Oxalate Dumping - a Probiotic Solution?

Oci

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That is the upper level you should be aiming for but really it is what is tolerable to you. And as @Gondwanaland says biotin and pantothenic acid may also be important.

Essentially it is antioxidants and B6 that might help overcome the enzyme problem that lead to endogenous oxalate production. B1, B5 and biotin help address other enzyme problems secondary to oxalate accumulation.

Personally I'm not a Yasko fan - she has made too many serious errors and I wasn't impressed with the quote from Nancy Mullins.
That sounds like gobbledegook to me.

Oxaloacetate, not oxalate is part of the Krebs cycle. They are different molecules with completely different roles. There is an obscure link which we talked about somewhere earlier in this thread, but it is obscure.

Many thanks, Gondwanaland, Alicec, Sidereal and Dannybex. I too have had many doubts about Yasko but was so impressed with her credentials...especially on paper! I have appreciated people pointing out her gobbledegook ie Susan Oakes. I tuned into a phone call with Nancy Mullen and was shocked at how disorganized she was and how she went on and on telling someone how awful their genetics were.

That is why I so appreciate this group over any others I have found. Such intelligent and well informed and caring people posting. Many thanks!

As for my current problems with vaginal itch and bladder discomfort, I'm thinking that probably both candida and perhaps the enterobacter cloacae that were identified in the May CDSA report are still a problem in spite of the things that I have been taking. I was traveling for 2+ weeks and so diet was all over the map as I visited various people.

I suspect that oxalates are likely a problem too as my sister has had vulvodynia for years and finds relief with a low oxalate diet. But I don't want to follow a low ox diet for years...I want to correct the underlying causes. I have had these symptoms before and they have gone away. However I don't know what I did to turn them off!

@alicec I am wondering what antioxidants you would recommend - I am COMT++ and so don't tolerate a lot of methyl donors. I did have an ION test done some years ago and it indicated that I had a lot of oxidative stress.

Since I suspect oxalates, I am more limited in what veggies and other foods I might otherwise eat.

Thanks again! Oci
 

alicec

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As for my current problems with vaginal itch and bladder discomfort

These could well be symptoms of oxalate accumulation and/or dumping.

I am wondering what antioxidants you would recommend - I am COMT++ and so don't tolerate a lot of methyl donors.

For antioxidants again it is what you can tolerate. A mixture of different types would be good but be careful with vitamin C - high doses can contribute to oxalate formation. Be careful too about the dogma about COMT++ and tolerance of methyl donors. The latter does indeed seem to be a problem for some people but it may not have anything to do with the former.

This seems to be something of a self-fulfilling prophecy. Somebody theorised that having COMT++ might result in intolerance of methyl donors so people with COMT ++ were not given methyl donors just in case. Then it became an accepted fact which is now endlessly repeated with very little evidence. Some people, me included, have ignored the dogma and tried it out and found that the relationship doesn't necessarily hold. I have several COMT++ snps and don't seem to have any trouble with methyl donors.

Since I suspect oxalates, I am more limited in what veggies and other foods I might otherwise eat.

You do need to be very careful with nuts, grains and grain substitutes but there are plenty of low ox fruit and veg. Don't restrict these.
 

Oci

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Thanks, Alicec, I really don't know how to determine whether the problem is oxalates or candida or possibly both. My plan at the moment is to continue with the antifungals (as yeast has been a problem determined through testing off and on for years) and to also follow a lower oxalate diet. Then hope the problem goes away as it has with the past episodes. I am also increasing the B vitamins and will gradually add antioxidants.

I was considering doing the Great Plains Oat test but then read...
"The OAT is designed to measure various metabolites in the body so that an understanding of the overall function can be assessed. It's up to you and your doctor to determine if you want an assessment of the body under the current metabolic conditions with supplements or without the aid of supplementation. Supplements themselves do not directly interfere with the OAT unless they contain apples, grapes, pears, or cranberries.

It is important to note that the body can take weeks to reestablish its metabolic functions after supplementation has been removed or introduced. If the supplements have recently been added or removed, the OAT will give a picture of the metabolism in transition and is difficult to assess from a clinical standpoint. If you determine that you want to cease or add supplementation, two weeks is the recommended period of time to wait before testing.

And also...
"Antibiotics and antifungal will not directly interfere with the OAT unless they contain apples, grapes, pears or cranberries. It is important that the patient and practitioner consider why the test is being administered in order to determine whether or not the patient should refrain from antibiotics and antifungals. For example, a practitioner may want to know if a certain therapy is effective. In this example, it would be perfectly acceptable to remain on the therapy during collection. Separately, a patient may want to understand their metabolic condition without the aid of therapy. In this case, it is best to remove the antibiotics or antifungals for 1-2 weeks prior to testing."

