RE: Candida (fungus) and oxalate issues

June 4, 2007

Wow ,

You would make a

great teacher. I feel like I just took a summer class. I have a

question about a supplement I love for my son and it’s the entire reason

I have not looked farther into LOD. OPC-3 it’s called with pinebark

extract, grapeseed extract, red wine extract, bioflavniods, etc. These

are all high Os right? Would I have to abandon this in order to comply?

Thanks, -

From: mb12 valtrex [mailto:mb12 valtrex ] On Behalf Of Owens

Sent: Monday, June 04, 2007 3:16

PM

To: mb12 valtrex

Subject: Candida

(fungus) and oxalate issues

Stan,

The Valtrex does seem to be a " biggy " for my daughter, so she is

still on

it, though not at a really high dose considering she is at her adult size

now. I just wish I had done the Valtrex years ago, as I did have the

impression even back then that she might have been exposed so early that it

kept her from making anti-CMV antibodies. I am really glad to be here and

I've appreciated the help.

Regarding the antifungal versus diet issue with oxalates, there are many

reasons I don't think fungus is " it " for the oxalate issues in most

kids. My biggest reason for this suspicion is that using antifungal

medication is extremely old news, for the practice of using antifungal

medication routinely has been in place by our DAN! doctors since the first

DAN! conference which I attended when I was a graduate student back in

1996. At this conference, Bill Shaw told us how he had been asked to leave

his position at Children's Mercy Hospital because the hospital had gotten

crosswise over his research into autism and looking at metabolites in the

organic acid test that were thought to come from candida and other

microbes. At this first DAN! conference, a collection was taken up for Dr.

Shaw so he could get his lab started.

The improvements the DAN! community started to see when antifungal therapy

was introduced were a huge step back then, but those improvements do not

seem to fit as well with the superset of changes we are seeing now with the

oxalate-reduced diet: things like catch-up growth, putting on muscle and

weight, big improvements in gross and fine motor skills, big increases in

energy, improvements in sleep (which makes everyone sleep better) and loss

of GI problems that had not improved on all previous DAN! therapy including

(for many listmates) constant antifungal therapy or even the GI meds that

the doctors put people on after scoping them.

Our poll last year showed us that GI problems have been the most common

improvements on LOD as a group. Losing various areas of " autismness "

on LOD

had happened for about 80% of the respondents to that poll. I don't

remember hearing of this cluster of changes and the improvements in

cognition in children on antifungal therapy, especially change that stayed

with the child when he went off the medication. If the fungus WAS the

source of the extremely high levels of oxalate, then the things that change

on antifungal therapy should be the same list with the same type of

prevalence we see on LOD, I would think! I certainly invite people to make

comparisons of what changes with these two different strategies!

At the beginning of our oxalate project, a lot of the parents started

reporting that their own children who had been constantly on antifungal

therapy for years (because once they went off the medication, the symptoms

came back) were losing completely those symptoms they had learned to call

" yeasty symptoms " . In fact, the parents found that their children who

had

been on a constant antifungal merrygoround could now go off antifungal

therapy and antifungal supplements without symptoms coming back. Parents

on our list were beginning to express doubt that what they had seen in the

past were yeast issues because now they were speculating that the symptoms

had been oxalate issues all along.

Were the parents right about this? I don't know, for I we don't have

experimental data to distinguish this oxalate vs. yeast question, but I do

know that oxalates can impair the function of the immune system's key way

to identify bacteria and fungi, which is by their lipopolysaccharide

coat. Most of the immune system works by recognizing pieces of protein, or

peptides, but this lipopolysaccharide means of recognition has its own

molecules for recognition (cd1d) and this system does not work as it should

when high oxalate is in the environment of this receptor's expression.

Oxalates also impair the function of carboxylase enzymes which are the

enzymes that use biotin as a swinging arm to move substrate within the

enzyme. This movement is ruined by high levels of oxalate, and would make

you lose some degree of action of all the carboxylase enzymes that use this

same structure in whatever compartment oxalate concentration got high

enough. (The association of this mechanism with the cell's key means of

getting energy is a big reason we think children get these astonishing

changes in energy and strength on LOD like the child I heard about last

week who is now bicycling through the mountains each morning, but was so

impaired when he was two that he couldn't stand up on his legs!)

This is an animation that shows how this swinging arm works:

http://www.rpi.edu/dept/bcbp/molbiochem/MBWeb/mb1/part2/gluconeo.htm#animat1

The very same enzymes will lose activity if biotin is scarce. The most

commonly known reason for this scarcity is biotinidase deficiency, which is

genetic. Biotinidase is an enzyme that helps attach biotin to

biotin-dependent enzymes. So biotinidase deficiency is a pure disorder

where carboxylase acitivity is known to be impaired. In this condition,

the patient is a sitting duck for yeast infections and specifically

candida. This is all over the literature.

Our project suspects that this loss of biotin dependent enzyme function is

why no one can get over these problems with yeast overgrowth when they are

absorbing excess oxalates or have high oxalates for other reasons.

Let's step back and look at this as objectively as we can. Everybody has

yeast in their body. What could be different about lots of kids with

autism that would make it where they seem to need antifungal medication to

keep certain symptoms away? Why do most people tolerate the presence of

yeast at levels which the GI docs say in autism is THE SAME as the level of

yeast that everybody else has? {(That has been what the GI docs have said

all along to the irritation of the clinical DAN! docs who have seen so much

improvement on antifungal medication!)

I don't know if you remember this, Stan, but Sophie Roseneau, one of the

doctors at the Royal Free Hospital studying children with autism, presented

data on this many years ago at a succession of DAN! conferences. She said

the level of yeast in the stool was the same in autism as in controls. At

the time, that information was not very happily received! She also showed

that antibiotic treatment that targetted anaerobic gram-negative bacteria

produced only temporary relief, but that relief of symptoms proved to be

exceedingly wonderful behaviorally for the kids on the

antibiotic. Unfortunately, her study followed up on these children and

found that the problem came right back just as bad as it had ever been when

the antibiotic was discontinued. (Sound sort of familiar?)

Both of these issues with fungi and bacteria might be evidence that the

real defect in kids with autism with these issues is immune recognition of

these microbes via the cd1d lipopolysaccharide receptor that presents this

type of antigen to the immune system...a receptor that won't function

properly in an environment of high oxalate. Of course, the oxalate we are

talking about here is oxalate still in the GI tract changing antigen

presentation that should be recognized by the gastrointestinal lymphoid

system!

We do know that candida can make d-erythroascorbic acid out of arabinose.

This cousin of vitamin C (like vitamin C) is only one step away from oxalate.

We still don't know WHERE the arabinose is coming from that is so prevalent

in autism, but my highest suspcion is that it is produced from the huge

increases of hyaluronic acid that occur in an inflamed gut. In oxidative

conditions, some of the sugars in hyaluronic acid are converted into

arabinose. If this is what is happening, then arabinose may be a pretty

good marker for an inflamed gut, but this is speculation. I have no

experimental data specific to autism to show that this happened with

hyaluronic acid.

Even if this complex carbohydrate molecule is not the source of the

arabinose, the literature is clear that arabinose is a food and not a

product of yeast. Also, (and this is more obscure) if certain changes

have been made in the phospholipid content of red blood cells because of

changes in phospholipase activity (something that changes in inflammation),

then the transport of arabinose in red blood cells is impaired. That might

be relevant as to why arabinose levels go up in urine. You can see we have

a crying need for some better basic science in this area to get rid of the

speculations.

Anyway, Stan, what may need restoring in autism is immune recognition of

microbes, but this recogntion would get very difficult when oxalate is

elevated because then all you can rely on is the presentation of peptide

antigens from the proteins in these critters instead of the more specific

recognition of antigens made of fat and sugar.

