Re: starting valtrex --upset belly

[Guest guest]

If your child is on valtrex he must also be on an antifungal, preferably diflucan. The valtrex causes yeast. To: mb12valtrex Sent: Thursday, January 31,

2013 9:12 AM Subject: starting valtrex --upset belly

We just started valtrex and my son's GI trac has been very upset... we have not dealt with GI issues in a long time... he is having a pretty constant diarrhea. Although hei is stillthe wanting toto eat andit drink normally...has anyone else experienced this? Could it be dying off or I am wondering if he is having a reaction to the medication... this is something other kids and families have dealt with, or if I should be worried.

Thanks kristen

[Guest guest]

Thanks for replying ...he is on difflucan!

 

If your child is on valtrex he must also be on an antifungal, preferably diflucan. The valtrex causes yeast.

 

To: mb12valtrex

Sent: Thursday, January 31,

2013 9:12 AM Subject: starting valtrex --upset belly

 

We just started valtrex and my son's GI trac has been very upset... we have not dealt with GI issues in a long time... he is having a pretty constant diarrhea. Although hei is stillthe wanting toto eat andit drink normally...has anyone else experienced this? Could it be dying off or I am wondering if he is having a reaction to the medication... this is something other kids and families have dealt with, or if I should be worried.

Thanks kristen

[Guest guest]

Curious,could she use charcoal for upset belly? To: "mb12valtrex " <mb12valtrex > Sent: Thursday, January 31, 2013 9:27 AM Subject: Re: starting valtrex --upset belly

If your child is on valtrex he must also be on an antifungal, preferably diflucan. The valtrex causes yeast. To: mb12valtrex Sent: Thursday, January 31,

2013 9:12 AM Subject: starting valtrex --upset belly

We just started valtrex and my son's GI trac has been very upset... we have not dealt with GI issues in a long time... he is having a pretty constant diarrhea. Although hei is stillthe wanting toto eat andit drink normally...has anyone else experienced this? Could it be dying off or I am wondering if he is having a reaction to the medication... this is something other kids and families have dealt with, or if I should be worried.

Thanks kristen

[Guest guest]

and ,

I just took a look at pubmed, and there doesn't appear to be any evidence of an

association between valtrex and candida infections, Valtrex and similar drugs

are used so widely that I believe there really would be a literature on this

association if this relationship was real. Valtrex is used so much in the HIV

world where people often have to deal with immunosupression and herpetic

infections. If anyone was going to make that observation with data to support

it, it would have happened there.

So could these very real changed symptoms you noticed actually mean something

else?

What I have continually seen in analyzing what has now been 680 of the Great

Plains Organic Acid tests, doing complicated statistics on this data, is that

on before and after OATs when people report they were put on diflucan, their

next OAT is frequently an oxalate disaster....often with oxalate levels

doubling, and also evidence that they are now in much worse oxidative stress.

That can break a lot of things.

The OATS also show evidence (that often was not there before) of making

endogenous oxalate. This doesn't mean the oxalate markers went over the

reference ranges. We see evidence of endogenous oxalate going up at around 40

mmole/mol creatinine, which is far below the reference range from Great Plains.

Why would increases in oxalate that your body makes happen after diflucan?

Diflucan is well known to be very hard on the liver, causing so much stress to

the body that the PDR recommends doctors do liver functon tests. When the liver

gets in oxidative stress, B6 dependent enzymes won't work properly.

Unfortunately, as a study I've mentioned below on rats and oxalate showed, AST

and ALT cannot rise after a B6 functional deficiency happens and that situation

also leads to increased production of oxalate.

In the cases where I've seen oxalate increase after diflucan, this is not

dietary oxalate but is oxalate the body makes because the enzymes that usually

process the intermediate glyoxylate to something harmless, are no longer

working. This probably happens because of the oxidative stress caused by the

drug.

What happens instead? Glyoxylate (which isn't on the OAT) builds up

intracellularly, and is converted into oxalate by lactate dehydrogenase, At the

same time, some of the increased level of glyoxylate is also converted to

glycolic acid and glyceric acid via other routes. Glycolic acid and glyceric

acid, like oxalate, are on the OAT and it is not hard to notice the levels of

all three of these going up together when that happens before and after some

treatment.

Sometimes, though, the fact that these analytes have gone up is not obvious

because increases in oxalate can be accompanied by stepped up creatinine

secretion.

How does that work?

Since everything on the test is ratioed to creatinine, raising the size of the

denominator makes the whole ratio fall. This affects everything on the test, so

it can make everything on the test suddenly fall low, and below the reference

ranges, and that might make your doctor think that he just solved a lot of

problems.

