The timeframe for observing the effects of vitamin B12 supplementation varies depending on the individual’s deficiency level, the mode of administration (oral, injection), and the underlying cause of the deficiency. Individuals with severe deficiencies may experience noticeable improvements within days or weeks, while those with milder deficiencies might require a longer period to perceive any tangible benefits. The specific timeline depends on the body’s ability to absorb and utilize the supplemented vitamin.
Adequate vitamin B12 levels are crucial for numerous bodily functions, including red blood cell formation, neurological function, and DNA synthesis. Addressing a B12 deficiency can lead to improvements in energy levels, cognitive function, and overall well-being. Historically, pernicious anemia, a condition caused by the inability to absorb B12, was a life-threatening ailment. The discovery and subsequent treatment of B12 deficiency have had a significant impact on public health.
The subsequent discussion will delve into the factors influencing the absorption and utilization of vitamin B12, the different methods of supplementation, and the typical timelines associated with each approach. Furthermore, it will address conditions that may impede B12 absorption and potentially prolong the time required to observe noticeable improvements.
1. Initial Deficiency Severity
The initial severity of vitamin B12 deficiency is a primary determinant of the time required to observe therapeutic effects following supplementation. The magnitude of the deficit directly influences the duration needed to replenish depleted B12 stores and subsequently reverse or mitigate the associated physiological impairments. For example, an individual presenting with severe neurological symptoms, such as paresthesia or cognitive dysfunction resulting from prolonged B12 deprivation, will generally require a more extended period of consistent supplementation before experiencing significant symptomatic relief compared to an individual with a milder, subclinical deficiency detected through routine blood work.
The underlying mechanism involves the saturation of various B12-dependent enzymatic pathways. In severe deficiencies, the body’s reserves are critically low, impairing vital processes like DNA synthesis and myelin formation. Supplementation initiates the replenishment of these reserves, but the restoration of optimal enzymatic function is a gradual process. Furthermore, the extent of cellular damage caused by prolonged deficiency also impacts the recovery timeline. For instance, if neurological damage is extensive, even with adequate B12 repletion, some symptoms might resolve slowly or incompletely. Individuals with milder deficiencies, having smaller deficits to overcome, may experience faster improvements in energy levels and overall well-being.
Therefore, accurately assessing the initial severity of a B12 deficiency is critical for establishing realistic expectations regarding the treatment timeline. It allows clinicians to tailor supplementation strategies and provide patients with informed prognoses. While prompt supplementation is crucial in all cases, the anticipated timeframe for observable benefits will inevitably vary depending on the pre-existing level of B12 depletion. Recognizing this relationship underscores the importance of early detection and intervention to minimize the potential for long-term complications and accelerate the recovery process.
2. Administration Route
The method of B12 administration significantly affects the time required for its therapeutic effects to manifest. Oral supplementation, while convenient, necessitates a functional intrinsic factor within the stomach for absorption in the ileum. This process can be compromised by factors such as atrophic gastritis, autoimmune disorders targeting intrinsic factor (pernicious anemia), or surgical removal of the stomach or ileum. Consequently, oral B12 may prove ineffective or require prolonged use to achieve adequate serum levels, especially in individuals with impaired absorption. Conversely, intramuscular B12 injections bypass the digestive system altogether, delivering the vitamin directly into the bloodstream. This route guarantees 100% bioavailability, leading to a more rapid elevation of serum B12 levels and, potentially, faster symptom resolution, particularly in cases of severe deficiency or malabsorption.
Sublingual administration presents another alternative, allowing B12 to be absorbed directly into the bloodstream through the mucous membranes under the tongue. This method avoids the intrinsic factor pathway but may still be less efficient than injections. Furthermore, the effectiveness of sublingual B12 can vary depending on the formulation and an individual’s ability to hold the tablet under the tongue long enough for adequate absorption. Real-world examples illustrate this point: Patients with pernicious anemia often require lifelong B12 injections to maintain adequate levels, as oral supplementation is unlikely to be sufficient. Similarly, individuals undergoing gastric bypass surgery frequently benefit from injectable B12 to circumvent absorption issues resulting from the altered digestive anatomy.
