Heidi Kong Good morning. I’d like to thank Lita for the invitation toe here today and talk to you about our work and how it relates with our HMP demonstration project on atopic dermatitis. We’ve heard a lot about the gut microbiome, and I think it was nicelyanized that Susan’s talk about the skin and wound healing segues very well into my focus on the skin microbiome.

And one of the overarching questions that has developed in our time in looking at the skin microbiome is Do skin microbes influence host skin immunity I’m going to go give some background for those who are not familiar with the skin microbiome work in order to be able to talk about the microbiome in eczematous skin. I’m highlighting here a series of experiments by a collaborator, Yasmine Belkaid’s group, to highlight some of the differences that we see in that this not only is the skin microbiome different than other body sites, but that the skin immunity and the skin microbial relationship is also distinct. Here, Trudy, who was a graduate student in Yasmine’s lab, she treated SPF mice these are all experiments in mice with antibiotics and what we can see in the gut, that after antibiotic treatment, there is a significant shift in the microbialmunities, but you don’t see those significant changes in the skin microbialmunities. Also, Trudy looked at the immune cells that were in the gut IL17 LMA, as well as interferon gammaproducing cells in the gut. And, aspared to the skin, once there was treatment with antibiotics, there was a significant reduction in the interferon gamma in IL17Aproducing cells. So there are, in distinct epithelia, there are differential responses to antibiotic treatment, at least in these mice.

So, Trudy then went on, and inparing SPF mice and germfree mice, SPF mice here, germfree mice, looking at IL17A producing Tcells in the gut and the skin, we see here that there are reduced IL17A producing Tcells in the germfree gut and skin. However, what she then did was topically monoassociate staph epidermidis in the germfree mice, and interestingly, there were no changes in the IL17Aproducing Tcells in the gut however, in the skin, there was an increase in the IL17Aproducing Tcells in the skin after application of staph epidermidis. So we can see here that skin microbes do influence the immune system, but is there a function Is there a biological result when you do that So, what then Trudy did was use a Leishmania major infection model. She infected the ears of these SPF mice and germfree mice, and inparing these two, you see that there is a local cutaneous response in the SPF mice, aspared much larger than the germfree mice, but also so you see increased interferon gammaproducing Tcells in the SPF mice, aspared to the germfree mice. So then when she topically associated staph epidermidis in these germfree mice, you see an increase in the local cutaneous response, as well as interferon gammaproducing Tcells that are in the ear. And these resemble what you see in the SPF mice. But also, here we see in parasite burden, that you have a decrease in the parasite burden when you treat or topically associate staph epidermidis. So skinmensals can restore immunity to Leishmania major infection in germfree mice.

So summarizing this part, the host immunity and microbial interactions in skin are distinct. In mice, skin microbes can tune the skin level of activation and function of skinresonant Tcells, promote immunity to pathogens, and drive responses locally that are distinct and independent from the gut flora. But what about human skin immunity and microbial interactions Unfortunately, we don’t have a lot of germfree humans walking around that we can do these types of experiments, but what we have done is started to look at what are the microbes that are on human skin. So, again, this is a background for those who are not as familiar with human skin microbiome surveys. These are highly selected due to limited time that I’m not going to go into all the surveys that have been done.

You’ve seen this figure before, but the reason why I’m showing it again is I want to emphasize that in skin, here in pink, there is a wide variation in the microbiome that you see in skin, aspared to the other body sites. And that is because the skin’s surface is highly heterogeneous, and that is one of the reasons why, in this study, we selected 20 skin sites. These are distinct microenvironments on the skin’s surface, but I also selected them because they were sites of predilection for skin disease, specific skin diseases for which microbes have been postulated to potentially have a role. And David Relman showed this figure earlier, so I won’t go into it in detail, but relative abundance of predominant bacteria appear to be dependent on the microenvironment.

