Hello everyone. Welcome to another episode of the Overcoming Chronic Illness podcast. My name is Dr. Brian Reid and I'm a naturopathic doctor. And today I am joined by Dr. Penny Kendall Reid. Uh Dr. Kendall Reed is a fellow naturopathic doctor and she developed a number of years ago a uh genetic um decoding software program um known as or uh report I should say known as um Gan Rx. Um Gan RX is a report that looks at A number of different genetic snips um single nucleotide polymorphisms. We'll get into the you know jargon if you're not
familiar with genetic reports or what snips are. I'm sure we'll get into that in the interview coming up. Um, and uh, I was really, um, to be perfectly honest, when I first heard about, you know, first saw one of her reports, um, I I didn't know that she had, um, I I saw the report, a patient brought it in. I didn't know exactly who, you know, Didn't um, realize that it was, you know, one of her reports. I was like, ah, it's like it's another genetic report. There are so many companies out there that are
offering these reports. Um, you know, once upon a time there were just a couple of options. Now, there are dozens of different options and quite frankly, I've seen a lot of these reports from a lot of different companies and a lot of them are, in my opinion, and in my experience, not Really all that useful. Um, you know, they'll have these, you know, reports that look really nice. You know, the graphic designers did a great job. Then you look at what they're reporting on and it's either not that many genes or the genes that they
do report on, they make these grandiose claims saying like, "Oh, you've got this polymorph polymorphism here, this polymorphism there." and you know that means that you should be doing this with your diet that Means this about your microbiome that means this this or that supplement or whatnot. And when you actually dig into the research literature um there's very very very little research. It might be just on you know some uh you know animal studies or um it might be um they're basically making a lot of extrapolations. Um, so when I first saw um one of
the um G&RX reports, I was like, "Ah, all right. It's probably another one of those reports." And so, You know, took a look at it. I was like, "Oh, she's actually reporting on a lot of genes that are not commonly talked about." And so, um, one of my colleagues actually did a really deep dive into her uh into her reports. And well, I I I started poking around at a few genes and saw that like, oh, there's actually a lot of research, like a lot of human clinical trials, sometimes like gigantic like largecale human clinical
trials looking at the relevance of these genes. And so I asked one of my colleagues to, you know, look into this more. She, you know, went through the entire report and there's just oodles and oodles of research backing up what is in this report. So I was really encouraged. Um, started looking into it in more detail myself. um you know took a look at my colleagues write up on that and um it was uh I was very very impressed. Um so um I started recommending this for my patients and I reached out to Dr. Penny
Kendall Reed and asked if she would be willing to chat with me on my podcast. She graciously said yes she would and so I'm really excited about having that chat. So, um, we'll get into the obviously all the all the weeds of it coming up soon, but, um, I think that there's a lot in those reports that, um, are a lot in her reports that are, uh, certainly relevant to folks with complex chronic illness. Um, you know, things related to inflammation levels, blood Sugar regulation, uh, metabolism issues, etc. Um, but then also, um, I think
there's a lot of really useful information in there for just folks in general. So, if you're listening to this because you know some of my podcast episodes are more maybe a little bit more biohacking focused or um if you were once suffering from complex chronic illness, you're a lot better all the way better and you're just wanting to health optimize. Um there should be I think Something in here for just about everyone. Um and I'm really excited to to get into it soon. So, um I will pause the recording and I'll be joined again in
just a moment by Dr. Penny Kendall Reed. All right, everyone. Well, welcome back to the podcast. I'm now joined by Dr. Penny Kendall Reed. Uh, Dr. Kendall Reed, thanks so much for joining me today. Thank you for having me. I'm It's a topic that's near and dear to my Heart, so I'm excited to share everything with it. Awesome. Well, looking forward to it. Um, well, just before we jump into the, you know, nitty-gritty of, you know, what are SNIPS and genomics and, you know, some of the ins and outs of the report, uh, that you
offer, uh, would you mind just telling folks who you are and just like a little little background on on who you are and why how you got into this? Absolutely. So, um I'm Dr. Penny Kendall Reed. I'm a naturopathic doctor in Toronto, Canada. Um gosh, I've been in practice for way too many years, almost 30 years. And um love it. Feel so blessed to be in in naturopathic medicine. It it and genetics takes it to uh an even bigger level because as our core as naturopathic doctors is get to the root cause of the problem,
right? Don't just look at the symptoms, get to the cause of it. How much closer can we get than our genetics? we see our Potential. Uh then you marry it with symptomatology and see which gene is turned on or turned off. And we'll get into all of that, but it it literally is genetics to me is like an intracellular MRI. It's like I get to see what's going on on that little level. And I I first got into it uh probably 19 or 20 years ago now. Um because I would see two patients come through
the office, same symptomatology, similar backgrounds, and you probably see this all the time and The same protocol would be fantastic for one person and it would aggravate another person or just not do anything. And I would say, well, like why don't you fit in the box? You have all the symptoms. Why can't I just tick that off? And more and more of that started happening. Um, and then I just read an article on genetics one day and that's started me down that path and I I spent many years researching it before I even tested my
own genes because I wanted to Know, well, is it valid? Is there a point in this? Are you just going to tell me something scary and then go, "Good luck with that. There's nothing we can do about it cuz I'm not interested in that and I'm not interested in that for a patient." Um, but years and years of research went went down the road and then I started testing different supplements and nutrients and things and did that make a difference with that gene and here we are many years later. Cool. Very cool. Yeah. So, you
were basically into genomics before it was cool. Yeah, exactly. Awesome. That's really great. Well, um just uh I know a lot of the folks who listen to or watch these episodes um of the um Overcoming Chronic illness podcast, they're they're pretty well educated. They're, you know, it's not their first rodeo. Um but uh that being said, genomics is like it's a little bit of a special category or topic, I guess, and that it's a little More maybe heady or uh a little more nuanced or detailed than maybe certain other topics. So, just to make sure
we're all on the same page, would you mind just giving us a quick little crash course and like, you know, what what are genomic reports actually looking at? like what is a snip? Um what's the relevance of looking at these things? If you could give us a little crash course in that please. Absolutely. Um so the best way sort of describing it if if we Think about our gene we know that we take half a gene from mom and half a gene from dad and that makes up our gene and and we all sort of
understand that concept that half a gene is called an alil. Um so we take one al from mom, one al from dad and that makes our gene or uh per se and tells us how we're going to code for it. However, every time a cell turns over, we should have those same two alals being turned over, it should make an identical replication of Itself. Sometimes it replicates into a different gene, or sometimes it can have a big stressor on it, so it replicates into a different shape or a different coding. The purpose of a gene
