Being on an omnivorous diet and regularly supplementing with B vitamins, I was being a bit quite curious where my levels would land at, so I pulled cobalamin in the most recent bw I had.
Because of the above, I was a bit dismayed to discover I have borderline levels - 254 pg/ml (187 pmol/l) over a lower range of 200. By modern standards, this already shows moderate deficiency.
Going a tad backwards in time, I did pull B12 two yrs ago, levels scored at 700 but I had been taking 1000mcg methyl-B12 tablet for about three months prior to bloodwork. From there on, I stopped those and relied on regular B vitamins complex.
Considering both supplementation and dietary intake from animal protein I should have been able to maintain average levels. It seems rather abnormal to me that such fall in levels occurred in a relatively short frame of time. Occording to medical literature, the liver should store about three-to-five years worth of B12 if intake stops. It's like I've been assimilating nothing.
I readily started IM cyano injections but I believe I do need to do further testing to understand what might be going on.
Possible causes for selective B12 malabsorption include atrophic gastritis (due to lack of IF), small bowel pathology (celiac sprue, IBD), and SIBO (small intestine bacterial overgrowth).
I checked antibodies for coeliac disease a while ago and came out negative. I feel I can exclude Chron's (though some family members have it) and other forms of IBD because symptoms of inflammation would be easily discernable and I got none.
Athrophic gastric can be autoimmune in origin and has higher incidence in hashimoto's patients (I'm one). I should have already looked for IF and parietal cells antibodies long ago, positivity isn't sufficient for diagnosis but might point in the right direction.
If these came out negative, I sense I should rather look into SIBO and perhaps run a trial of normix (rifaximin). Bacterial overgrowth in the small bowel might also well explain why Iron status too is at stale despite supplementation.
This is a good informative page about the functions of B12 in the body:
Vitamin B12 | Linus Pauling Institute | Oregon State University
The major enzyme families requiring cobalamin as co-enzyme are MS (methionine synthase) and MCM (Methylmalonyl-CoA mutase).
Methionine synthase catalyzes the recycling of homocysteine into methionine and MCM converts MMA (Methylmalonic acid) into Succinyl-CoA. Thus, tissue-level deficiency will lead to accumulation of these metabolites in the blood and can be used as markers of "true" B12 deficiency. This is very important to know because, according to modern research, this can be present despite normal, "in range" cobalamin levels, and can help with early diagnosis.
For the average public, I found this to be a good informative site: B12 Deficiency : Welcome
All in all I'm glad I've detected this issue early, I suspect I might have developed serious issues in the months ahead if I didn't correct this now. Being also affected by a genetic, benign "disease" that causes microcytic erythrocytosis (small red cells but higher in number), plus supplementing with folate/iron and with TRT supporting hematopoiesis it would have been quite hard to develop pernicious anaemia, the most prominent (and clinical) feature of B12 deficiency characterized by larger-than-normal red blood cells, reduced counts and haemoglobin, that means, the whole thing would have been perfectly masked and unrecognizable...
Reply With Quote
Originally Posted by bizzarro
