The Apparent Connection Between Microscopic Colitis 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

References:

1. Dolhun, R. (2014, December 08). Gut check on Parkinson’s: New findings on bacteria levels. [Web log message]. Retrieved from https://www.michaeljfox.org/foundation/news-detail.php?gut-check-on-parkinson-new-findings-on-bacteria-levels

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 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4747781/

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 https://www.ncbi.nlm.nih.gov/pubmed/26735311

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 http://www.jbc.org/content/277/18/16116.long

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 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3077063/

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 https://www.ncbi.nlm.nih.gov/pubmed/23415143

 

 

 

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.

References.

  1. Advantages of magnesium bisglycinate chelate buffered. (n.d.). Albion Laboratories, Inc. Retrieved from http://www.albionminerals.com/human-nutrition/magnesium-white-paper
  2. Koskela, R. (2011). Microscopic colitis: Clinical features and gastroduodenal and immunogenic findings. (Doctoral dissertation: University of Oulu). Retrieved from http://herkules.oulu.fi/isbn9789514294150/isbn9789514294150.pdf
  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 http://journals.lww.com/ibdjournal/Abstract/2016/03001/P_064_Impact_of_High_Dose_Vitamin_D3.89.aspx

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.