is to make a protein. That protein can do something good like increase your metabolism or make serotonin or happy hormone. it can do something bad like increase inflammation or push estrogen to a cancerous form. So that those two alals they determine the recipe if you will of That protein that's going to be made. The every gene has a very specific recipe. A snip though is when that recipe gets changed. So that that basic functioning of the gene has a different recipe and now it produces either too much inflammation or not enough serotonin. So the purpose
of testing genetics is what's inside your cells? What how much what possibility of inflammation or serotonin etc. and all the different pathways do you have? And Then what can we do about it? If it's too much, how do we bring it in? If it's not enough, how do we boost it up? Perfect. Great. Thank you very It's like you've said that before once or twice. Um and then could you just uh before we kind of get into, you know, um some of the more specifics of what the report looks at, um could you give us
a just a little backstory in terms of how this Test was developed? like you I know you've been in this quite some time but like how did you go from like you know kind of uh dabbling 20 some odd years ago to you know like now you have this G&RX um absolutely so um after I finished testing them on myself and literally genetics saved my life so it's something that I I do hold dearly and and tested it out on family and friends that's when I started using it with patients um but at that time
there there Wasn't a platform that I could upload a testing profile like a 23me me into and get the information that I needed. Um, and and the information I need is is the interaction between genes and and what each gene meant once it was decoded. So, I used to spend 7 8 hours per patient pulling out gene by gene from 23 and me which one I wanted. Then I would write a blurb to that patient. what does this gene mean and how it interacts with the next gene and what are we going to do About
that and marry it to their symptoms and about a year and a half later I was I was just way overworked from spending too many hours on this so I created um G&RX which is is the company and it's it's the first algorithmic program and that part was really important for me because all of the testing platforms that are out there they treat gene by gene so a really good example there is let's look at carbohydrates. There are three really Important genes which talk about how much insulin you make to carbohydrates, but also do you
create inflammation in your GI tract through carbohydrates. Do you feed cancerous pathways through carbohydrates? Like they each have different points as well. Treating gene by gene would say, let's say you code perfectly for the first gene. Great, you get to eat carbs. It'll say you can have carbs. And then the second one, let's say you're hetereroygote for that gene. So you have one normal alil making that normal amount of protein, one variant al making making less of that protein. H you're not so good with with carbohydrates. You need to eat less carbohydrates. And then let's
say the third gene you're variant for then it's going to say you can't have carbohydrates. Well, what does that mean? Do I get them? Do I not? You have to integrate them all together. And what does that mean? Are you creating Inflammation? Do you stimulate cancerous pathways? you can have this exact amount of carbohydrate per meal. And that's the sort of protocol that I wanted to create across all of genes for people. Um, so you've kind of touched on this next question already, but I'll just ask you more straight out here. Um, so, um, how
does the G&RX report differ from other reports like o over and above the, um, uh, the algorithmic kind of component? Um, and what other ways does It differ from other reports? for sure. So, it's it's long, it's intense, it's like 65 pages. Um, it gives a really good definition first of each gene. So, if somebody's new to genes, if um you can really learn about that gene because you're not just getting a oneliner about it and then it'll tell you key variant uh key points with the variant gene. But the biggest part is it gives
you full treatment protocols. So, after it does the integration of different genes, it Does a full explanation of what that integration means. And then what do you do about it? It gives you an 8week protocol because it takes about 8 weeks to reset a gene. So it could be this supplement at this dose for 8 weeks and then we get to drop the dosing down to this for another 8 weeks or you can come off of it or you need to stay on it at that lower dose. Um the report is also editable. So in
each treatment section um let's say you wanted to put somebody On something to boost up serotonin but they were already on a pharmaceutical. So this is where you can edit the report as a healthc care practitioner and say I know that we don't need to do this, you're already on it or this is why you're actually on this medication and it is well suited for you. Um you can change dosings for patients. You can change companies if you want to use the different company. Um in terms of the supplements, it's a very it's a very
Userfriendly report. So it gives you the full treatment pro programs but then you can also just add in little details for your patients. Great. Um, and since you haven't said it because you're probably just being kind and diplomatic and and Canadian like like I tend to be, I I will just say that uh you know, having looked at many many other uh reports out there, um what I was really really impressed by, I mentioned this in the introduction, but Just uh going to say it again because it just really warmed my heart when I learned
this um that your reports are just very very very like heavily evidence-based, like just ridiculous amounts of research backing up um each of these snips um these single nuclei polymorphisms that are that are looked at. Um so that is um something I would say that really notably sets your report apart from a lot of other ones too if I may say. Thank you. Yeah, it's something That's very important to me. Um when I was doing the research for each of the genes, um people often ask me how did I choose the genes and how did
I know which were clinically relevant. Um, I had a rule where I would h I would need seven different um, studies or seven different sites with clinical research behind it that all said the same variable about the gene because we all know that we can get one study and we can make a study say pretty much Anything that we want. So, I needed seven independent studies that were all saying the same thing. Not just that Snipedia had a slew of them. It had to be u very sort of sound research papers and all with the
same messaging system and then that's when I would take into credence. Yes, you can you can't just go by the number of people that have that snip. It has to be clinically relevant and it has to be the correct RS number for that gene. So I spend a great deal Of times the I'll often get docs um asking for the actual studies and I have a a document which is over 68 pages of just lines and the lines are just links to research paper. I mean there's so many research papers that went into it and
then I continue to update it. Um as new information comes out I'll change I'll change the algorithms. I will change I shouldn't say that I've added new algorithms. I haven't changed any of the older ones, but I've changed Treatment protocols. As new products come out, as new research comes out, um I'm always updating the the program and if I add in new genes, the reports automatically propagate those new genes and the treatment protocols as you go along and um so it's a very user friendly and scientifically grounded platform. It's really great and uh yeah, very
very refreshing in this field if I do say so. Um so as far as the application of this Report goes um I mean I I kind of mentioned also in the intro that um there's in my opinion to my understanding and you know better than me which is I'm going to ask you um so I think that there to my understanding there are applications to folks who are dealing with complex chronic illness you know whether it's fibromyalgia chronic fatigue syndrome um autoimmune conditions you know maybe mold illness chronic infections like lime and whatnot Um but
then there's also, I think, applications for just all of us in general because like we all have a metabolism. Um, we all have, you know, uh, cholesterol levels and blood sugar and all these things. Um, and so I'd like to ask you about sort of the application to certain conditions. Um, but I'll, um, just kind of like phrase the question or pose the question, but then, uh, that's kind of the ultimately like folks listening to sort of have a Sense of, okay, if I have X, Y, or Z condition, how might this apply to me?
