBC)

lysate. NAC administration also resulted in a significant improvement of thiol

content in RBC lysate via increasing reduced glutathione content and maintaining

its redox status. Oxalate-caused alteration of cholesterol/phospholipid ratio

(determining membrane fluidity) was also rebalanced by NAC administration.

Further, after NAC administration, electron microscopy showed improved cell

morphology presenting its prophylactic properties. Above results indicate that

NAC treatment is associated with an increase in plasma antioxidant capacity and

a reduction in the susceptibility of erythrocyte membranes to oxidation. Thus,

the study presents positive pharmacological implications of NAC against

oxalate-mediated impairment of erythrocytes.

PMID: 19734276

Eur J Pharmacol. 2008 Jan 28;579(1-3):330-6. Epub 2007 Oct 16.

Mitochondrial dysfunction in an animal model of hyperoxaluria: a prophylactic

approach with fucoidan.

Veena CK, phine A, Preetha SP, Rajesh NG, Varalakshmi P.

Department of Medical Biochemistry, Dr. ALM. Post Graduate Institute of Basic

Medical Sciences, University of Madras, Taramani Campus, Chennai - 600 113,

India.

Abstract

Oxalate/calcium oxalate toxicity is mediated through generation of reactive

oxygen species in a process that partly depends upon events that induce

mitochondrial damage. Mitochondrial dysfunction is an important event favoring

stone formation. The objective of the present study was to investigate whether

mitochondria is a target for oxalate/calcium oxalate and the plausible role of

naturally occurring glycosaminoglycans from edible seaweed, fucoidan in

ameliorating mitochondrial damage. Male albino rats of Wistar strain were

divided into four groups and treated as follows: Group I: vehicle treated

control, Group II: hyperoxaluria was induced with 0.75% ethylene glycol in

drinking water for 28 days, Group III: fucoidan from F. vesiculosus (5 mg/kg

b.wt, s.c) from the 8th day of the experimental period, Group IV: ethylene

glycol+fucoidan treated rats. The tricarboxylic acid (TCA) cycle enzymes like

succinate dehydrogenase, isocitrate dehydrogenase, malate dehydrogenase and

respiratory complex enzyme activities were assessed to evaluate mitochondrial

function. Oxidative stress was assessed based on the activities of antioxidant

enzymes, level of reactive oxygen species, lipid peroxidation and reduced

glutathione. Mitochondrial swelling was also analyzed. Ultra structural changes

in renal tissue were analyzed with electron microscope. Hyperoxaluria induced a

decrease in the activities of TCA cycle enzymes and respiratory complex enzymes.

The oxidative stress was evident by the decrease in antioxidant enzymes,

glutathione and an increase in reactive species and lipid peroxidation in

mitochondria. Mitochondrial damage was evident by increased mitochondrial

swelling. Administration of fucoidan, decreased reactive oxygen species, lipid

peroxidation (P<0.05), mitochondrial swelling and increased the activities of

antioxidant enzymes and glutathione levels (P<0.05) and normalized the

activities of mitochondrial TCA cycle and respiratory complex enzymes (P<0.05).

From the present study, it can be concluded that mitochondrial damage is an

essential event in hyperoxaluria, and fucoidan was able to effectively prevent

it and thereby the renal damage in hyperoxaluria.

PMID: 18001705

J Urol. 2005 Feb;173(2):640-6.

Citrate provides protection against oxalate and calcium oxalate crystal induced

oxidative damage to renal epithelium.

Byer K, Khan SR.

Department of Pathology, Immunology and Laboratory Medicine, University of

Florida, Gainesville, Florida 32610-0275, USA.

Abstract

PURPOSE: Oxalate and calcium oxalate (CaOx) crystals are injurious to renal

epithelial cells. The injury is caused by the production of reactive oxygen

species (ROS). Citrate is a well-known inhibitor of CaOx crystallization and as

such it is one of the major therapeutic agents prescribed. Since citrate

increases cellular reduced nicotinamide adenine dinucleotide phosphate and

glutathione (GSH), we hypothesized that exogenously administered citrate should

act as an antioxidant and protect cells from oxalate induced injury.

MATERIALS AND METHODS: We exposed LLC-PK1 and MDCK cells to 500 microM/ml

oxalate or 150 mug/cm calcium oxalate crystals for 30, 60 and 180 minutes with

or without 3 mg/ml citrate in the medium. We determined cell viability by

lactate dehydrogenase release and trypan blue exclusion, ROS involvement by

changes in hydrogen peroxide and GSH, and lipid peroxidation by quantifying

8-isoprostane.

