331: Resiliency Radio with Dr. Jill: Immune Resilience: The Future of Longevity w/ Dr. Isaac Melamed
Watch on YouTubeVideo summary
In this episode of Resiliency Radio, Dr. Jill welcomes Dr. Isaac Melamed, a distinguished immunologist and founder of Vera Health, to explore the critical link between immune resilience and longevity. Dr. Melamed shares his forty-year journey from neurosurgery in Israel to becoming an expert in immunology, driven by his discovery of the connection between nerve growth factor and B cells. He argues that the immune system should not be viewed as a collection of fragmented parts but rather as a complex symphony involving essential partners like mast cells, complement systems, and innate immunity, which are frequently overlooked in mainstream medicine. This holistic perspective is vital because current medical approaches often treat symptoms, such as chronic pain managed by opioids, without addressing the root causes that can lead to decades-long health struggles.
The discussion identifies three primary areas where immune dysfunction manifests: a history of infections, autoimmune or inflammatory conditions, and cancer. Dr. Melamed explains how interactions between specific infections, including Epstein-Barr virus, strep, and post-COVID states, can trigger autoimmune diseases, neurological symptoms, and psychiatric issues like anxiety, OCD, and depression. A key mechanism behind these failures is often low Toll-like receptor signaling within innate immunity, which allows pro-inflammatory mononuclear cells to become overactivated. These rogue cells can compromise the blood-brain barrier and affect microglia, leading to widespread systemic issues. To counteract this, Dr. Melamed highlights Intravenous Immunoglobulin (IVIG) as a therapeutic "red wine" derived from plasma that restores balance between pro- and anti-inflammatory cells by mimicking dysfunctional receptors and preventing super antigens that cause cytokine storms.
Beyond IVIG, the conversation touches on the role of albumin in binding and clearing inflammatory markers, with potential advancements in "super albumin." Dr. Melamed emphasizes that effective treatment requires addressing epigenetic triggers such as stress, nutrition, sleep, and environmental factors like mold exposure. He notes significant limitations in current treatments for chronic pain in patients with Ehlers-Danlos Syndrome or hypermobility, where standard care often relies on medications without resolving underlying immune dysregulation. Furthermore, he explores theories linking childhood stress events to increased nerve growth factor production and subsequent autoimmune conditions, suggesting that practical lifestyle interventions are essential for reducing stress and supporting overall immune function.
Ultimately, Dr. Melamed advocates for a paradigm shift from crisis management to early diagnosis and prevention to address pain, cognitive decline, and psychiatric issues rooted in immune dysfunction. He expresses his deep passion for helping patients as his professional legacy while acknowledging the intricate complexity of psychoneuroimmunology. By integrating insights on muscle activation, complement systems, and the interplay between stress and neuroimmune function, he offers a comprehensive approach to healing that goes beyond symptom suppression. For those seeking further information on his clinic or IVIG treatments, resources are available through immunoehealth.com or veroshealth.com, inviting individuals to explore these advanced therapeutic options for their long-term health.
Read the full video transcript
Hey everybody, welcome to Resiliency
Radio, your go-to podcast for the most
cutting-edge insights in integrative and
functional medicine. I'm your host, Dr.
Jill, and with each episode, we dive
into the heart of healing and personal
transformation. Join me as I interview
medical experts, thought leaders,
innovators of all types helping you on
your journey to healing and optimal
performance. Today is no different. You
will want to stay tuned if you have any
questions about the immune system or
IVIG. We're talking to one of the
world's leading experts and my personal
immunologist, Dr. Isaac Melamed. I'll
introduce him in just a moment, but I
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Okay, let me introduce my colleague, Dr.
Isaac Melamed. He's a nationally
recognized immunologist, physician, and
researcher with more than 35 years of
clinical experience and over two decades
dedicated to advancing the understanding
of immune-related diseases. Founder of
Vera Health, he's known for his
pioneering work in primary and secondary
immune deficiencies and the critical
connection between the immune system and
the nervous system, which we're going to
talk about today. He has authored more
than 100 scientific publications,
lectured internationally, and received
numerous honors for his contributions in
clinical immunology. Let's welcome one
of my favorite people in the world, Dr.
Isaac Melamed.
Dr. Melamed, you have been a very
special person in my life because you
have been my personal immunologist, and
I say this very publicly, so often I
really believe you've been part of
saving my life after cancer and all the
things I've been through. So, you have a
very special place in my heart because
the complexity and fascination with the
immune system is so profound, and you
are one of the few brilliant physicians
who I feel really understands and
continues to learn and study and pull in
all of the things that we're finding out
about the immune system. So, today we're
going to talk about that. But, before we
jump into the immune system, I want to
know just a little bit about you and
your personal journey into medicine and
then into immunology.
>> So, that Thank you, Jill, and it's my
honor to help you and many other
patients that what I'm doing for almost
40 years.
Um how I started my life, um I you can
see from my accent that I was born in
Israel.
And in Israel, you have to go to the
Israeli Defense Force.
I was lucky that I went to medical
school before, and I served as a
physician in the army.
And in the last two years um of my army,
I was involved in research.
And um I my plan in medicine was
neurosurgery. I started when I was 15
years old.
