1. Why B12 Brain Fog Happens Even With “Normal” Levels
What if your blood test says your B12 is fine—but your brain is already slowing down?
For millions of adults, especially over 50, this isn’t hypothetical.
Research is uncovering that even within the so-called “normal range,” low B12 levels can already be impacting the brain’s white matter, reducing processing speed, and accelerating cognitive aging. You might still be functional on paper—but deficient where it matters most: your brain.
You might have the vitmain B12 deficiency brain fog—a subtle but real signal that cognitive function is already slipping.
Vitamin B12 is best known for preventing anemia and supporting energy production. But its role in brain health runs much deeper. It helps maintain the protective myelin sheath around neurons, supports neurotransmitter synthesis, and enables the DNA methylation required for healthy brain function.
Without it, memory falters. Processing slows. Brain tissue shrinks.
And yet, the clinical threshold for deficiency remains based on outdated population averages—not on neurological & brain health outcomes.
In this article, we’ll look at new science that challenges these outdated definitions.
You’ll see how even moderate B12 levels—well within the “normal” range—have been linked to structural brain changes, vitamin B12 dementia risk, and cognitive impairment.
We’ll also explore the gap between total B12 and its functional form, holo-transcobalamin, and why standard blood panels often miss early decline.
In Part 2, I’ll share how to test your B12 status the right way, what markers matter most, and how my own B12 levels zigzagged dangerously—until I changed how I approached testing and supplementation.
But first, here’s the study that made us rethink what “normal” B12 really means—especially when it comes to brain health.
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2. The UCSF 2025 Study: B12 Brain Fog and White Matter Loss at Normal B12 Levels
In early 2025, researchers at UC San Francisco published a landmark study that directly challenges how we define “normal” vitamin B12 levels—especially when it comes to brain health.
The study followed 231 healthy older adults (average age 71). Only two had B12 levels below the conventional deficiency cutoff of 148 pmol/L, but their functional markers were normal, so they were included in the analysis. The median B12 level across the cohort was 414.8 pmol/L, with an interquartile range of 282.7 to 557.0 pmol/L—indicating that while most were well above the clinical cutoff, some still fell into a lower-normal range.
And yet, the results showed something concerning: even within that range, people with lower B12 had measurable signs of neurological damage.
Participants with lower levels of active B12—specifically holo-transcobalamin, the form actually usable by cells—performed worse on cognitive tests, had slower visual processing speeds, and showed more white matter hyperintensities (WMH) on brain MRI scans—patterns often linked to what people describe as B12 brain fog in early cognitive decline.
These white matter changes are linked to dementia risk, stroke, and long-term cognitive decline.
Meanwhile, higher levels of holo-haptocorrin—an inactive form of B12 that builds up when B12 transport is impaired—were associated with elevated levels of Tau, a known marker of neurodegeneration.
🧠 Key takeaway: Even when total B12 looks adequate, the brain may already be underperforming if the active fraction is too low or if transport pathways are impaired.
What this study revealed is that total serum B12 alone is a poor predictor of brain health and neurological risk. Two people can have the same B12 level—yet one may already show signs of cognitive decline while the other remains neurologically intact.
The authors emphasized the need to revisit clinical thresholds and argued that functional B12 status—not just total concentration—should guide care, especially in older adults.
This shift in perspective has real implications for longevity & cognitive performance.
Someone with a B12 level of 400 or even 500 pmol/L could still be losing white matter, slowing cognitively, and heading toward preventable decline.
And unless they’re asking their doctor to check markers like holo-transcobalamin or homocysteine—or testing for them directly—it might not be caught in time to prevent cognitive decline, vitamin B12 dementia or long-term white matter loss.
(By the way, Vitamin D can drive similar brain changes through a different mechanism—chronic inflammation and calcium imbalance. If you’re exploring other nutrient-related risks for cognitive decline, I’ve broken that down here.)
3. How Does Vitamin B12 Support Brain Health and Prevent Brain Fog?
Vitamin B12 is essential to brain function—not just as a metabolic cofactor, but as a structural and regenerative nutrient.
Its most critical neurological role is in maintaining and repairing the myelin sheath, the protective layer surrounding nerve fibers. This sheath allows electrical signals in the brain to travel quickly and accurately. When vitamin B12 is insufficient, the insulation deteriorates, signal conduction slows, and—over time—b12 brain fog symptoms like memory lapses or mental sluggishness may emerge.
