By Wayne Persky
Founder and President of the Microscopic Colitis Foundation
*Note that this article is so long that it is being published in two parts. This is part one.
Because the practice of medicine is based on the concept that every disease is diagnosed and treated as if it were independent of all other diseases, medical researchers rarely consider the interdependence of various diseases. Consequently, they tend to overlook common connections that might be primarily responsible for the development of an entire class of diseases, such as autoimmune (AI) diseases, for example.
What type of pathological issue might possibly lead to the development of all autoimmune diseases?
Based on published medical research, it's common knowledge that chronic inflammation is the common thread associated with all autoimmune diseases, suggesting that chronic inflammation might be implicated in the development of all autoimmune diseases (Storrs, 2022, September 16; Bennett, Reeves, Billman, and Sturmberg, 2018).1, 2 And the primary sources of chronic inflammation typically tend to be food sensitivities, infections, certain vitamin and mineral deficiencies, such as deficiencies of vitamin D and magnesium, and stress, whether individually, or in combination.
The accepted medical viewpoint incorrectly blames AI disease on corrupt immune system events.
So it's not surprising that conventional medical wisdom claims that AI diseases are caused by a complex interplay of genetic, environmental, and immune system factors that lead to the immune system attacking the body's own tissues and organs. While issues such as vitamin deficiencies or food sensitivities can exacerbate AI symptoms and trigger flare-ups in some cases, they are presumed to not be associated with the development of AI diseases, in general. However, many major medical websites do acknowledge that managing food sensitivities may be an important part of managing AI diseases for some individuals (on an individual disease basis).
Part of the medical community's AI description is at least a half-truth.
Research has not demonstrated that AI diseases may develop because of a common issue (although a few articles, such as the ones cited above, do suggest that possibility), such as food sensitivities, vitamin or mineral deficiencies, or chronic stress, so it is true that these issues have not been shown to be the root cause of AI diseases. Of course, that may simply mean that the connections have never been researched. And as is well established, AI syndromes can only continue to develop into chronic diseases, if they are fueled by chronic inflammation.
Arguably, the primary sources of chronic inflammation are infections, parasites, vitamin or mineral deficiencies, food sensitivities, and stress. Infections, whether bacterial, viral, or due to parasites, are typically easily ruled out during the early stages of conventional medical disease diagnosis. In other words, resolving infections and parasite problems are standard parts of conventional medical diagnostic procedures. By contrast, chronic problems such as vitamin D and magnesium deficiencies, food sensitivities, and chronic stress levels, are either inadequately addressed, or completely ignored during conventional diagnostic workups.
The evidence suggests that all AI diseases may be associated with leaky gut.
Research has shown that deficiencies of vitamin D, zinc, or magnesium, can cause increased epithelial porosity of the intestinal barrier (Yeung, et al., 2021; Wan, and Zhang, 2022); Nielsen, 2018).3, 4 ,5 As is well established by research, increased porosity of the epithelial barrier (leaky gut) perpetuates inflammation (Luissint, Parkos, and Nusrat, 2016).6 And, as most of us are well aware, stress is a well known cause of inflammation (Sun, et al., 2019; Liu, Wang, and Jiang, 2017).7, 8
Food sensitivities are caused by a leaky gut.
And most of us are well aware that although microscopic colitis (MC) and other inflammatory bowel diseases (IBDs) aren't usually caused by food sensitivities, the inflammation that accompanies all IBDs leads to increased intestinal permeability (leaky gut), and leaky gut leads to the development of food sensitivities. Consequently, it's the frequently repeated exposure to these food sensitivities that continues to generate the inflammation that perpetuates the clinical symptoms associated with active IBDs, including MC.
Once a food sensitivity develops, it becomes permanent.
Once the process is initiated, it becomes a vicious cycle, so that the inflammation, and the symptoms of the disease, become chronic. And note that certain medications can cause the creation of antibodies, also, so that continued use of the medication can lead to chronic inflammation, resulting in a continued reaction against it. Sometimes, stopping the medication, will stop the reaction, if it's done before significant intestinal damage has occurred.
Here's why the basic medical description of AI disease is flawed.
