Exercise creates free radicals in your body, which creates oxidative stress. COVID thrives on oxidative stress, so working out will create lots of free radicals that can "fan the flames" of COVID.
It's also important NOT TO DRINK ENERGY DRINKS when you have COVID, because it makes your bloodstream very ACIDIC. Soft drinks and energy drinks are HIGHLY acidic, creating free radicals in the body that can make it extremely difficult to get rid of COVID, once and for all. You can see just how acidic soft drinks really are, via the video on this page (scroll to the 3:24 mark if you want to go directly to the part where they show a test with several beverages and sports drinks).
Have a look at the excerpt from this study, below. Here's the link for the original:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2880768/
Soft drinks consumption and nonalcoholic fatty liver disease
Patients on a high fructose or sucrose diet show a greater uric acid response to a bolus of fructose[70,71] consistent with the upregulation of KHK activity. Finally, uric acid levels can predict the development of NAFLD[72]. There is also increasing evidence that the rise in uric acid may also have a potential role in causing features of the metabolic syndrome[73], in part by the ability of uric acid to deplete endothelial nitric oxide levels[74] and by activating adipocytes[68]. What does fructose become in our liver? Fructose becomes free fatty acids (the building blocks of all lipids), becomes VLDL lipoproteins and TGs (the nasty lipids most associated with cardiovascular disease), and becomes uric acid (oxidative stress, vascular inflammation, Figure Figure55).
Spike Proteins In Immune Cells - Dr. Bruce Patterson Discusses COVID Long Haul
From the YouTube transcript:
03:02
that's that's such a great question
03:04
um and you know our our big paper just
03:08
came out last week in frontiers in
03:10
immunology
03:11
and it really uh set out um
03:15
who is a long hauler and what is a long
03:17
hauler
03:18
and really the the gist of the paper was
03:22
that
03:22
we used machine learning to look at a
03:25
variety of different biomarkers
03:27
uh we started with probably over a
03:30
hundred
03:31
we narrowed it down to 14 and then we
03:34
used those 14
03:35
to see what the difference was were
03:37
between
03:38
uh long haulers severe coveted
03:42
mild to moderate covet and normal
03:44
individuals
03:46
and indeed there it was a very very
03:48
distinct
03:49
set um you know 99
03:52
distinct from active covid um
03:56
and it was truly uh its own immunologic
03:59
signature
04:00
and we developed the long hauler index
04:03
so that we could quantify
04:06
non-subjectively who is a long-hauler
04:10
from a diagnostic standpoint and most
04:12
importantly monitor them on therapy
04:14
because i know you you know very well
04:18
dr bean when you talk to these
04:20
individuals their stories are
04:22
completely different um and they have
04:25
day-to-day variations which
04:27
we'll talk about in a moment and to try
04:30
and grasp
04:33
any uh information in terms of recovery
04:36
treatment uh how they're feeling what
04:39
they're feeling
04:41
and they've been debilitated for months
04:42
on end so what's the
04:44
what's the contribution of having to be
04:47
debilitated
04:48
uh in terms of their symptom complex is
04:51
so complicated um that i know we
04:54
couldn't do it without um
04:56
the machine learning and and computer
04:58
assistance
05:01
got it thank you very much for this and
05:03
uh cool beans we're gonna continue to
05:05
discuss and go deeper and deeper
05:07
i hope that you would come along and and
05:10
have that
05:10
fascinating discussion one more question
05:13
uh
05:14
bruce the long haulers the ones that
05:18
i've been managing i'm sure that the
05:20
ones that you are managing
05:21
they go through this hills and valleys
05:24
so there was a cool bean here simple
05:25
garden who asked this question
05:27
that there are flare-ups do you know why
05:30
that happens
05:32
we do now i mean i think with the paper
05:35
