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I'm not sure what any of this means but I had low B12 in my blood test so my Neurologist ran a homosystine test and it was high. After taking supplements for B12 for 2 months, it all went back to normal. My last blood test showed high B12. I wonder if the homosystine would be really low?
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Not necessarily. The methylation cycle has many critical points and is part of the Citric Acid cycle which has many more.
Here's the thing about serum levels of B12 by our wonderful docs out there. The serum B12 measurement indicates that you don't have an
absolute B12 deficiency, but it does not rule out a
functional B12 deficiency. Many will show high serum B12 levels and it is known that the serum B12 or the absolute value measured, is dominated by the fraction of B12 that is bound to haptocorrin, and has been exported
from the cells. It does not show levels
in the cells, where we need it (
or the functional value). If Vitamin B12 just floats along in the blood because it is bound to haptocorrin, and none gets
into the cells, where the mitochondria use it, then even though one has a high serum level or an absolute value, one can still have a functional B12 deficiency. So one would have to find why the B12 can't get into the cells, and that is usually due to other critical points that are deficient.
The treatment Freddd suggests @ PR board, bypasses all the normal B12 absorption, transport, and intracellular processing of B12, and as such, it is effective in both absolute and functional B12 deficiency states of all sorts.
You didn't mention which form of B12 you took, which is important to many, but not all. Some can process the other forms, many cannot. To further define other forms, those would be hydroxycobalimin and cyanocobalimin, two popular forms found in most supplements on the shelves.
A functional B12 deficiency versus an absolute deficiency depicited by serum tests available today can also be the result of a methylfolate deficiency. There is a reason why B12 has become low. I'll get to the homocysteine in a minute. Bear with me, a lot of information all at once, and I am trying to make it understandable to as many as I can. The body can measure adequate serum levles or absolute levels, but the CSF and hence CNS doesn't have sufficient mb12 and/or adb12. They are finding in the diseases that had a generally "low" CSF cobalamin level with normal or high body serum cobalamin level; CFS, FMS, Alzheimer’s, Parkinson's, ALS, MS and others, specific markers for dramatically low levels of either of the two active b12s - adb12 and mb12 - in the form of elevated MMA and/or Hcy (homocystiene) in the CSF.
This occurence appears to proceed disease diagnosis by 20+ years. These depressed CSF cobalamin levels have “non-specific” and at first, quite subtle and apparently unconnected symptoms, with different symptom sets for mb12, adb12 and the combination. Further out of those common sets of symptoms, most people only have some fraction of them, possibly connected to how they use
folic acid, folinic acid and food folate, among other things. Which is why my identification of the MTHFR C677T mutation is quite important to me.
The test for elevated homocystiene, will specifically identify low levels of mb12 SPECIFICALLY (and possibly methylfolate and/or P-5-P, other critical points). By the time a person has elevated uMMA and/or Hcy they have already suffered damage, Finding elevated MMA
in the CSF appears to indicate the ongoing damage that leads to Parkinson’s. Finding elevated
Hcy in the CSF appears to indicate the damage leading to MS. Finding elevated Hcy and MMA in the CSF appears to indicate the damage leading to ALS. Meagan, I have neurolgical damage, I am not sure if you do. Actually through the course of all this, I didn't realize just how much I had incurred.
Dr. Joseph Chandry, treating Vitamin B12 deficiencies for 30 years, has made the observations that by the time symptoms are recognised and diagnosis given, there may be damaged transport proteins and utilization pathways (these are the "other critical points" I referred to above); and states that these people may need to maintain a very high blood serum concentration of B12 in order to function and maintain their current health status. And in my own opinion, this may also mean methylfolate.
Here's another point of contention I have with serum testing of B12 is the current age...
I included the functional and absolute deficiency above as a learning tool, and to help define the differences between what is in the serum, and what is actually getting into the cells. But differentiating between “functional” or “absolute” deficiency is based on a flawed definition of deficiency. And it is flawed because when these "limits" and "reference levels" were established it was only based on hydroxycobalimin and cyanocobalimin, and does not take into account the individuals ability to convert those particular forms into forms in which the body can actually utilize and get into the cells and CSF. These forms are considerd to be inactive forms, as it takes conversion in the body to produce the active forms in which is actually used, those active forms being methyl b12 and adenosyl-B12.
Half the people in this country are “functionally” deficient as defined by standards based on inactive cobalamin and pernicious anemia in Vitamin B12 studies. Serum cobalamin level doesn’t indicate the amount of active b12s available to the cells. The serum levels were set in reference to pernicious anemia and very enlarged red blood cells. They were NEVER set with the entire range of body active b12 deficiency symptoms.
A realistic lower limit for being asymptomatic is probably in the area of 3000-6000pg/ml. Further, even a serum level of 6000pg/ml might very well not be sufficient to correct the low cobalamin in the CSF/CNS. Whether it is enough to prevent neurological breakdown and differentiation into multiple diseases would require a 20-30 year trial depending upon a host of factors.
So any of the studies thus far in Vitamin B12 deficiencies have been based in the past on serum levels, not CSF levels and in which only address the enlargement of the red blood cells and pernicious anemia, and on inactive forms of Vitamin B12, not the active forms of Vitamin B12, that being methyl B and adenosyl, in which many do not have the capability to convert the inactive forms into the active forms. And it is due to this lack in studies and the pervasiveness of high serum B12 results in which propagate the "hidden" and stealth occurence of Vitamin B12 deficiency and does not take into account the role of folic acid/folinic acid/methylfolate status.
As far as your homocysteine levels dropping, that is good in the close up picture but may not be in the bigger picture. If too much homocysteine is being converted to methionine and not going to cystiene and glutithione, well then you would have found another critical point.
This stuff isn't easy by any means, nor explaining it either. Nothing I have responded back to you is to lend to a feeling of wellness or lack there of. There is just so many considerations, and I guess what I am really trying to convey by giving you all this information, is that perhaps you may want to pursue additional avenues in finding why your vitamin B levels were low in the first place. And that perhaps, since your test results show what was the original intent of the treatment, that maybe there may be additional avenues in which you would want to explore or atleast have your physician explain to you as to why or why not he/she may not want to, even though you have acquired the expected result.
Frito
June 1st, 2011, 05:17 PM
Had Genetic Testing Done 
Please stay tuned as I will be posting my results over the next few weeks.
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