May 25, 2024 • 26 mins
You have likely heard the headlines: cognitive impairment and Alzheimer’s and other forms of dementia are on the rise. Part of the increase is due to an aging population. But there are reasons that are adding to the increase beyond this. The epidemics of insulin resistance (recall that dementia is often labeled “type 3 diabetes,” meaning that the brain becomes insulin resistant), SIBO endotoxemia, the ubiquity of heavy metal toxicity, and deficiencies of important nutrients such as omega-3 fatty acids and vitamin D are likely making their own contributions.
There are a number of strategies that you can adopt, however, that hold potential for reducing your risk for developing cognitive impairment, or at least delay its onset. There are also various factors that you can supplement, some of which hold potential for improving cognition and, in some cases, slow or help prevent cognitive impairment and dementia. But this area is filled with imprecise thinking and, sadly, misleading marketing. To help you get your arms around these ideas, let me introduce you to a concept that makes gaining an understanding of what works and what doesn’t that can keep you on track and avoid pitfalls that waste time, effort, money, and have little to no benefit for brain health. It is to understand what factors provide nootropic and thereby temporary effects vs neurotrophic factors that actually generate healthy improvements in brain health and physiology.
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Episode Transcript
Available transcripts are automatically generated. Complete accuracy is not guaranteed.
Speaker 1 (00:05):
You've likely heard the headlines Cognitive
impairment and Alzheimer's andother forms of dementia are on
the rise.
Part of the increase is due toan aging population, but there
are reasons that are adding tothe increase beyond this the
epidemics of insulin resistanceRecall that dementia is often
labeled type 3 diabetes, meaningthat the brain becomes insulin
(00:28):
resistant SIBO, endotoxemia, theubiquity of heavy metal
toxicity and deficiencies ofimportant nutrients Such as
omega-3 fatty acids and vitaminD Are likely making their own
contributions.
There are a number ofstrategies that you can adopt,
however, that hold potential forreducing your risk for
(00:48):
developing cognitive impairmentor at least delay its onset.
There are also various factorsthat you can supplement, some of
which hold potential forimproving cognition and, in some
cases, slow or help preventcognitive impairment and
dementia.
But this area is filled withimprecise thinking and, sadly,
(01:10):
misleading marketing.
To help you get your armsaround these ideas, let me
introduce you to a concept thatmakes gaining an understanding
of what works and what doesn't.
That can keep you on track andavoid pitfalls that waste your
time, effort, money and havelittle to do with benefit for
brain health.
The key is to understand whatfactors provide nootropic, and
(01:35):
thereby temporary, effectsversus neurotrophic factors that
actually generate healthyimprovements in brain health and
physiology.
And later in the podcast, I'dlike to tell you about Defiant
Health's sponsors Paleo Valley,our preferred provider for many
excellent organic and grass-fedfood products, and BiotiQuest,
(01:58):
my number one choice forprobiotics that are
scientifically formulated,unlike most other commercial
probiotic products availabletoday.
This is a very importantconcept.
I'd like to help you understandthat, when you get it, a lot of
things make sense in the worldof trying to preserve your
(02:18):
cognitive health and trying toavoid the prospect in your
future of Alzheimer's, dementiaor other forms of dementia.
Surprisingly though, this isgoing to seem obvious, once you
hear this distinction, once youhear this idea, you're going to
find that many neurologists,certainly many primary care
physicians and other peopleinvolved in dementia and
(02:38):
cognitive preservation oftendon't understand this
distinction.
This is even true in the worldof pharmaceuticals For
Alzheimer's disease.
You're going to find that thepharmaceuticals that are
commonly prescribed, likerivastigmine or Aricept, really
have almost no impact on thedisease itself.
They may improve memory alittle bit or other aspects of
(02:59):
cognition, but they have nomaterial effect on the
progression of the disease, andso people think that it may be
beneficial.
Doctors think that those drugsmay be beneficial, but all they
do is improve memory orattention or other aspects of
cognition a little bit, with noimpact on the disease.
So the distinction is to beable to tell the difference
(03:21):
between what are callednootropics and neurotropics.
Now that sounds kind ofcomplicated, but it's really not
.
Nootropics, very simply, arefactors that improve various
measures of cognition.
It could be better memory, itcould be greater creativity.
It could be improved dataacquisition, learning new things
.
It could be improved dataacquisition, learning new things
(03:44):
.
It could be better datasynthesis, that is, putting
together ideas or data to comeup with new conclusions.
The problem with these theseare good things, right.
Improved cognition can be agood thing.
If you're trying to write apaper or meet a work deadline,
it's a good thing to haveimproved cognition.
But what you should not do isinterpret this to mean that your
(04:04):
brain is somehow healthier,because it's a good thing to
have improved cognition.
But what you should not do isinterpret this to mean that your
brain is somehow healthier,because it's not.
More often than not, it's nohealthier.
How do these nootropic agentswork?
Well, they work primarily byincreasing neurotransmitters,
that is, chemicals in the brainthat transact thought and memory
and attention and the otheraspects of cognition.
(04:25):
These are neurotransmitterslike acetylcholine or
norepinephrine or dopamine.
What nootropics do not do isdecrease the measures, the
phenomena associated withcognitive impairment and
dementia.
They don't.
Nootropics, for instance, donot decrease the beta amyloid
plaque and the tau protein, thephosphorylated tau proteins.
