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PRESENTERS 2017
David Perlmutter, MD: The Dynamic Brain
Interview by Craig Gustafson
Facilitated by The Institute for Functional Medicine Annual International Conference, to be held June 1 to 3, 2017, in
Los Angeles, California.
David Perlmutter, MD, is a board-certified neurologist and
fellow of the American College of Nutrition. He received his
MD degree from the University of Miami School of Medicine,
where he was awarded the Leonard G. Rowntree Research
Award. He has published extensively in peer-reviewed
scientific journals, including JAMA Neurology,
Neurosurgery, and the Journal of Applied Nutrition, and
he is a frequent lecturer at symposia sponsored by such
medical institutions as Columbia University, Scripps
Institute, New York University, and Harvard University. He
serves as an associate professor at the University of Miami
Miller School of Medicine.
Dr Perlmutter has been interviewed on many nationally
syndicated television programs, including 20/20, Larry King
Live, CNN, Fox News, Fox and Friends, The Today Show,
The Oprah Winfrey Show, The Dr Oz Show, and the CBS
Early Show. He is the recipient of the Linus Pauling Award
for his innovative approaches to neurological disorders. He
is also the recipient of the 2006 National Nutritional Foods
Association Clinician of the Year Award and was awarded
the Humanitarian of the Year award from the American
College of Nutrition in 2010. In 2015, Dr Perlmutter was
awarded both the Media Award from the American College
of Nutrition and the Healthy Living Award from the
Invisible Disabilities Association.
Dr Perlmutter is a 4-time New York Times bestselling
author, and his books have been published in 27 languages.
His 2013 bestseller, Grain Brain: The Surprising Truth About
Wheat, Carbs, and Sugar,1 has more than 1 million copies in
print. Other New York Times bestsellers include Brain
Maker: The Power of Gut Microbes to Heal and Protect
Your Brain—For Life,2 and his latest book, The Grain Brain
Whole Life Plan,3 published in November 2016.
Integrative Medicine: A Clinician’s Journal (IMCJ): This
year’s Annual International Conference is focused on the
dynamic brain and neuroplasticity, so let’s start off with:
When did the modern theory of neuroplasticity become
verified by the literature?
Dr Perlmutter: The first real landmark work came from
Donald Hebb, PhD, a Canadian researcher. He was puzzling
over what it is that allows brain cells to connect. He is the
one who, 68 years ago, postulated that some factor is
22 Integrative Medicine • Vol. 16, No. 2 • April 2017
operative when nerve cells communicate with each other
that allows them ultimately to connect. He proposed the
theory that, paraphrased, states: “Neurons that fire
together wire together.” Basically, the more that you do
something, the more it will ultimately form a more
indelible relationship between neurons and neural
networks.
IMCJ: Then if this groundbreaking work was done more
than 60 years ago, why has clinical practice been so slow to
catch up with the accepted evidence?
Dr Perlmutter: I think that clinical practice really focuses
on interventional types of things: “What can we do to
make things better?” for example. I think that Dr Hebb,
being a psychologist, was more involved in the research,
trying to understand how it is that neurons ultimately
connect in what is now called Hebbian learning. He wrote
a book back in 1949 called The Organization of Behavior,
and, in that, he proposed this theory whereby these factors
conspire to allow neurons to connect to each other.
Your question, I think, deals with clinical interventions
to perhaps enhance that process and understanding how
that activity might influence cognition, for example. I
think that has been only a relatively recent development,
which, to a significant degree, parallels the science of
neurogenesis, the growth of new brain cells. Interestingly,
the same trophic factors are involved in both neuroplasticity,
the connection of neurons, and the development of new
neurons, which we call neurogenesis.
Certainly what is getting the most attention these
days is brain-derived neurotrophic factor, or BDNF, as at
least one of the components of the nervous system that
enhances the activity both of the genesis of new brain cells,
as well as the way that they connect. These days, certainly,
the person who is well-deserving of the title the “father of
neuroplasticity” is Michael Merzenich, PhD. And he is, in
fact, one of the speakers at The Institute for Functional
Medicine conference this year.
