Chapter 9. Ulcerative Colitis and Crohn’s Disease
“About 25 percent to 40 percent of ulcerative colitis patients must eventually have their colons removed because of massive bleeding, severe illness, rupture of the colon, or risk of cancer.”
Ulcerative Colitis; National Institutes of Health [1]
Think outside the box
Ulcerative colitis and Crohn’s disease are characterized by inflammation and ulceration of the intestinal mucosa, or the inside upper layer of the intestinal walls (epithelium). In turn, inflammation blocks primary intestinal functions—the absorption of water, electrolytes, and nutrients from the chyme. Naturally, an accumulation of too many unabsorbed fluids in the lumen (the cavity of a tubular organ) causes diarrhea. In turn, the loss of essential fluids and nutrients leads to severe dehydration, malnutrition, loss of electrolytes, and associated complications.
Mainstream medical references classify ulcerative colitis (UC) and Crohn’s disease (CD) as Inflammatory Bowel Diseases (IBD). While ulcerative colitis is localized exclusively inside the large intestine, Crohn’s disease may extend into both the large and small intestines. According to The Merck Manual of Diagnosis and Therapy, the “groupings and subgroupings [of both conditions] are somewhat artificial. Some cases are difficult, if not impossible, to classify.”[2]
In other words, the most apparent symptoms (abdominal cramps, pain, diarrhea, bleeding, fever, dehydration, malnutrition, and weight loss) of ulcerative colitis and Crohn’s disease appear to be similar, and their respective treatments (diet, medication, rehab, etc.) are also similar. For these reasons, the overview of both conditions is combined into one chapter. For the record, there are significant morphological differences between the two conditions, but they aren’t relevant for a treatment and prevention overview. To streamline the narrative, the term “inflammatory bowel diseases” may be used in place of the repetitive “ulcerative colitis and Crohn’s disease,” unless noted otherwise.
Inflammatory bowel diseases rarely happen out of the blue—they may follow years of Irritable Bowel Syndrome, gastroenteritis, and the other functional disorders of the GI tract described throughout this book. Symptomatically, constipation may or may not be an apparent precursor, because it is often latent, i.e., hidden from view, and isn’t recognized. But that doesn’t mean that it isn’t there. In fact, this book’s central theme, the critical role of latent constipation in the pathogenesis of intestinal inflammation, is confirmed by the following remarkable fact:
The Merck Manual of Diagnosis and Therapy: About 1/3 of patients [diagnosed with Crohn’s disease] have a history of perianal [around the anus] disease, especially fissures and fistulas, which are sometimes the most prominent or even initial complaint. In children, extraintestinal [perianal] manifestations frequently predominate over GI symptoms.[3]
An anal fissure is a laceration of the anal canal mucosa that won’t heal. An anal fistula is a duct from the anal canal into the perianal region that was formed from the initial ulceration of the anal mucosa. Let’s think outside the box about the connections between fissures, fistulas, constipation, inflammation, and Crohn’s disease:
Q. What causes an anal fissure or fistula?
The extreme straining that’s required to expel dry, hard (not necessarily large) stools. Anyone who’s ever experienced a fistula or fissure will tell you that they are extremely painful, especially during defecation, and that they bleed often.
Q. What does this pain do to a person, especially a child?
Pain causes the delaying or withholding of stools to avoid further pain and bleeding. Children may withhold stools for days, even weeks at a time.
Q. What happens when a person delays or withholds stools?
Formed stools inside the large intestine get impacted from the rectum all the way back to the cecum.
Q. What happens when the stools get impacted and accumulate throughout the entire length of the large intestine?
They extend all the way back into the small intestine (ileum) and cause intestinal obstruction, which is actually a prominent symptom of Crohn’s disease.
Q. And what happens when this occurs?
The presence of feces in the small intestine causes mucosal inflammation. Inflammation causes profuse diarra. Diarrhea is often followed by severe constipation.
After that, it’s simple: constipation is either not treated at all or it’s treated with fiber. In both cases stools accumulate and impact. Depending on the diet, it may take up to a month to accumulate enough impacted stools to obstruct the small intestine again. At this point diarrhea kicks in again. After this cycle repeats itself several time, a person develops chronic intestinal inflammation or bleeding ulcers, and that’s when Crohn’s disease or ulcerative colitis are finally diagnosed.
