The Problem With Vitamin E Supplements (tocopherols) for People Who Are Sensitive to Soy

This is a glimpse of some of the information that will be discussed in my next book.  Please be aware that the details of this text are subject to change in the final version when the book is published.  This post is for informational purposes only, and should not be considered to be medical advice.  While this information is thought to be correct, some of it may be incomplete, and at this point it may not be verified by published medical research data.


Vitamin E can be found listed on labels in various forms, including d-alpha tocopherol, dl-tocopherol, alpha tocopherol acetate, mixed tocotrienols, tocopheryl acetate, and vitamin E succinate. Most of these (other than the first two) are very ambiguous terms. The topic of the safety of vitamin E for anyone who is sensitive to soy comes up often.

Natural vitamin E (in food) occurs in eight different chemical forms, called isomers:

alpha tocopherol
beta tocopherol
delta tocopherol
gamma tocopherol
alpha tocotrienol
beta tocotrienol
delta tocotrienol
gamma tocotrienol

Note that the first 4 are tocopherols, while the other 4 are tocotrienols. It was initially thought that only alpha tocopherol is needed for human nutrition. So supplements that contain natural vitamin E typically only contain alpha tocopherol, and this is designated on labels as d-alpha-tocopherol. Unfortunately most of those supplements are derived form soy oil because of its relatively low price.

But about 99 % of the vitamin E supplements that are available, use synthetic alpha-tocopherol, designated as dl-alpha-tocopherol. Research shows that most synthetic vitamin E supplements are very poorly absorbed, so most health advocates shy away from synthetic vitamin E supplements. Synthetic forms of vitamin E are only about half as effective as natural forms of vitamin E. And unfortunately, virtually all vitamin E supplements (whether natural or synthetic) contain only a single isomer of vitamin E (based on alpha tocopherol).

But research shows that gamma tocopherol is actually the most common isomer found in food. In fact, roughly 70 % of the vitamin E found naturally in food is in the form of gamma tocopherol. That predominance in itself suggests that totally ignoring this isomer in vitamin E supplements is probably counterproductive. It’s certainly counterintuitive at the very least. Why is this important? Because when only alpha tocopherol is supplemented, this tends to significantly deplete gamma tocopherol levels in the body because gamma tocopherol is needed by the body in order to reduce inflammation and regulate certain factors that protect against certain diseases (including certain cancers) (Moyad, Brumfield, &Pienta, 1999, Jiang, Christen, Shigenaga, & Ames, 2001).1, 2 Gamma tocopherol is also known to activate genes that protect against Alzheimer’s disease.

So clearly, virtually all vitamin E supplements (whether natural or synthetic) are contraindicated for the prevention of certain diseases, including cancer and Alzheimer’s, simply because they exclude gamma tocopherol, and because of that shortcoming, they tend to deplete existing supplies of gamma tocopherol in the body. The obvious goal should be to try to get vitamin E from food, not from supplements, and not from processed foods that are enriched with vitamin E in the form of various tocopherols.

Vitamin E is available in various foods, including almonds, sunflower seeds and oil, safflower oil, olive oil, spinach and other dark green leafy vegetables, broccoli, squash, shellfish, many fish, avocados, and certain fruits and berries. Most people who have MC can tolerate many of those foods, so it shouldn’t be necessary to use any vitamin E supplements. And of course vitamin E is also available in peanuts and soybean oil, and in tomatoes, but most of us find it necessary to avoid those foods.

But most people who have MC are not concerned so much with getting enough vitamin E from food — they’re much more concerned about accidentally ingesting a form of tocopherol derived from soy. As far as processed foods in general are concerned, far too many of them are “enriched” with some form of vitamin E, and the trick is to figure out which form of vitamin E is used, to determine whether or not it’s safe to use. A “Soy-Free” banner on the label of the product cannot be relied upon, because most label designers do not recognize natural forms of tocopherols as a derivative of soy.

