 We're live on Facebook with Dr. Richie Shoemaker who's here in audio today and I am really excited to introduce a longtime colleague and someone I respect just because of all the pioneering work he has done in the field of mold related illness, sears, and anything related to biotoxins. What we're going to go today deeper into is the genie test that he's developed along with colleagues and we're going to dive into what that actually looks like and why this is ground breaking research including the recent published review article that I have here on my desk from trends and diabetes and metabolic disease about hypometallizm so we're going to dive into that and I will let Dr. Shoemaker explain. Before I dive into that just a few housekeeping you can find us here this will be recorded you can watch it later if you miss it the first time and be sure to check out my youtube channel all free videos just interviews with other physicians that have great content for you. So Dr. Shoemaker, Dr. Richie Shoemaker is a recognized leader in patient care research and education and a pioneer in the field of biotoxin related illness. He has dedicated his life and career to uncovering the link between the toxic slew found in many of our buildings and homes and the vast amount of misdiagnosed as any of you who have been in this world as patients or have family members that have been sick you know how this goes you get shuffled around from doctor to doctor to doctor and then no one really understands what's happening or finds solutions for you so this has been really groundbreaking because he has been an absolute leader and one of the first to pioneer what's actually happening with patients who are exposed to biotoxins. So this we often assigned this pyromyalgia chronic fatigue and again hypometabolism waking etc and we put them in these categories but we're not really looking for the root cause so again Dr. Shoemaker has been absolutely instrumental by uncovering the real sciences behind these illness and attacking the problem with clinical studies and sound research. The other thing he does is he's publishing he's actively researching and publishing peer reviewed in the literature for the things that we're talking about today which is exciting because that's what really brings the science forward he led the way in not only identifying the true cause of these afflictions but also curing many in his community that were deemed incurable he truly feels it's imperative that patients educate themselves and now he's committed his time and resources to providing the tools so his website is surviving mold.com if you've been around for any sort of time i'm sure you've seen his website tons of resources there lots of research you can do a visual contrast test there you can just download all kinds of great information and i know you're continuing to keep that up to date. So Dr. Shoemaker thanks for that long introduction welcome and thank you for joining me today. Well thank you for having me this is quite a pleasure appreciate the invitation. Yeah it truly is it really really is i like i was telling you before and just to be public i have the utmost respect you really truly were one of the pioneers that started to name what was happening and describe for the rest of us physicians some of the underlying mechanisms that before that were not understood and we're not put together as far as how it could relate to an environmental exposure and again what we're finding now and what i want to learn from you today is it's not just mold it's this water damage slew that includes all kinds of things that activate the cytokine response before we jump into that i want to hear a little bit about i know your story many people do but tell us a little bit about way back when you first got into biotoxin illness and how that all happened in your life. Well it's 25 years now my my silver anniversary since the days when i was a very happy rural primary care physician and solo practice beautiful neck of the woods here in the bottom of the eastern shore on the east side of the Chesapeake Bay we can see Washington someday oh no that's Sarah Palin can see Russia i thought i got that wrong we can't quite see Washington but we can certainly see beautiful scenery and it's an idyllic place to live and raise a family and i was pleased to be a primary care physician and doing what i wanted to do is an outpatient practice and long come some looming disaster in the waterways the pokemoak river drains into the Chesapeake Bay there's 22 other estuaries that we were worried about as it turns out but something happened they our habitat changed fish that normally would swim away rapidly when here comes a boat or somebody else started acting erratically and swimming in circles and there were a few fish kills in 1996 and people who worked around the fish kills harvesting live fish we call them watermen you might want to call fishermen but they get crabs and oysters and that's how you say oyster it's oysters i gotta be proper here but specifically these folks had direct contract with with droplets of water and and fish with with skin problems called lesions and you know fish are always are getting lesions and the scales and slime don't really fix them all the time so this was not a true surprise but the illness was new the illness was not just i'm tired it was i'm tired and my brain doesn't work i'm tired my brain doesn't work and my joints hurt and to that diarrhea and secretory diarrhea was a real facet of them of this problem the skin problems there were diversity of lesions that we saw biopsy just showed some lymphocytic infiltrate not a not a real clue along the way but these people were were acutely affected and guess how much of the world's literature there was on people like this one zero so were they were they just a gomer and you remember what a gomer is right get out of my emergency room you know these these these folks are people i knew i would see them in walmart i'd see them along the street we'd build a nature trail with them so these these are good and honest hardworking people they're not making things up they're not trying to get out of work the story is