(04:47):
Those are the two factors thataccumulate such a gunk in your
brain that messes up yourcapacity for clear thought and
memory.
So nootropics do not decreasethese factors, nor do they
increase what are called trophicfactors.
These are hormones that workwithin the brain to increase the
proliferation andinterconnections of brain cells
(05:10):
and increase the synapticrichness, that is, the
interconnections between braincells, and support other cells
like glial cells that supportbrain cells.
So nootropics do not increasetrophic factors, and these are
factors that go by names likevascular endothelial growth
factor or BDNF, brain-derivedneurotrophic factor or
(05:31):
IGF-1-alpha, insulin-like growthfactor-1-alpha or neuronal
growth factor.
Don't memorize all those Justknow that these so-called
trophic or growth factors in thebrain support brain cells, the
proliferation and health ofbrain cells, and encourage a
richer interconnection orsynapses between brain cells.
Nootropics do not impact thisat all and so they don't reduce
(05:55):
the accumulated gunk in yourbrain, like beta amyloid plaque
or tau protein.
They do not increase trophicfactors and nootropic agents
also don't prevent atrophy.
So when you have cognitiveimpairment and dementia, certain
parts of the brain undergoatrophy.
They shrink and decay.
The hippocampus is the primaryarea that we watch for the
(06:17):
progression of dementia.
The hippocampus is a small partway inside the brain that is
the part of the brainresponsible for converting
short-term memory into long-termmemory and that becomes
atrophied and shrunken insomeone with dementia.
And that's why people withdementia often have intact
long-term memory, for instancewhat happened in their childhood
(06:38):
or teenage years or youngadulthood, but have almost no
memory for what happened thismorning, what they had for
breakfast, what they had fordinner, what they did yesterday.
So short-term memory isimpaired because they're
incapable, because ofhippocampal atrophy, and
converting short-term memoryinto consolidated long-term
memory.
Other parts of the brain canalso undergo atrophy, such as
(06:59):
the cerebral cortex, white andgray matter or the frontal lobe
or the temporal lobe, usually inmore advanced forms of dementia
, also in other forms ofdementia besides Alzheimer's.
But nootropic agents don't haveany impact on the progression
of atrophy either.
Now, these agents, theseso-called nootropic agents
there's many of them.
Some of them work, some of themdon't work so well.
(07:21):
Some of them don't work at all,but they coat by names you
likely never heard of, likeciticoline or
dimethylaminoethanol orhuperzine.
Those are three that, by theway, work by increasing the
level of acetylcholineneurotransmitter in your brain
transiently.
There's other factors likeselegiline or ergoloid mesolates
that increase dopamine in thebrain.
(07:43):
And then there's factors liketyrosine, the amino acid
tyrosine, that increases levelsof norepinephrine.
And then there are nootropicsthat work by uncertain
mechanisms, such as paracetam,aniracetam, prameracetam and my
favorite, vimpocetine.
It's my favorite because itworks.
It tends to increase yourcapacity for focus, attention,
(08:04):
creativity, synthesis of ideas.
I'll sometimes take Vin Postine, for instance, when I'm on a
deadline for a book or otherproject, and 30 milligrams
really increases your capacityfor thinking more clearly and
producing for a few hours.
Then it's gone.
Another analogy that helps youunderstand this idea of no
tropic effects is caffeine.
So you have coffee.
(08:25):
Especially when you firststarted drinking coffee when you
were younger, you notice thatyour focus, your attention was
intensified.
Your capacity to think andmemorize was improved for a
little while.
So that's called a nootropiceffect, because after a few
hours it wears off and you mayend up being more tired than you
were at the start.
But that's nootropic.
(08:45):
If you drink a cup of coffeeand your memory is a little bit
better, your creativity andenergy and focus are a little
better, do you say to yourself.
My brain must therefore behealthier, I must have less beta
amyloid plaque.
No, of course not.
So that is a nootropic effect.
And I made this importantdistinction because there are
people who try to sell youthings or try to tell you that
(09:06):
this or that nootropic becauseit improves, let's say, focus or
memory, temporarily ortransiently.
It must therefore mean thatyour brain is healthier and that
you are protected from dementia.
That is absolutely not true.
Now, while it's a good thing tohave improved cognition, better
memory and focus, etc.
It does not mean you should notinterpret that to mean that
(09:30):
your long-term potential fordementia is somehow reduced,
because it is not.
Yet this doesn't stop manyretailers or manufacturers from
telling you or selling youproducts where they say things
like if your memory is better,your brain is healthier.
That is simply complete fiction.
You cannot rely on thatnonsense.
(09:51):
Now, neurotrophics are somethingdifferent.
These are factors that actuallyimprove brain health and brain
physiology.
Now the list of things thatachieve this is shorter.
There's lots and lots ofnootropics.
There's not that many thingsthat have been discovered to be
neurotrophic.
The list is growing gradually.
Again, we have to be careful.
(10:11):
There's a lot of misinformation, false advertising, other
claims and false products,misleading products that you
want to avoid.
But just understand thatthere's a big difference between
nootropics and neurotrophics.
So what factors distinguishsomething as neurotrophic?
Well, first of all, aneurotrophic can also have
nootropic effects.
(10:32):
A neurotrophic factor can alsoincrease memory, attention,
focus, data acquisition, etcetera.
But it also should reduce betaamyloid plaque and the tau
protein that accumulate in thebrains of people with cognitive
impairment.
