This DOCTOR Knows What Causes Alzheimer’s and How You Can PREVENT It | Jay Lombard on Health Theory
Watch on YouTubeVideo summary
Dr. Jay Lombard presents a comprehensive theory linking neurodegenerative diseases like Alzheimer's, Parkinson's, and ALS to underlying infectious processes rather than viewing them solely as genetic inevitabilities or purely age-related decline. He argues that these conditions are fundamentally vascular-based issues where inflammatory mechanisms, infections (such as *C. diff*, Lyme disease, fungal pathogens), and lifestyle factors converge on the endothelium of small blood vessels. This convergence leads to ischemia—interruption of blood flow—which prevents essential supplements from reaching brain regions in need. Consequently, misfolded proteins accumulate within these compromised vascular systems, forming plaques similar to atherosclerosis or clots that the immune system cannot effectively clear due to lysosomal failure and bacterial inhibition mechanisms. Central to Lombard's hypothesis is the concept of "lysosomal failure," where the body's cellular cleanup crew becomes overwhelmed by modern pathogens and lifestyle stressors. He explains that heat shock proteins, which act as chaperones to identify misfolded proteins for degradation in acidic lysosomes, are often insufficient because patients cannot mount a fever or due to aging. Furthermore, certain bacterial infections actively inhibit lysosomal enzymes to ensure their own survival, creating chronicity. Lombard emphasizes the critical role of periodontal disease over "leaky gut" as the primary gateway for pathogens entering the brain via the blood-brain barrier, noting that the oral cavity's proximity to sinus cavities makes it a more direct staging ground for neurological invasion than the gastrointestinal tract alone. To prevent these conditions and manage them effectively, Lombard advocates for risk factor management identical to cardiovascular disease prevention, focusing on epigenetic regulation through methylation and acetylation. He recommends specific lifestyle interventions such as intermittent fasting (typically 16 hours) to reduce liver stress and increase heat shock proteins without inducing hypoglycemia in diabetics. His dietary approach suggests a balanced plate consisting of vegetable-based proteins, high-quality fats like olive oil and avocados, and complex carbohydrates rich in polyphenols from colorful fruits and vegetables, while avoiding processed sugars that drive insulin resistance. He also highlights the importance of natural antimicrobial mouthwashes for oral hygiene to mitigate periodontal risks associated with Alzheimer's disease. Beyond physical interventions, Lombard integrates a profound spiritual dimension into his clinical practice, challenging therapeutic nihilism by emphasizing purpose, faith, and social connection as vital biological necessities. Citing Victor Frankl’s logotherapy, he demonstrates that existential hopelessness biologically shuts down the production of neurotrophic factors like BDNF (brain-derived neurotrophic factor), while a sense of purpose activates survival pathways. He asserts that love is biology itself, increasing endorphins to help patients endure pain and noting that strong social support systems significantly improve prognoses for conditions like ALS. Ultimately, his goal is not necessarily curing the disease but helping individuals live with it by addressing vascular health, managing infections, optimizing lysosomal function through diet and fasting, and fostering a mindset of purposeful living.
Read the full video transcript
But I think what people most forget is
that the the the closest proximity
of infectious diseases to the blood
brain barrier is in periodontal
diseases and that's been
strongly associated with with
Alzheimer's disease.
[music]
Everybody, welcome to another episode of
Health Theory. I am joined today by Dr.
Jay Lombard. Jay, thank you so much for
joining me today.
It's a pleasure to be here. Thank you.
Dude, I'm really excited to go into
this. You are bringing together a lot of
different things in your field. I'm used
to dealing with holistic people when it
comes to nutrition, when it comes to
metabolic health, but you're sort of the
first person I've come across
that's bringing similar areas together
when we look at neurological conditions.
And so as a I guess a flag post here for
everybody in the audience, we're going
to go on a pretty epic journey I think
today regarding what impacts the brain
negatively, some of the neurological
disorders that are cropping up like mad
and what we can do to fix them. And
let's get really specific about what
your core hypothesis is and it'll be
interesting to see because there's
actually for how impressive I find you,
there is precious little
um
interview material out there on you. And
so I could watch your thinking evolving
in real time as I you know, watch these
interviews. And so the sort of last
guide post that I had in terms of what
you were talking about publicly was that
hey, I think that we what we may have is
um
a pathogenic
problem in the gut that is making its
way to the brain through leaky brain and
that may be causing I mean you you very
specifically said I have a hypothesis
that ALS is caused by
C. diff.
And that was as as of last guide post
was the thing that you said that people
were really pushing back on.
