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.

Stuck in the Predni-Zone

Hello, friends.It has been not even a whole month since GUTS has really opened for public viewing but the viewership, response, and contact from enthusiastic contributors has been more than I could have hoped for, thus far. I’ve gotten to develop some fun content and hear from some amazing people who fight disease everyday. Here is to a new year and to keeping the train a-rollin’ on!

In other news, here is an update from myself about life with IBD:

2, January, 2017 – Stuck in the Predni-Zone

So, it has been a long and winding road for my Crohn’s Disease the past months. Since the summer, I have gone through several massive life changes, largely in part to the condition of my health. Back in June, around the time my lease was ending in Blacksburg, Virginia, I was still working my previous laboratory position. This was at an institute I had  been working at for many years. In the years during that time after graduating from University, I had a bunch of battles with my Crohn’s. I could’t seem to shake it. So many vicious flares, new doctors (a couple I just couldn’t seem to see eye to eye with), and a constant fatigue that seemed to follow me around like a dark storm cloud everywhere I went. My lease was ending and it struck me that I would have to make a hard decision to benefit my health long term. It was short notice, but I decided to leave my job and move back to northern Virginia with my family temporarily to focus on getting my Crohn’s to a better place. It was often extremely stressful and required an unmatched dedication to the lab, but I loved Inflammatory Bowel Disease research and the people I worked with. It pained me to leave them behind. Ultimately, I knew that I was ignoring major issues that could cause me to get serious intestinal surgery if gone unchecked, and I was never going to fully commit to making myself better. There could be no competing priorities in that regard. And for my work at the lab, I would not be able to live up to the rigor of the research and required day to day excellence expected of the people who work there. I was, often times, a zombie walking the halls of the institute. I would let my colleagues down and hold them back in the state I was in. 

Next thing I know, I am letting my boss and mentor know that I was going to have to take my leave, began training others on necessary management responsibilities of the lab, packing up my maroon Honda CRV (Virginia Tech colors even when I drive, Go Hokies) and heading back to Northern VA. During the next few months, I rested, hid from much of the world, saw doctors, got prescribed LOTS of drugs, and asked myself “where do I go from here?” Well, after a few months I managed to get myself to a state where I felt I was healthy enough to jump on job offers and stop bothering my parents since I am a grown-ass man. Eventually, I started my current position with a contract research organization coordinating large molecule pharmaceutical studies and I accepted my offer to start a Masters at George Washington University. So, life has been getting back on track. The problem is, I have been taking Prednisone in my therapeutic regimen. 

Since July. 

That is 6 months on Prednisone. I was supposed to wean off it quite a while ago but I can’t seem to find myself feeling well enough without it.

I’m stuck in the Predni-Zone…

For those of you that are not familiar with prednisone, it is a steroid that is used by millions of people with inflammatory diseases to get their problem under control when it is severe. Most people with Crohn’s have a complicated relationship with prednisone. It often gets the job done, keeping you out of the bathroom or making your abdominal cramps disappear, but it has side effects like no other. In the long term, you really don’t want to deal with that crap. It is bad, believe me; I am a pred-vet. So now, I have to find a therapy that will get me out of the vicious cycle. But it is not easy. I have a strong aversion towards anti-TNF biologic use (i.e., Humira, Remicade) and the recently approved Stelara gives me similar discomforts. All of the sudden my options seem…limited. I am already taking Imuran with my pred, and it is just not enough. After talking with my GI, I will be looking potentially into getting involved in the anti-MAP antibiotic clinical trial and see how that works for me. I am not high on long term antibiotic use as a treatment approach but I am willing to say that it concerns me less than what I believe are massive unknown implications of biologic use. We’ll see…

Until then, thanks for reading my IBD journal update everyone and I appreciate you all coming to the site. I will update again soon to discuss where I have gone to try and escape the horrid Predni-Zone. Make sure to check out other articles on the site, read stories by our contributors, and share or comment on anything that resonates with you.

All the best to you and yours,



An Invisible Disease

Reddit user /u/ProfessorChaos_ shares her story of her recent Crohn’s Disease diagnosis as an adult, and how it quietly effected her years beforehand:

Almost 2 years ago, I started feeling really intense abdominal pain. The pain was so intense that I was unable to walk without hunching over. The next day I went to urgent care and was lucky enough to see my primary care physician. After an examination and a few tests, she sent me to another clinic across town to get a CT scan. After several hours of pain and vomiting (the contrast they made me take for CT scan did not agree with me), she called with my results. They were inconclusive, but she said that they showed pretty bad inflammation in my bowels. She said that I needed to get to the ER immediately.

My then boyfriend (now husband) and I waited for over 5 hours in the ER. 5 hours. Eventually, my name was called and we went to my little bed. Nurses and doctors came in and out of the room asking me what was wrong. All I could say that I was in really bad pain and I had a CT scan earlier, my results should have been sent earlier. Eventually, I was admitted to the hospital. I had my own little room where I was poked with needles all night. I have a heart palpation, so they were also checking my vitals every hour. Doctors kept telling me that they thought I have Crohn’s Disease but I’d have to have a colonoscopy for sure. So at age 23, I had my first colonoscopy.