Something that is neurotrophicshould be shown to increase
those trophic factors like BDNF,igf-1-alpha, vegf and neuronal
(10:57):
growth factor.
Some studies have shownincrease in activity in the
hippocampus and related areas asidentified by functional MRI.
That's a little bit sketchy.
It's not quite clear ifincreased activity means there's
better brain health, but it'ssomething that's emerging and
being explored.
And then, something that isneurotrophic should decrease
atrophy, that is, decay,degeneration of the hippocampus,
(11:19):
the cerebral cortex, frontallobe, temporal lobe and other
brain areas.
In other words, it actuallystops the decay of brain anatomy
and physiology.
So when we come back from ourmessage from our sponsors, let's
talk about the factors andstrategies that have known or
fairly well establishedneurotrophic effects.
(11:41):
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Now let's get back to ourdiscussion.
So what factors have been shownto have neurotrophic effects?
(14:38):
At the top of the list areomega-3 fatty acids, but
specifically the DHA, not somuch the EPA, because the brain
is largely made of DHA, and thatevidence is pretty good.
It's been shown that the DHAsupplemented tends to improve
cognition and preserve reducedlikely progression of cognitive
(15:00):
decline, especially ifintroduced early or taken
preventively.
If you have well-establisheddementia and you're in assisted
living or memory center and youtake DHA, the benefits are small
to minimal.
So the key is to startsupplementing earlier in life,
before cognitive impairment setsin, and certainly no later than
the beginning of cognitiveimpairment.
Now the dose is importantbecause there are other benefits
(15:23):
to omega-3 fatty acids, such asthe activation of the enzyme
intestinal alkaline phosphatasein the intestinal lining that
tends to deactivate partiallydeactivate the
lipopolysaccharide toxin fromfecal microbes that typically
infest the small intestine inmany Americans nowadays.
So taking both EPA and DHA arebeneficial For that reason also.
(15:47):
There may be cardiovascularbenefits, of course, and a
reduction of triglycerides andpostprandial or aftermeal
lipoproteins such as VLDL andchylomicrons topic for another
day.
Except that omega-3 fatty acidshave a range of benefits modest
benefits.
So I advise taking both the EPAand the DHA, but at higher
doses, typically minimum of3,000 milligrams per day of the
(16:11):
combination or more.
3,600 milligrams of thecombination is probably ideal
and if you are concerned aboutcognitive impairment you can
always increase the DHA evenfurther.
There's no downside to takingmore, except the cost it's a
little bit costly.
Another very importantneurotrophic strategy is to
follow a diet that reduces orminimizes insulin resistance and
(16:34):
glycation.
Let's talk about that.
So insulin resistance is thesituation in which your body's
cells, such as brain, muscle,liver, don't respond well to
insulin, typically because ofrepeated insults from high blood
glucose, high blood insulin.
Those repetitive cycles triggerinsulin resistance.
Also, deficiency of numerousnutrients like magnesium,
(16:55):
vitamin D all the factors in myprograms that leads to insulin
resistance.
Also, deficiency of numerousnutrients like magnesium,
vitamin D all the factors in myprograms that leads to insulin
resistance.
And insulin resistance is acommon thread through all forms
of dementia.
Whether it's Alzheimer'sdementia, early cognitive
impairment, frontotemporal lobedementia, parkinson's disease,
lewy body disease, they allshare insulin resistance.
(17:16):
So insulin resistance is amajor common factor in all forms
of dementia.
So you want to minimize that.
So follow my programs where weeliminate wheat, grains and
sugars.
We never restrict fats.
We restore nutrients likevitamin D, magnesium, iodine,
omega-3, fatty acids.
That conspire, that synergizeto minimize insulin resistance
(17:39):
and you have great improvementand protection as a neurotrophic
strategy in preventingcognitive impairment and
dementia.
Another thing about diet is youwant to minimize glycation.
Remember this Glucosemodification of proteins.
So the proteins in the brainare subject to glycation.
When brain proteins becomeglycated, they become useless,
(18:01):
essentially become junk, andjust gum up your brain.
So you don't want to glycate.
How do you do that?
Don't eat foods that raiseblood glucose Wheat, grains and
sugar.
Address nutrients that arelacking in modern life, that
allow higher blood glucoses onceagain vitamin d, magnesium,
iodine, omega-3 fatty acids.
So follow my program as writtenand you end up minimizing
(18:25):
insulin resistance and glycation.
And when you do that, you alsominimize inflammation, because
inflammation is another drivingforce in cognitive impairment.
So diet can be viewed assomething that has very potent
neurotrophic effects.
Now know that there have beenstudies in such things as the
Mediterranean diet and othersimilar diets.
(18:46):
They do not.
They have not been shown toaffect improvements in brain
health.
They are not neurotrophic.
They are at best, are notneurotrophic.
They are at best and unevenlynootropic.
So don't fall for this ideathat if a Mediterranean diet or
similar is better than astandard American diet, which is
terrible, it does notnecessarily mean that the
(19:06):
Mediterranean diet is ideal.
It's not.
So we're going to go towards adiet that we think is ideal and
thereby exerts betterneurotrophic effects by
minimizing insulin resistance,by minimizing glycation, by
reducing inflammation.
Physical exercise, butespecially resistance training,
is likely a neurotrophicstrategy.
