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Crohn’s and Colitis Awareness


I have many strong males and females in my family. And I don’t necessarily mean strong in the physical sense, though many of them are that, too. I mean strong as in stalwart, devoted, and disciplined.

Per the sake of this blog post, I want to focus on the males in my family.


My Father

For the past twenty-five years, my father has woken up at 4:00 a.m. for work. He does not miss a day, even when he is sick.

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My Grandfather

He is now 81. He fought in the Korean War.

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My Little Brother

He fights a silent battle every single day, yet one would never know since he does not complain. His life was turned upside down in the fall of his senior year of high school. My brother is physically tough, but mentally, he is even stronger. Everyday, he endures the pangs of ulcerative colitis, a condition that, according to him, “is so powerful it can make you drop to your knees and keep you inside your home for weeks on end.” 

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IBS (irritable bowel syndrome), Crohn’s Disease, ulcerative colitis…?

I’m sure you’ve seen the commercials about these illnesses. Cue depressing music and people grimacing while experiencing excruciating pain. On the contrary, the symptoms are actually much worse than these commercials could ever depict on a small screen.

The following information is provided by the Crohn’s and Colitis Foundations of America.

Below, most of the language is graphic. The description contains emotive language that elicits pain.

 

Readers, beware.

Inflammatory bowel diseases are a group of inflammatory conditions of the intestines. Crohn’s disease and ulcerative colitis are two inflammatory bowel diseases that cause chronic inflammation in the gastrointestinal (GI) tract. The GI tract is responsible for digestion of food, absorption of nutrients, and elimination of waste. Inflammation impairs the ability of affected GI organs to function properly, leading to symptoms such as persistent diarrhea, abdominal pain, cramping, rectal bleeding, and fatigue. With both Crohn’s disease and ulcerative colitis, patients go through periods of being symptom-free (remission) alternating with periods of having active disease symptoms (flare). While ongoing inflammation in the GI tract occurs in both Crohn’s disease and ulcerative colitis, there are important differences between the two diseases.”

Crohn’s disease

Crohn’s disease can affect any part of the GI tract, from the mouth to the anus. It most commonly affects the end of the small intestine (the ileum) where it joins the beginning of the colon. Crohn’s disease may appear in “patches,” affecting some areas of the GI tract while leaving other sections completely untouched. In Crohn’s disease, the inflammation may extend through the entire thickness of the bowel wall of the affected area.

Ulcerative colitis

Ulcerative colitis is limited to the large intestine (colon) and the rectum. The inflammation occurs only in the innermost layer of the lining of the intestine. It usually begins in the rectum and lower colon, but may also spread continuously to involve the entire colon.


Who is at risk for developing IBD, Crohn’s, or colitis?

At this moment, there are theories about possible causes, such as interaction between genes, the immune system, and environmental factors. Medical professionals generally cannot specify what causes the onset of these diseases.

There is medical literature which suggests that certain gene polymorphisms are associated with IBD, including ulcerative colitis. According to the article “A polymorphism in the IL11 gene is associated with ulcerative colitis” published in Genes and Immunity, “The IL11 [interleukin 11] gene is therefore a good candidate involved in genetic predisposition to IBD…Altered expression of IL11 appears to be involved in the genetic predisposition of UC.

Gastroenterology  also published an article, “Association between the C3435T MDR1 gene polymorphism and susceptibility for ulcerative colitis,” which tested for gene polymorphisms in the lower intestine. Their results suggest that an alteration in the C3435T MDR1 gene can make individuals more likely to develop UC.

Scientists also speculate that too much serotonin in the gut may affect the onset of the disease. In which case, they theorize that supplementation (under doctor’s supervision, of course) with Vitamin D3 may help.

Overall, IBD is a grey area, but one thing that medical professionals definitively do know is that IBS, Crohn’s, and colitis affect about 150–200 [people] per 100 000 in Western countries. Generally, people between the ages of 15-60 develop these illnesses. My brother was 17 when he was diagnosed.


Luck of the Draw?

If our fate lies in the hands of our genes, then are we sort of helpless? I’m not sure how to answer that question. Optimistically, I want to believe that epigenetics can increase our odds. 

