May 28, 2025 • 12 mins
In this episode of Daily Value, we look at recent research suggesting that the B12 levels we’ve always accepted as "normal" might silently be failing our brains. New data reveals that standard B12 thresholds may not adequately shield us from subtle neurological decline. Are current diagnostics overlooking hidden deficiencies? We go into how B12 truly supports your nervous system, the overlooked significance of active B12, and why traditional treatments might need reconsideration, particularly for those struggling with absorption. Perhaps the path to preserving cognitive health lies in rethinking what we thought we knew about vitamin B12.
00:00 Introduction: Rethinking Vitamin B12 Levels
00:33 Understanding Vitamin B12
01:24 The Role of B12 in Neurological Health
01:57 Causes and Consequences of B12 Deficiency
03:00 Reevaluating B12 Sufficiency Standards
04:40 New Research Insights on B12 and Cognitive Health
07:30 Dietary Sources and Bioavailability of B12
08:50 Supplementation and Treatment Strategies
10:50 Challenges in Treating B12 Deficiency
11:55 Conclusion: Towards Optimal Cognitive Health
PMID: 39927551
PMID: 36774098
PMID: 38987879
Mark as Played
Transcript
Episode Transcript
Available transcripts are automatically generated. Complete accuracy is not guaranteed.
Speaker 1 (00:00):
Are your vitamin B12 levels truly protecting your
brain?
Well, new research ischallenging our assumptions,
revealing that so-called normalB12 levels could quietly
contribute to cognitive declineand hidden neurological changes.
In today's episode, we'llexplore why standard
recommendations might not go farenough and how redefining
(00:20):
optimal could transform yourcognitive health as you age.
Vitamin B12, scientificallyknown as cobalamin, is an
(00:41):
essential water-soluble vitaminnecessary for proper functioning
of the nervous system, dnasynthesis and the formation of
healthy red blood cells.
B12 is unique in that it isexclusively synthesized by
microorganisms like bacteria andarchaea.
The latter are a group ofsingle-celled microorganisms
that, like bacteria, lack anucleus, but they are
(01:01):
genetically and biochemicallydistinct from bacteria.
B12 is naturally found inanimal-derived foods such as
meat, fish, eggs and dairy,especially those of ruminant
origin, meaning animals likecows, sheep, etc.
That have specialized stomachswith microbes that synthesize
B12 they store in their tissuesand use.
(01:23):
B12 plays a particularlyimportant role in maintaining
the myelin sheath, that's theprotective coating around nerve
fibers that acts as insulationon a wire ensuring efficient
communication between nervecells.
As of now, it's not entirelyknown how exactly B12
contributes to myelination orprevents demyelination, but what
(01:45):
we do know is that insufficientB12 can lead to neurological
issues due to impaired myelinintegrity, resulting in symptoms
such as numbness, tingling,muscle weakness and difficulties
.
Deficiency typically arisesfrom inadequate dietary intake
or impaired absorption due togastrointestinal issues,
surgeries or conditions likepernicious anemia caused by
(02:07):
atrophic gastritis.
This is an autoimmune-likecondition in which chronic
inflammation of the intestinescauses the loss of parietal
cells.
These are special cells thatproduce stomach acid, as well as
a protein called intrinsicfactor, which is essential for
absorbing B12 in the smallintestine.
Without parietal cells, you canabsorb B12 properly, which can
(02:28):
lead to deficiency andconditions like pernicious
anemia.
This is a type of anemia wherered blood cells are fewer in
number but also larger thannormal, but they're not as
effective as carrying oxygen.
The body does store vitamin B12,as carrying oxygen.
The body does store vitamin B12, approximately 1 to 5
(02:49):
milligrams, mainly in the liver.
Most people only lose about 2to 4 micrograms of B12 daily,
which means that these reservescan delay symptoms for years,
making early detection ofdeficiency syndrome challenging.
Low B12 levels are associatedwith increased white matter
hyperintensities in the brain,which are indicators of
microstructural brain changeslinked to cognitive decline.
