Marnie
Frequent Contributor (5K+ posts)
Member # 773
posted
and MnSOD is too high.
CoQ10 is an enzyme that carries hydrogen INTO the cells, from what I understand.
It has been said if we can get hydrogen INTO any cell, it can heal that cell.
Also...watch closely the dopamine -> epinephrine (adrenalin) connection.
We KNOW steroids make lyme worse...spell disaster.
This might be why very high doses of CoQ10 made a HUGE difference in experiments (trials) with those suffering with Parkinson's.
Here's some information:
The biosynthesis of CoQ10 from the amino acid tyrosine is a multistage process requiring at least eight vitamins and several trace elements.
What happens if there is too little tyrosine? A lot less energy.
When Parkinson's patients were given a lot of CoQ10, the energy production of the cells picked up.
High fatigue levels have been correlated with low succinic acid and asparagnine excretion and
reduced tyrosine
and phenylalanine serum levels. Not surprisingly CFS patients, in contrast to controls, exhibited a similar pattern.
This data suggests that increased catabolism (breakdown) of asparagnine and phenylalanine and
possibly tyrosine
results in
increased glycolysis in CFS patients! (Boy, that would make Bb happy!)
That serum glucose and succinate excretion are positively correlated suggests that
glycolysis is upregulated (anerobic phosphorylation)
and oxidative phosphorylation (aerobic phosphorylation) is inhibited in CFS.
(If asparagnine, phenylalanine and tyrosine are reduced in CFS then the output of the last half of the citric acid cycle is reduced.)
(To make matters worse) the precursors of catecholamines appear to be *broken down* by this mechanism. (Catecholamines are neurotransmitters; epinephrine, norepinephrine and dopamine. They are all derived from tyrosine.
The authors earlier noted that tyrosine levels were reduced in CFS patients relative to controls.) Reduced catecholamine levels may lead to many of the sympathetic nervous system associated symptoms found in CFS.
tyrosine into dopamine ->
DOPA decarboxylase converts DOPA to dopamine, dopamine b-hydroxylase converts dopamine to norepinephrine and phenylethanolamine N-methyltransferase converts norepinephrine to epinephrine.
Norepinephrine is also called noradrenaline and epinephrine is called *adrenaline*.
Melatonin functions by *inhibiting* the synthesis and secretion of other neurotransmitters such as dopamine and GABA...the feel good (dopamine..hey let's go to Vegas!) and the brakes (GABA)...
Tryptophan -> serotonin -> melatonin.
See the tyrosine-tryptophan ``defect''? Too little tyrosine, too much tryptophan. This is due to too little Mg IN the cells.
Tyrosine is a ``lowly amino acid''. It normally has to compete to go into the cells. If Bb is using tyrosine to stimulate glycolysis, not enough is available to fuel the mitochondria.
By giving CoQ10 (which also functions as an antioxidant), we would be ``conserving'' tyrosine because then we don't have to make it from tyrosine + other nutrients.
AND...the enzyme, CoQ10 is formulated with either soybean or rice bran oil which contain the nutrients to power the cell...specifically Mg and B6....
Restarting the Mg-ATP pump would drive oxidative phosphorylation...oxygen into the cell to make more ATP.
So long Bb..
Additionally...
extracellular calcium suppresses *tyrosine* phosphorylation by
decreasing the availability of intracellular ATP
When Mg -ATP levels drop, Ca rises and tries to go into the cells. The thyroid can be impacted, so TNF alpha steps in to try to stop this.
Manganese oxide, produced by Corynebacterium sp. in liquid medium was found to be amorphous, probably hydrated and was readily
reduced by neutral quinol.
C oQ- Q Uinol
Side note...besides the estrogen link, here's another reason why there are fewer men with lyme:
increased iron stores (ferritin levels) are associated with *decreased manganese absorption* The finding that men generally absorb less manganese than women may be related to the fact that men usually have higher iron stores than women
How about 1200mg of CoQ10...300mg 4x/day?
We don't know how much of this enzyme we really make. We make it when we...EXERCISE...provided we have the nutrients to make it...starting with Mg and B6.
Note (read carefully):
In the present study, we investigated the relationship between oxidative stress and breast cancer development in tissue level. Breast cancer is the most common malignant disease in Western women. Twenty-one breast cancer patients, who underwent radical mastectomy and diagnosed with infiltrative ductal carcinoma, were used in the study.
We determined coenzyme Q10 (Q) concentrations, antioxidant enzyme activities (mitochondrial and total superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase), and malondialdehyde (MDA) levels in tumor and surrounding tumor-free tissues.
RESULTS: Q concentrations in tumor tissues significantly decreased as compared to the surrounding normal tissues p < 0.001. Higher MDA levels were observed in tumor tissues than noncancerous tissues p < 0.001. The activities of MnSOD, total SOD, GSH-Px and catalase in tumor tissues significantly increased p < 0.001 compared to the controls.
CONCLUSIONS: These findings may support that reactive oxygen species increased in malignant cells, and
may cause overexpression of antioxidant enzymes and the consumption of coenzyme Q10.
Posts: 9424 | From Sunshine State | Registered: Mar 2001
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Vermont_Lymie
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posted
Thanks for the information and analysis Marnie! Made me reach for my Mg and CoQ10 after reading your post.
Posts: 2557 | From home | Registered: Aug 2006
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Thanks for the easy to follow post. As a vegetarian, I'm starting to realize how important it is to supp w/ amino acids.
I did have the catecholamines, metanephrines, 5-HIAA Quant, and cortisol panels (24 hr urine) run in the first 6 months of this illness because of the symptoms I was having.
The only abnornal value wa the 17-OH-corticost was slightly elevated. Can't imagine why???
It was suspected I had an adrenal tumor.
With the estrogen link, it should make one pause about birth controls pill, HRT, and not to think of livestock that have been fed w/ hormones to beef them up.
Off to make make my protien shake, take my supp including CoQ10, and some almonds to munch on......
Stella Marie
-------------------- Stella Marie Posts: 694 | From US | Registered: Apr 2005
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Jellybelly
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Member # 7142
posted
Good info Marnie! I have been using 300-400 mgs of CoQ10 for years now. It is one of about 5 things that I won't give up. I could totally see the difference.
Unfortunatly CoQ10 is not easily absorbed. The powder forms are absoultely useless. CoQ10 is very expensive, so, you should get the most bang for your buck.
I discovered Q-Gel which is highly absorbable. There is some really, really good information in the book the Sinatra Solution, by author of the same name. The book is really about heart disease, but he focuses on getting the needed elements to the cells so that they can produce the needed energy we are all lacking. This is energy on a VERY cellular level.
The book is really good at explaining all of this, and since so many of us have heart involvement it is a must read in my opinion. Even if you don't, understanding energy at the level of the mitochondria is need to know stuff.
You can get Q-Gel from numerous places on the internet. I think I get mine from Vitacost, and I buy like 8 bottles at a time. We all take it, and don't even waste our money on the other forms. It may be more expensive, but you get what you pay for, and so absorb more of it. Ordering on the net makes it actually less expensive then the better brands you will find at most healthfood stores. So it's really a bargin.