In summary, the choice of administration route is a critical factor influencing the timeline for B12 to exert its effects. While oral supplements are appropriate for individuals with normal absorption, intramuscular injections offer a more reliable and faster route to repletion in cases of malabsorption or severe deficiency. Understanding the limitations and advantages of each method allows for tailored treatment strategies that optimize therapeutic outcomes and minimize the time required to address B12 deficiency-related symptoms. This highlights the importance of carefully considering individual patient characteristics and underlying medical conditions when determining the most suitable B12 supplementation approach.
3. Absorption Efficiency
Absorption efficiency stands as a critical determinant in the timeline for observing the effects of vitamin B12 supplementation. The body’s capacity to extract and utilize B12 from ingested or administered sources directly influences the speed and extent of therapeutic response. Impaired absorption delays or diminishes the benefits, irrespective of dosage or administration route.
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Gastric Acid Production
Gastric acid facilitates the release of B12 from food-bound proteins, a crucial initial step in absorption. Conditions such as atrophic gastritis or the use of proton pump inhibitors (PPIs) reduce gastric acid production, hindering B12 liberation. This reduction extends the time necessary to replenish B12 stores, as a smaller proportion of ingested B12 becomes available for absorption. Elderly individuals, who often experience diminished gastric acid secretion, may require higher doses or alternative administration methods to achieve adequate B12 levels.
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Intrinsic Factor Availability
Intrinsic factor (IF), produced by parietal cells in the stomach, binds to free B12 and facilitates its absorption in the ileum. Pernicious anemia, an autoimmune condition targeting parietal cells or IF itself, leads to IF deficiency and severely impaired B12 absorption. In such cases, oral B12 supplementation is largely ineffective, and injectable B12 becomes necessary to bypass the IF-dependent absorption pathway, resulting in a more rapid and reliable increase in B12 levels.
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Ileal Function
The ileum, the terminal section of the small intestine, is the primary site of B12 absorption via the IF-B12 complex. Conditions affecting ileal integrity, such as Crohn’s disease or surgical resection, compromise B12 absorption, irrespective of IF availability. Individuals with these conditions may experience delayed or incomplete response to oral B12 supplementation and often require injectable B12 to circumvent the impaired ileal absorption, expediting the restoration of adequate B12 status.
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Transcobalamin II Capacity
Transcobalamin II (TCII) is a transport protein that carries B12 in the bloodstream to various tissues. Genetic variations or deficiencies in TCII can impair B12 delivery, even with adequate absorption from the gut or via injection. While less common, TCII deficiencies can slow the utilization of B12 by cells, potentially extending the time needed to observe therapeutic effects. Monitoring TCII levels can provide insights into the body’s capacity to effectively transport and utilize absorbed B12.
The interplay between these facets of absorption efficiency underscores the complexity of B12 metabolism and the variability in individual responses to supplementation. Addressing underlying factors that impair absorption, such as optimizing gastric acid production, bypassing IF-dependent pathways via injections, or managing ileal disease, can significantly influence the speed and completeness of B12 repletion. A comprehensive assessment of absorption efficiency is therefore essential for tailoring B12 supplementation strategies and accurately predicting the timeline for therapeutic benefits.
4. Individual Metabolism
Individual metabolism represents a crucial, yet often overlooked, factor influencing the timeframe for vitamin B12 supplementation to exert its effects. Metabolic processes dictate the rate at which the body processes, distributes, and utilizes B12, subsequently affecting the speed with which deficiency-related symptoms resolve. Variations in metabolic efficiency can therefore explain the diverse responses observed among individuals receiving similar B12 treatments.
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Genetic Polymorphisms in B12 Transport Proteins
Genetic variations affecting the function of transcobalamin II (TCII), the primary B12 transport protein, can significantly alter B12 delivery to tissues. Individuals with less efficient TCII variants may experience slower B12 uptake by cells, leading to a delayed response to supplementation, even with adequate serum B12 levels. Similarly, polymorphisms in other B12-related transport proteins, such as haptocorrin, can affect the bioavailability and distribution of B12 within the body, further influencing the response timeline. Identifying and understanding these genetic factors can provide insights into personalized B12 supplementation strategies.
