Inflammatory Bowel Disease: An Autoimmune Conundrum

Inflammatory Bowel Disease: An Autoimmune Conundrum
Assessing Traditional and Modern Treatment Paths, and How to Look Forward

by CT Heltzel


In Western society, people’s immune systems are becoming increasingly unstable, and their guts more sensitive. A major contributor to this is the rising number of people in the world who suffer from Inflammatory Bowel Disease (IBD). An estimated 1-1.3 million people in the US live with IBD, with as many as 70,000 new cases every year. IBD refers to a group of several autoimmune conditions that affect the colon or entire gastrointestinal tract. The two major classifications of IBD are Crohn’s Disease (CD) and Ulcerative Colitis (UC). Physicians diagnose a comparatively small portion of IBD patients with various types of “indeterminate” colitis. Both CD and UC present similar symptoms resulting from an overactive immune response in the GI tract, and commonly require similar medications for treatment. However, significant differences exist between the conditions that both physicians and patients must take into account when deciding upon treatment. Expressed symptoms specific to UC and CD create a need for alterations and selectivity to the types of inflammation ameliorating drugs patients decide to use. Modern medical treatments of IBD vary widely in approach to relieving inflammatory symptoms. Many of these treatments successfully relieve patients of their symptoms, often to the point of total remission. Despite this, nearly 70% of CD patients and 35% of UC patients will require major surgery after diagnosis1. Further, the medications required to treat IBD often cause dangerous side effects.

People with the condition are often on long term regimens of steroids and immunosuppressive biologics. In accordance with this, medical costs skyrocket and biologics have shot up to the top of the drug market. This is indicative of the impact autoimmunity is having on the US population. Millions of people pay extreme amounts to manage symptoms, but are never truly healthy. IBD is an emergent disease that is increasingly more threatening to population health in the US and other highly developed nations by forcing large groups of people to live immunocompromised and chronically ill. Fully understanding the current state of IBD research and treatments requires thorough investigation of several key subjects. Immune pathways and pathogenesis of the disease, modern treatments, and current research should be analyzed.

Pathobiology and Immunological Mechanisms

Among the many issues associated with IBD diagnosis and treatment is the lack of a primary source of known pathogenesis. Like many autoimmune conditions, IBD is described as a multifactorial disease, having several potential contributing actors and no easily recognized, common origin. These factors are broadly categorized as genetic predisposition, environmental triggers, and immune system disruption. Population studies demonstrate many common characteristics between people who have IBD, but they are not consistent as people may have one or a combination of many of these factors while maintaining similar or differentially severe pathogenicity as other patients. Examples of these factors include intestinal microbiome compositions, genetic mutations, lifestyle choices like smoking, or disease triggered after infection or injury.

Patients with active IBD show greater infiltration and activation of innate (e.g., macrophages) and adaptive (i.e., B and T cells) immune cells in the intestinal mucosa. The intestinal mucosa consists of the top epithelial layer of cells, or intestinal epithelial cells (IEC), in the gastrointestinal tract. Hyperactivity of immune cells causes heightened production and recruitment of more inflammatory agents in the mucosa. Proteins that signal immune cells to react in various ways, referred to as cytokines, represent the most relevant agents causing inflammatory proliferation. Specific cytokines of interest include tumor necrosis factor alpha (TNF-α), interferon-γ (IFN-γ), and cytokines associated with the interleukin-23—Th17 pathway2. These cytokines and cytokine receptors associate with T-cells via secretion or expression on the cell membrane. IBD research and treatment focus primarily on modulation of CD4+ T-cells, or helper T-cells (Th). Cytokine receptors can bind to various biological subunits and activate the differentiation of naïve (unactivated) CD4+ T-cells into several sub-types of helper T-cells. Differentiation into specific Th cells depends n activation by respectively associated interleukins (IL), cytokines that foster growth and differentiation of T-cells. Dysregulation of CD4+ T-cell differentiation into Th1, Th2 and Th17 holds a heavy implication in the pathogenesis of IBD3. Current research and treatment focuses heavily on the function of these immune cells as a potential route for therapeutic target discovery.