So we’ve talked about this throughout yesterday and some this morning, how there are carefullydefined cohorts that we’ve looked at most of these are adults. We’ve talked about what happens, there have been the studies by Maria Gloria, looking at the neonatal period, but what happens after that Ruth Ley talked about the at least for the gut microbiome, how that can transition in the first two and a half years, but what about the skin We don’t know thatrmation. In the other next transition puberty. This is a turbulent period of time for our bodies. What happens between as we transition into adulthood There’s something called a Tanner stage. For those of you who aren’t clinicians, the Tanner stage is used by pediatricians to assess the level of sexual maturation in an individual child. This is based on development of breast tissue, as well as genitalia, pubic hair, but it ranges from one to five one being prepubertal, five being fullydeveloped adult.

So, what we have here is we had cohorts of patients that were ranging from two to adulthood, so what Julia Oh did in our in Julie Segre’s lab was take these data andpare them with each other. And based on Tanner stages one, two, three, four, and five, we see the striking difference between Tanner stages one, two, three, and tanner stages four and five. This is from the nares, but we see a similar separation in other body sites in other skin sites.

What drives that Here we see a relative abundance chart, which you’ve seen a lot in these talks leading up to now. And here is Tanner stages one, two, three, and then here is four and five. I do acknowledge that the ends are pretty low in these populations, but what we see in Tanner stages one, two, three, that we have increased proteobacteria, and more lipophilic bacteria in Tanner stages four and five. That makes sense for anybody who’s gone everybody who’s through puberty you recognize that your body is changing dramatically, and one of the things that changes is the further maturation of our sebaceous glands, or oil glands in our skin. So it’s very possible this is one of the reasons why we have more lipophilic bacteria, because they can thrive in that type of environment.

So we’ve talked a lot about 16S taxonomic surveys. We’ve heard some about the virome, and several of the investigators looking at that. But what about the fungal microbiome So, more recently, we’ve published a project looking at sequencing the fungalanisms on the human skin surface, but in order to do this, we had to go back from the beginning and figure out how do we optimize sample collection. And this refers back to the conversation we had in the open floor session yesterday What are the protocols to use Optimizing DNA extraction, we had to deviate from the standard protocols for extracting DNA in order to optimize extractional fungal data using beadbeating, opening the fungal cell walls. What primers would we use There are individuals who use 18S, some who use 28S. There is the ITS region here ITS1, ITS2. That stands for internal transcribed spacer region. And so based on our analyses, for us, at least for skin, that ITS1 provides more taxonomic resolution. This alludes back to Jacques Ravel’sment yesterday that just because it works for the gut or for the vagina, it may not work for the skin. And so this is for, at least in our experience, ITS1 worked better for taxonomic resolution.

So what we did was we had 10 healthy volunteers. I selected 14 sites. These are not identical to the ones that we did in the bacterial survey, because these are, again, sites that reflect sites of predilection for skin diseases for which fungal contribution may be playing in a role. So in 10 healthy volunteers we see here. Then we if you look at the relative abundance charts, each of these horizontal lines represent one body site. Each of these vertical bars represents one of the healthy volunteers. And one of the most striking this that you can observe here is that malassezia predominates in 11 out of the 14 sites. That’s the purple. That’s why there’s so much purple. But on the heel, toenail, and toe web space, so on the feet, there is much greater diversity. We have fungi everywhere, but it’s just a different population depending on where you are.

One of the things that you may notice is that healthy volunteer seven is a bit different. This individual, again talking about protocol standardization, our eligibility was no one could take have taken an oral antifungal or an oral antibiotic within six months of being sampled for this protocol. And this individual hadpleted a course of oral antifungal six, seven months prior to being sampled. And so it’s not clear whether the differences we see are related to residual effects of taking an oral antifungal, or whether or not the person’s predisposition they were taking for a toenail infection whether a predisposition for a toenail infection represents some difference in their fungal microbialmunities. Interestingly, I don’t have the data right here, but their 16S survey for this particular individual, HV7, was similar to the others. So the bacterial microbiome was resembled any other healthy volunteer.

