Peptides & Optimum Health Webinar

Welcome everybody, and I really like those people who are always on time. And thanks Sanjay, thanks Dr. Alok, thanks Dr. Visalam, Sushma, uh, and everybody who has joined us on time to talk about this interesting and very, very innovative topic. As Dr. Thomas was sharing with me, you know, just before we started, that— okay, Rohit, please mute yourself. Perfect. That peptides is one area which is growing at a phenomenal rate, and I really like the title which Dr. Thomas has put here: Working with Nature, Not Trying to Outsmart It or Fight It. Dr. Thomas comes from a very, very rich background. Actually, when I was introduced to him— and thanks, Dr. Visalam, for introducing him and, you know, helping us learn from him— he comes from a psychology background, so he understands human beings and human potential to the core. He is a medical doctor. He is certified in anything and everything which we do in functional medicine. And has huge success rate in working with cancer patients in addition to the other patients he deals with. And when I was speaking to Dr. Thomas, he shared that, you know, peptides are his area which he's very passionate about teaching because he feels, and he has seen that, that it's a very, very safe therapy to do and it can benefit lots of people from doing anti-aging to, you know, better sexual life, to looking young, and also helping people reverse or manage cancer better. So, Dr. Thomas, without wasting any more time, I am going to hand it over to you. We are very, very excited to learn from you on peptides and implement in our practice. Over to you, Dr. Thomas.

Very nice, thank you. Thank you very much. Um, I'm about, about 4 or 5 days ago I got really sick, and I haven't been sick. And last time I was sick was about 30 years ago with, uh, well, I got the flu. Nowadays I think they call it other things. I think they, they, they think it's this visitor from the planet Omicron. And then they also think it's, uh, it's other things. So anyway, whatever they're calling it nowadays, it's, it's just a fluke. So anyway, and but according to the statistics, I should be dead since I'm 70. Shouldn't I be dead? Well, this is day 4 and I'm here, more energy than ever. So wow. Anyway, so here I am. And so what I tried to do just today, because— and then my computer didn't work. I mean, the Internet went down, so I had a big problem here getting, getting this done, so this might be a little scrambled, please forgive me, and I certainly can't cover everything because there is, the field of peptides is exploding, it's exploding in every area, whatever your area is, you're going to see that, I'm just going to, I'm going to give you little bits of it, so, and I'm not going to, try not to go into things too deeply. So let me just— okay, now remember, this, this is for just non-physicians as well as physicians. Anyway, you all know amino acids, and you all know that there are 20 amino acids, right? You know that, and you know that there are essential amino acids that we must get in our diet. Um, and then you, uh, are probably told by, um most of the people that, um, you have to eat dead animals if you want to get all your protein. You know, that's what they would tell me in Texas if I was in Texas. Um, it turns out that even mushrooms give me all the essential amino acids. Fruits, vegetables, nuts, grains, legumes give me all the essential and non-essential. Sorry, but every time I talk to people, I have to throw in the fact that just because I want to eat, it doesn't have to mean that someone must die. So here's some more complete proteins. Wow. More. Wow. Wow. Okay, now peptide bond is really— it's a dehydration bond, okay? Two amino acids, water is removed, and you've got a peptide bond, okay? Peptides and proteins. I mean, this is the definition. With these is extremely arbitrary. In fact, no man's land is between 50 and 100. So anything under 50 is definitely a peptide, and anything over 100 is definitely a protein. So they never clarify anywhere what is— what 50 to 100 is, right? But most of the peptides that are found in the human body are around 20. Okay, the names of peptides, and you all know this, um, it's just basic, uh, Greek— no, Latin— hexa, hexa, hepta, octa. Now, um, the types and actions of peptides. So just to give you an idea of the variety, you have antibiotic peptides and others. Our body produces these peptides as, um, to interfere with bacteria and, um, and funguses and other microorganisms from colonizing a particular area. Okay, so we've got that within us. We have bacterial peptides, brain peptides, cancer, anti-cancer, cardiovascular, endocrine, fungal, venom, vaccine, respiratory, As you can see, it's an extremely broad field, but just to have an understanding of the basic function of peptides is that peptides are basically ways in which the body communicates. You know, you figure we have anywhere from 60 to 100 trillion cells in our body, and they're all working as one unit. Now you have one, and in the end, all these right? You have all looked into the biochemistry, right? The biochemistry that occurs in one organelle in one cell is mind-blowing. Okay, so to imagine this whole thing working together and coming out with me, with you, right? Okay, so who's running the show? Well, we all know who's running the show. That's of course, um, divinity. We are divine beings. But, uh, the way in which these cells communicate with each other so that they can function like that is also divine. And we have what are called hormones. As you know, we have a central nervous system, peripheral nervous system, and these are pretty much the main ways in which the body communicates with itself. And, um, so, and as you know, hormones— there's steroid hormones and there's peptide hormones. So basically, the whole— these peptides are signaling molecules. They, they land on a cell and they signal. So just to show you some of the, the peptide hormones— I mean, the peptide hormones that we're already aware of are these, and we're all familiar with these: insulin, leptin, oxytocin. I will make these slides available, so if you all want them, so you don't have to take notes or anything, you can just enjoy the show. Um, but anyway, as you can see Yeah, these are peptides. Now, you know, the human body produces about 30,000 proteins and about 293,000 peptides. It's interesting, the human genome contains 20,000 genes, about 1.2% of the total genome. That means the other 98.8% is what we used to call junk DNA. There's the arrogance, the audacity of the human to think that God would make anything junk. God doesn't make junk and he doesn't make whipped cream. He only makes things— or he, she, it— it only produces things that are necessary. The law of the universe, as we know, is not a moral universe. It's a necessary unit. Everything that happens happens out of necessity. So, you know, you can stop asking the question why. Well, why did this happen? It's— I don't understand it, but it's this. So anyway, how peptides work, okay? They land on the receptor of a cell, and some go— some go right in and have their action directly in the nucleus. Others land on it and stimulate a process with what— which just should be well known to you— is the G-protein coupled receptors. There are over 1,000 different types of these receptors, and this was the Nobel— 2012 Nobel Prize in Chemistry. But anyway, so when a peptide hormone binds to the receptor, it activates the G protein, right, and then which triggers a cellular response. So basically, just to remind us that these pro— and the beauty of using peptides is that you're using substances that occur naturally in the body so that the cells— our cells are going to recognize them and we're going to have receptors for them. So it's kind of like— now, can you do too much? Yeah, you can definitely overdose on insulin. We know that. We know that. So you could do too much, right? So, but, but basically what we want to keep in mind is that, um, uh, for the most part, like for example, if you had too much insulin, which is a peptide by the way, if you had too much insulin, um, if you could tolerate the effects for a while, if you— if someone could keep your blood sugar up for a while, you would be fine. The extra insulin will be broken down into amino acids. So the, the, the, uh, and all of these peptor— peptide medicines that we're going to talk about, uh, um, really have no serious adverse effects. None of them. And you'll see that when we look at side effect profiles. So the history of it, uh, this is interesting. It must be interesting to you guys. In 326, uh, Indian soldiers used arrows dipped in Russell's viper against Alexander the Great. They didn't like that at all. This was the first medical use of a venom being used in 37 BC when Mithridates was bleeding to death and his neighborhood battlefield physician was there. And of course, if he didn't save his life, he'd be dead. So he had to make sure he did. So he was an out-of-the-box thinker. He said, well, let me get some venom of this venom because what does this venom do? It causes the whole body to coagulate. So let me just put that right in his leg. And of course it was healed, it stopped bleeding. So anyway, the venoms from snakes, toads, scorpions, spiders have been used for millennia. Okay, um, here in 1970, angiotensin inhibitor of captopril was developed based on bradykinin potentiating peptides, etc. Okay, now insulin was the first peptide hormone discovered in 1921. And as you know that— I'm not sure if you know, there was some controversy about the Nobel Prize. Uh, it was supposed to go to two people, it only went to one, uh, which was really sad. It's really sad because, uh Shouldn't happen. So anyway, it's considered a peptide with 51 amino acids. It's got an alpha chain and a beta chain. Okay, yeah, they ignored BEST. Hey, I'm not sure what the stuff— what the politics was behind that. Sorry about this noise, I apologize. Um, so now peptides are one of the newest big things in medical research. I was talking about that before in therapeutic. Uh, they're natural, they're, they're usually very specific because they have a, they have a receptor, so they have, they have a specific response. It's not like, uh, these new targeting, um, uh, monoclonal antibodies that are used in what they're calling oncoimmunology. Um, it's not immunology at all. It's, it's a, it's a fancy word for chemotherapy. It's a fancy word for poisoning people. Um, because it's not something that occurs naturally, therefore it— is it going to have side effects? Those are not side effects, those are effects. So those are the effects. Um, but anyway, with this, you know, you know what you're going to get. You got to— like, you give insulin, you know what's going to happen. So anyway, these are more— they're more potent, they're safe for the most part. You know, insulin overdosing is not safe. Whoops. Um, and when it breaks down, as I said, you just add to your amino acid pool. Okay, um, now these, these peptides that we— that are produced, uh, and you'll see how they're produced, um, mimic the behavior of the natural ligand. The natural signal. It interacts with the receptor on an enzyme or a cell to produce a biological effect. Therefore, it's precise. It doesn't have side effects. There's no unexpected effect. The only effects that we ever see from peptides are maybe, um, flushing or warm, warm, or Maybe some of them are painful when they get injected, and I avoid those. Anyway, the early peptides in the early part of the century— oxytocin, 9 amino acids, vasopressin, 9 amino acids. Amazing. Imagine, it's just 9 amino acids. We're talking about very small. Um, now science finally approved After 1,000 years, the FDA approved the use of leeches in 2004. And so leeches help heal wounds and restore circulation in blocked veins. Um, that's amazing that we have to have the FDA approve such a thing. You know, I deal with cancer all the time, and I've had women, uh, who have come in with breast tumors that were so large and necrotic. I mean, they kind of look like cauliflower. I'm not sure if you've ever seen that, but it's— it had that kind of, you know. And this is, uh, usually, uh, it's, it's, it's an inflammatory breast cancer, but it can even be just another non-inflammatory that breaks through the skin and just grows. Anyway, all the outside becomes necrotic, and the, the, the, the smell is— you can't tolerate it. You know, and you wonder how— when I meet these people and they come in for the first time, you wonder how could they have lived with it for and let it get that far. But they do. People are afraid and they live with it. So, uh, what did we use? How can you get rid of necrotic tissue and not damage healthy tissue? Again, call on God. God gave us these beautiful little creatures called maggots. So it's called medical maggot therapy. You put the maggots on, you cover them with cellophane, and you wait about 2 or 3 days, and then you let the flies fly. And when the flies go, you've got nothing left but, um, beautiful pink skin, um, dirt, you know, underlying tissue. And by the way, I don't think, I don't think the FDA has approved maggots yet, so be careful. Science is always harnessing nature. So here you've got 8 drugs, FDA-approved drugs, from the Gila monster— peptide hormones. Okay, now this one here I like a lot. Um, this is from the deathstalker scorpion. It's 36 amino acids. It specifically binds to glioma cells, glioma cells. So what's really, um, important is in surgery, if you're trying to identify which cells are, are, are malignant and which are not, and you're a neurosurgeon and you've already got your specs on and you're looking very, very tightly, you— have you had— if you have used this, this chlorotoxin, what happens is it only binds to the abnormal cells. It's like it paints it. So, but it also— so now the surgeon can easily remove what's what, what it— what he needs, he or she needs to remove. Um, but also when the binding of this substance also prevents its growth. This is old, I can't remember the number now, but as you can see, in 2018 There were 60 peptide drugs approved in the U.S., Europe, and Japan, over 150 in active clinical development, and 260 have been tested in human clinical trials. And here, this is just important to notice, is that if you look across the decades, you'll see that most of the peptides being researched and obviously brought to market are the ones that are under 10 amino acids. So summary: naturally occurring bioregulatory chemicals that control hormone, cell-to-cell communication, cell signaling. Less than 50 amino acids. Natural, bioidentical, or altered, right? They can— they do alter them, um, but it's okay, you're still coming up with, um, amino acid peptides. So almost 300,000 in the body and over 7,000 in clinical use. At this point. So addresses immunity, inflammation, chronic illnesses, sleep, sexuality, reproduction, and aging. And, and, and, and, uh, so anyway, these are not all the peptides that will be discussed. I didn't, I didn't include a couple of these, and I think I include a couple that are, that are not in here. And, and you'll see, it just takes a long time. So, um, just, uh, this is one of my favorite, is, um, is, um, produced by the pineal gland, epithalamus. So, so here it is. It weighs less than 0.2 grams. And, uh, accumulates fluoride, calcium, and phosphorus crystals, right, that accumulate with age and with you— whoops— and with those who use— if you have a government that, uh, puts fluoride in the water, or you have— you're buying fluoridated toothpaste, then you're in trouble. Or if you go to a dentist that uses fluoride, then you're in trouble. But anyway, it's a photosensitive timekeeper for the human body. It produces about 30 micrograms of melatonin a day in sighted people, not in people that are blind. People that are blind have much more melatonin production and much less cancer. Um, anyway, it also, uh, you know, melatonin regulates circadian rhythm, etc. Uh, it also— the pineal gland also produces dimethyltryptamine, which is also known as ayahuasca, uh, and it's produced neocortex and hypothalamus. It is where it has its effect. And we won't go into the DMT, but the other thing is this 4-amino acid peptide called epithalamine, also called epithalin. Okay, the potent biological regulated peptide involved in growth, puberty, fertility, immunity, and aging. It actually oversees the management of the pineal gland. Okay, it, it will increase melatonin production. It is an antioxidant. Okay, it inhibits the formation and growth of cancer, and it elongates telomeres by 33%. I'll show you the study in a minute. Attenuates inflammation, regulates endocrine activity in the body, combats the negative effects of stress, and regulates pineal secretions. Okay. So, and so, so that you can see, if someone, um, wanted to make us vulnerable, uh, other than feeding us fast food and, uh, and lies, uh, they would probably do everything they could to damage our pineal gland. So now, this is also called epithalamine. So epithalamine stimulates telomerase increases telomere length by 33%. Okay, now this is a Russian, uh, Russian researcher who found this out. And by the way, a friend of mine got in touch with him and said, hey, you never mentioned in any of your research, um, how long you can use this for. And he said, well, when I first discovered it and first started working with it back, uh, I think— I don't know, I forget the year, but he said when my, my mother was, um, 60, um, I've been giving it to her twice a year now. Um, she's now in her late 80s and she looks the same as to me as she did when I started working with her. So here's a study with, um, that he did, uh, and they did epithalamin increases lifespan of mice and rats to the equivalent of 100.7 human years without the development of, of cancer. That's a very important point, because usually when the longer you live, the more likelihood you're going to get cancer. Okay, so elderly with heart disease, a 15-year study, 79 participants aged 60 to 69. So the Group 1, standard care with apixaban, um, twice a year for 3 years. Group 2, standard care. Okay, now 10 milligrams IM every 3 days times 5 days. Right, so that was it. Okay, you do this every 6 months. You don't need to do it more than that. What they found was that the epithalamus group, cardiovascular deaths 46.2% as opposed to 83% in the control group. Survival 66.7% compared to 40% in the control group. And you got to understand that these were people that ate pretty bad food, like, like most people do. They probably stayed up late. They probably didn't move around a lot. I mean, so all they did was to give them epithalamin. And by the way, these are very easy to use. You get little vials, you reconstitute it with sterile water, and then you take out the amount you need with an insulin syringe. 31 needle, I mean, uh, and then you just grab a piece of your belly or your thigh and you inject it. Um, now, but several are— there's a few orals that are available, and, um, there's even more nasal, which are nice, the intranasal sprays. And then the rest are the injections, but the injections are no big deal unless it happens to be one that is painful. Okay. So there we go, 10 milligrams and 2 milliliters. I had saline here, but it's not— it's good. What I found is that they say saline or sterile water, but what I have found is a lot of times if I use saline, um, it'll precipitate, we can't use it. So sterile water always prevents that. So optional dosing is— yeah, so there's different ways. You can do it. Uh, if anyone's in— by the way, I, I just want you all to know that, um, um, we're lucky because there's a, there's a company called Tailormade, uh, and I, I'm not the expert on, on, on these at all. Uh, in fact, the guy that is a— that is an expert, um, is somebody I would like to bring on, uh, one time and have him give a lecture. Or not one time, as many times as he'll be willing Uh, I've never met anyone more— know more about peptides than this guy. Anyway, he's the starter. He's one of the founders of— co-founders of, uh, TailorMade. And, uh, anyway, they've— the, the FDA, you know, the federal death authority, well, they have, um, uh, made it, uh, difficult for, for, for peptides to be used in the U.S. Um, even though they have— many of them have FDA approval. And one of the reasons is, is because TA-1, um, thymosin alpha 1, which we'll talk about a little while, uh, has great effect against the, uh, COVID-19. Um, so anyway, so for that reason it's now very hard to get, even though I think it's improved— it's approved in 130 countries. It's FDA approved. It's— it was— it's the brand name was Zydaxin. So anyway, so they're having— so what they do is they ship, like, they can ship to Europe, Europe, they can ship to India, they can ship to Thailand, they can ship. So for my clinic in the US, they have to ship to me and then I ship back to them, to my clinic. So, uh, it's just more hoops. Um, Anyway, so if you're all interested, at all interested, I could work out an arrangement where we could find out, maybe one of you could become, who's interested in doing, taking over the business. But yeah.