And
um and one of the question that
they
>> [clears throat]
>> presented to me while I was in the army,
so soldier with splenectomy,
how's the immune system after
splenectomy if they can continue to
serve? So, I tried to figure who's the
expert in immunology and splenectomy and
then found my mentor that passed away
and his name Professor Shapiro. And I
can say that definitely his mentor in
terms of how to approach patient for
many, many years. And he is as a mentor
as he said, "You know, Isaac, you really
need to go to to be my successor in
immunology."
We end up he sent me to uh Canada to
Toronto to continue one of my
fellowship.
And actually in Toronto when I started
to work on the immune system with the
hope to get back to Israel, the chairman
from
uh in Toronto just moved to National
Jewish. And he said, "Isaac, before you
get to Israel, just be in National
Jewish for another 2 years." And the
reason I came,
which actually is the introduction for
what I like to discuss with you today,
is that I found two kind of a major area
in the immune system. The first one,
find a receptor that's called NGF, which
is nerve growth factor.
And I found that this nerve growth
factor is existing on the immune cells,
on B cells.
And actually more than that, we found
that there is a genetic mutation of
patient that it's called CIP, which is
CIP A,
which actually it's a summary of
congenital insensitivity and pain.
And this mutation of this NGF actually
started for me a journey, a 40-year
journey, of two major stories. One of
them is the cross talk between nervous
and immune system.
And the second one to try to look at the
immune system as a core uh mechanism to
different disease that I will share with
you today.
But the chairman of National Jewish the
chairman from Canada moved to National
Jewish and he say Isaac just come to
National Jewish to be an attending in
the National Jewish and I came.
Just as a personal disclosure my son
started medical school and he's a
neurosurgeon today and the family
decided to stay in
in the in Colorado.
But I switch my
being just in academic life to a private
which we develop over the last 40 years.
And there are two I will say key element
from the story that I share with you
Jill.
As I mentioned one of them is this NGF
that's crosstalk between nervous and
immune system. What's the meaning?
>> Yes.
>> The second one is that the immune system
is a core that for our discussion today
because if you look at the mainstream
medicine today one of the challenge of
mainstream medicine today
is actually it's a very
this it's it's a health care that really
focus on your symptoms and your organ.
So if we speak about disease that can be
chronic fatigue if we speak about
disease as pain if we speak about
cognitive changes the approach is how we
can help you with the symptoms.
We all know in United States we are
dealing with an epidemic that cause pain
and the answer is opioid.
>> Yes.
>> And the question is what's the
underlying for the pain? That's kind of
the question.
And then
so that's took me kind of this crosstalk
between the nervous and immune to the
question is what's the cause? What's the
underlying disease? And as my I will say
focus is immune system I focus on the
immune system as a core.
The immune system as a presentation
actually We are talking about three
major presentation.
One of them is in the infection history.
The second one is in the autoimmune or
inflammatory condition, and the third
one is in cancer.
>> Yeah.
>> And you just discussed Jill in your uh
patient journey that as a patient
disclosed it with all the audience. This
is unfortunately a story today in 2026
that we do have patient that going
almost 20 years in this journey.
>> Yes.
>> It start with cancer or infection and
autoimmune disease.
And and the reason is that the medicine
today
maybe it's going to change with AI. AI
may be a very sophisticated story to try
to bring all of them together to look at
the cause. But today we are very very
focused on the symptoms inside.
So that's how I started my journey. Um
and another thing that I like to share
with you, which is kind of interesting
for the history.
>> Yes.
>> One of the physician, Jim Jones, that
has been in National Jewish
that is a faculty um
and being sharing a room with me, and he
told me, "Isaac, I don't know why,
but everybody with chronic fatigue
syndrome does have allergies."
And that's what I like to share with
you, Jill, today that when we say the
definition of immune system,
>> Yes.
>> what we see today and what's unique
today is actually the partner of the
immune system. I really like to really
emphasize
that when we say immune system 20 years
ago, 30 years ago,
in terms of B cell and T cell, that's
the only player. And now we say there's
some other partner.
>> Yeah.
>> And long time ago, when he mentioned
that chronic fatigue is connected to the
allergies,
30 years fast forward, I would say that
the allergies as a partner of the immune
system is a key story in some evolution
of how we look at disease. When you ask
me about what's the role of mast cell
activation,
>> Yeah.
>> what's the role of EDS in terms of the
immune system, what's the role of
disease that we call them angioedema,
and then my answer is that all of them
connected because the immune system is
not fragmented. Right. It's specifically
that they talk with each other, and the
beauty is to look at all this symphony
and to divide it in three category in
the immune system. One of them, which is
a challenge,
is what are the epigenetic trigger that
leads to the activation of the immune
system,
what's the partner of the immune system
that respond to this epigenetic, and the
consequential this interaction is
basically what we call it today the
consequent, which is autoimmune disease,
cancer, or infection.
And I will use one of the disease that
is the most common immune deficiency,
but the most unknown immune deficiency
today.
And I would like to quote a sentence
that can represent what I'm trying to
share with the audience. It's a disease
that we call it CVID or common variable
immune deficiency.
And this disease is actually the people
describe it is
an old disease with new faces.
>> Yes.
>> What are the new faces? The new faces
that we are the talking today
is we see some new faces that they
present with a different presentation.
You can see patient that I see that
present with autoimmune first,
>> Yes.
>> and then the infection. Some people can
present with cancer that have leukemia
and then infection and then autoimmune.