When natural forms of vitamin E are used (d-tocopherol), unless the source of the ingredient is otherwise specified, it’s safest and usually most accurate to assume that the source is soy (because that’s what it’s usually made from). When the type of vitamin E is listed on the label as dl-alpha-tocopherol, or as synthetic vitamin E, then it does not contain any soy derivatives.

Any ingredient “extracts” should also be viewed with suspicion because in many cases the extraction medium used is soy oil. A good example of this is the rosemary extract found in most processed turkeys these days. Pure rosemary should be safe for most people who have MC, but rosemary extract may cause problems for anyone who is sensitive to soy.

Here are references 1 and 2 for this post:

1. Moyad, M. A., Brumfield, S. K., &Pienta, K. J. (1999). Vitamin E, alpha- and gamma-tocopherol, and prostate cancer. Seminars in Urologic Oncology. 17(2), 85–90. Retrieved from

2. Jiang, Q., Christen, S., Shigenaga, M. K., & Ames, B. N. (2001). Gamma-Tocopherol, the major form of vitamin E in the US diet, deserves more attention. American Journal of Clininical Nutrition, 74(6) 714–722. Retrieved from

The Apparent Connection Between Microscopic Colitis or other IBDs and Neurodegenerative Diseases

Here is a quoted section from chapter 9 of my new book on Microscopic Colitis.  Please be aware that the details of this text are subject to change in the final version when the book is published.  This post is for informational purposes only, and should not be considered to be medical advice.  While this information is thought to be correct, some of it may be incomplete.

The brain fog that often develops with MC may have a sinister side.

MC appears to be associated with neurodegenerative diseases such as Alzheimer’s, Parkinson’s and amyotrophic lateral sclerosis, or ALS. This association hasn’t yet been proven, but all of these diseases seem to have a gastrointestinal connection. For example, patients who have Parkinson’s disease have been shown to have different gut biomes than people who do not have the disease. Furthermore, Parkinson’s patients have been shown to have had gastrointestinal issues decades before their Parkinson’s symptoms developed.

According to The Michael J Fox Foundation, almost 80 % of Parkinson’s patients have constipation that usually begins several years prior to the development of Parkinson’s symptoms (Dolhun, 2014, December 08).1 Furthermore, not only do Parkinson’s patients have altered gut biomes, but Parkinson’s patients with different types of motor symptoms, have unique populations of gut bacteria that coordinate with the types of symptoms. For example, Parkinson’s patients with more severe balance and gait problems have more Enterobacteria than others.

All Parkinson’s patients have fewer Prevotella bacteria than normal people (Ghaisas, Maher, & Kanthasamy, 2016).2 So do autistic children, incidentally. Interestingly, this bacterium normally helps to produce thiamine and folate vitamins. Perhaps this is a clue.

According to The Michael J Fox Foundation, a protein that’s found in clumps in the brains of all Parkinson’s disease patients (known as alpha-synuclein) can be found in certain other locations in the body outside of the brain, including the enteric nervous system —the nerves that control the digestive system, sometimes called the second brain (Dolhun, 2014, December 08). The question yet to be answered concerns whether alpha-synuclein might develop first in the gut and then eventually spread to the brain where it causes motor symptoms.

Delayed gastric emptying is a common symptom for Parkinson’s disease patients.

Working from the prior knowledge that Parkinson’s patients have lower vitamin D levels than people who don’t have Parkinson’s, Kwon et al. (2016) showed that vitamin D deficiency may be a common cause of delayed gastric emptying in untreated Parkinson’s patients.3

Could these neurodegenerative diseases be consequences of decades of chronic vitamin D and magnesium deficiencies?

Looking at the associations of neurodegenerative diseases with decades of digestive disorders that are often connected with and typically caused by vitamin D and Magnesium deficiencies suggests to me that these syndromes are not diseases at all, but rather they are symptoms of ignoring chronic vitamin D and magnesium deficiencies for decades.

The brain fog that’s often associated with MC certainly illustrates the ability of digestive system inflammation to cause serious neurolological problems. And the fact that resolving MC symptoms resolves brain fog tells us that resolving these chronic deficiencies may be the key to preventing the development of neurodegenerative diseases.