But it was frustrating to see so much purple. There’s a lot of malassezia that’s not that helpful. But one of the questions we had was, what happens if you speciate Getting down to the speciation level, how do we do that Well, we couldn’t do that based on the databases that were available, so we had to cultivate our own malassezia and do genomic sequencing to actually populate the databases for us to be able to speciate. So when you do that, you again see there is striking site specificity for skin. Sarkis was talking about how there’s specificity in the gut, but also we see that for the skin, with regards to the fungal microbiome as well. So we can see in this area here, the external ear canal, behind the ear, the forehead, that malassezia restricta predominates. But in other sites, we have the upper back, the back of the scalp, the inside hip, those are you have malassezia globosa. So even though they’re all malassezia, there is specific species that we’re seeing at these different body sites.

So I did mention that we did 16S, so from these same clinical samples, we did ITS1 sequencing as well as 16S sequencing from these samples, and what you see here is interesting anatomically, in that those central body sites from the head and neck, or core body sites listed here, they have a relatively limited number with regards to richness, relatively limited numbers of different types of bacteria and fungi. Whereas on the arms here’s the palm, the forearm, and the inside elbow there’s a higher richness, a greater richness, with regards to bacteria, but still relatively limited for fungi. That’s different for the feet. Here, the heel, toe web, and toe nail relatively limited richness for bacteria, a much greater richness for fungi. So there are these regional differences that cannot be explained just by sebaceous, moist, and dry, and that it’s going to require a lot more understanding about human physiology and skin physiology to be able to explain these differences.

So just summarizing this beginning portion, the skin bacterial microbiome is highly dependent on the sampled skin site the neonatal skin bacterial microbiome varies based on mode of delivery. We’ve talked about that. That there are dramatically major shifts that we see in the Tanner stages one, two, three, versus Tanner stages four and five. And that fungalmunities over the skin’s surface differentially vary from the bacterial microbiome.

Now, I’m going to shift into what my charge was, into talking about eczematous skin, specifically atopic dermatitis, and then briefly I’ll talk about some data from other groups and our group about primary immunodeficiency syndromes and why that’s interesting. So for background, those who are not familiar with atopic dermatitis, it’s a chronic, itchy inflammatory skin condition. It is not considered an infectious disease, it’s an inflammatory skin disease, yet these individuals respond relatively well to antimicrobials, so there is something going on that suggests a role of microbes. It affects 15 percent of U.S.

children at a high cost financially as well as socially. The quality of life in these children and in these families is severely adversely affected. And I mentioned before, there is this association with microbes we observe, and when we take care of these patients, that disease flares are associated with increased colonization and infections of staph aureus, but also a subset of these patients are at high risk for severe spread of herpes simplex virus infection, and if theye into contact with smallpox vacinis spelled phically.

There is something that’s been termed the atopic march, in that there are 40 to 70 percent of those with severe atopic dermatitis over time go on to develop asthma and then hay fever. So these three diseases are termed the atopic triad. The incidence of these atopic diseases have doubled in the last three decades in industrialized countries, suggesting there may be a possible external factor, and this alludes to some of thements yesterday by Marty, and again today, that it is unlikely that our human genome can change in that period of time, and that an external, possibly microbial, contribution may be playing a role. Interestingly, in mirroring studies, skin exposure to antigens can result in subsequent mucosal sensitization to those antigens, suggesting that if we could somehow modify what happens in atopic dermatitis, could we then go on and abrogate the development or the disease severity of asthma, which has significant morbidity and potential mortality, as well as hay fever. So understanding the triggers of atopic dermatitis may allow us to modify the development of AD and atopic disorders, and potentially develop therapeutic targets. So atopic dermatitis is aplex disease. It looks very simple here, but this is not the whole story. But just emphasizing, we’ve talked about barrier, the gut barrier earlier today, but emphasizing I won’t talk about it here, but it is important in atopic dermatitis.