While it may be true that the immune system produces antibodies against its own tissues, in certain situations, this behavior is not idiopathic, as the medical description implies. Just because the medical community does not understand the cause, does not mean that the cause cannot be found. There's a reason for everything that happens — we simply have to discover it.
The immune system requires adequate nutrition.
If the immune system is deprived of adequate nutrition, for example (a deficiency of vitamin D3 and/or magnesium), it cannot operate properly. It can be shown that in virtually all cases, the immune system's seemingly aberrant behavior is actually a normal reaction, directed against one or more food sensitivities, or, the immune system's behavior is due to a vitamin or mineral deficiency, that prevents the immune system from functioning normally.
Magnesium deficiency promotes inflammation.
Published research shows that magnesium deficiency causes chronic inflammation (Maier, Castiglioni, Locatelli, Zocchi, and Mazur, 2021; Nielsen, 2018).9, 10 Published research also shows that magnesium can be used to reduce rheumatoid arthritis severity and joint damage (Laragione, Harris, Azizgolshani, Beeton, Bongers, and Gulko, 2023).11 In addition to fibromyalgia syndrome (FS), chronic fatigue syndrome (CFS), myofascial pain syndrome (MPS) and eosinophilia myalgia syndrome (EMS), magnesium deficiency has been shown to be associated with systemic lupus erythematosus (SLE) (Romano, 1997).12
Nutrient deficiencies can compromise intestinal barrier integrity.
In fact, published research shows that many nutrients are associated with the regulation of intestinal permeability, and intestinal inflammation (Farré, Fiorani, Abdu Rahiman, and Matteoli, 2020).13
With proper nutrition, the immune system functions flawlessly.
The point is, any compromised behavior of the immune system is not due to an idiopathic cause. Additionally, if the food (or foods) that triggered the reaction are removed from the diet, or the vitamin or mineral deficiency is corrected, the symptoms will stop. If the reaction were truly autoimmune (as the medical community claims), by definition, this could not happen. That is to say, the reaction would not stop, simply because an external trigger was removed from the diet.
Therefore, AI diseases are incorrectly defined.
Diseases claimed to be due to "autoimmune" reactions are not actually true autoimmune reactions. Instead they are due to chronic inflammation perpetuated by an external trigger (such as a food sensitivity, or a vitamin or mineral deficiency). Therefore, it should be possible to control AI diseases without medications, or other medical intervention, simply by removing the external triggers from the diet.
What does this imply?
If all AI diseases are the result of the body's response to the same basic set of issues, it's likely that AI diseases in general are not actually diseases. Rather, they constitute the presentation of an array of various symptoms that are the result of those issues (vitamin or mineral deficiencies, food sensitivities, or stress). In other words, they are symptoms, not diseases. Although this point of view might seem far-fetched, when compared with with the prevailing medical description, it's actually a more logical explanation, and it fits the boundary conditions imposed by these syndromes.
Most doctors routinely fail to look for issues that can cause inflammation,
even during so-called "annual wellness exams". In other words they don't check for deficiencies of any vitamins or minerals, nor do they consider any food sensitivities or stress levels. And even in the few cases where doctors do check vitamin D and magnesium levels, for example, their goals are not consistent with optimum health conditions (as shown by numerous published research articles).
Our immune system requires vitamin D.
If doctors check vitamin D, most doctors consider 20 mg/dL (50 nmol/L) to be sufficient, and 30 mg/dL (75 nmol/L to be more than adequate, when in fact, research shows that a 20 mg/dL level is only sufficient to prevent rickets, and even 30 mg/dL is not sufficient to assist in the control or prevention of infections or most diseases. Many authorities believe that a vitamin D level in the range of 40 to 60 mg/dL (100 to 150 nmol/L) is a much better choice, especially for someone who has a chronic disease. Doctor Amy Myers, a functional medicine doctor, recommends 60 to 90 ng/mL (150 to 225 nmol/L) for preventing disease (Myers, n.d.).14
Here's why vitamin D recommendations for patients who have a chronic disease are way too low.
Recommended daily allowances (RDAs) of vitamin D are way too low simply because those who would benefit the most from higher supplemental levels are almost always disqualified from participating in research trials. Typically, any potential candidate for most such studies who has a history of chronic disease, or oral glucocorticoid use is automatically excluded from such studies.
Likewise, most doctors have historically ordered the wrong magnesium test.