Even if these microbes were present in normal levels, if they are making

oxalate in their immediate environment out of a readily available food,

arabinose, then it may be that their constantly churning out oxalate in

their vicinity (even if it did not raise blood or urine levels

significantly) would make it difficult for the immune system to recognize

and get rid of them. So, our tack on the LOD list is to get rid of the

easily controlled oxalate in the gut first, and then maybe the immune

system can deal with candida in the same way it does in normal

people...ie., the yeast is there, but it isn't out of control.

If any listmates want to help me get experimental data to address this

issue, then they can write me offlist if they have GPL OATS that they did

before and after a round of successful antifungal medication. If I get

enough of these reports, then the data might speak as to whether the

medication changed the level of oxalate in the report. I need GPL OATS

because they also track oxalic acid which is what you measure to track

oxalate. If anyone is interested in supplying to me these before and after

antifungal medication data, just write me at LWO@....

Thanks!

Biochem Biophys Res Commun. 1995 Jul

6;212(1):196-203.<http://www.ncbi.nlm.nih.gov/entrez/utils/fref.fcgi?PrId=3048 & itool=AbstractPlus-def & uid=7612007 & db=pubmed & url=http://linkinghub.elsevier.com/retrieve/pii/S0006-291X%2885%2971956-0>

df7e8a9b.jpg

Links

Conversion of D-arabinose to D-erythroascorbic acid and oxalic acid in

Sclerotinia sclerotiorum.

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Loewus%20FA%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstractPlus>Loewus

FA,

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Saito%20K%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstractPlus>Saito

K,

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Suto%20RK%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstractPlus>Suto

RK,

<http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=Search & Term=%22Maring%20E%22%5BAuthor%5D & itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_RVAbstractPlus>Maring

E.

Institute of Biological Chemistry, Washington

State University,

Pullman

99164-6340, USA.

D-glycero-Pent-2-enono-1,4-lactone (trivial name: D-erythroascorbic

acid)

occurs in the phytopathogen, Sclerotinia sclerotiorum (Lib.) de Bary, where

it has a potential role as precursor of oxalic acid. On Glc/yeast/malt

medium, S. sclerotiorum produces only nominal amounts of D-erythroascorbic

acid but even partial replacement of Glc by D-Ara increases production of

erythroascorbic acid and oxalic acid. Use of D-[1-14C]-, -[3-14C]-, or

-[6-14C]Glc and D-[5-3H]-, -[2-14C,5-3H]-, or -[uL-14C]Ara provide

additional information on erythroascorbic acid biosynthesis and cleavage.

The latter process resembles that obtained by peroxygenation of

erythroascorbic acid in alkaline solution. An unknown erythroascorbic

acid-like compound also occurs in both Glc- and Ara-based cultures.

PMID: 7612007 [PubMed - indexed for MEDLINE]

: Biochim. Biophys. Acta. 1996 Sep 13;1297(1):1-8.

D-arabinose dehydrogenase and biosynthesis of erythroascorbic acid in Candida

albicans.

Kim ST,

Huh WK, Kim JY, Hwang SW, Kang SO.

Department of Microbiology, College of

Natural Sciences, Seoul National

University, South Korea.

D-Arabinose dehydrogenase was purified 2750-fold from the cytosolic fraction of

Candida albicans to apparent homogeneity, with an overall yield of 3%, by a

purification procedure consisting of ammonium sulfate precipitation and

DEAE-Sepharose A-50, Sephacryl S-200, Cibacron blue and phenyl-Sepharose CL-4B

chromatographies. Gel-filtration chromatography gave an apparent molecular mass

of 41 kDa and SDS-PAGE showed only one protein band corresponding to a

molecular

mass of 42 kDa, indicating that the enzyme is a single polypeptide. The enzyme

was optimally active at pH 8.0 and the pI value of the enzyme was 5.0. The

enzyme

was relatively stable from pH 4.5 to 7.5. The optimal temperature for the

enzyme

activity was 30 degrees C. The activity of the enzyme was inhibited by Hg2+,

Fe2+, Zn2+, Cu2+, Mg2+, Mn2+, N-ethylmaleimide and p-chloromercuribenzoic

acid.

The enzyme catalysed the oxidation of D-arabinose, L-fucose, L-xylose and

L-galactose, which have the same configurations of hydroxyl groups at C2- and

C3-positions, with apparent K(m) values of 29.2, 28.9, 37.1 and 91.3 mM at pH

8.0, respectively, with 50 microM NADP+. The enzyme used NADP+ as a coenzyme.

Apparent K(m) value at 60 mM D-arabinose for NADP+ was 44.6 microM. NADPH

inhibited the enzyme activity competitively with respect to NADP+ (Ki = 78.6

microM). The amino-terminal sequence of the enzyme was

Met-Lys-Leu-Ala-Thr-Glu-Ile-Asp-Phe-X-Leu-Asn-Asn-Gly-.

The reaction

product was

D-arabinono-1,4-lactone, judged from gas-liquid chromatography/mass

spectrometry.

In C. albicans, D-erythroascorbic acid was formed from D-arabinose by

D-arabinose

dehydrogenase and D-arabinono-1,4-lactone oxidase.

Publication Types:

Research Support, Non-U.S. Gov't

PMID: 8841374 [Pubmed - indexed for MEDLINE]

2: Biochim Biophys Acta. 1980 Aug 14;600(3):860-9.

Dual effect of membrane cholesterol on simple and mediated transport

processes in

human erythrocytes.

Grunze M, Forst B, Deuticke B.

The influence of cholesterol on simple and facilitated transport processes

across

the membrane of intact human erythrocytes was studied after graded depletion or

enrichment of membrane cholesterol by incubation of the cells in

phospholipid or

phospholipid/cholesterol suspensions. 1. The carrier-mediated transfer of

L-lactate and of L-arabinose proved to be enhanced in this effect....

PMID: 7407148 [Pubmed - indexed for MEDLINE]

3: Biochim Biophys Acta. 1979 Jul 5;554(2):400-9.

Influence of enzymatic phospholipid cleavage on the permeability of the

erythrocyte membrane. II. Protein-mediated transfer of monosaccharides and

anions.

Wilbers KH, Haest CW, von Benthem M, Deuticke B.

In order to investigate the influence of membrane lipids on transport via the

protein domain of the erythrocyte membrane, a number of facilitated diffusion

processes was studied by tracer flux techniques in whole cells after

cleavage of

up to 65% of the phosphatidylcholine or the sphingomyelin by phospholipase A2

from Naja naja or bee venom, or by sphingomyelinase, respectively. The mediated

fluxes of L-arabinose, which is transported by the glucose carrier, and of

L-lactate, which uses a specific monocarboxylate carrier, were markedly

inhibited

by cleavage of either phosphatidylcholine or sphingomyelin. ...

PMID: 486450 [Pubmed - indexed for MEDLINE]

Curr Protein Pept Sci. 2003

Jun;4(3):217-29.<http://www.ncbi.nlm.nih.gov/entrez/utils/fref.fcgi?itool=AbstractPlus-def & PrId=3152 & uid=12769720 & db=pubmed & url=http://openurl.ingenta.com/content/nlm?genre=article & issn=1389-2037 & volume=4 & issue=3 & spage=217 & aulast=Jitrapakdee>

Click here to read

Links

The biotin enzyme family: conserved structural motifs and domain

rearrangements.

