Pernicious Anaemia/B12 Deficiency Support Group - Page

06/07/2026

Radiculopathy – chronic pain disorder is often misdiagnosed in Pernicious Anaemia or B12 Deficiency Patients

Radiculopathy is a medical condition where a nerve root in the spine is pinched, irritated, or inflamed. This creates radiating pain, numbness, or weakness that travels along the path of the nerve into your arms or legs. Common examples include sciatica or a "pinched nerve”.

Key Types & Symptoms
Symptoms depend on which part of your spine the nerve is pinched.
Cervical (Neck): Causes pain in your neck, shoulders, and arms. You might feel "pins and needles" in your fingers.

Thoracic (Upper Back): Pain and numbness wrap around your chest or stomach. (This is the rarest type).

Lumbar (Lower Back): Sharp, shooting pain travels from your lower back, down your buttocks, and into your legs or feet.

Common Signs: Numbness, loss of reflexes, and muscle weakness in the arms or legs. The pain often gets worse with sudden movements like coughing or sneezing.

Vitamin B12 deficiency can directly mimic or worsen Radiculopathy by damaging the protective coating on your nerves called myelin. This causes numbness, tingling, and nerve pain. Correcting a B12 deficiency is crucial, as it often reverses nerve damage and dramatically improves chronic pain.

The B12 Effect: Your body needs B12 to create and maintain myelin. Think of myelin like the rubber coating on an electrical wire. Without enough B12, the "coating" wears away.

Overlapping Symptoms: B12 deficiency can cause severe nerve problems. The symptoms look a lot like a pinched nerve. These include "pins and needles", muscle weakness, and shooting pain in the arms or legs.

The Danger: A missed B12 deficiency can lead to irreversible spinal cord damage, even resulting in misdiagnosed cases where patients receive unnecessary spinal surgeries.

Some links to articles on B12 deficiency and radiculopathy
Vitamin B12 deficiency presenting as neck pain and cervical radiculopathy
https://pmc.ncbi.nlm.nih.gov/articles/PMC11043693/

AN UNUSUAL CASE OF VITAMIN B12 DEFICIENCY: LESSONS LEARNED
https://shmabstracts.org/abstract/an-unusual-case-of-vitamin-b12-deficiency-lessons-learned/

Pernicious Anaemia and or B12 Deficiency sufferers are often diagnosed with Radiculopathy without B12 levels ever being tested. Symptoms for this condition can overlap with symptoms of B12 Deficiency because both conditions present with nearly identical symptoms of nerve pain, numbness, tingling, and muscle weakness.

While anyone can experience a pinched nerve due to everyday triggers like poor posture, heavy lifting, or a minor sports injury, a true mechanical compression typically heals relatively quickly. Over 85% of acute radiculopathy cases naturally resolve within 4 to 12 weeks through standard conservative care, such as physical therapy, rest, or heat and cold therapy.
In stark contrast, when nerve pain is caused by a vitamin B12 deficiency, the underlying issue is actual chemical degradation of the protective myelin sheath shielding your nerve fibers. Consequently, even after corrective B12 therapy normalizes blood levels, repairing this microscopic nerve damage is a exceptionally slow physiological process; neurological recovery typically takes 3 to 12 months, and longstanding damage can occasionally become permanent if treatment is delayed.

06/03/2026

The B12 Alliance is hosting a Parliamentary Reception on September 10, 2026 at Westminster London, UK.

This is important because it raises the questions again, with the UK government, about inconsistency by GP’s with the NICE guidelines, individualized treatment will be discussed and many other issues that each and every one of you deal with, day in and day out.

They are asking for donations to help cover the costs. This kind of awareness helps us. If you can donate, please do. If you cannot, please share. Each donation and each share helps.

The B12 Alliance Parliamentary Reception at Westminster 2026 unites MPs, clinicians, researchers and patient advocates to advance vitamin B12 deficiency awareness, policy and patient care in the UK.