So, the new faces is the evolution of
the immune system in presentation can be
over years.
And one of the challenge is that
actually even you speak about physician,
there's no training or there's no
fellowship that's called autoimmune
disease.
>> Right.
>> It's a disease it's kind of a looking at
different disease from an eyes of an
immunology
and try to understand it.
And that's what I've been doing for 40
years.
>> Hey guys, just a quick interruption to
this incredible interview with Dr.
Melamed to remind you that my book
Unexpected talks about my own journey
through my strange immune system with
cancer, Crohn's disease, mold-related
illness, and all of the things in
between. It's a deep dive into a true
immunology case like mine and I often
get comments from patients that it was
encouraging just to help them on their
journey. I share a lot, I share deeply,
I share authentically about all areas,
spiritual, physical, emotional, and
healing on all levels. And there's
practical tips if you're suffering from
autoimmune disease or immune deficiency
or anything in between. So, check it
out. You can get a copy at
readunexpected.com. You can get one on
Amazon, anywhere books are sold. And if
you want a signed copy from me, go to
drjillhealth.com.
Okay, back to our show. Amazing how you
put that together because and again, I
don't mind sharing my personal history.
I've talked about it before. So,
anything we want to share here that's
relevant because I am a prototype of
this having had cancer at 25, multiple
autoimmune diseases, Crohn's and
Hashimoto's thyroiditis, and other
autoantibodies, and then also multiple
infections that have been under control
with your treatment and the IVIG. But
what's interesting is like you
mentioned, we can have this present any
number of those could be the forefront,
the first thing that we see. And what's
in in some ways kind of counterintuitive
that you would have an overactive
autoimmune attack of self and an
underactive, maybe T or B cells for
fighting infection can all occur at the
same time. Can you talk a little bit
about what we know, the state of the
research as to what might be some of the
mechanistic causes or um besides just
genetics, are there other things that
are contributing to this in our
patients? Is it increasing in in
incidence?
>> So, first of all, it's a great question
and in kind of a quick answer,
there's a lot that we don't know.
>> Yes.
>> And we continue to explore.
I will share with you um first in terms
of uh as a patient that you just
disclosed.
>> Yes.
>> And I always remember a lecture that was
in Budapest. And there was a lawyer from
England, very similar to your story,
very very similar to your story. Again,
Crohn's disease, cancer disease, and
autoimmune and autoimmune that you have.
And what she done was diagnosed with
immune deficiency 20 years later.
And she described her condition as a
prison of her disease.
And the problem on this, and I think
this sentence always for me is a huge, I
would say, drive force to try to help
the patient. And I say, "How can I help
you to get out of this prison and to get
seen?"
Because it's kind of the the challenge
is, and I will share with you somewhere
we're going to the research area,
but there's a lot of, I would say, area
of um
timing between science in medicine,
practice of medicine,
>> Yes.
>> and also insurance companies. So, the
vision of some of in the American
community, some in the insurance, some
of the patient, there's a lot of kind of
a not clear.
And uh and one of the question that we
always have to ask ourselves and we may
come to this later is what do we we feel
is the reason that some of the impact of
autoimmune disease and longevity in
United States is different from European
and different from other states? What
what is the role of the immune system in
this discussion? So, go back to your
first question is where the science is
going today.
I will start with the research that we
are involved in the last
almost 15 years in terms of the symphony
of the immune system in one major
question that we have.
>> [snorts]
>> And that's the interaction between I I
like to use the name infectious and
immune
>> Yes.
>> in various autoimmune or neuroimmune.
And I think that the model that I'm
talking about this interaction between
infectious and immune in the science it
actually started long time ago and
there's a paper in 1926 we're talking
many years ago.
And that was in related to a child, a
teenage that has been exposed to strep
infection and develop some tics and some
movement disorder. But in the same time
develop some type of psychiatry in terms
of anxiety and OCD and depression. That
was many years ago.
Then the concept of Korea has been
described connected to the strep.
Fast forward, we've been talking about
EBV and the connection of EBV to chronic
fatigue syndrome.
>> Yes.
>> One of we are my
um organization has doing a quite an
extensive collaboration with Stanford
and with LSU in New Orleans.
In Stanford there is a very famous
scientist named Larry Steinman and Larry
Steinman is looking at the connection
between EBV and the immune system
leading to multiple sclerosis.
>> Mhm.
>> Which is
unclear that multiple sclerosis is an
autoimmune condition and all the therapy
that we have today is really try to
target some of the uh lesion but not
really to understand the immune
underlying disease.
So, when we speak about the connection
between EBV and the immune system,
almost 30 years of research and we are
not clear.
Then we came to the COVID and the COVID
actually has been leading with a high
percentage of patient that develop
multi-organ effects specifically with
neurologic symptoms.
And those multi-organ can be cardiac and
joint, pulmonary, and GI.
And the question is, is this
uh COVID is one of the interesting
interaction between infection and immune
that leads to pandemic of autoimmune
disease specifically neurologic
symptoms. So, all the connection between
EBV and COVID and there was a lot of
work and discussion about Lyme and
post-Lyme and immune system.
>> Yes.
>> And by
by various research. So, this
interaction between infectious and
immune system is one of the research
that we are working.
And part of the work that in the
research we also explore that it's not
just the B cell and the T cell.
>> Yes.
>> We do have some other partner that we
have seen involved like what you just
mentioned, the mast cell activation.