setting the stage last week of what is a
05:38
long hauler
05:39
and and in fact um we were able to get
05:42
data
05:42
into our paper uh that in frontiers of
05:45
in
05:45
immunology that suggested that long-haul
05:49
long covid is caused by vascular
05:52
inflammation
05:53
you know and and the fact that vascular
05:55
inflammation you know happens all over
05:57
the body
05:58
um is really a unifying hypothesis
06:02
that brings together you know the 215
06:05
plus different symptoms
06:07
that these long-haulers experience now
06:10
the
06:10
sequel to that paper which we just
06:13
submitted
06:13
uh this morning to the pre-print service
06:17
uh really showed that it's because
06:20
uh non-classical monocytes
06:23
carry covid s1 protein
06:27
up 15 months after
06:30
diagnosis these cells bind to
06:34
blood vessel walls and endothelial cells
06:38
through a fractal kind and the fractal
06:41
kind receptor that's expressed on
06:43
non-classical
06:44
monocytes and causes inflammation and
06:47
these cells can cross the blood brain
06:48
barrier of course
06:50
and cause vascular inflammation in in
06:52
the brain
06:53
the most exciting thing that we found um
06:56
in the literature uh and i have to um
07:01
throw kudos to dr yogendra on this one
07:04
uh is that uh these non-classical
07:08
monocytes
07:09
are mobilized by exercise
07:13
and activity and so here you have a cell
07:16
carrying
07:17
covet protein and no rna by the way we
07:20
just
07:20
had a first round of um sorting
07:23
experiments
07:24
and next gen sequencing uh
07:27
today as a matter of fact to show that
07:30
there really isn't any um protein in
07:33
these cells yet they express the s1
07:35
protein
07:36
but they are mobilized by exercise
07:39
and so of course we to a person
07:43
who's a long hauler they get worse
07:46
after activity worse after exercise
07:49
we've had individuals who've
07:51
gotten back to pre-covet levels and and
07:53
some individuals who were just
07:56
absolutely bedridden who felt well
07:58
enough to
07:59
you know to work in the yard and take
08:02
their kids to
08:02
sporting events that overdid it and
08:06
um you know had a relapse and the fact
08:09
is you know if these cells
08:11
still contain s1 protein are still
08:13
circulating
08:14
a little bit of exercise um you know
08:17
more than
08:18
just a mile or two walk uh they're
08:21
they're going to get a
08:21
a flare up of their of their symptoms
08:24
and that's why you see this
08:25
waxing and waning and when we talk about
08:28
therapy in
08:29
our therapeutic approach um
08:32
we'll talk about how that can mitigate
08:35
these flares and and and help eliminate
08:39
these cells from the circulation
08:43
that is an important point and i'm going
08:44
to very quickly
08:46
if you don't mind this is such an
08:48
important topic
08:49
and the i think
08:53
i just want to very quickly show this
08:54
that so cool means if this is a blood
08:57
vessel
08:58
and there are endothelial cells here
09:01
dr patterson is talking about monocytes
09:03
that are sitting near the blood vessel
09:05
wall
09:06
and they are patrolling the blood vessel
09:08
boundaries they actually patrol
09:10
all boundaries and one important one is
09:13
the blood vessel boundary and they are
09:15
in an
09:15
m2 state or as dr peterson said
09:19
non-classical state that means they are
09:22
sort of in a eat and repair state
09:25
and then so uh dr so bruce
09:29
do they have s1 protein in them or are
09:32
they just
09:33
expressing it yes they have they have s
09:36
they are exp they are antigen presenting
09:38
cells
09:39
basically and so they are um
09:43
essentially doing what they're supposed
09:44
to be doing which is presenting
09:46
foreign antigens and so um yes there's a
09:49
s1 proteins on the surface which we
09:51
showed by flow cytometry
09:53
then we sorted those cells and again
09:55
i'll show a couple slides in a moment
09:57
and confirmed using high sensitivity
10:01
mass spectrometry
10:03
that these cells had a single spike
10:06
um spike in the mass spec
10:09