The skin barrier, we know if you have a mutation in the skin epidermal protein filaggrin, it’s highly associated with the development of atopic dermatitis, particularly the kind that goes on to develop asthma and hay fever. We know the immune system is deranged in these individuals, and that they have extremely high IgE levels, and antimicrobial peptides in the skin are reduced. But and we’ve also talked about the microbes, and that is just oneponent of thisplex disease. So our study, we recruited pediatric patients with moderate to severe disease, and healthy age match controls. I sampled them in characteristicallyaffected sites. As I mentioned before, dermatological diseases have sites of predilection where we find them, and that helps us in the diagnosis of these diseases. But it typically occurs in the antecubital fossa and the popliteal fossa, that being the inside elbow and behind the knee. We selected the volar forearm, or the inner forearm, as a control site, because it is less often affected in moderate disease, and it’s an adjacent site. We also sampled the nares, because that is a site of carriage for staph aureus. And I sampled them during the baseline, flare, and postflare time points, and these are just SCORAD scores, which is just a method for assessing severity in these patients. And you can see that, over time, their SCORAD increases during the flare and decreases after they’ve been treated. This figure just demonstrates that when you have more severe disease, that we observe a decrease in the bacterial skinmunities. But that drop in diversity is not everywhere, it is very site specific again, it is at the sites where we see disease appear the inside elbow and behind the knee but not at all time points. This, in particular, are disease flares. These are the natural true natural history of the disease, where they have not been putting anything on their skin. These the blue flares are individuals who put on topical steroids potentially two days before seeing us, or sometime within the seven days before they were sampled. So these flares are truly the natural history of the disease. But what are the bacteria that seem to be driving this decrease in diversity So looking down to the genus down to the genus level, here are the healthy controls. These are the baseline time points for the atopic dermatitis, the flare time points, the no treatment ones versus the intermittently treated ones, and the postflare time point. And what you can see is there’s a dramatic increase, a significant increase in the pink, the staphylococci in the skin of these patients during a flare, but we do see increased staph in proportion, or relative increase in some of these individuals. So that was quite a concern. Again, we had to go down to speciation level, because there’s staph epidermidis, staph aureus. Staph epidermidis, again, is a known skinmensal staph aureus is a fairlymon pathogen.

And so it was important to us, at least at the genome level they’re very similar, so we had to know which one was which, because it makes a difference, at least clinically. And so what we did, if you focus primarily on the pink, the staphylococci, and we speciated those, it was reassuring to see that most of the staph we see in the healthy controls, those are staph epidermidis staph hominis, known skinmensals. But what we do observe is, yes, there is an increase in the staph aureus we see, even at base line, but it is a dramatically increase during the flare, the natural history of disease we see, increased staph aureus, but also staph epidermidis. That was not something we did expect to see, but there is that is one of the benefits of looking at the whole microbialmunity with regards to disease progression. And then it decreases once patients had been treated.

And one of the questions that people often ask Well, you gave them antibiotics, but often the majority of these patients were limited their treatment was limited to topical steroids, or some of them do take dilute bleach baths, which is like having a small swimming pool in your own tub. So that’s what we observed, but what is what remains a question is our correlations What happens to get from this point to this point Or what can we do so that these you never you remain a control you don’t go on to develop atopic dermatitis. Those are questions that remain.

We did look at the fungalmunities on the skin. Julia Oh looked at this. These are baseline flare and postflare for a few of our patients who had atopic dermatitis, and although you see fluctuations in the bacteria, we don’t see that type of fluctuation in the fungalmunities on the skin. So I’m going to shift gears a little bit and talk about primary immunodeficiencies. There are some cohorts of primary immunodeficiency patients who have eczematous skin disease, and the benefits here are they genotypically have the same mutation. They are monogic disorders, and some of these patients have atopic dermatitislike skin eruptions, and these eruptions can be antibiotic responsive again. And so that was one of the reasons why we pursued these cohorts, and asking, domon and rare diseases with similar clinical phenotypes, do they share skin microbiome features And how does the innate and the adaptive immunity shape the skin microbiome We haven’t been able to ask all of these questions, but these are some of the reasons we were led down this path. I’m just going to talk about two of these diseases in the rest of the time that I have, talking about hyper IgE syndrome, which have STAT3 mutations, as well as another paper that was recently published by Dirk Gevers and colleagues, looking at STAT1 mutations with chronic mucocutaneous candidal infections. So a STAT pathway is important it’s a biochemical pathway, and it’s involved in so many things. But these patients have are at risk for infections on hyper IgE syndrome, they have staphylococcal skin, and lung infections, candidal infection, and they can develop secondary aspergillosis lung infections. So this is the paper I just mentioned, by Dirk Gevers and colleagues, where they looked at STAT3 and STAT1 mutations. It’s hard to see, but these the leftmost groups, these are the STAT1 mutation patients the middle group are the hyper IgE syndrome patients, or STAT3 mutations, and these are their controls. But, in general, what you see, just summarizing everything this little corner, at the genus level, you see increased corynebacterium species in the STAT1 mutations. You have decreased corynebacterium species in the STAT3 mutations.