Yeah, so Dr. Thomas, we already have question regarding this, where to source it from and is it legal to use in India?

Okay, so epithalin. Epithalin?

Yeah, or maybe peptides.

Well, no, peptides, they're all different. They're, they're, you know, it was in 19— I forget what the year was, 1962 I think was when they, uh, they finally came up with a way to make peptides. You know, they figured out it was a good, a good system for sequencing them and putting them together. 'Cause they have to be produced. They have to be produced from amino acids, but that's all they are. You got— keep in mind that when you're talking about a patented drug, what you've done is you've taken a natural substance and you've added something to it that's not natural, and now you can patent it, okay? You cannot patent peptides because they're just what they are, unless you've modified the peptide from its natural. So the, you'll see, F-O-X-O-4, FOXO4-DRI is modified, so it can be, it could be, um, um, it could be, uh, patented, right? Right. So, uh, so these are what I'm saying is these are an amino acid, isn't— I mean, tryptophan is tryptophan, right?

Uh, we can't patent it, right?

So, so, so there, yeah, this can't be patented. So they're made in a laboratory, uh, because you— I certainly, especially nowadays, don't want to get any excretions or secretions or extractions from any human being. Do you? You want to get it?

Yeah, natural, definitely natural, Dr. Thomas.

Well, then you've got to get, get it extracted from a human being. You want to go and— do you want to do that? How many human beings do you know were smart enough to avoid genetic engineering? Not many.

Not many.

Not many. So what are you gonna— what, there's no more natural in when it comes to glandulars and things like that. And especially to get this one here, you would have to, you would have to extract it from a, from the pineal gland, which I'm sure would not, not possible, not be possible. So in this case, and in many of the cases They've got, well, like for example, think about it, this is only 4 amino acids, so you just have to make 3 peptide bonds.

Right.

