Tue, Jan 03, 2023 4:51PM • 1:51:46
SUMMARY KEYWORDS
angiotensin, receptor, cells, ace, pathways, upregulate, atherosclerosis, oxidative stress, endothelial, endothelial cells, induces, polarize, nitric oxide, activated, plaques, triggers, leads, homeostasis, patients, renin angiotensin system
SPEAKERS
Bill Clearfield
00:38
I guess we’re the first person on
00:45
let’s let’s horizon Hey Joe Are you gonna hold well?
01:37
Call me back
01:38
on oh here we go
01:55
941-400-3675
02:10
Robert Joe
02:16
well I’m calling about my wife’s phone I’m calling you on my phone it will not make calls or receive Paul’s. It seems to do our own on the internet and stuff. It just doesn’t have service as
02:30
far as I’m concerned okay Hi there. I’m sorry I didn’t understand how are you?
Bill Clearfield 03:07
Still can’t hear you.
03:10
Can you hear me now what it is? It’s me. Okay.
03:11
All right.
Bill Clearfield 03:14
Yeah, it was me okay.
03:17
How are you?
Bill Clearfield 03:18
I’m doing great. How about you? Did good guys through the holidays. Okay.
03:23
Yes, thank goodness and you
Bill Clearfield 03:26
were still here. So yep, we got through the holidays. Okay, and we’re doing okay.
03:33
Looks like he lost weight.
Bill Clearfield 03:36
I’m trying.
03:38
So that’s a good thing through the holidays. That’s a challenge.
Bill Clearfield 03:41
It is a challenge. So trying so that’s good. We have our own proprietary weight loss shot so someone’s got to try it out. So I just got word from AMG. They want me to present it at their Miami meeting coming up. So that’s
04:00
good. That’s good.
Bill Clearfield 04:02
So we’ll be doing it there.
04:05
I have I want to I want to order your course for
04:10
the hormones.
04:13
I have to find the email again.
Bill Clearfield 04:16
Okay, I’ll put it in the chat when once we get started. Okay. Okay. Okay. It’s actually one of the on the flyer every, every week, the last couple of weeks. It’s at the bottom of it.
04:28
And I still don’t get the emails.
04:30
You don’t know.
04:33
This is an old one from 2021. I still have so it still
04:37
works. I don’t know why.
04:41
Because the J module doesn’t work at all and the Nobel had
04:45
to come to your meeting because I’m gonna have to go in the other room when
04:51
I must be Fred.
04:53
I have it up here. I guess. I’ll turn the phone on. I mean, TV on.
05:03
Okay. Okay, okay. Yeah. Hey, hi. So it’s, um, it’s your control board on the package unit. I can get one right now. It’s going to be and I can write you up in the invoice but it’s gonna be about $1,150.
Bill Clearfield 05:26
Can I do? I can get it done tonight. You can’t. Yes, sir. Go for it. Okay,
05:31
I’m on my way. I’m gonna go grab it and then come back Okay, let’s see.
Bill Clearfield 05:46
So we got Jackie’s can hear we can hear you again. So where are we?
05:51
Now? Um, I sent you the Nova email again, because you said that will
05:54
work. But you’re still not getting it? No.
Bill Clearfield 06:00
All right. Did you send that to my email?
06:02
I put it in the chat right now.
06:07
Do you? RM 184. Yeah. Well, once we get going, I’ll try and fix it. Okay, no problem. Thanks. For what school you’re at.
06:23
Nova Southeastern.
06:26
You’re teaching there what do you teach?
06:32
Physical diagnosis principles or clinical medicine? medical procedures. The first and second years?
Bill Clearfield 06:40
Maybe maybe what have you give us a talk with I think we all forgot about that. Look at Dr. Burgess down there. He doesn’t know anything about that. I guess
06:49
I excited every Tuesday night and now we got another star joining us. This is wonderful. Yeah. How far is this? How far is the school from Miami?
07:00
It’s an Davie. There’s two campuses, one in Davie, which is Fort Lauderdale area, and then one in Tampa. Which is Clarets Clearwater, Clearwater Tampa.
07:12
My mom’s place.
07:14
Where are you? I’m in Tampa.
07:19
My family? My family has been there. 200 years.
07:22
Yeah. So if you come visit, give me a goal. The campus
07:27
thank you and by the way, I announced everybody hear my rumor is that there’s going to be a new osteopathic medical school started about 2030 minutes from me here. Oh, that gives us some more opportunities to step in. Bill and all you other guys because all we’re trying to do is share good information. But anyway, I go see my senators and about whenever a week or two. Then I have heart surgery. And then I tried to get my foot in the door the AOA in this medical school. I’m still trying to make you look good bill.
Bill Clearfield 07:59
Still trying to make me look good. Again, stop it. Well, one of the one of the one of the architects of our demises as left the AOA has gone to work for a Hospital Corporation of America.
08:12
Isn’t that what does that tell you? Hey, boy. So it’ll work out good. At Jack Jacqueline. Thank you for joining us.
08:24
know,
08:25
I’ve been I usually try to make it every week. We’ve been here before.
Bill Clearfield 08:29
Yeah. It’s those mushrooms John. You know,
08:35
that’s what I’m promoting. Yeah. By the way, the by the way, I’ll just mention I don’t know how many here are familiar with Ibogaine to get people off dope opiates. It’s 1000 milligrams and you’re off. You have no withdrawal the rest of your life. Within six hours. I tell you get people off heroin. Anyway, I just got notified by our Caribbean Ibogaine services that they are now providing psilocybin vacation relaxing things, you know, for depression and such. So yeah, since you Brett bring up mushrooms. They’re now being provided in and now in Nassau, isn’t that Nestle? That’s the Bahamas right so that’s where it is so that’s all good news. And then we go to talk to our senators about Ibogaine here
09:29
pretty soon. Okay, well,
Bill Clearfield 09:32
that’s great. So it’s a little bit after five.
09:37
Dr. Joseph is with us. And
Bill Clearfield 09:42
she here where are you at, sir?
09:45
What’s that? Sorry. I was getting. We were calling you. You were calling me.
Bill Clearfield 09:53
We’re looking for your
09:55
expertise here. Oh, calling from my ex. Otherwise, we’re
Bill Clearfield 09:59
going to be listening to Dr. Burgess. expound on the on the joys of Ibogaine and ayahuasca.
10:09
Nice. Well that’s a that’s enlightening to ya. So So, I’m gonna share the screen here. So I can get to the slideshow.
Bill Clearfield 10:21
So Dr. Joseph. James Joseph is our speaker tonight and I’m gonna let him introduce himself. I’ll let folks in as they show up. And I hope everybody had a good holiday. And this year is going to be better than the last Right? Right.
10:42
Absolutely. This year is going to be better than the last. And you know my whole thing is somebody asked me well, how are you dealing with everything that’s going on in the world? And I said, actually great. I think I do better in this kind of world then the delusional world before this, so I guess that’s how I feel about it. But I think with everything that’s going on, for me, it really makes me it makes me come alive. And, you know, the reality is, is I think it’s better to have that kind of attitude in general, because, you know, we can only control so many of the things that are happening. And I’ve come to the conclusion that pretty much what’s going to happen, it’s going to happen. And I’m okay with that because it’s game time. You know, it’s time to put on put on our superhero outfits and be our best versions of ourselves and take life to the max while we’re here.
Bill Clearfield 11:54
Okay, all right. You hear that Dr. Burgess? No. More fooling around. No more fill in the rags. No.
12:04
Go ahead. Go ahead.
