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First try at Active Protocol and have questions.

Chocolove

Tournament of the Phoenix - Rise Again
Messages
548
@JasonUT Here's to hoping your low aldosterone....low adrenal function is caused by insufficient B vitamins rather than some other agent. Making sure your body has sufficient nutrients for adrenal function and enough to support the HPA axis is a good square one step. However you can see why it's a good idea to check out other possibilities as well.
 

JasonUT

Senior Member
Messages
303
BUN Brainstorming: This is not a new topic. I have discussed the relationship between elevated BUN equals increased symptoms in post #13 and #14 and #92. I have yet to figure out a theory or root-cause of this relationship. However, I thought I would dive into it again.

This article suggests that:
A BUN test is done to see how well your kidneys are working. If your kidneys are not able to remove urea from the blood normally, your BUN level rises. Heart failure, dehydration, or a diet high in protein can also make your BUN level higher. Liver disease or damage can lower your BUN level.

This article suggests that a high creatinine level is a sign of kidney dysfunction. My creatinine levels have always been good.

So why would my kidney's have trouble removing Urea from the blood?

I was on an all meat diet due to SIBO test prep for 12 hours. This might explain my high ER BUN value. But how do I explain all the other 20+ data points I have?

I don't think I have heart failure, but I was diagnosed with POTS which is associated with low blood pressure and blood pooling. Is it possible my Urea is getting backed up, because the kidneys can't filter the blood fast enough due to poor blood flow? How can I safely improve blood flow through the kidney's?

Is my increased thirst my body's attempt at trying to increase urination to get rid of the high Urea?

Or, is my Urea high because I have high Ammonia production?

What are proven methods to reduce BUN? Will this translate to improved symptoms?
 
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Chocolove

Tournament of the Phoenix - Rise Again
Messages
548
@JasonUT Perhaps you should try another BUN test if you have gone off the high meat diet. That may be a simple way to put to rest some of the worry. Being dehydrated can raise BUN. Know that your doctor uses various diagnostic protocols to help decipher all the test results. You may want to look up such:
https://www.google.com/search?q=understanding+medical+lab+results&ie=&oe=
http://www.kidney-symptom.com/high-bun-level/362.html
https://www.livestrong.com/article/526406-how-to-reverse-high-bun-levels/
 

renski

Senior Member
Messages
338
Location
Honolulu
B2 and B5 Brainstorming:
In post 67, I struggled with B2 specifically. I couldn't reconcile the idea that SpectraCell shows high B2, but OAT shows low B2. Then it dawned on me that B vitamins work as a team. Maybe because it's teammates are out of the game injured. I have read that B1, B2, and B3 work as a team. I am functionally deficient in B1 and B3; therefore, is it possible that B2 can't be metabolized (i.e. metabolites don't show up in urine)? Could this explain why it is showing up high on SpectraCell, but low on OAT? Perhaps balancing B1 and B3 will help balance the other B's?

@JasonUT, thanks for posting all of this, it's been helpful for my own troubleshooting.

I think on the OAT test (at least for Great plains lab) B2 is an indirect marker (so it isn't a measurement of B2 itself), but that is strange if it's low on your test. My Glutaric is still within range but on the higher end of the scale, meaning I'm deficient in B2. My Nutreval also showed B3, B2, B6 deficiency, B1, Biotin was also very close to deficiency.
 

JasonUT

Senior Member
Messages
303
@renski Thanks for the feedback. It's been an interesting journey.

I am continuing to tweak things. I feel like I am on a seesaw now. I fixed B1, B6, and B9, but now need to shift gears to B3 and B5. It appears B5 competes with Biotin and ALA for absorption via sodium-dependent multivitamin transporter (SMVT) [Source]. B3 and B5 are both needed for Acetyl-Coa and CoQ10 production [Source].

With that said, I started experimenting with larger doses of pantothenic acid and niacinamide. I discontinued the CoQ10 experiment for now. CoQ10 increased energy, but lowered my blood pressure too much making me potsy. I also dropped my extra B-Right. My working theory at this time is to fix B3 and B5 and hope that fixes CoQ10, Biotin, and Hormones.
 

