KIDNEY CRI Signs, Symptoms, Solutions
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I was first diagnosed with Parkinson’s in 2008.  I have tried a lot of things; some of which worked.  However some did not work or had very bad side effects.  This is a compilation of what I found works to help me improve my condition.  Parkinson’s is the result of insufficient Dopamine which is normally produced in the brain to cause muscles to contract.  With Parkinson’s those contracted muscles then cannot relax adequately for normal function.  My emphasis of therapy is to first of all avoid drugs as much as possible. My preference is to pursue any and all natural means possible.  This would include all forms of physical therapy in the broad definition of the word (see below). 


The primary general issue in dealing with Parkinson’s revolves around medication, circulation and pain control:

A.      Parkinson’s Medication

·         Sinamet (Carbidopa-Levadopa) – This has been the mainstay medication for the last 40 years.  I have not found any other medications acceptable due to adverse side effects.

·         Extended Release Sinamet (Carbidopa-Levadopa Extended Release) - used at bedtime.


B.      Pain Control & Circulation

It is necessary to improve circulation and decrease pain throughout the body in order to enable Dopamine to function.  Consequently, pain determines whether you can walk normally or not at all, regardless of how much Dopamine medication you take. 

Pain control includes not only physical pain but psychological stress.  Pain and stress effectively incapacitate the effect of Dopamine.  Stress can come not only from psychological pain but physical pain as well.  Typically muscles that lock up (contract), becoming tighter and tighter with increasing pain, much like a cramp.  Stress can also be caused by the body being too tired to fully function.  Therefore, any efforts in exercise must be balanced with muscle relaxation.  In other words, be sensitive to what your body is telling you and be careful not to overdo it.  This includes being aware of the cyclical effects of your medication.

Methods of Controlling Psychological Pain which results in Physical Pain 

·         Stress Relief

o   Sleep

o   Herbal - Chamomile Tea for calming of shaking extremities

o   Nutrition:

SAM-e Supplement for Seratonin (for feel-good mood support), (in contrast to drugs that supposedly do similar effects of Seratonin)

CoQ-10, an OTC supplement enabling increased energy production in the body which will reduce achiness and increase energy

Vitamin D3 – you should be tested by your doctor to determine the amount of Vitamin D your body needs; also increases energy.

        High-potency Multivitamin

        50 mg Multi Vitamin-B Complex

        See Nutrition Schedule for additional vitamins


o   Hormones

DHEA for muscle development

Testosterone – This hormone affects your energy level and decreases with age.  Men should be tested by their doctor to determine the amount of testosterone their body needs.  The doctor can implant hormone pellets beneath the skin that are effective for 8-12 weeks.  Important: DO NOT use OTC products for “male enhancement”!

·         Psychological Counseling

·         Discussions with Support/Help Groups

·         Stay organized and be Proactive

·         Research Options

Methods of Controlling Physical Pain

Pain-Control Topical Lotions

·         Bio-Freeze (Non-Prescription)

·         Voltaren Gel (Prescription)

·         Gabapentin-based Pain Solution Cream (Compound Pharmacy)

Pain Control – Medical Instruments

·         Ultrasound treatment – followed up by application of Bio-Freeze

·         TENS Unit – Electric muscle stimulation

·         Pneumatic Compression Devices for Limbs

Pain Control Drugs:

·         Hydrocodon-Acetaminophen (Narcotic)

·         Gabapentin (Prescription Pain Control)

·         Tizanidine HCL (Prescription Muscle Relaxant)

·         Advil or Aleve (OCT Products)

Pain Control / Physical Therapy:

·         Exercises – Treadmill, Bicycle, Walking:

Use in conjunction with forms of muscle relaxation, e.g. stretching, etc.

o   Stretches

·         Massage Therapy –Electric Massage Tools

·         Vibrating Foot Pad

·         Hand-held Massage Units

·         Massage Therapist

·         Hydro-Therapy

·         Swimming Pool Exercise

·         Jacuzzi Spa with Water Jets

·         Water Massage Table

·         Ice Packs or Wraps

·         Home Walk-in Handicap Bathtub with Air Jets – can be used with Epsom Salts to relax the muscles

·         Jacuzzi Spa

·         Pneumatic Compression Devices for Limbs

Other Factors:

                Medical Equipment that may be needed:

·         Cane

·         Walker

·         Rollator

·         Knee Walker/Roller

·         Wheelchair or Power Chair

·         Stairlift

·         Shower hand grips and/or seat

·         Caregiver

o   Tendonitis/Bursitis

o   Occupational Therapist Consultation

o   See YouTube Videos

o   Gait Belt

·         Nutrition Drinks

·         Water, Ionized or Filtered; see Water Ionizer link

·         Beds

·         Memory Loss: Stay organized; keep lists of things to do; keep logs of medication due/taken

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Source Brand Supplement Bill Dosage Dosage/Tab Qty.
$ Per

Caps per day

$ Per
$ Per
30 days
Amazon Source Naturals ENADH - NADH 4 T / day AM    5 mg  (TR) 90  $ 45.89 4 $2.04  $     61.19
Costco NatureMadeCo-Enzyme Q101 T /day AM
200 mg  $ 37.672$    0.84  
Costco NatureMade Ubiquinol Co Q 10 1 T 2x/day - AM PM 100 mg 120   2  $    0.84  $     25.11 Source Naturals LifeForce Multi-Vitamin  1  T / day  AM Blend
180  $ 29.51 1  $    0.16  $       4.92 Country Life ALCAR   (with B-6)
Acetyl L-Carnitine 
1  T / day -  AM 500 mg 120  $ 36.56 1  $    0.30  $       9.14