IMCJ: You mentioned that neurogenesis as being a more
recent concept. How did the validation of that theory
change the game for neurology?
Perlmutter—Presenters
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Dr Perlmutter: There was a huge reluctance to accept the
fact that growth of new brain cells could occur in humans.
There are many reasons that that was the case, but at the
time, it was ultimately discovered and published by Peter
Eriksson, MD, PhD.4 This idea—published in November
1998 in the journal Nature Medicine, volume 4, issue 11—
had been well proven in rodents and in primates. But there
was almost a religious rejection of the notion that we
could grow new brain cells as humans.
Dr Eriksson, working with Fred Gage, PhD, at the
Salk Institute in California, in a very clever way was able
to demonstrate neurogenesis in humans. There were a
group of patients being followed who had squamous cell
carcinoma of the face. They were being given a chemical
that marks cells in division, BRDU, bromodeoxyuridine,
which labels cells during the process of mitosis—which is
obviously upregulated in cancer.
Several of these patients died, and Dr Gage and
Dr Eriksson looked at their brains, specifically at the area
where neurogenesis had been found in primates—the
hippocampus, the brain’s memory center. Lo and behold,
they found cells labeled with BRDU in humans of various
ages—well into adulthood—showing active genesis of new
cells, essentially stem cells being formed in the
hippocampus. This was revolutionary.
As a matter of fact, he wanted to publish this
breakthrough finding but was rejected by multiple peer-
reviewed journals, again, who just basically dug in their
feet because they could not accept this change in paradigm;
that neurogenesis does occur in humans. Ultimately, he
not only demonstrated that neurogenesis is occurring in
humans, but that these newly formed neurons actually
develop and differentiate into fully functional neurons, by
doing a special type of staining called TUJ staining. This
was landmark, groundbreaking research that went directly
against the teachings that formed many of my
contemporaries’ training in terms of medical school and
in residency—this notion that brain cells are terminally
differentiated and we do not gain any new population of
brain cells. Nothing could be further from the truth.
Now we fully understand that, and we have come to
the point where we do get right back to the clinical arena
and recognize that this process, this incredible process of
neurogenesis, can be enhanced by making simple lifestyle
changes. That is the part that really lends itself wonderfully
to those of us who are working with patients and trying to
change their ability to influence their health destiny as it
relates to their brains.
IMCJ: With regard to neurogenesis, you mentioned the
hippocampus, in particular. I was recently reading an
article that referred to a study where they compared cab
drivers versus bus drivers…
Dr Perlmutter: Exactly, and they found significant
differences in that these individuals did appear to be both
Perlmutter—Presenters
laying down and retrieving information and there were
clearly brain changes associated with that. Right?
IMCJ: Right, and they found that the taxi drivers had
larger hippocampi than the bus drivers that they attributed
to the fact that the taxi drivers had to learn the entire city
and divine what the specific route was going to be for a
given fare at a given time of the day, versus the bus drivers
who had a set route that they drove consistently.
Dr Perlmutter: That is right. The study that you are
referring to was published, actually, in a journal that is
called Hippocampus. The study was done in London. It
was published, actually, quite a while ago, in 2006,5 and
they did indeed demonstrate that there were patterns—
changes in the patterns of hippocampal gray matter seen
in taxi drivers. It really brings to mind the question, “Now
what is happening?” Because none of us is really in a
position of needing to learn directions anymore because
we have apps, like Waze and Google Maps, that basically
take the guesswork out. We do not have to remember
phone numbers, addresses, or how to get anywhere
anymore because your iPhone is going to tell you where to
go. I think that clearly there are changes that might not
necessarily be positive now that we have off-loaded so
much of our brain power.
IMCJ: What potential do these theories of neuroplasticity
and neurogenesis hold as a clinical tool to support health
and well-being?
