Very high B12! On methyl supps, so what's next to get it down??

[Basilico]

Just wanted to throw out something, in case it's at all helpful. Since I have a chronic iron deficiency problem that tends to become anemia, I've spent a lot of time researching how to do the opposite of what you need to do (increase iron absorption). So perhaps you might want to do the opposite of my protocol.

Combining iron with vitamin C (ascorbic acid) INCREASES absorption (as does alcohol, and sugar in general, even from fruit)

Combining iron with calcium DECREASES both heme and non-heme iron absorption. (so does eggs and a few other things).

Here is a link that has a little more information about what inhibits/increases iron absorption: http://www.irondisorders.org/diet/

 

[grapes]

Which mutations?

Valentijin, the FUT2 mutations. I mentioned three specific ones starting with rs above in my reply to keenly.

 

[Valentijn]

...of which two are shown as significant: rs492602 GG and FUT2 rs602662 AA. THAT could explain this high B12...

I found this about my homozygous FUT2 rs601338

rs492602 isn't doing anything. It's homozygous only because rs601338 is homozygous, and it's not adding to its effects. rs601338 means that the gene's product is prematurely terminated and non-functional, so that's really the only relevant mutation.

But it sounds like FUT2 doesn't have anything to do with uptake of B12 into the cells. Rather the presence of the mutation results in more B12 being absorbed in the gut. So that can certainly raise B12 blood levels, but doesn't indicate any functional deficiency further down the line.

 

[grapes]

Just wanted to throw out something, in case it's at all helpful. Since I have a chronic iron deficiency problem that tends to become anemia, I've spent a lot of time researching how to do the opposite of what you need to do (increase iron absorption). So perhaps you might want to do the opposite of my protocol.

Combining iron with vitamin C (ascorbic acid) INCREASES absorption (as does alcohol, and sugar in general, even from fruit) Combining iron with calcium DECREASES both heme and non-heme iron absorption. (so does eggs and a few other things).

Hi Basilico. Thank u. My problem is that I could either be absorbing too much (such as a variant for hemochromatosis) or not absorbing enough (due to methylation variants). Either can show high blood serum iron. My challenge is figuring out what is causing all this--both high iron and high B12!!

 

[grapes]

rs492602 isn't doing anything. It's homozygous only because rs601338 is homozygous, and it's not adding to its effects. rs601338 means that the gene's product is prematurely terminated and non-functional, so that's really the only relevant mutation.

But it sounds like FUT2 doesn't have anything to do with uptake of B12 into the cells. Rather the presence of the mutation results in more B12 being absorbed in the gut. So that can certainly raise B12 blood levels, but doesn't indicate any functional deficiency further down the line.

The information I'm getting is contrary to what you stated.

i.e. with homozygous rs492602, livewello states: Among generally well-nourished women, a study1 found that common variation in the FUT2 secretor gene was associated with plasma vitamin B12 at high levels of statistical confidence. Women homozygous for the rs492602[G] allele had higher B(12) levels.

Re: FUT2 rs601338....According to the information presented to me in livewello and in research I found, it means I don't have great intestinal microbiota diversity, and especially need bifidobacteria, which I am now on.

 

[Valentijn]

The information I'm getting is contrary to what you stated.

i.e. with homozygous rs492602, livewello states: Among generally well-nourished women, a study1 found that common variation in the FUT2 secretor gene was associated with plasma vitamin B12 at high levels of statistical confidence. Women homozygous for the rs492602[G] allele had higher B(12) levels.

rs492602 isn't capable of having an impact, because it's a synonomyous mutation. So having either allele means you create exactly the same protein.

In the research where they found that risk, they also explain that the effect is actually due to the stop-gain mutation at rs601338. The two SNPs are in strong linkage disequilibrium, which means that people get both variants, or they get neither. So if someone researches either mutation, they find exactly the same effect for both of them, because they are basically only one mutation that is having an impact. If both are studied together, they have no additive effect.

 

[grapes]

**SNAP** I got on 5 mg lithium after reading it helps get B12 to the cells, helps COMT, helps MTRR, etc. I moved up to 10 mg max, and after six days, voila....I started detoxing copper about 48 hours ago. So here's hoping that means the lithium might be one missing puzzle piece in all this to improve my methylation (along with so many other supplements I'm on, including SAM-e, which I restarted several days ago)

 

[pattismith]

@grapes ,

if you are still around, how did you fixed your B12 and Iron issue?

I have found studies about high B12 blood levels associated with B12 insuficiency, when an auto-antibody binds Transcobalamin II (this prevent the release to the cell)


Circulating antibody to transcobalamin II causing retention of vitamin B12 in the blood
http://www.bloodjournal.org/content/49/6/987.short?sso-checked=true

Transcobalamin deficiency can also be genetical.

"Homozygous or compound heterozygous mutations in the transcobalamin II gene (TCN2) on chromosome 22q12.2 that contains 9 coding exons are known to cause transcobalamin II deficiency, including deletions, nonsense mutations, and a mutation resulting in activation of a cryptic intronic splice site"

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4805327/

I do have myself two unfrequent missense mutations (heterozygous) on the TCN2 gene (of unknown incidence)

rs35915865 TC (this one is classified as "uncertain significance" )
rs4820889 GA (this one is quoted as "likely benign", but is associated with lower B12 blood levels and increase CAD risk in an Indian study)

https://www.researchgate.net/profil...onary-artery-disease-in-Indian-population.pdf

https://www.ncbi.nlm.nih.gov/clinvar/RCV000353236/

edit: I had my insaturated Transcobalamin II tested in 2011, which was 351 pg B12/ml (lab normal ranges were 400-1800)

 

[grapes]

pattismith, yes, I'm still around and that is very interesting! Just checked, the only variant of that gene I have is rs4820886 and only heterozygous. So not sure how strongly this mutation would explain my high B12.

I did finally get my iron down, but the serum B12 stays stubbornly high now the entire year i.e. over 2000. A bit crazy. That's with taking folate in higher amounts.

 

[grapes]

Also just found out my selenium is high..

 

[pattismith]

Hydrogen Sulfide depletes potassium, and I think we all have a problem with that.

Can you explain? I'm not familiar with hydrogen sulfide - is it in food or? and what sort of problems does it cause?

I would be interested as well, as I didn't find evidence or anecdotal reports for that...

 

[keenly]

I would be interested as well, as I didn't find evidence or anecdotal reports for that...

Have your own levels measured. HS interferes with mitochondrial function.

 

[pattismith]

Have your own levels measured. HS interferes with mitochondrial function.

Yes I know that hydrogen sulfide inhibit OXPHOS, but I didn't find anything about potassium. So I wonder if you have a link to propose?