Pernicious Anaemia/B12 Deficiency Support Group - Page

05/11/2026

Do you have that cough that just won’t go away. You have taken OTC cough remedies, your doctor has tried antibiotics but nothing works. You are still coughing. Despite many visits to the doctor, no cause can be found for it.

Unexplained, chronic, and typically dry coughs can be a symptom of vitamin B12 deficiency, which may cause sensory neuropathy and increase airway sensitivity. Research indicates that correcting this deficiency with supplementation can significantly improve or resolve this type of persistent cough.

The B12-Cough Connection:
Mechanism: Vitamin B12 deficiency may lead to increased Nerve Growth Factor (NGF) levels in the pharyngeal mucosa, causing sensory neuropathy and heightened sensitivity in the upper airways. Study Findings: A study found that among patients with unexplained chronic cough, a significant percentage were B12 deficient (serum levels below 300 pg/mL).

When to Suspect B12 Deficiency: If common causes of chronic cough (smoking, asthma, reflux, ACE inhibitors) have been ruled out. If you are vegetarian, vegan, elderly, or using long-term acid-suppressing drugs.

Abstract
Background: Chronic cough is characterized by sensory neuropathy. Vitamin B-12 (cobalamin) deficiency (Cbl-D) causes central and peripheral nervous system damage and has been implicated in sensory neuropathy and autonomic nervous system dysfunction.
Objective: We evaluated whether Cbl-D has a role in chronic, unexplained cough.

Cbl-D is cobalamin deficiency
Conclusions: This study suggests that Cbl-D may contribute to chronic cough by favoring sensory neuropathy as indicated by laryngeal hyperresponsiveness and increased NGF expression in pharyngeal biopsies of Cbl-D patients. Cbl-D should be considered among factors that sustain chronic cough, particularly when cough triggers cannot be identified.

Unexplained chronic cough and vitamin B-12 deficiency
Caterina B Bucca , Beatrice Culla, Giuseppe Guida, Savino Sciascia, Graziella Bellone, Antonella Moretto, Enrico Heffler, Massimiliano Bugiani, Giovanni Rolla, Luisa Brussino
American Journal of Clinical Nutrition, 2011 Mar;93(3):542-8.
https://pubmed.ncbi.nlm.nih.gov/21248188/

05/10/2026

Do you wake up in the night, drenched in sweat. Night sweats can be linked to many conditions and causes however, B12 deficiency is most often overlooked as a cause of night sweats.

Vitamin B12 Deficiency - Some Observations, Some Misconceptions
Rehman HU
Eur J Gen Med 2015; 12(3):261 -266

ABSTRACT
Functional vitamin B12 deficiency is a syndrome where a wide variety of symptoms in the presence of “normal” serum levels of the vitamin respond to vitamin B12 therapy. A series of patients with functional vitamin B12 deficiency are described whose presenting features were drenching night sweats and fatigue. Reliance on serum vitamin B12 levels as a diagnostic test would have obscured the cause of their symptoms. Serum homocysteine and/or methlymalonic acid levels should be done in all patients with suspected B12 deficiency. Normal levels of these metabolites do not exclude diagnosis and empirical treatment may be justifiable in certain cases. Author also argues that oral vitamin B12 treatment results in suboptimal clinical response in a vast majority of patients and intramuscular route should be preferred in most patients.

CASE 1
A 57-year old man was referred for assessment of 3-4 years history of drenching night sweats needing replacement of bed-sheets almost on a nightly basis. The sweating involved only the upper portion of his body from top of the head to mid chest around the level of the ni***es and seemed to be worse after drinking alcohol. He denied any bowel symptoms, weight loss, fever, cough or skin rash. His past medical history was significant for hypertension treated with hydrochlorothiazide.
Vitamin-B12 injections 1000mcg daily for 7 days followed by monthly injections were prescribed on the basis of elevated homocysteine levels. His serum B12 level was normal. His homocysteine level was 14.9. Celiac antibodies, antibodies to parietal cells and intrinsic factor were negative. Patient reported a dramatic response of his sweating after the second injection of vitamin-B12 and remained asymptomatic at 3 months follows up.