Modern medical treatments for IBD vary widely in mechanisms of action and biological targets. In essence, certain medications perform more effectively for ther CD or UC and for different severities and locations of disease symptoms. 5-Aminosalicylates (5-ASA), for example, provide greater symptom amelioration for UC since the medication mostly effects the colon. 5-ASA binds and activates the anti-inflammatory receptor Peroxisome proliferator-activated receptor-γ (PPARγ) in colon-based IECs4. Figure 1 highlights the differences between the diseases relevant to treatment.

The main types of drugs used to reduce IBD symptoms in current treatments fall under a few specific categories. From least to most extreme, physicians and researchers commonly group treatments as 5-aminosalicylates (5-ASA), corticosteroids, immunomodulators, or biologics. Physicians regularly prescribe all of these medications, sometimes in a combination treatment including more than one. However, physicians must balance medication effectiveness with harmful side effects. The balance between the two fuels a controversial argument in the scientific community: which treatment path best leads to long-term remission with the lowest potential for negative side-effects? The treatment paths in question for IBD generally fall under two schemes known as “Step-up” and “Top-down”5.

The former represents the traditional approach in which treatment uses weaker medications followed by harsher medication in accordance with increasing symptom severity. Top-down involves first utilizing the most powerful immunosuppressive drugs, such as biologics and immunomodulators, to eliminate symptoms quickly. Subsequently, physicians treat with weaker medicines as the patient moves towards remission6. The top-down approach becomes increasingly popular as more patients see positive results from use of biologics. However, many physicians and scientists are not supportive of such an approach, seeing the dangers of immune system suppression as an unethical first-line of defense. The most common immunosuppressive biologics commercially available include anti-TNFα antibodies, such as infliximab (Remicade®) or adalimumab (Humira®). These antibodies locate and bind to the TNFα cytokine and inhibit its activity7. This approach provides effective amelioration of IBD symptoms since TNFα is greatly overexpressed. However, lowering function of this cytokine lowers overall immune function and T-cell development which can be unhealthy and leads to potential infections.

Biological Target and Drug Efficacy

The uncertainty towards a superior therapeutic treatment method within the scientific community suggests significant room for innovation in the realm of IBD medications. Deciding on what constitutes a high efficacy biological target forms the first major hurdle in the research process. Measurability of the target in question can make pursuing research either plausible or unlikely very early on. Time and expenses limit the necessary devices and techniques at a laboratory’s disposal to measure a potential target, as well as the feasibility of measuring it based on biological and chemical characteristics. Beyond financial and experimental obstacles, the most important criteria relate to biological function. Specificity of a target to the disease process probably counts as a main feature of significance towards efficacy. Preferably, the target is unique to the condition’s mode of action and has a potent effect on symptoms without unwanted inhibition of other physiological processes. A target proximal to symptom initiation holds a similar importance to specificity. Proximity refers to closeness to disease related symptom initiation. Affecting the target hopefully does not affect other, possibly unrelated, processes prior to symptom initiation in the inflammatory cascade. Another scenario for good proximity involves prevention of symptoms, rather than clearing the aftermath. For the purposes of IBD treatment, a target that has high systemic expression instead of local expression to one part of the GI tract can be of great interest to researchers. Some targets fail to be useful, as they do not have great presence in all possible areas of inflammation.

The types of compounds composing drugs used to treat inflammation are also relevant to the quality of a treatment. The difference between a small molecule and large molecule drug can make a great difference in the comfort of a patient. Currently, anti-TNF-α biologics represent the most potent drugs on the market. These antibody-based medications are large molecules and patients apply them via injection/infusion. Small molecule drugs commonly utilize oral delivery, a preferable method for most patients. For the sake of easy application to the patient, a small molecule with potent effects on inflammation makes for a desirable compound to research. Most importantly, a drug should have low toxicity. Additional short or long-term side effects from therapy essentially defeat the purpose of researching a new IBD drug. The negative side effects researchers observe in preclinical trials root out potential drugs early on.

