What can Babies tell us about Alzheimer’s?
In 1906, Dr. Alois Alzheimer requested to
examine the brain of a patient named Auguste
Deter who appeared to have no sense of time
or place and could barely remember basic details
of her life.
In her brain he found abnormalities that remain
to be the hallmarks of Alzheimer’s disease
today, making Auguste the first known patient
with the disease.
“Now here’s the even more striking thing.
If Auguste had instead been alive today, we
could offer her no more help than Alois was
able to 114 years ago.”
In a 2015 TED talk, Samuel Cohen points out
that despite having discovered the disease
more than 100 years ago, no real progress
has been made in the fight against it.
Cohen explains that Alzheimer’s is certainly
not a part of normal aging and it is a disease
that can be cured. “…we’ve managed to identify
a critical step in the process and are now
testing a new class of drugs which should
specifically block this step and stop the
However, while Cohen and his team’s work
will surely be productive, it’s very unlikely
that a single drug will cure the disease.
That is not to say that the disease cannot
be treated, but… why is this?
And what does Alzheimer’s have to do with
And finally: What do babies, coconut oil and
breast milk all have in common?
To understand, let’s start with a story
from Dr. Mary Newport.
In May 2008, her husband Steven received a
MRI and was diagnosed with Alzheimer’s disease.
That same year, Mary took Steve to the University
of South Florida – hoping that he’d be able
to qualify for a new vaccine study that might
help his condition.
Unfortunately… he was unable to achieve
the necessary score of 16 on a mental state
examination to qualify for the study – he
only scored a 12.
Around this time, Mary had heard of an upcoming
drug called Ketasyn, or AC-1202 which had
brought about significant improvement over
a 90-day period in half of subjects with a
specific genetic profile.
In a pilot study, some Alzheimer’s patients
improved on memory testing with the very first
Mary then learned that the promising ingredient
in Ketasyn is MCT oil and that the dosing
was just 20 grams.
Mary found out that the MCT oil was derived
from coconut oil and calculated that 35 grams
of coconut oil should contain 20 grams of
MCT oil and so she put this amount – a little
more than two tablespoons, in Steve’s morning
Four and a half hours after having his breakfast,
Steve went again to University of South Florida
to be retested for the same trial mentioned
This time he scored an 18 on the mental state
examination …two points higher than the
60 days after Steve began taking coconut oil
for its MCT content, Dr. Newport wrote this
case study, commenting that “He is able
to concentrate on things that he wants to
do… and stay on task, whereas before coconut
oil he was easily distractible and rarely
Here are three clocks he drew as part of a
mental examination, one the day before he
started taking coconut oil, one just two weeks
after and one 37 days after.
Now, this is just one anecdote and the MCT
in coconut oil did not “cure” Steve’s
Alzheimer’s, but he did improve significantly.
MCT, or “medium chain triglycerides” are
not usually a significant part of the average
adult’s diet, a baby however would be getting
a reasonable amount of them from breast milk.
In fact, MCT’s are added to commercial infant
formulas to mimic the composition of breast
And MCTs are even stored in babies’ fat
What is interesting about MCT oil is that
it acts as a different source of fuel for
the brain, rather than glucose.
(Just to be clear, blood glucose is the same
as blood sugar, which rises when you eat carbohydrate)
Late last month I had the chance to interview
Amy Berger, author of the Alzheimer’s Antidote
where she explained the significance of not
having to rely on sugar, that is – glucose,
“So, um, yea, I would say Azheimer’s is
a fuel shortage or an energy crisis in the
And where that comes from is that the major
problem in the brain of somebody with Alzheimer’s
is that neurons in affected parts of the brain
lose the energy to effectively metabolize
So they’re basically starving.
They’re starving for energy, they’re withering,
they’re shrinking, you can see the volume
of the brain shrinking on an MRI, you can
see that it’s smaller.
And all that comes because the brain is starved
for fuel and the brain is what we call an
Energy Intensive Organ, it only accounts for
about 2% of an Adult’s Body weight but it
uses between 20 and 25% of all the glucose
So the brain, you cannot have an interrupted
fuel supply to the brain or you’re going to
be in major trouble.”
In her book, Amy explains that “compared
to healthy people, Alzheimer’s Disease patients
have shown up to 45 percent reductions in
cerebral metabolic rate of glucose” – essentially
up to a 45% reduction in the rate the brain
uses glucose for energy.
And, It’s almost always observed that the
Alzheimer’s brain is under metabolizing
So what is going on here?
