Read more about Wormwood and other plants and herbs in the Herbal Materia Medica.

DO’S & DON’TS: First off, I’ll give you a list of “helper” foods and a list of “avoid” foods. What you want to do is gradually increase the amounts of the helper foods and decrease the others. This is the easiest way to get started.

HELPERS: beets, radishes of all kinds, carrots, lemon juice, watermelon with black pepper, onions, melons (always eat melons alone), olives, raw vegetables, papaya, bananas, grapefruit, yogurt, Yogi Tea, black salt, black pepper, turmeric, and cardamom.

AVOID: all fried foods, cooked oil, caffeine and other stimulants, fried grains, all processed foods, cheese, meat, eggs, animal fat, alcohol, any food that is heavy or difficult to digest (taking more than 20 hours to pass).

LIVER TONICS: Another easy addition to your program is to start your day, the very first thing in the morning, with 8 ounces of cold, plain Yogi Tea. Take the Yogi Tea before you drink or eat anything else, sipping it slowly and mixing it with saliva well before swallowing. This is a well-known yogic liver tonic. In the alternative, you could sip unsweetened lemon juice and water (the juice of one lemon with 12 ounces of water). I would recommend sipping the lemon water through a straw to best maintain tooth enamel.

ONE-DAY AND ONE-WEEK MONO-DIETS/FASTS*: Once you are getting accustomed to the “helper” foods and life with less of the “avoid” foods, try a one-day fast or mono-diet of beets only. This is a good way to give your digestive system a “rest” and your liver a little tune up. Choose one day a week (Monday works for me) and have that be your cleanse day. You can try the beets different ways (see simple serving suggestions below), cooked or raw. Also, on your fast day, you can have as much plain Yogi Tea as you like, lemon juice (great squeezed over the beets) and, of course, lots of water. A little more aggressive approach would be doing the same fast for one full week, every 1-3 months.

CLEANSING DIETS*: Over the years I have tried numerous cleansing diets. I did well with the long-term strict mono-type diets when I was younger (40-day beet fast, banana fast, melon fast… more about these fasts another time). I’m better now with a little more variety and find that sticking to a regimen of pretty much only the foods on the “helper” list (and eliminating entirely the “avoid foods”) is very effective. Start with one week. Then next time, try it for two weeks, and then shoot for completing 40 days. Remember to drink lots of water.

When you have completed the diet, you should gradually introduce other foods. The best food to break the fast with and to give your body nutrients it has been lacking during the fast, is Mung Beans & Rice with Vegetables. This is a very easy-to-digest source of high-quality balanced protein, vegetables and fiber. It is a good alkaline food that is nurturing and rebuilding. Depending on how long you did the cleansing diet, you should have Mung Beans & Rice with Vegetables as your main food for several days to two weeks.

DEALING WITH CRAVINGS AND DEPRIVATION: Whatever program you choose to follow, if you find yourself beset with cravings for the foods you “can’t” have, try shifting your mind-set, so that it is a choice you have made, rather than a restriction put upon you. Usually within a week (often, just 1-2 days) the cravings subside, and you are feeling the effect of the diet: feeling more energy, lighter, and increased mental clarity, Importantly, if you go ahead and have that cup of coffee, or doughnut, or whatever, don’t feel guilty about it. You will probably find that whatever you ate or drank really wasn’t so satisfying after all. Let yourself feel renewed with inspiration to keep up!

Once, when I was on a long melon fast, every time there was a special meal, party, or feast with any food that I wished I could have… I took one serving and put it in the freezer. At the end of my fast I had a freezer full of cake, lasagna, pizza… you name it. And, you know what? I ended up not eating ANY of it; I had so lost the desire to eat that food. But, knowing I had some treats in the freezer for later did help me, in my weaker moments, from feeling deprived.

POSSIBLE OUTCOMES: You may start cleansing in ways you had not anticipated. Skin is the greatest organ we have for elimination, and it is not uncommon to have outbreaks of acne when on a cleansing program. Along the same vein, you may experience (actually, others may experience) increased body odor with an even less-inviting aroma. Also, your colon may go through some changes. Although beets help with regularity, you may find yourself with a little constipation or even runny stools. This is why it is important to drink lots of water and also drink Yogi Tea. Also, adding ground cardamom to the beets will help with your elimination. If you are going on the one-week mono diet, keep in mind it is a week to cleanse, heal, relax, meditate, and do yoga. Choose yoga postures that are for the liver and digestion. It is not a time to go mountain climbing, run five miles a day, work out for two hours in the gym, or work under stress. If you are accustomed to a protein-based diet, you are not likely to have the stamina for any type of strenuous exercise.

AND DON’T FORGET FRESH JUICES: Carrot, beet and radish juice are also excellent for liver detox. Start with a combination of 6 oz. carrot, 1-2 oz. beet and 1-2 oz. radish (any type radish will do, daikon is a good choice) juice. The beet and radish juices are very potent and you should only very gradually increase their proportion. The radish juice, especially, is best taken immediately after juicing. (It’s flavor quickly deteriorates.) Always mix juices very well with saliva. They are a very concentrated food and need that saliva to digest the best and to give you their full effect. Chew your liquids and drink your solids is an old saying. Simply put: chew chew chew.

*As always, never undertake any fast or diet program without the approval and/or guidance of your health practitioner.

SIMPLE BEET RECIPES

HOW TO COOK: Steam whole beets (with skins, roots, stem ends, and all) until just tender (the skins will blister a little bit and they will pierce fairly easily with a fork or knife). Depending on size (I cut the large ones in half) they will take about 25-30 minutes to cook. Test one beet by running it under cold water and removing the skins. The skin should easily slide off. If not, cook the beets a little longer (be sure there is enough water in there so they do not scorch). When done, remove the skins from all the beets and cut off the root and stem ends. 2 lbs of beets will make about 4 cups of cooked beets. For a one-day fast, you will need 3-5 pounds of beets. Just cook them all up in the morning or the night before.

SERVING SUGGESTIONS:

• Cut cooked beets into slices or ½” cubes and drizzle with lemon juice and pepper.
• Make a Black Salt Lassi to enjoy with your beets: Blend in a blender 1 cup low-fat plain yogurt, ¼ teaspoon black salt, and 2-3 ice cubes. Add more salt if desired.
• Mash beets and mix with ground cardamom, pepper, little black salt and lemon juice.
• Baja Borscht:
  
  2 cups cooked beets
  
  3” gingerroot, sliced thinly, boiled for 20 minutes in:
  
  4 cups water; then strain for ginger tea
  
  1 Tbsp. lemon juice
  
  2 tsp. fresh mint, finely minced
  
  little salt or black salt
  
  Blend 2 cups cooked beets until smooth. Add 1½ cups ginger tea, lemon juice, mint and salt to taste. Serve cold or heated.
• Grate raw, peeled beets. Garnish with lemon juice, chopped cilantro, pepper
• DAIKON RADISH: Peel and slice into sticks (like carrot sticks). Sprinkle with black salt. Great for snacks.
• COOKED DAIKON: Steam whole (or in big chunks) and then peel. Slice or chop as desired. Add lemon juice and black salt, maybe a little cilantro.
• RADISHES & RICE: a great combination. Use 1 cup basmati rice to 2 cups water. Bring water to a boil, add the washed and well drained rice, 1 bunch of red radishes (whole or chopped), 1-2 tsp. turmeric, ½ tsp. pepper, and about ¾ tsp. black salt. You can add other seasonings too (poppy seeds, celery seeds, green chilies). Return to boil, cover, turn to low, and let steam for 10 minutes. Keep covered, remove from heat, and let stand another 5-8 minutes.

Mungbeans & Rice with Veggies
Yield: approximately 1 gallon (8-12 servings)

This sort of curried stew is a great staple for the vegetarian/yogic diet.
Mungbeans and Rice together make a balanced protein which, when cooked in
this way, is very easy on the digestive system. This dish is so nurturing
and satisfying. It is one of the best foods for breaking a fast or special
cleansing diet and any circumstance where the body needs replenishing (such
as in illness recovery and the first few days after child birth). It is one
food I never tire of! Serve it as is, or dressed up a little bit with a
spoonful of fresh salsa on top! Sometimes I add water and take it more like
a soup (adjust flavor with a touch of tamari or Bragg Liquid Aminos). Or,
make it on the thick side and roll up in a flour tortilla (like a burrito)
with chopped onion and lettuce. My favorite way is to have a simple bowlful
with a little chopped cilantro and crushed red chilies on top.

The seasoning in this recipe is mild. To spice it up a bit, add 1/2 to 1
tsp. of crushed red chiles and used rounded measurements for the other
spices (instead of leveled measuring spoons). You may also increase the
ginger and garlic per your taste. From start to finish, you can have this
ready to serve within 60-75 minutes (depending on how fast you chop!). Make
a potful, and enjoy it for several days for lunch and/or dinner.

It will keep refrigerated up to five days (but is always best fresh), and
does not freeze well.

4 quarts water
1 cup mung beans, sorted and rinsed well
2 medium onions, chopped
2″ piece gingerroot, peeled and finely chopped
2 tsp. turmeric
1/2 tsp. ground black pepper
1/2 tsp. ground cardamom
3/4 tsp. cumin seeds
2 tsp. curry powder or garam masala (optional)
2 Tbsp. minced garlic
6 cups chopped assorted vegetables (celery, chard, broccoli,
carrots, cauliflower, mustard greens.. whatever you like)
1 1/4 cup basmati rice, sorted and rinsed well
2 Tbsp. butter or ghee (optional)
salt, tamari soy sauce or Bragg Liquid Aminos to taste

Bring water to boil in a 6-quart soup pot. Add mung beans and cook at a
light boil, uncovered. Add onions and ginger as they are prepped. Add
spices. When beans begin to split open add garlic, vegetables and rice. Cook
15-20 minutes over medium-high flame, stirring occasionally, and more as it
thickens. Add butter or ghee and season with salt, tamari or Braggs. Remove
from heat and let it sit another 15 minutes (it will thicken up a little
more).

__________________________________
Based on the teachings of Yogi Bhajan

]]> 6682 https://healthy.net/2000/12/06/turmeric-the-golden-healer/?utm_source=rss&utm_medium=rss&utm_campaign=turmeric-the-golden-healer Wed, 06 Dec 2000 13:28:52 +0000 https://healthy.net/2000/12/06/turmeric-the-golden-healer/

Turmeric has been recognized by yogis and ayurvedic healers since ancient times for its many healing properties. Grown mainly in India, the turmeric root is a close cousin to ginger root. It is dried and ground into a fine powder, brilliant gold in color, and used in many Indian recipes (this is what makes curry yellow). Commercially, turmeric is used for its color and as a thickener (yellow prepared mustard, canned soups, many processed foods contain turmeric!). Little do those food manufacturers know of this amazing root’s qualities!