Current IBD Treatments

As described previously, physicians prescribe several types of medications to treat IBD. Each classification differs greatly in biochemical mechanism and there are many drugs on the market within these classifications for physicians to utilize. A patient with severe IBD symptoms commonly begins treatment with corticosteroids. A typical beginning of treatment shared by many IBD patients involves use of the drug Prednisone. Corticosteroids such as Prednisone bind to glucocorticoid receptors and proceed to downregulate gene transcription for various inflammatory agents8. This corticosteroid has uses in many conditions outside IBD and thus has the negative attribute of many side effects unrelated to inflammatory relief. Physicians avoid use of prednisone and other steroids as a long-term solution. Once patients achieve short-term symptom relief by use of steroids, physicians attempt design a new treatment regimen for long-term stability.

Physicians commonly prescribe 5-ASA as a next step after steroids, or possibly before if symptoms start out mild. This progression falls in line with the top-down treatment path. As stated earlier, 5-ASA acts as a ligand, binding to PPARγ and activating its anti-inflammatory effects in IECs. 5-ASA drugs commonly prescribed by physicians include Asacol and Pentasa. These drugs act locally in the gut, which make them very effective for UC and mild-moderate cases of CD. The local predominance allows for minimal systemic side effects, leaving the most common ones related to digestive organs. Such side effects could include diarrhea, flatulence, or cramping. Despite minimal side effects, the inability of 5-ASA to cause potent anti-inflammatory effects outside colonic IECs makes these drugs ineffective in severe cases of CD. A preemptive colonoscopy allows physicians to find areas of inflammation local to the colon. Observing severe inflammation outside the colon may cause a physician to bypass 5-ASA treatment.

Chemical immunomodulators cause potent immunosuppressant effects to reduce inflammation, often in relief of or in conjunction with 5-ASA usage. Thiopurines such as mercaptopurine (6-MP) and azathioprine (AZA) act as small molecule immunomodulators that suppress the immune system much like biologics. They are used for more moderate IBD symptoms and have less potent effects9. 6-MP functions as a competitive antagonist of GTP, binding to a small GTPase protein, Rac1. Binding to Rac1 suppresses activation of the protein in gut CD4+ T-cells, and causes cell apoptosis10. This reduction of CD4+ T-cell activity creates significant anti-inflammatory effects throughout the GI tract. However, thiopurines have many faults outside of immunosuppression that make them ineffective as a final treatment for many patients. Not all sever cases of IBD appear to associate with Rac1 based T-cell proliferation, often causing patients to use biologics as a powerful alternative.

Physicians prescribe biologics such as Remicade (infliximab), Humira (adalimumab), and Cimzia (certolizumab) in cases of severe CD, often when all other medications fail to relieve symptoms. All the biologic medicines above consist of monoclonal antibodies that work as TNFα antagonists. The antibodies bind TNFα and inhibit its ability to signal, lowering development and recruitment of various inflammatory agents. With the FDA approval of Humira as a CD medication in 2007 and for UC in 2012, biologics will continue to rise to the top of the IBD drug market11. Negative side effects such as risk of infections due to high immunosuppression and the possibility of increased lymphoma occurrence (uncommon in short term use) present significant issues with anti-TNFα biologics12. Despite this, the usual high remission rates using these medications often outweigh any negatives for IBD patients. Non-TNF based biologics such as ustekinumab (Stelara) and vedolizumab (Entyvio) have hit the market in recent years, as well, and provide potential alternatives in the realm of powerful large molecule drugs. Stelara binds to the p-40 subunit shared by the IL-12 and IL-23 cytokines. This keeps p-40 from binding to these cytokines, making it unable to send a signal for T-cells to differentiate into inflammation promoting Th17 cells13. Entyvio blocks lymphocyte trafficking and adhesion in the gut through its recognition and blocking of the α4-β7 integrin glycoprotein on B and T-cells14. This does not appear to cause systemic immune suppression in the rest of the body, making the drug a potential safe alternative to anti-TNFα antibodies. Still, immunosuppression in general is an unhealthy practice, leaving significant room for innovation in future IBD treatments.

