March 31, 2020
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all right so good morning my name is dr. Paul Mason and I’m from Sydney and today I’m going to talk to you about a protein that’s found in plants called lectins and how they can have a massive impact on our health and understanding lectins I believe fills in a massive chasm in conventional medicine when it comes to treating a myriad of chronic diseases and certainly for me understanding their impact has improved the care that I deliver to my patients as with all of my lectures nothing contained here within should constitute personal medical advice so the story begins in 1976 in England when nine school boys ate some kidney beans that had been soaked but not boiled and within one and a half hours all nine of them ended up with profuse diarrhea and vomiting and some of them had only consumed four kidney beans and further illustrating the toxic potential of kidney beans is a diet containing only 1% kidney beans will kill a rat in two weeks so the problem of uncle kidney beans was considered so serious in England back in this period that the government started issuing written warning labels on uncooked kidney beans so then that leaves us with the question what earth is in uncooked kidney beans that will do that so this is a kidney plant being plant here it doesn’t have any claws it can’t run away so it’s pretty defenseless well you’d be wrong it’s not at the complete mercy of any caterpillar that wants to come along because it engages in some very potent chemical warfare and the chemical warfare that plants use one of them is called lectins and the particular lectin contained in kidney beans is called phyto hemagglutinin and in fact there’s over a hundred known sources lectins and many of these are toxic to humans each lectin is a protein with a unique structure and it’s a protein that has the ability to bind to carbohydrates all of our cells in the body have these glycoproteins which protrude up from the cell membrane and they contain a carbohydrate moiety on the end of it and lectins can bind to that carbohydrate moiety and that means lectins can therefore bind to our human cells now leptons are resistant to cooking in the case of red kidney beans it’s recommended that you should soak them for five hours and then boil them for at least 10 minutes to reduce the lectins to a less dangerous level and as well as being heat stable lectins are often very very resistant to the normal digestive enzymes that we have lining our gut and it’s to the point where a lot of lectins provide no nutritional value at all they often excrete it completely unchanged and often on the way through the intestinal tract these unchanged lectins can often bind to the walls of our intestine and do significant damage including killing the cells so the way to think about it is our intestinal tract is a hollow tube from mouth to anus and ideally it should allow absorption of nutrients across the wall while not allowing entry of any toxins and the lining of the intestinal tract has this basic structure firstly there’s a mucus layer on top indicated in green here and then beneath that you’ve got these epithelial cells which had joined together side by side by what are called tight junctions and on top of the epithelial cells here you’ll see that little frill layer and that’s called micro villi now on the very tip of these micro villi we have something called a glycocalyx and this has a glucose or a sugar or a carbohydrate component which means that lectins can actually bind to this part of the intestinal membrane so if we take something like wheat German gluten and that will actually bind to the internal lining of a car and damage it and that causes something called leaky gut now once you’ve got this single layer of cells if you then fold it in a way you can get these finger-like projections here which we now call villi and this is what villi look like under an electron microscope now coming back to the general function of the gastrointestinal tract if we had a toxin like a lectin hopefully it would pass straight through us without being absorbed but occasionally we can ingest a toxin and we have leaky gut or intestinal permeability which allows the toxin to actually enter the body and this is a graph here that demonstrates the potential of these toxins these lectins to enter our body so seven participants consumed 200 grams of peanuts and this test was actually measuring the amount of peanut lectin within their blood and you can see that within half an hour the level started to rise and within an hour there was a significant amount of this leptin seen in the circulation and the ability remember of these lectins to bind to the surface of cells means that after entering our circulation they can actually bind ourselves in many different organs depending on what particular affinity the leptin has for a particular kind of cell so this image was done from a study that was done on females with unexplained fertility and this is a sample of the endometrium the lining of the uterus and what you can actually see is indicated by the arrows is they’re actually demonstrating soybean agglutinin electon actually bound to some endometrial tissue now unfortunately the consumption of lectins in our diet is actually increasing significantly so in part this is due to natural selection selective breeding and genetic modification of crops which tends to select for species that are natural resistant to pesticides and that natural resistance comes from lectins so let’s take a look at the specific health consequences that these lectins can have beginning with obesity has anybody ever noticed that when they cut plant foods out of their diets that they lost weight even if you’re already on a low carbohydrate diet so why is that I know several people of lost over ten kilograms and it’s because lectins can