Inflammatory Bowel Disease

Inflammatory bowel disease (IBD) is a term that is used to describe three distinct albeit related conditions of the bowel. Irritable bowel syndrome, also called mucous colitis or spastic colon,refers to a hypermotility of the small and large intestines, characterized by abdominal pain that is often relieved by moving the bowels (Anderson 1994, 848). It can have a variable course, and the condition may undulate between periods of diarrhea and constipation. Diarrhea with blood and mucus however are generally not a component of the disease, as they are with the IBDs.

Crohn’s disease

Crohn’s disease is chronic inflammatory bowel disease (IBD) that typically affects the distal portions of the small intestine (i.e. the ileum) and/or proximal regions of the colon (i.e. the ascending colon). About 45% of Crohn’s patients suffer from both ileal and colonic inflammation, whereas about 35% involve the ileum only, and 20% involve only the colon. In some cases the entire small intestine may be involved, and in rare cases the stomach, duodeum and esophagus. In about 10-15% of patients the anorectal fistulas are the dominant presentation. (Berkow 1992; Rubin and Farber 1990)

The cause of Crohn’s disease is idiopathic, with a number of theories to suggest its prevalence, including chronic infection and autoimmunity. Epidemiological evidence suggests that Crohn’s is for the most part a disease of industrialized, Western nations and has a strong familial predisposition. Although much neglected by medical researchers, the data suggests that environmental factors such as diet are very important.

The inflammation of Crohn’s disease typically involves all layers of the bowel wall, and is thus called a transmural inflammatory disease. The inflammation however is discontinuous, interrupted by normal patches of intestinal tissue. The earliest lesion of the disease is intestinal crypt injury which progress to aphthous ulcers, often located over lymphoid nodules. In some cases the lesions regress, but in others the inflammatory process continues, with the local proliferation of inflammatory cells. The continued spread of inflammation eventually leads to mucosal edema and a thickening of the bowel wall from fibrosis. As the condition progresses further the mucosa develops a cobblestone appearance, comprised of both longitudinal and transverse ulcers with intervening mucosal edema. (Berkow 1992; Rubin and Farber 1990, 379-389; Gowan 1990, 403-4)

Patients with Crohn’s disease typically present with abdominal pain, fever, anorexia, weight loss, and a very tender right lower quadrant mass or fullness upon palpation. Up to a third of patients may also have a prior history or present with anal fissures or fistulas. The disease also has extra-intestinal manifestations, and is closely associated with ankylosing spondylitis and other arthropathies (e.g. sacroilitis), apthous stomatitis, primary sclerosing cholangitis and anterior uveitis. (Berkow 1992; Rubin and Farber 1990, 379-389; Gowan 1990,403-4)

Crohn’s disease is characterized by periods of exacerbation and remission, which can be spontaneous and in many cases idiopathic. Dietary factors, stress, and other illnesses appear to have an influence but a cause and effect relationship can be difficult to establish. While the surgical resection of the affected bowel portions is a rather drastic method of putting the condition into ‘remission,’ in many cases the disease will begin to manifest in adjacent regions of bowel, suggesting the continuous of the caustive factors that promote the disease. Patients with long-standing Crohn’s disease of the small bowel are at increased risk of small-bowel cancer, and patients with Crohn’s disease of the colon have a long-term risk of colorectal cancer equal to that of ulcerative colitis. (Berkow 1992; Rubin and Farber 1990, 379-389; Gowan 1990, 403-4)

Ulcerative colitis

Similar to Crohn’s disease, ulcerative colitis is a chronic, inflammatory bowel disease, but unlike the former, is confined to the colon, usually affecting the distal portions of the bowel. While its cause or causes are unknown, it has a similar prevalence and distribution as Crohn’s, with a familial pattern, more commonly found in Europe and North America and much less frequently in Africa and Asia. (Berkow 1992; Rubin and Farber 1990, 381-82; Gowan 1990, 418-20)

The inflammation and ulceration of ulcerative colitis can extend from the most distal part of the rectum all the way to the proximal regions of the colon, but generally not into the small intestine. Unlike Crohn’s, which is a transmural disease, the ulceration extends only to the mucosa and not the deeper layers of the colon.