The consequences of low vitamin B12 show up across the lifespan.
In infants, deficiency can derail brain development.
One case study described a 14-month-old child of vegetarian parents who presented with profound hypotonia, developmental delay, and visible brain atrophy. MRI scans revealed severe myelination deficits—later reversed following B12 repletion. The child’s motor skills and cognition improved in parallel with structural recovery on imaging.
In adults, B12 continues to play a regenerative role.
Studies on traumatic brain injury (TBI) in animal models show that B12 promotes remyelination, restoring structural integrity to white matter and boosting the expression of myelin proteins like MBP. These effects were dose-dependent and enhanced further when combined with treatments that reduced endoplasmic reticulum stress. In other words, B12 didn’t just slow damage—it supported visible tissue repair.
This regenerative support also extends to the peripheral nervous system.
Here, vitamin B12 works in concert with thiamine (vitamin B1) and pyridoxine (vitamin B6) to direct the response to nerve injury. Together, these neurotropic B vitamins protect neurons from oxidative damage, stabilize neurotransmitter function, and promote the regrowth of damaged axons and myelin. When this system is under strain—whether due to age, inflammation, or deficiency—the nervous system may default to Wallerian degeneration, a breakdown pathway seen in neuropathy. But when B1, B6, and B12 are sufficient, the process can shift back toward nerve regeneration.
These mechanisms also shape long-term brain health & cognitive resilience.
Specifically, vitamin B12 supports DNA methylation and neurotransmitter synthesis—both essential for memory, focus, and neural repair. Without enough B12, these processes gradually erode. Early signs of dysfunction, like B12 brain fog related signs including slower thinking or trouble concentrating, often appear before traditional deficiency thresholds are crossed.
One of the markers of this process is white matter hyperintensity (WMH)—lesions on brain MRI that increase with age and are closely tied to cognitive slowing, B12 brain fog and dementia risk. In the UCSF 2025 study, researchers found that total B12 wasn’t predictive of WMH volume. What mattered was the level of holo-transcobalamin, the active form of B12 delivered to cells. Lower Holo-TC was associated with a higher burden of these white matter lesions (panels B and C).
That distinction is important.
Even if a lab report shows a “normal” B12 level, a lack of active B12 at the cellular level can still leave the brain vulnerable.
Understanding that gap—between total and functional B12—is essential for protecting the longevity of cognitive performance & long-term brain health. And when it comes to vitamin B12 brain health, functional markers like holo-transcobalamin are key.
🧠 Think Your B12 Is “Normal”? Your Brain Might Disagree.
Even with “normal” levels, early decline can start.
This panel tests what standard labs miss—so you can act before symptoms escalate.
4. Other Research on Vitamin B12 Dementia Risk, Memory and Brain Fog
Beyond structural brain changes, researchers have begun to map how vitamin B12 status—particularly its active and inactive forms—tracks with biomarkers of neurodegeneration.
In the same 2025 UCSF study, investigators went further by measuring a panel of well-established markers tied to Alzheimer’s risk, neuronal damage, and glial activation. Their goal: to understand whether subtle imbalances in B12 metabolism could leave a biochemical fingerprint long before clinical symptoms appear
B12 and Brain Fog: How Functional Deficiency Links to Vitamin B12 Dementia
As part of their investigation, the UCSF researchers measured a panel of biomarkers tied to early neurodegeneration and Alzheimer’s risk—including markers of tau pathology, axonal damage, and glial activation.
These included:
- T-Tau: a marker of neurofibrillary degeneration
- UCH-L1: a marker of neuroaxonal injury
- GFAP: reflecting astrocyte activation
- Aβ42/Aβ40 ratios: associated with amyloid plaque risk in Alzheimer’s
- NfL: indicating axonal damage
When B12 fractions were analyzed:
- Total B12 correlated positively with T-Tau
- Holo-HC (the inactive haptocorrin-bound B12) also showed a strong positive association with both T-Tau and UCH-L1
- Holo-TC (the active B12 fraction) showed no significant association with neurodegenerative markers
This implies that an elevation in total B12—when skewed toward inactive forms—might track with increased neuronal stress, rather than protection, and can explain why vitamin B12 and brain fog can appear even when blood levels seem fine. In essence, high B12 doesn’t always mean effective B12, especially in aging adults where transport and uptake pathways may be compromised.