The other probable path to either condition is a matter of just plain bad luck. Accidental food poisoning, travelers’ diarrhea, viral infection, or a food allergy may bring along intestinal inflammation, vomiting, and diarrhea. The outcome—a ride to hell or a full recovery—depends on the treatment of the original cause.
- The prudent approach: a brief (24 to 48 hours) fast following the attack (you wouldn’t have an appetite anyway). Then, a low-density recovery diet for a week or two (no fiber, no known food allergens, and no hard-to-digest foods). After that, the mucosa heals, and you are as good as new.
- The imprudent approach: taking drugs to suppress vomiting and/or diarrhea (just recall those happy-go-lucky TV ads), so you can continue eating as if nothing happened. This is, unfortunately, the more typical “protocol,” which keeps the intestinal inflammation raging on, and on, and on. Then, at the first sign of diarrhea and blood, the treatment of ulcerative colitis or Crohn’s disease starts in earnest, and the ride to hell begins.
You may wonder why two diseases, both culminating with severe diarrhea, are included in this book. The answer is obvious—they may begin with diarrhea, but, actually culminate with equally severe constipation. In other words, as much as constipation may cause ulcerative colitis or Crohn’s disease, both of them cause constipation too. Directly, when the recovery is spontaneous, and indirectly as well, after a treatment with prescription drugs and/or fiber.
This book provides ample evidence that the generally accepted treatment of ulcerative colitis and Crohn’s disease-related constipation with dietary fiber is THE CAUSE of the next round of diarrhea, and behind the gradual progression (worsening) of both diseases, namely more mucosal inflammation, more ulcerations, more anorectal damage, more blood loss, and more drugs to treat the ensuing diarrhea. This is followed by more fiber to alleviate constipation, and (surprise, surprise) the diarrhea-constipation cycle repeats itself.
The previous chapter (Chapter 8, Irritable Bowel Syndrome) provided equally ample evidence that constipation, hidden or not, is one of the leading causes of ulcerative colitis and Crohn’s disease.
The origins of ulcerative colitis and Crohn’s disease: Debunking uncommon nonsense
You’ve probably heard this truism time and again: to cure a disease, you must first eliminate its causes. That’s common sense, right? The bad news is: ulcerative colitis is still “incurable,” because its causes are still “unknown:”
National Institutes of Health: Theories abound about what causes ulcerative colitis, but none have been proven. The most popular theory is that the body’s immune system reacts to a virus or a bacterium by causing ongoing inflammation in the intestinal wall. [4]
Equally bad news: the etiology of Crohn’s disease remains as enigmatic as ulcerative colitis:
The Merck Manual of Diagnosis and Therapy: The fundamental cause of Crohn’s disease is unknown. Evidence suggests that a genetic predisposition leads to an unregulated intestinal immune response to an environmental, dietary, or infectious agent. However, no inciting antigen has been identified.[5]
The good news is: I don’t buy any of that. Let’s put aside the theories, and deal with facts. The fact is, there’s nothing mysterious or complicated about ulcerative colitis or its causes. The mucosa is the mucosa is the mucosa. The same forces that cause inflammation and ulceration inside one’s mouth or stomach may cause similar inflammation and ulceration inside one’s intestines, small and large. No difference, except when the stomach is affected, one vomits, and when the intestines are affected, one gets diarrhea.
And there is nothing complicated or mysterious about the treatment of mucosal inflammation or ulcers, either. If, for example, you have bleeding ulcers inside the mouth, you change to a liquid or semi-soft diet to minimize chewing, you exclude spices to avoid contact with hypersensitive tissues, you avoid hot drinks to prevent burns, you don’t put anything harsh in your mouth to prevent abrasions, you treat cavities and gum disease to eliminate potential sources of infection, and you don’t kiss anyone or engage in oral sex, etc.
And if those ulcers don’t heal in few weeks time, you take a doctor-prescribed broad-spectrum antibiotic for a week or two to eliminate probable pathogens. Soon, the ulcers are gone, and hopefully you won’t repeat doing the same stupid things that caused inflammation and ulcers in the first place. That’s just common sense, right?
It’s the same with stomach ulcers. You take a drug or two to inhibit the secretion of hydrochloric acid, you are placed on a low-density diet, you don’t smoke or drink alcohol, and, if tests show H.pylori infection, you take antibiotics and antacids to wipe it out. Soon, the ulcers are gone, and hopefully you won’t repeat doing the same stupid things that caused them in the first place. That’s also common sense, right?