(03:11):
New research suggests thattraditional testing for B12
sufficiency may deceive us bymeasuring only total serum
levels, missing the veryimportant active fraction known
as holotranscobalamin.
This is the form of B12 boundto protein in the bloodstream.
This is the only form of B12that has a specific receptor for
cellular uptake.
Thus it's considered the activefraction of bodily B12.
(03:35):
It turns out that the boundariesof normal might be dangerously
narrow, particularly for agingbrains.
Current guidelines definedeficiency as 148 picomoles per
liter, that's 200 picograms permilliliter.
These thresholds are comingunder scrutiny as evidence
mounts that our cognitive healthrequires levels far beyond what
(03:55):
we've accepted as adequate.
In fact, the threshold forvitamin B12 deficiency was
developed as a simplecalculation of three standard
deviations below the average USintake.
Interestingly, in 2010, theAmerican Society for Nutrition
argued that 5% of patients whohave a syndrome consistent with
(04:16):
B12 deficiency who respondpositively to B12
supplementation, have levels ofB12 over those considered to be
adequate as of right now.
Could it be that the standarddefinition of vitamin B12
sufficiency is failing us,quietly allowing neurological
decline?
Perhaps it's time to questionthese boundaries and redefine
what truly constitutes optimalvitamin B12 status.
(04:40):
A very recent study published byBaudry, richard et al suggests
that beneath the surface of whatwe consider normal vitamin B12
levels, there is a cognitiverisk.
Participants in this study withlower levels of active B12
showed greater volumes of whitematter hyperintensities.
Again, these are markers onbrain scans that hint at subtle
(05:01):
structural damage.
These lesions could reflectunseen disruptions in vascular
permeability and the quiet lossof oligodendrocytes.
These are cells responsible formaintaining the brain's
protective myelin sheath that wetalked about.
The negative effects didn't endthere.
Older adults within the studydemonstrated a clear functional
(05:22):
link between lower B12 levelsand slower cognitive processing
speed.
Interestingly, the study showedsomething unexpected Higher
total B12, specifically thebiologically inactive fraction,
that's, b12 bound to haptocorin,correlated with elevated tau
protein.
That's a marker connected withneurodegenerative disease like
(05:43):
Alzheimer's.
The biological implications ofthis relationship remain elusive
, raising questions.
Does excess inactive B12trapped by haptochorins somehow
diminish the brain's ability touse active B12, inadvertently
facilitating tau-mediatedneuronal injury?
Vitamin B12 is normally knownfor helping inhibit the
(06:04):
formation of misfolded tauproteins.
Thus, if haptochorin-bound B12is indeed reducing the brain's
access to usable B12, could itbe silently contributing to
these destructive accumulations?
These findings shine a new lighton the limitations of
traditional guidelines.
Population-based definitions ofmicronutrient adequacy might
(06:25):
have unknowingly overlookedsubtle yet important
neurological deficits appearingat both extremes of the B12
continuum levels, historicallydismissed as clinically
irrelevant Without sensitivediagnostic tools.
These nuanced neurologicalsymptoms have long remained
hidden and unexplained, oftenleaving patients frustrated.
(06:45):
Even after standard treatmentsseemingly succeed in addressing
hematological or blood-relateddeficiency syndrome, it's
actually a very commonoccurrence for people to request
more B12 to deal with theneurological symptoms after the
blood-related symptoms clear.
So we have to ask why do somepatients continue to demand
higher B12 doses to managelingering neurological symptoms,
(07:07):
despite having fully resolvedhematological issues?
Perhaps it is time toreconsider what we truly
understand as a normal vitaminB12 level?
Perhaps the answer tosafeguarding our cognitive
futures lies hidden precisely inthese subtler signals we've
neglected to acknowledge.
So what does this all mean foryou, especially if you're older,
(07:27):
plant-based or simply assumingyour level are fine?
First let's talk diet.
We know that what you eat andhow much B12 it contains is only
half the story.
Bioavailability matters, andit's currently thought that
approximately 50% of B12 isabsorbed from food.
Dairy, it turns out, leads theway in bioavailability.