T / day -  AM 25 mg 100  $ 23.00 1  $    0.23  $       6.90

Curcumin T / day -  AM 1000   mg
Bob's Red Mill Bob's Brand                         96 tsp per
Lecithin Powder (16oz bag)
1 x / day - AM 2 Teaspoon 96  $   9.77 2  $    0.20  $       6.11
Costco Kirkland Fish Oil/Omega 3 * 3 T 2x/day - AM PM  1000 mg   * 400  $ 10.39 6 0.16  $       4.68 Source Naturals Eve.Primrose Oil  * 1 T 2x/day - AM PM  1350 mg   *   120  $ 13.44 2 0.22  $       6.72 Source Naturals Folic Acid  1 T 2x/day - AM PM  800 mcg 1000  $ 11.64 2 0.02  $       0.70
           Source Naturals Vitamin D-3 1 T 2x/day - AM PM  2K  IU"s 600  $ 15.07 2 0.05  $       1.51 Puritan's Pride Green Tea Extract 1 T 1x/day -  PM 500 mg 120  $    11.99 1 0.10  $       3.00 NSI Saw Palmetto  1 T 2x/day - AM PM 540 mg 300  $ 14.98 2 0.10  $       3.00
Harvest Moon Barlean Flax-Oil Caps (w / Lignans) 1 T 1x/day - AM 1000 mg * 250  $ 28.46 1 0.11  $       3.42
Costco Tru-Nature CoEnzyme Q10  1  T / day - PM 100 mg    130  $ 20.45 1 0.31  $       9.44 Puritan's Pride B Vitamin             TR 1  T / day - PM 50 mg 100  $      6.73 1 0.07  $       2.02 Source Naturals Vitamin E  T / day - PM 400 I.U. 250  $ 15.06 1 0.06  $       1.81 Puritan's Pride Probiotic Acidophilus 1  T / day -   PM 100 mg    100  $   5.99 1  $    0.06  $       1.80
WalMart Equate Fiber powder 1/2 t/day w/drink .083 oz 16 oz.   1    
            TOTAL COST:    $      7.48  $     224.33

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Flax Oil

Fish Oil

Source Naturals
Evening Primrose


Total MG.
Per 3 Caps:


Per Daily

Per Daily




Dosage of 3 Caps Provide:







3 caps - 2x/day

3 caps - 3x/day

1 cap    3x/day










Flax Seed

Fish Oil




O - 3




































Alpha Linolenic
















































O - 6








































































O - 9






































Multi Vitamin

Plus Additional  Minerals  &  Herbs  (1 pill)

William R. Miller  

            Vit.A – 12,500 I.U. (75 I.U. as Beta Carotene, 5000 I.U. as palmitate)

            Vit.C – 500 mg (as ascorbic acid & ascorbyle palmitate)

            Vit.D-3  - 200 I.U. (as cholcalciferol)

            Vit.E  - 200 I.U. (as natural d-alpha tocopheryl)

            Thiamin (Vit.B1)                                                                                 50 mg

Riboflavine (Vit.B2)                                                                             50 mg

Niacinamide 35 mg & Niacin 15 mg                                                     50 mg

Vit.B6 (as pyridoxine HCL)                                                                 50 mg

Folate (as Folic Acid)                                                                       400 mcg

Vit.B12 (as cyancobalamin)                                                             100 mcg

Biotin                                                                                            150 mcg

Pantothenic Acid (as calcI.U.m d-pantothenate)                                 50 mg

CalcI.U.m (as calcI.U.m chelate, citrate & malate)                            100 mg

Iodine (from kelp)                                                                          100 mcg

MagnesI.U.m (as magnesI.U.m chelate, citrate & oxide)                    100 mg

Zinc (as zinc citrate & monomethionine [OptiZinc])                           100 mg

Copper (as copper sebacate)                                                            1 mg

Manganese (as manganese citrate)                                                100 mcg

ChromI.U.m (as chromI.U.m polynicotinate) [ChromeMate]               100 mcg

Molybdenum ( molybdenum chate)                                                 100 mcg

PotassI.U.m (as potassI.U.m citrate)                                                50 mg

Plus:    N-Acetyl Cysteine                                                                         100 mg

Hawthorn Berry                                                                             75 mg

Tumeric Root                                                                                72 mg

Milk Thistle Seed Extract (yielding 60 mg silymarin)                         72 mg

L-Tyrosine                                                                                    50 mg

Choline (as bitarate)                                                                      50 mg

Inositol                                                                                         50 mg

            DMAE (as bitrate)                                                                         25 mg

            Alpha-Lipoic Acid                                                                         25 mg

            MSM (Methylsulfonylmethane)                                                      25 mg

            Grape Seed Extract (proanthodyn)tm                                              25 mg

            Coenzyme Q10                                                                            20 mg

            Ginko Biloba Leaf (24%  -  50:1 Extract)                                         10 mg

            Bilberry Standardized Extract                                                        10 mg

            Pepper Fruit Extract  (Bioperine) tm                                                  3 mg

            Boron Amino Acid Chelate                                                              2 mg



CAVEAT:  The following is neurotransmitter nutritional research, attempting to specifically address all possible nutritional needs to help offset MY specific Parkinson’s disease (PD) symptoms and causes: 

The following is a compilation of personal research notes that MAY, OR MAY NOT BE APPLICABLE TO MY PERSONAL CONDITION, and is compiled from MANY web sites resources including, all from which this author provides NO assurances of accuracy OR applicability; for others to apply to their specific conditions. 