06/02/2026

Eye Health Matters in Pernicious Anaemia & B12 Deficiency

Many people are surprised to learn that vitamin B12 deficiency and pernicious anaemia can have serious effects on vision. Because B12 is essential for healthy nerves and blood vessels, low levels can quietly damage the eyes long before a diagnosis is made — and sometimes even after, if treatment is delayed or inadequate.
Common Eye‑Related Issues Linked to B12 Deficiency

Blurred or fluctuating vision
Low B12 can affect the optic nerve and the small vessels supplying the retina, leading to intermittent or persistent blurriness.

Roth Spots
These small retinal haemorrhages with pale centres are sometimes seen in severe B12 deficiency. They indicate fragile blood vessels and reduced oxygen delivery to the retina. If you have these spots on your eye, your eye doctor should be able to give you a diagnosis of B12 Deficiency.
https://europepmc.org/article/MED/22696623

Optic Neuropathy
One of the most serious complications. Damage to the optic nerve can cause blind spots, colour‑vision changes, and progressive vision loss. Early recognition and proper treatment are essential to prevent permanent harm.

Macular Degeneration‑like Changes
B12 deficiency can cause or worsen changes in the macula — the part of the retina responsible for sharp, central vision.
This happens because:
Retinal nerves lose their myelin, making them vulnerable to damage
Homocysteine rises, harming the tiny vessels that feed the macula
Reduced oxygen delivery from anaemia stresses the highly oxygen‑dependent macular tissue

These changes can mimic age‑related macular degeneration (AMD), but unlike typical AMD, B12‑related macular changes may improve with proper treatment if caught early.

⚠️ Hereditary Leber’s Optic Neuropathy (LHON): A Critical Warning
Individuals with Hereditary Leber’s Optic Neuropathy (LHON) — a mitochondrial condition that causes rapid, severe central vision loss — must be especially careful with the form of B12 they receive.
Cyanocobalamin MUST NOT be used in LHON
Cyanocobalamin releases cyanide during metabolism, which places additional stress on already vulnerable mitochondria.
This can worsen optic nerve damage in people with LHON or those carrying LHON‑associated mitochondrial mutations.

Hydroxocobalamin is the appropriate form to use. Hydroxocobalamin binds cyanide and supports mitochondrial function, making it the preferred form of B12 in LHON and in individuals at risk. This distinction is vital — especially because LHON can be misdiagnosed as “just B12 deficiency” or vice versa.

Note: It has been my experience over the years to have noticed that LHON seems to be more prolific in the Dutch population. (PK).

If you live with pernicious anaemia or B12 deficiency, any change in vision — even mild — deserves attention. Eye symptoms are not rare, and they are not “in your head.”
Early recognition and proper treatment can prevent long‑term damage, and in some cases, even reverse it.
Let’s keep raising awareness so no one is left struggling with preventable vision loss.

05/31/2026

A good example of a piece of research that can be misinterpreted from a not so good research article.

Over the past week, this article has been floating around the internet. Some health and wellness sites have picked it up and rather than posting the complete title, post High B12 levels a concern in cancer. I caution every person who reads an article from a health and wellness site or a health food site, to actually look for the study and read the study. For example, Science Daily posts a scaremongering title…”Scientists are raising new questions about vitamin B12 and cancer.”

This is the actual title of the article.
Vitamin B12 Intake and Cancer Risk: Findings from a Case-Control Study in Vietnam
Ngoan Tran Lea,b*, Yen Thi-Hai Phamc,d*, Y-Thanh Lue*, Linh Thuy Lef*, Nhi Yen Ngoc Huynhg,Hang Viet Daoh, Dai Duc Nguyeng, Kathryn Demanelisc, Toan H. Hai, Suresh V. Kuchipudii andHung N. Luu

The research article refers to dietary B12 and does not mention B12 deficiency except in reference to some study subjects having low B12. In fact the highest amount of Vitamin B12 intake was only 3mcg which isn’t much. The study does not demonstrate that Vitamin B12 causes cancer. It demonstrates an association between estimated dietary B12 intake and cancer diagnoses in a specific population. Those are very different conclusions.