12:07
Let’s be careful now. Yeah, we have to do everything as my commander said, discretion. We’ll just stick with him that yeah, that’s
12:20
that’s what I mean by our superhero outfits. You know, we’re gonna get out there and do do the right thing and, and, and help people and make an impact on people. And that’s just simply the case and we’re going to do it in the most sophisticated way. way I see it is the the lectures I’ve been doing recently, are it’s stuff that we already have learned. But still at the end of the day, I still have questions about like the renin angiotensin system and how COVID triggers oxidative stress triggers the interleukin six and polarization of the immune system. And so by doing these lectures, it’s kind of like a way of saying, You know what, let’s get it down pat. And then we’re pretty much done. And then we do the next lecture like vitamin D, and we see how that ties into it. And pretty soon we start having all the puzzle pieces that really make sense, and we’re not pretending to make sense. And so, I will start nowadays it is already established that hypertension is a modifiable risk factor for cardiovascular diseases and reduction in blood pressure. It’s accompanied by a reduction in cardiovascular risk. Well, this by the way, this this article was actually written before COVID And so we get to look at this without any connection to COVID. So this is this is what they’re talking about is the connection between the ROS system leading to atherosclerosis as really the primary way that it’s happening, but the root of what’s actually happening, versus some of the other things is just, oh, it’s hypertension. Oh, it’s this it’s that, well, what if it’s really the renin angiotensin system? On the other hand, the persistent burden of cardiovascular events despite a high effective control of conventional risk factors suggests that other mechanisms might underlie a proportion. These events. As previously reviewed by us and by others, atherosclerosis consists of an of an inflammatory response of the arterial wall to injuries. The inflammation is often initiated by endothelial dysfunction and progresses to cellular adhesion molecules. Expression adhesion of circulating leukocytes to the endothelial cells, leukocyte migration and formation of a fibrous cap, lipid core which compromises the vascular lumen so okay all basic stuff. We all know this. In addition to its traditional role in hypertension, the long term blood pressure control system, the renin angiotensin system, Ross is directly involved in the development of atherosclerotic lesions due to its effects mainly on endothelial function. Inflammation, fibrosis, coagulation balance, plaque stability, and structural remodeling. And so they’re already looking at the Ross system is, is directly causing the problem along with the classic cascade of renin angiotensin system, which involves the conversion of angiotensinogen to angiotensin one by rennen, followed by its cleavage to angiotensin two by angiotensin converting enzyme ace, other peptides and enzymes related to the renin angiotensin system are important. And Anthro. Genesis. Angiotensin two is the main effector All right. So over the past two years, learning about COVID realizing I was weakened I thought I knew more but I there were a lot of intricate pathways that I didn’t realize, and when I learned them, everything started to make a lot more sense. And now that we’ve got sort of some focus points, and I really think that the renin angiotensin system is a focus because we can tie everything else into it. And we have to because it’s the main problem with COVID. And the fact that it’s downregulating the ACE two receptor and an angiotensin two is, is dominant. The effects of angiotensin two are mediated by its binding into the angiotensin type one and type two receptors. So it’s either going to bind to type one and type two, or both in equal amounts, which which would give a balanced effect. So the type one, angiotensin type it angiotensin two type one receptor is the inflammation route. And the other one, the type two receptor is the anti inflammatory. So we got the yin and the yang and that’s the one thing I always look for is, you know, for every, for every one thing, there’s there’s the equal and opposite in the body. It has been shown that angiotensin two directly induces endothelial dysfunction and increases endothelial oxidative stress through the production of reactive oxygen species, such as superoxide anions. Derived from the complex enzyme nicotinamide adenine dinucleotide phosphate oxidase, otherwise known as its NOx. You can put stuff on yours. Some of these Yeah, somebody’s mic microphone is still on. We can hear you. This predominantly through the interaction with endothelial angiotensin type one receptor, which mediates increase in calcium concentration in endothelial cells promoting activation of calmodulin and interaction with KNOX five calcium calmodulin binding domain, really Camogli and just means calcium modulation. So the angiotensin two if there’s overabundance of it, it’s going to be stimulating angiotensin type one receptor. Too much things are things are out of balance. The angiotensin two is not being converted to its other form angiotensin one seven, which would activate another receptor actually, very similar to the type two receptor called the moss receptor, which is the anti inflammatory route. So when it goes down pathway number one and I have a picture of this calcium concentration goes up, and it may be that it’s being released from intracellular stores. Or perhaps it’s a calcium channel, letting calcium in, but that interaction between calcium calcium modulation molecule interacting with knots, five which is within the cellular membrane, triggers the production of superoxide anions. Okay, so that’s where all the oxidative stress, the beginning of the oxidative stress, the cytokine storm, that’s where the storm is actually starting. That’s what they’re talking about with oxidative stress and why we’ve got to buffer that because that leads to all the other oxidative stress pathways. Activate activation of NOx five mediated by angiotensin two produces superoxide like the ultimate free radical activates ROA and leads to subsequent stimulation of rho associated kinase in human umbilical arterial endothelial cell culture. Now, these ROA and all these these terms I you know, I always try to look them up and see if there’s a way to maybe it means something that’s that’s relevant because I don’t like to just remember, you know, random words that have no meaning. But you’ll see with all the different cellular pathways, ROA and roc, they all sort of start with an R, and they’re all a part of this Ross family. And Ross means rat,
21:38
rat sarcoma, and that was an that was obviously named that because that was one of the pathways that they found sarcoma in when they did studies on the laboratory mice. So that’s how I sort of remember that it’s probably not a good pathway. That’s, that’s how I see it. Now the rho rock pathway, or you know, part of the Ross family the RET sarcoma. The bad pathway is an upstream regulator of mutagen activated protein kinases. And when you think of mutagen, just think of mitosis because you’ll see ma p k overexpression, or you’ll see it involved with proliferation mitosis proliferation. Now, it’s not a bad pathway, if it’s imbalanced with the other pathway, okay, so this would be the part that triggers cellular division and growth of the endothelial cells, but the problem is is it’s overstimulated and over overstimulation promotes an imbalance of NF or triggers NF Kappa, NF kappa B, which is a transcription factor. So everything has been happening in the cytoplasm. And then NF kappa B gets activated. And that’s sort of goes into the nucleus and triggers the transcription of various genes. And this is these are the ones so NF kappa B. regulates the expression of numerous genes such as cytokines, tumor necrosis factor alpha, interleukin six chemokine, things like that, which is just, you know, things that attract other immune cells so monocyte chemoattractant, protein adhesion molecules, those are there like to put the brakes you know, that like I see them as like little ropes to catch the, the circulating monocytes that are attracted that grab them and pull them in. And the the antium during the inflammatory enzyme, Cox two which is really just part of inflammation. In general, the the pathway that is blocked by NSAIDs, non steroidal anti inflammatories, and then I guess it does produce angiotensinogen which can then give rise to more angiotensin angiotensin two and stimulate that pathway even more if phase two is downregulated or blocked. Moreover, activation NF kappa B seems to be an important signal transducer and signal transducer. I found it fascinating. It just means it’s one form of energy is being transferred to another form of energy and amplified. So it’s literally just like, if somebody plays a guitar, the there’s the wires that connect to the to the speaker and the sound that comes out. You could you could say that the speaker is the transducer. So it’s taking the signal from the from the electric guitar and and changing it and amplifying it at the same time. And this causes an upregulation of oxidized low density lipoprotein mediated angiotensin one expression. So it basically they’re the receptors it triggers the receptors to oxidize circulating low density lipoproteins. That’s or or the light or the LDL that is gets within gets in between the endothelial cells and embeds itself in the intima of the vasculature. It is likely that TNF alpha released upon angiotensin two stimulation of angiotensin II type one receptor, in combination with interleukin four acts as a paracrine molecule inducing selective adhesion of mononuclear cells to the arterial endothelial through increased expression of Pam and release a various various chemo kinds involved in the recruitment