Vitamin B12 deficiency: frequently underestimated

“I feel constantly tired – am I perhaps missing something?” Enquiries like this reach you daily. Vitamin B12 is rarely the customer’s first thought, but frequently the decisive one. The deficiency develops insidiously, the symptoms are non-specific, and those affected usually have no inkling of their risk. This is precisely where the pharmacy’s strength lies: you see the long-term medication, you know the dietary habits, and you are often the first professional to raise the subject at all.

This guide follows four recurring situations at the counter. First, the essentials on physiology and diagnostics – because the most frequent follow-up question, “should I have my level measured?”, can only be answered cleanly with a knowledge of laboratory logic.

B12 in 90 seconds: what counts for the consultation

Cobalamin is involved in cell division, blood formation and the myelination of nerves. The body stores it for years – hepatic reserves typically last three to five years. That explains why a deficiency long goes unnoticed and why the neurological consequences often appear before the macrocytic anaemia detectable in the laboratory.

Decisive for the consultation are the two routes of uptake. Active absorption runs via intrinsic factor from the stomach and is limited to around 1.5–2 µg per meal. Alongside this, cobalamin reaches the blood by passive diffusion, independently of intrinsic factor – but only around 1 % of the administered dose. This second route is the key to high-dose oral therapy: from a 1,000 µg tablet, around 10 µg are thus absorbed – enough to correct a deficiency even when active absorption is impaired, for instance when intrinsic factor is absent.[12]

The estimated value for adequate intake derived by the German-speaking nutrition societies (DGE, SGE, ÖGE) has since its revision stood at 4.0 µg per day for adults (previously 3.0 µg); for pregnant women 4.5 µg, for breastfeeding women 5.5 µg.[1] Since B12 occurs in appreciable amounts only in animal foods, a purely plant-based diet without a supplement does not cover requirements.[1]

The laboratory sticking point: what the measurement really says

The question about “the B12 level” is trickier than it sounds. Total vitamin B12 in serum captures, to 80–90 %, cobalamin bound to haptocorrin and not directly available metabolically. It is inexpensive and therefore still the screening parameter, but as a sole marker it is sluggish: it falls only late.[6]

Three additions are more informative: holotranscobalamin (holo-TC) reflects the active, cell-available fraction and indicates depletion of stores early. Methylmalonic acid (MMA) and homocysteine are functional markers that confirm a metabolically relevant deficiency. No single marker is conclusive in itself – history, clinical picture and risk factors remain part of the diagnosis; current guidelines recommend a stepwise approach.[2] [3] A combined index investigated in Switzerland (4cB12) improves the detection of subclinical deficiency states compared with single values.[6]

A practical reflex that guards against errors: folic acid can mask the haematological signs of a B12 deficiency – but not the neurological ones. Anyone recommending B-vitamin combinations with high folic acid indiscriminately can create the appearance of a normal blood count while neurological damage progresses. MMA remains normal in pure folate deficiency and helps to separate the two.[2]

Case 1: “I’m constantly tired”

A customer in her late forties wants “something to build her up”. She has felt weak and listless for weeks.

Fatigue is the most non-specific of all symptoms – here restraint in promising and care in contextualising are called for. Three short clarifications make sense, without unsettling the customer: dietary pattern (vegan/vegetarian), long-term medication (metformin, proton pump inhibitors) and age or gastrointestinal history. If one or more risk factors apply, you can bring B12 to the fore with good reason.

If risk factors are absent and the customer is otherwise healthy, a low- to medium-dose oral preparation is defensible as a trial – combined with the clear note that fatigue has many causes (sleep, iron, thyroid, stress) and that if it persists over some weeks a medical assessment should follow. Do not promise a rapid “energy effect”: if there is no deficiency, supplementation brings no benefit.

Case 2: the customer living vegan

A young man has been eating a vegan diet for two years and asks whether he needs “something with B12”.