Vitamin B12 Dementia: Cognitive Impairment and Decline That Looks Like Aging
A separate multicenter study looked at 202 patients with mild cognitive impairment who also had biochemical signs of B12 deficiency.
Participants were stratified by severity of deficiency:
- Moderate (100–200 pg/mL): 56%
- Mild (200–350 pg/mL): 28.7%
- Severe (50–100 pg/mL): 15.3%
A key finding: homocysteine levels were elevated in the majority of these patients:
- 21% had levels >20 µmol/L
- 50% were in the 15–20 µmol/L range
These elevations matter. Homocysteine is a methylation byproduct that accumulates when vitamin B12 is too low to support normal cellular function—even if serum B12 appears “borderline.” High homocysteine is a red flag for functional B12 deficiency, and it’s strongly linked to brain shrinkage, white matter damage, and accelerated cognitive decline, a subtle imbalance that contributes to vitamin B12 dementia over time.
After B12 supplementation and follow-up:
- 78% of participants improved in both cognitive testing (MMSE) and subjective symptoms
- An additional 13% improved on MMSE alone
- Only 8.9% showed no measurable improvement—primarily women over 50, hinting at possible overlapping metabolic or hormonal influences
🧠 Memory complaints in adults are often not just aging—they’re correctable. When homocysteine is elevated and B12 is borderline, identifying and treating functional deficiency can lead to meaningful, measurable recovery
Vitamin B12 and Brain Fog: Why Timing Is Everything
While some randomized controlled trials on B12 supplementation have shown mixed results, a closer examination reveals a pattern: timing matters. Late-stage neurodegeneration is less responsive to intervention, but in individuals with early memory decline and elevated homocysteine, outcomes improve more consistently.
This aligns with a prevention-first framework:
- Monitor homocysteine and active B12 (Holo-TC)
- Don’t rely solely on serum total B12
- Address borderline levels proactively—especially in aging populations
Together, the biomarker correlations and clinical results underscore the same point: the relationship between B12 and brain health is more nuanced than it appears on standard lab reports.
🧩 Functional markers like homocysteine, Holo-TC, and neurodegeneration biomarkers offer a more complete picture—and may hold the key to earlier, more effective intervention.
5. Why the Current Reference Range for Standard Vitamin B12 Tests Miss Brain Fog and Functional Deficiency
The standard clinical definition of vitamin B12 deficiency hasn’t kept up with what we now know about vitamin B12 brain health.
In most countries, including the U.S., deficiency is diagnosed when serum B12 falls below 148 pmol/L (~200 pg/mL). But that cutoff wasn’t based on neurological data—it was derived statistically, as three standard deviations below the average of a broader population. It doesn’t reflect when symptoms begin or when brain tissue starts to change.
Clinical studies tell a different story.
🧪 Understanding B12 Ranges: Why “Normal” Isn’t Always Optimal
| Vitamin B12 Range (pmol/L) | Category | What It Means | Research Notes | Functional Markers | Additional Context |
|---|---|---|---|---|---|
| <148 pmol/L | Deficient | Below standard cutoff | Triggers diagnosis and treatment. Symptoms (e.g., brain fog) often start earlier. | Holo-TC low, homocysteine/MMA elevated. | Common in vegetarians, elderly with malabsorption. |
| 148–250 pmol/L | Low-normal / borderline | May appear “normal” on labs | Elevated homocysteine and cognitive symptoms common. Often missed. | Holo-TC may be insufficient, homocysteine rising. | Borderline in UK/Germany; consider supplementation if symptomatic. |
| 250–400 pmol/L | Suboptimal | Still within reference range | Measurable brain changes (e.g., WMH) and treatment benefits observed. | Holo-TC variable, monitor homocysteine. | UCSF study links low Holo-TC to deficits at median 414 pmol/L. |
| 400–500 pmol/L | Average | Median in many cohorts (e.g., UCSF = 414) | Brain fog, WMH, and elevated Tau noted even here. | Holo-TC low or Holo-HC high may indicate risk. | Check functional status despite “normal” total B12. |
| >500–550+ pmol/L | Longevity-optimized | Target for neurological health | Functional B12 more likely sufficient. Recommended for aging adults. | Holo-TC adequate, homocysteine low. | Japan’s cutoff; longevity focus due to absorption decline with age. |
| >1000 pmol/L | Potentially Excessive | Above typical upper limit | May indicate high Holo-HC, linked to Tau elevation; monitor for toxicity. | Holo-HC dominant, assess MMA/homocysteine. | Rare; excess from supplements may pose risks (research ongoing). |
People with B12 levels above 148 pmol/L can still experience memory loss, white matter changes, and elevated homocysteine. Some show measurable improvement with B12 treatment, despite having values considered “normal” on paper.
