3 months into stage 1 diet, still struggling w/ D

[RanchGal424]

Hi all,

I am hoping to provide an update on where I am at with my diet and get your thoughts on the next steps that I plan to pursue in my quest for remission.

For the past 3 months I’ve been following a strict diet based on the stage one eating plan suggested here and also based on my results from Enterolab. However, I am still having watery D anywhere from 3-6 times per day. Although this is an improvement, I still know that something is not quite right.

I get about 80% of my calories from quality “safe” protein (grass fed, organic, and/or wild meats) and 20% from veggies (mainly squash, zucchini, carrots, potatoes) cook everything myself, use only California olive oil or pork or duck fat, or coconut oil for cooking, and use only salt for seasoning. I drink some coffee in the morning with coconut milk (the canned kind with zero gums or additives) and a small amount of turbadino sugar (sugar in the raw). I take magnesium and vitamin D in liquid form. I drink a little bit of soda water with stevia to drown out the bad taste of the liquid magnesium.

Really, that’s it. I occasionally have a banana, and sometimes a Lara Bar that has only peanut and dates if I’m somewhere where I cannot access a protein based breakfast (ex. work travel) My Enterolab test results showed I am not sensitive to soy, so this is why I occasionally eat peanut based bars (but never whole peanuts as I know these are tough to digest).

I am so tired of the 100% liquid watery D. There is still urgency during the day and at night. As a next step, I think I am going to try eliminating all lectins- no peanuts, squash, soy, or potatoes- for 30+ days and see if I see any remote improvement.

What do you think of this plan? I am not looking for remission yet, but at least some slight change in the consistency and urgency of my D.

Thank you everyone, I am so grateful for your insights!

Ranch Gal

[tex]

Here's my 2 cents worth: I believe you're certainly on the right track, and you might just need more healing time, but I believe I would skip the magnesium (especially in liquid form — that can be potent stuff) for a day or so, to see what effect that might have. Brandy has demonstrated by personal experience that sometimes we have to avoid all supplements during a flare in order to break out of the flare (reach remission).

I agree that minimizing lectins in your diet should help. They are definitely inflammatory for our digestive system. This may be TMI, but if you want to consider inflammation caused by other anti-nutrients, here's a quote from Understanding Microscopic Colitis that provides some insight into this issue:

What type of antinutrients are likely to cause problems?
There are many known different types of these defensive mechanisms, but the most notable examples tend to cause symptoms ranging from irritating to toxic. Some of the antinutrients for which research data have been published include (but are not limited to) lectins, chitins, benzoxazinoids, and amylase trypsin inhibitors (ATIs) Because predators (including humans) typically learn to avoid plants that cause obvious symptoms, those plants are usually avoided, or not even considered to be food. It's the plants that cause more subtle or delayed symptoms that tend to be the most troublesome, because the cause of the problem may not be easily recognized.

Lectins are a well-known cause of digestive problems.
They can bind to cell membranes and they can cause sugar molecules to stick together, a process known as agglutination (Sullivan, 2016, October 5).14 Over three decades ago the wheat germ agglutinin (in wheat) was shown to be a lectin (Kolberg, & Sollid, 1985).15 The agglutinating properties of gluten are what make the molecules in bread dough stick together and allow it to be kneaded. Lectins normally are not affected by gastric acid or digestive enzymes, so they tend to remain undigested. That means that they retain their antagonistic properties while passing through the digestive system. They can bind to cell membranes in intestinal walls, arteries, and organs, resulting in irritation and possible cellular damage.

Do lectins cause leaky gut?
Clearly, because wheat germ agglutinin is a lectin, that implies that at least some lectins can cause leaky gut. Some of the most common sources of lectins are grains, legumes, dairy, and nightshades. And it's probably not a coincidence that the 8 most common allergens (wheat, dairy, soy, eggs, peanuts, tree nuts, fish, and shellfish) contain some of the highest amounts of lectins. Lectins are probably the main reason why a low-carbohydrate diet works so well to prevent heartburn, gastroesophageal reflux disease (GERD), and sometimes other digestive system problems (because a low-carbohydrate diet reduces lectin intake). Fortunately the problems caused by many lectins can often be minimized by proper cooking methods, but some of them cannot be degraded sufficiently by cooking, so they still cause problems for many individuals.

Certain carbohydrates (specifically mono and oligosaccarides) can bind specific lectins and prevent them from attaching to cell membranes (Sullivan, 2016, October 5). N-acetyl-glucosamine (aka N-acetyl-D-glucosamine, GlcNAc, or NAG) is an enzyme occurring naturally in the body. It's the main binding target of wheat lectin. Therefore it seems reasonable to suspect that this may be the reason why glucosamine compounds have the ability to protect cells in cartilage and possibly in the intestines from inflammation damage associated with gluten-induced arthritis. If the lectins bind to a glucosamine supplement, they can't bind to cells in the body. This implies that the arthritis symptoms associated with MC and other IBDs may be reduced by taking an over the counter (OTC) glucosamine product. In practice, many MC patients and others who suffer from gluten-induced arthritis have found that glucosamine does indeed help to relieve joint pains.

