Kate,

I appreciate you sharing your experience and concern. A few clarifications that may help readers:

Gut bacteria and B12: Humans don’t rely on B12 made in the colon; it’s produced too far downstream to be absorbed. Dietary/supplemental B12 is absorbed in the terminal ileum via intrinsic factor; a small fraction (about 1–2%) is absorbed anywhere along the gut by passive diffusion from high‑dose supplements.

Testing: Total serum B12 alone can miss functional deficiency, but modern practice uses better markers rather than abandoning testing. Methylmalonic acid (MMA) is the most specific functional marker; holotranscobalamin (holoTC) can help; homocysteine is supportive. The Schilling test is obsolete.

Long COVID: It’s linked to gut dysbiosis and barrier issues, but there’s no solid evidence that long COVID uniquely blocks passive diffusion, and only case reports (not population data) suggest it increases pernicious anemia. If deficiency is present without dietary cause, intrinsic factor and parietal cell antibodies, gastrin/pepsinogen, and sometimes endoscopy can confirm autoimmune gastritis/pernicious anemia (source).

Treatment: High‑dose oral B12 (e.g., 1,000 mcg/day cyanocobalamin) is usually effective even with malabsorption because of passive diffusion. Injections are appropriate for severe neurologic symptoms, very low levels, intolerance, or adherence concerns. Evidence for transdermal B12 patches is limited.

Forms: There is robust evidence for cyanocobalamin (via supplements) and hydroxocobalamin (via injections) correcting deficiency.

Practical advice for readers with symptoms (fatigue, macrocytosis, neuropathy, glossitis):
Test: serum B12 + MMA (or holoTC), consider homocysteine.
If low/indeterminate and not explained by intake: test intrinsic factor antibodies; if negative but suspicion remains, parietal cell antibodies and supportive gastric markers; consider GI evaluation.
Treat promptly (oral high‑dose or IM) and recheck labs/clinical response.

I’m dropping into the comments almost exactly eight years after the last one, because I just learned that the B12 tests in common use now are nearly useless for some people, and that there really is no one perfect test to determine deficiency of active B12, or its cause. It seems I was one of the post-SARS patients with markers like macrocytosis, lymphopenia, etc. that was deficient.

Fascinating writeup on the tests here: https://www.sciencedirect.com/topics/biochemistry-genetics-and-molecular-biology/schilling-test

This means, that a person can continue to get normal B12 tests in their labwork while they might be seriously B12 deficient. This can go on long-term, and be missed by doctors. Patients may develop macrocytosis/megaloblastic anemia, lymphopenia, nerve and muscle weakness and/or pain, nerve damage, brain damage, dementia.. it’s really an awful list.

Several things place people who fared poorly after SARS-COVID-19 infections (especially multiple infections) in danger of acute B12 deficiency. Most “Long COVID” patients have significant damage to their digestive tracts, stomachs and intestines. “Long COVID” cases are in the hundreds of millions now worldwide, and there could be a large population being left behind by the faulty modern assays, and because B12 deficiency isn’t front and center in our doctors’ minds. The days of only missing people with pernicious anemia is over, and now how many hundred million Long COVID and ME/CFS patients are suffering from what appears to be autoimmune injury, cognitive damage (“Brain Fog”), dementia, SARS/AIDS, leukemia, Addisons, immune damage, recurring cancers… another terrible list?

SARS-COVID leaves viral segments, active virus and antibodies in the blood, triggers latent other viruses (especially herpesviri like Epstein-Barr, herpes simplex, chickenpox/shingles, etc.) and antibodies alone can interfere with modern B12 tests. COVID also destroys stomach and gut bacteria, rendering people incapable of accessing the active B12 they normally would produce in our ileum, intestines and colons. People with SARS damage could be dangerously ill from long-term deficiency. I know that I was, and after one month of active B12 supplementation, I am strongly recovering. My labs are showing repair. None of my doctors were aware that the tests were not working for me (or people like me)- nor did they know about why, or how much of the population it affects.

Many papers suggest that the number of people left behind by modern B12 tests could be 25% or higher (which is insanely high for our doctors not to be on this) but if one adds in the number of people harmed by multiple SARS infections, that number could be staggering- certainly more than 50%. After all, most people have had COVID more than twice, and do not mask in public (I do). Absolutely great article here, from 2008:

https://pmc.ncbi.nlm.nih.gov/articles/PMC2696961/

While there are no good tests to offer the huge numbers of people who could be deficient, there are active B12 patches and liquids out there to trial- look for METHYLATED B12- this will show as cyanocobalamin or methylcobalamin on the labels.

If people are malabsorbing B12, though, liquids, pills or patches probably won’t help repair damage, and they could need B12 injections to improve. A doctor’s scrip is needed for that (in the US) and a course of injections could be needed. So fellow LC/ME/CFS patients, please ask your nutritionist, trainer, or doctor to help (I see a great link above for plant-based dieticians) or consider trialing active B12 patches.

Supplementing with active Vitamin B12 while our doctors catch up could save our lives.

Hi Dustin–

Thank you for your comments and paying such close attention to this article.

1. I’m not sure why I cited Refsum et al. for the idea that B12 deficiency is rare in India—the study certainly doesn’t suggest that and I’ve removed that citation and modified the statement. Thanks for catching that.

2. I was reporting the percentages of healthy subjects with elevated homocysteine and MMA as listed in Table 1 of Refsum et al. Go to the bottom of the table and you’ll see I copied the percentages just as they list them. Regarding the average B12 level, I converted 160 pmol/l to 216 pg/ml (conversion factor of 1.35). I list B12 values in pg/ml throughout the VeganHealth.org site. I’ve now added the measurement to table header to prevent confusion.

I had a few questions for you based on the information you have presented here:

1. You said: “B12 deficiency has been found with relatively high frequency among vegetarian Indian immigrants in England, while it is supposedly uncommon among native Indians with identical dietary patterns (3, 4).”

Question: Your fourth citation, Refsum et al., indicates that B12 deficiency is common in India but here you state that it is “uncommon among native Indians”. Is this just a typo? Should it not read that it is common? Or did you mistakenly include Refsum et al. there when in reality you just meant to include Albert et al. (the third citation) there?

2. You indicate that Refsum et al. used 27 lacto-ovo subjects and 36 non-veg subjects. I feel this is also a mistake because it states, in their article, that the subjects on a vegetarian diet involved 27% of the 63 healthy subjects. Thus, I feel as if the correct number of lacto-ovo healthy subjects should have been listed at 17 rather than 27 lacto-ovo healthy subjects, as 17 represents 27 percent of the 63 healthy subjects. This would then mean that 47 healthy subjects would have been non-veg. Or am I missing something here?

Additionally, for the lacto-ovo and non-veg healthy subjects you list their combined average serum B12 at 216. I was just wondering if you could explain to me how it was you arrived at this figure? In Refsum et al.’s study, on table 1 of page 235, it states that this figure should be 160.

Lastly, it would be greatly appreciated if you could please explain to me how you concluded that 46% of the healthy subjects had a serum B12 < than 203.

Thanks in advance for your response. Look forward to hearing from you.