(07:48):
In a Quebec-based new age study, older adults consuming over 4
micrograms a day of food-derivedB12 without any supplements had
significantly reduced odds ofbiochemical deficiency using the
current B12 thresholds.
Notably dairy-derived B12,not-meat or organ meats had the
strongest association withbetter B12, not meat or organ
(08:10):
meats had the strongestassociation with better B12
status.
Interestingly, dairy's B12seems to be absorbed more
efficiently approximately threetimes more bioavailable than B12
from meat or fish.
This means that a cup of milkwith 1.3 micrograms of B12 may
actually be more useful than athree-ounce portion of beef
containing 2.4 micrograms.
In practical terms, a dailyintake of 6 to 10 micrograms B12
(08:31):
, mostly from natural foodsources, appears to saturate
biomarkers of sufficiency likeholotranscobalamin.
That intake of 6 to 10micrograms is 2.5 to 4 times
higher than the current USrecommended dietary allowance of
2.4 micrograms per day.
And what about supplements?
Here's where things get morenuanced.
(08:52):
Supplements provide B12 in freeform, not bound to protein, and
bypass the need for gastricacid and pepsin.
However, absorption efficiencydrops dramatically with dose
size due to intrinsic factorsaturation.
That's the protein that bindsto B12 in the small intestine
and helps it be absorbed.
Below 2 micrograms of B12,absorption can reach 50%, but at
(09:16):
higher doses, like 500micrograms or 1 milligram, it
plummets to 2 to 1.3%.
This means a 500 microgramtablet delivers roughly 10
micrograms absorbed still enoughto saturate knees, but far less
efficient than most peoplethink when it comes to
correcting B12 deficiency,especially in the context of is
roughly 10 micrograms absorbedstill enough to saturate knees,
but far less efficient than mostpeople think.
When it comes to correcting B12deficiency, especially in the
context of malabsorption, foodand oral supplements may not be
(09:37):
enough.
The preferred route is usuallyintramuscular hydroxycobalamin
at 1,000 micrograms per.
When it comes to correcting B12deficiency, especially in the
context of malabsorption, foodand oral supplements may not be
enough.
The preferred route is usuallyintramuscular hydroxycobalamin,
1,000 micrograms per injection,or 1,000 to 2,000 micrograms a
(10:01):
day orally for those that canabsorb vitamin B12 in the small
intestine.
According to US, british andeven Dutch clinical practice,
initial treatments often startwith twice-weekly or
alternate-day injections forfive weeks until neurological
symptoms stabilize.
After that, injections aretapered based on clinical
(10:21):
response, not lab markers.
Importantly, symptom resolutionmay take months or even years
and in many cases fullresolution never even occurs.
Up to 50% of patients requiremore frequent injections than
the standard two-monthmaintenance dose.
Many remain symptomatic unlesstreated every two to four weeks,
with some people needing weeklyinjections long-term.
(10:44):
The idea that symptoms resolvein parallel with biomarker
normalization is a bitmisleading.
Symptoms resolve in parallelwith biomarker normalization is
a bit misleading.
B12 levels often normalize farearlier than clinical
improvements and symptom relapsefrequently does occur without
any drop in serum B12 levels.
Interestingly enough, this hassparked growing support for the
therapeutic trial approach.
(11:04):
If a patient presents withneurological or cognitive
symptoms suggestive of B12deficiency, even with normal
serum B12, they may benefit froma 3-6 month trial of
intramuscular B12 therapy.
In such cases,holotranscobalamin,
methylmalonic acid and evenserum B12 are poor predictors of
(11:25):
response.
The only reliable endpoint issymptom resolution.
And what of oral therapy formalabsorption?
While high doses may normalizelabs through passive absorption,
real-world efficacy variesdramatically.
In fact, passive B12 absorptioncan be as low as 0.1 to 0.5
percent in some individuals.
(11:46):
This is where there iscurrently no clinical consensus
that oral therapy can safelyreplace injections in patients
with confirmed malabsorption ofB12.