My guess is that yeast is still a component and I don't want to be off of antifungals for a couple of weeks just now. So, I guess I just carry on! If this does not clear up in due course then I can still do the test. Likely I will anyway at some later date. What I need to determine is why I have these fairly chronic candida problems. It looks like a worthwhile test.

Thanks so much, Oci
 

Gondwanaland

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Is polycystic ovarian syndrome a risk factor for urolithiasis?
Urolithiasis
August 2013, Volume 41, Issue 4, pp 361-362
Date: 21 Apr 2013

Abstract
Urinary stone disease is a complex multifactorial disorder influenced by both intrinsic and environmental factors. It is generally known that age and sex are risk factors for urinary stone disease. Also men have higher mean urinary oxalate concentrations than women. In addition, in animal and human studies, testosterone has been shown to increase the formation of urinary stones. This suggests that sex hormones are considered to be involved in the pathogenesis of stone disease. Polycystic ovary syndrome (PCOS) is one of the most frequent endocrine disorders of women in the reproductive age, affecting 5–10 % of women in this life span. It is characterized with chronic anovulation\oligo-ovulation, clinical or biochemical evidence of hyperandrogenism and polycystic ovaries on ultrasound examination. Hyperandrogenism, the main feature of PCOS, may trigger the urinary stone formation besides hirsutism, alopecia and acne. Therefore, we hypothesize that PCOS accompanied by hyperandrogenism may be a risk factor in the formation of urinary stone disease.

I don't have PCOS, but from reading this short review, I concluded that FIRST I will have to raise my estrogen, then NEXT I will have better chances of raising T by eventually tolerating K2-MK4.

Edit -- It is very intriguing that in this thread the people with oxalate trouble are women.
 
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alicec

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maybe you have something more to report before I start?

I had intended to take one twice a day but after the first one realised that I was a bit sensitive to the FOS, so have just been taking one 2-3 times weekly. No problems with this. I do intend to increase but have been struggling with other issues so haven't got around to it.

I have just been looking for negative issues for my initial assessment. In terms of benefits I imagine this might not be obvious in the short term. There could be increased oxalate dumping - this might be unpleasant but is definitely a sign that they are working. I haven't experienced this but maybe am not taking enough yet.

In the longer term I'm hoping to see O. formigenes appear in my uBiome tests and maybe find that I can tolerate more oxalates in food.
 

Avengers26

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@alicec This is something I had asked before but never quite got a sure answer. Does oxalobacter even show up in the ubiome test? My ubiome test doesn't show any oxalobacter either. May be, I don't have it or may be the test itself doesn't show it.

If I understood it right, the ubiome test only shows a limited no. of species. Has any one's ubiome test shown oxalobacter species so far?
 

alicec

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If I understood it right, the ubiome test only shows a limited no. of species. Has any one's ubiome test shown oxalobacter species so far

No, uBiome tries to sequence all bacterial DNA in a sample, ie all species in the gut. If Oxalobacter is present it will show up, however there does appear to be a lower threshold. I don't understand enough about the technical issues that limit this threshold of appearance since the technique is sensitive enough to report single counts (ie a single organism) for some species. Maybe it is something to do with sampling - ie there is not an even distribution of species and a certain threshold level is necessary for one organism to be present in the portion of the gut sampled.

In any case if Oxalobacter doesn't show on the test it doesn't necessarily mean it is entirely absent but if it is present it would be at an extremely low level.
 

Asklipia

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There could be increased oxalate dumping - this might be unpleasant but is definitely a sign that they are working. I haven't experienced this but maybe am not taking enough yet.
Thanks for the report @alicec !
I was wondering about this. If Oxalobacter eats up oxalates, what happens then? On the one hand, more Oxalobacter in the gut, OK I can understand that, and less oxalic acid around.
Then, does Oxalobacter exit the gut by the lower end and we can say bye to this oxalic acid,
or does this constitute another oxalic acid store that can cause oxalate dumping the first time the Oxalobacter are killed by whatever is in the food, antibiotics or even preservatives?

I suppose our Oxalobacter count will act as a buffer when eating high oxalate foods.
Delaying the pain somehow.

But will it lower the oxalate load in the body? What do you think?

The second thought I had is : if Oxalobacter eats up the oxalic part, will it free the other part of the oxalates, that is calcium, magnesium etc whatever they are bound to, and could this cause a problem?