is heard over and over again but interestingly in 1997 a tv announcer from channel seven out of washington named brad bell sent a water sample from the pokemon down to a lab in run north carolina at nc state where joanne berkholder had been looking at an organism called fisteria sounds like hysteria but fisteria we had been active in the panico sound and news river and what have you and there are lots of problems with fish kills and anybody who said they were sick was almost hounded into silence so no cases no studies no human illness and lo and behold we had fisteria in the pokemon river well what this little organism does is normally have a very slow moving you know phase of its life where it kind of crawls along the bottom of the river but if another fisteria comes along and releases a toxin that toxin is actually a pheromone it's a signal for feeding and breeding so you would get suddenly a bloom of fisteria organisms they would make a system drop back in the river in the way they went well what happened that this new monster with multiple life forms could grow in our in our river nutrients had no change and they ended up being blamed of course government officials like to do that but what was new were additives to the water column a blue mold was now wiping out tomatoes wiping out tobacco in areas where water would be runoff during rain events into the north canola sounds what have you into the news river in the pokemon river would be where we would see a sudden bloom that would come and go feeding and breeding and next and it turned out what was toxic in the in the water was copper in that it would kill things that the slow moving phase of fisteria would like to eat and then there also were diethiocarbomates special old-fashioned fungicides that killed off the things that ate fisteria so you had a double whammy that says this organism is going to be fast moving in the water column and it's going to not have any predators so it made toxins more and more and more and more people got sick and i got inundated with people richick you got to do something so secretory diarrhea well you and i are old-time family docs we know full well that colis styramine a non-absorbable anion binding resin with the anion radius of 1.4 angstroms will bind very nicely to negative charge anions and make life easy because the match of what we saw in toxins later on was a ring a negatively charged ring of about 1.43 angstroms that matched to 1.4 angstroms where the side chains of positive side chains of colis styramine we had a mechanism now to stop what's called entero hepatic or gi gastrointestinal liver recirculation to go the toxin be made come out secreted against the gradient in a bile down into the duodenum reabsorbed in the jejunum and on you go people did not self heal unless very strange things happen but you know there's diarrhea i couldn't fix i tried everything you know mo trend and steroids and you know anything that anyone would do in practice would think about but i said why not use something to stop the secretory diarrhea give people some sleep for god's sake so they're not going 10 times in the middle of the night and lo and behold the very first patient in 1997 called me back two days later says boy that stuff is great stop my diarrhea well of course that's that i gave it to you for that reason i'm glad to hear that she goes but you know like my memory is back in my car my coughs gone and and i can breathe through my nose and i'm not short of breath i'm going wait a minute wait a minute well i had a bunch of people almost in the charts sitting on my desk saying i haven't been able to help this person because the labs are all the same yeah nothing nothing abnormal at all just like we know today normal said rates you know we didn't know then why high viscosity gave normal said rights but that's for another day but specifically what happened is that i was faced with a decision am i going to be firing shotguns from a family practice gun that says i'm going to give people medicine even if i don't know the physiology even if i don't know the pathophysiology but if i can make them better will i do something like that kind of like with kovat people what are they going to do and well maybe we'll have time to talk about vip and kovat but it's a great story and uh secretory physiology you tell you what but with that in mind over 200 patients later i had a winner because i still didn't have the physiology but i had a mechanism that i could help people who are adversely affected well guess what there was some criticism amazing you know it's a free country so you can criticize ritchie you know but that was done and needed to say when i said copper and i thought carbon mates nobody ever heard of such a thing and yet when you disrupt chemical chemically disrupt i mean you're you're a big end to round up and all that stuff and i can argue with you and you argue with me so there we go but specifically if we are looking at an environmental source an environmental disturbance would that be different if it was a different organism besides a dinoflagellate well here came the phone call from the st lucy river we've got a problem through the crypto paradigmiopsis for 25 years i can still remember that name how about that that's good person man woman camera tv right okay oh no that's somebody else you don't know that joke uh-huh maybe you and me only but all right anyway but anyway sure enough what happened in the st lucy river which is on the east coast of florida is that when lake okie chubby fills up the water that's breaching the the top of 18 feet down of lake okie chubby's got to be vented and you can't put in the everglades and the cape sable sparrows as you can't put it down in the clues to hatch you so they sent it through all the channels and canals into the st lucy and as soon as they opened the c73 lock you knew that three days later there was going to be a bloom of dinoflagellates and guess what was in that pore water that florida proof mariland never did it was copper and i thought of carbon mates so here we have the same thing so blooms next in lake okie chubby well my goodness look at what's going on there of