Here the message is unambiguous: a purely plant-based diet permanently requires a B12 supplement; algae, fermented products or “natural sources” are not a reliable supply and in part contain ineffective analogues.[1] This is prophylaxis, not therapy – and thus a classic self-medication topic.

On dosage: because of the limited active absorption, an amount well above the nutritional estimated value is advisable for oral administration. As a maintenance dose on a purely plant-based diet, around 50–100 µg daily applies; alternatively, higher doses work less frequently (for instance 1,000 µg two to three times a week).[13] In practice, lozenges, drops or sprays are as suitable as tablets; sublingual and oral forms are comparable in effectiveness.[5]

Particular attention is due to pregnant and breastfeeding vegan women as well as breastfed infants of vegan mothers – here a secure supply is essential, with medical supervision when in doubt.

Case 3: metformin and PPI in long-term medication

A regular customer, 72, is filling her prescription: metformin for type 2 diabetes, plus a proton pump inhibitor she has taken for some time.

This constellation is perhaps the most important – and most frequently overlooked – occasion for B12 counselling. Metformin inhibits active B12 absorption in the gut; up to 30 % of patients on metformin show a deficiency.[7] At daily doses above 2,000 mg the risk almost triples.[8] A deficiency can conceal or aggravate an existing diabetic neuropathy.[8]

Proton pump inhibitors reduce the gastric acid needed to release B12 from food. Taking them for at least two years raises the risk of deficiency by around 65 %.[9] Where metformin and a PPI coincide, the effects add up.

Raise the risk actively – but in a way that creates neither anxiety nor a compliance problem. Do not question the medical prescription, but offer a determination of B12 status (ideally holo-TC) with the treating physician and point out the possibility of simple oral substitution. Those affected are usually unaware of their risk – and it is precisely here that counselling competence shows.

Case 4: “Can you give me a B12 injection?”

A customer wants a B12 injection – “it works better than tablets, doesn’t it?”

Two things need clarifying here. First, the legal position: the injection preparations Vitarubin Inj and Vitarubin Depot are assigned to dispensing category B (prescription-only) in Switzerland; an injection is initiated by a doctor.[11] Second, the widespread misconception that the injection is inherently superior.

The evidence speaks against it: high-dose oral B12 is for most patients just as effective as intramuscular administration as regards normalisation of serum values and clinical response.[4] An international Delphi expert consensus (2024) as well as a recent meta-analysis (2025) confirm the equivalence; for long-term therapy the oral high dose is preferred, and patient preference should be taken into account.[2] [5] Since B12 is water-soluble and excess is excreted renally, high-dose administration is very safe.[12]

Your answer can therefore be: for most situations a tablet is just as good, simpler and cheaper. Practically relevant: the oral high dose (Vitarubin Oral) can be dispensed as a List D preparation without a prescription – reimbursement, however, is tied to a medically confirmed deficiency (LIM).[12] Parenteral therapy remains reserved for certain cases (see below) and belongs in medical hands.

Therapy and choice of preparation in the Swiss range

Therapeutically, B12 is usually supplied as cyanocobalamin or hydroxocobalamin – both prodrugs that are converted in the body into the active forms.[11] Hydroxocobalamin binds more strongly to plasma proteins and remains longer in the organism (depot effect); cyanocobalamin can also be given subcutaneously – relevant in patients on oral anticoagulation, in whom intramuscular injection is avoided.[14]

Note: preparations, dispensing categories, SL status and prices change – before dispensing, please check the current entry in the Compendium or the specialities list.[12]

Established dosing schemes

• Oral high dose (standard for most): 1,000 µg/day over 8 weeks, then 1,000 µg/week; monitoring closely at first (compliance), then after 6 and 12 months.[10]
• Parenteral (severe/acute or neurological deficiency): initially frequent doses (e.g. 1,000 µg every 2 days until improvement), then monthly maintenance; in severe neurological manifestation, hydroxocobalamin initially.[10] [2]
• Prophylaxis in a vegan diet: around 50–100 µg/day orally (not reimbursed).[13]