Because of the aforementioned success of biologics in diminishing the symptoms of people with IBD, as well as millions of others suffering from autoimmunity, these drugs are more and more likely to be prescribed and have risen to top grossing positions in the pharmaceutical market15. With this comes the implication that millions of people are also being critically immunocompromised over significant periods of time, causing dysregulation of the body’s innate bio-molecular mechanisms. Such blanket treatments could be viewed as unethical on that large of a scale without looking forward to new methods. But what could be done to better regulate this system of treatment? How can we better meet patient’s needs? One answer is using precision medicine as a path towards pinpointing disease pathogenesis on a person by person basis. The concept of precision medicine utilizes multiple avenues of modern clinical research tools to personalize the treatment path for patients. This method seeks to combine pharmaceuticals, nutraceuticals, bioinformatics/genomics, and microbiology to understand and approach the driving force behind a patient’s condition16. IBD is one of the most practical areas to start using precision medicine because of its multifactorial nature. Computational models of the intestinal immune response can be developed that use patient data on microbiome and immune cells and molecules as a baseline and are calibrated to an individual using their specific bacteria, mutations and disease pathology as input parameters. The outputs of such a model would inform clinicians on the best types and amounts of therapy needed to return someone to a healthy immunological baseline. In order to do this, however, massive epidemiological studies must continue to be conducted on willing patients through public health initiatives that involve numerous practitioners, hospitals, and testing sites. Using the collected data, researchers will be more capable of creating refined and accurate models of disease that can be turned into a reliable clinical tool17.  This data will also be critical in determining what initiatives must be put forward to focus on preventive measures. Big epidemiological data can lead to pathological origin trails that may inform what needs to be regulated or removed from typical human consumption. It is likely this will involve limitations on regulations on human exposures to antibiotics, food pesticides, preservatives, and other chemicals that we come into contact with on a daily basis that could be brought to light via connections made in the computational model of disease. If bioinformatics continues to progress as quickly as computational systems typically do in modern times, there may yet be hope for a world unburdened by chronic inflammatory bowel disease in the near future.

Autoimmune conditions like IBD remain difficult to control because of the high complexity of human immunity. Diagnosis rates for the condition grow yearly, and more individual must learn to manage crippling intestinal damage or depleted immune systems. Current medicines provide effectiveness relief for many patients, but have the potential to be much safer. For this reason, it is important that research on new therapeutic targets and treatment paths for IBD treatment continue to develop.

  1. Maggiori, L.; Panis, Y., Surgical management of IBD–from an open to a laparoscopic approach. Nature reviews. Gastroenterology & hepatology 2013, 10 (5), 297-306.
  2. Abraham, C.; Cho, J. H., Inflammatory Bowel Disease. New England Journal of Medicine 2009, 361 (21), 2066-2078.
  3. Abraham, C.; Medzhitov, R., Interactions Between the Host Innate Immune System and Microbes in Inflammatory Bowel Disease. Gastroenterology 2011, 140 (6), 1729-1737.
  4. Iacucci, M.; de Silva, S.; Ghosh, S., Mesalazine in inflammatory bowel disease: a trendy topic once again? Canadian journal of gastroenterology = Journal canadien de gastroenterologie 2010, 24 (2), 127-33.
  5. Hanauer, S. B., Positioning biologic agents in the treatment of Crohn’s disease. Inflammatory bowel diseases 2009, 15 (10), 1570-82.
  6. Blonski, W.; Buchner, A. M.; Lichtenstein, G. R., Inflammatory bowel disease therapy: current state-of-the-art. Curr. Opin. Gastroenterol. 2011, 27 (4), 346-357.
  7. Pollack, P. F.; Hoffman, R. S.; Renz, C., Uses and compositions for treatment of Crohn’s desease. Google Patents: 2013.
  8. Emilie, D.; Etienne, S., [Glucocorticoids: mode of action and pharmacokinetics]. La Revue du praticien 1990, 40 (6), 511-7.
  9. Goracinova, K.; Glavas-Dodov, M.; Simonoska-Crcarevska, M.; Geskovski, N. In Drug targeting in IBD treatment-existing and new approaches, InTech: 2012; pp 301-332.
  10. Neurath, M., Thiopurines in IBD: What Is Their Mechanism of Action? Gastroenterology & hepatology 2010, 6 (7), 435.
  11. FDA FDA approves Humira to treat ulcerative colitis.
  12. Williams, C. J. M.; Peyrin-Biroulet, L.; Ford, A. C., Systematic review with meta-analysis: malignancies with anti-tumour necrosis factor-alpha therapy in inflammatory bowel disease. Aliment. Pharmacol. Ther. 2014, 39 (5), 447-458.
  13. Frleta, M.; Siebert, S.; McInnes, I. B., The Interleukin-17 Pathway in Psoriasis and Psoriatic Arthritis: Disease Pathogenesis and Possibilities of Treatment. Curr. Rheumatol. Rep. 2014, 16 (4), 8.
  14. Ghosh, N.; Chaki, R.; Mandal, S. C., Inhibition of Selective Adhesion Molecules in Treatment of Inflammatory Bowel Disease. Int. Rev. Immunol. 2012, 31 (5), 410-427.
  15. FDA FDA approves Humira to treat ulcerative colitis.
  16. NIH, All of Us Research Program.
  17. MIEP, Computational Models.