Are we seeing that the brain cells have died
or is it that they are alive and just unable
to utilize glucose?
If the cells were dead, then – as Dr. Stephen
Cunnane points out here, those cells shouldn’t
be able to use any sort of fuel.
As he shows on this slide, you can see that
as indicated by less red shading, glucose
uptake progressively reduces as you progress
from mild cognitive impairment to Alzheimer’s
However, the Alzheimer’s brain has no problem
using ketones for energy.
Not only that, as he shows here, the Alzheimer’s
brain actually uptakes ketones better than
Very simply put ketones are a source of energy
naturally produced in the body from fat when
dietary carbohydrate is restricted enough.
So, if the key problem with Alzheimer’s
is that the brain is lacking adequate fuel
due to an inability to utilize glucose, then
it makes sense that providing an alternate
fuel would cause improvements.
The significance of the earlier mentioned
medium chain triglyceride, MCT oil – is that
MCTs are quickly transported from the gut
to be rapidly oxidized in the liver and turned
For example, In comparison to the long chain
oleic acid, the medium chain caprylic acid
is oxidized 5 times faster in liver cells.
To highlight this point, here’s Dr. Stephen
Cunnane showing that after 6 months of 30g
of MCT oil supplementation, people with mild
cognitive impairment show a doubling of the
uptake of ketones in the brain.
However, this doesn’t matter if getting
more MCT oil into the stomach and getting
more ketones into the brain doesn’t improve
But… it does.
Dr. Cunnane shows here that 6 months of MCT
supplementation improves scores on a battery
of cognitive tests in people with mild cognitive
Before we continue, I’m guessing that if
you are into reading about health and dieting,
ketones are probably starting to feel like
cranberries in the year 2000 … “I don’t
know what’s going on with cranberries, but
they’re getting in all the other juices!”
“Showing up everywhere – hey what do you got
Put some cranberries in it, we’ll call it
cran-apple go 50-50.
What do you got, grapes?
How ’bout cran-grape?
What do you got mangoes?
It seems that with anything from weight loss
to diabetes to arthritis, to brain fog you’ll
find someone saying that the ketogenic “keto”
diet is the answer.
However, while ketones and ketosis may seem
like the new fad being sold as a panacea,
ketosis is not a new thing at all because
virtually every human has been in ketosis
at the start of their life.
As Dr. George Cahill showed in this 2006 paper,
newborns are essentially starting out in ketosis
at a level of about 0.5 millimoles, which
is considered nutritional ketosis.
By comparison, an adult, depending on their
diet, would have to fast for at least 13 hours
to produce that same level of ketones, and
a newborn can reach more than that initial
level simply by not eating for a little more
than 3 hours – something that would take more
than an entire day of fasting for an adult
As this 1986 paper reveals “ketone bodies
could account for as much as 25% of the neonate’s
basal energy requirements in the first several
days of life.”
And it has been shown that ketones can provide
up to 60% of the energy requirements for an
Babies may be living on ketones even before
In his book on the health potential of ketones,
Dr. Muneta Tetsuo, director of Muneta Maternity
Clinic in Japan explains that pregnant women,
whether they are restricting carbohydrate
or not are producing higher than normal levels
By comparing the mother’s blood with the
newborn’s umbilical cord blood, he found
that out of 416 cases, 70% of babies were
born with even higher levels of ketones than
that of the mother.
By analyzing the villi that provide contact
with the mother’s blood to the fetal membrane,
Muneta deduced that the fetus must be living
in an environment of elevated ketones from
the start of pregnancy.
And, even a month after birth, babies on average
had a blood ketone level 5 times higher than
that of a normal person.
And, while the older you get, the harder it
is to get into ketosis, humans are generally
much better at getting into ketosis than other
Amber O’Hearn explains this in her talk
at Low Carb Houston 2018,
“You might think that a dog would be in ketosis
A dog eats a low carb diet but in fact, if
you want to get a dog into ketosis, you have
to either deprive them of calories or put
them through some intense exercise, or you
can give them MCT oils and that would work
But even if you completely fast a dog, it
takes longer for a dog to get into ketosis
and they never get into the deepest levels
that a human would get into.”
So what’s interesting about human babies’
brains is that while they have an even higher
demand for energy, as much as 3 times as what
the adult brain requires, they are relying
on ketones, a fuel that modern people rarely
utilize, because fasting or heavy carb restriction
are necessary to get an adult into ketosis.
And, while Alzheimer’s patients are having
trouble using glucose for energy, their brains,
like a baby’s brain, can run just fine on
But of course, most people have no trouble
running their brains on glucose – In fact
it was thought for a while that the brain
could only run on glucose.
