I had a few blood tests done this week at a private lab and got some very unexpected results back. Before I give them, here's a little basic information about B12: There are three carrier proteins that are bound to B12 in the serum. When B12 is bound to transcobalamin I, also known as haptocorrin, it is considered to be inactive. The purpose of haptocorrin bound B12 in serum is not well understood despite normally comprising 75-80% of all serum B12. B12 bound to transcobalamin II is the active form. It binds to the B12 receptors on cell membranes and is taken up by the cells. For completeness, there is a third binding protein, transcobalamin III. Again, this form is not well understood and is rarely mentioned. The proportion of active B12 in the serum is generally considered to be about 20-25% of the total B12 but it does vary and can be much lower. Therefore, total B12, although a reasonable indicator of B12 status, is not always reliable. I had my total B12 measured about six years ago and it was around 350 pmol/L. This is considered sufficient in the UK and many other countries. Japan changed their reference range some time ago and anything below 500 pmol/L is deemed a deficiency. Shortly after my previous test, I started taking 1000mcg of methylobalamin sublingually, and did respond in a way that some would consider a sign of existing neurological damage being repaired - a burning sensation in the soles of my feet and increased tingling in my fingers. Methylcobalamin also helped me to sleep (which is reported by a minority of people taking it) and I have continued to use it sporadically whenever I have phases of troubled sleep. This generally means taking a lozenge every evening over the course of about a week. The last time I did this was about two months ago and it was only for three or four days. I'd always intended to get my active B12 measured but had never gotten round to it. However, my 83 year old mother has been showing potential signs of significant neurological damage over recent months and in the absence of any other diagnosis, I decided to get us both tested. These are my results: Total Vitamin B12: 352 pmol/L (IN RANGE) (Deficient <140 / Insufficient 140 - 250 / Consider reducing dose >725) B12-Active: 167.9 pmol/L (MARGINALLY HIGH) (25.1 - 165) Serum Folate: 4.25 nmol/L (DEFICIENT) (8.83 - 60.8 nmol/L) Note that the active B12 is 47% of total serum B12. Serum folate is deficient but my haemoglobin and mean cell volumes are mid range. Potentially relevant neurological symptoms: Tingling in feet, occasional tingling in fingers, poor sense of balance, twitchy muscles and tinnitus but all these have been present for years. Recently, walking has become more awkward in that it feels stilted and I almost trip up quite frequently. (I feel like I'm walking now at 48 similar to my mother did when she was about 65.) So far not really all that interesting apart from the unusual active B12 percentage. Now we come to my mother's results. Total Vitamin B12: 352 pmol/L (IN RANGE) (Deficient <140 / Insufficient 140 - 250 / Consider reducing dose >725) B12-Active: 216.2 pmol/L (VERY HIGH) (25.1 - 165) Serum Folate: 8.3 nmol/L (MARGINALLY DEFICIENT) (8.83 - 60.8 nmol/L) The sharp-eyed will notice that my mother's total B12 is identical to mine. She also has an identical mean cell volume (91 fl) and we are both on the border of a vitamin D3 insufficiency, being separated by only 1 nmol/L. Her results showed a haemoglobin deficiency which is consistent with what we already know. So similar were most of the results that I was worried that a mistake had been made. We have been reassured that this is not the case. My mother's active B12 is 60% of the total. When I asked about our unusual percentages, the doctor replied: My understanding is that haptocorrin's function is to protect B12 in the stomach. Low stomach pH is required to release the B12 but once released the B12 is at risk of being denatured until it can be absorbed. In the absence of all other factors it seems surprising to me that someone deficient in TCN1 could ever end up with a high active B12 even though most of their B12 would be in the active form. He's right that I eat a lot of meat but my mother doesn't. She has also never supplemented and she is showing signs of a potentially severe deficiency yet she has an even higher level of active B12 than I do. Her symptoms are: Severe mobility problems over the past few months. It doesn't seem to be a simple weakness, although that's certainly true on occasion. It appears more like her legs aren't obeying her. Balance is terrible. Her vision appears to be getting worse all of a sudden although there could be an alternative explanation for this. She is extremely fatigued and mostly stays in bed. Appetite has declined. Frequent nausea. Has dry retched a couple of times (no bile). Breathless at the slightest effort (sometimes even without any effort). Tachycardia - always either in the 100s or 110s at rest. Yellowish tinge to the skin on her body. Face is very pale. Bouts of confusion and disorientation. Poor short term memory / concentration problems Pale diarrhoea which has persisted for months. Tremulousness To an extent, a lot of the above symptoms are not unexpected in an 83 year old but what concerns me is the speed with which it has happened. She'll be seeing her GP on Thursday. I am dreading bringing up this topic. For myself, the next step will be to test homocysteine and methylmalonic acid to try to get an idea of what is happening within the cells. Does anyone have experience of getting these tests done privately? Any advice? For those who are knowledgeable about B12, is it possible that my mother and I could have a problem with cellular uptake? Could this explain the relatively high active B12 in the serum even though we appear to have an apparent a likely genetic variation that would otherwise be expected to lead to an apparent deficiency? Anyone else have odd active B12 findings?