This was a case control study and not a causation study. The researchers compared people who already had cancer with people who did not have cancer and then estimated their Vitamin B12 intake from food questionnaires. This design can identify correlations but cannot establish cause and effect.

Many cancers can cause high B12 levels especially if the kidneys and liver are involved. That does not mean that B12 caused the cancer, rather it means that cancer caused the high B12 levels. Again I refer to those individuals who were never deficient in B12. For example lung cancer does not occur because someone develops a cough. The cancer causes the cough.

Again, I just urge caution whenever you see an article, with a title, that screams high B12 levels linked to cancer, to actually look at the medical research, itself.

As for this article, I truly hope it gets withdrawn. In my opinion, it is nothing but a piece of garbage.

Vitamin B12 has long been seen as a health hero, helping the body make red blood cells, repair DNA, and keep nerves functioning properly. But scientists are discovering that the story may be more complicated than simply “more is better.” While too little B12 can damage DNA and raise cancer risk,...

05/29/2026

Have you just started treatment?

If you are just beginning treatment or taking over your own care through self-injecting, please keep the following in mind.

It took years — often 3 to 5 years or even longer — for your body to become deficient in B12. Vitamin B12 is present in every cell and every nerve in the body. Because of this, it is unrealistic to expect one, two, or even ten injections to completely replenish your body’s B12 stores. Healing and replenishment take time.

There are billions of cells in the human body, and restoring adequate B12 levels throughout the body can take years. B12 deficiency damages nerves by eroding the myelin sheath, the protective fatty insulation surrounding the nerves. As the myelin sheath deteriorates, nerves become exposed and can eventually die. This damage is what causes many of the symptoms associated with Pernicious Anaemia and B12 deficiency.

The peripheral nervous system is usually affected first. Tingling, numbness, and pins-and-needles sensations in the hands and feet are often among the earliest signs of B12 deficiency.

As the deficiency progresses, the central nervous system can become affected. At this stage, memory problems, balance difficulties, and coordination issues may develop. You may notice that you cannot shower safely with your eyes closed because you lose your balance. Walking in the dark may become difficult, and you may find yourself constantly looking down at your feet while walking. Even stepping off a curb may suddenly require conscious effort because you need to visually guide your foot placement.

This loss of awareness is known as proprioception — the body’s ability to sense its own position and movement. B12 deficiency can impair this important neurological function.

The foundations of healing are B12 together with either folic acid or folinic acid. If you are injecting daily or every other day, many PA/B12 deficient sufferers find they require approximately 5 mg of folic acid or folinic acid daily as well.

Any information suggesting that you must first “raise your B12 level” before taking folate is incorrect. B12 and folate are completely interdependent. B12 requires folate, and folate requires B12 in order for both to function properly within the body.

Iron supplementation should only be added if it is genuinely needed. Before supplementing iron, it is important to know your iron studies and ferritin levels.

A B-complex vitamin can also be helpful, but there is usually no need to introduce it immediately. Your body is already adjusting to finally receiving the B12 it has long been deprived of. Many people find it better to introduce a B-complex gradually, usually within a few weeks to a month after beginning self-injections. Note: the B6 in a B complex must not exceed 10mg.

One symptom of B12 deficiency that is rarely discussed is an extreme lack of patience and heightened frustration. I have seen it repeatedly in group members, and I experienced it myself while helping my daughter through treatment. Your frustration is understandable. I hear you. However, expecting rapid improvement after starting injections can often lead to even greater disappointment.

Try not to expect dramatic changes in the early stages of treatment. Improvement is often very gradual. Significant healing may take six months to a year, and in some cases even longer.

