Vitamin B12 deficiency

Vitamin B12 does two jobs that explain everything else about it. It is needed to build DNA, which is why the fast-dividing cells of the bone marrow suffer first and produce large, immature red cells. And it is needed to maintain myelin, the insulating sheath around nerve fibres, which is why prolonged deficiency damages nerves, spinal cord and brain.

India carries an unusually heavy burden of it. Indian studies report deficiency in anywhere from a quarter to well over half of the populations they sample, and estimates vary widely — because the cut-off used differs between studies, because the populations studied differ (urban professionals, rural communities, pregnant women, older adults), and because assay methods vary. Rather than settling on one figure, the honest summary is that a large minority to a majority of Indians have low or borderline B12, and that vegetarians sit at the higher end.

The reason is dietary. B12 is made by bacteria, not by plants, and it is essentially absent from plant foods. Dals, vegetables, fruit and grains carry none. Fermented foods and unwashed produce contribute negligible amounts. For a lacto-vegetarian, dairy is the only real source, and the quantity of milk and curd in a typical Indian diet falls well short of the requirement. Jain diets, which additionally restrict root vegetables, and strict vegan diets, carry the highest risk of all.

Absorption is where the rest of the causes live, and the pathway is worth following. B12 in food is bound to protein. Stomach acid and pepsin release it. Intrinsic factor, made by parietal cells in the stomach lining, then binds it and escorts it the length of the small intestine to the terminal ileum, where a specific receptor takes it up. A break at any point produces deficiency in someone whose diet is perfectly adequate.

That explains the list. Pernicious anaemia is autoimmune destruction of the parietal cells, so intrinsic factor is lost; it clusters with other autoimmune conditions, particularly autoimmune thyroid disease, which is why the two are worth thinking about together. Atrophic gastritis and H. pylori infection reduce acid and damage the same cells. Long-term acid suppression with proton pump inhibitors — often taken for years without review in India — limits the release of B12 from food. Long-term metformin impairs uptake at the ileum, an effect that is real, dose-related, and under-communicated to patients. Crohn's disease, coeliac disease, ileal resection and bariatric surgery remove or damage the absorbing surface itself.

Two groups deserve specific mention. Pregnant and breastfeeding vegetarian women pass on their status: maternal deficiency is associated with low infant stores, and infant B12 deficiency can affect growth and neurological development at a stage when it matters most. And older adults become deficient through reduced stomach acid even on a mixed diet, which is why age alone raises the risk.

ⓘThis information is educational and not a diagnosis.

The single most valuable thing on this page is this: neurological damage can begin before anaemia appears, and if left long enough it may not fully reverse. Waiting for the blood count to change before acting is the wrong order.

The nerve symptoms usually start in the feet and hands and move inward — tingling, pins and needles, a glove-and-stocking pattern of numbness, burning soles that are worse at night. Loss of vibration and position sense follows, and with it a subtle unsteadiness that is worse in the dark or with the eyes closed, because the feet are no longer reporting reliably. Later there can be weakness, a stiff or spastic gait, and falls. Alongside this, people describe a tiredness that rest does not repair, memory slipping, a foggy difficulty holding concentration through a working day, and low mood or irritability that they had attributed to stress.

The mouth gives an early clue that is easy to overlook: a smooth, red, sore tongue, and sometimes ulcers or a burning sensation.

When anaemia does develop it is macrocytic — large red cells, a raised MCV — and it can be profound before it is noticed, because it develops slowly enough for the body to adapt. Pallor with a faint yellow tinge is characteristic, because ineffective red cell production releases bilirubin.

There is one trap worth naming plainly. Folic acid corrects the anaemia of B12 deficiency while the nerve damage continues underneath, unseen. Folate is added to many supplements and is routinely given in pregnancy, so the anaemia can quietly resolve while the real problem progresses. This is precisely why B12 status is worth establishing before folate is given in someone with unexplained anaemia.

What makes all of this easy to miss is the pace. B12 stores last for years, so deficiency arrives over months rather than days, and the body adapts as it goes. People attribute the tiredness to work, the forgetfulness to age, the tingling to sitting cross-legged, and the low mood to circumstances. It is often a family member who notices the change first, or a routine blood report that arrives before anyone has connected the symptoms to each other.

The features listed below suggest the nervous system is actively involved and warrant prompt assessment rather than a routine appointment.