RESULTS: The presence of citrate was associated with significant decrease in

lactate dehydrogenase release (p <0.001) and staining with trypan blue (p

<0.05). In addition, there was a significant increase in GSH (p <0.005) and a

decrease in the production of hydrogen peroxide (p <0.05) and 8-isoprostane (p

<0.0005) secretion into the culture medium when citrate was present in the

medium.

CONCLUSIONS: Citrate protects cells from oxalate and CaOx crystal induced injury

by preventing lipid peroxidation through a decrease in ROS production. The

results provide additional data for the beneficial role of citrate therapy for

CaOx nephrolithiasis.

PMID: 15643280 [

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> What's is the best way to decrease oxalates and oxaditative stress

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September 20, 2010

Oxalates rise in response to yeast overgrowth. Reduce yeast and the oxalates

will follow. I once read a study that suggested reducing them without dealing

with the underlying problem isn't recommended, because the oxalate rise has to

do with something in the body working to protect itself. I don't remember the

details, because the study was very hard to read (blurry copy) so I only go bits

and pieces of it. I think it was from the Autism One conference.

We have never attempted to reduce our son's oxalates, we just work to treat the

underlying cause of the yeast and bacteria overgrowth.

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> What's is the best way to decrease oxalates and oxaditative stress

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> Sent from my iPod

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September 20, 2010

I didn't read this whole thing, just had time to skim it, but I wonder if anyone

addressed the possibility of heavy metals at the root of these things. With

heavy metals comes high pathogenic loads and when you test an individual, their

yeast and bacteria loads tend to correlate to their oxalate levels. I am sure

there are other disorders out there that may not relate to this at all, but when

you connect the autism link, high pathogenic loads are ALWAYS involved, so are

heavy metals....just a thought! Remove the heavy metals and the rest follows...

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September 20, 2010

This is a very good article on oxalates, it combines pretty much all of the

things mentioned on this post, lol. It's from Great Plains Labs.

http://www.greatplainslaboratory.com/home/eng/oxalates.asp

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September 20, 2010

I don't know the specifics, that is 's arena, but metals bond to oxalate. And the converse can also be said, reduce oxalate, and you may see the metals go bye bye, without need for "chelation.", I didn't mention the B6 because high B6 will increase phenol sensitivity, I thought, but P5P does not do this.... didn't know the reasons and I didn't want to have to expand on it, other than the B6 impairs some enzyme. Also, many of the people here are using B6 or P5P, I don't want them to think that is all they need to do to work on their oxalate issue. FWIW, there is a steep learning curve to this diet, if you want to ramp up to it, start now. LOL It still makes my head spin :-) --- ToniTo: mb12 valtrex Sent: Mon, September 20, 2010 1:09:48 PMSubject: Re: Oxalates

I didn't read this whole thing, just had time to skim it, but I wonder if anyone addressed the possibility of heavy metals at the root of these things. With heavy metals comes high pathogenic loads and when you test an individual, their yeast and bacteria loads tend to correlate to their oxalate levels. I am sure there are other disorders out there that may not relate to this at all, but when you connect the autism link, high pathogenic loads are ALWAYS involved, so are heavy metals....just a thought! Remove the heavy metals and the rest follows...

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September 20, 2010

,

There is ABSOLUTELY no evidence that yeast infections produce physiologically

relevant levels of oxalate no matter what you heard at AutismOne. This was

conjecture. I think the paper you read was a blog post that I also had people

send to me, and it was also conjecture. There is unfortunately no science to

support it. Just look in pubmed!

No scientist has found that the body makes oxalate in response to any condition

except vitamin deficiencies that ruin the regulation of the enzymes designed to

protect us from the toxicity of oxalate that comes from food. B6 is one of

those vitamins, as is thiamine.

What is known is that yeast can make a precursor to oxalate from arabinose

called d-erythroascorbic acid, and it puts you at the same risk for making

oxalate as taking vitamin C...no more, no less. That conversion is more or less

the same conversion. Yeast won't use arabinose as food unless other forms of

sugar are not available. Using arabinose is a stress reaction for yeast. Check

the literature!

At this conference I attended, one scientist reported that ordinary commensal

bacteria only degrade oxalate in the gut if their normal food is not available,

like in a stress response. This may be why the " anti-candida diet " that reduces

sugar may persuade microbes in the gut to degrade oxalate that would ordinarily

leave oxalate alone. Changes in the diet aimed at " killing yeast " may have

worked actually by stressing bacteria so that they degraded oxalate!