Symptoms often improve in the reverse order in which they appeared. The newest symptoms are frequently the first to improve because they have caused less long-term damage. Healing usually happens slowly and in stages, sometimes so gradually that improvements are barely noticed at first.

It is also possible to develop new or temporarily worsening symptoms after starting treatment. This does not necessarily mean treatment is failing. It often reflects the fact that the body is still replenishing depleted B12 stores and that damaged nerves are beginning to reactivate.

Keeping a symptom diary can be extremely helpful. Record your symptoms daily and rate them from 1 to 10. If a symptom is a 10 today and an 8 tomorrow, that is progress — even if it may not feel dramatic at the time.

Lastly, many people find that symptoms temporarily worsen before improvement begins. Your body is adjusting to a vitamin it has desperately needed, and nerves that have been dormant for a long time are beginning to wake up. As healing begins, those nerves can become painful and overactive, which may temporarily intensify symptoms.

Healing from Pernicious Anaemia/B12 deficiency is often a long journey, but improvement will occur. Just hang in there. It truly does get better.

The photo lists only a few symptoms. As everyone knows, there are many more.

05/25/2026

Pernicious Anaemia and B12 Deficiency have so many symptoms. What were your symptoms and how did it impact your life.

Pernicious Anaemia and Vitamin B12 Deficiency can affect nearly every system in the body, which is why symptoms are often so varied, confusing, and frequently overlooked. Many people initially experience extreme fatigue that does not improve with rest. Everyday activities such as climbing stairs, grocery shopping, concentrating at work, or even holding a conversation can become exhausting. Weakness, shortness of breath, dizziness, heart palpitations, pale skin, and headaches are also common. Because the body relies on vitamin B12 to produce healthy red blood cells and maintain proper nerve function, a deficiency can gradually leave individuals feeling physically and mentally depleted.

Neurological symptoms are among the most concerning aspects of B12 deficiency and pernicious anaemia. Many people report numbness, tingling, burning sensations, “pins and needles,” electric shock sensations, muscle twitching, poor balance, unsteady walking, and muscle weakness. Some individuals develop significant mobility problems and may require walking aids. Nerve involvement can also affect vision, causing blurred vision, light sensitivity, visual disturbances, or eye pain. Cognitive symptoms are equally impactful and may include brain fog, memory loss, confusion, difficulty concentrating, poor word recall, and slowed thinking. Some people are incorrectly told they have anxiety, depression, burnout, or even early dementia before the underlying deficiency is recognized.

The condition can also have a major emotional and psychological impact. Mood changes are frequently reported, including anxiety, irritability, panic attacks, emotional instability, low mood, and depression. In more severe cases, hallucinations, paranoia, or psychosis can occur. Sleep disturbances are also common, with individuals experiencing insomnia, vivid dreams, restless sleep, or waking unrefreshed. These symptoms can deeply affect relationships, employment, and overall quality of life. Many people struggle with the frustration of appearing “well” on the outside while silently coping with debilitating symptoms every day.

There are also many lesser-known and unusual symptoms associated with B12 deficiency and pernicious anaemia that are often dismissed or misattributed to other conditions. These may include burning mouth syndrome, mouth ulcers, a swollen or smooth tongue, altered taste, tinnitus, sound sensitivity, internal vibrations, tremors, temperature regulation problems, excessive sweating, and feelings of internal buzzing or vibrations. Some people experience bladder issues, urinary urgency, interstitial cystitis–like symptoms, bowel disturbances, nausea, appetite loss, or unexplained weight changes. Others report hair loss, skin changes, easy bruising, infertility issues, or worsening symptoms around hormonal fluctuations.