(19:28):
So exercise, typically 150minutes per week of some aerobic
exercise, or 75 minutes perweek of at least moderate to
strenuous exercise, has beenshown to achieve neurotrophic
effects such as preservation orincrease in hippocampal size and
an increase in those trophicgrowth factors.
It's important to know that themost important kind of exercise
(19:51):
is resistance training, not tosay that resistance training
alone is sufficient, butresistance training in
combination with other aerobicactivities like riding your bike
, walking a treadmill, evenbetter.
Walking outdoors, gardening,digging in your garden, raking
the leaves, cutting the grassAll those things really add up
to preserve brain health andhave been shown to minimize or
(20:15):
even reverse hippocampalshrinkage and other forms of
atrophy in the brain andincrease trophic factors in the
brain.
Be aware of something calledexergaming.
This is a new kind of ideawhere you combine cognitive
exercise.
Cognitive exercises likeplaying sudoku or chess or
crossword puzzles or learning anew language or learning another
(20:36):
new skill like a new musicalinstrument probably does not
have neurotrophic effects.
They do have cognitive benefits, that is, nootropic effects.
But if you combine thecognitive benefits of cognitive
exercises like those things Imentioned with some form of
exercise.
It could be a stationary bikewhile you play a video game and
(20:57):
you get the best of both aerobicexercise and cognitive exercise
.
Of course, there's no strengthtraining there.
It's hard to do strengthtraining while you're playing a
game.
But be aware it's an easy andreally fun way to acquire the
benefits of cognitiveimprovement and maybe a bit of
neurotrophic benefit.
A very important neurotrophicstrategy is to reduce or
(21:20):
minimize endotoxemia.
If you've been following myconversations, you know that
about half of the Americanpublic has something called SIBO
, that about half of theAmerican public has something
called SIBO small intestinalbacterial overgrowth a situation
in which we've lost numerousbeneficial microbes.
That has therefore allowed theascent of fecal microbes like E
(21:40):
coli and salmonella into the 24feet of small intestine, where
they don't belong, where thosetrillions of fecal microbes
infesting the small intestinelive and die rapidly.
When they die, they releasetheir toxins, such as endotoxin,
that is able to penetrateacross the intestinal wall, the
small intestinal wall, and intothe bloodstream.
That is a process calledendotoxemia and, in my
(22:04):
estimation, half the USpopulation has this and it is a
major driver of insulinresistance inflammation and
damage to the US.
Population has this and it is amajor driver of insulin
resistance inflammation anddamage to the brain.
It actually causes atrophy ofthe brain.
So getting control over SIBO andendotoxemia is critical.
I see many people saying, oh,this is too difficult, it's too
hard to understand.
(22:24):
Some of the strategies tocontrol are too complicated.
Please don't do that.
If you bury your head in thesand, not only are you increased
risk for cognitive impairmentand dementia, but also multiple
sclerosis, parkinson's disease,migraine headaches, rosacea,
psoriasis, eczema, fibromyalgia,restless leg syndrome, weight
(22:45):
gain, obesity, type 2 diabetes,breast cancer.
In other words, uncorrectedSIBO and endotoxemia has major
implications for your long-termhealth beyond even just
cognitive impairment.
So addressing so, if you don'tknow what I'm talking about,
please see prior episodes ofthis Defiant Health podcast or
my many thousands of posts in mydrdavisinfinitehealthcom blog,
(23:09):
as well as my books, especiallythe Super Gut book.
Now, an added bonus is when weengage in restoring the microbe
lost by nearly everybody,lactobacillus roteri that we
know is able to colonize the GItract and send a signal to your
brain to release the hormoneoxytocin.
Oxytocin is very powerful andamong its effects relevant to
(23:33):
brain health is that it reducescortisol dramatically.
Cortisol is damaging to yourbrain, so prolonged stress, for
instance, can damage your brainfrom sustained elevated levels
of cortisol.
Well, the oxytocin boost youget from lactobacillus roteri
blunts that rise dramatically.
L-roteri is also unique in that, you may recall, it colonized
(23:56):
the small intestine and that'swhere SIBO occurs, that's where
endotoxemia originates.
So when L-roteri takes upresidence in the small intestine
it produces bacteriocins.
These are natural antibioticseffective against fecal microbes
and Elroderi.
Thereby, in addition toproducing oxytocin, also reduces
(24:16):
endotoxemia that drivescognitive impairment.
Oxytocin can also increasetestosterone, which helps males,
because an increase intestosterone, especially if it's
low, can reduce abdominalvisceral fat.
That's a driver of inflammation.
It causes a return of muscleand muscle is a major advantage
in anybody.
(24:36):
The restoration of L-reuterinoxytocin also increases a sense
of optimism and generosity andsociability that likely also
contribute to beneficial braineffects.
So I hope you now understand thedistinction between nootropics
factors that make you a littlebit smarter, a little bit more
clever, a little bit morecreative, a little more
(24:57):
attentive, but don't necessarilyimprove brain health by
addressing all those factorsthat cause cognitive impairment.
But neurotrophic factors reallydo have potential for preserving
brain health, even increasinghippocampal size and preventing
brain atrophy, increasing thosetrophic factors and also, in
addition, having cognitivebenefits, nootropic effects.
(25:19):
Understand this distinction andyou're protected from all the
silly claims often made forproducts.
You know that most of thethings that are neurotrophic, by
the way, are not beingadvertised, and that's one of
the problems we have inhealthcare that if something
doesn't make a lot of money,like a dementia drug, you won't
hear much about it.