You have increased gramnegatives that you observe in these patient populations, decreased prevotella and decreased fusobacteriales spelled phically. So you we observe that there are taxonomic differences that we observe on the skin of these patients with primary immunodeficiency syndrome. This group went on to do some studies of challenging PBMCs. These are PBMCs from healthy volunteers.

What they initially did was they prestimulated them with either corynebacterium, acobacter, or staphylococcus, and then they challenged them to candida albicans or staph aureus. And what this essentially shows is that if they were initially exposed to acobacter baumannii, there was a decrease TNFalpha, interferon gamma, and IL22 that was produced upon exposure with staph aureus and C. albicans in these healthy volunteer PBMCs. So exposure to certain skin microbes may alter PBMC skin cytokine response to pathogens, such as C.

albicans and staph aureus. This is just a snapshot of some of our work looking at patients with hyper IgE syndrome, STAT3 mutations, but due to the limited amount of time, I will direct you to Poster 31, where Julia Oh will walk you through her analyses that she’s looked at STAT3 mutation patients, but other primary immunodeficiency syndromes as well.

So, briefly, going through summarizing this part,AD flares are associated with shifts in the skin bacteria. We talked about the different species. The specific primary immunity deficiency patients harbor a distinct skin microbiota, and that altering the skin microbiome may alter the PBMC’s response to specific microbes, but we need more studies. Quickly, moving into the gaps, needs, and challenges, since I’m running out of time.

These are knowledge gaps. And then I’ll go into as Owen charged us with finding things that frustrate us on a daytoday level. But knowledge gaps here are evolution of the skin microbiome over life stages, what are the physiological factors that contribute to the skin microbiome differences, getting down to understanding skin microbiome and immunity interactions. Trying to expand on what has been done now, but to explore that to a greater degree and fully understand how our immune system interacts with our skin microbes. And again, the importance of human and animal models. We’ve talked about this, but moving from correlation to causation, but also, as our recent survey has highlighted, the magnitude of interaction between fungi and bacteria, and the role in health and disease. But one of the bigger challenges that I don’t think I’ve seen anything been able to ovee this one challenge is skin metagenomics, and that is due to the low biomass on skin. So I do have a caveat. These are my views they do not represent the views of the government.

But these are some of the frustrations that we encounter on a daytoday basis. Standardization of protocols. We’ve talked about this, but particularly for skin, I did a nonscientific survey of some of the people who do skin work here, and we have different protocols. I will admit that we don’t follow the HMP protocol, we have our own protocol that we’ve been doing, and we’ve had to modify that from time to time. So we are just as guilty of not having following a standardized protocol. The importance of phenotyping patients, making sure are the really healthy, or are the normal What diseases, particularly atopic dermatitis, has several different phenotypes, how do we define what is the phenotype we’re studying, and how do we especially you do that when you’re at different, multiple sites. Which sampling sites do you do How frequently What is the skin prep The time since antibiotics What sampling method Is swabbing still the best way What are the critical metadata fields that are needed And it might change depending on the disease state you’re looking at.

DNA extraction. This is really critical, looking at especially when you have low biomass. It’s easily contaminated when you’re talking about skin, but then when we’re looking at fungalanisms, we had to modify DNA extraction. But the primers, PCR conditions, just looking at various abstracts of the past and manuscripts, they’re all over the place. Quantitation. This is a key question that I always get askedHow do you know Can you quantify what’s there And we can’t at this point, and that is a major frustration, I think, not just for skin, but in the entire microbiome field. More microbial characterization, where including genomes, where we had to, you know, sequence our own malassezia in order to figure out speciation. Metagenomics analytical tools, particularly if you have low biomass.