Unfortunately, the sudden decrease of everything on the test is an artifact that

happens because of the change in creatinine secretion.

What does that mean?

Creatinine secretion increasing when oxalate increases is documented in an

animal study on rats, and in so many OATs I've seen where the concentration of

everything looked like it fell together. For the study, please see

https://www.jstage.jst.go.jp/article/biomedres/27/3/27_3_93/_pdf.

Not knowing about the shift in creatinine is why it is so easy for doctors not

to see what is going on and that is why your doctor might miss noticing the

increase in oxalate markers on the GPL test, but these are not measured in tests

from Metametrix or Genova.

But why might increased oxalate cause GI symptoms and behavioral symptoms at the

same time?

Scientists in the last four years have been busy characterizing the transporters

oxalate uses to cross the membranes in the body, so how it enters and exits

cells. They have learned that these transporters get involved with the movement

of water, regulation of pH, and the movement of other molecules important to

autism, like sulfate, and iodine, and chloride. The science has not come far

enough for us to understand all the signaling mechanisms that change how oxalate

transport works, but a big focus of their research is the gut.

Scientists still cannot tell us why the changes in movement of oxalate come on

suddenly, but one of the signals that has been characterized is angiotensin II,

which also regulates your appetite for salt and water, but it causes a sudden

shift in oxalate secretion to the gut.

In the first year of the Autism Oxalate Project, a survey of changes parents

reported in their children on a low oxalate diet amounted to huge improvements

in autistic symptoms (the biggest being sociability) and also huge improvements

in GI function. That was also associated with improved motor skills, growth

when they needed it, and loss of pain and many other things.

In other populations (and we are monitoring the diet now also in many other

populations in adults) oxalate is associated with increased pain of all sorts.

Also, some people have noticed that when oxalate " dumping " occurs, when the body

starts to release oxalate stores from the body, it can be accompanied by a

change in attitude or perception that amounts to a failure to be able to notice

or understand someone else's point of view...like a lot of unreasonable

responses to situations.

So if you really want to distinguish the " yeast versus oxalate " issues, then do

two very objective things. The first is, get a stool culture for that very

moment you saw the changes in behavior.

Two peer reviewed articles on autism found no difference in the amount of

candida in autism in the stool compared to controls, and both of these studies

were conducted by people who are " friendly " to DAN! approaches, but their data

did NOT support a " yeast is a big deal " autism model.

The other thing to do is take a urine sample and freeze it, and then send it for

a new OAT from Great Plains so you can check the oxalate markers.

A study in Poland published in the European Journal of Paediatric Neurology last

year found that 35 out of 36 children with autism who were not on special diets,

had no kidney issues, and no seizures (all which could associate with high

oxalate) were higher than ALL the control children in blood, in urine, or in

both and as a group they were two and a half to three times higher.

This oxalate data is some of the strongest and most consistent data that has

ever been seen in autism, and it went virtually unnoticed. Did your doctor

realize what it meant?

Anyone can read the study here:

autism.org/content/PDF_files_newsletters/oxalate_and_autism.pdf.

It has been hard to communicate to the autism community how seriously damaging

oxalate is known to be to the body, and especially to the mitochondrion.

Something about autism, as the Polish study showed, seems to offer some

protection to the kidneys compared to what happens in primary hyperoxaluria at

the same levels of oxalate.

But even though it isn't causing kidney stones, the oxalate being that high in

the body is still harmful....just not as much to the kidney.

So if your doctor is NOT on board with the oxalate story, find out why not?

He may not be aware that oxalate causes oxidative stress and mitochondrial

dysfunction. Its toxicity can well account for issues that we've seen go away

in children who have been able to reduce oxalate.

But the diet isn't at all the whole thing. At AutismOne two years ago, I

presented data from ten OATs on a child I received after the fact, from someone

whose doctor ordered all these tests. This child had been on a low oxalate diet

the whole time, but between her fifth and sixth OAT, her oxalate and

pyroglutamate levels soared. (Pyroglutamate is a marker of oxidative stress.)

The mom told me that what they had changed between those OATs was introducing

diflucan and nystatin, and in the next two years, the oxalate levels in this

child did not go down, despite diet, but stayed in dangerous territory,

It is important to know that some of the biomed treatments over time can lead to

worsened oxalate situations and this is a dilemma for everybody. I've been

involved in autism research since 1995 and have labwork on children since the

early days, and I keep seeing that children whose original OAT I have, after

being treated with rounds and rounds of antimicrobials have gotten OATs that get

worse and worse on the oxalate front the longer they've been treated with

antimicrobials. I'm seeing this perspective in some kids over ten years.