stimulate the insulin receptor insulin is a hormone that stimulates fat storage and lectins can stimulate this this graph here is from a 1983 study and it compared active fat storage between wheat germ agglutinin and insulin so down the bottom here this is what happened to fat storage when insulin alone was given this is what happened to fat storage when insulin plus a leptin in the form of wheat germ agglutinin was given and this is what happened when you just give lectin alone and the point is that it stimulates the insulin receptor in a far more prolonged fashion than even does insulin so this is a concern if you’re trying to lose weight but it’s not only wheat German gluten and that has this ability in the same study they actually looked at two other lectins as well and you can see ability to produce persistent lipogenesis creating fat and it seems like lectin can also impact on another hormone critical to fat storage and this hormone is leptin with a P not to be confused with leptin and the hormone leptin is essential in regulating appetite satiety and energy balance have a look at these two mice the one on the left has no leptin demonstrates the importance of leptin functioning effectively and lectins with a C can actually bind to the leptin receptor and interfere with it causing resist and this here is a study showing of another lectern come carnival an a that leads to leptin resistance and when we test this in animal studies using isocaloric diets that simply eliminate leptons that leads to significant weight loss in the animals now what about reflux we’re all familiar with reflux that’s what happens when you have stomach acid in the stomach that ascends up the esophagus it’s often called heartburn well you might be surprised to learn that lectins can also cause this because they can stimulate excess and acid production so this is a mast cell here and it can secrete a chemical called histamine and if it secretes histamine that then leads to acid production in the stomach and lectins can come along and bind to these molecules on the outside of the Marcelle called IgE molecules and that stimulates the histamine release and through this mechanism you can actually increase the acid and this is one study where it showed a dramatic reduction in the acid levels in the esophagus within six days of starting a low carbohydrate diet and that’s simply because when you go on a low carb diet you often come out the lectin rich grains and cereals so they actually had probes down into the esophagus that were sitting there for 24 hours and measuring the acid level constantly and you can see that in a matter of six days there was a significant reduction in the acidity within the esophagus and this is why symptoms of reflux often improve incredibly rapidly and when we go on a plant free diet now I’d like to make a very important point here so far I’ve only talked about plant lectins but lectins actually do exist in animal foods as well and other foods the reason i’m only talking about plant lectins is that they’re far more likely to be problematic doesn’t mean that animal-based lectins can’t be problematic as just they’re so much less likely to do it in this study here this is a study looking at histamine release from 16 different lectins and you can see the four that had the most significant response we’re all plant-based lectins so that’s why I’m tending to focus on them now I just like to focus we’ll turn our attention to a condition called Parkinson’s disease now this is a movement disorder I’m sure you’ve all heard of it you familiar with it you end up with a tremor you end up with rigidity and slowed movement and there’s evidence now that this is caused by lectins you see if you ingest a lectin and this sounds crazy it can actually ascend up to the brain by traveling along nerves and the nerve in particular is called the vagus nerve so theoretically if that was true if you just simply cut the nerve you would interrupt the highway which the lectins are sent to the brain and you should be able to reduce the risk of Parkinson’s disease makes sense right so they did it so this is an example this is a picture of the two vagus nerves and when you cut them it’s called a the gotta me so in one study it was published in 2015 they compared every patient in Denmark who had this procedure between 1977 and 1995 and this is what they found they found that by cutting the vagus nerves the risk of developing Parkinson’s disease dropped by 47% and then this is a more recent study that was able to actually confirm the mechanism it was able to demonstrate that lectins were actually able to travel to the neurons in the brain which are affected in Parkinson’s disease and this graphic here shows the ingested P lectin sitting on top of a neuron in the brain that makes dopamine this is the problem in Parkinson’s disease so now I want to turn our attention to autoimmune disease and in autoimmune disease the body attacks its own tissues and the particular tissues attacked determine what specific autoimmune disease it is because you’ve got a choice there’s heaps of them more than you can pocus different examples of them might include different types of inflammatory arthritis might have pernicious anemia you might even have multiple sclerosis type 1 diabetes inflammatory bowel disease lupus and the list goes on but the point is that all autoimmune diseases are characterized by the body’s immune system attacking itself and one of the defining features is called Auto antibodies so this y-shape structure here in the middle is what we call an antibody and it’s one of the main features of the immune system and normally antibodies are used to defend against foreign invaders pathogens if you have a bacteria the antibody will have a strong affinity for the bacteria and when it attaches to it that then stimulates or initiates an immune response that