course the okie chubby and in florida that part is full of phosphate in the water and you're going to be giving nurturing and nutrients to cyanobacteria and every single sage has got cyanobacteria we think about the pond scum but sure enough they had the same symptoms for steroid patients did they had the same lab abnormalities they were all zero and by this time we finally had a diagnostic test visual contrast sensitivity thanks to ken hud now that that's brilliant that because that's such a even though it's not specific it's such a great tool how did that come about was that research that you had found for biotoxins or how did you find that visual contact was was a neurotoxicologist for the usepa he was based in research triangle park and he had studied by some you know organic compounds affecting the visual pathways yeah and he could show a defect in dry clean workers who's opposed to you know tetrachlorothylene and all these other things and there's lots of stuff that i don't know about that they used hydrocarbons would also cause a problem with ability to see an edge where gray meets gray you lose the ability to see an edge where black equals white then you can see an edge but if you turn down the black and make it grayer and you're darken up the white to make it grayer you'll find a point of extinction that you can't see a line that has a certain shade and that point of extinction became the point that we could put on a graph and we could do the same test in multiple places and show the same abnormality and then when we found that infisteria because i called up ken because he was the first person in the world to publish on vcs infisteria i said ken i can fix this illness and he said well look let's do before and after vcs and bingo within four days we had an answer we now have the first biomarker but how come some people were swimming in williams point there's 10 people three people got sick and seven people didn't well it couldn't be drinking beer everybody in summers accounting drinks beer you know that and you know what is cigarettes or age or disease no no no it wasn't till 2000 i started reading up on hla and look at this here was immune response genes oh my god there was no teaching back then in medical school and we knew about hla b27 but not hla dr but anyway sure enough that was the answer and we needed to collect enough data to prove that there was a genetic susceptibility as shown by increased incidence in cases compared to incidence in controls and when that ratio exceeded 2.1 it's going to be 2.0 to 1 we had then relative risk so we had now symptoms we had normal laboratories we had hla we had bcs what else was there well it turns out here comes along 1998 people with Lyme disease well they had the same visual contrast deficits same symptoms i'll give them colostyramine same way i always do and hopefully didn't get constipated and hope all the good things happen well they didn't they weren't were able to take it long enough to get to to figure it out they did they got slammed they could barely lift their heads off the pillow and sure enough this was the first clue that cytokines were involved when cytokines were involved i started reading about vegef and now low vegef was involved and now mmp9 told us about endotoxins and one after another i think i have been the original publisher on 25 different biotoxin biomarkers for sir's illness chronic inflammatory response disease and we have two more that were coming out next week let's specifically what we now we're seeing was the commonality among exposure to biotoxins which are small compounds less than a thousand daltons teeny tiny little things they had the ability to move from cell to cell but more importantly they had the ability to be secreted against the gradient out of bile to dump into the duodenum and if we had colostyramine more thanks to ray stricker ray was the first from lime to say try well call and he was right that worked we could now come after these folks but not everybody got better and tim roberts from australia was working with me on a different case and tell me about this marcon's well tim told me about marcon's and sure enough we had it too and as time has gone on marcon's have been a real flashpoint and it separates me and you here just jill just to tell you the truth because use of particular medications and antifungals especially will induce horizontal gene transfer and create massive antibiotic resistance and marcon's and marcon's are boy are they ubiquitous and they love to breed with anybody else and share little bits of DNA and antibiotic resistance factors we knew from burn units as soon as you use antifungals and antibiotics together in a bad burn guess what you had resistant fungi and resistant staffs the same antibiotic resistance factors wow amazing and that's true to this day so i'm going to argue by antifungals there i'm really going to get you when we come to genie but that's all right as time went on i'm very good i'm glad to hear your opinion and this and the science because i really i mean i want to be the best scientist that i can what i've seen that makes a difference is we have immune compromised and that makes those people are the subclass that really is a different treatment group and those people are full of optimistic infections like fungal infections and i find antifungals and immunocompromised to be life-saving so tell me what the definition of immunocompromise is yeah so deficiency of total IgG and now the literature is supporting even deficiencies in IgM or IgE that's brand new definition but classically they combine gamma gamma globulinopathies those are pretty severely ill people that cannot my boy good good luck finding a lot of those cases i used to track my immune globulin panels and finding gamma globulin deficiency or any of the four times of IgG was was rare but there's very different though see that's why i think there is a difference in this and i really like i just have nothing but respect so i i love talking about this in a respectful way because i do believe right they're overused but on the other hand i actually do have a large percentage of immune compromised patients i