Introducing: Drugs, in Review

Hello friends and Crohnies!

I would like to introduce the new weekly section of GUTS, Drugs, in Review:

This section is a weekly feature about a pharmaceutical or nutraceutical currently in use by practitioners or being researched for treating IBD and other autoimmune condtions. Each article will go over the specifics on the drug, how it helps people, how it might not be so helpful, and other insights about the state of the drug in today’s market.

This week’s post will be about Imuran (aka Azathioprine) and its sister drug, 6-MP

Do you take Imuran/6-MP? Sound off in the comments and look out for the post in Drugs, in Review on GUTS this week.

Best to you and yours,

The Hardest Pill to Swallow

In honor of Crohn’s and Colitis Awareness Week, as well as my brother, Will, who suffers from Type 1 Diabetes:

Wake up, its 2 AM. Bathroom time. Number 10 on the night. Good news, looks like you’re in competition for the world record in trips to the porcelain throne. Tomorrow’s pre-calc exam can’t hold a candle to that.

Bad news is you’re 16 years old, and this is your life now.

But hey, don’t sweat it, you’ve just joined one of America’s biggest clubs. And membership is growing every day.

That teenager was me. Seven years ago. My name is Chase Heltzel. I have Crohn’s Disease. And frankly, I’m a bit upset.

For those of you unfamiliar with Crohn’s Disease (CD), allow me to enlighten you on the situation. Crohn’s is a form of Inflammatory Bowel Disease (IBD), an umbrella term for a series of autoimmune diseases that cause inflammation in the gastrointestinal tract. Among these are Crohn’s, Ulcerative Colitis, and any other number of indeterminate forms of colitis. All of these are shitty conditions to have (pun intended). To gain a basic understanding of CD, I’ll put it like this:

The human bowel is an extremely busy and hyper-complex breeding ground for microbiological activity. Since I have CD, mine does not handle this all too well. Our guts are covered in a community of bacteria known as the microbiome, the hottest topic in microbiology and immunology these days. A normal immune system intricately operates within the gut mucosa to regulate the composition of the microbiome and remove any potential pathogenic invaders. In order to do this immune cells often are required to initiate a cascade of signals that cause inflammation at the site of pathogenic microbes. After that, natural healing processes begin. The issue is, my immune cells don’t like to quit causing inflammation when the job is done, and those involved in healing don’t like to show up for work. This could happen at anytime, anywhere in my gastrointestinal tract. It is pretty awful.

