Oxalate Toxicity

[Dutchie]

I am using energin around my navel. Energin is the first B complex with B6 I’ve been able to handle. When I tried B6 orally (even very low doses, <1mg, of P5P spread throughout the day) I would have a really bad oxalate dump and get peripheral neuropathy after 2d of use. My serum levels were never tested high. I think it has to do with the liver picking up most of the Bs when taken orally.

Thanks.
I've looked around but there are no shops here selling a product with the name Energin, however I did see various liquid b-complex supplements but it's still for oral use and it has other ingredients which I'm not crazy about.
The thing is that I don't notice any negatives from taking the b-complex orally,but it's just that I seem to have become very sensitive to endogenous production and I don't know why this is/keeps happening.

 

[Recoen]

Thanks.
I've looked around but there are no shops here selling a product with the name Energin, however I did see various liquid b-complex supplements but it's still for oral use and it has other ingredients which I'm not crazy about.
The thing is that I don't notice any negatives from taking the b-complex orally,but it's just that I seem to have become very sensitive to endogenous production and I don't know why this is/keeps happening.

Energin is from idealabs.

Are you dumping more?

Are you getting enough sleep, reduced stress, etc?

It’s hard to say if there’s a food or supplement causing it because you really don’t know if you made a lot until you dump.

 

[Dutchie]

Energin is from idealabs.

Are you dumping more?

Are you getting enough sleep, reduced stress, etc?

It’s hard to say if there’s a food or supplement causing it because you really don’t know if you made a lot until you dump.

I've read about dumping in the tlo fb group,but it's still unclear to me when I'm dumping. The only time I can tell is when my urine is cloudy,which now typically happens when I have some collagen or glycine powder. I also get an overactive bladder and can hardly hold up my pee.
Those are symptoms to me that my oxalates are high.
Looking back at the previous years,I've definitely have had major dumping episodes (hairloss, teeth worsening and tartar built up etc.)

My life is very low to no stress at the moment,so those things can't be it

 

[Recoen]

I've read about dumping in the tlo fb group,but it's still unclear to me when I'm dumping. The only time I can tell is when my urine is cloudy,which now typically happens when I have some collagen or glycine powder. I also get an overactive bladder and can hardly hold up my pee.
Those are symptoms to me that my oxalates are high.
Looking back at the previous years,I've definitely have had major dumping episodes (hairloss, teeth worsening and tartar built up etc.)

My life is very low to no stress at the moment,so those things can't be it

Dumping usually means you’ve actually lowered your total oxalate load. So the body now feels “safe” to rid itself of it. I would try to slow the dumping if it’s making you uncomfortable with some chocolate or something a little higher ox.

 

[somuch4food]

Has anyone tried upping copper? It seems like copper status is important for zinc and B6 retention.

signs of a low copper deficiency?

Spoiler

Haem production (using iron) works only if Cu is available. If insufficient copper, then Zn and B6 lost from the body. So treating with Zn and B6 supplements is treating a symptom, not the cause.

(He didn't mention copper toxicity in this - but that's not an issue for us)

When people are short of bioavailable copper, they won't make enough dopamine, leading to cravings for sugar and alcohol to boost dopamine.

He seems to advocate food sources above supplements.

 

[Recoen]

Has anyone tried upping copper? It seems like copper status is important for zinc and B6 retention.

signs of a low copper deficiency?

Spoiler

Haem production (using iron) works only if Cu is available. If insufficient copper, then Zn and B6 lost from the body. So treating with Zn and B6 supplements is treating a symptom, not the cause.

(He didn't mention copper toxicity in this - but that's not an issue for us)

When people are short of bioavailable copper, they won't make enough dopamine, leading to cravings for sugar and alcohol to boost dopamine.

He seems to advocate food sources above supplements.

It could also be the Cu is stuck in the cell. B1 has been shown to get it and Fe moving again. Really anything that helps with ATP/CO2 production should. I’ve been eating chocolate, oysters, liverwurst, and some claim vitamin C from food has Cu in it.
Do you supplement Cu?