So it's really simple. So, and as I said, because they're specific and they have a receptor, they therefore have known consequences, known results. There's no surprises. That's the beauty of it. Yeah. So here's the pineal gland, and, uh, and as you— I'm sure you all know that, being doctors, you all know that. But, you know, here we are early on in life, and as we get older, it— so does it, right? So here I am. So do I need epithalamin? Absolutely. Do I do it twice a year? Yes. So how do you decalcify the pineal gland. Avoid fluoridated water, use fluoride-free toothpaste, eat organic fruits and vegetables, raw chocolate, melatonin, and epithalan, which I think are all stimulate the pineal gland. Eliminate mercury fillings and meditate. All of this has been proven to decalcify the pineal gland. Epithalan actually has a reparative effect on the pineal gland by stimulating its activity and increasing the production of melatonin. Okay, yeah, so here it is. It was 1965. 1965, scientists from China completed the synthesis of insulin, which is the first— the world's first synthetic peptide. Okay, so 1902, we got secretin. 1931, substance P. 1953, oxytocin. Uh, and then here it was at the end of the 1950s that Robert Bruce Merrifield invented solid phase peptide synthesis. Very important because now, now they're able to be produced. And that, since that time, we've seen an explosion in research. Now, cerebral lysin. Now I'm going to talk about neuropeptides first. Cerebral lysin is actually a combination of neurogrowth factors. Which all come together to repair, repair, and to recover nerve cells in the brain and peripheral nervous systems. So they are brain-derived neurotrophic factor, nerve growth factor, and kephalin, orexin, CN, cerebral nerve growth factor, and p21, which you may know is, uh, one of the signaling pathways in our cells. Okay, so that's what Cerebelysin is. It's basically a combination of these peptides. Okay, as I said, neuroprotective and neuroregenerative. It has a low molecular weight, so it can, it can cross the blood-brain barrier and the blood-CSF barrier. Okay, very important. It's a peptidergic drug with neuroprotective, neurorestorative properties. Anyway, they— some of them some of these neuropeptides demonstrate cross-reactivity with antibodies against several trophic factors, such as glial cell line neurotrophic factors, ciliary neurotrophic factor, IGF-1, and IGF-2, suggesting their potential capacity to bind receptors of these factors. And indeed they do. It's just, this was just some, what's the word, indirect evidence. So what it does is cerebrolysin acts as, uh, has pleiotropic positive effects on amyloid beta and tau pathologies, neuroinflammation, neurotrophic factors, oxidative stress, excitotoxicity, neurotransmission, brain metabolism, neuronal apoptosis, degeneration, neuroplasticity, neurogenesis, as well as cognition. Now, and this has been shown in human studies. So what is amazing about this now is that I have— there's a doctor named Pam Smith in the US who pretty much specializes in this, all the neurological peptides, uh, and she's pretty much like a maestro with it. But she, she is— it takes, it takes a good year, but she can really reverse people, uh, many people, not everyone. who have traumatic brain injury, which you know is a serious situation. Okay, so again, in pharma— in pharmacodynamics studies, it's been shown that it reduces brain amyloid beta deposition, tau phosphorylation, and amyloid beta and tau-related neuropathologies. Okay, modulates neuroinflammation, etc. Reducing elevated serum TNF-alpha, TNF receptor. Anyway, I won't go into all of these details. Protects against oxidative and exotoxic damage. One of the most important things about this and the Cmax and the Clank that I want to talk about is that in addition to restoring, repairing, and stimulating— nootropic, stimulating their growth— they also chelate, and they also get rid of— they're also neurological antioxidants. So in even, uh, the person who is aging, and let's say you're 55, you're 60 years old, your memory is not what it was, start on it. Not this one, I would start on the CMAX and the C-Link, which is what I do. By the way, just so you all know, I did, uh, I gave myself 1 milligram of CMAX this morning because when I woke up, this was again day 4 of this horrible flu, and I hadn't been out of bed in 3 days. So I was sitting up here looking at the computer and I was kind of, huh, I gave myself the CMAX. Here I am 8 hours later. So it's amazing. Um, so it protects against oxidative and excitotoxic damage by inhibiting lipid peroxidation and calpain activation, influences synaptic transmission mediated, mediated by GABA-B, adenosine A1, and glutamate receptors, enhances the supply of glucose to the brain and ameliorates the slowing of brain bioelectrical activity, promotes neuroplasticity, and prevents dendritic and synaptic loss. I mean, it's, you know, these things almost sound like someone's making it up. It can't be true, but it's— this is all proven in the literature. Stimulates neurogenesis, probably through AKT activation, improves learning and memory. Okay, therapeutic uses so far: concussions, traumatic brain injury, Alzheimer's, dementia, strokes, Parkinson's, MS, mood disorders. Um, yeah, and I should add in here— I don't know why I didn't— but cognition, memory, um, very, very important. Now we're going to talk about, uh, adrenal cortical ACTH. And other POMC peptides. I'm sure you're familiar with the pro-opiomelanocortin. You may be. It's a, um, it's a very large, I think 267 amino acid protein that's produced in the brain, and then it is cleaved and broken down into smaller ones. I'll show you in a moment. But anyway, ACTH The first evidence that ACTH had an effect on behavior in animals was obtained in the mid-'50s. At that time, David Weed and colleagues studied the influence of ACTH and its fragments on the learning abilities of animals and showed that the removal of the glandular lobe of the pituitary resulted in disturbed formation of conditioned responses that could be restored completely with administration of ACTH. Okay, so here is the, uh, the propiomelanocortin and its derivatives. Okay, and as you can see, the beta-endorphin, gamma-lipotropin, alpha, uh, melanostimulating hormone, which is from the ACTH. So differential cleavage of POMC occur in different tissues where it is expressed, resulting in diverse biological functions. Yeah, so this is an amazing, um, protein here, and pre-proprio melanocortin. In fact, it exists, it's made as a pre, I think, and it has— an enzyme comes in and removes 12 amino acids and turns it into the proprio melanocortin derivative. Now let's talk about C-Max because this is what This is the area. So in the late 1970s, a research team headed by Dr. um, Maya Sadove and Ashmorin, they initiated studies to produce a nootropic peptide preparation based on ACTH, because they had seen that when they took out the pituitary gland of these rats, they were able to restore the function with the ACTH, of the cognitive function. The problem is that the, the effects produce shortness of breath, so they had— they were limited on how— what they could use, right? And it's probably because of the effect on the adrenal glands. Um, anyway, so what they found— and then they finally came down to this fragment here— the ACTH 4 to 10 was as short as— the effect was only 30 to 60 minutes. Okay. And even by increasing the dose, it had yielded no effect. So, the study of the nootropic activity of some analogs with various C-terminal region modifications showed that the analogs carrying a replacement of the 3-terminal amino acids Pro-Gly-Pro— now this is important, because it's found in other peptides, too, where they actually add in this 3 amino acid sequence, and it, it can modify the activity a little bit. Okay, so anyway, this new peptide— oh, sorry about that— this new peptide— where am I? Ah, okay, so this, this new peptide which, um, uh, where they added the ProGlyPro, as you can see at the end there, okay, uh, was, was called CMAX, and it exhibited nootropic effects of its natural product, but its effects lasted for 20 to 24 hours. That's the important part. So it lasted 20 to 24 hours, and it did not cause any other problems associated, because this is a derivative from the, uh, melanocyte stimulating hormone alpha. Because the reason you, you want to avoid the, the— whoops— you want to avoid the side effects from that, or you want to avoid the effects of that, is because, um, you get the corticotropic, um, because you don't get the melanocyte stimulating activities, right? Um, as you'll see, there are, there are, there's another group of peptides from the same parent that make you turn extremely dark. So, um, in fact, one of them, the melanotan-1, can be used with vitiligo. So if you have any people with vitiligo, this will help restore that. So that's a very, uh, nice effect where you wouldn't want to eliminate that effect. You wouldn't want to eliminate that. So, so the CMAX, what does it do? It elevates expression of the brain-derived neurotrophic factor and increases the TRKB, tyrosine kinase beta receptor, activates dopaminergic and serotonergic stem cells. Okay, so in the brain, you're, you're active, you're activating the, the stem cells that produce dopamine and serotonin. Okay. All very, very much important for antidepressants and anxiolytics, attenuates chronic stress. So the biological activity of CMAX, okay, shown to increase brain-derived neurotrophic factor, nerve growth factor, tyrosine kinase B type 2. Um, yeah, anyway, so this is the study. Now, so what they did was they exposed neurons to glutamate, which as you know is toxic to neurons, and they improved that, uh, neuronal survival by an average of 30%. Okay, so as I said, anti-inflammatory, neuroprotective, remyelination, and neurorestoration. It also chelates, um, heavy metals. It also, uh, it also stimulates— where was it? Oh yeah, it also chelates heavy metals, especially copper. Um, and, um, as you know, it's the copper toxicity. Uh, we all know of Wilson syndrome, but you can have copper toxicity. And copper toxicity, if you're having copper toxicity, remember, it will be— it's the same double-edged sword as iron toxicity, right? Because both copper and iron exist as, uh, in a, in a ick valence of 3+ and an us valence of 2+, okay? And being in an ick condition, they're easily reduced and they produce hydrogen peroxide and other reactive oxygen species and can cause severe damage. All right, so it's very important that the CMAX actually does this, um, prevents that from happening. So 15-year experience published in 1997, significantly improved memory and attention in healthy men under extreme conditions of activity, and they were using it as intra— intranasal administration. Now we have, um, when I first started working with peptides a few years ago, we only had injectable, but now many are— we're now getting many that are intranasal. And, uh, so what do we have intranasal now? We have several of them. I'll try to mention them as we go through them, but one is Semax. The other one is C-Lanc. And the, the, the beauty of C-Max and C-Lanc is since they're nootropic, they're going to go right into the nose, right through the cribriform plate, and they have direct administration access to the brain, right? Which is exactly why you don't want, when going to a public place, anyone to stick an unknown substance deep into your nasal cavity with the excuse that they're testing for something. So CMAX for stroke— study of 30 patients with acute ischemic strokes. CMAX improved the recovery of the stroke clinically and by EEG. 12 milligrams for moderate, 18 milligrams, and the course was 5 to 10 days. Pretty amazing. Uh, CMAX clinical effects. Attention and memory. The work of Kaplan et al. using human volunteers showed that intranasal administration significantly increased attention and short-term memory of the subjects during testing. Okay, it had a helpful effect on non-proliferating diabetic neuropathy, stroke, hypoxia, glaucoma, optic neuropathy, analgesic and opioid attenuation, and ADHD. In fact, I have a, I have an 80-year-old male here, um, in Phuket who happens to be a billionaire. I thought billionaires were smart, but anyway, he's been on Ritalin for 30 years. I asked him why. He said, was it they put his son on it when his son was, uh, teenager or something, so whatever that means. Um, anyway, so he's been on it now, the father, and he said, I, I don't want to take this anymore, I don't think it's good for me. I said, good thought, let me get— so I gave him the C-Lanc, the C-Max, and something called Dihexa. And he's using these natural substances and just stopped cold turkey after 30 years of, uh, of Ritalin. And, uh, he's perfect attention, all that sort of thing. He's in, he's in his mid, mid to late 80s. So the method of administration, sub-q or nasal. As you can see, it's low dose, 100 micrograms, 750 micrograms. Timing as needed. Now the suggestion is, um, 3 to 1,000 micrograms sub-q twice a week, and you can alternate with C-Lanc so that you could be doing it 4 times a week. But you can also do it daily, there's no problem. The only concern is tachyphylaxis, that you might— your body might become used to it. And if it does, you stop for a day or two. Okay, so C-Lanc. Heptapeptide, nootropic, anxiolytic, synthetic analog of the human peptide tuftsind. Now, Selenc has exactly the same cognitive, um, benefits as Semax except that it is much more anxiolytic. So therefore, let's say— and these are good for— these are good to use. You keep the little spray bottles near you, you know, you give yourself a squirt when you, you know, if you're working on a project, if you're, uh, or if you know, if you have patients, if you have patients who are actually losing their memory and stuff like that. I actually find that I like— I, I, the effects last longer when I give myself the sub-q of the and up to c-max. Um, but, uh, the, uh, so the c-length would be probably more indicated in the person who had an anxious cognitive decline. For example, somebody, you know, a lot of times you'll see in people with, uh, with Alzheimer's early onset or other kinds of dementias, they know what's happening to them, and it makes them extremely anxious and uncomfortable and all that sort of thing. And just that anxiety now contributes more, so now they can't think, because we know, we know that one of the things that anxiety is, on the release of epinephrine and cortisol kicks our, our consciousness away from our prefrontal cortex into our hindbrain so that we can just be response mechanisms and not think. Because, you know, when you got a guy with a gun coming after you, or a guy with the thing he wants to put in your nose coming after you, you don't have time to think, hmm, should I go this way or that way? You got to just run, right? And so that's why, um, it's the stress response on steroids is what it is. Um, so anyway So if your memory— if you're having trouble with cognition, thinking, decision-making because you're under a lot of stress and you're anxious about it, then the C-Lanc would be good. And you can alternate them, as you say. So it also modulates IL-6 and balances T helper cell cytokines, elevates BDNF in the hippocampus, influences on monoamine neurotransmitter, and diminishes breakdown of enkephalins. So all basically the same. Okay, therapeutic applications: major depressive disorder, generalized anxiety disorder. Non-sedating, non-addictive, and no cognitive impairment. Okay, so if you just wanted to use it rather than an— rather than a benzodiazepine— why do I say that? Because the allostatic— allosteric modifier of the GABA receptor amplifies affinity of the receptor for GABA. Benzodiazepines are allosteric modulators of the Type A GABA receptor, so it increases inhibitory action of GABA, right? That's what this does, and that's what the benzodiazepines— except it's not sedating. It doesn't make you sleepy. I do it, and I'll do it, and I'll I'm— I, I can concentrate for hours. So it's not sedating and not addicting, of course. See, like, immunological effect regulates inflammatory response. Bcl-6 protein serves as an important transcriptional regulator of the immune system. Pivotal role of the Bcl 6 is in regulating B and T cell development, and it also has antiviral activity. So you'll see that if we can use this and a few other peptides, we can really restore and balance the immune system in people with cancer, autoimmune conditions, chronic fatigue, uh, you know, any condition that is debilitating and, and serious. Prevents weight gain. It's an anticoagulant, fibrinolytic, and antiplatelet. And that's due to this, and that's the reason why, um, I mean, it— and it decreases glucose, so it's a hypoglycemic and an anticoagulant. And that is— both CMAX and C-LINK have it, which is due to the pro-gly— uh, proline glycine proline sequence. Sea Lanc and gastric ulcer— it accelerates gastric ulcer healing, improves blood supply and lymphatic circulation to the gastric mucosa. Dosing— as, as I said, you can combine it synergistically with SeaMax. Again, 300 to 1,000 micrograms sub-q once a day, 2 times per week, alternate with SeaMax. And the intranasal is available. However, Yes, you can be doing one or the other every day, and that's important when you got an older person who's, um, starting to lose it. All right, no, nothing part-time is going to work for them. But of course you're going to change their diet, you're going to balance their hormones, you're going to get rid of their toxicities— dental toxicities, medical toxicities. Metal, metal toxicities, etc., etc., etc. Um, there's some great homeopathic— as you— sure, I'm talking to the, to, to the, the right group here— some great homeopathics to get rid of some of the, um, chemical toxins we have from living in the 21st century. Now, the range— the renin-angiotensin system in the brain is believed to be involved in the process beyond mere hydroelectric, electro— electrolytic homeostatic control. It has been implicated in the process of learning and memory and neuronal differentiation and nerve regeneration, okay, as well as the pathophysiology of various diseases. All right, dysregulation in the brains, RAS, has been reported in studies of patients with Alzheimer's, Parkinson's, and X-linked intellectual disability. Okay, so, um, the point I wanted— I don't want to read all of this to you, but the point I wanted to make here was, yeah, so for example, the hexapeptide angiotensin IV and its various analogs have been found to exert antigambosan effects in animal models on epilepsy, protect against cerebral ischemia, improve endothelial function in animal models of atherosclerosis, and enhance long-term potentiation in vitro and in vivo. So one of the ones that— where's the— I don't have the name of it. I wanted to show you the name. Anyway, but it's called Dihexa, and Dihexa is fortunately in an oral form. You can take it, you can take 2 pills in the morning, and you'll be, you'll be clear and focused most of the day. Most of the day. My, um, one of my former nurse who lives here also in Thailand who is part of— is part of— very much responsible for bringing peptides to Thailand, has been using dihexa daily. You know, the only potential problem with it is that it's been shown to increase angiogenesis. So theoretically, if someone has cancer or is at risk for cancer, they should avoid it. Now, that being said, there's no data, and there's been a lot of research with it too. Um, so anyway, uh, learn to avoid this. Further studies of ANG-4 and several ANG-4 analogs have shown these peptides to facilitate long-term potentiation, learning and memory consolidation, increase in cerebral blood flow, and neuroprotection. Okay, so, uh, they were— and the one of the analogs that we're talking about, DiEXA, reverses deficits in dementia models induced by treatment with cholinergic muscarinic receptor scopolamine, um, kainic acid injections into hypothalamus, perforant path cuts, ischemia resulting from transient 4-vessel occlusion. Nice thing to do. But anyway, despite such promising results, various physiochemical properties of these peptides have hindered their development. ANG IV is susceptible— ANG-4 is susceptible to metabolic degradation and too big to cross the blood-brain barrier. Therefore, they came up with this, and it has 10 million times the potency of BDNF. That's a pretty potent brain-derived neurotrophic factor. It mimics HGF, um, hepatocyte growth factor, and activates c-Met, which is a pathway for growth and proliferation. So for these reasons, they're saying, well, thank God, if you have a tumor, it could really stimulate it. It said, but in animal models, DiHEX has been shown effective in reversing or limiting almost every model of cognitive dysfunction. So it's, it's available orally. The transdermal looks like it's going to be actually better, usually 10 milligrams for preventative, 50 to 70 for a neurodegenerative condition. And although it activates the c-Met pathway, there has been no link to cancer at all, and there's been a lot of studies. I can send you some, and you can also just look it up and you'll see that, uh There's been a lot of work in this area. So the combination— this is what I've been doing with this, with this 80-year-old, 80-something-year-old, uh, to get him off 30 years of Ritalin was Selank, C-Max, and, uh, Dihexa. Dihexa orally and the Selank and the C-Max nasally. Okay, switching gears. And there are— listen, there are many, many more. There's a few others that I really wanted to talk about that are very important, but we just don't have time regarding, um, cognitive problems, regarding traumatic brain injury, regarding stroke, cerebral vascular accidents. Okay, so just a quick review of cytokines. Secreted primarily white blood cells, T cells, epithelial cells. Two groups based on, um, the effect they have on lymphocytes: Th1 and Th2. So as we know, um, because we study— this is the stuff we study and we like— the Th1 dominant is, is best when you're— and it's what you have— whoops— when you're younger in life. Where was that? Yeah, uh, promotes cell-mediated immunity. Right? And then the, the Th2 is the humoral immunity, okay? So, and the cell— the cellular immunity is the killer cells, the activated lymphocytes, CD8, natural killer cells, etc., okay? So a failure of the Th1 arm, or in other words, to get the polarizations over to Th2, results in these chronic conditions— AIDS, chronic fatigue, candidiasis, multiple allergies, multiple chemical sensitivities, viral hepatitis, Gulf War syndrome, cancer, etc. So see, Th1 cytokines such as interleukin-2, interleukin-12, gamma interferon, and IgA support mucosal immunity. I, when I'm working with somebody with cancer, I use all— I use some peptides that directly kill the cancer and a few peptides that stimulate the immune system and bring it back to the Th1. Uh, and we can measure that by measuring the interferon gamma. We find interferon gamma actually increased. The other thing we do is we do a blood test called a lymphocyte subset so that we can um, look at the before and after to see what, what changes. I'm sure you're all familiar with that test, but it looks at the different, um, the relative proportions of the lymphocytes that we have, including CD56 natural killer cells. So with that in mind, So since before birth, the thymus gland is instrumental in the production of maturation of T lymphocytes. So that's why it's called T— they're called T cells because, um, they're— they, they all go to, uh, they all go to undergraduate school in the, um, in the bone marrow, and then some get accepted into the University of Thymus. They get to the University of Thymus, and it's kind of like the CIA headquarters. They graduate as, uh, as trained assassins called T cells, but they haven't been given a target yet. So they're what they call— we call naive, and they're naive. So what do they need? Well, they have two friends called dendritic cells and macrophages that are out there looking for targets. As we all know. But anyway, this gland shrinks, right? It becomes surrounded by fat, and the actual parenchyma of the gland shrinks to the point of being largest at puberty, 25 grams at 25, 60, and then you get down to me, just 5 grams. So do I do— do I use TA-1? Absolutely. I love T cells. I love natural killer cells. Thymus— thymic involution. Thymic involution results in Th1 to Th2 shift, which decreases thymosin alpha 1 and thymosin beta 4, which results in increased risk of opportunistic and intracellular infections, autoimmunity, inflammation, and risk of cancer. Also, the decreased telomere length in the, in the immune cells. So if your T cells and your B cells are— have short telomeres, they can't divide anymore. And as you know, if something is encountered that requires a powerful immune response, you've got to have clonal expansion. But if you don't have short telomeres on your B cells, these T cells, natural killer cells, nothing's going to happen. Now, thymosin alpha 1 is the one I was talking about to you before that has such a good effect with, with the COVID-19. It's a 28-amino acid. It enhances T cells, dendritic cells, and antibody responses, modulates cytokines and chemokine production. It enhances natural killer cell system and stimulates the immune response by stimulating stem cells and augmenting the production of new immune cells. So when we were using it with cancer, we were giving it concomitantly with 5-FU, um, or, or after radiotherapy. And we're able to maintain the NK activity of the spleen, which is very important. And what I was also going to say a moment ago— excuse me one second. I'm so sorry, there's an emergency, but some patient's having a problem. Okay, anyway, I hope she's okay.