uh lingo that showed that it was indeed
10:12
s1 protein and and what they do
10:15
is you know as you mentioned m2
10:18
phenotype
10:20
it's a pro-inflammatory phenotype so
10:22
these cells are still making tnf alpha
10:25
and what's very interesting which i'll
10:26
show in a slide in a moment
10:28
is that when they when these monocytes
10:30
bind to
10:32
the endothelial cells through fractal
10:34
kine
10:35
and the fractal kine receptor they
10:37
produce
10:38
vegf which we see elevated in almost
10:41
all long haulers
10:44
and they cause vasodilation
10:48
why is that important because i'm sure
10:50
you've seen this
10:51
uh dr bean is that they'll complain of
10:54
a fullness in their head and and
10:57
dilated blood vessels and
11:01
and headaches and migraines which we all
11:03
know are caused from
11:05
vasodilation not vasoconstriction
11:07
so once again there's there's there's
11:11
very little we can't explain now that we
11:14
understand
11:15
this mechanism that's at play in the
11:18
long haulers
11:19
this is so important even this morning
11:24
and yesterday i was speaking with a
11:26
patient
11:27
young woman 25 years old and she kept
11:30
saying it seems like i have pressure in
11:32
my head
11:33
and i cannot see correctly and i
11:36
become confused and if i go out and look
11:38
at the bright lights or
11:40
or computer screen i start my vision
11:42
does
11:43
weird things that's how she described it
11:46
so are these related to the issue here
11:49
wizard dilatation absolutely and um
11:54
you know uh i'll pull up uh a couple of
11:56
slides now and show
11:58
um the cool beans what um uh some of our
12:01
data and what we're talking about
12:03
um uh i hope you can all see this screen
12:07
um this plot
12:11
really shows on the far left this these
12:13
are classical monocytes
12:15
the cd14 high cd16 negative monocytes
12:19
they have absolutely no um uh
12:22
s1 protein which is interesting because
12:25
as we say in the paper
12:28
classical monocytes express very high
12:30
levels of the ace2 receptor
12:32
and almost no ccr5
12:36
intermediate monocytes express very high
12:38
levels of ccr5
12:41
and high levels of ace2 receptors yet
12:44
maybe
12:44
uh you know occasional uh infection of
12:48
of these cells in both the severe uh and
12:51
the long hauler
12:52
patients but it's really over here on
12:55
the far right
12:56
when you look at the non-classical
12:59
monocytes
13:00
which express no h2 receptor
13:03
they express ccr5 and they express
13:06
high levels of the fractal kind receptor
13:09
and that's where you're seeing all the
13:11
s1
13:12
positive cells in these
13:15
individuals now this is the mass spec
13:19
analysis
13:20
it's it's rather small but it's in the
13:21
new paper
13:23
but this top panel here this top
13:25
rectangle
13:26
shows this single spike in this blue box
13:30
that's store-bought s1 protein
13:33
we bought it from a company it's highly
13:36
purified
13:37
it's it's it's the full length
13:40
s1 protein and if you look at these next
13:44
six panels every single one of these
13:47
long haulers between 12 and 15 months
13:50
has the identical spike which
13:53
represents the s1 protein and if you
13:56
look over here
13:58
in these two graphs which are
13:59
representative of
14:01
you know of the specific sequence
14:05
of amino acid that uh is 40 percent
14:09
analogous um to the spike
14:12
i mean 40 of the spike one uh
14:16
protein so we confirmed by two different
14:19
technologies
14:21
uh that these non-classical monocytes
14:24
uh are carrying uh the s1 protein
14:28
also we went back and looked at the s1
14:31
protein
14:32
in the cells the cd14 positive
14:36
uh cd14 low cd16 positive
14:39
s1 protein positive cells
14:42
and guess what they're expressing
14:45
cx3 cr1 um
14:49
which is the fractal kind receptor
14:52
and of course that is what allows them
14:54
to bind to
14:56
uh the vascular epithelium
14:59
which this isn't as good as your diagram
15:03
dr bean but it shows just the propensity
15:06
of of these three monocyte subsets
15:11