Dr Perlmutter: I think it is a question that needs a lot of
attention because, in the recent work of Kirk Erikson, PhD,
they demonstrated what we have known for a long time—
that physical exercise has a dramatic effect in terms of
upregulating the transcription of BDNF, relating to
increased serum level of BDNF, increased size of the
hippocampus, and improved cognitive function to the
extent that his recent publication and editorial that
followed it indicated that people who regularly engage in
aerobic exercise may have as much as a 50% reduced risk
for developing Alzheimer’s disease.
That is profound in the context of (1) the fact that we
have no meaningful treatment for that disease, (2) that
5.4 million Americans are already affected by that, and
(3) that the number is projected to triple by the year 2050.
Here is a powerful intervention that costs nothing and
nobody is talking about. What we see on the evening news
are commercials for medications, cholinesterase-inhibiting
medications or NMDA-receptor antagonists that do not
work. That is what people think they need to do: Basically
live their lives, come what may, and then hope that
medical science has developed a cure for this disease,
which we now recognize is highly preventable between
engaging in aerobic exercise on a daily basis and keeping
your blood sugar low or not becoming a type 2 diabetic.
Integrative Medicine • Vol. 16, No. 2 • April 2017 23
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These 2 factors alone have a profound effect in terms of
lowering an individual’s risk for becoming an Alzheimer’s
patient regardless of their APOE status.
IMCJ: What role might environmental toxins play in
Alzheimer’s risk?
Dr Perlmutter: We are just beginning to look at why that
might be an event. When you understand the Functional
Medicine Matrix, you realize it is sort of like a carousel and
that you can jump onto that carousel at multiple points.
We have genetic predisposition, we have early life factors,
and we have triggering events. Many of these triggering
events, I think, are things that people are becoming much
more aware of.
For example, a new understanding is that even the air
we breathe might significantly increase a person’s risk for
cognitive decline and even full-blown Alzheimer’s disease.
A study6 that was published just in January of this year in
the journal Science looked at the risk for developing
dementia in relationship to how close somebody lived to a
busy street. When you live near a busy street, you are
exposed to what are called PM2.5. What that means in
scientific jargon is particle size of around 2.5 micrometers
or less. These are things that are strongly associated with
oxidative stress and we know that these particles are
associated with other inflammatory issues like asthma,
lung cancer, and coronary artery disease. Now new
research indicates that through multiple mechanisms,
these same particles are associated with a dramatically
increased risk for developing dementia.
The Lancet reported a study7 indicating that those
people who live within 50 meters of a major roadway have
a 10-fold increased risk of dementia compared with those
people who live at least 150 meters away from a busy
roadway. This was looking at a population of around
6.6 million subjects, basically all of those living in Ontario,
Canada. It was a really incredible study that builds on
Harvard research that looked at the Framingham data and
showed significant shrinkage or decline in brain volumes,
again, in individuals who have had this PM2.5 exposure.
We add this to the list that includes exposure to
environmental mercury, other heavy metals, and now the
very air that we breathe as being a potent environmental
risk factor for cognitive decline and risk for dementia. I
would say, “Who knew?” but we had to suspect that.
IMCJ: Earlier you mentioned that at the moment there is
not a recognized cure for Alzheimer’s, but there has been
some significant progress in mild cognitive impairment
and moderate cognitive impairment and the ability to
actually reverse that, hasn’t there?
Dr Perlmutter: Well, not from a pharmaceutical
perspective, no, there has not. By and large, pharmaceutical
approaches have focused on 3 areas: NMDA receptor
24 Integrative Medicine • Vol. 16, No. 2 • April 2017
antagonism, anticholinesterase therapy based on the
so-called acetylcholine hypothesis that deficiencies of
acetylcholine lead to brain degeneration—which I think
we all recognize now is basically absurd—and, third, the
notion that the approximate cause of cognitive decline in
the Alzheimer’s brain or even prior to the diagnosis is this
accumulation of beta-amyloid plaque.