um but without you know having three days to talk to you non-stop and going through like every you know known medical condition under the sun u maybe we can kind of just generally um categorize them sort of so I guess for for folks who are dealing with say um let's I'll just start broad you know folks who are dealing with complex chronic health issues so you know uh Fatigue and or pain and or neurological symptoms a lot of inflammation um maybe related to things like you know mold lime uh other co- infections viruses is SIBO,
etc. Like just uh just just kind of imagine like your um I say this affectionately, but like your classic like dumpster fire, a patient who's got everything under the sun and every symptom under the sun. Um what uh elements of the report would you say would you say would be the most useful Or relevant to a case like that? Absolutely. So initially I think what would have got that person into a problem would be the inflammatory genes, the detoxification genes and the miogenic genes along with autophagy. So um genes as mentioned they interact with one
another. So the inflammatory genes right off the bat if somebody is variant for those genes they're making up to 85% more inflammation every time it is called upon. So let's say they are Exposed to a mold or they are exposed to lime. Their inflammatory load rather than being this is this and then that inflammation begets more inflammation. inflammation like cortisol turns 90% of genes to their adverse position. So let's say they had an a weaker stress gene here. Now that inflammatory load is now going to turn on the stress genes and then the stress genes
augment the inflammation again. um detoxification if it is if they have poor particularly oh No both fa if it's too fast for phase one and too slow for phase two that's the most inflammatory state somebody can be in so if someone's exposed to mold or toxins or a bacteria and that that toxin goes intracellular or pathogen goes intracellularly too fast phase one means they are pulling it out really quickly and dumping it into the extracellular where phase two should then pull it But if phase 2 is really slow, it can't Get it out. So now
you've just dumped it from being quiet inside the cell to outside the cell where it's active and now it can't get out. And that's where we see these massive differences between two people being exposed to a mold or a toxin. They have a hyperinflammatory reaction to it and then they can't get it out of the body and it keeps creating caveat after caveat after caveat. that then starts to trigger um their stress genes which also impairs their sleep Genes. So now they don't go into deep sleep and they they have decreased energy levels from both
of those pathways. Those are all the offshoots. But for most chronic issues, it begins in those inflammatory mixed up phase one phase 2 detoxification states and then the mess occurs. It can occur from low autophagy as well and it can occur particularly what I saw during COVID. Um there's a a gene IR5 which talks about how quickly does your immune system see A virus or a bacteria jump on top of it and then start to destroy it. Some people if they're varant for that gene they don't see it quickly at all. So that pathogen comes
into the body it's invading. it's now replicating and your immune system is just kind of hanging out and then suddenly the immune system goes oh god there's something in here I've got to do something about this but by that time the pathogen has taken hold and those are the people again comboed With high IL6 because we know co really targeted IL6 had such bigger effects um and and this is why I I love gene genetics because you can see the potentials in all people almost all disease comes from an aberrant pathway that is in GRX.
It's not going to jump out and say lime, but you're going to look at the pathogen associated one. You're going to look at the detoxification one. You're going to look at the inflammatory one. You treat those Guys. You're treating almost all of the side effects with it. Again, miogenesis or mitochondrial function can have an out can have a an effect there too, but it's usually secondary to the mold or the pathogen itself. Um could you speak a little bit to the kind of mitoenesis related genes? Yeah, absolutely. One of the biggest ones um is sod
or superoxide dismutase 2. So this is a phase 2 detoxification gene as well, but it's right within the Mitochondria itself. So it's decreasing the production of inflammatory markers or ROS's and cleaning out the mitochondria so that they can keep um replicating themselves as well as keep making ATP to have every function going. There's also C 6 and BDNF both which also play a role in mitochondrial function. They're a little bit more specific for neural repair. So they're when they're low, they're that's really involved in a lot of the different uh Neurodeenerative diseases, Alzheimer's, dementia, um
Parkinson's, MS, etc. So with sod 2, would that be primarily related to keeping up that um kind of balancing out like all the prooxidants that are or the proxidative pathways that are involved in ATP production like trying to keep those neutralized so that you know I I always explain it to my patients as mitochondria being little combustion engines that are like doing work like making energy but you would Never run like you know say a a gas powered generator in the middle of your house cuz you would kill yourself from all the exhaust. So we
need to neutralize that exhaust preventing you know lipid oxidation and peroxidation and things like that. Um so with this the SOD2 is that primarily is is there some other function that it serves over and above neutralizing free radicals in the mitochondria? Yes, it actually directly increases Miogenesis. So the the replication and the repair of the mitochondria themselves outside of ROS reduction and oxidation. Okay, great. Cool. Um, and then just for folks listening, um, so you know, talking about like, okay, so someone's listening thinking like, okay, like I'm I'm that, you know, affforementioned dumpster fire. Um,
and I've got all these things going on and okay, so I do this test and I find out that I've got imbalances with my phase One and phase 2 detox and my mitoenesis abilities and all these different things. Um, so are there things that I can actually do about it? um or and uh not that we need to get into specific protocols and sorry I meaning to meant to mention this earlier as per usual we're not offering any medical advice during this podcast this is all forformational purposes only if you need healthcare if you need