>> Yes.
>> Like the complement system that we have.
Like alpha-1 trypsin that we've seen.
And we've seen some in- some other
player like the innate immunity.
>> Mhm.
>> So, the innate immunity, the I N N A T E
immunity
which was an immune system including the
complement that we basically ignored it
for years and years and years we say
yes, but it's a very
basic immune system that is really a
core in our future research and why?
>> Yes.
>> The reason is that if we speak about an
immune system
I want to bring two kind of the area of
the research that are relevant to our
store.
The first one is the question is that
this relationship between infections and
immune system
does it play a major role in some
autoimmune disease, but what is the
relevant in terms of longevity for
example?
And I will give you one example.
Is why do we give a vaccine against
shingles as you get older?
And the answer is that your immune
system that has been educated how to
respond to the shingle is losing its
mind or losing its memory to the shingle
and suddenly you need to renew the
shingle the vaccine and to re-re-educate
the immune system to this vaccination to
the shingle.
That's a memory defect that depends on
the innate immunity that lost the
immunity to the shingle
but this loss of the immunity to the
shingle can happen to you earlier in
life.
>> Mhm.
>> And I defined it in one of the paper I
published, I used the name Alzheimer of
the immune system.
>> Ah, brilliant.
>> And and and the it's a very interesting
because a paper just recently published
about they say and they saw that people
who get the vaccine against shingle has
less incidence of Alzheimer and we will
come back to this connection that serve
with Alzheimer.
So I saying that our research is trying
to understand
that actually the innate immunity
respond to different type of epigenetic
and what are the partner that may lead
to this Alzheimer? If it's the
complement, if the mast cell, if the
alpha-1-antitrypsin,
and part of this dysfunction between the
infection and the immune system is
actually leading to this area that we
have interest, which I like to call it
neuroimmune.
>> Yes.
>> So, I'll give you a few example in the
clinical setup. The first one is
actually this paper that was published
more than 100 years ago on the Korea and
the children with type of
anxiety and even in this paper he
mentioned increase in suicide um
attempt.
So, 10 years ago, um we started to get
explore to a condition that we see in
teenage
and children.
And the story with the children is that
they get sick.
And after they get sick, the mother is
telling, "You know, it's not the same
child."
>> Yes.
>> I know my child. This is not the same
child.
And the child is getting anxiety, the
child is getting tics, getting OCD, he
doesn't want to school, he gets in the
middle.
And the first response that I want to
mention it to you, Jill, and this is
what I'm trying to teach new residents
and new students, and I try to teach
them
something that from me being 40 years in
medicine and for there are few things
that you know.
When somebody when the mother is telling
you a story and he tells you, "Well,
this is my child."
Just listen to the mother. The mothers
knows the child better than everyone
else. Even that you are physician and if
you don't know the answer, it doesn't
mean it doesn't exist. It just mean that
we just don't know. We need to do more
research and we need to understand.
But don't tell the mother it's just in
your head and and it's not an issue.
It took me many many years and we're
doing quite a lot of research with as I
mentioned with Stanford
and with um Dr. Frankovich and Dr. Verso
passed away in this area. And the point
is that what we try to understand
if this connection between strep
and the immune system leading to some
psychiatry is the immune system is
involved.
And fast forward for almost 10 years of
research, the answer is yes and we found
in the research that basically what
happened
we do have the interaction between the
infections and the immune system.
And that's what I want to go back to
what I share with you. One of the
failure most probably is the innate
immunity
which we evaluate it's called toll-like
receptor that we look at the signaling
of toll-like receptor.
And we see that the TLR is actually low
in the patient with infection.
And as it is being low, what happened is
the immune system is producing
pro-inflammatory
mononuclear cells. So there is in the
immune system a balance between
pro-inflammatory mononuclear cells and
anti-inflammatory mononuclear cells. So
basically when you do have this
interaction between the infection immune
those pro-inflammatory cells are over
activated.
We see now that they are moving to the
brain to the blood-brain barrier. So
those type of mononuclear cell
can affect the permeability of the blood
brain barrier.
>> Mhm.
>> And from the blood brain barrier, they
are getting to the microglia.
They're affecting the microglia.
And we see that using IVIG, for example,
that knows how to immunomodulate the
system,
those anti-inflammatory
monocytes get upregulated and able to
reduce and get the balance. And that's
how we see the clinical response and
But that's The point is that I want to
share with the Jill that this is science
that speaks about an interaction between
infections and immune
in the straight condition, but presented
with a psychiatry world, which is
anxiety, depression, and OCD. And as
this patient mentioned so many years
ago, which is suicide.
>> Yes.
>> Which brings a question to the
scientific world. And there's a lot of
science that we are involved in all
other places in the world from different
psychiatry
that speaks about a condition that we
define it psychiatry, which is
depression, anxiety, and fatigue that
actually it's an inflammatory condition
that the immune system is involved. And
we just need to continue to understand
and research and how we can model it.
So, that's one area that uh we've been
in in our
relationship between infections and
immune.
The second one that I want to mention in
our research is actually this the COVID
and the interaction with COVID and
immune system.
And here we really evaluated few
partner, which is the complement system
and um other system of the immune system
that as I mentioned the alpha-1
antitrypsin and the innate immunity.