When they occasionally check magnesium levels, most doctors order the serum magnesium test. But that test is only useful for emergency department setting, since it measures the amount of magnesium in circulation in the blood at the moment that the blood draw is made. Blood levels of magnesium are automatically regulated by the body, within a narrow normal range, because magnesium is an electrolyte, so the level in circulation is critical for the proper functioning of many organs. A serum magnesium test will only yield a low result if most cells in the body are almost completely depleted of magnesium, which is a a situation that carries a high risk of a cardiovascular event.
The proper magnesium test to order is the red blood cell (RBC) magnesium test. And many authorities believe that the "official" normal range for RBC magnesium reserves is too low for optimum health considerations. Therefore, if a patient's RBC magnesium result is in the lower part of the normal range, a magnesium supplement might be beneficial.
Let's look at how MC develops, for example.
Microscopic colitis (MC) normally does not initially develop because of one or more food sensitivities. Presumably, that rarely happens. There can be many issues that lead to the development of MC. However, in essence, the disease develops because of chronic inflammation, and if the inflammation persists for a long enough period of time, it will eventually lead to digestive system consequences that can cause permanent food sensitivities, that in turn, regenerate the inflammation each time those foods are eaten.
Food sensitivities perpetuate the disease.
Once they develop, the food sensitivities perpetuate the inflammation, and that perpetuates the disease. Were it not for the development of food sensitivities, the disease might never become chronic, in most cases, because the initial issue that caused the inflammation, normally would eventually fade away, with or without intervention. Food sensitivities, once they develop, never fade away, so the disease becomes chronic.
Avoiding our food sensitivities can stop the symptoms.
As many of us have found, if we diligently track down all of our food sensitivities, and meticulously eliminate them from our diet, we can achieve remission from our MC symptoms, and maintain remission indefinitely, as long as we're careful not to allow any of those food sensitivities in our diet.
AI disease tends to lead to additional AI diseases.
Most of us are well aware that most MC, and other IBD patients tend to have one or more additional AI diseases. In other words, AI diseases seem to attract additional AI diseases. Surely, this isn't just coincidental. In the school of hard knocks, most of us have learned that there's a reason for everything, and as previously noted, if we search for that reason, we can often find it. This situation appears to fit the old saying, "If it quacks like a duck . . ." Food sensitivities appear to be a common thread that causes the perpetuation of most (or all) so-called AI diseases.
For example, atopic dermatitis has been linked to an increased IBD risk.
An online Medical News article reported a study showing that kids who had atopic dermatitis, had a 44% increased risk of developing IBD, whereas adults in the study had a 34% increased risk of developing IBD (Chiesa Fuxench, et al., 2023).15 What does that suggest? It suggests that the inflammation associated with atopic dermatitis eventually leads to the development of IBD, in many cases.
And research shows that a magnesium and zinc deficient diet can lead to symptoms of atopic dermatitis (Makiura, et al., 2004).16 Similarly, research shows that stress can cause atopic dermatitis (Suárez, Feramisco, Koo, and Steinhoff, 2012).17
Are food sensitivities a problem for other AI disease patients?
It doesn't take much imagination to visualize how other AI diseases might involve a similar process, because all AI diseases involve inflammation. Therefore, it's certainly possible, and might even be likely, that other AI diseases involve increased intestinal permeability, and the resulting generation of food sensitivities, which then perpetuates the symptoms of the disease. Obviously, all this is speculation, and unproven by medical research. But although it probably won't happen anytime soon, there's certainly at least a reasonable possibility that eventually, researchers will make the connection and get around to proving this association with food sensitivities, medications, or something else in the diet that's triggering the so-called "AI" reactions.
This article will be continued in part two.