The only fungal infection that has been noted to produce damaging amounts of

oxalate is aspergillus infections of the lung which have huge fungal balls in

the lungs that can be detected. Nothing subtle.

I've had multiple conversations with Bill Shaw about this. If large enough

amounts of oxalate were produced by yeast, then recognition of oxalate issues in

patients with candidiasis that is fatal or near-fatal would have been noted in

the literature! It is not there.

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> > What's is the best way to decrease oxalates and oxaditative stress

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September 20, 2010

,

I think you skimmed too quickly!

I was reporting on people who are known to have A GENE DEFECT that causes them

to MAKE oxalate that goes all over the body. Their oxalate is not a secondary

condition to anything.

You've mentioned people who are suggesting that oxalate is a secondary issue to

some other things seen in autism, but our experience and that of the Vulvar Pain

Foundation is that the arrow is likely going the other direction!

Many on LOD lose the need for treatments for yeast and treatment of heavy metals

without using the medicines or supplements. Once the diet has worked in this

area, it seems to be a more or less permanent change.

Even before our project started, we heard that the Vulvar Pain Foundation

noticed that their members with chronic yeast issues also lost their chronic

yeast problems on the diet and tendency to urinary tract infections and no

longer needed ANY treatment for these issues after they had experienced

sometimes decades of treatment.

It is so hard to shift models when people have been thinking so hard that the

causation arrow goes one way, when an ASSOCIATION does not tell you which part

of that association came first.

Even among scientists where I spend most of my time, what people already believe

(doctrine that never had proof in the first place) ends up being the biggest

block to learning or grasping the significance of something new. This is

exactly what kept the kidney doctors from recognizing the autistic tendencies in

primary hyperoxaluia patients BECAUSE they believed without proof that oxalate

damaged the kidneys before it could damage the rest of the body. Because of

this they ignored the other issues that were already in their patients, like

their GI issues, their fibromyalgia, their interstitial cystitis, and

apparently, their autism. They never dreamed these issues were related to

oxalate!

Previous models about yeast and heavy metals have kept many people from

listening to how different the oxalate issue is from previous models. Some

people only listened long enough to get a " sound bite " and then ran off in their

own direction advancing theories as if they were facts. Be careful to notice

who has references and which points are referenced by scientific studies and

which are not! People on my listserve know I am a bear about furnishing

references, for I want people to know what has the solid backing of clinical and

basic science research.

Treating yeast is not news in autism. I was there fifteen years ago when Bill

Shaw first presented his theories on yeast to the first DAN! conference and

talked about anti-fungal therapy. I was a graduate student at the time. DAN! has

done this sort of treatment ever since then, but the recurring problems with

yeast didn't go away with treatment and it wasn't long before the same scenario

had to be repeated again.

If treating yeast would solve the oxalate issue, then we wouldn't have those who

went on the anti-fungal parade and got only better during treatment and then

crashed off treatment, and never got rid of the tendency to NEED treatment, but

who after this went on LOD and lost the need for antifungal treatment and

improved in other areas as well. The same thing happened at the Vulvar Pain

Foundation. Women who experienced chronic yeast lost that tendency on the low

oxalate diet.

Why? There is an easy explanation. Oxalate impairs carboxylase activity. That

loss makes it difficult for the body to keep yeast within normal bounds. This

is why those with several different genetic defects that all impair carboxylase

issues ALSO have yeast problems. That's in the literature and it makes sense

why after being on reduced oxalates, yeast issues that were caused by oxalate go

away.

Better science tells us not what will keep patients dependent on supplements and

medicines for the rest of their life, but it tells us how to get their bodies to

heal and regain independence!

For anyone who had a child who regressed, identifying the mechanism of the

regression will point to a solution that should get the child back to normal

where he won't need the props. The count of the biomedical treatments that are

necessary right now in a child is a pretty good measure of the distance someone

is from finding and solving the PRIMARY problem. You can chase secondary

problems until you are blue in the face and until the child feels like he will

never be independent of all this stuff.

I recently talked with a mom of a little girl who was one of our early people on

the low oxalate diet. At one time her school district called this girl 67%

impaired. This now pre-teen young lady not only lost her diagnosis of autism

years ago after about two years on LOD, but she lost the need for special

education or accommodation at school. This summer she went to a primitive scout

camp for two weeks with no supplements, and had a BLAST. In fact, now she has

for several months had no supplements at all. Her mother was scared to stop the

supplements that we recommend on LOD, but becoming independent of all the pills

and micromanagement had become a passion for this child. This young lady is so

proud of losing the burden of all that intervention and now she can start to

feel normal! So far, it is working and the mother keeps being astonished at how

her daughter is planning ahead, venturing into unknown territory, exploring

friendships, and discovering her own heart, etc.