 

[Dutchie]

Dumping usually means you’ve actually lowered your total oxalate load. So the body now feels “safe” to rid itself of it. I would try to slow the dumping if it’s making you uncomfortable with some chocolate or something a little higher ox.

I think the past years I've been massively dumping. I don't think I really dump much if at all anymore.
However what I described with the urine and bladder,only happens when I've had collagen or glycine powder. So it's an endogenous production issue and that's what I don't get,why this keeps happening despite daily supplementing.

 

[somuch4food]

It could also be the Cu is stuck in the cell. B1 has been shown to get it and Fe moving again. Really anything that helps with ATP/CO2 production should. I’ve been eating chocolate, oysters, liverwurst, and some claim vitamin C from food has Cu in it.
Do you supplement Cu?

I'm not supplementing. I'm trying to find a eating pattern that support my health. I'm upping liver and oysters. I was upping fruits, but that fails. I will keep to a few low fructose ones a day.

I've felt good a few times. I just need to find balance.

 

[Recoen]

I think the past years I've been massively dumping. I don't think I really dump much if at all anymore.
However what I described with the urine and bladder,only happens when I've had collagen or glycine powder. So it's an endogenous production issue and that's what I don't get,why this keeps happening despite daily supplementing.

That’s interesting. I wonder if the collagen/ glycine is really helping the body to release already stored oxalate? I say this because people seem to dump with B1, B2, etc supplementation. The vitamins are obviously helping ATP/CO2 production and making the body “stronger/healthier” and reducing endogenous production. So I wonder if a similar thing is happening.

 

[Dutchie]

That’s interesting. I wonder if the collagen/ glycine is really helping the body to release already stored oxalate? I say this because people seem to dump with B1, B2, etc supplementation. The vitamins are obviously helping ATP/CO2 production and making the body “stronger/healthier” and reducing endogenous production. So I wonder if a similar thing is happening.

I'm sorry,I'm not sure what you're trying to say.
Collagen and glycine trigger endogenous production, so I dont think the cloudy urine
happens bc the body releases oxalates,it produces it so it seems.
When I dont take collagen or glycine my urine is clear.

 

[Recoen]

I'm sorry,I'm not sure what you're trying to say.
Collagen and glycine trigger endogenous production, so I dont think the cloudy urine
happens bc the body releases oxalates,it produces it so it seems.
When I dont take collagen or glycine my urine is clear.

Yes, they say if you don’t have enough B6 then glycine becomes oxalate. However, they also say people don’t dump but store oxalate, until their body burden decreases. And taking supplements like B1, B2, even vit K2 causes dumping because your body has more ATP, SOD, GSH, etc to deal with the dump. Because glycine/ collagen causes you to have characteristic dumping signs to me that means it’s beneficial for you, because your body is letting go of the stored oxalate. If it were converting to oxalate endogenously then from what all the low ox people seem to say, it’ll stay in your body until conditions are such that it’s safe to dump.

 

[Dutchie]

Yes, they say if you don’t have enough B6 then glycine becomes oxalate. However, they also say people don’t dump but store oxalate, until their body burden decreases. And taking supplements like B1, B2, even vit K2 causes dumping because your body has more ATP, SOD, GSH, etc to deal with the dump. Because glycine/ collagen causes you to have characteristic dumping signs to me that means it’s beneficial for you, because your body is letting go of the stored oxalate. If it were converting to oxalate endogenously then from what all the low ox people seem to say, it’ll stay in your body until conditions are such that it’s safe to dump.

From what I gathered is that oxalates get stored when they can't be taken out of the body. It doesn't automatically get stored....and I'm not sure if only dietary oxalates get stored.
Anyway,what I experience after taking glycine is definitely from production and not released oxalates.