of mononuclear cells. So what’s new we the common theme here is TNF alpha. And interleukin six actually is is the bigger thing. And we may get to interleukin four. So I believe interleukin four triggers the the T helper cells to polarize towards th two Okay, so that’s important because if you imagine a COVID infection, you’ve got interleukin six, which is going to polarize the the T helper cells, or at least the T, the T regs will polarize towards th 17. And so yeah, well you have two different kinds of T helper cells, you got the teeth, th 17 helper cells, and the th 17. Arms are in the th two helper cells and they get activated they start off as naive and they get triggered by those specific interleukins. Okay, so I’m gonna go blow this up a little bit. So we’ve got basically two sides of a coin here. On the left, we have angiotensin type one receptor, and on the right, we’ve got the angiotensin II type two receptor and the MAS receptor. And at first I was confused. When I looked at looked at this, I’m like, Well, if angiotensin two binds to both, well, why would one be more more dominant? Well, the answer is because your if and if ace two is suppressed or blocked, say by COVID or for other reasons. Then angiotensin one seven will not be created to interact with with the mass receptor. And apparently, it also triggers the the ACE two receptor. And so if you’re not getting that stimulation, then you’re going to have an overabundance of angiotensin two stimulating that the type one receptor in relation to the moss receptor, which is not being activated. So again, so we’ve got on the left side all the bad stuff, endothelial dysfunction, cytokines, TNF alpha, interleukin six, interleukin four, we’ve got the chemokine attracting the monocytes you know that will present to the to the naive T cells. We’ve got the adhesion molecules, oxidative stress, super superoxide anion, recruitment of mononuclear cells osteopontin. I see that as sort of like a bridge builder if when when a plaque is being formed, and the mononuclear cells are, are invading the space along with oxidized LDL, osteopontin sort of creates the structure that holds everything together. Sort of an osteo means obviously, oh, well, I still literally means bone and Pong. Pawns actually means bridge. So that’s that’s how I remember it. And you can think of it as the pawns of the of the midbrain or I’m sorry of this brainstem is sort of the bridge between the brain and and spinal cord. I won’t say all the other stuff but everything on the on the right side is the opposite. Just notice that there is nitric oxide is increased and, and that’s relevant to this whole system. Okay, so, moving on angiotensin two. This induces the expression of osteopontin a multifunctional protein found in many cell types, including macrophages, endothelial cells, smooth muscle cells, which is part of the the vasculature intima and epithelial cells angio to angiotensin two also up regulates the locks gene, and I believe the locks gene is that’s what really is up regulating the receptors that oxidize LDL. Lots of the transmembrane glycoprotein that serves as a receptor for oxidized LDL or it attracts them and brings them in
31:39
the endothelial binding of oxidized LDL and lox causes increase in leukocyte adhesion molecules activates apoptosis pathways and increases reactive oxygen species and induces endothelial dysfunction. So the way I see it in the extreme cases, you might have apoptosis, for example, like with COVID in the lower lungs, you’re having in the microvasculature, you’re having apoptosis, destruction of some of the endothelial cells and apparently that causes a release of von Willebrand factor into the micro vasculature. Which may be responsible for all the micro clotting. So this, you know, this is why I like this. It’s starting to tie things together how the things relate.
32:39
According to experimental and clinical data, ACE inhibitors, and ARBs. The angiotensin receptor blockers appear to have beneficial anti atherosclerotic effects. It has been shown that the Angiotensin Receptor Blocker olmesartan significantly reduced vascular inflammation in hypertensive patients with a significant reduction in serum levels of many inflammatory markers such as C reactive protein, TNF alpha, interleukin six and the monocyte, chemo, taxes, protein. It’s all of those things, really. I mean, it’s blocking that type one receptor. So it’s, it’s inhibiting that effect of the angiotensin two leading to that whole cascade of events, triggering oxidative stress, apoptosis, NF kappa B. The first evidence of a relationship between ace two and atherosclerosis was demonstrated in 2006. So not that terribly long ago 2008 found AES two overexpression on aortic plaques attenuate the pur aggression of early lesions and rabbits that underwent that had endothelial injury and received an atherogenic diet probably by conversion of angiotensin two, two angiotensin one seven and so the plaques may have, I’m not sure if they induced the ace to overexpression or or the vessels we’re trying to produce more ace two receptors in order to try to balance everything. Likewise, overexpression of ACE two and APR II knockout mice attenuated atherosclerotic lesion size and improve endothelial homeostasis, at least in part through a mechanism that involves reduction of angiotensin two induced reactive oxygen species generation. Now a bo II that’s a whole you know, I got back into looking at some of these concepts and that’s, that’s a whole nother system and, you know, they’re involved with, I guess binding to some cholesterol and in this situation, if, if it was knocked out
35:30
it led to an overexpression of AES two, and then the the atherosclerotic lesion size improved. So, so there’s a direct correlation between ace to increase ace to and and improvement of atherosclerosis. The production the protective role of Ace to atherosclerosis was also supported by the use of Ace to deficient vice model, ace to knockout AES two deficiency in both LDL receptor deficient mice and APR II knockout backgrounds resulted in larger atherosclerotic lesions when compared to the respective controls. So what they’re saying is that the biggest the biggest thing here is not the LDL. It’s not April II and you know, as a carrier of LDL and other cholesterol molecules as to is is the biggest thing. And so, that that means a lot 2008 It was demonstrated the presence of AES two and humans they detected AES two protein and human veins healthy and atherosclerotic arteries expressed in endothelial cells, smooth muscle cells and macrophages. Well, that’s relevant because that means then that COVID can invade macrophages, and they can invade smooth muscle cells. I don’t know what the relevance exactly is with that. But that’s significant. In 2016, it was found that baseline circulating ace to activity was enhanced in chronic kidney disease. Patients with atherosclerotic plaques when compared to patients with no plaque suggesting that higher circulating ace to activity is associated with higher risk for silent atherosclerosis, meaning that the silent atherosclerosis is in the process. And the cells are trying to produce more ace two receptors in order to create homeostasis, and some of those receptors end up in the bloodstream. I guess they’re cleaved or, you know, I don’t think they even mentioned why but the the elevated level indicates that the body’s trying to get back into homeostasis by producing more ace two receptors. AES two is an integral cell membrane protein that can undergo cleavage or shedding and release its catalytically active eco domain into the surrounding milieu. So yeah, so there it is. It is cleaved, it’s shredded, and perhaps it’s trying to bind in a sense, other engines you know, other angiotensin two in circulation, you know, stop it before it even gets to the cell. The main promoter of bass to shedding is a disintegrin and metalloprotease. Adams 17. And, you know, I just sort of remember these things is look at this. It’s disintegrating. Something, you know, therefore, it’s, you know, cutting something or cutting something off and a receptor and that’s, that’s really how I remember that. So that might be up regulated, and then causing those ace two receptors to shed and maybe bind some of the other milieu, bind up some of that angiotensin two before it gets there. Some therapeutic strategies for atherosclerosis targeting ace two have been thought of either with new drugs or drugs already used in the clinic. A recent study has demonstrated that the overexpression of ACE by plasmid mediated transfection and both primary monocytes and th P one cell THP. One cells are what are what are basically the monocytes that they they study in the in vitro that’s just another name for them, leads to a marked decrease of Ace to messenger RNA expression and induces a pro atherogenic phenotype with elevated gene expression of the cellular adhesion molecules. I can be cam and macrophage colony stimulating factor. You know, that that says something, so, they had a plasmid mediated transfection that decreased ace to messenger RNA expression. So, look like they could create some sort of infection that could that could manipulate the system. All these effects were partly reversed by Captopril and Losartan. It was interesting, and this is just these are just facts. When I looked at Losartan closely, in regards to COVID. This was later in 220 20. Right at the beginning of the year, it was actually before the beginning of the year, they they had taken Losartan off off the market and other ARBs because they discovered that a batch was was causing cancer or could cause cancer. So, it was unfortunate because, you know, that could have maybe have helped a lot of people. Anyways, and in that context, this is in 2015. They show that Losartan inhibited the evolution of atherosclerotic plaques and high cholesterol fed rabbits as well as increased the ace to protein expression. In plaques.
