Pernicious Anaemia/B12 Deficiency Support Group - Page

10/25/2025

An excellent article that every doctor should read. Moving this up from lower down the page.

https://www.facebook.com/PAB12DSupportGroupPage/posts/724632403031550

Excellent article on B12. One that you may want to show your doctor.

https://www.bmj.com/content/383/bmj-2022-071725

10/19/2025

Good article on how B12, folate and iron work together in the formation of red blood cells. Of interest, the iron clinic says the same thing about folate that I keep preaching about. Folate levels can drop quickly, if you are injecting daily or EOD and you do not supplement. Folate only stores for 4 months. B12 stores can last for years but you need intrinsic factor to access them.

"Vitamin B12 intake averages just 1 microgram daily, but liver stores (≈2–5 mg) can last for years, while folate stores deplete within months if intake falls."

How iron, folate, and vitamin B12 sustain red blood cell formation

Iron, folate, and vitamin B12 are essential nutrients that work together to make and mature red blood cells. Their metabolism is tightly controlled because even small deficiencies can impair oxygen delivery and DNA synthesis, leading to anemia.

1️⃣ Iron intake and absorption
Most adults need 10–20 mg of dietary iron per day, but only 3–15% is absorbed in the small intestine. Iron from meat (heme iron) is absorbed more efficiently than iron from plants (non-heme iron). Stomach acid helps convert ferric iron (Fe³⁺) to its absorbable ferrous form (Fe²⁺).
🟢 Example: Vitamin C enhances absorption by reducing Fe³⁺ to Fe²⁺, while phytates in grains or excess calcium reduce uptake.

2️⃣ Iron transport and storage
Once absorbed, iron binds to transferrin, the blood’s transport protein, and is delivered to tissues like the bone marrow for red blood cell production. Surplus iron is stored in the liver as ferritin and hemosiderin. The hormone hepcidin from the liver regulates iron export—high levels block release, preventing overload.
🟢 Example: In chronic inflammation, hepcidin rises, trapping iron in macrophages and leading to “anemia of chronic disease.”

3️⃣ Iron recycling
When red blood cells break down, macrophages in the spleen and liver recover the iron from hemoglobin and return it to circulation. This recycling process supplies most of the daily iron needed for new red blood cell formation.
🟢 Example: The body recycles about 25 mg of iron each day, far exceeding the amount absorbed from food.

4️⃣ Folate and vitamin B12 absorption
Folate is absorbed in the small intestine, while vitamin B12 requires intrinsic factor from the stomach for uptake in the ileum. Both nutrients are stored in the liver and used for DNA synthesis in developing red blood cells.
🟢 Example: Vitamin B12 intake averages just 1 microgram daily, but liver stores (≈2–5 mg) can last for years, while folate stores deplete within months if intake falls.

5️⃣ Shared role in erythropoiesis and DNA synthesis
Inside bone marrow, folate and B12 cooperate to generate tetrahydrofolate, a cofactor for DNA and red cell production. Without them, cells enlarge without dividing properly, producing megaloblastic anemia.
🟢 Example: B12 deficiency traps folate in its inactive form (“methyl-folate trap”), halting DNA replication and leading to fatigue, pale skin, and neurological symptoms.

Efficient red blood cell production depends on the seamless interaction between iron supply, folate metabolism, and vitamin B12 activation. When any link in this triad breaks, oxygen transport falters and anemia develops—a sign that cellular energy and repair are being starved at the molecular level. #

10/18/2025

Vitamin B12 Levels Association with Functional and Structural Biomarkers of Central Nervous System Injury in Older Adults

Abstract
Objective
Vitamin B12 (B12) plays a critical role in fatty- and amino-acid metabolism and nucleotide synthesis. While the association between B12 deficiency and neurological dysfunction is well-known, the exact threshold for adequacy remains undefined in terms of functional impairment and evidence of injury. The objective was to assess whether B12 levels within the current normal range in a cohort of healthy older adults may be associated with measurable evidence of neurological injury or dysfunction.

Methods
We enrolled 231 healthy elderly volunteers (median age 71.2 years old) with a median B12 blood concentration of 414.8 pmol/L (as measured by automated chemiluminescence assay). We performed multifocal visual evoked potential testing, processing speed testing, and magnetic resonance imaging to assess neurological status. Moreover, we measured serum biomarkers of neuroaxonal injury, astrocyte involvement, and amyloid pathology.

