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Speaker 1: (00:01)
Welcome to pushing the limits, the show that helps you reach your full potential with your host, Lisa Tamati, brought to you by Lisatamati.com

Speaker 2: (00:13)
Hey team. We're this week I have an absolutely superstar, the world's number one leading functional genomic specialists, Dr. Mohammed from Toronto and Canada. Dr Mansoor, Mohammed has two guests now. He is a scientist and entrepreneur in the field of genomics and is regarded as one of the most innovative leaders in the emerging personalized medicine and lifestyle genomic space. Dr Mohammed is a PhD and president and scientific officer at the DNA company and is really considered to be a pioneer medical genomics. He's a classically trained molecular immunologist who has received academic and industry awards, published numerous papers and holds patients in the general fields of molecular diagnostics in genomics. Now functional genomics is about understanding the DNA and how it behaves in every definition and this Dr. Mentor was very different than many of the other DNA companies that I've looked at recently and that he doesn't just look at the single litters, if you like, of the DNA, but it looks in combinations of genes.

Speaker 2: (01:22)
And how they're playing out. And this makes him very, very different. This, he sees DNA like a language rather than a vocabulary and language that has grammar, sentence structure, Syntex and nuances. And you've got to be able to read genetic structure at the holistic level. Now I'm super excited about document's all his work and I'm studying functional genomics at the moment and it is the next level in personalized health. I'm really, really excited to bring this interview to you. It's taken me months to get documents or on this podcast and I'm hoping later on the year to get Dr. Mansoor Down to New Zealand for a lecture tour to speak to functional medicine practitioners down here as well as the public. So if you'd like to know more about that, please reach out to me and let me know. I'm just like to remind you before I hand over to Dr. Mansoor that my book launch is happening just next week over the time of this recording is the 6th of March and on the 11th of March.

Speaker 2: (02:26)
So by the time this recording actually comes out, my book will be live. It's called relentless and it tells the story of bringing my mum back after a major aneurism myth. You're fighting for a life and lift her in and basically not much over a vegetative state. Massive brain damage at the age of 64 and what I did to beat all the odds and bringing my mum back to health, all of the CRPS I used, the protocols, the attitude, the mindset, the obstacles that we had to overcome, the problems that I've discovered in our medical system in on it goes. So this book is really, I'm, I'm so pleased to be able to bring it out. It's taken me two years to get this together and to bring it to the public, but I really want to pay it forward and I want to help thousands and thousands of other people facing difficult challenges to take them are hit on with the right mindset to overcome great obstacles.

Speaker 2: (03:18)
So if you'd like to check that out, we can head over to my website. I have Lisatamati.com Hit the shop button and you'll see all of my books there and my jewelry collections. But make sure you check out the neatness. It's really going to be worth a read for anyone who has major medical problems at the moment. Or of course anyone who has a stroke aneurysm Alzheimer's dementia, and wants to know about brain rehabilitation or optimizing your brain function and who isn't interested in that as well as the whole mental attitude and mindset that it takes to do all this. So without further ado, over to Dr. Mansoor Mohammed. Well, hi everybody. Lisa Tamati here at pushing the limits. It's fantastic to have you back again. Now I am just grinning from ear to ear. I can't stop smiling because I've been waiting for this interview for weeks. I have a very, very special guest, Dr. Mansoor Mohammed, all the way from Toronto in Canada. Dr. Mansoor How are you going?

Speaker 3: (04:17)
I am great, Lisa. And likewise, it's been something that I've been looking forward to, to the audience. Please forgive me. I'm a little bit sleepy from Jeff blog from last night, but Lisa has been pumping me up and so we're going to have some fun of this

Speaker 2: (04:31)
Now. I know what it's like when you're a little bit jetlagged and you have a main very much in demand. So I'm just so excited to have a little bit of time with you now. Dr Mansoor, I do the whole introduction on a separate recording, but dr Mansoor, can you give us a little bit of background about your what you did your PhD in your, your, a little bit of a brief history of your back.

Speaker 3: (04:55)
Sure. genes. Genetics has always have always been my love. The study of how this operating manual, just just thinking, just, just dialing it back and thinking that the human being, we've got this operating manual that by every definition of the word it behaves like an operating manual. And to think that it's there and to think that one date might be accessible and that we could read this and we could read it intelligently and just simply understand myself much less, much less. Anyone else has always been my love. And so I started, my PhD is in applied molecular genetics and immunology. So I was looking at the genetics of the immune system. I was very, very fortunate to have an awesome mentor. She was then the chair of molecular biology at UCLA invited me to UCLA. So I had an awesome couple of postdocs there where I got deeper and deeper involved in eugenics.

Speaker 3: (05:47)
But a real pivotal point happened when I was done, invited to come to Baylor college of medicine and Houston, Texas. And it was that heavy time just about the human genome project, its, you know, sort of pinnacle. And I was asked because of the work that I had been doing with UCLA to come over to Baylor and start a company, the goal of this company was to begin looking at multiplex genomics. In other words, to really do the, you know, the barrage searches into the human genome. Not one gene at a time, but looking at the entire genome in pathway type manners. Now initially we applied this knowledge to cancers. We apply this knowledge to developmental disorders syndromes, Prader, Willi syndrome, autistic spectrum disorders and so on and so forth. And about 15 years ago, after many years of doing what I call disease genomics, looking at the operating manual, looking at when the operating money was broken out of what happens from a disease perspective.

Speaker 3: (06:45)
Then I sort of thought, okay, well that was fun. That was good. That was, but why should I not look at the operating manual? But nothing is purportedly broken, but just the operating manual. So then still we can tell presumptively healthy individuals how to stay healthy or how to get over the type of chronic illnesses. So this is what I've been doing for the last 15 years, studying, researching and applying the knowledge of the human genomic operating manual. So we've been, we can just simply understand it. How does the body work, which clearly there's an individuality to that, obviously. I mean, we are human beings. We all, our cells, our organs, our bodies, all have to accomplish the same jobs that we do. These jobs with nuance differences, some of us less optimal, more optimal, more efficient, less efficient. And when we can zone into that, when we can read this operating manual from that perspective, really Lisa miracles happened with the sort of insights that you get, the nuances that you can tease out. It really has transformed the clinicians. We train the patients, we work with the transforms, it empowers the individual to understand how their body works and what they might do to obtain that optimal health.

Speaker 2: (07:59)
This is, and this is a super exciting and I can feel your passion coming through despite the jet lag for this area and it's now mind you, passion is of the last maybe two months or six weeks or however long it is now that I've been diving into this world and just going, Oh my gosh. Oh my gosh, this is just, this is just the next level and the information that I've been searching for to try to understand because everything seems so generic. And this a personalized house and yeah, doctor man saw you the president and founder of the DNA company, which is offering direct to public and in conjunction with conditions. A couple of reports. So our full genomic report in a hormone report and I want to tease apart a little bit today, why should people even consider having a look at these, the sort of testing what benefits they can get out of it.

Speaker 2: (08:58)
And I'd like to also tease a little bit about looking at other, like I've, I've looked at a lot of gene companies and that do gene DNA testing. And you had an analogy on a Bulletproof radio that I heard you on the same show who's amazing Dave and his work that was about the most people are looking at it DNA as a vocabulary and not a language. And that just seems them light bulb up in my head where I realized, okay, so it's not the siloed genes looking at them individually, but looking at cascades and pathways and combinations of genes as we are then interpretation has been missing today.

Speaker 3: (09:43)
Oh, 100%. So I always say, you know, Lisa, anyone that is in the data business, regardless of whatever data you're collecting, data is really quite dumb. Data in and of itself doesn't mean anything unless you know what to ask of the data unless you know how to triage, how to approach the data. So when we use the analogy as DNA, the operating manual, the genome, it really meets all the classifications and descriptions of a language. Thus far we've been looking at DNA and genetics from a language perspective purely as a vocabulary exercise. The more words we know, the better we presume to think we know the language. And as much as that is important as per the analogy that I drew with on Dave, show a person simply knowing more vocabulary by no means mean they understand the language. And so when it comes to DNA, when it comes to genetics, when it comes to how this awesome operating manual, the architecture of it, it's not just about vocabulary, it's not just about the individual genes.

Speaker 3: (10:51)
So here are the two layers implicit in your question that we do a bit differently and why we need to do that differently and why it's important that it's done this way. The first is this. When you're looking at the DNA, if the person are either genetic makeup, the vast, vast majority of companies right now, they're looking at things called snips, single nucleotide polymorphisms. In other words, they're looking at places which is absolutely important. They're looking at spelling variations in this operating manual. And of course these spelling variations, these single nucleotide polymorphisms will impart to you mean Jane, Paul, Peter, the same cellular job that we all want to do. These spelling differences can impact the efficiency with which we do that job and that is important to know, but while we're at that point of spelling, you see per any language, if I wrote a paragraph, I might have spelling errors in that paragraph, but there are examples where I may have inadvertently deleted a sentence or deleted a couple of sentences in that paragraph.