“For nearly a century after the term “epigenetics” first surfaced on the printed page, researchers, physicians, and others poked around in the dark crevices of the gene, trying to untangle the clues that suggested gene function could be altered by more than just changes in sequence.

Today, a wide variety of illnesses, behaviors, and other health indicators already have some level of evidence linking them with epigenetic mechanisms, including cancers of almost all types, cognitive dysfunction, and respiratory, cardiovascular, reproductive, autoimmune, and neurobehavioral illnesses.

Epigenetics literally means ‘in addition to changes in genetic sequence.’ The term has evolved to include any process that alters gene activity without changing the DNA sequence, and leads to modifications that can be transmitted to daughter cells. Known or suspected drivers behind epigenetic processes include many agents, including heavy metals, pesticides, diesel exhaust, tobacco smoke, polycyclic aromatic hydrocarbons, hormones, radioactivity, viruses, bacteria, and basic nutrients” (Weinhold 160-64).

I mean, I used to suffer from asthma. I struggled to run 1/4 of the mile-run in grammar school. It was humiliating to watch my friends run laps around me. My body wanted to run, but I was unable to breathe normally. I thought that I would never be able to run. Well, guess what? I no longer have asthma. I can sprint. I can jog. The only thing that drastically changed in the meantime was my diet. Read the full story here.

My mother taught my brother and I about the importance of basic nutrients (i.e. macronutrients and micronutrients). Nutrition is something that we believe we can control because we have the ability to choose our food and feed ourselves.


My Brother’s Case Study

My brother is not a passive victim; he does not want to cover up his condition with a band-aid and “forget about it.” After doses of prednisone, he was over being ornery. He researched the illness, and so did my mother and I.

We came across blogs such as Roost, Against All Grain, Comfy Belly, etc. Via these social media platforms, we discovered the Specific Carbohydrate Diet (SCD) by Dr. Haas and biochemist, Elaine Gottschall.  “The Specific Carbohydrate Diet™ is predicated on the understanding that Ulcerative Colitis, Crohn’s Disease, Irritable Bowel Syndrome, and gluten therapy resistant Celiac are the consequence of an overgrowth and imbalance of intestinal microbial flora. By altering the nutrition we take in, we can effect the constitution of our intestinal flora, and bring it back into balance, healing our digestive tracts and restoring proper absorption.

Let me break down the diet for you: it is essentially ALL whole foods. Nothing processed: no candy, packaged food, boxed food, microwavable food, sulfites, pizza, or takeout. Oh, and no alcohol, caffeine, or other stimulants because these substances are shown to cause damage and stress inside the body, on a cellular level.

Alcohol, in particular, has no nutritional value or benefits from consumption. It’s essentially toxic and is known to cause oxidative stress. In the article “Alcohol, Oxidative Stress, and Free Radical Damage,” Wu, et al, elucidate alcohol’s harmful effects:

“Alcohol promotes the generation of reactive oxygen species (ROS) which are small, highly reactive, oxygen–containing molecules that are naturally generated in small amounts during the body’s metabolic reactions and can react with and damage complex cellular molecules such as fats, proteins, or DNA. ROS and/or interferes with the body’s normal defense mechanisms against these compounds through numerous processes, particularly in the liver… alcohol can alter the levels of certain metals in the bodyalcohol reduces the levels of agents that can eliminate ROS (i.e., antioxidants). The resulting state of the cell, known as oxidative stress, can lead to cell injury…Both acute and chronic alcohol exposure can increase production of ROS and enhance peroxidation of lipids, protein, and DNA, as has been demonstrated in a variety of systems, cells, and species, including humans.”

My brother was in high school when he developed the condition. Like I said, we don’t know what caused it. Perhaps there was too much serotonin being produced in his gut. Maybe he could have avoided the condition by reducing the stress caused by excessive alcohol or caffeine consumption. We do not know. We cannot know. At first, all we were able to do was try to alleviate his pain and control the inflammation.