Gondwanaland

Senior Member
Messages
5,092
larger doses of pantothenic acid
From my own experience this is a potent antagonizer of bile acids (esp. endogenous Taurine synthesis). Since I do not tolerate Taurine supplementation (it lowers aldosterone horribly), I am looking into improving endogenous Taurine. Carcinine does that and in my case it depleted all the raw materials... I haven't found a reputable source for it yet though
https://bebrainfit.com/taurine-benefits/
The amino acids cysteine and methionine must be present along with zinc, vitamin A, and vitamin B6
 

JasonUT

Senior Member
Messages
303
From my own experience this [pantothenic acid] is a potent antagonizer of bile acids (esp. endogenous Taurine synthesis).

Interesting. These articles seem to suggest B5 helps Bile Acid production via Acetyl-CoA. I wounder what is happening.
http://healthandscience.eu/index.ph...-pantothenic-acid&catid=54&Itemid=327&lang=en
http://mccordresearch.com/vitamin-b5-pantothenic-acid
http://www.syrianclinic.com/med/en/ProfSupplements/VitaminB5PantothenicAcidps.html
https://nootropicsexpert.com/vitamin-b5-pantothenic-acid/
https://www.drlam.com/blog/about-vitamin-b5/1235/

coa_pathways.gif


Since I do not tolerate Taurine supplementation (it lowers aldosterone horribly)...

Interesting, I'll need to research taurine's affect on aldosterone, hypotension, POTS, vasodilaiton, etc.
 

JasonUT

Senior Member
Messages
303
Nutritionist Appointment, 10/6/2017:
  1. Concerned about Metabolic Disorder around processing proteins. Recommended a Metabolic Disorder Panel test.
  2. Felt that I may have some form of Urea Cycle abnormality. This is based on the idea that my urea levels are elevated when symptomatic and I struggle to supplement with Glutamine which is one of the primary amino acids of Ammonia and Urea [Source]. Glutamine avoidance and Essential Amino Acid and BCAA supplementation is one of the primary treatments for urea cycle disorders such as Ornithine Transcarbamylase Deficiency.
  3. I may be struggling with low B3 levels because my body is having trouble processing proteins, specifically tryptophan amino acid. My tryptophan metabolite 5-HIAA has been historically low on my OAT. Tryptophan pathways.
  4. As a result, he recommended I try to lower animal protein intake, avoid glutamine, and try BCAA supplements that are free of added glutamine.
There appears to be a lot of discussion on Phoenixrising around BCAA's. I'll need to dive into these existing discussions.

Here are a few studies on Urea Cycle disorders and Amino Acids:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3565665/
Supplementation with essential amino acids (particularly branched-chain amino acids) at these times should be considered

https://www.ncbi.nlm.nih.gov/pubmed/15050979
These findings suggest that better titration of protein restriction could be achieved with branched chain amino acid supplementation in patients with UCDs who are on alternative route therapy.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3488504/
Plasma levels of branched-chain amino acids (BCAAs, a subgroup of the EAAs) are decreased in patients taking high doses of sodium PBA [112], suggesting the potential need of BCAA supplementation [113,114]. It has been advocated that EAA supplements should be rich in BCAAs but not in the neurotransmitter precursor amino acids tryptophan, phenylalanine and tyrosine [114]. BCAA supplements are available as single amino acids or complete mixture and as per EAAs given as a divided dose.
Since glutamine levels change with the fasting/feeding status, being highest after the overnight fast [169]...
Interesting. Not sure what to make of this statement.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5260006/
Finally, these BCAA metabolites are catabolized by a series of enzyme reactions to final-products (acetyl-CoA from leucine, succinyl-CoA from valine, and both acetyl-CoA and succinyl-CoA from isoleucine), which enter the TCA cycle.

https://en.wikipedia.org/wiki/Branched-chain_amino_acid
The BCKDH complex converts branched-chain amino acids into acyl-CoA derivatives, which after subsequent reactions are converted either into acetyl-CoA or succinyl-CoA that enter the citric acid cycle.[15]

We have a suspicion that I struggle with low Acetyl-CoA levels. I wounder if BCAA supplements will help.
coa_pathways.gif
 

JasonUT

Senior Member
Messages
303
BCAA's and Ammonia Detox: I cherry picked a few studies to elicit some discussion and brainstorming.