So what is going on that messes up the brain’s
ability to take up glucose?
I can’t share the whole picture in this
one video, but for starters, consider this:
it’s estimated that 80% of Alzheimer’s patients
have insulin resistance or Type 2 diabetes.
(Just to clarify insulin resistance is what
leads to diabetes) And, women as young as
24 years old with a form of insulin resistance
due to polycystic ovary syndrome have reduced
metabolism of glucose in the brain that looks
strikingly similar to what you’d see in
a 65 year old brain.
In fact, Alzheimer’s is frequently referred
to as Type 3 diabetes.
Though… it’s not as simple as you first
get Type 2 diabetes and then you progress
to Type 3 diabetes from there.
I guess the logical step would be…
OK you get type 2 diabetes and then you progress
into Type 3 diabetes… is that accurate?”
“Partly but not fully.
So, having type 2 diabetes is a risk factor
for Alzheimer’s or cognitive decline, so you
are at increased risk to have dementia later
in life, if you’re a type 2 diabetic, but,
not everybody with type 2 diabetes will develop
Alzheimer’s and not everyone who has Alzheimer’s
had or has type 2 diabetes.
So the thing is: When we talk about type 2
diabetes, we only ever talk about blood sugar
– blood glucose.
They never look at insulin, so there’s a lot
of people walking around right now with totally
normal blood sugar, but the blood sugar is
only normal because it’s being kept in check
by sky high insulin.
And in a lot of modern illnesses, what we
call non-communicable diseases – meaning not
something you can catch like a cold or flu,
not something contagious, some kind of chronic
illness that’s not … – like type 2 diabetes,
like obesity, PCOS, cardiovascular disease,
So many of these are driven by chronically
high insulin, even when blood sugar is normal.
So you can get any of those things, whether
its hypertension, pcos, gout, all these things
that are driven by insulin, even people’s
sugar is normal.”
“The same thing is true for Alzheimer’s.
Chronically high insulin is a major risk factor
for Alzheimer’s, regardless of what genes
To simplify a very complex issue, chronically
high insulin is what drives insulin resistance.
When you eat carbs, insulin is secreted to
transport glucose into the cell.
When insulin is constantly being secreted
in response to excessive low fiber carb intake,
your cells become resistant to the effects
of insulin, similar to how frequently drinking
alcohol makes you resistant to the effects
As Dr. Georgia Ede explains here, insulin
has many important functions in the brain
other than just glucose regulation.
And, there are insulin receptors on the blood
brain barrier to get insulin into the brain
so it can perform those functions.
But when the blood brain barrier is constantly
flooded with insulin, it becomes resistant
to it by downregulating insulin receptors.
So, you can reach a state where you have plenty
of glucose in the brain, but not enough insulin
to use it.
The hippocampus, the region of the brain largely
responsible for memory formation, has a particularly
high glucose demand.
And while many brain cells have Glut-3 receptors
which don’t require insulin, the hippocampus
also has Glut-4 receptors which do require
And, one of the earliest detectable traits
of Alzheimer’s disease is a compromised hippocampus.
And Of course memory problems are a well understood
sign of cognitive impairment or Alzheimer’s
Now, there is one more point about insulin
I want to share and it has to do with beta
amyloid, which I’m sure you’ve heard of
if you spent any time looking into Alzheimer’s
disease as beta amyloid plaques are one of
the hallmarks of the disease.
“I think, some people who might be a little
bit more into this topic, they might’ve heard
of Amyloid Plaque and they might be saying
‘Oh, maybe it’s the Amyloid Plaque that is
like choking neurons and so they can’t get
Is that accurate or is it not, and can you
comment on that?’.”
“It’s, it is accurate but the implications
are not what we’re normally told about this
So um, I don’t know how much time we have
to get into detail, but amyloid or beta amyloid
is this protein that the neurons secrete that
even healthy people’s brains secrete, it’s
not specific to Alzheimer’s.
The problem in Alzheimer’s is that these proteins
are not cleared away properly, so when they’re
secreted they just build up and build up….
and form these infamous plaques.”
“We were talking about…
Amyloid plaque seems to be kind of choking
the neurons ability to utilize glucose.
Is there a mechanism around that that you
can talk about?”