Since my brother lived at home, my mother made him the  SCD “legal” foods in the initial stages of his healing process. For example, she made him batches of nurishing bone broth until he was ready to try other foods, such as gelatin (only sweetened with honey) and homemade yogurt.

We suspected that his large doses of steroid therapy (i.e. prednisone) heavily taxed his gut’s microbiome. The yogurt is a probiotic and thus replenishes microbes. The homemade yogurt is beneficial for someone with colitis specifically because, according to Department of Agriculture,

additional milk solids including lactose and protein are added to commercial yoghurt and then subjected to the short fermentation. Because of so much lactose in it from the very beginning, what happens is that the little good guys (bulgaricus and thermophilus start doing their work and when they have converted half of the lactose in the original vat, there is lactic acid produced and the acidity (acid=acidity)(the pH) reaches a critical point of about 3.5. At this point, our little guys’ enzymes cannot work because of the acidity and there is still 50% more lactose remaining (remember they added milk solids at the start). You end up with as much, if not more, lactose as in a glass of milk. Subjecting the yoghurt to more time would not change anything. The cultures’ machinery (enzymes) cannot work in such an acid environment” (Elaine Gottschall).

After months on the diet, consuming ONLY the aforementioned foods and supplementing with additional vitamins (under his doctors supervision), my brother wanted to introduce some fat and protein into his diet. Yes. Don’t be afriad of fat, or protein, for that matter, although I think that fat is the most feared macronutrient. We all metabolize fat differently (see: PPARγ), and we all require different amounts and variations, yes; however, steroids (i.e. cholesterol, phytosterol, and stigma sterol) and fatty acids (i.e. EPA, DPA, DHA) are basic, essential nutrients. WE NEED THEM.

Fat is essential for survival. We need it for energy, development, vitamin absorption (i.e. A, D, E, K, and carotenoids), and cell membrane maintenance. Of course, if you have only eaten low-fat your entire life, then you will have to learn which fats will serve you best.

 There are many studies involving various lipid types. In relation to inflammation, Daniella DeCoffe’s article, “Dietary Lipid Type, Rather Than Total Number Of Calories, Alters Outcomes Of Enteric Infection In Mice,”  which I’ve referenced below, states that,

Olive oil diets resulted in little colonic pathology associated with intestinal alkaline phosphatase, a mucosal defense factor that detoxifies lipopolysaccharide. In contrast, while both corn oil and milk fat diets resulted in inflammation-induced colonic damage, only milk fat induced compensatory protective responses, including short chain fatty acid production. Fish oil combined with milk fat, unlike unsaturated lipid diets, had a protective effect associated with intestinal alkaline phosphatase activity. Overall, these results reveal that dietary lipid type, independent of the total number of calories associated with the dietary lipid, influences the susceptibility to enteric damage and the benefits of fish oil during infection.”

My family likes LOVES fish. My brother, in particular, also loves his cheese. The first time my brother met my (now) fiancé, he was nibbling on a block of parmesan. No joke. My brother was almost in remission from his colitis, so the parmesan sat well with him. Needless to say, my brother has no problem choosing fish and milk fat over corn oil. Obviously, you will want to listen to your body before you slice through a block of parmesan cheese.

Oh, vegetable oils, like olive oil, should only be consumed at room temperature, whether you have colitis or not. The article, “Heated vegetable oils and cardiovascular disease risk factors,” by Chun-Yi Ng, et al, explains why:

the quality of dietary oils and fats has been widely recognized to be inextricably linked to the pathogenesis of [cardiovascular disease]. Vegetable oil is one of the essential dietary components in daily food consumption. However, the benefits of vegetable oil can be deteriorated by repeated heating that leads to lipid oxidation. The practice of using repeatedly heated cooking oil is not uncommon as it will reduce the cost of food preparation. Thermal oxidation yields new functional groups which may be potentially hazardous to cardiovascular health. Prolonged consumption of the repeatedly heated oil has been shown to increase blood pressure and total cholesterol, cause vascular inflammation as well as vascular changes which predispose to atherosclerosis. The harmful effect of heated oils is attributed to products generated from lipid oxidation during heating process.”