Speaker 3: (12:00)
Now, if the analogy here is that the gene is the paragraph, so your operating manual are these 23 volumes. Think of it. Think of a 23 volume and psychopathic set these awesome, huge volumes. Now we're going to inherit two of these 23 volumes. One from mom, one from dad, and these volumes are properly arranged and when we open up any page, let's say we go to volume three from mum volume three from dad, we open up page four on each of those volumes and we look at paragraph five page four, volume three we, I see the same paragraph. We're going to see the same information from dad's gene paragraphs of genes and mom's gene. We're going to see the same information, but when we look really carefully, when we look at those paragraphs, really collect carefully, we might find that there's some spelling differences. Those are the snips.

Speaker 3: (12:57)
We may also find that on either dad or mom's paragraph, a sentence was missing and I just taught this over the weekend. So I was in the auditorium and I said, okay, here's an instruction that was waiting for me coming to this auditorium to give this lecture, Dr Mansoor, go to auditorium B and to the left door approach to podium from the right side, press the enter button, begin your lecture. That's an instruction. That's a paragraph. That's an instruction and that's the equivalent of a gene. Now in that paragraph they make has been a few spelling errors or changes that may have confused me a little as to what the instructions are. But when I look at it carefully, I could sort of still figure it out. Okay. But if in that paragraph, the sentence that says go to auditorium B was missing at, of course there are multiple auditoriums, all of the other parts of the instructions are there.

Speaker 3: (14:03)
But I can really be confused as to what is the ultimate thing that I'm supposed to do. It's called an indel. So in our genes, not only do our genes have slips, many important genes actually have places within them that I'm missing. So until we test for those type of changes, we're by no means getting the full picture of what is happening. The third thing is this, not only do we have slips, not only do we have in Dells, there are occasions where the entire gene is missing is show I'm supposed to show up. I got to the hotel where the conferences are and the instruction just telling me what it's just not even there. So here I'm in the lobby going, I don't know what I'm supposed to do. This example is a genetic phenomenon keeping the analogy, this is called this C and V copy number variation.

Speaker 3: (15:03)
We see because we were supposed to have two copies of that. Paragraph five page four, volume three. Sometimes believe it or not, when we go to page four we've opened up mum's volume three dad's volume three. There they are. We're going to read both of the instructions cause that's what yourself has to do at any given moment. When there's a job to be done, your cell goes and pulls the volume that has that instruction, takes down a mum's copy, takes down, dad's copy, opens up and reads the instruction. Now in the case of a CMV copying of the variation, we can open up mum's volume three page four there is paragraph one, paragraph two, paragraph three paragraph four paragraph six. Oops, wait a minute. Where's part of our five? It's gone. There's part of four. There's part of six. I look over a dad. He's got all of the paragraphs or vice versa.

Speaker 3: (16:02)
Sometimes Lisa, both paragraph fives are gone. Okay. So the point of the first answer to your question, why we do things a bit differently is we're not just in the business of collecting data for data's sake. We're collecting data. Are you were doing gene testing to understand a process. When we designed genetic tests, we don't begin with genes. We begin in a whiteboard saying, what is the thing in the human body that we want to study? What is the thing that we want to study? Genetics, just good old fashioned medical textbook, human physiology. Do we want to study the way the newer chemicals are produced and bonding and response? Do we want to study how the human body makes sex hormones? Something we should talk about when it comes to human performance. So how does the male and female body makes progesterones androgens Astros? And then we mapped that out.

Speaker 3: (16:56)
Forget genetics, which is not about how does the human body do that? No, of course, if the human body's having to do something, then it means there are genetic instructions for that film. So only when we map out the cellular, the cellular biology, the cascade, only when we met that out, then we come in and we pencil it. This gene is responsible for here. This gene is responsible for there such that at the end of the exercise, we've got a genetic test that already tells a story. The result from that genetic test is telling you the entire cascade. Step one, step two. We look at each of those genes that are telling us the story and we ask are these snips that are important? Are there entails that are important? Are the CNVs that are important because all three make a wow. And so the first part to the answer to your question is if you've been looking at genetic tests that are only reporting snips, you are dramatically limiting the variations that you and I and every other person have within our genome. So you're missing the nuances that are in your language to clarify the job to be done. Does that make sense?

Speaker 2: (18:16)
Absolutely. So that actually puts them together in my head because I've been starting this, I don't know, like for example, the GSTT one gene and the detox and antioxidant pathway, one of those types of genes that can be completely done.

Speaker 3: (18:31)
Completely. Totally said, absolutely. And of course it belongs to super family. So there are multiple G S T genes, but two minutes on that. If you're going to design the human body and you're going to say, listen, one day we're going to make this thing called human being and we're going to put him or her in this wonderful world, but mind you, he or she is going to have to deal with some toxic insults, both from without and from within. Where would you, and you know that, where would you put your detox defenses? Well, they're about four places. If you're an intelligent designer, you would put your detox, different defenses at least in four places. You would say, how and where do things get into the human body, dermal skin, the nose, nasal Bronxville lung, the GI track. Okay. So those are how things get it.

Speaker 3: (19:23)
And unsurprisingly you would want to make sure your detox genes and the things that you'd want to make sure there's super active in those places. And then you, you'd also say, well look, at the end of the day, things are always going to get past borders inside of the body, their waste products. So then I'm also going to put a detox organ. The liver, when we go to the human body, this is where we find these detox genes expressing themselves. And each of the GST is have sub specialties. Some of them are more important in the nasal bronchial track, some of them more important in the GI track and so on and so forth. So when you know the story that you want to read about the body, you know how to read the manual and interpret, is the GST T one gene deleted or not? This is a massive implication to the human body.

Speaker 3: (20:16)
Can you imagine the GSTT one gene is one of, if not the most important bio transforming antioxidizing enzymes in the body per its name and its gene and its enzyme. And if a person doesn't have it, literally it's not in mere manual. The GSTT one gene is on volume 22 and if that paragraph you have not inherited it from either mum or dad, you are missing an enzyme in your body. That is one of the most important detox. Now doesn't mean that you're not compatible with life, but it most certainly means you could not be the person who says, well you know what do you have a metals mean after all they're not that bad. Oh you know what, my uncle smoked until he was 80 years old. I'm going to smoke as well. Well you can't compare yourself to that person cause you don't have one of the most awesome detox genes.

Speaker 2: (21:13)
You don't have a good defense mechanism. And so like the detox is actually the first port of call before the immune system even does this job. So I'm, I'm excited to get my tests back cause I haven't gotten gotten through the reports yet. I'm, I'm suspecting that I have a problem in my GC jeans because I'm a very young age. For example, I've been the next medic as a, as a severe asthmatic, as a child, and I'm very hypersensitive to smells and anything. So I'm like a Canary one C one, which is theta. Yes,

Speaker 3: (21:54)
Very important in the liver. Key one PI GSTP one is the one that's really important in your nasal bronchiolar lung cavity. Individuals with a suboptimal P one are at extreme risk of early ectopic asthmas. They're the ones that if they go into the shopping mall, you know, the perfume resection, they've got to avoid the perfume resection. Right? Those are the GSTP ones.

Speaker 2: (22:21)
Wow. I'm obey. Fascinating to see if that's what comes back. And so if you want it deleted into them, we'll get onto hormones next because I really want to dive into there, but just to, to to look at the GST genes. If you don't have, you either have only one inherited GST, one gene, your mother or your father and you're missing the other ones or you're missing both altogether, are you more likely to have you're more likely to have toxins coming in that you can't deal with as well. And then your immune system is this way or auto-immune or part of the

Speaker 3: (22:57)
Brilliant, brilliant question. Just before we answer that, I had mentioned there were two layers to differentiate yourself, so just so that we close the chapter on what we do differently. So I'm going to come back and, and so now we will take it forward. We just mentioned that there you have to be mindful of the three different layers of variations, snips in Dalles with pieces of the genome missing and CNVs where the whole gene may be missing. The other quick differentiator, bringing back the analogy of a language, bringing back the story of the human body, it's this, and I told the audience this, there was an audience of clinicians in Phoenix this weekend. I said, have you ever read a really good, you know, suspense novel and not suspense novel, the novel that the author's painting the character and you're thinking he's the bad guy, you know, and he's falling around the heroin and he knows he looks a bit shady.

Speaker 3: (23:51)
And then until or unless you've read the entire book, you only find out that he was a protector or he was something. He was a guardian and words. He wasn't about that guy. Now what the heck does this have to do with genes? The second player, when we mentioned that we do things differently, we said that DNA is really a language by all of its definitions, with its nuances is this, there are many genes, Lisa, where if you were to look at that gene as a standalone and if you was to look at the genotype of that gene, in other words, what version do you have? You think you have either the best version or the worst version depending, and you may think you have the best version for example, but it is not until you look at a completely independent gene that has nothing to do with this gene, that the version of that independent gene wow colors, whether your actual optimal version of gene a will stay optimal or not.