don't know if that's just because of the people i treat so it is a different ballgame for them they they require antifungals in order to overcome because they cannot amount to response innately well it's time you publish that yeah you're right you're right because i'm gonna want to see it period and what what are the data show and if you have this is this is something new and if it's legit it'll stand up to peer review and certainly that's where you go but to go back to where we were talking it became clear that in 1998 the first persons that i saw who had a hysteria like illness who didn't have hysteria exposure they were nowhere near the pokemon river all they had was a closet that was full of this black stuff that was growing with the roof leaked wow so how many years between the first river exposure and the actual this mold how how how long did that how many years 1997 and 1998 so by by that time we had our first mold patients before we had Lyme patients but we had dinoflagellates and cyanobacteria is the first but then there were some people that didn't get better marcon's had to be eradicated back then we could use big spray varies with great results not anymore but then it became clear that we fixed the the colostyramine deficiency or well-called deficiency fixed that and and marcon's was gone people still were not getting better well what else will hear mmp9 elevation oh my god i can fix that too it's a marker for for th1 cytokines and then we had this the insight will have a low veg f and then along came c4a oh my goodness was c4a the big player and finally in 2008 i begged finally beg beg beg because all the time but for example with mmp9 there was a lab called esoterics outside denver that agreed to do mmp9s for me i was the only person in the country that had that data i was the only person at hla i was the only person treating this with colostyramine now a few others came along later and they said they were the first but you know i published first anyway having said all that the same approach to classical science of looking at data of cases versus controls prospective reexposure trials to prove risk that's the only way you can prove risk is prospective studies so we had the sequential activation of need immune elements and multiple papers along that way and in litigation and i hope you're doing litigation but specifically we needed a voice to not only convince physicians but also convince the attorneys because you don't change the law if you don't change the attorneys the laws are dastardly but anyway the whole issue is that along with the legal testimony work along came multiple publications and suddenly we had a robust literature so the robust literature has continued to grow and in 2003 and four the human genome project was going you remember you know billion dollars and what in the hell in the world are they doing all this not understand all this but you know having said all that uh transcriptomics started evolving in 2005 and differential gene activation was sort of first got attention in cancer a little bit in vascular disease but still it's it's it's a it's a rosetta stone that's that's unscratched and along comes jimmy ryan who's a transcriptomist brilliant man he started working with me and we see jimmy said well we need to raise a million dollars sure let's do first connect how did you connect with siguitero dinoflagellis jimmy was working at the national marine biotoxin lab in charleston and i went down to give some talks on fisteria and siguitero and he was doing stuff with john ranchdale that i didn't know about and they didn't know about the human health center why don't we work together and so that got started you know with the mold pieces but in in 2010 when we published a paper on on siguitero which is a marine dinoflagell that makes people sell be sure to ask if people have had fish from the grower reef part of your differential diagnosis but having said that nobody does at any rate when jimmy was able to convince me to raise the money to buy a aluminum sequencer next generation sequencing an rna seek we could see of the 50 000 genes that we could sequence in seris patients there were 2000 they were always abnormal we went to those 2000 genes look with the greatest signal to noise ratios and looked at diversity we wanted cytokine pathways we want a coagulation pathways and we wanted to look at what was going on with lack of ribosomal rna ribosomes weren't working right we couldn't get mrna to attach to start making a protein we couldn't make you know amino acid added to a daisy chain for so we didn't have the elongation we didn't have termination these these these this rna was not there what was suppressing it that led to discovery of the sarsen ricin loop and remember ribosomes have two big structures the large subunit and the small subunit they're sandwiched around a little tiny piece which is where all this protein and amino acid stuff works sarsen most people haven't heard of sarcoma inhibitors but they have heard of ricin a plant toxin and ricin works by splitting off the adenosine moiety at position 15 on this loop that's necessary for this whole structure to work and every single living creature you name one every single living creature has a sarsen ricin loop and four billion years ago look at the bio warfare we had fungi dealing with spirochetes my gosh sigma terror is coming spirochetes dealing with dinoflagellates all this stuff going to cyanobacteria making the first oxygen in the environment these organisms made ribotoxins that would take the the adenosine moiety out they also made ribosome inhibitory proteins and those compounds are with us today they are creating the hypometabolism that starts with ribosomes in the cytoplasm but extends the ribosomes in mitochondria mito ribosomes so if you got a ribosome well that in the mitochondria there's got to be a gene to program for RNA right well there were a thousand genes from mitochondria now there's 37 at last count 37 where'd the other thousand go well you know they migrated to the nucleus and they are nuclear encoded mitochondrial genes and they're subject to transcription factors so the same transcription