But the end results now brings to a very
interesting um
panel that I think that the future
is is the cognitive changes and all what
we see in the cognitive and the
deterioration to the disease like
Alzheimer and the cognitive change
is the immune system is involved and I
think that the answer is yes.
Some of the area that we don't
understand but more science is coming
and more and more that it's coming
uh to the concept that we use the name
mitochondria and that's the mitochondria
that we are bringing to the picture is
is just imagine that you have the innate
immunity
that as like a bridge that is trying to
support all the different epigenetic
and you know very well because you
describe it many well and you doing much
better
and describe it the innate immunity
about the stress and epigenetic that and
nutrition and other component that lacks
in the innate immunity
and as a failure we get
some inflammasome or we get some
inflammation area
that's affect the mitochondria
and affect the mitochondria and suddenly
a paper that just published in nature by
my corporation in LSU that showed
that those mitochondria injury and
fragmentation
can actually move and lead to some of
the effect on the cognitive.
So that's all those are the area that in
the neuroimmune is focused on my
research from
as he described it I like to describe
myself as a translation medicine taking
the patient story and going to the
science and try to get some answer.
>> Wow, that was so much great information
and what I really love is you're also
teaching medical students and residents
to really listen to the patient and the
mother because I know in my own journey
of being a physician, so often if I'm
just curious and I listen, even if it
doesn't make sense from the training, we
can start to learn because we're like,
"Huh, that's an interesting pattern that
we're seeing. Let's look deeper." And
then what happens is over time we start
to find the reasoning, which you just
described, you know, way back in the
day, early days in the 1920s of first
describing this neuro
psycho-neuroendocrinology
and the connection between
Um so, one thing that I think patients
uh suffer from is there's inflammation
in general and then there's um weak
immune system fighting infections and
then there's also um autoimmunity. Uh
and the one of the big tools that you
have used is IVIG, which is um
intravenous immunoglobulins. Can you
tell us a little bit about the story and
the history of IVIG because I feel like
you're one of the world leading experts
and it can it's not always the uh
answer, but many, many times it can be
very powerful.
>> Sure. Um first of all,
I like to talk always I compare to the
patient the IVIG to red wine.
>> Uh-huh.
>> And the reason I compare it to red wine
is A, we start with the same grape
>> Mhm.
>> and end up with a different wine.
>> I love it.
>> What happened between the grape and the
red wine, we just don't know.
>> Yes.
>> And and the research of IVIG has been
almost more than 35 years and some of
the leading research that we collaborate
to try to understand the mechanism of
IVIG has been going for almost 35 years
and the beauty is
that this is nature. I like to call it
holistic nature that produced the IVIG
and we really don't um understand and I
will share with you um a first of all,
what's IVIG?
So, one of the thing that if we look at
the immune system,
um I like to kind of uh speak about a
little bit for for all the audience.
Some part of the basic mechanism of the
immune system.
And um, the immune system actually, if
you look at the cell, you can imagine
that the cell has some membrane, which
is the cover of the cell. And it has a
nucleus.
And what I published many years ago that
actually even the structure of the cell,
which is called cytoskeleton,
plays a role in transition of signal.
So, just imagine that you have a cell
and you have a cover of the cell. You
have the nucleus in.
So, the signal between the membrane into
the nucleus, which we use the name
signal transduction,
this has been the focus on research
almost the last 40 years.
And um, many many protein involved in
this transaction of signaling from the
membrane to the nucleus.
But the end result of this journey that
takes only few minutes from the membrane
to the
nucleus
is the end point of two major thing that
I would like to which I think it's
basic.
One of them we use the name apoptosis.
So, the name apoptosis, just imagine
that every cell in our body supposed to
die. This is the nature. And the cell
needs to die and to rejuvenate with a
new cell.
So, the process of rejuvenation,
it's a normal nature process.
As we get older, this process, which is
controlled by the immune system, is
getting weaker and weaker.
And as the apoptosis process get weaker
or dysfunction,
you basically end up as a result to an
inflammatory consequence. Basically,
just imagine that you have a very long
his journey that the immune system
supposed to clear the junk. Let the
inflammation.
And it doesn't matter if the junk or
inflammation is the skin or it's in the
joint, or it's in the brain, or it's in
the cardia, or in the in your any organ,
it's the same process, inflammation
process.
Then the second
story from the membrane to the nucleus,
it's the signal that leads in the
nucleus what we use the name activation.
So, activation of the nucleus, it has
about few, at least seven that we know
today, but maybe more, which it's called
check and balance.
>> Mhm.
>> So, the immune system is doing check and
balance on this activation.
And sometimes that you get some
dysfunction in the check and balance,
that's what you end up with cancer. So,
you see two major process that we call
apoptosis and activation of the cell
controlled by the immune system.
Now, all this what I share with you,
which is a very complicated and continue
on the research,
start most probably in some receptor
that sits on the surface of this
membrane.
And some of this receptor sitting in
many different cell. And this receptor
has a name FC. So, this receptor is
called FC receptor.
So, just imagine it to for simplicity,
so this FC receptor is like a key.
So, now you have a relationship of a key
and a lock relationship. So, if the
infection is the
is the key, and this FC is the lock, you
have a key and a lock relationship. So,
suddenly the relationship between the
key and the lock are dysfunction for
some reason.