Now, if you find this a littlebit too overwhelming, I invite
(25:40):
you to join my programs, such asmy drdavisinfinitehealthcom
inner circle, where we have lotsand lots of learning materials,
including videos, and ourtwo-way Zoom meetings where we
discuss all these issues andhelp you succeed.
Now, if you learned somethingfrom this episode of the Defiant
Health Podcast, I invite you tosubscribe to your favorite
podcast directory.
(26:01):
Post a review, post a comment.
Do your part to grow thismovement of self-empowerment in
health and minimizing ourreliance on a flawed healthcare
system.
Thanks for listening.
You've likely heard the headlines Cognitive
impairment and Alzheimer's andother forms of dementia are on
the rise.
Part of the increase is due toan aging population, but there
are reasons that are adding tothe increase beyond this the
epidemics of insulin resistanceRecall that dementia is often
labeled type 3 diabetes, meaningthat the brain becomes insulin
(00:28):
resistant SIBO, endotoxemia, theubiquity of heavy metal
toxicity and deficiencies ofimportant nutrients Such as
omega-3 fatty acids and vitaminD Are likely making their own
contributions.
There are a number ofstrategies that you can adopt,
however, that hold potential forreducing your risk for
(00:48):
developing cognitive impairmentor at least delay its onset.
There are also various factorsthat you can supplement, some of
which hold potential forimproving cognition and, in some
cases, slow or help preventcognitive impairment and
dementia.
But this area is filled withimprecise thinking and, sadly,
(01:10):
misleading marketing.
To help you get your armsaround these ideas, let me
introduce you to a concept thatmakes gaining an understanding
of what works and what doesn't.
That can keep you on track andavoid pitfalls that waste your
time, effort, money and havelittle to do with benefit for
brain health.
The key is to understand whatfactors provide nootropic, and
(01:35):
thereby temporary, effectsversus neurotrophic factors that
actually generate healthyimprovements in brain health and
physiology.
And later in the podcast, I'dlike to tell you about Defiant
Health's sponsors Paleo Valley,our preferred provider for many
excellent organic and grass-fedfood products, and BiotiQuest,
(01:58):
my number one choice forprobiotics that are
scientifically formulated,unlike most other commercial
probiotic products availabletoday.
This is a very importantconcept.
I'd like to help you understandthat, when you get it, a lot of
things make sense in the worldof trying to preserve your
(02:18):
cognitive health and trying toavoid the prospect in your
future of Alzheimer's, dementiaor other forms of dementia.
Surprisingly though, this isgoing to seem obvious, once you
hear this distinction, once youhear this idea, you're going to
find that many neurologists,certainly many primary care
physicians and other peopleinvolved in dementia and
(02:38):
cognitive preservation oftendon't understand this
distinction.
This is even true in the worldof pharmaceuticals For
Alzheimer's disease.
You're going to find that thepharmaceuticals that are
commonly prescribed, likerivastigmine or Aricept, really
have almost no impact on thedisease itself.
They may improve memory alittle bit or other aspects of
(02:59):
cognition, but they have nomaterial effect on the
progression of the disease, andso people think that it may be
beneficial.
Doctors think that those drugsmay be beneficial, but all they
do is improve memory orattention or other aspects of
cognition a little bit, with noimpact on the disease.
So the distinction is to beable to tell the difference
(03:21):
between what are callednootropics and neurotropics.
Now that sounds kind ofcomplicated, but it's really not
.
Nootropics, very simply, arefactors that improve various
measures of cognition.
It could be better memory, itcould be greater creativity.
It could be improved dataacquisition, learning new things
.
It could be improved dataacquisition, learning new things
(03:44):
.
It could be better datasynthesis, that is, putting
together ideas or data to comeup with new conclusions.
The problem with these theseare good things, right.
Improved cognition can be agood thing.
If you're trying to write apaper or meet a work deadline,
it's a good thing to haveimproved cognition.
But what you should not do isinterpret this to mean that your
(04:04):
brain is somehow healthier,because it's a good thing to
have improved cognition.
But what you should not do isinterpret this to mean that your
brain is somehow healthier,because it's not.
More often than not, it's nohealthier.
How do these nootropic agentswork?
Well, they work primarily byincreasing neurotransmitters,
that is, chemicals in the brainthat transact thought and memory
and attention and the otheraspects of cognition.
(04:25):
These are neurotransmitterslike acetylcholine or
norepinephrine or dopamine.
What nootropics do not do isdecrease the measures, the
phenomena associated withcognitive impairment and
dementia.
They don't.
Nootropics, for instance, donot decrease the beta amyloid
plaque and the tau protein, thephosphorylated tau proteins.
(04:47):
Those are the two factors thataccumulate such a gunk in your
brain that messes up yourcapacity for clear thought and
memory.
So nootropics do not decreasethese factors, nor do they
increase what are called trophicfactors.
These are hormones that workwithin the brain to increase the
proliferation andinterconnections of brain cells
(05:10):
and increase the synapticrichness, that is, the
interconnections between braincells, and support other cells
like glial cells that supportbrain cells.
So nootropics do not increasetrophic factors, and these are
factors that go by names likevascular endothelial growth
factor or BDNF, brain-derivedneurotrophic factor or
(05:31):
IGF-1-alpha, insulin-like growthfactor-1-alpha or neuronal
growth factor.
