Eureka! We have a cure for PD!
 

Where's the other post?
 

Imad,

Don't keep us hanging in suspense...where is your other post on your difference in taking coconut oil?!?!

Laura

while we are waiting...
 

My mind has been running the same direction and perhaps this would combine nicely with MCT-


1. Am J Physiol Regul Integr Comp Physiol. 2009 Apr;296(4):R1071-7. Epub 2009 Feb
11.

Quercetin increases brain and muscle mitochondrial biogenesis and exercise
tolerance.

Davis JM, Murphy EA, Carmichael MD, Davis B.

University of South Carolina, Department of Exercise Science, Columbia, SC 29208,
USA. markd@mailbox.sc.edu

Quercetin is one of a broad group of natural polyphenolic flavonoid substances
that are being investigated for their widespread health benefits. These benefits
have generally been ascribed to its combination of antioxidant and
anti-inflammatory activity, but recent in vitro evidence suggests that improved
mitochondrial biogenesis could play an important role. In addition, the in vivo
effects of quercetin on mitochondrial biogenesis exercise tolerance are unknown.
We examined the effects of 7 days of quercetin feedings in mice on markers of
mitochondrial biogenesis in skeletal muscle and brain, and on endurance exercise
tolerance. Mice were randomly assigned to one of the following three treatment
groups: placebo, 12.5 mg/kg quercetin, or 25 mg/kg quercetin. Following 7 days of
treatment, mice were killed, and soleus muscle and brain were analyzed for mRNA
expression of peroxisome proliferator-activated receptor-gamma coactivator
(PGC-1alpha) and sirtuin 1 (SIRT1), and mitochondrial DNA (mtDNA) and cytochrome
c. Additional mice underwent a treadmill performance run to fatigue or were
placed in voluntary activity wheel cages, and their voluntary activity (distance,
time, and peak speed) was recorded. Quercetin increased mRNA expression of
PGC-1alpha and SIRT1 (P < 0.05), mtDNA (P < 0.05) and cytochrome c concentration
(P < 0.05). These changes in markers of mitochondrial biogenesis were associated
with an increase in both maximal endurance capacity (P < 0.05) and voluntary
wheel-running activity (P < 0.05). These benefits of querectin on fitness without
exercise training may have important implications for enhancement of athletic and
military performance and may also extend to prevention and/or treatment of
chronic diseases.


PMID: 19211721 [PubMed - indexed for MEDLINE]

(Note that full text is available)



1. Med Sci Sports Exerc. 2009 Jul;41(7):1467-75.

Effects of quercetin and EGCG on mitochondrial biogenesis and immunity.

Nieman DC, Henson DA, Maxwell KR, Williams AS, McAnulty SR, Jin F, Shanely RA,
Lines TC.

Department of Health, Leisure, and Exercise Science, Appalachian State
University, Boone, NC 28608, USA. niemandc@appstate.edu

PURPOSE: To test the influence of 1000 mg of quercetin (Q) with or without 120 mg
of epigallocatechin 3-gallate (EGCG), 400 mg of isoquercetin, and 400 mg of
eicosapentaenoic acid and docosahexaenoic acid (Q-EGCG) on exercise performance,
muscle mitochondrial biogenesis, and changes in measures of immunity and
inflammation before and after a 3-d period of heavy exertion. METHODS: Trained
cyclists (N = 39) were randomized to placebo (P), Q, or Q-EGCG and ingested
supplements in a double-blinded fashion for 2 wk before, during, and 1 wk after a
3-d period in which subjects cycled for 3 h x d(-1) at approximately 57% Wmax.
Blood, saliva, and muscle biopsy samples were collected before and after 2 wk of
supplementation and immediately after the exercise bout on the third day. Blood
and saliva samples were also collected 14 h after exercise. RESULTS: Two-week
supplementation resulted in a significant increase in plasma quercetin for Q and
Q-EGCG and granulocyte oxidative burst activity (GOBA) in Q-EGCG. Immediately
after the third exercise bout, significant decreases for C-reactive protein
(CRP), and plasma interleukin 6 (IL-6) and interleukin 10 (IL-10) were measured
in Q-EGCG compared with P. Granulocyte colony-stimulating factor and CRP were
reduced in Q-EGCG 14 h after exercise. No group differences were measured in
muscle messenger RNA expression for peroxisome proliferator-activated receptor
gamma coactivator alpha, citrate synthase, or cytochrome c. CONCLUSIONS: Two-week
supplementation with Q-EGCG was effective in augmenting GOBA andin countering
inflammation after 3 d of heavy exertion in trained cyclists.


PMID: 19516153 [PubMed - indexed for MEDLINE]

ordering coconut oil tommmorrow!