Serum B12 is the standard test and is honestly imperfect. It measures total B12, most of which is bound to a protein that does not deliver it to cells, so the number can look adequate while cells are short. Values clearly below about 200 pg/mL indicate deficiency; values above about 400 pg/mL usually exclude it. Between those lies a wide grey zone in which the result settles nothing on its own, and in which a great many Indian reports land.

Methylmalonic acid and homocysteine resolve that ambiguity. Both accumulate when cells lack B12, so they measure function rather than concentration. Homocysteine also rises in folate deficiency and kidney impairment; methylmalonic acid is the more specific of the two. Both are more expensive and less widely available in India than a B12 assay, which is often the practical reason they are not sent.

The full blood count adds a great deal, and one interaction matters especially. A raised MCV points to B12 or folate deficiency, but coexisting iron deficiency shrinks red cells and can pull the MCV back into the normal range, hiding both. Mixed deficiency is common in Indian vegetarian diets. A blood film showing hypersegmented neutrophils and cells of markedly uneven size is a useful clue when the indices look unremarkable.

Where diet does not explain the deficiency, the search turns to cause: anti-intrinsic factor and anti-parietal cell antibodies for pernicious anaemia, serum folate alongside, thyroid function where autoimmune disease is suspected, coeliac serology, and a review of metformin and acid-suppressing medicines.

On cost and access: a serum B12 assay at an Indian chain laboratory typically runs to a few hundred rupees, and it is bundled into most routine health packages, which means many people discover a borderline value without any symptom prompting the test. That is not a reason to dismiss the result — but it is a reason to interpret it against how you actually feel rather than against the printed range alone.

Replacement is straightforward; what varies is route, dose and duration, and those are decisions for your doctor rather than a shelf in a pharmacy.

Injections. Intramuscular hydroxocobalamin or cyanocobalamin is the established approach where absorption is impaired or where nerve symptoms are present. Loading doses given close together over the first weeks are used because the aim is to refill depleted stores quickly and to saturate the transport proteins, rather than to top up gradually. Maintenance then continues at longer intervals, often indefinitely where the cause is permanent.

Oral B12. High-dose oral supplementation works for many people, including some with absorptive causes, because roughly 1% of an oral dose crosses the intestinal wall by passive diffusion that does not require intrinsic factor at all. Trials comparing high-dose oral with intramuscular replacement have found comparable correction of blood markers in many settings. Where the deficiency is purely dietary, oral replacement is usually the sensible route.

Which form. Methylcobalamin is marketed aggressively in India as the superior molecule. The evidence for that superiority is weak. Cyanocobalamin is more stable and has the larger evidence base; hydroxocobalamin is retained longer in the body and is preferred for injections in many countries. Formulation matters much less than being on adequate replacement at all.

Diet and fortification. For someone continuing a vegetarian diet, dairy alone rarely suffices. Fortified foods — some breakfast cereals, fortified milk and plant milks, nutritional yeast — help, though India's fortified food supply remains limited. The realistic framing for a lifelong vegetarian is that B12 is an ongoing requirement, not a course to be completed.

A word on testing first. B12 tablets, sublingual sprays and injections are all available over the counter in India, and starting one before testing is common. It raises the measured level within days while leaving the reason untouched, so the question of whether this is dietary, autoimmune or absorptive becomes considerably harder to answer for months afterwards. Where symptoms suggest deficiency, establishing it first gives a clearer answer and a plan that fits the cause.

Monitoring and expectations. Blood counts respond within weeks, and the reticulocyte rise is often visible within the first week. Tongue soreness and fatigue improve early. Nerve symptoms recover far more slowly, over months, and recovery is more complete the earlier treatment begins — which is the whole argument for not waiting. Potassium can fall as new red cells are produced rapidly, which is one reason severe cases are monitored rather than simply supplied.

B12 is the deficiency where the number on the report tells you the least. A value of 240 pg/mL in a lifelong vegetarian with tingling feet means something quite different from the same value in someone with no symptoms at all.

If you would like to work through how to read your own blood report — the grey zones, how iron and B12 deficiency mask each other, and which results genuinely warrant a follow-up — the Learning Session below covers it in a small group, with time for questions.

If you have nerve symptoms, a borderline result, or a history that includes long-term metformin or acid-suppressing medicines, that is a conversation for a consultation rather than an article.