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Methylation Cycle Efficiency
B12 plays a vital role in the methylation cycle, a fundamental metabolic pathway involved in DNA synthesis, neurotransmitter production, and detoxification. Variations in the efficiency of the methylation cycle, often influenced by genetic factors such as MTHFR polymorphisms, can affect B12 utilization. Individuals with less efficient methylation cycles may require higher B12 doses or specific forms of B12 (e.g., methylcobalamin) to overcome metabolic bottlenecks, thereby accelerating the restoration of optimal function and reducing the time to observe therapeutic benefits.
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Liver Function
The liver serves as a primary storage site for B12. Impaired liver function, due to conditions such as cirrhosis or fatty liver disease, can affect the storage and release of B12, influencing its availability to other tissues. Individuals with compromised liver function may experience delayed B12 repletion following supplementation, as the liver’s capacity to store and release B12 is diminished. This underscores the importance of assessing liver function when evaluating B12 status and treatment responses.
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Kidney Function
The kidneys play a role in the excretion of excess B12. Individuals with impaired kidney function may experience altered B12 clearance, potentially leading to higher serum B12 levels but not necessarily faster symptom resolution. Reduced kidney function might also affect the metabolism and utilization of B12 within renal tissues, influencing the overall therapeutic response. Monitoring kidney function is therefore relevant when assessing B12 status, particularly in individuals with renal disease.
These multifaceted aspects of individual metabolism highlight the complexity of B12 utilization and the variability in treatment responses. Factors ranging from genetic predispositions to organ function significantly influence the rate at which B12 exerts its therapeutic effects. Accounting for these individual metabolic characteristics is essential for tailoring B12 supplementation strategies, optimizing treatment outcomes, and providing realistic expectations regarding the timeline for symptom improvement. Comprehensive assessment encompassing genetic testing, liver and kidney function evaluation, and methylation cycle analysis can facilitate personalized approaches to B12 management, ultimately enhancing treatment efficacy and patient satisfaction.
5. Underlying Conditions
Pre-existing medical conditions exert a significant influence on the duration required for vitamin B12 supplementation to demonstrate efficacy. These conditions can impair B12 absorption, increase B12 requirements, or interfere with its metabolic utilization, thereby prolonging the time to observe therapeutic benefits. Recognizing these underlying factors is critical for tailoring treatment strategies and setting realistic expectations.
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Autoimmune Disorders
Autoimmune conditions, such as pernicious anemia (affecting intrinsic factor production) or autoimmune gastritis (damaging parietal cells), directly impede B12 absorption from the gastrointestinal tract. In these scenarios, oral B12 supplementation proves largely ineffective, necessitating intramuscular injections to bypass the impaired absorption pathway. Even with injections, the underlying autoimmune process can fluctuate, influencing the overall B12 status and potentially extending the timeframe for achieving and maintaining optimal levels. For instance, individuals with active autoimmune gastritis may experience intermittent improvements in B12 absorption, leading to variable responses to supplementation.
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Gastrointestinal Diseases
Conditions affecting the small intestine, such as Crohn’s disease, celiac disease, or small intestinal bacterial overgrowth (SIBO), can compromise B12 absorption by damaging the intestinal mucosa or interfering with intrinsic factor-B12 complex uptake. These diseases often lead to malabsorption syndromes, requiring higher B12 doses or alternative administration routes to compensate for the reduced absorption efficiency. Furthermore, active inflammation in the gastrointestinal tract can increase B12 requirements, further prolonging the time needed to replenish deficient stores. Real-world examples include patients with Crohn’s disease who require regular B12 monitoring and supplementation adjustments to maintain adequate levels despite ongoing treatment.
