Is PD the long lost brother to diabetes?
 

Come with me on a flight of fantasy for a minute and entertain a radical idea. Suppose that there is, for lack of a better term, a "metabolic pattern" built into our DNA that produces both PD and diabetes (and perhaps other conditions as well) when certain conditions exist.

I ran across an article in Science Daily. I am going to take some major liberties and completely recycle the article by substituting PD for diabetes:
"<PD> is caused by an inability of the <neurons> in the <substantia nigra> to produce enough of the <neurotransmitter dopamine> to meet the body's needs.

Central to this is a loss of <neuronal> function and mass as a result of <dopamine> resistance (the inability of cells in the body to respond appropriately to <dopamine>).

New insight into how <dopamine> resistance leads to loss of <neuronal> mass has now been provided by studies .....

In the study, in the absence of the protein <"X">, the symptoms of <PD> improved in two mouse models of the disease....

<"X"> is a protein that is involved in promoting the death of a cell that is under stress because it is producing more <dopamine> than it is able to handle.

The authors therefore propose that <dopamine> resistance causes <neurons> to make more <dopamine> than they can handle, such that the stress signaling pathways that activate <"X"> are initiated and the <neurons> die....

Mere musings, but does dopamine resistance exist?

May not be totally off the wall...
 

the question is
 

is it related to hypoglycemic -low blood sugar?

I have hypoglycemia, when I take my sinemet/ carbi dopa levo dopa, sometimes I feel as if my blood sugar gets too low, so I must be careful,
not to take - if I have not eaten,or if I do eat an hour before meds

in our brains we must have level blood sugar, and oxygen...

Along the same lines....
 

Rick,

As you know, I have been clinging to the parathyroid and thyroid connections, or rather, Parkinsonian manifestations to these disorders when undetected and/or untreated for a long time. Then I ran across a new case of a woman who developed a rather quickly developing Parkinsonism that was reversible...blah blah...this sort of thing always pops up, now an anti-epileptic drug implicated. In researching Parkinsonism, we find neurological signs that look like PD but originate with use of drug therapies, (channel blockers, anti-psychotics, etc.) metabolic disorders, nutritional or electrolyte deficiencies, immune disorders, not to mention the usual garden variety that springs up with the ingestion of exotic, neurotoxic native plants.

In trying to find a link say between say parathyroid and PD, I was making too big a direct leap. I get that we have primary, idiopathic PD and then we have secondary Parkinsonism related to something else. I am saying how they know what any of us primarily has? Often they'll say that responsiveness to levodopa differentiates us. Not so, there are cases of parathyroid induced Parkinsonism that are dopa responsive...same with drug and neurotoxin induced secondary PD.

It seems we could learn a lot from exploring why we even have what mimics PD without the neurodegeneration? If we are primarily losing dopamine, or have lost near 80% for emergence of motor symptoms, what in the world is going on inside a person who is suffering from manganese or copper toxicity- the latter is not neurodegenerative; there is no permanent or substantial loss of dopamine. What, for example, is the neurometabolic cause of a hyperthyroid tremor...it certainly is not a dopamine-acetylcholine imbalance but it can sure look like one. I guess I can't figure out how it can all look the same, but be so vastly different at the same time. Or is it really not so different after all?

Could the common link be autoimmune response? This is the only thing that makes remote sense to me. If we have idiopathic PD, we are SOL and our T cells continue unabated. If we have a response in our brain that just looks like PD then reverses, that says we have a normal immune response . I may be way off center tonight...just sort of riffing some thoughts. Or is this just saying that we are all experiencing the same sort of channelopathy- a dopamine blockade that begins on different paths but leads to the same sorry looking state? We are running on fumes while others only appear to be approaching "E" because of a temporary fuel pump glitch?

Way off track here, sorry. I ran across this when researching the endocrine link in the last few days and received responses from two members of our forum who have links between PD and Vitiligo. Which leads me to my next big question...the role of Melanin.

From eMedicine's web site, on Polyglandular Autoimmune Syndrome, where an unfortunate person ends up with 2-3 endocrine disorders, the whole syndrome is further linked to other diseases like:

Other disorders associated with PGA-II include the following:

* Hypogonadism (usually autoimmune oophoritis) and hypopituitarism
* Idiopathic thrombocytopenic purpura
* Myasthenia gravis
* Parkinson's disease
* Vitiligo
* Alopecia
* Seronegative arthritis

What is striking is that every other disorder on this list has a known autoimmune component except Parkinson's?!?

Laura