Hopefully she will be.

Yeah, yeah. Um, um, oh, anyway, what I wanted to say before— let me go back here and, uh, where was it? Where was it? Yeah, here. So what I was going to say is that I, in addition to giving all the peptides that I give, I give interleukin-2. Um, and there's an amazing, uh, article, uh, if you— anybody works with cancer, of the combination of TA-1 and interleukin-2, both low dose. Now IL-2 is used— interleukin-2 is used in high doses with cancer, much like they used to use— you all remember with hepatitis B, they used to use interferon and they gave such high doses that the people said, I'd rather die than take that again, or I'd rather die from—

Sorry, I think Gaurav unmuted by mistake. Extremely sorry about that, Dr. Thomas.

No, no, no problem, no problem. But anyway, so anyway, if anybody ever, ever helped, gave a patient that with hepatitis B, I think way back 30 years ago, right? The patient said, I forget it, I want to die. I don't want to take this medicine again. Well, it's the same kind of thing with the interleukin-2. You know, they give like 90,000 units, 100,000 units, right? We give 3,000. Yeah, well, I'm sorry, they give 90 million, 100 million. We give 3 million. Small dose and only 6 days a week for 4 weeks. But that— what does it do? Interleukin-2 is one of the ways in which the immune system is woken up. So it's part of the febrile response to awaken our, um, to awaken, awaken our, um, our immune system, to activate it, right? To get it out of a surveillance mode and into an active clonal expansion mode. Right? So interleukin-2 is very important. So you combine that with the TA-1, and you have an amazing improvement in your, uh, Th1. You turn back on your Th1. And you can see, this is not only for cancer, this is for, you know, everything. Now, just a reminder, here is the, uh, again, the drug, the name of the drug when they got it, um, the TA1 was called zidaxin, right? And it was in, I forget how many countries, and now it's hard to get. Um, but anyway, you can see what it does. Okay, stimulates dendritic cells, which act— and macrophages. So it activates the dendritic and macrophage complex. Very, very important, right? It also stimulates the precursor T cell to become an activated Th1, right? And it also, uh, activates, uh, the cytotoxic T cells. And natural killer cells. So basically every part of the immune system that is essential for viruses and cancer are activated by thymus and alpha-1. Restores NK cell activity. So this is all very important. We use this also when people This is very important with people who have gone through radiotherapy or gone through chemotherapy. All of this stuff is very, very important. In fact, what I like to do is to use it concomitantly. So I never— I rarely recognize— recommend it or agree with radiotherapy. And, you know, but sometimes it's necessary, absolutely. And, um, so when it is— or, uh, but high-dose chemo is never necessary. You get not only the same benefits, but you get no side effects, and you get immune stimulation by low-dose chemo, what they call metronomic chemotherapy. Okay, and then if you add insulin, you're walking on water already. All right, so, uh, um, yeah, so anyway, these are very, very important. And I think anybody undergoing— right now we see that the world is gripped by fear, and as we know, fear shuts off natural killer cell activity completely. You can't even find the interferon gamma in most people nowadays. This is what fear does. So this was the study in 2019, reduced— it's not 20, it was in 2020. I don't have the date here. But anyway, TA1 reduced the mortality of severe That's when they call it coronavirus 2019. By restoration of lymphocytopenia and reversion of exhausted T cells. So TA-1 treatment significantly reduced mortality of severe blah blah blah. These patients with counts in circulation less than 400 or 650 respectively gained more benefit from the TA-1. Improves tissue repair and healing, improves host defense to infections, improves microcirculation, and inhibits viral replication. Increases chemotactic response and phagocytosis, normalizes immune balance, and promotes Th2 to Th1 shift. Back to that. The reason I'm spending so much time is, is probably it's— there's no contraindication at all. Almost anybody can benefit by it, and it can be used prophylactically. Usually the way we, uh, we give it is, um, if someone's really sick, you give it daily subcutaneously, uh, for 10 days and then twice a week. And it's 1.6 milligrams, so the vials are 10 milligrams, and then you, you put in, you reconstitute with the water, sterile water, and then so you get what, is it 4.5, 4.5 doses, or I forget, I think like that, um, which is because you get 3, 6, you get 6 doses out. Yeah. Yeah, so it's very, it's very good, um, which means it's— and now if, um, if you're doing it twice a week, that's going to last you quite a long time. But if someone's sick, trying to get through something that, that's— they're in trouble, then you just keep giving it to them daily. But even with cancer patients, we give it 10, 14 days at the most, and then twice a week, or maybe 3 times a week, because remember that even, uh, uh It's pretty much eaten up, degraded by the body, but the effects stay around for about a week. So slow— these are, these are the biomarkers of thymosin alpha deficiency: slow and difficult wound healing, increased inflammatory markers, and low CD4/CD8. Reduces inflammation, improves tolerance to stress, reverses immunosuppression. By chronic fatigue, fibromyalgia, Lyme, increases antioxidant and glutathione production, approved in 35 countries. That's what it is. No documented adverse effect. It's considered a vaccine adjunct. Prior to the whole, uh, the worldwide hoax, uh, it was used for HIV, hepatitis B, hepatitis C. And it was approved as an orphan drug in the U.S. Thymosin beta-4— this is the one that does stimulate, um, because it— this is— you find this being produced in wounds. If you were to evaluate the chemicals produced in a wound, you would find that they have much more thymosin beta-4 than, uh, normal tissue. Okay, because it stimulates healing. And what do we know is one important part of healing, and that is angiogenesis. So, but one of the benefits is, is it actually can restore, um, hair growth. And I've seen that with a, with a kid who had, um, alopecia totalis. It took about a year and a half and his hair was— so, reactivates progenitor cells to repair damaged tissue, promotes rapid wound healing, potent anti-inflammatories, reduces acute and chronic pain, supports tissue stem cell to heal and regenerate the tissue, works in muscle to protect against sarcopenia. So it's really good. So many things. But if you do have cancer, then you can't use it because it does stimulate angiogenesis. The mechanism of upregulation is, is with actin and myosin, as you know, which are the, uh, components of muscle, the contractile components of muscle. Enhances collagen deposition, upregulation of actin to promote healing, cell growth, cell migration, cell proliferation. And because of its low molecular weight, it's able to when it leaves the thymus, it goes to any cell in the body that needs it. Now, going back to the pro-opiomelanocortin, um, each is, uh, each is packaged in larger dense core vesicles. Okay, so here's just as a reminder here, we've got the alpha melanocyte— melanocyte stimulating hormone functions with other hormones in the regulation of appetite. Um, by causing satiety. The alpha MSH also coordinates sexual behavior, which we'll be talking about. Alpha MSH from the intermediary lobe of the pituitary regulates melanin. ACTH regulates the secretion of glucocorticoids from the adrenal cortex— DHEA, aldosterone. And then the beta endorphins we see over here are produced in the brain for— in pain. So, mechanisms of sexual arousal. Sexual excitation involves the activation of neurotransmitters such as noradrenaline, oxytocin, which stimulates sexual arousal, and dopamine, and melanocortins, which stimulate attention and desire within the regions of the hypothalamus and limbic system in response to sexual cues and stimulation. So, the activation of those neurochemical systems blunts the influence of the inhibitory mechanisms such as endogenous opiates, which are released into the cortex, limbic system, hypothalamus, midbrain during an orgasm or sexual reward, and endocannabinoids, which mediates sedation and serotonin, which is released in those regions to induce refractoriness and sexual satiety. Okay, so it blocks those as well as turns on the noradrenaline, the oxytocin, the dopamine, turns off those. So So the sexual excitation can be primed internally by steroid action or externally by sexual incentives or drugs. But of note, very important note here, is that if you've had any male patients with erectile dysfunction, you'll find that they have— they get to a point where the Viagra or Cialis or the Lavitra, um, stop working. You give them this and they are 16 years old again. And no kidding, it's, yeah, pretty amazing. So the melanocortins, and for that reason you do not mix the, um, which we'll talk about, the PT141. You don't mix it with any of the, um, you know, Viagra or the other PDE inhibitors because you can wind up with priapism. So you— because you don't need it anyway, you don't want it. Okay, so neuropeptides derived from pro-opio include beta-endorphin, ACTH, alpha-melanocytes. Of those, the MC3 and MC4 subtypes exist in hypothalamic and limbic regions of the animal brain. Estradiol increases the alpha-MSH levels in the medial basal hypothalamus of female rats, suggesting that alpha-MSH release may be one of the several intermediates of estrogen activity. Okay, and because we all know that, and we all remember that the way God designed us was that, uh, the rise and peak of estrogens and then the quick deceleration which results in ovulation— that peak in the estrogen and what we're seeing here with the alpha MSH, um, is probably a significant reason why women are around ovulation become more arousable, more inclined to want to have sex. So it's very interesting, you know, God thought of everything, everything. We don't have to come up with stuff, he thought of it. Anyway, so the system arises in the arcuate nucleus of the hypothalamus, and projects dorsally to hypothalamic limbic forebrains. The system potentiates sexual desire through an interaction with dopamine. Now, the thing that's important to realize is that this is a centrally mediated, centrally activated modification of the sexual response. This is much different than any drug. Now, but I'm going to show you in a moment that this is not just for men. In fact, the PT-141 has finished FDA testing and was approved in 2019 as the female Viagra. Um, so now the MSH analogs, melatonin 2 and 1, and bremelanotide, which is also called PT-141, okay. So there's 5 different members of these receptor systems, and there you can see them there. But so it's the MC1R that's associated with pigmentation genetics, right? People have taken this and you get very dark. So it's— it's people with vitiligo, like full-body vitiligo, like this a lot. So these, these two are for the ACTH alone. Um, anyway, so the development of melanotan 2 for aphrodisiac effects, it's estimated that— I don't know the— oh, by the way, I never answered your question. Is it legal in India, um, the epithelon? Um, I, I, I, I don't, I don't know why not. I mean, I, I really don't know, but I I think we could find out. And also, if I can connect one of you to this company that we use in the US, yeah, one of you, one of you to become the distributor, then you could— they would— maybe they know because they're— they, they distribute worldwide and they, they know what's, um— now just to let you just know, so Dr.