And one gripe about data submission When we’re submitting a manuscript and having to do dbGaP and SRA, that is a major frustration. Again, my own opinions. So then, if I can move on to the acknowledgements, if they will it’s not there we go. I’d like to acknowledge my close collaborator Julie Segre, and I have underlined here, as well as photos of the post docs’ work who I’ve highlighted here, but there are many collaborators within my group, but then also collaborators across different institutions, but especially our patients and volunteers. Thank you very much for your time.

applause Female Speaker Thank you so much for that great talk. So we do have time for a question if there is one out there. Oh,e on. Go ahead. Male Speaker That was a lovely talk. In your discussion about the areas we need to work on methods, I think today, as I was talking with a colleague, we’ve seen very few slides, actually, on the methods that are used in any of the studies, particularly in humans, whether it was a wet cotton swab, whether it was a brush. You know, I think that as part of the methodological discovery process, we all need to disclose or discuss exactly what the methods are as we’re going forward, even in we’re presenting data such as we have here. I know from the papilloma virus field, we went through decades of methodological considerations that were critical. So I applaud your, you know, pointing these out, and I encourage everybody to start including more specifics on exactly how they’ve collected the specimens, processed, stored, et cetera, so we can understand that as we’re interpreting the data.

Heidi Kong Thank you for yourments. Female Speaker Thanks for a nice talk. When you showed the results, you show the fungi changes Heidi Kong affirmative Female Speaker and you went very fast, basically you didn’t do muchments, but I think I saw malassezia globosa increasing in the skin of the in the flare. Can youment on that Heidi Kong Are you talking about the atopic dermatitis one This one Or were you talking about Female Speaker That one.

Heidi Kong Yeah. So this one I willment, this particular individual was Tanner stage four, and so what we see is it’s possibility related to, although this was a pediatric patient, that they had already transitioned through puberty and had more oils on their skin, and so that’s why we see that malassezia globosa is dominating potentially in this individual. Or it may be something unique to this individual, and we just small, and it’s hard for us to tease that out. Thank you for that question.

Skin Tag Removal in 15 Mins Home!

Wee to SKIN TAGS! Skin tags can be removed with one easy 15 minute treatment at home! The Skin tag removal kit contains all you require to remove 30 to 40 skin tags.

and skin healing cream containing pearl oil Here we have a young lady with a skin tag on her neck. she is very aware of it and wants it removed. After cleaning the area with a sterile pad, here we can see the emery board being used to roughen the surface of the skin. to allow the active ingredients to prate into the body of the Skin Tag to destroy it The applicator is used to coat the skin tag with the solution A mild stinging sensation is normal at this stage Any excess cream should be wiped away The cream is left in place for 15 minutes in some cases a second application may be needed where the skin tag is old and thick Fresh water is used to remove the dried cream and clean the treated area We can see as the area is cleaned that the whole skin tag has turned black! A sure sign that the treatment has been successful The skin around the treated area is quite red, this should be expected There may even be slight swelling around the base of the skin tag, but this is temporary The healing cream containing pearl oil is then applied to the treated area and surrounding skin.

After a short time, the redness around the area has greatly reduced leaving only local redness. After 24 hours we can see there is a little redness around the treated area and the skin tag has be darker and smaller 2, 3 4 days pass. the skin tag bes gradually smaller and hardens Finally, after 5 days the skin tag has fallen off.

stem cell glue heals arthritis

Stem cell glue mixture may heal arthritis Mirand Hitti writing for WebMD reported on a study where scientists used stem cells to repair arthritis damage in mice. They tweaked the stem cells’ genes to pump up production of a bonebuilding protein called BMP4. When mice with knee injuries got those stem cells, their knees healed better than other mice with the same injuries. The findinges from doctors including Ryosuke Kuroda, MD, PhD, of Children’s Hospital of Pittsburgh and the University of Pittsburgh.

Kuroda’s team took stem cells from mouse muscles, placed the stem cells in chemical glue, and used the mixture on mice with knee injuries. Some mice got stem cells that had been gically altered to make more BMP4. Others got stem cells with normal genes. A third group just got the chemical glue with no stem cells. The mice that got the gically altered stem cells healed best by the study’s end. They made glossy, white tissue that repaired the joint damage quite well. Healing attempts didn’t go as well in the other mice. Their joint repairs were rougher and didn’t last as long.