Not all cautions and adverse effects are known or included, therefore consult your doctor first before adding any of the below listed supplements to your diet. 


Product name: SAM-e (Sold As)    S-Adenosyl Methionine 

Note Serotonin Syndrome  (Extreme Caution)







NAC is the derivative of L-Cysteine and precursor to glutathione

The following is neurotransmitter nutritional research, attempting to specifically address all possible nutritional needs to help offset MY specific Parkinson’s disease (PD) symptoms ONLY.  

Not all cautions and adverse effects are known or included, therefore consult your doctor first before adding any of the below listed supplements to your diet. 



5 – HTP Tryptophan

DAT  (dopamine active transporter):

Acetyl L-Carnitine (ALCAR)

R-Alpha Lipoic Acid (R-ALA)

L-Tyrosine  (TH)

NADH  -  NicotinamideAdenineDinuleotid

Vitamin D 3

GDNF family of ligands


Omega-3   DHA  (Fish Oil)


Melatonin is non-toxic except with MAOIs that prevent breakdown of Melatonin.

Melatonin is an endocrine hormone with antioxidant properties to protect Nuclear & Mitochondrial DNA.  Synthesized from Tryptophan, via Serotonin in penial gland at center of brain. Crosses cell & blood brain barrier. No redox Rx,  with 10:1 neutralization of free radicals.  In PD, cancer & viral infection it is effective protection of cell DNA.  Also stimulates T Lymphocytes.  Prevents hyperphosphorylation of tau protein in Alzheimer's. 

5 – HTP Tryptophan

5-HTP is an intermediate metabolite between L-tryptophan and serotonin.   It is also a precursor to Melatonin.

Supplement one capsule per day at PM.   

Seratonin (5-HT) is a monoamine neurotransmitter synthesized in serotonergic neurons in CNS. 

5-HT receptors are the receptors for serotonin.  Serotonergic action is terminated primarily via uptake of 5-HT from the synapse.  This is through the specific monoamine transporter for 5-HT. 

Various drugs are used to modulate the 5-HT system, including specific antidepressants through use of specific MAOIs.  MAOIs prevent the breakdown of monoamine neurotransmitters (including serotonin), and therefore increase concentrations of the neurotransmitter in the brain.  Extremely high levels of serotonin can have toxic and potentially fatal effects.  Such toxic levels are essentially impossible to reach through an overdose of a single antidepressant drug, but require a combination of serotonergic agents, such as an SSRI with an MAOI. 

Because neither the amino acid L-tryptophan nor the SSRI-class antidepressants raise blood serotonin levels, they are not under suspicion to cause the syndromes described. 

However, 5-Hydroxytryptophan (5-HTP) does raise blood serotonin levels.  5-HT receptors are located in the cell membrane of nerve cells and other cell types including smooth muscle. 

5-HT receptors affect the release and activity of other neurotransmissers such as glutamate, dopamine, and GABA. 

Monoamine neurotransmitters are derived from tyrosine, tryptophan and thryroid hormones.  Examples: dopamine, melatonin, serotonin (5-HT). 

DAT  (dopamine active transporter):

Specific protein transporters called monoamine transmitters exist that transport monoamines into or out of a cell.  These are the dopamine transporter (DAT), serotonin transporter (SERT), etc. 

Monoamine oxidase (MAO) is an enzyme that breaks down monoamine neurotransmitters after they have been released into the synapse. 

The dopamine transporter (DAT) is a membrane-spanning protein that binds the neurotransmitter dopamine and performs re-uptake of it from the synapse into a neuron.  DAT is present in the peri-synaptic area of dopaminergic neurons where dopamine signaling occurs.  DAT terminates the dopamine signal and is implicated in many dopamine-related disorders. 

DAT is an integral membrane protein that removes dopamine from the synaptic cleft and deposits it into surrounding cells, thus terminating the signal of the neurotransmitter dopamine. 

DAT is a symporter that moves dopamine across the cell membrane.  DAT was found to be enriched in dendrites and cell bodies of neurons in the SUBSTANTIA NIGRA.  This pattern makes sense for a protein that regulates dopamine levels in the synapse. 

Results suggest that dopamine re-uptake may occur outside the synaptic specializations once dopamine diffuses from the synaptic cleft.  In the substantia nigra, DAT appears to be specifically transported into dendrites where it modulates the entra-cellular and extra-cellular dopamine levels of nigral dendrites. 

The rate at which DAT removes dopamine from the synapse can have a profound effect on the amount of dopamine in the cell, best evidenced by motor abnormalities.  Decreasing levels of DAT expression are also associated with aging and likely are underlying reasons for decreases in dopamine released as a person ages. 

Acetyl L-Carnitine (ALCAR)

There are no harmful side effects.  ALCAR is non-toxic. 

It is also known as Vitamin BT.  It is synthesized from Lysine and Methionin but enough B1 (Thiamine) and B6 (Pyridoxine) must be available. 

It is used for fatty acid transport (FAT) and is required for entry into the mitochondria and removal of organic acids which frees the entramitochrondrial coenzyme.  It is used for energy supply within the cell, muscles, assists in prevention of fats in the muscles.  It improves antioxidant affect of Vitamins C & E. 