and their functions the classical
15:12
monocytes phagocytosis
15:15
the intermediate monocytes
15:19
antigen presentation regulation of
15:22
apoptosis
15:23
trans endothelial migration
15:26
and then of course the non-classical uh
15:28
monocytes which as you suggested
15:31
their function is to patrol the blood
15:34
vessels
15:35
uh they are also phagocytic and they
15:37
also present
15:38
uh antigen which is exactly what's
15:41
causing
15:41
all the vascular inflammation in long
15:44
covid
15:46
as you can see here on the closer up
15:48
these cells bind through
15:50
fractal kind and the fractal kind
15:52
receptor
15:53
and in the process produce a th1
15:56
response
15:58
which as the cool beans know the th1
16:01
response is a
16:02
classical antiviral response that
16:05
consists of interferon gamma and
16:08
interleukin-2
16:09
well you know what goes into our
16:11
long-haul or index
16:13
interferon gamma levels and il-2
16:16
divided by cxcl4 which is of course a
16:19
ligand
16:20
for ccr5 but it
16:24
we didn't know this when we were coming
16:25
up with the algorithm or the computer
16:27
was helping us come up with the
16:29
long-haul or index but when we started
16:31
looking at the mechanism
16:33
that causes long haulers we found
16:36
amazing correlation with what we had
16:40
published last week in terms of
16:42
the bioinformatics and the vascular
16:46
inflammation
16:47
theory and then again over here you see
16:50
when
16:50
these vascular monocytes bind to
16:54
the endothelial cells through
16:57
cx3 cr1 which is the fractal kind
17:00
receptor
17:01
and fractal kine which is another name
17:03
for it is cx3
17:05
cl1 messenger rna what does it do
17:09
promotes angiogenesis through vegf
17:13
and it causes vasodilation which of
17:16
course
17:17
accounts for this head fullness
17:19
headaches
17:20
migraines etc maybe even the brain fog
17:25
and so um why is that important well
17:29
these monocytes express ccr5
17:33
and they're mobilized by exercise and so
17:36
from a therapeutic standpoint
17:38
we recommend ccr5 antagonists
17:41
we've been using moravarak laurentlimab
17:44
is another example that's been talked
17:46
about on this show a lot
17:48
it's another ccr5 antagonist is still
17:50
awaiting
17:51
uh approval but they are critical
17:54
in keeping these monocytes from
17:57
migrating
17:58
all over the body in response to ranties
18:02
and people always say i talk about
18:05
ranties all the time well you know what
18:07
in the long haulers ranty's is elevated
18:11
and over 80 percent
18:12
of long haulers so we still have a
18:16
rante's driven disease and in fact in
18:19
one long hauler
18:20
uh last week their ranty's level was
18:23
900 000 when normal is 10 thousand
18:28
and the highest we saw in our first
18:30
studies of acute covid back
18:32
in february 2020 in severely critical
18:37
patients was three hundred thousand so
18:40
at times the levels of
18:42
ranties in long haulers is even higher
18:45
than
18:45
uh the most severe cases of acute covet
18:48
and then effect in fact the angiogenesis
18:52
and vasodilatation
18:53
play a part but we can also interrupt
18:56
uh this fractal kind fractal kind
18:59
receptor
19:00
uh pathway with statins
19:04
so the hallmark of our treatment regimen
19:06
now
19:07
um that we recommend is a ccr5
19:10
antagonist
19:11
and statins and of course uh ivermectin
19:15
we have found
19:16
uh as as you've used extensively and
19:19
and dr corey as well we find it to be
19:22
very very useful
19:24
in our combinations uh we tend not to
19:27
use it uh
19:28
alone because now that we understand the
19:30
mechanism
19:32
behind long covid um
19:35
we want to interrupt the pathway we want
19:39
to treat the cause
19:40
and not the symptoms but by no stretch
19:43
of the imagination
19:45
do we think that ivermectin isn't
19:47
important in its immunomodulatory
19:49
effects
19:51
that complements uh the ccr5 antagonists
19:54
uh and fractal kind and excited
19:58
i'll go go ahead i have a couple of very
20:01
important questions so i don't want to
20:02