The outer shell (exoskeleton) of insects and crustaceans is made of a polymer known as chitin.
Some authorities claim that because chitins consist primarily of long polymers of n-acetyl-glucosamine (the primary binding target of wheat lectin), they are functionally equivalent to wheat gluten (Mercola, (2011, July 5).16 If that's the case, then foods that contain significant amounts of chitin, such as barley, rye, rice, tomato and potato should cause major digestive problems. And of course barley and rye do indeed cause the same intestinal damage and clinical symptoms as wheat (because they are closely related to wheat).

But for most people (including MC patients) of all the grains, white rice is typically the least likely to cause inflammation or digestive problems. The same cannot be said for brown rice. The difference between brown rice and white rice is primarily in the husk, which is removed from white rice. And of course the husk contains most of the chitin. Tomatoes are not well-tolerated by many MC patients, but this may be because they are actually a citrus fruit, and citrus fruits are not well-tolerated by the majority of MC patients. While potatoes cause digestive problems for some MC patients, many can tolerate potatoes quite well. So in the real world, while chitins may be a problem for some, they may or may not be a category of antinutrients that cause a significant level of digestive problems for most people (or most MC patients).

Do chitins cause leaky gut?
Based on the effects on the digestive system of foods that contain significant amounts of chitin, it appears that the jury is still out, because the food-based evidence appears to be inconclusive. We already know that barley and rye cause leaky gut, but rice, potato and tomato have not been shown to do so.

However, certain pathogenic organisms that sometimes invade the digestive system may be examples of how chitins can cause leaky gut. All pathogenic fungi contain chitin in their cell walls (Lenardon, Munro, & Gow, 2010).17 The outer wall of the mycelia (roots or feeding tubes) of Candida albicans are made of chitin. And it's well known that Candida roots penetrate the epithelial layer of human intestines. It's also well known that Candida causes leaky gut. So there is no question that certain situations associated with chitins lead to leaky gut.

Sprouted grains are touted by many as beneficial for health.
But Mercola (2011, July 5) warns of the dangers of sprouted grains, pointing out that they contain benzoxazinoids (Bas), known to be a toxin, and sprouted whole wheat contains some of the highest amounts of wheat lectin. While it's true that the cereal grains (including wheat, rye and corn (maize) contain Bas that are utilized as a defensive mechanism primarily against certain insect pests and competing weeds, rye has by far the most potent effect (Makowska, Bakera, & Rakoczy-Trojanowska, 2015).18 Corn can cause digestive problems for a relatively small percentage of people, but compared with other foods known to cause significant digestive issues, corn appears to rank somewhat low on the overall scale.

Do benzoxazinoids cause leak gut?
While there doesn't appear to be any medical proof that they do, their presence certainly doesn't enhance digestion in any way. And it's possible that the additional stress that they impose on the digestive system, when added to the accumulated issues caused by other antinutrients in the same foods, or in other foods in the diet, may at least contribute to the development of leaky gut.

Do amylase trypsin inhibitors cause leaky gut?
Amylase enzyme is produced and used by the body to digest carbohydrates, and trypsin enzyne is produced and used by the body to digest proteins. It's been known for decades that legumes (including various beans and soy) contain not only lectins, but also inhibitors of amylase and trypsin (Savelkoul, van der Poel, & Tamminga, 1992).19 But more recent research data published by Junker et al. (2012) has shown an association between wheat amylase trypsin inhibitors and the activation of toll-like receptor 4 (TLR4).20 TLR4 is known to promote inflammation.

This discovery has prompted renewed interest in the cause of celiac disease. On the Internet there are even blogs claiming that gluten is not the cause of celiac disease. Instead, amylase trypsin inhibitors are claimed to be responsible. At least one blog even claims that celiac disease is due to the selective breeding techniques used half a century ago to create genetic changes in wheat intended to improve pest resistance.

While that sounds like a plausible observation, it totally ignores the history of medicine.
Celiac disease was first described in the medical literature approximately 2,000 years ago, not 50 years ago (Guandalini, 2007, summer. p. 1).21 In fact, prior to the 1920s, the medical community didn't have the foggiest idea what caused celiac disease, so they had no idea how it should be treated. For a relatively simple disease (gluten sensitivity), with a simple cure (avoid gluten), why has it taken the medical community almost 2,000 years to figure it out, and why are they still not sure they've figured it out?

