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Levodopa Medications, Vitamin B6, and the Hinz protocol

For the purposes of this post, levodopa medication refers to prescription medications like Sinemet, Rytary, or Madopar that contain carbidopa or benserazide. For simplicity when I refer to carbidopa that also includes benserazide .

According to Marty Hinz, carbidopa will deplete your vitamin B6 and cause declining health. This is a bit of an exaggeration. It is true that if a molecule of B6 encounters a molecule of carbidopa they will bind together irreversibly and thus disable each other. That will happen if you take them close together in time - they will meet up in your stomach or small intestine. So do not take vitamin B6 and levodopa medication together! Allow at least two hours between one and the other, and if possible five hours after taking a timed release version of levodopa, before taking B6.

Once the B6 is clear of your GI tract the carbidopa will meet up with the enzyme that converts levodopa to dopamine, and disable it, which is what is supposed to do. Some carbidopa may get into circulation, bind to and disable some B6, but this doesn't matter as long as you have plentiful B6 in circulation.

Case in point, in the morning I take a multivitamin with 40 mg of B6, and B complex with 50 mg of B6, and I wash it down with Emergen-C which has another 10 mg of B6, for 100 mg of B6 in all. In the evening I take C/L 50/200 for a total of 50 mg of carbidopa daily. So I have an abundance of B6 in circulation that will never be disabled by the carbidopa. Nonetheless the carbidopa does what it is supposed to do because circulating B6 is not a problem. It only interferes with carbidopa when it is in the GI tract. If I am going to be social and want to show no sign of tremor during the day, I can take a morning dose of levodopa medication if I wait two hours after taking my B6.

If the Hinz protocol is working for you that's great, no harm done, but it is not necessary to preserve your vitamin B6.


Interested readers should also see Silvestrov's well-informed commentary below and my additional comment there regarding the anti-cancer properties of carbidopa.

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Interesting and clearly explained thanks.


Nice. I’m taking uridine after a post by WackaMole about a year ago. Park Bear, what about other vitamin depletion’s ?

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Not that I am aware of at this time. Yes, I just saw that uridine post and read up on it. Do you think it has been helpful?


Too early to say. If I never get dyskinesia then we might be on to somerthing! Google it?


Park_Bear you are wrong and looking at only the small picture. Carbidopa and benserazide both bind irreversibly (not neutralize) vitamin B6 and the B6 enzymes. Your statement of, "as long as you have enough B6" in the system is not correct. If you give enough B6 to compensate for the carbidopa, you induce a naked L-dopa state where all the problems of L-dopa that the carbidopa was intended to be used for are once again present. In the naked L-dopa state you need six times more L-dopa to get the same effects as you do with carbidopa. This means giving six times more carbidopa and six times more vitamin B6. You are that point are officially chasing your tail. The bottom line, if you are using carbidopa and getting benefits from it you are in a state of depleting your vitamin B6 and B6 enzymes with all the problems that go with this drug induced nutritional deficiency. You must remember that the enzyme which catalysis metabolism of L-dopa to dopamine is a B6-enzyme. As you deplete this enzyme it can appear that Parkinson is getting worse.

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You are guilty of selectively quoting one word out of context. What I actually wrote was: "bind together and neutralize each other." The meaning of this is clear. You say:" bind irreversibly (not neutralize) " - A distinction without a difference. Lest anybody else be similarly confused, I added the word "irreversibly" to my text , and changed "neutralize" to "disable".

" If you give enough B6 to compensate for the carbidopa, you induce a naked L-dopa state where all the problems of L-dopa that the carbidopa was intended to be used for are once again present."

Did you even read what I wrote? If so, you evidently failed to comprehend it or could not be bothered to try. The carbidopa is needed to do its work in the GI tract. If allowed to do so, and the B6 is ingested at a different time, the carbidopa is not interfered with. A plenitude of B6 then gets into general circulation where it is needed. If you are taking more B6 than carbidopa that guarantees you will always have unbound, active, vitamin B6 available in general circulation.

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My post is a response to that article.


The problem I have with Hinz's hypothesis as to carbidopa causing death in PD is its laziness. They authors rely on the timeline of levodopa as therapy versus levodopa plus carbidopa and compare their respective death rates. It is too simple and does not explain the following:

Aspiration pnuemonia is the number one cause of death in PD and how does carbidopa cause aspiration pnuemonia (AP)? AP is also the leading cause of death for Progressive supranuclear palsy, Huntington's disease and is common in Multi system atrophy.

What do all these diseases have in common? Brain stem degeneration. So how does carbidopa cause brain stem degeneration? And it should be noted L-dopa is not a therapy for Huntington's disease. They actually use haloperidol which causes drug-induced parkinsonism.

As an aside low dose haloperidol may be a future therapy for PD:


Are there any studies supporting a deficiency of pyridoxine leads to pneumonia? Yes, one study from 1949... (not a rock solid argument)..

The effect of diet on the susceptibility of the mouse to pneumonia virus of mice; influence of pyridoxine administered in the period before as well as after the inoculation of virus.