break your stream of thought so please
20:04
complete your thought and i would
20:06
ask the questions yes i just i want to
20:09
uh show one last slide and i'm excited
20:12
to get back to the questions because
20:13
this has been such
20:15
a key question uh out there in
20:18
social media and and from our patients
20:21
and that is the post-vaccination uh
20:24
long-haulers or the the people who have
20:27
never had covid
20:29
um and three or four months after
20:31
vaccination they have long
20:33
hauler symptoms well i think we've
20:36
enrolled
20:37
um you know a hundred or maybe even
20:40
close to 200 now
20:42
and we're starting to input the data
20:44
into our machine learning
20:46
algorithm and we had fascinating results
20:49
from the first
20:50
20 or 25 that we fed into the machine
20:54
learning
20:54
where we saw a very heterogeneous group
20:58
there was one individual who was normal
21:01
by the severity score which we use in
21:04
acute covid
21:05
and negative by the long hauler square
21:08
which we use in long haulers
21:10
we found four um
21:13
individuals who had a uh
21:16
inflammatory profile that looked a lot
21:19
like
21:20
um covid and severe active covet
21:23
although it wasn't and then the rest
21:26
look exactly like long haulers from the
21:30
long hauler index
21:32
so and then we went to a binary
21:35
uh bioinformatics models they all
21:38
uh qualified as long haulers so
21:42
indeed immunologically they resemble
21:46
very much like long haulers we've
21:48
treated them as such
21:50
and we've been very successful in
21:52
treating them so as much as it's
21:55
a side effect of vaccines i think it's
21:58
not something to
21:59
be too concerned about it's treatable
22:02
um and uh it's not something that will
22:05
that will stick for forever so we're
22:09
very pleased to um
22:11
to take a look at that so that is
22:13
excellent i actually have a question on
22:15
one of your slides as well but let me
22:17
ask a few questions that are
22:19
even burning questions for me too so
22:22
first
22:22
question reema are these monocytes or
22:26
macrophages
22:28
they are monocytes and you know there's
22:30
been some reports that
22:32
macrophages in the gut it's and in the
22:34
lungs on autopsy contain
22:37
um you know covalent sars and i i don't
22:40
i don't doubt that um that's just
22:44
a part and parcel to the fact that
22:46
macrophages
22:47
function in the tissues they're gonna
22:49
have um
22:50
residual um virus i don't think it's
22:53
replicating
22:54
the the the key point about our
22:57
discovery
22:58
is it's in a highly mobile
23:02
cell that's in the blood they are true
23:05
monocytes um non-classical monocytes but
23:09
monocytes nevertheless
23:12
and they have the capacity to go all
23:15
over your body
23:16
and cause inflammation and that is what
23:19
is
23:19
so key about this finding relative
23:22
just uh to autopsy findings where you're
23:25
going to find
23:26
you know bits and pieces of virus and
23:29
you know in
23:29
terminally differentiated uh macrophages
23:34
thank you very much i want to share a
23:36
thought with the with the cool beans
23:38
cool beans for the today's talk i was
23:41
thinking that
23:43
the whole world population became stuck
23:46
with this
23:46
covet seven billion and more people
23:50
and then there are people who invented
23:53
divermectin or discovered it
23:56
and now they're they are not but there
23:58
are people who are pushing it like dr
24:00
pierre corey they are the people who are
24:01
saving
24:02
billions of people similarly vaccines
24:05
are actually saving billions as well
24:07
and i was thinking about dr bruce
24:09
patterson and his discovery
24:12
it is at the same level of saving
24:15
billions of people because this misery
24:17
i can tell you today while talking with
24:20
one of the patients i was so
24:22
angry he he has post-covered
24:25
long-haul and he himself is a research
24:29
worker and a health care professional
24:32
and he goes to doctors he knows them he
24:35
himself is a healthcare
24:36
