GF or Elimination diet? Which do I try first

[Jean]

Where to begin to find your food intolerances
There are two different ways to approach finding your food intolerances. You can begin on a gluten free diet and then go on to test for other food intolerances if you need to. Or, you can start by eliminating all possible offending foods on the elimination diet. There are advantages and disadvantages to both ways. It depends on you and your body. You have to decide what will work best for you.

Gluten Free First
There are some good reasons to consider starting on a gluten free diet before trying the elimination diet. If you are already gluten free, skip to Reasons for Starting with the Elimination Diet.

Gluten seems to be the common offending food in people who are multiple intolerant. The odds are that if you have food intolerances, gluten is one of them. Beginning with a gluten free diet will give your gut time to heal. As your gut heals, you will notice that your symptoms start to improve. For the elimination diet to work, it is important to be able to distinguish your normal symptoms from a food reaction. For example, if you have chronic diarrhea, it will be pretty hard to tell if you are reacting to a certain food, because your reaction will probably be diarrhea. Staying gluten free until you have solid stools will make your reactions much more obvious.

If you start the elimination diet before your gut has had time to heal, you may get false positives. That means that you will seem to react to foods that you aren’t truly intolerant of. They are just aggravating an already distressed digestive system. For example, people with frequent diarrhea often find that they can’t tolerate vegetables, especially raw ones. A few months on a gluten free diet usually makes those same veggies quite tolerable. It would be a shame if you considered them a food intolerance and avoided them for years. Remember, the point of the elimination diet is to only eliminate the foods we absolutely have to.

Another good reason to start with gluten is that there is a huge learning curve associated with eliminating foods from your diet. It is easiest to start with one. Once you have mastered gluten, it is much easier to eliminate other foods. Gluten is one of the most common and well-known food intolerances. It is one of the easiest to find information on. Some restaurants even have gluten free menus. Celiac organizations have done an excellent job of making the public aware of their disease. I bet as soon as you tell a few people that you are following a gluten free diet, you will find someone who is gluten intolerant. When I mentioned it at work, I found out that a friend’s mother has Dermatitis Herpetiformis. She turned out to be a wonderful person who brought me gluten free treats, took me to Celiac meetings and helped me get started on my diet.

When you undertake this diet, it is important to ask yourself what you are willing to do and when. Eliminating foods from you diet is a difficult thing to do. If you let yourself get overwhelmed, it is much more likely that you won’t stick to your diet. If you cheat on the elimination diet, intentionally or accidentally, you will have to spend more time on it or start over. Nobody wants to stay on the elimination diet any longer than they have to!

If you have been tested and have been diagnosed as gluten intolerant, it would be wise to start with the gluten free diet. There is a good chance that gluten is your only food intolerance. If you have also tested positive for other foods, you should definitely eliminate them at the same time. You may find that these are all of your intolerances, and you will never need to go on the elimination diet.

In my opinion, you should start on the gluten free diet first if your symptoms are rather severe. I would also take into consideration how long you have had symptoms. The longer you’ve been ill, the longer it will probably take for you to see improvement. Expect to be on the gluten free diet for three to six months before you’ll know if you need to look for other food intolerances.

Reasons for Starting with the Elimination Diet
One good reason to start with the elimination diet is that you are already gluten free and one or more things have happened. First, you had initial improvement but some of your symptoms have returned. Second, you feel better on the gluten free diet, but you don’t feel great. Third, you had no improvement on the gluten free diet. Before you start the elimination diet, be sure that you are not getting any hidden forms of gluten. You may want to check the list on gluten sources just to make sure you haven’t missed anything.

If you decide to start with the entire elimination diet, you will probably get better much faster. I think this is a good option for someone who has less severe symptoms. I also think it would be good for someone who has recently become ill. The important thing is to be able to tell when you are reacting to a food that you are testing.

[mjgarr]

I have been gluten free for about 3 weeks. I still have D. I have MC/LC. When should I expect to see some results? I have been tested by Enterolab. I am 13 on gluten, 1+ corn & chicken, 2+ oat. I think I am gluten free.

mjgarr

[tex]

The time can vary from a few days to a year or more for some of us. It took me about a year and a half. Without budesonide to mask the symptoms, it usually takes most people from a few weeks to 6 months or more to start showing signs of improvement. The time required depends on a lot of things, such as the amount of damage that has to be healed and how "clean" the recovery diet is. The gut heals very slowly.