[snorts]
And I'm curious, is that still where
you're at or
Uh well, it's evolved since then. So,
I'm glad to have this interview right
now because I I think C. diff uh one of
the issues with uh correlating
infectious disease with neurological
diseases uh is is there's two questions,
basically. The first question is
uh are they comorbid conditions? Not
necessarily being causal. Meaning that
you can see patients that have
infectious disease like C. diff. Uh it
doesn't necessarily mean that that those
infectious diseases are causing
neurological problems. So, one of one of
the gaps in our understanding is how
specifically do infectious diseases
actually lead uh to neurological injury?
That's sort of, you know, one big step
that has had evolve in my thinking uh to
establish, you know, uh
I will I won't say the word causality,
but but pathogenic mechanisms that
overlap uh between infectious diseases
and neurological problems. And the
second thing that I I kind of have to
backpedal on, I thought that it was C.
diff was the primary smoking gun. Uh
that's why I'm glad that I'm on this uh
call with you today because I don't
think it's a single infection. Um I
think it's a multitude of chronic
infectious diseases uh
whether it's a combination of bacterial,
uh fungal, as well as viral diseases,
Lyme disease. Uh I'm a I'm an astute
listener to my patients. So, when my
patients tell me that there's a
connection between
uh when they developed uh
a hepatic infection or Lyme disease and
thereafter developed, you know, MS
symptoms,
uh I started paying attention and not
being dismissive uh of what patients
told me they thought the connection was
between infectious disease and a
neurological problem.
Yeah, so if your former hypothesis and
and you were very clear that this was a
hypothesis, and every time I've ever
heard you speak, you're very metered, um
which I love, but I also like that
you're not afraid to have a hypothesis
that you're pursuing. So, is now your
thinking that basically that we're
getting these neurological symptoms, we
think that we need to focus entirely on
the brain, but really the effects in the
brain are merely a uh
a symptom of a pathogen that has
intruded somewhere else, whether it be
from a tick bite and it's Lyme disease,
or whether it be from your diet and um
you're you've caused disruption in your
microbiome, and now C. diff
overpopulates.
Is is that the idea that all of this is
pathogen-related, or is there
potentially something else?
Yeah, so first of all, I'm glad that
that uh
that this is a hypothesis. This is a
theory, right? And it's it's it should
not I I do not want to be credited for
this theory. I mean, there's plenty of
publications from in nature, from all
sorts of esteemed journals that have
actually asked this question, you know,
is Alzheimer's an infectious disease? Uh
and other neurodegenerative diseases
Parkinson's. So, I I don't want to take
credit for this theory.
Uh that's number one. Number two is I
think that the way my thinking has
evolved regarding this hypothesis is to
try to explore
how specifically
uh does any infection
uh produce neurological problems? So, my
in regards to how my thinking is
involved, uh I think that these
conditions are ultimately
vascular-based.
Uh meaning that
uh inflammatory conditions, infectious
diseases,
uh bad lifestyle, insulin resistance,
hypertension, uh all converge on the
endothelium, on on blood vessels,
basically, in the walls of blood
vessels. Uh and that is sort of the
underlying mechanism of neurological
injury uh that connects all these
epigenetic factors to neurological
diseases like ALS, Parkinson's, and
Alzheimer's disease. So, you know, in
the old days back, uh,
you know, in the 1990s when I finished
my neurology residency, we would see on
on MRI studies when they first came out
because it was, you know, that in those
days MRI was just being introduced, uh,
we would see all sorts of of changes,
ischemic changes, changes like like what
we call mini strokes, uh, or vascular
changes, uh, in various areas of the
nervous system. So, for instance, in
Parkinson's disease patients, we would
see, you know, evidence of what's called
small vessel ischemic disease. Uh, you
know, the
ischemic mean?
Ischemic means lack of blood flow,
interruption of blood flow.
Um, and we still see these changes. If
we do, uh, MRIs on Alzheimer's patients
or in patients with ALS,
uh, we see what what are called these
unidentified bright objects, these UBOs,
uh, that the radiologist, uh, kind of
comment on and they they say
differential diagnosis could be
vasculitis, it could be Lyme disease,
uh, it could be just age-related white
matter changes. But what what all those
things actually mean in principle is
that whatever the provoking factor is,
whether it's inflammatory mechanisms,
uh, infectious mechanisms,
uh, or some combination of of various,
uh, interruptions, traumatic brain
injury is another example that can
produce these vascular changes.