Speaker 3: (24:52)
Or conversely, whether you thought you had the suboptimal version of a bad guy, you read the full story, something else tells you what you fought was the bad guy was not the bad guy. Wow. And this is what it's called at peace basis. You see we're all concerned about epigenetics, which is important. FP genetics. How are we reading? Are we actually going to read that paragraph on the page or are we not going to read? That's at the genetics, but nobody's talking about epi. Stacy, this is Stacy. This is often, we've read the page after we've read the paragraph. We cannot yet make a conclusion until we read 10 pages later, 15 pages later, something there. We'll bring it to life. We'll color what we read on page three.

Speaker 2: (25:48)
Yeah, so, so for example, if you're, if you're looking at a specific gene and it has an, that is say the faster for the sip, 79A1 gene and the hormone a kiss guide. If it's a fast one that's not in and of itself a good or a bad thing. It depends on the other things. It depends on the, so that's what you're meaning. So one of

Speaker 3: (26:14)
The best examples of that is this, the BDNF gene, the BDNF gene, brain derived neurotrophic factor. What are the most important genes in the brain? Well, in the whole human genome that tells the brain how to secrete this awesome thing that heals the brain. You and I were having a conversation about a loved one, so that loved ones B, D and F was going to be hugely important. And how that loved one recuperated from the challenge that she had met BDNF. Now the beating of gene has an important variation. A snip this time, which is either a G version or a version. Okay. TheG version, Jews and George as in guanine is the optimal version of BDNF, the optimal version. So if you're a GG blessed, that's good. You are naturally predisposed. You have the in Harrods, the innate ability to make more BDNF.

Speaker 3: (27:13)
And let me tell you that's a good thing. Any which way you slice it. Wow. An independent gene, the TPH to gene the trip to five hydroxylase gene to TPH, two gene, which is involved in how the body deals with serotonin. K two has a sip. It comes in a G version and a T version G as in George T as in Thomas. The G version is considered optimal but hold on. If you happen to be GG fatigue, pH two and GG for BDNF ostensively both those genotypes for each affair genes are optimal, but if you were GG for both, it creates a haplotype. It creates a combination that is an act risk combination and it is, it is the negative combination. It is the, it is the deleterious combination when it comes to certain aspects of human behavior. These individuals, when you're GGGG, they exhibit poor inhibition of negative emotional stimuli.

Speaker 3: (28:28)
In other words, when something negatively emotionally affects them, their ability to kinship, the ability to say, you know what, I'm not going to focus. I'm not going to hamster wheel constantly play that over and over over again. They haven't, they have a hard time giving up that when something gets under their skin. So to speak emotionally, they have a really hard time getting over it so they have a strong imprint. The memory imprint, very strong EMI, emotional memory imprint and of course the stronger you EMI emotionally memory imprints, the easier you emotional memory recall EMR is because the deeper something is imprinted then the smallest cue. You have a love, you have a partner and you know you love each other to bits, but like human beings, you're going to have your ups and downs. I mean it's where human beings after all, and on one particular evening you were both getting on each other's nerves and she was wearing that beautiful red dress and that was the evening that you both said things you shouldn't have said and it hurts the person who has this phenomena.

Speaker 3: (29:36)
Whenever he sees his wife, would that red dress down the road, everything's perfect. You, you're going up for a birthday party, you're both happy, it rises back up. He remembers that evening more than he should. It brings back to the surface and vice versa. This is that Paul, inhibition of negative emotional stimuli that lead to profound memory imprinting and therefore profound memory. Recall. The point of all of this and the reason I mentioned this is, and we're going to come back to the GSTT one, was to clarify, you see Lisa, it's not just about even the type of things you're looking for. What matters is the interpretation we sell the combination, we are reading the manual, not just flipping, picking words out.

Speaker 2: (30:24)
This is we have a calmer is well we are the, the apostrophes are this is someone that is what they would be more prone to PTSD

Speaker 3: (30:36)
100 that's the point actually and that is further exacerbated based on the no adrenergic pathway which dramatically increases the risk of PTSD. It is exacerbated based on how quickly they are removing their dopamine and noradrenaline via content. So what happens is you begin to pixelate a picture and you've got a low resolution picture and then the more intelligence information you put in, you start to increase the resolution of that picture. You start to get a clearer picture of the person that you're looking at. But to do so, you've got to know where to pick slate. If I'm trying to get a better look at what Lisa's face look like, I don't really be pixelating your toes. I need to pick slick your face and this, this ability to read intelligently. Lisa, I stress intelligently. Riyadh, human genome. Yeah, that's what we do. We do

Speaker 2: (31:35)
That is absolutely insane. And they've vacations because yeah, I would have seen, Oh, you've got a G G G is good, but I've just understood that nuance, that combination of things. And now I can't wait to get my reports and my family reports so I could because this helps us also understand like the speed in which you are dopamine is processed and gotten rid off or the speed of which we're saratonin tone and all of these things have a fixed on your personality and that we're not 100% to blame for some of our differences.

Speaker 3: (32:12)
Oh gosh, no. Gosh, no. In fact, what this needs to do on the one hand, it creates the empathy of appreciating, look, this is how some of this is their predisposition. Now, on the other hand, it is not to create a sense of fatalism. While that's the way I am, I know I have found and I have done. The only thing that I've done, probably somewhat unique and special Lisa, is I have reviewed thousands upon thousands of profiles. In terms of my in the world, most of my peers that work at the level I do would say Dr. Mansoor Probably reviewed the most genomic profiles in the world. I don't know if that's true or not, but I certainly have reviewed several thousand meaning meeting the patient, speaking with their doctor, looking at their health profiles and looking at underlining genetic phenomena to see if we can understand what's going on.

Speaker 3: (33:00)
You know what I found, at least as a fellow, when you empower a person to understand a predisposition, you, you might think that leads to fatalism, but when you explain the functional reality, it actually does the opposite. It gives the person a sense of ownership and then they can finally say, you know, I have dumped with my entire life, I've been this way and I just, I didn't even know why it was that way. Now that I can even understand what's going on, it gives me some closure. Yes, but it now gives me something to appreciate. I can, I can envision how this is working, how my emotions are working. I can now go, you know what? As soon as I see that stimulus that would have got me on that slippery slope, I'm going to stop. I'm not going to go down that slippery slope because I know if I do, there's no coming back for the next two weeks.

Speaker 3: (33:52)
So what we've found is that this crew all around it just creates empowerment. Which brings me now to the question that you asked about GSTT one and you are, your connections are on point, Lisa, the connection between the detox mechanism of the body. Here's the threefold, and of course it's a bit more complicated, but it's also remarkable. You can take complex systems, break them down to building blocks and keep the acuity. So there are three building blocks we need to look at when we connect detoxification pathways in the body and the immune system. And the, the only thing missing is the inflammatory system. So the triangulation between toxins and immune responses goes like this. The human body's insulted with whatever. It's insulted with the intentional, the unintentional of our daily lives, those toxins enter the body or they try to enter the body. Step number one, how individually efficient is that person at negating bio transforming, neutralizing those toxins either before they can enter the body, such as in the mucosa of the lung, the alveoli lumen, the the lining of the lung, such as the GI mucosa and so on.

Speaker 3: (35:16)
And so what can we, can we neutralize it so the toxin doesn't even get into the bloodstream? And of course to the degree that it gets into the bloodstream, can we live a hepatic re detoxified so that at least it does not by you accumulate in the body so that at least it does not reach levels that are unsafe. First step number one now too, there are genes, there are whole gene families, their whole cellular processes, GSTs, glutathione, ionization, UGI, Ts, glucuronidation, methylation, self, phonation and acetylation. These are the major enzymatic steps linked to genetic genes that are responsible for bio transforming neutralizing things in our body, okay? So what we need to do is we say, what is the lifestyle environmental context of the person? What are they getting exposed to? I'll be living in a home that has written with mold, are they living and so on and so forth.

Speaker 3: (36:17)
Okay, step number one, step number two, how good are they at individually neutralizing those toxins so as to not bio accumulate them to the degree that those, whatever. The answer to that question is we're going to have an individualization and with some individuals are better at getting rid of toxins and others are not. If a person is not genetically, innately efficient, optimal at getting rid of their toxins, then what happens? Well, what do toxins do? Toxins cause cellular inflammation, okay? And they cause inflammation via any number of methodologies. They can inflame cell surface receptors, they can get into the cell and create overproduction of oxidants as they can hamper the energy modules, the mitochondria. That's one of the places you'd never want toxins getting to. And of course they can get into the nuclear eye. They can get into the libraries of the operating manual and they can start to change gene expression.