And while corticosteroids such as budesoide can mask the symptoms while the diet changes are stopping the inflammation and healing the gut, corticosteroids actually slow down the healing process by stopping the inflammation. Believe it or not, inflammation is the first stage of healing and it's a necessary part of healing. It seems like a long time, but in most cases, the damage has been accumulating for a long time.

Tex

[Gabes-Apg]

what do you mean -

"I think I am gluten free"

if you are having bland safe proteins and safe veges, avoiding processed food items, (food and drink) then the risk of gluten in your eating plan is very low.
what is your current eating and drinking plan?
have you checked toothpaste, lipbalms, makeup etc for Gluten?
do you share the kitchen with others that are eating gluten?

[mjgarr]

My eating and drinking are as follows: One to two cups coffee and the rest of the day plain water. I have chicken broth, turkey broth. Some white rice, very soft carrots. Very soft squash. Rice cakes. Rice checks. I still have D.

mjgarr

[Gabes-Apg]

with the coffee,
are you having it black? or with creamer or milk etc
what type of coffee? some instant coffee can have gluten

you are having the chicken and turkey broth, but are you having servings of meats / proteins?
the broths - are they home made?
how are you cooking the vegetables? just with water or bone broth and plain salt?

the rice cakes and rice checks - I am not sure what rice checks are?


do you share the kitchen with others? are they having gluten based products?
did you get new cookware, chopping board, utensils when you started gluten free eating?

[mjgarr]

I have my coffee black and no instant coffee.

The broths are home made. I have servings of meats also. My vegetables are mostly cooked in water. Some in broth with plain salt.

Rice checks are cereal.

I share a kitchen with my sig. other who doesn't have gluten based products. I didn't get new cookware or anything else when I started gluten free eating.

mjgarr

[tex]

If you meant Rice Chex (by General Mills), they should be safe. If that's what you meant, your diet sounds safe. You probably just need more healing time. You may see improvement any day.

If you are having watery D, something is wrong. But if it's just ordinary D, you're probably on track.

Tex

[mjgarr]

My D is watery. I don't know why. It is Rice Chexs by General Mills.

mjgarr

[tex]

OK, now we're getting somewhere. It might be the chicken (and chicken broth). Turkey or lamb would be safe substitutes. Even though EnteroLab rates chicken as just a 1+ sensitivity for you, chicken can become a high-histamine food as it ages and your symptoms may be triggered by the excess histamine. This is especially true if you sometimes experience itching, a rash, sneezing, runny nose, watery eyes, a facial or chest flush, or any other common allergy symptom immediately after eating chicken or chicken broth.

I know it's possible because I have that problem. Chicken is fine when I eat it immediately, but when it ages a day or so, I begin to react to it (or soup or broth), and it gets worse and worse with each passing day, because the histamine level skyrockets with each additional day of aging.

A few people react to the Chex cereals, so that's a remote possibility. That used to happen, but I'm not sure if it happens any longer. General Mills may have cleaned up their act in recent years.

Tex

[mjgarr]

You are so right on. During and after chicken or the broth I get watery eyes, sneezing, etc. I also get that with turkey sometimes. I was not tested with Enterolab for turkey. What other stuff has high histamines? Corn was also 1+ sensitivity. Should I stay away from that also?

mjgarr

[tex]

Corn is probably safe. It's normally not a high-histamine food. Turkey might be a problem because of the histamines, though it shouldn't be as bad a problem as chicken.

You can Google high-histamine foods for a list, but mostly they include fish, chicken, ripe bananas and other ripe fruit, and pickled, dried, smoked, or fermented foods. Many of the foods listed as high-histamine are only high-histamine under certain conditions

Here's a quote from the book I'm currently working on. This is just a first draft, it's not necessarily the final edited version. But you may find it helpful for understanding the problem.

Histamine is responsible for most of the classic allergy symptoms that we experience if we have a pollen allergy or some other type of allergy. The runny nose, watery eyes, itching, and in severe reactions, the anaphylactic symptoms such as airway restriction and breathing difficulties are caused by the release of histamine from mast cells, basophils, and eosinophils. The redness and swelling that develop following a mosquito bite or a wasp sting are due to the release of histamine in the tissues surrounding the bite or sting.

