Vitamin B12 deficiency can develop gradually, often going unnoticed until symptoms become pronounced. Recognising the signs of lack of B12 early is crucial, as prolonged deficiency can lead to serious neurological complications, some of which may become irreversible. Common indicators include persistent fatigue, pale skin, a sore tongue, and neurological symptoms such as pins and needles or balance problems. Certain groups—including vegans, older adults, and those with pernicious anaemia or gastrointestinal conditions—face higher risk. This article explores the key signs of B12 deficiency, who is most vulnerable, and when to seek medical advice for prompt diagnosis and treatment.

Common Signs of Vitamin B12 Deficiency

Vitamin B12 (cobalamin) is an essential water-soluble vitamin that plays a crucial role in red blood cell formation, DNA synthesis, and neurological function. When the body lacks adequate B12, a range of symptoms can develop, often gradually over months or years.

Early signs of B12 deficiency frequently include persistent tiredness and fatigue that doesn't improve with rest, alongside generalised weakness. Many people notice a pale or slightly jaundiced (yellowish) complexion due to ineffective erythropoiesis or mild haemolysis. Glossitis—a sore, red, swollen tongue—is a characteristic feature, often accompanied by mouth ulcers or a burning sensation in the mouth.

Digestive symptoms are also common. These may include loss of appetite, constipation, or occasional diarrhoea. Some individuals experience unexplained weight loss. Cognitive changes such as difficulty concentrating, memory problems, or a general sense of mental fog can occur even in the early stages of deficiency.

It's important to recognise that B12 deficiency symptoms can be non-specific and overlap with many other conditions. The insidious onset means symptoms may be attributed to stress, ageing, or other health issues. Because the body stores B12 in the liver (typically enough for 2–5 years), deficiency develops slowly, and symptoms may not appear until stores are significantly depleted.

Importantly, taking folic acid supplements without addressing B12 deficiency can mask anaemia while allowing neurological damage to progress. If you experience several of these signs persistently, particularly if you have risk factors for B12 deficiency, it's advisable to consult your GP for appropriate investigation.

Neurological Symptoms of Low B12 Levels

Vitamin B12 is essential for maintaining the myelin sheath—the protective coating around nerve fibres. Prolonged deficiency can lead to demyelination and potentially irreversible neurological damage if left untreated. Neurological manifestations of B12 deficiency can occur even before haematological changes (anaemia) become apparent.

Peripheral neuropathy is one of the most common neurological presentations. Patients typically experience paraesthesia (pins and needles) or numbness, usually starting in the feet and hands in a symmetrical pattern. This occurs because B12 deficiency affects the peripheral nerves and posterior columns of the spinal cord. Some people describe a sensation of walking on cotton wool or difficulty sensing where their feet are in space (proprioception loss).

Balance and coordination problems may develop, leading to an unsteady gait or increased falls risk. This condition, known as subacute combined degeneration of the spinal cord, affects both sensory and motor pathways. Cognitive and psychiatric symptoms can be particularly distressing and include depression, irritability, mood changes, and in severe cases, confusion or memory impairment that may mimic dementia in older adults.

Vision disturbances, though less common, can occur if B12 deficiency affects the optic nerve (optic neuropathy). Patients may notice blurred or disturbed vision, reduced colour perception, or visual field defects.

The neurological complications of B12 deficiency represent a medical priority. Early recognition and treatment are crucial because some neurological damage may become permanent if deficiency persists untreated for extended periods. If neurological symptoms are present, urgent treatment with hydroxocobalamin injections should be initiated while arranging further assessment. If you experience any neurological symptoms alongside other signs of B12 deficiency, prompt medical assessment is essential.

Who Is at Risk of B12 Deficiency?

Certain groups face significantly higher risk of developing vitamin B12 deficiency due to dietary, physiological, or medical factors. Understanding these risk categories helps identify individuals who may benefit from screening or prophylactic supplementation.

Dietary factors play a major role, as B12 is found naturally only in animal products (meat, fish, dairy, eggs). Vegans and strict vegetarians who don't consume fortified foods or supplements are at substantial risk. The NHS and British Dietetic Association recommend that people following plant-based diets take regular B12 supplements or consume fortified foods.

Pernicious anaemia is the most common pathological cause of B12 deficiency in the UK. This autoimmune condition destroys gastric parietal cells, preventing production of intrinsic factor—a protein essential for B12 absorption in the terminal ileum. Testing for intrinsic factor antibodies is the most specific diagnostic test, while parietal cell antibodies are less specific. Pernicious anaemia typically affects older adults and has a genetic component, being more common in people of Northern European descent and those with other autoimmune conditions.

Gastrointestinal disorders significantly impair B12 absorption. These include Crohn's disease (particularly affecting the terminal ileum), coeliac disease, and atrophic gastritis. Surgical interventions such as gastrectomy or ileal resection remove or bypass the sites of B12 absorption, necessitating lifelong supplementation.