42:00
So, I mean, it’s doing all the right things. That’s in cholesterol fun rabbit. So again, it’s the the issue is Ace two and angiotensin two A’s to activating drugs and seem promising with emphasis on Dimas. Dima, then, then min Nazim Okay. Guys, which has several protective effects such as improvement of metabolic profile and reduction of lipogenesis in mice antihypertensive effects in renal vascular hypertensive rats and improvement of pulmonary endothelial function in Sprog dolly rats. Now, the cool thing is, I just did a lecture yesterday on vitamin D. And guess what vitamin D actually up regulates, as to you know, so the question is, do we really need the magazine or can we just optimize our vitamin D, and you’ll see that vitamin D does basically the reverse of everything that COVID is doing. For the most part, Vitamin D is, is it’s all of its actions. work against COVID on many different levels. Angiotensin one seven was investigated three decades decades ago, as an important counter regulator component of the renin angiotensin system promoting hypotension and bradycardia. After micro injection in dorsal motor nucleus of the vagus. So this was three decades ago. They were testing angiotensin one seven. Well, we have a peptide called di hexa. That’s what it is. And so they hexa would be another way to balance out the renin angiotensin system and perhaps help reduce blood pressure. The formation of angiotensin one seven in vascular endothelial was first identified by using human aortic and human umbilical vein endothelial cells. Robust studies have shown the angiotensin one seven induces the mass receptor that we saw on that slide a G protein coupled receptor. There’s only like four types of receptors in G protein coupled receptors is one of them. pi k, a key tape pathway leading to phosphorylation of endothelial nitric oxide synthase. You know, so how how to really remember that, the, the, that’s phospho inositol. That’s what the Pei stands for, and kinases is just sort of, you know, part of the passing on of phosphorus you know, from one molecule to the to another that has a higher affinity, kind of like the electron transport chain. I remember pi k because the cell wall the reaction is happening, really in the cell wall and phosphor inositol is it’s linked to the to the cell wall that is, is a phospholipid. Okay, so that’s kind of how I see it. And otherwise, I don’t really have any other way to remember. But it is the good side of things in this situation. And it’s leading to activation of nitric oxide synthase producing nitric oxide, more nitric oxide and that is having an inhibitory effect on NF kappa B. So it’s balancing out what’s going on with the other side of things. Angiotensin one is able to one seven disabled also to promote angiotensin two receptor endothelial activation, which stimulates the brain keinen nitric oxide cascade. Nitric oxide is one of the most important factors released by the endothelial so it’s contributing to so it’s working alongside the boss receptor. This gas is involved in vascular homeostasis, and its decrease induces endothelial dysfunction, which is the key factor in atherogenesis. So it’s playing, it’s playing more of it’s more than just you know, when you think of nitric oxide, I mean, for me, it was just basal dilation. But when you realize that it has more to do with homeostasis, on the intracellular level, then the I’m seeing it more like a communication signal. I’m seeing it differently
47:35
think I already know I guess this is like okay studies have demonstrated that angiotensin one seven stimulates endothelial cell function restoration by increasing nitric oxide but by availability. Angiotensin one seven down regulates the you know it’s having the opposite effect downregulates I can be cam in the endothelial by preventing both the phosphorylation of P 38 ma PK, an expression of again, NF kappa B. So it’s just blocking that whole pathway. Moreover, angiotensin one seven induces proliferation of endothelial progenitor cells in the injured vascular tissue triggered by atherogenesis.
48:30
So it’s already blocking all of the proliferation and the formation of the plaque. During the vascular inflammation, many cytokines and inflammatory cells are required to begin and maintain atherosclerosis progression. So we know that there’s all of these things that are happening as a result. In this context, angiotensin one seven has been described to induce anti inflammatory phenotypes which contribute to restrain vascular lipid accumulation. And that’s, I mean, that’s really the name of the game. In contrast to angiotensin two induce proliferation and hypertrophic effects, angiotensin one seven inhibits the migration and proliferation of vascular smooth muscle cells. So you don’t have all of the smooth muscle cells sort of closing in on that area? This effect was described in 2013. Showing the angiotensin one seven induces activation of the moss receptor and jak stat pathways. Just remember moss I think that’s just the most important part leading to nitric oxide in vascular smooth muscle cells to mitigate the atherosclerotic plaque formation
50:09
so that’s actually happening in the smooth muscle cells. Okay, so not not the endothelial cells, but stopping Well, let me look at this again, showing that angiotensin one seven induces activation, these pathways in vascular smooth muscle cells to mitigate okay to mitigate so it’s stopping all the migration further. Furthermore, angiotensin one seven has demonstrated a potential to negatively regulate the vascular fibrosis as can be noticed by decreasing in matrix Metalla proteases in atherosclerotic plaques. So it’s reducing the fibrosis and that’s kind of part of what the metallic proteases do. Accordingly, angiotensin one, the seventh treatment promoted a reduction in the Neo intimal layer growth by structural recovery of endothelial and showed atheroprotective properties attributed to the binding to both angiotensin type two receptor and mass receptor. So I mean, it’s actually causing leading to healing. Angiotensin one, seven reduce so again, so I’m thinking we need to take a keep looking at the hexa because if that’s angiotensin one, seven, and it’s reducing all these things well, I can’t think of AI to me that would be really relevant. And that’s just my conclusion. It just makes sense to me. That’s the logic. Why would we not be using the hexa as part of our balancing act because we’re trying to create homeostasis, and we, if the root of our problems now stem from downregulated, Ace two receptors? Well, we need to address that directly. We need to look at vitamin D and make sure that our levels are optimal. Not just a little bit above normal, because that’s going to upregulate a stew and then throw in the hexa. In You know, I think peptides they kind of they get used as they’re needed. And if we don’t need them, then they don’t use them. I and then if that’s going to stop the polarization of the immune system, towards th 17 Which leads to autoimmunity a cancer Well, this is why I’m going through this stuff. Again. I mean, it’s kind of honestly it’s a little bit painful to go through this and in this kind of detail, but it leads us leads to a conclusion that we need to address these components of the renin angiotensin system and we need to realize that we have tools already that we can use to do that. And of course, you know, buffer the redox and it’s good to have something you know, especially with all these viruses happening all at the same time, it seems like I take methylene blue, five milligrams twice a day, and then I take more when everybody’s getting sick around me. And then I have my I’ve got a wrist red light with an intra nasal connection. And you know if I feel like I’ve been exposed that day, then i i take my methylene blue and then 45 minutes later I do I do the wrist light, which absorbs into the the radial and ulnar arteries. So anything that passes there that stained by methylene, blue is going to get zapped. And the nose right now seems to be colonized quite readily with Omicron. Seems as though it causes headaches. And so in what we could do, we do have a spray methylene blue spray that we can use or we’ve got the methylene blue the oxytocin combination that we can spray and then if we review the oxytocin pathways, those are also counter acting COVID and many different ways and and creating homeostasis and and also increases the the mucus layer secretions are increased. It’s reducing sympathetic tone, increasing parasympathetic tone, and all these things make it more difficult for COVID to get inside our bodies. And I’m at the point now where I think well the name of the game is to prevent COVID In my opinion, because every single time at least for me, every time I get it, even if it’s like oh, it’s just a cold. I ended up right back with with the fatigue. And nothing good comes from this infection. It’s like every time we get infected, we get knocked down another level. So what if we could actually just be the people that don’t get it? Everybody else gets it but we don’t because we’ve got all of these different modalities that are very specific now talk about not shooting in the dark, but we know exactly why we’re doing what we’re doing. We’re taking di hexa to counter regulate the overabundance of angiotensin two to heal any atherosclerotic plaques, but at the same time to buffer any of the negative effects that COVID is going to have in triggering oxidative stress. And polarizing the immune system in the wrong direction. And then up regulating the ACE two receptors, so that angiotensin two can convert over to angiotensin one seven in concert working with di hexa as well to ensure then we’ve got a reason to actually check our vitamin D levels. And actually make sure just taken 5000 units of vitamin D probably isn’t going to do it because it might not be absorbed. If you’re in the north if you’re north of the 35th latitude 35th degree latitude which is anything above the the northern border of Georgia or the southern border of Tennessee, or the border of Arizona, California and Nevada. Once you go north of there, you’re getting less and less sun and less vitamin D photosynthesis. Yeah, just like the plants we photosynthesize it and that’s a very energetic molecule as I have learned to understand. And one of the things that does is upregulate a stew. It does other things. It enhances autophagy of all things it turns on autophagy especially within the immune system, so that when the immune cells phagocytose the virus or the virus gets in it can be quickly degraded by autophagy. Perhaps even before it inhibits autophagy I don’t know exactly what the virus is doing. But I do know that enhancing autophagy may help clear the virus so that it’s not sticking around. Theoretically that that would make sense. In addition, angiotensin one, reduce that atherosclerotic lesion by decrease in college and accumulation through activation of angiotensin II type two receptor So apparently there’s collagen over too much collagen. Conversely, it was described an increase in collagen content after angiotensin seven administration resulting in the increase in plaque
59:27
stability.