Uh, the the smoking gun, if you will,
uh, is really based upon disruption, uh,
in these very very small blood vessels
that are responsible to perfuse the
brain
because without perfusion of the brain,
you could take any supplement you want,
uh, but if you don't have adequate
perfusion,
uh, you're not going to have a healthy
brain.
Meaning you no longer have the
functioning vasculature to get said
supplement to the regions of the brain
that actually need it.
Exactly.
So, all neurodegenerative diseases,
whether it's ALS, Parkinson's,
Alzheimer's, are characterized by the
production of of proteins that are
misfolded. Uh so, think of these
proteins as basketballs
uh that need to be inflated a certain uh
volume so you can dribble correctly,
right? Once once that that basketball
becomes deflated
uh as a protein, we call these misfolded
proteins. So, there really there really
are two challenges uh in our approaches
to ALS and other conditions. One is to
uh
figure out how to block the production
of these proteins cuz these proteins
will continuously be misfolded uh based
upon genetic abnormalities that a person
uh has acquired as a result of these
conditions. And the second challenge is
once those misfolded proteins are
actually um
uh created, how do you degrade them?
Because at they these proteins are
pathological, and they build up like
atherosclerosis. In fact, we now there's
there's plenty evidence right now
uh that these conditions uh you know,
ALS, Parkinson's, uh
and Alzheimer's disease uh have these
plaques uh in the vascular system.
There's a condition called amyloid
angiopathy, which which speaks to that.
So, in other words, I the way I the way
I've been thinking about uh
neurology right now is the way that I
think cardiologists began thinking about
heart disease uh back in the '70s,
meaning that that, you know, unless
you're at the stage where you need sur-
surgery, right? To remove whatever
plaques are building up, the best bet is
identifying who has these conditions,
number one,
uh and number two, uh putting a a
preventive program
uh with the same risk factor management
as we do for cardiovascular disease
because like you said, you know, the the
pathology manifests based upon where a
person's most vulnerable. People with
genetic risk for Alzheimer's, that's
where this pathology is going to show
up. But the pathology itself is very
similar. I mean, you know, misfolded
proteins are basically what clots are,
right? Clots are basically protein
aggregates that are misfolded and
therefore can't be removed by the body's
immune system. So,
uh what I what I mean to say is that I
think that, you know, our our goals here
are to to manage these as chronic
diseases. I I tell people, my goal as a
clinician is to help you live with ALS,
not die from the condition.
That's that's what I, you know, try to
encourage people to think about.
Very interesting. So, do you think that
all of these chronic diseases, whether
it's cancer, whether it's heart disease,
Alzheimer's, ALS, do you think that they
all have
um
What I was going to ask is do you think
they have the same set is probably the
right word of underlying conditions, or
do you think it's just that the body
only has so many
uh make-or-break mechanics and things
impact those make-or-break mechanics in
different ways?
That's that's a fantastic question, by
the way. Fantastic question. So, I think
that
we need to understand sort of uh a
little bit more in depth about how the
body normally handles these proteins
because there are
uh cellular mechanisms uh within our
cells that are endogenous mechanisms
that help us break down these proteins.
Uh it's an area of the cell called the
lysosome, uh which is a very acidic
environment that takes a degraded
protein
uh and literally breaks it down so that
it's no longer pathological. Basically,
you know,
the body has to find a housekeeping
effect to essentially dissolve these
pathological proteins. So, a lot of
leading investigators in all sorts of
fields, cardiology, basic science of
cardiology,
basic science in oncology, basic science
in neurology have identified lysosomal
failure. Uh meaning an inadequacy of the
ability of lysosomes to degrade these
pathological proteins regardless of what
disease a person particularly has.
Meaning that there's an overlapping
mechanism of reduced ability for our
bodies to break down these pathological
proteins.
Do you think that is due to the amount
or due to the type of misfolding that
maybe the lysosome doesn't understand?
Because when I think about things like
that in our body, I I am truly dazzled
that there is a part of our body that
goes
I know I recognize you. You're a good
protein. I'm going to leave you alone.
Ooh, you look weird. You're damaged in
some way and now I'm going to dissolve
you cuz they have to be selective.
Right.
So, is the system just being overwhelmed
or is there a way to misfold that is due
to a modern lifestyle that the lysosome
is just not familiar with?
Uh
it's a combination of various things.
So,
the the proteins responsible to identify
misfolded proteins are called heat shock
proteins. These are proteins that are
elevated by hyperthermia. So, that's
sort of the original principle of why
hyperthermia may be an efficacious
biophysical approach to conditions like
this by elevating these heat shock
proteins.