If the deficiencies continue to remain untreated as the decades pass, then whether or not a neurodegenerative disease may develop is very likely determined by whether or not the individual under consideration has certain predisposing genes. In other words, genetics will determine which type or types of neurodegenerative issues may develop due to unresolved nutrient deficiencies. At this point, this is strictly a theory. Time will tell whether or not it will eventually be proven by medical researchers to be valid. In support of my theory, however, I would point out that magnesium has been shown to prevent the clumping of alpha-synuclein (Golts et al., 2002).4 So a chronic magnesium deficiency would surely allow the clumping of alpha-synuclein.

And to add to the support for this theory, vitamin D and vitamin D receptors have been shown to be important in the treatment of Alzheimer’s and Parkinson’s disease (Butler et al., 2011).5 Both Alzheimer’s and Parkinson’s patients are known to have lower vitamin D levels than the general population (Zhao, Sun, Ji, & Shen, 2013).6

There may also be a connection between IBDs and neurodegenerative diseases by way of MTHFR gene mutations (which cause methylation issues).

But this is a separate issue and a hugely complex subject that is poorly understood by most physicians, including gastroenterologists and other medical specialists.  But the fact that methylation issues are common with MC and other IBDs, and often complicate recovery, and they frequently result in neurodegenerative symptoms for IBD patients, certainly illustrates that there is a strong connection.


1. Dolhun, R. (2014, December 08). Gut check on Parkinson’s: New findings on bacteria levels. [Web log message]. Retrieved from

2. Ghaisas, S., Maher, J., & Kanthasamy, A. (2016). Gut microbiome in health and disease: Linking the microbiome-gut-brain axis and environmental factors in the pathogenesis of systemic and neurodegenerative diseases. Pharmacology & Therapeutics, 158, 52–62. Retrieved from

3. Kwon, K. Y., Jo, K. D., Lee, M. K., Oh, M., Kim, E. N., Park, J., . . . Jang, W. (2016). Low serum vitamin D levels may contribute to gastric dysmotility in de novo Parkinson’s disease. Neurodegenerative Diseases, 16(3-4), 199205. Retrieved from

4. Golts, N., Snyder, H., Frasier, M., Theisler, C., Choi, P., & Wolozin, B. (2002). Magnesium inhibits spontaneous and iron-induced aggregation of alpha-synuclein. Journal of Biological Chemistry, 277(18), 16116–16123. Retrieved from

5. Butler, M. W., Burt, A., Edwards, T. L., Zuchner, S., Scott, W. K., Martin, E. R., . . . Wang, L. (2011). Vitamin D receptor gene as a candidate gene for Parkinson disease. Annals of Human Genetics, 75(2), 201–210. Retrieved from

6. Zhao, Y., Sun, Y., Ji, H. F., & Shen, L. (2013). Vitamin D levels in Alzheimer’s and Parkinson’s diseases: a meta-analysis. Nutrition, 29(6), 828–832. Retrieved from




Diarrhea caused by bile acid malabsorption (BAM) may be due to inadequate cortisol

While experimenting with mice that had been specially altered to have no glucocorticoid receptors in their livers, a group of researchers discovered that the mice lost weight when fed the same diet on which normal mice were able to maintain their normal weight (Rose et al., 2011).1 They lost weight because they weren’t able to properly digest fats — they also weren’t able to recycle bile acids. Furthermore, they developed gallstones.

Normally, the gallbladder stores an adequate supply of bile so that bile will be available as needed by the digestive system whenever a meal is eaten. As we become hungry, cortisol (which is a glucocorticoid hormone) is released to attach to glucocorticoid receptors in the liver. The liver responds by producing bile and storing it in the gallbladder to gear up for digesting the next meal. As the next meal is eaten, bile is released through the common bile duct into the small intestine. Lipase from the pancreas is also added to the common bile duct to mix with the bile. The bile emulsifies the fat in the food (breaks it into small globules) and the lipase breaks the globules into much smaller particles.

