Coenzyme Q10?

[ashleyk]

Hi, I saw my neurologist this week and was told there has not been much change in my PD over the past 9 months. Good news. I take low amounts of Sinemet and Mirapex. I also take other supplements, one of them being 200mg of coenzyme Q10 for the past year. My doctor told me to take the max Q10 for PD which I guess is 1200mg. I am wondering if this is the right thing to do. From what I know, there have been one or two Q10 studies done on small groups of people with PD. Are there any more or recent studies that say Q10 slows PD? Does anyone take 1200mg of Q10 and can you say it works and is worth the expense?
Ashley

[reverett123]

I have wondered about CoQ10, especially its cost effectiveness. If I understand it right, it is acting as an antioxidant and/or an anti-inflammatory. In both categories there are cheaper and more effective alternates. Curcumin and green tea extract for example.

[jeanb]

Ashley,

i try to take 1600mg :eek: of coq10 per day (...often less than that though because i frequently miss taking doses throughout the day). i do believe it works, but it is pretty expensive.

my doctor writes a prescription for me, which i keep with tax receipts. arizona allows it as a medical expense, so i get some of that cost back in the form of a tax refund.

[caya]

There has been a study at the University of San Diego a couple of years ago headed up by Dr. Clifford Shults and the results were amazing. The folks with early stage PD who took 1200 mg per day for 16 months showed 44%
LESS decline in symptoms. (Go on line and look up Dr. Shults and/or just CoQ10). The CoQ10 acts on the mitochondria in the brain cells which are deficient in CoQ10 in PD patients. My Movement Disorder Specialist put me on 1200 mg of CoQ10 on August 22nd and I go in for my first check up February 16th which I think is going to be a good one. This stuff really gives me a lot of energy. It is expensive, but worth it. In the CoQ10 arena, one must be very careful about what type you take. For it to be effective inn PD treatment it must be formulated to have the capacity to cross the Blood Brain Barrier. Most CoQ10 soft-gels do not do this. What I take is a chewable wafer form and is the one that was used in the trials at UC San Diego........that is University of California at San Diego.....not Univ. of San Diego as I wrote above. CoQ10 is something we will all be hearing more about in the near future. But the most important thing to remember is the formulation. It MUST be formulated in a manner that it will cross the Blood Brain Barrier.........or it won't do one bit of good.

Caya

[CTenaLouise]

co -enzyme B is much better!
:)

[olsen]

coenzyme q10 is a co-factor in the chemical reaction that takes place within the mitochondria of our cells to produce energy for our cells. that energy is "ATP" or adenosine triphosphate, and is generated from foodstuff substrates through a process(oxidative phosphorylation) involving the "electron transport chain" (ETC)that is in the mitochondrion itself. this ETC consists of 5 complexes (actually more than 5, though most references list the 5 well known ), complexes 1,2,3,4 and 5--the end result is both ATP for cellular energy and a "few" rogue oxygen species that are uncoupled (known as free radicals). these free radicals can inflict much damage to the cell (known as "oxidative stress), eventually resulting in death of the cell.

coenzyme q10 is part of complex 1, 2 and 3--it is a necessary factor for energy to be made efficiently within our cells. coq10 also functions as an anti-oxidant within the cell--it "neutralizes" free radicals--uncoupled oxygen--thru its ability to donate an electron to the rogue molecule. thus it serves 2 major purposes within every cell of the body--major co-factor in production of ATP thru oxidative phosphorylation and as an electron donor to reactive oxygen species and thus an anti-oxidant..

Parkinson's is theorized to be due to several pathophysiological problems; the first 2 mentioned are frequently: mitochondrial dysfunction and oxidative stress--in both, coq10 is involved.