factors oh boy when I tell you about TGF-81 oh my goodness the same transcription factors that are differentially associated with gene replication or activation or suppression remember there's four layers and the disease we're talking about is that disease is lack of regulation of lack of regulation of lack of regulation of lack of regulation of DNA transcription and if you understand that you'll see why nuclear transcription factors micro RNA some of the long non-coding RNAs and then housekeeping genes are regulatory for gene transcription you know I see you'll hear a lot of people talking about you know methylation all this stuff and I just kind of yon because you're missing the boat if you're thinking about methylation because there's more deep methylators and there are methylators there's more acetylators and deacetylators but there's both of those are constant so epigenetic stuff is four different structural layers of gene transcription don't don't start me on methylation and it'll ruin a good day having said all that to go a little further what we found is that or jimmy found not we jimmy found is that a collection of mitochondrial encoded nuclear genes control ATP synthesis and look at what we want we want pyruvate to be broken down from glycogen and from glucose we want glucose to be taken up by glucose transport proteins one and four there's solute carriers incomes glucose into the cell there's other mechanisms as well but there is the vital role of insulin and illicit receptors than insulin receptor substrate two this is regulating metabolic back to the past like crazy and don't you know jimmy found abnormalities in metabolism as well so we had ATP synthesis you don't make ATP the poor mitochondria is being victimized people are saying this a mitochondrial disease for god's sake no it's not it's just lack of ATP synthesis and look at ectinomyces oh my goodness look what they do pyrocyne A knocks out complex one oligomycin knocks out complex three we can affect the electron transport turn chain with actinose found in water damage buildings oh my who never heard of such a thing well just wait do you see volatimicin and monansin and nigericin because those block the voltage dependent anion channel now you know and i'm going to use some of the other what else do you do now is that this little pore sits on the outside wall the outer membrane of the mitochondria and if it's open you will have migrating inside the cell ions okay that's a good idea solutes okay adp ah that's where you make ATP from ATP and pyrovate ah that's how pyrovate gets into the inner mitochondrial space and then the transport protein will take it from the inner membrane and put it into the electron transport chain and cribs cycle that's where you use all your ATP but if your pyrovate doesn't get in what happens to it it stays in the cytoplasm and pyrovate cannot be sitting around because it's going to cause trouble and pyrovate gets converted into what lactic acid oh no lactic acid is secreted against the gradient but glucose is still being pumped in making new compounds and there will be diversion of those new compounds into the building blocks that the cell needs to reproduce oh so let me talk really quick Dr. Shoemaker this is brilliant i'm following you every bit of the way but for an average listener there's two things i want to talk about because i think you just mentioned basically for if you're listening and wondering this biochemistry that i find fascinating that Dr. Shoemaker's explaining and brilliant what what he's talking about is the cellular energy makers this the energy producers in each cell they're broken and what we get from that is this exercise intolerance he's talking about lactic being in the cytoplasm and when that accumulates you'll have that muscle soreness the fibromyalgia the chronic fatigue so what he's describing is on a chemical biochemical level what happens when you after you get exposed to mold or some of these other biotoxin pathways the chronic fatigue the fibromyalgia the muscle pain the exercise intolerance where you're sore two to three days later this is the biochemical pathways if i if i'm right Dr. Shoemaker of what we see in the clinical practice so it's so relevant there's way more yeah way more i'm on a roll going let me get back on it you're you're right to clarify thank you so the question then comes if we've got pyruvate being made into lactic acid and secreted against the gradient is there a medical condition for which we see extra lactic acid yeah it's called metabolic acidosis and if the cell is getting ready to divide making all these extra building blocks that kind of physiology is called proliferative physiology so proliferative physiology means you only get two molecules of the ATP from each bit of pyruvate and for total for that whole situation but you make building blocks and along comes this whole mechanism lack of energy storage so you're now that metabolic acidosis and proliferative physiology what else goes with that now i i know that you've had some health issues in the past and used to talk about in public so i'm not breaking any secrets not at all i was disabled by pulmonary eye pretension in 2012 the reason i stopped with medicine because the cardiologist said put your things in order what's kind of nice words to hear wow so where did my pulmonary eye pretension come from so i started looking at people we could identify proliferative physiology i'm going to get to that in just a sec and we said if they got metabolic acidosis what else do they have well lo and behold 80 percent of that pulmonary eye pretension 80 percent of them have T regulatory cell deficiency yes they all do yes i agree they all do we see that and that's where that they also get injury to gray matter nuclei injury to cortical gray and enlargement of superior lateral ventricle we can show the mechanism objectively without any guessing without any ridiculous psychological exams we can show in black and white the definable objective pattern of injury and we published a paper in 2017 showing we can fix that and we still can't we're on a roll with that so now we've gone from physiology of hysteria