professional and he's a research worker
24:38
and he goes to doctors and they have no
24:40
idea
24:41
and when he says we should try this or
24:42
we should test that they have no idea
24:44
and they have no
24:46
other than a few they have no even
24:49
interest
24:50
and i was becoming so angry to say if
24:52
this is what vaccines are going to do
24:54
and then we are going to break people
24:56
and then we have no help for them
24:57
then what is really the help there so
25:00
once again thank you very much for your
25:01
work
25:02
i wish everyone in the world can once
25:05
know that there is
25:06
a team that has discovered it and they
25:08
have a solution
25:09
and be able to use that now there is
25:12
another
25:13
question here which is important simple
25:15
garden says
25:16
will the system eventually equalize and
25:19
return to normal
25:21
that's you know these are just the the
25:24
the best questions that get to the heart
25:26
of the matter
25:27
and the fact is these cells have a
25:30
definitive lifespan
25:32
and you know if you look at classical
25:35
monocytes
25:36
intermediate monocytes and non-classical
25:39
monocytes
25:40
in normal human beings you're talking
25:42
about you know
25:43
life spans in the order of days and
25:45
weeks
25:47
what happens though in pathologic
25:50
conditions
25:51
is uh a whole set of mechanisms
25:55
that prevent cell death
25:58
come into play that make them more
26:00
long-lived
26:02
than in normal individuals that said
26:06
using the combination of ccr5
26:08
antagonists and
26:10
and statins and ivermectin
26:13
we've seen by doing serial monitoring of
26:17
these cells
26:18
we've seen the levels go down so we
26:21
are very very hopeful and optimistic
26:25
that eventually these cells get cleared
26:27
we are
26:28
we've already shown people in
26:32
patients in our program that we've
26:34
gotten their immune systems back to
26:36
normal
26:37
absolute normal every one of the 14 plex
26:41
cytokines in our panel is normal and
26:45
you know that was the goal you know
26:47
restore the immune system
26:49
to normalcy you know sometimes there's a
26:53
lag in the symptoms
26:55
but and then also there's there's
26:57
symptoms that just
26:58
are a function of being debilitated for
27:01
12 months
27:02
i mean if you broke your hip and and you
27:04
were laid up on the sofa
27:06
for eight months and all of a sudden
27:08
your hip was better
27:09
you know you would have aches and pains
27:11
and be out of shape and not be able to
27:13
do what you used to do and have
27:15
have fatigue um so i think it's
27:18
reassuring that we can say to these
27:20
individuals
27:21
hey your your immune profile is back to
27:24
normal
27:25
um usually their their symptoms are
27:28
right along with that
27:30
um but some may have some symptoms that
27:32
remain and
27:33
so we get them to 90 to 95 percent
27:36
of their pre-covet levels and we still
27:38
have five to ten percent to go but i
27:40
think that five
27:41
to ten percent is a function of being
27:43
debilitated for so long
27:46
and maybe just normal effects of being
27:49
sedentary or even you know bedridden for
27:52
so long
27:53
that we have to start stepping up their
27:55
exercise now that we've
27:57
you know eliminated these these cells
28:00
stepping up their activity
28:02
um and um getting them back to you know
28:05
getting them back to a normal life
28:06
there may be setbacks but what i tell
28:08
them is
28:10
we were able to get your immune system
28:12
back to normal we have a target like a
28:14
like a bow and arrow um we know
28:18
where the bullseye is and we know how to
28:20
get you back there so go ahead
28:22
you know we'll step up your exercise
28:25
go get vaccinated if you want to get
28:28
vaccinated
28:29
um we'll deal with the consequences
28:32
of increased activity and other
28:34
perturbations
28:36
of the immune system because we know how
28:38
to get you back to where you were
28:40
and that's our message got it thank you
No comments:
Post a Comment
Note: Only a member of this blog may post a comment.