medical advice please talk to your healthcare provider To get that advice um so not getting into specific protocols but could you maybe give us like a hypothetical example of like okay someone's got all these symptoms they've got maybe a phase one phase 2 imbalance or they've got a mitoenesis issue you know around SOD2 or certain one or whatever it is uh that happens to be. Could you give us an example of like what they would actually actionably do with this um information? Absolutely. So, let's say their phase One is too too fast um as mine
is. Um curcumin will actually slow it down. So, curcumin slows down phase one detoxification. Really important because if you're already slow for phase one detoxification, this just a little side note, curcumin is bad for you. It slows down your slow down phase one too much and that's actually pro-inflammatory for myself or someone whose phase one is too fast. It's a fantastic anti-inflammatory and it slows down phase one. So does Caffeine. Coffee, yay for me, good for me. Um, in fact, two to three cups of coffee a day will reduce my risk of having a heart
attack by 68%. through regulating phase one detoxification. Uh we can upgrade mitochondrial output sodu specifically with aazanthin or NAC glutathione. Lots of different ways that we can you know upgrade that one specifically we can even a ubiquininal what I'll often do is try to cross cover multiple genes with less supplements. So NAC and ubiquininal or sorry NAC and glutathione they will upgrade sod activity but they'll also upgrade GSTP1 and NQ1 the other phase 2 ones. So that way we can cover more with less things to upgrade um mitoenesis. We can also use uh rveratrol and
then we can also use spermadine. We also for these patients though we have to look at because by the time they come to us and I you see this too it's not just their inflammation and detoxification that's Off. Those pathways have now triggered their adrenals. So we have to look to their stress genes and trying to treat these patients and not treat their adrenals or their stress genes at the same time or all the offshoots they will not heal. So yes we we see the cause of it in the report but then you also see
all the potentials of where it can go to um particularly so we look at the sleep genes um you know how well do you transition into deep sleep? Do we need To fix that as well? because that can also be a big part of it. And we can easily reset stress genes with a casein decipeptide and atheine combo. We can easily reset the sleep even just by using highdosese melatonin comboing it with some pacifa depending on which those genes are. So we have to make sure that our healing pathways are also reset not just our
pathological pathways that are off. I'm just curious with curcumin um is That so that slows down phase one that's great for me but not great if you're slow right so um is that largely because it just like preoccupies your cytochrome P450s 100% so yeah it it's decreases the amount of cytochrome P4501 uh 1a2 the the main enzyme that needs to go inside of it bind to that toxin and take it out. So, you're leaving intracellular toxicity here. Um, and if you're slowing that down even more, the inflammatory Load gets higher and higher and higher. Um,
and sorry not to bleer the point, but is it just because it um curcumin just um preoccupies a lot of the um CYP450 resources or is it that it actually downregulates? actually downregulates the CYP1 A2 specifically. Okay. Yeah. Okay. Interesting. Is it does it use I think it uses 3A4 as well for its metabolism. 3A4 as well. 1 A2 massively. 3A4 it does. Um 3A4 is not quite as strongly associated with Curcumin as the 1 A2 is. Um but 1 A2 for sure. Okay, cool. Um so um I I'd like to ask you about a
few other um applications or you know conditions that might benefit from having um a G&RX report done but um anything else you'd want to add as far as the um like more like complex chronic illness um applications would go. I think I think it's been quite a bit but you know it better than me so yeah. No Again like when I when I'm doing anything with a patient I'm sort of also going back to our naturopathic roots of diet. Um, so diet and exercise because we we all can understand how there's not one diet for,
you know, keto can work for weight loss for somebody and high carb, lowfat can work for somebody and now we know why it's genetics and this will dictate it. But diet can be just as damaging. So you know we always want to go back to that and also exercise doing The wrong form of exercise can also generate a lot of um toxic byproducts and inflammation etc. So, knowing those two basics, just sort of getting back to our naturopathic foundation there. Also, I'll always include those no matter what the case is. Um, and just kind of
a related question, just a little bit of a side question out of curiosity. Um, so I know in my practice, I've had, you know, many patients that have come to see me over The years and, you know, just where, you know, I have a reputation for treating folks with, you know, chronic infections and mold and heavy metals and all all the things been mentioned. Um, and you know, in many cases, they come in and we test them and they have those issues and we treat them and they they feel better. Um, I've also had, you
know, quite a few patients though over the years. I haven't been at it for 30 years. It's only been 16 for me, so halfway there. I'll get there eventually. Um but um I I've I've had a number of patients over the years where you know they come in saying you know like I I just had a new patient actually uh very just yesterday I think or the day before yesterday and you know she has seen like all these great doctors you know these like really you know very well-versed you know very smart functional medicine docs.
She's been treated for like eight years or something like that for you know lime Molds you know everything under the sun. Um you know she's had you know other genomic testing done whatnot. every supplement you can think of. Uh, you know, fancy pants like you know, more new fangled things like well kind of old I was going to say methylene blue is not new. Methylene blue drug that was I think approved by the FDA if I'm not mistaken once upon a time but anyways um lots and lots of different things and yet um you know
still having still Having symptoms. Um, and in a case like hers where, you know, we're we're going to do some additional testing, you know, see see what's going on. But, um, in cases where it's like patients are saying, well, I've got all these, you know, you know, infections and this and that, but like I've been treated for years and I'm still not better. U, maybe I've hopefully improved somewhat at least, but like I'm still not better. And so, like, you know, I've had lime For 10 years. I've been treated for, you know, however many years.