It reduces the risk of poor fat metabolism.  In long-term administration in rats, it restores a synaptic pattern comparable to that of young rats. 

Antioxidant concentrations are shown to be low in the substantia nigra with most severe neuron depletion with age.   Acetyl L-carnitine is being investigated as a determinant of neuronal longevity.  ALCAR can counteract the age-dependent reduction of several receptors in the CNS of rodents such as neurotransmitters and others, thereby enhancing the efficiency of synaptic transmission and appears to reverse age-associated deficits in cellular function, in part by increasing cellular ATP production.  

It transports fatty acids into the mitochondria and increases the rate in which fat is burned.   It contributes positive effects on muscles, heart immune cells, brain nerves, and sperm. 

R-Alpha Lipoic Acid (R-ALA):

Typical dose: 100-200 mg three times per day.  There are no significant side effects.  Food sources include spinach, broccoli and potatoes.  Lipoic acid (R-ALA) is non-carcinogenic and shows no evidence of target organ toxicity.

It is found in every cell in the body.  It is thought that certain nerve diseases are at least partially caused by free radical damage.  Free radicals are hypothesized to play a role in neuropathy.  In diabetes, nerve cells leading to the arms and legs become damaged, resulting in numbness, pain, etc.  It neutralizes free radicals in both fatty and watery regions of cells. 

It increases levels of glutathione (an antioxidant in the brain).  It is produced by the body and decreases with age.  It acts as a coenzyme in cellular energy production.  It chelates heavy metals and recycles vitamin E and C.  The R form of R-ALA is biologically active and native to the body.  It significantly reduces inflammations.  It is immediately available to cells in the R-ALA form.  It is a co-factor in aerobic metabolism, specifically the pyruvate dehydrogenase complex.  R-ALA has the ability to modify gene expression by stabilizing a transcription factor for treatment of various cancers. 

Lipoic acid is able to regenerate (reduce) antioxidants such as glutathyione, Vitamin C & E, thus maintaining a healthy cellular redox state.  Studies of rat aging suggest that R-ALA and L-Carnitine result in improved memory and delay mitochrondrial decay.  As a result, it is helpful for Parkinson’s disease and Alzheimer’s.   R-ALA chelates mercury intoxication.  It can penetrate the blood-brain barrier and cell membrane.  Lipoic acid is essential to oxidative decarboxilization of keytones.  In pyruvate dehydrogenase, complex lipoic acid links with a Lysine residue and results in reversible ring open/closing in the oxidation of A-keto acids. 

Deficiency of lipoic acid results in:  reduced muscle mass, failure to thrive, brain atrophy, and increased lactic acid accumulation.  Lipoic acid is involved in the conversion of carbohydrates to energy.  When sugar is metabolized in the production of energy, it is converted to pyruvic acid.  When there is plenty of oxygen available to the cell, pyruvate is broken down by an enzyme complex that contains lipoic acid, thiamine and niacin.  When the oxygen supply is low, the cell converts pyruvate acid to lactic acid.  During exercise, lactic acid tends to accumulate and leads to muscle fatigue.  Lipoic acid supplementation may help improved energy metabolism as an antioxidant.  It improves diabetic neuropathy. 

It also aids in stimulating the regeneration of nerve fibers.  It increases glucose uptake by muscle and nerve cells and protects cells from glycation.  R-ALA prevents excess glucose reaction with proteins to create cross-links that damage vital proteins, including the myelin sheath of neurons. 

With decreased bodily production of lipoic acid with age mitochondrial energy production becomes less efficient and more free radicals are generated.  Lipoic acid protects cells, particularly in the mitochondria where most oxygen damage occurs.

L-Tyrosine  (TH):

Caution:  MAOIs may result in hypertensive crisis.  The potentiation of sympathomimetic substances and related compounds by MAO inhibitors may result in hypertensive crises.  Individuals taking phenelzine should avoid sympathomimetic drugs (including amphetamines, cocaine, methylphenidate, dopamine, epinephrine and norepinephrine), or related compounds (including methyldopa, L-dopa, L-tryptophan, L-tyrosine and phenylalanine).  Tyrosine increases sensitivity to stimulants.  Other drugs which tyrosine may interact with include: opiates and L-dopa.

Dosage:   Daily dose divided into 3 or more doses daily.  Sensitivity side affects are observed in as low a dose as 200-500 mg.  Recommend starting at 100 mg, 30 minutes prior to a meal.  Do not exceed 4 grams per day.  N-Acetyl Tyrosine has inferior bioavailability. 

Foods containing tyrosine include cheese, which is also an extremely high source of glutamine because casein inhibits protein breakdown in the body.


Tyrosine converts to L-dopa to dopamine to norepinepherine to epinephrine.  Tyrosine as a precursor to L-dopa, a precursor to dopamine and requires biopterin (a folate derivative).  H4biopterin, the co-enzyme of TH, is reduced to about 50% in the brain of PD patients. 

The key enzyme in H4biopterin  biosynthesis is the quinoidH2pteridin reductase.  H4biopterin is formed from H2pterin by an enzyme called quinoiddihydropteridinreductase (DHPR), an enzyme that needs NADH as a central co-factor.


Tyrosine is therefore one of the possible rate-limiting enzyme for the creation of dopamine.  Increasing tyrosine availability could have the ability to increase dopamine synthesis.  Tyrosine increases all catecholamine levels and increases plasma neurotransmitter levels.  Some neurons become more sensitive to tyrosine availability. 