Posts: 1251 | From california | Registered: Apr 2005
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"Coenzyme Q10 is synthesised naturally in humans and is also found in foods, such as vegetables and fish. It acts as a cofactor in the electron transfer pathway which produces energy (in the form of adenosine triphosphate - ATP) within the mitochondria of human cells. The energy is used for muscle contraction and other vital functions. It is also an antioxidant which may have a sparing effect on vitamins C and E in situations of oxidative stress.
Diminished concentrations of coenzyme Q10 have been reported with increasing age, on statin medication and in various disorders including cardiovascular disease and cancers. [Gold top tube (SST)] �21.00"
My result was 0.33, normal range is 0.55-2.00. I noticed quite a big difference in overall energy and heart function after starting 300mg a day for a few months. I now take 100-200mg daily.
P.S) I take Lamberts 100mg CoQ10, don't know if it is available in the U.S, but it is supposed to be very good.
Posts: 263 | From UK | Registered: Mar 2006
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johnnyb
Frequent Contributor (1K+ posts)
Member # 7645
posted
google search seemed to point to UK for Lamberts...
Since CoQ10 seems to be very important, yet expensive, lets do some research for brands that work well but aren't super-pricey (if such an animal exists).
As I mentioned, consumerlabs.com tests supplements.... any other services we can check?
- JB
Posts: 1197 | From New Jersey | Registered: Jul 2005
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Jellybelly
Frequent Contributor (1K+ posts)
Member # 7142
posted
This is the place I get my Q-gel. $28.77 for a highly absorbent form, good to me.
posted
I buy COQ10 at BJ's. 120 gel caps, 100mg. each, for $35.99. It is sold under the BJ brand called Berkeley & Jensen.
I have been taking 30 mg. of zinc daily and 600mg. daily of CoQ10 and have been feeling more energy and stamina now after several months. Am off all abx now. Hoping to add mangosteen juice soon.
MetaMetrix lab can test CoQ10 levels and also lipid peroxides. With adequate CoQ10 supplementation lipid peroxide levels should improve -- may still not be in normal range, but can get closer. With 400 mg of CoQ10 hubby's lipid peroxides fell from 4.9 to 1.1 in a couple of months -- 1.0 was normal on the test at the time. This was before any antibiotics and before his diagnosis.
If you are not currently taking CoQ10 then you should ramp up slowly -- can cause headaches if increase too quickly.
If you can afford it I would suggest the ION panel from MetaMetrix -- hopefully you can find a doc who does not mark up the cost and will let you pay directly for the test or bill to your insurance.
Hubby has been taking 400 - 800 mg of CoQ10 for about 5 years now since early in his illness. A very good neurologist (not Lyme literate unfortunately) prescribed the CoQ10. We buy the Life Extension brand. I feel that the CoQ10 is one of the reasons hubby has had less brain fog than many others seem to report. That is just my opinion and not medical advice.
Bea Seibert
Posts: 7306 | From Martinsville,VA,USA | Registered: Oct 2004
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posted
To Summarize : Our cells seem to function best when supplied with adequate amino acids, magnesium, CO Q 10 ( and of course other basic minerals and fatty acids ) .
treepatrol
Honored Contributor (10K+ posts)
Member # 4117
posted
Corynebacterium is a genus of Gram-positive, facultatively anaerobic, non-motile actinobacteria. Most do not cause disease, but are part of normal human skin flora.
Some nondiphtheria species of Corynebacterium produce disease in specific animal species, and some of these are also human pathogens. Some species attack healthy hosts, and others attack immunosuppressed hosts. Some of their effects include granulomatous lymphadenitis, pneumonitis, pharyngitis, skin infections, and endocarditis. Endocarditis caused by Corynebacterium spp. is particularly seen in patients with indwelling intravascular devices.
Infection by diphtheroids tend to occur in elderly, neutropenic, or immunocompromised patients, and those who have indwelling prosthetic devices such as heart valves, neurologic shunts, or catheters.
Certain Corynebacterium species are used in the industrial production of amino acids such as lysine.
-------------------- Do unto others as you would have them do unto you. Remember Iam not a Doctor Just someone struggling like you with Tick Borne Diseases.
posted
Just got my LIfe Extension magazine today(must be December issue it's not on internet yet) and there was an article about a new breakthrough from Japan. A more absorbale CoQ10 product......You take less mg and get more than before!!
I AM NOT PUSHING LIFE EXTENSION, but this is the first good news i've heard in increasing it's capacity for absorption.
Life Extension Super BioActive CoQ10 Ubiquinol 50 mg, 100 softgels........$52.65 for members
Now, Japan's largest CoQ10 producer has patented a form of CoQ10 that offers unprecedented bioavailability--capable of increasing human blood levels up to 8 times more efficiently than the higher-absorption CoQ10 products on the market today.
In studies from Japan, this superior new form of CoQ10 has shown remarkable antiaging effects. In one study, it was 40 percent more effective than conventional CoQ10 in slowing markers of aging in middle-aged mice.1 In a study of aged rats, this new form of CoQ10 demonstrated anti-fatigue effects that were 2.5 times greater than conventional CoQ10 supplements
The reason this new form of CoQ10 is so effective is that scientists have succeeded for the first time in producing a stabilized ubiquinol capsule form of CoQ10. While CoQ10 exists in both ubiquinol and ubiquinone forms, the ubiquinol form has been shown to be vastly more bioavailable than conventional ubiquinone CoQ10. In a study measuring absorption in humans supplementing with 150 mg and 300 mg , far lower doses of ubiquinol CoQ10 produced blood plasma levels of CoQ10 that were equivalent to those produced by much higher doses of ubiquinone.3 In fact, it would take up to 8 times more ubiquinone than ubiquinol to raise CoQ10 blood levels to the same level.3
Each capsule of Super BioActive CoQ10 Ubiquinol provides 50 mg of this novel ubiquinol form of CoQ10. With its superior absorption and ability to remain bioavailable over much longer periods of time, most healthy people will need to take just one capsule twice daily to obtain significantly higher blood levels of CoQ10.
References 1. Exp Gerontol 2006 Feb;41(2):130-40. 2. Kaneka Corporation study. Treadmill test with the age rat at the age of 61-63 weeks. 2006 3. Regul Toxicol Pharmacol. 2006 Aug 17; Absorption Comparison Using Different Form of CoQ10.
Gail
-------------------- Strength does not come from physical capacity. It comes from an indomitable will ~ Gandhi Posts: 562 | From Wellsville, PA, USA | Registered: Jan 2004
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Marnie
Frequent Contributor (5K+ posts)
Member # 773
posted
In the Parkinson Disease trials, the CoQ10 was given
WITH
vitamin E.
If I remember correctly, WE first identified this enzyme, but the Japanese developed the supplement.
Posts: 9424 | From Sunshine State | Registered: Mar 2001
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klutzo
Frequent Contributor (1K+ posts)
Member # 5701
posted
For those who agree that CFIDS is usually caused by Lyme, please read Dr. Cheney's new article on "CFS and Cardiac Issues" at:
He says COQ10 is needed, but unless other things are in balance first, COQ10 will cause more damage.
Klutzo
P.S. Before someone jumps on me, I have listed his full last name because, though he acknowledges infections like Lyme as triggers of CFS, he is not an LLMD.