Um, so when if a patient like that shows up at your doorstep, um, I'm wondering, um, how how many times or have you seen cases where, you know, they've had all these diagnoses, all the things they've been treated for, they're still not better, and then you find something within the G&RX report or some multiple things within the G&RX report where it's like, okay, the things that actually finally Cracked that case were that it was about figuring out the phase one phase 2 imbalance or it was, you know, getting them on the right type of diet
that was um designed for their individual um you know genetics or you know something else that you found within that report that had nothing to do with that magic antibiotic or that magic binder for mold or that magic nasal spray or whatever it was. So um hopefully I articulated that well. Yes. No, perfectly. Um actually do See I work I do a lot of work with a medical doctor in the US um helping her like I I'll go through her patients genetics for her in exactly the same arena that you're in. Um, and generally what
I see with those patients is it's really slow phase one. Um, and they are on curcumin. They're slowing it down further because everyone thinks it's this great anti-inflammatory for everything across the board. Um, so they're not actually doing anything Beneficial or they're they may be increasing phase one, but if they have the curcum in there, it's it's a it's a moot point moot point. They're also hyperthylating. Um, and I see this and this is a big pet peeve of mine is um people methylation needed. Uh, it is a catalyst. It speeds speeds up reactions. Um,
and it's one of the first areas within genetics that was sort of brought to the forefront. So, everybody loves to focus just on Methylation. Um, you can't specifically turn on methylation though and say, you know what, I would just like to upgrade that pathway and that pathway and not that one and that one. you turn on methylation, it's like the Christmas tree. Every light bulb goes on. So, if you do that before you turn off the stress pathways and the inflammatory pathways, all the studies show us that you upgrade those pathways even more. So, you're
making those pathways way Worse. And everybody, every patient of that description I've seen is on methylators. Um, so we have to pull them off. And I pull every patient initially off of any any methylator um particularly if their methylation genes are strong. I had a patient today there's a cancer patient who was put on so many methyl like methylators and she got perfect methylation. So she's just hyperthylating from day one. So I see that as a as a big issue. I also see the Stress genes um no matter what their position even if they're slightly
weak or really weak that is a big blocker for those patients because as mentioned stress and inflammation block the treatment of over 90% of genes. So you could do everything perfectly in every other section and if you don't properly treat stress and inflammation or you leave one area of them untreated, it's going to stop all treatment. So we need to not just Decrease the excess release of cortisol, adrenaline and noradrenaline with our ad adaptogenic herbs. We need to stop the blockage of the stimulation of the stress pathways at the hypothalamic and pituitary level. And that's
with like the casein decipeptides etc that unblock um those receptors turn FKBP5 off the gene that makes the protein that's blocking those receptors and then we also have to look at all forms of inflammation. So diet as you spoke about GIPR are you making a ton of inflammation in your GI tract through disaccharides or carbohydrates. So if you're not addressing that side here's another version of inflammation. If you're not going into stage four sleep, leaving even sleeping seven versus eight hours a night starts to increase inflammation in five days. So just that alone. So we
have to treat all of the areas of inflammation and all of the areas of stress. Watch out for phase one Detoxification with that chronic patient and watch out for hyperthylation. Um, are there genes in your report that um indicate that there is hyperthylation? No, just tells you how you methylate, but the report will say if you're perfect, don't do this. Makes sense. Um, and I know you've mentioned the case decapide a few times now. Um, bearing in mind that this is not a CME accredited u podcast episode, So I'm assuming we're talking about lactium. Yes,
we're talking about lactum. So either serenitin plast or stress reset. Okay, great. Um and sorry I keep for you between CE and Yeah. Yeah. Yeah. No, no, I appreciate it. Um I I do the same thing, but um so with with lactium slash I think Casey and Decaeptide sounds cooler, but anyways. Yeah, would you mind um just because I think uh a lot of folks are not aware of the existence of that at least, you Know, here in Canada anyways. I don't I I didn't I'd never heard of it until I had a patient who
had consulted with you and I was like, "Oh, what's this stuff?" And I was like, "Uh, like I maybe I'm getting skeptical in my, you know, whopping 16 years of practice, but um I was like, I wonder if it's just it's like, wow, there's so much research on this thing." Like, so much research on it. It's so cool. I'm using it all the time now. Yeah, it's it's phenomenal. So, it's a it's a casein deck peptide. So, it is a 10 amino acid sequence which is isolated from milk. Um, it's lactosefree. For anybody who is
allergenic to milk, it's still fine because the immune system can only see something that is 10 amino acids in length or sorry, 12 amino acids or or longer. This is 10 amino acids. So, it kind of scoots under the radar of the immune system. So, even my anaphylactic dairy patients have no issue with it. Um What it does is so when as for listeners and I know that you know this but just for listeners just in case um when we have a stressor our adrenal glands make adrenaline nor adrenaline and cortisol once we've dealt with
that stressor those hormones bind into receptors in the hypothalamus in the pituitary and that's a signal to the nervous system say great I'm done with this stressor tell my adrenals to stop making more stress hormone and take me back to Campfire parasympathetic we need that binding of those neurotransmitters into those receptors in order to to stop making more stress hormone. If there is if that messaging doesn't happen, your adrenals don't know that they need to they can stop making the hormone. They just keep making more and more and more. So, there's a gene FKPP5 which
makes a protein which blocks those receptors. Um, and then there's another gene which tells you how many of Those receptors you make. But what lactium does is it goes in and it kind of kicks out FKBP5 out of those receptors. So now they're open up again. So now we can have the our own hormones come in and turn off engage negative feedback in that HP axis again. The same time it turns off the FKVP5 gene. It binds into the GABA A1 receptor immediately which is the calming receptor in the brain but it doesn't bind to
the GABA PBR receptor which is The sedating receptor. So, a benzo binds into both of those. Um, this only binds into the calming one. Um, and there are zero side effects. We we isolated, we've discovered it in breast milk that babies that suckled with mom, their cortisol levels dropped. They thought, well, is it cuz they're suckling with mom or is there something there? So, they put formula in a bottle, breast milk in a bottle, and regular milk in a bottle. the breast milk baby, their levels Dropped most rapidly, started playing around with it in the
lab, and lo and behold, there's the sequence. Um, so with the lactium, um, is it, um, how long does it typically take to see a response in a patient who's taking that? Honestly, 48 hours if you get the right dose. Um, what you have to do is get the right dose. Most people do one a day. No, no. Uh I'm generally starting everybody at two twice a day usually unless um and then how quickly they drop Down is is according to their genetics. Um or they take it with food and then it's going to be
completely blocked. You have to take an empty stomach. Um that's like if you take it with food, it's like saying I'm going to increase eggs in my diet, so I'm going to eat cake. Yep, there is an egg and cake. But we don't eat cake and our body doesn't go egg to go do this. You have to take this this protein peptide on its own away from food. Well, You can mix it with other empty stomach supplements, but if you mix it with food, it just gets lost in the food as like a little bit