will lead to the eventual destruction of that bacteria and if this was a healthy cell here well hopefully that has no affinity for it so on the surface of the cell here you see what’s called an antigen that’s a particular molecular identifying feature either on a cell or a bacteria and the specificity of that antigen and the receptor on the antibody will depend whether they bind together or not and in the case of autoimmune diseases antibodies have receptors that can actually bind to healthy cells and then that can lead to your healthy tissue is starting to be destroyed and the presence of these also antibodies is actually what I use to diagnose autoimmune diseases it’s one of the major things I use and there’s over a hundred different antibodies that I can now test for back home in Australia when I’m trying to diagnose an autoimmune disease now leaky gut this can test all permeability that allows lectins to enter into the circulation is a key contributor to autoimmune disease and gluten is one of the major causes of leaky gut so about 80% of the total protein contained within wheat gluten and that’s significant but just from one fact because it means that 80% of the protein is useless in weight so you’re not getting as much protein as you think you are but the gluten is also very damaging to the intestinal barrier so this graph here demonstrates the intestinal barrier as assessed by something called trans epithelial electrical resistance the higher the line the better the top line shows barrier function in celiac intestinal cells that haven’t been exposed to gluten when we expose them to gluten this happens and you can see it happens rapidly within 15 minutes any people with celiac disease this increase in intestinal permeability will persist for up to a week but here’s the thing that a lot of people don’t know it’s not only celiacs who are affected by gluten this top line here is non celiac cells not exposed to gluten this one here non celiac cells exposed to gluten there’s still a significant impediment to intestinal barrier function gluten impairs the intestinal barrier in everybody not to celiacs now let’s have a look exactly how gluten can do this so the top layer in green here represents a mucous layer and the bottom layer here in blue is something called the lamina propria this is the the tissue layer of the intestines where the immune system lives you’ve got blood vessels and lymphatic vessels and a few other things kicking around there and this here is gluten now when it gets ingested it can get broken down partially into these smaller parts called gliadin but no further and this Caladan then combined to a special receptor called CXC r3 and once it binds to that that leads to signaling within the cell that produce leads to the production of a molecule called zon Yulin and this is on Ulan can then come and act on a receptor which leads to the breakdown of these proteins here called the tight Junction or gap Junction which actually hold the cells together and when that gets disrupted the cells are able to physically separate and this is what causes leaky gut this is what leaky gut is and then these lectins that have been ingested as well as any bacteria that might exist in the intestines can actually pass between the cells and get down to the lamina propria where it gets exposed to the immune system and it’s able to interact with the immune system now because lectins are offensive essentially foreign particles we often mount an immune response to get them so we often end up developing antibodies that will target them so let’s say here in purple that that’s selectin and if you have a look at the antigen on the surface in green you can see that it’s the same as part of an antigen on a healthy cell so that means if we develop an antibody response against selectin we can also develop an antibody response against a healthy cell and this is called molecular mimicry and this is thought to underpin most autoimmune disease now lectins aren’t the only cause of molecular mimicry and autoimmune disease we can also have cell wall fragments from bacteria that look very similar to our healthy cells that will trigger this molecular mimicry Typex response and certainly this has been shown to be the case in rheumatoid arthritis and a couple of other very specific inflammatory conditions now in addition to molecular mimicry these bacteria can also exacerbate symptoms of inflammatory conditions like arthritis because they secrete toxins called lipopolysaccharides now you can see dotting the surface of the bacterium here and circled here what’s called the lipopolysaccharides and when the bacteria enter the circulation they’re then able to release these lipopolysaccharides into the circulation which then will stimulate inflammation and it stimulates information because the lipopolysaccharide can bind to this receptor up here called the toll-like receptor for and that then initiates an inflammatory cascade which ends up having a whole lot of deleterious downstream effects but here’s a key point and I often hear people talking about the importance of lipopolysaccharides in inflammation but they’re not all the same some lipopolysaccharides will stimulate this toll-like receptor and some won’t some will block it you can have pro-inflammatory lipopolysaccharides and you can have anti-inflammatory ones as well so in general lipopolysaccharide produced by this group of bacteria the bacteria deities phylum is actually quite inhibitory of this inflammatory cascade and reassuringly when we’re in good health it’s this phylum of bacteria which produces most of our lipopolysaccharide and further if we’re on a healthy diet often a ketogenic diet a high saturated fat and animal protein diet those diets have actually been shown to increase the proportion of bacterial deities which is actually falls within the phylum of the the larger phylum