<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubmed_AbstractPlus & term=%22Jitrapakdee+S%22%5BAuthor%5D>Jitrapakdee

S,

<http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed & cmd=Search & itool=pubmed_AbstractPlus & term=%22Wallace+JC%22%5BAuthor%5D>Wallace

JC. Department of Biochemistry, Faculty of Science, Mahidol

University,

Bangkok, Thailand. scsjimahidol (DOT) ac.th

The biotin carboxylase family is comprised of a group of enzymes that

utilize a covalently bound prosthetic group, biotin, as a cofactor. These

enzymes, which include acetyl-CoA carboxylase, pyruvate carboxylase,

propionyl-CoA carboxylase, methylcrotonyl-CoA carboxylase, geranoyl-CoA

carboxylase, oxaloacetate decarboxylase, methylmalonyl-CoA decarboxylase,

transcarboxylase and urea amidolyase, are found in diverse biosynthetic

pathways in both pro-karyotes and eukaryotes. The reactions catalyzed by

most members of this group of enzymes share two common features: (1)

carboxylation of biotin, apparently via the formation of a carboxyphosphate

intermediate, followed by (2) transcarboxylation of CO(2) from biotin to

specific acceptor molecules to yield different products. Structural

determinations by NMR and X-ray crystallography, complemented by

mutagenesis studies, have identified some motifs that are structurally or

catalytically important. Analysis of the amino acid sequences of a number

of biotin carboxylases not only shows remarkable similarities within

certain domains but also that there appears to have been domain

rearrangements between groups of carboxylases. Acyl-coenzyme A derivatives,

which bind either as substrates or as allosteric regulators of the biotin

carboxylases, do not appear to share any of the CoA binding motifs that

have been identified in other CoA-SH/acyl-CoA binding proteins. Further

comparisons of biotin-dependent carboxylases with other groups of enzymes

in the protein data bank reveal that this family of biotin enzymes has

strong similarities in specific domains to a number of ATP-utilizing

enzymes and to the lipoyl-containing enzymes. These structural homologies

are so extensive as to be highly suggestive of evolutionary relationships

between biotin carboxylases and these other enzymes.

PMID: 12769720 [PubMed - indexed for MEDLINE]

At 01:45 AM 6/3/2007, you wrote:

>Quite a list of questions.

>

>I'll leave the SCD+LOD questions to but the simple answer is yes.

>

>My view about LOD (without trying to offend who I deeply respect and

>I'm happy is

>playing in our group and playing with antivirals) is that a significant

>source of oxalates is

>fungus. My philosophy is going after fungus first and then seeing if the

>gut normalizes. If

>it doesn't then you may have to step up to LOD.

>

>Eggs are very common IGG issues and I stay away from them until an IGG

>food allergy test

>by blood comes back negative. The same goes with banannas. More than half

>the IGG

>labs I have read have raised bananna.

>

>My son was 28 to 32 lbs and was on 250mg of Valtrex three times a day and

>50mg of

>Nizoral at night.

>

>Natural antifungals are not typically effective in this community when

>Valtrex is onboard.

>It's very interesting and telling if you ask me... and unfortunately true.

>

>Stan

>

> >

> > i had the pleasure of sitting at stan's table at the menteur mom

> > dinner last week at the autism one conference but didn't get the

> > details of the anti-viral/anti-fungal protocol. i need some

advice

> > before we begin. my son is 3 and weighs 27#. he has been on SCD for

> > 8.5 mos and started dmsa 2.5 mos ago. he was limited to applesauce,

> > eggs and juices this entire time. we go through 3/4 bushel apples

> > every wk so we haven't gone organic on the apples yet due to the

> > cost. we are hoping to get him off apples & get him to eat

veggies &

> > a limited amount of organic fruit by going caveman. he did finally

> > eat a bite of a carrot the other day and will now eat an scd almond

> > banana pancake w/o coaxing (the chelation is working). we had to pull

> > the raisins and porkrinds 2 mos ago because his gutt wasn't healed

> > enough and he was getting addicted but now he is finally showing

> > interest in other foods. i want to go low-oxolate and caveman but

> > still follow scd guidelines. he has 36 igg intolerance. i am unsure

> > if we can make juice drinks with raw spinach, apples and fruit since

> > scd says produce needs to be cooked until the gutt is healed. maybe

> > he is ready for raw after 8 mos but i am not sure. is their a list of

> > basic foods to avoid and to use on the low-oxolate diet which are

> > also scd legal? is it better to use raw egg yolk and cooked egg

> > white? is their any reason to avoid eggs and bananas? i noticed that

> > ethan is avoiding those 2 items but i wasn't sure if those were igg

> > intolerances specific to him or if they were not allowed on the lo-

> > oxolate diet.

> >

> > what tests should i have done before starting the protocol? what dose

> > of valtrex and nizoral should a 3 yr old be on? is there a natural

> > alternate anti-fungal we can use that is effective for the valtrex

> > protocol? how long on average are kids staying on the meds?

> >

> > what would be a sample 2 day caveman menu? any interesting juicer

> > recipes that a 3 yr old would like? is there a caveman/scd/lo-oxolate

> > cookbook coming out? is it possible to do lo-oxalate and scd?

> >

>

June 4, 2007

,

I'm not sure any of these have been tested. Anything that comes from a

plant source, though, has the potential to be high oxalate.

Believe me, it has been a challenge in the autism world, to cope with using

a diet that has only been used for people on a very ordinary diet. There

has been more effort to test TV dinners than to test herbs or guar gum or

xanthan gum or some of the flours people use that are gluten free. I was

so elated that at the FASEB oxalate conference, I met a botanist who was

excited about testing all these things, and we raised money and bought him

an HPLC to do the testing. Then between demolishing the science building

and starting over and then campus politics that made our botanist lose his

job, we were left with an HPLC and no one to run it!

So, right now we are scrambling to find a home for this machine with

someone with the expertise and interest who could do this testing for us

and some of us are trying to get some foods tested for a " pay by item "

basis from a commercial lab.

At any rate, I think OPC-3 would fall pretty far behind a lot of other

foods and herbs in our priority for testing, but you could order it tested

yourself. If this really is your holdup, maybe it would be worth it.

I'm glad what I wrote made sense to you!

>Wow ,

>

> You would make a great teacher. I feel like I just took a summer

> class. I have a question about a supplement I love for my son and it's

> the entire reason I have not looked farther into LOD. OPC-3 it's called

> with pinebark extract, grapeseed extract, red wine extract, bioflavniods,

> etc. These are all high Os right? Would I have to abandon this in order

> to comply? Thanks, -

>

--

No virus found in this outgoing message.

Checked by AVG Free Edition.

Version: 7.5.472 / Virus Database: 269.8.7/830 - Release Date: 6/3/2007 12:47 PM

June 4, 2007

Susam:

I'd be interested to hear your thoughts on the Fat Soluble Vitamin

(Vitamin K) protocol to bring down oxalate levels. They seem to think

that the oxalate production is tied to a " granumalatous " Vitamin D

immune response upsetting calcium channels in the body and that the

LOD will not help with mitigating that problem. Or do we need to do

both?

Gayatri

> > >

> > > i had the pleasure of sitting at stan's table at the menteur mom

> > > dinner last week at the autism one conference but didn't get the

> > > details of the anti-viral/anti-fungal protocol. i need some

advice

> > > before we begin. my son is 3 and weighs 27#. he has been on SCD

for

> > > 8.5 mos and started dmsa 2.5 mos ago. he was limited to

applesauce,

> > > eggs and juices this entire time. we go through 3/4 bushel

apples

> > > every wk so we haven't gone organic on the apples yet due to the

> > > cost. we are hoping to get him off apples & get him to eat

veggies &

> > > a limited amount of organic fruit by going caveman. he did

finally

> > > eat a bite of a carrot the other day and will now eat an scd

almond

> > > banana pancake w/o coaxing (the chelation is working). we had

to pull

> > > the raisins and porkrinds 2 mos ago because his gutt wasn't

healed

> > > enough and he was getting addicted but now he is finally showing

> > > interest in other foods. i want to go low-oxolate and caveman

but

> > > still follow scd guidelines. he has 36 igg intolerance. i am

unsure

> > > if we can make juice drinks with raw spinach, apples and fruit

since

> > > scd says produce needs to be cooked until the gutt is healed.

maybe

> > > he is ready for raw after 8 mos but i am not sure. is their a

list of

> > > basic foods to avoid and to use on the low-oxolate diet which

are

> > > also scd legal? is it better to use raw egg yolk and cooked egg

> > > white? is their any reason to avoid eggs and bananas? i noticed

that

> > > ethan is avoiding those 2 items but i wasn't sure if those were

igg

> > > intolerances specific to him or if they were not allowed on the

lo-

> > > oxolate diet.