Thomas, I know of some doctor who uses peptides in India in onco cases. And I will connect with you after this and see what we can do. If it is not available in India, how can we make it available, and whether it's legal or not.

Yeah, yeah, okay. And as I said, the Zidaxin should be legal. It's legal in 35 countries. One of those countries must be India, I hope.

Should be, because I know of some doctors who are using it. So I will also check with them how they are doing it. And meanwhile, I'll connect with you and this company and see how we can bring it.

Beautiful, beautiful. And what they— what the company does is they send over the raw material to a compounding pharmacist who then gets the formula from this company and can turn it into a nasal, because not all of them are— some of them are too big to be used nasally. But all of those that can be used nasally, of course, is much preferable because people don't like to give themselves injections every day, or at least minimize the number of injections.

So perfect. Yeah, yeah, Dr. Thomas, there are a few more questions. Can I take them now before we continue, or you would want to take them at the end?

Um, well, I don't see— where are we? How many slides do we have? I guess we're okay. Let's, let's do quickly.

Perfect.

Yeah.

Could I ask you the questions, Dr. Thomas?

Yeah, yeah, please.

Okay, so, uh, there's this question: what peptides do you use in autoimmune disorders? And does thymosin have any role in autoimmunity?

Yes, yes, yes, yes, yes, because remember, autoimmunity, like, um, is TH2 dominant, right?

Right.

So this, this brings it back. In fact, all of the ones that we've been talking about bring back and reverse that fundamental problem with the immune system. So absolutely, um, yeah, I would definitely use, use the TA1. Now, somebody with a severe, um, a severe autoimmune condition, like, uh, you know, like, um, you know, anyone that was, that was very acute and extremely uncomfortable for the person. I would do it daily, the 1.6 milligrams daily, but I would also use small amounts of maybe even only 1 million units of the IL-2, just a little bit, because you want the IL-2 to kind of— see, what happens is, um, when we look at chronic inflammation, we look at a chronic inflammatory a condition, we see that there's a switch to Th2. We also see the macrophages switch to an M2, and everything goes into this chronic phase. And in that chronic phase, what we have is tissue proliferation and pathological growth of all sorts of things. Okay, so one of the ways that the body— that God gets us out of that is God gives us a fever, and we start producing all these acute cytokines that just stick us back like without, without any warning, stick us right back into Th1 and get rid of all that stuff. In fact, that's what Dr. William Coley did 100 years ago. As you know, it's at Memorial Hospital in New York, which is now Sloan-Kettering Memorial. He found that the people who had sarcomas, you know, his job as a surgeon was to go in and amputate, and he kept finding people that they were— they healed spontaneously and left. He tracked them all down and found out they all had a a serious infection with, um, with erysipelas, and they had shaking chills for 2 weeks and it was gone. So, Coley's toxin, all that sort of thing. So we have to shift the body out of this chronic inflammatory, uh, allergic autoimmune kind of condition and bring it back to the Th1, which fights. So yeah, absolutely.

Thank you, Dr. Thomas. Dr. Thomas, another question we have is, does dihexa cause hypertension?

Does which one?

Dihexa. Dihexa.

Yeah. Oh yeah, does it have an effect on hypertension? Yeah, yeah. So somebody with hypertension would, um, uh, would want to monitor it. Um, now, um, I have had Oh, I don't know, 30, 50 people on it, and none of them have had high— I mean, none of them have had a problem with their blood pressure, um, and we follow them pretty closely. So I think, yeah, that's true. And I think if someone had uncontrolled hypertension and they weren't treating it at all, that you would say, well, listen, let's get this— let's get your hypertension controlled first and treat it. And then when you start them on it, start them out with one a day Right. And then monitor and take it on carefully. But there's no reason why you can't use it.

Perfect. Thank you. So, Dr. Thomas, another question we have is what peptides are bad and are there some peptides which need to be avoided in certain group of patients? And is there a group— sorry, is there a group of peptides which supports gut microbiome health?

Yes, yeah, so what I will try to do is, not what I try to do, what I will do is that as we go through each peptide, I'll mention whether or not there are contraindications, right, and then, but what I also would like to get everyone to agree on is, and hopefully he'll give us a talk, um, is that I think the, the— you'll be blown away when he, when he gives a talk on peptides. You, you can't— you don't even want to take notes. It's like listening to a, to an, to a symphonic orchestra of beautiful intellect. It's amazing. So he's a brilliant guy. But anyway, he could give us the, uh, the answer. He could probably give us lists in every category of what shouldn't be used. He has a broader— because he, he's the one, he's one of the founders of of TaylorMade in the US. So let's get him to get some, some of those specific— those are all great questions.

Sure. And any peptides you use to support gut health, Dr. Thomas?

Yes, there is a BPC-157, and I didn't include it this time, but, um, this is pretty amazing. I have people that come in with bloated stomach, bloated abdomens, um, you know, they're uncomfortable, they can't eat much of anything because they get bloated, um, and of course because of all the gas they're constipated, uh, or they have, uh, yeah, so they've got basically a dysbiosis, right? You take these, you take 2 of these, and they're orally fortunately. Used to be when we first started there was only injectable, but they're orally. You take 2 of them a day for 3 months Okay, you got a flat belly. You got a flat belly. It really helps with the dysbiosis. But keep in mind something— how did we get dysbiosis? We have to keep that in mind. So whatever we're being exposed to in our environment that's killing the healthy bacteria, we have to stop that exposure, number one. And number two, perhaps even more importantly, if we want to have a certain— if I want to raise horses What do I need? I need to have pasture land with good grass, hay, alfalfa. That's what I need. I don't need anything else. I need that. If I want to raise lions, then I got to have a jungle full of animals. So in other words, each organism requires the food that it requires in order to grow and propagate. So the bacteria that live on a fast food diet are not the same bacteria that would benefit our health, right? So if you're— let's say I was eating fast food but I was taking probiotics all day long and I took the BPC-157. I, I, you understand, I couldn't— I wouldn't be able to feed the new guys, right? There wouldn't be any food for them. So we have to remember, you limit your exposure to anything that's going to kill them And number 2, you make sure you're feeding them well. And what do they like? Vegetables, fruit, nuts, seeds. They love it. And, um, you know, if you— anyone looks and studies anatomy and physiology of the human being, that our gut is in one sense like an herbivore and in another sense, um, like a primate. But we have a longer small intestine. So even though we have a longer small intestine, uh, which allows us to get a quick energy from fruit and things like that, we also do some hindgut fermentation, right? So we— that's why we have a cecum and we have a colon, and we, we do that because gorillas, for example, get 30% of their energy from hindgut fermentation, right? Much less than the orangutans and the chimps. But anyway, we're in that same group, as you know, phylogenetically. And so, yeah, but anyway, the point is, is that by eating the foods that we were designed to eat by God, by nature, then what happens is that everything turns out to work perfectly.

Right. Dr. Thomas, last question is, are these peptide intakes safe for kidney stage 4?

Yeah, yeah, um, yeah. So stage 4, are you, are you meaning already on dialysis?

Yeah. No, he's saying no, no, not yet.

Okay, so they're not yet on dialysis. Yeah, it's not going to— they're not going to impair. You know, if you think about them, what they're doing is, remember, they don't have— they're not drugs, so they don't have extra effects that you don't know about. You know, if this is like CMAX for cognitive function, that's what it'll affect. It won't affect kidney function at all, right? And if it's, uh, yeah, and if it's for sexuality, it's not going to affect anything except the sexual response. It's not going to affect the kidneys. It has no effect on the kidneys.

Oh, that's good news.

Yes.

Yeah, because otherwise, you know, more than half the time we are thinking about what are the other effects this thing we love, right?

And, and the beauty is, the beauty is that, um, only the organs— since it's, uh, especially the, the melanotan derivatives, um, all of the organs involved centrally, from the hypothalamus, limbic system, down to the genitalia, all of the systems are not the kidney system and not the liver. It's not the liver. So it's only going to affect that system. And that's the beauty of peptides, right? They don't have— they're not greedy. They don't grab everything. They just do what they— they're looking for their receptors. It's beautiful.

Thank you. Yeah, we can continue, Dr. Thomas. Thanks for answering these questions so beautifully. You're very welcome.