Apart from the chemical and antioxidant functions of coq10 that "should" theoretically help, there have been independent studies showing lower coq10 levels in platelets and serum of patients with PD. all of the above constitutes the reasons (as i understand it) that shults, beal, et al did the original study utilizing megadoses of coq10 for patients with PD. it was a very small study--80 patients total--but the results showed a decrease in the progression of PD symptoms in patients with early stage PD. because of the theories about coq10's usefulness in mitochondrial dysfunction and oxidative stress, it is currently being used in clinical studies in multiple centers for patients with huntington's and alzheimer's. seems to me i remember reading it is being used in a study with patients with ALS, also. The highest dosage I have read about is 3000 mgm/day-used in the alzheimer's study. there is a study at present for PD patients--or it was supposed to start soon.

Is any of this correct? thus far, no one seems to know. (Most physicians caution people to wait until it has really been proven effective--the cost is so prohibitive that it may end up a waste of a considerable amount of $$$.) the use of coq10 scientifically sounds "reasonable"--though as anyone in science (NIkki, RLS, zucchini, carolyn, Ron, etc.) can tell you, you frequently cannot reason your way to the answer in science.....with the above knowledge, and with the consent of his neurologist, my husband decided to try the coq10--its primary drawback has been the cost!! the only side effects I have read about are GI--?maybe diarrhea, though i am unsure if that was it specifically... my husband has suffered no side effects from it, and felt that it made a major difference for him. mostly in his energy levels--he went from wanting to nap 2-3 times/day to having energy to work a full day and work out for 1 to 1 1/2 hrs/5 days a week. It has had no effect upon his tremor or slow movement.

all of the above is my interpretation of the science i have read--the errors are mine alone.

[Shelley]

Is it over the counter or prescription?

[olsen]

it is a supplement and over the counter. friend who is a pharmacist told me that sam's coq10 was "pretty" absorbable---and considerably less expensive.

[Shelley]

Thanks Olsen!:D

[reverett123]

Mitochondrial problems are, as stated above, one of the key prolems of PD and it is wise for us to know a little about them. This abstract gives a good bit of information but you really should go to Medline and search using the document number at the end. This will give you the opportunity to download the entire PDF (click on the logo at the right of the page) which is extremely well written for such a complex subject. And it's free.

1: Altern Med Rev. 2005 Dec;10(4):268-93.

Neurodegeneration from mitochondrial insufficiency: nutrients, stem cells,
growth factors, and prospects for brain rebuilding using integrative management.

Kidd PM.

University of California, Berkeley, USA. dockidd@dockidd.com

Degenerative brain disorders (neurodegeneration) can be frustrating for both
conventional and alternative practitioners. A more comprehensive, integrative
approach is urgently needed. One emerging focus for intervention is brain
energetics. Specifically, mitochondrial insufficiency contributes to the
etiopathology of many such disorders. Electron leakages inherent to
mitochondrial energetics generate reactive oxygen free radical species that may
place the ultimate limit on lifespan. Exogenous toxins, such as mercury and
other environmental contaminants, exacerbate mitochondrial electron leakage,
hastening their demise and that of their host cells. Studies of the brain in
Alzheimer's and other dementias, Down syndrome, stroke, Parkinson's disease,
multiple sclerosis, amyotrophic lateral sclerosis, Huntington's disease,
Friedreich's ataxia, aging, and constitutive disorders demonstrate impairments
of the mitochondrial citric acid cycle and oxidative phosphorylation (OXPHOS)
enzymes. Imaging or metabolic assays frequently reveal energetic insufficiency
and depleted energy reserve in brain tissue in situ. Orthomolecular nutrients
involved in mitochondrial metabolism provide clinical benefit. Among these are
the essential minerals and the B vitamin group; vitamins E and K; and the
antioxidant and energetic cofactors alpha-lipoic acid (ALA), ubiquinone
(coenzyme Q10; CoQ10), and nicotinamide adenine dinucleotide, reduced (NADH).
Recent advances in the area of stem cells and growth factors encourage optimism
regarding brain regeneration. The trophic nutrients acetyl L-carnitine (ALCAR),
glycerophosphocholine (GPC), and phosphatidylserine (PS) provide mitochondrial
support and conserve growth factor receptors; all three improved cognition in
double-blind trials. The omega-3 fatty acid docosahexaenoic acid (DHA) is
enzymatically combined with GPC and PS to form membrane phospholipids for nerve
cell expansion. Practical recommendations are presented for integrating these
safe and well-tolerated orthomolecular nutrients into a comprehensive dietary
supplementation program for brain vitality and productive lifespan.