Certain medications interfere with B12 absorption or metabolism. Metformin, commonly prescribed for type 2 diabetes, can commonly reduce B12 levels, with risk increasing with dose and duration of treatment. Proton pump inhibitors (PPIs) and H2-receptor antagonists reduce stomach acid production, which is needed to release B12 from food proteins. For those on long-term use of these medications, monitoring B12 status is advisable if symptoms develop or other risk factors are present.

Nitrous oxide exposure, whether from recreational use or medical procedures, can cause functional B12 deficiency by inactivating vitamin B12.

Older adults (over 60 years) face increased risk due to reduced stomach acid production (achlorhydria) and higher rates of atrophic gastritis. NICE guidance suggests considering B12 status in older patients presenting with cognitive impairment or unexplained anaemia.

When to See Your GP About B12 Symptoms

Recognising when to seek medical advice is crucial for preventing potentially serious complications of B12 deficiency. While mild, non-specific symptoms might initially seem insignificant, certain presentations warrant prompt GP consultation.

You should arrange a routine GP appointment if you experience persistent tiredness and weakness that doesn't improve with rest, especially when accompanied by other signs such as pale skin, sore tongue, mouth ulcers, or mild cognitive changes like difficulty concentrating. If you belong to a high-risk group—particularly if you follow a vegan diet, have a gastrointestinal condition, take metformin or long-term PPIs, or have a family history of pernicious anaemia—discuss B12 screening with your GP even before symptoms develop.

Seek same-day medical attention if you develop neurological symptoms. Paraesthesia (pins and needles), numbness in hands or feet, balance problems, coordination difficulties, or unexplained vision changes require prompt assessment. These symptoms suggest potential nerve damage, which may become irreversible without timely treatment. Similarly, significant cognitive or psychiatric symptoms—such as marked confusion, memory loss, depression, or personality changes—warrant urgent evaluation, particularly in older adults. Recent nitrous oxide use with neurological symptoms also requires immediate assessment.

If you experience severe symptoms such as extreme weakness, significant breathlessness, rapid heartbeat, chest pain, or signs of severe anaemia, contact your GP immediately or seek same-day assessment. Very rarely, severe B12 deficiency can cause serious complications requiring urgent intervention.

When consulting your GP, provide a comprehensive history including dietary habits, medications, previous gastrointestinal surgery, and family history of autoimmune conditions or pernicious anaemia. This information helps guide appropriate investigation and ensures you receive timely, targeted treatment. It's advisable not to start high-dose B12 supplements before testing unless advised by a clinician, as this may affect test results.

Early diagnosis and treatment of B12 deficiency typically leads to excellent outcomes, with most symptoms reversing completely when addressed promptly.

Diagnosing and Treating Vitamin B12 Deficiency

Diagnosis of B12 deficiency involves clinical assessment combined with laboratory investigations. Your GP will take a detailed history and perform a physical examination, looking for characteristic signs such as pallor, glossitis, or neurological findings.

Initial blood tests typically include a full blood count (FBC) and serum B12 level. The FBC may reveal macrocytic anaemia (enlarged red blood cells with raised mean cell volume), though anaemia isn't always present, particularly when neurological symptoms predominate. Serum B12 levels below the laboratory's reference range generally indicate deficiency, though reference ranges vary between laboratories. Some UK labs use holotranscobalamin (active B12) as a more specific marker.

When B12 levels are equivocal, additional tests may include methylmalonic acid (MMA) and homocysteine levels, which become elevated in B12 deficiency. Testing for intrinsic factor antibodies and gastric parietal cell antibodies helps diagnose pernicious anaemia, though negative results don't exclude it. Your GP may also check folate, ferritin, thyroid and liver function, and coeliac serology if indicated.

Treatment depends on the underlying cause and severity. For pernicious anaemia or malabsorption disorders, the British National Formulary (BNF) recommends hydroxocobalamin injections. The standard regimen involves 1 mg intramuscularly three times weekly for two weeks, then maintenance injections every two to three months for life. When neurological symptoms are present, more intensive initial treatment is required: 1 mg on alternate days until no further improvement occurs, followed by maintenance injections of 1 mg every 2 months.

For dietary deficiency without malabsorption, oral supplementation with cyanocobalamin (50–150 micrograms daily) is usually effective. Cyanocobalamin tablets are available over-the-counter, though prescription may be needed for higher doses.

It's important to note that if B12 deficiency is suspected, any folic acid supplementation should only be started concurrently with B12 treatment, as folic acid alone can mask anaemia while allowing neurological damage to progress.

Response to treatment is typically monitored with a reticulocyte count and FBC after 7–10 days, with clinical review by 4–8 weeks. Fatigue and cognitive symptoms often improve within days to weeks, whilst neurological symptoms may take several months to resolve. Some long-standing neurological damage may be permanent, emphasising the importance of early treatment. Routine B12 level monitoring is not required for patients on regular injections, though patients should report any symptom recurrence. Those with pernicious anaemia require lifelong treatment and should be advised that this is a chronic condition requiring ongoing management.

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