what in the hell is that to the molecular biology of proliferative physiology as opposed to energy storage associated with metabolic acidosis associated pulmonary eye pretension associated t-rig cell where's the oral immunity come from where's all the tissue based inflammation lack of t-rigs oh my gosh t-effector cells are beautiful i want to just pause really quick to clarify that again just for the lay person so we have th 17 and t-rig cells and then we have th 1 and th 2 but t-rig cells are like the body guards they're like hey calm down don't overreact we don't need to react to too much out there everything's okay and they help us not to be either over reactive to pathogens or over reactive to self and create auto immunity they're really important if you don't have t-rig cells you're going to be a on fire for auto immunity and on fire for inflammation and cytokine production and most people in this illness have elevated tg f beta which drives th 17 and a reduction in t-rig cells which is what dr schumer there's there's more you haven't listened to me recently there's way more oh yes there's more i'm trying to keep it really simple go ahead let's let's let's go back to what else did jimmy ryan show us i talked about vdac this poor it turns out translocases and if you don't know what a translocase is join the club i didn't know but it sounds like it moves from moves from one location to another a translocase this protein is necessary to move mitochondrial proteins through the poor and through this complex into the inner membrane of the mitochondria and if your translocases are depress or deficient if you don't have that mrna will you get mitochondrial proteins coming in to the inner matrix of the mitochondria the answer is no so we've talked about actinose and i mentioned probably too quickly that actinose disrupt vdac they do translocases affect vdac as well and it turns out the more genes that jimmy started looking at we started looking at beta tubulin and tubulin a4a when we looked at the the associated findings of people with abnormalities of these two cytoskeleton structures these microtubule structures we found that they had a mean of 6.15 gramantre nuclear atrophy and area atrophy out of a total compared to controls that would have 0.9 so they were hugely abnormal what do those tubulins do jill can you answer my question is what do they do to the vdac no tell me they block it okay so proliferative physiology now when we fix vdac we also can fix gray matter nuclei we're using vip in my protocol for the further to fix gray matter nuclear atrophy didn't know we were fixing vdac but specifically we now had the the the the poker hand that 90 percent of people with chronic fatigue illnesses whether they're serous patients heart failure patients cancer patients renal failure patients psychiatric fatigue patients they if they have proliferative physiology they have hypometabolism now the met hypometabolism is made worse if irs2 is elevated why let's talk to jimmy care hypometabolism you and i know what that is let's just describe for the average person what does that actually mean what is molecular hypometabolism or mhm is not the same as hypometabolism i try to save time but this is suppression of rna genes suppression of mitochondrial genes suppression of might arrive with some on nuclear genes so all these gene suppression due to impairment of the sarson rice and loop is where this illness comes from it's real simple it's real simple and all this gobbledygoo it's real simple if you've got hypometabolism you're going to have proliferative physiology if you've got proliferative physiology you will do worse if you start having problems with insulin receptor substrate that opens the door to let more glucose in therefore more pyruvate therefore more lactic acid and if you say i'm going to use a keto diet my cringe buzzword you either get glycolysis if you got irs2 glycolysis is going nuts either you glycolysis or you've got fatty acid oxidation yes and if you got fatty acid oxidation glycolysis will be depressed but if you get glycolysis up regulation which we do if you're if you're proliferative the keto diet's not going to work you'll get a lot of placebo effect but in terms of glycolysis and in physiology you won't get what you want well i want to comment because in clinical practice what i have seen is exactly what you're describing i completely understand there's a percentage of people that do not do well on a keto diet nor should they be doing it because they don't have the ability to utilize the alternatives for fuel don't use keto if you've got molecular hypometabolism later on what if irs2 is suppressed you keto works fine but if irs2 is up it doesn't work fine there's a reason for that and this is also why we're basically seeing the induction of pre-diabetes diabetes metabolic there's multiple mechanisms including remember these assimilation pathways i was telling you that lucas can can use to to make cell division you also will have the exosaminidase synthetic pathway that results in creation of insulin resistance now that's why by action on on on on fat cells not by glucose so we need to change our thoughts there also is intracellular insulin resistance from monansin and nigericin which is something that for another day but that's that's what actinomycetes do so there's multiple ways to impair glucose metabolism but here we go now what else do we see in genie apoptosis of programmed cell death is a mechanism to take care of cells that are programmed to die and grants i'm sure will label a cell saying it's your time to go and here come natural killer cells provided they've got a t-cell synapse and they don't insert uh-huh well apoptosis again just to clarify for those of you listening apoptosis is how we don't get cancer it's how we take dead cells and tell them hey get out of here don't be uh nuisance don't cause trouble when their cell life is over for simplistic more remember when you when you make it easy remember the apoptosis starts with mitochondrial changes mitochondria rules the classical pathway for apoptosis because they're targeted when they're mitochondrial dysfunction for