> > >

> > > what tests should i have done before starting the protocol?

what dose

> > > of valtrex and nizoral should a 3 yr old be on? is there a

natural

> > > alternate anti-fungal we can use that is effective for the

valtrex

> > > protocol? how long on average are kids staying on the meds?

> > >

> > > what would be a sample 2 day caveman menu? any interesting

juicer

> > > recipes that a 3 yr old would like? is there a caveman/scd/lo-

oxolate

> > > cookbook coming out? is it possible to do lo-oxalate and scd?

> > >

> >

>

> No virus found in this outgoing message.

> Checked by AVG Free Edition.

> Version: 7.5.472 / Virus Database: 269.8.7/830 - Release Date:

6/3/2007 12:47 PM

>

June 4, 2007

Gayatri,

The issue of granulomas is very near and dear to my heart, for my father

had a granuloma when I was a child that required lung surgery. It ended up

that what they thought was cancer ( and what later on Xray was very scary

to his physicians his whole life) was a granuloma that formed because my

father had inhaled mineral oil that he was taking because of his messed up

GI tract. (There is a similar reference below talking about oxalate getting

involved with a granuloma induced by mineral oil!)

My dad almost died on two different occasions from ulcers that went all the

way through his GI tract and spilled blood and the contents of his bowel

into the rest of his body. It has not escaped my attention that the degree

of gut inflammation my father experienced his whole life may have led to a

hyperabsorption of oxalate that may have damaged a lot of tissues. When I

was in college, he almost died when his gall bladder exploded and he got so

sick from this that the doctor had advised us to plan his funeral. It ends

up that some gall bladder stones are made from oxalate. Right before this

happened, my father's sleep cycle was very disturbed. He called me one

time at 3:00 in the morning all chatty, and it was very bizarre to have him

call me at all, but especially in the middle of the night in my dorm! A

lot of the children on LOD have lost the tendency to wake up in the middle

of the night and be wide awake. Maybe it is related.

My father was a HUGE responder to both the g/f c/f diet and epsom salts

therapy. which both were critical to his quality of life in his last four

years. I wish he were still alive so that I could see what his oxalate

levels may have been or if he would respond to the low oxalate diet.

He did have awful fungal issues. The nail on his toes were about a quarter

of an inch thick and yellow and crumbly. He was the grandfather that Bill

Shaw mentioned in his book that responded with neurological improvements to

diflucan..though Dr. Shaw got it wrong about his having a grandchild with

autism. My daughter never had autism.

My father lost the last ten years of his life to dementia, and part of my

quest all these years has been to avoid the same fate that has been in my

family for several generations. I have wondered how much of his dementia

came from oxalates getting into his brain and creating the oxidative stress

that now is being understood as being central to Alzheimers. My father

also had mini-strokes. Those possibly could have been caused by oxalates

building up and damaging the vascular tissues in his brain. Just today, I

read an article about oxalate collecting in the blood vessels of the

intestine and causing ulcerations and perforations and finally hemorrhage

in the intestine that ended up fatal in this patient.

How many parallels were there with my father? I don't know, but I do know

how long his intestinal issues had been with him because I found a letter

his father wrote to the services about these issues when he was drafted for

World War II when he was a very young man!

Anyway, if you read the articles I've put below about oxalates and

granulomas you will see how many different tissues this process may affect,

because oxalates can travel all over the body and do bad things. Another

little curiosity is that the formation of giant cells in response to

oxalate (that is mentioned below) also may be seen in tissues after measles

infection, though the literature on this relationship to measles (139

articles) never mentions oxalate. I cannot imagine how these things could

be linked, but I find the association to be intriguing given the

association of autistic regression in some to the MMR.

I don't see how any of this has anything to do with vitamin K, though, and

it sounds like 's theory has been doing a bit of migrating.

As far as I can tell from any literature I have been sent or have found on

my own, there is no direct relationship between oxalate issues and Vitamin

K other than they both have some effects on calcium trafficking and another

issue I'll mention below. I don't like to speak beyond the literature

other than to say what needs to be studied more.

To me, a great deal of harm has been done by the suggestion that taking

vitamin K could get rid of the oxalate issues in people whose oxalates most

likely came from hyperabsorption from food due to the inflammation of the

gut. I have no problems at all with taking vitamin K to make up for a

deficiency that is known to develop in those with gut inflammation. I am

sure that correcting such a deficiency was a very good thing, but it has

nothing to do with oxalates that has been characterized so far. I can say

that I think we need to see far more basic science research on what oxalate

does biologically and any other role it may play in calcium and other

mineral trafficking, for I would be surprised if its only good role is

trafficking calcium into the endoplasmic reticulum.

At any rate, I think it is time to look at those who stopped the low

oxalate diet when Tamaro proposed that vitamin K therapy made it

unnecessary, and see how the children following her strategy have done now

that it has been nine months since she proposed her theory. That's long

enough to grow a baby! The list of changes people see on low oxalate diet

are recorded on our website at Trying_Low_Oxalates . If

those taking vitamin K have seen the same list of improvements, and the

same degree of improvement, I would like to know!

One of the issues I raised back when because it had been discussed at the

FASEB oxalate conference and the urolithiasis conference I attended this

past fall, is that a vitamin-K dependent enzyme is involved with making

oxalate crystals form in tissues and it is stimulated in the presence of

oxalate. Gamma-glutamyl carboxylase is the name of this vitamin K

dependent enzyme.

From a study below:

Lipid peroxidation positively correlated with cellular oxalate, oxalate

binding, gamma-glutamyl carboxylase, and calcium level and negatively

correlated with GSH, vitamin E. ascorbic acid, and total protein thiol.

That means in those raising vitamin K levels at the same time as eating

high levels of oxalate with a leaky gut, that one would expect stepped up

utilization of this enzyme and stepped up formation of oxalate crystals and

increased oxidative damage in tissues. Is that a benefit??? Would it not

be better to take vitamin K (to correct a deficiency) at the same time as

LOWERING oxalate absorption from the diet?

If there is any lowering of urinary oxalate that comes from vitamin K when

the exposure to oxalate is held steady, then it may be that the oxalate

instead of being secreted into the urine and the lumen of the gut, is

instead encouraging the formation of crystals either in the kidney, or

elsewhere in the body. The crystals are far more toxic than the free

oxalic acid because of how they are handled by cells.

==================

On gamma-glutamyl carboxylase:

Blood. 2007 Feb 27; [Epub ahead of print][] Links

Fatal hemorrhage in mice lacking {gamma}-glutamyl carboxylase.

Zhu A, Sun H, RM, Furie BC, Furie B, Bronstein M, Kaufman RJ,

Westrick R, Ginsburg D.

Medical Institute, University of Michigan, Ann Arbor, MI,

United States.