If carbidopa/benserizide are the cause of death in PD then all PD patients should develop peripherol neuropathy prior to death and PN develops in 1/5 PwP. In addition (form the Death Rate article):

"Systemic vitamin B6 concentrations inversely correlate with mortality induced by coronary artery disease, colorectal cancer, stroke, heart failure, and atherosclerosis."


"This study shows a significantly increased risk of ischemic stroke in PD patients. Further studies are required to investigate the underlying mechanism."


An older study:

"The carotid duplex scanning results could not provide a potential explanation for the relatively low occurrence of stroke in Parkinsonian patients, because most strokes are related to carotid atherosclerotic lesions while the TCD results might reflect a diminished blood supply secondary to a decline in tissue metabolism."


Missing link in Parkinson's disease found: Discovery also has implications for heart failure

Heart disease:

"Researchers at Washington University School of Medicine in St. Louis have described a missing link in understanding how damage to the body's cellular power plants leads to Parkinson's disease and, perhaps surprisingly, to some forms of heart failure."

The author's note that mitochondrial dysfunction is the connecting point between developing PD and heart failure in PwP.


Colorectal cancer?


"Parkinson’s disease is inversely associated with CRC risk."


There is not doubt that Sinemet/Benserizide are imperfect drugs and much maintenance is required to have them work properly. In B12 and folate must be taken to prevent the rise of homocysteine and methylmelonic acid levels (which are associated with peripheral neuropathy). Other methy donors like betaine hydrochloride and choline should be considered too. L-dopa methylates parkinsonsnewstoday.com/201... And EGCG from green tea should be considered as adjuvant L-dopa therapy because it can 'modestly' inhibit levodopa methylation: europepmc.org/articles/PMC2...

Etc, etc....

Here is the proverbial 'kicker'. PwP have lower rates of certain cancers, like colorectal cancer, with the exception of melanoma/non-melanoma skin and breast cancer(s). Surprisingly, there is some evidence that carbidopa has anti cancer activity:

Carbidopa Reduced Tumor Growth in Lab Studies of Cancer


"The most widely reported reduced risks in PD patients are cancers of the prostate, lung, bladder, stomach, colorectal, blood, and uterus (Table 1). While the lower risks of lung, bladder, and colorectal cancer, all smoking-related cancers, in PD patients are generally undisputed, stomach, leukemia, and uterine cancers fail to achieve significance in some studies for a clear inverse association."

"Evidence also links PD to an increased prevalence of a few cancers (Table 1), in particular non-melanoma skin cancer."


If anyone reading this is interested in lowering their non-melanoma skin cancer risk, take 2 x 500 mg of niacinamide/nicotinamide per day:

"Oral nicotinamide was safe and effective in reducing the rates of new nonmelanoma skin cancers and actinic keratoses in high-risk patients."


But this reduction of cancer rates in the west seem to be different with those from people of Chinese descent (a Taiwan study):

"The researchers found Parkinson's was not related to an elevated risk of developing thyroid, ovarian or breast cancer. However, the people with Parkinson's were found at an increased the risk for 16 other forms of cancer, including lung, urinary tract and brain cancer, as well as leukemia and melanoma."


Could carbidopa use be a contributing factor in the inverse relationship between PD and cancer in western society and not using carbidopa in Taiwan the cause of the increased rate of cancer? (Assuming they don't use carbidopa/levodopa.)

Everyone who has read my posts know I am pro vitamins, minerals, amino acids, fatty acids, herbs as either primary or adjuvant therapies for PD, but, after reading the Hinz article I was dissatisfied with their hypothesis.

I have communicated with people on the Hinz protocol and like any other therapy for PD, it can help improve PD symptoms but its results are variable. Some people cannot take the high dose of levodopa due to cramping and nausea. It helps some people more than others but it is a viable therapeutic alternative.

Oh well here is my two bits.

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"Carbidopa inhibited pancreatic cancer cell proliferation both in vitro and in vivo"

worth noting. They used human pancreatic cancer cells in an animal model.


" We believe that the reduced incidence of most cancers in Parkinson’s disease patients is due to carbidopa.”


Sinemet/madopar are not the best drugs (I hope they are soon replaced) but this could be one of their benefits. I read the Hinz death rate hypothesis and thought it is a weak argument. Like I wrote, show me how the major cause of death for PwP, aspiration pneumonia, is caused by a pyridoxine deficiency and I am all ears.


Rich - thanks for the well reasoned reply. Any idea how Mucuna compares with Carbidopa/ Levadopa with regards to B6 absorption? Thanks- John G


I posted a thread which featured an article showing the equivalent dose of sinemet to mucuna pruriens and mucuna pruriens to madopar:


As for taking P5P/pyridoxyl 5 phosphate/B6 with mucuna P. they obviously cannot be taken simultaneously but P5P is used with the proverbial 'Hinz protocol':

"...the following cofactors were administered daily: 1) vitamin C 1,000 mg; 2) calcium citrate 220 mg; 3) vitamin B6 75 mg; 4) folate 400 mcg; 5) l-lysine 500 mg; 6) l-cysteine 4,500 mg; 7) selenium 400 mcg."


