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
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), 199–205. 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