 

[Amazoniac]

We associate hydrocraponate in the gut with stomach and its protection against acidity, yet it's present throughout it. A defective barrier due to overwhelming insults can result in compromised cellular respiration that might not yield enough hydrocraponate for proper mucus organization. Perhaps this makes someone prone to absorb too much oxalic acid because a superficial layer with lower acidity will create an environment that favors the loss of hydrogen ion from oxalic acid; ionized molecules are more difficult to move freely, which might prevent excessive absorption. Also, since the process of unfolding involves killcium liberation, it could be a coordinated effect that promotes the complexation of oxalate with killcium.

- Slimy partners: the mucus barrier and gut microbiome in ulcerative colitis

"Stratification of the mucus layer has been shown to be indirectly influenced by the gut microbiome (Fig. 1a). An increase in pH and removal of N-terminally bound single calcium ions are necessary for the conversion of the inner firm mucus layer to the outer loose mucus layer, the so-called mucus layer stratification[50]. In general, colonocytes are mainly dependent on adenosine triphosphate produced by the β-oxidation of butyrate, a metabolite of the gut microbiome, which is accompanied by the generation of CO2 that can be converted by carbonic anhydrase into HCO3−[51]; this is the ideal physiological solution for precipitating calcium and raising the pH at the epithelial surface[52]. The absence of HCO3− at the intestinal epithelial surface or inhibition of HCO3− transepithelial transport decreases the amounts and rates of stimulated mucus release in vitro and in vivo[53]. For instance, facultative anaerobic bacteria such as pathogenic E. coli and Salmonella expand and invade the surface epithelium, thereby subverting colonocyte metabolism from β-oxidation of SCFAs to anaerobic glycolysis to promote their own luminal growth in competition against the gut microbiota by increasing the luminal bioavailability of oxygen (O2), lactate, and additional electron acceptors, including tetrathionate (S4O62−) and nitrate (NO3−)[51,54]. The resultant decrease in HCO3− in the lumen creates a high-H+ environment, enhancing the Ca2+-binding of mucin polymers and making them more adhesive to each other in condensed mucin granules[55]. As a result, the structure of mucus layers is impaired, and host susceptibility to pathogens and even UC incidence increases; therefore, UC was postulated to be an energy-deficient disease resulting from a failure to utilize butyrate[56]."​

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"There are two key transport systems for HCO3− extrusion into the colonic lumen: Cl−/HCO3− and SCFA/HCO3− exchangers[79] (Fig. 1b). Several lines of evidence indicate that SCFA/HCO3− exchangers mediate ionized SCFA entry into colonocytes concomitant with an increase in luminal pH and a decrease in oxygen tension in both human and rodent colons80, which are vital for the stratification of the secreted mucin complex and colonization of obligate anaerobes, respectively. Treatment with live Bifidobacterium and its culture supernatants stimulated the expression of Slc26a3, a Cl−/HCO3− exchanger[81]. Inflammation in the mid-distal[82] or distal colon[83] in Slc26a3-deficient mice was related to the loss of mucus secretion resulting from a remarkably low surface pH microclimate[83], a more aggressive microbiota[82] and/or reduced microbiome diversity[83]. A luminal microenvironment with higher oxygen and lower pH could change the gut microbiota composition and drive an uncontrolled luminal expansion of E. coli and Salmonella[84]."​

- Deep breathing for fixing constipation
- What would you choose if you were eating starch?

 

[Amazoniac]

- Effect of alanine supplementation on oxalate synthesis

The Primary Hyperoxalurias (PH) are rare disorders of metabolism leading to excessive endogenous synthesis of oxalate and recurring calcium oxalate kidney stones. Alanine glyoxylate aminotransferase (AGT), deficient in PH type 1, is a key enzyme in limiting glyoxylate oxidation to oxalate. The affinity of AGT for its co-substrate, alanine, is low suggesting that its metabolic activity could be sub-optimal in vivo. To test this hypothesis, we examined the effect of L-alanine supplementation on oxalate synthesis in cell culture and in mouse models of Primary Hyperoxaluria Type 1 (Agxt KO), Type 2 (Grhpr KO) and in wild-type mice. Our results demonstrated that increasing L-alanine in cells decreased synthesis of oxalate and increased viability of cells expressing GO and AGT when incubated with glycolate. In both wild type and Grhpr KO male and female mice, supplementation with 10% dietary L-alanine significantly decreased urinary oxalate excretion ~30% compared to baseline levels. This study demonstrates that increasing the availability of L-alanine can increase the metabolic efficiency of AGT and reduce oxalate synthesis.