Sometimes referred to as the “poor man’s saffron” because of the golden color it imparts, the similarity ends there. Taken internally, turmeric is a friendly healer to the liver and stomach, promoting healthy mucus membranes and skin. Yogis know that it also helps with stiff or creaky joints and arthritis. It is also used as a digestive aid. There is also some evidence that it is even helpful in lowering cholesterol. Turmeric also has a drawing quality, to draw out toxins, dry up secretions, and to heal.

Now, how to get that rather bitter tasting powder into your body?

First of all, cook it. You can either boil it in water for 8-10 minutes to make Turmeric Paste or Golden Milk or sizzle in a little ghee or olive oil for 20-30 seconds. This takes out the bitter taste and also releases the essences of the turmeric into the oil or water. It must be cooked!

You can also get turmeric in capsules at the natural foods store. Usually the capsules contain a greater concentration of curcumin, its active ingredient.

Here are a few yogic remedies:

Sore Throat (especially with mucus/phlegm stuck in throat): Take about ½ teaspoon of thick turmeric paste and form into a ball. Pop it into the back of your throat and swallow with a glass of water. You can do this a few times a day or as often as every hour if desired.

Creaky or Stiff Joints: Take at least 1 cup of Golden Milk every day for 40 days.

Stomach & Digestive Problems: Golden Yogurt, a total of at least 1 cup a day. This is also good for intestinal candidiasis; the yogurt brings in the good bacteria for healthy intestinal flora and, since turmeric is a natural anti-fungal, it helps to counter the yeast overgrowth.

About 15 years ago, during a very stressful time, I developed gastritis. Yogi Bhajan suggested I take a daily concoction of yogurt, banana and 1 Tbsp. of turmeric paste. I found this really quite helpful.

And, you can add turmeric to so many foods. Keep a jar of turmeric paste in the fridge (it keeps for a couple of weeks), and add a spoonful to your breakfast cereal, smoothies, and even spread on toast with a little honey. Also, it’s easy to add a spoonful to cooking foods, such as rice, tofu, and vegetable dishes.

Its benefits do not stop yet! Turmeric is used externally as well.

Skin Conditions: The juice of fresh turmeric is prized as a cure/soother for many skin conditions, including eczema, chicken pox, shingles, poison oak/ivy, and scabies. Turmeric paste makes quite a satisfactory substitute! Apply the paste directly to the affected area, cover lightly with gauze or loose cotton clothing (that will likely be ruined with stain). This is known to help dry the blisters up and accelerate the healing process. For shingles, one ayurvedic remedy calls for first spreading a light coating of mustard oil on the shingles rash, and then spreading the turmeric paste over that. (Skin condition such as those described above are seen in Ayurvedic and Chinese medicine as originating from liver congestion/toxicity. You can help your rash from the inside out, by also ingesting turmeric. Also, see my September 2000 column, Eating for a Healthy Liver.)

Sores/Wounds: Keep turmeric in your first aid kit! It acts quickly to help stop bleeding, plus because of its anti-bacterial quality, will help prevent infection. For cuts, pile on the turmeric, cover with gauze, and apply pressure to the area to stop the bleeding. Of course, serious wounds require immediate medical attention.

Douche: Made with fresh plain yogurt, turmeric and water, this is especially helpful in countering odor and yeast problems, and is the best douche to use following the menstrual period. Use 8-10 parts water, 1 part yogurt (be sure it has active acidophilus cultures), and 2-3 tsp. turmeric. Blend it up in the blender until smooth.

Turmeric Paste

3 Tbsp. turmeric

3 cups water

Bring turmeric and water to a boil. Let it boil until it forms a thick paste. It must boil at least 8 minutes. If necessary, add more water. Once it starts to thicken slightly, you must stir it constantly to prevent scorching. Store in a glass jar (it will stain a plastic storage container) in the fridge.

Golden Milk

Recipe by Yogi Bhajan

(as it appears in my cookbook, From Vegetables With Love)

1/8 tsp. turmeric

½ cup water

1 cup milk

1-2 Tbsp. almond oil (optional)

honey to taste

Boil water and turmeric in small saucepan over medium-high heat for 8 minutes (the turmeric must be fully cooked). Meanwhile, bring the milk and almond oil to boiling point in a separate pan and remove from heat. Combine the two mixtures and add honey to taste.

Now, what I don’t say in the cookbook is that you can easily make more than one serving at a time and keep it in the fridge. Also, I really prefer it with a lot more turmeric. It certainly can’t hurt to use more. I suggest using ½ tsp. per cup. And, if you have Turmeric Paste made, you can just heat up the milk and almond oil with a teaspoon of turmeric paste. Try adding a little freshly grated nutmeg, too. Mmmm!

Golden Yogurt

You can make Golden Yogurt from scratch (this is the best way), or simply add a spoonful of Turmeric Paste to plain yogurt (be sure the commercially prepared yogurt is made with active acidophilus and/or bifidus cultures, and does not contain gelatin, stabilizers, or added milk solids). A favorite breakfast of mine is ½ cup of Golden Yogurt, 1/2 cup organic apple sauce, and ½ cup (or less) of granola. Mmmm. Here’s how to make your own:

1 Tbsp. turmeric

1 ½ -2 cups pure water

1 quart whole milk or low-fat milk

2 Tbsp. plain yogurt (save some from your last homemade batch, or use commercially prepared yogurt as described above)

Bring water to boil with turmeric over high heat. They must boil together at least 8-10 minutes until forming a thick paste. Once it starts to thicken, stir constantly. When it is quite a thick paste, add the milk. Stir until smooth. Stir frequently until the milk just comes to the boiling point. Immediately remove from heat.

Immerse the pot of turmeric milk in a basin of ice water to quickly cool it and avoid that scald film forming on top. It must cool to about 118 degrees. I never use a thermometer! Put your clean finger into the warm/hot milk. If you can hold your finger in there for 30 seconds (it should feel pretty warm) and be able to hold it in without it feeling ‘hot’, it is ready. Now, to avoid grit, you can strain the warm/hot milk through a fine tea strainer. Or, just keep all that turmeric in there. Stir in the yogurt (I use a wire whisk to gently take out yogurt lumps). Pour this into a clean (sterile) quart size glass jar (or plastic container will do). Cover.

You need to maintain the warm temperature. You can do this several ways:
1. Use a heating pad set at LOW. Place one or two layers of towel over the heating pad. Put the yogurt container on that, and then wrap the towel around the container to maintain the heat.

2. OR, use your gas oven that has a warm pilot light on. (This only works in older ovens.) Turn the oven on for 5 minutes to get it hot in there. Turn the oven off. Wrap the yogurt container in several layers of towels or a blanket to contain the heat, and put on a rack in the oven. Close the oven door.

3. OR, use a yogurt maker! Pour the turmeric milk into the yogurt cups and follow the instructions that came with your appliance.

The yogurt needs to sit undisturbed and be kept warm for 6-8 hours. Once it is done, you can keep in the fridge easily for several weeks. For stronger acidophilus content, let the yogurt sit out at room temperature for 3-6 more hours (the longer it sits out, the sourer it will become). The liquid that forms on top will be rich in acidophilus. It will not go bad sitting out like this. Believe me, you will KNOW when yogurt has gone bad because it molds and smells disgusting. It is supposed to be at least a bit sour!

]]> 6683 https://healthy.net/2000/12/06/acne/?utm_source=rss&utm_medium=rss&utm_campaign=acne Wed, 06 Dec 2000 13:28:02 +0000 https://healthy.net/2000/12/06/acne/

Acne is a skin condition marked by pimples, such as white heads, blackheads, or even raised, red ones that hurt. These pimples show up on the face, neck, shoulders, and/or back. Acne mostly strikes teenagers and young adults. For some, acne, or the scars it can leave, persist into adulthood. Acne results when oil ducts below the skin get clogged with secretions and bacteria. Factors that help cause acne include:

• Normal increase in the levels of the hormone androgen during adolescence.
  
• Changes in hormone levels before a woman’s menstrual period or during pregnancy.
  
• Rich moisturizing lotions or heavy or greasy makeup.
  
• Emotional stress.
  
• Nutritional supplements that have iodine.
  
• Cooking oils, tar, or creosote in the air. Creosote is often used as a wood preservative.
  
• Putting pressure on the face by sleeping on one side of the face or resting your head in your hands.
  
• Birth control pills, steroids, anti-convulsive medications, and lithium (used to treat some forms of depression).
  

Time is the only real cure for acne, but these tips can help:

• Keep your skin clean. Using a clean washcloth every time, work the soap into your skin gently for a minute or two and rinse well.
  
• Try an astringent lotion, de-greasing pads, or a face scrub.
  
• Ask your doctor for the name of a good acne soap.
  
• Leave your skin alone! Don’t squeeze, scratch, or poke at pimples. They can get infected and leave scars.
  
• Use an over-the-counter lotion or cream that has benzoyl peroxide. (Some people are allergic to benzoyl peroxide. Try a little on your arm first to make sure it doesn’t hurt your skin). Follow the directions as listed.
  
• Wash after you exercise or sweat.
  
• Wash your hair at least twice a week and keep it off your face.
  
• For men: Wrap a warm towel around your face before you shave. This will make your beard softer. Always shave the way the hair grows.
  
• Don’t spend too much time in the sun. Don’t use a sun lamp.
  
• Use only water-based makeup. Don’t use greasy or oily creams, lotions, or makeups.
  

Questions to Ask

Is your acne very bad and do you have signs of an infection with it, such as fever and swelling?
Are the pimples big and painful?
Have you tried self-care and it doesn’t help or does it make your skin worse?

The liver is probably the body’s most versatile organ. Among its many tasks are the following:

• Makes bile (a substance that aids in the digestion of fats)
  
• Produces blood proteins
  
• Helps the blood to clot
  
• Metabolizes cholesterol
  
• Helps maintain normal blood sugar levels
  
• Forms and stores glycogen (the body’s short-term energy source)
  
• Makes more than 1,000 enzymes needed for various bodily functions
  
• Detoxifies substances (e.g., alcohol and certain drugs)
  

To make matters worse, people who regularly overindulge in alcohol generally have poor nutritional habits. When alcohol replaces food, essential vitamins and minerals can be missing from the diet. Malnutrition makes cirrhosis worse.

Alcohol abuse is the most common cause of cirrhosis. Hepatitis, taking certain drugs, or exposure to certain chemicals can also produce this condition.

Signs and Symptoms


Early signs and symptoms are vague, but generally include:

• Poor appetite
  
• Nausea
  
• Indigestion
  
• Vomiting
  
• Weight loss
  
• Constipation
  
• Dull abdominal ache
  
• Fatigue
  

• Enlarged liver
  
• Yellowish eyes and skin and tea-colored urine (indicating jaundice)
  
• Bleeding from the gastrointestinal tract
  
• Itching
  
• Hair loss
  
• Swelling in the legs and stomach
  
• Tendency to bruise easily
  
• Mental confusion
  
• Coma
  

(See “Places to Get Information & Help” under “Liver Diseases” on page 376.)

I spoke to representatives from three different laboratories around the country about the latest in laboratory technology. We discussed various trail-blazing tests, and what symptoms or situations were indicated for each. Ask your doctor about these eight lab tests so you can truly practice preventative health care.