59:29
Interestingly increase in plasmatic angiotensin one has been involved in regulation of lipid metabolism. And perhaps it’s decreasing inflammation and that perhaps inflammation is what triggers more release of our creation of of different lipid particles from the liver. It promoted a reduction in triglycerides and cholesterol levels together with a decrease in adipose tissue mass as well as an improvement of glucose metabolism. That’s that’s a lot. The authors have suggested and they’re not talking about that hexa they’re just talking about it you know, if you could give angiotensin one seven. They suggested and involvement of adiponectin in the regulation of glucose and lipid metabolism induced by angiotensin one seven. I don’t know exactly how it does that. I’m not sure if it’s the endothelial cells would be producing adiponectin or Angiotensin one seven is having an effect on fat cells. That That one is unclear. I apologize for that. Some therapeutic strategies have been validated to positively modulate the renin angiotensin system. Statins we all know these have emerged too, due to its pleiotropic properties demonstrating additional effects apart from those of decreasing cholesterol levels. Treatment with this is the article This is none of this is me. I’m just interpreting what I see. Treatment with statins such as a torx. Avastin have promoted an upregulation of Ace to angiotensin one access, reducing the proliferation of vascular smooth muscle cells and intimal thickening respectively effects that are closely related to atherogenesis Well, there you go. Well, we’ve got other strategies if, if, if we don’t want our patients to be on statins you know, for various reasons. Well, we’ve got other ways to upregulate that the ace to angiotensin one axis. The role of statins on the renin angiotensin system components also have been observed in clinical trials as shown 2014 For the first time and increase in angiotensin one seven level in hypercholesterolemic subjects after a torx bit statin treatment. Altogether, those responses suggest an important role of statins on the renin angiotensin system. components, including a decrease in angiotensin two and apparently an upregulation in the ace to angiotensin one axis.
1:02:56
So also decrease in a angiotensin two this fact could be crucial to atherosclerosis and cardiovascular diseases therapy. Now I thought I thought I had another picture. Actually, no, we, we actually not sure if we saw I’m gonna see if if I have it here. Give me a quick second.
1:03:52
Okay, so let’s let’s see if. That’s hiding from me okay, it’s cookie here. Just saw it Okay, all right. So
1:04:59
this also gives us a look at the you can see the on the right side, all the good things that are counterbalancing the production of nitric oxide which blocks the NF kappa d and the the the MA P K’s. Okay. But you also get a chance to see how the oxidized LDL in the intima gets magicite posed by the macrophages, you know the monocytes that come to the area get brought into the intima you know, turned into macrophages and then just the the LDL oxidized LDL and that’s the that forms the foam cells. You know, and I don’t know if that just makes it makes it expand. But but that’s that’s literally what’s happening to the LDL. Yeah, it’s also showing that that there’s the angiotensin one and mass receptors in the smooth muscle cells and the angiotensin one, you know, prevents them from migrating and proliferating or enclosing in. Other things that are important to notice again, is you see the production of or the transcription activated by NF kappa B have interleukin six and doesn’t have the interleukin four but just know that that’s the reason why acute COVID polarizes the immune system to th 17 and in th two and we need th one because that’s what activates or causes the differentiation of CDA eight cells and because we need CDA eight T cells to kill the virally infected cells to get rid of the virus. And so the virus is is making it so that the immune system thinks it’s fighting something else. Fighting a bacteria because that because th 17 leads to neutral philia. And so, hopefully now and we’re at the end of this lecture, hopefully now, if if you weren’t clear yet that you’re more clear, because it really is as complicated as these pathways can be. It’s really straightforward and explains exactly what’s happening. And then what can we do about it and by buffering the redox perhaps with methylene blue and with other modalities, and by considering they hexa which is something I do and also at the same time up making sure vitamin D levels. It probably through the use of cod liver oil i And that’s been mentioned in the articles because it absorbs the or we’re able to absorb that better. You’ll see and I will if you want me to I’ll do the lecture on vitamin D. And again, it’s because and I can really I guess I can only speak for myself every time. If I were to if somebody were to ask me well, how does vitamin D actually work? I would have to give like a superficial answer. Oh, it’s anti inflammatory. But that’s all that’s all I understood after all these years. So I finally just dug deep with it and actually made sense of it. And it ties in nicely to what we talked about today. And you’ll see how it produces capitalist buttons that can punch holes and in. In bacteria, you’ll see how it how there’s anti how it can block viral entry into cells. How it triggers a tapa G, how it will buy up regulating the ACE two receptor, it’s modulating the entire renin angiotensin system. And so yeah, and it’s now I got it, I understand it now. And so I’ll do a lecture on that. If you guys want. But with that, any questions
Bill Clearfield 1:10:02
thank you so much, Dr. Joseph.
1:10:04
Sure. Great pleasure.
Bill Clearfield 1:10:07
Um, let’s see in the chat here. We’re gonna get to
1:10:13
Marist Excellent, thank you, Dr. Joseph.
1:10:16
Thank you. Yeah, no, I hope I hope at least her a couple you know, something clicked or maybe it you know, like it really created Oh, now I got it now or
1:10:27
you know what? I think tonight was your Martin Luther lecture. You nailed it on the door. And you have established the truth and thank you very much. It was wonderful. Thank you.
1:10:41
Appreciate that.
Bill Clearfield 1:10:45
You want to you want to elaborate on that one, John.
1:10:49
And he’s putting it together. I’ve been watching Dr. Joseph for a while and darned if he really didn’t honestly, link some very important things. And if you’re watching the television or the news or sports broadcasts, you understand how important what he’s you know, we’re saying people dying by the 1000s from NGO problems. With that about and then it was in the news yesterday when a football player went down and the truth is creeping through. And what Dr. Joseph is doing is telling the truth, just appreciate it. And important.
Bill Clearfield 1:11:28
All right. You know what you say?