Don't memorize all those Justknow that these so-called
trophic or growth factors in thebrain support brain cells, the
proliferation and health ofbrain cells, and encourage a
richer interconnection orsynapses between brain cells.
Nootropics do not impact thisat all and so they don't reduce
(05:55):
the accumulated gunk in yourbrain, like beta amyloid plaque
or tau protein.
They do not increase trophicfactors and nootropic agents
also don't prevent atrophy.
So when you have cognitiveimpairment and dementia, certain
parts of the brain undergoatrophy.
They shrink and decay.
The hippocampus is the primaryarea that we watch for the
(06:17):
progression of dementia.
The hippocampus is a small partway inside the brain that is
the part of the brainresponsible for converting
short-term memory into long-termmemory and that becomes
atrophied and shrunken insomeone with dementia.
And that's why people withdementia often have intact
long-term memory, for instancewhat happened in their childhood
(06:38):
or teenage years or youngadulthood, but have almost no
memory for what happened thismorning, what they had for
breakfast, what they had fordinner, what they did yesterday.
So short-term memory isimpaired because they're
incapable, because ofhippocampal atrophy, and
converting short-term memoryinto consolidated long-term
memory.
Other parts of the brain canalso undergo atrophy, such as
(06:59):
the cerebral cortex, white andgray matter or the frontal lobe
or the temporal lobe, usually inmore advanced forms of dementia
, also in other forms ofdementia besides Alzheimer's.
But nootropic agents don't haveany impact on the progression
of atrophy either.
Now, these agents, theseso-called nootropic agents
there's many of them.
Some of them work, some of themdon't work so well.
(07:21):
Some of them don't work at all,but they coat by names you
likely never heard of, likeciticoline or
dimethylaminoethanol orhuperzine.
Those are three that, by theway, work by increasing the
level of acetylcholineneurotransmitter in your brain
transiently.
There's other factors likeselegiline or ergoloid mesolates
that increase dopamine in thebrain.
(07:43):
And then there's factors liketyrosine, the amino acid
tyrosine, that increases levelsof norepinephrine.
And then there are nootropicsthat work by uncertain
mechanisms, such as paracetam,aniracetam, prameracetam and my
favorite, vimpocetine.
It's my favorite because itworks.
It tends to increase yourcapacity for focus, attention,
(08:04):
creativity, synthesis of ideas.
I'll sometimes take Vin Postine, for instance, when I'm on a
deadline for a book or otherproject, and 30 milligrams
really increases your capacityfor thinking more clearly and
producing for a few hours.
Then it's gone.
Another analogy that helps youunderstand this idea of no
tropic effects is caffeine.
So you have coffee.
(08:25):
Especially when you firststarted drinking coffee when you
were younger, you notice thatyour focus, your attention was
intensified.
Your capacity to think andmemorize was improved for a
little while.
So that's called a nootropiceffect, because after a few
hours it wears off and you mayend up being more tired than you
were at the start.
But that's nootropic.
(08:45):
If you drink a cup of coffeeand your memory is a little bit
better, your creativity andenergy and focus are a little
better, do you say to yourself.
My brain must therefore behealthier, I must have less beta
amyloid plaque.
No, of course not.
So that is a nootropic effect.
And I made this importantdistinction because there are
people who try to sell youthings or try to tell you that
(09:06):
this or that nootropic becauseit improves, let's say, focus or
memory, temporarily ortransiently.
It must therefore mean thatyour brain is healthier and that
you are protected from dementia.
That is absolutely not true.
Now, while it's a good thing tohave improved cognition, better
memory and focus, etc.
It does not mean you should notinterpret that to mean that
(09:30):
your long-term potential fordementia is somehow reduced,
because it is not.
Yet this doesn't stop manyretailers or manufacturers from
telling you or selling youproducts where they say things
like if your memory is better,your brain is healthier.
That is simply complete fiction.
You cannot rely on thatnonsense.
(09:51):
Now, neurotrophics are somethingdifferent.
These are factors that actuallyimprove brain health and brain
physiology.
Now the list of things thatachieve this is shorter.
There's lots and lots ofnootropics.
There's not that many thingsthat have been discovered to be
neurotrophic.
The list is growing gradually.
Again, we have to be careful.
(10:11):
There's a lot of misinformation, false advertising, other
claims and false products,misleading products that you
want to avoid.
But just understand thatthere's a big difference between
nootropics and neurotrophics.
So what factors distinguishsomething as neurotrophic?
Well, first of all, aneurotrophic can also have
nootropic effects.
(10:32):
A neurotrophic factor can alsoincrease memory, attention,
focus, data acquisition, etcetera.
But it also should reduce betaamyloid plaque and the tau
protein that accumulate in thebrains of people with cognitive
impairment.
Something that is neurotrophicshould be shown to increase
those trophic factors like BDNF,igf-1-alpha, vegf and neuronal
(10:57):
growth factor.
Some studies have shownincrease in activity in the
hippocampus and related areas asidentified by functional MRI.
That's a little bit sketchy.
It's not quite clear ifincreased activity means there's
better brain health, but it'ssomething that's emerging and
being explored.
And then, something that isneurotrophic should decrease
atrophy, that is, decay,degeneration of the hippocampus,
(11:19):
the cerebral cortex, frontallobe, temporal lobe and other
brain areas.
In other words, it actuallystops the decay of brain anatomy
and physiology.