The carboxylation of glutamic acid residues to gamma-carboxyglutamic acid

(Gla) by the vitamin K-dependent gamma-glutamyl carboxylase

(gamma-carboxylase) is an essential post-translational modification

required for the biological activity of a number of proteins, including

proteins involved in blood coagulation and its regulation. Heterozygous

mice carrying a null mutation at the gamma-carboxylase (Ggcx) gene exhibit

normal development and survival with no evidence of hemorrhage and normal

functional activity of the vitamin K-dependent clotting factors IX, X, and

prothrombin. Analysis of a Ggcx+/- intercross revealed a partial

developmental block with only 50% of expected Ggcx-/- offspring surviving

to term, with the latter animals dying uniformly at birth of massive

intra-abdominal hemorrhage. This phenotype closely resembles the partial

mid-embryonic loss and postnatal hemorrhage previously reported for both

prothrombin and Factor V (F5) deficient mice. These data exclude the

existence of a redundant carboxylase pathway and suggest that functionally

critical substrates for gamma-carboxylation, at least in the developing

embryo and neonate, are primarily restricted to components of the blood

coagulation cascade.

PMID: 17327402 [PubMed - as supplied by publisher]

3: Eur Urol. 1998;33(1):116-20.

Enhanced renal vitamin-K-dependent gamma-glutamyl carboxylase activity in

experimental rat urolithiasis.

Angayarkanni N, Selvam R.

Department of Medical Biochemistry, Dr. A.L. Mudaliar Postgraduate Institute of

Basic Medical Sciences, University of Madras, Taramani, India.

OBJECTIVE: To detect the role of the enzyme gamma-glutamyl carboxylase in an

experimental stone-forming condition. METHODS: Urolithiasis was induced in

experimental rats by (i) oral feeding of 1% ethylene glycol (EG) and (ii)

feeding a calculus-producing diet containing 3% sodium glycolate. RESULTS: A

significant enhancement in the activity of renal vitamin-K-dependent

gamma-glutamyl carboxylase was observed in both groups of experimental

urolithic

rats. Dicoumarol as well as EG treatment enhanced the accumulation of the

endogenous substrate for the enzyme. The carboxylase activity was stimulated by

sodium oxalate as well as calcium oxalate in vitro. A positive correlation was

observed between lipid peroxidation and the renal gamma-glutamyl carboxylase

activity. CONCLUSION: The enhanced carboxylase activity observed in the

hyperoxaluric condition is suggested to be due to stimulation of the enzyme by

oxalate/calcium oxalate, increased concentration of endogenous carboxylase

substrate and lipid peroxidation.

Publication Types:

Comparative Study

In Vitro

Research Support, Non-U.S. Gov't

PMID: 9471053 [PubMed - indexed for MEDLINE]

1: Chin Med J (Engl). 2003 Apr;116(4):569-72.

Decreased renal vitamin K-dependent gamma-glutamyl carboxylase activity in

calcium oxalate calculi patients.

Chen J, Liu J, Zhang Y, Ye Z, Wang S.

Department of Urology, Wuhan First Hospital, Wuhan 430022, China.

jhch800@...

OBJECTIVE: To study the activity of vitamin K-dependent gamma-glutamyl

carboxylase in patients with calcium oxalate (CaOx) urolithiasis compared with

healthy individuals and to assess its relationship to the renal calcium oxalate

urolithiasis. METHODS: Renal parenchymas were harvested from urolithic patients

and renal tumor patients undergoing nephrectomy. The renal carboxylase activity

was evaluated as the radioactivity of [(14)C] labeled sodium bicarbonate in

carboxylic reactions in vitro using beta-liquid scintillation counting.

RESULTS:

Significantly reduced activity of renal vitamin K-dependent gamma-glutamyl

carboxylase was observed in the urolithic group as compared with normal

controls

(P < 0.01). CONCLUSION: It suggests that the reduced carboxylase activity

observed in the urolithic patients may play an important role in the course of

renal calcium oxalate urolithiasis.

Publication Types:

Research Support, Non-U.S. Gov't

PMID: 12875724 [PubMed - indexed for MEDLINE]

2: Urol Res. 2002 Mar;30(1):35-47.

Calcium oxalate stone disease: role of lipid peroxidation and antioxidants.

Selvam R.

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

Medical Sciences, University of Madras, Taramani, Chennai, India.

drselvamr@...

Membrane injury facilitated the fixation of calcium oxalate crystals and

subsequent growth into kidney stones. Oxalate-induced membrane injury was

mediated by lipid peroxidation reaction through the generation of oxygen free

radicals. In urolithic rat kidney or oxalate exposed cultured cells, both

superoxide anion and hydroxyl radicals were generated in excess, causing

cellular injury. In hyperoxaluric rat kidney, both superoxide and

H2O2-generating enzymes such as glycolic acid oxidase (GAO) and xanthine

oxidase

(XO) were increased, and hydroxyl radical and transition metal ions, iron, and

copper were accumulated. The lipid peroxidation products, thiobarbituric

acid-reactive substances (TBARS), hydroperoxides, and diene conjugates were

excessively released in tissues of urolithic rats and in plasma of rats as well

as stone patients. The accumulation of these products was concomitant with the

decrease in the antioxidant enzymes, superoxide dismutase (SOD), catalase,

glutathione peroxidase (GPx), and glucose-6 phosphate dehydrogenase (G6PD) as

well as radical scavengers, vitamin E, ascorbic acid, reduced glutathione

(GSH),

and protein thiol. All the above parameters were decreased in urolithic

condition, irrespective of the agents used for the induction of urolithiasis.

Oxalate binding activity and calcium oxalate crystal deposition were markedly

pronounced, along with decreased adenosine triphosphatase (ATPase) activity.

Lipid peroxidation positively correlated with cellular oxalate, oxalate

binding,

gamma-glutamyl carboxylase, and calcium level and negatively correlated with

GSH, vitamin E. ascorbic acid, and total protein thiol. Antioxidant therapy to

urolithic rats with vitamin E, glutathione monoester, methionine, lipoic acid,

or fish oil normalised the cellular antioxidant system, enzymes and scavengers,

and interrupted membrane lipid and protein peroxidation reaction, ATPase

inactivation, and its associated calcium accumulation. Antioxidant therapy

prevented calcium oxalate precipitation in the rat kidney and reduced oxalate

excretion in stone patients. Similarly, calcium oxalate crystal deposition in

vitro to urothelium was prevented by free radical scavengers such as phytic

acid

and mannitol by protecting the membrane from free radical-mediated damage. All

these observations were suggestive of the active involvement of free

radical-mediated lipid peroxidation-induced membrane damage in the pathogenesis

of calcium oxalate crystal deposition and retention.

Publication Types:

Review

PMID: 11942324 [PubMed - indexed for MEDLINE]

4: Calcif Tissue Int. 1993 Oct;53(4):242-8.

The effect of warfarin on urine calcium oxalate crystal growth inhibition and

urinary excretion of calcium and nephrocalcin.

Worcester EM, Sebastian JL, Hiatt JG, Beshensky AM, Sadowski JA.

Nephrology Section, Zablocki VA Medical Center, Milwaukee, Wisconsin.

Urine contains inhibitors of calcium oxalate (CaOx) crystal growth. One such

inhibitor is nephrocalcin (NC), a glycoprotein which is made in the kidney and

contains several residues of gamma-carboxyglutamic acid (Gla) per molecule. The

presence of Gla may be important to its ability to inhibit crystal growth.

Several studies suggest that vitamin K-dependent proteins may also play a role

in renal calcium (Ca) handling, and that vitamin D deficiency may lead to

excess

urinary Ca loss, but the effect of the vitamin K antagonist warfarin on urinary

Ca excretion and CaOx growth inhibition in humans is not known. We studied 11

men while they were taking warfarin for a mean of 252 days, and again a mean of

64 days after its discontinuation. Urinary Ca excretion did not differ between

those on or off warfarin, or between those on warfarin and normal controls. The

ability of the subjects' urine to inhibit CaOx crystal growth did not differ on

or off warfarin, or from that of control urine, and the excretion of

immunoreactive NC also did not differ between these groups. NC was found to be

responsible for approximately 16% of the CaOx growth inhibition seen. These

results do not suggest that vitamin K-dependent proteins play a major role in

renal Ca excretion in men, or that interference with vitamin K alters NC

excretion or inhibitory activity of the urine.