Signs and symptoms are typified by a recurrent, bloody diarrhea interspersed with asymptomatic periods. The degree of symptoms can vary, and often have a discrete onset, beginning as a mild diarrhea that gradually becomes more intense, accompanied by LLQ pain, and blood and mucus in the stool. In some patients however the onset can be acute, with a very watery diarrhea accompanied by fever and indications of peritoneal inflammation. Other clinical features may include malaise, fever, anemia, anorexia, and weight loss, while laboratory investigations reveal leukocytosis, hypoalbuminemia, and an elevated ESR. One particularly severe complication of ulcerative colitis is a toxic megacolon, which occurs when the ulceration results in intestinal obstruction and peritoneal inflammation. As this condition progresses the colon begins to dilate over a period of hours or days, and the patient presents with fever, and severe abdominal pain.(Berkow 1992; Rubin and Farber 1990, 381-82; Gowan 1990, 418-20)

The incidence of colon cancer in ulcerative colitis is increased when the entire colon is involved and when the disease lasts for more than 10 years, at a rate of about 0.5 to 1% per year. Although the cancer incidence is highest when the ulceration involves the entire colon, the risk is significantly increased when any portion beyond the sigmoid is involved. Similar to Crohn’s disease, extra-intestinal manifestations include inflammation of other tissues including the joints, muscles, skin and eyes. While classified separately based upon the target and characteristics of inflammation and ulceration, most gastroenterologists group ulcerative colitis and Crohn’s disease together as Crohn’s-colitis, which accounts for the similar prevalence, distribution and etiological factors. (Berkow 1992; Rubin and Farber 1990, 381-82; Gowan 1990, 418-20)

Medical Treatment of Inflammatory bowel disease

There are no curative treatments for any of these conditions, and various drugs are used to alleviate the symptoms, including:

  • Aminosalicylates, containing the active drug 5-ASA that has topical antiinflammatory effects, e.g. sulfasalazine, mesalamine, and olsalazine. Aminosalicylates are taken orally or by suppository. Sulfasalazine is used with caution in renal or hepatic impairment, blood dyscrasias, or urinary obstruction; frequently causes a reversible decrease in sperm count and motility; therapy is discontinued if a rash or hemolytic anemia occurs.
  • Antibiotics, to inhibit the gut ecology, e.g. metronidazole. Destroys the gut ecology and predisposes the body to reinfection.
  • Corticosteroids, to suppress inflammation, e.g. hydrocortisone, methylprednisolone. Regular use is associated with hyperglycemia, edema, osteonecrosis, myopathy, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, myasthenia gravis, growth suppression, and infections
  • Immunomodulants, to modulate the immune response. One of the more common drugs is azathioprine, which exerts its effect by antagonizing purine metabolism and inhibiting the synthesis of DNA, RNA, and proteins. This is thought to decrease the proliferation of immune cells, which results in lower autoimmune activity. Azathioprine is associated with a significant risk of pancreatitis and myelosupression.
  • Anti-TNF drugs, to neutralize the cytokine TNF-alpha and inhibits its binding to TNF-alpha receptor, e.g. infliximab. Anti-TNF drugs can promote immune dysregulation and severe infection. The cost of Anti-TNF agents is very expensive.
  • H2-receptor antagonists and proton pump inhibitors. H2-receptor antagonists block the binding of histamines to H2 receptors in the gastric parietal cells, e.g. ranitidine, famotidine and nizatidine. Proton pump inhibitors inhibit gastric acid secretion by inhibition of the H+/K+/ATPase enzyme system in the gastric parietal cells, e.g. omeprazole, lansoprazole and esomeprazole.
  • Antidiarrheal drugs, to inhibit diarrhea, e.g. loperamide, diphenoxylate and atropine
  • Antispasmodic drugs, to relieve bowel spasm, e.g. dicyclomine, hyoscyamine (Berkow 1992, 833-34, 837-39)

Additional treatment includes the usage of tranquilizers and antidepressants for any accompanying anxiety or depression. As many Crohn’s patients become malnourished from damage to the absorptive epithelium, some kind of intravenous nutritional therapy is provided to ensure adequate nutrition and give the bowel a rest. Severe ulcerative colitis is usually recommended to surgery, with a total protocolectomy with ileostomy being considered a permanent “cure.” The prognosis for Crohn’s however is quite poor even with surgery. (Anderson 1994, 413).

Holistic Treatment of Inflammatory bowel disease

Although the diagnostic features of Crohn’s and ulcerative colitis are distinct, they are really considered to be the same condition in holistic circles, at least in regard to treatment. The primary approach to the treatment of inflammatory bowel disease is to treat the patient for intestinal permeability, reduce inflammation, support detoxification, enhancing immunity, promote a healthy bowel flora, and repair damage and reduce further insult to the gut epithelium. Please refer to the general protocols listed under the treatment for autoimmune disease.