I totally acknowledge that these treatments may cause quick behavioral

improvements, but I'm wondering, rather than producing improved behavior from

killing something, they may be " behaviorally effective " because of stopping the

detox process of oxalate.

What do I mean by that? It may be acting in a similar way to how, for an

alcoholic, taking another drink stops delirium tremens. Our listserve already

learned years ago that the way to stop an oxalate " dump " is to get more oxalate,

and then the " dump " stops, and so do the symptoms, but we've learned that

stopping that process just delays the problem and sets someone up for worse

problems later.

This is the real bugabear about how oxalate works and how the body detoxes from

it and i'm sure it is confusing to everybody.

Anyway, please don't assume that every behavioral meltdown is yeast. From what

I've been able to see so far, the evidence (objective lab tests) really don't

support that very strong belief, especially after you start understanding the

science of how oxalate is handled and affects symptoms.

I'm not on this listserve much, but the subject got my attention today, and I

really want parents to realize there is another way of interpreting these

symptoms that is tied very strongly to objective labwork.

You can get more information about oxalate at www.lowoxalate.info or you can

come join our yahoogroup at Trying_Low_Oxalates that now has

almost 7000 members. This listserve is still growing at a furious rate after

eight years of work in this area. We find new studies almost every week that

offer plausible explanations for what people have observed changing in their

children.

>

> > **

> >

> >

> > If your child is on valtrex he must also be on an antifungal, preferably

> > diflucan. The valtrex causes yeast.

> >

> >

>

[Guest guest]

, you know I heart you. :)I thought I'd add a bit to the discussion. It's been a while for me too. ;)You're welcome to look at the antiviral 101 link in my signature for some answers and 3 rat studies. I haven't done any digging for human studies since then. My son is recovered so I really haven't been that involved anymore, aside from maintaining this list.Valtrex switches the immune system from TH1 to TH2 (or vice versa, I can never remember off the top of my head, it's in the link). This is a known fact within the medical community. TH1 cytokines are what control yeast. I don't believe the yeast issue is strictly candida since we are talking about a systemic inability to control yeast appropriately while on antifungals. There's never been any hidden fact that liver function tests should be done while on systemic antifungals. It's always been out in the open. It can be hard on the liver, and no one has ever contested that. In the 6 years my son has been on antifungals, he's never had an issue with his liver though. Some have issues the first month.I don't honestly know much about HIV treatment, but I do know that many HIV patients do take antivirals and antifungals concurrently because they are immunosuppressed. I'm not sure if it would be something that is worth studying to them if it's a known fact that antivirals switch TH1 to TH2 cytokines. Especially since NK cells are already low in HIV. I can really only speculate, and I don't have a lot of time to do any digging on google, but thought I'd at least offer up some studies. But all infections are a rather large concern so, again, I'm not sure it would even be an issue for study since it's already known to suppress the immune system and they are already suppressed from the very nature of HIV. I'm not sure they could even pinpoint what would cause the suppression of cytokines with HIV patients. (I should also add that I'm not a scientist, so I fully expect that maybe they could, and I just don't know it.)You are the oxalate girl, so I can't comment on oxalates. What you've said about oxalates stopping oxalate dumps certainly makes sense, but I don't know that I would disregard all yeast concerns. And really, what does it mean for someone like ME in the position of what I know of my child?What I KNOW of my child:If I take him off antivirals, he regresses with ASD symptoms. Symptoms he currently does not have.If I take him off antifungals, but remain on the antiviral, he behaves with what I've come to identify with yeasty behavior based upon the observations and labs we're previously had. Could that, in fact, be oxalates? I dunno. I suppose so. But we also had yeast in our labs that went away with antifungals.If I take him off antivirals and remain on antifungals, it does NOT stop the regression back to ASD symptoms.If I stop both, he does both regressions.If I stop none, he remains status quo recovered.I'd be hard-pressed to change what's working. Is there even a way to transition from one protocol to the other without too much of a regression? How long do you give it? And what happens if it doesn't provide the expected results? Do we continue to leave what's working in favor of something that isn't? I dunno. Like I said, I'd be hard pressed to even try.BUT I do agree that we can't blame everything on yeast all the time. It took me a while to learn to distinguish yeast from ammonia from bacteria in my son's behavior because of spending too much time blaming yeast.

* * * Cheryl * * * ~ Antiviral Therapy 101~~ Make a biomed book ~~ gryffinstail.wordpress.com ~~ @Gryffins_Tail ~~ Join the MB12Valtrex Yahoo! Group ~

and ,

I just took a look at pubmed, and there doesn't appear to be any evidence of an association between valtrex and candida infections, Valtrex and similar drugs are used so widely that I believe there really would be a literature on this association if this relationship was real. Valtrex is used so much in the HIV world where people often have to deal with immunosupression and herpetic infections. If anyone was going to make that observation with data to support it, it would have happened there.