The mark of finding the culprit is when what you have done to fix something

really fixes it and puts you in a position to lose the need for boatloads of

supplements and all the doctors and all the chasing after each year's new autism

intervention!

>

> I didn't read this whole thing, just had time to skim it, but I wonder if

anyone addressed the possibility of heavy metals at the root of these things.

With heavy metals comes high pathogenic loads and when you test an individual,

their yeast and bacteria loads tend to correlate to their oxalate levels. I am

sure there are other disorders out there that may not relate to this at all, but

when you connect the autism link, high pathogenic loads are ALWAYS involved, so

are heavy metals....just a thought! Remove the heavy metals and the rest

follows...

>

September 20, 2010

Toni,

Oxalate binds both lead and mercury and makes the body RETAIN them in a highly

insoluble form. If your blood is high in oxalate BEFORE your exposure to these

metals, then oxalate may compromise your ability to excrete these metals. The

kidneys are where you have a high concentration of metals collecting and high

concentrations of oxalate and they are where most chelators work. But if metals

are bound to oxalate, they are not likely to be impairing enzymes, although the

oxalate that bound them could be in the company of other oxalate that is free

and impairing a long list of enzymes.

Years ago, a DAN! doctor in Spain, Dr. Jesus Clavera started putting all

her autism patients on reduced oxalate diets and found that the same chelation

program she had been using on them for sometimes years was suddenly producing

(after the diet) such higher elevations of metal excretions that she was worried

about it and reduced the chelating agents in fear that the higher levels being

excreted would cause harm.

Because oxalate that is in BLOOD may change the way the kidney secretes fluids

and adjusts pH, that means changes on any urine tests that are reported ratioed

to creatinine can be misleading if no one notices whether and WHEN the analytes

as a group shift down or up. You cannot tell if that shift has occurred in a

Metals test done in isolation because there are no normal ranges for these

toxins.

This is why I studied 224 Great Plains organic acid tests collected over a

period of about ten years. In that group, there was only one boy in which

repeat tests did not show shifts in average urine concentration that were as

great as three-fold over repeat tests. This shift, if it is as common in autism

as it appears to be from this database, should effect the interpretation of all

urine tests ratioed to creatinine including metals tests. I presented on this

problem to the thinktank a couple of years ago.

In other words, something shifts the ratio of creatinine to water and everything

else in the urine, and a big suspect is oxalate that is being detoxified by the

body, so moving from blood into the kidney for excretion.

Let me give you an example. A parent sent me two organic acid tests done twelve

hours apart on her son. When I asked her why the two tests were so close

together, she told me the test was repeated after he was given a vitamin C IV

and ended up in a metabolic crisis hours later that landed him in the Emergency

Room.

His oxalate level (vitamin C converts to oxalate in high amounts) had increased

about twenty-fold in those hours, but his overall urine concentration of all the

analytes on the test dropped three-fold in the twelve hours between the two

tests. In other words, the analytes that shift in response to oxalate's enzyme

inhibition in the mitochondrion were dramatically different, about a third way

higher (as much as forty times higher), and a different third had dramatically

shifted down in ways that could be understood by how oxalate impairs certain

enzymes. After calculating the shift in the AVERAGE concentration, the other

analytes were completely stable that wouldn't be affected by oxalate getting

into the mitochondrion of cells.

What was so shocking is that the effect of the higher oxalate in his blood would

have made a metals test done at the same time look like the metals had fallen

three fold! This is why I always recommend someone do an organic acid test at

the same time as a metals test so that you can calculate that shift as I always

do now on organic acid tests.

Making this correction is how I've found a lot of children with fatty acid

disorders and other things that the doctor didn't see from the " shifted " report.

Tony, vitamin B6 is critical to the oxalate-protecting metabolism and also to

the sulfur chemistry in helping us make sulfate and taurine. The lack of

sulfate is what leads to PST problems, as they were studied by Dr. Rosemary

Waring at the University of Birmingham in England many years ago.

If anyone need more info on that, I suggest they read the archives on

sulfurstories, a yahoogroup I set up after speaking on sulfur at DAN!

conferences to the science and in another year to the regular sessions many

years ago. One of those times was right after 9/11!

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September 20, 2010

Thank you ,

Does this child still need the diet, even if she is off of the supplements? And

if so, what then gets to the root of the problem, chelation? And my question

pertains to children who have high oxalates, but no other markers suggesting

it's a genetic disorder.