Posts: 1269 | From Clearwater, Florida, USA | Registered: May 2004
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klutzo
Frequent Contributor (1K+ posts)
Member # 5701
posted
I Copied this from another forum where I posted it long ago. I don't remember the source, sorry. I take COQ10 (240 units/day) but am worried about all this, since I have proven brain hypoxia by BEAM scan.
- - - - - - - - - - - - - - - - - - - - - - - - Idebenone - The ultimate anti-aging drug? by James South MA
Idebenone (pronounced eye deb eh known) is a synthetic analog (variant) of one of life's most essential biochemicals, coenzyme Q10 (Co Q10). Co Q10 is an important antioxidant component of the lipid (fatty) membranes that surround all cells, as well as the lipid membranes surrounding the various organelles ("little organs"), such as mitochondria and microsomes, inside cells.
Co Q10 is also an important member of the "Electron Transport Chain" (ETC) within mitochondria, which are the "power plants" of the cell. Most of the oxygen we breathe is used inside the electron transport chain to produce much of the ATP bioenergy that powers virtually every activity of our cells and bodies.
Without CoQ10, or a good substitute, human life quickly ends, and Idebenone is a "better Co Q10" that has been extensively researched the past 15 years.
Co Q10's pro-oxidant action
When blood flow is seriously reduced to any part of the body, as in a heart attack, stroke, trauma, shock, or chronic poor blood circulation- cellular/ mitochondrial oxygen (O2) levels quickly drop in the affected region. Yet because oxygen is seven to eight times more soluble in the lipid zones of cell membrane, compared to the watery compartments of the cell, there is still sufficient oxygen remaining in the membranes of cells and organelles, as well as in the electron transport chain, to auto-oxidize Co Q10.
As the Co Q10 auto-oxidizes, hydrogen peroxide, superoxide and hydroxl free radicals are rapidly formed in massive numbers. These free radicals quickly damage cell/ organelle structure and function, as well as rapidly halt ATP energy generation by the electron transport chain.
Brain and spinal cord cells are especially prone to such damage, and may be irreparably damaged or even destroyed within minutes.
Why Idebenone is superior to Co Q10
Enter Idebenone to the rescue! Studies have shown that under the same cellular low oxygen conditions that cause Co Q10 to act as a pro-oxidant producer of damaging free radicals, Idebenone prevents the free radical damage and maintains relatively normal cell ATP levels.
In short, while Idebenone can effectively substitute for Co Q10's positive and life essential functions, it doesn't have Co Q10's free radical producing and energy crashing "dark side" which occurs under hypoxic (low oxygen) conditions.
Idebenone's potential benefits fall into five categories; antiaging, energy enhancement, cognition enhancement, organ protector and protector against excitatory amino acid neurotoxicity.
Idebenone - The anti-aging benefits
The mitochondrial power plants produce over 90% of all cellular ATP bioenergy. They are also generally the richest sites in Co Q10 (or Idebenone). Mitochondrial DNA (mtDNA) allows mitochondria to reproduce them-selves.
While the DNA in a cell nucleus comes from both our parents, mtDNA comes exclusively from our mother's mtDNA.
There are typically two or three copies of mtDNA in each mitochondrion, with average 1000 mitochondria per cell. Because mtDNA exists in the "heart of the fiery furnace" where electron "sparks" are constantly leaking as ATP is produced in the electron transport chain, mtDNA is far more prone to free radical electron damage than is the DNA in our cell nuclei that contains the "blueprint" for our entire organism.
At the same time, the repair capacity of mtDNA is much less than that of our cell nucleus DNA. As a consequence, over the course of a lifetime our mtDNA becomes ever more damaged, and the mitochondria produced therefrom become ever more ineffective at energy generation.
Studies comparing heart tissue from young people with that from elderly people have shown almost no significant mitochondrial dysfunction in young hearts, with significant, often severe mitochondrial dysfunction in elderly hearts.
The cells that are most susceptible to mitochondrial energy depletion with advancing age are the brain, skeletal muscle and heart muscle cells. Idebenone thus offers a prime anti-aging effect here in several ways.
Unlike Co Q10, even under the low oxygen conditions that may occur periodically over a lifetime, Idebenone will serve as a powerful mitochondrial free radical quencher, lessening the ever-increasing mtDNA damage that occurs with age.
Idebenone will work even better than Co Q10 within the electron transport chain to keep energy production high, even under hypoxic conditions. This is especially critical to brain and heart cells that may be rapidly damaged during low ATP production episodes that occur due to poor tissue oxygenation.
Idebenone - Energy enhancement
Iron is a "dual edged sword." It is absolutely essential for life, it plays a central role in ATP generation in the electron transport chain. Yet iron can also be a powerful initiator of free radical production and cell structural damage, especially under low oxygen conditions.
This occurs, for example, during stroke, and during the gradual onset of Parkinson's disease. Studies have shown that Idebenone can tightly couple oxidation to energy production. This prevents iron ions from wastefully and toxically, diverting oxygen to producing free radicals inside the mitochondria, instead of energy.
Studies have shown that Idebenone can almost completely eliminate this, diverting 10% of cellular oxygen away from toxic iron induced free radical generation, to beneficial ATP energy production under hypoxic conditions.
Mild cellular hypoxia can occur even from intense exercise, or even from mild exercise done by out of shape "couch potatoes."
Idebenone - Cognition enhancement
A variety of studies using brain cells, (animal and humans) have shown Idebenone's ability to enhance brain structure and function.
Human and animal studies have demonstrated that Idebenone can enhance serotonin production, even under far less than optimal conditions, as e.g. with a very low tryptophan diet, or in patients with cerebrovascular dementia.
Idebenone has enhanced cholinergic nerve function and consequent learning ability even under hypoxic conditions, or when an anti-cholinergic drug (Scopolamine) was administered.
Idebenone has increased cellular catecholamine (dopamine, adrenalin and noradrenanlin) production by enhancing cellular uptake of the precursor amino-acid tyrosine.
Idebenone enhances long term potentiation in hippocampal nerve cells, a key part of memory formation and consolidation. Idebenone has restored glucose (brain fuel) utilization and ATP production in ischemic (poor blood flow) rat-brain.
Idebenone has been shown to enhance general cerebral metabolism, lessen the damage from strokes, and has been used to treat Alzheimer's and other dementias.
And like the original nootropic drug; piracetam, Idebenone has been shown to promote information transfer across the corpus callosum, the membrane separating the right and left brain hemispheres.
This is turn may promote the union/ integration of the logical (yang) and intuitive (yin) halves of the brain/ mind.
Idebenone - Organ protector
As our organs age or are damaged, we age and are damaged. Over a lifetime, blood flow to our organs diminishes due to arteriosclerosis and less efficient heart pumping. This reduces oxygen dependent energy production needed for repair, reproduction and normal function of the organ cells. Free radical damage accumulates over time, leaving ever more dead, dying or dysfunctional cells within organs.
At some point a critical threshold is reached when too many cells within an organ are dysfunctional, and they can no longer sustain the organ's life and function. Then the organ- heart, brain, liver etc. fails.