Today we've looked at thehidden complexities surrounding
vitamin B12 status, uncoveringevidence that challenges
established thresholds andtreatment guidelines.
It appears increasingly clearthat current normal reference
(12:08):
ranges may inadequately reflectoptimal cognitive and
neurological health.
To truly protect cognitivefunction across the lifespan, a
more precise, individualizedapproach, considering dietary
patterns, absorption capacity,supplementation strategy and
clinical symptoms, may benecessary.
Given these new insights,perhaps it's time to question
(12:29):
whether conventional guidelinesadequately protect our most
vital asset, our cognitivehealth.
Normal, it seems, may no longerbe enough.
Thank you for joining me todayon Daily Value.
As always, stay healthy.
Are your vitamin B12 levels truly protecting your
brain?
Well, new research ischallenging our assumptions,
revealing that so-called normalB12 levels could quietly
contribute to cognitive declineand hidden neurological changes.
In today's episode, we'llexplore why standard
recommendations might not go farenough and how redefining
(00:20):
optimal could transform yourcognitive health as you age.
Vitamin B12, scientificallyknown as cobalamin, is an
(00:41):
essential water-soluble vitaminnecessary for proper functioning
of the nervous system, dnasynthesis and the formation of
healthy red blood cells.
B12 is unique in that it isexclusively synthesized by
microorganisms like bacteria andarchaea.
The latter are a group ofsingle-celled microorganisms
that, like bacteria, lack anucleus, but they are
(01:01):
genetically and biochemicallydistinct from bacteria.
B12 is naturally found inanimal-derived foods such as
meat, fish, eggs and dairy,especially those of ruminant
origin, meaning animals likecows, sheep, etc.
That have specialized stomachswith microbes that synthesize
B12 they store in their tissuesand use.
(01:23):
B12 plays a particularlyimportant role in maintaining
the myelin sheath, that's theprotective coating around nerve
fibers that acts as insulationon a wire ensuring efficient
communication between nervecells.
As of now, it's not entirelyknown how exactly B12
contributes to myelination orprevents demyelination, but what
(01:45):
we do know is that insufficientB12 can lead to neurological
issues due to impaired myelinintegrity, resulting in symptoms
such as numbness, tingling,muscle weakness and difficulties
.
Deficiency typically arisesfrom inadequate dietary intake
or impaired absorption due togastrointestinal issues,
surgeries or conditions likepernicious anemia caused by
(02:07):
atrophic gastritis.
This is an autoimmune-likecondition in which chronic
inflammation of the intestinescauses the loss of parietal
cells.
These are special cells thatproduce stomach acid, as well as
a protein called intrinsicfactor, which is essential for
absorbing B12 in the smallintestine.
Without parietal cells, you canabsorb B12 properly, which can
(02:28):
lead to deficiency andconditions like pernicious
anemia.
This is a type of anemia wherered blood cells are fewer in
number but also larger thannormal, but they're not as
effective as carrying oxygen.
The body does store vitamin B12,as carrying oxygen.
The body does store vitamin B12, approximately 1 to 5
(02:49):
milligrams, mainly in the liver.
Most people only lose about 2to 4 micrograms of B12 daily,
which means that these reservescan delay symptoms for years,
making early detection ofdeficiency syndrome challenging.
Low B12 levels are associatedwith increased white matter
hyperintensities in the brain,which are indicators of
microstructural brain changeslinked to cognitive decline.
(03:11):
New research suggests thattraditional testing for B12
sufficiency may deceive us bymeasuring only total serum
levels, missing the veryimportant active fraction known
as holotranscobalamin.
This is the form of B12 boundto protein in the bloodstream.
This is the only form of B12that has a specific receptor for
cellular uptake.
Thus it's considered the activefraction of bodily B12.
(03:35):
It turns out that the boundariesof normal might be dangerously
narrow, particularly for agingbrains.
Current guidelines definedeficiency as 148 picomoles per
liter, that's 200 picograms permilliliter.
These thresholds are comingunder scrutiny as evidence
mounts that our cognitive healthrequires levels far beyond what
(03:55):
we've accepted as adequate.
