My Health: explaining my low homocysteine

With my specific DNA mutations in the methylation cycle a high homocysteine level is to be expected. Making me deficient for SAM-e and flooding my cells with sulfur.

pic by J. Gabriel

But much to my surprise the other day my blood test resulted in LOW levels of homocysteine. Too low, according to the lab. (“below six! Alert! should be 5-15”)

Now, having looked at my mutations, it is entirely possible my levels were substantially lowered in these few months that I started to supplement with methyl-B12.

I have two busted genes, one called MTR and one called MTRR.

Having MTR busted up properly, meaning a homozygous mutation, rendering the DNA useless to make its enzyme, is a rare mutation. Less than 1% of people have it.

Well, ain’t I the pretty spesiul snowflake!

 pic by J. Gabriel

Genic Genie -that wonderful program that will interpret your DNA results for you when it comes to Methylation and Detoxing- tells me this:

“Mutations in MTR have been identified as the underlying cause of methylcobalamin deficiency. Megaloblastic anemia can occur as a consequence of reduce methionine synthase activity.

A homozygous mutation of MTR A2756G is relatively rare (<1%). ”

Methylcobalamin is vit B12 once it enters your cells, y’all. Even though regular old B12 looks good in my blood levels there’s not enough of it in my cells. I have a vitB12 deficiency that doesn’t show up in blood tests.

Now, what is this MTR supposed to do anyway?

pic by Jefta

MTR grabs any a homocysteine particle and tries to glue a folate to it. With this new building block all kinds of wonderful things are done. Especially clearing the cells of all kinds of debris and heavy metals. So: important!

This glueing action by MTR requires homocysteine, folate, glue, scissors and a piece of mB12. Its friendly enzyme buddy MTRR makes this mB12.

MTRR is a special kind of enzyme, though, its like a brake. It does its thing in a slow, regulated way. Because hey, there’s other enzymes wanting a bit of mB12 too!

Here you can read a difficult piece of how it all works together. I don’t understand it myself. Yet. But the stuff has to do with proper DNA repair. And dopamine. And ATP and cortisol and moon phases. And they all long for mB12.

But my MTRR is broken…. no mB12 for any of you! This results in high homocysteine and all kinds of nastiness. And a sad little MTR who’s got nothing to glue.

But as soon as I started to supplement mB12 my MTR got going, grabbing homocysteine and folates left and right. Because my MTRR is broken too, there’s nothing to keep it in pace. My MTR floored it!

pic by Myles Davidson

As soon as I provided the mB12 my MTRR doesn’t make, MTR put the pedal to the metal. Quickly clearing my whole system of homocysteine. Resulting in the low levels that showed up in my blood work.

It may not be a bad thing per se. Wonderful stuffs are made from homocysteine-with-a-folate-glued-to-it. Stuffs such as SAM-e and Methionine (which I have not studied yet but they sound wonderful)

Homocysteine itself is a powerful yet dangerous thing I hear. Dr.Yasko compares it to a prison chain gang such as known in the US of A. A group that can do good and helpful things for the community. But they need to be monitored and supervised carefully.

Anyway, I do feel better on mB12. I take about 1mg per day (B12 felt not ok, neither did folate acid. Folinic acid doesn’t seem to do much either way, indicating that my heteryzugous MTHFR C677T is probably not expressed, meaning it functions alright and ignores the faulty half of the DNAladder.)
Next time I’ll get my methionine checked.

I wonder how the other enzymes are faring, the ones who’d like a bit of mB12 for themselves. Do they get any? How can I find out? How can I aid them?

to remind myself, this is what Heartfixer says about MTR/MTRR:
“The MTR A2756G defect is an up regulation. The enzyme is always on, grabbing every homocysteine and 5-methyl folate molecule that it can get its hands on, processing them to methionine and THF. Methyl-B12 is required for normal function of MTR, and with each spin of the MTR enzyme, one molecule of methyl-B12 is degraded.

MTRR (Methionine Synthase Reductase) serves the needs of MTR, regenerating methyl-B12 from available methyl donors and B12. Without methyl-B12, MTR cannot convert homocysteine in to methionine. Needed downstream methyl donors such as SAMe will not be generated. Methylation fails, so does your biochemistry, and there goes your health. ”

pic by Joel Kingsbury

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