So could these very real changed symptoms you noticed actually mean something else?

What I have continually seen in analyzing what has now been 680 of the Great Plains Organic Acid tests, doing complicated statistics on this data, is that on before and after OATs when people report they were put on diflucan, their next OAT is frequently an oxalate disaster....often with oxalate levels doubling, and also evidence that they are now in much worse oxidative stress. That can break a lot of things.

The OATS also show evidence (that often was not there before) of making endogenous oxalate. This doesn't mean the oxalate markers went over the reference ranges. We see evidence of endogenous oxalate going up at around 40 mmole/mol creatinine, which is far below the reference range from Great Plains.

Why would increases in oxalate that your body makes happen after diflucan?

Diflucan is well known to be very hard on the liver, causing so much stress to the body that the PDR recommends doctors do liver functon tests. When the liver gets in oxidative stress, B6 dependent enzymes won't work properly. Unfortunately, as a study I've mentioned below on rats and oxalate showed, AST and ALT cannot rise after a B6 functional deficiency happens and that situation also leads to increased production of oxalate.

In the cases where I've seen oxalate increase after diflucan, this is not dietary oxalate but is oxalate the body makes because the enzymes that usually process the intermediate glyoxylate to something harmless, are no longer working. This probably happens because of the oxidative stress caused by the drug.

What happens instead? Glyoxylate (which isn't on the OAT) builds up intracellularly, and is converted into oxalate by lactate dehydrogenase, At the same time, some of the increased level of glyoxylate is also converted to glycolic acid and glyceric acid via other routes. Glycolic acid and glyceric acid, like oxalate, are on the OAT and it is not hard to notice the levels of all three of these going up together when that happens before and after some treatment.

Sometimes, though, the fact that these analytes have gone up is not obvious because increases in oxalate can be accompanied by stepped up creatinine secretion.

How does that work?

Since everything on the test is ratioed to creatinine, raising the size of the denominator makes the whole ratio fall. This affects everything on the test, so it can make everything on the test suddenly fall low, and below the reference ranges, and that might make your doctor think that he just solved a lot of problems.

Unfortunately, the sudden decrease of everything on the test is an artifact that happens because of the change in creatinine secretion.

What does that mean?

Creatinine secretion increasing when oxalate increases is documented in an animal study on rats, and in so many OATs I've seen where the concentration of everything looked like it fell together. For the study, please see https://www.jstage.jst.go.jp/article/biomedres/27/3/27_3_93/_pdf.

Not knowing about the shift in creatinine is why it is so easy for doctors not to see what is going on and that is why your doctor might miss noticing the increase in oxalate markers on the GPL test, but these are not measured in tests from Metametrix or Genova.

But why might increased oxalate cause GI symptoms and behavioral symptoms at the same time?

Scientists in the last four years have been busy characterizing the transporters oxalate uses to cross the membranes in the body, so how it enters and exits cells. They have learned that these transporters get involved with the movement of water, regulation of pH, and the movement of other molecules important to autism, like sulfate, and iodine, and chloride. The science has not come far enough for us to understand all the signaling mechanisms that change how oxalate transport works, but a big focus of their research is the gut.

Scientists still cannot tell us why the changes in movement of oxalate come on suddenly, but one of the signals that has been characterized is angiotensin II, which also regulates your appetite for salt and water, but it causes a sudden shift in oxalate secretion to the gut.

In the first year of the Autism Oxalate Project, a survey of changes parents reported in their children on a low oxalate diet amounted to huge improvements in autistic symptoms (the biggest being sociability) and also huge improvements in GI function. That was also associated with improved motor skills, growth when they needed it, and loss of pain and many other things.

In other populations (and we are monitoring the diet now also in many other populations in adults) oxalate is associated with increased pain of all sorts. Also, some people have noticed that when oxalate "dumping" occurs, when the body starts to release oxalate stores from the body, it can be accompanied by a change in attitude or perception that amounts to a failure to be able to notice or understand someone else's point of view...like a lot of unreasonable responses to situations.

So if you really want to distinguish the "yeast versus oxalate" issues, then do two very objective things. The first is, get a stool culture for that very moment you saw the changes in behavior.

Two peer reviewed articles on autism found no difference in the amount of candida in autism in the stool compared to controls, and both of these studies were conducted by people who are "friendly" to DAN! approaches, but their data did NOT support a "yeast is a big deal" autism model.