Now you may find yourself asking “Wow, Chase. How did your nasty ass intestines get so messed up? Eat too many of those sugar free Haribo gummy bears?” No. The reality of the situation is that there IS NOT A KNOWN SINGULAR CAUSE FOR INFLAMMATORY BOWEL DISEASE. Excuse my yelling. It’s just a bit frustrating. The best understanding we have of the origins of CD is a multifactorial paradigm involving microbiome composition, environmental influences, and genetic predisposition. These all have different commonly occurring instances show up in CD populations, such as similar gene mutations or types of bacteria in the gut, but there are many patients and nobody has it exactly the same. It really is tough. Often times, we know what processes are messed up, we just don’t have a good understanding of the trigger. But you know what is really messed up? Its not just CD patients. Its not just IBD patients. This is the case with a shocking number of autoimmune diseases in general. It’s Type 1 Diabetes. It’s Rheumatoid Arthritis. It’s god damned Multiple Sclerosis. Our immune systems are attacking us and WE DON’T KNOW WHY. This brings me to the major purpose of my ranting:

Autoimmune diseases are a modern epidemic in the industrialized world. And nobody is talking about it.

The rapid increase in autoimmune deficiency is alarming and likely happening at an exponential rate. This is not a case of better criteria for diagnosis, but a full on wave of sick individuals that would not have been in previous decades. Diseases that would only see a handful of patients in the hospital every year now bring in hundreds of unfortunate men, women, and children every day. The American environment is toxic. Our people are consuming the scum of the earth, daily. We are stuck in a destructive marriage with the ways of our society and will tumble down into a dark abyss along with them. In sickness and in wealth, the bottom line today is a priority over the human lives of tomorrow.

In order to combat this bleak situation that is becoming increasingly dire, we need to make massive changes to how we currently approach them as a risk to society. For starters, there are two areas in which need to do this

1. Federal research funding towards autoimmunity as a condition.

2. Public health initiatives related to environmental health and healthcare policy that focus on the potential prevention of autoimmunity

Again, these are massive undertakings, more easily said than done. But autoimmunity has become a problem with such momentum that we can only stop it if we make big leaps. Small steps in the right direction are no longer something we have time for. It is likely that ~50 million Americans or more suffer from autoimmunity. Currently, The National Institutes of Health (NIH), the largest financial supporter of biomedical research in the United States, funds cancer research the most at somewhere greater than $5 billion a year. Cardiovascular disease and stroke funding from the NIH comes to ~$2 billion a year. Autoimmunity gets about half a billion. However, in all likelihood, Cardiovascular disease and Cancer patients combined don’t even reach the same number of total people living with autoimmune disorders. Let me pile on here a few more stats, if you don’t mind?

Healthcare burdens for Cancer in the US stand at $9 billion annually. Autoimmune diseases are costing around $100 BILLION EACH YEAR. And believe me, that differential is only going to grow wider and wider. It is essential that funding for research programs in autoimmunity gets more support. Yes, Cancer is terrible. But we have so much more to lose once we become a society of sick, overly medicated sad sacks. In fact, people are getting cancer from having autoimmune diseases. IBD patients are faced with the significantly increased risk of colorectal cancer to go along with that delightfully uncomfortable gut we get to live with, already. And I am not even going to get started on the long term implications of immunosuppressive therapeutics used to treat most patients with these conditions. That is a whole other article worth writing, and a lot more dedicated biomedical research needed.

Now, to my second area of need: Public Health Reform

This one is big. We need to change the way we live. We need to put forth initiatives that flip society as we know it. And this needs to happen now. The American public can not be allowed to continue ingesting the unnecessary toxins and chemicals they are blindly absorbing on a daily basis. The current state of what enters the majority of the public’s bodies is an environmental, medical, and moral disaster. First, we need to consume more holistically. The fewer non-whole ingredients in your diet, the better. You want things looking more or less in their original form. No strange, unrecognizable chemicals ingredients. Your body is easily naturally capable of handling these whole ingredients, while many of these stray chemicals are likely having unknowable interactions any number of things in your metabolism. The FDA and other health regulatory agencies need to come down hard on what we consume. This sounds harsh but we cannot play around like these aren’t severe issues on the brink of catastrophe. Health organizations need to focus on promoting truly healthy consumption and finding ways to get better food and lifestyles in the grasp of the middle and lower socioeconomic classes. Not every blessed American man and woman can have the honor of shopping at Whole Foods every week. Some people (hell, too many people) are living on that Wonder bread and Arby’s diet. That can’t fly anymore.