And common sense dictates doing exactly the same things if you have inflammation and bleeding ulcers inside your small intestine (Crohn’s disease) and/or large intestine (ulcerative colitis). But that’s not what’s being done. Quite the opposite. Besides drugs that are supposed to stop diarrhea, patients are advised to take indigestible fiber to prevent the constipation that (surprise, surprise) results from the diarrhea treatment. As in this example by the famous Mayo clinic:
Experiment with foods high in fiber (fresh fruits, vegetables and whole grains).[6]
If you follow this advice, here is what happens next:
- Indigestible fiber (a.k.a. “bulking agent,” “roughage”) expands four to five times from its original shape and weight, and enters the intestines.
- While the expanded fiber slowly crawls through the inflamed and ulcerated sections of the small and large intestine, the bacterial fermentation produces fatty acids that are obviously acidic, and gases that are obviously expanding. (To overcome fiber fermentation, many patients are instructed to take potent antibiotics indefinitely instead of eliminating fiber.)
- Expanded fiber remains in permanent contact with inflamed and ulcerated mucosa throughout the entire journey. This fact is meaningless, unless you recall that human intestines were not intended to transport indigested food, only liquid chyme. That, incidentally, is why intestinal obstructions are so common among patients with Crohn’s disease.
- Patients who get “treated” with fiber-rich whole grains ingest profound quantities of dietary gluten, a plant protein and potent food allergen that causes intestinal inflammation known as celiac disease. This is one of the precursors (surprise, surprise) of ulcerative colitis and Crohn’s disease.
So there we have it: (a) large chunks of bloated fiber are chafing and scraping an inflamed and ulcerated mucosa; (b) profuse gases are pressing on the intestinal walls because they can’t escape by the inflamed mucosa; (c) astringent fatty acids are burning the bleeding ulcers because they can’t get absorbed past the inflamed mucosa; and (d) the voluminous fiber keeps accumulating inside the intestines, because to relieve the pain from (b) and (c), patients take muscular relaxants, which block intestinal peristalsis altogether, stall the “traffic,” and cause the obstruction.
When this situation becomes unbearable, the body responds with violent diarrhea again, and the whole cycle starts anew. Uncommon nonsense, right? So let’s now apply common sense to the same problem, namely the inflammation and ulceration of intestinal mucosa.
What’s the number one rule of first aid care? Keep inflammation and ulcers (cuts, wounds, abrasions) clean and protected from the elements! So why, then, doesn’t this rule apply to intestinal inflammation and ulcers? Why should the insides of the intestines scrape against impacted stools that are full of decaying fibers, nauseating gases, and burning acids? Obviously, one isn’t going to earn a PhD or win the Nobel Prize by writing a two-line thesis:
Keep Intestinal Inflammation And Ulcers
Clear Of Congested Crap!
Of course not! So countless researchers are earnestly struggling to develop fancy theories, harsh treatments, and ever more potent drugs to accomplish the impossible: to heal mucosal inflammation and ulcers inside small and large intestines loaded to the rafters with rotting fiber, large stools, and everything else that comes along.
Impossible! While this “research” continues, hapless patients are still having their colons routinely amputated:
National Institutes of Health: About 25 percent to 40 percent of ulcerative colitis patients must eventually have their colons removed because of massive bleeding, severe illness, rupture of the colon, or risk of cancer. Sometimes the doctor will recommend removing the colon if medical treatment fails or if the side effects of corticosteroids or other drugs threaten the patient’s health.[7]
Not fun, but still better than dying.
But how about this for first aid: relieve your intestines, both large and small, of congested “crap” and keep them “clean.” If done in time (before rupture, or something to this effect) the ulcerative colitis and Crohn’s disease will take care of themselves. Or, as they say: no cause—no disease!
Of course, it isn’t just fiber, fiber, and fiber. As ulcerative colitis and Crohn’s disease advance, other factors, mentioned by the NIH, contribute to their worsening outlook. There are two major theories related to their pathogenesis:
- Bacterial and viral theory. Each round of antibiotics decimates intestinal flora, and leaves the large intestine defenseless from endogenous (remaining inside) and exogenous (brought from outside) pathogens. We now know from clinical experience that the restoration of intestinal flora alone cures ulcerative disease in many patients, regardless of the stage.
