The other day, I had a follow up with my endocrinologist because I have been concerned about a slowly increasing sugar levels as well as HgA1C (glycosylated Hemoglobin used to detect sugar levels in the last 3-6 months to help diagnose diabetes and then gauge management) possibly being caused of increased night sweats and overall sweating.
Although I am not diabetic, I am becoming slowly at risk…which initially I attributed my increase glucose levels to the number of steroids I have received over the past 12 months for treatment of various other illnesses.
Then I began to wonder if this process had anything to do with my Parkinson’s?
I then seemed to remember reading something about dopamine increasing sugar levels and tried to recall by first year of medical school when we discussed physiology.
After my visit my doctor confirmed that I was becoming glucose intolerant and would be best to start treatment to avoid developing diabetes. Well of course this was not a pleasant experience to add yet another medication to my already long list of medicines but more importantly sent me in search of answers?
What I discovered to my great astonishment and chagrin was that indeed there is a connection between having Parkinson’s, dopa intake and developing insulin resistance leading to diabetes. What amazed me the most was study after study detailing this information dating back to the late seventies; yet no one in neurology or Parkinson’s specialty much less others outside this field have ever made any comments, concerns, or indications to monitor a patient’s sugars or discuss risk of diabetes!!!!
In the presence of high sugars, dopamine stimulates insulin secretion from pancreatic cells. (1)
The substancia nigra plays a crucial role in controlling structure and activity of these pancreatic islet cells which produce insulin. When lesions occur in this area of the brain or there is loss of dopamine there is a decrease in the content of insulin thus unable to properly regulate blood glucose levels causing an increase? This process is mediated via D2 receptors in the pancreas. However, as with all things pertaining to the brain things are not always straight forward. At increased concentrations outside of the brain it has an inhibitory role while it stimulates insulin at lower concentrations.
This perhaps can be the simplest explanation of why Parkinson’s patients have increased chocolate cravings particularly when off or low on dopamine, as has been my experience, in an attempt not only to increase dopamine but more importantly to increase glucose levels. This information again perhaps is one of the reasons a blood glucose modifying agent was studied to see its effects on PD as disease modifying. (2)
Studies have shown higher fasting blood glucose levels in 50 to 80% PD patients than in normal (non-PD) patients suggesting again that there may be an impairment in glucose tolerance (or glucose intolerance) problem. This problem may be further exacerbated by levodopa therapy (3); yet to date this issue has been mostly ignored leaving the risk of developing diabetes in a Parkinson’s patient completely undefined. I highly believe that high glucose intolerance merits high scrutiny as well as further research considering the irreversible damage diabetes can cause in an already fragile health system leading to increase dyskenesias, poorly controlled motor symptoms and less than effective treatment with levodopa.