Secondly, we need to adopt a new philosophy in the treatment of patients, especially those with autoimmune diseases. Medicine needs to become more personalized. Every individual is different and has diverse needs that can be met with the numerous clinical research tools we have available today. No more one size fits all. No more throwing antibiotics at it, no more “when in doubt, debilitate the immune system!” What we need is Precision Medicine. Personalized treatment that realizes these conditions are multifactorial and benefit most from a versatile, combination approach. Using research data such as massive scale health informatics, genomic information, pharmaceutics/nutraceutics, and microbiome assessment, we should be able to tailor a treatment plan to each and every patient. Crohn’s Disease, with its particular combination of microbial, genetic, and environmental factors, is the perfect testing ground for the precision medicine approach. This is so much the case that the Crohn’s and Colitis Foundation of America (CCFA) has started a program called IBD Plexus, which is working to help make the use of precision medicine in IBD a reality. Putting efforts towards the creation of initiatives that support this sort of medical methodology and the research needed to make it happen must become a priority.

Now its getting late, and I am a bit tired of rambling, but I have a few more things to say. To all the people reading this, normally healthy or not, please do everything you can to live by example and make healthy decisions for you and the future of our people. Hell, if anything, do it for your kids, your grandkids. We can only change as a group.

Every day since I was 16, I have had to take between 6-10 pills just to keep myself in some semblance of well being. I still feel awful much of the time. Like many Crohn’s patients, I wear a smile that has been perfected to hide the pain I feel oh so often. Still, that is not the worst thing. What is truly disheartening is that with the rate society is going, my plight could become that of the majority. That my friends, is the hardest pill to swallow.

And to all my fellow IBDers who made themselves #IBDvisible this week, and to all who suffer from autoimmune conditions:

Never give up. Get angry, but don’t give in to it. Use it. Be angry about what has happened to you and fight every single god damned day to make a difference. Fight to make sure no one HAS to ever understand how you feel. Fight because you feel that wretched growl in your bowel and you want to shut it up. Get up every day and dig through the blood, the crud, the pain and the shame and come out the other side a stronger person. You are not broken. You are not worse than anyone else. You are visbible.

Howdy, friends!

Hello, all, and welcome to my first public blog! Thanks for checking it out and reading whatever ramblings I have decided to put on display. I decided to initiate this site as a sort of personal outlet for me and others to talk about and discuss things that are important that we see in the world today regarding public health, immunity, inflammatory bowel disease, and any other nonsense that has been rattling back and forth in my mind. This is new territory for me, so I hope I can create some content that might provide some enjoyment or inspiration to people. If only a single person other than myself gets something positive out of it, I believe I would feel pretty good about that. And if I end up just sitting here every day typing to myself, that’s probably fine too. Writing can be nourishing for the mind and soul and I haven’t done too much of it (outside of a scientific research setting…) in the past years.

Generally, I will be trying to post significantly about topics related to public health and science associated with autoimmune diseases and the need for initiatives that will help prevent the massive threat they quietly pose to society. As a person with Crohn’s Disease, this is something I am very passionate about and will talk about often. I am attempting to delve in to higher graduate studies and research in the fields of epidemiology and pubic health so an audience to read and give feedback on my posts and articles would be amazingly helpful! Constructive criticism, well wishes, and even saying you find something posted interesting or informative could provide invaluable insight on perfecting my craft and how I could make it better, or even gain new knowledge and perspectives myself! I think the best case scenario is that I could facilitate a realm of constructive discussion and information sharing through this site and I think it would be just delightful if that came to fruition.

Other than the serious stuff, I am a classical nerd and science fiction junkie, a hopelessly cursed DC sports fan, and a bit of a sucker for a little pop culture trivia and history lessons. So occasionally I will probably rant about those types of things (My secret side ambition/dream is to be a science fiction writer…maybe getting into a little writing here on this blog will spark an inspired idea for this. Who knows? )

So, once again welcome to my blog and thanks for checking in! I’ll try my best to create content and not be too much of a insufferable dork.

All the best to you and yours,