Discussion
Our results suggest that in a cohort of healthy elderly individuals, lower B12 associates with a delay in VEP latency, and that it is specific to the biologically available fraction of serum B12 bound to transcobalamin (Holo-TC). Low levels of Holo-TC also associate with slowed spatial processing speed in an age-dependent manner. On MRI, participants with lower Holo-TC have a higher burden of T2 WMH. Remarkably, we find that high levels of Holo-HC, the biologically unavailable fraction of B12, associate with an increase in the levels of T-Tau proteins in the serum, a biomarker for neurodegeneration. These findings suggest that current parameters for defining adequate B12 levels may be inappropriate when considering neurophysiological, neuropsychological, serological, and neuroradiological outcomes.

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Sentences from above article of interest (PK)
• The plaques seen in Alzheimer's disease contain hyperphosphorylated Tau proteins, and B12 plays a role in preventing these aggregations by inhibiting the fibrillization of Tau.59, 60

• Therefore the retention of vitamin B12 by haptocorrin may decrease the bioavailability of B12 in the brain thus favoring Tau-mediated neuronal injury. Haptocorrin is a glycoprotein that binds to vitamin B12 (cobalamin) in the stomach and other secretions, protecting it from degradation and assisting its absorption in the intestine. Also known as transcobalamin, it is a major carrier of vitamin B12 in the blood, acting as a temporary storage molecule.
• Another element of the underlying mechanism for our observed effects may lie in the genetic variability for B12-related proteins, for example, the transcobalamin 1 (TCN1) and 2 (TCN2) gene variants, which may affect the levels of B12 measured in the blood between individuals and affect cognitive outcome as previously shown
• Our findings are of critical importance for rethinking the “biologically sufficient” B12 levels. The population-based studies that defined healthy micronutrient levels may have missed the subclinical manifestations of low or high B12 at the extremes of the population distribution that can affect people without causing overt symptoms. While the clinical features of unambiguous B12 deficiency are well defined as predominantly hematological (most conspicuously macrocytic anemia) and neurological, the condition can manifest with either hematological or neurological syndromes in isolation.
• Without sensitive tools to detect subtle neurological deficits, the heterogeneous nature of the symptoms remained unexplained. Notably, during and following B12 repletion therapy, patients often request higher dosing of B12 to treat their neurological symptoms, even after their hematological symptoms have resolved.62 Our findings support the idea that subtle neurological deficits manifest at higher levels than the current threshold defined for deficiency, and most importantly, it could provide an explanation for the often-reported discrepancy between hematological and neurological symptoms.
• Revisiting the definition for healthy B12 levels could promote earlier intervention and prevention of cognitive decline, especially in the elderly carrying increased risk for B12 malabsorption and insufficiency.67, 68 A study on an aging population previously argued for a broadening of the reference range for B12 levels in elder people, and our results further support such a shift to account for age.69 The elderly population may be particularly vulnerable to the effects of declining B12 availability and may benefit from a change in guidelines for what is currently defined as healthy levels of vitamin B12.
• The theoretical model we are proposing with this work is that inadequate amounts of vitamin B12 could induce neurological deficits at a threshold that is higher than the one in current use (Graphical abstract). Moreover, we should work on defining a cutoff for higher B12 and study how haptocorrin might be associated with or could induce neuro-axonal damage. Accordingly, our current understanding of optimal serum B12 may have to be revisited to account for the clinical manifestations of B12 inadequacy at both ends of the spectrum.
End of notes - PK
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We all know the reference ranges for B12 are too low. We also know that when neurological damage has occurred, a higher B12 level is needed to help heal the symptoms. Maintenance dosage of either hydroxocobalamin or cyanocobalamin is just not sufficient to heal neurological symptoms. This paper suggests that B12 needs to be revisited and a clear definition of a cutoff for higher B12. It further suggests that Haptocorrin should be studied to find out if Haptocorrin could induce neuro-axonal damage.

Full article available at the link below…a pdf can be saved from the site.

At low levels of B12, specifically when bound to transcobalamin for cellular uptake, evidence of slower conductivity in the brain could point toward impaired myelin. At high levels of B12, specifical...