CASE 4
A 45-year-old man was diagnosed with multiple sclerosis and vitamin B12 deficiency in 2009. He had been on vitamin B12 injections for 2 years but than switched to oral vitamin B12 1000µg daily. He presented with 4-month history of drenching night sweats primarily affecting head and face. He denied cough, fevers, or weight loss. He drank very little alcohol and did not smoke. Examination revealed pulse rate of 74/min and blood pressure of140/90mmHg. Rest of the physical examination, including neurological examination was normal. Urea, creatinine and electrolytes were in the normal range. Gastric parietal cell antibodies and intrinsic factor antibodies were negative. Oral vitamin B12 was replaced with intramuscular vitamin B12 1000mcg monthly. When reviewed 4 months later, his symptoms had resolved completely.

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This also supports our statement that oral cobalamin is not effective to treat a B12 deficiency caused by malabsorption.

05/08/2026

Sensory Symptoms of B12 Deficiency

Vitamin B12 deficiency can cause demyelination - the myelin sheath is damaged. This damage impairs the conduction of signals in the affected nerves. In turn, the reduction in conduction ability causes deficiency in sensation, movement, cognition, or other functions depending on which nerves are involved. Altered sensations (sensory symptoms) are a type of nerve (neuropathic) pain and may be classified as dysaesthesia, paraesthesia or allodynia.

Some examples are
Burning
Tingling
Pins and needles
Crawling
Numbness
Prickling
Sensitive skin
Wetness – a feeling of wetness on the body, could be face, arms, hips.
Stabbing
Electric shock
Itching
Trickling

Allodynia: where something, like a light touch, feels painful even though it shouldn’t cause pain. It is a type of neuropathic pain where typically non-painful stimuli (like light touch, clothing, or lukewarm water) cause pain.

Paraesthesia: which is an annoying unusual sensation, like tingling or numbness, which may be triggered or just happens spontaneously. It can be caused chiefly by pressure on or damage to peripheral nerves.

Formication: is the sensation that resembles that of small insects crawling on (or under) the skin. It is one specific form of a set of sensations known as paraesthesias, which also include the more common prickling, tingling sensation known as "pins and needles". It is a tactile hallucination defined by the sensation of insects crawling on or underneath the skin, despite there being no actual bugs present.

Dysaesthesia: which is a more intense, sometimes painful, feeling which happens spontaneously. It is a neurological symptom defined as an abnormal, unpleasant, or painful sensation, often caused by nerve damage. It is an abnormal physical touch sensation without outside cause. It often involves painful, itchy, burning, or restrictive sensations.

05/05/2026

. Have you noticed your voice gets hoarse. Do you find it can be difficult at times to speak for any length of time. Does your voice get raspy. Have you lost your voice?
If so, you might want to ask your doctor to order a Vitamin B12 test.

Unusual neurological presentations of vitamin B12 deficiency

T.-B. Ahna,d, J.-W. Choa and B. S. Jeona, Department of Neurology, Seoul National University College of Medicine; Department of Neurology and Clinical Research Institute, Seoul National University Hospital; Department of Neurology, Kyung Hee University Hospital, Seoul, South Korea

Case reports
A 41-year-old man was admitted because of progressive difficulty in walking. He first noticed numbness and tingling sensation on his hands and feet 15 years ago. At that time he felt difficulty in walking, which was more severe in the dark. He visited a local hospital, where he was diagnosed as having anemia and prescribed with some medication. Anemia resolved and gait disturbance mildly improved. Two years later he discontinued medication without medical advice. Gait disturbance gradually worsened. There was no bulbar dysfunction. Two years before admission, he couldn’t feel touch sensation below the level of umbilicus. Three months before admission, hoarseness developed and was hard to be heard. At the time of admission he was unable to stand unassisted. On inquiry, he denied any remarkable medical history other than the above. He was neither a vegetarian nor a habitual alcoholic.

Laryngoscopic examination revealed bilateral vocal cord paralysis. Parenteral B12 injections reversed the vocal cord paralysis.

Case 2
A 53-year-old man was admitted with progressive difficulty in walking for 11 months. Eleven months prior to admission, he first noticed numbness and paresthesia of his feet and hands. Gradually, difficulty in speech and gait developed. He became confined to his home because of gait disturbance. He denied any history of diabetes mellitus, hypertension and gastrointestinal disease. He was not a vegetarian. He drank a small amount of alcohol beverage once or twice a week.