Daily living can become profoundly affected when symptoms are severe or long-standing. People may struggle to maintain employment, drive safely, exercise, socialize, or manage household responsibilities. Simple tasks such as reading, cooking, following conversations, or remembering appointments can become difficult. Chronic exhaustion and neurological symptoms can leave individuals isolated and misunderstood, especially when blood results appear “normal” despite ongoing symptoms. Many patients describe feeling as though they have “lost themselves” before receiving appropriate diagnosis and treatment.

One of the challenges with pernicious anaemia and B12 deficiency is that symptoms can develop slowly over months or years, making it difficult for individuals to recognize how unwell they have become. Symptoms also vary widely between people. Some individuals may develop significant neurological symptoms with little or no anaemia, while others experience profound fatigue or gastrointestinal problems first. Early recognition and treatment are important because prolonged deficiency can lead to permanent neurological damage in some cases. This is why many patients and advocates continue to call for greater awareness of the broad and often misunderstood presentation of these conditions.

05/23/2026

Some other causes of genetic B12 deficiency aside from the exploited MTHFR gene.

- Cobalamin A Deficiency,
- Cobalamin B Deficiency,
- Cobalamin C Deficiency,
- Cobalamin D Deficiency,
- Cobalamin E Deficiency,
- Cobalamin F Deficiency,
- Cobalamin G Deficiency,
- Cobalamin J Deficiency
- Cobalamin X deficiency. Cobalamin x deficiency is found only in newborn male babies.

Cobalamin deficiency disorders are identified and diagnosis is confirmed by identification of biallelic ( Referring to both alleles of a gene pair. Biallelic variants may be homozygous or compound heterozygous) pathogenic variants in one of the following genes (associated complementation groups indicated in parentheses):MMACHC (cblC), MMADHC (cblD-combined and cblD-homocystinuria), MTRR (cblE), LMBRD1 (cblF), MTR (cblG), ABCD4 (cblJ), THAP11(cblX-like), ZNF143(cblX-like), or a hemizygous variant in HCFC1 (cblX, which can show a cblC complementation class).

Cobalamin A Deficiency – gene is MMAA
Cobalamin B Deficiency - gene is MMAB
Cobalamin C Deficiency – gene is MMACHC
Cobalamin D Deficiency – gene is MMADHC
Cobalamin E Deficiency – gene is MTRR
Cobalamin F Deficiency – gene is LMBRD1
Cobalamin G Deficiency – gene is MTR
Cobalamin J Deficiency – gene is ABCD4
Cobalamin X Deficiency – gene is THAP11, ZNF143 or a variant in HCFC1 which can look like a Cobalamin C deficiency – note: Cobalamin X Deficiency will only appear in newborn male babies. It is the gene HCFC1 that dysregulates the gene MMACHC which provides instructions for making a protein that helps convert vitamin B12 (also called cobalamin) into one of two molecules, Adenosylcobalamin or Methylcobalamin.

Cobalamin A deficiency causes elevated methylmalonic acid levels, leading to methylmalonic acidemia. It is an autosomal recessive disorder, which means an affected child inherits one mutated gene from each parent. Testing for this condition is included in the newborn screening panel.

Cobalamin B (cblB) deficiency is a rare inherited metabolic disorder caused by mutations in the MMAB gene. This gene also elevates methylmalonic acid (above range) resulting in methylmalonic acidemia.

Cobalamin C Deficiency – variants of the MMACHC gene can elevate both MMA and Homocysteine causing both homocystinuria and methylmalonic acidemia. It causes a buildup of homocysteine and methylmalonic acid and decreased methionine. When methionine is low, the conversion process or recycled homocysteine, via folate, to methionine, stalls and this creates what is called the methylfolate trap. A methionine deficiency directly reduces S-adenosylmethionine (SAMe) levels because methionine is the essential biological precursor required to synthesize SAMe in the liver. Without enough methionine, the body cannot produce adequate SAMe, which impairs vital methylation processes and increases the risk of cellular stress and liver dysfunction. Although Cobalamin C Deficiency is now included in the newborn screening panel, individuals who were born before 2005, and who believe they are deficient in B12 with no cause being found, should be tested for this gene.