Because those are the the chaperones
that say, "Hey, you're a misfolded
protein. It's time for you to leave the
cytoplasm. Come with me to lysosome.
Don't worry.
We're not going to get rid of you. We're
just going to recycle you."
So, they these heat shock proteins take
uh misfolded protein, they send it to
the lysosome, the lysosome then digests
the protein, breaks it down, then it
sends it to the what's called the
endoplasmic reticulum, which is another
cellular structure that helps to kind of
recycle all those pathways. So, this
sort of uh
combination of a sort of a three-hit
hypothesis is one that there's not
enough heat shock proteins uh because
aging itself
uh
and you know, one of the things that
that I think I spoke about on with Dr.
Hyman is one of the things that is a
very classic history I hear from
patients is that they're unable to mount
a fever.
Mhm. Uh very often, you know, oh yeah,
I've had C. diff or I've had, you know,
Lyme, I've had sinusitis, but I never
get a fever. That means that the the
body's endogenous
mechanisms to increase heat shock
protein 70 are defective. Uh then you
have a second hit, which is that the
lysosome
So, think of a lysosome like as a as a
pool, right? And you have to put just
the amount of chlorine in the pool or
salt if you're not into chlorine, right?
Uh but if you put too much salt in the
pool,
uh your eyes are going to burn. Meaning
that if it's too acidic, uh
that's also unhealthy for the cell. But
if you don't put any salt into the pool,
you're going to have overgrowth of mold,
overgrowth of of these various
uh
infectious diseases. In fact, one of the
most interesting things I just recently
found in my research is that bacterial
infections actually inhibit lysosomes.
They actually inhibit lysosomes. Part
part of their survival mechanism
uh is based upon inhibiting the enzymes
that are normally required to digest
them. Cuz don't forget
You can take me to the swimming pool,
but the pool's not going to kill me.
That's exactly right.
Yep.
Wow.
Sure. Take me to the pool, but you know
what, guys? I'm going to hang out here.
And that's And that's what sort of
creates the this the chronicity of
infectious diseases is that the lysosome
is unable to digest them properly cuz
the immune system saying, "Hey, okay, we
found, you know, something that doesn't
belong to human DNA. This is, you know,
a bacterial antigen or a fungal antigen,
uh you know, a protein that doesn't look
like us." Okay, great. The heat shock
protein has to uh bind to that
particular pathological protein, right?
If the heat shock protein
uh is not elevated enough because a
person can't mount a fever,
then the the infection will remain
because it's not able to be carried to
the lysosome. But let's say you it does
take it to the lysosome, the lysosome
says, "Hey, guys, I'm out of acid. I
have no more enzymes uh to degrade this
this protein. So, you know, you're
you're looking at at at many
pathological steps
uh in the pathology these conditions
that are that are disrupted
uh and and why, you know, my research is
so focused on trying to figure out ways
of actually improving the immune system
by enhancing lysosomal function.
Wow. Okay, so I've heard of heat shock
proteins a bazillion times. I have never
heard anybody explain what they do, only
that this may be the reason that saunas
are
connected. I'm not even sure if people
are making the bold claim that there
there's a causation, but that they're
connected to lowered risk of um heart
disease.
Yes.
Do you think that's why?
I I think it's definitely why. And and
the other the other thing I want to
bring up cuz, you know, everyone is sort
of, you know, uh
kind of puts this gut-brain problem
uh into things like SIBO
uh or dysbiosis or, you know, um
you know, hyperpermeability of the gut,
but I think what people most forget is
that the the the closest proximity
of infectious diseases to the
blood-brain barrier is in periodontal
diseases. And that's been
strongly associated with with
Alzheimer's disease.
It's It's It's, you know, the the the
oral cavity is directly proximal to the
sinuses of the brain. So, that anywhere
where you're going to see a leaky
mucosal barrier, it's in people that
have periodontal disease, because that's
the the first area of of staging of the
battle between these various infectious
diseases and the immune system. So, what
happens is that the immune system is
activated, right, to try to break down
these pathogens. And by the way, I used
to think, cuz I'm not a dentist, I used
to think that, you know, periodontal
disease is all bacterial. But in fact,
periodontal disease has association with
candida,
fungal infections.
It's It's not just bacteria that that
causes periodontal disease. But the
point is that that they're so close to
the blood-brain barrier that they have
an easier ability to migrate into the
brain and produce inflammatory reaction
in the brain than leaky gut does. So, I
think that, you know, one of the
take-home messages I would have for your
listeners is that, yes, I think that
leaky gut is is a very important aspect
of, you know, a functional medicine
approach to any condition, but I think
the first and foremost point of
assessment would be assessing
periodontal disease in those patients.