 

[Amazoniac]

- Fat-reduced diet in the treatment of hyperoxaluria in patients with ileopathy

Thirteen patients with ileopathy were studied under metabolic ward conditions, first on a 100-g fat diet and later on a 40-g fat diet. Ten of the patients were studied after three to 27 months on a fat-reduced diet. Ten of the patients had a high urinary oxalate excretion on the high-fat diet compared with a control group. The patients with a faecal fat output of more than 15 g a day showed a reduction in oxalate excretion when the fat intake was decreased and in the follow-up study the oxalate excretion was low in all patients except in one with a remaining steatorrhoea. There was a correlation between urinary oxalate excretion and faecal output of fatty acids. It is postulated that a low intraluminal calcium ion concentration, mainly caused by the high fatty acid content, explains the hyperoxaluria. The low fat diet, which also reduced the diarrhoea and increased the urinary output, was acceptable to the patients. The diet is recommended for patients with ileopathy in order to reduce the risk of formation of renal calculi.

 

[Lollipop2]

Interesting @Amazoniac and whodonethunkit? Free fatty acids showing as part of the problem ?

 

[Amazoniac]

- Interactions Of Vitamin E And K

- Low-vitamin E diet exacerbates calcium oxalate crystal formation via enhanced oxidative stress in rat hyperoxaluric kidney

Vitamin E was previously reported to reduce calcium oxalate (CaOx) crystal formation. This study explored whether vitamin E deficiency affects intrarenal oxidative stress and accelerates crystal deposition in hyperoxaluria. The control (C) group of rats received a standard diet and drinking water, while the experimental groups received 0.75% ethylene glycol (EG) in drinking water for 42 days. Of the latter, one group received a standard diet (EG group), one received a low-vitamin E (LE) diet (EG+LE group), and the last received an LE diet with vitamin E supplement (4 mg) (EG+LE+E group). The C+LE and C+LE+E groups were the specific controls for the last two experimental groups, respectively. In a separate experiment, EG and EG+LE rats were studied on days 3–42 to examine the temporal relationship between oxidative change and crystal formation. Urinary biochemistry and activity/levels of antioxidative and oxidative enzymes in glomeruli and tubulointerstitial specimens (TIS) were examined. In EG rats, CaOx crystal accumulation was associated with low antioxidative enzyme activity in TIS and with increased oxidative enzyme expression in glomeruli. In the EG+LE group, marked changes in antioxidative and oxidative enzyme levels were seen and correlated with massive CaOx deposition and tubular damage. The increased oxidative stress seen with EG+LE treatment was largely reversed by vitamin E supplementation. A temporal study showed that decrease in antioxidative defense and increased free radical formation in the EG+LE group occurred before crystal deposition. This study shows that low vitamin E disrupts the redox balance and causes cell death, thereby favoring crystal formation.

- Supplementation of vitamin E and selenium prevents hyperoxaluria in experimental urolithic rats

Renal injury is considered as one of the prerequisites for calcium oxalate retention. In order to determine the role of lipid peroxidation related effects for hyperoxaluria, we evaluated the alterations in lipid peroxidation, antioxidants and oxalate synthesizing enzymes in lithogenic rats with response to vitamin E + selenium treatment. In kidney of lithogenic rats, the level of lipid peroxidation and the activities of oxalate synthesizing enzymes were found to be increased whereas the levels/activities of non-enzymatic and enzymatic antioxidants were found to be decreased. The urinary excretion of both oxalate and calcium were significantly elevated. Supplementation of lithogenic rats with vitamin E + selenium decreased the levels of lipid peroxides and the activities of oxalate synthesizing enzymes like glycolic acid oxidase (GAO), lactate dehydrogenase (LDH), xanthine oxidase (XO) with a concomitant increase in the activities of enzymatic antioxidants like superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glucose-6-phosphate dehydrogenase (G6PDH) and increased levels of non-enzymatic antioxidants like ascorbic acid, alpha-tocopherol and reduced glutathione (GSH). The urinary excretion of oxalate and calcium were normalized. The antioxidants vitamin E + selenium thereby protected from hyperoxaluria.