TLR4 activation has been shown to cause leaky gut.
It has long been known that chronic alcohol exposure causes increased intestinal permeability, and Li et al. (2013) showed that the mechanism by which this occurs is associated with the activation of TLR4.22

Chronic ethanol treatment significantly elevated blood endotoxin levels, intestinal permeability, and the expression of TLR4 in the ileum and colon. Moreover, ethanol exposure reduced the distribution of phosphorylated occludin in the intestinal epithelium because of PKC activation. In conclusion, chronic ethanol exposure induces a high response of TLR4 to lipopolysaccharide (LPS), and TLR4 increases intestinal permeability through down-regulation of phosphorylated occludin expression in the intestinal epithelial barrier, accompanied by membrane PKC hyperactivity. (p. 459)

Therefore, amylase trypsin inhibitors promote leaky gut.
So it appears that it's likely that lectins, chitins, benzoxazinoids, amylase trypsin inhibitors, and possibly other antinutrients may play a role in the development of leaky gut. Whether their respective individual effects are major contributors to the development of digestive system disease, or they turn out to be relatively insignificant, remains to be seen. But one thing we know for sure — grains are associated with all of these issues and legumes are associated with the most potent offenders such as lectins and amylase trypsin inhibitors. In view of all the possible ways by which leaky gut can be induced by the foods that most people eat every day, is it any wonder that food sensitivities are so common?

TLR4 has been shown to be associated with IBDs.
The association of amylase trypsin inhibitors with TLR4 activation appears to have special significance for IBD patients. In research data published in 2005, Oostenbrug et al. showed that TLR4 is associated with both Crohn's disease and ulcerative colitis.23 Using mice that had been genetically modified to overproduce the active form of TLR4 in the epithelium of the intestine, Fukata et al. (2011) showed that this characteristic increased the vulnerability of the mice to chemically-induced colitis.24 Mice that have been genetically modified to overproduce TLR4 are known as villin-TLR4 mice. Furthermore, Fukata et al. (2011) concluded that the regulation of toll like receptors affects the outcome of both colitis and associated cancers, and therefore it might have potential as a way to help prevent or treat colitis and the cancers that have been shown to be associated with IBDs.

The discovery that amylase tripsin inhibitors provoke the activation of TLR4-based inflammation fully validates non-celiac gluten sensitivity.
Whether the propensity of amylase trypsin inhibitors to activate TLR4 turns out to be the primary mechanism by which wheat promotes the pattern of inflammation known as celiac disease remains to be seen. But regardless of whether or not that's the case, the potential inflammatory effects of not only amylase trypsin inhibitors, but possibly all of the antinutrients discussed here should equally apply to non-celiac gluten sensitivity. Why? Because TLR4 is part of the innate immune system. That makes it an equal opportunity inflammatory agent, independent of the HLA-DQ2 and HLA-DQ8 genes commonly associated with celiac disease. In other words, it's not necessary for the immune system to develop a sensitivity to any foods that provoke a TLR4 response because all humans are born with that sensitivity.

In support of the above claim (about the ability of other antinutrients to provoke an innate immune system response), it should be noted that both lectins and chitins bind to TLR4 (Unitt, & Hornigold, 2011, Koller, Müller-Wiefel, Rupec, Korting, & Ruzicka, 2011).25,26 This could well be a game-changer for the understanding and treatment of inflammatory bowel diseases and autoimmune diseases in general, because they are all associated with the inflammatory consequences of food sensitivities.

Here are references 14–26 from that quote:

14. Sullivan, K. (2016, October 5). The lectin report. Krispin's Komments on Nutrition and Health. Retrieved from http://www.krispin.com/lectin.html

15. Kolberg, J., & Sollid, L. (1985). Lectin activity of gluten identified as wheat germ agglutinin. Biochemical and Biophysical Research Communications, 130(2),867-72. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/3839672

16. Mercola, J. (2011, July 05). These five foods may cause problems very similar to wheat. Mercola.com, Retrieved from http://articles.mercola.com/sites/artic ... ealth.aspx

17. Lenardon, M. D., Munro, C. A., & Gow, N. A. R. (2010). Chitin synthesis and fungal pathogenesis. Current Opinion in Microbiology, 13(4), 416–423. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2923753/

18. Makowska, B., Bakera, B., & Rakoczy-Trojanowska, M. (2015). The genetic background of benzoxazinoid biosynthesis in cereals. Acta Physiologiae Plantarum, 37(1), 176. Retrieved from http://link.springer.com/article/10.100 ... 015-1927-3

19. Savelkoul, F. H., van der Poel, A.F., & Tamminga, S. (1992). The presence and inactivation of trypsin inhibitors, tannins, lectins and amylase inhibitors in legume seeds during germination. A review. Plant Foods for Human Nutrition, 42(1), 71-85. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/1372122