The other thing to do is take a urine sample and freeze it, and then send it for a new OAT from Great Plains so you can check the oxalate markers.

A study in Poland published in the European Journal of Paediatric Neurology last year found that 35 out of 36 children with autism who were not on special diets, had no kidney issues, and no seizures (all which could associate with high oxalate) were higher than ALL the control children in blood, in urine, or in both and as a group they were two and a half to three times higher.

This oxalate data is some of the strongest and most consistent data that has ever been seen in autism, and it went virtually unnoticed. Did your doctor realize what it meant?

Anyone can read the study here: autism.org/content/PDF_files_newsletters/oxalate_and_autism.pdf.

It has been hard to communicate to the autism community how seriously damaging oxalate is known to be to the body, and especially to the mitochondrion. Something about autism, as the Polish study showed, seems to offer some protection to the kidneys compared to what happens in primary hyperoxaluria at the same levels of oxalate.

But even though it isn't causing kidney stones, the oxalate being that high in the body is still harmful....just not as much to the kidney.

So if your doctor is NOT on board with the oxalate story, find out why not?

He may not be aware that oxalate causes oxidative stress and mitochondrial dysfunction. Its toxicity can well account for issues that we've seen go away in children who have been able to reduce oxalate.

But the diet isn't at all the whole thing. At AutismOne two years ago, I presented data from ten OATs on a child I received after the fact, from someone whose doctor ordered all these tests. This child had been on a low oxalate diet the whole time, but between her fifth and sixth OAT, her oxalate and pyroglutamate levels soared. (Pyroglutamate is a marker of oxidative stress.) The mom told me that what they had changed between those OATs was introducing diflucan and nystatin, and in the next two years, the oxalate levels in this child did not go down, despite diet, but stayed in dangerous territory,

It is important to know that some of the biomed treatments over time can lead to worsened oxalate situations and this is a dilemma for everybody. I've been involved in autism research since 1995 and have labwork on children since the early days, and I keep seeing that children whose original OAT I have, after being treated with rounds and rounds of antimicrobials have gotten OATs that get worse and worse on the oxalate front the longer they've been treated with antimicrobials. I'm seeing this perspective in some kids over ten years.

I totally acknowledge that these treatments may cause quick behavioral improvements, but I'm wondering, rather than producing improved behavior from killing something, they may be "behaviorally effective" because of stopping the detox process of oxalate.

What do I mean by that? It may be acting in a similar way to how, for an alcoholic, taking another drink stops delirium tremens. Our listserve already learned years ago that the way to stop an oxalate "dump" is to get more oxalate, and then the "dump" stops, and so do the symptoms, but we've learned that stopping that process just delays the problem and sets someone up for worse problems later.

This is the real bugabear about how oxalate works and how the body detoxes from it and i'm sure it is confusing to everybody.

Anyway, please don't assume that every behavioral meltdown is yeast. From what I've been able to see so far, the evidence (objective lab tests) really don't support that very strong belief, especially after you start understanding the science of how oxalate is handled and affects symptoms.

I'm not on this listserve much, but the subject got my attention today, and I really want parents to realize there is another way of interpreting these symptoms that is tied very strongly to objective labwork.

You can get more information about oxalate at www.lowoxalate.info or you can come join our yahoogroup at Trying_Low_Oxalates that now has almost 7000 members. This listserve is still growing at a furious rate after eight years of work in this area. We find new studies almost every week that offer plausible explanations for what people have observed changing in their children.

>

> > **

> >

> >

> > If your child is on valtrex he must also be on an antifungal, preferably

> > diflucan. The valtrex causes yeast.

> >

> >

>

[Guest guest]

Cheryl,

You are so sweet! I heart you, too!

Believe me, I know how difficult this subject is, and nobody would have gotten

kids on these antifungal protocols if it didn't seem that it was keeping the

symptoms at bay.

Have you done any GPL organic acid tests on your son through all this use of

antifungals?

Did you catch that the animal study showed that AST/ALT enzymes CANNOT rise if

you get into the sort of B6 problem that leads to endogenous oxalate? A study

below explains why.

When I went to an oxalate conference, the reasons for how that works became

clear. The problem is that enzymes that use pyridoxine are formed in an

apoenzyme form (without the cofactor) before they bind the pyridoxine. AGT, the

important B6 dependent enzyme involved with oxalate, for instance, won't have

any activity, and won't get in the right compartment if it hasn't first bound

pyridoxine.

The binding makes them a holoenzyme. The mechanisms for trafficking the enzyme

or recognizing its formation, are for the holoform, so if you are low in B6, or

if because of oxidative stress, B6 cannot properly bind its enzyme, then the

levels of AST and ALT in the holoenzyme will plummet. Does that make sense?