- One estimate suggests that 5–10% of people with neurological symptoms have B12 levels above 148—but still benefit from supplementation.
- In the UCSF study, median B12 was 414 pmol/L, yet participants still showed cognitive slowing and white matter abnormalities.
- These issues were more strongly linked to holo-transcobalamin, the active form of B12, rather than total serum B12.
📊 A lab result of 400 pmol/L may look acceptable—but if active B12 is low, cognitive risk can still be present.
Some countries have responded by adjusting their cutoffs.
Japan, for instance, defines deficiency at a much higher level—closer to 500 pmol/L. Many longevity-focused advice recommend maintaining levels above 500–550 pmol/L, especially as we age, where absorption and transport efficiency decline.
But even total B12 doesn’t tell the whole story.
Standard serum B12 tests measure both the active (holo-transcobalamin) and inactive (holo-haptocorrin) forms. However, only the active form is available for cellular uptake and directly supports neurological and metabolic function. The inactive portion may inflate total B12 levels without reflecting what’s actually usable by the body.
From a longevity perspective, this distinction is critical. Two individuals may have identical total B12 levels, yet their biological risk profiles can differ significantly depending on how much of that B12 is active. Without measuring functional markers, early deficits that affect memory, cognitive performance, and long-term brain health may go undetected.
This is where homocysteine testing becomes essential. Homocysteine rises when B12, folate, or B6 are insufficient at the cellular level—often before B12 drops below standard thresholds. It provides a functional snapshot of how well methylation, DNA repair, and neurotransmitter pathways are running.
🧬Why Homocysteine Matters: B12 is needed to convert homocysteine into methionine. When B12 is low, homocysteine rises—triggering neuroinflammation, oxidative stress, and long-term cognitive risk.
So why hasn’t the reference range changed?
Partly inertia. Partly cost. And partly because most clinicians aren’t taught to look beyond standard serum markers unless symptoms are severe.
For people looking to maintain long-term brain health, that approach can miss early changes that are both measurable and addressable—if you know what to look for.
🌍 How B12 Deficiency Cutoffs Vary by Country
| Country / Region | Deficiency Cutoff | Unit | Notes |
|---|---|---|---|
| United States | 148 pmol/L (≈200 pg/mL) | pmol/L | Based on 3 SDs below mean; symptoms often missed above this level. |
| Canada | ~150 pmol/L | pmol/L | Aligns with U.S.; anemia-based, may miss functional deficiency. |
| United Kingdom | <150 pmol/L (borderline 150–200 pmol/L) | pmol/L | Borderline flagged but treatment often delayed unless anemia/neuropathy. |
| Germany | ~200 pmol/L (functional <250 pmol/L) | pmol/L | Functional deficiency suspected below 250; Holo-TC increasingly used. |
| Japan | 500–550 pmol/L | pmol/L | Higher threshold for neurological protection; proactive approach. |
| India | ~150–200 pmol/L | pmol/L | Common due to diet; underdiagnosed, varies by lab. |
| WHO / Global | ~150 pmol/L | pmol/L | No universal cutoff; many countries adopt ~150 pmol/L statistically. |
| Scandinavia (Nordic) | ~150 pmol/L (functional up to 300 pmol/L) | pmol/L | Aligns with U.S./UK; research suggests >300 pmol/L for optimal health; focus on biomarkers. |
6. Can B12 Brain Fog and Dementia Symptoms Be Reversed?
While symptoms like memory issues and slowed thinking often come first, research also points to a physical consequence of low or borderline B12: vitamin B12 brain atrophy.