Speaker 3: (37:23)
So toxins do all of these things. Ultimately, you see Lisa 15 not even 15 years ago, 10 years ago, if you told that a medical conference, there's this concept of inflammation. You'd have a lot of professionals. Well, come on, you gotta be more specific than that. We actually now know that there is a phenomena called chronic inflammation, and regardless of what stimulated that inflammation, bat bacterial toxin B, it's an inorganic chemical. It be it a physical inflammation. It does not matter the way the sun looks, the way the cell begins to behave when it has been insulted with toxins, with exposures, remarkably is the same regardless of the stimulus. Because chronic inflammation has hallmarks that are similar regardless of the stimulus. Now at that juncture, when the cell is inflamed, when the machinery in the cell isn't doing the job that it's meant to do properly, that cell now starts to be like this pulsing red thing just by analogy.

Speaker 3: (38:35)
In other words, the body is looking at it going, something's happening in there. It's not behaving the way it should. Okay, so now we're going to have two steps. The body now has an anti inflammatory set of steps to quiet us, to bring the cell back into line cause they Whoa, Whoa, hold on. You're starting to misbehave. There's too much inflammation. This is where it's selling the process known as methylation comes in. Cellular methylation can be viewed. It's a detox reaction by the way, but it is a cellular cascade that is radically responsible for bringing your soul from that humming, inflamed, you know, ticking bomb type of modality back down to acquire essence behavior. That's cellular methylation. Now, to the degree that you're able to do that, because suddenly methylation is a multigene cascade, multiple places where things could be not as optimal as we would like.

Speaker 3: (39:36)
So to the degree that we then triage, we stratify the patients based on their detox potential. We then stratify them based on their anti inflammatory potential. Now, to the degree that we are not quite yessing that chronic inflammation, this is where the immune system can be activated. Immune system was meant to be activated in acute episodes, not chronic episodes. The more you ask the cell to produce antibodies, IgG, IGA is IGMs, particularly IgGs. The more you keep telling that the body pump out IgG, something's not working right, something is there, which is why chronic infections are now very well understood to be linked to autoimmune diseases. The infection did, did not go away, constantly demanded of the body to produce antibodies. And somewhere along the line those antibodies begin to forget what was the bacteria or what and what was the self. And now we just start shooting friend and foe alike. Wow. This is the triangulation that has become now a focal point of so many diseases. Some diseases being more relevant to the whole, you know, things like lying disease. Do you guys have lung disease down in New Zealand?

Speaker 2: (41:05)
I think, yes, we do. And I think you know we have a massive problem with like thyroid, Hashimoto's sort of autoimmune diseases, crones, IVs. So this is, this is where the body is actually going in overdrive. So the, the original detox genes haven't been able to do their job because combination.

Speaker 3: (41:26)
There's that one. Exactly. There's inflammation. Yup.

Speaker 2: (41:33)
Yes.

Speaker 3: (41:33)
Methylation didn't do the job that was supposed to do and now we're triggering. So there are meta-analyses meta-analyses that show the deletion of the GSTT one gene or overall poor Ghouta finalization has been strongly linked with ulcerative colitis, Crohn's disease, IBD, strongly linked with ectopic asthma, particularly GSTP one in early childhood asthma. Then of course, if you, if you double down on poor math on poor detoxification with poor methylation, you really start seeing

Speaker 2: (42:10)
Clinical outcome. Yes. Yeah. So, so if we then we, we, we find out all this about ourselves. We find out we've got either the good or the bad and the ugly. And these combinations are not ideal. Then how, you know, we've got this information now, now we want to know what the heck do I do about this? I can't change my DNA. Of course, all things that these reports that your company does, for example, where it can actually lead to some successful outcomes. Obviously avoiding cigarette smoke or exhaust folk tunes and things your GPS deleted. But, but beyond that, nutraceuticals, new nutrients what can be done to help people.

Speaker 3: (42:52)
So it starts with, so the first thing I would have to say is we take our reports only so far. So the actual report, we take it to the point of explanation of what's happening. And there are certain recommendations, but the real magic must still come from a trained population, you know? So what, so what we do is through also training a certain class of healthcare providers. We might call them the, the new modern day biohackers. The healthcare providers who are really sniff, they're no longer just, you know, pill pushers. They're looking. So I just wanted to clarify. We take the reports, we explain the systems, we explain what's happening, but we also have to be careful so that people aren't jumping to conclusions and self-treating based. So you still want to have someone who understands the bigger picture. And by the way, that's the second part of what our company does.

Speaker 3: (43:47)
As per my travel schedule, I'm constantly traveling, teaching people, teaching auditoriums full of doctors who are now saying, listen, if I keep practicing medicine the way that I'm practicing, I'm just dealing with a disease population. I'm not healing people. Okay, so with that minor clarification, now we come to, let me paint a picture, paints a thousand words not to be, you know, blahzay here's what I like people to picture and here's what you would want to picture for yourself. Lisa. Picture slide. Okay, so there's a slide your screen, okay, and a circle. And then picture a circle on that screen somewhere on your screen. There's a circle. Now because you're a human being, your circle is going be on the screen. In other words, this is the screen of all human beings and your circle, you, your circle is somewhere on the screen or what does the circle represents? It represents your genetic makeup, which represents a part of your genetic makeup for whatever biochemical process we were studying. So this circle is Lisa's genomic pathway. Okay.

Speaker 3: (44:56)
I want you to then think of an equilateral triangle that equal three sided triangle that just perfectly encompasses your circle just perfectly. Your circle is perfectly encompassed just right in that triangle. And the emphases of this triangle are labeled environment, lifestyle and nutrition. Yes. What we're learning and what we're recognizing more and more is other than extreme cases, other than extreme cases, and there are mind you extreme cases where a particular genetic combination was really just a real doozy. And in other words, we're going to see some, you know, with the best of efforts, we're going to see some probably deleterious outcomes. Fair enough. But other than those extreme cases, for the vast majority of us, the spite, any inefficiencies we might have if we find the right triangulation of lifestyle, nutrition and lifestyle, nutrition and environment. If we could figure that out and it perfectly matches, I would circle.

Speaker 3: (46:08)
This is optimal health. So image, the image of optimal health is when you can find your genomic makeup, your circle for whatever you're studying and contextualize it perfectly within the right for you. For Lisa Laughlin, sir, not for Joanne Felisa. What is leases? Optimal lifestyle, nutrition and environment. Now the problem is, Lisa, when we begin working with a patient, obviously and clinicians with their patients, the vast majority of individuals, they do not know their circle. They don't know what's the economic influence. So they don't, and if you don't know your circle, your triangulation, choices of lifestyle choices, nutrition choices, and environmental choices offers skewed and they are not synergistic with your circle. So first objective of this, did you get that picture? Do you know when people say, well, it depends on your genes, your genes. It depends on how you're using your body. If you are, if you took, if you took five identical individuals, they were, you know, quintuplets identical, contemplative.

Speaker 3: (47:27)
If such a thing exists in today, the same genes and you give those five people at 35 years old, the exact diet. But if those five, one of them was an ultra marathon runner and extreme sports enthusiasts, the other was a couch potato, I don't know, doing whatever the other was a, you know, an accountant who had a nine to five job. We can exercise worrier, but from Monday through Friday really just goes to work, comes home, eats, goes to that and so on and so forth. Even with the same jeans, you can put the nutrition and an obviously not expect the same outcome because they got to know the genomic legacy. You've got to know what is the lifestyle context, what is the nutritional context, what is the environment or context? If one of the things quintuplets moved from your gorgeous country and move to massive metropolis with, you know, air quality, that breathing for one day is the equivalent of smoking a pack of cigarettes in your beautiful country.

Speaker 3: (48:36)
He or she may have gotten away with a GSTT one or GSTP, one suboptimal ability. He's living in those, you know, that wonderful country views. He's practicing otherwise good, not eating foods with pesticides and herbicides and so on and so forth. And he was going about life actually, not really realizing there was any suboptimal ability until one day his job took him to a big metropolis somewhere. He lost track of the quality of his foods. He's just so busy. He's day in, day out breathing the equivalent of a pack of cigarettes and then six months into this, all things ELLs as equal, his jeans are equal, but he now starts to show symptomologies that he would never have had any different environment and a nice clean environment. Right? So this triangulation is so important. Now coming back to the specifics, once we understand the pathways, we begin first with the dose.

Speaker 3: (49:31)
It may seem simple, but it actually enters Lisa into, it's not just about the obvious things that you might imagine. I give the example, Lisa, and by the way, it's relevant to the GSTT one gene. Now, juice, TT. Let's focus on the T one. It's the big sister in the glue, the fine fabric. So GSTT one no, it's what's called a phase two detox pathway. Phase two detox. Because when it talks and enters the human body, we typically go through two steps. We take toxin a, we converted into an intermediate B. Yup. We take B further, convert that to C. C is what leaves the body, the B to C part of the transformation. That's where the GSTs come in. The a to B. This is where your cytochrome P four 50s come in. That's the phase one. Bio transforming enzymes. Now if I were to ask you something, when you say fiber to say, would it be a good practice for person to start drinking a nice cup of green juice?

