What Have We Learned About Autoimmune Disease?

Well, welcome to 2017. Oh boy. This is already starting as one of those remarkable years. It's like we're all being shot out of a cannon with all the things that are happening right now across a wide spectrum, but certainly not the least of which is healthcare and biomedicine. So this year we're going to have a lot of news to use. We'll have a lot of new things to be sharing with you. And I want to start this year with a little bit of a walk down memory lane, because I had the opportunity just within the last week to go through archives of materials that we've been putting in storage since the late 70s, early 80s, which was really quite interesting to me to go through some of this information that we've been providing through our Functional Medicine Update and our seminar series and our publications going back into the early 80s. One of those things that I found, which I found very, very interesting, was a 1985 seminar series set of syllabi and audio tapes. Yes, there were those days of audio tapes entitled New Breakthroughs in Autoimmune Disease. And I thought, wow, 1985, how presumptuous to even talk about new breakthroughs. But as I reviewed, what I discussed in 1985 was the emerging understanding that autoimmune disease may not just be so simple as a person's genes coming dysregulated and producing reaction to their own proteins so that they become allergic to themselves. That that model seemed like it was fallacious based upon the fact that, number one, these disorders are not that genetically inherited, they're not monogenic, and number two, that there appeared to be ever increasing evidence that our body's tissues would undergo change as a consequence of different types of things like glycation, oxidation, phosphorylation that would make our body not like it used to be, so it would become a foreigner in its own land, for. For which the immune system then was capable of recognizing this alteration and generating antibodies in the inflammatory process and response. So that then in 1985 gave me the thought that maybe autoimmune disease was more than just a genetically pre programmed immune reaction to ourself, that it was really a consequence of the body responding to its environment and producing alterations in tissue structure that then the immune system responded to, meaning it could be modifiable by understanding what were the precipitating or triggering factors. So that was the context of 1985 seminar series. And I am amazed when I think now, going back now more than 1995, 2005, 2015, so we're now, 30 plus years later where we're starting to discover, with a fairly broad understanding across the field of immunology, that autoimmunity is more than just genetically pre programmed response to the body's own tissues, native tissues, that the environment and lifestyle play significant roles. Now with that as a context, now let me share with you a little bit of news to use in 2017. So in the January issue of the Lancet, this is actually the January 21 issue of 2017, there is a lead article talking about a new so called JAK1 inhibitor that is showing very great promise for the treatment of the autoimmune disease, Crohn's disease, which you know is a regional ileitis with inflammatory conditions that often lead to recurrence of problems, surgical resection and all sorts of very complicated medical therapy, including anti inflammatory and anti immune types of therapies. And so they go on to say that this study offers promise because it might provide a whole different approach towards blocking the inflammatory effects of Crohn's disease. And in 1932, it was the first time when Beryl Cohen and Leon Glinsburg and the Gordon Oppenheimer group had actually codified regional ileitis as a distinct clinical entity with its own pathophysiological characteristics that was later called Crohn's disease disease. And successive approaches have been able to achieve universal success against the relapsing nature of this illness, according to the Lancet. And research is not keeping up with the need. And this is where I think the next sentence is very important for us. It goes on to say, each year Crohn's disease snatches the quality of life for an increasing number of young adults in more and more countries. So why is it increasing? If it's genetically pre programmed, then you would think it would have a set kind of penetrance into the phenotype. But what we're really seeing, particularly in young women, is ever increasing numbers of that, not just in the United States, but as development of our society moves into other countries, then we start to see it become much more prevalent in countries where it was not even recognized before at all. So why is that? And I think that if you start to examine this at a little bit deeper level, you'll start to recognize that the microbiome, our diet, our lifestyle and our environment are starting to demonstrate to be principal features in determining many of these characteristics that we associate with autoimmunity of the gut. Crohn's disease, inflammatory bowel disease. And how does that then relate to systemic immune dysfunction and other autoimmune characteristics. So I want to segue just briefly if I can, to what might appear to be abstract, but I think it actually connects to the story and that is the connection of food allergy to diet. As you probably recognize, there's been a long standing recognition that certain types of foods, particularly things like peanuts and eggs, can produce allergic disorders in children leading to things like otitis media or middle ear infections and alter immunofunction so that children become more susceptible to certain immune related infections. So what is that all about and how does that relate to this concept of autoimmune disease? Well, as you probably recognize that there have been studies now that have been demonstrated that you can early on take a child that is susceptible to peanut allergy and you can start titrating their peanut sensitivity by neutralizing it with low dose therapy. So there's an actual approved therapy where you introduce specific types of peanut antigens at a very low dose to immunize that child against their peanut allergy. And similarly now we've seen in the Lancet another step towards prevention of allergy to foods which has in this case to do with eggs. And I'm now quoting again from the lancet, same issue, January 21, 2017 in which they talk about a two step egg introduction prevention of egg allergy in high risk infants with eczema. Now, eczema is not Crohn's disease, but eczema is a manifestation of a mucosal surface inflammatory condition associated with an an immune reaction to its environment. And so what do they find is by immunizing a child with this two step egg introduction, low dose first, to get low dose zone tolerance, just like you would immunize to any number of type of antigens, in this case it's low dose oral tolerance that you're really talking about. You can then prime the immune system to be tolerant to that antigen. Now what happens then when you kind of put into our environment 50,000 new chemicals and you start changing the nature of our food supply and you start changing the whole nature of use of various medications early in life because you treat the effect and not the cause by giving a lot of antibiotics to children, you change the microbiome. All of those factors then are doing the opposite than neutralizing the immune system by low dose priming. They are then overwhelming the immune system into an inflammatory state. So I think we're witnessing the emerging of a very new view of where these atopic conditions, these things like asthma, allergy, eczema and now even going into inflammatory conditions of the gut and other mucosal surfaces and how they relate to environmental factors. Beyond that, just of saying it's determined because you have the genes and you've inherited this risk. This is a major breakthrough, I believe, that will make the whole construct of lifestyle medicine the whole construct of making sure that we're asking the right questions, interrogating. Right. And also using the immunization potential of certain foods at low dose to produce a tolerant outcome in a infant or a child at risk. It's a very, very exciting chapter in our emerging, I think, advancing understanding how to treat and prevent these conditions without just suppressing symptoms using immune blocking agency.