1. Restore digestion through diet

  • eliminate immunogenic cereals (e.g. Triticum, Hordeum, Avena, Zea), legumes, milk, refined sugar, and excess fruit (> one serving daily)
  • establish digestion through a graduated approach, applied over 3-7 days, using broth as the primary medium, moving progressively through the phases as signs and symptoms improve:
    • phase one (1 day): lightly salted vegetable and non-fat meat broths (e.g. chicken, goat)
    • phase two (2-3 days): add well-cooked starchy (peeled) vegetables (e.g. carrot, rutabaga, sweet potato, winter squash) and grains such as well-cooked white basmati rice to the broth that are low in resistant starch, as the appetite gets stronger
    • phase three (1-2 days): introduce steamed tender green vegetables (e.g. baby kale, chard, baby bok choy), as well as small amounts of fermented vegetables (begin with 1 tsp of brine, working up to eating the actual pickle)
    • phase four (2-3 days): gradually add in high quality proteins such as poached fish, basted/poached eggs, shredded chicken, stewed goat meat; to support digestion, serve separately from carbohydrates
    • phase five (2-3 days): gradually introduce small amounts of foods higher in resistant starch and fiber, e.g. fruit, beet root, non-grass cereals (e.g. quinoa, buckwheat), brown rice, well-cooked legumes (e.g. mung, adzuki)

2. Relieve intestinal spasm, enhance digestion

  • aromatic carminatives and stimulants: Fennel (Foeniculum vulgare), Dill (Anethum graveolens), Yavani (Trachyspermum spp.), Caraway (Carum carvi),Cardamom (Elettaria cardamomum), Nutmeg (Myristica fragrans), Ginger (Zingiber officinalis), etc.
  • antispasmodics: Wild Yam (Dioscorea villosa), Hops (Humulus lupulus), Belladonna (Atropa belladonna)

3. Repair damage to intestinal wall

  • hemostatics: Sanqi (Panax notoginseng), Shepherd’s Purse (Capsella bursa-pastoris), Witch Hazel (Hamamelis virginiana), Oak (Quercus spp), Goldenseal (Hydrastis canadensis), Kutaja (Holarrhena antidysenterica), etc.
  • demulcents: Marshmallow (Althaea officinalis), Slippery Elm (Ulmus fulva), Licorice (Glycyrrhiza glabra), DGL
  • vulneraries: Marigold (Calendula officinalis), Self Heal (Prunella vulgaris), Chickweed (Stellaria media), Plantain (Plantago spp.), Licorice (Glycyrhiza glabra), Shatavari (Asparagus racemosus), Bala (Sida cordifolia)
  • trophorestorative nutrients: A, C, E, zinc, MSM, bioflavonoids, NAC, glucosamine, glutamine

4. Support liver function and enhance detoxification

  • hepatic trophorestoratives: Milk Thistle (Silybum marianum),Turmeric(Curcuma longum), Huang Qin (Scutellaria baicalensis)., Katuka (Picrorrhiza kuroa), Guduchi (Tinospora cordifolia),Wu Wei Zi (Schizandra chinense),Bhunimba (Andrographis paniculata), etc.
  • cholagogues: Barberry (Berberis vulgaris), Burdock (Arctium lappa), Dandelion (Taraxacum officinalis), Fringe Tree (Chionanthus virginicus),Radish (Raphanus spp), etc.
  • lymphagogues: CleaversGalium aparine),Redroot(Ceanothus americanus),Poke Root(Phytolacca americana), etc.

5. Inhibit system inflammation (e.g. arthritis, skin inflammation) without hepatotoxic NSAIDs or immunosuppressive corticosteroids

  • omega 3 fatty acids: 2-3 g daily
  • full spectrum digestive enzymes: 2-3 caps with meals
  • antiinflammatory botanicals: Turmeric (Curcuma longum), Devil’s Claw(Harpagophytum procumbens), Huang Qin (Scutellaria baicalensis), Chai Hu (Bupleurum falcatum), Willow (Salix spp), Ashvagandha (Withania somnifera), Licorice(Glycyrrhiza glabra), etc.