Diagnosis of B12D was made and he was treated with intramuscular injection of cobalamin (1 mg). EOM limitation began to improve in 5 days. Gait disturbance gradually improved over several months. Neurological examination performed at 12 months later revealed full range of EOM, no dysarthria (motor speech disorder) , no dysmetria on cerebellar function test. There still remained mild sensory deficit, mild ataxic gait, and increased reflexes.

Dysarthria (motor speech disorder) as an Isolated Neurological Manifestation of Vitamin B12 Deficiency: An Unusual Presentation.
(The only symptom of B12 Deficiency was dysarthria and no indication via haematology indices of anaemia).

Abstract
Vitamin B12 (Vit. B12) is an important cofactor for the cellular metabolism and myelination. Vit. B12 deficiency can manifest as hematological, neurological, or gastrointestinal (GI) abnormalities. The following case had a unique manifestation of Vit. B12 deficiency in the form of dysarthria without any evidence of hematological involvement. From this case, we can infer that, in young patients with isolated neurological manifestation, Vit. B12 deficiency can always be a differential diagnosis. A26‑year‑old female presented with complaints of fever, odynophagia, and dysarthria. She was vitally stable and had no neurological deficits.

Her blood investigations showed leukopenia and thrombocytopenia. She was positive for dengue immunoglobulin M, her Vit. B12 levels were low, and her hemoglobin electrophoresis was suggestive of sickle‑cell trait. She was subjected to an upper GI endoscopy which was suggestive of antral gastritis. Her magnetic resonance imaging findings were within normal limits. Upon intravenous supplementation of Vit. B12, her dysarthria resolved. From the clinical course and investigation, we consider that dysarthria is an isolated neurological manifestation of Vit. B12 deficiency.

This case of Vit. B12 deficiency had two interesting points; it presented with neurological manifestation without hematological involvement and the neurological manifestation also was only dysarthria. The patient responded promptly with the supplementation of Vit. B12 with full recovery within few days. This case emphasizes the importance of increased index of suspicion of Vit. B12 deficiency in young patients presenting with isolated neuropathic symptoms as if detected early and treated adequately in time, the patients have fast and full recovery.
https://www.researchgate.net/publication/331350359_Dysarthria_as_an_isolated_neurological_manifestation_of_Vitamin_B12_deficiency_An_unusual_presentation

05/04/2026

Could a vitamin deficiency cause ‘double-jointedness’ and troubling connective-tissue disorder?

Tulane University researchers have discovered a possible genetic cause for hypermobility (commonly known as double-jointedness) and a range of associated connective tissue disorders such as Ehlers-Danlos syndrome, according to preliminary findings published in the journal Heliyon.

You may know someone with overly flexible joints, a friend or family member who can easily slide into a split or bend limbs to impossible angles. But hypermobility is a more serious condition than being “double-jointed.”

For those with hypermobile Ehlers-Danlos syndrome (EDS), the same conditions that create fragile connective tissue can cause a range of symptoms that, on the surface, can seem unrelated: physical conditions such as joint pain, chronic fatigue, thin tooth enamel, dizziness, digestive trouble and migraines; and psychiatric disorders, such as anxiety and depression. Women with hypermobile EDS may also be at increased risk for endometriosis or uterine fibroids.

For years, researchers have struggled to find the cause of hypermobility and hypermobile EDS. Of the 13 subtypes of EDS, hypermobile EDS comprises more than 90% of the cases. But until this study, hypermobile EDS was the only subtype without a known genetic correlate. As a result, symptoms have often been treated individually rather than as the result of a single cause.
Researchers at Tulane University School of Medicine have linked hypermobility to a deficiency of folate – the natural form of vitamin B9 – caused by a variation of the MTHFR gene.

“You’ve got millions of people that likely have this, and until now, there’s been no known cause we’ve known to treat,” said Dr. Gregory Bix, director of the Tulane University Clinical Neuroscience Research Center. “It’s a big deal.”
https://www.sciencedirect.com/science/article/pii/S240584402302594X
Treat with folinic acid.