Looking for Osteoporosis

Once you hit 35, gradual bone loss is inevitable. This trend is accelerated by smoking, poor diet, lack of exercise, genetics or race and may eventually result in osteoporosis. Full-blown osteoporosis is painful; losing bone is not. While we should all take steps to prevent or slow bone thinning, you may want to take extra precautions if you’re an unusually fast bone loser.

Special X-rays are usually used to detect brittle bones. However, this pricey test isn’t sensitive enough to see if or how rapidly you’re losing bone. By the time bone loss is noticed it may be too late.

Fortunately, labs like Meridian Valley Clinical Laboratories in Kent, Washington now offer a simple, inexpensive (around $70.00) urine test that measures a bone loss protein called Type I collagen. The higher your levels, the faster you’re losing bone.

Bone is continually breaking down and rebuilding itself, says Karen Wissinger, Meridian Lab’s Administrative Director. In 10 days, the osteoporosis or NTx test tells your doctor how fast you lose bone, not merely how much is gone. Prevention against further bone thinning can then be taken.

The NTx test should be performed on women (or men) 30 years and older who are at high risk of developing osteoporosis. This establishes a baseline reading. The test can be repeated every year or two to see if bone loss rate has changed. Treatment effectiveness can also be assessed by repeating this osteoporosis test six to eight weeks–the time it takes for bone loss patterns to change–after the initial NTx.

The Parasite Test

About five to 10 percent of the general population have parasites, estimates Dan Lukaczer, ND, Assistant Director of Educational Services at Great Smokies Diagnostic Laboratory in Ashville, North Carolina. This is much higher than what most conventional doctors report.

Increased world travel and a rise in immigration to this country may explain why pinworms, giardia, disentamoeba and other protozoan parasites or worms are more common. “Or it might be parasites have been prevalent for a long time but not detected before,” suggests Lukaczer. Unlike conventional doctors, inquiring about parasite-like symptoms is standard protocol among many natural health physicians.

Diarrhea, cough, itching, skin rash, bloody stools, unexplained fever and abdominal pain all strongly suggest an intestinal parasitic infection. However, these bugs can launch symptoms like headaches, chronic fatigue and joint pain too. Food allergies and autoimmune disease may stem from parasites. You can also be infected and feel nothing unusual.

Most laboratories offer parasite testing. But at Great Smokies, specialists in digestive lab tests, searching for parasites is a passion. “Our lab techs are well trained and well versed in these bugs,” says Lukaczer. “We do around 500 parasite tests per week, much more than the average lab. In addition, we run extra specialized tests that the normal reference lab doesn’t. So we pick up infections not normally detected.”

One to three stool samples are required to check for parasites. The cost varies from $55.00 to over $200.00 depending on many samples are submitted and whether other analyses are made. Parasite results are available within one week.

Nutrient Function Test

Numerous studies have confirmed the relationship between nutrient deficiencies and disease. For instance low zinc levels may play a role in diabetes (1) and insufficient body reserves of vitamin E can increase your risk of angina (2). Laboratory tests designed to find vitamin and mineral deficiencies are essential to prevent or delay nutritionally-related ailments.

“The typical serum test looks for the amount of nutrients in your blood,” says Cyrene Vacanti, Marketing Manager of SpectraCell Laboratories, Inc. in Houston, Texas. “We use a test called the Essential Metabolics Analysis (EMA) to measure how well nutrients work in the cells. That’s what matters, not vitamin and mineral blood levels.”

The EMA test begins with a blood collection. At SpectaCell’s lab, white blood cells called lymphocytes are removed from the blood sample and grown in a series of special dishes whose contents varies depending on which nutrient is being tested. An assortment of vitamins, minerals, amino acids, and fatty acids can be tested for. “Normal results (available within two weeks) are different for each nutrient,” explains Vacanti. Cost ranges from $70 to $465 depending on how many nutrients are tested.

Comprehensive Digestive Stool Analysis

Good nutrition is vital for good health. However, a great diet is useless if your body can’t digest, absorb or utilize the food you eat. First developed by Meridian Labs, the Comprehensive Digestive Stool Analysis (CDSA) employs a series of tests to evaluate digestion.

Meat and vegetable fibers are measured in your stool as are fats to gauge absorption. Lab technicians look for blood and mucus in your stool (both should be absent), and record stool color. Stomach acid is measured along with enzyme levels and bile. Even a predisposition to colon cancer can be detected.

The healthy intestine houses over 400 bacteria and other bugs. A simple stool sample reveals what and how many yeast, bacteria and parasites live inside you, and whether this population coexists in a healthy balance. An abnormally high ratio of pathogenic bacteria and other microbes creates an unhealthy state called dysbiosis.

A CDSA is certainly warranted if you suffer from chronic diarrhea, indigestion or other gastric complaints, or if you spot undigested food in your stools. However, poor intestinal health doesn’t stop with indigestion. The CDSA provides helpful information for a variety of health concerns ranging from asthma to arthritis. Also offered by Great Smokies and other labs, a CDSA panel takes one week to complete and costs around $300.

Intestinal Permeability Test

“The Intestinal Permeability test is performed when a doctor suspects the small intestine has problems, but there are no or few gut symptoms,” says Lukaczer. Often performed along side the CDSA, this $85.00 test evaluates how permeable or “leaky” your small intestine is.

A healthy small intestine permits mostly small fully-digested food particles to pass into general circulation, while excluding large partially digested food molecules, chemicals and other toxic compounds. A damaged or sick intestine can turn sieve-like, also to as “leaky gut syndrome”.

This test requires you fast overnight and then drink a beverage the next morning containing lactulose and mannitol, sugars that don’t break down during digestion. Six hours later urine is collected and sent to the lab where urinary mannitol and lactulose are measured. Within one week, you receive results. Low levels of both sugars indicate malabsorption; high amounts point to a leaky gut. High lactulose and low mannitol means both conditions exist.

Various types of arthritis have been linked to a leaky gut, as have food allergies, skin conditions and celiac disease. Inflammatory bowel disease or other intestinal conditions including infections, injuries and dysbiosis may increase intestinal permeability. Alcoholism, aging and certain medicines like aspirin and ibuprofen aggravate this problem.

“The gut is the source of a lot of health problems,” says Lukaczer. “It’s like the roots of a tree, if the roots are poor, the whole system suffers.”

Functional Liver Detoxification Test

The gastrointestinal tract does its best to screen out harmful toxins. The liver catches then detoxifies and eliminates most toxins that sneak over the intestinal wall. However, a leaky or dysfunctional gut, or over-exposure to noxious compounds can overwhelm the liver and ultimately creep into the bloodstream.

Fatigue, headaches and other symptoms signal liver overload as well as conditions like Alzheimer’s or Parkinson’s Disease, food allergies, multiple chemical sensitivities and premenstrual syndrome.

Rather than check for liver damage (which is difficult to repair), the $100.00 and up Functional Liver Detoxification test determines how well the liver filters out toxins. Urine and saliva samples are collected after you ingest several pills including one containing caffeine. A complex printout returns in one week with results, for instance, as follows. Elevated salivary caffeine usually means high toxin exposure; low levels may indicate an inefficient liver.

Checking for Free Radicals

If you’re wondering how well your body manages free radicals, for $70.00 to $100.00 you can find out. Free radicals are highly reactive molecules that, when exceedingly high, speed up aging and promote cancer by harming cells and tissues. This damage may be silent, or contribute to one of over 100 diseases ranging from ulcerative colitis to rheumatoid arthritis.

Your body produces free radicals to help white blood cells disable germs, and aid in liver detoxification. However, pollution, too much sun, pesticides, radiation, some drugs, alcohol, cigarettes and rancid fats push free radicals above comfortable levels, and use up free radical-fighting nutrients called antioxidants.

With the same lymphocyte technique used in their Essential Metabolics Analysis test, the Spectrox test from SpectraCell Labs inspects blood to see how well your body’s antioxidants and repair mechanisms resist free radical damage.

Great Smokies Lab offers similar information with its Oxidative Stress test. Technicians examine your blood or urine sample for glutathione, an antioxidant found in your body, and lipid peroxide (free radical) levels. High glutathione means your body’s working overtime combatting free radicals. Elevated lipid peroxides signal excessive oxidative or free radical damage.

It’s a good idea to test both antioxidant body stores and free radical damage, states Lukaczer, so you know how much antioxidant supplementation is needed to offset current oxidative harm. Lukaczer suggests running the Functional Liver test together with the Oxidative Stress test since a dysfunctional liver increases free radical production. Test results take from one to two weeks.

Food Allergies

ELISA isn’t the name of a girl; it’s an acronym for enzyme linked immunosorbent assay, a food allergy test. For as low as $40.00, this simple blood test will tell you what foods are causing allergic symptoms.

There are two types of food allergies. The fixed or immediate kind produce hives, stuffy nose or even life-threatening anaphylaxis usually within hours or even minutes after eating an allergic food. Common offending foods include shellfish, strawberries, peanuts, nuts and others. Conventional (and alternative) allergists readily accept fixed food allergies, a diagnosis easily confirmed through not only symptoms but a variety of lab tests including ELISA.

Delayed, cyclic, masked or hidden food allergies are more controversial. Symptoms run the gamut from headache, bedwetting and mental confusion to ear infections, asthma and joint pain (3). No body system is exempt from adverse food reactions. Again, ELISA is an appropriate test for this form of food allergies.

There are several kinds of ELISA allergy tests on the market. Make sure the one you choose detects increases in both immunoglobulin E (IgE) and immunoglobulin G (IgG)–the antibodies that increase in response to fixed and delayed food allergies respectively. Results should be available to you with two to five working days.

Lab results are just one piece of evidence used by a doctor to diagnose health conditions. Physical exam and detailed questions are also vital. Remember too that lab tests aren’t perfect: sometimes they miss a problem, other times they falsely say you’re sick.

If you think the above laboratory tests will help you, take this information to your doctor for consideration. All of these tests should be instigated under your physician’s supervision. For free brochures on these and other laboratory tests, call:

Great Smokies Diagnostic Laboratories

800-522-4762

Meridian Valley Clinical Laboratory

800-234-6825

SpectraCell Laboratories, Inc
800-227-5227

Candida


This yeast can be measured in the gastrointestinal tract, vagina, throat or other suspected infected areas. Candida infection symptoms include fatigue, indigestion, mental confusion and others.

DHEA levels


Low levels of the adrenal hormone dehydroepiandrosterone has been linked to various ailments including fibromyalgia and rheumatoid arthritis. If levels are low, your doctor can prescribe DHEA medication.

Hair Analysis


Laboratories can assess heavy metal exposure (lead, cadmium, for example) from a lock of hair. Lead toxicity in children causes mental confusion.

Glucose-Insulin Tolerance Test


This test is used to assess suspected refined carbohydrate intolerance, or what many refer to as hypoglycemia. If you have essential hypertension, ask your doctor about performing this test. High blood pressure is associated with defects in insulin, glucose and lipoprotein metabolism in some people.