> >

> > I didn't read this whole thing, just had time to skim it, but I wonder if

anyone addressed the possibility of heavy metals at the root of these things.

With heavy metals comes high pathogenic loads and when you test an individual,

their yeast and bacteria loads tend to correlate to their oxalate levels. I am

sure there are other disorders out there that may not relate to this at all, but

when you connect the autism link, high pathogenic loads are ALWAYS involved, so

are heavy metals....just a thought! Remove the heavy metals and the rest

follows...

> >

>

September 20, 2010

Wow, this is so confusing and I consider myself fairly literate in biomedicine

after more than two years of research, but this is like a foreign language, lol!

So what would you be looking for in an OAT and what would it mean?

I had one done when we started this with our son. He's not autistic, but his

health mirrors that of an autistic and he has anxiety/yeast/bacteria/probably

viral problems/GI disturbances/SPD. Our two year old has never been tested, but

he seems pretty similar in many ways.

How does all of this relate to the many children who have been recovered with

slow oral dose chelation (Andy Cutler)? They don't need diets, supplements,

treatments, etc.

And then there is the topic of recovery by homeopathy which seems to be pretty

popular and successful too.

It all just makes my head spin, how can there be so many directions which you

can address the same problems, or are they not the same in the end?

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September 20, 2010

LOL ... whenever posts something, I feel like I don't know anything about this diet at all. :-)I just keep trying the diet and hoping for the best. --- ToniTo: mb12 valtrex Sent: Mon, September 20, 2010 9:39:13 PMSubject: Re: Oxalates

Wow, this is so confusing and I consider myself fairly literate in biomedicine after more than two years of research, but this is like a foreign language, lol!

So what would you be looking for in an OAT and what would it mean?

I had one done when we started this with our son. He's not autistic, but his health mirrors that of an autistic and he has anxiety/yeast/bacteria/probably viral problems/GI disturbances/SPD. Our two year old has never been tested, but he seems pretty similar in many ways.

How does all of this relate to the many children who have been recovered with slow oral dose chelation (Andy Cutler)? They don't need diets, supplements, treatments, etc.

And then there is the topic of recovery by homeopathy which seems to be pretty popular and successful too.

It all just makes my head spin, how can there be so many directions which you can address the same problems, or are they not the same in the end?

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> > > > What's is the best way to decrease oxalates and oxaditative stress