Wow. Okay, we're starting to understand
some of the mechanisms that are causing
the issue here.
How does one improve their oral health?
Like, is this just what you eat? Is this
better brushing and flossing? Like, what
do we actually need to do?
So,
uh it's it's
a uh both a simple question and a and a
complicated question to answer because
obviously, you know,
um I'm not a periodontist, so I don't
want to speak out of turn about, you
know, how to manage periodontal disease.
But, um
you know, I I think the the first point
is yes,
uh you know, oral hygiene is critically
important. Uh
there's lots of various types of
mouthwashes and like tea tree oil, for
instance, which has, you know, very good
antimicrobial effects. Um so, I I think
that uh you know, a strategy that both
includes, you know, very good oral
hygiene, but also some type of of
natural antibacterial
um
mouthwashes
uh really makes sense to me as well.
Okay, so now going beyond the mouth,
what are we doing on a lifestyle basis
to live as optimally healthy, high
cognition, avoid things like
Alzheimer's? Like, what do we need to be
doing?
I think people should watch your show
more often. That's my
my first recommendation.
Um
Good advice.
You know, so
um
I I think that you know, first of all,
people should, you know, identify uh
whether they have these risk factors,
right? So, if people have a family
history of of cardiovascular disease or,
you know, heart disease or or lung
disease,
uh
uh inflammatory diseases or neurological
diseases, uh they're the ones that
really need to pay attention
uh to preventive strategies going
forward. I mean, we all do, obviously,
but we know that the those people have a
high genetic risk because their family
members have had similar diseases. So,
you know, Ben Franklin said an ounce of
prevention is worth a pound of cure,
right? So, I I think the same
recommendations that we have for
cardiovascular disease are are equally
warranted for prevention of neurological
conditions. There There are There are
two uh phenomena that regulate
epigenetics.
Okay? So, regardless of what gene you
have, cuz everyone everyone has bad
genes for for something, right? I mean,
you know, there's an old workup, you
know, what's a healthy person? Someone
who hasn't had a a full diagnostic
workup yet, right? Because
we all have,
you know, genes that are going to lead
to something down the road. Uh but
epigenetic expression uh is modified by
two processes. One is called
methylation,
uh which is why, you know, high doses of
methylfolic acid have proven to be very
effective in a variety of clinical
conditions like depression, uh uh but
also the second process is called
acetylation.
So, methylation
uh and acetylation uh are able to kind
of repress uh pathological genes from
expression.
But, people have done a lot of uh work
on the methylation processes, but
there's much less understanding of how
nutraceuticals
uh and certain pharmaceutical agents
promote what's called uh
uh inhibiting the deacetylation,
the breakdown of of acetyl groups that
are responsible to prevent the
pathological expression of a bad
protein. Think of a mummy, right? Uh the
mummy's got all this stuff wrapped
around him, right? Uh the the
methylation and and acetylation help to
keep that mummy under wraps.
And what's under the wrapping is our
DNA, correct?
The expression of the DNA, correct.
Yep.
What do you mean the expression? So, in
in the what
my layman's understanding of DNA goes
like this, it's this tightly wound
thing, and depending on how much it's
wound, any given gene is wound up will
determine its level of expression. So,
when a gene gets turned on by something
in our environment that loosens the
winding, and now that gene can be read,
and therefore it expresses.
Now, I get that that's probably super
clumsy, but if that's sort of the rough
idea,
is that not then inside the wrapping is
our DNA?
Correct. So, what's what wraps the DNA
is something called chromatin,
uh
which is just a way it it keeps
it it basically regulates the expression
of genes,
right? So, and by the way, just as as a
shout-out to what you just said, so
there's many non-pharmaceutical
uh nutraceutical um compounds that
prevent uh
the deacetylation, the the breakdown of
the mummy wraps to help uh prevent the
expression of pathological genes. Uh
some of this work was done by uh Andy
Zimmer, who's
a pediatric neurologist. I think he was
at Hopkins at one point that
demonstrated that um
certain isothiocyanates from broccoli
and from uh other uh healthy foods
um actually uh have um neuroprotective
effects by actually preventing the
expression of pathological genes in
autism.
All right, this is uh man, this stuff is
so complex, but the fascinating thing is
the more I interview amazing minds like
yours, I I'm actually starting to piece
this stuff together. It's pretty crazy.
