I have been diagnosed with auto-immune hypothyroid disease for just over a year, but have had symptoms since early 2014. I have just had the results back from a private blood test, which among other things, reveals that both my b12 and folate levels are low:
Active b12 34.3 (25.1-165)
Folate serum 5.68 (2.91 - 50)
The helpful peeps over at the Thyroid UK forum have suggested that at that low level I should ask my GP if I can be tested for Pernicious Anaemia.
I am a dedicated meatatarian and also consume plenty of eggs and milk, so I figure I must have some issue with absorption. I'm surprised my folate level is so low as I do eat green veg and chick peas quite frequently, but honestly, I could probably do better here.
Should I ask to be tested? The problem is that my GP already thinks I'm a nut-job for insisting that my Hypo medication is not resolved, so I am reluctant to try to convince him of yet another thing wrong if there is a sensible alternative.
What are the forum's thoughts on b12 nasal sprays, for example. Are these absorbed by-passing the digestive system as I assume they are? If a conceivable alternative, what sort of dose should I consider?
For info, I'm 42, female and otherwise fit and healthy.
Thanks in advance x
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Laundretta
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Neither of your folate or B12 is low. Both are well within the normal limits. The folate test is very accurate (better than 10%). The Active B12 test is supposed to be much more accurate than the normal serum test (20%).
So no doctor is going to think you’re deficiency in either from those numbers.
An MMA and hCys test will find if there’s enough B12 and folate getting into the cells.
Nasal sprays do nothing for me. The B12 molecule is too large and too hydrophilic to get across the buccal membrane.
You’ll find loads of people on this forum saying how much more accurate the active test is tha the normal serum test. You can’t jus throw all that away and decide, with no evidence at all, that it’s not more accurate.
36% above the lower limit might be considered borderline for the serum test. But there’s no way it could be described as ‘low’ for the active test.
I’ve never questioned the accuracy of the active test - did you read my post properly? You erroneously exclaim that 35 is considered well within range. I say this with some confidence following further reading of several academic studies, all of which conclude that active b12 measured under 35 should be referred for MMA testing. Much of the research sets the bar somewhat higher in fact. The viapath labs at St. Thomas will refer for MMA <70.
The semantics are irrelevant. Testing for MMA wouldn’t be considered if 35 was normal enough to not implicate potential deficiency. From my reading since my first post I feel justified in my alarm at such a low result considering my diet, despite your unhelpful comment.
Is this the general consensus? What levels are you looking at before PA is a possibility? Where in the scale do you aim to be once medicated? 34.3 feels pretty low where the scale tops out at 165!
I have read that b12 stores can take 3 years to deplete. My diet is rich in b12. Any suggestions as to what could be causing lack of absorption?
If I wanted to raise the levels assuming absorption is an issue for whatever reason, what would people suggest?
Hiya! Just started figuring out all this stuff myself. I didn't use them for my active B12 test, but the active B12 range Viapath at St Thomas Hospital use is >70*; * between 25-70 referred for MMA, so if you would have tested with them they would have followed up with a MMA test with your results. viapath.co.uk/our-tests/act...
They do testing for the NHS, so your GP can make the request to them. My active B12 was 45.1 (serum 251, 221, 247 range 211-900) and I used this information to help get my GP to consult a hematologist and start me on loading doses and follow the treatment protocol for neurological symptoms. Hope that helps!
Not only does the latest BMJ research summary below state there is NO reliable test, but the Dutch links on the r/h side of the forum state this too. The fact is that you have already tested quite low, are at higher risk (having Hashimoto's thyroid disease) and have reason to believe there may be an absorption problem, in which case, any neurological symptoms should be treated with injections without delay to avoid permanent damage.
You'll see from BMJ summary that symptoms are paramount but MMA test is the most likely to be reliable. Testing homocysteine is not recommended if you have thyroid disease. The other test for absorption issues is Intrinisic Factor but many find this is only 40% reliable. So you can see why it is so hard to get urgent and sufficient treatment in these times when medicine is so test based with many medics not aware of the serious consequences of undertreated B12deficiency and not keeping up with the latest research. This is why so many of us on the forum resort to self injecting.
b12deficiency.info/. Lots of information on neurological symptoms, as well as on writing to your GP. Joining the PAS means you will also have access to articles for professionals on the PAS website - information in r/h side of the forum.
I don't know if this research link might help convince your GP (posted originally by John Midgley, TUK). It highlights the connection between Hashimoto's Thyroid disease and PA, - how gastric atrophy (often silent) in HT leads eventually to malabsorption of essential nutrients, including vitamin B12, and PA:
"The natural history of HT is the progressive reduction of thyroid function till overt hypothyroidism (24) with a rate of progression of 2–4% per year (23), while that of gastric atrophy features the progressive reduction, till disappearance, of parietal cells, leading to reduced or absent acid production (3, 22). These alterations interfere with absorption of essential nutrients leading, at first, to iron-deficient anemia, followed by PA if the self-injurious process involves the IFA (13)."
"A well-described clinical feature of thyrogastric syndrome is represented by the presence of an iron-deficient and/or a PA. In fact, it has been demonstrated that an iron-deficient anemia, refractory to oral iron therapy, in patients with HT, may be due to chronic atrophic gastritis (13). The clinical signs of this disease appear after several years of its onset, when the progressive reduction to disappearance of the parietal cells leads to atrophy of the gastric mucosa, impairing the absorption of iron, vitamin B12 (cobalamin), folate, and other nutrients."
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