Cobalamin D deficiency can lead to high levels of homocysteine or MMA. It is caused by mutations in the MMADHC gene. This gene provides instructions for proteins that help transport and convert vitamin B12 (cobalamin) into its two active, usable forms in the body. Types of cblD: Because the MMADHC gene can mutate in different areas, the disease manifests in three distinct ways: cblD-homocystinuria: Leads to elevated homocysteine levels. cblD-methylmalonic aciduria: Leads to elevated methylmalonic acid (MMA) in the urine. cblD-combined: A more severe form where both MMA and homocysteine are elevated. These gene variants cannot break down certain proteins and fats causing a buildup of methylmalonic acid and or homocysteine or a combination of both.
Cobalamin E deficiency ( gene MTRR) and Cobalamin G deficiency(gene MTR) usually will result in a high homocysteine level and a disorder called homocystinuria which is buildup of homocysteine and an inability to process homocysteine to methionine.

Cobalamin F deficiency – variants in the gene, LMBRD1, can result in a combination of high homocysteine levels and Methylmalonic Acid leading to the disorders of homocystinuria and methylmalonic acidemia. Again it causes a buildup of homocysteine, methylmalonic acid and decreased methionine.
Cobalamin J Deficiency – variants in the gene ABCD4. Description is the same as for Cobalamin F Deficiency.

Cobalamin X – occurs only with newborn male babies, variants in the genes THAP11, ZNF143 or a variant in HCFC1 results in a combination of high homocysteine and methylmalonic acid levels.

Methylmalonic acid and homocysteine testing should be performed in all of the deficiencies listed above, as failure to carry out these investigations could result in a missed diagnosis. It is also essential that genetic testing for these conditions is conducted by a qualified medical practitioner with expertise in metabolic genetics. In these cases, hydroxocobalamin is the recognized form of B12 treatment, alongside folinic acid, whereas cyanocobalamin is considered contraindicated. Newborn screening panels now test for homocystinuria. In addition to hydroxocobalamin, other supplements that are or may be necessary to take, are folinic acid (leucovorin), Betaine (also known as cystadane), L-Methionine and L-Carnitine.

Note: While MMA is not included in a newborn screening panel, Propionylcarnitine (C3) is included. If Propionylcarnitine (C3) is elevlated, then MMA is tested.

Some of the information taken from
https://www.ncbi.nlm.nih.gov/books/NBK1328/
And this article is one that suggests Cobalamin C deficiency sufferers should strive for a serum B12 level of 1,000,000.
https://pubmed.ncbi.nlm.nih.gov/36543571/

05/20/2026

Frequently Reported Misconceptions and Misbeliefs Regarding Vitamin B12 Deficiency

From the article, The Many Faces of Cobalamin (Vitamin B12) Deficiency, written by
Bruce H.R. Wolffenbuttel, MD, PhD; Hanneke J.C.M. Wouters, BSc;
M. Rebecca Heiner-Fokkema, PhD; and Melanie M. van der Klauw, MD, PhD

On some of your visits to a doctor, in your long journey to diagnosis, have you ever been told the following: All of which are nonsensical statements to make so do not accept what your doctor tells you when it is so wrong.

Diagnosis:
You do not have vitamin B12 deficiency because:
You have no anemia (one does not have to have anaemia to be deficient in B12)

You have no macrocytic anemia (the same as above)

Your serum vitamin B12 level is within the reference range of 140 to 450 pmol/L (it is well docmented that B12 deficiency can occur with serum B12 levels in the 400's)

Your serum vitamin B12 level is only moderately low (a moderately low B12 level is a deficiency)

Your serum vitamin B12 level may be low, but your plasma level of methylmalonic acid is completely normal (MMA can only determine a deficiency, it cannot determine how low your B12 is)