Bile acid malabsorption (BAM).
The body usually recycles about 95 % of the bile that’s released into the intestine. The reabsorption (recycling) takes place in the terminal ileum, which is the last segment of the small intestine. Any bile that is not recycled, stays in the intestine and passes into the colon. And since it shouldn’t be there, if too much remains, it may cause diarrhea. This scenario is known as bile acid malabsorption (BAM) and it can be a major cause of diarrhea not only for MC patients, but others as well.

But if bile acids are not being properly recycled, the liver may not be able to produce enough bile to maintain a normal level in the gallbladder. If that happens, the digestive system may not be able to digest fat properly, and the patient may begin to lose weight. And too much undigested fat in the stool causes diarrhea. Energy levels will also probably be decreased.

The researchers were able to verify that this effect also apples to humans. The adrenal glands are responsible for producing cortisol. Patients who have been diagnosed with a rare disorder known as Addison’s disease are unable to produce normal amounts of cortisol. Their immune system attacks their adrenal glands and this interferes with their ability to produce normal amounts of cortisol. The researchers discovered that when they analyzed blood samples taken from Addison’s disease patients before and after eating, the samples showed that bile acid recycling was also compromised similar to the mice that had no glucocorticoid receptors in their livers. So therefore cortisol must also control bile acid recycling in humans.

This might have interesting implications for MC patients.
Some patients tend to gain weight during a flare, while others lose weight when their MC is active. It would seem that this scenario might suggest that those MC patients who are unable to properly recycle bile acids might be among those who are more likely to lose weight during a flare. And conversely, those who are able to properly recycle bile acids are less likely to lose weight. This might also imply that those patients who lose weight (or lose it more rapidly) are more likely to respond to cholestyramine treatments than those who are less prone to losing weight during a flare. Please keep in mind that this is strictly speculation at this point, as there is not yet any published research that verifies it as a fact.

It’s highly likely that this explains why corticosteroids are so effective for treating MC and other IBDs. When patients take a corticosteroid, it boosts their ability to recycle bile acids, thus eliminating (or at least minimizing) a major cause of diarrhea. Anti-inflammatory products such as budesonide (Entocort or Uceris) have potent glucocorticoid activity, so they are capable of providing a significant cortisol boost to enhance bile acid reabsorption. This also should explain why so many patients tend to gain weight while taking budesonide or some other corticosteroid.

1. Rose, A. J., Berriel Díaz, M., Reimann, A., Klement, J., Walcher, T., Krones-Herzig, A., . . . Herzig, S. (2011). Molecular control of systemic bile acid homeostasis by the liver glucocorticoid receptor. Cell Metabolism, 14(1), 123–130. Retrieved from

What causes MC to become a chronic disease?

Microscopic colitis patients tend to either be deficient in vitamin D and magnesium or they soon become deficient once the disease becomes active. Published research shows that about two-thirds of magnesium absorption normally takes place in the ileum and the colon, precisely where the inflammation associated with MC is known to be the most severe (Albion Laboratories, n.d., Koskela, 2011).1, 2

Not only does the malabsorption problem associated with the disease cause vitamin D and magnesium deficiencies, but the most popular medical treatment prescribed to treat the disease (budesonide) depletes vitamin D. All corticosteroids deplete vitamin D. And since the diet changes required to gain remission from MC should also include a reduction in the amount of vegetables eaten, especially raw, green, leafy, vegetables, magnesium intake is likely to be restricted as a result of diet changes associated with treating MC. Dr. Norman Shealy, a well-known neurosurgeon and pioneer in the field of pain medicine, once pointed out that every known disease is associated with magnesium deficiency.

So what are the consequences of these deficiencies? Could vitamin D and/or magnesium deficiency possibly interfere with our ability to heal? Yes it could. One of the primary functions of the immune system is to control the various stages of healing. Published research verifies that certain vitamins and minerals are so important to the immune system that they can speed up the healing process. And conversely, a deficiency can slow down the healing process. If the deficiency is severe enough, healing might be so compromised that it is not even possible until the deficiency is corrected.