Speaker 3: (50:38)
You know, like some juice, juice, broccoli and some maybe put a little bit of a baby spinach in there. A bit of ginger, maybe some cute, cute curcumin at the end of it. Would that be a really healthy drink? Yes. Something I do every day. Beautiful, beautiful. And it is healthy generally speaking. So now someone puts a blog together giving this recipe of something that's ostensibly so healthy and there's this mechanic who works in a shop all day with fuse and so on and so forth. He read this blog, she read this blog and she decides that before she goes to work, she's going to have this beautiful juice. This green juice that they read was so healthy and it was a detox juice and they feel good about themselves. Hold on, hold on. Many of the ingredients and not green juice. Many of the ingredients in that green shoes turn on certain phase one sip four 50 enzymes so as to accelerate the conversion of a to B.

Speaker 3: (51:54)
Now some of the toxins a that this mechanic was facing in her shop, in the, in the, in the mechanic shop that she was working at, when she converts a to B, we know that the B, the intermediate is truly more toxic than wow. And by the way, she did not know she was a GST one deleted individual. Oh, so what did we do to this young woman? We encourage the things that is that we're getting into her body. When she drove that beautiful healthy green juice, she more rapidly converted her A's into B and then ups B's and to CS very well. Wow. Even something that would ostensibly be really healthy by normal standards. Do you see that's a healthy nutrition on the triangle, but we did not ask what was the environment on the triangle and so now we have skewed her triangle away because her genetics circle, she does not have the GSTT one. Do you get that picture? This is a little bit frightening for people who are listening to this or who might be going well, what's the point being?

Speaker 3: (53:16)
This is weird. The reports have the super value, isn't it? That's the point. It's, it's actually not discouraging. It's, it's finally, and this is all gold. It's finally meant to unravel those nuances that there is such a thing. Have you been? How many of us, you know, we do something that 20 or the coworkers swore was the best thing since sliced bread and then we tried it and not only did it not work, we actually felt like crap or less healthy, and we, we're all aware of this until it's what is it led? It's led for most of us to become numb. We're just kind of get to that point where we're like, well, I don't know what's right for me or run for me. Plus today it says one thing tomorrow it says another thing. So creating some sanity from this confusion is what this goal is about and it can be done.

Speaker 3: (54:11)
Lisa, when you take your time to read things, intelligent meals, explain things. That's why we've got these epiphany moments that constantly, I like my consults with patients because I feed off of the energy. When a patient just, you see that epiphany admission and they light up and they go, Oh, that's why this hasn't been working with. That's why that was better for me. That's why I took methyl B12 because everyone's telling me methyl B12 is the best version. But every time I take methyl B is it just in my head. I get a headache every time I take micro B12 I get a, and then I go, no, actually I got one too. I can't take methyl before. That's an actual thing. I can't take methyl B12 because my methylation cascade is inconsistent with me taking methyl Beto when I take a dental Sobe 12. Oh, completely different.

Speaker 2: (55:07)
Wow. So this is getting really granular for each individual. And this is what makes me so excited. And, but before we go on, we have to go and cover off the hormone report. This is something that I and, and this is, you know, for me and any woman, but I wanted to focus a little bit more in on the woman. We've got very complicated hormones, households, but this was the cascade for men and women is very, very similar, isn't it? Yes

Speaker 3: (55:33)
It is. It's just remarkably, this is what we taught at the cost on the weekend after introducing genomics, it was the first open to eyes that the cascade, the circadian rhythm with which the human body converts progesterones into androgens, androgens to estrogens, men, we do not have a monopoly over androgens. Women, you do not have a monopoly over estrogens. In fact, your estrogens come from androgens. Men, we have estrogens. It's just a matter of the circadian rhythm. When is it happening? How quickly is it happening? And of course, ultimately how much of any of these hormones are produced. And then the final component is how responsive are you, the the woman's body, all things equal. She's designed with the estrogen receptors to be more responsive to estrogen. She responds to androgens as well. Conversely, for men. Now keep in mind something as simple as, I can't believe how many clinicians do not realize how an androgen or estrogen receptors.

Speaker 3: (56:32)
Now let's stop there for this cascade. We can talk about all of the things about how hormones are produced and how they're metabolized and so on and so forth. But ultimately, how is estrogen affecting your body? Lisa, you're a young woman. You're making estrogen as if you're menstruating or if you want hormone replacement, there's likely some estrogens in your body, one way or the other when estrogen binds to your estrogen receptor. And to the degree that that can happen, mind you, because there are variations to that fidelity, this complex estrogen. So the estrogen receptor androgen to Stastrom, DHT to the androgen receptor. These complexes are some of the most potent DNA transcribing complex. They go into the nucleus and the churn on genes. This is how estrogen and testosterone impacts the human body. They live. They're not just, I don't know, causing breast development or, or, or, or Andrew demise in the book.

Speaker 3: (57:39)
They do that by churning on the genes that cause the cells to behave in a more underutilized manner or more estrogen. So the first thing I want, our audience needs, our clinicians, we need to re re climatize reacquaint ourselves with that. These hormones potently DNA transcribing, they go into the nucleus and they turn on and off genes. That is why they are not to be dealt with trivially. Number one. Number two, in a menstruating woman. Now I just told you when estrogen enters a cell, I did binds its receptor. It's not just staying in the, in the Maloo of the South, it's going in to the volts, the nuclear volts and churning on and turning off genes. Wow. When you look at the ministerial cycle of, of a, of a relatively normal, repeatable menstrual cycle, you will notice something radically important over the course of 28 days.

Speaker 3: (58:43)
The human female body isn't exposed to estrogen at the same amount every day, not at all. The human female body in 20 days only has about a six day or so window in which your estrogens that are really elevated and then it comes down. In other words, what is this telling us from a human biology perspective? It's saying that the type of gene expression changes the epigenetic phenomena that estrogens cause on your operating manual. You don't want that to be consistent and constant across the month, and this is very frightening when you look at contraceptive pill or hormone replacement therapy. So it's most certainly very frightening. That is not, let me be clear. That is not to say that there isn't a place or a time for these things. You know they are absolutely a young woman has to have the right to how she treats her body and what she does.

Speaker 3: (59:47)
But there is a place in time you at least be equipped, at least be empowered before you make this decision as to a knowing what it's doing for you. Say, okay, look for these few months of my life, for these couple of years of my life, this is going to be a bit more important that I take these precautions, for example, but you should know that to do so indefinitely, month after month, year after year. Now they've got clinicians encouraging young woman not to even have a bleed through. There's no point for even the bleed. So just stay on the, you know, constant level, 24 seven three 65 15 years. How is this compatible with normal human physiology? When you understood what I just said? Yep. Now let's go a step further than that. You see estrogens do what we just said. They bind their receptors, they go into the cell so they go into the nucleus.

Speaker 3: (01:00:47)
They change gene expression as they're meant to for brief periods during the month. Fair enough. Now, once those estrogens have done what they've done for those days, then the point of it is there's a circadian rhythm. The body breaks down those estrogens metabolizes them by a transforms them so that they're no longer active. They've been neutralized, and then we hit repeat, rinse and repeat, and we start a new cycle. But here's the point. Every a woman, Lisa, every a woman, a man for that matter, but let's focus on the ladies when she made her estrogens or she took her estrogens, because even whether you take it or whether you make it innately or you take it, it doesn't matter. You've got to metabolize the estrogen. Now, every young woman can metabolize estrogens into three byproducts. I estrogen 400 Z estrogen, 16 hours for hydroxy estrogen. Every human being does this, and this is a crucial point.

Speaker 3: (01:01:49)
Absolutely. But these three metabolites do not impact yourselves in the same way you say. If you thought of it, you've made the estrogen small window. Now you want to neutralize it so that the body isn't under its constant influence. So you want this metabolite, this estrogen, this hub light to have lost bind to the receptor. You want it to last. It's estrogen Ising properties. Lo and behold, four estrogen, one of those three metabolites retains the ability to bind the estrogen receptor. In fact, some studies show it might be an even more potent comm when it, when it binds and it creates this, this common, a tutorial, Leiden and receptor, it's DNA. Transcribing effects are even more potent, much like the analogy between DHT and the androgen receptor versus testosterone. DHT dihydrotestosterone, which is a metabolite of testosterone, has a higher potency binding affinity to the androgen receptor.