Yes, so ACTH and alpha MSH generate sexual stimulation and penile erection in various animal species, including rats, rabbits, dogs, and monkeys. Both melanotan-1 and melanotan-2 are analogs of the alpha melanocyte stimulating hormone. It's the melanotan-1, as I was saying before, that makes people very dark. So unless, like, maybe an albino— I wonder what it would do to an albino because they simply don't have melanocytes. So, but, uh, So they could, they could simply, they could easily use this for other purposes because it still has all the other, the sexual response. Um, so the melanotan-2 and the bromelanotide, um, 2 is 7 amino acids. It's a derivative of melanotan-2. It's a potent initiator of erection with minimal side effects. Again, the MC3 and the MC4 receptors in the brain which activate the penis, the erection. Now it activates the endogenous pathways involved in the sexual response, centrally mediated, fast acting, okay? And it binds to these receptors. So, um, it's very interesting. I, you know, when you think of For example, when you think of some men that are unable to get an erection, it's because of the, um, you know, they just have— they have system-wide atherosclerosis, right? And so they just can't get blood into the penis anymore, right? And so that's why these, uh, these drugs that increase nitric oxide expand that and allow the blood to rush through. So here you have— here you have something that's not even dealing with that. And you get the erection. So that's, that's important to know. That's why it reminds me, it keeps me reminded that sexuality, the sexual response, the sexual experience is more in here than out here, you know. Because if you think about it, if you think about it, people that have fetishes for whatever kind of object How could the object do anything, right? How did the— how can an object elicit an arousal? It's all here. It's all here. So anyway, um, but this is kind of a reminder that sexuality, probably we think of the most primal of physical activities, is not at all physical. I mean, it is, it is, but okay. So here, now this was a very important, uh, libido peptide for females. Study in premenopausal women with sexual arousal disorder. It was only 18 women. This was back in 2006. This is what led to the FDA investigating it, okay? More women reported moderate or high sexual desire following treatment versus placebo. 20 milligram intranasal dose. Now, here we had 400 premenopausal women diagnosed with female sexual arousal disorder, hypoactive sexual desire disorder, or both were enrolled in multi-centered randomized placebo-controlled parallel group dose-ranging trial. Patients were treated for 16 weeks and randomized to one of four double-blind treatment groups receiving placebo or subcutaneous bromotriptyline Bremelanotide doses of 0.75, 1.25. Responder analysis showed there is a statistically significant increase in the percentage of women whose total score on the Female Sexual Index, 69% versus 46% for placebo. Now that's pretty good for placebo. I mean, 46% for placebo just hones right into the point of how much sexuality is a, is a, is this, is a psychological process, okay? Because placebo, if you think this is going to work and you unleash whatever type of inhibitory mechanisms you have going on psychologically that you're not even aware of, then here you go. Anyway, so 50% increase in satisfying sexual events versus 12 percent with placebo. Therefore, in 2019, the drug's name is Vylesi, which is called the female Viagra. So they had 30 clinical trials with over 2,500 patients. Anyway, it's now, it's now considered a female Viagra, and it, it gives, um And of course, you know, women, it has nothing to do with, with erections or anything like that. So it's just basically the sexual response, the libido. Neurohormone acting at the CNS level, binding to melanocortin receptors in the hypothalamus. Rapid onset of arousal, erection achieved within minutes. Found to induce erection in 80% of males who did not respond to PDE5s. Inhibitor drugs. And flushing, nausea, gastrointestinal— again, penile erection. If, if you're giving this to a male, do not give them Viagra with it. Yeah, anyway, the study of a failure with sildenafil with PD— PT-141. Okay, so they were given 10 milligrams as an intranasal spray 45 minutes or 2 hours prior to sexual stimulation, and they used at least 16 doses or attempts. Minor side effects: nausea, flushing, headaches. Patients in the group reported significantly greater intercourse satisfaction than those in the placebo group. Sometimes it takes 2 to 6 hours, uh, depends on the person. I would say a minimum of an hour, 2 hours. Oxytocin has been best known for its roles in female reproduction. It is released in large amounts during labor, as we all know, and after stimulation of the nipples. It's a facilitator for childbirth and breastfeeding. However, recent studies have shown that it is involved in orgasm, social recognition, bonding, and maternal behavior. So it's a 9-amino acid peptide, um, and it's, it's also now believed to be very much involved in physiological and pathological functions such as sexual activity, penile erection, ejaculation, pregnancy, uterine contraction, milk ejection, maternal behavior, social bonding, stress, which makes oxytocin and its receptor potential candidates as targets for drug therapy. I hate when they do that, just use the hormone. Anyway, this looked into the different kinds of female orgasms. And, um, as you can see, this one down here looks pretty nice— ecstasy. Anyway, it's a very interesting study. It's worth reading. But, uh, this is also part of how it became FDA approved. Orgasm in men— one of the main and now well-characterized peripheral oxytocin targets is erectile tissue, the corpus spongiosum. And carbon monoxide. It's— moreover, it's thought to be associated with ejaculation by increasing sperm number and contracting ejaculation tissue, especially prostatic urethra, bladder neck, and ejaculatory duct. By the way, if you've got older men who have BPH, one of the reasons for BPH is a lack of ejaculation. Their testosterone levels go down, they stop having sex, they don't ejaculate, they wind up with getting engorged, um, prostates. So you got to write a prescription: must ejaculate once a day. Anyway. So the dosing can be sublingual or nasal. 50 to 150 micrograms is needed. Okay, uh, this one we won't spend much time on because I have— I've been disappointed. But kisspeptin— um, puberty begins with a kiss. This is the peptide, neuroendocrine peptide that was found to initiate puberty, and it was discovered in Hershey's, Pennsylvania, so they called it KISS-peptin. Isn't that clever? KISS-peptin is a peptide that is encoded by the KISS-1 gene. Now, it was originally identified as the human metastasis suppressor gene for melanoma and breast cancer. Okay, so suppressor of metastasis and melanoma and breast. Anyway, I won't go into much with this, but basically it increases LH, it increases FSH, it increases testosterone. 5 men 60 years and older, testosterone increased with kisspeptin, but not— but less compared with younger men age 29. So if you got a young man who doesn't have quite— and we see a lot of young men now with who, who are having low testosterone— instead of giving them exogenous testosterone, perhaps give them kisspeptin and let them produce their own. Now there are several antidepressant peptides, but I'm only going to use this one. Today. So depression, as you know, depression— if you've ever seen a major depression, it's devastating. And it's said to affect 20% of the world's population. And despite some benefit from the SSRIs, um, there's some pretty serious side effects from that. So Spaten, which is PE1228 is an endogenous peptide with antidepressant activity. It specifically blocks the TREK-1 channel. TREK-1 channels are ubiquitous potassium channels that play a pivotal role in stabilizing membrane potential and thus prevent cellular excitability. Okay, so they're used— they have— there's lots of pharmacological, um, benefit with, with pain, epilepsy, stroke, and depression. Okay, in mice, the deletion of the TREK1 gene results in a depression-resistant phenotype that mimics antidepressant treatments. It is also associated with enhanced serotonergic neurotransmission and an increased neurogenesis in the hippocampus, specific for TREK1 and devoid of any TREK1-related side effects. Very important. The monoamine hypothesis of depression was expanded to other recent hypotheses, mainly blah, blah, blah, blah. In other words, such as the brain-derived neurotrophic factor. Um, classical antidepressants take several weeks to produce their effect. This one can— this works within 4 days, and you can do it nasally. And it has very, very similar effect as ketamine, except that ketamine uses the mTOR pathway whereas spaten does not interfere with mTOR signaling. And that's important because, you know, as you know, mTOR signaling can stimulate cancer. So small enough for nasal absorption, 4 milligrams per milliliter in a 6 milliliter spray, 2 sprays daily, and results should be seen within a few days. So I'm jumping all over the place.

I apologize, but no, no, we are, we are really liking it because if you won't have jumped, we would have many more questions.

Oh, okay, okay. So sleep and not sleep, CJC 1295. Promotes slow-wave sleep, which is delta-wave sleep. And, um, as you know, basically there are two, uh, two types of sleep. There's restorative sleep and there's REM sleep. And prior to about 2 AM, our 90-minute cycles are dominated by restorative sleep, maybe 80%, and only 20% to REM. And then after about 1 or 2 AM, whatever our particular reset point is, it reverses. So we wind up having predominant REM and less restorative, which is why going to bed early is imperative, not negotiable. But anyway, so a lot of people can't get into delta sleep This little baby here, completely Delta. So just a reminder, you know, right now we're all in Beta, hopefully. Uh, this is watching TV, listening to music, whatever, just hanging out. Theta is when we're dreaming, we're just watching. Remember, when you're dreaming, you don't edit your thinking. You're just watching it happen. Same thing happens when you're jogging. If you're a jogger or a— or do you do anything long, long and repetitive, you will not, um, your thoughts just go by. And so meditation is somewhere between alpha and theta. And they say that people that have been meditating for decades can be in complete meditation in delta. So delta sleep-inducible peptide was discovered in 1974 from the blood of a rabbit. Yeah, uh, 9 amino acid has been found in both free and bound forms in the hypothalamus, limbic system, the pituitary. However, the gene for DSIP and where it is made from is still unknown. So we can find the peptide, but we can't find the gene. So this is a very small study, but 6 chronic insomniacs— these are people that didn't sleep for 20 years— it improved their sleep quality. That's a big deal if you've ever had anybody who really doesn't sleep. And the problem, the reason you can't do it every night, is the tachyphylaxis. So give it maybe 2 nights a week. I would say 2 nights a week, and then use melatonin and stuff like that. Maybe 3 nights a week for a while. It don't be— they're all of the, you know, they always put the indications on to give you minimal. Forget the minimal. You want to get it maximum. Okay, so now The hallmarks of aging: dysregulated nutrient sensing, loss of proteolysis, proteosasis, altered intracellular communication, stem cell exhaustion, telomere attrition, mitochondrial dysfunction, cellular senescence— a big one— and epigenetic alterations. And here they all are. This is what happens when we see aging. Now, uh, you may know about this guy. If you don't, please get this book, um, David Sinclair, um, The Revolutionary Science of Why We Age and Why We Don't Have to. Amazing, amazing book. Where is it? I have it here somewhere. Um, Anyway, so his conclusion is this, and this guy's a scholar. His conclusion is that the dysregulation of cell cells contributes to aging by causing them to lose their genetic and epigenetic identity. This happens because sirtuins are distracted by damage and are unable to regulate the epigenetic genome changes. You all know what sirtuins are, I'll talk about them in a moment. This results in all the hallmarks of aging listed above. So sirtuins are a class of proteins that deacetylate, or actually turn off transcription of certain genes. They control the epigenome, the proteomics, and the DNA repair. Okay, humans have 7 sirtuins. Okay, 1, 6, and 7 shuttle between nucleus and cytoplasm. 3, 4, and 5 control mitochondrial function. Sirtuins are activated by NAD+. As you age, NAD levels decrease. Dr. Sinclair believes that when sirtuins are distracted, they are unable to regulate the epigenome and it becomes dysregulated and cells slowly lose their identity. Keeping sirtuins healthy and active can prevent aging. What I wanted to show you here was Ah, yeah, was here. This is the biological functions. The SIRT1 is the one we're talking about, with results to epigenetics, cancer, cardiovascular, metabolism, neuronal, inflammation, and stress. The SIRT1, okay, all turned on by the NAD to NADH ratio, the NAD+ to NAD ratio. That is how that is kept healthy. Okay, and there are different sirtuins that do different things, but this is what I wanted to point out right now. Now, with caloric restriction, a decrease in caloric intake by 10 to 40% without malnutrition has been shown to increase lifespan and healthspan in all organisms. In which it has been tested. The benefits of caloric restriction on metabolism and other cellular functions such as cognition depend on NAD+ sensing by SIRT1. Okay, that's how powerful that is. So if you look here in the middle, you see the NAD+, right? You see the, the— in the diet, right, we get nicotinic acid, it goes through these pathways and can produce NAD+. Then we have de novo biosynthesis. This happens by the keralian— I think it's pronounced keralian— keralian pathway, which is part of the tryptophan pathway. If you all remember that tryptophan, the first step in tryptophan metabolism produces serotonin. And then as soon as the lights go out, then it stops producing the serotonin and continues down the pathway to produce melatonin. Okay, but when there's stress and unusual stress or whatever, block, the circadian rhythm is disturbed, then it diverts into what's called the carillan pathway, which produces NAD+. The, the sad thing is, is that we make less and less NAD+ as we age. And if we do that, we're just not gonna— there's nothing, there's nothing we can do. Okay, so what are the NAD+ consuming enzymes? The sirtuins, the PARP, CD38, and CD157. Okay, so here we have the PARP. And as you can see, this is the one when we talk about in cancer, PARP inhibitors has to do with DNA repair, epigenetic repair, RNA processing, uh, circadian rhythm. Each of these use up NAD. Okay, the certain ones use up NAD. Right, and then the CD38, which is responsible for inflammation, cell adhesion signaling, and all of that, uses up the NAD+. And then epigenetic metabolism. Now, um, So recent preclinical studies demonstrate diversified pharmacological activities of NMN in cardiac and cerebral ischemia, Alzheimer's, diet- and age-induced type 2 diabetes and obesity, all of which are linked to the deficiency of NAD+. Supplementing, supplementing with NMN and NR, we can increase NAD+ levels, which can help activates your TUN function and PARP function, which leads to repair in DNA and regular, better regulation of epigenetic identity. Okay, so, um, the— let me see. Well, anyway, as you can see, it's a very complex system. It reminds me of, uh, NF-kappa beta. NF-kappa beta kind of sits right in the center of the whole inflammatory cascade, right? If you can turn off NF-kappa beta, you're gonna— which curcumin does, which a lot of botanical medicines do. If you can turn up— vitamin C does. Uh, if you can turn off NF-kappa beta, you can stop the, uh, the whole inflammatory process. Well, NAD, if you can increase NAD in any way, you can extend life and improve everything. It's pretty, pretty amazing. So why is this— why is this here? Anyway, well, there we go. Okay, so nicotinamide mononucleotide supplementation promotes neurovascular rejuvenation in aged mice. Okay, so transcriptional footprint of SR, SIRT1 activation, mitochondrial protection, anti-inflammatory, and anti-apoptotic. Now I don't know if it's, if it's big in India yet. Let me know if it is. Uh, but here it's like everybody's got intravenous NAD+.