Fatigue during exercise is contributed in part to the increase of serotonin and increase in the ratio of serotonin to dopamine.  Tyrosine may help decrease this ratio and compete with tryptophan (the precursor to serotonin).  Increased dopaminigeric activity may decrease the perception of fatigue. 

Tyrosine has been reported in the treatment of Parkinson’s to elevate dopamine as measured by levels of a dopamine metabolite. 

One study associated combined administration of tyrosine, 5-HTP, and cardbidopa.  Tyrosine can potentiate the effects of various drugs, allowing a lower dose to be equally effective.  No toxicity levels have been observed. 

Tyrosine is involved in the synthesis of neurotransmitters in the brain.  Tyrosine is a precursor to L-dopa, dopamine, and others.  Tyrosine requires biopterin (a folate derivative), NADPH and NADH (forms of niacin), copper and Vitamin C.  Conversion of tyrosine requires Vitamin B-6, folic acid and copper.  It may serve as a valuable adjunct therapy in the treatment of Parkinson’s disease.  Tyrosine is used by cells to synthesize proteins. 

Tyrosine functions in part of the signal transduction process; which is transmitted by using glutamate; as the nitrogen source.   Tyrosine phosphorylation is considered to be one of the key steps in signal transduction and regulation of enzymatic activity.

NADH  -  Nicotinamide Adenine Dinuleotid:

NADH is known as CoEnzyme -1 or as Co-E1.

Requires Enteric-coated NADH capsules produce time-released action, increasing bioavailability absorption.

Stimulates manufacture of Dopamine, Noradrenaline & Serotonin by stimulating Tyrosine to L-Dopa,  NAD+ (Redox reduced to NADH) synthesized from tryptophan (Quinolinic acid).

NADH stimulates cellular production of the neurotransmitters of dopamine, noradrenaline and serotonin.  It is directly involved in the cellular immune defensive system and DNA repair.   

NADH is the reduced form of NAD with high-energy hydrogen (H), which provides energy to the cell.  Hydrogen, in its biologically active form (the negative charged hydrogen ANION), is what gives energy to your body’s cells, activating cell metabolism and cell regeneration.  The negatively charged hydrogen, with its extra electron, is a highly efficient antioxidant, which is able to neutralize free radicals.  NADH is the natural biological carrier of H-. 

It is effective in combating disorders such as fibromyalgia and chronic fatigue syndrome. 

NADH Study #1:

Biosynthesis of dopamine could be blocked at the metabolic conversion from tyrosine to L-dopa.  The enzyme catalyzing this reaction is tyrosine (TH).  The activity of which is considerably diminished in substantia nigra of Parkinson’s.  H4biopterin, the co-enzyme of TH, is reduced to about 50% in the brain of PD patients.  Taking this into account, we consider a new concept to overcome the dopamine deficit, namely to stimulate TH activity in order to increase L-dopa biosynthesis.  However, H4biopterin does not show any beneficial effects with PD.  The failure of this approach was the impermeability of the blood-brain barrier for H4biopterin.  Therefore, this substance cannot reach its target, the substantia nigra. 

The question is whether it is possible to stimulate the H4biopterin biosynthesis in the brain.  If a diminished biosynthesis H4biopterin is the cause of TH defect, stimulation of H4biopterin biosynthesis should elevate the enzyme activity. 

The key enzyme in H4biopterin  biosynthesis is the quinoidH2pteridin reductase (10).  This enzyme needs NADH as a co-enzyme.  The idea was to stimulate H4biopterin biosynthesis by applying NADH, which increases quinonoidhtpteridine reductase activity.  Owing to this NADH may stimulate endogenous L-dopa biosynthesis. 

NADH  Study Group #2:

To investigate the concept, 800 PD patients were treated with NADH.  NADH has been studied in a dopamine producing neuroblastema cell-line.  

Results of study group:  The maximum improvement of orally applied NADH was 60%.  The motoric ability improved considerably. 

When neuroblastoma cells were incubated with NADH, dopamine production was observed.  The stimulation was independent from the tyrosine supplied, indicating that the substrate tyrosine is not the limiting factor, but the enzyme or the co-enzyme respectively was the limiting factor. 

When TH (L-trosine) activity was measured directly after NADH had been added to a culture medium, a 75% increase could be observed.  This finding indicates that NADH is able to stimulate TH activity directly. 

L-dopa biosynthesis may occur via enhanced production the TH enzyme H4biopterin.  Levels of H4biopterin in the brain of PD patients are reduced by 50%.  If the deficit of H4 is due to a decreased biosynthesis, the biochemical mechanism of NADH may be explainable.  H4biopterin is formed from H2pterin by an enzyme called quinoiddihydropteridinreductase (DHPR), an enzyme that needs NADH as a central co-factor.  There is indirect evidence that DHPR influences TH activity via H4biopterin biosynthesis, because substances which completely inhibit DHPR such as MPTP induced PD symptoms. 

Therefore, we have to rely on indirect evidence, one of which is the metabolic product of dopamine and homovanillinic acid (HVA).  The level of this substance increases after NADH treatment. 

Furthermore, tissue culture experiments show that NADH is able to increase dopamine production.  Indirect evidence for this assumption is derived from the assumption that dopa inhibitors such as carbidopa in combination with NADH yield a better and longer-lasting clinical improvement. 