1:11:32
Yeah, and then, you know, I was gonna, I was gonna say, you know, the vitamin D lecture they do talk about its effects on the cardiovascular system. And, and its anti inflammatory effects, which may have a protective effect on you know, some of the sudden issues that are happening, I don’t have I’d have to look at it a little bit more. closely, but there may be a protection aspect involved, but again, the vitamin D levels have to be optimal. Not you know, and if we don’t know, I was gonna say that John Schwarz he did his lecture. On the, on the on the supplements, and, you know, he’s, you know, he’s a sales guy that understands, you know, a level of, of the products. I’ve dug in deep into the products, looked at the data studies. It makes sense to me, because part of our issue is not absorbing vitamin D, and not getting enough sun. But what are you going to do? I mean, it’s freezing up here in Chicago, run around naked and in the middle of the winter. And so, carotenoids vitamin A. They do make sense. There’s some gene regulation mitochondria upregulation. Activating of certain genes that are favourable. I like to go in and take a second look at these and just kind of like that, like the angiotensin or the renin angiotensin system. Get it a little bit more precise, but the the message is still the same. Vitamin D is a big player in because it does all the opposite of what COVID is doing. But it’s the absorption is is the main issue. So carotenoids, vitamin A, cod liver oil all make sense. In that respect right now I’m just doing the cod liver oil and doing injections but I, I did do the supplements. And that’s something that’s measurable. You can actually measure that and I wonder too, and there may be a connection because the current noids they build up in the skin and there was literature that skin health improves. Well, as we age, our skin thins and produces less photosynthesis of vitamin d3. Okay, so there may be a connection there. And I say that because everything I do any supplement I take, I want it to be extremely relevant. I don’t want to just you have to take this take that but you know, we we’ve got to be different. We have the opportunity to be different to know exactly what we’re doing and why we’re doing it. And as Dr. Colossus says, not shooting in the dark, I think gives us a an incredible advantage. But even with the supplements I think it’s a good idea to really have that realization like okay, that’s why I’m taking the crowd noise so guy now I get it’s because the skin and I need more absorption of the sun and photosynthesis because vitamin D is doing all of these things. In fact, it’s even modulating or creating homeostasis in our skeletal system which is really what they what they call us steel immunity. Because if your skeletal system if your bones are getting weak, you can imagine like the Tribeca lay on the inside are becoming hollow. Well, what do you think is going to happen to your bone marrow, the originator of your immune system? Well, it’s going to stop replicating to a certain degree. And so then you have immunosuppression on top and that’s exactly what if there was a motive behind you know, polarizing of the th 17 moving everything away from T cell immunity. Well, if you if you throw on top of that immunosuppression at the same time, well, you’re just you’re just the, you know, on your way to bad things. So if we think sort of bigger with and using the modalities that affect, you know, we can’t take 1000 things so if we take you know, a handful of things that are all relevant, they’re all handling all the different pathways and everything that’s most relevant or it upregulate something that has an effect on all the other systems. That’s, that’s the place where I’m at now. And that’s the place where I like to be confident when for anything I do. I don’t want to take something just to take it you know, Oh, it sounds good. I want it to be I want to fit the piece you know put the pieces together have a grand picture and and then you know, get that gives us the advantage. So we can think clearly and that go down there if we go down the bad road, because what I see, you know, talking to most people that are oblivious to any of this stuff is they’re just leaving everything to chance, essentially. And every time I turn around, somebody’s got cancer somebody’s I mean, it’s I mean, it’s my mother up in Michigan. I mean they have tons of cancer, like every time they turn around somebody else’s cancer and you’re white, why leave things to chance? So that’s, that’s the purpose. That’s, that’s where I’m coming from. And the other comments
1:17:57
I have a comment. Sure. Hi. Hi. So I was thinking that perhaps taking inositol 500 milligram capsules would help to upregulate the photo enhances the phospho inositol kinase that work in the cell wall and it will help to build the the nitric oxide since that since the days and it will hear it the NF k bit.
1:18:42
Exactly so So is there a letter is Is this just calm is this sort of
1:18:50
that this I mean site
1:18:53
Yeah, well, I’ve never known what enough to tall really did but I wonder if it has something to do with helping to upregulate the the mass pathway and you know, because of the pi k and enzyme kinase upregulate that leading to more and I think that again, I think that’s the those are the things I like to look at because every time I turn around, then it brings up questions like this, and then I go on PubMed, I look up a nice atoll and sure enough, I wouldn’t be surprised if something shows up there. Now, I personally I try not to get caught up in one chemically one molecule you know, because there’s probably multiple molecules of supplements, I guess, you know, so always then if I’m taking a supplement that has, you know, multi things in it, then I’m looking to see if it has inositol and if I see it then it’s like okay, well now we’re we’re we’re even adding more good things, you know, for all the right reasons, and it will give me at least a logic behind, you know, reinforce why I’m using a supplement. You know, if I can find multiple reasons that, you know, other than just a bunch of stuff in it, and I don’t really know what, you know, I just, I don’t know for sure what it’s doing. Yeah, so I’d be Yeah, I’d like to look into that. Thank you. Yeah. And then yesterday, you had mentioned the vitamin K Right, correct. Yeah, no, I that was great, because we talked about that afterwards. And I didn’t, I just wasn’t aware. But yeah, I mean, the fact that it reduces calcifications like literally you know, we were talking about it in the context of, you know, what if, what if he had too much vitamin D? You know, could it cause contribute to calcification sets? It’s involved with calcium homeostasis. But, yeah, I mean, the fact that the say if he had fibrocystic disease with breast disease, with with calcifications and and Vitamin K, a good supplement bicep can literally almost like bind to that calcium or bring it out. I don’t know exactly how it does it. That’s that’s a big deal. Yes, so So yeah, so that’s another one for myself. Just have to go look. Gotta look it up and and read it because I’d much rather you know, it’s a pain sometimes I like doing it. It’s just the language sometimes. It can get in get twisted up in in some of the literature, but I always find that if I just stick with it, I can come out the other end with with a nice clear understanding. And, you know, I tried to break things down to basics and tie it and see the commonalities because I think there’s there’s a basic method to all this at the same time. It’s just that the language gets confusing. But But that’s, that’s how I go about these things. I go through an article and then I find out oh, gosh, I really don’t know this, or maybe they’re talking about something that’s a component and then I’ve got to go look it up. But in the end, in the end, I’m telling you, it’s a clarity, actually, you know, it’s things become more clear. And then I don’t feel like I’m pretending to to know things and again, you know, if I had to think about how was the pre COVID I probably did more pretending I mean, I had intuition and, and I knew what I was doing, but I couldn’t I couldn’t give you any deeper precision. And I’m convinced now that that’s what we’re supposed to do. You know, we’re supposed to, we’re, well, we’re not going to do it. Who else is and I think this is the way doctors have used to always be, you know, but I think I think the system has caused us to become, you know, especially that the newer physicians, you know, they’re they’re becoming protocol, jockeys, and they’re not. They can’t question the protocols because they don’t have enough time to really dig into the literature and draw their own conclusions.
1:24:06
Yeah, I remember many years ago, or not so many years ago, I was in practice. And I was the director and the founder of the women’s wellness Institute, in Bethesda, Maryland. And I will see many patients and I also have become a naturopathic doctor because I was trying like you to understand the basis of how people get sick, and how to get rid of whatever it is they have, through nutrients and through vitamins and through natural interventions. And I was an OB GYN, so many patients came to me who were seeing other doctors and including patients with cancer who were survivors. And some of them were taking inositol. And I was always wondering, why is this patient taking inositol and, and another doctor had to prescribe it for cancer but also inositol causes the need nitric oxide to go up so it’s beneficial
1:25:29
interesting.