So when we come back from ourmessage from our sponsors, let's
talk about the factors andstrategies that have known or
fairly well establishedneurotrophic effects.
(11:41):
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Now let's get back to ourdiscussion.
So what factors have been shownto have neurotrophic effects?
(14:38):
At the top of the list areomega-3 fatty acids, but
specifically the DHA, not somuch the EPA, because the brain
is largely made of DHA, and thatevidence is pretty good.
It's been shown that the DHAsupplemented tends to improve
cognition and preserve reducedlikely progression of cognitive
(15:00):
decline, especially ifintroduced early or taken
preventively.
If you have well-establisheddementia and you're in assisted
living or memory center and youtake DHA, the benefits are small
to minimal.
So the key is to startsupplementing earlier in life,
before cognitive impairment setsin, and certainly no later than
the beginning of cognitiveimpairment.
Now the dose is importantbecause there are other benefits
(15:23):
to omega-3 fatty acids, such asthe activation of the enzyme
intestinal alkaline phosphatasein the intestinal lining that
tends to deactivate partiallydeactivate the
lipopolysaccharide toxin fromfecal microbes that typically
infest the small intestine inmany Americans nowadays.
So taking both EPA and DHA arebeneficial For that reason also.
(15:47):
There may be cardiovascularbenefits, of course, and a
reduction of triglycerides andpostprandial or aftermeal
lipoproteins such as VLDL andchylomicrons topic for another
day.
Except that omega-3 fatty acidshave a range of benefits modest
benefits.
So I advise taking both the EPAand the DHA, but at higher
doses, typically minimum of3,000 milligrams per day of the
(16:11):
combination or more.
3,600 milligrams of thecombination is probably ideal
and if you are concerned aboutcognitive impairment you can
always increase the DHA evenfurther.
There's no downside to takingmore, except the cost it's a
little bit costly.
Another very importantneurotrophic strategy is to
follow a diet that reduces orminimizes insulin resistance and
(16:34):
glycation.
Let's talk about that.
So insulin resistance is thesituation in which your body's
cells, such as brain, muscle,liver, don't respond well to
insulin, typically because ofrepeated insults from high blood
glucose, high blood insulin.
Those repetitive cycles triggerinsulin resistance.
Also, deficiency of numerousnutrients like magnesium,
(16:55):
vitamin D all the factors in myprograms that leads to insulin
resistance.
Also, deficiency of numerousnutrients like magnesium,
vitamin D all the factors in myprograms that leads to insulin
resistance.
And insulin resistance is acommon thread through all forms
of dementia.
Whether it's Alzheimer'sdementia, early cognitive
impairment, frontotemporal lobedementia, parkinson's disease,
lewy body disease, they allshare insulin resistance.
(17:16):
So insulin resistance is amajor common factor in all forms
of dementia.
So you want to minimize that.
So follow my programs where weeliminate wheat, grains and
sugars.
We never restrict fats.
We restore nutrients likevitamin D, magnesium, iodine,
omega-3, fatty acids.
That conspire, that synergizeto minimize insulin resistance
(17:39):
and you have great improvementand protection as a neurotrophic
strategy in preventingcognitive impairment and
dementia.
Another thing about diet is youwant to minimize glycation.
Remember this Glucosemodification of proteins.
So the proteins in the brainare subject to glycation.
When brain proteins becomeglycated, they become useless,
(18:01):
essentially become junk, andjust gum up your brain.
So you don't want to glycate.
How do you do that?
Don't eat foods that raiseblood glucose Wheat, grains and
sugar.
Address nutrients that arelacking in modern life, that
allow higher blood glucoses onceagain vitamin d, magnesium,
iodine, omega-3 fatty acids.
So follow my program as writtenand you end up minimizing
(18:25):
insulin resistance and glycation.
And when you do that, you alsominimize inflammation, because
inflammation is another drivingforce in cognitive impairment.
So diet can be viewed assomething that has very potent
neurotrophic effects.
Now know that there have beenstudies in such things as the
Mediterranean diet and othersimilar diets.
(18:46):
They do not.
They have not been shown toaffect improvements in brain
health.
They are not neurotrophic.
They are at best, are notneurotrophic.
They are at best and unevenlynootropic.
So don't fall for this ideathat if a Mediterranean diet or
similar is better than astandard American diet, which is
terrible, it does notnecessarily mean that the
(19:06):
Mediterranean diet is ideal.
It's not.
So we're going to go towards adiet that we think is ideal and
thereby exerts betterneurotrophic effects by
minimizing insulin resistance,by minimizing glycation, by
reducing inflammation.
Physical exercise, butespecially resistance training,
is likely a neurotrophicstrategy.
(19:28):
So exercise, typically 150minutes per week of some aerobic
exercise, or 75 minutes perweek of at least moderate to
strenuous exercise, has beenshown to achieve neurotrophic
effects such as preservation orincrease in hippocampal size and
an increase in those trophicgrowth factors.
It's important to know that themost important kind of exercise
(19:51):
is resistance training, not tosay that resistance training
alone is sufficient, butresistance training in
combination with other aerobicactivities like riding your bike
, walking a treadmill, evenbetter.
Walking outdoors, gardening,digging in your garden, raking
the leaves, cutting the grassAll those things really add up
to preserve brain health andhave been shown to minimize or
(20:15):
even reverse hippocampalshrinkage and other forms of
atrophy in the brain andincrease trophic factors in the
brain.