that produces these anti-inflammatory lipopolysaccharides so a healthy diet might actually increase the amount of lipopolysaccharides but it will produce anti-inflammatory lipopolysaccharides and this is a point that’s often missed in the research now one of the conditions that’s linked to type 1 diabetes is one of the is the gluten consumption rather so if you consume gluten it’s been shown that your risk of developing type 1 diabetes gluten Hashimoto’s thyroiditis these other clusters of autoimmune diseases is significantly increased and this recent study encapsulate that risk with maternal gluten consumption looking at the risk of developing type 1 diabetes in the offspring so they looked at over a hundred thousand pregnancies in Denmark and what they found was there was a reliable linear increased risk of type 1 diabetes with gluten consumption and for the highest group of gluten consumption the risk of your offspring developing type 1 diabetes was doubled and that we have papers like this which indicate that commencing a gluten-free diet soon after diagnosis of type 1 diabetes can significantly alter the prognosis so this study looked at what happened to a boy who was placed on a street gluten-free diet soon after diagnosis a type 1 diabetes and it compared him to a group of 21 other children as a control and what you can see he he is down in red his insulin level his insulin usage was far far less and his blood sugar control was far far better it had him in the sub 6 group rarefied air and his diabetes was still in remission 20 months later when this study was actually published now just a little bit of a semi related point I’d like to raise we cannot assume that only children develop type 1 diabetes we don’t call it that in adults we use the term latent autoimmune diabetes of adulthood which is a pretty cumbersome name but it’s essentially the same it’s diabetes of autoimmune origin and in fact up to 14 percent of cases of type 2 diabetes which are diagnosed in adults actually have an autoimmune component and this is huge because it means there’s a potential intervention that we might be able to do for these other people that we’re missing out on and unfortunately we very very rarely test for autoimmune diabetes in adults despite the fact that the chances are more than 1 in 10 of type 2 diabetics actually have this condition and it doesn’t matter if you’re overweight and have other metabolic risk factors you still could have this autoimmune type of adult onset diabetes so it’s probably time to pause for a moment and ask why not everybody has an autoimmune disease because we’ve all consumed lectins in the past right so I find it helpful to apply the Swiss cheese model of accident causation here and that states that accidents only happen when deficiencies in the defense’s lineup so if we have a think about autoimmune diseases you need to pick the wrong parents you probably need to have some aspect of intestinal permeability which may or may not be triggered by lectin consumption and then you may also need to be consuming lectins or have some other kind of antigenic stimulus like certain bacteria within your gut so unless all of those three line up then chances are you probably won’t develop an autoimmune disease but for people that have picked the wrong parents these next two layers become very important so let’s pay a bit more attention to intestinal permeability or leaky gut now so this chart here was derived from a genome Association study looking at you lament free bowel disease and it found that having inflammatory bowel disease or the genetics for it increased the risk of 23 other conditions most of them autoimmune diseases so this should suggest that there’s something about inflammatory bowel disease which is inherently associated with increased intestinal permeability that is problematic in autoimmune disease so let’s start with a few factors of things that we can actually do to reduce or increase intestinal permeability other risk factors alcohol’s a big one so clearly here you see that intestinal permeability is far higher consuming ethanol than not what about anti-inflammatory medications likewise this is diclofenac this is the active ingredient found in voltaren so it’s been understood for a long long time that taking anti-inflammatory medication increases intestinal permeability and to add insult to injury these are the medications that doctors often prescribe to people with joint pain for in a group of arthritis called the seronegative spondyloarthropathies or even rheumatoid arthritis ease other conditions that as a root cause will often have intestinal permeability contributing now let’s have a look at our processed foods so they’re full of a myriad of ingredients that they’re always homogenized and the reason is because they contain emulsifiers and this study here it was done in mice but it actually compared a couple of emulsifiers at one percent of their food intake so it wasn’t big compared to the amount of emulsifiers that an average person on a processed food diet consumes this is actually quite modest but what you can see the addition of emulsifiers in the second or the third column here leads to a significant thinning of the mucus shown in green and it actually allows increased bacterial penetration of the mucus so you can see the red dots there the bacteria they’re now able to get very close to the intestinal wall and if we actually have a look at what the consequences are of this in the same study we find that exposure to the emulsifiers increased volitional food intake we didn’t tell the mice to eat more they just did so the second and third columns there and predictably this then led to a significant increase in fasting blood glucose levels and perhaps even more predictably the mice got fatter the authors of this paper basically said it was emulsifier induced metabolic syndrome