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September 20, 2010

wow , what a wealth of information. Fascinating to me right now as my son was just diagnosed with pyrroluria -so his body dumps out all of his B6 and Zinc, therefore with no B6 he is then in a bad situation with oxalates, I see. He was just diagnosed with a Long Chain Fatty Acid defect and now it looks like Mito deficiency partial complex I and III....I wonder how much of this mess is all about oxalates? Alison M Re: Oxalates Rhonda,Oxalates themselves cause an enormous amount of oxidative stress and lipid peroxidation, depleting glutathione, and shutting down the energy metabolism in cells where oxalate gets into the mitochondrion. For more info on this, see the studies I've put below on oxalate's effects on red blood cells and the mitochondrion and the kidney.I've recently gone to the primary hyperoxaluria conference in NYC where they discussed the genetic condition where an enzyme defect makes their liver churn out high levels of excess oxalate and there, I found autism.The field is RUN by kidney doctors who only start treating these patients after they get in kidney failure, but they have failed to recognize other things that happen in these patients earlier. Included there would be horrible GI problems and GI pain, bone pain, and according to one doctor I talked to from Canada, a list of the same conditions we see getting better on the low oxalate diet outside autism, like fibromyalgia, interstitial cystitis, and vulvodynia.They had a mixer where the people at the patient conference could mingle with the scientists who attended the scientific conference, so in talking to the families and to the only person who has done a clinical study on a large group of these patients, I learned about undocumented autism that seems it could be common in this genetic disease. (There are only about 500 cases of primary hyperoxaluria that have been identified in the whole world. Because of their gene defect oxalate levels in blood and urine and tissues soar.) The first family I met had a son with primary oxaluria who had OCD and Aspergers. The next family with a toddler had an uncle with autism and the mother had hydrocephalus. That was striking to me because one of the most dramatic improvements on the diet has been a child with autism who had failed to develop past infancy and had hydrocephalus and was given a shunt, but his development arrested there. He only began "infant" development at age five once he was on the diet.A fifteen or so year old boy sat by himself at my table and never looked up as I got up, sat down, got up over and over again, but he was immersed in a game toy he was playing with during the whole hour and a half of the party. That seemed "spectrumish" to me, although I didn't talk to him since I never got eye contact. Later, I had lunch with a scientist who is developing the orphan drug probiotic oxalobacter formigenes. She has been doing Phase II and III drug trials on this product which is the only treatment study that has ever been done in primary hyperoxaluria aimed at reducing oxalate. When I told her all the families I had met that seemed to have autism in the family, she said, "Oh yes. They are not normal." (She's a microbiologist...so you wouldn't expect her to be able to diagnose autism, but what she said told me that the kidney doctors also had been ignoring this issue, just like doctors and psychiatrists for so many years ignored the GI issues in autism.)Rhonda, our listserve has had people with other genetic diseases comorbid with autism that have genetic reasons for gut permeability and their autism symptoms have improved on the diet just like the "regular" autism kids.There may be polymorphisms for oxalate issues that increase risks of not being able to "handle" oxalate. A study in France found that most patients given a drug that contains large amounts of oxalate developed neurotoxicity, but the level of neurotoxicity appeared to be determined by the presence or absence of a polymorphism in the AGT gene, which is the B6 dependent gene that causes primary hyperoxaluria. I hope we can do a genetic study like theirs in the autism population.Why was the autism and why have their GI issues and metabolic issues been ignored in primary hyperoxaluria?There was a complaint at the conference from a scientist who had done mouse studies that the "field" was ignoring the rest of the body and especially the blow that oxalate makes on the general metabolism, and the lack of treatments beyond liver transplants. I talked to him and gave him the good news that the Autism Oxalate Project at ARI HAS developed treatments that aide in the detoxification of oxalate. It is when detoxing oxalate that you see the worst symptoms, both in autism and in primary hyperoxaluria after they have a transplant.The detox process occurs in the body in earnest ONLY AFTER the sources of excess oxalate have been reduced...such as diet, and correcting vitamin deficiencies that lead to our cells making oxalate.The biggest issue on the vitamin front is pyridoxine (vitamin B6). Bernie Rimland studied B6 and magnesium therapy in autism for decades but he didn't know that these nutrients are critical to keep people from making oxalate metabolically. Enzymes that handle oxalate function in an organelle called the peroxisome, but until that enzyme binds B6, it cannot be imported into the peroxisome, so it cannot work properly. A scientist at the conference reported there is one mutation in primary hyperoxaluria where they found giving 400-600 mgs of pyridoxine a day pretty much solved the oxalate problem in that group! That's higher amount of B6 than anyone has gone for studying its effects in autism.So Rhonda, you asked a simple question, but the answer involves much more than Toni offered, though what she said was good. What Toni mentioned will help in reducing how much oxalate you absorb, but on our listserve I get into the particulars of which supplements have been documented as reducing the oxidative stress that comes from oxalate's effects on cells. There was lots in the literature to help us and it is incorporated into the recommendations I make on the listserve.Oxalate knocks out every important complex in the electron transport chain, at the same time as compromising glycolysis, gluconeogenesis, and the TCA cycle because of other enzymes it knocks out. Mitochondrial scientists do not know this literature as I learned while attending the United Mitochondrial Disease Foundation meeting this summer. Oxalate knocks out the enzyme that uses pyruvate to make citrate at the entrance into the Krebs cycle. People with high oxalate tend to be low citrate, and correcting the citrate will help reduce oxidative stress as the article below states! This is why the preferred form of calcium used is calcium citrate.If you want to know more, join our listserve where we discuss all this and have great helps for "newbies".I do not recommend people reducing oxalate without getting the benefit of the discussions on our listserve where you get the latest science as it happens. I cannot tell you how many people come to our listserve saying they've been LOD, but they were not getting the information they needed to get the results that they did get once they joined. This has happened because DAN! has not provided access for me to train ANY of the nutritionists/dieticians in Defeat Autism Now! that are trying to train others or advice patients on how to use the diet. Unfortunately, the ones who are giving out advice on LOD don't know what they don't know!Hum Exp Toxicol. 