So, now what you do, you take an IVIG,
which is build the same story. IVIG also
has an FC receptor. And this FC receptor
is coming to this FC receptor that you
are in this dysfunctional immune system.
And one of the mechanism can be in this
dysfunctional reason, it has a name,
it's called mimicking.
>> Yes.
>> So, what's a mimicking? The mimicking is
that let's use what I discussed a little
bit before on EBV.
And let's say that your FC receptor,
which is the lock, is looking at EBV as
a key and says, "I want to produce a
good relationship, but somebody is get
confused." Yes. So, instead of producing
a um [clears throat] response to the
key, is doing a mimicking and producing
antibodies again your brain, again your
joint, again that's what we call
autoimmunity.
>> Mhm.
>> So, now the FC is coming to this
receptor and try to train the FC how to
behave and how to really produce the
antibodies in a normal way. That's one
mechanism.
Second mechanism that has been as a
potential,
if you look at the key and the lock
relationship on the FC,
so basically the FC suddenly from key
and the lock become a master key.
>> Yes.
>> So, now instead of one key, you have
master key. All the keys are the same.
So, the key can be opened by this EBV as
a key can open all the keys. And then we
use the name super antigen. So, this
super antigen leading that we use it in
the immunology, in the post-COVID people
are using a lot of the name which is
called cytokine storm.
>> Mhm.
>> What is cytokine storm? Is basically
imagine that the immune system producing
an inflammatory storm.
>> Yes.
>> And this inflammatory storm can be an
autoimmune, joint, brain, and cardiac,
and etc.
So, then the IVIG is coming and training
this key to behave and not don't be a
master key, just be a
So we're using a name in the IVIG, we're
using a name in two property. One of
them that it's used immune replacement,
>> Yes.
>> prevent infection and immune modulation.
And the immune modulation, what I share
with you is trying to really modulate
the immune system.
And and I will share with all of you
many of the area is that even that
started, I'll give you two example here
that happened and I was involved
actually 40 years ago in the research on
both of them when I was in Canada with
the rheumatology team.
The first disease that I would like to
share with you is called Kawasaki.
>> Mhm.
>> And the Kawasaki story is mean in the
80s.
And the Kawasaki story, we saw children
that had some exposure maybe to
infection, we're not clear.
But they showed a full autoimmune
inflammatory skin and joint and high
fever.
We had no clue what is going on. There
was a lot of speculation in the 80s and
research in different and people tried
to do steroid, people treated, we had no
clue what is going on.
And when we've been in Canada and and
was a good immunology rheumatology team
together, we say maybe it's an immune
related is maybe.
>> Yes.
>> So we use IVIG as a as a holistic
approach. If it's an immune system,
let's use it and see what happen.
We gave the first infusion of IVIG and
immune modulation and
and I will never forget the child who
was with a high temperature, with joint,
he's been overnight is getting better.
>> Wow.
>> And so IVIG now it's a been a treatment
of choice. Now
I will share with you one interesting
story that happened.
So, we gave the IVIG to the Kawasaki,
but not everybody agree and not
everybody So, years later, maybe 10
years later,
we have seen teenage that playing
basketball
and they suddenly fall and die from
cardiac arrest.
>> Mhm.
>> So, children has been dying from cardiac
arrest
and nobody could understand why.
So, the science went back and found the
children that died from cardiac issue
actually had Kawasaki early age in life
>> Wow.
>> and never been treated with IVIG.
>> Yes.
>> So, what interesting is that the immune
system doesn't stop with the Kawasaki,
it just it continually lead to some
cardiomyopathy and cardiac issue. And
now, it's a mandatory when you have a
Kawasaki to treat you with IVIG.
>> Mhm.
>> You'll ask me, Jill, do we know
what is the actual mechanism in Kawasaki
that happened today? We don't know.
>> Yeah.
>> But what I'm trying to say is not only
is
the full science will give you all the
answer.
>> Yeah.
>> The question is that we like to do is to
try to figure if the immune system is
involved. And now, it's a mandatory
rule.
The same happened about the pandas. The
other example would also happen in
Canada
and I will never forget it. That's
another disease which we call
Guillain-Barré.
>> Mhm.
>> And Guillain-Barré is a disease that you
get exposed to an infection,
unknown infection, and you get
paralyzed. You just get paralyzed.
So, you're speaking about the connection
between infection and immune system that
the paralysis.
And IVIG has been shown
to really the recover all the
neurological doing. It's a mandatory now
in Guillain-Barré.
But still, we don't [clears throat]
understand the mechanism of the IVIG in
gambling.
And it doesn't mean that it doesn't
work. So, I think that IVIG that I am
looking at IVIG is in two kind of a
statement.
>> Yeah.
>> Is your disease immune?
>> Mhm.
>> And we will do all the efforts
scientifically with all the signs that
we are trying to understand who are the
player of the immune system. And I think
that that's a beauty. We are going to
learn more and more about the immune
system.
And then to try to have the tool how to
do the immuno rehabilitation. And IVIG
is a is one of them.
And now there are many interesting
because the prediction that we are going
to see what I call
biologic therapy in all immune related
there are flaring because the immune
the industry is understanding that the
immune system is a key player.
>> Mhm.
>> So, now you have so many new biologic
that really focus on the immune system.
In the allergy world, and if it's an
asthma, if it's hives, if it's a chronic
hives, if it's any disease that's affect
the
connection between allergies and immune
system.