In fact, the threshold forvitamin B12 deficiency was
developed as a simplecalculation of three standard
deviations below the average USintake.
Interestingly, in 2010, theAmerican Society for Nutrition
argued that 5% of patients whohave a syndrome consistent with
(04:16):
B12 deficiency who respondpositively to B12
supplementation, have levels ofB12 over those considered to be
adequate as of right now.
Could it be that the standarddefinition of vitamin B12
sufficiency is failing us,quietly allowing neurological
decline?
Perhaps it's time to questionthese boundaries and redefine
what truly constitutes optimalvitamin B12 status.
(04:40):
A very recent study published byBaudry, richard et al suggests
that beneath the surface of whatwe consider normal vitamin B12
levels, there is a cognitiverisk.
Participants in this study withlower levels of active B12
showed greater volumes of whitematter hyperintensities.
Again, these are markers onbrain scans that hint at subtle
(05:01):
structural damage.
These lesions could reflectunseen disruptions in vascular
permeability and the quiet lossof oligodendrocytes.
These are cells responsible formaintaining the brain's
protective myelin sheath that wetalked about.
The negative effects didn't endthere.
Older adults within the studydemonstrated a clear functional
(05:22):
link between lower B12 levelsand slower cognitive processing
speed.
Interestingly, the study showedsomething unexpected Higher
total B12, specifically thebiologically inactive fraction,
that's, b12 bound to haptocorin,correlated with elevated tau
protein.
That's a marker connected withneurodegenerative disease like
(05:43):
Alzheimer's.
The biological implications ofthis relationship remain elusive
, raising questions.
Does excess inactive B12trapped by haptochorins somehow
diminish the brain's ability touse active B12, inadvertently
facilitating tau-mediatedneuronal injury?
Vitamin B12 is normally knownfor helping inhibit the
(06:04):
formation of misfolded tauproteins.
Thus, if haptochorin-bound B12is indeed reducing the brain's
access to usable B12, could itbe silently contributing to
these destructive accumulations?
These findings shine a new lighton the limitations of
traditional guidelines.
Population-based definitions ofmicronutrient adequacy might
(06:25):
have unknowingly overlookedsubtle yet important
neurological deficits appearingat both extremes of the B12
continuum levels, historicallydismissed as clinically
irrelevant Without sensitivediagnostic tools.
These nuanced neurologicalsymptoms have long remained
hidden and unexplained, oftenleaving patients frustrated.
(06:45):
Even after standard treatmentsseemingly succeed in addressing
hematological or blood-relateddeficiency syndrome, it's
actually a very commonoccurrence for people to request
more B12 to deal with theneurological symptoms after the
blood-related symptoms clear.
So we have to ask why do somepatients continue to demand
higher B12 doses to managelingering neurological symptoms,
(07:07):
despite having fully resolvedhematological issues?
Perhaps it is time toreconsider what we truly
understand as a normal vitaminB12 level?
Perhaps the answer tosafeguarding our cognitive
futures lies hidden precisely inthese subtler signals we've
neglected to acknowledge.
So what does this all mean foryou, especially if you're older,
(07:27):
plant-based or simply assumingyour level are fine?
First let's talk diet.
We know that what you eat andhow much B12 it contains is only
half the story.
Bioavailability matters, andit's currently thought that
approximately 50% of B12 isabsorbed from food.
Dairy, it turns out, leads theway in bioavailability.
(07:48):
In a Quebec-based new age study, older adults consuming over 4
micrograms a day of food-derivedB12 without any supplements had
significantly reduced odds ofbiochemical deficiency using the
current B12 thresholds.
Notably dairy-derived B12,not-meat or organ meats had the
strongest association withbetter B12, not meat or organ
(08:10):
meats had the strongestassociation with better B12
status.
Interestingly, dairy's B12seems to be absorbed more
efficiently approximately threetimes more bioavailable than B12
from meat or fish.
This means that a cup of milkwith 1.3 micrograms of B12 may
actually be more useful than athree-ounce portion of beef
containing 2.4 micrograms.