Uh okay, so
All right, so you were explaining
epigenetics and how those were the two
elements of epigenetics, and we were
ultimately trying to get to like what
those lifestyle things are that we can
do that are going to make sure that we
don't end up expressing
um some you mentioned autism now, and I
do want to get into that, but first I
want to sort of finish this lifestyle
aspect. Um
I I've heard you talk about ketogenic,
so I know you have
familiarity with at least the byproduct
of certain diets. I'm curious to know
like where you come down on
veganism versus carnivore and things
like that. Like do you have a take on
what lifestyle gives us the sort of
optimal results?
Yes.
Regardless of whether you live it or
not. That I'm not worried about that at
all.
[laughter]
Full disclosure, right?
Uh no, so I I practice fasting on a
regular basis. Um
The The only reason why I do it though
is not not because of the health issues.
It's because I'm so busy that I have no
time to eat from like 6:00 in the
morning till like 8:00 at night. So I
think fasting is one of the most healthy
things people can do
as long as they don't have, you know,
diabetes or or, you know, a risk of
developing hypoglycemia.
Ooh, let's see if the layperson can
really get himself in trouble here. So
if somebody came to me and said, "I have
diabetes." I would say, "The first thing
you need to do is fast."
And you're saying that that is a
dangerous answer.
It could be because if they need to have
proper amounts of glucose in their
bodies,
they can actually have, you know, a fair
fairly serious consequence of having too
low blood sugar. But just in in a, you
know, a broader spectrum, what fasting
does
is it actually increases heat shock
proteins. Um so it's
Why are they called heat shock?
Ah, very good question.
Excellent question, by the way. So what
happens when a person is under stress or
when a plant is under stress, right?
The plants also make heat shock
proteins.
It's really the wrong word, heat shock
proteins. They're basically
environmental shock proteins, meaning
that that extreme temperatures of either
kind, hot or cold, will activate those
proteins. But anyway, so fasting I think
is a great idea.
Um I am very much uh a uh
a believer in protein-based
uh veget- vegetarian protein-based diets
as opposed to
Sorry, real fast before we move off of
um fasting, the one thing I wanted to
note, when you say fast, you you talking
16 hours, 24 hours, 48 hours? Like what
duration do you then consider to fast
and not just being a space between
meals?
Um I usually start fasting uh like
around 6:00 uh at night.
And then I will eat something very light
uh for breakfast, and then I won't eat
anything again for until dinner time.
And the reason that it's healthy is that
it produces less stress, uh particularly
on the liver, which is, you know,
primarily responsible uh to metabolize
the proteins that we ingest. You know,
one of the problems with the
high-protein diets,
not that I'm against high-protein diets,
but that it produces a lot of stress on
the liver to actually uh
you know, to break down those proteins
properly. And if the liver is impaired
in some way,
uh when a person has a high-protein
intake, that may increase something
called ammonia, uh
which is a byproduct of protein
metabolism. So, you know, one of the the
ideas here is that, you know, by resting
the hepatic function uh through uh
less consumption of of you know, foods
on a regular basis, uh reduces something
in the body called uh ER stress,
endoplasmic reticulum stress, which is
at the level of the liver.
So, you know, by the way, a lot of a lot
of patients that I see have evidence of
fatty liver in association with uh
neurological diseases,
uh which is why I'm very encouraged with
something I mentioned uh
with Mark Hyman on last podcast I did
about Tudca. Tudca is a a secondary bile
acid that promotes hepatic metabolism
that has been shown to have potentially
beneficial neuroprotective effects on a
variety of of conditions like ALS.
Very interesting. Okay, so we're we know
we're doing fasting. You were about to
say then what we want to eat.
What do we want to eat? Right. So I I I
generally recommend the following: a
third, a third, a third.
A third of protein. So think about like
three fists of food on your plate.
One fistful should be, and again this is
my opinion only,
vegetable-based proteins. Um two are,
you know, high-quality fats from, you
know, nuts, avocados, uh olive oil,
those those types of foods. And then the
third from complex carbs like, you know,
fruits and vegetables that are very
colorful that contain a a wide variety
of what are called polyphenols, uh which
are the things that like broccoli,
cauliflower are able to uh repress
pathological genes through the process
we discussed, um as well as folic acid.
Okay, so what would be um
what would be a complex carb? That that
that is the one at least for me that I
have found just
essentially avoiding.
So would like where do you fall on sweet
potatoes,
which would be my favorite, but I find
that I put on fat when I eat them.
Right.
What are your thoughts on that or do you
have a better complex carb that you
recommend?