Publication Types:

Research Support, U.S. Gov't, Non-P.H.S.

Research Support, U.S. Gov't, P.H.S.

PMID: 8275352 [PubMed - indexed for MEDLINE]

===========================

On oxalate-induced granulomas

1: J Laryngol Otol. 2001 Jun;115(6):514-6.

Calcium oxalate granuloma of the nose of a chronically dialysed nephritic

patient.

Böör A, Jurkovic I, Friedmann I, Benický M, Kocan P.

Institute of Pathology, Medical Faculty, P. J. Safárik University, Kosice,

Slovak

Republic.

The patient was a 54-year-old woman who had been suffering from chronic

tubulo-interstitial nephritis for about seven years, requiring haemodialysis.

More recently, she developed a polypoid mass in the left nasal cavity causing

discomfort on breathing and slight epistaxis. The tumour was of gritty

consistency and measured 28 x 8 x 5 mm. Microscopy showed a lobulated almost

cystic structure composed of granulation tissue with comparatively few plasma

cells and many multinucleated giant cells lining the spaces filled with

crystalline deposits of calcium oxalate.

Publication Types:

Case Reports

PMID: 11429084 [Pubmed - indexed for MEDLINE]

2: Sarcoidosis Vasc Diffuse Lung Dis. 2000 Jun;17(2):140-50.

Calcium oxalate and iron accumulation in sarcoidosis.

Ghio AJ, Roggli VL, Kennedy TP, Piantadosi CA.

Department of Medicine, Duke University Medical Center, Durham, NC 27710, USA.

BACKGROUND: In many patients with sarcoidosis, the granulomas contain inclusion

bodies within giant cells. Many giant cells contain crystalline oxalate that

chemically coordinates iron on the surface of the crystal. If this iron is

incompletely coordinated and capable of redox cycling, then oxalate might

contribute to granuloma formation in the lung. METHODS: Using human tissues,

isolated alveolar macrophages and respiratory epithelial cells, we measured the

ability of calcium oxalate to sequester iron, stimulate cytokine release and

cause granuloma formation. We then studied the effects of in vivo oxalate

instillation on pulmonary granuloma formation over 3 to 6 months in rats.

RESULTS: Calcium oxalate present in human sarcoid granulomas sequesters

significant amounts of iron and ferritin. In alveolar macrophage cultures,

oxalate accumulates iron and stimulates ferritin production and giant cell

formation. In cultured respiratory epithelial cells, calcium oxalate increases

the release of two interleukins (IL), IL-8 and IL-6, involved in granuloma

formation by 8 to 10 fold within 24 hours. Intratracheal instillation of

calcium

oxalate crystals into the lungs of rats is associated with pulmonary iron and

ferritin accumulation and organic carbonyl formation consistent with sustained

oxidative stress. These exposures were accompanied by influx of alveolar

macrophages, giant cell formation, and a granulomatous response in the lung.

CONCLUSIONS: These results support an association between calcium oxalate

deposition in the lung, iron mediated oxidative stress and formation of some of

the granulomas of sarcoidosis.

PMID: 10957762 [Pubmed - indexed for MEDLINE]

3: Histopathology. 1998 May;32(5):481-2.

Comment in:

Histopathology. 1999 Aug;35(2):181-3.

An unusual granulomatous form of chronic pyelonephritis mimicking tuberculosis.

Bouzourene H, Bouzourene N, Francke ML.

Publication Types:

Case Reports

Letter

PMID: 9639129 [Pubmed - indexed for MEDLINE]

4: Histopathology. 1995 Nov;27(5):423-9.

Calcium oxalate crystal deposition in epithelioid histiocytes of granulomatous

lymphadenitis: analysis by light and electronmicroscopy.

Symmans PJ, Brady K, Keen CE.

Department of Histopathology, ham Hospital, London, UK.

In this study of 55 cases of granulomatous lymphadenitis of various

aetiologies,

both haematoxylin and eosin stained and unstained sections were examined by

light

and polarizing light microscopy for crystals within epithelioid

histiocytes. This

investigation was prompted by a case of granulomatous lymphadenitis in

which the

identification of ovoid birefringent structures within epithelioid histiocytes

led to an initial false suggestion of foreign body reaction. Identical single,

small, ovoid or biconvex, intensely birefringent crystals, invisible by

ordinary

light microscopy, were found within the cytoplasm of mononuclear epithelioid

histiocytes in 37 cases. There was only minor crystal loss with routine H & E

staining. The sections were also examined by scanning electronmicroscopy in

secondary and backscattered electron imaging modes and 27 cases were found to

contain biconvex crystals which were shown on X-ray energy dispersive

spectroscopic microanalysis to be consistent with calcium oxalate. There was a

good quantitative correlation between light and scanning electron microscopy.

Tissue from the index case was also examined by transmission

electronmicroscopy,

and electron dense crystals were identified. We confirm the previous

findings of

ovoid oxalate crystals in a variety of granulomatous conditions including

Mycobacterial infection, sarcoidosis and Crohn's disease. Ovoid crystals of

calcium oxalate, a common finding in granulomatous lymphadenitis, appear to be

endogenously derived, and should be more widely recognized in order to avoid

misdiagnosis of foreign body reaction.

Publication Types:

Case Reports

Review

PMID: 8575732 [Pubmed - indexed for MEDLINE]

5: J Clin Pathol. 1994 May;47(5):470-1.

Secondary oxalosis and sperm granuloma of the epididymis.

Coyne J, al-Nakib L, Goldsmith D, O'Flynn K.

Department of Histopathology, University Hospital of South Manchester, UK.

A 30 year old man with a 20 year history of chronic renal failure who presented

with a testicular lesion is described. The lesional pathology, secondary

oxalosis, and associated sperm granuloma of the epididymis was clinically

considered to be an intrascrotal tumour. The oxalate crystal deposition was

present within the rete testis, the ductuli efferents, and the epididymis along

with sperm granulomata. This seems to be a rare complication of secondary

oxalosis associated with chronic renal failure and having both clinical and

pathological implications.

Publication Types:

Case Reports

PMID: 8027405 [Pubmed - indexed for MEDLINE]

6: J Urol. 1993 Dec;150(6):1800-2.

Stone granuloma: a cause of ureteral stricture.

Dretler SP, Young RH.

Kidney Stone Center, Massachusetts General Hospital, Boston.

Ureteral stricture is a recognized complication of ureteroscopy and ureteral

stone fragmentation. Although most strictures are either asymptomatic or easily

dilated, there are some strictures that result in progressive ureteral

obstruction, do not respond to ureteral dilation and require operative

intervention. A review of 125 percutaneous nephrostolithotomies for staghorn

stone disease and 652 ureteroscopic stone fragmentations revealed 5 cases in

which refractory ureteral strictures developed, requiring operative

intervention.

In 4 patients a " stone granuloma, " embedded particles of calcium oxalate

associated with macrophages and foreign body giant cells, was found with

surrounding fibrosis and ureteral obstruction. In the remaining patient a

suture

granuloma from a recent ureterolithotomy was the source of the stricture.

In each

instance of stone granuloma the particles of calcium oxalate had become

embedded

in the wall as a consequence of ureteroscopic stone fragmentation and partial

ureteral wall disruption. During ureteroscopy and intracorporeal lithotripsy

every effort should be made to prevent calcium oxalate particles from becoming

embedded in the ureteral wall. They are not inert and may cause irreversible

stricture formation. To our knowledge, stone granuloma is a previously

undescribed phenomenon and should be suspected when ureteral strictures that

occur following ureteroscopy do not respond to endourological methods of

management.