1:25:31
It a other other patients came with with the taking the vitamin D, but but also taking the the K grouping and they say the K I’m supposed to take it alone, not with the other vitamins because it works better when when it’s taken by itself. So I sort of acquired experience that that this this patients share what other doctors said, but also I have been trying to figure out on my own. And during the past years, I never had a group to ask to ask questions to write. I was doing it on my own. And right now with this group, it is possible to find like minded physicians and just come to a consensus of why do we do what we do.
1:26:35
So the pieces of the puzzle are coming in faster. You know, if you don’t have you have some of the pieces and then me or somebody else throws some more pieces, and they start they started clicking together 100% And the other reason why we have to be more precise is you know these patients now at least the ones that I attract then they have multiple things going on, you know, you know, imagine there’s some some mold toxicity there. There may be a secondary chronic viral infection. There’s COVID and then there’s, there’s influenza, PCT is exactly and so when you have multiple things going on, then you have to have this to me you have to have these things mastered. Because, you know then then it’s then you’re thinking in terms of wall, well this is causing that but this is causing that you know and how is it overall affecting things because you know, certain things will polarize the immune system in one direction or polarize it in another direction. So, so far, you know, for now, the lymphocyte map has been big, I mean, it shows exactly where your immune system is polarized. And then and then of course, besides treating the underlying condition you know, because people and this is where I think where the peptides have their place because you know if the body is overwhelmed, or there’s too much chronic disease to the point where providing it with all of the nutrients, appropriate nutrients that it needs. Still does not allow it to reach homeostasis, then we can directly push some of the buttons with with peptides and and you know we can use thymus and alpha diamond sunbae the Ara to 90 and other modulators to upregulate a part of the immune system that that is downregulated and create immune balance that way which will ultimately reduce inflammation which will break the cycle or reduce th 17 polarization which can become amplified. You know it can it can turn into a wildfire and not only produce more autoimmune disease, but that’s that’s really according to one of the articles I presented and I may have to present it again is really the true reason for cancer along with you know the the genetic component predisposition but it’s that amplification of of that interleukin six really is called the interleukin six amplification. And that that basically what you’re having is a double stimulation of map or the mutagen or the MA PK pathways and NF kappa B pathways. And, and that what starts to happen is is if there’s any dysfunction within those pathways, there’s going to be disruption of there’s going to be a change in cellular division. And that’s going to lead to cancer or you could say the adaptations of the cells to to a hostile environment, if you think about it that way. But you know, to me it makes more sense because now it’s going to survive better with less oxygen, more oxidative stress. And you know, and you know, and I do think that there’s probably it seems like an intelligent process. So it’s not you know, I don’t see very many accidents in the body anymore. So, knowing that that’s, that’s where things go, well then we need to have a map so you can see where you stand and that and that again, you know, it goes to the are we going to just leave everything to chance or are we going to know where we stand for ourselves and for our patients so that we can address the issues. Again, having a clear understanding of where did this functions are and why we’re doing what we’re doing ultimately, in like a doctor of philosophy says that. There’s really three main things at the end of the day we’re trying to, we’re trying to do we’re trying to buffer the redox that’s on the chemical level. We’re trying to create immune balance, because if we don’t again, if it’s th 17 polarized, it’s going towards cancer. And we’re trying to optimize mitochondrial function. And either one of those will affect if you’re if you optimize mitochondrial function, you decrease oxidative stress. If you improve immune function, you’re going to optimize the mitochondria as you have less inflammation, less oxidative stress. So that’s another sort of lens I kind of look through when I’m treating somebody you know, usually it’s going to be one or two things to start. It’s like well, if anything, I know exactly what I’m treating, and am I addressing those three things at the same time? Because that’s sort of like the three overseers of of all these, that’s the biggest picture. You know, if we have those imbalance, we’re healthy. I mean, nothing’s going to happen. The way I understand it
1:32:57
any other any other questions?
Bill Clearfield 1:33:00
Couple of questions in the chat. Could Allah scarin tekturna work similarly to ARB. I rent an inhibitor
1:33:14
Yeah, I don’t know. What trying to look for it here. Oh, you’re talking about the the repurposing are tell telmisartan
1:33:42
Oh, well.
Bill Clearfield 1:33:43
No, this is this one up here. Oh, sorry. Nick Turner. Ellis Karen.
1:33:50
Okay. Yeah, so I don’t know and I in fact, I really have never, it looks familiar. I’ve seen that somewhere. I think that’s one of those ones to look up and find out.
Bill Clearfield 1:34:03
Okay, so Steve Hartman has here some articles on talent telmisartan for cardiac protection, that’s what these are here.
1:34:15
Also fat mobilization helps them lose fat.
1:34:19
Okay. See, oh, the the which one the Alice? skerin telmisartan. Oh, okay. And that’s causing weight loss just simply because of the reduction in inflammation and oxidative stress or maybe it’s the the effects
1:34:35
on actually be a decent treatment for non alcoholic fatty liver disease that helps mobilize visceral fat. But besides that, I started using it on all my guys on gear. My theory is that these guys who are on gear and training hard, they’re growing muscle, but they’re also growing heart muscle, and we want to prevent that and telmisartan specifically seems to prevent this cardiac remodeling.
1:35:04
So using it in high performance athletes, is that yes. Okay. Yeah, I mean, and I wonder if it has to do with the, again the adiponectin that, you know, maybe you know, an ideal I should have, I didn’t think to look into it, but I still get fuzzy with adiponectin exactly, but it was linked to you know, at least in the slideshow. Linked to better glucose metabolism, insulin sensitivity, I believe. Not sure. But, you know, I’m sure that that might be the the reason for the connected to the weight loss because otherwise I don’t really see exactly why. I mean, besides reduction in inflammation and oxidative stress in general. But again, one of those things that take a second look at and look up and get a get a clearer understanding. Yeah, that’s a good one. Yeah. You have an interesting population. Weren’t you doing other a lot of funky like, detoxing, like different modalities as far as I see, or?
1:36:30
Yeah, no, I see them all. There’s nothing I don’t do. But I do see a decent amount of are they occasionally like crazy body builder on a bunch of gear and my job is to make sure they don’t kill themselves. You know, they’re not gonna stop what they’re doing. But I have to check to make sure they do it safely.
1:36:49
And you’re in Florida like what part like Melbourne? Melbourne. Okay. You’re right you’re right up there with with Dr. beamer then close by. Oh, yeah. Okay.
1:37:02
Yeah.
1:37:06
Are you still seeing you had a patient before that had more like Lyme like the sound like they were more like somebody with like heavy metal toxicity and Lyme and mold? Or you? Was that just you just happen to get one of those patients or do you see patients as well?
1:37:26
No, not so much like I see the vaccine injured and the lung colors.
1:37:33
Okay, so some of the modalities you have you have like, I’m sorry, do you have hyperbaric?
1:37:38
I’m looking at buying that I’m gonna install some cool stuff this year in my office.