No, I think sweet potatoes is an
excellent. Look, I strongly believe that
if nature produces these types of foods,
right? Grapes, artichokes,
uh sweet potatoes, onions, cauliflower,
uh you know, that these that have, you
know, complex carbs as part of their
uh, makeup that they're not they're not
unhealthy. It's just it's you know,
what's unhealthy are are simple sugars,
not complex carbohydrates
uh, that produce insulin resistance
going forward. So, I I I strongly am a
proponent uh, of those types of dietary
factors being incorporated into a diet.
So, basically the punchline there is if
you're eating whole food, you're
probably fine.
But, where you're going to get yourself
into trouble is when it's been processed
and the sugar's been refined out and
then added back into something. Is that
accurate?
Correct. And the same thing is true with
with meats and fish as well because you
have to look at not just the the the
uh,
the the the the quality of the food, but
the processing process that goes from
you know, from farm to table. That has
to be looked at as well.
Mhm. Yeah, one thing that I never
thought would matter is what your food
ate.
Yep. Absolutely. And the same thing is
true for fish, by the way, as well. I
think we we pay, you know,
not enough attention to to fish as a as
a source of of course of omega-3 fatty
acids, which are essential.
Uh, but many fish uh, people that
consume a lot of fish uh, may have high
mercury uh, as a result of consuming
fish. Um,
so, it's you know, like everything else
uh, in life, uh, these kinds of issues
are very very complex uh, and there's a
lot of variables that go into those
decisions uh, for each person that
decides to follow whatever diet that
they want to follow. So, I'm I'm not,
you know, to be honest with you, I'm I'm
a traditional physician. Uh,
I you know, usually refer people to a
dietitian for questions about what I
think is is optimal dietary approaches
to to these conditions.
Um, so, uh, Uh, but I I have sort of a
broad understanding
uh, what I think are the proper
dietary consumptions that a person
should have in general.
Jim, I'm sad that you don't do more
interviews.
I will say that you are not a
traditional clinician.
Uh, and I think what you're saying now
is and I I completely understand and
because I'm so
much more ignorant than you, I am so
comfortable making guesses and drawing
conclusions.
Um,
but while I get that you're not a
dietitian and all that and you're, you
know, hedging your bets about those
aren't my areas of expertise,
what makes you so amazing, dude, is the
way that you're pulling these different
threads together and saying there might
be something here. You need to look at
that. There might be something here. And
so, for instance, if I were diagnosed
with ALS tomorrow, you would be my first
phone call.
If for no other reason than you're
looking at things that not a lot of
other people are looking at.
And so, tying this now sort of finally
back into lifestyle,
um,
how do you think about these sort of
hopeless neurological cases that for,
like, autism, in fact, let's let's go
with that one. That for so long people
just threw their hands up and, you know,
once it happens, it happens and there's
nothing you can do and it's purely
genetics.
Um, how do you think about a problem
like that?
Uh,
let's talk about ALS. I've moved into a
dimension uh,
in my mind and in my practice
that where where people who
will not give up hope uh,
and and believe that that whatever
condition that they have, whether it's
Parkinson's or or ALS or, you know, I
see some of the most difficult cases in
the world, to be honest with you. And
what I find most
humbling
uh, to me as a physician, uh, is their
sense of of not accepting nihilism, uh,
and their their sense of purpose, uh,
cuz many times I've heard I've heard my
patients say to me that I feel that
Parkinson's is a gift.
And I'm like, "Really?" I mean, I I
would ne- I would be so angry at at at
God if I got, you know, Parkinson's or
ALS. I I don't know how I would come to
accept that uh, as a condition. But, uh,
they've done studies and we've actually
looked at people who had uh,
long-term survival from ALS who were
given a prognosis of like 3 to 5 years
who are still living.
Uh, and I've spoken to some of those
those particular folks myself. Uh,
and I want to give a big shout-out, by
the way, to, uh, a nonprofit called
Everything ALS uh, that has really
helped uh, the community of ALS
patients, uh, realize that that
we're not going to go down without a
fight on their behalf. So, Everything
ALS is just, you know, an extraordinary
organization uh, that is working towards
uh,
the ability to to not accept the
therapeutic nihilism,
uh, that comes with the diagnosis of
ALS. Um, and what the the common thread
of of long-term survivors has been a
sense of purpose and faith uh,
in the ineffable. Whatever You can You
can call it God, you can call it a
higher calling, you can call it
It doesn't have a name, basically, but
it's a sense of of a spiritual
connection to oneself and and and the
rest of the world that helps them
endure,
uh, as a mind-body method of helping
patients, uh, deal with these
conditions. Um, and it's something that,
you know, I'm glad you reminded me about
because that's sort of, you know, where
I come from as a clinician.