This new therapeutic principle, namely the stimulation of the endogenous L-dopa biosynthesis could overcome the drawback of the L-dopa treatment in the sense that it could avoid further destruction of the residual Ingra cells caused by the action of radicals, which are formed in considerable quantities by oxidation of L-dopa. 

Vitamin D 3:

The role of Vitamin D3 in degenerative diseases is becoming more obvious every year.  Vitamin D3 is obtained from sunlight and stays longer in the body than supplements. 

Parkinson’s Disease is a result of selective loss of dopamagenic neurons in the substantia nigra region of the brain.  In PD, the cause and mechanism of continued neuron cell death is currently unknown.  We hypothesize, based upon several lines of evidence, that documented chronically inadequate Vitamin D intake is a significant factor in the pathogenesis of PD.  This hypothesis implies that a dietary aid for prevention and therapy for PD is possible.  Currently the tolerable upper intake level tolerance is approx. 2000 IUs per day (50 mcg).  There’s evidence of lack of adverse affects in clinical trials that used intake of 1250 mcg/day Vitamin D3.  In a test tube, Vitamin D3 increased cell output of GDNF.

GDNF:This is the abbreviation for the Glial cell-Derived Neuropathic Factor (GDNF).  This small protein promotes survival of many types of neurons.  This gene encodes a highly conserved neurotropic factor.  A form of this protein has shown to promote survival and differentiation of dopaminergic neurons in culture, and was able to prevent apoptosis of motor neurons. 

A mature form of the protein is a ligand.  The most prominent feature of GDNF is its ability to support the survival of dopaminergic and motor neurons.  These neuronal populations die in the course of Parkinson’s disease. 

The GDNF family of ligands (GFL) consists of four neurotropic factors: GDNF, NRTN, ARTN & PSPN.  GFLs play a role in cell survival, neurite outgrowth, cell differentiation and cell migration.  In particular, signaling by GDNF promotes the survival of dopaminergic neurons. 

GFLs are distantly related to the transforming growth factor super family of proteins and belong to the cystine knot protein family. 

GFLs function as homodimmers at the cell surface of target cells.  At the cell surface, a signaling complex forms composed of a:  GFL, dimmer, a receptor tyrosine, and a cell surface bound co-factor.  Consequential phosphorylation of these tyrosines then initiate intra-cellular transduction processes. 

GFLs are an important therapeutic target for several conditions:  GDNF has shown promising results in Parkinson’s disease clinical trials.  GDNF is a potent survival factor for central motor neurons. 

NRTN can also be used for Parkinson’s disease therapy to promote survival of basal forebrain cholinergic neurons and spinal motor neurons.  Given the huge spectrum of possible therapeutic applications, the modulation of GFR receptor complex activity is of great interest. 

However, as GFLs are unable to penetrate the blood-brain barrier, creation of agonists for development of effective therapies against neurological diseases are desired.


Lecithin’s side affects include anorexia, nausea, abdominal bloating, gastrointestinal pain and diarrhea.  Medications of high niacin to treat high cholesterol can deplete choline (a derivative of lecithin).

Toxicity: No toxicity.  Recommended dosage: 100-600 mg daily

Lecithin breaks down to choline, which reacts to form acetylcholine or phosphatidylserine which breaks down to form phosphatidylcholine.

Choline supplementation is also used therapeutically to reduce cholesterol levels.

Lecithin is usually used as a synonym for pure phosphatidylcholine.  Phosphatidylcholine is an important component of the mucous layer or mucosa in the large intestine.  The mucous layer forms the mucosal barrier, protecting the large intestine from attacks by bacteria.  Lecithin is an essential part of cell membranes and can be easily and totally metabolized. 

The major source of lecithin is soybean oil.  The main phosolipids in lecithin from soy and sunflower are phosphatidylcholine, phosphatidylinositol, phosphatidylethanolamine, and phosphatidic acid. 

Choline is essential in the manufacture of the neurotransmitter acetylcholine and is the main component of our cell membranes, such as phosphatidylcholine (lecithin) and sphingomyelin.  Choline supplementation also increases the accumulation of acetylcholine within the brain. 

Choline is also required for the proper metabolism of fats.  Choline, like Vitamin B12, SAM-e and folic acid, acts as a methyl-donor.  It's essential for proper liver function.  It’s required for the export of fat from the liver.  Choline as a methyl-donor also helps conserve carnateine and folic acid. 

Choline also provides liver support, by increasing solubility of cholesterol and inhibiting platelet aggregation as a result of its high content of linoleic acid. 

Alzheimer’s Disease is characterized by the general destruction of nerve cells in several key areas of the brain.  It’s possibly related to the decrease of available acetylcholine, which functions as a transmitting agent in the brain. 

Phosphatidylserine, a derivative of choline (Lecithin derivative), is mostly found in neural cell membranes.  The serine molecule in phosphatidylserine is attached mostly to DHA (Omega-3 fatty acid) – (Fish Oil).  Phosphatidylserine in soy is basically serine attached to fatty acids.  Phosphatidylserine is the major phosholipid of brain synaptic membranes.  It plays a crucial role in several membrane-linked activities such as:  enzyme activation, liposome function, ion permeability, maintenance of the cell’s internal environment, secretory vesicle release, cell-to-cell communication, and cell growth regulation. 