Sex Hormone Profile


This urine test measures various sex hormones including DHEA, testosterone and progesterone. It also calibrates estrone, estriol and estradiol (the three different estrogens) ratios, one way to judge breast cancer risk.

1. Niewoehner CG et al. Role of zinc supplementation in type II diabetes mellitus. The American Journal of Medicine 1986;81:63-68.

2. Riemersma RA et al. Risk of angina pectoris and plasma concentrations of vitamins A, C, and E and carotene. The Lancet 1991;337:1-5.

3. Pizzorno J & M Murray. A Textbook of Natural Medicine®. Seattle: Bastyr College Publications, 1985.
   

Arginine has several important functions. It is essential to the metabolism of ammonia that is generated from protein breakdown. It is also needed to transport the nitrogen used in muscle metabolism. Arginine is one of the body-building amino acids and also influences several hormone functions. L-arginine has been shown to stimulate the pituitary gland to produce and secrete human growth hormone in young males, at a dose of more than 3 grams daily. Human growth hormone helps in muscle building, leading to increased muscle strength and tone, and enhances fat metabolism (increases the burning of fats), which may help with weight loss. Growth hormone in general seems to increase metabolism and energy. L-arginine has a positive effect on the immune system, mainly by stimulating thymus activity, and also helps the body heal from wounds. Some research has shown that high doses of L-arginine may increase male fertility by increasing sperm production and motility.

L-arginine has several possible uses. The most common use, in part promoted by Pearson and Shaw’s book Life Extension, is as a growth hormone stimulant. Body builders supplement L-arginine along with L-ornithine for its muscle-building effects. Recent research has suggested that L-arginine and L-lysine together have a similar effect, possibly at lower dosages. L-arginine supplementation, at a dosage of 4 grams daily, has been successful in improving fertility in men by increasing low sperm count and motility. Arginine has been shown to help speed wound healing in rats, possibly as an aid to collagen formation. Other possible uses for L-arginine as seen in animals are to improve decreased liver functions, to lower cholesterol levels, and to inhibit the growth of certain tumors (it may also stimulate the growth of certain tumors).

L-arginine, available in 500 mg. capsules, is usually well tolerated in doses as high as 3–6 grams, although side effects such as diarrhea, nausea, and, rarely, ataxia (unsteadiness) may occur in some people. Dosages of less than 2 grams daily are usually handled without problems. A dosageof 3–4 grams daily is needed for the growth hormone effect. L-arginine and L-ornithine, or L-arginine and L-lysine, can be supplemented at 500–1000 mg. of each twice daily, or 1000 to 1500 mg. of each before bed. To improve male fertility, a dosage of 2 grams twice daily is suggested. Children and teenagers should avoid supplementation of L-arginine for growth stimulation or body building. People with diabetes must be careful because of arginine’s effect on insulin and carbohydrate metabolism. Supplementation should not be done continuously for a long period. I suggest that it be used for two to three weeks, followed by a break of one to two weeks. A balanced amino acid supplement can also be used.

Compromised intestinal barrier function can also cause disease directly, by immunological mechanisms.[6-9] Increased permeability stimulates classic hypersensitivity responses to foods and to components of the normal gut flora; bacterial endotoxins, cell wall polymers and dietary gluten may cause “non-specific” activation of inflammatory pathways mediated by complement and cytokines. [10] In experimental animals, chronic low-grade endotoxemia causes the appearance of auto-immune disorders.[11-13]

Leaky Gut Syndromes are clinical disorders associated with increased intestinal permeability. They include inflammatory and infectious bowel diseases [14-19], chronic inflammatory arthritides [9, 20-24], cryptogenic skin conditions like acne, psoriasis and dermatitis herpetiformis [25-28], many diseases triggered by food allergy or specific food intolerance, including eczema, urticaria, and irritable bowel syndrome [29-37], AIDS [38-40], chronic fatigue syndromes [Rigden, Cheney, Lapp, Galland, unpublished results], chronic hepatitis [41], chronic pancreatitis [4, 5], cystic fibrosis [42] and pancreatic carcinoma. Hyperpermeability may play a primary etiologic role in the evolution of each disease, or may be a secondary consequence of it which causes immune activation, hepatic dysfunction, and pancreatic insufficiency, creating a vicious cycle. Unless specifically investigated, the role of altered intestinal permeability in patients with Leaky Gut Syndromes often goes unrecognized. The availability of safe, non-invasive, and inexpensive methods for measuring small intestinal permeability make it possible for clinicians to look for the presence of altered intestinal permeability in their patients and to objectively assess the efficacy of treatments. Monitoring the intestinal permeability of chronically ill patients with Leaky Gut Syndromes can help improve clinical outcomes.

Triggers and Mediators of the Leaky Gut

Leaky Gut Syndromes are usually provoked by exposure to substances which damage the integrity of the intestinal mucosa, disrupting the desmosomes which bind epithelial cells and increasing passive, para-cellular absorption. The commonest causes of damage are infectious agents (viral, bacterial and protozoan) [43-46], ethanol [47, 48], and non-steroidal anti-inflammatory drugs [20, 49, 50]. Hypoxia of the bowel (occurring as a consequence of open-heart surgery or of shock) [51, 52], elevated levels of reactive oxygen metabolites (biliary, food-borne or produced by inflammatory cells) [53], and cytotoxic drugs [54-56] also increase para-cellular permeability.

The Four Vicious Cycles

Cycle One: Allergy

The relationship between food sensitivities and the leaky gut is complex and circular. Children and adults with eczema, urticaria or asthma triggered by atopic food allergy have baseline permeability measurements that are higher than control levels [57-59]. Following exposure to allergenic foods, permeability sharply increases. Most of this increase can be averted by pre-treatment with sodium cromoglycate [32, 34, 57-59], indicating that release from mast cells of atopic mediators like histamine and serotonin is responsible for the increase in permeability. It appears that an increase in intestinal permeability is important in the pathogenesis of food allergy and is also a result of food allergy.

Claude Andre, the leading French research worker in this area, has proposed that measurement of gut permeability is a sensitive and practical screening test for the presence of food allergy and for following response to treatment [57]. In Andre’s protocol, patients with suspected food allergy ingest 5 grams each of the innocuous sugars lactulose and mannitol. These sugars are not metabolized by humans and the amount absorbed is fully excreted in the urine within six hours. Mannitol, a monosaccharide, is passively transported through intestinal epithelial cells; mean absorption is 14% of the administered dose (range 5-25%). In contrast, the intestinal tract is impermeable to lactulose, a disaccharide; less than 1% of the administered dose is normally absorbed. The differential excretion of lactulose and mannitol in urine is then measured. The normal ratio of lactulose/mannitol recovered in urine is less than 0.03. A higher ratio signifies excessive lactulose absorption caused by disruption of the desmosomes which seal the intercellular tight junctions. The lactulose/mannitol challenge test is performed fasting and again after ingestion of a test meal. At the Hospital St. Vincent de Paul in Paris, permeability testing has been effectively used with allergic infants to determine which dietary modifications their mothers needed to make while breast feeding and which of the “hypoallergenic” infant formulas they needed to avoid in order to relieve their symptoms [60].

Cycle Two: Malnutrition

Disruption of desmosomes increases absorption of macromolecules. If the epithelial cells themselves are damaged, a decrease in trans-cellular absorption may accompany the increased para-cellular absorption. Because nutrients are ordinarily absorbed by the trans-cellular route, malnutrition may occur, aggravating strucutural and functional disturbances [61]. Under normal conditions, intestinal epithelium has the fastest rate of mitosis of any tissue in the body; old cells slough and a new epithelium is generated every three to six days [62, 63]. The metabolic demands of this normally rapid cell turnover must be met if healing of damaged epithelium is to occur. When they are not met, hyperpermeability exacerbates [64, 65].

Correction of nutritional deficiency with a nutrient-dense diet and appropriate supplementation is essential for the proper care of patients with Leaky Gut Syndromes. Specific recommendations are made in the last section of this review. Because of the association between hyperpermeability and pancreatic dysfunction, pancreatic enzymes may also be required.

Cycle Three: Bacterial Dysbiosis

Dysbiosis is a state in which disease or dysfunction is induced by organisms of low intrinsic virulence that alter the metabolic or immunologic responses of their host. This condition has been the subject of a recent review article [66]. Immune sensitization to the normal gut flora is an important form of dysbiosis that has been implicated in the pathogenesis of Crohn’s disease and ankylosing spondylitis[67-81]. Recent research findings suggest that bacterial sensitization is an early complication of altered permeability and exacerbates hyperpermeability by inducing an inflammatory enteropathy [82, 83]. This has been most studied in the response to NSAIDs. Single doses of aspirin or of indomethacin increase para-cellular permeability, in part by inhibiting the synthesis of protective prostaglandins [20, 49, 50, 84, 85]. Hyperpermeability is partially prevented by pre-treatment with the prostaglandin-E analogue, misoprosterol. Chronic exposure to NSAIDs produces a chronic state of hyper-permeability associated with inflammation, which can not be reversed by misoprosterol but which is both prevented and reversed by the administration of the antibiotic, metronidazole [83, 86]. The effectiveness of metronidazole in preventing NSAID-induced hyperpermeability probably reflects the importance of bacterial toxins in maintaining this vicious cycle. A single dose of bacterial endotoxin, administered by injection, increases the gut permeability of healthy humans [87]. Chronic arthritis can be induced in rats by injection of cell wall fragments isolated from normal enteric anaerobes[88]. Patients with rheumatoid arthritis receiving NSAIDs have increased antibody levels to Clostridium perfringens and to its alpha toxin, apparently as a secondary response to NSAID therap[89].

There is ample documentation for a therapeutic role of metronidazole and other antibiotics in Crohn’s disease and rheumatoid arthritis[90-98]. The mechanism underlying the response has been in dispute. In the case of tetracyclines, one group has asserted that mycoplasma in the joints cause rheumatoid arthritis, others have countered this argument by demonstrating that minocycline is directly immunosuppressive in vitro [99]. Because all patients with arthritis have used NSAIDs, and because NSAID enteropathy is associated with bacterial senisitization, it is possible that the the antibiotic-responsiveness of some patients with inflammatory diseases is a secondary effect of NSAID-induced bacterial sensitization which then exacerbates the Leaky Gut Syndrome. Altering gut flora through the use of antibiotics, synthetic and natural, probiotics, and diet is a third strategy for breaking the vicious cycle in Leaky Gut Syndromes. With regard to diet, patients whose disease responds to vegetarian diets are those in whom the diet alters gut ecology; if vegetarian diets does not alter gut ecology, the arthritis is not improved[100].