Publication Types:

Case Reports

PMID: 8230508 [Pubmed - indexed for MEDLINE]

7: Br J Dermatol. 1993 Jun;128(6):690-2.

Cutaneous oxalate granulomas in a haemodialysed patient: report of a case with

unique clinical features.

Isonokami M, Nishida K, Okada N, Yoshikawa K.

Department of Dermatology, Osaka University School of Medicine, Japan.

We report a patient undergoing haemodialysis, who developed multiple

subcutaneous

nodules. Histology showed that the nodules were composed of deposits of

crystals

in the dermis, with an associated foreign-body reaction. The crystalline

deposits

were identified as calcium oxalate by histochemical staining, polarizing

microscopy, and analytical electron microscopy.

Publication Types:

Case Reports

PMID: 8338754 [Pubmed - indexed for MEDLINE]

8: Rev Rhum Mal Osteoartic. 1991 Nov 30;58(11):763-9.

[bone involvement in primary oxalosis. Study of 20 cases]

[Article in French]

Benhamou CL, Bardin T, Tourlière D, Voisin L, Audran M, Edouard C, Lafage MH,

Sebert JL, de Vernejoul MC, Wendling D.

Service de Médecine F, Hôpital de la Source, Orleans.

The authors report 20 cases of primary oxalosis with bone involvement, late

revealed in adults in 19 cases. They have studied the clinical,

radiological and

histological manifestations of this bone oxalosis. 19 cases had an end stage

chronic renal failure, either treated by maintenance hemodialysis, or by renal

(or liver-renal) graft. 17 patients complained of bone pain after starting

hemodialysis; 3 had vertebral crush fractures, and 1 multiple spontaneous

fractures. Diffuse bone sclerosis (with a homogeneous pattern on axial skeleton

and a patchy appearance on the peripherical skeleton), bone translucency,

subperiosteal phalangeal resorption were the main radiological symptoms.

Oxalate

crystals surrounded by a giant cells granuloma were always observed on bone

biopsy (16 cases). Bone resorption was observed in 9 cases, hyperparathyroidism

in 14 cases and osteomalacia in 7 cases. Hyperparathyroidism does'nt

explain all

the clinical and radiological manifestations (especially bone resorption). Bone

resorption as other radiological and clinical manifestations can be found

without

hyperparathyroidism and can increase despite parathyroidectomy; so, bone

resorption seems to be partly due to the granulomatous reaction around oxalate

crystals rather than hyperparathyroidism.

Publication Types:

English Abstract

PMID: 1780651 [Pubmed - indexed for MEDLINE]

9: Lancet. 1991 Feb 23;337(8739):502-3.

Comment in:

Lancet. 1991 Apr 6;337(8745):854.

Unusual particles and crystals in Crohn's disease granulomas.

Roge J, Fabre M, Levillain P, Dubois P.

Publication Types:

Letter

PMID: 1671513 [Pubmed - indexed for MEDLINE]

10: Endocrinol Metab Clin North Am. 1990 Dec;19(4):839-49.

Urinary calculi in hypercalcemic states.

WC.

University of Florida College of Medicine, Gainesville.

In this brief review of various hypercalcemic disorders and the likelihood of

renal calculus formation, it is clearly evident that renal calculi occur much

more often in hyperparathyroidism than in the other hypercalcemic states.

Dystrophic calcification and nephrocalcinosis are common to all of the

hypercalcemic disorders, including hyperparathyroidism, when the

hypercalcemia is

marked and the limit of solubility of calcium and phosphate in serum is

approached. Interestingly, in sarcoidosis there are calcium oxalate crystals in

variously distributed sarcoid granuloma, and the renal calculi are composed of

calcium oxalate. By contrast, in hyperparathyroidism, the calculi composed of

calcium phosphate predominate. This indicates a subtle and as yet undefined

alteration in oxalate metabolism in sarcoidosis. An increase in urine pH occurs

in hyperparathyroidism, and this enhances formation of crystalline calcium

phosphate. However, the striking disparity between the frequency of calculus

formation in hyperparathyroidism and that in other hypercalcemic disorders,

several of which may be of relatively long duration, suggests that there indeed

may be increased promoters of crystal formation in the urine of

hyperparathyroid

patients.

Publication Types:

Research Support, U.S. Gov't, P.H.S.

Review

PMID: 2081514 [Pubmed - indexed for MEDLINE]

11: J Am Acad Dermatol. 1990 Feb;22(2 Pt 1):316-8.

Cutaneous oxalate granuloma.

Sina B, Lutz LL.

University of land School of Medicine, Department of Medicine, Baltimore

21201.

Publication Types:

Case Reports

PMID: 2312818 [Pubmed - indexed for MEDLINE]

12: Am J Clin Pathol. 1988 Nov;90(5):545-58.

Calcium oxalate in sarcoid granulomas. With particular reference to the small

ovoid body and a note on the finding of dolomite.

Reid JD, Andersen ME.

Pathology Department, Memorial Hospital, Ravenna, Ohio.

The nature, prevalence, and specificity of birefringent calcific particles in

granulomas of sarcoidosis have been examined, including histochemical

reactions,

single particle, and microchemical analyses. Particular attention was paid to

small ovoid forms of which most were calcium oxalate monohydrate. Larger

crystals, those within giant cells, and the birefringent component of a

Schaumann

complex were also calcium oxalate. Small ovoids appeared to originate in

macrophages and to be precursors of other forms; they were found in 86% of

lymph

nodes and 73% of surgical lung specimens. They were not specific for

sarcoidosis.

Organisms could not be certainly identified in them. Their origin is

discussed in

relation to activated macrophages, calcium, and oxalate metabolism, and the

role

of calcium oxalate in granulomas is considered. Four particles from two cases

were dolomite and two were a calcium-sulphur compound. The biologic origin of

dolomite is reviewed.

Publication Types:

Research Support, Non-U.S. Gov't

PMID: 3177273 [Pubmed - indexed for MEDLINE]

13: Mod Pathol. 1988 Nov;1(6):415-9.

Significance of crystalline inclusions in lung granulomas.

Visscher D, Churg A, Katzenstein AL.

Department of Pathology, University of Alabama, Birmingham.

We describe six examples of nonnecrotizing lung granulomatosis in which there

were numerous polarizable crystalline inclusions. The crystals were easily

visible in routine H & E-stained slides and were so prominent that the

question of

a pneumoconiosis or other exogenous source was raised. There was no clinical

history to suggest an inhalational source, however, and no patient used

intravenous drugs. In one case, an atypical mycobacterial infection was

proven to

be etiologic, while sarcoidosis was documented in three. A review of 63

additional consecutive lung biopsies and 24 extrapulmonary biopsies showing

nonnecrotizing granulomatous inflammation demonstrated crystals in almost

two-thirds of cases. X-ray spectroscopy and histochemistry demonstrated

that the

crystals contained mainly calcium oxalate and calcium carbonate and thus

represented products of cellular metabolism. These findings emphasize that

crystalline inclusions are common in lung granulomas of varying etiology. They

may be numerous, and their presence does not necessarily indicate a

pneumoconiosis or other exogenous source.

PMID: 2851787 [Pubmed - indexed for MEDLINE]

14: Heart Vessels Suppl. 1985;1:262-70.

Granulomatous inflammation of the heart.

Ferrans VJ, Rodríguez ER, McAllister HA.

Morphologic characteristics of granulomatous inflammation in the heart and

pericardium are discussed. In rheumatic fever, two types of myocardial

lesion are

present--a nonspecific myocarditis and a specific lesion characterized by

granulomas known as Aschoff's nodules. The latter undergo a cycle of

development

and resolution; in their mature stage, they contain Aschoff's cells which are

uni- or multinucleated histiocytes with a serrated nuclear chromatin bar.