more milk. So, it has to be empty stomach. But generally I see most people start to feel a difference in two days unless there's a great deal of inflammation in the body blocking receptors and then which case 10 days to 2 weeks um I've never not seen somebody but don't forget that inflammation makes a big big difference with anything Binding particularly in the brain and that's because of that lock and key fit. Right? So every neurotransmitter has a lock and key fit with its receptor. If this is the receptor and it's this shape, inflammation comes
along, makes it look like this. Doesn't matter how much ingredient you have to go in here, it can't get in there anymore. So you got to open up the receptor by reducing the inflammation and then stuff can go in. Um with lactium on an empty stomach. I'm just thinking for folks who are taking it at nighttime to go to sleep like is it okay to like would taking melatonin or theine or other things like that would that interfere or that's No, absolutely. In fact, um there's some great products that put all of those together. So
yes, empty stomach is just 30 minutes or more before food or 2 hours or more after, but it can be with other empty Stomach nutrients. No problem. Okay. Um I think we should probably move on from the uh the complex chronic illness patient. Um just because I want to ask you about a couple of other things here unless there's any final thoughts that you wanted to share on that. Okay. Um, so yeah, one of the things that I was really fascinated with with the G&RX report when I, you know, dug into it was um just
so much uh so many snips, like so much research literature looking at Some of these genes as they relate to um challenges with weight loss. And uh one of the reasons that I have premature gray hair is that I've just had so many patients over the years where like they've done everything right and they cannot seem to lose weight. Um, and like patients who are like, you know, fasting like crazy, like, you know, carnivore diet, keto diet, you know, they'll swing the other way, like just going full vegan, like exercising regular, like Just still can't
seem to lose weight. Um, so thankfully that's not a majority of patients, but like they're they're they're out there as your smart Absolutely. Um, so could you speak a bit to uh some of the things that you've seen in practice um in terms of using the data from the G&RX report and how that's translated into cracking some of these like very challenging like weight loss resistance cases? 100%. There are so many different weight loss books out There like like you go into a store there's like rows and rows and rows and rows. You go on
to Amazon to try to look up one and there's bajillions. They all work for somebody. They don't work for all of us. I've written many of those books. I don't even keep them around anymore because they're obsolete. It all comes down to our genetics. So our our metabolism is almost entirely controlled by three hormones. Leptin, adipeneectin, and ghrein. They ultimately dictate how Much insulin you're going to make. They dictate GLP1. They dictate all of those guys. Our hunger, our satiety, our rate of lipolysis and lipogenesis. So how much fat we're breaking down and how much
fat we're creating. those three adypocines or those three hormones. They they control the majority of it. Um Grex has six different genes which talk about how much of each of those you make and in different scenarios when you're on a weight loss diet, when you're not and Etc. Um so just in terms of getting the metabolism working, you have to know how much of those hormones you're making and then push it one way or the other. A perfect example, I am what's called FTO variant. So I have the slowest metabolic rate through one of the
biggest metabolic genes called FTO. Um I have always known that I had to eat less than the average individual. I required less calories. I felt absolutely fine. Didn't mean it was fun, but I always needed Less to maintain a specific amount of weight. Now I was very blessed. I grew up in an incredibly healthy environment. my mom fed us organic, you know, that's 50 years ago, more then, um, etc. So, I I didn't I was exposed to a very clean diet that didn't fully trigger my FTO gene to its own position. Now that I know
it, I have retrained that gene, kept all of my metabolic genes in their off position um, so that I don't do this. If I eat what my husband eats Because he needs carbohydrates, my genes don't, I will start doing this. Um, I I need more fats than he does not ketogenic. So, everybody's different, but your genes will dictate how much insulin you are making to um to carbohydrates. It will dictate from saturated fats. At what gram level do you start kicking in fat storing um or increased inflammation? What are your hunger cues? What are your
satiety cues? How quickly do you break it down? And You can't just you can't you can't guess it. Um you know, especially when somebody goes on a ketogenic diet, at first they cut out all sugar and then they lose weight and then they're like, "Oh, this is it. This is the one for me." And then like three, four weeks into it, it starts to slow and then they hit that plateau at like a month and then it can even start to go up and everybody will lose weight and feel good from pulling out sugar. The
question is Are you supposed to for to do that for long term and at what extreme? Doing an extreme in any diet increases the stress hormones and the stress hormones themselves will make you put on weight. So, you have to know where where your diet is at in terms of fat burning potential, satiety, and hunger cues. What's going to increase or decrease inflammation? What is going to increase or decrease cortisol? Not everybody's designed for intermittent fasting. If if Their metabolic genes are really strong, fasting is actually a stressor on their body and increases cortisol. So
the the report gives you all these clues into your very specific genetic diet. Some people are way overloading protein that's just turning into inflammation. So it's it's very individualized. Um would you be able to give us maybe an example from your practice or um some example of what that might look like for someone? like um just kind of a maybe an Example of someone who was you were working with uh they were having a heck of a time losing weight and then like what u what an actual protocol looked like for them like give or
take. Yeah, absolutely. So um I had one individual who was put on a an GLB1 agonist. So she was about 200 lb overweight. She wasn't responding with the GLP-1 agonist. didn't change her. She w was on a ketogenic diet while she was on this. We did her genetics and her metabolic genes Were actually quite strong. Um she was catered towards a higher carb, lower fat diet. The problem was is that she had had an awful lot of trauma as a child and her stress genes were really weak and they will take stress will take a
good gene and turn it to its off position. So her strong metabolic genes were in the off position. So I actually didn't need to play around with her her adypines, her grein leptin adactin. I needed to change her diet to A higher carb, lower fat. needed to actually pull her off the GLP1 agonist and fix the stress genes and she's actually lost two I just saw her last week 230 lbs so even more than she had wanted to but other individuals who have come in and they've tried every diet under the sun but their FTO
and their MC4R genes are turned on and particularly with MC4R FTO you can diet your way out of FTO and turn that gene off MC4R you cannot Once that gene is Triggered, you will you cannot turn it off without a supplement. So for that individual, I actually didn't change their diet at all. They were eating perfectly just by chance to what their genetics wanted them to. All we had to do was put in something called TMC or try metatabolic control which is a LC carnosine not carnitine bourberine resveratrol combo which resets a dipenectin leptin and
ground but the MC4R gene and all of her weight started Coming off for the first time in years. So it can come from a lot of different places. Um, but don't don't underestimate the power of stress to turn off a good gene just as much as it can turn on a bad gene. Very very interesting. Um, okay. Um, uh, anything else you want to share on the weight loss uh, front before we move on to another? Yeah, also again look to the inflammatory and detox genes. um inflammation and and toxins are stored Inside of our