so anybody’s still clinging to the calories in calories out hypothesis but even those on a ketogenic diet shouldn’t get too comfortable right now this is cream and it contains these emulsifiers and they’re also found in things like coconut cream – so please check your labels and so they’re not often stated so polysorbate 80 it’s nice if they say that but it’s often does listed as e3 433 so check your labels if you’re having processed foods polyethylene glycol is another substance that can really thin the mucus layer so that’s often used as an anti foaming food additive or it’s often used to manage your treat constipation in things called Mobe call that’s actually made of polyethylene glycol and in this study here we can see what happened when you add polyethylene glycol to a sugar mixture it must see how it impacts a thickness of the mucus layer there now another additive in food which has a potential to damage the intestinal barriers one that might surprise you and that’s titanium dioxide nanoparticles now we’re used to talking about titanium dioxide in sunscreens when we worry about it but you can probably relax because it doesn’t seem to penetrate to the deeper layers of the skin to the dermis where it can actually interact with the immune system but if you ate it that’s a different story and it’s an approved food additive and you might well be eating it so it’s often in sweets and chewing gums and studies have actually shown in animals that regular consumption for a period of 10 days will actually lead to detectable accumulations in organs so what we’ve got here is a stick of sugar-free and gluten-free chewing gum and as an aside it’s so effective at penetrating the gut barrier that drug companies use it for drug delivery they try and complex a drug molecule with a nanoparticle because they know man a nanoparticle can actually get past the intestinal wall now we move to pesticides and pesticides of all sorts of being associated with a whole lot of autoimmune disorders neurological defects developmental disorders and what we can see here is a study on pesticides so you can see there in green these are tight junctions of proteins that hold the epithelial cells together and they’re being highlighted by something called immunofluorescence and this is a sample that hasn’t been exposed to pesticides and this is a sample from a mouse that has been exposed to pesticides tight junctions are gone and associated with this loss of tight junctions is increased passage of bacteria into the circulation so this is from the same study and this graph demonstrates the percentage of rats following pesticide exposure who had different classes of bacteria in their circulation so the gray bars demonstrate the rats exposed to pesticides and the white bars demonstrate the rats who weren’t and here’s the problem any of her foodstuffs are actually contaminated with pesticide residues this is one that might surprise a lot of people we’ve all heard about people moving to the mountains and the inflammatory bowel disease got better or something like that and pollution may be to blame so particularly the really small particles called the PM tents and they’ve actually been shown to increase gut permeability and in this graph here in control mice we have a and mice exposed to PM 10 you can see there’s a significant increase in intestinal permeability especially in the colon and the reason it’s worse in the colon is probably because the residue spends the longest time in that part of the gastrointestinal tract and they can also induce free radical damage the which then has a holding up another list of consequences in terms of oxidative stress and free radical production what about chemicals found in plastic you’ve all probably heard of BPA and we know that BPA is damaging to the gut lining but it’s being taken out of the the food packaging now right so that’s got to be a good thing well it’s being replaced by something called bps it basically has the same effect we think except it has it really been studied but now 80% of Americans actually have detectable levels of BP s in their urine so maybe stay away from plastics now let’s have a look at things that you can do things that are good now the consumption of fats has actually been shown to significantly improve the function of the mucus layer in the intestines and the effect was significant so when we compared it we had 200 nanometer spheres and we measured the passage of those across a barrier the consumption of fats immediately preceding that reduced to passage by at least 10 times and possibly more than a hundred times there’s something else we can take possibly and that’s called glutamine this is one of the most abundant amino acids in the body’s and it’s used as a main fuel source by the intestinal cells and that significantly contributes to the structural integrity of the intera sites and in animals if we give a mouse indomethacin we can see a lot of the cells die and when we give them indomethacin plus glutamine we see that it’s restored to baseline so as yet human trials and they’ve been a couple they haven’t quite has dramatic results but I’m still I’m still waiting our suspect it probably will be beneficial bovine colostrum claustrum is the the milk moon this is a milk curd cows are making the first few days after birth and this is a randomized control trial on seven male volunteers who took 50 milligrams of indomethacin three times a day for five days and what they found was that before they took into medicine and after they took indomethacin if they had colostrum there was no change in their intestinal permeability but if they didn’t take the colostrum and they took a surrogate a whey protein then there was a significant increase and it’s thought to be that there’s growth factors in their classroom in particular transforming growth factor beta which is thought to support