That's what I was saying is that the study found when B6 was deficient at the

same time as oxalate was high, AST could not rise. If that is happening

eventually on long term diflucan therapy, this makes the AST/ALT test not work

as a measure of liver toxicity. So years of having AST and ALT within reference

ranges (ie, under the reference range) wouldn't mean that the diflucan was not

having toxic effects on the liver. When I saw the study that showed this issue,

I was shocked, realizing how much confidence the doctors put in that test.

I wish there were a better study looking at diflucan particularly, especially

after using it over a long, long time.

What I am seeing on OATs is that in the OATs done after long years of

intervention, the biochemistry is getting pretty desperate trying to find a way

to get energy, since oxalate blocks so many mitochondrial pathways. The body

looks like it may be starting to use an energy cycle that has barely been

studied in people, though there has been a lot of work in microbes and plants.

It is not a pathway in the mitochondrion. It is in the peroxisome.

This pathway hasn't been studied in animals for about thirty years, though there

is one researcher still looking at it in Russia.

There has just been a lot going on underneath everything that we didn't know was

going on.

I think the better people to ask your question to would be people on our

listserve who spent a long time on antifungals and after that did the diet, and

found that high dose biotin kept the yeast issues away without the need for

antifungals, but after the body detoxified from oxalate, the need for high dose

biotin went away. Wouldn't it also be nice not to have to pay the cost of

antifungals any more?

It is not just our project that has made that observation.

We heard from the Vulvar Pain Foundation before we even started our autism

project, that their experience was that when their members had been on the low

oxalate diet for a long time, that the chronic vaginal yeast infections they had

experienced went away.

Their Pain Project never considered biotin's connection to this, but I got into

that area because back when the DAN! manual was written, I wrote a section on

biotin for that book before I even started looking at oxalate. Once our oxalate

project started, we found the sorts of improvements on high dose biotin therapy

that became oddly parallel with the improvements we started seeing on LOD.

Later, I ran into a study that talked about how oxalate inserts itself in biotin

dependent enzymes called carboxylases, That breaks them. These enzymes don't

function either when someone has biotinidase deficiency or holocarboxylase

deficiency and the result in those genetic conditions is that lack of biotin

activity in those enzymes leads to chronic yeast problems. That is why we

thought it likely that solving the oxalate problem would solve the yeast

problem, and it has done that for a lot of people...and not just autism.

But the problem is that IF the " killing the yeast " protocol is what keeps your

oxalate level high, then you can't win because you still have to keep giving

this treatment because without it, the problem comes back. You start to dump,

the high oxalate impairs biotin dependent enzymes, and then the immune system

loses its partner that keeps yeast at bay. Then it comes back. That happens

because the medicine is not dealing with the source of the REAL problem but it

is just treating a secondary problem while maybe prolonging the primary problem,

which may be the oxalate.

Does that make sense?

I invite you to come look at our archives on TLO and read the stories from

parents on this and on how biotin worked for them and how after reducing

oxalate, they didn't have to worry about yeast.

This isn't just an autism issue. We have listmates with all sorts of chronic

conditions that are very frequently treated by antifungals.

Mostly, we see some people come onto our list who just cannot let loose of the

chase-every-symptom- with-some-sort-of-antimicrobial approach. They don't seem

to do as well as those who just let the body detoxify from the oxalate and then

see where that puts them using biotin to strengthen the immune system effort

against yeast.

The awful part of this is that oxalate does store in the body, and it seems to

come out in dumping periodically even if you aren't doing the diet. The body

seems to be built to recognize that the only reasonable direction for oxalate is

out, so it quickly chooses that route the second it has a chance. This is how

we came to recognize that those who reduced oxalate would often begin to have

their first dump after only a day or two of reducing oxalate. We've seen that

thousands of times now. If antifungals raise oxalate levels, then removing

them would reduce oxalate levels, and that might induce a dump of oxalate from

tissues, and then the symptoms come on again.

Cheryl, it requires a new way of thinking to get to this understanding. As long

as yeast is seen as the " enemy " , it will be hard to recognize that it is doing

its usual role in nature, which is to expand to clean up the damage when

something isn't healthy. That's what yeast always does...helps sick and dead

stuff get recycled. If what you are doing is making the body healthy, then

yeast should go away without the antifungal being necessary because there is

nothing, then, to keep it going.

Another little rough spot in this requiring a philosophical shift is that the

stress pathway that I seem to be seeing reflected on OATs is also a stress

pathway in Candida. This is where it goes for survival when its usual " food " is

gone, such as when it has been endocytosed by a macrophage trying to kill it.