Matt already understood the concept of oxidation, as well as the concept of “good” and “bad” fats. My mother explained it to us when we were younger.

Anyway, when my brother felt that his body could handle slightly more than the bland foods he’d been eating, he began to incorporate several plain tablespoons of pure, extra virgin coconut oil per day. Coconut oil contains β-Tocopherol and α-Tocopherol, which are both antioxidants. Coconut oil also contains phytosterols, which have been shown to improve serum lipid (cholesterol) profiles. He also added in broiled fish (i.e. salmon and flounder). Broiling appears to be “better” than grilling because grilling causes mutagenic activity, as does burning/frying any food source.

Overall, my brother saw improvement with these big, fat additions to his diet ;). As time went on, he slowly and gradually added in other foods that are SCD legal, too.


After the Diet (and Medication)

As I said before, my brother’s healing process was slow and gradual. It required time, positive thinking, patience, research, as well as critical thinking.

After strictly adhering to the diet for many months, it seemed my brother’s symptoms had been completely alleviated. So my brother went on to college. He lived on campus and he played for the club hockey team. An eighteen year old freshman in college… you can guess what his every day environment looked like–stressors of all sorts: alcohol, caffeine, and test anxiety. Unfortunately, after living the college lifestyle for quite sometime, his symptoms returned and he experienced another flare. Thus my brother had to repeat the Specific Carbohydrate Diet again, from scratch.


Concluding Words

In my brother’s case, he has found that an eating style filled with nutrient dense foods is most beneficial for him. Then again, shouldn’t everyone eat for nutrition? I mean, our bodies are so amazing; they are like intricate machines. They just need to be cared for via proper nutrition, movement, and conscious acknowledgement.

Most importantly, I am happy to say that, at the moment, my brother is in remission.

Should you have any questions about colitis or Crohn’s, please contact me at glutenfreedee@hotmail.com. My brother welcomes questions about his condition and symptoms.


 Research

While learning about my brother’s condition, our research expanded from food blogs to medical journals involving studies in vitro and in vivo. On a daily basis, in order to understand and learn, I read about biochemistry, genetics, immunology, gastroenology, bacteriology, microbiology, and various branches of biology.

Below, I will link to medical journals that I have referred to either directly or indirectly throughout this post.