Have you recently had your B12 and folate levels tested.

Ehlers-Danlos Syndrome (EDS) and Vitamin B12 deficiency are two distinct conditions that frequently overlap, creating a complex clinical picture for many patients. EDS is a group of genetic connective tissue disorders primarily characterized by joint hypermobility and skin hyperextensibility. While the root causes differ—one being genetic and the other nutritional—they share several overlapping symptoms, such as chronic fatigue, brain fog, and neurological issues like tingling or numbness. For those living with EDS, a B12 deficiency can significantly exacerbate existing symptoms, making it a critical area of focus for managing overall health.

The link between these conditions is often found in the gastrointestinal (GI) tract. Up to 90% of people with hypermobile EDS suffer from GI challenges, including gastroparesis, irritable bowel syndrome (IBS), and slow motility. These issues can lead to significant malabsorption of essential nutrients like Vitamin B12, even if the person consumes a diet rich in the vitamin. When the gut cannot properly process or absorb B12, levels drop, leading to deficiencies that further weaken the body's systems.

Beyond absorption issues, some research suggests a deeper biochemical connection involving collagen production. Vitamin B12 is a necessary co-factor in the methylation cycle, which ultimately supports the production of glutathione—an essential component for processing iron in cells. Iron is required for the enzymes that cross-link collagen, the body's "glue." A functional B12 deficiency can therefore interfere with these processes, potentially leading to the production of weaker, more "lax" collagen, which is a hallmark of the EDS phenotype.

Neurologically, the two conditions can mimic or mask one another. EDS is often associated with dysautonomia, including conditions like Postural Orthostatic Tachycardia Syndrome (POTS), which can cause dizziness and palpitations. Interestingly, low B12 levels have also been linked to autonomic dysfunction and POTS-like symptoms. When both conditions are present, a patient might experience severe neurological decline, including impaired proprioception (the sense of where your body is in space) and cognitive impairments. Addressing a B12 deficiency through targeted supplementation or injections often provides a significant boost in energy and mental clarity for EDS patients.

Managing EDS requires a multidisciplinary approach that includes monitoring nutritional health. Because the symptoms of B12 deficiency so closely mirror common EDS "flares," it can easily go undiagnosed. Routine screening for B12, along with other common deficiencies like iron and vitamin D, is often recommended by specialists to ensure that patients are not struggling with treatable nutritional gaps. By optimizing B12 levels, many individuals with EDS find that they can better manage their chronic fatigue and improve their day-to-day quality of life.

05/03/2026

What causes your symptoms. B12 deficiency, of course. But how do the symptoms develop. Many of the neurological symptoms you have are caused by the breakdown or erosion of the myelin sheath. Wherever the erosion occurs on the myelin sheath, the exposed nerve dies and then your symptoms start. Below is a good explanation of the myelin sheath. Note the sentence wherein the author says, the damage occurs before any sign of anaemia.

Every nerve in your body is wrapped in myelin, a multilayered lipid sheath that insulates the axon and lets electrical signals travel fast. B12 maintains this sheath through two separate pathways, and both fail at the same time when B12 drops.

The first pathway runs through methionine synthase. B12 (as methylcobalamin) converts homocysteine into methionine, which becomes SAMe. SAMe provides the methyl groups needed to build phosphatidylcholine, one of myelin's major lipid components. When B12 is low, SAMe drops and myelin lipid synthesis stalls.

The second pathway runs through methylmalonyl-CoA mutase. B12 (as adenosylcobalamin) clears methylmalonyl-CoA by converting it to succinyl-CoA. Without B12, methylmalonic acid (MMA) accumulates and abnormal fatty acids get incorporated into the myelin sheath itself, weakening its structure from the inside.

What makes this dangerous: the nerve damage can appear before anemia does. In the Lindenbaum NEJM study, 28% of patients with neuropsychiatric symptoms from B12 deficiency had completely normal blood counts. No anemia, no macrocytosis. The myelin was already degrading with nothing on the CBC to flag it. If caught early, repletion can reverse it. If caught late, the demyelination can become permanent.

Scalabrino, Prog Neurobiol, 2009.
Lindenbaum et al., NEJM, 1988.