Coconut oil, Really?

I find it hard to believe that after 193 years since James Parkinson published his paper on The Shaking Palsy and many many years of medical research and millions and millions of dollars the the key to curing Parkinson's disease is coconut oil. Then again, I am not surprised at all. I have felt since I was first diagnosed that it had to be something simple at the cellular level. I have even been chastised on the old Braintalk forum and in this very forum for suggesting that someone who knows what they are doing goes back to basic biology and start from the beginning. I will be keeping an eye on this for sure.

GregD

The drugs used for diabetes do not heal mitochondria.

Taking supplements that facilitate mitochondrial processes however, will enhance any use of coconut oil.

These are acetyl carnitine, CoQ-10 and lipoic acid.

Avoidance of drugs that damage mitochondria is important, and some common drugs do this:
statins,
fluoroquinolone antibiotics (Cipro, Levaquin, Avelox)

This post gives a more complete list:
http://neurotalk.psychcentral.com/ar.../t-122889.html

Insulin resistance and alterations of insulin also are problematic.
A specific form of inositol, called d-chiro inositol is known to improve insulin actions at the cellular level. This tends to be expensive, but fertility doctors are using in in women who have PCOS, and elevated insulin, called insulin resistance.

http://www.chiralbalance.com/
Anyone can buy this, as it is over the counter, but it is still costly.

Using coconut oil without consideration of these other factors, affecting mito metabolism, is not likely to succeed if toxic substances are used that continue to damage the mitochondria.

looks like pharma interested
 

Ketogenic diet, modified atkins, etc
 

drugs to repair the mitochondriya
 

MrsD:
My statement that existing drugs to treat diabetics may be used to deal with (heal) the mitochondria failure to accept glucose is based on my understanding of the following article. My terminology may not be scientifically accurate.
Any way, my understanding is that the "faulty" mitochondria (as far as accepting glucose) can still accept ketones without the need of any drugs!

http://www.msnbc.msn.com/id/39541782...ealth_library/
The brain cells of patients with Parkinson's disease undergo a shutdown of their energy powerhouses, the mitochondria, according to a new study. Because this shutdown probably occurs early in Parkinson's cases, the finding could lead to therapies that stop the disease before too much damage has been done.
Researchers identified 10 groups of genes — called gene sets, each carrying out one biological process — associated with Parkinson's disease. Many of these gene sets are involved in helping the mitochondria do their job. Even in people whose autopsies revealed early Parkinson's — who did not have clinical symptoms, but whose brains showed signs of the disease — these gene sets were not expressed properly, meaning the mitochondria in those cells probably weren't working.
The loss of working mitochondria, which produce most of the cell's energy, may contribute to the onset of the disease, the researchers said.
All of these gene sets are controlled by a single gene, a "master regulator" called PGC-1alpha that switches the gene sets on or off. This gene could be a target for future therapies to treat or prevent the disease, the researchers said
Their results are published today in the journal Science Translational Medicine.
Parkinson's genes
Parkinson's affects about 5 million people globally. The disease kills brain cells that produce the chemical dopamine. This impairs patients' movements, causing symptoms such as tremors, muscle stiffness and impaired balance and coordination. The cause of the disease is not known.
Clemens Scherzer, of Brigham and Women's Hospital and Harvard Medical School, and his colleagues analyzed genetic data from 17 studies involving a total of 322 human brain tissue samples and 88 blood samples. Of these, 185 were derived from the dopamine-producing brain cells of deceased patients with Parkinson's.
They initially found 28 gene sets to be associated with Parkinson's. Further research looking into the genomes of patients with early Parkinson's narrowed the field to 10 gene sets.
Some of these gene sets contain the genetic code to make proteins involved in the electron transport chain — a set of reactions inside the mitochondria that produce energy. Defects in the electron transport chain would severely affect the ability of the brain cells to generate energy, the researchers said.
It's possible that genetic and environmental influences, along with aging, have a combined impact on the expression of the mitochondrial genes, Scherzer said.

Future drugs
Medications that activate the PGC-1alpha gene already have been approved by the U.S. Food and Drug Administration for treatment of other diseases, such as diabetes. This means pharmaceutical companies may be able to develop new drugs for Parkinson's by tweaking already developed drugs rather than by starting from scratch, the researchers said.
The study was funded by the National Institute of Neurological Disorders and Stroke, the National Institute on Aging, and the Michael J. Fox Foundation, among others.
cheers
Imad

Ahhhh
 

Do people who live in a country where the diet is naturally high in coconut oil have less cases of Parkinson's than other countries where other fats are used?
I am certainly not anti coconut oil as we use it as our main fat in food I make, as I believe in its healing properties.