In India it's not big right now.

You got to get it, you got to get it. Yeah, this is important, NMN, right? And the NR. Um, but, uh, because this is a precursor, and I'll show you, it's a precursor and you can take it orally, but still the IV is that when people get it, they really can see the difference.

They actually say, wow, yeah, they go, they go, wow, their energy is back.

I mean, it's everything. So the point is, um, yeah, so I mean, if, if you can— I know of a guy in the UK who's, who is it, take, brings it all over the world and he's got really good quality.

If you, if you need to try to get it into the country Um, I will check with you because I got a very small batch, uh, recently, but, and, um, I've not reordered again because we are not doing it too much in India.

Ah, and he's got all the protocols. He's developed all the protocols.

So I'll connect with you.

Yeah, yeah, yeah. Okay, so the nicotinamide mononucleotide treatment attenuates oxidative stress, rescues angiogenic capacity, blah blah blah blah. Rescues cerebral microvascular endothelial function. So in other words, it's pretty, it's pretty amazing. Um, but why did that happen? You know what, I think I, when I was making this, I kind of, I finished, I finished that section down, so forgive me. Somehow I'll finish that later. Yeah, all right. Okay, anyway, let's talk about cancer for a minute. We won't spend a lot of time because I don't think, I don't think many of you deal with cancer specifically, right?

I think a lot of us do have cancer patients, but I'm not sure if somebody's exclusively working with cancer.

Oh, okay. Well, if you do, then it would be— yeah, you'll, you'll really you'll really appreciate it.

Right.

Excuse me one second. Okay, I got it. So the different targeting effects on cancer. So Anyway, the 3 major parts of the, of cancer are the lymph node, the blood, and the tumor microenvironment. That's why when, uh, they, uh, go in there and they say, oh, we removed 37 lymph nodes Uh, 5 were positive. Well, if they're positive, that means the lymph node was doing its job, right? Unless the lymph node has been completely obliterated, completely taken over, and it's no longer a functional lymph node, then it's doing its job. It's developing an immune, an immune response. It's the headquarters. It's— this is how the immune system works. Anyway, but, uh, anyway, I just wanted to bring that up. I won't go into all of this about cancer. Okay, this is one that we like. It's opioid growth factor MET5. Uh, it's known as metenkephalin. This is, uh, it's an endogenous pentapeptide opioid growth factor. Um, regulates cell growth in normal and abnormal. Okay, it can control the cell cycle. So OGF, OGF-R upregulation at the translational level produces oncostatic and oncosuppressive effects, and that's what we try to do. So the OGF-OGF-R axis regulates cell proliferation by altering the, the cell cycle. Through p16 and p21 cyclin. So it's, it's called metankephalin, it's called Met5, it's called OGF, but it stimulates the inhibitory pathways of cancer cell division. So imagine you do this while you're giving the TA-1 and the IL-2. So you're turning on the ones you want to, and you're, and you're turning off the ones you don't want. Okay. They found it to kill colon, pancreas, squamous cell, neuroblastoma, renal, triple negative breast, ovarian in vitro. Phase 1 human trials in 16 pancreatic cancer patients showed improved survival over standard 5-FU or gemcitabine with good pain control. Okay, so it's, it's just, it's tragic that those are the only two choices the patient gets. They don't give them talk to them anything about all the other things we know that are important— diet, going to sleep early, you know, balancing hormones, meditation, all the stuff. That's why you're doing research, I believe, is unethical. You don't do research on human beings or animals either. You just do everything possible. Well, how do you know what's possible? Well, you figure it out. You figure it out, but you don't do experiments on human beings. Yeah, what if that human being happened to be your mother or you? Is that okay? You want us— you want to be— you want to be in the, uh, control group? I think I'd rather be in the control group than the— than in the therapeutic arm, from what I know about the fantastic allopathic medical world. I'm a recovering allopath. Our findings in vivo or in vitro show that that treatment, either in vivo or in vitro, could upregulate the percentages of CD8 T cells, induce markers of activated T cells, increase cytotoxic activity against the S180 tumor cells, and increase secretion of interferon gamma. Okay, here's another study. Melanoma. The tumor volume and weight with the, with the metenkephalin-treated group were lower than those in the control group and naltrexone. So they gave low-dose naltrexone plus the, um, uh, men— M-E-N-K. And here was one with, um, regulating dendritic cells. Via the metenkephalin. Thus, it is concluded that metenkephalin could exert anti-tumor effects through precisely regulating opioid receptor-mediated function of dendritic cells. In addition, the MK-treated DC cells may serve as a new immunotherapy approach against the tumor. So I just use this on everybody. And then here we go with, uh, improves lymphocyte cell population in human peripheral of 50 cancer patients by inhibiting regulatory T cells, Tregs. As you may know, Tregs are— you want to inhibit those because otherwise they actually turn off the immune system, right? Because they're regulating it, they turn it down, they dial it down, and that's not what you want, right? You want to do that when you've got autoimmune, things like that. You want to get it up. Opioid growth factor improves clinical benefit and survival in patients with advanced pancreatic cancer. Again, of the subjects surviving more than 8 weeks, 62% either a decrease or stabilization tumor cell by CT. Median survival 65.5 versus 21 days. But you can see With all— I mean, that was just manipulating this one particular peptide. But imagine the way one works with cancer, and the one way one works with anyone, is not by doing one thing and seeing how it's going to work. The way we work with human beings, because we are human beings and we took an oath to save their lives and relieve their suffering, we don't say, well, I'm going to try this on this person but not this. No, the hell— I shouldn't have been given my medical license if I'm going to do something like that. Sorry if you're researchers out there, but I don't think it's ethical to do experimentation on human beings. So I give everybody everything, and if it's not working, it's not working. And I add it in. That's why I don't have the— all the data I have is very global data, you know. Um, but, uh, yeah, but, but again, everything I use has a ton of science with it, all science. But as you can see, when we're looking at here, we're looking at just what, an extra 30 days, 40 days? Okay, um, and there was less pain. But you know, we could— and do much better. Well, what I— I've had advanced stage 4 cancers go home, back to work. I had an orthopedic surgeon from California in Arizona when I was in Arizona He came in and he said, look, I don't have time for this, I got a busy practice. I said, okay. He was home in 6 weeks. Now this one I like a lot, PNC 27. Um, there are HDM2 proteins expressed on cancer cell membranes that this binds to on solid tumors and induces a transmembrane pore formation. So it doesn't happen in normal cells. It doesn't have this membrane— this protein. And it also stimulates it because p53, if it gets phosphorylated, which it does, it gets phosphorylated in most cancers, and that kind of stops it from being active, right? So this also gets that activated. Here's ovarian cancer. Conclusions: these findings show for the first time the efficacy of PNC27 on freshly isolated primary human cancer cells. Our results indicate that the potential of PNC27 peptide as an efficient alternative treatment of previously untreated ovarian cancer as well as ovarian cancer. Now, one thing I have to say about this, because it has a direct killing effect and not necessarily apoptosis, a lot of times it's, it's cytotoxic cell death. There is a high potential for, uh, tumor necrosis syndrome. And so with these people, uh, we wind up giving 1 milligram subcutaneous to the person. They can do it at home. Like 5 times a day, and that's a minimal kind of dose, but it's, it's enough. Ideally, you would give it to them really in slow amounts, low amounts, over 8 to 12 hours, but no one's going to do that because it's got to be every day for a while. But people will get tumor necrosis, so it could actually, it could actually preclude the need for many other therapies. But if you're adding it and you give the person the The, uh, you get— they give them the peptide, they do it at home. It's— you can do a few at the office while you're at your office. Okay, and you just measure uric acid, you know, you look for, um, and you start to see a rise in uric acid or any other signs of tumor necrosis syndrome, then you just slow down. Here's an anti-cancer peptide. The results indicate expressed in the membrane of non-solid tumors. Yeah, okay. GHK. Now this is someone who can also look— you know, I didn't get a chance at all today to put in the body restructuring and, um, the beauty aspect of it because I just didn't get around to it because we're already late. But this GHK, GHK-Cu actually, has amazing utility in anti-aging— what's the word— cosmesis, cosmetics. Cracks go away. Collagen increase and all that sort of thing. But, but, so it protects skin cells from UV radiation, but it also suppresses RNA production in 70% of the 54 genes overexpressed in cancer patients. So it kind of resets, turns off the oncogenic, um, model that's been established. So that's why I use that. And a side effect is they wind up looking beautiful. No established dose, 2.5 milligrams sub-q 3 times a week. No one knows because they just— it's not— there's not money, you know. Mitochondrial dysfunction underlies heart failure, cancer, neurodegenerative process. We all know that cancer is a result of loss of mitochondrial function. If myocardial function is restored, cancer cells no longer ferment and are therefore no longer cancer cells. So one of the things that I learned in, in Japan when I studied with Dr. Kobayashi Tsuneo was how to do a type of hyperthermia that lasts 6 hours, and you give certain IVs while you're doing it. The person is kept at a very strict 40.5 for that period of time. You're measuring cardiac— you're monitoring the cardiac rhythm. You've got a central— you've got a rectal thermometer in. Anyway, what happens is at that temperature, it stimulates the production of heat shock proteins, and heat shock proteins in turn stimulate mitochondrial proliferation. So Dr. Kobayashi had done biopsies of tumor cells prior to treatment and then looked at them with an electron micrograph, and after treatment did a biopsy and looked at them with the electron micrograph. And the difference was that before the hyperthermia, the cell had very few and small shrunken-down mitochondria. After the protocol, it was plush with big, fat, healthy mitochondria. So in effect, since cancer is a metabolic condition— that is, it lost its mitochondria, so it has to ferment in order to produce energy— it no longer has to ferment, therefore it's no longer cancer. It's pretty simple. It's called cancer reversal. Now, uh, to give him some credibility, Um, uh, he— meticulous records, 40 years, 45 years. Over 40 years, and he's got meticulous records. Uh, 70% of his patients have long-term remission. He does more than just the hypothermia, but And one day I'll have to talk about him because he's amazing. Yeah. And by the way, we have to grab his— we have to grab his mind before he dies.