fat cells. And when that level starts to rise up, um the fat cell, no matter what you do, even if you're treating all the other sections, won't give up any of the fat around it because the fat or atapose itself acts as a buffer to the toxicity of the inflammatory substrate or the toxin inside of it. So, it actually wants to sort of hold on to it. If you do a crash diet um and then you release that fat, that fat cell will die. So then it Quickly usurps um even more fat and it rebounds
back up. So opening those pathways is also really important. Okay. Um is it easy? Knocked over my mic. Sorry, one sec. Okay. Um so um is there an application of the G&RX report to folks who are um dealing with um maybe I'll say kind of like idiopathic dysipidemia um and translating that for people into English. Um so there's some folks where They seem to be you know eating a reasonable diet. They're you know exercising regularly you know they're not you know holding on to like significant amounts of excess body weight etc. and um yet they
seem to have well they they have elevated cholesterol levels um you know elevated LDL total cholesterol etc. um sometimes and and maybe so I'm wondering if the G&RX report um has an application to folks like that and then maybe a follow-up or A sec second uh a related question to that would be um some folks who have elevated cholesterol like total cholesterol maybe LDL's up a bit but then their HDL is also really quite high like say their HDL is maybe like a you know 2.3 or 2.5 or something like that where if only their
HDL was lower their total cholesterol would be in range you know somewhat ironically it's like there's too much of the good stuff. So, um have you seen uh cases Like that as well? And does that um does the G&RX report um have an application of those cases? Yeah. So, there is actually a whole cholesterol section um within the G&RX report and the genes there talk about how many receptors you have on the liver to break down and recycle LDL. So, the true idiopathic um cholesterol is not so much about the formation of cholesterol, it's about
the inability to break down the cholesterol and recycle it. And that's with less of Those receptors. And then there's also one that talks about how much of an enzyme do you make in order to break it down. So you need both a receptor and the enzyme there. Um for those people we need to most often use a red yeast rice extract which will function similarly to a statin in terms of HMA reductase but without any the sort of inflammatory or myopath myopathy side effects. most often. I have over the years seen a few people with
the the myopathy side Effects with that. Um, cortisol also uh has receptors right on the liver too to increase LDL production, which is why you'll often see um even in people with great diets, LDL go up right after a stressful period of time or a prolonged stressful period of time. So again, don't don't forget about those genes, not from turning off the cholesterol genes, but just from a direct receptor point of view for those people. Um, then again, we look at the saturated fats. So That's where the dietary part comes in. And some some people
particularly for a 2, if they're variant for that gene. Um, this is the gene which says when I'm eating saturated fats, how at what threshold do I then start making cholesterol and inflammation and store fat and etc. That's at 22 g. Um, so 22 g can be pretty easy to achieve if you're eating a square of dark chocolate, which is 9 oz. 1 oz is 9 g of saturated fats. Um, 1 tspoon of coconut oil is 13 g of Saturated fat. So that already puts you up over the the 22 g. And then it's going
to go into then if you have some fish which has both good and bad saturated and unsaturated fats in it then you're going to start making cholesterol LDL from the fish the fat and the fish. So you do need to look at that threshold and sometimes people aren't quite paying attention to that. An easy way to negate that just don't have any MCT oil bulletproof oil or Coconut oil and you've really dropped it down. Do watch you know the dark chocolate. Um, but a serving of of steak for most individuals is anywhere from 3 and
12 to 4 oz or 3 and 1 half to 4 g of saturated fat versus that 1 oz of dark chocolate or 1 tbsp of coconut oil which is so much higher. So if we just sort of get back to real food um we can we can negate it. But from a a um idiopathic point of view, we have to look at the number of receptors to break down and Then the production of the enzymes to recycle that LDL. So, um, are there certain genetic, uh, patterns that you might see where to get the cholesterol
panel looking within range, shall we say, that you pretty much have to go on a statin medication in some cases? Or is it maybe notwithstanding like, you know, familial hyper cholesterolmia or something like that? But um is are there certain like just very unlucky subsets where you're Just probably going to need to go on a statin or is there is that I've had two patients in in all of my years who I'm they just they had to go on a statin okay down and then we just high dose ubiquinol with them. Um to circle back
to your HDL question. I'm actually okay. My HDL is 2.7 um but my LDL is two. So, um you know the bigger part is is the ratio as you know and um I actually had to fight with insurance companies uh for patients before because of HDL being Really high bumping it up over the numbers even though their LDL was nice and low and that is a more protective point of view. So I'm not too too excited about that. It's generally a more protective point of view. Um, but there are some genes that are not in
in genre X called LIPC and things like that. And they talk about how much um, uh, HDL you make for exercise. So if people who exercise a great deal, and I do, and I code normally for that gene, I Make a a ton of HDL through exercise. Um, I'm not going to say to myself or someone, don't exercise to lower your HDL. Um the other thing with respect to LDL is fraction it out right do the NMR test where you look at the particle size of LDL. Is it small or is it large? What is
the what is the ratio and therefore what is the impact of this? And then I also say get an angiogram and just see how much of it is is is it doing any damage because we know that if this is Our blood vessel what makes anything to glum onto it cholesterol or calcium etc is stickiness and what makes it sticky is inflammation. So we can we can really decrease a lot of the risk factors associated with higher cholesterol. um because I'm not a huge fan of bringing people's cholesterol down to zilch, which is what they
often do in traditional medicine and then cognitively they're struggling later on. Yeah. Um so just kind of a general Question um in I'm paraphrasing here, but you mentioned said something I think a couple of times to the effect of you know it's going to take uh I think like eight weeks or something to that effect to kind of like you know reset that gene or kind of recalibrate that gene. Um, just so that we're all on the same page, I'm I'm ascertaining that you're not insinuating that you're going to turn like, you know, a T
a G or a C to an A. Um, but, uh, would you mind just Elaborating on what you mean by resetting a gene? For sure. So, um, every gene is like a light switch that has an on and an off position, but that light switch always looks the same. It's just is it on or is it off? So, if a gene is on, it's making that protein to do whatever. Um, if the gene is off, it's not making that protein to do whatever. So, if it is a gene that makes a protein to make inflammation,
I want to turn that gene off. If it is a gene That makes a protein to make more leptin for our metabolism, I want to turn that gene on. So, it's really about um triggering the expression of that gene to make that protein or to not make that protein. And just to maybe get a little more hyper technical here because I just want to know for my sake um and and for the most learned of listeners out there um like are we talking about like gene like methylation or acetylation or things Like that? Are we
talking about transcription factor transcription factors? Okay. Yeah. 100% transcription factors. Gotcha. Okay. Yeah. Um so I know our time is winding down. Um but um yeah, I've got maybe a couple other questions I could ask, but um are there other things about the G&RX report that um you think would be most useful to share? Um yeah, for me by the you know, if you treat the all the areas that are in G&RX, we're treating the underlying Pathology of almost all disease. um whether it's um you know MS whether it is the plaque in the brain