Idebenone protects organs in many ways, it cushions them against hypoxic (low oxygen) and/ or ischemic (poor blood flow) damage. Idebenone enhances both normal and hypoxic ATP energy generation.
Each cell in our organs must produce the energy it needs for life and health, cells cannot "borrow" energy from each other.
Idebenone - The free radical quencher
Idebenone is a powerful antioxidant, more so than Co Q10, and in some studies is 30 to 100 times more effective, than vitamin E or vinpocetine as a free radical quencher within the brain cells.
Idebenone lessens the free radical induced mtDNA damage that accumulates acceleratingly over a lifetime, slowing organ damage and aging.
A 1995 study in the Journal of Transplantation compared the organ preserving effects of Co Q10 and Idebenone. The study measured various factors, such as free radical membrane lipid damage, cell protein damage and cellular energy production under hypoxia conditions.
The results showed Idebenone to be dramatically more effective than Co Q10 at preserving liver tissue under conditions identical to that endured by whole livers "harvested" and stored (briefly) before transplant to another person.
The study recommended using Idebenone to increase the transplant viability of human livers donated for organ transplant. Why not use Idebenone to increase your own organ viability, while you still have the use of them!
Protection against excitatory amino acid (EAA) neuro toxicity
Glutamic acid and aspartic acid are the two chief excitatory amino acid neurotransmitters in the human brain. Without them we would be "mental vegetables."
Yet under certain conditions, e.g. stroke or traumatic brain injury- excessive amounts of excitatory amino acids accumulate in the fluid surrounding brain cells, causing damage and even death to nerve and glial cells through free radical mechanisms.
Excitatory amino acid toxicity is at least partly responsible for the neurotoxicity of the recreational drug "Ecstasy or MDMA." Studies over the past 30 years have also shown that excessive dietary intake of excitatory amino acids may also damage brain structure/ function, especially in children or excitatory amino acid sensitive adults.
The two main dietary sources of excitatory amino acids are the flavor enhancer MSG (monosodium glutamate) and the artificial sweetener aspartame (Nutrasweet). Also many processed foods (e.g. canned soups, dry roasted spiced peanuts, beef/ chicken bouillon, canned tuna, spices etc.) contain "hydrolized vegetable protein, yeast extract, soy protein isolate" and similar ingredients that are mostly excitatory amino acids.
In studies with various types of nerve cell, as well as oligodendroglial cells (which make up the protective myelin sheaths surrounding many nerves, the so-called "white matter" of the brain). Idebenone has shown dramatic protective effects against glutamate toxicity.
Summary
With all these powers, Idebenone should now rightfully take its place in the first rank of anti-aging/ nootropic/ energizer drugs, along with Hydergine, piracetam, vinpocetine, deprenyl and GH3/ KH3 (and it's one of my personal favorites!)
So who can benefit from Idebenone? The answers are,
1. Healthy people wishing cognitive enhancement and brain energizer effects (it synergizes well with piracetam, vinpocetine and Hydergine). 2 or 3 tablets (45mg each) daily.
2. Stroke victims wishing to improve memory, emotional or speech disturbances. 3 to 6 tablets (45mg each) daily.
3. Alzheimer's and cerebrovascular dementia patients. 4 to 6 tablets (45mg each) daily.
4. Those preparing for major surgery, especially brain, heart, liver or kidney. Synergizes well with Hydergine. 4 to 6 tablets (45mg each).
5. People with heart energetics problems, e.g. cardiomyopathy, ischemic heart disease, congestive heart failure. 3 to 6 tablets (45mg each) daily.
6. People with myelination problems, e.g. multiple sclerosis or "white matter" stroke injury. 3 to 6 tablets (45mg each) daily.
7. Those seeking to increase their general energy and vitality levels. 2 to 3 tablets (45mg each) daily.
8. People with especially high endurance energy needs, e.g. cross country skiers, long distance runners, cyclists, swimmers etc. 3 to 4 tablets (45mg each) daily.
9. Those at risk of excitatory amino acid brain damage, e.g. people who routinely consume large amounts of aspartame sweetened foods/ drinks, or those who routinely eat MSG or "hydrolyzed vegetable protein" containing restaurant or prepared foods. 2 or 3 tablets (45mg each) daily.
10. People wishing to enhance the brain serotonin benefits of tryptophan or 5-hydroxy-tryptophan supplements or SSRI drugs, such as Prozac, Paxil, Zoloft, or Luvox etc. 2 to 4 tablets (45mg each) daily.
11. Those suffering acute or chronic liver damage from poison mushrooms, toxic chemicals, hepatitis etc. 2 to 4 tablets (45mg each) daily.
12. People desiring a "long haul" broad-spectrum anti-aging drug. Synergizes well with deprenyl, Hydergine, GH3/ KH3. 2 or 3 tablets (45mg each) daily.
Because of its synergy with other life extension drugs, those also taking any or all of Hydergine, piracetam (and its analogues), vinpocetine, deprenyl, GH3/ KH3 may benefit from even just one 45mg tablet a day, especially if taken regularly on a long-term basis. Because idebenone is fat soluble, it is best taken with a fat rich meal, or with lipid absorption enhancing agents such as lecithin or phosphatidyl choline.
Numerous studies have shown that idebenone is well distributed through-out the body after absorption, accumulating in cellular and organelle membranes, as well as in the electron transport chain, exactly where it does the most good!
___________________
Posts: 1269 | From Clearwater, Florida, USA | Registered: May 2004
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clairenotes
Frequent Contributor (1K+ posts)
Member # 10392
posted
With the onset of puberty my daughter experienced sudden brain chemistry issues. PEA and dopamine and epinephrine and norepinephrine were way off.
We were able to address much of the imbalance through products from Neuroscience out of Wisconsin but they are expensive. They are basically made up of specially formulated aminos and minerals.
My question was always... yes but... what caused this extreme imbalance in the first place? I am never satisfied when it comes to health, and this was not normal.
A THOUSAND THANKS for these posts on CoQ10 and Mg deficiencies. Perhaps another mystery unlocked.
Also, Life Enhancement as opposed to Life Extension also has a supplement called Pegysomal CoQ10. It is also supposed to be more easily absorbed. Have not tried it myself and I am also not, in any way associated with the organization. My husband has been telling me about the different pegysomal products for awhile.
Claire Posts: 1111 | From Colorado | Registered: Oct 2006
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clairenotes
Frequent Contributor (1K+ posts)
Member # 10392
posted
Also... would it not help to go after the corynebacterium to reduce manganese oxide among other possibilities?
Claire
Posts: 1111 | From Colorado | Registered: Oct 2006
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Marnie
Frequent Contributor (5K+ posts)
Member # 773
posted
Even though I am not a "fan" of abx., I did post this:
Magnesium-containing antacids and laxatives
and the ***antibiotic medication, tetracycline, may decrease the absorption of manganese***
if taken together with manganese-containing foods or supplements (22).
That's not a good situation to be in...given the fact that Bb uses Mn.
Posts: 9424 | From Sunshine State | Registered: Mar 2001
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klutzo
Frequent Contributor (1K+ posts)
Member # 5701
posted
I hate to sound so negative, but please be careful with the NeuroSciences products. I had their testing. Predictably, it was way too low, since their "norms" are far different than the conventional medical norms for the same tests, and I was put on NeuroReplete and CysReplete.