Histamine causes increased permeability of the small blood vessels (capillaries) in the area in order to allow white blood cells to pass from the capillaries into the surrounding tissues to engage any pathogens or toxins that might be present. The inflammation resulting from the histamine and the white cells, along with the fluids from the bloodstream that also flow into the area, cause the redness and swelling.

In the body, histamine is derived from histidine, which is an essential amino acid. Because humans cannot produce histidine, it must be present in the diet. However, certain species of gut bacteria can produce histidine, and it's conceivable that the evolutionary changes that have taken place in our gut bacteria profiles in recent decades due to increased antibiotic use and the expanded use of ingredients and chemicals in processed foods may play a part in the trend toward increasing histamine problems.

Many authorities have long suspected that MC may be caused by gut bacteria imbalances.
But to date, no researcher or research team has ever been able to verify that this is even a valid possibility, let alone likely. What follows is a theory (my own) — a description of a mechanism by which this might occur.

If histamine can cause increased permeability of blood vessels, then it doesn't take much of a stretch of the imagination to recognize that it may well also be capable of causing increased permeability of the intestines, because the epithelial lining of both blood vessels and the intestines are quite similar. And because the intestines are specifically designed so that nutrients can pass from the lumen (the interior volume of the intestines) into the blood vessels present in the intestinal walls, for distribution throughout the body, similarity of design of the 2 interfaces in order to accommodate this vital function would be expected.

We learned in the first edition of Microscopic Colitis that increased intestinal permeability is a side effect of gluten sensitivity that leads to the development of food sensitivities, so now we can see how excess histamine in the intestines could easily trigger existing food sensitivities, or possibly promote the development of additional food sensitivities. So now all that is lacking in this scenario in order to provide the potential for excessive histamine levels capable of causing a leaky gut and triggering intestinal inflammation is a gut bacteria population shift toward higher percentages of histidine-producing species, and a mechanism for promoting the conversion of histidine to histamine.. And it just so happens that such a mechanism happens to be very, very common in IBD patients — a magnesium deficiency.

Here's a little more information from my notes, but this will surely be edited in the final version. I'll copy it here because this includes an explanation of how histamine is created in the body and how the amount of histamine is managed. And I'm including it here mostly because you may be a perfect example of an MC patient for whom this applies.

Many MC cases that are unresponsive to treatment may be associated with an undiagnosed magnesium deficiency.
Magnesium deficiency is very common in the general population. In fact, many authorities insist that a majority of the population in developed countries are magnesium-deficient. And magnesium deficiency is even more likely among MC (and other IBD) patients because not only do both the malabsorption problem and diarrhea associated with the disease deplete magnesium, but the most common medical treatment used to suppress the inflammation, corticosteroids, also depletes magnesium.

Histidine decarboxylase is the enzyme used by the body to convert histidine into histamine. It's known that a magnesium deficiency increases the activity of histidine decarboxylase, thereby increasing the conversion of histidine into histamine. But a magnesium deficiency can lead to a double whammy in this situation, because it also reduces the activity of diamine oxidase enzyme (DAO). As we discussed in the first edition of Microscopic Colitis, DAO is the enzyme primarily used by the body to purge unused or excessive amounts of histamine in circulation, in order to prevent the possibility of a potentially harmful histamine buildup.

So with the potential for a significant increase in histamine production, and a reduced ability to remove excessive amounts of histamine from the body, clearly a magnesium deficiency is likely to significantly increase the risk of a histamine buildup that can lead to various problems with the digestive system and elsewhere. And this can occur with or without a shift in the gut bacteria population balance to an increased percentage of histidine-producing bacteria. Obviously if gut bacteria begin to promote an increase in histidine production concurrent with a magnesium deficiency, this could create the potential for a perfect storm of inflammation due to an inappropriate level of mast cell activity. And the likelihood that this would become a chronic condition means that it would impose a significantly increased risk of triggering and/or perpetuating a microscopic colitis flare.