Vitamin B12 deficiency only occurs in elderly people (B12 deficiency occurs in infants, children, young adults, middle aged adults and the elderly)

Vitamin B12 deficiency never occurs in children (of course it does, babies can be born lacking intrinsic factor)

Treatment
Oral therapy is as good as or even better than painful injections to alleviate neurologic symptoms;
You may stop treatment because your serum vitamin B12 level has normalized;
You must stop treatment because your serum vitamin B12 level is elevated;
You must stop after 5 injections because vitamin B12 can have serious adverse effects;
You must stop the injections because your symptoms have worsened;
We must measure your serum vitamin B12 level after 3 injections to see whether the treatment is successful; and
We must stop vitamin B12 injections now that you are pregnant.

The above answers for treatment are all obviously incorrect. Prof. Wolffenbuttel is well educated on the pitfalls of diagnosing and treating Vitamin B12 Deficiency and is relating answers that he hears from patients who are experiencing or have experienced the minefield of trying to get a B12 Deficiency diagnosis and proper treatment.

Abstract
Although cobalamin (vitamin B12) deficiency was described over a century ago, it is still difficult to establish the correct diagnosis and prescribe the right treatment.
Symptoms related to vitamin B12 deficiency may be diverse and vary from neurologic to psychiatric. A number of individuals with vitamin B12 deficiency may present with the classic megaloblastic anemia.
In clinical practice, many cases of vitamin B12 deficiency are overlooked or sometimes even misdiagnosed. In this review, we describe the heterogeneous disease spectrum of patients with vitamin B12 deficiency in whom the diagnosis was either based on low serum B12 levels, elevated biomarkers like methylmalonic acid and/or homocysteine, or the improvement of clinical symptoms after the institution of parenteral vitamin B12 therapy. We discuss the possible clinical signs and symptoms of patients with B12 deficiency and the various pitfalls of diagnosis and treatment.

Conclusion
Patients with low serum vitamin B12 levels may have no symptoms (yet). Nevertheless, they are at high risk for development of symptoms. There is a tendency among physicians to consider a serum vitamin B12 level higher than 140 pmol/L as normal, but many symptomatic patients may present with such levels, for instance because of taking oral vitamin supplementation. This does not mean that their tissue vitamin B12 levels are normal as well.

Methylmalonic acid and homocysteine are not very sensitive biomarkers, but there is currently no good alternative, although systematic evaluation of more advanced metabolic factors may lead to the application of better biomarkers.
When serum total vitamin B12 levels are low or questionable, the combination of total vitamin B12, active vitamin B12, MMA, and homocysteine may be the best strategy, but the validity of this combined biomarker approach needs to be validated in larger prospective studies and especially validated against objective markers of treatment response. In case of doubt, when results of biomarker measurements are equivocal, a trial with parenteral hydroxocobalamin injections may be considered, as was done in patients B and D. Because symptom improvement in long-standing (subclinical) vitamin B12 deficiency may take some time, we usually advise a treatment regimen of twice weekly hydroxocobalamin injections for 3 months, after which a thorough re-evaluation is performed with systematic evaluation of symptom score as demonstrated in patient B. There is no proof in large prospective, double-blind studies that oral supplementation is as effective in reducing symptoms associated with vitamin B12 deficiency as parenteral treatment.
https://pubmed.ncbi.nlm.nih.gov/31193945/

05/18/2026

Pernicious Anaemia/B12 Deficiency and Non Alcoholic Fatty Liver Disease (NAFLD).

Research indicates a complex bidirectional link between vitamin B12 and non-alcoholic fatty liver disease (NAFLD). Lower serum B12 levels are frequently observed in NAFLD patients, while adequate B12 helps regulate hepatic lipid metabolism and may prevent the progression of liver inflammation and scarring.