20. Junker, Y., Zeissig, S., Kim, S.-J., Barisani, D., Wieser, H., Leffler, D. A., . . . Schuppan, D. (2012). Wheat amylase trypsin inhibitors drive intestinal inflammation via activation of toll-like receptor 4. Journal of Experimental Medicine, 209(13), 2395–2408. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3526354/

21. Guandalini, S. (2007, summer). A brief history of celiac disease. Impact, The University of Chicago Celiac Disease Center. 7(3). Retrieved from https://www.cureceliacdisease.org/wp-co ... .News_.pdf

22. Li, X., Wang, C., Nie, J., Lv, D., Wang, T., & Xu, Y. (2013). Toll-like receptor 4 increases intestinal permeability through up-regulation of membrane PKC activity in alcoholic steatohepatitis. Alcohol, 47(6), 459–465. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/23871536

23. Oostenbrug, L. E., Drenth, J. P., de Jong, D.J., Nolte, I. M., Oosterom, E., van Dullemen, H. M., . . . Jansen, P. L. (2005). Association between Toll-like receptor 4 and inflammatory bowel disease. Inflammatory Bowel Diseases, 11(6), 567-575. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/15905704

24. Fukata, M., Shang, L., Santaolalla, R., Sotolongo, J., Cristhine Pastorini, C., España, C., . . . Abreu, M. T. (2011). Constitutive activation of epithelial TLR4 augments inflammatory responses to mucosal injury and drives colitis-associated tumorigenesis. Inflammatory Bowel Diseases, 17(7), 1464–1473. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3117047/

25. Unitt, J., & Hornigold, D. (2011). Plant lectins are novel Toll-like receptor agonists. Biochemical Pharmacology, 81(11), 1324-1328. Retrieved from https://www.ncbi.nlm.nih.gov/pubmed/21420389

26. Koller, B., Müller-Wiefel, A. S., Rupec, R., Korting, H. C., & Ruzicka, T. (2011). Chitin modulates innate immune responses of keratinocytes. PLoS ONE 6(2), e16594. Retrieved from http://journals.plos.org/plosone/articl ... ne.0016594

If doing that doesn't help significantly, I would ask my doctor for a prescription for cholestyramine (the original Sandoz version, not some other brand, and definitely not a "Lite" version), and experiment with the dosing for at least a few weeks, or until I saw significant improvement [(in case Bile Acid Malabsorption (BAM) is causing the continued WD]. Your GP should be willing to phone in a prescription to your pharmacy of choice without requiring an office visit, since you have a diagnosis of MC. If you do this, be aware of the need to separate taking the cholestyramine from meals or taking any other medications because it will bind most meds and nutrients. The cholestyramine should be taken at least 4 hours before any meal (or before taking any other medication), or at least 2 hours after a meal, or after taking other medications.

I hope this helps. Maybe someone else has some better suggestions.

Tex

[brandy]

Hi Ranch Girl,

Sorry you are suffering. I'd eliminate the oral magnesium for 7 days and the liquid D for a couple of days.
I'm not sure where you live. If in warmer climates try to get some sun mid day. In lieu of the oral magnesium
you can switch to epsom salt baths or lotion mag (in the epsom salt area) from walmart. I prefer the
epsom salt foot baths or baths over the lotion mag as the lotion mag makes me itch but others swear by the
lotion mag.

You should see improvements pretty quickly eliminating the oral mag. Like in several days.

Utilize meditation tapes/ prayer. I found WD itself rose my stress levels so when I have WD I try to do a 3-5 minute
meditation/prayer every 2 hours (I set my cell alarm). This keeps my stress down.

If you decide to go prescription drug route the cholysteramine (not spelled right) is more benign and less side effects than the
budesonide. (I've used both.)

IT IS POSSIBLE TO GET TO NO WD WITHOUT DRUGS. My first time I got to "soft serve" once a day through diet alone.
I went on budesonide from pressure from my boss.

My second 9 month reflare I got to remission from diet alone but eliminating oral supplements was key. I was struggling
until I eliminated the oral magnesium.

Good luck, keep us posted. Jean (JFR) went into remission eating mostly protein. You can read her story on the success story area.

[RanchGal424]

Tex, Brandy:

Thank you so much for your insight and advice. It is greatly appreciated! I love that this group is so supportive- having MC can be very lonely since others directly around me don’t really understand the struggle. I will try your suggestions and keep you posted on my progress!

Ranch Gal

[brandy]

Hi Ranch Gal,

I took a look at your food plan and it is generally safe. I can probably eat a lara bar now but it would be problematic with WD.
Believe me I get it that travel work breakfasts are tough. Can you eat hard boiled eggs and a banana for a travel work breakfast?
A lot of times I'll eat bacon on travel work breakfasts. Also avacado and bananas, also hard boiled eggs.

Keep us posted.