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Metabolic Disorders
Certain metabolic disorders, such as diabetes mellitus or chronic kidney disease, can affect B12 metabolism and utilization. Diabetes, particularly when poorly controlled, can impair B12 transport and increase its excretion, leading to lower B12 levels and a delayed response to supplementation. Chronic kidney disease can also affect B12 metabolism and increase the risk of deficiency, necessitating higher doses and closer monitoring. Furthermore, medications commonly used in these conditions, such as metformin for diabetes, can interfere with B12 absorption, further complicating the treatment response.
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Medications
The use of certain medications can significantly impact B12 absorption and metabolism, influencing the timeline for supplementation to take effect. Proton pump inhibitors (PPIs), commonly used for acid reflux, reduce gastric acid production, impairing the release of B12 from food-bound proteins. Metformin, a common diabetes medication, can interfere with ileal B12 absorption. Other medications, such as colchicine and neomycin, have also been linked to B12 malabsorption. Individuals taking these medications may require higher B12 doses or alternative administration routes to overcome the drug-induced absorption impairment, which will affect the time it takes for B12 supplementation to improve their levels. Monitoring B12 levels is crucial in individuals taking these medications to ensure adequate supplementation and minimize the risk of deficiency.
In summary, the presence of underlying medical conditions introduces significant variability in the time required for B12 supplementation to yield noticeable improvements. By carefully evaluating an individual’s medical history, assessing potential absorption impairments, and considering the impact of medications, clinicians can tailor B12 supplementation strategies to optimize treatment outcomes and provide patients with more accurate prognoses regarding the expected timeline for symptom resolution. This personalized approach acknowledges the complex interplay between underlying health status and B12 metabolism, ultimately leading to more effective and efficient management of B12 deficiency.
6. Form of B12
The specific form of vitamin B12 administered significantly influences the time required to observe therapeutic effects. Different B12 forms exhibit varying degrees of bioavailability, metabolic conversion requirements, and tissue utilization, directly impacting the rate at which B12 deficiency-related symptoms improve.
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Cyanocobalamin
Cyanocobalamin, a synthetic form of B12, is widely used in supplements and fortified foods due to its stability and cost-effectiveness. However, it requires conversion to methylcobalamin and adenosylcobalamin, the active forms of B12, within the body. This conversion process can be less efficient in some individuals, particularly those with genetic polymorphisms affecting methylation pathways or impaired liver function. Consequently, cyanocobalamin may exhibit a slower onset of action compared to pre-converted forms. For example, an elderly individual with reduced liver function may experience a delayed response to cyanocobalamin supplementation compared to a younger individual with normal liver function.
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Methylcobalamin
Methylcobalamin is a naturally occurring, biologically active form of B12. It is readily utilized by the body without requiring conversion, making it potentially faster-acting than cyanocobalamin. Methylcobalamin plays a crucial role in the methylation cycle, supporting neurological function and detoxification processes. Individuals with methylation defects or neurological symptoms may experience a more rapid improvement with methylcobalamin supplementation. For instance, a patient with peripheral neuropathy attributed to B12 deficiency might observe a quicker reduction in nerve pain with methylcobalamin compared to cyanocobalamin.
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Adenosylcobalamin
Adenosylcobalamin is another biologically active form of B12, primarily involved in energy production within mitochondria. It supports cellular function and is crucial for the conversion of methylmalonyl-CoA to succinyl-CoA, a key step in the citric acid cycle. Adenosylcobalamin is often used in combination with methylcobalamin to provide comprehensive B12 support. Deficiencies in adenosylcobalamin can manifest as fatigue and reduced energy levels. Supplementation with adenosylcobalamin, either alone or in combination, may lead to a faster improvement in energy production compared to cyanocobalamin alone.
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Hydroxocobalamin
Hydroxocobalamin is a naturally occurring form of B12 that is closely related to cyanocobalamin, methylcobalamin, and adenosylcobalamin. It possesses a high binding affinity to transport proteins, which leads to a longer retention time in the body. This can lead to more sustained B12 levels in the blood. It is often used for B12 injections and can be particularly effective in people with cyanide poisoning because it binds to cyanide in the blood and forms cyanocobalamin, which is then excreted in the urine. Hydroxocobalamin supplementation can result in a gradual and sustained increase in serum B12 levels.