And so many in the area of angioedema
and so many other example.
And the other area that we are going to
see more and more in the future is the
concept of cancer.
>> Mhm.
>> And the immunotherapy in terms of the
cancer.
The second I would say protein in our
body which is a very interesting body
that all is well needs more research and
more understanding, but I like to bring
in to your question on IVIG is called
albumin. And I think the albumin is
another
interesting protein that sits in your
major plasma.
And the albumin has many interesting
binding sites to the
And those binding
actually seats is a nature issue to say,
"Okay, I understand that your immune
system is not doing so well.
>> Mhm.
>> You're getting old. You are your immune
system is not doing well as you would
like to see. And the end result is this
inflammation that we discussed. So, we
are bringing the albumin is produced and
circulated and continuing with the
binding site to
get and get your bind get get all those
inflammatory
that I just mentioned from the
mitochondrial failure and the
inflammation failure and really get all
of them clear and get them clear from
you.
And the albumin is also a been target in
terms of research to say, "What can be
done?
Let's speak about super albumin. The
albumin has more binding site. The
albumin is more effective.
And there was a kind of a very
interesting
paper in the New York magazine New York
Time magazine about albumin in terms of
our body is like oil change. You are
basically
this is the oil that you need to change
your machine.
And this is a world that has been
involved. People have been using it
today in longevity or other reason in
normal that we have.
>> So, that's a perfect transition to talk
about something that you and I've been
really excited about is bringing some of
these services. What happens and maybe
you can speak to this as well as there
are certain covered indications for IVIG
and unfortunately I think a lot of the
indications that may have use are not
always covered and I know one of your
things in your clinic is for the
patients who really need it. For
example, a Crohn's or colitis patient
that isn't a typical indication for
IVIG, but you and I have shared several
patients who have benefited from the
indication and if it can get covered.
So, one of the things with plasma
exchange with albumin or IVIG or even um
IVs with vitamins or nutrition or
glutathione. We have both seen a big
need for these offerings to patients to
be able to pay for the kinds of things
that they want to get. And I'd love for
you to talk just a little bit about your
vision and and what we sat down and had
a a discussion about your legacy, which
I really love because I think no greater
thing than we leave a legacy in the
world. And I I really love your heart
around this in creating a whole new
entity for providing these services for
patients who want them.
>> No, thank you uh Jill uh for my your
nice work. Um
I think that the the are two
few area that I like to focus when we
mention
>> Yeah.
>> what I'm doing for so many years and
legacy. I think that number one issue
is the patient that I see and I feel
that they are frustrated um in terms of
the complex. But let's speak about I'm
saying three major area today
>> Mhm.
>> that we see uh that there is some
challenge in health care.
And we can speak about number one is
pain that we can speak we can speak
about cognitive deterioration.
>> Yes.
>> And we can speak about a question is why
we still see
the story of depression and suicide.
>> Mhm.
>> So just my granddaughter that she is in
high school and she's 16 years old
just called me 2 days ago about a child
16 years old in her high school
committed suicide. And just four kids in
her
high school committed suicide. So I
assume that the question is
>> Yeah.
>> from medicine standpoint is that I
brought all those three area that we
have.
>> Mhm.
>> From a concept is we from my approach is
to try to understand
the role of the immune system in the
three area that I share with you, which
is the pain, the psychiatry, and the
cognitive issue.
And when I say the immune system, the
immune system is not an isolated
everything that I share with you. The
complexity of the immune system is
something that we need to learn and to
research and to understand and to work
with the manufacturer to develop some
new drug and new super algae or super
albumin and to try to help the patient.
But in the same token is what you are
contributing and that the huge
interaction and complement with you're
doing and we're trying to do is
I always compare it to the gun. The gun
can be loaded with your gene, but if you
don't trigger the gun, it's not be
active.
So, the trigger is that we all speak
about the epigenetic that
>> Yes.
>> I can talk about them, but you are the
expert and and them how to really do it.
So, we all agree that this immune system
is really and the gene that you have is
really responsing very very
intimate to stress.
>> Yes.
>> Very intimate to all nutrition, very
intimate to your physical activity, very
intimate to the sleep, very intimate to
the other environmental if it's a mold
or other environment. All of them are
very very important over the time
and a very important is to discuss how
they work with the immune system and
more and more study to have and discuss.
So, this epigenetic is a key element in
terms of the complement that the two of
us can do to understand the interaction
between epigenetic and immune.
We'll do our best to understand the
immune system and I think that the
cellular immunity, the mitochondria
immunity,
the the player of the immune to
understand it's just the diagnostic the
next
years that we'll have more and more to
information.
And the next one that is very important
I think
that all what I mentioned to you, that
the pain and the cognitive change and
the psychiatry,
I think that the approach that we need
from a patient standpoint to listen them
to early
>> Yes.
>> as much as we can get to the early
diagnosis of the patient and focus on
the prevention concept
>> Mhm.
>> versus to go to the crisis mode.
>> Yes.
>> Because we all know very very well we
know it.
When you do have a patient with
Alzheimer's disease and he does have the
plaque,
all the area that we call plaque
delivery or plaque distribution, it's
not working.
>> Mhm.
>> And we know that. And the question is,
who is in the age of 30, 40 to 50 that
we know and what do we need to do to
change it from immune system and
epigenetic to to change it?