Cycle Four: Hepatic Stress

The liver of Leaky Gut patients works overtime to remove macromolecules and oxidize enteric toxins. Cytochrome P-450 mixed-function oxidase activity is induced and hepatic synthesis of free radicals increases. The results include damage to hepatocytes and the excretion of reactive by-products into bile, producing a toxic bile capable of damaging bile ducts and refluxing into the pancreas [4, 5]. In attempting to eliminate toxic oxidation products, the liver depletes its reserves of sulfur-containing amino acids [101]. These mechanisms have been most clearly demonstrated in ethanol-induced hepatic disease [47]. Sudduth [102] proposes that the initial insult is the ethanol-induced increase in gut permeability which creates hepatic endotoxemia. Endotoxemia can further increase permeability, alter hepatic metabolism, and stimulate hepatic synthesis of reactive species which are excreted in bile. This toxic bile, rich in free radicals, further damages the small-bowel mucosa, exacerbating hyperpermeability.

A Practical Approach

Suspect a pathological increase in gut permeability when evaluating any patient with the diseases listed in Table 1 or the symptoms listed in Table 2. Measure permeability directly using the lactulose/mannitol challenge test. Indirect measures of gut permeability include titres of IgG antibody directed against antigens found in common foods and normal gut bacteria. These tests may be useful but cannot substitute for the direct permeability assay, especially when one is following the response to treatment.

IF ALL COMPONENTS OF THE LACTULOSE/MANNITOL TEST ARE NORMAL, repeat the challenge after a test meal of the patient’s common foods. If the test meal produces an increase in lactulose excretion (signifying hyperpermeability) or a decrease in mannitol excretion (signifying malabsorption), specific food intolerances are likely and further testing for food allergy is warranted. Once the patient has been maintained on a stable elimination diet for four weeks, repeat the lactulose/mannitol challenge after a test meal of foods permitted on the elimination diet. A normal result assures you that all major allergens have been identified. An abnormal result indicates that more detective work is needed.

IF THE INITIAL FASTING MANNITOL ABSORPTION IS LOW, suspect malabsorption. This result has the same significance as an abnormal D-xylose absorption test. Look for evidence of celiac disease, intestinal parasites, ileitis, small bowel bacterial overgrowth and other disorders classically associated with intestinal malabsorption and treat appropriately. After eight weeks of therapy, repeat the lactulose/mannitol challenge. An improvement in mannitol excretion indicates a desirable increase in intestinal absorptive capacity. The lactulose/mannitol assay has been proposed as a sensitive screen for celiac disease and a sensitive test for dietary compliance [46, 103-106]. For gluten-sensitive patients, abnormal test results demonstrate exposure to gluten, even when no intestinal symptoms are present. Monitoring dietary compliance to gluten avoidance by testing small bowel permeability is especially helpful in following those patients for whom gluten enteropathy does not produce diarrhea but instead causes failure to thrive, schizophrenia or inflammatory arthritis [107-115].

In the case of relatively mild celiac disease or inflammatory bowel disease, mannitol absorption may not be affected but lactulose absorption will be elevated. A recent study published in the Lancet found that the lactulose-mannitol ratio was an accurate predictor of relapse when measured in patients with Crohn’s disease who were clinically in remission [116].

IF THE INITIAL FASTING LACTULOSE IS ELEVATED, OR IF THE INITIAL FASTING LACTULOSE/MANNITOL RATIO IS ELEVATED, consider the possibility of mild inflammatory bowel disease or gluten enteropathy. There are four other primary considerations:

(A) Exposures. Does the patient drink ethanol, take NSAIDs or any potentially cytotoxic drugs? If so, discontinue them and have the lactulose/mannitol challenge repeated three weeks later. If it has become normal, drug exposures were the likely cause of leaky gut. If it has not, bacterial sensitization may have occurred. This may be treated with a regimen of antimicrobials and probiotics. My preference is a combination of citrus seed extract, berberine and artemisinin (the active alkaloid in Artemisia annua), which exerts a broad spectrum of activity against Enterobacteriaceae, Bacteroides, protozoa and yeasts [117-120].

If the patient has no enterotoxic drug exposures, inquire into dietary habits. Recent fasting or crash dieting may increase permeability. Counsel the patient in consuming a nutritionally sound diet for three weeks and repeat the test.

Patients with chronic arthritis may have difficulty stopping NSAIDs. Alternative anti-inflammatory therapy should be instituted, including essential fatty acids, anti-oxidants or mucopolysaccharides[121-125]. Changing the NSAID used may also be helpful. NSAIDs like indomethacin, which undergo enteroheaptic recirculation, are more likely to damage the small intestine that NSAIDs that are not excreted in bile, like ibuprofen [126]. Nabumetone (relafen) is a pro-NSAID that is activated into a potent NSAID by colonic bacteria; the active metabolite is not excreted in bile. Nabumetone is the only presently available NSAID that does not increase small intestinal permeability.

(B) Infection. The possibilities include recent acute viral or bacterial enteritis, intestinal parasitism, HIV infection and candidosis. Stool testing is useful in identifying these. Repeat the permeability test six weeks after initiating appropriate therapy.

(C) Food allergy. Approach this probability as described in the section above on food allergy in patients with normal fasting test results. The difference lies in degree of damage; food intolerant patients with abnormal fasting permeability have more mucosal damage than patients with normal fasting permeability and will take longer to heal.

(D) Bacterial overgrowth resulting from hypochlorhydria, maldigestion, or stasis [41, 127, 128]. This is confirmed by an abnormal hydrogen breath test. Most of the damage resulting from bacterial overgrowth is caused by bacterial enzyme activity. Bacterial mucinase destroys the protective mucus coat; proteinases degrade pancreatic and brush border enzymes and attack structural proteins. Bacteria produce vitamin B12 analogues and uncouple the B12-intrinsic factor complex, reducing circulating B12 levels, even among individuals who are otherwise asymptomatic [129, 130]. In the absence of intestinal surgery, strictures or fistulae, bacterial overgrowth is most likely a sign of hypochlorhydria resulting from chronic gastritis due to Helicobacter pylori infection. Triple therapy with bismuth and antibiotics may be needed, but it is not presently known whether such treatment can reverse atrophic gastritis or whether natural, plant-derived antimicrobials can achieve the same results as metronidazole and ampicillin, the antibiotics of choice.

Bacterial overgrowth due to hypochlorhydria tends to be a chronic problem that recurs within days or weeks after antimicrobials are discontinued. Keith Eaton, a British allergist who has worked extensively with the gut fermentation syndrome, finds that administration of L-histidine, 500 mg bid, improves gastric acid production in allergic patients with hypochlorhydria, probably by increasing gastric histamine levels [personal communication]. Dietary supplementation with betaine hydrochloride is usually helpful but intermittent short courses of bismuth, citrus seed extract, artemisinin, colloidal silver and other natural antimicrobials are often needed. The first round of such treatment, while the patient is symptomatic, should last for at least twelve weeks, to allow complete healing to occur. Repeat the lactulose/mannitol assay at the end of twelve weeks, while the patient is taking the antimicrobials, to see if complete healing has been achieved. The most sensitive test for recurrence of bacterial overgrowth is not the lactulose/mannitol assay but the breath hydrogen analysis.

Atrophic Therapies

Many naturally occurring substances help repair the intestinal mucosal surface or support the liver when stressed by enteric toxins. Basic vitamin and mineral supplementation should include all the B vitamins, retinol, ascorbate, tocopherol, zinc, selenium, molybdenum, manganese, and magnesium. More specialized nutritional, glandular and herbal therapies are considered below. These should not be used as primary therapies. Avoidance of enterotoxic drugs, treatment of intestinal infection or dysbiosis, and an allergy elimination diet of high nutrient density that is appropriate for the individual patient are the primary treatment strategies for the Leaky Gut Syndromes. The recommendations that follow are to be used as adjuncts:

(1) Epidermal Growth Factor (EGF) is a polypeptide that stimulates growth and repair of epithelial tissue. It is widely distributed in the body, with high concentrations detectable in salivary and prostate glands and in the duodenum. Saliva can be a rich source of EGF, especially the saliva of certain non-poisonous snakes. The use of serpents in healing rituals may reflect the value of ophidian saliva in promoting the healing of wounds. Thorough mastication of food may nourish the gut by providing it with salivary EGF. Purified EGF has been shown to heal ulceration of the small intestine [131].

(2) Saccharomyces boulardii is a non-pathogenic yeast originally isolated from the surface of lichee nuts. It has been widely used in Europe to treat diarrhea. In France it is popularly called “Yeast against yeast” and is thought to help clear the skin in addition to the gut. Clinical trials have demonstrated the effectiveness for S. boulardii in the treatment or prevention of C. difficile diarrhea, antibiotic diarrhea and traveler’s diarrhea[132, 133]. Experimental data suggest that the yeast owes its effect to stimulation of SIgA secretion[134]. SIgA is a key immunological component of gut barrier function.

Passive elevation of gut immunoglobulin levels can be produced by feeding whey protein concentrates that are rich in IgA and IgG. These have been shown to be effective in preventing infantile necrotizing enterocolitis[135].

(3) Lactobacillus caseii var GG is a strain of lactobacillus isolated and purified in Finland. Like S.boulardii, Lactobacillus GG has been shown effective in the prevention of traveller’s diarrhea and of antibiotic diarrhea and in the treatment of colitis caused by C. difficile. Lactobacillus GG limits diarrhea caused by rotavirus infection in children and in so doing improves the hyperpermeability associated with rotavirus infection.[136-139] The mechanism of action is unclear. The ability of other Lactobacillus preparations to improve altered permeability has not been directly tested, but is suggested by the ability of live cultures of L. acidophilus to diminish radiation-induced diarrhea, a condition directly produced by the loss of mucosal integrity.

(4) Glutamine is an important substrate for the maintenance of intestinal metabolism, structure and function. Patients and experimental animals that are fasted or fed only by a parenteral route develop intestinal villous atrophy, depletion of SIgA, and translocation of bacteria from the gut lumen to the systemic circulation. Feeding glutamine reverses all these abnormalities. Patients with intestinal mucosal injury secondary to chemotherapy or radiation benefit from glutamine supplementation with less villous atrophy, increased mucosal healing and decreased passage of endotoxin through the gut wall[140-143].

(5) Glutathione (GSH) is an important component of the anti-oxidant defense against free radical-induced tissue damage. Dietary glutathione is not well absorbed, so that considerable quantities may be found throughout the gut lumen following supplementation[144]. Hepatic GSH is a key substrate for reducing toxic oxygen metabolites and oxidized xenobiotics in the liver. Depletion of hepatic glutathione is a common occurence in Leaky Gut Syndromes contributing to liver dysfunction and liver necrosis among alcoholics and immune impairment in patients with AIDS. The most effective way to raise hepatic glutathione is to administer its dietary precursors, cysteine or methionine. Anti-oxidant supplementation for Leaky Gut Syndromes should therefore include both GSH and N-acetyl cysteine. Because protozoa are more sensitive to oxidant stress than are humans and because most anti-parasitic drugs and herbs work by oxidative mechanisms, high dose anti-oxidant supplementation should be witheld during the treatment of protozoan infection, especially during treatment with Artemisia.