2009 Apr;28(4):245-51.Oxalate-mediated oxidant-antioxidant imbalance in erythrocytes: role of N-acetylcysteine.Bijarnia RK, Kaur T, Singla SK, Tandon C.Department of Biotechnology and Bioinformatics, Jaypee University of Information Technology, Waknaghat, India.AbstractThe present in-vivo study was to observe the effect of N-acetylcysteine (NAC) on oxalate-induced oxidative stress on rat erythrocytes. A total of 15 Wistar rats were divided into three groups. The control group received normal saline by single intraperitoneal injection. Hyperoxaluria was induced by single intraperitoneal (i.p.) dose of sodium oxalate (70 mg/kg body weight in 0.5 mL saline) to a second group. The third group was administered single i.p. dose of NAC according to 200 mg/kg body weight dissolved in 0.5 mL saline, half an hour after oxalate dose. NAC administration normalized antioxidant enzyme activities (superoxide dismutase and catalase) and reduced malondialdehyde content (indicator of lipid peroxidation) in hyperoxaluric rat's red blood cell (RBC) lysate. NAC administration also resulted in a significant improvement of thiol content in RBC lysate via increasing reduced glutathione content and maintaining its redox status. Oxalate-caused alteration of cholesterol/phospholipid ratio (determining membrane fluidity) was also rebalanced by NAC administration. Further, after NAC administration, electron microscopy showed improved cell morphology presenting its prophylactic properties. Above results indicate that NAC treatment is associated with an increase in plasma antioxidant capacity and a reduction in the susceptibility of erythrocyte membranes to oxidation. Thus, the study presents positive pharmacological implications of NAC against oxalate-mediated impairment of erythrocytes.PMID: 19734276Eur J Pharmacol. 2008 Jan 28;579(1-3):330-6. Epub 2007 Oct 16.Mitochondrial dysfunction in an animal model of hyperoxaluria: a prophylactic approach with fucoidan.Veena CK, phine A, Preetha SP, Rajesh NG, Varalakshmi P.Department of Medical Biochemistry, Dr. ALM. Post Graduate Institute of Basic Medical Sciences, University of Madras, Taramani Campus, Chennai - 600 113, India.AbstractOxalate/calcium oxalate toxicity is mediated through generation of reactive oxygen species in a process that partly depends upon events that induce mitochondrial damage. Mitochondrial dysfunction is an important event favoring stone formation. The objective of the present study was to investigate whether mitochondria is a target for oxalate/calcium oxalate and the plausible role of naturally occurring glycosaminoglycans from edible seaweed, fucoidan in ameliorating mitochondrial damage. Male albino rats of Wistar strain were divided into four groups and treated as follows: Group I: vehicle treated control, Group II: hyperoxaluria was induced with 0.75% ethylene glycol in drinking water for 28 days, Group III: fucoidan from F. vesiculosus (5 mg/kg b.wt, s.c) from the 8th day of the experimental period, Group IV: ethylene glycol+fucoidan treated rats. The tricarboxylic acid (TCA) cycle enzymes like succinate dehydrogenase, isocitrate dehydrogenase, malate dehydrogenase and respiratory complex enzyme activities were assessed to evaluate mitochondrial function. Oxidative stress was assessed based on the activities of antioxidant enzymes, level of reactive oxygen species, lipid peroxidation and reduced glutathione. Mitochondrial swelling was also analyzed. Ultra structural changes in renal tissue were analyzed with electron microscope. Hyperoxaluria induced a decrease in the activities of TCA cycle enzymes and respiratory complex enzymes. The oxidative stress was evident by the decrease in antioxidant enzymes, glutathione and an increase in reactive species and lipid peroxidation in mitochondria. Mitochondrial damage was evident by increased mitochondrial swelling. Administration of fucoidan, decreased reactive oxygen species, lipid peroxidation (P<0.05), mitochondrial swelling and increased the activities of antioxidant enzymes and glutathione levels (P<0.05) and normalized the activities of mitochondrial TCA cycle and respiratory complex enzymes (P<0.05). From the present study, it can be concluded that mitochondrial damage is an essential event in hyperoxaluria, and fucoidan was able to effectively prevent it and thereby the renal damage in hyperoxaluria.PMID: 18001705J Urol. 2005 Feb;173(2):640-6.Citrate provides protection against oxalate and calcium oxalate crystal induced oxidative damage to renal epithelium.Byer K, Khan SR.Department of Pathology, Immunology and Laboratory Medicine, University of Florida, Gainesville, Florida 32610-0275, USA.AbstractPURPOSE: Oxalate and calcium oxalate (CaOx) crystals are injurious to renal epithelial cells. The injury is caused by the production of reactive oxygen species (ROS). Citrate is a well-known inhibitor of CaOx crystallization and as such it is one of the major therapeutic agents prescribed. Since citrate increases cellular reduced nicotinamide adenine dinucleotide phosphate and glutathione (GSH), we hypothesized that exogenously administered citrate should act as an antioxidant and protect cells from oxalate induced injury.MATERIALS AND METHODS: We exposed LLC-PK1 and MDCK cells to 500 microM/ml oxalate or 150 mug/cm calcium oxalate crystals for 30, 60 and 180 minutes with or without 3 mg/ml citrate in the medium. We determined cell viability by lactate dehydrogenase release and trypan blue exclusion, ROS involvement by changes in hydrogen peroxide and GSH, and lipid peroxidation by quantifying 8-isoprostane.RESULTS: The presence of citrate was associated with significant decrease in lactate dehydrogenase release (p <0.001) and staining with trypan blue (p <0.05). In addition, there was a significant increase in GSH (p <0.005) and a decrease in the production of hydrogen peroxide (p <0.05) and 8-isoprostane (p <0.0005) secretion into the culture medium when citrate was present in the medium.CONCLUSIONS: Citrate protects cells from oxalate and CaOx crystal induced injury by preventing lipid peroxidation through a decrease in ROS production. The results provide additional data for the beneficial role of citrate therapy for CaOx nephrolithiasis.PMID: 15643280 [>> What's is the best way to decrease oxalates and oxaditative stress > > Sent from my iPod>