The choice of B12 form therefore impacts the timeline for achieving optimal B12 status and experiencing symptom relief. While cyanocobalamin remains a cost-effective option, methylcobalamin and adenosylcobalamin may offer faster and more efficient repletion, particularly in individuals with specific metabolic challenges or neurological symptoms. Hydroxocobalamin can offer a longer, more sustained increase in B12 levels. Understanding the nuances of each B12 form enables clinicians to tailor supplementation strategies to individual patient needs, optimizing treatment outcomes and minimizing the time required to address B12 deficiency-related symptoms.
7. Dosage Consistency
Dosage consistency represents a fundamental factor influencing the timeframe for vitamin B12 supplementation to achieve its desired effects. Regular, uninterrupted administration of the prescribed B12 dosage is essential for maintaining stable serum B12 levels and facilitating the gradual replenishment of depleted tissue stores. Fluctuations in dosage, whether due to missed doses or inconsistent adherence to the treatment regimen, disrupt this process, prolonging the time required to observe noticeable improvements. This is because therapeutic efficacy hinges on achieving and sustaining a sufficient concentration of B12 within the body to support B12-dependent metabolic processes.
Intermittent B12 supplementation introduces variability in serum B12 levels, preventing the body from establishing a steady state. The erratic supply of B12 hinders the saturation of B12-dependent enzymes, delaying the restoration of optimal cellular function. For example, individuals prescribed weekly B12 injections who occasionally skip a dose will experience periodic declines in serum B12 levels. These declines interrupt the process of replenishing B12 stores in the liver and other tissues, extending the overall time needed to alleviate deficiency symptoms such as fatigue, cognitive dysfunction, or neuropathy. Similarly, inconsistent oral B12 supplementation can lead to fluctuations in absorption, further complicating the attainment of stable B12 levels. A person might be taking 1000 mcg of B12 supplement per day. However, their compliance might be on/off making the b12 level unstable and less predictable the time it would work effectively.
In summary, the importance of dosage consistency cannot be overstated. Consistent adherence to the prescribed B12 dosage ensures a steady supply of the vitamin, enabling the body to gradually replenish depleted stores and restore optimal metabolic function. While other factors such as absorption efficiency and individual metabolism play a role, dosage consistency provides the essential foundation for effective B12 supplementation. Practical significance lies in educating patients about the importance of adherence and providing strategies to maintain consistent dosing schedules. Addressing challenges related to adherence, such as pill burden or injection anxiety, can significantly improve treatment outcomes and minimize the time required to achieve the desired therapeutic benefits.
Frequently Asked Questions
The following questions address common concerns related to the timeframe for experiencing the benefits of B12 supplementation.
Question 1: How Long does it take b12 to work for energy levels?
The timeframe for experiencing improved energy levels following B12 supplementation is variable. Individuals with severe deficiencies may notice changes within a few weeks, while those with milder deficiencies might require several months to experience a tangible difference. Consistent supplementation and addressing underlying absorption issues are important.
Question 2: How Long does it take b12 to work on neurological symptoms?
The improvement of neurological symptoms, such as numbness or tingling, can be a prolonged process. Nerve regeneration is slow, and significant improvement may take several months, even with consistent B12 supplementation. Early intervention and addressing the underlying cause are critical for optimal outcomes.
Question 3: How Long does it take b12 to work with injections versus oral supplements?
B12 injections bypass absorption issues and deliver the vitamin directly into the bloodstream, generally leading to a faster response compared to oral supplements. While oral supplements may be effective for mild deficiencies, injections are often preferred for individuals with malabsorption issues or severe deficiencies.
Question 4: How Long does it take b12 to work if I have pernicious anemia?
Pernicious anemia, characterized by impaired intrinsic factor production, necessitates B12 injections for effective treatment. Oral B12 supplementation is typically insufficient. With consistent injections, improvements in red blood cell production and neurological function can be observed within weeks to months.
Question 5: How Long does it take b12 to work for mood and cognitive function?