I think we now recognize that this is not a disease that is
caused by a single variable. Multiple issues conspire to
ultimately lead to the decline in cognitive function that we
then call dementia. Now, reversing that is, in fact, possible,
but not by pharmaceutical means as yet. Dale Bredesen, MD,8
and his work published in the journal, Aging in 2014,
demonstrated actual reversal of full-blown Alzheimer’s
disease in 9 of 10 patients, not by providing one
intervention, but by using, ultimately, as many as
36 different leverage points including change in diet,
increase in aerobic activity, optimizing vitamins and
nutrients including vitamin D and DHA, going on a
gluten-free diet, and stress reduction. Multiple factors
allowed those patients to actually recover, many of whom
were able to return to gainful employment.
Now, as it relates to mild cognitive impairment, there
are multiple studies that demonstrate significant
improvement in cognitive function just by introducing an
exercise regimen to the extent that the Mayo Clinic
proceedings several years ago indicated—that physical
exercise should be considered as a therapeutic prescription
in the treatment of cognitive decline. It is really taking us,
I think, significantly away from this notion of looking for
and needing a pill, but, rather, recognizing that there are
some lifestyle issues that are critically important.
Again, what the Mayo Clinic published was the idea
that moderate-intensity physical exercise should be
considered as a prescription for lowering risk for cognitive
decline and slowing cognitive decline across the age
spectrum. That was published in the Mayo Clinic Proceedings
back in September of 2011.9 When there is an Alzheimer’s
drug or a drug that has utility in treating mild cognitive
impairment, to get back to your question, I am going to be
thrilled. That will be wonderful. However, this should be a
very inclusive approach as opposed to being an approach
that just focuses on monotherapy. I think that even
Dr Bredesen’s approach does, in fact, welcome the utility of
pharmaceuticals as part of a more wide-ranging spectrum
in dealing with, and even averting, brain-function decline.
IMCJ: You mentioned that Dr Bredesen’s approach has
36 different access points in the protocol. If I understand
it correctly, there is a tipping point. A patient incorporates
enough of the access points and there will be a point at
which things begin to go the other way. So a given patient
does not have to adhere to all 36 access points.
Dr Perlmutter: That is right. Beyond that, there is some
degree of personalization of the program by, really, all of
Perlmutter—Presenters
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us who are involved in Functional Medicine. That is
“What might that person specifically need based upon his
or her biometrics, his or her genetic predisposition?” for
example. I think, again, one of the primary tenets here is
to not lock into a specific recipe for a specific medical
problem. Be very open to the notion that these protocols
need to be very malleable and very much personalized
with reference to the uniqueness of the individual patient.
IMCJ: Is there a difference between approaches for
remission of conditions or repair of an injury versus
something that is more targeted toward prevention and
wellness?
Dr Perlmutter: I was once criticized online by somebody
indicating that I have extrapolated between those 2 ideas:
that prevention versus intervention should be considered
very different approaches. I tend to reject that because I
think that we are trying to undo these processes and target
these mechanisms preemptively in the preventative
protocol and interventionally when dealing with
established diseases. However, the processes are, in fact,
the same.
Ultimately, from a broad mechanistic perspective,
they are inflammatory and mediated through the action of
oxyradicals and nitrogen radicals. Oxidative stress and
inflammation are indeed the cornerstone mechanisms
that can be targeted in both a preventive scheme and also
from an interventional perspective once disease has
manifested. Having said that, we need to take a step back
and ask, “What is it in our physiology that enhances this
feed-forward inflammation and oxidative stress that
ultimately leads to the penultimate event in
neurodegeneration and mitochondrial dysfunction and/or
failure?” The ultimate event, of course, being what is
induced by this mitochondrial dysfunction, and that is
apoptosis or actual loss of brain cells.
We can get to that endpoint through multiple channels,
and I think we’ve got to address what those common
channels are that both lead to disease and also help to
propagate it once it has manifested. That takes us back to
lifestyle issues. We know that, for example, glycation of
proteins is a seminal event in initiating both oxidative stress
as well as inflammation. This relates, then, back to diet and
other lifestyle issues. It is why, for example, type 2 diabetes
is associated with as much as a quadrupling of the risk for
developing Alzheimer’s disease. That is, by and large, a
preventable condition based upon lifestyle choices. It is why
we focus so heavily on diet and on lab parameters like
hemoglobin A1c, fasting insulin, fasting blood sugar, and
fructosamine as giving us some sense as to where this
individual might be on the risk scale.