cell death well i'm going to disagree with that one that's right i've got a nice lecture showing the mechanisms that will go along with that they're a little separate activation of capsaic signals are are not not not the same specifically what we're looking at is programming a cell to die and packaging cell components like dna and rna and mitochondria and you know endoplasmic reticulum and ribosomes packaged in them inside of a membrane so that when they're released into circulation that membrane protects the contents from being recognized as a foreign invader like dams and dams like damages this uh pathogen sure but what we're looking at at 15 percent of serous patients and 15 percent of chronic illness patients have defective apoptosis and they only have ripk1 a gene that goes in that interacts with ripk3 that will kill the cell now covid uses this pathway hiv uses this pathway so it's pay attention this cell will be killed if it's harboring a virus most commonly the virus can block apoptosis but the cell says okay you've blocked apoptosis mr virus i'm going to kill you i'm going to commit suicide with necroptosis there's 12 of these apoptosis or and specifically what will happen here is that there will be a release of the cell contents without membrane packaging so you have an endogenous inflammatory cascade like crazy yes this is a this is a cell danger response that dr nevo wrote about well we're going to talk about that because what comes first the gene activation or gene suppression or mitochondrial response so that's that's still and by the way when when dr navio was writing about that he was saying that that is part of the dour physiology this this nematode called c elegans he has been well studied that goes in dour as a stage of hibernation that is not what we call oxidative glycosylation it's deoxidated so it's it's anaerobic so aerobic glycolysis versus anaerobic glycolysis so what bob was talking about is anaerobic glycolysis effect this is aerobic glycolysis it's very important to make that distinction so now we're looking at other elements of cheney how about coagulation we've been jimmy's published and i've been co-authoring of papers since 2015 that in biotoxin illnesses coag genes are upregulated and lo and behold here is this ton of work out of rochester rockefeller university uh in new york city looking at the vascular hypothesis for neuronal injury and i'm sure you're familiar with that because here we have coagulation elements will be bound to a bo b excuse me uh web locket be bound to one of the precursors in alzheimer's to bind to make a clot in the vascular bed that clot will create a distal hypoxia so that more of bad guys more tall will be made and this so that we've got apo a and b and all these these just amazing but what if you've got coagulation genes upregulated will you make more coag products to be bound in the brain yes and you can look at the difference between the 10 genes we look at for coag if you've got two upregulated you'll have two or three genes that are that are that are too small but if you've got four genes upregulated for coag the mean number of gray matter nuclear atrophy is 4.5 just just from the coag genes now i told you a couple times that i wanted you to go back to be thinking about tgf beta one as it turns out because we're running out of time as it turns out if we are looking at the fundamental difference between you and me i see exposure you see exposure i see immune reactivity i'm not sure you do and the difference is exposure who so what who cares if you're exposed it turns out if you have a proteomic response that person should care but if you have the immune response that illness is very very different in much worse for years i have said i cringe when i see certain hla types 4353 and 11352 b saying these are the dreaded well as we turns out the link from exposure and we can measure hopefully you're using a lab that will measure of species abundance not not just one species not not just streptomyces grisius that you get for from micrometrics there's nothing wrong with that but we're looking for species abundance we use evirobiomics i have no no plug for them there's no no conflict of interest but if we look at ectinos in this whole situation what we are looking at is mechanisms to show exposure and then we can look at particular immune markers and that's proprietary that will show us that there has been a reaction to the ectino compounds these are intracellular compounds ectinos make more compounds than anything else it's a it's the biggest species of all or biggest genius of all in microbiology but ectinos if they are exposed and there is immune response there will be activation of tgf beta one receptor one two or three and that receptor links to smad all the different smad is nuclear transcription factors so now we've got the mechanism more common in 4353 by far 22 times what normal population is in people with exposure and reactivity but if you get activation of this receptor the downstream pathways not just smad not just nuclear transcription but they also are the same basic building blocks that insulin receptors do it is the link of metabolism to inflammation in a brand new way and this is stuff we published the first time next week so it is it's uncanny so now we're looking at the link and saying all right do you have a link for ectinos yes do you have a link for mycotoxins yes do you have a link for endotoxins oh yeah we do cd14 and tol4 well which is more common in a thousand mold patients now what's more common is those links that turn on if you're exposed to mycotoxins no they're not first ectinos are first how about mycotoxins being number two no endotoxins are number two mycotoxins are seven percent of the problem seven percent of the immune responses so activity of this whole metabolic structure of the basic difference between proliferative physiology versus energy conservation should make sense biology has limited mechanisms to to act upon we don't have a million different genes we got 50 000 that's that's plenty but specifically go go ahead i got one more point to me no i just didn't say i want to link to because lps endotoxin