whether it's the low autophagy or the low mioenesis that leads to those whether it is cancerous um in terms of pi3k pathways or mtor pathways or autophagy or hormone stimulation so even though the report doesn't jump out and say you know Lyme disease this is what you do for it or cancer this is what you do for But um all of the Answers are in there. And often as practitioners when for somebody first starts into genetics, it seems kind of overwhelming. You're like, "Oh my god, these illes, what am I doing in just go back
to our foundation? We know what detoxification is. We know what it has, what impact it has on the body. We know how to treat it. We just got to see what's the strength within those systems. We understand the HP axis. We understand autophagy. And so that's why, you know, it's um especially that's why I love lecturing with with NDEs versus any other group um of docs because we have the foundation in this. Um our whole education is about using natural supplements to, you know, manipulate genes. That's what we've been doing. We just didn't know which
gene we were manipulating and in what direction. And sometimes it worked and sometimes it didn't. Sometimes it backfired those patients that had the adverse side Effects, but um the synthesis with the information is is so much faster um with our our crowd and and the educated public who is now also doing their research on this. Um, it's a very good segue into this the next question I want to ask uh or the after the next uh question I'm going to ask. Um, because I'm sure a lot of folks listening are like, "How do I how
do I access this test?" So, I'd like to get into that in just a minute. Um, just the One question that came to mind though that uh, if you don't mind my asking. Um, so you know, with the G&RX test, um, you know, it's your genes, so you really only, to my understanding anyways, only ever need to do this test once because it's it ain't going to change, um, over time for for better or for worse. Um, I'm wondering, um, are there kind of peripheral tests, if you will, or adjunctive tests that you uh, use
regularly to kind of track progress. um Where if you know the genes and especially the way you have it laid out which I again really really appreciate um where it's very much like this like action plan it's not just you know the blueprint and then like ah what do we do with this information it's very very actionable which is lovely um with that being said you know are you measuring people's you know leptin levels are you measuring their you know homo IR scores for insulin resistance are you measuring Their um yeah what what are you
measuring um absolutely um so I do a bit of both it depends on depends on the patient. Um certainly things like cholesterol or homoir or even just fasting insulin levels like all of those I absolutely if it is um cancer and looking at the CT scans and things like that and and requesting you know those through their oncologist obviously if it is hypertension we can look at their their blood pressure but for a lot of Things I don't use blood or saliva anymore and the reason genetics is what's led me into that. Um, so a
really good example is I have very few B12 receptors. I I am mostly vegetarian. I just don't like meat. It's just a taste thing. It's not anything else to do with that. I don't I don't take a B12 supplement. I get little bits of B12 from from egg. I do do eggs and things like that. Um, my B12 in my is always skyrocket high, but It's skyrocket high because I have very few receptors for it to be bound into. That doesn't mean I have good B12 activity. That means I have a lot of B12 useless
hanging out in my blood not doing anything because for it to have an effect, it's got to be bound into a receptor. So when we look at, you know, uh neurotransmitter levels in the blood, when we look at a lot of different nutrient levels in the blood, it's it's the extra. So is it in your blood Because you don't have enough receptors? Is it in your blood because you don't transport that nutrient or neurotransmitter to the receptor? Or is it low because it's all bound up into the receptor having a really great effect? And that's
where we have to marry the genetics. Okay, I see that you don't transport really well. Um, so and and you do make a lot. That's why your levels are so high, but that's why you still have the symptomatology as if you Didn't make any. Um, so it's really genetics has really changed how I add extra testing into it if it is a reliable test. And for it to be reliable, it also has to be longer term. like TSH TSH goes up 150% 12 times over a 12-h hour period. Not reliable. And you know, so we
have to again I'm going to look at the gene that talks about how much TSH you're making on a daily basis. The normal amount, a lower amount, a higher amount, like that sort of thing. It gives me the patterns that I can then marry with the the patient and their symptoms. makes a lot of sense. Um, so how can folks access this test? Um, so Genrex is is a platform that is for healthcare practitioners only. So if you're not a healthcare practitioner, you need to go to your health care practitioner such as yourself and say,
"I'd like to do this test." Um, and that's because there's a lot of medical information. Um, we're Talking about, you know, altering people's serotonin and their dopamine and and I don't know if they're on a medication or not. and they may not know if it's going to interact with the medication that they're on. So, I always want that to be overseen by a healthcare practitioner. Um, the first step is to get your raw your your genes tested. Get your raw data tested. Um, the genes that I use are really unique. So, there's only two tests.
Um, 23 and me health and Ancestry, which has gone through its ups and downs. Um, and it has to be the Health and Ancestry or DNA Allure um, which is a Canadian company um, based out here out of in Toronto. So they have a test called the ultimate genomics and that will both of those tests have all the genes that um GRX uses. So you get those tested, send that text file to your practitioner who then just creates account with GRX and then drags and drops it into the account. It it it is Very easy
on the practitioner level just today. So yeah, once you have that TXT file, you're uh you're a tech idiot, so it had to be easy. I said to my chat guy, you you need to make it so I can do it. There we go. Well, I'm glad you set the bar low for that because that's that's good. I do. Yes. Um well, I I really appreciate the time you spent chatting with me today, uh Dr. Kendall Reed. It's been uh yeah, very very informative. I'm really Excited about the test. I've been starting to use it
with patients and um yeah, just excited to use it even more after our chat today. Um fantastic. Are we are there um any uh social media platforms or online offerings or anything that uh folks or folks want to work with you? Um could you let us know where they can find you or anything you have? So I'm going to date myself here again. I don't have any social media handles. Um that's and I sort of have Enough ways of of people being able to contact me. Um I am actually as of July 1st which will
be 30 years in practice. I'm actually closing my practice to patients. I am only working with healthcare practitioners helping them with their genetics cases. So um unfortunately as a patient they can absolutely um get in touch with me my uh on my website pkrhealth.ca they can email me and I can set them up with a naturopath that's near them um to To go through genetic testing and and and do this. Um but from a time point of view because I already run the company and then I do a lot of lecturing and things like that.
Um it was sort of my next level of getting the information out there at a higher level. Um because I really do see a difference in treatment with patients when we do genetics and when we don't. So the more I can get that information out there by helping the docs who can then help so Many more people than I could touch personally. Um that's my next goal. Makes sense. So um so gnrx.ca CA I believe is the platform for docs to for docs. Yeah. This the software and then pkrhealth.ca for uh contacting you if they
want to get in touch with the doc that work. Exactly. Awesome. Great. Well, I'll put that in the show notes and uh yeah, thank you so much again for taking the time to chat with me today. It was uh Very very enlightening. I really appreciate it. It was my absolute pleasure. Thank you for inviting me. Well, uh, we hope that you enjoyed this episode of the Overcoming Chronic Illness podcast, and please stay tuned for the next