It almost killed me, and I do not exaggerate. I ended up on a portable heart monitor, barely able to walk across a room.
Your neurotransmitter levels change from moment to moment. In fact, they change with every thought you have! I don't know how they can claim that levels taken at 10:30 am are reflective of the way you are all the time.
Tyrosine and 5HTP can dramatically increase blood pressure. 5HTP is a potent vasoconstrictor. That is fine unless you are a part of the late-stage Lyme minority like me who have high blood pressure already. Then it's a disaster.
I am very glad it helped your child, but it took me months to get over what it did to me. Also ,the withdrawl was worse than withdrawl from prescription antidepressants. I cried for weeks after stopping it, because the supplements had prevented my body from making it's own serotonin.
Klutzo
Posts: 1269 | From Clearwater, Florida, USA | Registered: May 2004
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clairenotes
Frequent Contributor (1K+ posts)
Member # 10392
posted
Klutzo,
No... your not being too negative. Wish that all the people who disagree were that polite.
I am very sorry to hear about your experiences with Neuroscience products. Never in my wildest dreams would I have thought that their products could do so much harm! I am not familiar with the two products you took, only Serene plus, Travacor, and Adrecor, which address serotonin, dopamine, and low adrenal function.
I was mainly trying to point out that a strong mineral/amino imbalance occurred, and mentioned the products because many of them are minerals and amino 'replacers' to simplify it to some degree. If Bb causes extreme mineral imbalances, etc., my daughter's experience supports that. It was not necessarily meant to be an endorsement of the products.
But they did bring my daughter's extreme hyper-reactiveness down to a more normal level. For example, if I said to her "the sky is so blue today..." she no longer took me to task on it. The change was also sudden, going from receiving frequent positive comments about her, to suddenly having to apologize for her behavior (very humbling experience). Her situation was very real. Neuroscience addressed her issues, but nominally. We still had to provide other supplements and some things that were told to us, that would resolve, didn't. And still... I never felt that the true cause was really being addressed. We did do anti-microbials in the summer because I have read about the microbial connection to illness, in general. Just didn't know about LD, in particular.
I do agree with you that the body is always in a constant 'flow' state (at least one would hope), and things change inside from moment to moment. I see this from a several years observing bio-resonance data. I like that saying, "if we place our foot in a river one minute and then again a minute later, is it the same stream?" I really agree with you on your thinking and even asked my practitioner about this prior to the test. It would not surprise me if the numbers were skewed somehow or sometimes... we know it wouldn't be the first time a manipulation has occurred in the health field, alternative or otherwise.
Still have to read and re-read the information provided here. Just saw your longer post.
Hope you are better now.
Claire
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clairenotes
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Marnie,
So it sounds like you might agree that we need to go after corynebacterium? Maybe with Abx, though not your first choice?
I suppose I was thinking out loud that if corynebacterium is causing some of the problems, why not go after 'it.' Had not considered by what means, yet, alternative or mainstream. Just wanted to know if that was something that could/should be done.
Thanks.
Claire
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Marnie
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I feel Bb is the biggest threat.
Abx. will take care of the LPS layer pathogens later.
Go after the leader.
Even if co-infected with babesia.
BECAUSE...high levels of melatonin is "saving" the RBCs from destruction.
Now, I have to try to remember which file that is in!
Lyme alone can cause anemia. It has to do with PFK levels...dropping. This happens to our astronauts.
When PFK levels drop, I SUSPECT the body goes into an "iron save" mode....as it will be stored out of use of the pathogens that DO use iron to replicate.
It looks like tryptophan triggers amylase release from the pancreas which triggers tyrosine (to go into the cells) which triggers glycolysis.
If we can temporarily halt amylase (and lipase) release...
I ran across creatine info. again today as I was looking at the amino acids again.
klutzo
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posted
Dear Clairenotes, I went and looked at NeuroSciences web site. It really changed a lot! It has been at least 5 years since I took their products, and it appears they no longer sell the two that caused me such trouble, though a search of their site provided 42 hits on the names of one of the products.
However,both Serene Plus and Travacor have 5HTP in them, and Adrecor has Tyrosine, so the warning about high blood pressure would apply to all 3 products, with an additional warning about arterial spasms for the first two, esp. relevant, since people with Bb tend to be Mg deficient, which makes arterial spasm more likely.
I believe over 200 Neurotransmitters have been discovered to date, and messing with just the few we know a little bit about is scary to me. Like many here, I am desperate enough to try it though.
What is really confusing is that the NeuroReplete, which was supposed to get rid of my PSVT attacks, actually made them much worse, while the prescription drug Luvox, which has the same function, totally controlled the attacks for 3 yrs. before I became tolerant to it.
Both products were supposed to do the same thing, but the natural product should increase the NT's themselves, by providing precursor aminos, while the drug just keeps existing NT's in play longer by making neurons over-fire. The drug also seemed to be killing off my over-firing neurons and slowly turning me into an idiot, or maybe it was just coincidental progression of Lyme into my brain, I do not know.
Food and vitamin precursors in much larger amts. than those provided in NeruoSciences Products have failed to do anything for me,so maybe the ingredients I cannot tolerate are the magic ones, though they are safe only for those with low BP.
The only thing that really helps stem the attacks for me is Daylight Savings Time, so I tried one of those light visors for people with Seasonal Affective disorder, which I wear for 45 mins. each morning. That is not helping either. I tried extra vitamin D, which also did not help.
I know how frustrating these bizarre sx can be,and it must be so much harder for a child, so I am thrilled you found something helpful.
With empathy, Klutzo
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Marnie
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Let's add another nutrient, another co-enzyme to the stew...
Co-E1 or NADH which comes from niacin.
NADH, biologically known as Coenzyme 1 (as it is the most important co-enzyme, also known as Co-E1 ), is the reduced form of nicotinamide adenine dinucleotide (NAD) with high energy hydrogen (H) which provides energy to the cell.
In the organism, NADH or Coenzyme 1 is the natural biological carrier of H-minus.
In oxidative phosphorylation, the hydrogen atoms stripped off from these macronutrients in the Krebs cycle are transferred to the cytochrome system within the mitochondrial membrane by nicotinamide adenine dinucleotide (NAD) and flavin adenine dinucleotide (FAD), derived from the B-vitamins niacin and riboflavin, respectively.
As the hydrogen electrons are shuttled down the cytochrome chain (similar to traveling down a staircase) from a high level of energy to lower levels of energy, the difference between each step is given off as free energy, which can be used to recouple adenosine diphosphate (ADP) with phosphate to form more ATP.
Like all other tissues, the substantia nigra of the brain requires an adequate supply of ATP energy to survive and function normally.
Within the mitochondrial membrane, CoQ10 acts as a hydrogen electron shuttle that literally escorts the hydrogen electrons from one cytochrome to the next (from one step in the staircase to the next).
It specifically functions as an electron acceptor for complex I and complex II within the mitochondrial membrane. As such, a decline in CoQ 10 levels within the mitochondrial membrane results in a decreased ability to synthesize ATP, resulting in development of the type of cellular dysfunction and death found in Parkinson's disease.
