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 https://www.ncbi.nlm.nih.gov/pubmed/10332921

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 http://ajcn.nutrition.org/content/74/6/714.long

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.

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