We all know that any cancer and what
cancer and how it's involved. Yes, gene
is gene, but there are some other effect
that can affect it.
So, I think that the pain is a great
example is, do we understand why the
pain is there?
And what are we want to do with the
pain?
And and are we going to tell the patient
the only thing that you have an option
is use opiate?
>> Yeah.
>> And you get to the opiate crisis?
Or to try to say, "You know what? I
agree that you have pain. Let me try to
figure that thing."
>> Yes.
>> And I want to bring the pain as a
something new in our research that we
are collaborating with South Carolina.
And that's a condition that I I don't
have an answer
>> Uh
>> to explain you why.
Maybe because we have more patient that
come to It's a new condition. We call it
hypermobility or EDS.
>> Yes. Yes.
>> So, this EDS and hypermobility that we
start to see more and more,
young female
that have a history of hypermobility and
some
joint dysfunction.
And all of them have some pain.
>> Yes.
>> And the pain also being diagnosed by
neurology by a condition called small
fiber neuropathy.
>> Yes.
>> Meaning you have a biopsy and you have
an evidence that small fiber neuropathy
is there.
And you do have pain too.
And And I will say from our approach on
the medical
we have no approach.
>> Mhm.
>> The only thing is get on tramadol or any
opioid.
Do physical therapy and live with it.
>> Mhm.
>> And I can see I'm speaking about young
female
that I can see them in wheelchair.
Um and they cannot function.
And and we are trying to figure what is
going on. So, there is very interesting
now signs that we are involved in all of
this.
We start to understand with the genome
and all the testing I'm doing that
actually there are few partner of the
immune system that are involved. And
we're trying to explore if this
partnership of the involved is leading
to this EDS and how we can address it.
The question comes is to that I had a
discussion
with Dr. Maitland. Her name is professor
in South Carolina and she is seeing a
lot of patient with a with a EDS one of
the image she sent me, you know, we've
been
going to the same direction for many
years. She is working on the muscle
activation and the complement and we are
getting together in this EDS and it's
interesting.
So, my a proposal was because I'm
interested in doing a lot of research on
the connection between infectious and
immune is the COVID really trigger some
of this
immune underlying leading to the EDS is
that kind of the underlying.
She raised a very interesting point that
I like to bring to you, Jill, and uh
because it's kind of a a one of the
leading in this theory
that she is claiming that some
childhood
stressful event
is leading to some autoimmune.
>> Mhm.
>> So, I'm sure that you know more than
person, Professor Maté from Budapest.
>> I think he's very famous and he done a
lot of work about childhood stress and
autoimmune condition.
>> Yes. Yes.
>> The reason I'm mentioning is that I
absolutely believe Dr. Maté. I believe
with others.
And that I'm going back to the first
what I share with you about what I my
disclosure about this NGF.
And it's clear
>> Yeah.
>> that when you get exposed to stress
your NGF production
is much higher in some susceptible
immune system.
>> Yes.
>> So, this NGF production
is linked to stress.
>> Mhm.
>> And this NGF we have now more data how
it's related to neuroimmune and pain and
others. So, it's very interesting that
we all agree
>> Mhm.
>> that stressful environment
is a very important point either from
childhood stress that we had in terms of
life
or from ongoing stress that we have
daily in life.
>> Yes.
>> And I think that again in medicine when
you see your physician
he can mention that stress is important,
but how we reduce it?
How what is the lifestyle that we need
to have?
Which brings another point that you
raised it before and I agree with you.
And just to mention that
as much as I will focus on the immune
system, I cannot ignore
the stress
and the physical therapy that is
associated with reduction of the stress
because this is a tool
simple tool.
>> Yeah.
>> Physical activity.
>> Mhm.
>> Keep your lifestyle.
>> Yes.
>> Keep everything that you're doing help
your immune system to function in a
better way.
>> Yeah.
>> So, lifestyle and nutrition and stress
relief and everything that you can do
I cannot give you advice because I
myself lives in in this stressful
environment. Um I never found any
recipe.
But I will share with you. My answer is
I love what I do.
>> Yes.
>> I love to help patient and that's my
legacy and that's what keep me
and to help people and to continue to do
what I'm doing.
>> What a beautiful synopsis of this thing
we call psychoneuroimmunology and all
the ways the systems interact and and
really even though we have so much more
information, we're still kind of at the
doorway of the complexity of the system
and like you said, maybe AI will start
to even bring more research to the table
and and and we'll understand it better.
But I just want to say first of all,
thank you for your 40 plus years of work
and all the many many patients. We've
shared many and you and I'm one of them
that you have helped. I'm super excited
about the immuno wellness concept that
we're going to hopefully bring to the
Denver area. And if you want more
information, um I think they can find
information about your clinic at
immunoehealth.com
or veroshealth.com.
Is that correct?
>> That's correct and thank you again,
Jean. It is it was a pleasure
to work with you and to have
I I the beauty with you is really is
from your experience as a patient. You
took it to help other people in the
world. And I think that that's
it that's a great great um Thank you
again for inviting me and thank you.
>> You're welcome. I look forward to our
future collaborations. Hey guys, hope
you enjoyed that fascinating deep dive
into immunology with Dr. Isaac Melamed,
one of my favorite humans and someone I
deeply respect for his own role as a
physician in my health and recovery from
cancer and Crohn's.
If you haven't yet subscribed on
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