The impact of B12 supplementation on mood and cognitive function varies. Some individuals may experience improvements in mood and concentration within a few weeks, while others may require a longer period. The presence of other contributing factors, such as stress or underlying mental health conditions, can influence the response.
Question 6: What factors influence How Long does it take b12 to work?
Numerous factors influence the time required for B12 supplementation to take effect, including the severity of the deficiency, the route of administration (oral vs. injection), underlying medical conditions, medication use, and individual metabolic factors. A comprehensive assessment is essential for tailoring supplementation strategies and setting realistic expectations.
The response to B12 supplementation is highly individualized and influenced by a multitude of factors. While some individuals experience rapid improvements, others may require a more extended period to observe tangible benefits. Consulting with a healthcare professional is crucial for determining the appropriate dosage, administration route, and monitoring B12 levels to optimize treatment outcomes.
The next section will address potential side effects associated with B12 supplementation and strategies for managing them effectively.
Maximizing B12 Supplementation Effectiveness
The following guidelines aim to optimize B12 supplementation strategies, potentially influencing the timeframe for observing positive effects.
Tip 1: Ascertain Baseline B12 Levels: Prior to initiating supplementation, measuring serum B12 levels is essential. This provides a reference point for monitoring treatment progress and determining the severity of the deficiency. Comprehensive testing, including methylmalonic acid (MMA) and homocysteine levels, can further assess B12 status.
Tip 2: Select Appropriate B12 Form: Consider the various forms of B12 available, such as cyanocobalamin, methylcobalamin, and adenosylcobalamin. Methylcobalamin, being the active form, may offer faster results for some individuals compared to cyanocobalamin, which requires metabolic conversion. Consulting with a healthcare provider is advised.
Tip 3: Optimize Administration Route: For individuals with suspected malabsorption, intramuscular B12 injections circumvent the gastrointestinal tract, ensuring direct delivery into the bloodstream. This approach can expedite B12 repletion and potentially reduce the time to symptom improvement.
Tip 4: Address Underlying Absorption Issues: Identify and address any underlying conditions that may impair B12 absorption, such as atrophic gastritis, Crohn’s disease, or celiac disease. Managing these conditions can improve B12 absorption efficiency and enhance the response to supplementation.
Tip 5: Maintain Dosage Consistency: Adhere to the prescribed B12 dosage consistently. Missed doses can interrupt the repletion process and prolong the time required to achieve optimal B12 levels. Implementing strategies to improve adherence, such as setting reminders, can be beneficial.
Tip 6: Monitor Medication Interactions: Be mindful of medications that may interfere with B12 absorption, such as proton pump inhibitors (PPIs) or metformin. If taking such medications, consider alternative B12 administration routes or discuss potential dose adjustments with a healthcare professional.
Tip 7: Evaluate Dietary Factors: While supplementation is often necessary, ensuring a diet rich in B12-containing foods, such as meat, fish, and dairy products (if tolerated), can support overall B12 status. For vegetarians and vegans, fortified foods or supplements are crucial.
Adhering to these strategies can potentially optimize B12 supplementation effectiveness, possibly influencing the timeframe for experiencing the benefits. Early diagnosis and intervention are crucial for maximizing outcomes.
The concluding section will summarize key findings and provide a final perspective on B12 supplementation.
Conclusion
The preceding discussion has explored the multifactorial nature of “how long does it take b12 to work”. The response to B12 supplementation is not a fixed entity, but rather a dynamic process influenced by the severity of the deficiency, the administration method, individual absorption efficiency, metabolic processes, pre-existing medical conditions, the form of B12 utilized, and adherence to a consistent dosage. Understanding these variables is paramount for tailoring effective treatment strategies and managing patient expectations.
Given the complex interplay of factors influencing B12 absorption and utilization, a personalized approach to supplementation is crucial. Healthcare professionals must conduct thorough assessments to identify the root cause of B12 deficiency and to implement appropriate interventions. Continued research and clinical vigilance are vital to refine B12 supplementation protocols and to improve outcomes for individuals with B12 deficiencies.