- Autoimmune response theory. When the intestinal mucosa is healthy, it is well protected from the by-products of digestion. When it is inflamed, it is not protected, and may develop antibodies to once-benign components of food, mainly proteins, both plant and animal. The longer the inflammation, the more the antibodies may develop. This means that affected patients may experience strong allergic reactions—histamine release directed by antibodies—to once perfectly acceptable food. These reactions, which may appear just like another relapse of ulcerative colitis or Crohn’s disease, are manifested by inflammation and diarrhea. Unfortunately, there is no way to eradicate antibodies, except by suppressing the immune system itself. For obvious reasons, it isn’t a wise strategy, although it’s commonly employed. A far better strategy is to avoid trigger foods, and these antibodies will eventually wear off just like the antibodies to most vaccines do.
But again, these issues are secondary next to the fundamental rules of treatment and prevention of inflammations and ulcerations: keep the affected organs “clean.” I put the clean in quotes here, because in the case of the intestines I mean it figuratively, not literally: let the intestines perform their innate task of transporting fully digested liquid chyme, rather then stuffing them up and down with loads of indigestible, bulky, and rough fiber. Never!
Mission impossible: The conventional treatment of ulcerative colitis and Crohn’s disease
The treatment of both conditions is intended to stabilize patients and suppress the symptoms. Neither the doctors nor the patients really have much choice. The patients are temporarily satisfied because there is less diarrhea, pain, suffering, and bleeding, and the side effects of medications take time to develop. Here are the most popular treatment options:
- Antibiotics to destroy bacteria. Broad spectrum antibiotics provide temporary relief because they terminate the fermentation of dietary fiber, formation of gases, and fatty acids by wiping out intestinal flora along with the suspected pathogens. It should, of course, be the other way around—fiber, soluble as well as insoluble, must be excluded to terminate fermentation. It’s worth repeating that clinical and practical experience indicates that the restoration of intestinal flora alone is often all that is needed to cure ulcerative colitis for good, and by extension, Crohn’s disease. Obviously, antibiotics have their uses, and shouldn’t be shunned when prescribed for a real cause, rather than for “just in case.”
- Aminosalicylates to reduce mucosal inflammation. Unfortunately, these drugs have digestive side effects, such as nausea, vomiting, heartburn, and (surprise, surprise) diarrhea. Not surprisingly, they may work for some patients, but not for long. And the next step is...
- Corticosteroids to reduce mucosal inflammation. These hormonal drugs cause typical side effects such as rapid weight gain, elevated blood pressure, depression, anxiety, and risk of infection. Because they impact the body’s hormonal balance, they also cause severe acne and rapid growth of facial hair among women. And the next treatment is...
- Immune system suppressants to reduce inflammation by literally turning the immune system off. These “killer” drugs are euphemistically called immunomodulators. They open the body to a host of other opportunistic infections, from flu to pneumonia, that can easily turn deadly. The immunomodulators may cause permanent damage to the liver, pancreas, and bone marrow. This is especially likely in patients already weakened by ulcerative colitis and Crohn’s disease.
- Anticholinergics to stop peristalsis. These are systemic (body-wide) muscular relaxants that suppress the effect of acetylcholine, a neurotransmitter that stimulates muscular contractions. These drugs alleviate diarrhea-related muscular cramps and spasms, but unfortunately they also stop the flow of nutrients throughout the entire length of the digestive tract, and cause indigestion, intestinal obstruction, and constipation. Also, these drugs affect other organs that are controlled by muscles, including the heart, salivary and sweat glands, and genitourinary organs.
- Fiber laxatives to bulk up stools. Here is a direct quote from The Merck Manual: “Hydrophilic mucilloids (eg, methylcellulose or psyllium preparations) sometimes help prevent anal irritation by increasing stool firmness.”[8] Of course, we already know what happens with firm stools when they are applied to immobilized, inflamed, and ulcerated intestines.
Inevitably, and for obvious reasons, these drugs fail, or their cumulative side effects overwhelm patients, and radical surgery to remove the colon and/or affected sections of the small intestine is the usual next step:
National Institutes of Health: In severe cases, a patient may need surgery to remove the diseased colon. Surgery is the only cure for ulcerative colitis.[9]
And not just to stop the diarrhea and bleeding:
National Institutes of Health: About 5 percent of people with ulcerative colitis develop colon cancer. The risk of cancer increases with the duration and the extent of involvement of the colon. For example, if only the lower colon and rectum are involved, the risk of cancer is no higher than normal. However, if the entire colon is involved, the risk of cancer may be as much as 32 times the normal rate.[10]
Considering the hardship of living without a colon, calling surgery a “cure” is, of course, a euphemism. Unfortunately, for many people surgery is the only option, because the alternative is death.