Be aware of something calledexergaming.
This is a new kind of ideawhere you combine cognitive
exercise.
Cognitive exercises likeplaying sudoku or chess or
crossword puzzles or learning anew language or learning another
(20:36):
new skill like a new musicalinstrument probably does not
have neurotrophic effects.
They do have cognitive benefits, that is, nootropic effects.
But if you combine thecognitive benefits of cognitive
exercises like those things Imentioned with some form of
exercise.
It could be a stationary bikewhile you play a video game and
(20:57):
you get the best of both aerobicexercise and cognitive exercise
.
Of course, there's no strengthtraining there.
It's hard to do strengthtraining while you're playing a
game.
But be aware it's an easy andreally fun way to acquire the
benefits of cognitiveimprovement and maybe a bit of
neurotrophic benefit.
A very important neurotrophicstrategy is to reduce or
(21:20):
minimize endotoxemia.
If you've been following myconversations, you know that
about half of the Americanpublic has something called SIBO
, that about half of theAmerican public has something
called SIBO small intestinalbacterial overgrowth a situation
in which we've lost numerousbeneficial microbes.
That has therefore allowed theascent of fecal microbes like E
(21:40):
coli and salmonella into the 24feet of small intestine, where
they don't belong, where thosetrillions of fecal microbes
infesting the small intestinelive and die rapidly.
When they die, they releasetheir toxins, such as endotoxin,
that is able to penetrateacross the intestinal wall, the
small intestinal wall, and intothe bloodstream.
That is a process calledendotoxemia and, in my
(22:04):
estimation, half the USpopulation has this and it is a
major driver of insulinresistance inflammation and
damage to the US.
Population has this and it is amajor driver of insulin
resistance inflammation anddamage to the brain.
It actually causes atrophy ofthe brain.
So getting control over SIBO andendotoxemia is critical.
I see many people saying, oh,this is too difficult, it's too
hard to understand.
(22:24):
Some of the strategies tocontrol are too complicated.
Please don't do that.
If you bury your head in thesand, not only are you increased
risk for cognitive impairmentand dementia, but also multiple
sclerosis, parkinson's disease,migraine headaches, rosacea,
psoriasis, eczema, fibromyalgia,restless leg syndrome, weight
(22:45):
gain, obesity, type 2 diabetes,breast cancer.
In other words, uncorrectedSIBO and endotoxemia has major
implications for your long-termhealth beyond even just
cognitive impairment.
So addressing so, if you don'tknow what I'm talking about,
please see prior episodes ofthis Defiant Health podcast or
my many thousands of posts in mydrdavisinfinitehealthcom blog,
(23:09):
as well as my books, especiallythe Super Gut book.
Now, an added bonus is when weengage in restoring the microbe
lost by nearly everybody,lactobacillus roteri that we
know is able to colonize the GItract and send a signal to your
brain to release the hormoneoxytocin.
Oxytocin is very powerful andamong its effects relevant to
(23:33):
brain health is that it reducescortisol dramatically.
Cortisol is damaging to yourbrain, so prolonged stress, for
instance, can damage your brainfrom sustained elevated levels
of cortisol.
Well, the oxytocin boost youget from lactobacillus roteri
blunts that rise dramatically.
L-roteri is also unique in that, you may recall, it colonized
(23:56):
the small intestine and that'swhere SIBO occurs, that's where
endotoxemia originates.
So when L-roteri takes upresidence in the small intestine
it produces bacteriocins.
These are natural antibioticseffective against fecal microbes
and Elroderi.
Thereby, in addition toproducing oxytocin, also reduces
(24:16):
endotoxemia that drivescognitive impairment.
Oxytocin can also increasetestosterone, which helps males,
because an increase intestosterone, especially if it's
low, can reduce abdominalvisceral fat.
That's a driver of inflammation.
It causes a return of muscleand muscle is a major advantage
in anybody.
(24:36):
The restoration of L-reuterinoxytocin also increases a sense
of optimism and generosity andsociability that likely also
contribute to beneficial braineffects.
So I hope you now understand thedistinction between nootropics
factors that make you a littlebit smarter, a little bit more
clever, a little bit morecreative, a little more
(24:57):
attentive, but don't necessarilyimprove brain health by
addressing all those factorsthat cause cognitive impairment.
But neurotrophic factors reallydo have potential for preserving
brain health, even increasinghippocampal size and preventing
brain atrophy, increasing thosetrophic factors and also, in
addition, having cognitivebenefits, nootropic effects.
(25:19):
Understand this distinction andyou're protected from all the
silly claims often made forproducts.
You know that most of thethings that are neurotrophic, by
the way, are not beingadvertised, and that's one of
the problems we have inhealthcare that if something
doesn't make a lot of money,like a dementia drug, you won't
hear much about it.
Now, if you find this a littlebit too overwhelming, I invite
(25:40):
you to join my programs, such asmy drdavisinfinitehealthcom
inner circle, where we have lotsand lots of learning materials,
including videos, and ourtwo-way Zoom meetings where we
discuss all these issues andhelp you succeed.
Now, if you learned somethingfrom this episode of the Defiant
Health Podcast, I invite you tosubscribe to your favorite
podcast directory.
(26:01):
Post a review, post a comment.
Do your part to grow thismovement of self-empowerment in
health and minimizing ourreliance on a flawed healthcare
system.
Thanks for listening.
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