This refers to measurable shrinkage in brain tissue—especially in regions involved in memory and processing speed—that has been observed in people with lower B12 status and elevated homocysteine. These changes can begin before B12 falls outside the standard range, and in some cases, studies have shown that early intervention may help reduce the rate of loss or support partial recovery.
How vitamin B12 Brain Fog and Homocysteine Accelerate Brain Aging
One of the early signs that B12 status is impacting brain structure is a rise in homocysteine—a functional marker that often increases before B12 drops outside the normal range.
Homocysteine (Hcy) is produced as part of the methylation cycle, a critical process for DNA repair, neurotransmitter synthesis, and detoxification. B12, folate, and B6 act as cofactors that help convert homocysteine into other essential compounds. When these nutrients are low, homocysteine accumulates.
Elevated homocysteine has been associated with:
- Increased oxidative stress and reduced cellular resilience
- Disruption of the blood-brain barrier
- Smaller hippocampal volume on MRI
- Accelerated brain atrophy
- Faster cognitive decline in domains like memory and processing speed
- Earlier symptoms of B12 brain fog, even when standard B12 levels appear normal
- Increased risk of vitamin B12 dementia, especially in adults with poor methylation capacity
These effects appear to be dose-dependent and are more pronounced in older adults.
The connection between B12, homocysteine, and cognitive symptoms becomes even clearer when looking at brain imaging over time. Several studies have tracked how early B12 insufficiency—before overt deficiency—can lead to measurable brain shrinkage.
Vitamin B12 Brain Atrophy: How Early Deficiency Impacts Brain Structure & Brain Shrinkage
Longitudinal imaging studies have shown that brain atrophy rates are higher in individuals with low-normal B12 status and elevated homocysteine.
In one 5-year study, participants with B12 levels in the lowest third (<308 pmol/L) had up to 6 times more brain volume loss than those in the highest range. Two key predictors of this decline were:
- High homocysteine
- Elevated methylmalonic acid (MMA)—a sign of low cellular B12
These findings reinforce the connection between B12 and brain fog, and hint at vitamin B12 dementia risk long before classic deficiency thresholds are reached.
Importantly, the strongest associations were found in people with:
- Low holo-transcobalamin (the active B12 fraction)
- Homocysteine >13 μmol/L
- Mild cognitive symptoms, but not yet advanced neurodegeneration
Vitamin B12 Dementia: What Clinical Trials Say About Reversing Cognitive Decline
One trial in particular helps explain why timing matters.
The VITACOG study looked at older adults with mild cognitive impairment and homocysteine levels above 13 μmol/L—a group at higher risk for brain atrophy. Over two years, participants received high-dose B-vitamin supplementation, including B12, B6, and folate.
The results were compelling:
- MRI scans showed slower gray matter loss
- Cognitive performance improved in key areas like memory and executive function
- Some participants even improved their Clinical Dementia Rating (CDR) scores—shifting out of the mild impairment category
These changes weren’t seen in participants with more advanced neurodegeneration, highlighting the importance of acting early—especially when homocysteine is elevated and functional B12 is low.
Reversing B12 Brain Fog and Cognitive Impairment: What the Evidence Shows
Another clinical study helps drive the point home: early intervention works—if you catch it before deeper damage sets in.
In this 2022 trial, adults with low serum B12 and mild cognitive symptoms received targeted supplementation and were tracked over several weeks. The improvements were measurable:
The findings were striking:
- Mean homocysteine (Hcy) levels dropped from 22.9 ± 16.9 to 11.5 ± 3.9 µmol/L (p < 0.001), reflecting restored methylation capacity.
- Serum B12 levels rose from 135.8 ± 27.5 to 721.0 ± 523.1 pmol/L—a fivefold increase confirming effective physiological repletion.
- Cognitive scores improved significantly: Mini-Mental State Examination (MMSE) scores rose from 20.5 ± 6.4 to 22.9 ± 5.5 (p < 0.001; effect size r = 0.73), within 21–133 days.
Statistical analysis confirmed these changes weren’t due to chance or external factors like age, sex, or education. Interestingly, the degree of B12 increase didn’t directly predict the homocysteine drop—underscoring the importance of tracking functional markers like homocysteine itself.
When B12 correction happens early—before structural brain damage takes hold—both cognitive longevity and metabolic function can improve in parallel.