Speaker 3: (01:03:00)
Four hydroxy estrogen is to the estrogen receptor as DHT is to the androgen receptor. Wow. The ability innate tendency of a young woman when she's faced with estrogens to make either the two hydroxy which is considered protective because has lost or the four hydroxy that inmate differentiation is radically genetically determinable. Now, if something as simple as that, Lisa, when you stitch these things together, when you understand, look, estrogen should be my body needs security and rhythm. I do not want estrogen is constant. When I break down those estrogens, I want my body to have had a break from them. And you did not know whether you were four hydroxy dominant or not. If you had a tendency to make more of the four hydroxy than the two and why is four hydroxy so naughty? Three reasons. A, it binds the estrogen receptor, not giving your body a break from the estrogen ization one to four hydroxy estrogen if you are not flushing it out of the body and how do you flush out for drugs, the estrogen through methylation, the comp gene, which is catechal methyl transfers an oops.

Speaker 3: (01:04:29)
Can you imagine if you were innately genetic info, hydroxy dominant and have the slow comps because now you're making too much four hydroxyestrone you have a tendency to do so. You do not have the enzymatic ability to get rid of it. Now you buy your stagnate, your four hydroxy Astrid. Do you know what full hydroxy estrogen does other than binding the estrogen receptor and Quinones? Quinones? Listen, my God, you're speaking more than some of the best medical biologists that I've spoken to. So the, the decompose into Quinones and do you know what Quinones do? They get into your DNA. They stick to, they are mutagens. They stick to your DNA, causing the DNA to not be able to unravel and repair itself and by the Quinones then cause accidents. So here's what you don't want to be. You don't want to be the young woman who is genetically predisposed to overly produce four hydroxy estrogen simultaneously, have a poor comp, simultaneously, have a low GSTT one GSTP one, which was the thing, Quinones, and then have a poor mitochondrial superoxide dismutase or antioxidation to get rid of the oxidants

Speaker 2: (01:05:52)
And add to that. You're in your forties or your 50s and you're making more EstroZen,

Speaker 3: (01:05:57)
Which is a breast tissue because it's not in the liver anymore. The liver organ, at least it was designed for that type of metabolism. You're doing this in the breasts, you know, God forbid. Okay,

Speaker 2: (01:06:10)
This is where the cancers can come in

Speaker 3: (01:06:13)
This is weird and just why we have the the epidemiologic rise during that shift where the woman's body shifts from doing that grunt work in her liver, which was designed for it to doing that grunt work in such as breast tissue, cervical tissue, an ovarian tissue and so on and so forth. Which of course the human body, the female body does not express estrogen receptors, the same level for every cell type. You know, when you were, we lobby at nine years old and you could have gone outside, you know, flat chested like any other boy and you know, and then when, when men awe kits and the body changed your elbows and forms didn't change, it was suitable zone. Those are the zones that have more estrogen receptors.

Speaker 2: (01:07:03)
And this is so this is how we can see like when you're looking at the phenotype, if we can go look like the the the hormone cascade just for people that are listening, it's going from producer owns and pregnenolone's into testosterone's which can sometimes go into DHT and which then go into the estrogen. Is thrown in your estradiol if you're pregnant when you're older you have more strokes coming in which are, that's coming from the the other top of testosterone isn't it? One on one and then it's means a lighter than these three path rates into the two hydroxy four hydroxy and 16 alpha hydroxy, two hydroxy being the good pathway and anti inflammatory. The four hydroxy being the dangerous one and this is where you've got a lot of PMs symptoms. If you've got your breast tissues like talking person on the end, this is probably too much information, but month like I've been on hormone replacement therapy and this is why I'm so excited about the hormone situation because obviously I've been put on a standard dose all the way through. It's DHT.

Speaker 3: (01:08:16)
Now all of those can turn into, other than the DHT, the progesterones testosterone, even D H E A to the estrogens. The DHT will have gone past a pathway that it's not going to come back to estrogen. It can, by the way, reverse pathway affects certain things. They send signals back up the chain, the body. Oh yes, absolutely. The body is always looking for, you know, but I mean that's the whole way in which the hormone in which the pill, the contraceptive pill works, that when you give estrogens to the female body, the female body says, well, hold on. If I'm getting it from somewhere, I no longer need to make it internally because it's just showing up. We don't know where it's showing up from the body speaking to itself, which by the way is why when a lot of women, when they take the, they go on the pill, they find certain degrees of waking, loss of libido.

Speaker 3: (01:09:12)
Why? Because when you took this premade us, of course, this is not for all women because it depends on the genetic cascade, but for some women you give them estrogen premade and the body goes, well, I know mama need to make estrogens. If you don't, if you no longer need to make estrogens, what were you making? Estradiol from testosterone. And so if I go give the female body just extra dial and she goes, well, I no longer need to make my own Estradal do you know what? Ellis is not going to be made very efficiently. You have to start strong. That's why so many young women, they go on the pill, they find not all. They find the libido tanks on them. They find that they gain weight, they find that their body goes into an estrogen dominance and of course they OBG or they go, Oh no, that's, don't worry.

Speaker 3: (01:09:58)
No, that's just normal occurrence. Well, it's not a normal occurrence on this. You know what your pathway is. Are you shutting it down permanently? Like if you're on the pill box, these are, these are epigenetic feedback phenomena, right? Because remember when that extra dial enters the gene expression profile. So think of a think of a Rubik's cube, okay. And think of a Rubik's cube that has been mixed up. Okay. And it's, you know, it's been, it's been altered in whatever way, all of the combinations of the colors of that Rubik's cue in that time and that mode that's representative of the genes that are on and off at a given period of time. And so think of a particular Rubik's cube and that particular mix is what happens when there's estrogen izing going on. Okay. Now the Rubik's cube needs to go back to its pre solved mode where everything is nice and set, okay.

Speaker 3: (01:11:02)
The time with which the gene expression, the time with which it can revert. This is a critical phenomena. It does revert, but it tends what the storylines, so for example, the gene expression, the pro inflammatory gene expression changes caused by the insulin insulin receptor complex, almost an identical phenomena. When insulin binds to the insulin receptor, it leaves the cytoplasmic membrane, goes into the nucleus, just like the AR testosterone, ER estrogen receptor and causes gene expression, the insulin insulin receptor motif. The gene expression that it causes is very pro inflammatory, very proinflammatory. Now the body can return to its non-interest inflammatory status within hours to days for the estrogens and the hormone cycle. It takes longer.

Speaker 2: (01:12:06)
So you can this will be affecting woman's fertility. I mean, I've had fertility issues and I was ill from the age of 13 because I had issues. So they put me on the pill to mask these issues. Now what I'm expecting to see in my reports when they come back, and I don't know that I have a dominance of four hydroxy because I've had fibroids and so on and infertility and, and all of these sort of concomitant sort of problems. Now I just want to go in a little bit deeper into this. What is your take then? Is it possible to have hormone replacement therapy? Because obviously there are benefits to having these hormones in our body. The aging, can I, will I be able to, you know, and not just me, but will I be able to tweak it so that I can get the right amounts on the right days of the produced around the insurgence and the DHI and be able to do that safely without causing cancers and so on.

Speaker 3: (01:13:07)
So it's a brilliant question. Now we've must answer that question is, and so let me just say this, and this is not just to be a blanket disclaimer. I am absolutely emphasizing being on a birth control, whether it's a pill or not being on hormone replacement, BHRT or versions of it. Not only is it appropriate in certain separate circumstances, it's lifesaving. It's life transformative in a positive way. In many circumstances, we were by no means saying, or even trying to hint that it should, that women, young women meant menopausal, but should be deprived of this by God. No first to begin with, despite any evidence of the O the other. That's a young woman's body. She makes the decision what's happening to her body. So no two ways. We're not tenting of that. What we're saying is everyone and the scientific literature, we understand that the outcomes of these things, the outcomes of a hundred young woman going on the same birth control pill, a hundred young, middle aged woman going and home and replacement, we absolutely know that there are differential outcomes visiting risks for certain deleterious outcomes, be the strokes on the pill, be the country effects or others on hormone replacement.

Speaker 3: (01:14:25)
We know this happens. So what we're trying to say is do we just leave it as a statistic? Do we just say there's a 10% risk increase? Or do we say, look, you fall in the bucket where we can really tease out, are you specifically the person that is at risk or conversely beautifully, you're not the person that is at risk. So if you do choose to be in BHRT, you can do so now without necessarily that ghostly whisper, a fear that many young women have even when they choose to go. So it works both ways. Now. Now to answer your question, when you understand that these hormones are causing gene expression changes and these gene expression changes are what bolters cell behavior to any number of outcomes, we need to stop looking at hormone replacement. If we're going to do it intelligently, we've got to start to understand that the human body is a cicadas Ian creature.