Ultrastructural studies do not suggest a relationship between these cells and

cardiac or smooth muscle cells. In metabolic disorders, granulomas occur in

Farber's disease (lipogranulomatosis), gout (in which tophi are associated with

calcific deposits and with a foreign body cellular reaction), the various

syndromes of oxalosis (in which oxalate deposits also lead to a foreign body

reaction), and in chronic granulomatous disease of childhood. Foreign body

giant-cells can also be found in association with calcification of necrotic

myocytes and in the syndromes of " cholesterol pericarditis. " Well-developed

granulomas occur in sarcoidosis, giant cell myocarditis, as a reaction to

foreign

bodies and devices implanted within the cardiovascular system, and in certain

diseased caused by infective agents (tuberculosis, fungal and parasitic

disorders). Infiltration of the heart by nongranulomatous masses of histiocytes

can occur in Whipple's disease, Niemann-Pick disease, the

hyperlipoproteinemias,

Gaucher's disease, and in proliferative disorders of the mononuclear phagocyte

system (juvenile xanthogranuloma, Chester-Erdheim syndrome, and malignant

histiocytosis).

Publication Types:

Review

PMID: 3916477 [Pubmed - indexed for MEDLINE]

15: Mt Sinai J Med. 1980 May-Jun;47(3):255-7.

Sarcoid-like granulomas in secondary oxalosis: a case report.

Fayemi AO, Ali M.

Publication Types:

Case Reports

PMID: 6967173 [Pubmed - indexed for MEDLINE]

16: Arch Pathol. 1973 Nov;96(5):320-6.

The nature of yellow-brown bodies in peritoneal lymph nodes.

Doyle WF, Brahman HD, Burgess JH.

PMID: 4126348 [Pubmed - indexed for MEDLINE]

17: Fertil Steril. 1964 May-Jun;15:278-89.

MINERAL OIL GRANULOMAS OF THE UTERUS AND PARAMETRIUM AND GRANULOMATOUS

SALPINGITIS WITH SCHAUMANN BODIES AND OXALATE DEPOSITS.

CAMPBELL JS, NIGAM S, HURTIG A, SAHASRABUDHE MR, MARINO I.

PMID: 14156905 [Pubmed - OLDMEDLINE for Pre 1966]

18: Nippon Jibiinkoka Gakkai Kaiho. 1963 Jun;66:788-803.

[OSTITIS OR OSTEOMYELITIS TEMPORALIS CHRONICA (OTITIS MEDIA IN THE BROAD SENSE)

WITH CHOLESTERIN GRANULOMA.]

[Article in Japanese]

NIHO S, MURAKAMI I, DOTA T, SAEKI M, SASAKI Y, SAKAMOTO T.

PMID: 14055978 [Pubmed - OLDMEDLINE for Pre 1966]

At 05:57 PM 6/4/2007, you wrote:

>Susam:

>

>I'd be interested to hear your thoughts on the Fat Soluble Vitamin

>(Vitamin K) protocol to bring down oxalate levels. They seem to think

>that the oxalate production is tied to a " granumalatous " Vitamin D

>immune response upsetting calcium channels in the body and that the

>LOD will not help with mitigating that problem. Or do we need to do

>both?

>

>Gayatri

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June 4, 2007

Hi :

Thanks for sharing your father's story, it sounds painful and I am

sure he would have appreciated all that you are doing to gain

knowledge and share it with others.

If you have ever looked at classical homeopathy, ulcers and mini-

strokes are to be found in those that are syphilitic. The syphilinum

miasm causes destruction of tissue. In case you are wanting to take

care of your own and your daughter's long-term health.

On the presence of oxalates after a measles infection, one time I

took my son to the EAV naturopath - he was quite sick. What came up

on his machine were 2 miasms, Medorrhinum and Syphilinum and the

remedy that was covering both of those was also one for suppressed

measles. I thought that was interesting since about 80% or more of

the ASD kids have the measles in their gut. Those with Medorrhinum

have arthritis, asthma, or diabetes in their family.

Thanks again for taking the time out to reply and give all these

citations, I'll hopefully get back to re-reading those carefully

sometime soon.

Gayatri

> >Susam:

> >

> >I'd be interested to hear your thoughts on the Fat Soluble Vitamin

> >(Vitamin K) protocol to bring down oxalate levels. They seem to

think

> >that the oxalate production is tied to a " granumalatous " Vitamin D

> >immune response upsetting calcium channels in the body and that the

> >LOD will not help with mitigating that problem. Or do we need to do

> >both?

> >

> >Gayatri

>

> --

> No virus found in this outgoing message.

> Checked by AVG Free Edition.

> Version: 7.5.472 / Virus Database: 269.8.7/830 - Release Date:

6/3/2007 12:47 PM

>

June 5, 2007

Gayatri,

I really didn't mean to go on so about my father, but the more I started

thinking about his history, and all his GI issues, the more these things

seemed to fit a pattern. Oh, how I wish that earlier in his life someone

could have figured out how to heal his gut! He had so many brushes with

death because of these issues, but still managed to live to be 82! Taking

care of him in his old age was one of the greatest priviledges (and

burdens) of my life.

I do hope you found what I wrote about the vitamin K issues below what I

wrote about my father. It is so important to understand the science and

what is known about how these molecules interact in such complex ways.

Homeopathy seems to be built on tradition and the reputation of some

well-respected observers who defined all these categories and the

treatments. There is not a lot that someone used to a scientific model

(ie, getting information based on experimental data) can grasp when the

information that is presented about homeopathy is confined pretty much to

" When you see this, do this one thing, or this set of things... " . It seems

so rare to hear any discussion of why those relationships were ever

anticipated by those who set these traditions long ago.

At 01:16 AM 6/5/2007, you wrote:

>Hi :

>

>Thanks for sharing your father's story, it sounds painful and I am

>sure he would have appreciated all that you are doing to gain

>knowledge and share it with others.

>

>If you have ever looked at classical homeopathy, ulcers and mini-

>strokes are to be found in those that are syphilitic. The syphilinum Gar

>miasm causes destruction of tissue. In case you are wanting to take

>care of your own and your daughter's long-term health.

>

>On the presence of oxalates after a measles infection, one time I

>took my son to the EAV naturopath - he was quite sick. What came up

>on his machine were 2 miasms, Medorrhinum and Syphilinum and the

>remedy that was covering both of those was also one for suppressed

>measles. I thought that was interesting since about 80% or more of

>the ASD kids have the measles in their gut. Those with Medorrhinum

>have arthritis, asthma, or diabetes in their family.

>

>Thanks again for taking the time out to reply and give all these

>citations, I'll hopefully get back to re-reading those carefully

>sometime soon.

>

>Gayatri

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June 5, 2007

Thanks ,

Since I wrote

this question to you I decided to look at the foods to see how many he might be

having that are high O. I was surprised to find that not many things he eats

are high O and only a couple of things on the medium list (oranges). A

lot of the things on the high O list either 1 or all 3 of my kids are allergic

to. I thought it was interesting. Maybe their reactions are because

of the oxalates. Even celery (which I thought was a strange allergy) is

on my daughter’s allergy list. All nuts are in my whole family

(mine and my kids have the worst reactions to almonds). So all along I’ve

been concerned about not looking into oxalates we’ve been pretty much

limiting them anyway. I was very interested in the probiotic being

developed as well. Is there are progress on that?

Good luck with

all of the testing. And keep up the great work. Thanks,

From: mb12 valtrex [mailto:mb12 valtrex ] On Behalf Of Owens

Sent: Monday, June 04, 2007 5:10

PM

To: mb12 valtrex

Subject: RE: Candida