05/02/2026

B12 Deficiency presenting as Epilepsy or Seizures

We have several members of the group who were diagnosed with Intractable Epilepsy (seizures not responding to anti seizure meds), only later to find out aggressive treatment with B12 injections stopped the seizures. B12 deficiency can cause seizures in babies and children. One of our members suffered seizures for years, her parents were her carers. They had to help her into and out of bed. With aggressive B12 treatment, daily injections of hydroxocobalamin, she recovered, got her life back and is employed.

Recurrent seizures: An unusual manifestation of vitamin B12 deficiency

S. Kumar Neurology Unit, Department of Neurological Sciences, Christian Medical College Hospital, Vellore - 632004, India

The present report highlights an unusual presentation of vitamin B12 deficiency— recurrent seizures in a 26-year-old man. His symptoms responded to parenteral vitamin B12 therapy.
Vitamin B12 deficiency causing neuropsychiatric manifestations such as peripheral neuropathy, subacute combined degeneration of cord, dementia, ataxia, optic atrophy, psychosis and mood disturbances is well known.1-3 We report a case with recurrent seizures resulting from vitamin B12 deficiency.

A 26-year-old man presented with recurrent episodes of complex partial seizures of three weeks duration. He had developed behavioral changes one year ago characterized by social withdrawal and memory impairment. Prior to admission, he had neglected self-care, had become severely withdrawn and was disoriented. He was treated with risperidone and carbamazepine. (These medications both lower B12 levels.).

In conclusion, seizures rarely occur in patients with vitamin B 12 deficiency. ( I disagree here as they are occurring more frequently and most likely not diagnosed properly). Serum B12 levels should be checked, especially in those patients who present with other known neuropsychiatric features of vitamin B12 deficiency. Early withdrawal of antiepileptic drugs should be attempted as long-term antiepileptic use is not warranted and may be associated with adverse effects in such cases. Chronic carbamazepine therapy has been found to lower the levels of vitamin B12 and folate.

Intractable Epilepsy as the Presentation of Vitamin B12 Deficiency in the Absence of Macrocytic Anaemia

∗Meng Lee, ∗Hong-Shiu Chang, ∗Hsiao-Ting Wu, †Hsu-Huei Weng, and ∗Chiung-Mei Chen ∗Second Department of Neurology and †Department of Radiology, Chang Gung Memorial Hospital and College of Medicine, Chang-Gung University, Taipei, Taiwan
We report a patient with vitamin B12 deficiency presenting as intractable epilepsy in the absence of macrocytic anemia. The seizure attacks and all other symptoms/signs of vitamin B12 deficiency resolved after an intramuscular administration of cobalamin.

A 76-year-old man began to experience frequent generalized tonic–clonic seizures 3 years before visiting our hospital. The frequency was ∼3–5 times monthly. The initial investigations in a local hospital were normal except for mild normocytic anemia. He was diagnosed with epilepsy of an unknown etiology, and phenytoin (PHT), 300 mg once daily, was given to prevent seizure recurrence. In spite of a plasma drug concentration of 15.4 µg/ml (target concentration, 10–20 µg/ml), the frequency of seizures was still ∼3–5 times monthly. Valproate (VPA), 500 mg twice daily, was added, but without an improvement in seizure control.

One year later, he felt numbness at the plantar area of both feet. The abnormal sensation ascended to the knees within a few months. Because of these problems, he was admitted to our hospital in March 2003. The laboratory survey showed a low cobalamin serum level of 55 pg/ml (normal, 160–970 pg/ml). Homocysteine was elevated to 175.5 µM (normal,

04/30/2026

B12 Deficiency in Children

Note: Before the 1970s, there was relatively little research specifically focused on vitamin B12 deficiency itself. However, pernicious anaemia was already a well-recognized disease, even though its connection to vitamin B12 deficiency was not always fully appreciated in clinical practice. Much of the earlier medical literature discussed pernicious anaemia rather than “B12 deficiency,” because pernicious anaemia was the classic and most recognized cause of severe B12 deficiency at the time. Therefore, when searching older medical articles or historical research, it is often more useful to search for pernicious anaemia (or pernicious anemia) rather than vitamin B12 deficiency.