These kinds of gains suggest that B12 brain fog isn’t just reversible—it may be a warning sign with a window for action.
Key Point: Vitamin B12 Dementia Risk May Begin With Brain Fog
Cognitive decline doesn’t usually start with a diagnosis. It starts with small shifts: slower processing, more frequent forgetfulness, moments of lost clarity.
Often, these symptoms appear while blood B12 levels are still technically normal.
That’s why recognizing and addressing functional deficiency—through markers like homocysteine and holo-transcobalamin—may offer one of the most practical ways to protect long-term brain health. Early detection opens the door for targeted support—before irreversible loss begins.
🧠 Ready to Catch B12 Brain Fog Before It Escalates?
Low B12 doesn’t always show up on standard labs—but the brain often knows first.
Our Longevity Essentials Panel tests homocysteine, methylmalonic acid, and more—no doctor’s visit needed.
FAQ: B12 Brain Fog, Dementia, and Cognitive Function
Is vitamin B12 dementia reversible?
In early stages, cognitive decline due to B12 deficiency may be reversible with targeted support—but not in advanced dementia.
B12 deficiency can mimic or contribute to dementia-like symptoms, including memory loss and confusion. When caught early—especially with elevated homocysteine or methylmalonic acid—B12 supplementation has been shown to improve cognition and slow brain atrophy. However, in late-stage Alzheimer’s or advanced neurodegeneration, benefits seem to be limited.
Does vitamin B12 improve cognitive function?
Vitamin B12 improves brain function when deficiency is present—especially in people with high homocysteine or early signs of B12 brain fog.
Studies show that supplementing B12 in deficient individuals can improve memory, focus, and processing speed—particularly in older adults with mild cognitive symptoms. The most robust results are seen when homocysteine levels are >13 µmol/L and intervention occurs before significant brain atrophy.
What are early signs of B12 deficiency in the brain?
Early signs of B12 brain fog include mental fatigue, forgetfulness, mood changes, and trouble concentrating—even with “normal” B12 levels.
These subtle symptoms often show up before serum B12 falls below standard thresholds. Functional markers like holo-transcobalamin (active B12) and homocysteine are more sensitive to early neurological changes and can reveal vitamin B12 brain health risks missed by basic blood panels.
Is B12 deficiency linked to dementia?
Yes—vitamin B12 deficiency is associated with dementia, especially when it causes elevated homocysteine or brain atrophy.
Clinical research shows that B12 insufficiency—particularly low holo-transcobalamin and high methylmalonic acid—can accelerate white matter loss, cognitive decline, and raise the risk of vitamin B12 dementia symptoms. In early stages, this may look like typical aging or mild forgetfulness, but the root cause is often underrecognized.
Curious how other nutrient deficiencies affect brain aging? Vitamin D plays a different role—especially in managing inflammation and maintaining synaptic function. There’s a full breakdown here if you want to explore that side too
What level of B12 is considered optimal for brain health?
For optimal vitamin B12 brain health, aim for serum B12 levels above 500–550 pmol/L and homocysteine below 10 µmol/L.
The standard cutoff of 150 pmol/L misses early neurological issues. Functional B12 tests—especially holo-transcobalamin and homocysteine—offer a clearer picture of brain fog, methylation function, and cognitive risk. These markers help identify functional B12 deficiency before permanent decline occurs.
Conclusion: B12 Brain Fog Starts Before Vitamin B12 Deficiency Shows Up
The science shows that cognitive decline tied to B12 can begin long before levels fall outside the “normal” range. Often, the brain is already changing—slowing, shrinking—while standard labs say everything looks fine, even as early signs of vitamin B12 dementia begin to take hold.
Older adults, vegans, people on metformin or antacids, peopel with certain gut issues… even health-conscious people who test regularly can miss the warning signs—or see changes that don’t show up on standard labs.
I didn’t have high homocysteine, and I didn’t experience obvious symptoms. But when I changed my nutrition, my B12 levels shifted dramatically—and so did my perspective on what “normal” really means.
In Part 2, I’ll break down exactly how this shows up in lab work (including my own), who’s most at risk, and what to test—so you can catch problems before they escalate. You’ll also see how I stabilized my B12 status, what I’d do differently now, and how to approach vitamin B12 brain health proactively
🧠 If you’ve ever been told your B12 is “fine,” don’t miss it.
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