In other words, NADH changes Coenzyme Q-10 in the body into an antioxidant; hence, Coenzyme Q-10 needs NADH to become effective. Additionally, CoQ10 concentrations may be increased with NADH supplements.
NADH stands for nicotinamide adenine dinucleotide. NADH is an activated form of the B vitamin niacin.
Enzymes also need helpers, and these helpers are called coenzymes. Most of the coenzymes are partly made from vitamins, such as vitamins E, C, lipoate, and riboflavin (vitamin B2). NADH, known as nicotinamide adenine dinucleotide, is a coenzyme, partly made from nicotinamide (vitamin B3).
NADH, through a series of reactions with acetyl and oxygen, is able to produce energy. This energy is in the form of ATP (adenosine triphosphate).
Therefore, a good supply of NADH optimizes energy production in the body. Another function of NADH is its ability to help transform an amino acid called tyrosine into the important brain chemical dopamine. Dopamine is involved in mood, energy, sexual drive, concentration, memory and muscle movement.
NADH is normally found in meat, fish, and poultry. The content of NADH in fruits and vegetables is minimal.
(Interesting since niacin looks to work similarly to NO as far as dilating the vessels.)
Okay...so to boost this...NADH + CoQ10? (perhaps less CoQ10 would be necessary?) Why did the doctors use vitamin E with CoQ10? Did you catch the above re: the vitamins as coenzyme helpers?
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clairenotes
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Klutzo,
Glad you pointed out the HTP issue for those who have high blood pressure. Again, please know that I am not necessarily endorsing those products.
It seems like you are going about your treatment in a thoughtful and careful way, and it is unfair that many of the avenues taken have not brought more positive results.
I know from dealing with my father-in-law, it takes very little to cause changes in his blood pressure. We gave him a protein drink (he is too thin), which we thought would only give support... instead, caused his BP to rise.
From his experience I know a little of how frustrating it would be to have the "magic" vitamins or food precursors to neurotransmitter balance cause high BP.
It seems the number one issue is to get your BP down?
I wonder if anyone else has any advice here. I have not dealt with this issue, myself (and then, of course, I am not a doctor).
Could we narrow down what microbes are involved? I know that Dr. K's ART system is supposed to be helpful in this regard. And there are lab tests, some of which I am sure you have done.
Also, does CoQ10 cause your BP to go up? I still have not had a chance to read your other post with the research.
Homeopathics did help me with neurotransmitter issues, both for depression, and over-thinking. But not my daughter -- she needed more raw materials.
Once, earlier on in this mess, a practitioner told me to spend time outside. Did not get to ask why. But I know sunlight helps me in a way I cannot describe. I spent a lot of time gardening last summer.
My bed looks like a science library!! But this is how it has to be for now. We have to just keep researching and asking the right questions until all of the answers are in. I am kind of stubborn and I don't listen to "no" very well when it comes to health. And I don't think anyone should.
Maybe in the summer, I will move my 'library' outside. With a safe insect repellent.
Claire
[ 29. March 2007, 01:58 PM: Message edited by: clairenotes ]
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clairenotes
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And now more to research from Marnie...
She sure keeps me busy.
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lymeinhell
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Thanks for this post Marnie!
Although I am among the better crowd, I still have a few slight issues. Blood pressure is one of them. I've been on a beta blocker 3 yrs now and can't get off. I've been taking CoQ10, but only 100mg.
For the last 3 days, I've been taking 300mg, 4x, and tonight immediately after coming home from work, my pressure was 110/71!! (It's typically around 130/80 at that time of the day)...
I have NADH in the shelves from when I needed it most (when I went off abx) - it's a REAL energy boost. Holy cow!! I might just have to add that back in with the CoQ10 and see what happens.
Thanks again!!
-------------------- Julie _ _ ___ _ _ lymeinhell
Blessed are those who expect nothing, for they shall not be disappointed. Posts: 2258 | From a better place than I was 11 yrs ago | Registered: Sep 2003
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Marnie
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Wow...this gets complex...but here goes:
While further researching, trying to figure out why the researchers gave those with Parkinson's vitamin E + CoQ10...it looks like vitamin E provides hydrogen.
While NADH is already "complete"???
Which made me pause.
Hydrogen to combine with free oxygen radicals or does hydrogen to combine with NAD (from niacin) -> NADH?
So it comes down to:
CoQ10 + Vitamin E
or
CoQ10 + NADH?
NORMALLY either would be good...but perhaps the first is better?
or
CoQ10 + NAD (i.e., niacin - B3) to lock onto the hydrogen in the cells -> NADH?
Or just CoQ10 alone?
The following may explain it better. Scroll down to the end...this gives me pause...
Supplements of coenzyme Q10 significantly
enhanced the anti-inflammatory effect of vitamin E in a new animal study.
It was found that excess vitamin E significantly increased the uptake of CoQ10; deficient vitamin E and CoQ10 in excess did not affect the uptake of vitamin E.
CoQ10 has been proposed as a regenerator of vitamin E. When cellular situations call for the use of vitamin E somehow it needs to be regenerated. If CoQ10 is important in this process, then this would explain the increased absorption of CoQ10 into the tissues when excess vitamin E is present.
The lack of additional CoQ10 uptake when vitamin E is deficient shows that CoQ10 is not a substitute antioxidant for vitamin E, but is involved in separate reactions. It was found that vitamin E decreases slowly in all tissues but in comparison, CoQ10 decreases at a relatively faster rate.
This rapid disappearing act may be due to the metabolic use of CoQ10, or just effective maintenance by the tissues. All cells produce their own CoQ10, utilization of external sources is not necessary, and therefore the breakdown of dietary CoQ10 occurs quite rapidly.
The biosynthesis of CoQ10 from the amino acid ***tyrosine*** is a multistage process requiring at least eight vitamins and several trace elements.
(Tyrosine is being used for a NUMBER of things!)
What is CoQ10?
It is a fat-soluble vitamin-like substance present in every cell of the body and serves as a coenzyme for several of the key enzymatic steps in the production of energy within the cell.
It also functions as an antioxidant which is important in its clinical effects. It is naturally present in small amounts in a wide variety of foods but is particularly high in organ meats such as heart, liver and kidney, as well as beef, soy oil, sardines, mackerel, and peanuts.
To put dietary CoQ10 intake into perspective, one pound of sardines, two pounds of beef, or two and one half pounds of peanuts, provide 30 mg of CoQ10.
CoQ10 is also synthesized in all tissues and in healthy individuals normal levels are maintained both by CoQ10 intake and by the body's synthesis of CoQ10. It has no known toxicity or side effects.
All CoQ10 available today in the United States is manufactured in Japan and is distributed by a number of companies who place the CoQ10 either in pressed tablets, powder-filled capsules, or oil-based gelcaps. CoQ10 is fat-soluble and absorption is significantly improved when it is chewed with a fat-containing food.
The antioxidant or free radical quenching properties of CoQ10 serve to greatly reduce oxidative damage to tissues as well as
significantly inhibit the oxidation of LDL cholesterol (much more efficiently than vitamin E) (60,61).