We see strong correlations that demonstrate, for
example, a very powerful relationship between a person’s
A1c and the degree of atrophy of their hippocampus. That
is a powerful relationship published in the Journal of
Perlmutter—Presenters
Neurology.10 When we see that information, it tells us that
doing our very best to control blood sugar is going to go a
long way to keeping the brain from degenerating. There
are multiple other mechanisms that are involved with
sugar metabolism that have a role to play in the brain, not
the least of which is the role of insulin, but, that said, I
think that my opinion is: We can certainly explain this
dramatic increase in Alzheimer’s incidents based upon a
correlation with increased incidents of type 2 diabetes.
As an Alzheimer’s preventative approach, it is
incumbent to keep blood sugar levels in a range that is
good for the body and good for the brain. I think that the
so-called normal levels of blood sugar need to be reassessed
through the lens of what is an optimal level. We let people
get away with a blood sugar of 100 when clearly we see
published in the New England Journal of Medicine in
September of 2014 an article aptly entitled “Glucose Level
and Risk for Dementia” demonstrating that even a level of
100, which is considered normal, is already associated
with increased risk for developing dementia.11 We need to
really revise that and pay close attention to those
biomarkers because they have implications not just for the
development of type 2 diabetes, but for inflammatory
diseases across the spectrum, which do, in fact, include
Alzheimer’s as well as coronary artery disease, obviously
diabetes, and even cancer.
IMCJ: It really is amazing that we allow that threshold to
be so high.
Dr Perlmutter: Well, we look at normal ranges that are
developed from large numbers of people. Our norms are
an extrapolation of averages. That does not take lab work
and bring it into the clinical arena in terms of what is best.
It is time that we look not at normal levels but at optimal
levels. Then, from an interventional perspective with an
established patient, someone who already is manifesting
disease—what then should we do based upon just the
simple notion of blood sugar being detrimental to the
brain? And that is a far more aggressive approach. By
placing that patient on a ketogenic diet, powering the
brain with fat as opposed to carbs, the result is far more
efficient production of ATP, far less production of free
radicals associated with oxidative phosphorylation, and,
ultimately, amping up of the body’s production and
availability of beta-hydroxybutyrate. This is far more than
a cellular fuel, but actually a messenger molecule
stimulating G-protein receptors that augment antioxidant
protection, reduce inflammation, and also act as what we
call a histone deacetylase inhibitor, which has some very
powerful effects in a positive way in terms of viability and
preservation of brain cells.
IMCJ: In the very first interview I ever did in this field, I
talked to a gentleman about insulin sensitivity, glycation,
and related issues. He said, “Even at the blood glucose
Integrative Medicine • Vol. 16, No. 2 • April 2017 25
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level of 90, you have got damage going on in your body. It’s
just not good.”
Dr Perlmutter: Well, that is right. We have seen well
beyond cognitive impairment, even Parkinson’s disease,
which is considered a motor event, be profoundly affected
by the intervention of placing people on a hyperketonemia
diet—actually pushing them into ketosis. This is not news.
The first report of this was published way back in 2005 in
the Journal of Neurology.12 What we know is that in
Parkinson’s, for example, the mitochondrial defect is in
what we call complex one of the electron transport chain.
It is why, for example, coenzyme Q10, which can bypass
that defect, has been so heavily investigated.
We also know that ketone metabolism, using ketones
as a mitochondrial fuel, might actually bypass that
mitochondrial defect. The first study done back in 2005
was actually very small. It involved only 5 patients,
Parkinson’s patients on medication, and they were placed
on a very strongly ketogenic diet for a 28-day period. They
measured a bunch of parameters that make up what is
called the Unified Parkinson’s Disease Rating Scale. That is
a common scale used by neurologists to measure how a
Parkinson’s patient is doing, looking at things like
mentation and mood, activities of daily living, motor
function, and whether there are any complications from
the treatment that they might be receiving.