The B12 and NAFLD Connection
Lower Levels in NAFLD: Multiple studies, including a prominent analysis from the National Center for Biotechnology Information (NCBI), indicate that patients with NAFLD tend to have significantly lower serum vitamin B12 levels compared to healthy individuals.
Role in Fat Metabolism: The liver is the primary storage organ for B12. B12 acts as a vital cofactor in lipid and 1-carbon metabolic pathways. When B12 is deficient, the liver's ability to process and export fat is impaired, promoting fat accumulation and oxidative stress. (This is why some B12 deficient patients develop non alcoholic fatty liver disease, (PK)).

Progression of Fibrosis: While early fatty liver might maintain B12 storage capacity, advanced forms of the disease—such as non-alcoholic steatohepatitis (NASH) or fibrosis—correlate with lower serum B12 levels and impaired liver.

Shared Risk Factors: Having NAFLD does not inherently cause a B12 deficiency; rather, the two conditions frequently share common causes and exacerbating factors:

Metformin Use: Long-term use of metformin (common for type 2 diabetes, which frequently co-occurs with NAFLD) is a well-documented cause of B12 malabsorption.

Medications and Diet: Proton pump inhibitors (PPIs) and strict plant-based diets lacking adequate animal products increase deficiency risk.

Summary: Fatty liver disease does not directly cause Vitamin B12 Deficiency, but associated conditions and medications commonly increase deficiency risk.
Simple fatty liver typically preserves B12 storage capacity; advanced disease may impair hepatic function and alter B12 binding proteins.
Metformin, proton pump inhibitors, and dietary restrictions frequently coexist with fatty liver and independently increase B12 deficiency risk.
Serum B12 levels may appear misleadingly normal or elevated in chronic liver disease due to altered binding proteins.
Neurological symptoms (neuropathy, cognitive changes) require urgent assessment and same-day parenteral B12 treatment if deficiency is confirmed.
MHRA guidance (2022) recommends B12 monitoring for patients on long-term metformin therapy.
Treatment involves hydroxocobalamin injections for confirmed deficiency and lifestyle modification for fatty liver disease management.
https://www.frontiersin.org/journals/endocrinology/articles/10.3389/fendo.2024.1426103/full

https://www.boltpharmacy.co.uk/guide/can-fatty-liver-cause-vitamin-b12-deficiency

High Prevalence of Autoimmune Gastritis in Patients with Non-alcoholic Steatohepatitis (NASH)
Conclusion
The prevalence of NASH with concomitant autoimmune gastritis was high, highlighting the need for upper endoscopy for the diagnosis of autoimmune gastritis and gastric malignancies.
https://www.jstage.jst.go.jp/article/internalmedicine/58/20/58_2693-19/_article/-char/ja/

Folate and B12 Levels Correlate with Histological Severity in NASH Patients
Abstract:
Background: The correlation between abnormal vitamin serum levels and chronic liver disease has been previously described in literature. However, the association between the severity of folate serum levels (B9), vitamin B12 and non-alcoholic steatohepatitis (NASH) has not been widely evaluated.
Therefore, the aim of this study was to investigate the existence of such a correlation in a cohort of NASH patients.
Conclusion:
Our study demonstrated a statistically significant correlation between low levels of folate and Vitamin B12 with the histological severity of NASH. These findings could have diagnostic and therapeutic implications for patient management and follow-up.
https://www.mdpi.com/2072-6643/10/4/440

B vitamins can potentially be used to treat advanced nonalcoholic fatty liver disease
Summary:
Scientists at Duke-NUS Medical School in Singapore have uncovered a mechanism that leads to an advanced form of fatty liver disease -- and it turns out that vitamin B12 and folic acid supplements could reverse this process.
Scientists have found that elevated blood levels of an amino acid called homocysteine correlate strongly with the severity of an advanced form of non-alcoholic fatty liver disease. They also found vitamin B12 and folic acid could be used to prevent and/or delay disease progression.

https://www.sciencedaily.com/releases/2022/08/220805091251.htm