PMID: 16366737 [PubMed - indexed for MEDLINE]

[rosebud]

A friend of mine who is a pharmacist has been after me to take it for awhile, about two years. I told him the cost is out of my league. He told me a year ago that there is a new formulation of it that is cheaper and more condensed so you don't need as much. Yesterday he sat with me through one of my off spells and he said "you've got to do this, there has to be a way." He was stunned by the intensity of my legs tremoring and the anxiety attack that comes along with it. Sweating etc. He says he has some of his regular PD patients on it and they get it direct from a supplier in the States. He also said it takes about 8 or more months before the benefits really start to show. That is not unusual for natural supplement type nutrients.Natures way to titrating up the ladder and natural adjustment. We are spoiled by drugs that work within days and don't stick with it for the payoff when we have to wait. The other thing that has thrown me is I got "generic Sinemet" last perscription refill, and it is REALLY BAD!!!! I'm going to the pharmacy to get this one corrected, whatever I have to do!

[RLSmi]

in directly shuttling electons in mitochondrial oxidative metabolism, an additional function of coenzyme Q10 has been discovered. This process is currently being studied by a research group at Yale led by Tamas Horvath.

It has been known for some time that the mitochondria in brown fat (plentiful in hibernating animals and newborn babies) contain a protein that allows some hydrogen ions which were pumped out across the inner mitochondrial memberane to "leak" back into the inner matrix rather than re-entering via passage through the inner membrane enzyme ATP synthase. This process is called "uncoupling" because it allows oxidation to occur without being coupled to phosphorylation, the synthesis of ATP from ADP and phosphate. In mitochondrial oxidation, a series of electron transport proteins embedded in the inner matrix membrane uses energy released as electrons from fuel molecules are passed down the chain to pump protons (hydrogen ions) out of the inner matrix space to create a proton concentration gradient across the membrane. The energy of that gradient is released when the protons either pass through the ATP synthase enzyme complex to be conserved as high energy phosphate bonds, or as heat if re-entering through the uncoupling protein.

The brown fat mitochondrial protein, uncoupling protein 1 (UCP1), permits some proton leakage, allowing this tissue to generate heat, in addition to making ATP. This is an adaptation to protect the newborn from the thermal shock of birth and to provide other animals with heat during hibernation.

It turns out that there are a couple of different but similar uncoupling proteins, UCP2 and UCP3. UCP2, which occurs primarily in mitochondria of central nervous system cells, is activated by coenzyme Q10. When mitochondrial oxidative phosphorylation is partially uncoupled by UCP2 and CoQ10, the production of reactive oxygen species such as superoxide is decreased, and the uncoupling also stimulates the formation of more mitochondria. This seems to be counterintuitive, since less ATP formation would seem to result in less energy available for nerve function. Horvath's group suggest that the additional mitochondria compensate for any resulting loss of ATP production.

A fascinating hypothesis proposed by this group is that the heat released by local, selective mitochondrial uncoupling in specific neurons enhances the diffusion of neurotransmitters such as dopamine released from pre-synaptic cells to receptors on post-synaptic cells.

Robert

[reverett123]

...but in case you missed it earlier, this is the link to the full eight minute video collaboration between Harvard's biology department and some top animators. Robert's post just made me appreciate anew what an incredible thing we are and this video is one of the best ways to get a glimmer of what is really going on. It's so darned beautiful under the hood...

http://multimedia.mcb.harvard.edu/anim_innerlife_hi.html