But 70% reversal is a very, very, very, very good percentage. Difficult to believe?

Impossible to be— I mean, because I've worked with cancer and I can't imagine.

Right. So 70% is like Specially we know that these patients reach our doorsteps only when they've lost all hope from all other sciences.

Exactly.

Then giving 70% reversal, I would definitely agree with you that, you know, we need to catch hold of his brains and learn.

Yeah, I've studied with him. I've gone back and forth to Japan for the last 25 years, you know, spending time with him and training with him. But, you know, he's at the point now where he's getting senile. Oh, by the way, can you see this? Yeah, that's the C-Link. So you take this off, you take that off, and then—

Wow, great. I have one question for you, Dr. Thomas. Here is, do you combine OGF and MENK in cancer?

Yeah, well, no, they're the same. They're the same. They're different.

They're the same, right? Perfect. Great.

So, um, anyway, so that's, that's one of the things. It's great. So what I like about this is if you, um, can restore mitochondrial function. So, so I'm going to talk about a couple of mitochondrial peptides, but these peptides, understand are important for somebody with anything, um, chronic fatigue, um, aging, uh, anything, you know, the mitochondria are everything, right? So, right, okay. So MOTC is produced in the mitochondria in response to metabolic stress, diabetes, and insulin resistance, okay? So during that time, uh, the mitochondria— it's a mitochondrial peptide and it translocates to the nucleus of the cell, which then turns on all the antioxidant enzymes of the cell to block this, uh, the stress. Okay, so that's what this does. And of course, we don't make a lot of it as we get older. Um, so, so mitochondrial DNA, there are 37 genes, 2 RNA, 22 tRNAs, 13 polypeptide subunits. MOTC is a 16-amino acid peptide produced by mitochondria. So anyway, it regulates the antioxidant response elements, and you can see that there. Now the thing that's very important about this is that longevity, exercise, diabetes, and cancer. Okay, so, all right, metabolic imbalance, right? Um, putative functions. It blocks— if this is increased, it blocks your purine synthesis, which stimulates AKAR and AMPK, which also gets stimulated with exercise, which turns on PGC-1 alpha, which then in turn stimulates mitochondrial biogenesis. Now I know you're not going to believe it because I didn't, but one injection of this gives you the increase in ATP production equivalent of 6 months of, um, uh, what's, what's the word?

HIIT training.

Yeah, yeah, training, you know, like power, high intensity, high intensity training. Yeah. And I— so when I, when I learned that from, from the guy, the doctor at, um TaylorMade. I had to see that. What are you talking about? And it's true. So I'll get that study to you, but that— it's just pretty amazing. So, um, anyway, it improves insulin sensitivity, protection against obesity, but it blocks AKAR. I mean, the blocking the de novo purine synthesis allows AKAR, AMPK, uh, you know, which is AMP kinase, and all of this to go up, right? Aging stops this. Right? So aging blocks this. So the MOTC is kind of critical in here. If you can do that, you can bypass it. So, but imagine doing that and exercising daily. Uh, so activation of AMPK has been found to oppose tumor progression in several cancer cell types. Hypoxia, hypoglycemia with exercise or fasting, and mitochondrial biogenesis. That's what happens when, when the PGC-1 alpha stimulates mitochondrial biogenesis. So you're increasing the number of mitochondria you have. So 5 milligrams subcutaneously every other day or daily, or some people do 10 milligrams 3 times a day. Depends on your, on your budget. So the maximum is, uh, 20 milligrams a day.

But now And for how many days?

Well, they say about 6 weeks, 8 weeks, and then give it a break. Now this here is on the inner mitochondrial membrane. There's a folding in here, and if you can see the orange here and the orange down here and the orange here. This is cardiolipin. Cardiolipin is a phospholipid that's produced only in the mitochondria, and it being here actually keeps this mitochondrial fold of the inner membrane tight. And it also, right here in that place at the center, is where the actual whole Krebs cycle goes on. And that's where all the ATP is produced. So as my— as, as, uh, now cardiolipin has— is a— has 4 phospholipid groups, and they're all omega-6, not omega-3. They're all omega-6s. Anyway, they become oxidized as we age, and when they become oxidized, that fold in there starts to open up. And when it opens up, less and less ATP are formed. Okay, so that's what that happens. So, so the inner mitochondrial membrane, mitochondrial contact site ATP synthase is localized at the cardiolipin. It oxidizes with age, the curve gets looser, and energy production decreased. Ah, this is the one, this is the one. Sorry, one injection, same as 6 months endurance training. So SS31 has a dimethyl, dimethyl tyrosine residue allowing it to scavenge free radicals and inhibit linoleic acid oxidation. Because remember, we're talking about omega-6s, so linoleic acid. So it inhibits uh, it blocks the peroxidation of those lipids. Okay, so it binds to the cardiolipin like a glue, tightens the curve, and then you have better ATP production. So SS31 eliminates reactive oxygen species, increases ATP production in mitochondria, thus maintaining membrane— mitochondrial membrane potential. Okay, so anyway, and then you know that this is for everything from neurodegenerative diseases Everything, everything. So the name of the— what they call it in addition to SS31 is elamprutide. Elamprutide. No contraindications, no serious adverse events, mild aches or flatulence or abdominal pain with very high doses. Some have used 100 milligrams daily IV or 40 subcutaneous in clinical trials. 1 milligram daily is most widely used for people who have no problems. 10 milligrams per day for cancer. I, I do, uh, I do about 10 milligrams 4 or 5 times a week now. This was a very— there's a very important— because if you work with people with cancer, eventually you're going to find someone that's going to become cachexic. And, uh, you know, it's very difficult to treat cachexia because, um, it just is. Usually they're not hungry either. Anyway, um, anyway, they use oxaliplatin and 5-FU high doses to, to put mice into a state of cachexia. Um, anyway, so what the conclusion was, the results suggest that targeting mitochondrial function may be as important as targeting protein anabolism. Yeah, so in other words, yeah, you need the protein, you got to get protein into the body, right? Because you gotta, you, you need that, but you also need the other nutrients, and you need the energy. Because the first job of all cells is to make enough energy just to maintain its shape, to maintain its sodium-potassium pumps, to maintain its shape. Then it can do any kind of work. So here it is. It prevented cisplatin-induced acute kidney injury by regulating mitochondrial ROS. In conclusion, our study revealed that NLRP3 inflammasome might act as a pivotal regulator promoting the process of CP-AKI. SS31 could reduce oxidative stress and apoptosis in these mice and therefore resist renal injury, which might be due to the inhibition— inhibition— activation of mitochondrial— I hate science talk. Now, The last topic that's very important, because we're really out of time, um, is cellular senescence. Mitochondrial peptides can increase cellular senescence. Cellular senescence is also increased with chemotherapy. Cellular senescence is also increased with aging. Okay, so many things can trigger senescence. The problem with senescence is once the cell becomes— it's on pause, it's no longer functioning, it's just on pause, but it's not dead— it starts leaking anti-inflammatory cytokines. It's called senescence-associated secretory phenotype, SASP. Okay, it stimulates inflammatory cytokines. It's called inflammaging. And it underlies everything we see in aging, from, from dementia to osteoporosis to everything, you name it, it's underlined by this. So we need senolytic therapies. So the senescent-associated secretory phenotype, it pauses the secrete— the inflammatory cytokines IL-1, IL-6, NF-kappa beta, etc., are increased As these increase with inflammation, low-grade chronic aging, you get atherosclerosis, fibrosis, osteoarthritis, and insulin resistance. You get the whole thing. Telomere erosion causes it, epigenetic factors, mitochondria. So the risk for geriatric syndrome, including frailty, immobility, mild cognitive impairments, and incontinent urine, these conditions also cluster within individuals and are associated with age-related chronic diseases, blah, blah, blah. Fundamental aging processes include chronic sterile low-grade inflammation. By the way, and, and look at this here, they just transplanted a small number of senescent cells around a knee joint and it caused osteoarthritis. Now, by the way, one of the most powerful anti-inflammatories is to eat uncooked food. Cooked food stimulates inflammation. Raw food does the opposite because it's not viewed by the body as being something that is unnatural and needs to be eliminated. You can look up that research by Dr. Luigi Fontana, MD, PhD, at Washington University, um, in, uh Where's that? I forget. Anyway, Luigi Fontana, MD, PhD. Everybody that was on raw food for 3 years or more consistently, whether they were 80 years old and 16 years old, had an undetectable CRP. So, synolytic treatment: fisetin, rapamycin. Rapamycin is not really synolytic, it's, uh, static. Metformin, quercetin, resveratrol, NMN, NAD+ that we talked about, the foxofar DRI, and the 5-amino-1Q. These are some of the senolytics, but it should be in use in any— anybody who's aging, uh, who's having— especially having a symptomatic aging, or how about someone that doesn't want to age and they're not quite symptomatic? So the FOXO4 relation to senescence— FOXO4 transcription factors have been shown to downstream effector molecules of IGF-1. The absence of insulin and the PI3K is inactive, so the FOXO homolog is able to translate to— translate to the— so what happens is basically that it winds up blocking— this is very similar to the PNC27 binding to the MDM2. This is very similar because it does the same thing. So in a cell, let me see if I can see right here. In a cell, where is that? Hmm, okay. Well, any— anyway, in a cell you have the p53, and then you have the thing that puts the brakes on to the p53, because the p53, which we know is tumor suppressor, right, and, and produces apoptosis, right? But if it was activated in all cells, it would cause apoptosis, we would die. So we have this MDM2 that counteracts it. It's like estrogen and progesterone, okay? So they counteract each other. So, um, uh, what happens is the FOXO4, uh, binds to the p53, which prevents it from being phosphorylated, and it can be activated. Pretty cool. So, and again, remember we were talking about modifying peptides a little bit. So, um, research on peptide chemistry usually is the natural L-peptides, okay, but the D-amino acids are in retro-reverse sequence. Modification of peptides to a D-retro-inverso isoform can render peptides new chemical properties which may improve their potency. And that's exactly what the DRI is. So the FOXO4 can regulate expression of the p53, and through this activation, uh, wind up increasing and turning back on p53. You, if you worked with cancer, you know that one of the big problems with cancer is p53 being downregulated. It's like 50% of cancers, and probably even more. So this is a big deal. But it also cleans up senescent cells. It gets rid of senescent cells. That's very, very important. So here's a study where they gave high doses of doxorubicin to these rats, and guess which one got the FOXO4 DRI? Yeah, his hair came back full, he grew, had a good— okay, in other words, he didn't have the accumulation of senescent cells. So it counteracted the loss of renal function, uh, in regular aging mice as well. So if you have someone with stage 4 renal cancer, definitely anybody with any aging problem, or it's due to diabetes, it's due to a metabolic problem, the FOXO4 and the NMN and the all the other, uh, I found a product Here, fisetin, rapamycin, metformin, quercetin. I found a product online that is called— huh, I can't remember, but it's a fantastic combination of fisetin, quercetin, uh, whatever it was, like 4 or 5. And then quercetin, it was NMN. You know, it was pretty amazing. I gotta— I'll find it and I'll send it to, to you so that you can share it with the group. Okay, but, um, it's pretty amazing. I'm gonna, I'm gonna order it myself and get it. Um, whoops. So I guess that's it. You know, I, I apologize again. I didn't, I didn't, I didn't organize this. I, I just did this all in one day.

So no, thank you, Dr. Thomas. It was very, very informative. Interesting and very crisp and clear. I'm sure all the participants are feeling like, you know, when can we start using it, right, right, right? So I will connect with you and take the contact numbers and speak to them how we can make it available in India. Also, we'll plan few more sessions with you and the other guys you were recommending. Have an amazing time and let 2022 be the year of functional medicine in India and helping and healing people.

Yes.