September 20, 2010

Could you give more details on the diet pls the information isGreat still need to research it all.... Thank youSent from my iPod

Toni,

Oxalate binds both lead and mercury and makes the body RETAIN them in a highly insoluble form. If your blood is high in oxalate BEFORE your exposure to these metals, then oxalate may compromise your ability to excrete these metals. The kidneys are where you have a high concentration of metals collecting and high concentrations of oxalate and they are where most chelators work. But if metals are bound to oxalate, they are not likely to be impairing enzymes, although the oxalate that bound them could be in the company of other oxalate that is free and impairing a long list of enzymes.

Years ago, a DAN! doctor in Spain, Dr. Jesus Clavera started putting all her autism patients on reduced oxalate diets and found that the same chelation program she had been using on them for sometimes years was suddenly producing (after the diet) such higher elevations of metal excretions that she was worried about it and reduced the chelating agents in fear that the higher levels being excreted would cause harm.

Because oxalate that is in BLOOD may change the way the kidney secretes fluids and adjusts pH, that means changes on any urine tests that are reported ratioed to creatinine can be misleading if no one notices whether and WHEN the analytes as a group shift down or up. You cannot tell if that shift has occurred in a Metals test done in isolation because there are no normal ranges for these toxins.

This is why I studied 224 Great Plains organic acid tests collected over a period of about ten years. In that group, there was only one boy in which repeat tests did not show shifts in average urine concentration that were as great as three-fold over repeat tests. This shift, if it is as common in autism as it appears to be from this database, should effect the interpretation of all urine tests ratioed to creatinine including metals tests. I presented on this problem to the thinktank a couple of years ago.

In other words, something shifts the ratio of creatinine to water and everything else in the urine, and a big suspect is oxalate that is being detoxified by the body, so moving from blood into the kidney for excretion.

Let me give you an example. A parent sent me two organic acid tests done twelve hours apart on her son. When I asked her why the two tests were so close together, she told me the test was repeated after he was given a vitamin C IV and ended up in a metabolic crisis hours later that landed him in the Emergency Room.

His oxalate level (vitamin C converts to oxalate in high amounts) had increased about twenty-fold in those hours, but his overall urine concentration of all the analytes on the test dropped three-fold in the twelve hours between the two tests. In other words, the analytes that shift in response to oxalate's enzyme inhibition in the mitochondrion were dramatically different, about a third way higher (as much as forty times higher), and a different third had dramatically shifted down in ways that could be understood by how oxalate impairs certain enzymes. After calculating the shift in the AVERAGE concentration, the other analytes were completely stable that wouldn't be affected by oxalate getting into the mitochondrion of cells.

What was so shocking is that the effect of the higher oxalate in his blood would have made a metals test done at the same time look like the metals had fallen three fold! This is why I always recommend someone do an organic acid test at the same time as a metals test so that you can calculate that shift as I always do now on organic acid tests.

Making this correction is how I've found a lot of children with fatty acid disorders and other things that the doctor didn't see from the "shifted" report.

Tony, vitamin B6 is critical to the oxalate-protecting metabolism and also to the sulfur chemistry in helping us make sulfate and taurine. The lack of sulfate is what leads to PST problems, as they were studied by Dr. Rosemary Waring at the University of Birmingham in England many years ago.

If anyone need more info on that, I suggest they read the archives on sulfurstories, a yahoogroup I set up after speaking on sulfur at DAN! conferences to the science and in another year to the regular sessions many years ago. One of those times was right after 9/11!

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September 20, 2010