The study was really quite dramatic because it
demonstrated improvements pretty much across the
board—dramatic improvements—in these parameters,
especially in terms of motor function. Over the brief
study—28 days—the participants achieved an average
reduction of 43% in their UPDRS or Unified Parkinson’s
Disease Rating Scale rating with one patient having an
81% decline on the UPDRS scale, which is far better than
what you can typically achieve with medication. This was
just by placing them on a diet that cut their carbs, cut their
sugar, and favored healthful fat.
Now, these days we would want to amp that up, of
course, by adding coconut oil and MCT oil, and being very
strict on the carbs. It is so unfortunate that there is still such
a reluctance to embrace anything nutritional. Here this was
published in the Journal of Neurology, which is arguably the
most well-respected neurology journal on the planet. It is
actually the journal published by the American Academy of
Neurology. This was 12 years ago, and no one has paid any
attention to it since that time. But now we are seeing all
kinds of work that is really starting to popularize ketosis. A
recent comprehensive book by Thomas Seyfried, PhD,13
looking at the metabolic basis of cancer, is one example.
We are really seeing a lot of new information that is going
to be difficult for mainstream medicine to turn its back on.
IMCJ: What topic will you be focusing on in your
presentation at the conference?
26 Integrative Medicine • Vol. 16, No. 2 • April 2017
Dr Perlmutter: Well, my opening key note is going to take
a very broad overview of where we are in the neurosciences
today, the challenges we face in terms of the sheer numbers
across multiple disease spectrums, and what the notion of
prevention is all about as it relates to the brain. I am then
going to introduce, by way of their presentation, each of the
speakers and talk about what they are going to present and
how their specific topic uniquely fits into the Functional
Medicine Matrix. Then I am going to explore a little bit
further the notion of neurogenesis and neuroplasticity and
ultimately a talk about how just thought in and of itself,
even without action is able to change the brain in terms of
its network and also in terms of its functionality. I am doing
a workshop, as well, which is where I will do more
discussion about the role of the microbiome.
IMCJ: Research in that area, the gut-brain connection, has
exploded in recent years.
Dr Perlmutter: That is for sure. It is like we have just come
upon this, but, truthfully, medicine has lived in a world of
reductionism, of looking upon the body and its constituent
parts as basically a machine, as described by Descartes.
That is: The brain is the computer and the lungs are the
bellows and the heart is the pump. But now we recognize
that this integrative view, this holistic view of the human
body, is really going to give us the most powerful leverage
points to be aggressive and successful in keeping people
healthy, but also in reversing disease. We are just beginning
to see gut-targeted therapies that have profound effects in
terms of brain function as it relates to mood, as it relates to
cognition, and even as it relates to motor activity.
Beyond that, we are just beginning to fully appreciate
that the mitochondria within each and every neuron—and
there are thousands of mitochondria in every nerve cell—are
really deeply involved in regulating cellular or neuronal DNA
expression. It is a very humbling notion that the mitochondria
are actually involved, for example, in regulating the nuclear
genes that deal with whether a cell will live or die. Mitochondria
regulate the action of what are called caspase enzymes, which
are involved in cellular apoptosis.
To a significant degree, we have to look upon the
mitochondria as wielding the Sword of Damocles,
determining who lives and who dies. We are now
understanding—in recent research, published last week—
that ultimately autism may be, in fact, a mitochondropathy,
a mitochondrial event, and that there may be some
influence upon neuronal mitochondria from things going
on in the gut whereby, for example, changes in gut bacteria
that may have been induced by the herbicide, glyphosate,
may ultimately relate to mitochondrial changes within the
brain. This correlation could well explain why autism is
increasing so dramatically in its incidence worldwide.
For more information on the Institute for Functional
Medicine 2017 Annual International Conference, visit
http://IFM.org/AIC/.
Perlmutter—Presenters
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Perlmutter—Presenters Integrative Medicine • Vol. 16, No. 2 • April 2017 27