Are there alternatives to colon resection (surgical removal)? Absolutely. Ulcerative colitis is an acquired disease, not a congenital one. Just like with any other disease, the treatment must start from removing the causes, instead of treating the symptoms. But I am repeating myself.
The information presented in this book should help you eliminate some of the preceding conditions—namely, constipation and reliance on dietary fiber to treat it, which contribute to the development of ulcerative colitis and Crohn’s disease. Depending on the stage, these measures may not be enough to arrest these diseases, and a doctors’ involvement is absolutely critical for a patients’ recovery. And this means:
Respect thy doctor
Please note one very important distinction: dietary fiber is just one of many factors in the etiology of ulcerative colitis and Crohn’s disease. The subject of this chapter is the adverse role of fiber for persons who are already affected with either disease.
This chapter is not about the treatment of the ulcerative colitis or Crohn’s disease themselves. The diarrhea and blood loss alone are life-threatening conditions, and patients must continue working with their doctors. I’m confident that no doctors will be hostile to the suggestions and conclusions made in this book once they’ve had a chance to review them.
Furthermore, once their patients begin recovering, doctors will happily apply similar approaches to their other patients, because nobody wants to see their patients suffering or dying.
You may ask a reasonable question: why aren’t doctors denouncing fiber? The answer is really simple—they simply may not know about its ill effects yet. Just like a decade ago doctors didn’t know that calcium deficiency may cause kidney stones, or, most recently, that Vioxx may cause heart attacks, doctors don’t yet know that dietary fiber is detrimental in the treatment of ulcerative disease and Crohn’s disease.
And the question “You make it so obvious, why can’t doctors figure it out?” isn’t fair, because of the following considerations:
- Communication skills. The ability to express complex concepts and ideas in an accessible format and language is the domain of professional medical writers, not practicing doctors. It takes years to master the art of writing, and, on top of that, a writer must have medical education, life experiences, analytical skills, motivation, time, resources, and the guts to tackle these complex and controversial subjects. That’s simply not the domain of doctors, unless, of course, they become medical writers and still possess all of the above.
- Training and ethics. Practicing doctors aren’t scientists, researchers, or analysts trained to analyze and investigate the causes of diseases. They are confronted with preexisting medical conditions and are trained to take care of them to the best of their abilities. For the same reason you don’t expect a policeman to write, or, even worse, decide the laws, you shouldn’t expect practicing doctors to be know-it-all scientists or, even worse, conduct experiments and research on unwitting patients.
- Rules of engagement. Medical doctors are in one of the most tightly regulated professions. To avoid harm to patients and malpractice suits, they rely on the generally accepted treatment protocols taught in accredited medical schools, and described in blue-chip medical books and references. In general, that’s what we all want them to do. And if all of those authoritative sources recommend dietary fiber to treat constipation, they too will recommend this approach to their patients, and will apply it to themselves, and to their family members without the slightest hesitation or doubt in its safety and efficacy. That’s the reality.
- Personal experience. Doctors may not suspect the connection between dietary fiber and IBD, because they may believe that they themselves benefit from fiber, and, for a while, they don’t experience any of its side effects. Indeed, it takes decades for fiber’s impact to become apparent in healthy people. But by the time it does, it’s hard to determine what hit you—age, bad luck, or fiber. Personal experience and subjective judgment play an important role in medicine. If you don’t feel it, you don’t pay as much attention to it.
- Risk aversion. Independent analysts (such as myself) aren’t restricted or limited to any dogma and leave no stone unturned while seeking out better solutions. And, once they believe that they’ve found better ones, they publish their findings, and stake their reputation and livelihood on the results. That’s the kind of risks that doctors don’t take, and shouldn’t be expected to take.
- Theory of relativity. The human body isn’t as mysterious as it was once thought to be, but it’s still as unpredictable as the weather in early spring. Hence, there is no absolute truth, but many “truths.” And reasonable people have the right and obligation to doubt anything that isn’t “absolute.” And they will. It means that even the best-intentioned doctors may not instantly accept this or that method, regardless of its merits. That’s human nature.
- Inertia. The field of inflammatory bowel diseases isn’t any different from any other field of science or medicine. Not long ago, the top scientists of their day believed that the world was flat. It takes time for old beliefs to wither and die, and new ones to take hold.