As usual the roof is in the pudding of the guinea pig, I shall know more after trying, but I would be grateful for your thoughts on this.
:)
 

alicec

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If Oxalobacter eats up oxalates, what happens then? On the one hand, more Oxalobacter in the gut, OK I can understand that, and less oxalic acid around.
Then, does Oxalobacter exit the gut by the lower end and we can say bye to this oxalic acid,
or does this constitute another oxalic acid store that can cause oxalate dumping the first time the Oxalobacter are killed by whatever is in the food, antibiotics or even preservatives?

The bacterium digests the oxalate as an energy source - it is its preferred food. The oxalate is completely broken down so if one had a plentiful supply of bacteria in the gut, oxalates from foods would be readily digested and there would be little or none left to be taken up into the body and stored.

But will it lower the oxalate load in the body? What do you think?

It could do that in two ways. With less oxalate being taken up from food, blood levels will fall which is turn is a signal to cells to release oxalate stores. Then there is the not fully understood mechanism whereby the gut signals that oxalate digesting bacteria are present so the body dumps stored material there (this is why I thought starting the probiotic could precipitate oxalate dumping).

if Oxalobacter eats up the oxalic part, will it free the other part of the oxalates, that is calcium, magnesium etc whatever they are bound to, and could this cause a problem?

I think the main form in foods is oxalic acid but I guess with some foods like spinach there could be a significant amount of calcium associated with it. In this case it might be a good thing since the calcium is now nutritionally available.

I honestly don't know enough about what happens to mineral bound oxalates if the body decides to reduce oxalate stores. Does the whole mineral complex get dumped? I suppose so. This means that when the complex hits the gut and is digested by O. formigenes, the free metal would be released. This could be a good or bad thing, depending on the metal and how much there is.

Mind you not all oxalate in the body is mineral bound - the oxalate anion alone is responsible for all the metabolic havoc.

Sorry I can't entirely answer your questions. O. formigenes as a probiotic is so new that there is little known about what happens when the bacterium is introduced into someone deficient in it and with significant oxalate stores. Presumably the Ox-thera people and the Indians who have developed the preparations now on sale in India have done some studies but they don't seem to be available yet.
 

alicec

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if Oxalobacter eats up the oxalic part, will it free the other part of the oxalates, that is calcium, magnesium etc whatever they are bound to

I've been thinking about this and really don't recall reading anything about how O. formigenes deals with mineral salts of oxalate. I've had a quick look and found a recent paper reviewing what is known about the bacterium in light of the complete sequencing of its genome - see here The mechanism that is understood is how the bacterium takes up the free (soluble) oxalate anion via an anion transporter on its surface. They do know that the bacterium can also deal with crystalline (insoluble) oxalates, eg calcium oxalates, but not how. The assumption is that the organism can somehow dissolve or otherwise breakup the crystal and take up the oxalate anion by the usual means. That would mean, as we have speculated, that the free metal is then lying around in the gut.

I couldn't find anything about what the body does about dumping crystalline oxalates (though didn't look very hard) - apart from the obvious expulsion of relatively large kidney stones. Again what is known is how anion transporters are used to transport soluble oxalate anion out of cells - including across the gut wall. By draining away free oxalate does this mechanism simply change the equilibrium and eventually lead to slow dissolution of these crystals or is there some other way these stores can be released?

I did find a bit more about the signalling mechanism for oxalate dumping. If there's not enough oxalate around in the gut, clever O formigenes stimulates these anion transporters in the gut wall so they'll deliver it a feed from body stores.

Finally I did find a study about the OxThera product and presumably why all has gone quiet with them - see here . The product was unable to reduce urinary oxalate levels in patients with the genetic disease primary hyperoxaluria in a double blind trial, in contrast to a previous smaller pilot study. They did say they had changed the formulation in between trials - maybe it had something to do with this or maybe it is more complicated.
 

Asklipia

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999
Great finds @alicec ! Even though you bring up more unexplained mysteries along with fantastic information. No doubt some answers to our problem lie this way. Let's hope that more research comes to light.

The OxThera product is not the same as the Oxalobact. And the Oxalobact is on the market and has been used for a few years, it must have enough good results to warrant three different pharmaceutical brands.
Or maybe not?
Because the Oxalobact contains other probiotics apart from the O. formigenes, maybe it becomes more effective? Maybe taking VSL3 and Miyarisan release oxalates (which I found true in my case) by virtue of the same mechanism?
That is, maybe the other probiotics break up the soluble oxalate and the O. foreignness gobbles up the oxalic part? In that case taking O. formigenes alone would not work so well?

Maybe it is possible to break up the insoluble crystalline oxalates in certain circumstances, for example if there is a particular pH, which might happen when there are no soluble oxalates around? Just a fantasy.