the intestinal wall now by definition lectins can bind to sugars because remember their carbohydrate protein so the theory is that perhaps if we’re consuming lectins we can consume sugars at the same time and these sugars will serve as a decoy and a bind to the lectins before they can hit our intestinal wall and do the damage and what you can see here in this study on mice is that if they were giving a lectin on its own there’s significant increase in intestinal permeability but when they gave it co consumption of sugar plus selectin the damage was reduced and there’s also theories that giving glucosamine supplement will do the same so we can actually do a dacoit now the really interesting thing to consider here is that if you’re a vegetarian on a low carbohydrate diet then you may actually be getting more damage from the lectins and somebody’s still you know totalling down all the tim tams and whatever shield retreats you guys have over here now let then is a unique substance so this is often used as a natural emulsifier in foods but it’s a good guy so it actually contains something called phosphatidylcholine and more than 70% of the phospholipids in a mucous membrane is made as phosphor a phosphatidylcholine and orally ingested liquor –then has actually been shown to adhere to the mucous layer and strengthen it and in one randomized control trial that led to more than 50 percent improvement in symptoms in more than 90% of patients with inflammatory bowel disease and this was in a population that was refractory to steroids and other medications and in fact 80% of patients who were on steroids were able to have them withdrawn because of the liquor –then now we’ve already seen a significant association between bacterial populations in the gut and intestinal permeability so the question is well can we replace can we supplement with bacterial populations in the form of probiotics and several strains of bacteria have actually been shown to be beneficial to the intestinal lining and this includes lactobacillus plantarum which is found in a medical-grade probiotic supplement called the earth bsl-3 that we often use in inflammatory bowel disease one of the issues is though the need to nourish any introduced bacteria if the food supply or the nutrients available for the bacteria which we introduce is not favorable to it it’s likely to be out competed by other bacteria and that just means that when we’re going to need to have a continual delivery now as you know there’s some debate about whether we should have dairy foods and a lot of the debate goes around whether we should have a 1 or a 2 proteins so basically a 1 protein which is found in some milks can lead to the formation of a peptide called b c m7 and these has certain opiate type effects that can bind to opiate receptors in the brain possibly lead to cognitive dysfunction and it can often it’s thought that might also cause intestinal inflammation and several other things and there are some studies that actually show comparing a1 and a2 milks that eliminating the a one protein led to a reduction in systemic inflammation and improving cognitive performance and several other things but there is a take-home point here because putting that to one side both the milks still led to a low-grade inflammatory response the type of which is often seen in conditions what we call a tepee allergic type conditions asthmatic type conditions so it’s probably reasonable here to err on the side of caution if you have a genetic susceptibility for developing allergies or autoimmune disease then avoiding cow’s milk for the first period of your life is certainly highly recommended and possibly ongoing so just to wind up the question is with all of this theory does avoiding these plant-based lectins actually help auto immune conditions and the answer is yes this was a study that was published in 2017 and it looked at a cohort of 15 patients with inflammatory bowel disease and remember inflammatory bowel disease was at the center of this diagram of all the other autoimmune diseases and the average duration of inflammatory bowel disease in the study participants was 19 years and 7 of the 15 actually relied on expensive what we call biological therapy monoclonal antibodies to try and help control their disease so they were placed on a diet that was called the autoimmune protocol so they avoided gluten refined sugar grains legumes nightshade vegetables because there they carry a lot of lectins a lot of people don’t realize so your potato your capsicum you guys call them bell peppers you eggplants tomatoes chilies very rich in maintance so we cut out the nightshades Bridget no dairy no eggs no coffee no alcohol no nuts no seeds no food additives and they also gave them a little bit of lifestyle advice you know optimize his sleep exercise a little bit so what would the results well 11 of the 15 subjects had clinical remission by six weeks and they maintained it for the duration of the study and remember the average duration of inflammatory bowel disease entering the study was 19 years now by virtue of the small study size the laboratory measurements didn’t reach statistical significance but they did show a trend for improvements take for example fecal calprotectin this is a marker of bowel inflammation they get shed off into the feces and it’s a very reliable test of inflammatory bowel disease and in actual fact it’s one of my preferred tests for this condition that I do in the clinic and the average reduction was from 471 to 112 now it didn’t reach statistical significance by virtue of the small sample size but certainly if there’s reductions like that I’d consider that clinically significant and these kind of results mirror what the results that I actually see in my patients I think we should wind up there so thank you

Randall Smitham

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