Natural vitamin E exists in eight different forms or isomers, four tocopherols and four tocotrienols. All isomers have a chromanol ring, with a hydroxyl group which can
donate a hydrogen atom to reduce free radicals
and a hydrophobic side chain which allows for penetration into biological membranes.
The incubation of SHR aortas with different concentrations of vitamin C (10 to 100 �mol/L) and specifically with high concentrations of vitamin E (100 �mol/L) improved endothelial function, reduced superoxide production as well as NAD(P)H oxidase activity, and increased eNOS activity and NO generation in SHR aortas to the levels observed in vitamin C- and E-treated WKY aortas.
Our results reveal endothelial NAD(P)H oxidase as the major source of vascular O2- in SHR and also show that vitamins C and E are critical in normalizing genetic endothelial dysfunction through regulation of eNOS and NAD(P)H oxidase activities.
NADH is the reduced form of NAD+, and NAD+ is the oxidized form of NADH.
NAD is used extensively in glycolysis and the citric acid cycle of cellular respiration. The reducing potential stored in NADH can be converted to ATP through the electron transport chain or used for anabolic metabolism. ATP "energy" is necessary for an organism to live.
Cells produce NAD from niacin, and use it to transport electrons in redox reactions. During this process NAD picks up electrons and is therefore reduced to NADH, releasing one proton (H+).
MH2 + NAD+ → NADH + H+ + M: + energy, where M is a metabolite.
Two hydrogen ions (a hydride ion and an H+ ion) are transferred from the metabolite. One electron is transferred to the positively-charged nitrogen, and one hydrogen attaches to the carbon atom opposite to the nitrogen.
In this process, the complex translocates protons across the inner membrane, helping to build the electrochemical potential used to produce ATP. The exact catalytic mechanism remains unknown.
NADH is the abbreviation used for Nicotinamide Adenine Dinucleotide, one of the most important coenzymes in the human brain and body.
A coenzyme is the active, or working form of a vitamin. NADH is the reduced (electron- energy rich) coenzyme form of vitamin B3, while NAD is the oxidized (burned) coenzyme form of B3.
NAD and NADH are converted into each other in numerous different metabolic activities. In some metabolic reactions it is NAD which is the needed catalyst, with NADH a useful by-product, in other reactions the situation is reversed.
NAD and NADH also serve to activate various enzymes, NAD for example,
activates alcohol dehydrogenase and acetaldehyde dehydrogenase that are the two enzymes needed to detoxify the alcohol
we drink into carbon dioxide and water.
NADH is the first of five enzyme complexes of the electron transport chain, where much of the ATP bioenergy that runs every biological process of our lives is formed.
NADH its vital chemical role As already noted, NAD(H) is the coenzyme or active form of vitamin B3. The chemistry of NAD(H) is some of the most complex in the human body.
NAD(H) is necessary to oxidize (burn) all foodstuffs (fats, sugars, amino-acids) into ATP bioenergy. There are three interlinked energy production cycles: the glycolytic (sugar burning) and Krebs' citric acid cycles (aminos and fats are "burned" through the Krebs' cycle), and the electron transport side chain.
A glycolytic cycle "waste" end product- pyruvic acid- helps power the Krebs' cycle, while electron "sparks" released from the step by step slow "burning" that occurs in the Krebs' cycle provide the fuel used by the electron transport side chain to generate much of the ATP bioenergy that literally powers our life.
NAD(H) is involved in all of these different cycles, as well as in the conversion of the pyruvate end product of the glycolytic cycle into the beginning fuel of the Krebs' citric acid cycle.
It is NADH, which captures the electron "sparks" thrown off during Krebs' cycle oxidation and shuttles them to the electron transport side chain energy production cycle.
Each unit of NADH is capable of generating three units of ATP energy. In a very real sense, NADH is the "energy of life" coenzyme.
NAD(H) is a relatively large and complex molecule, as coenzymes go. It is vitamin B3 (niacinamide) combined with a ribose (5-carbon sugar), a phosphate group and an adenine nucleotide (a DNA component). NAD(H) can be made in the liver and other cells from vitamin B3.
It can also be
made from the amino acid L-Tryptophan at the "expensive" ratio of 60mg tryptophan for 1mg B3.
Taking in exogenous (from outside the body) B3 or NAD(H) may spare the scarce amino acid tryptophan, which is the least plentiful amino in any normal diet. Tryptophan is the precursor of one of the most important antidepressant neurotransmitters, serotonin.
NADH's role in Parkinson's disease J.D. and W. Birkmayer of the Birkmayer Institute have pioneered the clinical use of NADH only in the last decade for Parkinson Therapy, Vienna, Austria.
The Birkmayers' are the first to develop a stable and absorbable oral tablet form of NADH. They have also conducted groundbreaking research on the use of NADH in Parkinson's disease, depression, Alzheimer's dementia and fatigue.
In a series of scientific papers published between 1989 and 1993 the Birkmayers have related their clinical success with NADH in Parkinson's, as well as provided supporting biochemical experiments and rationale for their success with NADH.
Parkinson's disease, one of the most common neurological diseases of aging, involves the gradual and even more severe destruction of the dopamine using neurons, in a brain region called the substantia nigra. Parkinson's involves movement disorders, speech difficulties, depression and cognitive dysfunction.
The traditional medical therapy for Parkinson's is L-dopa, the amino acid precursor of dopamine. However, this therapy has serious drawbacks.
After a period of use, even higher L-dopa doses are required, and these eventually cause severe side effects. In addition the dopamine formed through L-dopa therapy is prone to auto-oxidation to free radical forms that eventually "burn out" what few dopaminergic neurons are left.
(Parkinson's disease begins when the substantia nigra neuron population has dropped to 20-30% of normal).
Dopamine is usually made inside the neurons that use it through a two step process.
The amino acid tyrosine is first converted to L-dopa through an enzyme called tyrosine hydroxylase. L-dopa is then converted to dopamine. Research has shown that it is the activity of tyrosine hydroxylase, which is the rate-limiting controller of dopamine synthesis, and tyrosine hydroxylase activity is considerably lower in Parkinson's patients than healthy people.
Research has also shown that giving Parkinson's disease patients L-dopa diminishes their already weak tyrosine hydroxylase activity, thus further limiting their own L-dopa production and increasing the need for L-dopa supplements in an ever worsening vicious spiral.
The Birkmayers discovered that the coenzyme that activates tyrosine hydroxylase- tetrahydrobiopterin (H4BP) is reduced 50% in the brains of Parkinson's patients compared to age matched healthy controls.
They further discovered that NADH activates the enzyme, which helps produce H4BP.
Cell culture studies showed that NADH could elevate H4BP production, tyrosine hydroxylase activity and dopamine production.
The Birkmayers thus decided to try a therapy that might increase the brain's own production of dopamine, rather than suppress it as L-dopa therapy eventually does.
The Birkmayers' treated a group of 885 patients with NADH, 415 with intravenous (IV) NADH and 470 with oral NADH (Acta Neurol Scanda, 1993, PP 32-35).
Both groups showed overall good response to treatment, especially in motor improvements, walking, pushing, posture and speech. They also noted cognitive and emotional improvements in some patients, and surprisingly, the improvement figures for both IV and oral NADH were almost identical, and the maximum total improvement was actually shown by oral NADH users.