Phosphatidylserine supplements are made by enzymatically preparing soybean lecithins and L-serine by a phosphilipase reaction.  Toxicity: No toxicity.  Recommended dosage: 100-600 mg daily

Phosphatidylserine modifies: glucose metabolism in the brain, catecholamine, and acetylcholine release, NMDA receptor density and function and muscarinic acetylcholine receptor density.  The primary mechanism is the enhancement of cholinergic transmission. 

In rats, Phosphatidylserine restores acetylcholine and increases acetylcholine receptor density. 

Phosphatidylserine increases cholinergic function in multiple ways:  

First, it maintains membrane potential. 

Second, it increases calcium uptake, as this is important in neurotransmitter release. 

Third, Phosphatidylserine affects exocytosis of neurotransmittors by interacting with membrane-binding proteins.   Phosphatidylserine increases turnover of dopamine in the brain and in the striatum.  It also increases dopamine released in the limbic area and cerebral cortex.  Phosphatidylserine also prevents age-related deficits in NMDA receptor function in the forebrain. 

Phosphatidylserine mediates a variety of processes related to synaptic plasticity, information storage, and glutamatergic transmission.  

It also acts as an antioxidant, suppresses cytotoxic factors & interacts with nerve growth factor (NGF). 

It reduces circulating levels of stress hormone cortisol.  It decreases post-exercise cortisol levels and reduces muscle soreness. 

Omega-3   DHA  (Fish Oil)

A brain phospholipid lowers triglycerides.  Low levels result in low serotonin; it is 40% of brain fatty acids, and 50% of neuronal membrane.  It modulates the carrier of choline, glycine, and taurine. 

Phosphatidylserine (PS) controls apoptosis, and low DHA levels lower neural cell PS and increased neural cell death.  DHA can be derived from EPA (Omega 3) – Flax seed oil .  It also suppresses tumor growth.




SAM-e    S-Adenosyl Methionine  -  NoteSerotonin Syndrome  (Extreme Caution)

SAM-e    S-Adenosyl Methionine

Adverse Effects: Serotonin syndrome--there is concern and one report of the potentially fatal serotonin syndrome in association of SAM-e with other medications.

Serotonin Syndrome:

Serotonin Syndrome is a rare but potentially life threatening adverse drug reaction.  It is a consequence of excess serotonergic activity at the central nervous system (CNS) and peripheral serotonin receptors.  Symptoms range from barely perceptible to fatal.  It is a result of over-stimulation of 5-HT1A receptors. 

Drugs that may contribute to over-stimulation include: St. John’s Wort, Anti-depressants such as MAOIs, TCAs, SSRIs, SNRIs, Mirtazapine and Bupropion; also CNS stimulants, 5-HT1 agonists as triptans and others such as tryptophan and 5-HTP supplements.

The combination of MAOIs and other serotonin agonists or precursors possess a particularly severe risk of life-threatening serotonin syndrome.  Serotonin agonists and MAOIs should be avoided in combination with serotonin.  Most frequently (and perhaps the only) combination of drugs likely to elevate serotonin to a fatal degree is the combination of MAOIs with SSRIs. 

Symptoms:  Onset is usually rapid within minutes of self-poisoning.  There is no lab test for serotonin syndrome and no antidote.  Management is by removal of participating drugs and the administration of serotonin antagonists (Cyproheptadine or Methysergide).  If the symptoms are mild, treatment may consist of giving benzodiaepines and waiting for symptoms to resolve within 24 hours.

SAMe Increases Serotonin.  Is made of ATP & methionine.  Most SAM-e is produced and consumed in the liver. 

SAMe involves methyl group transfer from SAM-e to various substrates such as nucleic acids, proteins and lipids which are hydrolyzed to homocystine and adenosine with homocystine recycled back to methionine.  Methionine is then converted back to SAM. 

SAM is required in synthesis of neurotransmitters dopamine and serotonin.  Therapeutic use:  SAM-e used for liver disease and osteo-arthritis.  Low levels may cause Alzheimer's Disease (AD).  SAM disulfate tosylate by Nature-Made is liable to degradation with oral bio-availability at possibly 5%, thus the need for enteric-coated tablets.

Possible Side Effects of SAM-e & Homocysteine:  Once SAM-e donates its methyl group to choline, creatine, carnitine, DNA, RNA, norepinephrine, and other conpounds, it is transformed into S-adenosyl-homocysteine (SAH). 

Under normal circumstances, homocysteine, in the presence of Vitamin B6, B12, and folic acid (SAM-e's main co-factors) will eventually be converted back into methionine, SAM-e or cysteine, glutathione, and other useful substances. 

However, if adequate amounts of these vitamins are not present, SAM-e will not break down properly.  As a consequence, the full benefits of SAM-e will not be obtained, and homocysteine may increase to unsafe levels.  High levels of homocysteine have been associated with atherosclerosis (hardening and narrowing of the arteries), as well as an increased risk of heart attacks, strokes, liver damage, and possibly Alzheimer's Disease.  Therefore, Vitamin B supplements should be  taken along with SAM-e.  These vitamins help metabolize the homocysteine into other useful compounds.

Methionine: Its derivative SAM serves as a methyl donor.  Methionine is an intermediate in the biosynthesis of cysteine, carnitine, taurine, lecithin, phosphatidylcholine, and other phospholipids.  Improper conversion of methionine can lead to atherosclerosis. 

Methionine is one of only two amino acids encoded by a single condon (AUG) in the standard genetic code (tryptophan, encoded by UGG, is the other).  The condon AUG is also significant, in that it carries the "Start" message for ribosome that signals the initiation of protein translation from mRNA.  Methionine is synthesized via a pathway that uses both aspartic acid and cysteine.