1:37:44
Yeah, I mean, now I had a colleague when I went to the a forum conference a few weeks ago, there was a natural path out of Washington State, who very passionate and knowledgeable who said he was having success with combining hyperbaric ozone, you know, repeated therapies, in getting rid of chronic fatigue, and that it really doesn’t make sense. I did the hyperbaric training. It’s like an extra day before the conference a full day of trading on hyperbaric and I see hyperbaric is very, very relevant. And the reason is, is it can reverse immunosuppression bone marrow suppression. And, and it seems like the lymphopenia that people are getting, maybe the result of bone marrow suppression are partly a result of bone marrow suppression. And the logic is that there’s an article that COVID and chemotherapy have very similar properties. And anybody while chemotherapy is well known to cause immunosuppression, the problem is when you have immunosuppression, it stays, okay and that that was the basis of another lecture. I did. And we’re not talking about progenitor cells, which is distinct of the family of immune cells and red cells and T cells and B cells and all those precursor cells. We’re talking about the he met and Humana poetic stem cell the one that’s in the most quiescent state that needs to keep reproducing, producing a daughter cell and and a progenitor cell and the daughter cell and the progenitor cell, because that’s how we just continue to live. If that’s not replicating your, your, you’re running on borrowed time. And so, and you may not know that you’re immunosuppressed okay. And I can say this because when I when I had a lymphocyte map done after about four months after having the first Omicron don’t quote me on that because it may have been after the second on the prime I think it was after the the first Omicron which was not a big deal. I mean, omicron wasn’t that sick but my my lymphocyte map, I mean, I had severe lymphopenia My CD four count was extremely low. I mean, it looked like somebody with AIDS, and I’ve got no problem saying it because it is what it is. But that’s scary. My my limp. Lymphocytes were like 1000 Something I was at the level where you know if you know if I needed surgery, they probably wouldn’t have done surgery. It doesn’t make sense I’m you know, I consider myself to be a healthy person, but I did have severe post COVID fatigue. I mean, I didn’t have the first COVID But it obviously got into my system. And later I found out I’m genetically prone to have the the fatigue because of my genetic susceptibility to inflammation and difficulty and detoxifying which means that I need to address those issues. Okay. Again, knowing what I’m doing, and not just guessing but if, if my lymphopenia was coming from immunosuppression, bone marrow suppression, then there’s only a few things that are going to reboot that peptides are going to do it and fasting for 48 hours. That’s, that’s one that I found in the literature 48 hours or longer. And it has to do with you’re really flipping those the switch from a NPK or, you know, mTOR and a NPK. Those sorts of Yang’s you have to go into a NPK and shut off insulin like growth factor, which is really what’s taking it into the activating mTOR. You got to go into healing and regeneration versus growth and proliferation. For a long enough time to produce enough stress to be able to reach the hematopoietic stem cells because they’re in such a quiescent state. They’re hard to reach. It’s hard to promote enough stress to activate them and and by fasting long enough, it will be starved of insulin like growth factor long enough that that it will it will flip it will switch. It will go into healing and regeneration. And then when you finally eat, it will turn on into growth and proliferation. Hyperbaric does the same thing. And is because it’s creating enough stress enough of an oxidative burst by sort of pushing the oxygen into the mitochondria is it’s kind of like pushing turbo boost. On a sports car and by boosting the mitochondria, you’re able to well, you’re actually producing oxidative stress. I mean that thing but you’re producing a burst of oxidative stress because I mean mitochondria even though you’re optimizing it in your you know think about the car you know when you often slam the the gas down and open up the air valve, you’re going to have a lot more. You’re going to have a burst and and it’s that burst at that’s able to again stimulate the hematopoietic stem cell activated because it needs a nice enough stress to flip a flip a switch and turn it back on. And then you can combine fasting with with hyperbaric and then according to, you know, this professional in Washington state he is having results by adding the ozone to it. And and I I believe that that’s also adding an oxidative burst. In fact, even getting out of the hyperbaric chamber is another oxidative burst. And so it’s really all about the burst. And it’s really all about flipping switches. And at the basic level, it’s all about flipping switches between a NPK and mTOR. Because on a basic biological level, we’re either in growth and proliferation or we’re in healing and regeneration. The problem is we’re in growth and proliferation too much because we’re unhealthy Americans, unless we do restricted eating, only eat eight hours a day and fast for 16 hours, which is what I do now. Or like the athletes, those high performance athletes we talked about. They are exercising so much and so intensely, that they’re essentially doing the same thing. But everything is about flipping those switches and everything in those switches require a burst. And so that’s another sort of rule of thumb. I’ve started to realize and so even if we’re bringing in all the right nutrients, and we’re taking the appropriate peptides because we know the pathway there there still needs to be some sort of activation mechanism, you know, a spark of some sort. And so that’s where these modalities are, I’m sure even cryo cryotherapy that’s that’s sort of a burst. You know, ozone gives you that first because it’s got that extra free radical hyperbaric because you’re going into turbo boost. Fasting, exercising is a burst and so that’s that’s the lens I look through. When I think of okay, how am I going to get from here to there and I’ve got the pathways covered now I’ve got to have it I got to turn the ignition
1:46:54
- So I hope that I mean, that’s that’s what I’ve concluded so far, you know, tying in all of the other, you know, why this or why, and that just thinking of just one thing, you know, it’s not like everything’s all about ozone, or it’s all about No, I mean, these things all have their place and ozone has its place because it you know, it’s probably it’s anti infectivity, you know, that free radical that, you know, has a direct effect on maybe some of the chronic pathogens that are, you know, that are part of the problem as well. And so that’s, that’s the thinking process. Yeah, and then Dr. Dan, you had said, Oh, gear you had asked, by the way, thanks. said something about gear or what was your main?
1:47:55
Yeah, that was my comment. Yes. So as running home and oh, say just the basics right. So you got your 500 a test you got your DECA you got your HGH maybe you some echo boys, you know, maybe master own you guys are throwing the kitchen sink at their bodies.
1:48:14
But but but your gear literally stands for
1:48:19
that that’s just what the body builders call it.
1:48:22
Oh, they Okay, okay, okay. Oh, yeah, I got my gear. All right. You gotta buy goods.
1:48:27
Or like, you see a guy Jim is like, Oh, he’s on gear.
1:48:31
Okay. Because he looks like Arnold Schwarzenegger or something.
1:48:34
They don’t even look like that anymore. There’s they’re bigger than that.
1:48:38
Oh by Arnold’s nothing that That’s old school. It’s not good. No, make sense. Well, I feel pretty good about tonight. Any other questions?
1:48:54
Yeah, I’m ready to go.
1:48:57
All right. Well, thanks, guys.
Bill Clearfield 1:48:58
Thank you for having
1:48:59
- And yeah, happy to I’m happy to do more of these, you know if they create some aha. So
Bill Clearfield 1:49:07
okay, we’ll have you back. The vitamin D is
1:49:10
falling. Okay. All right. Sounds great.
Bill Clearfield 1:49:13
Next week, we have Nima. What’s her last name? She’s from all your rich. You Are you a Gu Rex, they do. auto immune testing. So she’s going to show us some water. I mean, we had it. We had a gal from another outfit a couple of months ago. So what’s going on here? Can we close that? out somehow? So
1:49:46
what? Okay,
Bill Clearfield 1:49:50
stop that. There. Yeah. Okay. All right. So a gal named New York. That’s her name. And she’ll be talking about some auto immune testing.
1:50:05
Next week, okay. Okay. That was great.
Bill Clearfield 1:50:09
That’s next week and in two weeks. Just to give you a little heads up, we have we have Felice Gersh again, you know, everybody knows her. She’s our own gal and you know with Dr. Pam Smith is coming up. And Dr. Andrew Campbell is coming back also the next few weeks and so, so we have a pretty good lineup. Pass it on to your crew there Dr. Joseph and great as always, thank you anything, anything bad in
1:50:42
all is wonderful and good.
Bill Clearfield 1:50:44
Okay, again, everybody. Thank you. I hope you all had a good holiday season and anybody else has anything they ever want to present. Ron if you’d like to present something again, let me know. Dr. Dayton, Dr. Cruz like scenario and maybe Dr. woking since she teaches at the medical school physical diagnosis we go back to to that since most i don’t know i forgot most of it. I’m pretty sure So. So. Okay, any questions? Anybody? Everything will be up on our website as usual. Aos er d.org/webinars. Awesome. Slash webinars. And thank you so much, and we’ll be in touch. See you. Next week. Same time, same station.
1:51:40
Awesome. Awesome. Good night.
1:51:41
Thank you.