(6) Flavonoids are potent, phenolic anti-oxidants and enzyme inhibitors with varied effects depending on the tissues in which they act. Quercetin and related flavonoids inhibit the release of histamine and inflammatory mediators. Taken before eating, they may block allergic reactions which increase permeability. Catechins have been used in Europe to treat gastric ulcerations. The flavonoids in milk thistle (silymarin) and in dandelion root (taraxacum) protect the liver against reactive oxygen species[145].

(7) Essential fatty acids (EFAs) are the substrates for prostaglandin synthesis. Differential feeding of EFAs can profoundly affect prostanoid synthesis and the systemic response to endotoxin. In experimental animals, fish oil feeding ameliorates the intestinal mucosal injury produced by methotrexate and, additionally, blunts the systemic circulatory response to endotoxin[146]. The feeding of gamma-linolenic acid (GLA), promotes the synthesis of E-series prostaglandins, which decrease permeability. EFAs should be consumed in the most concentrated and physiologically active form to avoid exposure to large quantities of polyunsaturated fatty acids from dietary oils. Consumption of vegetable oils tends to increase the free radical content of bile and to exacerbate the effects of endotoxin[147].

(8) Fiber supplements have complex effects on gut permeability and bacterial composition. Low fibre diets increase permeability. Dietary supplementation with insoluble fibre, such as pure cellulose, decreases permeability. Dietary supplementation with highly soluble fibre sources, such as fruit pectin or guar gum, has a biphasic effect. At low levels they reverse the hyperpermeability of low residue diets, probably by a mechanical bulking effect which stimulates synthesis of mucosal growth factors. At high levels of supplementation, they produce hyperpermeability, probably by inducing synthesis of bacterial enzymes which degrade intestinal mucins[148-151]. For maximum benefit with regard to intestinal permeability, dietary fibre supplementation should therefore contain a predominance of hypoallergenic insoluble fibre.

(9) Gamma oryzanol, a complex mixture of ferulic acid esters of phytosterosl and other triterpene alcohols derived from rice bran, has been extensively researched in Japan for its healing effects in the treatment of gastric and duodenal ulceration, thought to be secondary to its potent anti-oxidant activity[152, 153].

Summary

Altered intestinal permeability is a key element in the pathogenesis of many different diseases. Hyperpermeability initiates a vicious cycle in which allergic sensitization, endotoxic immune activation, hepatic dysfunction, pancreatic insufficiency and malnutrition occur; each of these increases the leakiness of the small bowel. Effective treatment of the Leaky Gut Syndromes requires several components: avoidance of enterotoxic drugs and allergic foods, elimination of infection or bacterial overgrowth with antimicrobials and probiotics, and dietary supplementation with trophic nutrients. Direct measurement of intestinal permeability allows the clinician to plan appropriate strategies and to gauge the effectiveness of treatment, using objective parameters.

Inflammatory bowel disease

Infectious enterocolitis

Spondyloarthropathies

Acne

Eczema

Psoriasis

Urticaria

HIV infection

Cystic fibrosis

Pancreatic insufficiency

AIDS, HIV infection

Hepatic dysfunction

Irritable bowel syndrome with food intolerance

CFIDS

Chronic arthritis/pain treated with NSAIDs

Alcoholism

Neoplasia treated with cytotoxic drugs

Celiac disease

Dermatitis herpetiformis

Autism

Childhood hyperactivity

Environmental illness

Multiple food and chemical sensitivities

Fatigue and malaise

Arthralgias

Myalgias

Fevers of unknown origin

Food intolerances

Abdominal pain

Abdominal distension

Diarrhea

Skin rashes

Toxic feelings

Cognitive and memory deficits

Shortness of breath

Poor exercise tolerance

NOTES:

1. Crissinger, K.D., P.R. Kvietys, and D.N. Granger, Pathophysiology of gastrointestinal mucosal permeability. J Intern Med Suppl, 1990. 732: p. 145-54.

2. Anderson, K.E., Dietary Regulation of Cytochrome P450. Ann. Rev. Nutr., 1991. 11: p. 141-167.

3. Paine, A.J., Excited states of oxygen in biology: their possible involvement in cytochrome P450 linked oxidations as well as in the induction of the P450 system by many diverse compounds. Biochem. Pharmacol., 1978. 27: p. 1805-1813.

4. Braganza, J.M., et al., Lipid-peroxidation (free-radical-oxidation) products in bile from patients with pancreatic disease. Lancet, 1983. ii: p. 375-378.

5. Braganza, J.M., Pancreatic disease: a casualty of hepatic “detoxification”? Lancet, 1983. ii: p. 1000-1002.

6. Deitch, E.A., The role of intestinal barrier failure and bacterial translocation in the development of systemic infection and multiple organ failure. Arch. Surgery, 1990. 125: p. 403-404.

7. Hazenberg, M.P., et al., Are intestinal bacteria involved in the etiology of rheumatoid arthritis? Review article. Apmis, 1992. 100(1): p. 1-9.

8. Peters, T.J. and I. Bjarnason, Uses and abuses of intestinal permeability measurements. Can. J. Gastroenterol., 1988. 2: p. 127-132.

9. Rooney, P.J., R.T. Jenkins, and W.W. Buchanan, A short review of the relationship between intestinal permeability and inflammatory joint disease [see comments]. Clin Exp Rheumatol, 1990. 8(1): p. 75-83.

10. Walker, W.A., Antigen absorption from the small intestine and gastrointestinal disease. Pediatr Clin North Am, 1975. 22(4): p. 731-46.

11. Bloembergen, P., et al., Endotoxin-induced auto-immunity in mice. I. Time and dose dependence of production and serum levels of antibodies against bromelain-treated mouse erythrocytes and circulating immune complexes. Int Arch Allergy Appl Immunol, 1987. 84(3): p. 291-7.

12. Bloembergen, P., et al., Endotoxin-induced auto-immunity in mice. II. Reactivity of LPS-hyporesponsive and C5-deficient animals. Int Arch Allergy Appl Immunol, 1988. 86(4): p. 370-4.

13. Bloembergen, P., et al., Endotoxin-induced auto-immunity in mice. III. Comparison of different endotoxin preparations. Int Arch Allergy Appl Immunol, 1990. 92(2): p. 124-30.

14. Katz, K.D., et al., Intestinal permeability in patients with Crohn’s disease and their healthy relatives [see comments]. Gastroenterology, 1989. 97(4): p. 927-31.

15. Pearson, A.D., et al., Intestinal permeability in children with Crohn’s disease and coeliac disease. Br Med J, 1982. 285(6334): p. 20-1.

16. Pironi, L., et al., Relationship between intestinal permeability to [51Cr]EDTA and inflammatory activity in asymptomatic patients with Crohn’s disease. Dig Dis Sci, 1990. 35(5): p. 582-8.

17. Munkholm, P., et al., Intestinal permeability in patients with Crohn’s disease and ulcerative colitis and their first degree relatives. Gut, 1994. 35(1): p. 68-72.

18. Hollander, D., et al., Increased intestinal permeability in patients with Crohn’s disease and their relatives. A possible etiologic factor. Ann Intern Med, 1986. 105(6): p. 883-5.

19. Teahon, K., et al., Intestinal permeability in patients with Crohn’s disease and their first degree relatives. Gut, 1992. 33(3): p. 320-3.

20. Jenkins, R.T., et al., Increased intestinal permeability in patients with rheumatoid arthritis: a side-effect of oral nonsteroidal anti-inflammatory drug therapy? Br J Rheumatol, 1987. 26(2): p. 103-7.

21. Mielants, H., Reflections on the link between intestinal permeability and inflammatory joint disease [letter; comment]. Clin Exp Rheumatol, 1990. 8(5): p. 523-4.

22. Morris, A.J., et al., Increased intestinal permeability in ankylosing spondylitis–primary lesion or drug effect? [see comments]. Gut, 1991. 32(12): p. 1470-2.

23. Smith, M.D., R.A. Gibson, and P.M. Brooks, Abnormal bowel permeability in ankylosing spondylitis and rheumatoid arthritis. J Rheumatol, 1985. 12(2): p. 299-305.

24. Sk:oldstam, L. and K.E. Magnusson, Fasting, intestinal permeability, and rheumatoid arthritis. Rheum Dis Clin North Am, 1991. 17(2): p. 363-71.

25. Juhlin, L. and C. Vahlquist, The influence of treatment on fibrin microclot generation in psoriasis. Br J Dermatol, 1983. 108(1): p. 33-7.

26. Juhlin, L. and G. Micha:elsson, Fibrin microclot formation in patients with acne. Acta Derm Venereol, 1983. 63(6): p. 538-40.

27. Hamilton, I., et al., Small intestinal permeability in dermatological disease. Q J Med, 1985. 56(221): p. 559-67.

28. Belew, P.W., et al., Endotoxemia in psoriasis [letter]. Arch Dermatol, 1982. 118(3): p. 142-3.

29. Jackson, P.G., et al., Intestinal permeability in patients with eczema and food allergy. Lancet, 1981. 1(8233): p. 1285-6.

30. Scadding, G., et al., Intestinal permeability to 51Cr-labelled ethylenediaminetetraacetate in food-intolerant subjects. Digestion, 1989. 42(2): p. 104-9.

31. Jacobson, P., R. Baker, and M. Lessof, Intestinal permeability in patients with eczema and food allergy. Lancet, 1981. i: p. 1285-1286.

32. F:alth-Magnusson, K., et al., Gastrointestinal permeability in children with cow’s milk allergy: effect of milk challenge and sodium cromoglycate as assessed with polyethyleneglycols (PEG 400 and PEG 1000). Clin Allergy, 1986. 16(6): p. 543-51.

33. F:alth-Magnusson, K., et al., Gastrointestinal permeability in atopic and non-atopic mothers, assessed with different-sized polyethyleneglycols (PEG 400 and PEG 1000). Clin Allergy, 1985. 15(6): p. 565-70.

34. F:alth-Magnusson, K., et al., Intestinal permeability in healthy and allergic children before and after sodium-cromoglycate treatment assessed with different-sized polyethyleneglycols (PEG 400 and PEG 1000). Clin Allergy, 1984. 14(3): p. 277-86.

35. Jalonen, T., Identical intestinal permeability changes in children with different clinical manifestations of cow’s milk allergy. J Allergy Clin Immunol, 1991. 88(5): p. 737-42.

36. Barau, E. and C. Dupont, Modifications of intestinal permeability during food provocation procedures in pediatric irritable bowel syndrome. J Pediatr Gastroenterol Nutr, 1990. 11(1): p. 72-7.

37. Paganelli, R., et al., Intestinal permeability in irritable bowel syndrome. Effect of diet and sodium cromoglycate administration. Ann Allergy, 1990. 64(4): p. 377-80.

38. Batash, S., et al., Intestinal permeability in HIV infection: proper controls are necessary [letter]. Am J Gastroenterol, 1992. 87(5): p. 680.

39. Lim, S.G., et al., Intestinal permeability and function in patients infected with human immunodeficiency virus. Scand J Gastroenterol, 1993. 28(7): p. 573-580

40. Tepper, R.E., et al., Intestinal permeability in patients infected with human immunodeficiency virus. Am J Gastroenterol, 1994. 89: p. 878-882.