But it won't die there, because in that environment, it turns on this

alternative way of getting energy that allows it to survive using fat from cell

membranes. This makes it more virulent, and it allows it to survive undetected

within our immune cells. And that's why it comes back when the stressor is

gone. That stressor could be diflucan.

So there is lots to think about!

But. Cheryl, have you had a GPL OAT done since your son has recovered even

staying on antifungal therapy? I'd love to see it, and I would like even more

to see a bunch of them over time on him. I could do the adjustment that gets rid

of creatinine, and then you could look at the changes from OAT to OAT and draw

your own conclusions.

That offer goes with anyone here who is trying to evaluate the effects of long

term antifungal therapy. This goes only for those who did the Great Plains Test

because they have the oxalate markers.

When I finally saw what was going on with the diflucan leading to endogenous

oxalate, that made me realize why it was the doctors who are such strong

believers in antifungal therapy who saw such ho-hum results when their patients

went on LOD. The diet obviously couldn't be effective when the body was

churning out much more oxalate endogenously than the diet contained. The proofs

of all this is in the lab tests.

The best time to have lab tests evaluating all this is during the meltdowns that

are thought to be yeast related. Let's see what those tests look like.

Effect of treatment with pyridoxine on aspartate aminotransferase activities in

pyridoxine-deficient rat tissues.

M Okada, T Kondo

In rat liver, 90% of the aspartate aminotransferase is present as the

holoenzyme. In pyridoxine deficiency, the ratio of holoenzyme activity to total

activity is markedly reduced, but after pyridoxine injection it was found to

rapidly increase, although the total enzyme activity remained low for a few

days. The activities of aspartate aminotransferase isozymes in

pyridoxine-deficient rat tissues and the effect of pyridoxine treatment on their

activities were examined. The intestinal enzyme activities of

pyridoxine-deficient rats were readily reconstituted in the presence of

pyridoxal phosphate in vitro, but the enzyme activities in liver and muscle in

the deficient rats required several days for complete recovery, suggesting that

active enzyme was synthesized de novo in these tissues.

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> > > >

> > > > If your child is on valtrex he must also be on an antifungal, preferably

> > > > diflucan. The valtrex causes yeast.

> > > >

> > > >

> > >

> >

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[Guest guest]

Comments within:

* * * Cheryl * * * ~ Antiviral Therapy 101~~ Make a biomed book ~~ gryffinstail.wordpress.com ~~ @Gryffins_Tail ~~ Join the MB12Valtrex Yahoo! Group ~

Cheryl,

You are so sweet! I heart you, too!You're the one who connected the dots for me on erythromycin so many years ago. We've had entirely too many overly-sciency conversations for me to do anything but love you. Especially when you start talking like a scientist, using chemistry terms instead of medical terms, thereby exceeding the height of my head. My favorite is when the statistician terms come in too. That totally gets me. Right in the ticker.

Have you done any GPL organic acid tests on your son through all this use of antifungals? Yes. But it's been a long time. I stopped doing the GPL tests a couple years ago. I've always found them to be only so useful because results are never reliable. And that's not just GPL, it's labs in general. I learned to just stick with using labs as more of a "take a look and see if things look any different" than a tool for diagnostics. They really just seem to give us an overall picture. We tried treating to labs with zero success.

Did you catch that the animal study showed that AST/ALT enzymes CANNOT rise if you get into the sort of B6 problem that leads to endogenous oxalate? A study below explains why.I'll def. take a look.

When I went to an oxalate conference, the reasons for how that works became clear. The problem is that enzymes that use pyridoxine are formed in an apoenzyme form (without the cofactor) before they bind the pyridoxine. AGT, the important B6 dependent enzyme involved with oxalate, for instance, won't have any activity, and won't get in the right compartment if it hasn't first bound pyridoxine.

The binding makes them a holoenzyme. The mechanisms for trafficking the enzyme or recognizing its formation, are for the holoform, so if you are low in B6, or if because of oxidative stress, B6 cannot properly bind its enzyme, then the levels of AST and ALT in the holoenzyme will plummet. Does that make sense? It does. Our biggest problem though is that Gryffin can't tolerate any B's. We've never been able to use any B's for long.

I wish there were a better study looking at diflucan particularly, especially after using it over a long, long time.Me too.

What I am seeing on OATs is that in the OATs done after long years of intervention, the biochemistry is getting pretty desperate trying to find a way to get energy, since oxalate blocks so many mitochondrial pathways. The body looks like it may be starting to use an energy cycle that has barely been studied in people, though there has been a lot of work in microbes and plants. It is not a pathway in the mitochondrion. It is in the peroxisome.