When the idea of using fiber for constipation relief was initially advanced in the first half of the 20th century, the average lifespan of Americans was still too short to observe its “global” harm. Besides, it takes decades for symptoms to develop, the diseases to take hold, the statistics to get collected, and for someone to question conventional wisdom.
Well, we know better now. Get on with it, and don’t blame doctors for not being clairvoyant. For all I know, doctors are victimized by the fiber scourge even more than the general public, because they start taking ‘good’ care of their bodies earlier then most of us. And, up to now, that has meant eating more fiber, drinking more water, and exercising the abdominal muscles. You already know the results all of those activities may cause, and hopefully, because of this book, most doctors will also know about them soon, and will declare a similar loud message:
FIBER ISN’T THE SOLUTION, IT’S THE PROBLEM!
Hence, respect thy doctor! When bloody diarrhea strikes, it isn’t the time to read a self-help book. You need a good doctor!
Summary
- Ulcerative colitis and Crohn’s disease are inflammatory diseases of the small and large intestines (IBD). Their causes, symptoms, and treatments are similar.
- Profuse diarrhea and blood loss from localized ulcers are the two primary outcomes of ulcerative colitis and Crohn’s disease. Both conditions require intensive medication and treatment to protect patients’ lives.
- Certain medicines used to arrest diarrhea cause constipation because they decimate the intestinal flora responsible for forming stools, and because they inhibit intestinal peristalsis, responsible for the propulsion of stools.
- Originally, ulcerative colitis and Crohn’s disease may be caused by factors other than constipation. The worsening of their outlook, however, is generally caused by constipation that stems from the treatment of their original causes.
- There is an unambiguous connection between Crohn’s disease and latent constipation. Fecal impaction, that causes anal fissures and fistulas, also causes Crohn’s disease.
- People with anal fissures and fistulas, particularly children, have the highest risk of Crohn’s disease.
- The use of dietary fiber to treat constipation worsens the outlook of inflammatory bowel diseases, because fiber’s mechanical and chemical properties aggravate inflammation and ulceration.
- Inflammatory bowel diseases aren’t congenital (genetic) conditions. The occurrence of the diseases among family members isn’t determined by genes, but by similar styles of nutrition, exposure to similar pathogens, and susceptibility to similar food irritants and allergens.
- People with inflammatory bowel diseases develop allergies to regular food because impaired mucosa may produce antibodies to otherwise benign components of these foods. This doesn’t happen when the mucosal membrane is intact.
- The treatment of constipation and other measures suggested in this book should help break the dependence on dietary fiber and medication, and lessen or eliminate the factors that provoke diarrhea.
- In most cases, the restoration of intestinal flora alone may be sufficient to cure ulcerative colitis and Crohn’s disease.
- The prevention of inflammatory bowel diseases in children and adults should begin with the elimination and prevention of apparent and/or latent constipation, because both conditions are by far the most dominant causative factors of ulcerated colitis and Crohn’s disease.
- Proper recovery from unrelated functional, infectious, viral, and autoimmune diseases of the GI tract is the second (after constipation) most important consideration for the prevention and treatment of inflammatory bowel diseases.
- Medical doctors may not be familiar with the negative role of fiber in the etiology of ulcerative colitis and Crohn’s disease because it hasn’t been described yet in mainstream medical literature.
- Doctors play an important, if not crucial, role in the treatment of and recovery from inflammatory bowel diseases, particularly during the acute stages of diarrhea and bleeding. In these situations proper diet and the removal of fiber may help, but this isn’t sufficient to prevent additional complications or the loss of life.
Footnotes
1Ulcerative Colitis; NIH Publication No. 03–1597 April 2003; [link]
2Inflammatory Bowel Diseases; 31:3;The Merck Manual of Diagnosis and Therapy; [link]
3Crohn’s Disease; 31:3; The Merck Manual of Diagnosis and Therapy; [link]
4 Ulcerative Colitis; NIH Publication No. 03–1597 April 2003; [link]
5 Crohn’s Disease; 31:3; The Merck Manual of Diagnosis and Therapy; [link]
6 Diet and Stress; Ulcerative Colitis; Mayo Clinic; [link]
7 Ulcerative Colitis; NIH Publication No. 03–1597 April 2003; [link]
8Crohn’s disease; 31:3; The Merck Manual of Diagnosis and Therapy; [link]
9Ulcerative Colitis; NIH Publication No. 03–1597 April 2003; [link]
10Ibid.