https://www.clinicalcorrelations.org/?p=3544
Furthermore, supplementation of BCAAs is thought to facilitate ammonia detoxification by supporting synthesis of glutamine, one of the non-branched chain amino acids, in skeletal muscle and in the brain as well as diminishing the influx of AAAs across the blood-brain barrier.[5]

https://www.ncbi.nlm.nih.gov/pubmed/23756281
The rationale for recommendation of branched-chain amino acids (BCAA; valine, leucine, and isoleucine) in treatment of liver failure is based on their unique pharmacologic properties, stimulatory effect on ammonia detoxification to glutamine (GLN), and decreased concentrations in liver cirrhosis.

https://link.springer.com/chapter/10.1007/978-1-4939-1923-9_9
Branched–chain amino acids (BCAA; Isoleucine, leucine and valine) have attracted particular interest as they are believed to support this muscle ammonia detoxification. Liver disease represents the field in which the potential ammonia lowering effect of BCAA has been most intensely investigated.

https://www.ncbi.nlm.nih.gov/pubmed/23315357
Branched-chain amino acids (BCAA) are used as a therapeutic nutritional supplement in patients with cirrhosis and hepatic encephalopathy (HE). During liver disease, the decreased capacity for urea synthesis and porto-systemic shunting reduce the hepatic clearance of ammonia and skeletal muscle may become the main alternative organ for ammonia detoxification.

https://www.ncbi.nlm.nih.gov/pubmed/23945292
Thus, BCAA supplementation may enhance detoxification of ammonia in skeletal muscle and may be a possible therapeutic strategy for HE/MHE.
 
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JasonUT

Senior Member
Messages
303
Inborn Errors of Metabolism (IEM) in Adults: My nutritionist speculated that I might have a Metabolic Disorder that might explain my peculiar response to protein and BUN plus my other symptoms. As a result, I started researching and here is what I have found so far.

Inborn Errors of Metabolism: Disorder of Adults?

They refer to single gene disorders wherein loss of function of a single enzyme results in abnormalities in synthesis or catabolism of proteins, carbohydrates or fats, which results in a disruption in a metabolic pathway. This results in toxic accumulations of substrates before the disruption, intermediates from alternative pathways, and/or defects in energy production and utilization. Nearly every metabolic disease has several forms that vary in age of onset, clinical severity and mode of inheritance.

A simple method classifies IEMs into disorders involving protein metabolism, carbohydrate metabolism, lysosomal storage, fatty acid oxidation defects, mitochondrial disorders, peroxisomal disorders.

Increase the residual enzyme activity: People with Group II IEMs can benefit by increasing the residual enzyme activity. This is done by administration of pharmacologic doses of the vitamin cofactor for the defective enzyme (Table 4).

We talk about pharmacological doses of vitamin cofactors a lot on this forum, but it is only 1 of 8 potential treatments mentioned in the article.

Inborn Errors of Metabolism in Adults: A Diagnostic Approach to Neurological and Psychiatric Presentations
 

Gondwanaland

Senior Member
Messages
5,092
@Gondwanaland, would that mean if you are low on B1 then the B2, B3, B6 need to be replenished first for the sulfur pathway to work? Nothing seems to be that simple though :/
Dr. Lonesdale recommends taking a B complex along with therapeutic doses of B1, + macrominerals like magnesium and potassium. Some people might also have some extent of deficiency in microminerals, which could be a limiting factor. I know I do, given my sulfite sensitivity.
 

renski

Senior Member
Messages
338
Location
Honolulu
Dr. Lonesdale recommends taking a B complex along with therapeutic doses of B1, + macrominerals like magnesium and potassium. Some people might also have some extent of deficiency in microminerals, which could be a limiting factor. I know I do, given my sulfite sensitivity.

Ideally.. I can barely tolerate Allithamine and regular Thaimine, Benfotamine is a bit better but still strong side effects. And I'm very low in B2, B3, B6 and a bit low in B1.
 

Gondwanaland

Senior Member
Messages
5,092
Ideally.. I can barely tolerate Allithamine and regular Thaimine, Benfotamine is a bit better but still strong side effects. And I'm very low in B2, B3, B6 and a bit low in B1.
Same here. I only tolerate Thiamine-HCl in a low dose B complex.
 

vortex

Senior Member
Messages
162
If I saw glutathione levels as low as yours I would suspect MTHFR, it would explain everything.
I looked through all your posts but dont see you mentioned your status anywhere?