The better way
(the only way)
|Written byDr. Marty Hinz|
|CARBIDOPAThe devil’s drug|
|Vitamin B6||THE ONLY STATED REASON for administering carbidopa with L-dopa is to address L-dopa induced nausea. Carbidopa is of no therapeutic value.|
|Vitamin B6 is required the function of over 100 enzymes in the body. No other vitamin or mineral in the body is involved in more chemical reactions.
In order to prevent depletion of associated systems when L-dopa and 5-HTP are administered concomitant administration of the following is also required in proper balance:
1. L-tyrosine, under lab guidance
2. A thiol (glutathione, L-cysteine, L-methionine, or S-adenosyl-L-methionine)
3. Cofactors vitamin C, vitamin B6, folate, and calcium carbonate.
USE OTHER DRUGS FIRST: L-dopa is the most effective drug for treating Parkinson’s disease. It is used last due to the severe side effects and adverse reactions it causes. The following classes of much less effective drugs are used for as long as possible prior to starting L-dopa in order to delay the onset of its side effects. These drugs are not needed if L-dopa is administered properly.
– Dopamine agonists
– MAO Inhibitors
– COMT Inhibitors
All of the drug classes listed immediately above have severe and potentially life threatening side effects associated with them.
Mechanism of action: Carbidopa binds irreversibly to the active form of vitamin B6 permanently deactivating it. Carbidopa is very effective at inducing a drug induced relative nutritional deficiency involving both the central and peripheral systems.
One nasty drug: The molecular weight of vitamin B6 is 244. The molecular weight of carbidopa is 247. The average adult male has 167 mg of vitamin B6 in the body. Daily carbidopa dosing values range from 25 mg to 250 mg or greater. The US-RDA for vitamin B6 is 2 mg per day. Carbidopa can easily deplete all peripheral and central vitamin B6 in the body.
It is the standard of care in medicine that all other drugs (which are marginally effective on Parkinson’s disease) are administered first and L-dopa is used last due to the side effects encountered with L-dopa.
The solution: Administration of proper levels of 5-HTP is absolutely effective in controlling L-dopa induced nausea. When proper levels of 5-HTP are administered with L-dopa, carbidopa is not needed.
THE PRIMARY REASON FOR PROGRESSION OF PARKINSON’S DISEASE IS NOT NEURODEGENERATION IT IS MULTIPLE NUTRITIONAL DEFICIENCIES THAT ARE NOT ADDRESSED PROPERLY
L-dopa is a nutrient required by the body for normal function. Improper administration can induce numerous nutritional deficiencies. It is these nutritional deficiencies that have been mis-interpreted as side effects.
Monoamine depletion: It is well documented that Parkinson’s disease is known to be associated with depletion of serotonin, dopamine, norepinephrine, and epinephrine, thiols (homocysteine, L-methionine, S-adenosyl-L-methionine, S-adenosyl-homocysteine, cystathione, L-cysteine, and glutathione), L-tyrosine, L- tryptophan, and catecholamines. Each of these depletions represent a relative nutritional deficiency since the amount of nutrients required by the system to correct the depletion cannot be obtained from a normal or optimal diet, see Table 1.
Administration of L-dopa is known to induce further relative nutritional deficiency associated depletion of serotonin, thiols, L-tyrosine and L-tryptophan, see Table 1.
Administration of a general decarboxylase inhibitor such as carbidopa or benserazide, through competitive inhibition of AADC, facilitates yet another relative nutritional deficiency induced depletion of peripheral serotonin, dopamine, norepinephrine, and epinephrine, see Table 1.
|Parkinson’s disease induces dopamine depletion. This represents a relative nutritional deficiency since the amount of dopamine precursor amino acids that can be obtained from normal or optimal diet is enough to meet the needs to the body.Therefore, L-dopa needs to be administered first not last.|
|Table 1Table 1: Depletions of centrally acting monoamines (serotonin, dopamine, norepinephrine, and epinephrine), thiols (homocysteine, L-methionine, S-adenosyl-L-methionine, S-adenosyl-homocysteine, cystathione, L-cysteine, and glutathione) L-tyrosine, and L-tryptophan associated with Parkinson’s disease, L-dopa administration, and administration of a general decarboxylase inhibitor.
Relative nutritional deficiencies occur when nutritional intake is normal or optimal and there is not enough nutrient intake to meet the needs of the system. All of the depletions listed in Table 1 represent relative nutritional deficiencies where with optimal dietary nutrient intake the systemic synthesis needs cannot be met. Preventing or correcting each of these depletions is dependent on nutrient intake higher that is than can be achieved on a normal or optimal diet. The current standard of care in medicine does not consider or address any of these relative nutritional deficiencies.
|TABLE 2 – Sampling of vitamin B6 dependent enzymes
Table 2: A listing of B6-dependent enzymes.
Carbidopa and benserazide irreversibly (permanently) bind to the B6 active site on the enzymes listed in Table 4. They also bind irreversibly to the B6 substrate required for activation of these enzyme. This is a powerful interaction where both the substrate and the enzyme are irreversibly deactivated. It has been noted that vitamin B6 is involved directly and indirectly in more chemical reactions in the body than any other vitamin, mineral, or amino acid, see addendum 1. Administration of carbidopa or benserazide has full potential to induce a profound B6 (vitamin B6) relative nutritional deficiency.