Wouldn't it also be nice not to have to pay the cost of antifungals any more?It would, but in the grand scheme of how much we've paid for recovery, antifungals are one of the cheapest things we pay for. The multivitamin costs more. Biotin costs more. But I do get what you're saying. We never saw anything with biotin either. We did biotin for at least a year. (I'd have to look at the biomed book to remember it all.) We've just NEVER seen anything with naturals or diet. Ever. I do suppose it's possible we weren't using enough biotin.

But the problem is that IF the "killing the yeast" protocol is what keeps your oxalate level high, then you can't win because you still have to keep giving this treatment because without it, the problem comes back. You start to dump, the high oxalate impairs biotin dependent enzymes, and then the immune system loses its partner that keeps yeast at bay. Then it comes back. That happens because the medicine is not dealing with the source of the REAL problem but it is just treating a secondary problem while maybe prolonging the primary problem, which may be the oxalate.

Does that make sense?Yes. But I do have a healthy dose of skepticism anytime I hear "getting to the real problem" because it's a catch phrase all doctors, with all their protocols, use. They all claim they get to the root of the problem when the reality is, no one is getting to the root of the problem. IF there's an oxalate issue that isn't caused by the antifungal, then what's causing the oxalate problem? Diet is effective in lowering oxalate intake but we've done LOD with no change (no diet has ever been effective for us). Again, we're still treating what we know, not why it got there. Now what I didn't do is LOD without an antifungal. So as you said, that's something to consider. But wouldn't I have at least seen something with the diet?

I invite you to come look at our archives on TLO and read the stories from parents on this and on how biotin worked for them and how after reducing oxalate, they didn't have to worry about yeast.I will! I don't have much time for the lists anymore but this and dehydration study has piqued my interest. So I'll probably join in a day or so to dig around the files.

This isn't just an autism issue. We have listmates with all sorts of chronic conditions that are very frequently treated by antifungals.It never is. None of what our kids are going through is strictly an autism issue. That's probably the most frustrating thing about autism.

Mostly, we see some people come onto our list who just cannot let loose of the chase-every-symptom- with-some-sort-of-antimicrobial approach. They don't seem to do as well as those who just let the body detoxify from the oxalate and then see where that puts them using biotin to strengthen the immune system effort against yeast.You know, my son has always been a pretty clear case of what works and what doesn't. We've never been able to chase it all. Not for lack of trying but because I'm a firm believer in doing what works. When things don't work, I don't keep doing it. It's probably the main thing I attribute to his recovery. I haven't loaded him up with things he doesn't need or benefit from and I'm meticulous about knowing if anything is happening. I just haven't had any luck seeing anything when dealing with oxalates.

The awful part of this is that oxalate does store in the body, and it seems to come out in dumping periodically even if you aren't doing the diet. The body seems to be built to recognize that the only reasonable direction for oxalate is out, so it quickly chooses that route the second it has a chance. This is how we came to recognize that those who reduced oxalate would often begin to have their first dump after only a day or two of reducing oxalate. We've seen that thousands of times now. If antifungals raise oxalate levels, then removing them would reduce oxalate levels, and that might induce a dump of oxalate from tissues, and then the symptoms come on again.So how long do you think it would take to dump the oxalates? I'd be willing to drop the antifungal for a while and see what happens. But I would need a relative (I know there are no absolutes!) time frame to wait before starting it up again. I would remain on the antiviral though. You'd REALLY have to work pretty hard to convince me to give that up. Yeasty behavior I can handle. ASD symptoms, not so much. But I'd like to know what I could expect as far as time frame. Should I expect a dumping to start within a week of stopping? And how long should I expect the dump to last? Removing the antifungal is not a problem for me to do. I have no qualms with giving it a shot simply because the antifungal is supporting the thing that's really needed - the antiviral. I've gone time without both though. Every year I try to drop them. Every year it fails miserably. From experience, I know he won't start showing yeasty symptoms for about a week or two. And then all hell breaks loose with yeast symptoms. I've gone as long as a month without an antifungal. So I can already assume that it's going to take longer than a month to dump excess oxalates. But. Cheryl, have you had a GPL OAT done since your son has recovered even staying on antifungal therapy? I'd love to see it, and I would like even more to see a bunch of them over time on him. I could do the adjustment that gets rid of creatinine, and then you could look at the changes from OAT to OAT and draw your own conclusions.I'm totally willing to send them to you. They're old. If I remember right, the oxalates are high too. I think that's why I started LOD in the first place. But I'll scan them in and email them to you in the next day or so. You can tell me what you think.