- Vitamin E Prevents Calcium Oxalate Stones

Objective: To determine whether vitamin E prevents hyperoxaluria-induced stone formation, using a new animal model of calcium oxalate stone disease, as our previous in- vitro and in-vivo studies showed that oxalate and hyperoxaluria induce free-radical generation, which results in peroxidative injury to renal tubular cells.

Materials and methods: Ethylene glycol (EG) was administered at 150 mg/day by gavage for 3 weeks to rats fed on diets with adequate (group 1), excess (group 2) or deficient (group 3) vitamin E. Several indicators of peroxidation, free radicals and enzymatic activity were then assessed.

Results: EG treatment in group 1 lead to increased lipid peroxidation, protein thiol, excretion of urinary enzymes, oxalate and decreases in urinary calcium, antioxidant enzymes and altered glutathione redox balance. Although renal function was not altered, there was increased water intake, urine volume and lowered urinary pH in these rats. These changes were more intense, with extensive calcium-oxalate crystal deposition, in rats in group 3, and prevented in rats in group 2, except for urinary oxalate levels, which remained high. Histopathological examination showed that there was no deposition of calcium oxalate crystals in rats in group 2.

Conclusion: This is the first study to demonstrate in-vivo evidence that hyperoxaluria-induced peroxidative injury induces individual calcium oxalate crystal attachment in the renal tubules. In addition, excess vitamin E completely prevented calcium oxalate deposition, by preventing peroxidative injury and restoring renal tissue antioxidants and glutathione redox balance. Therefore, vitamin E therapy might provide protection against the deposition of calcium oxalate stones in the kidney of humans.

 

[Lollipop2]

- Interactions Of Vitamin E And K

- Low-vitamin E diet exacerbates calcium oxalate crystal formation via enhanced oxidative stress in rat hyperoxaluric kidney

​

- Supplementation of vitamin E and selenium prevents hyperoxaluria in experimental urolithic rats

​

- Vitamin E Prevents Calcium Oxalate Stones

​

Hey interesting @Amazoniac - easy solution to oxalate problem.

 

[Blossom]

Hey interesting @Amazoniac - easy solution to oxalate problem.

I agree, that’s a great find. Too bad a just swore off any more experimenting for the next 40 days or I’d be trying this tomorrow. :)
I’ll have to put it on the agenda for later.

 

[tallglass13]

I am on day 10 of very low oxalate. It has basically brought me closer to a more Peaty diet. If you look at Danny Roddy's youtube video on Bioenergetic Eating sample, it shows a very low oxalate foods. Starches and veggies are the high foods. I was always eating tortillas and bread despite trying to eat a Ray Peat diet. Mostly dinner would include burritos, burgers, pizza. I have cut all of that out completely. Now I have no starch in my diet. No more beans either.
Results so far is that I am feeling fantastic, more limber, no aches or pains. I now can start working out soon. My skin is clearing up. I use to be a truck driver before I became a nurse, and had the worst kidney pains from drinking mocha coffees and eating bad foods like lots of flour bean burritos. Man, as someone who really cares about health, I sure did a lot of things wrong. I feel as if finding and learning about the dangers of the oxalate crystals cutting blood vessels and tearing into your kidneys, has really helped me clean up my diet.
Question for all of you, and @Blossom, What do you think about Coffee? Some reports show a very high Oxalate content, others like Sally Norton say it is only 3-4 mg per cup. I have decided to cut out coffee for now, since I like my beer. I only drink light bottled beer from Italy, so the content is just like coffee, at 3-4 mg per bottle.