The UK NICE guidelines for B12 Deficiency and Folate deficiency failed to provide guidance for children beneath 16 years, hence we now have doctors believing that B12 deficiency and or pernicious anaemia cannot occur in children. Doctors fail to read research because the first case of Juvenile Pernicious Anaemia was diagnosed in 1937, so how can they say it cannot occur. According to the UCLA Department of Medicine, the first case of Juvenile Pernicious Anaemia was reported in 1937, long before the discovery of cyanocobalamin.

"The disease is essentially one of old people, but it occurs occasionally in children. We have ourselves described a 10-year old girl with this disease (14) and Chanarin (2) mentions several pediatric cases. Congenital IF deficiency (IFD) has been known since at least 1937 (56). The gastric IF gene GIF had long been postulated to be implicated in IFD (57), and the defect was expected “to reflect the usual spectrum of nonsense and missense changes” (58). In 2004, the first GIF mutation was described (59) and a larger series of cases was identified by linkage analysis."
https://pmc.ncbi.nlm.nih.gov/articles/PMC3152595/

It is important that a diagnosis is made early, particularly for infants who may be deficient because the mother is breast feeding and the mother, herself, has an undiagnosed B12 deficiency. Of if the mother has pernicious anaemia via antibodies to intrinsic factor and those antibodies have crossed the wall of the placenta, leaving the baby lacking intrinsic factor. Or if you notice your child is feeling more tired and grumpy than usual, losing his/her appetite and just overall not feeling well. If there is a history of pernicious anaemia in the family or if you remember a distant relative having to get some kind of injections, then investigate by having B12 tested.

The authors of a paper published in February 2026 state that an early diagnosis in children is crucial because of global developmental delay (GDD) in infancy and early childhood.

Abstract
Background: Vitamin B12 deficiency is a recognized but frequently under-integrated cause of global developmental delay (GDD) in infancy and early childhood. Early diagnosis is critical because neurological impairment may be partially or completely reversible with timely treatment.

Conclusions: Targeted assessment of vitamin B12 status in children with GDD, together with evaluation of maternal status, represents a clinically relevant approach to identifying a potentially preventable and treatable cause of neurodevelopmental impairment. Integration of functional biomarkers into diagnostic pathways and the development of pediatric-specific reference standards are key priorities for future research and clinical practice.
https://www.mdpi.com/2072-6643/18/7/1098

If you think your child has b12 deficiency, have your child tested. If baby is young and you do not want to subject your infant to a blood draw, the uMMA test is very specific and accurate to diagnose a B12 deficiency. However, a serum B12 test will still have to be done as the uMMA test can only determine a B12 deficiency, it cannot tell you how deficient your child is.
Look at the photo for some of the symptoms of B12 deficiency in a baby or young child. In addition to the symptoms in the photo,
Further insist on testing if the child
• Has undergone any surgery (including dental surgeries) involving nitrous oxide. This substance, used as an anaesthetic agent and often administered during dental work or surgeries, such as insertion of ear tubes in children with chronic ear infections, can inactivate the body’s stores of B12 and cause severe neurological damage.
• Exhibits failure to thrive (poor appetite), poor growth and/or weight gain, general poor health
• Has a diagnosis of autism, mental retardation, developmental delay, learning disability, or neurological disorder
• Has severe food allergies or sensitivities
• Is diagnosed with Coeliac disease or gluten enteropathy
• Has a thyroid or other autoimmune disorder
• Has suffered a stroke or is diagnosed as having atherosclerosis
• Is diagnosed with any psychiatric or behavioural disorder of problem (schizophrenia, depression, bipolar disorder, suicidal behaviour, conduct disorder, anxiety disorder, attention deficit hyperactivity disorder.

04/29/2026

A Brief Overview of the Diagnosis and Treatment of Cobalamin (B12) Deficiency

I keep talking about symptoms because so many are overlooked. Our body fools us at times and tries to cover up symptoms by over compensating in other areas. I will also promote articles that make common sense as to why oral B12 tablets, spray and sublingual are not a replacement for B12 injections. A doctor in the Netherlands, Dr. Bruce H R Wolffenbuttel is a staunch B12 supporter. His medical field is endocrinology and the metabolic process of B12 overlaps in this field. He has published some excellent articles on B12 Deficiency.