For example, Narula, Cooray, Anglin, & Marshall, (2016) demonstrated that taking relatively large doses of vitamin D can help to prevent a relapse of Crohn’s disease.3 Compared with taking 1,000 IU of vitamin D daily, they showed that taking 10,000 IU of vitamin D resulted in no relapses in this group of subjects. By contrast, those taking only 1,000 IU daily had a 38 % relapse rate during the 12 month trial period. No one has investigated whether or not large doses of vitamin D might have any effect on MC, but it’s very likely that since all IBDs involve intestinal inflammation and compromised healing ability, the effect of vitamin D might be similar for MC patients.

And this makes a lot of sense, because the reason that microscopic colitis exists in the first place is because the inflammation that causes it becomes chronic. If the intestines just healed, as they should, the disease could not become chronic, and the symptoms would fade away after a few days. But our immune system is unable to heal the damage caused by the inflammation. Why are the intestines unable to heal? That’s a good question. And unfortunately medical science doesn’t seem to know the answer.

The initial cause of the chronic state of inflammation is continued exposure to foods that cause our immune systems to produce antibodies. But we also know from past experience that even after the diet is changed to avoid all known food and drug sensitivities, recovery can take a very long time. Logic tells us that making diet changes to avoid all foods that cause the inflammation in the first place is the best way to stop the inflammation, (which will stop the symptoms) since using this technique can be done with or without medications. So there’s no question that it works for most people. Now we realize that the next step in planning a treatment program that will optimize recovery from MC is to make sure that we are not deficient of vitamin D and magnesium.


  1. Advantages of magnesium bisglycinate chelate buffered. (n.d.). Albion Laboratories, Inc. Retrieved from
  2. Koskela, R. (2011). Microscopic colitis: Clinical features and gastroduodenal and immunogenic findings. (Doctoral dissertation: University of Oulu). Retrieved from
  3. Narula, N., Cooray, M., Anglin, R., & Marshall, J. (2016). P-064 Impact of High Dose Vitamin D3 Supplementation in Treatment of Crohn’s Disease in Remission: A Randomized Double-Blind Controlled Study. Inflammatory Bowel Diseases: Official Journal of the Crohn’s & Colitis Foundation. Retrieved from

Are Inflammatory Bowel Diseases Contagious?

This is a glimpse of some of the information that will be discussed in my next book.  Please be aware that the details of this text are subject to change in the final version when the book is published.  This post is for informational purposes only, and should not be considered to be medical advice.  While this information is thought to be correct, some of it may be incomplete.

Are inflammatory bowel diseases contagious?

Recent research by Dheer et al. (2016) has shown that increased toll-like receptor 4 (TLR4) signaling is associated with an increase in the population and translocation of gut bacteria, and an increase in intestinal permeability.1  The effects on gut bacteria characteristics imply that increased TLR4 activation might provide the mechanism needed to substantiate the long-held theory that IBDs may be the result of a bacterial infection. And it suggests the possibility of infectious transmission.

For decades, the medical community has denied that IBDs may be transmitted from one individual to another, but experience shows that while this is not common, plenty of examples exist to show where more than one member of a household has developed an IBD. With MC, for example, not only are there multiple IBD cases in some households, but there are also examples of cases where the disease appears to have been transmitted from a human to a pet. MC is actually somewhat common in dogs. While appearances can be deceiving, and it’s certainly possible that all these cases are merely coincidental, it’s worth noting that Dheer et al. (2016) pointed out that:

Interestingly, WT mice cohoused with villin-TLR4 mice displayed greater susceptibility to acute colitis than singly housed WT mice did. The results of this study suggest that epithelial TLR4 expression shapes the microbiota and affects the functional properties of the epithelium. The changes in the microbiota induced by increased epithelial TLR4 signaling are transmissible and exacerbate dextran sodium sulfate-induced colitis. Together, our findings imply that host innate immune signaling can modulate intestinal bacteria and ultimately the host’s susceptibility to colitis. (p. 798)

WT mice are “Wild Type” mice (with no genetic modifications).  Villin-TLR4 mice are genetically modified to overexpress TLR4, making them highly vulnerable to colitis and the physiological effects of colitis. While not conclusive evidence, this research certainly suggests that susceptibility to colitis, if not the disease itself, may be increased by close contact with someone who is highly susceptible to colitis. That potentially opens the door to possible contagious effects, though clearly the risk (if it exists) must be low, otherwise the transmission of IBDs between humans would be common.