Speaker 3: (01:15:29)
Yeah, we are. We are circadian within our 24 hours. We have circadian within monthly. It's why ancient wisdom talks about the moon cycles and so forth. There's actually wisdom in these things that the human body is a sick Cajun creature. Even the foods we eat, the different seasons. Often when you look really carefully, they, they and the people who were indigenous to that religion, it's speaks to certain nutrients that the body needs more at certain times versus other times. It's one of the reasons when we coach people, when we talk to people about taking micronutrients, we are by no means a four. In fact, we are against the one-ton, you know, 50 million things. If micronutrients every morning at 7:00 AM gobble, gobble, gobble. Because that's not how the human body was designed. You know, even if I told you you needed these 15 ingredients at these different concentrations within 24 hours that you need your body needs, that it doesn't mean that I can give you the 15 things all at once at 7:00 AM no, these nutrients, the body, because neutrals do what they get into the cells.

Speaker 3: (01:16:42)
They act as building blocks, but they also act to change gene expression. And again, I want you to to, to focus on the fact coming back to the hormones that these hormones are causing gene expression changes. So the first thing we have to do is we need to become better acquainted with what are the healthy changes that hormone replacement is accomplishing. Not just what is healthy, but when is it healthy and the amplitude of the changes. All three things are different, but yet correlated the what, the when, and the how much of the change. Okay? Now secondly, we have to understand that when we take hormones as part of an anti aging or or rejuvenating or simply actually therapeutic, forget auntie, just simply therapeutic. For this, for this menopausal young woman to be able to sleep, for heaven's sakes, and to be able to know these are things you can't tell this young woman, she shouldn't try a healthy BHRT protocol, but when did we realize what the home ones are doing?

Speaker 3: (01:17:53)
Think about it. Are we supporting the mitochondria? Are we changing gene expression causing the cells to behave differently? But we've paid no attention to other mitochondria. The energy power plants keeping up with the changes that we're bringing about because of the gene expression, because of the hormone replacement. Are we doing that? Are we are we accomplishing based on nutrient protocol that which was better suited for these changes? So the, that's the long lens. The short answer is this. Therefore most certainly can. We come to a genomic to a hormone replacement protocol, but we need to look at the individuality. You see, quick granularity. A woman converts her pregnant alone into her androgens via the gene sub 1781 CYP 17 alpha one. This gene and its associated enzyme comes in a faster version and a slow version. Slow here is not bad. Slow is actually desirable.

Speaker 3: (01:19:01)
It's the beneficial version. So in other words, by comparison to the fast version of the enzyme, the slow version of pregnant loaned to androgen is universally considered all things equal, healthier. No, just that one. This one piece of information a young woman has the fast sub 1781 a young woman has the slow sub 1781 I choose to put them on hormone replacement. She chooses to go home with a bracelet with pregnant alone progesterone. But by giving these two women the same progesterone dose, the potential that is brought about in the young woman who had the fast sub 1781 is more than the Andrew divinization potential than the young woman that had the slows, etc. And then of course I made my androgens, but then of course my sip 19 a one aromatase is going to take that to Stastrom and converted into extra dialogue or that understand beyond and converted into a strong, and by the way, the aromatase, 1981 comes in a faster medium and a slow version.

Speaker 3: (01:20:10)
Did I know which version this young woman has? So should she be on a protocol that is progesterone to SaaStr and the estrogen is she was, she had the fast 17 I'm fascinating. A woman that has a fuss sip 1981 and the fast sub 1781 and this put on a triad hormone replacement. She's going to be a young woman that quite likely we are all over estrogen [inaudible] because everything in that cascade, the progesterones are going to androgens. The androgens are going to estrogens, the estrogens. We're giving our estrogen problems, God forbid, and there will be a disaster for that. When a woman says she would be at risk for both, this is what we've clearly shown and repeatedly shown in the data at least I can't tell you how many young women fall into the buckets that they were four hydroxy dominant with poor content or poor detox and they should.

Speaker 3: (01:21:19)
Again, we're talking about we see thousands of patients, not tens or hundreds, thousands. And I can't tell you how many young woman, if that category came to the clinic thinking they had Lyme disease because it's a phenomena and it's a problem here in South Ontario, Northeast America. Why? Because four hydroxy estrogen and Quinones cause the same neuro inflammatory effects as newer Berlioz's you don't, I just had to ask them one question and they were convinced they had chronic Lyme disease and by the way, the tests were coming back negative, are you for Lyme testing at the most sensitive levels. And I said, have you been pregnant in the last six years that you taught? You had lying? And then the young woman said, yes. And I said, did you notice that while you were pregnant, your symptoms went away? And her eyes opened up and she began to cry and she goes, [inaudible], I actually told my husband, I wish I could just stay pregnant because when I'm pregnant I get a relief from all of my symptoms.

Speaker 3: (01:22:21)
And then I had to point out to her, when you're pregnant, you as trial dominance and your body isn't making the four hydroxy estrogen, what are you getting when you're pregnant? Is you getting a relief from extra toxicity if you had Lyme disease, Lyme disease, this doesn't take a holiday during pregnancy. Right? And so the estrogen dominance and estrogen toxicity, I was a two different, two different, absolutely. A woman can be estrogen dominant and be perfectly nontoxic. She, you know, she, she has a certain physiology that's consistent with her estrogen dominance. She lives her life perfectly healthy because when she makes those estrogens maybe a bit more, you know, body type, but she's breaking them down efficiently. She's methylating the two hydroxy efficiently and a little bit of four hydroxy. She's detoxifying the GSTs and the soup and she's as healthy as can we being all things equal her how her diet or lifestyle environment.

Speaker 3: (01:23:26)
So you first should determine what we call the androgen estrogen balance. So where are you on the, on on the spectrum from androgen dominance to estrogen dominance? Rubin, this is relevant to men and women. Okay. So where are you then off to that you go, depending particularly for the woman, depending on your estrogen dominance or not. Where are you with extra toxicity? See how many young woman Lisa, they were extra toxic, extra toxic, meaning they, they had the predisposition, there's sip one B, one surgical P for 51 B one which is the enzyme pathway to go to the full Hydrox agent that was dominant in them. They may or may not have had the low comp and other features. They will extra toxic, but they will, I'm sure dominant. Then we go. So that as a, as a teenager, these young women, they were more athletic, leaner. They did have some irregularities with their menstrual cycle. Mind you often times, but they were lean or they were able to put on, you know, not very, not much wisdom development, leaner cut, muscle strain and so on. And so they were Andrew dominance.

Speaker 3: (01:24:46)
But then because of wanting to normalize their menstrual cycles, sometimes they get, now during this period of time they were underdominance blessing, which was come a flashing, the extra toxicity. Now you put this young woman and you go and you give her premade estrogen, which her body had not been doing in an almost self preserve in this, in this beautiful, miraculous way in which things tend to occur in the right combinations. But now you go there for estrogens, what have you done? You have literally pulled the Komodo open and exposed her extra toxicity and then all the things that you start seeing happening. And by the way, we've had ideal thanks to brilliant young scientists, dr Dan Turner and his mentor before him and the Walsh at the red bull high-performance division. So of course you certainly know, but the red bull, high performance athletes, we, Dr. Turner and I, we have screened many of the most elite Redbull high performance athletes in a, in a, an amazing program, but that the chairman has put together, including the genetics and the genomics that we do.

Speaker 3: (01:26:06)
And along the way we met these, you know, goober, athletic young movement that works so high-performing, but at a certain point, you know, early twenties for other personal reasons, stuff went on the pill and all hell broke loose in terms of health body weight metrics and you know, per per performance that is only to very classically observe that she was the very fact that she was such a really good triathlon. Try athletic young woman per the body type was, she was a very unsure Dominic JIA woman. She was antra dominant but didn't realize she was extra toxic and that extra toxicity only showed its ugly head once she went on the birth control pill. Wow.

Speaker 2: (01:26:52)
And then does the sporting performance change? Do they get more hip FLIR brace development and new light? You know,

Speaker 3: (01:27:03)
I mean I'm somewhat embarrassed by the degree of accuracy. If I see a young woman's genomic profile without ever having seen them, I could actually predict body type. I can predict proclivity to Southern lights. These are not by the, these are not Lucy goosey. This is real post inflammation, vascular events, propensity for adipose tissue development. And that position, they're all driven to a large degree

Speaker 2: (01:27:33)
Awesome pathway. And this is where it's so frustrating, you know, when you're dealing with we, you know, we coach 700 athletes and we've got a lot of women who are athletes and who are striving with the weight despite perfect diet, what you would consider a very good diet, exercising crazily. And then they, they, they still putting on weight. They still got cellulite, they're still got, and they're like, what do I need to do? Why don't I look like that girl down the road? Who's exercise one iota? Like, you know, Elle McPherson? What is the difference? You know, it's very, there's a really

Speaker 3: (01:28:10)
Personal things that, that can really needle away, can really erode away at yourself. Confidence. Not because of not being body encompassing and being proud of yourself. No, that's not the point here. The point is to the degree of what you, a young woman or young man thinks they're putting in and they're not seeing what they perceive to be the outcome, you know, they begin to go,

Speaker 2: (01:28:34)
One, am I doing it?

