Vitamin D

Levels of vitamin D are lower in PD patients worldwide (1).  Several neurologic disorders are associated with vitamin D deficiency, including MS, stroke, and other neurodegenerative disorders.   We are not sure yet what this means, or what all of the functions of vitamin D are (though what is known is extensive).   It seems clear, however, that keeping a normal level is a good idea.

Doctors measure vitamin D with a blood test.  The test checks levels of 25-hydroxy D total, a combination of D2 and D3.  We get vitamin D2 from diet, and some conversion is made when we are exposed to sunlight and UVB enters the skin, helping us produce the active vitamin D3 form.  According to Mayo Medical Laboratories New England, 10-24 ng/mL = mild to moderate deficiency, and optimum levels in the normal population are 25-80 ng/mL.

Interestingly, vitamin D receptors are found all over the brain.  One location that is relevant here is the receptors on large neurons of the substantia nigra, the darkly pigmented structure of our upper brainstem, which produces dopamine.   These cells are unfortunately lost throughout disease in PD.  The progressive depletion of these neurons over several years ultimately results in enough of a dopamine deficiency for the first motor signs of PD to show (tremor, stiffness, slowness).   As disease progresses, one has fewer of the cells, and therefore, less dopamine.

I am going to get a little technical here.  One thing that vitamin D does in these cells is to increase an enzyme called tyrosine hydroxylase.  This enzyme converts the amino acid tyrosine into dopa, a precursor of dopamine.  Therefore, we may need vitamin D to make dopamine efficiently.

Researchers have shown in mice that knocking out the vitamin D receptor on these neurons will result in a PD-like motor impairment (2).  This led the same investigators to question whether low vitamin D might predispose people to neurodegenerative disease.  Further, they wanted to know if keeping levels in the high normal range would make a difference.   In a 12-month study with 114 PD patients who averaged a vitamin D level of 22.5 ng/dL, 56 were given 1200 IU of vitamin D daily and 58 were given placebo.  At the end of the study, the treatment group had a higher vitamin D level, with an average of 42 ng/dL.  The very simple Hoehn and Yahr stage was stable, but not the more detailed UPDRSIII motor score.  This is not an impressive result, but it was a limited study.

The jury is still out on vitamin D levels in PD.  A normal level is probably a good idea for many reasons, but it is not clear if it will have an effect on disease progression.  There is no data on high levels, except to say that taking too much can cause toxicity.  Acute vitamin D toxicity may cause confusion, excess urination and thirst, loss of appetite, vomiting, and muscle weakness.  Chronically high levels of vitamin D may result in kidney stones, loss of bone mineralization, and pain.  So, as with any vitamin, work with your doctor to make sure your level is normal.

REFERENCES

  1. Lv, et al.  Vitamin D Status and Parkinson’s disease” as systematic review and meta-analysis. Neurol Sci 2014;35:1723-30.
  2. Suzuki et al. Does vitamin D arrest the progress of PD?   American Journal of Clinical Nutrition. 2013;97:1004-13.

 

Published by

Bill Stamey, M.D.

A neurologist trained in movement disorders, Dr. Stamey has no relevant financial or nonfinancial relationships to disclose. His artistic rendering is by Emily Stamey. Maine PD News receives no outside funding. www.mainepdnews.org