1. Dheer, R., Santaolalla, R., Davies, J. M., Lang, J. K., Phillips, M. C., Pastorini, C., . . . Abreu, M. T. (2016). Intestinal epithelial toll-like receptor 4 signaling affects epithelial function and colonic microbiota and promotes a risk for transmissible colitis. Infection and Immunity, 84(3), 798-810. Retrieved from

How a chronic magnesium deficiency can cause inflammation, and how antibiotics can amplify the problem

This is a glimpse of some of the information that will be discussed in my next book.  Please be aware that the details of this text are subject to change in the final version when the book is published.  This post is for informational purposes only, and should not be considered to be medical advice.  While this information is thought to be correct, some of it may be incomplete, and at this point it may not be verified by published medical research data.

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 mosquite 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.

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 (in the new book — Edition II), 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 earlier in this article, 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.

Here are references 2 and 3 for this post:

2. Forbes, E. E., Groschwitz, K., Abonia, J. P., Brandt, E. B., Cohen, E., Blanchard, C., . . . Hogan, S. P. (2008). IL-9– and mast cell–mediated intestinal permeability predisposes to oral antigen hypersensitivity. Journal of Experimental Medicine, 205(4), 897–913. Retrieved from

3. Drago, S., El Asmar, R., Di Pierro, M., Grazia Clemente, M., Tripathi, A., Sapone, A., . . . Fasano A. (2006). Gliadin, zonulin and gut permeability: Effects on celiac and non-celiac intestinal mucosa and intestinal cell lines. Scandinavian Journal of Gastroenterology, 41(4), 408-19. Retrieved from

My next book

I’m currently working on Edition II of Microscopic Colitis.  A lot has happened since the first edition was published.  This edition will basically begin where the first one left off.  In other words, it will not include the information in the first book except in places where new or more detailed information has become available about topics that were included in the first edition.  I’ve already accumulated over 700 pages of notes, most of them related to new research data that have become available.

And because so much medical research these days is biased because of the fact that most research is sponsored by commercial interests that have a financial stake in the outcome of the research, one cannot simply take the conclusions reached in most medical research reports at face value.  Nor can one safely assume that all of the headlines in the medical press articles that are based on the press releases and the actual research articles are accurate and totally objective.  Often they are biased either by improper conclusions stated in the research articles, or by dissenting medical opinion (especially when the conclusions of the research reports contradict prevailing mainstream medical opinions or policies).

So sorting out all the data found in research reports, and weighing the various comments made about the research by other medical authorities who are often interviewed to get their thoughts on newly-published research, can often require a lot of careful reading and sometimes a bit of detective work.

Here is the current list of chapters.  Bear in mind that this list may change before publication.

Chapter 1 – Why Do Treatment Programs Fail?
Chapter 2 – Cross-Contamination and Other Dietary Issues
Chapter 3 – Nutritional Deficiencies
Chapter 4 – Methylenetetrahydrofolate Reductase (MTHFR) Gene Mutations
Chapter 5 – Magnesium Deficiency, Histamine, Gut Bacteria, Inflammation
Chapter 6 – BAM, SIBO, Low-Dose Naltrexone, GERD, Other Considerations
Chapter 7 – Depression, Inflammation, and Stress Associated with MC
Chapter 8 – Medical Diagnostic and Treatment Issues That Must Be Corrected
Chapter 9 – Recent Research

Projected completion time is Fall, 2017.  If you have any suggestions on topics that you would like to see addressed in the book, or any other comments, please feel free to post your thoughts.