41. Lichtman, S.N., et al., Hepatic injury associated with small bowel bacterial overgrowth in rats is prevented by metronidazole and tetracycline. Gastroenterology, 1991. 100(2): p. 513-9.

42. Mack, D.R., et al., Correlation of intestinal lactulose permeability with exocrine pancreatic dysfunction. J. Pediatr., 1992. 120: p. 696-701.

43. Lahesmaa-Rantala, R., et al., Intestinal permeability in patients with yersinia triggered reactive arthritis. Ann Rheum Dis, 1991. 50(2): p. 91-4.

44. Serrander, R., K.E. Magnusson, and T. Sundqvist, Acute infections with Giardia lamblia and rotavirus decrease intestinal permeability to low-molecular weight polyethylene glycols (PEG 400). Scand J Infect Dis, 1984. 16(4): p. 339-44.

45. Serrander, R., et al., Acute yersinia infections in man increase intestinal permeability for low-molecular weight polyethylene glycols (PEG 400). Scand J Infect Dis, 1986. 18(5): p. 409-13.

46. Lim, S.G., et al., Intestinal permeability and function in patients infected with human immunodeficiency virus. A comparison with coeliac disease. Scand J Gastroenterol, 1993. 28(7): p. 573-80.

47. Bjarnason, I., R. Wise, and T. Peters, The leaky gut of alcoholism: Possible route of entry for toxic compounds. Lancet, 1984. i: p. 79-82.

48. Worthington, B.S., L. Meserole, and J.A. Syrotuck, Effect of daily ethanol ingestion on intestinal permeability to macromolecules. Am J Dig Dis, 1978. 23(1): p. 23-32.

49. Bjarnason, I., et al., Effect of non-steroidal anti-inflammatory drugs on the human small intestine. Drugs, 1986. 1: p. 35-41.

50. Rooney, P.J. and R.T. Jenkins, Nonsteroidal antiinflammatory drugs (NSAID’s) and the bowel mucosa: changes in intestinal permeability may not be due to changes in prostaglandins [letter]. Clin Exp Rheumatol, 1990. 8(3): p. 328-9.

51. Ohri, S.K., et al., Cardiopulmonary bypass impairs small intestinal transport and increases gut permeability. Ann Thorac Surg, 1993. 55(5): p. 1080-6.

52. Ohri, S.K., et al., The effect of intestinal hypoperfusion on intestinal absorption and permeability during cardiopulmonary bypass. Gastroenterology, 1994. 106(2): p. 318-23.

53. Grisham, M.B., et al., Effects of neutrophil-derived oxidants on intestinal permeability, electrolyte transport, and epithelial cell viability. Inflammation, 1990. 14(5): p. 531-42.

54. Bjarnason, I., et al., Intestinal permeability to 51Cr-EDTA in rats with experimentally induced enteropathy. Gut, 1985. 26(6): p. 579-85.

55. Lifschitz, C.H. and D.H. Mahoney, Low-dose methotrexate-induced changes in intestinal permeability determined by polyethylene glycol polymers. J Pediatr Gastroenterol Nutr, 1989. 9(3): p. 301-6.

56. Berg, R.D., The translocation of the normal flora bacteria from the gastrointestinal tract to the mesenteric lymph nodes and other organs. Microecology Therapy, 1981. 11: p. 27-34.


57. Andr:e, C., [Food allergy. Objective diagnosis and test of therapeutic efficacy by measuring intestinal permeability]. Presse Med, 1986. 15(3): p. 105-8.

58. Andr:e, C., F. Andr:e, and L. Colin, Effect of allergen ingestion challenge with and without cromoglycate cover on intestinal permeability in atopic dermatitis, urticaria and other symptoms of food allergy. Allergy, 1989. 9: p. 47-51.

59. Andre, C., et al., Measurement of intestinal permeability to mannitol and lactulose as a means of diagnosing food allergy and evaluating therapeutic effectiveness of disodium cromoglycate. Ann Allergy, 1987. 59(5 Pt 2): p. 127-30.

60. Barau, E. and C. Dupont, Allergy to cow’s milk proteins in mother’s milk or in hydrolyzed cow’s milk infant formulas as assessed by intestinal permeability measurements. Allergy, 1994. 49(4): p. 295-8.

61. Doe, W.F., An overview of intestinal immunity and malabsorption. Am J Med, 1979. 67(6): p. 1077-84.

62. Williamson, R.C., Intestinal adaptation (first of two parts). Structural, functional and cytokinetic changes. N Engl J Med, 1978. 298(25): p. 1393-402.

63. Williamson, R.C., Intestinal adaptation (second of two parts). Mechanisms of control. N Engl J Med, 1978. 298(26): p. 1444-50.

64. Lunn, P.G., C.A. Northrop-Clewes, and R.M. Downes, Recent developments in the nutritional management of diarrhoea. 2. Chronic diarrhoea and malnutrition in The Gambia: studies on intestinal permeability. Trans R Soc Trop Med Hyg, 1991. 85(1): p. 8-11.

65. Behrens, R.H., et al., Factors affecting the integrity of the intestinal mucosa of Gambian children. Am J Clin Nutr, 1987. 45(6): p. 1433-41.

66. Galland, L. and S. Barrie, Intestinal dysbiosis and the causes of disease. J. Advancement Med., 1993. 6: p. 67-82.

67. Avakian, H., et al., Ankylosing spondylitis, HLA-B27 and Klebsiella. II. Cross-reactivity studies with human tissue typing sera. Br J Exp Pathol, 1980. 61(1): p. 92-6.

68. Ebringer, R., et al., Ankylosing spondylitis: klebsiella and HL-A B27. Rheumatol Rehabil, 1977. 16(3): p. 190-6.

69. Ebringer, A. and M. Ghuloom, Ankylosing spondylitis, HLA-B27, and klebsiella: cross reactivity and antibody studies [letter]. Ann Rheum Dis, 1986. 45(8): p. 703-4.

70. Ebringer, A., The relationship between Klebsiella infection and ankylosing spondylitis. Baillieres Clin Rheumatol, 1989. 3(2): p. 321-38.

71. Geczy, A.F., et al., Cross-reactivity of anti-Klebsiella K43 BTS 1 serum and lymphocytes of patients with ankylosing spondylitis: antipodean curiosity? [letter]. Lancet, 1985. 1(8438): p. 1169.

72. Geczy, A.F., et al., HLA-B27, molecular mimicry, and ankylosing spondylitis: popular misconceptions. Ann Rheum Dis, 1987. 46(2): p. 171-2.

73. Husby, G., et al., Cross-reactive epitope with Klebsiella pneumoniae nitrogenase in articular tissue of HLA-B27+ patients with ankylosing spondylitis. Arthritis Rheum, 1989. 32(4): p. 437-45.

74. Ilowite, N.T., et al., The rheumatoid factor cross-reactive idiotype in juvenile rheumatoid arthritis: role of the CD5-positive B cell. Clin Immunol Immunopathol, 1993. 67(3 Pt 2): p. S74-82.

75. Khalafpour, S., et al., Antibodies to Klebsiella and Proteus microorganisms in ankylosing spondylitis and rheumatoid arthritis patients measured by ELISA. Br J Rheumatol, 1988. 2: p. 86-9.

76. Phillips, P.E., Evidence implicating infectious agents in rheumatoid arthritis and juvenile rheumatoid arthritis. Clin. Exper. Rheumatol., 1988. 6: p. 87-94.

77. Ramakrishnan, T.P., et al., The major rheumatoid factor crossreactive idiotype and IgA rheumatoid factor in juvenile rheumatoid arthritis. J Rheumatol, 1991. 18(7): p. 1068-72.

78. Sullivan, J.S., et al., Cross-reacting bacterial determinants in ankylosing spondylitis. Am J Med, 1988. 85(6A): p. 54-5.

79. Trull, A.K., et al., IgA antibodies to Klebsiella pneumoniae in ankylosing spondylitis. Scand J Rheumatol, 1983. 12(3): p. 249-53.

80. Welsh, J., et al., Ankylosing spondylitis, HLA-B27 and Klebsiella. I. Cross-reactivity studies with rabbit antisera. Br J Exp Pathol, 1980. 61(1): p. 85-91.

81. Yu, D.T., S.Y. Choo, and T. Schaack, Molecular mimicry in HLA-B27-related arthritis [see comments]. Ann Intern Med, 1989. 111(7): p. 581-91.

82. Katz, K.D. and D. Hollander, Intestinal mucosal permeability and rheumatological diseases. Baillieres Clin Rheumatol, 1989. 3(2): p. 271-84.

83. Davies, G.R., M.E. Wilkie, and D.S. Rampton, Effects of metronidazole and misoprostol on indomethacin-induced changes in intestinal permeability. Dig Dis Sci, 1993. 38(3): p. 417-25.

84. Bjarnason, I., et al., Effect of prostaglandin on indomethacin-induced increased intestinal permeability in man. Scand J Gastroenterol Suppl, 1989. 164: p. 97-102.

85. Bjarnason, I., et al., Misoprostol reduces indomethacin-induced changes in human small intestinal permeability. Dig Dis Sci, 1989. 34(3): p. 407-11.

86. Bjarnason, I., et al., Metronidazole reduces intestinal inflammation and blood loss in non-steroidal anti-inflammatory drug induced enteropathy. Gut, 1992. 33: p. 1204-1208.

87. O’Dwyer, S.T., et al., A single dose of endotoxin increases intestinal permeability in healthy humans. Arch Surg, 1988. 123(12): p. 1459-64.

88. Severijnen, A.J., et al., Intestinal flora of patients with rheumatoid arthritis: induction of chronic arthritis in rats by cell wall fragments of Eubacterium aerofaciens strain. Br J Rheumatol, 1990. 29: p. 433-439.

89. Dearlove, M., et al., The effect of non-steroidal anti-inflammatory drugs of faecal flora and bacterial antibody levels in rheumatoid arthritis. Br J Rheumatol, 1992. 31: p. 443-447.

90. Alarcon, G.S. and I.S. Mikhail, Antimicrobials in the treatment of rheumatoid arthritis and other arthritides: a clinical perspective. Am. J. Med. Sci., 1994. 309: p. 201-209.

91. Brown, The puzzling problem of the rheumatic diseases. Maryland State Med. J., 1856. 2: p. 88-109.

92. Caperton, E.M., et al., Ceftriaxone therapy of chronic inflammatory arthritis. A double-blind placebo controlled trial. Arch. Intern. Med., 1990. 150: p. 1677-1682.

93. Brown, T.M., et al., Antimycoplasma approach to the mechanism and the control of rheumatoid disease. Inflammatory Diseases anbd Copper. edited by J.R.J. Sorenson., 1982. Humana Press, Clifton, N.J.

94. Porter, D., et al., Prospective trial comparing the use of sulphasalazine and auranofin as second line drugs in patients with rheumatoid arthritis. Ann Rheum Dis, 1992. 51(4): p. 461-4.