The Birkmayers also found increased urinary excretion of dopamine metabolites in the patients, indicating there was an actual NADH induced increase in dopamine production. They also were able to reduce and even eliminate other anti-Parkinson medications in some patients.
NADH and its anti-depressant abilities Based on their success with NADH treatment of Parkinson's patients, the Birkmayers decided to try NADH as an antidepressant in 205 depressed patients. There are multiple theoretical rationales for such use.
NADH increases brain dopamine and noradrenaline using brain cells use dopamine to make noradrenaline.
It is generally accepted that dopamine and/ or noradrenaline are frequently diminished in the brains of depressed patients, and drugs that raise brain dopamine/ noradrenaline levels will frequently end depression.
In addition, through NADH's sparing of tryptophan (discussed earlier in this article), more tryptophan would be left to end up as brain serotonin, another neuro-transmitter frequently reduced in depressives, and when drugs or tryptophan supplements raise brain serotonin, this frequently halts depression.
Lastly, it should be noted that the human brain must produce and use 20% of the body's total ATP bioenergy, and PET scans of the brains of depressed and demented people frequently show reduced brain energy production.
Thus, through its multiple roles in producing ATP energy, NADH might be expected to literally energize the brain, and depression may be in part the mental/ emotional direct experience of the brain's lowered energy status.
Not surprisingly therefore, the Birkmayers reported in their 1992 paper in New Trends in Clinical Pharmacology, a beneficial effect in 93% of the NADH treated depressed patients.
As with their Parkinson's patients, the Birkmayers found that NADH tended to induce serious improvement more in younger (less than 65 years old) than older patients. Their Parkinson's studies also showed shorter duration illness patients to benefit more than longer duration patients.
NADH and Alzheimer's disease Because many Parkinson's patients exhibit dementia as well as neurotransmitter problems, while many Alzheimer's patients exhibit neuromotor dysfunction as well as dementia, the Birkmayers next tried oral NADH on 17 Alzheimer's dementia (AD) patients (unpublished paper).
These patients ranged from mildly to severely demented. The results were nothing short of astounding! Not only did NADH halt the progression of Alzheimer's disease, it significantly reversed the cognitive and behavioral problems, even in the worst cases.
The NADH therapy was even able to restore some patients from being virtual "vegetables" to a semblance of normalcy. The Birkmayers also did before and after urinary analyses of dopamine and noradrenaline metabolites and found evidence indicating significantly improved brain dopamine/ noradrenaline activity.
While deficits in the function of acetylcholine neurons is the more well known pathology of Alzheimer's dementia, studies have also shown seriously diminished dopamine/ noradrenaline nerve activity in Alzheimer's dementia.
In several patients NADH was halted briefly to determine if the improvements would last without it. After several weeks absence of NADH (after a year's NADH treatment), deterioration began. Once again, NADH was started, and the previous improvements were regained.
NADH a possible fatigue fighter? In June 1997 W. Birkmayer was to announce the details of a successful trial using NADH to combat fatigue at a Las Vegas health convention. I was unable to get the details at the time of writing this article.
However, given the multi-dimensional roles of NADH in all aspects of human cellular ATP production, favorable results with NADH in fatigue situations is hardly surprising.
NADH doses and uses The standard dosage of NADH has been 10mg, taken with water 30 minutes before breakfast.
Animal studies suggest 1000mg per kilogram of body weight (70,000mg for a 154 pound human!) to be a tolerable dosage, so aside from the expense, there is no reason not to experiment with higher doses should 10mg not suffice to bring a hoped for benefit.
Those wishing to use NADH in Parkinson's cases might do well to accompany it with tyrosine and deprenyl.
Those wishing to try NADH for depression might add DLPA, tyrosine and/ or tryptophan or 5-hydroxy tryptophan.
Those wishing to try NADH for Alzheimer's dementia might include acetyl L-carnitine and DMAE or centrophenoxine with NADH.
In serious fatigue situations, B-complex vitamins, alpha-lipoic acid, Co Q10 or Idebenone and magnesium would be synergistic with NADH.
NOTE THIS!!!
In situations involving chronic alcoholism, however the cellular NAD/ NADH ratio is already detrimentally
skewed in favor of NADH, so NADH would not be appropriate.
Given the routine interconversions in all cells between niacin, niacinamide (2 forms of vitamin B3), NAD and NADH, as well as B3's sparing effect on tryptophan, it may be useful to add small (50-100mg) doses of vitamin B3 to any NADH regimen.
The lactic acid system is capable of releasing energy to resynthesise ATP without the involvement of oxygen and is called anaerobic glycolysis.
Glycolysis (breakdown of carbohydrates) results in the formation of pyruvic acid and hydrogen ions (H+). A build up of H+ will make the muscle cells acidic and interfere with their operation so carrier molecules, called nicotinamide adenine dinucleotide (NAD+), remove the H+.
The NAD+ is reduced to NADH which deposit the H+ at the electron transport gate (ETC) in the mitrochondria to be combined with oxygen to form water (H2O).
If there is insufficient oxygen then NADH cannot release the H+ and they build up in the cell.
To prevent the rise in acidity pyruvic acid accepts H+ forming lactic acid which then dissociates into lactate and H+.
Some of the lactate diffuses into the blood stream and takes some H+ with it as a way of reducing the H+ concentration in the muscle cell.
The normal pH of the muscle cell is 7.1 but if the build up of H+ continues and pH is reduced to around 6.5 then muscle contraction may be impaired and the low pH will stimulate the free nerve endings in the muscle resulting in the perception of pain (the burn).
This point is often measured as the lactic threshold or anaerobic threshold or onset of blood lactate accumulation (OBLA).
When the Mg-ATP pump is not working and the Na-K or Na-H pump is disrupted, the cells suffer from oxidative stress.
Too many free radicals are produced. These are primarily lone oxygen molecules as H2O2 (which we make all the time in the cells) -> H2O and O. This lone O is a serious problem.
Additional information here:
http://www.ncbi.nlm. nih.gov/entrez/query.fcgi?cmd= Retrieve&db= PubMed&list_uids= 1659205&dopt=Abstract
Posts: 9424 | From Sunshine State | Registered: Mar 2001
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I did buy NADH about a year ago before I knew I had Lyme but never took it in the end. My LLMD has put me on alot of the things mentioned above. 1000mg Mg 300mg CoQ10 1000iU Vitamin E 500mg Vitamin B3 And D-Ribose
I noticed quite a huge difference in energy levels - I also had SOD measured which was a bit low and was put on SODzyme. I was put on all the above after having a mitochondrial test which showed quite severe mitochondrial dysfunction, which my LLMD said is very common in Lyme. My ADP > ATP conversion was 22% (should be at least 60%) CoQ10 was very low, B3 was also low. I had a 73% block of the TL site, but haven't had the second test yet to see what is blocking it.
It's all interesting stuff, please keep posting what you find.
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clairenotes
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posted
Bringing this thread up again from the past for a follow-up note.
Though still a ways to go, CoQ10 has had a very positive impact on my neuro issues as well as my daughter's. I am still experimenting with higher doses.
The science is sometimes difficult to get through, but well worth it.
Thank you, Marnie.
Claire
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