            - linoleic acid (Omega 6)    Also in Evening Primrose oil.

Grape Seed Extract        


Side affects:  Abdominal pain, cough, headache, nausea, sore throat, soft stools or oily leakage from GI tract.  Dosage recommendation of extract: 50-200 mg per day.

Grape Seed Extract is an antioxidant known as polyphenols, including proanthocyanidines.  It blocks the effects of enzymes that process fats, including cholesterol.  Consequently, less fat may be absorbed and more may be eliminated from the body.  Research shows it may help in preventing damage to cells caused by drugs, pollution and other toxins. 

Polyphenols in grape seed extract are called resveratrols.  In laboratory tests, it appears to interfere with cancer cell growth and division, as well as causing some cancer cells to disintegrate faster.  It may also block enzymes that prolong the survival of several cancer cell types, including skin, prostate and breast cancer.  As a result, tumors may actually stop growing or may actually shrink. 

It may also increase the effectiveness and/or lower the side affects of drugs currently used for cancer chemotherapy.  It may also allow lower doses of cancer drugs to be effective, thereby limiting potential side affects. 

It is thought that it interferes with viral multiplication, possibly by preventing viral attachment to host cells.  Oil pressed from grape seed is used as a dietary supplement and contains a high amount of linoleic acid (Omega 6)    Also in Evening Primrose oil.



                                              ADD FOODS NOTED ESPECIALLY CHEESE FOR BETTER EFFECT

NAC is the derivative of L-Cysteine and precursor to glutathione




NAC is not absorbed well. 

NAC is a source of cystine, but subject to side affects. 

Caution:  Increases of blood pressure in the lungs and right ventricle of the heart could potentially cause damage to the heart and lungs with long term use when used as a body-building supplement. 

NAC acts to augment glutathione reserves to directly bind to toxic metabolites and modulates inflammations in Cystic Fibrosis and has a potential to counter intertwined redox inflammatory imbalances.  It’s used primarily as an inhaled mucous-dissolving therapy for respiratory conditions. 

Vegetable sources of NAC include: red peppers, garlic, onions, broccoli, brussels sprouts and oats. 

Natural source of cystine is undenatured whey proteins from milk (cheese).  Nutritional sources of cystine are virtually free of the toxic side effects associated with the singular molecule of cysteine (NAC).

NAC is the derivative of L-Cysteine and precursor to glutathione.  Cysteine is a component of many proteins and enzymes.  Cysteine is named after cystine, its oxidized dimer.  Cysteine is potentially toxic and is cannibalized in the GI tract and blood plasma.  Conversely, cysteine is absorbed through digestion as cystine, which is more stable in the GI tract.  Cystine travels safely and is promptly reduced to 2 cysteine molecules upon cell entry.  Cystine is the amino acid formed, when a pair of cysteine molecules are joined by a disulfide bond. 

Due to the ability of thiols to undergo redox reactions, cysteine has antioxidant properties expressed in the tripeptide glutathione.  Systemic availability of oral glutathione is negligible. 

Cysteine residues play a valuable role by cross-linking proteins, thereby increasing the protein stability in the extra-cellular environment.  Cysteine is an important source of sulfide in human metabolism.  Aside from its oxidation to cystine, cysteine participates in numerous post-translational modifications.  In nucleophilic thiol group allows cysteine to conjugate to other groups.  These roles are typically limited to intra-cellular milieu. 

Cysteine directly counteracts poisonous effects of acetaldehyde, which is the major byproduct of alcohol metabolism to produce acetic acid. 

Glutathione is a tri-peptide containing a peptide link between cystine and glutamate. 

It is an antioxidant.  Thiol groups are kept in a reduced state.  In effect, glutathione reduces any disulfide bonds formed within cytoplasmic proteins to cystines by acting as an electron donor.  Glutathione is found almost exclusively in its reduced form.  In fact, the ratio of reduced to oxidized glutathione within cells is often used scientifically as a measure of cellular toxicity. 

All cells in the body are capable of synthesizing glutathione by combining L-Cysteine, L-Glutamate and glycin.  Most eukaryotes synthesize glutathione.  Glutathione (GSH) is a substrate in both conjugation reactions and reduction reactions catalyzed in cytosol, microsomes, and mitochondria.  However, it is also capable of participating in non-enzymatic conjugation with some chemicals. 

Glutathione is also needed for the detoxification of methylglyoxal, a toxin produced as a byproduct of metabolism.  Glutatihion taken orally is not well absorbed across the GI tract.  However, glutathione concentrations can be raised by increased intake of the precursor cysteine.  Glutathione is diminished during anaerobic exercise, i.e. intense exercise.









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Product Specification Comparisons


Product pH And ORP Comparisons Tests

Ionized alkaline water and acid ionized water made by electrolysis have the following chemical characteristics:

(+)2H20  -à  O2 + 4H+ + 4e- + 1.229v(Eo)

(-)2H20 + 2e- -à H2 + 2OH-  + 0.828v(Eo)

With electrolysis, the water at the cathode or negative pole produces alkaline ionized water (OH-) and positively charged ionized minerals such as calcium, magnesium, sodium and potassium.

Consequently the anode (+) pole has hydrogen (H+) ions because the oxygen gas (O2) generates acidic ions such as chlorine, sulfur and phosphorus.