95. Porter, D.R. and H.A. Capell, The use of sulphasalazine as a disease modifying antirheumatic drug. Baillieres Clin Rheumatol, 1990. 4(3): p. 535-51.

96. Pybus, P.K., Metronidazole in rheumatoid arthritis. S. African Med. J., 1982. (February 20): p. 261-262.

97. Tilley, B.C., et al., Minocycline in rheumatoid arthritis. A 48-week, double-blind, placebo-controlled trial. Ann Int Med, 1995. 122(2): p. 81-89.

98. Wojtulewski, J.A., P.J. Gow, and J. Waller, Clotrimazole in rheumtoid arthritis. Ann Rheum Dis, 1980. 39: p. 469-472.

99. Kloppenburg, M., et al., Antibiotics as disease modifiers in arthritis. Clin. Exp. Rheumatol., 1993. 11 Suppl 8: p. S113-S115.

100. Peltonen, R., et al., Changes of faecal flora in rheumatoid arthritis during fasting and one-year vegetarian diet. Br J Rheumatol, 1994. 33: p. 638-643.

101. Whitcomb, D.C. and G.D. Block, Association of acetaminophen hepatotoxicity with fasting and ethanol use. JAMA, 1994. 272(23): p. 1845-1850.

102. Sudduth, W.H., The role of bacteria and enterotoxemia in physical addiction to alcohol. Microecology and Therapy, 1989. 18: p. 77-81.

103. Ukabam, S.O. and B.T. Cooper, Small intestinal permeability as an indicator of jejunal mucosal recovery in patients with celiac sprue on a gluten-free diet. J Clin Gastroenterol, 1985. 7(3): p. 232-6.

104. Cobden, I., J. Rothwell, and A.T. Axon, Intestinal permeability and screening tests for coeliac disease. Gut, 1980. 21(6): p. 512-8.

105. Hamilton, I., et al., Intestinal permeability in coeliac disease: the response to gluten withdrawal and single-dose gluten challenge. Gut, 1982. 23(3): p. 202-10.

106. Mulder, C.J., et al., Coeliac disease. Diagnostic and therapeutic pitfalls. Scand J Gastroenterol Suppl, 1993. 200: p. 42-7.

107. Hallert, C. and T. Derefeldt, Psychic disturbances in adult coeliac disease. I. Clinical observations. Scand J Gastroenterol, 1982. 17(1): p. 17-9.

108. Hallert, C. and J. Astr:om, Psychic disturbances in adult coeliac disease. II. Psychological findings. Scand J Gastroenterol, 1982. 17(1): p. 21-4.

109. Hallert, C., J. Astr:om, and G. Sedvall, Psychic disturbances in adult coeliac disease. III. Reduced central monoamine metabolism and signs of depression. Scand J Gastroenterol, 1982. 17(1): p. 25-8.

110. Hallert, C., J. Astr:om, and A. Walan, Reversal of psychopathology in adult coeliac disease with the aid of pyridoxine (vitamin B6). Scand J Gastroenterol, 1983. 18(2): p. 299-304.

111. Singh, M.M. and S.R. Kay, Wheat gluten as a pathogenic factor in schizophrenia. Science, 1976. 191(4225): p. 401-2.

112. Storms, L.H., J.M. Clopton, and C. Wright, Effects of gluten on schizophrenics. Arch Gen Psychiatry, 1982. 39(3): p. 323-7.

113. Wood, N.C., et al., Abnormal intestinal permeability. An aetiological factor in chronic psychiatric disorders? Br J Psychiatry, 1987. 150: p. 853-6.

114. Dohan, F.C., et al., Is schizophrenia rare if grain is rare? Biol Psychiatry, 1984. 19(3): p. 385-99.

115. O’Farrelly, C., et al., Association between villous atrophy in rheumatoid arthritis and a rheumatoid factor and gliadin-specific IgG. Lancet, 1988. 2(8615): p. 819-22.

116. Wyatt, J., et al., Intestinal permeability and the prediction of relapse in Crohn’s disease. Lancet, 1993. 341(8858): p. 1437-9.

117. Vanderhoof, J.A., et al., Effects of berberine, a plant alkaloid, on the growth of anaerobic protozoa in axenic culture. Tokai J Exp Clin Med, 1990. 15(6): p. 417-23.

118. Gupte, S., Use of berberine in treatment of giardiasis. Am J Dis Child, 1975. 129(7): p. 866.

119. Rabbani, G.H., et al., Randomized controlled trial of berberine sulfate therapy for diarrhea due to enterotoxigenic Escherichia coli and Vibrio cholerae. J Infect Dis, 1987. 155(5): p. 979-84.

120. Subbaiah, T.V. and A.H. Amin, Effect of berberine sulphate on Entamoeba histolytica. Nature, 1967. 215(100): p. 527-8.

121. Buchanan, H.M., et al., Is diet important in rheumatoid arthritis? [see comments]. Br J Rheumatol, 1991. 30(2): p. 125-34.

122. Darlington, L.G. and N.W. Ramsey, Is diet important in rheumatoid arthritis? [letter; comment]. Br J Rheumatol, 1991. 30(4): p. 315-6.

123. Darlington, L.G. and N.W. Ramsey, Review of dietary therapy for rheumatoid arthritis. Br J Rheumatol, 1993. 6: p. 507-14.

124. Prudden, J.F. and L.L. Balassa, The biological activity of bovine cartilage preparations. Sem Arthritis Rheumatism, 1974. 3(4): p. 287-321.

125. Sperling, R.I., Dietary omega-3 fatty acids: effects on lipid mediators of inflammation and rheumatoid arthritis. Rheum Dis Clin North Am, 1991. 17(2): p. 373-89.

126. Bjarnason, I., et al., Importance of local versus systemic effects of non-steroidal anti-inflammatory drugs in increasing small intestinal permeability in man. Gut, 1991. 32(3): p. 275-7.

127. Kirsch, M., Bacterial overgrowth. Am. J. Gastroenterol., 1990. 85: p. 231-237.

128. Stockbrugger, R.W. and U. Armbrecht, Bacterial overgrowth in the upper gastrointestinal tract and possible consequences: report of a workshop in Brussels, Belgium, 9-10 February, 1990. Microb. Ecol. Health Dis., 1991. 4: p. i-vii.

129. Brandt, J., B. L.H., and A. Wagle, Production of vitamin B12 analogues in patients with small-bowel bacterial overgrowth. Ann. Int. Med., 1977. 87: p. 546-551.

130. Giannella, R.A., S.A. Broitman, and N. Zamcheck, Competition between bacteria and intrinsic factor for vitamin B 12 : implications for vitamin B 12 malabsorption in intestinal bacterial overgrowth. Gastroenterology, 1972. 62(2): p. 255-60.

131. Playford, R.J., et al., Effect of luminal growth factor preservation on intestinal growth [see comments]. Lancet, 1993. 341(8849): p. 843-8.

132. Surawicz, C.M., et al., Treatment of recurrent Clostridium difficile colitis with vancomycin and Saccharomyces boulardii. Am J Gastroenterol, 1989. 84(10): p. 1285-7.

133. Surawicz, C.M., et al., Prevention of antibiotic-associated diarrhea by Saccharomyces boulardii: a prospective study. Gastroenterology, 1989. 96(4): p. 981-8.

134. Buts, J.-P., et al., Stimulation of secretory IgA and secretory component of immunoglobulins in small intestine of rats treated with Saccharomyces boulardii. 1990.

135. Eibl, M.M., et al., Prophylaxis of necrotizing enterocolitis by oral IgA-IgG: review of a clinical study in low birth weight infants and discussion of the pathogenic role of infection. J Clin Immunol, 1990. 10(6 Suppl): p. 77S-79S.

136. Siitonen, S., et al., Effect of Lactobacillus GG yoghurt in prevention of antibiotic associated diarrhoea. Ann Med, 1990. 22(1): p. 57-9.

137. Salminen, E., et al., Preservation of intestinal; integrity during radiotherapy using live Lactobacillus acidophilus cultures. Clin Radiol, 1988. 39: p. 435-437.

138. Oksanen, P.J., et al., Prevention of travellers’ diarrhoea by Lactobacillus GG. Ann Med, 1990. 22(1): p. 53-6.

139. Gorbach, S.L., T.W. Chang, and B. Goldin, Successful treatment of relapsing Clostridium difficile colitis with Lactobacillus GG [letter]. Lancet, 1987. 2(8574): p. 1519.

140. Klimberg, V.S., et al., Oral glutamine accelerates healing of the small intestine and improves outcome after whole abdominal radiation. Arch Surg, 1990. 125(8): p. 1040-5.

141. Souba, W.W., The gut-a key metabolic organ following surgical stress:Benefits of glutamine supplementation. Contem Surg, 1989. 35(5A): p. 5-13.

142. Souba, W.W., Glutamine: a key substrate for the splanchnic bed,. Annu. Rev. Nutr., 1991. 11: p. 285-308.

143. van der Hulst, R.R., et al., Glutamine and the preservation of gut integrity. Lancet, 1993. 341(8857): p. 1363-5.

144. Hagen, T.M., et al., Fate of dietary glutathione: disposition in the gastrointestinal tract. A,. J. Physiol., 1990. 259: p. G530-G535.

145. Cody, V., et al., ed. Plant Flavonoids in Biology and Medicine II. Biochemical, Cellular and Medicinal Properties. Progress in Clinical and Biological Research, Vol. 280. 1988, Aland R. liss, Inc.: New York. 481.

146. Vanderhoof, J.A., et al., Effect of dietary menhaden oil on normal growth and development and on ameliorating mucosal injury in rats. Am J Clin Nutr, 1991. 54(2): p. 346-50.

147. Stark, J.M. and S.K. Jackson, Sensitivity to endotoxin is induced by increased membrane fatty-acid unsaturation and oxidant stress. J Med Microbiol, 1990. 32(4): p. 217-21.

148. Eisenhans, B. and W.F. Caspary, Differential changes in the urinary excretion of two orally administered polyethylene glycol markers (PEG 900 and PEG 4000) in rats after feeding various carbohydrate gelling agents. J Nutr, 1989. 119: p. 380-387.

149. Gyory, C.P. and G.W. Chang, Effects of bran, lignin and deoxycholic acid on the permeability of the rat cecum and colon. J Nutr, 1983. 113: p. 2300-2307.

150. Shiau, S.Y. and G.W. Chang, Effects of certain dietary fibers on apparent permeability of the rat intestine. J Nutr, 1986. 116(2): p. 223-32.

151. Spaeth, G., et al., Food without fiber promotes bacterial translocation from the gut. Surgery, 1990. 108(2): p. 240-6.

152. Fukushi, T., Studies on edible rice bran oils. Part 3. Antioxidant effects of oryzanol. Rep Hokaido Inst Pub Health, 1966. 16: p. 111.

153. Yagi, K. and N. Ohishi, Action of ferulic acid and its derivatives as anti-oxidants. J Nutr Sci Vitaminol, 1979. 205: p. 127-135.