Speaker 3: (01:28:35)
Why am I doing it for right? And so to help them a have that epiphany, the epiphany moment it says, by the way, when I asked a young woman and I say, look, have you started noticing, well do you notice per your Pernod looking at their profile? So they're like, why are you asking me this? When I say, have you noticed the three to five days prior to your menstrual cycle, you really get a bit more breast tenderness and you know, nipple tenderness. Yes. So those three to five days prior to menstruation are the days that your body is particularly to the degree of your, the, the, the hydroxy, the four hydroxy two hydroxy, that's when those things are accumulating in the body. And if you happen to be more four hydroxy dominant, you're going to show profoundly more signs of inflammation. And of course as you get closer and closer to that pre perimenopause period when you become more estrogen dominant, and hence the four hydroxyl Strohn is showing up in the breast to Seymour and hence the symptomology, right?

Speaker 3: (01:29:36)
So once you can show these young woman that thought was that they just fought, were, you know, just a narrow personal, crazy perception, they just never could understand it. And you join the dots for them. What you've done here, Lisa, is you've empowered them and it's not fatalistic. And then brings to the last point to the degree that you see the pathway is to the degree that you might then often, not always, I want to be clear there, they're still phones. You know, when I teach Lisa, the first slide that I put up says humility have to have the humility that by no means do we understand everything far from it far from it. But should that leave us feeling and capable to act? No. Because of the things that we do know. And as we're continuing this, this has been the way that any type of health and medicine is practiced.

Speaker 3: (01:30:33)
You practice what you know to the best of your ability and the more you understand, you bring it in without choking on it. You bring it in bit by bit until you find that happy place where your body and, and the other thing, Lisa, is once you understand these gene expression changes, keep in mind the diet, the lifestyle that was potentially the work for those things that were potentially optimal few in your 20s you might often the not copies sitting in your forties going, well that's what worked for me in my twenties well the way in which your genomic manual was being used in the 20s is not the same. It's the same genomic millennial, but it's not being used in the same way 20 years later or 25 years later.

Speaker 2: (01:31:22)
Oh this is just absolutely mind. Like talk to me. So I could honestly, I'd love to just sit for days like this, learning from you.

Speaker 3: (01:31:33)
I've, I learned, I learned more honestly and I don't, I'm not just saying that because these are the conversations that you know, as you digest these things and this is what's going to happen, Lisa, God willing when you and you will, we will do your profile together. You are the N of one, right? So when you learn about these things, what happens is you, the person who then starts to sit in soup a minute, hold on, is this related to this is this symptomology, is this? And that's where the data comes from. That's the only that cause no one collects N of one data points. In fact, it's the variant of a meta analysis. It's the antithesis of that analysis. But data is at the end of one. That's where your data is out, you know. So for example, you know, this is a coolant and maybe as we wrap up with this I know ask individuals, I say, you know, do you happen to be one of those individuals?

Speaker 3: (01:32:32)
And when you get an insect by just, just a regular regular insect, like are you the person for whom that insect bite stays flared up? You know, it, she and ERC's some much longer than the average person as we know, some of us that have. And if you say yes, it's an awesome predictor that your methylation cycle is suboptimal. Oh wow. And not just that. It is almost always associated with the suboptimal SHMT one. And MTR suing hydroxy methyltransferase and methionine synthase. Those two genes when suboptimal in the methylation cascade is extremely closely correlated by asking a completely benign, completely mundane question, what insect bites you would be amazed by the acuity of the association. Because the inset back inflammation we said very early in the Columbus, inflammation is inflammation. It doesn't matter what initiates the inflammation. If you are unable to douse the fire of your inflammation, whatever caused it, be repetitive joint injury, be it surgery, be it bacteria, infection, viral infection, toxic inflammation, your methylation isn't working properly.

Speaker 2: (01:33:50)
Wow. So these, Oh man, these insights have just absolutely this, this is gonna change the entire one. I'm hoping it will. The entire medical model, you know, w drugs that we're taking, the hormone stuff that were taking [inaudible], I mean T S Wiley and the cyclic nature of the hormones. Going back to the hormones. I'm in the middle of her book at the moment and the whole cycle. And joining the dots. And then, you know, we, we do also epi epigenetics, which is again, another important piece of the puzzle.

Speaker 3: (01:34:25)
Hugely important, hugely important. Lisa in New Zealand. What's the first new one for fatiguing, baby teething and, and fevers. What's the first drug? What's the first do you guys use baby Panadol baby Tylenol?

Speaker 2: (01:34:40)
Yeah, Panadol. Panadol I think. Yup.

Speaker 3: (01:34:43)
So in, in North America more so. It's acetaminophen. BBC. You Tylenol. Okay. So here's a drug, Lisa, to this point, when you talk about honestly changing a mindset, so if you take as human beings, literally the first and most used drug in the human population is often a set of manifests from an Crawler is acetaminophen Tylenol is that pain? Is that analgesic thick? Antipyretic that we use from the earliest from BBT, they and fevers vaccination posts factors into adulthood. Okay, fair enough. Acetaminophen, what it is metabolized by sip to E one to Edward, one is converted into a noxious, it's in the same family as the Quinones, not Q. So acetaminophen, which is the analgesic when it is first metabolized from a to B by cytochrome P four 50 to Edward, one to Epsilon one gets converted into a potent liver toxin, not Q. Q remove from the body via GSTT one.

Speaker 3: (01:36:02)
Now, if he knew that you had the fast sip to E1 and the deleted GSTT one, do you really think you one Tylenol is your go to medication from the time you were four months old onto do you just just stop? One thing that one thing that when we open our medicine cabinets in developed countries or in any country, you open that cabinet, everyone's giving their children. Again, I am not saying don't treat a fever. I'm by no means say don't use Tylenol if you're in pain and it happens to be what's appropriate for you. But I am saying, can you imagine? We said we're not more intelligent about these things. Ibuprofen does not go through that pathway. So if you have this potential combo, consider using ibuprofen as your pain killer, not acetaminophen and so on and so forth. So these are all parts of the same puzzle. What is the puzzle? The human genome, what is the solution? Intelligent, non superficial, meaningful reading of the manual. That's what has to happen. That's what we've committed our lives to. And that's what I hope God willing to leave as my legacy.

Speaker 2: (01:37:24)
You're definitely doing that Dr. Mansoor I'm just a comic. So excited for that. What this will bring in the future, the suffering that this is gonna save the the people's lives. This is going to say and you know, I'm, as I'm as passionate and my way about this as well now and I'm, I'm going to be a part of this. I'm bringing this out to the world. So I'm super excited. We're going to try to get dr mentor those listening. We're trying to bring dr mentor down later on this year to New Zealand. My big goal, I've got to go and work out how the heck we make this happen. But you know, with oil there's a way,

Speaker 3: (01:38:01)
If you, if you invite me, I'll, you know, just it just, it's just I'm, I'm, I'm beyond honored. I'm, I'm tickled pink. I will find my way down there and, and to whomever would want to listen and, and just, you know, we're just, we're trying to create something that is based on good knowledge that is created on by flow of information and by flow energy. Just people that want to make a change and not, not make a change because, you know, there's sometimes we change just for change sake. No, we want to make a change where it matters and, and empower people and this is where it comes to. It ultimately comes down to empowerment. It comes down to your energy leases. Just awesome. It's such an honor speaking with you. Please. Whenever, if ever you need something from me or you feel like there's something else that I might be able to help with, it would be my single on her to help you.

Speaker 2: (01:38:53)
Oh, documents and what you just absolute gold. I can see like your passion comes through in your words and the abs. Talk to Sanjay, one of your colleagues that you have on your team and he just says, Dr. Mansoor Does not have any hobbies. This is his life. He is timesing the world and I totally get this guy and you have a, a massive vision and I can see that vision and I can see that this is going to help so, so many people. So thank you so much for your time today. Document or it's just been

Speaker 3: (01:39:26)
Absolute honor and to, to all of the, what do we call New Zealand is the Kiwi. There we go. So to all of the Kiwis and beyond the Kiwis, I have actually a different story, a different time. I have a, and I'm not saying this to be a locating or to be in, you know, self engendering to your community. I have a particular love. Someone that is exceedingly dear to me is from New Zealand and as a whole, it's that this love the people there. You got your governance there. It's just a different modality. And so if I ever come down though, if I have the honor to come in September, October, September, I think

Speaker 2: (01:40:02)
Maybe he's more, we're hoping for September. That's what we're aiming for. So I'd be the one that would be grinning from ear to ear to mid. So thank you so much for your time. I know you've been because Austin and you're still stuck on here for an hour. This is, I'm sorry my apologies. Fucking carried on too much.

Speaker 4: (01:40:23)
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Speaker 1: (01:41:13)
That's it this week for pushing the limits. Be sure to write, review, and share with your friends and head over and visit Lisa and her team at Lisatamati.com