Blood test for methylfolate

[bigmillz]

Getting this done up next week. Can anyone comment on a decent range to be in? I haven't found much aside from Ben Lynch saying it's useful in determining methylfolate dose (duh).

 

[TrixieStix]

Getting this done up next week. Can anyone comment on a decent range to be in? I haven't found much aside from Ben Lynch saying it's useful in determining methylfolate dose (duh).

Get a homocysteine blood test thru your doctor. It does require specific fasting and you need to eat a normal amount of protein during dinner the night before. If your level is good then your methylating just fine. At least that is what I concluded after months of reading up on MTHFR after finding out I had 2 mutations touted as "serious" by so-called mthfr experts. My homocysteine level came back perfect (10) so I know I'm methylating just fine.

I personally believe the mthfr thing is over-hyped and being used by many naturopaths to make $ from patients.

I found this resource just recently after my own travels down the mthfr road had already concluded.

https://sciencebasedmedicine.org/dubious-mthfr-genetic-mutation-testing/

 

[Mary]

Getting this done up next week. Can anyone comment on a decent range to be in? I haven't found much aside from Ben Lynch saying it's useful in determining methylfolate dose (duh).

One test to look at is the MCV - mean corpuscular volume - on the CBC (complete blood count) panel. If this number is high, it generally indicates a B12 and/or folate deficiency. The cells will become extra large, thus causing the high volume number, in order to compensate for the deficiency. My MCV was always in the normal range, but near the top of the range, and I had a noticeable increase in energy after starting methylfolate. I'd already been taking MB12 for many years.

BTW, my homocysteine numbers are always quite low, which is supposed to be a good thing. Homocysteine levels are not an indicator of folate or B12 levels.

And "science-based" medicine is not a credible source for health information. They go out of their way to criticize and debunk, often twisting themselves into impossible knots, anything not pushed by mainstream medicine. They want to revoke the ability of naturopaths to be licensed in California. They refer to integrative medicine doctors with quotes around "integrative" indicating that they are somehow not legitimate. It's a fraud, its name notwithstanding.

 

[bigmillz]

Get a homocysteine blood test thru your doctor. It does require specific fasting and you need to eat a normal amount of protein during dinner the night before. If your level is good then your methylating just fine. At least that is what I concluded after months of reading up on MTHFR after finding out I had 2 mutations touted as "serious" by so-called mthfr experts. My homocysteine level came back perfect (10) so I know I'm methylating just fine.

I personally believe the mthfr thing is over-hyped and being used by many naturopaths to make $ from patients.

I found this resource just recently after my own travels down the mthfr road had already concluded.

https://sciencebasedmedicine.org/dubious-mthfr-genetic-mutation-testing/

Definitely getting homocysteine tested.

Interesting read, and not really surprised. I've never been a fan of doctors selling their own supplements. It's a pretty perfect business concept.

 

[CFS_for_19_years]

The cells will become extra large, thus causing the high volume number, in order to compensate for the deficiency.

The cells are large due to a defect in maturation; they do not become large due to a deficiency.
It results from inhibition of DNA synthesis during red blood cell production. When DNA synthesis is impaired, the cell cycle cannot progress from the G2 growth stage to the mitosis (M) stage. This leads to continuing cell growth without division, which presents as macrocytosis.
https://en.wikipedia.org/wiki/Megaloblastic_anemia

The maturation defect can also be seen in neutrophils (white blood cells) that have hypersegmented nuclei, which also help establish the diagnosis of megaloblastic anemia.

 

[TrixieStix]

Definitely getting homocysteine tested.

Interesting read, and not really surprised. I've never been a fan of doctors selling their own supplements. It's a pretty perfect business concept.

Like I said I had made my own mind up about the mthfr business before reading that "skeptics" article. I'm not saying I agree with 100% of what it says but that's what critical thinking is about.

As for the ideal level of homocysteine, it doesn't seem to be exactly known, and some resources say "the lower the better", but there are some doctors online who say too low of a homocysteine level is also not good. But is seems to be accepted that above 10 is too high.

A 2008 study showed Homocysteine to be a better at predicting risk of death from cardiovascular disease in older people better than any conventional measure of risk including cholesterol, blood pressure or smoking.

https://www.patrickholford.com/blog...er-than-cholesterol-blood-pressure-or-smoking

 

[Mary]

The cells are large due to a defect in maturation; they do not become large due to a deficiency.
It results from inhibition of DNA synthesis during red blood cell production. When DNA synthesis is impaired, the cell cycle cannot progress from the G2 growth stage to the mitosis (M) stage. This leads to continuing cell growth without division, which presents as macrocytosis.
https://en.wikipedia.org/wiki/Megaloblastic_anemia

The maturation defect can also be seen in neutrophils (white blood cells) that have hypersegmented nuclei, which also help establish the diagnosis of megaloblastic anemia.

You said it more clearly. When I said to "compensate for a deficiency" was probably not the best way to say it; however, the defect in maturation and resulting large cells is most often due to a B12 or folate deficiency. And the way my doctor explained it to me was that the cells were extra large due to the deficiency. The deficiency causes the inhibition of DNA synthesis and so on.

The defect in red cell DNA synthesis is most often due to hypovitaminosis, specifically a deficiency of vitamin B12 and/or folic acid. Vitamin B12 deficiency alone will not cause the syndrome in the presence of sufficient folate, as the mechanism is loss of B12 dependent folate recycling, followed by folate-deficiency loss of nucleic acid synthesis (specifically thymine), leading to defects in DNA synthesis. Folic acid supplementation in the absence of vitamin B12 prevents this type of anemia (although other vitamin B12-specific pathologies may be present).

(from the same Wikipedia article cited above)

 

[Jimbo39]

I have high blood glucose. My doc says I have thick blood. Could this be a type of Megaloblastic anemia? If so, it would appear that B12 can correct this.

 

[CFS_for_19_years]

I have high blood glucose. My doc says I have thick blood. Could this be a type of Megaloblastic anemia? If so, it would appear that B12 can correct this.

"Thick blood" is not anemia. It is a combination of factors such as a high hematocrit (the opposite of anemia), red cell deformability, plasma viscosity and red cell sedimentation which is measured by an ESR (erythrocyte sedimentation rate).
Measuring Blood Viscosity to Improve Patient Outcomes
http://www.townsendletter.com/Jan2012/measureblood0112.html

Blood Viscosity and Diabetes
It is has been demonstrated by many investigators that diabetics have elevated blood viscosity. It is also known that red cell deformability and the osmolarity of the blood – both affected by uncontrolled blood glucose – mediate blood viscosity changes and the onset of small vessel disease. Diabetics have a higher proportion of red cells that are relatively nondeformable and which must pass through relatively long, narrow capillaries to deliver O2 and nutrients to cells. Capillaries can be smaller than erythrocyte diameter, resulting in injuries to the capillary walls. This injury is dramatically increased as erythrocyte deformability is impaired. Blindness, kidney insufficiency, and leg ischemia are the first comorbidities to appear because the associated organs are the most dependent on microperfusion for function.