Candida Case Study 7 Val With Chronic Asthma

Thank you for checking out my tutorial today. It’s going to be another case history. This case is going to be regarding a woman who’s now is her 70s and her name is Val. So I’m going to read a little bit from my book, Candida Crusher, and then I’m going to explain a bit about this case. Val came to my roomplaining of severe fatigue, burning and itchy ears, eyes burning and watery, and an irritable burning throat and many digestive problems. On top of her chronic and depilating fatigue, Val had childhood asthma and was placed on steroid drugs for just over 60 years and remained on them for almost 50 years. She’d spent countless hours over the years in various hospitals and she also had two epileptic fits. Finally, after consulting with more than 30 doctors, she decided she was going to have no more steroids after almost 50 years of continuous drug use.

Ventolin or salbutamol was taken for 25 years and other drugs like antibiotics were routinely prescribed on and off. Over the past 30 years, her sinus, nose, eyes and ears were getting worse by the day, but still the doctors persisted with the steroid drug rmendations. It is early days for Val, but things are already starting to look gray. I first rmended that all drugs be neatly flushed down the lavatory from this point forward and that we started Val on an adrenal fatigue treatment program. The results have been incredible, and it just goes to show that no matter how old the patient is, how debilitated they are or how screwed up they’ve be due to over chronic prescribing of drugs, the body keeps on maintaining the ability to restore its vital function. After six months of adrenal treatment, we have a staggering 40 percent improvement. But as I suspect, Val will need adrenal support for up to two to three years or even more to get a full recovery. If you look at this case carefully, Imended Val quite clearly. She’s a remarkable lady, a very nice person, and I saw her on numerous occasions. This poor woman had very bad thrush of the throat, but also she had vaginal thrush.

She had digestive thrush. She had itchy skin. She was a wreck. She was a train wreck this woman. Completely screwed up on drugs. You may be on medication for many years yourself, particularly steroid medications. Steroid medications are designed to suppress the immune function, whether you’re using topical on the skin, hydrocortisone for conditions like dermatitis, eczema, or psoriasis. Whether it’s an inhaled steroid, those puffers for asthma. Whether it’s an ingested steroid like prednisone for an auto immune disease like lupus or rheumatoid arthritis or any one of the hundred other diseases you might have that are auto immune related. These drugs are crap! They’re absolute crap because they wreck your body. If you keep on them long enough, they’re going topletely screw your system up. In the short term, they may be of benefit, but long term they’re going to destroy your body. It’s just not worth going there.

What happens when you suppress the immune system long enough is you’re a sitting duck for all kinds of infections. In Val, when she came to see me, she was literally rotating five or six antibiotics all the time in a rotating fashion. As her body would resist one, she’d switch to another one. I mean that’s just crazy. That’s like going from a Master Card to a Visa Card, all these damn cards, until you’ve maxed everything out and then you overmax things. Poor patients. I feel so sorry for so many people out there that are victims of these stupid drug crazed medical treatment regimes that they fall under. Long term, it’s almost like Russian roulette to me. You’re going to die. It’s only a matter of how many bullets have you got in the chamber. In Val’s case, my first aim was to try to boost her immune system up as much as I could, and I found that treating the adrenal glands was a very smart move. And in the early days, I didn’t really understand the connection between the adrenal gland and Candida, but now I do. In fact, a lot of my patients with chronic resistant, intractable Candida have severe adrenal fatigue. It’s not until we change their lifestyle, boost their adrenal function up, and power their immune system that we can actually fight this chronic infection. All the diets aren’t going to work if your immune system is in poor condition. Just remember that. All the diets are useless. You have to get your immune system powered up. It’s a very important point I want you to get from Val’s case history. The respiratory physician at the hospital was absolutely blown away when he looked at Val’s peak flow volumes, how that improved four or five fold literally within six months of adrenal treatment. He was staggered. And when I asked him if he thought this was a valid therapy, he said, Oh, absolutely. And then when I asked him if this would be possible in the hospital, he said, It’s impossible.


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