In practical terms, a dailyintake of 6 to 10 micrograms B12
(08:31):
, mostly from natural foodsources, appears to saturate
biomarkers of sufficiency likeholotranscobalamin.
That intake of 6 to 10micrograms is 2.5 to 4 times
higher than the current USrecommended dietary allowance of
2.4 micrograms per day.
And what about supplements?
Here's where things get morenuanced.
(08:52):
Supplements provide B12 in freeform, not bound to protein, and
bypass the need for gastricacid and pepsin.
However, absorption efficiencydrops dramatically with dose
size due to intrinsic factorsaturation.
That's the protein that bindsto B12 in the small intestine
and helps it be absorbed.
Below 2 micrograms of B12,absorption can reach 50%, but at
(09:16):
higher doses, like 500micrograms or 1 milligram, it
plummets to 2 to 1.3%.
This means a 500 microgramtablet delivers roughly 10
micrograms absorbed still enoughto saturate knees, but far less
efficient than most peoplethink when it comes to
correcting B12 deficiency,especially in the context of is
roughly 10 micrograms absorbedstill enough to saturate knees,
but far less efficient than mostpeople think.
When it comes to correcting B12deficiency, especially in the
context of malabsorption, foodand oral supplements may not be
(09:37):
enough.
The preferred route is usuallyintramuscular hydroxycobalamin
at 1,000 micrograms per.
When it comes to correcting B12deficiency, especially in the
context of malabsorption, foodand oral supplements may not be
enough.
The preferred route is usuallyintramuscular hydroxycobalamin,
1,000 micrograms per injection,or 1,000 to 2,000 micrograms a
(10:01):
day orally for those that canabsorb vitamin B12 in the small
intestine.
According to US, british andeven Dutch clinical practice,
initial treatments often startwith twice-weekly or
alternate-day injections forfive weeks until neurological
symptoms stabilize.
After that, injections aretapered based on clinical
(10:21):
response, not lab markers.
Importantly, symptom resolutionmay take months or even years
and in many cases fullresolution never even occurs.
Up to 50% of patients requiremore frequent injections than
the standard two-monthmaintenance dose.
Many remain symptomatic unlesstreated every two to four weeks,
with some people needing weeklyinjections long-term.
(10:44):
The idea that symptoms resolvein parallel with biomarker
normalization is a bitmisleading.
Symptoms resolve in parallelwith biomarker normalization is
a bit misleading.
B12 levels often normalize farearlier than clinical
improvements and symptom relapsefrequently does occur without
any drop in serum B12 levels.
Interestingly enough, this hassparked growing support for the
therapeutic trial approach.
(11:04):
If a patient presents withneurological or cognitive
symptoms suggestive of B12deficiency, even with normal
serum B12, they may benefit froma 3-6 month trial of
intramuscular B12 therapy.
In such cases,holotranscobalamin,
methylmalonic acid and evenserum B12 are poor predictors of
(11:25):
response.
The only reliable endpoint issymptom resolution.
And what of oral therapy formalabsorption?
While high doses may normalizelabs through passive absorption,
real-world efficacy variesdramatically.
In fact, passive B12 absorptioncan be as low as 0.1 to 0.5
percent in some individuals.
(11:46):
This is where there iscurrently no clinical consensus
that oral therapy can safelyreplace injections in patients
with confirmed malabsorption ofB12.
Today we've looked at thehidden complexities surrounding
vitamin B12 status, uncoveringevidence that challenges
established thresholds andtreatment guidelines.
It appears increasingly clearthat current normal reference
(12:08):
ranges may inadequately reflectoptimal cognitive and
neurological health.
To truly protect cognitivefunction across the lifespan, a
more precise, individualizedapproach, considering dietary
patterns, absorption capacity,supplementation strategy and
clinical symptoms, may benecessary.
Given these new insights,perhaps it's time to question
(12:29):
whether conventional guidelinesadequately protect our most
vital asset, our cognitivehealth.
Normal, it seems, may no longerbe enough.
Thank you for joining me todayon Daily Value.
As always, stay healthy.
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