It depends on the source of the "sweet" and how much of it you eat. Dried fruits like dates, figs, apricots ,raisens etc are very good for you..but you can over do it! For example I like apricots, but two or three at a serving is plenty. They are dried so the fructose (that's the name for fruit derived sugars) is more concentrated than if you would eat a regular apricot. And three apricots would certainly qualify as a serving of fruit. Also Apricots are rich in nutrients. So a few apricots is a good choice. It's when you eat the whole bag in one or two sittings, that you start to have a problem. Remember, the real glucose (sugar) problem is often those hidden sugars that are the long chain molecular structure, where you cannot taste the sweet.
Candy bars are bad because they are a combination of sweet and fats... and no there is not enough redemptive good in the chocolate. The only good chocolate is a dark semi-sweet and even that in moderation.

I'm a real party pooper aren't I?

..what you say makes sense to all, PD or no PD. My conclusion from your posts is to eat well and in balance and to watch it

I did a short search on hyperglycemia, PD & dyskinesia, to see what was in the literature on Rosebud's theory.
I came across the following, which says reducing your glucose level also improves your levodopa response, as well as curbing dyskinesia.
Ron


Int J Neurosci. 1993 Mar-Apr;69(1-4):125-30.Links
The relationship between diabetes mellitus and Parkinson's disease.Sandyk R.
NeuroCommunication Research Laboratories, Danbury, CT.

It has been reported that 50% to 80% of patients with Parkinson's disease have abnormal glucose tolerance which may be further exacerbated by levodopa therapy. Little is known about the impact of chronic hyperglycemia on the severity of the motor manifestations and the course of the disease as well as its impact on the efficacy of levodopa or other dopaminergic drugs. This issue, which has been largely ignored, is of clinical relevance since animal studies indicate that chronic hyperglycemia decreases striatal dopaminergic transmission and increases the sensitivity of postsynaptic dopamine receptors. In addition, evidence from experimental animal studies indicates that diabetic rats are resistant to the locomotor and behavioral effects of the dopamine agonist amphetamine. The resistance to the central effects of amphetamine is largely restored with chronic insulin therapy. In the present communication, I propose that in Parkinson's disease diabetes may exacerbate the severity of the motor disability and attenuate the therapeutic efficacy of levodopa or other dopaminergic agents as well as increase the risk of levodopa-induced motor dyskinesias. Thus, it is advocated that Parkinsonian patients should be routinely screened for evidence of glucose intolerance and that if found aggressive treatment of the hyperglycemia may improve the response to levodopa and potentially diminish the risk of levodopa-induced motor dyskinesias.

PMID: 8082998 [PubMed - indexed for MEDLINE]

Out of interest, having found the BBB dysfunction implicated in almost everything PD, I did another search , and found that high blood sugar levels damage the BBB!!!
See,
http://www.nature.com/jcbfm/journal/.../9600454a.html

"The purpose of this study was to examine what levels of hyperglycemia cause blood–brain barrier (BBB) disruption during permanent and transient middle cerebral artery occlusion in the rat and when the adverse effects of hyperglycemia occur. "

There is a lot of evidence for this, eg
"These results suggest that hyperglycemia appears to be an important risk factor for additional increase in BBB permeability"
in
http://www3.interscience.wiley.com/c...TRY=1&SRETRY=0

Now I must read up more on diabetes.... This is a full time job!!!
Ron

I have no patience for researching things, so it's a good thing we have the likes of Ron and Rick And Tena and ZF and all you others who have to go find the written documentation. So one more time for those of you who didn't get it YOU CAN DECREASE YOUR DYSKINESIA AND IMPROVE YOUR OVERALL RESPONSE TO MEDS BY AVOIDING THE HIGH G.I. FOODS AND BY NOT OVEREATING AND BY CUTTING BACK ON THE SWEETS!

Thank you Ron. The question is: will at least some of you do it???

I will quote from a medical text

Hypoglycemic brain damage

Roland N. Auer,
Departments of Pathology and Clinical Neuroscience, Faculty of Medicine, University of Calgary, 3330 Hospital Drive N.W., Calgary, Alta., Canada T2N 4N1

Available online 10 November 2004.



Abstract
Hypoglycemia was long considered to kill neurons by depriving them of glucose. We now know that hypoglycemia kills neurons actively from without, rather than by starvation from within. Hypoglycemia only causes neuronal death when the EEG becomes flat. This usually occurs after glucose levels have fallen below 1 mM (18 mg/dl) for some period, depending on body glycogen reserves. At the time that abrupt brain energy failure occurs, the excitatory amino acid aspartate is massively released into the limited brain extracellular space and floods the excitatory amino acid receptors located on neuronal dendrites. Calcium fluxes occur and membrane breaks in the cell lead rapidly to neuronal necrosis. Significant neuronal necrosis occurs after 30 min of electrocerebral silence. Other neurochemical changes include energy depletion to roughly 25% of control, phospholipase and other enzyme activation, tissue alkalosis and a tendency for all cellular redox systems to shift towards oxidation. The neurochemistry of hypoglycemia thus differs markedly from ischemia. Hypoglycemia often differs from ischemia in its neuropathologic distribution, a phenomenon applicable in forensic practice. The border-zone distribution of global ischemia is not seen, necrosis of the dentate gyrus of the hippocampus can occur and a predilection for the superficial layers of the cortex is sometimes seen. Cerebellum and brainstem are universally spared in hypoglycemic brain damage. Hypoglycemia constitutes a unique metabolic brain insult.

Keywords: Hypoglycemia; Metabolism; Brain; Necrosis; Excitatory amino acids; Running title; Brain in hypoglycemia



Forensic Science International
Volume 146, Issues 2-3, 16 December 2004, Pages 105-110
Forensic Neuropathology

http://tinyurl.com/2yl2en



there are many roads that may lead to brain damage/
yet these are well known
too high amounts of sugar - diabetic
very low blood sugar - hypoglycemia

here is a link that is for YOUNG ONSET PD
http://www.emedicine.com/neuro/topic635.htm

Your post on Hypoglycemia upholds everything I believe about the path that I took to the dx of PD. It may not be everyone's story but it sure is mine. Throw in a little extreme stress and you have a recipe for disaster. Thanks for posting that...I feel validated.

This hugs for you...(and Ron)