References
1 Storrs, C. (2022, September 16). Inflammation: A Driving Force of Autoimmune Disease. Global Autoimmune Institute, Retrieved from https://www.autoimmuneinstitute.org/articles/about-autoimmune/inflammation-a-driving-force-of-autoimmune-disease/
2 Bennett, J. M., Reeves, G., Billman, G. E. And Sturmberg, J. P. (2018) Inflammation–Nature's Way to Efficiently Respond to All Types of Challenges: Implications for Understanding and Managing “the Epidemic” of Chronic Diseases. Frontiers in Medicine, 5, 316. Retrieved from https://www.frontiersin.org/articles/10.3389/fmed.2018.00316/full
3 Nielsen, F. H. (2018). Magnesium deficiency and increased inflammation: current perspectives. Journal of Inflammation Research, 11, pp 25-34. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5783146/
4 Wan, Y., and Zhang, B. (2022). The Impact of Zinc and Zinc Homeostasis on the Intestinal Mucosal Barrier and Intestinal Diseases. Biomolecules, 12(7), 900. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9313088/
5 Yeung, C. Y., Chiang Chiau, J. S., Cheng, M. L., Chan, W. T., Jiang, C. B., Chang, S. W., . . . Lee, H. C. (2021). Effects of Vitamin D-Deficient Diet on Intestinal Epithelial Integrity and Zonulin Expression in a C57BL/6 Mouse Model. Frontiers in Medicine (Lausanne), 8, 649818. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8369235/
6 Luissint, A. C., Parkos, C. A., and Nusrat, A. (2016). Inflammation and the Intestinal Barrier: Leukocyte-Epithelial Cell Interactions, Cell Junction Remodeling, and Mucosal Repair. Gastroenterology, 151(4), pp 616–632. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5317033/
7 Sun, Y., Li, L., Xie, R., Wang, B., Jiang, K,, and Cao, H. (2019). Stress Triggers Flare of Inflammatory Bowel Disease in Children and Adults. Frontiers in Pediatrics, 7, 432. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6821654/
8 Liu, Y. Z., Wang, Y. X., and Jiang, C. L. (2017). Inflammation: The Common Pathway of Stress-Related Diseases. Frontiers in Human Neuroscience, 11, 316. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5476783/
9 Maier, J. A., Castiglioni, S, Locatelli, L., Zocchi, M., and Mazur, A. (2021). Magnesium and inflammation: Advances and perspectives. Science Direct, 115, pp 27–44. Retrieved from https://www.sciencedirect.com/science/article/pii/S1084952120301713
10 Nielsen, F. H. (2018). Magnesium deficiency and increased inflammation: current perspectives. Journal of Inflammation Research, 11, 25–34. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5783146/
11 Laragione, T., Harris, C., Azizgolshani, N., Beeton, C., Bongers,G., and Gulko, P. S. (2023). Magnesium increases numbers of Foxp3+ Treg cells and reduces arthritis severity and joint damage in an IL-10-dependent manner mediated by the intestinal microbiome. BioMedicine (The Lancet), 92, 104603. Retrieved from https://www.thelancet.com/journals/ebiom/article/PIIS2352-3964(23)00168-8/fulltext#%20
12 Romano, T. J. (1997) Magnesium Deficiency in Systemic Lupus Erythematosus. Journal of Nutritional & Environmental Medicine, 7(2), pp 107–112. Retrieved from https://www.tandfonline.com/doi/abs/10.1080/13590849762691
13 Farré, R., Fiorani, M., Abdu Rahiman, S., and Matteoli, G. (2020) Intestinal Permeability, Inflammation and the Role of Nutrients. Nutrients, 12(4), 1185. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7231157/
14 Myers, A. (n.d.). Vitamin D And Your Immune System. Retrieved from https://www.amymyersmd.com/article/vitamin-d
15 Chiesa Fuxench, Z. C., et al. (2023). Risk of Inflammatory Bowel Disease in Patients With Atopic Dermatitis. JAMA Dermatology, Published online. Retrieved from https://jamanetwork.com/journals/jamadermatology/article-abstract/2808972
16 Makiura, M., Akamatsu, H., Akita, H., Yagami, A., Shimizu, Y., Eiro, H., . . . Matsunaga, K. (2004). Atopic dermatitis-like symptoms in HR-1 hairless mice fed a diet low in magnesium and zinc. Journal of International Medical Research, 32(4), pp 392–399. Retrieved from https://pubmed.ncbi.nlm.nih.gov/15303770/
17 Suárez, A. L., Feramisco, J. D., Koo, J., and Steinhoff, M. (2012). Psychoneuroimmunology of psychological stress and atopic dermatitis: pathophysiologic and therapeutic updates. Acta Dermato-Venereologica, 92(1), pp7–15. Retrieved from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3704139/