Strange but thinking of this O. formigenes activates in me a special sound that I only hear when I am 100% right. Laugh as you like, but I feel I am on the right rack.
Lots of good wishes! :hug:

The bad news is that my parcel did not contain the desired Oxalobact, but a present sent by a friend. Arghh!
 
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Valentijn

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@Oci - VSL#3 is the only probiotic which seems to work well for me. I feel better on it than off it, and other probitics (including yogurt) make me feel worse. But I would expect that's different for different people.

It's being sold as Vivomixx instead of VSL#3 now, in at least some areas in Europe. It's available online from http://shop.vivomixx.eu/ (based in Switzerland).
 

Oci

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261
Interesting. Thanks. Something is exhausting me but not sure what. Guess I need to reduce supps and see. Or perhaps the fatigue/sleepiness is a sign that my body is mounting a response to whatever?
 

Gondwanaland

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I was reading this study
Effect of sex hormones on oxalate-synthesizing enzymes in male and female rat livers
Abstract
Purpose
We studied the effect of changes in sex hormones on oxalate metabolism in rats.

Materials and Methods
Adult male and female rats were administered a precursor of oxalate, and the relationship between dose and urinary oxalate was examined. Levels of sex hormones were varied in rats and glycolate oxidase (GO) and serine pyruvate aminotransferase (SPT) activities were measured under the conditions of being fed tap water or loading with 0.5% ethylene glycol. In addition, urinary oxalate excretion was evaluated.

Results
Ethylene glycol and glycolate increased urinary oxalate concentration in male rats dose-dependently but less in female rats. There was almost no change during glycine loading in either male or female rats. GO activity was significantly lower in intact female and gonadectomized male rats. SPT activity was slightly higher in the female than in the male controls. There were no differences in urinary oxalate excretions between male and female rats. During ethylene glycol loading, GO and SPT activities were similar to those with tap water intake. However, urinary oxalate excretion increased to two times the control value in male rats but only slightly increased in female rats.

Conclusions
Sex-related differences exist in the metabolic conversion of glycolate to oxalate in rats, and GO activity is promoted by testosterone. Although difference in GO activity has no physiological effect on oxalate synthesis, GO activity affects urinary oxalate excretion during ethylene glycol loading. We could also conclude that estrogen decreases GO activity in male rats from our results.
then I looked up glycolate oxidase on wikipedia:
This enzyme belongs to the family of oxidoreductases, specifically those acting on the CH-OH group of donor with oxygen as acceptor. The systematic name of this enzyme class is (S)-2-hydroxy-acid:eek:xygen 2-oxidoreductase. Other names in common use include glycolate oxidase, hydroxy-acid oxidase A, hydroxy-acid oxidase B, glycolate oxidase, oxidase, L-2-hydroxy acid, hydroxyacid oxidase A, L-alpha-hydroxy acid oxidase, and L-2-hydroxy acid oxidase. This enzyme participates in glyoxylate and dicarboxylate metabolism. It employs one cofactor, FMN ( @ahmo ).
then I looked up glyoxylate and dicarboxylate metabolism:
A compact graphical description of major biochemical reactions involved can be found at KEGG[1] ( KEGG is an interesting site @aaron_c ) This provides information on the relevant enzymes and details the relationship with several other metabolic processes: glycine, serine, and threonine metabolism which provides hydroxypyruvate and glyoxylate, purine metabolism ( @Violeta ) which provides glyoxylate, pyruvate metabolism which provides (S)-malate and formate, carbon fixation which consumes 3-phospho-D-glycerate and provides D-ribulose 1,5-P2, ascorbate and aldarate metabolism which shares tartronate-semialdehyde, nitrogen metabolism which shares formate, pyruvate metabolism and the citrate cycle which share oxaloacetate, and vitamin B6 metabolism which consumes glycolaldehyde.
The glyoxylate cycle describes an important subset of these reactions involved in biosynthesis of carbohydrates from fatty acids or two-carbon precursors which enter the system as acetyl-coenzyme A. Its crucial enzymes are isocitrate lyase and malate synthase.
I barely understood anything, but I thought someone could extract the meaning out of it.

If I understand at least a little of it, B2 (FMN) has a role on it all, but it is not recommended in the oxalate lowering lists of supplements.
 

Avengers26

Senior Member
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158
This thread has probiotics for oxalates. There are also probiotics out there for histamine problems. Sorry, for being OTT, but are there any probiotics for salicylates/phenols, or for sulfur (thiol) rich foods/sulfates, for those who don't tolerate them well (eg. epsom salt bath intolerance)?

Later this year, I plan to do an elimination diet. So, it will be handy to have probiotics at hand for experimentation for different known diet issues.
 
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