10/13/2025

Parkinson's disease and vitamins: a focus on vitamin B12

Abstract

Parkinson’s disease (PD) has been linked to a vast array of vitamins among which vitamin B12 (Vit B12) is the most relevant and often investigated specially in the context of intrajejunal levodopa infusion therapy. Vit B12 deficiency, itself, has been reported to cause acute parkinsonism. Nevertheless, concrete mechanisms through which B12 deficiency interacts with PD in terms of pathophysiology, clinical manifestation and progression remains unclear. Recent studies have suggested that Vit B12 deficiency along with the induced hyperhomocysteinemia are correlated with specific PD phenotypes characterized with early postural instability and falls and more rapid motor progression, cognitive impairment, visual hallucinations and autonomic dysfunction. Specific clinical features such as polyneuropathy have also been linked to Vit B12 deficiency specifically in context of intrajejunal levodopa therapy. In this review, we explore the link between Vit B12 and PD in terms of physiopathology regarding dysfunctional neural pathways, neuropathological processes as well as reviewing the major clinical traits of Vit B12 deficiency in PD and Levodopa-mediated neuropathy. Finally, we provide an overview of the therapeutic effect of Vit B12 supplementation in PD and posit a practical guideline for Vit B12 testing and supplementation.
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PK Notes: From the Abstract
"Vit B12 deficiency, itself, has been reported to cause acute parkinsonism"
Acute Parkinsonism is defined as a rare, yet critical, movement disorder emergency defined by the subacute to acute onset of core parkinsonian features, including bradykinesia and muscular rigidity, evolving over a timeframe ranging from minutes to week.

Bradykinesia is a symptom of slowness of movement, which can make voluntary and automatic motions slower and harder to perform. It is a key feature of Parkinson's disease but can also be caused by certain medications. Symptoms include reduced movement amplitude, difficulty with fine motor tasks, and changes in facial expression and speech. (PK)There is no mention of vitamin B12 deficiency as a cause in this definition.
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Introduction
Parkinson’s disease (PD) is a multicomplex, multi-neurotransmitter, progressive chronic disease which encompasses not only motor features (such as bradykinesia, rigidity, tremor, and gait disturbance) but also nonmotor features (including constipation, neuropathy, pain, and cognitive decline (Sauerbier et al. 2016).The exact pathophysiology of PD is likely multifactorial amongst which oxidative stress, neuroinflammation and mitochondrial dysfunction may play a role in the development and progression of PD. The involvement of vitamins and minerals in the context of PD is not well understood however, vitamins are micronutrients playing a pivotal role in neurogenesis, neurotransmission, and housing antioxidative properties essential in maintaining homeostasis within the body and brain (Kumar et al. 2022; Rai et al. 2021).

Vitamins are classified as either being fat-soluble or water-soluble vitamins. Fat soluble vitamins, vitamins A (Vit A), D (Vit D), E (Vit E), and K (Vit K), mainly bind to cellular nuclear receptors with the ability to affect the expression of certain genes (Chawla and Kvarnberg 2014, Pignolo et al. 2022). Water soluble vitamins, vitamin C (Vit C) and B-complex vitamins including vitamins B6 (Vit B6), B12 (Vit B12), and folate, affect enzymatic activity by acting as cofactors (Chawla and Kvarnberg 2014). Given the importance of vitamins in the function of the human body and its development, vitamin deficiencies can manifest with significant clinical symptoms and syndromes. Specific vitamin deficiencies can particularly manifest as parkinsonism features.