“Yea so I do think there is a physical aspect
to it that these plaques do build up outside
the cell and they actually block synapses,
they block neuronal signal transmission, but,
biochemically – so I’m gonna get a little
nerdy, hopefully the audience is not gonna
be bored here, but… this amyloid inhibits
an enzyme called pyruvate dehydrogenase, and
this enzyme, pyruvate dehydrogenase is the
connection between glycolysis and the krebs
cycle – so it’s two ways to produce energy
We convert glucose to pyruvate through the
process of glycolysis, and then we convert
pyruvate to acetyl-CoA, which then gets burned,
gets oxidized for energy, to produce energy
through the krebs cycle.
And pyruvate dehydrogenase is the connection
between those two.
And beta amyloid puts the breaks on this enzyme.”
“What is it that degrades the amyloid plaque,
what clears it out – you were saying that’s
one of the issues, it’s not getting cleared
“Yea this is really one of the most shocking
things I came across in my research on this
is that – remember I said these plaques, these
amyloid proteins are not really a problem
– even healthy brains secrete them.
The problem is that in Alzheimer’s, they build
up, they’re not cleared away properly.
There’s an enzyme that clears this stuff away
and it’s called insulin degrading enzyme,
I mean how weird is that?
So this enzyme, IDE, insulin degrading enzyme
has more than one target that it works on,
these – beta amyloid is one of its targets,
insulin is another of its targets.
And the thing is, enzymes have different affinities
– different sort of like favoritism for one
target, one substrate over another.
And the favorite of this enzyme is insulin,
the affinity of this enzyme for insulin is
so high that as long as there’s a lot of insulin
swimming around in the blood stream… this
enzyme is so busy going after all these insulin
that it’s going to ignore and neglect all
of its other targets, including this beta
And they know that in people that have hyperinsulinemia
who have chronically high insulin levels,
they have more beta amyloid buildup.”
“You can have Alzheimer’s disease without
a lot of plaque buildup in the brain and you
can have a lot of plaque buildup in the brain
and not have Alzheimer’s.
So um, we can’t pin everything on this amyloid
if not everyone who has Alzheimer’s even has
a lot of this plaque.”
This complexity of the disease that Amy Berger
has highlighted brings us back to my first
point that it’s very unlikely that a single
drug will cure the disease.
As Dr. Dale Bredesen, author of the “End
of Alzheimer’s” points out, the drug would
have to do the following 36 things:
That is not to say we need 36 different drugs
– Dr. Bredesen likens this situation to a
roof with 36 holes.
You can plug some of the holes with drugs,
but you’ll have to plug many more of them
with lifestyle interventions like adopting
a ketogenic or low-carb diet, consuming MCT
oil, making sure you are getting sufficient
amounts of certain vitamins and minerals,
getting sufficient sun exposure, optimizing
sleep, exercising, and more as part of his
Here is Dr. Bredesen explaining the case of
a physician – who was… basically a genius,
having gone to a major university when he
was only 15 years old, but as of 2014 was
suffering cognitive impairment.
As a classically trained physician he was
very skeptical of Dr. Bredesen’s approach…
“so, everything I would say he’d say ‘That’s
not important, that’s not important.’
So finally after a few minutes I said look,
give me six months, if I can’t make you better
then go elsewhere.
He said there is no place else.”
On the program he drastically reduced his
fasting insulin and made significant improvements
in other important markers.
More importantly his cognition improved significantly
– in just 3 months his wife called Dr. Bredesen
to tell him how much sharper he had become.
Dr. Bredesen wrote that in just 10 months,
he went from struggling to perform mentally
to seeing patients full time.
Interestingly, the volume of his hippocampus
increased – going from the 17th percentile
to the 75th percentile.
The neuroradiologist who did the second MRI
insisted the apparent increase in brain volume
was a mistake because they had never seen
that in the 75,000 scans they had done in
Dr. Bredesen took the films to be analyzed
elsewhere and confirmed that this person had
indeed increased the volume of their hippocampus
on the program.
This is just one person, but not the only
person who made improvements on the program.
Dr. Bredesen published a research paper in
2016 documenting 9 more case studies of patients
who improved biomarkers and their cognition
on his program, and there are still many more
Dr. Bredesen says that there are at least
3 types of Alzheimer’s, so if you are trying
to treat or prevent it, your approach will
be different depending on which type you have.
Alzheimer’s is, as you’d expect – complicated.
But that does not mean there is not plenty
of useful information out there.
Just because there’s not a single pill or
even a handful of pills we can hold up and
say is the cure to Alzheimer’s, that doesn’t
mean there’s no way to prevent, stall or
even reverse the disease.
If you’d like more information, check the
description for links to the books and lectures
I mentioned and stick around because I’ll
be releasing the full Amy Berger