Uh
is is based upon trying to
uh you know, for my in my own life to
come to accept that that whatever
problems that we have are are to learn
from those problems, to to grow as
individuals, and to and to deal with
them
uh without running away from the problem
itself.
Yeah, that that to me is sort of the
nexus of um
why I'm so fascinated by you
is really bringing these disparate
worlds together. So, right before I do
an interview, I always journal
essentially on, "Okay, what is it about
this person that's interesting or unique
or fresh?" And that was the thing I kept
coming back to you with you is there's
nobody else that's like pulling these
threads together. Like,
up until this moment of the interview,
no one would have any idea that you have
this sort of breathtaking expansive view
of
um God and our brain and sort of the
connection therein.
Because you're still utterly motivated
by evidence and science, but yet I could
have in this interview flipped it, and
this could have been totally about faith
and meaning and purpose, and you would
have been just as eloquent.
Um and I don't know, there's something
in that for me in the open-mindedness
that has allowed you to escape the
nihilism,
um which I find
useful and I think is really important.
But then we get into uh
connection and love and hope, and where
do you come down on that, and do you
think about that as a clinician?
Every second of my life.
Every second of my life. Um you know,
love love is is is is biology,
basically, right? Uh
when when we love, we increase our
endorphins, which helps us to uh
bear whatever pain that we're
experiencing with whatever condition.
My experience with people who have
conditions like ALS,
who have very strong social support
through their families and and their and
their friends,
have much much better
prognoses than the same patient, same
age, same condition without those social
support systems. And you know, just a
quick aside, Victor Frankl, who wrote a
book,
he was a he was a psychiatrist who wrote
a book about
logotherapy was it was what he
developed. He found evidence-based
that people were able to endure the
worst conditions in the Holocaust if
they had a sense of purpose. He said,
"Look, I'm going to survive this no
matter what because I know at the end of
the day I'm going to be reunited with my
my my kids or my my my my my parents."
And people who had lost hope completely
died.
So the idea that that we can infuse
medicine with a sense of of purpose
is I think of extraordinary value,
you know, for everybody to to
appreciate.
Yeah. Yeah, it's uh
I don't understand it.
I don't know why it's true,
but it is experientially self-evidently
true.
Right.
And you know, reading Man's Search for
Meaning by Victor Frankl was an utterly
transformational book for me. And I just
thought, "Wow!" Like to think about how
there is
something, some connection between the
brain and the body where when the brain
no longer has a sense of purpose in all
of this, you actually shut off
biologically.
Yes.
I wrote about that in the book, by the
way. I mean, there's actually
explanations about how that happens and
why that happens, as well.
Give it to us.
So, there are growth factors in the
brain.
Uh they're proteins uh that are called
neurotrophic factors, like BDNF is one
example.
Uh which, by the way, is what exercise
promotes and why exercise has an
antidepressant effect is because it
increases BDNF levels. Uh but, there's a
direct uh association
between experience uh
and cellular pathways uh that results in
a uh inability to produce adequate
amounts of these neurotrophic survival
factors. There clearly is a a biological
explanation for how uh existential
states of hopelessness
uh lead to, you know, premature death.
And how existential states of living a
life of purpose uh are able to overcome
uh those on a biological basis, meaning
that it's it's not like uh a game of
smoke and mirrors. It's There are
explanations about how that actually
occurs biologically.
Yeah. Jay, you are
so intriguing to me. I am so grateful
that you took the time to meet with me
today.
Uh you you are hard to find on the
internet, but where can people connect
with you?
Uh well, I have a a a website that's
pretty, you know,
not a great website, but it is what it
is. It's www.drjaylombard.com.
Uh www.drjaylombard.com.
I highly recommend that people uh follow
you, that they go to your website, read
your books. Um
I have thoroughly enjoyed my time
researching you and spending time with
you today. Uh really, really amazing,
man. Um thank you again for taking the
time.
Likewise, I've I've enjoyed speaking to
you as well.
Thank you. Guys, trust me, while he
doesn't put out a lot of social content,
this is somebody the content that's out
there is breathtaking, really
intriguing,
and I highly encourage you to check out
his books as well. Watch this interview
on a loop, and then hopefully we will
get him back again someday.
And speaking of things that you should
do on a loop, if you haven't already, be
sure to subscribe. And until next time,
my friends, be legendary. Take care.
Thank you guys so much for watching and
being a part of this community. If you
haven't already, be sure to subscribe.
You're going to get weekly videos on
building a growth mindset, cultivating
grit, and unlocking your full potential.