me has always been a big plug for me i really even with covid we see the underlying cytokine activation of my lps is underlying 90 of the illness in the united states and even in a water damage building i what you're saying is mold is not the primary trigger it's endotoxin it's not i actually want you to read i want you to read a little bit more about red blood cells ability to to bind endotoxins to endothelium so this whole idea every every time you had a bowel movement or you pee or you have some intimate activity there will be endotoxins in blood but red cells take care of it pretty fast so be be careful on that one i want to go back to a couple other all i want to say there though is the data on endotoxin me there's there is so much literature to support like you want to talk about the most research out there endotoxin mea has a lot of data to support it as the and the mechanism by which you get sustained endotoxin me has a very crummy literature yeah very small i would agree i totally i totally agree i just wanted to clarify because i think we agree on more than you think we do but so i know you have to go but why don't you go the last maybe five minutes or so kind of summarize then just for those of you listening dr shumaker is talking about the genie test i will include links on his recently published article and then when the next one comes out so i'll be sure and get those links from you dr shumaker and include those and then i will also include information on the test that you're talking about a lot of people are asking what's genie what they want to know more you'd have to work with your doctor to get it ordered is that correct dr shumaker yes the clear license will be coming around before long a couple things i wanted to touch on there are a lot of folks in the chronic fatigue world think that viral activation is a big deal and they say it is say it is say it is fortunately compounds made by neutrophils called defences will be activated if there are viral infections so we give you two defences it's all that you can actually with the genie help to identify which persons are more affected by viral activation or not viral or not viral it's it's actually about less than 10 percent of all of this total but similarly bacterial infection here's the easiest way to detect bartonella by the way lime the mechanisms that we use that were published in transcriptomics of lime in 2016 bouquet's paper was with john alcott and uh and charles chou from ucsf we we can tell you if you don't have lime disease in the last six months we can tell you if you're if you've been treated in the last six months it's kind of me the other thing that's bothered me for so long has been chemical sensitivity and i'm going to take just one minute i've seen plenty of people with chemical sensitivity i can recognize them when i talk to them but finding an accepted case definition for chemical sensitivity good luck you've seen people with with food sensitivities you've seen people with uh drug sensitivities it all turns out that if we look at icarus the anti-inflammatory pathway and add up accuracy because it's positive and vip r1 this vip receptor is negative those people are chemically sensitive and the low-dose vip protocol we got we'll fix that icarus vip and fix the chemical sensitivity we're going to publish that very soon but it's just fascinating the other piece for genie that people need to know is that the marker for sers the marker for persistent illness is lack of normal antigen presentation in defective antigen presentation we know about hla we've talked about hla but look at the antigen presentation of the dendritic cell professional antigen presenting cell to a naive t-cell aha cd3d boom we can look at that with one test we can look at cd48 what we're really looking at now has to do with histamine for folks who think they've got moment mass activation syndrome if the genes for histamine are up-regulated you don't have mass cell activation you've got genes that are the basis of histamine release that's why so many people with mass cell activation will have normal triptases and normal grand and aid because they don't have the disease they've got instead histamine release the last thing to say is that relapse one of the we stratify people by five stages stage one is treatment naive stage two is after my protocol stage three is after vip stage four is off vip cured but the fifth stage is relapse within two days 100% of patients with reexposure and reactivation of immune reactivity those people will have return a proliferative physiology we treat that infectively with the protocol it's so nice that you have that string and return of iris to up regulation within two days so the next prospective study is going to be take volunteers for usually those in litigation or will do anything and do the psi protocol that wins the legal cases very nicely but break down the reexposure on day one into four hour increments so we can see how fast does the proliferative physiology occur I think it'll be less than eight hours yeah eight hours that's all it takes unbelievable and yet I completely believe it I mean truly that's the that's fascinating so you've got the paper coming out as soon you'll have to be sure and send that to me and I'll share it with everybody who's listening and then as these come out we'll have to get on here again and talk about your your next data set with exposure and hypometabolism and how quickly that occurs and immuno reactivity yes yes the link the link between inflammatory illness and metabolic illness they go hand in hand you cannot deal with this illness without both the elements absolutely well Dr. Shoemaker thank you so much for your generous time with us today I know everybody's just really enjoying this there's lots of comments I'll have to go back and post I'll be sure and share with you the link here and then when it's on YouTube in case you want to share or use it in any way and I really do appreciate your time and your expertise and thank you as always for being such a leader in this field we greatly appreciate it well thank you for those kind words it's good words to go home on yeah okay bye bye