PD as Metabolic Disorder
 

Ketones are produced by the liver in response to famine as well as diabetes. In the case of the former, they serve as a replacement for glucose in providing fuel for mitochondria to convert to useable energy in the brain.

In PD, the mitochondria are damaged in such a way that they cannot burn glucose. But the damage seems not to interfere with their ability to burn ketones. In the thread about using diet to reduce symptoms, it may be that some of us are experiencing a form of this effect. Either way, this represents a new way of attacking PD. It also is not going to earn Big Pharma much money, so if it is going to bear fruit it will need our help.

You can cause your body to produce ketones by manipulating your diet. Fasting, for example, triggers their production. A diet extremely high in fat also does it. The latter has been a long used treatment for epilepsy in children. But it is a terribly hard diet to stick to and has some danger.

But there is a possibility that a compromise exists that can help PD. Could we eat our way to health?:)


1: Neurology. 2005 Feb 22;64(4):728-30.
Comment in:
Neurology. 2006 Feb 28;66(4):617; author reply 617.

Treatment of Parkinson disease with diet-induced hyperketonemia: a feasibility
study.

Vanitallie TB, Nonas C, Di Rocco A, Boyar K, Hyams K, Heymsfield SB.

Division of Endocrinology, Diabetes, and Nutrition, Department of Medicine, St.
Luke's-Roosevelt Hospital Center, New York, USA. tedvani@ewol.com

Ketones may bypass the defect in complex I activity implicated in Parkinson
disease (PD). Five of seven volunteers with PD were able to prepare a
"hyperketogenic" diet at home and adhere to it for 28 days. Substituting
unsaturated for saturated fats appeared to prevent cholesterol increases in four
volunteers. Unified Parkinson's Disease Rating Scale scores improved in all five
during hyperketonemia, but a placebo effect was not ruled out.

PMID: 15728303 [PubMed - indexed for MEDLINE]

Lewy bodies are the result of glycation
 

Another example of a serious aspect of PD that could be eased by diet. Within the power of each of us if we figure out the program to follow.

1: Biogerontology. 2004;5(6):365-73.

Glucose, glycation and aging.

Suji G, Sivakami S.

Department of Life Sciences, University of Mumbai, Santa Cruz (E), Mumbai 400
098, India.

Glycation, a deleterious form of post-translational modification of
macromolecules has been linked to diseases such as diabetes, cataract,
Alzheimer's, dialysis related amyloidosis (DRA), atherosclerosis and Parkinson's
as well as physiological aging. This review attempts to summarize the data on
glycation in relation to its chemistry, role in macromolecular damage and
disease, dietary sources and its intervention. Macromolecular damage and
biochemical changes that occur in aging and age-related disorders point to the
process of glycation as the common event in all of them. This is supported by
the fact that several age-related diseases show symptoms manifested by
hyperglycemia. Free radical mediated oxidative stress is also known to arise
from hyperglycemia. There is evidence to indicate that controlling hyperglycemia
by antidiabetic biguanides prolongs life span in experimental animals. Caloric
restriction, which appears to prolong life span by bringing about mild
hypoglycemia and increased insulin sensitivity further strengthens the idea that
glucose via glycation is the primary damaging molecule.

PMID: 15609100 [PubMed - indexed for MEDLINE]

interesting articles Rick. I guess I'll be doing some more reading, experimenting and asking questions. Big Pharma wouldn't like it much if it was that simple.

GregD