Note that this can happen independently of any T cell-based inflammation that might currently be present. Theoretically it can occur even if no T cell-based inflammation is present. Or it can occur when a combination of the 2 modes of inflammation exceed the threshold at which a reaction is triggered. It's possible that there might even be a synergistic effect between the 2 types of inflammation. And in such a situation, logic dictates that as long as the total sum of the inflammation exceeds the threshold at which a reaction is maintained, remission cannot occur.

And because diamine oxidase enzyme requires vitamin B-6 for activation, the deficiency of B vitamins that so commonly occurs over the long term because of the malabsorption problems associated with MC and other IBDs can significantly add to the problem of histamine buildup by preventing DAO from functioning properly. Laboratory experiments have shown that increased vitamin B-6 intake can result in higher DAO activity levels. Whether or not this correlates with improved performance in the real world remains to be seen.

Could it be that the combination of antibiotic use and a magnesium deficiency is the real key in many cases?
As mentioned earlier in chapter 3, many antibiotics and various other drugs tend to significantly deplete magnesium. And many MC patients point to antibiotics as the cause of their disease. So according to my theory, here is how this cascade of events unfolds to explain why antibiotics trigger microscopic colitis for so many people:

Antibiotics not only disrupt gut bacteria populations to provide the potential for histidine-producing bacteria to become better established, but they also severely deplete magnesium. And as we discussed a couple of pages back, magnesium deficiency not only increases the activity of histidine decarboxylase, thereby increasing the conversion of histidine into histamine, but it also reduces the activity of diamine oxidase enzyme thereby compromising the ability of the body to purge excess histamine from the body This sets up an ideal environment for significantly increased mast cell activity and and an inflammatory histamine condition.

Forbes et al. (2008) has demonstrated that when stimulated by interleukin-9, increased mast cell activity can cause increased intestinal permeability that leads to food sensitivities.2 Note that this basically mimics the action of gliadin peptides in wheat gluten, which activate zonulin to cause increased intestinal permeability independent of genetics associated with autoimmunity (Drago et al., 2006).3 In other words, gluten causes increased intestinal permeability in all individuals, not just in those who have a gene associated with celiac disease.

Likewise, the conditions described above appear to provide another mechanism that can lead to leaky gut. This opens the door to a totally independent way for food sensitivities to not only develop, but to be perpetuated, and this is essentially unexplored by medical researchers. And while this may occur independent of any genetic limitations, it seems likely that genetics may play a role due to the fact that MC tends to run in families. It's also possible that MC may run in families because of similar environmental associations, rather than genetic links.

But remember that a magnesium deficiency can promote the conversion of histidine to histamine without a gut bacteria population shift. Obviously a much more robust effect would occur if the use of an antibiotic promoted the proliferation of histidine-producing bacteria, but it also appears apparent that this mechanism should be capable of triggering MC independent of an event associated with the use of an antibiotic.

If this theory can be verified, it appears to define a mechanism by which MC can be triggered independently of T cell inflammation, which is currently considered to be the cause of the inflammation that's associated with the disease. Because lymphocyte-induced inflammation is a diagnostic marker for the disease (LC), this raises an interesting question. "Are there any undiagnosed cases of MC that involve only mast cell-induced inflammation (apart from mastocytic enterocolitis), or do all cases involve T cell inflammation?"

Lymphocytic infiltration is a diagnostic prerequisite for lymphocytic colitis, and it is virtually always present even in collagenous colitis cases. And if it is absent, and no collagen band thickening can be detected in colonic biopsy samples under the microscope, then neither LC nor CC can be diagnosed. But does that mean that MC cannot exist in such a situation? What if the mechanism I have described above is an alternative source of inflammation that can lead to the clinical symptoms normally associated with MC?

If all cases of MC involve lymphocyte-promoted inflammation (by definition), then either all cases initiated by mast cell inflammation soon lead to lymphocytic infiltration, or mast cell-based inflammation (as described above) is secondary to the lymphocyte-based inflammation typically attributed to MC. Otherwise, there is no way that it could be diagnosed under the current diagnostic criteria.

Tex

[rudi]

Hi Rudi again,
I was wondering if pasta made from corn is safe? Namely Burilla (sp?) brand.

[tex]

Yes. If corn works for you, that should be safe. Just check the label to make sure that it doesn't contain anything that causes you to react. The fewer ingredients, the better. I've never tried that particular brand, but I've tried others, and they were excellent when prepared according to the directions.

Tex