6. Support immune function and enhance non-specific resistance

  • immunomodulants: Reishi (Ganoderma lucidum), Huang Qi (Astragalus membranaceus),Ashvagandha (Withania somnifera), Amalaki (Emblica officinalis), Gokshura (Tribulus terrestris),Siberian Ginseng (Eleuthrococcus senticosus),Jujube date (Zizyphus jujuba), Saw Palmetto (Serenoa serrulata), Shatavari (Asparagus racemosa), Ginseng (Panax spp), Schizandra (Schizandra sinensis), Shilajit, Licorice (Glycyrrhiza glabra), Dong Gui (Angelica sinensis), Di Gu pi (Lycium chinensis), American Ginseng (Panax quinquafolium)
  • botanical antibacterials: Goldenseal (Hydrastis canadensis), Wild Indigo (Baptisia tinctoria), Neem (Azadirachta indica), Huang Lian (Coptis chinense), Purple Coneflower(Echinacea angustifolia), etc.
  • botanical antifungals: Pau d’Arco (Tabebuia spp.), Sweet Annie (Artemisia annua), Barberry (Berberis vulgaris), Toothache plant (Spilanthes acmella), Haritaki (Terminalia chebula), Neem (Azadirachta indica), Hing (Ferula asa-foetida),etc.
  • botanical antihelminthics: Garlic (Allium sativum), Haritaki (Terminalia chebula), Neem (Azadirachta indica), Hing (Ferula narthex), etc.

7. Correct bowel ecology

  • probiotics: 25-50 billion bacteria daily
  • gradually increase fiber rich in inulin and other fructo-oligosaccharides
  • supplement diet with naturally fermented foods, e.g. miso, apple vinegar, sauerkraut

8. Eliminate insult to gastrointestinal mucosa

  • limit use of NSAIDs
  • limit use of antibiotics
  • avoid drugs and especially alcohol
  • choose organically-grown, hormone-free vegetable and animal produce
  • increase consumption of antioxidant-rich foods (e.g. garlic, beets, broccoli, blueberries), and antioxidant vitamins and minerals

9. De-stress and resolve underlying emotional issues.

  • botanicals: Vervain (Verbena officinalis), Milky Oats (Avena sativa), Ashvagandha (Withania somnifera), Valerian (Valeriana officinalis), Brahmi (Bacopa monniera), Skullcap (Scutellaria lateriflora), Motherwort (Leonorus cardiaca),Catnip (Nepeta cataria), Jatamamsi (Nardostachys jatamansi), Gotu Kola (Centella asiatica), He Shou Wu (Polygonum multiflorum),Passionflower (Passiflora incarnata), Damiana (Turnera diffusa), Kava (Piper methysticum)
  • massage therapy
  • biofeedback
  • psychotherapy
  • yoga and meditation
  • vitamin L (love): recommended dose is 8-10 hugs daily

10. Enema therapy.

While both general and specific internal measures will be helpful, due to the location of the disease, treatment may also need to be applied via the anus, in the form of an enema (in Ayurveda, vasti karma). For this purpose, there are two basic forms of vasti: anuvāsana vasti, or ‘oil enema’, and nirūha vasti, or ‘decoction enema’ (also called āsthāpana vasti). The oil enema is the first type of vasti treatment to be implemented, and is used in an alternating fashion with the decoction enema. The length and scope of vasti therapy depends upon several factors. The longest vasti regimen is karma vasti, comprised of alternating oil enema and decoction enema over a twenty-four day period, followed by six days of oil enema to total thirty days. Kāla vasti is comprised of alternating oil enema and decoction enema for twelve days, followed by four days of oil enema to total sixteen days. Yoga vasti is comprised of alternating oil and decoction enema for six days, followed by two days of anuvāsana to total eight days of treatment.

The protocol for the decoction enema may include herbs that exert a hemostatic, antimicrobial, and vulnerary properties, prepared as an aqueous extract, mixed with equal parts oil and honey, with a little saindhava (pink salt). Examples of useful herbs include:

  • hemostatics: Sanqi (Panax notoginseng), Shepherd’s Purse (Capsella bursa-pastoris), Ashoka (Saraca indica), Nagakesara (Mesua ferrea), Oak (Quercus spp), Kutaja (Holarrhena antidysenterica), Manjishtha (Rubia cordifolia)
  • antimicrobials: Goldenseal (Hydrastis canadensis), Barberry (Berberis spp.), Coptis (Coptis spp.)
  • vulneraries: Calendula (Calendula officinalis), Plantain (Plantago spp.), Balm of Gilead (Populus trichocarpa bud oil extract), Licorice (Glycyrhiza glabra), Shatavari (Asparagus racemosus), Bala (Sida cordifolia)