I stayed at the hospital for 5 days. By the 5th day, I was officially diagnosed. I had 6 medications, a new diet, an outrageous hospital bill, and Crohn’s disease.
According to my doctors, my inflammation indicates that I had been living with the disease for years before I was diagnosed. Most of my health issues can be traced back to Crohn’s Disease. It is often called the “invisible disease” and for good reason. I might look completely healthy but feel like I’m dying inside. CD also affects other parts of my body. I stopped getting a regular menstrual period for over 2 years because I was so anemic and my body decided to use my blood cells to fight off the disease. As my doctor put it, “having babies becomes a luxury”. I am tired, ALL OF THE TIME. Fatigue is probably one of my worst symptoms, apart from the almost constant need to go to the bathroom and the pain.

Crohn’s is quite the lifestyle to get used to. I’ve been on all sorts of medications, none now, thanks to insurance complications. I am a firm believer in the medicinal properties of marijuana. I have a wonderful GI doctor, an amazing support system, and am a part of an online support group (the Crohn’s subreddit has been my go-to through all of this). Everyone has been so wonderful and helpful. I couldn’t do this without you. Thanks for reading my wall of text! 🙂

Thanks again to /u/ProfessorChaos_ for sharing! 

5 Holiday Gifts for that Special Crohnie in Your Life

Hi everyone,

It’s that magical time of year again and GUTS is here to give some lovely gift ideas to counteract the gift that keeps on giving; your inflamed bowels.

At GUTS, we have that knack for digestive gift giving that will make your butt hole say “thanks!” instead of DEAR GOD GET SOME SOFTER TOILET PAPER”, and we want to share it with you!

GIFT NO. 1 – A Squatty Potty

“If pooping with your pants still on is cool, then you can call me Miles Davis!”

Aw yiss. The Squatty Potty. The true natural, #1 way to go #2. Have you been saying your whole life, “Man, going poo really sucks and feels like a total hassle.” That’s because you’re doing it WRONG you ignorant rube. You were born to squat when you defecate. Your colon kinks and has difficulty passing stuff when you just sit on the toilet. Putting your legs up into a natural squatting angle makes your poo’s come out nice and smooth and can potentially even reduce your risk of colorectal complications later in life. Your buddy with the special bowels will be saying “Wow! My poops feel mad decent! Magical even!” But in the case of a Crohn’s patient, best you can hope for is regularly decent, I guess. We can all dream, right?

Wait, so if I was supposed to be squatting when I poop this whole time, maybe I wouldn’t have gotten such bad bowel problems…? Best not to think about it…

On to…

GIFT NO. 2 –  A Bidet!

“Toitlet used water gun. It was super effective!”

Thought your porcelain throne was already a perfect spot for your private moments? WRONG. Prepare to step your toilet accessory game another level, friends. Stop using so much toilet paper, stop your friends from using so much toilet paper. Do you hate the earth? Stop that. Have a bidet squirt water at your butt. Not only will it make your butt nice and clean without having to do some major handywork down there, it is just civilized. Get your beloved Crohnie a bidet, put your pinky out, and get sophisticated.

GIFT NO. 3 – A Fitbit!

“Aw, great. Someone else to tell me I’m being too lazy.”

Whether it’s to promote exercise that can help fight the sedentary depression that often washes over your pal, or to help them make those lifestyle changes they’ve been yammering on about, a Fitbit is a great way to have your wrist become your own personal coach. Now they can visually see a metric of just how much they are walking between their desk and the bathroom everyday! Great! Nothing like getting a notification on your phone saying you walked the entire distance of the city of Tokyo, entirely from bathroom trips! What a time to be alive!

GIFT NO. 4 – A Taco Bell Taco 12 Pack!

Lol. Just kidding this is a terrible gift idea. Friends don’t give friends with Inflammatory Bowel Disease Taco Bell. Be reasonable.

GIFT NO.5 – An Artificial Nano-bot Replacement Immune System!

“Sweet, an immune system run by computers! Just like the rest of my life!”

Here it is. The best gift for you fiery gutted friend. This will solve ALL their problems. Just get a sophisticated community of nanobots that run a complex and highly-functioning multi-scale computational model of the human immune system and intestinal mucosa, replacing the need for all those dysfunctional immune cells they have. You just won the holidays! You can pick one up at Amazon for only the small pric-

Oh wait. These don’t exist. Drats.

All Jokes Aside:

Interested in giving an actual really great gift to the Crohn’s and Colitis community this holiday season? Donate to the Crohn’s and Colitis Foundation of America to honor your friends with IBD. Until December, 31st, all donations made to CCFA will be DOUBLED by the foundation to support double research and double the health programs. Thanks for reading!

Donate to CCFA here!

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,