Sentences of interest from the following article.
- Diagnosis is often difficult due to diverse symptoms, marked differences in diagnostic assays’ performance and the unreliability of second-line biomarkers, including holo-transcobalamin, methylmalonic acid and total homocysteine.
- Clinical and patient experience strongly suggests that up to 50% of individuals require individualized injection regimens with more frequent administration, ranging from daily or twice weekly to every 2-4 weeks, to remain symptom-free and maintain a normal quality of life.
- ‘Titration’ of injection frequency based on measuring biomarkers such as serum B12 or MMA should not be practiced. There is currently no evidence to support that oral/sublingual supplementation can safely and effectively replace injections.
- In the case of B12 malabsorption, intramuscular injections of B12 are mandatory.
- symptoms may also be present in individuals with serum B12 above 148 pmol/L. Deficiency is therefore easily overlooked when total serum B12 is used as a the only status marker.
- Importantly, once started, B12 administration should be maintained for life.
- This whole paragraph is of interest to those who think oral B12 is effective. “Since the 1990s, the use of oral instead of parenteral administration of B12 has been hotly debated. It was suggested that passive absorption of B12 is about 1% to 2% of any oral dose. Hence, the use of sufficiently high doses (2000mg) could result in up to 10 to 20 micrograms absorbed daily,73 and this could allow serum B12 concentrations to normalize. However, early studies have shown that passive B12 absorption varies considerably between individuals, and may only be 0.1% to 0.5% in a significant proportion of patients.8
- Moreover, most studies assessing the effects of oral B12 supplementation focused on normalizing serum B12 concentrations, while the specific goal of treatment is alleviating symptoms. This is why we have so much difficulty getting a doctor to listen to us. As long as your B12 level is normal, it doesn’t matter if you have to crawl in to your doctor’s office on hands and knees, symptoms are still ignored.

Background: An increasing number of adult individuals are at risk of vitamin B12 deficiency, either from reduced nutritional intake or impaired gastrointestinal B12 absorption.

Objective: This study aims to review the current best practices for the diagnosis and treatment of individuals with vitamin B12 deficiency.

Results: Prevention and early treatment of B12 deficiency is essential to avoid irreversible neurological consequences. Diagnosis is often difficult due to diverse symptoms, marked differences in diagnostic assays’ performance and the unreliability of second-line biomarkers, including holo-transcobalamin, methylmalonic acid and total homocysteine. Reduced dietary intake of B12 requires oral supplementation. In B12 malabsorption, oral supplementation is likely insufficient, and parenteral (i.e. intramuscular) supplementation is preferred. There is no consensus on the optimal long-term management of B12 deficiency with intramuscular therapy. According to the British National Formulary guidelines, many individuals with B12 deficiency due to malabsorption can be managed with 1000 mg intramuscular hydroxocobalamin once every two months after the initial loading. Long-term B12 supplementation is effective and safe, but responses to treatment may vary considerably. Clinical and patient experience strongly suggests that up to 50% of individuals require individualized injection regimens with more frequent administration, ranging from daily or twice weekly to every 2-4 weeks, to remain symptom-free and maintain a normal quality of life. ‘Titration’ of injection frequency based on measuring biomarkers such as serum B12 or MMA should not be practiced. There is currently no evidence to support that oral/sublingual supplementation can safely and effectively replace injections.

Conclusions: This study highlights the interindividual differences in symptomatology and treatment of people with B12 deficiency. Treatment follows an individualized approach, based on the cause of the deficiency, and tailored to help someone to become and remain symptom-free.

A Brief Overview of the Diagnosis and Treatment of Cobalamin (B12) Deficiency
Bruce H. R. Wolffenbuttel, MD, PhD1 , Andrew McCaddon, MD, PhD2 , Kourosh R. Ahmadi, PhD3 , and Ralph Green, MD, PhD4

The full article is well worth reading and can be read at this link.
https://www.researchgate.net/publication/382172337_A_Brief_Overview_of_the_Diagnosis_and_Treatment_of_Cobalamin_B12_Deficiency