Works Cited/References

  1. Agrawal, Anurag, Meher Priyanka Mothey, and Anupam Reg. GastroenterologyPulse(2016): 70-71. Academic Search Premier. Web. 15 June 2016.
  2. Africa, Jonathan, et al. Lifestyle Interventions Including Nutrition, Exercise, And Supplements For Nonalcoholic Fatty Liver Disease In ChildrenDigestive Diseases & Sciences 61.5 (2016): 1375-1386. Academic Search Premier. Web. 15 June 2016.
  3. Anderson AFR. Ulcerative colitis- an allergic phenomenon. American Journal of Digestive Diseases1942;9:91–98. Web. 15 June 2016.
  4. Bo, Liang, et al. Effect Of Vitamin E And Omega-3 Fatty Acids On Protecting Ambient PM2.5-Induced Inflammatory Response And Oxidative Stress In Vascular Endothelial Cells. Plos ONE 11.3 (2016): 1-11. Academic Search Premier. Web. 15 June 2016.
  5. Brandes JW, Stenner A, Martini GA. Dietary habits of patients with ulcerative colitisZeitschrift fur Gastroenterologie1979;17:834–842. Web. 15 June 2016.
  6. Gilat T, Hacohen D, Lilos P, Langman MJS. Childhood Factors in Ulcerative-Colitis and Crohns-Disease – an International Cooperative Study. Scand J Gastroenterology. 1987;22:1009–1024. Web. 15 June 2016.
  7. Chun-Yi Ng, et al. Heated vegetable oils and cardiovascular disease risk factorsVascular Pharmacology, Volume 61, Issue 1, Page 1. Web. 15 June 2016.
  8. DeCoffe, Daniella, et al. Dietary Lipid Type, Rather Than Total Number Of Calories, Alters Outcomes Of Enteric Infection In MiceJournal Of Infectious Diseases213.11 (2016): 1846-1856. Academic Search Premier. Web. 15 June 2016.
  9. Gerasimidis K, et al. Micronutrient status in children with IBD: true deficiencies or epiphenomenon of the systemic inflammatory responseJ Pediatric Gastroenterology Nutr. (2013): 56(6):e50-1. Web. 15 June 2016.
  10. Hart AR, Bergmann M, Luben R, Camus J, Oakes S, Welch A, Bingham S, Khaw KT, Boeing H, Day NE. The role of diet in the aetiology of ulcerative colitis: A pilot study in a European prospective cohort study. Gut. 2002;50:287. Web. 15 June 2016.
  11. Hubbard, Catherine S., et al. Abdominal Pain, The Adolescent And Altered Brain Structure And Function. Plos ONE11.5 (2016): 1-30. Academic Search Premier. Web. 15 June 2016.
  12. Klein, W, et al. A polymorphism in the IL11 gene is associated with ulcerative colitis. Genes and Immunity (2002). Web. 20 July 2016.
  13. Mayberry JF, Rhodes J, Newcombe RG. Increased sugar consumption in Crohn’s disease. Digestion1980;20:323–326. Web. 15 June 2016.
  14. Okayasu, Isao, et al. Vitamin A Inhibits Development Of Dextran Sulfate Sodium-Induced Colitis And Colon Cancer In A Mouse Model. Biomed Research International (2016): 1-11 11p. CINAHL Complete. Web. 15 June 2016.
  15. Wang, Tingting, et al. Dectin-3 Deficiency Promotes Colitis Development Due To Impaired Antifungal Innate Immune Responses In The Gut. Plos Pathogens 14.6 (2016): 1-22. Academic Search Premier. Web. 15 June 2016.
  16. Reif S, Klein I, Lubin F, Farbstein M, Hallak A, Gilat T. Pre-illness dietary factors in inflammatory bowel diseaseGut1997 ;40:754–760. Web. 15 June 2016.
  17. Rodríguez-Bores L, Fonseca GC, Villeda MA, Yamamoto-Furusho JK. “Novel genetic markers in inflammatory bowel disease.” World J Gastroenterology (2007). Web 20 July 2016.
  18. Schwab, M, et al. Association between the C3435T MDR1 gene polymorphism and susceptibility for ulcerative colitis. Gastroenterology (2003); 124(1):26-33. Web. 20 July 2016.
  19. Swanson GR, Sedghi S, Farhadi A, Keshavarzian A. Alcohol. 2010 May; 44(3):223-8. doi: 10.1016/j.alcohol.2009.10.019. Web. 15 June 2016.
  20. Tragnone A, Valpiani D, Miglio F, Elmi G, Bazzocchi G, Pipitone E, Lanfranchi GA. Dietary Habits as Risk-Factors for Inflammatory Bowel-Disease. Eur J Gastroenterology Hepatol. 1995;7:47–51. Web. 15 June 2016.
  21. Wu, Defeng, Cederbaum, Arthur I. Alcohol, Oxidative Stress, and Free Radical Damage. National Institute of Alcohol Abuse and Alcoholism. Web. 15 June 2016.
  22. Yun-Hee Youm, Kim Y Nguyen, Ryan W Grant, Emily L Goldberg, Monica Bodogai, Dongin Kim, Dominic D’Agostino, Noah Planavsky, Christopher Lupfer, Thirumala D Kanneganti, Seokwon Kang, Tamas L Horvath, Tarek M Fahmy, Peter A Crawford, Arya Biragyn, Emad Alnemri, Vishwa Deep Dixit. The ketone metabolite β-hydroxybutyrate blocks NLRP3 inflammasome–mediated inflammatory diseaseNature Medicine, 2015.
  23. Zuk, Aleksandra, Tiffany Fitzpatrick, and Laura C. Rosella. Effect Of Vitamin D3 Supplementation On Inflammatory Markers And Glycemic Measures Among Overweight Or Obese Adults: A Systematic Review Of Randomized Controlled Trials. Plos ONE 11.4 (2016): 1-23. Academic Search Premier. Web. 15 June 2016.
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