Conclusions
Compelling evidence has been provided pinpointing that Vit B12 effectively hinders the formation of αSN fibrils and reduces neuronal cytotoxicity. Such conclusion was mainly established based on animal models of PD and invitro experiments. Furthermore, the question whether Vit B12 should be considered as symptomatic treatment in PD or as a disease modifying therapy remains triggering and unresolved. Thus, it is essential to approach such hypothesis with caution and aim to demonstrate it in case–control studies including PwPD. As for clinical correlates, Vit B12 deficiency and HHcy do predict more rapid motor progression and cognitive dysfunction among PwPD and thus modulate PD clinical phenotypic variability. We highlighted that PN is an underestimated problem among PwPD, especially among those receiving LCIG infusion. It remains crucial to regularly warrant a close monitoring of Vit B12, Hcy and MMA as well as the nutritional status of PwPD in general. We provided a guideline detailing the key aspects of managing LCIGtreated PwPD. In this context, the subcutaneous LDopa infusion pump could offer an intermediate approach between the two conventional administration routes of LDopa, potentially mitigating some side effects. Finally, while Vit B12 supplementation has practical implications in neurological diseases and seems to yield benefits in PD, the dearth for comprehensive understanding surrounding its CNS bioavailability and mechanisms of action presents an obstacle to elucidate among PD patients. As we move forward, it becomes increasingly evident that further interventional studies are essential to provide evidence-based valuable insights and recommendations regarding the monitoring of Vit B12 deficiency and its biomarkers and to establish accurate guidelines for Vit B12 supplementation in PD.
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Conclusion states that PD patients should be given B12 Supplementation.

The full article can be read at the link below. It is a very interesting article describing vitamin B12's role in Parkinson's Disease.

10/10/2025

09/30/2025

End of B12 Awareness Month

As B12 Awareness Month draws to a close, it is an important time to reflect on the ongoing struggles faced by those with Pernicious Anaemia and or B12 deficiency, particularly concerning the medical community's persistent failure to recognize and adequately treat the condition. All too often, patients present with debilitating symptoms of neurological damage, from tingling and numbness to cognitive impairment and balance issues, only to have their concerns dismissed or misdiagnosed.

The standard "one-size-fits-all" approach, which often involves minimal, maintenance dosage injections, proves woefully inadequate for many. This rigid adherence to a "starvation dosage" not only fails to halt the progression of neurological damage but also prevents any hope of improvement, as it ignores the fundamental truth that each individual's body has unique requirements for this vital nutrient. The current paradigm traps patients in a cycle of suffering, forcing them to navigate a system that often prioritizes rigid guidelines over individual patient needs. This must change. The guidelines must change to reflect individual requirements as opposed to “one size fits all”. The guidelines must also reflect symptom response. Doctors have to re-learn to put their patient first and not rely on blood test results that cannot determine a response to symptoms. Doctors, please listen to your patients.

I would also like to acknowledge two long time B12 advocates, Sally Pacholok and Jeff Stuart. Sally and Jeff’s books, the “Could it be B12” are a must read for any PA or B12 Deficient individual. Sally and Jeff have been promoting awareness of B12 in the United States for many years. Sally is an an ER nurse and in the early days of advocating about B12, suffered the consequences of being served with a Court Order, obtained by her employer, prohibiting her from speaking to any patient about B12, I am honoured to be friends with Sally and Jeff.
https://www.youtube.com/watch?v=OvMxJ6GRBNQ&list=PLkScFRcnM8K90GWzoBzIoFCfdAMlCr22O&index=1&t=34s
This is a link to their Awareness Site:
https://b12awareness.org/

However, in the midst of this frustration, we must also acknowledge the small but growing number of exceptional doctors who are challenging the status quo. These compassionate and forward-thinking practitioners listen to their patients, truly hearing their stories of persistent symptoms and recognizing the profound impact of B12 deficiency on their lives. They understand there is no harm in providing more frequent B12 injections when a patient's symptoms and personal history indicate a need for it. These doctors are not just treating a number on a lab report; they are treating a person and their unique constellation of symptoms. A heartfelt shoutout goes to these medical allies who demonstrate true patient-centered care and offer a beacon of hope to those who have felt abandoned by the system. Their willingness to deviate from the rigid protocol and trust their patients' lived experiences is a testament to what healthcare should be: a partnership built on trust, empathy, and a shared goal of restoring health and well-being. These doctors are very rare but they do exist.

Finally, a big thank you to each and everyone of you who shared posts, photos and notices from this page. It did make a difference. There were 1,603,907 views of this page this month and many were from non followers. This means that by sharing information, we did reach an audience that may have not known very much about B12. Thank you again

Over the next year, I am truly hoping for change to benefit all of us.
Pat Kornic

Raising awareness to the dangers of vitamin B12 deficiency by reeducating the medical community and educating the public. Promoting early diagnosis and treatment preventing neurologic injury, disability, poor outcomes, and premature death.

09/29/2025

Credit to Sally Pacholok