Comment: 400 mcg of selenium is the maximum safe upper limit daily amount. I take 200 mg/day of selenomethionine.

Large doses of standard pyridoxine can cause peripheral neuropathy so I do not use pyridoxine hydrochloride: ncbi.nlm.nih.gov/pubmed/363...

And P5P does not cause PN:

"The use of supplemental P5P has not been associated with toxicity, although the inactive form, pyridoxine, has been associated with reports of peripheral neuropathy.

Also. "The antituberculosis drug isoniazid can result in a functional vitamin B6 deficiency.

Anti-parkinsonian drugs benserazide and carbidopa cause vitamin B6 depletion by forming hydrazones."


Since P5P will decrease the effectiveness of mucuna pruriens levodopa if taken simultaneously, I would take it at bedtime (provided you do not take L-dopa at bedtime) because:

"B6 nutritional status has a significant and selective modulatory impact on central production of both serotonin and GABA – neurotransmitters that control depression, pain perception, and anxiety. P5P is a cofactor in the synthesis of these neurotransmitters."

Same link as above. Since serotonin and GABA can help induce sleep (and relieve stress), taking P5P at bedtime may help with your sleep. Many natural sleep aids have P5P as a component:


The dose of P5P supplements are at 20, 50 or 100 mg. Considering Hinz et al, use 75 mg, 50 mg/day should be fine.


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re "Large doses of standard pyridoxine can cause peripheral neuropathy" -can happen, rarely, with moderate doses:

"Case report A 49-year-woman, who had taken 75 mg B6 daily together with multivitamins*, zinc and magnesium for 2 years, and whose serum B6 level was > 34 ng/ml, complained of paraesthesia of hands at night, ‘biting ants up her legs, electric shock pains in her head’, numbness of her finger tips and itching between the shoulder blades. Examination revealed patchy areas of hypersensitivity to stroking with cotton wool on her back and lower limbs, especially her shins. Reflexes and muscle power were normal, and L‘hermitte’s test negative. On stopping B6 in July 1985 all symptoms eased within 3 months. She restarted 50 mg B6 in August 1986 and by November 1986 had a return of the same neurological symptoms, the same areas of hypersensitivity and her serum B6 was again > 34 ng/ml. She has again been advised to stop B6."

*multivitamin may have additional B6


I had a long week and am finally able to respond.

Like most things under the sun, B6 in Parkinson's therapy is not new. Previously I posted the doctoral presentation, "Beans, roots and leaves, A History of the Chemical Therapy of Parkinsonism", opus.bibliothek.uni-wuerzbu...

The author noted:

"In the 1950's, however, a number of European workers, particularily in Germany and Austria, recommended a high dose therapy in which the daily dose was set in the region of 600-1,400mg; up to 750mg/day was administered intravenously, while higher doses were required if taken orally. The major benefit was seen in the relief from rigidity and the reduction of tremor, accompanied by a general increase in physical strength and improvement in mood; Sigwald's group also found an effect on akinesia. Marked improvements in specific tasks, such as the co-ordination of movement and speech, were also noted with some surprise. The therapy was most effective for patients in the early stages of the disease and after a long period of treatment with the vitamin, as summarized by Finke (Neurological Clinic Neuemuhle, Kassel-Niederzwehren):"

"The vitamin B6 therapy must be seen as the preparation of choice for thetreatment of parkinsonism (especially of early identified cases). Significant objective improvement in cases which are 4 or 5 years old, however, cannot be expected even with high doses of becauue of the severity of damage to the globus pallidus and substantia nigra."

"Finke believed that the progression of the disorder could be slowed by pyridoxine therapy, so that is was not merely another symptomatic treatment. Some authors (for instance, Hartmann-von Monakow, who had employed the vitamin in the treatment of parkinsonism since 1945) found that pyridoxine could even be used alone in early cases; it was, however, worthwhile at any stage of the disease, as it could be combined with any other anti-parkinsonian medication, produced no side effects, improved the temper of the patient and increased his general physical fitness and resistance to infection."

Side effects were not noted in this high dose usage of pyridoxine for PD, though they are not recommended because, as you (along with the following article) have noted:

Revisiting the evidence for neuropathy caused by pyridoxine deficiency and excess.

"Pyridoxine deficiency and excess have been implicated as a cause for peripheral neuropathy. As a result, unrelated neuropathies are often treated with pyridoxine based on questionable evidence. However, neurological practitioners frequently discourage patients from taking pyridoxine in excess of 50 mg/d given concerns around the development of a toxic sensory neuronopathy. There is no systematic review to support either of the 2 practices. To address this gap in knowledge, we reviewed the available literature on neuropathy attributed to pyridoxine deficiency and excess. Based on the current limited data, it can be concluded that very low doses of daily pyridoxine are required to prevent peripheral neuropathy. There is inadequate evidence to support routine pyridoxine supplementation in patients with disorders of peripheral nervous system. Supplementation with pyridoxine at doses greater than 50 mg/d for extended duration may be harmful and should be discouraged."


As previously noted P5P, pyridoxyl 5 phosphate will not cause PN at 50 mg doses but it has to be used cautiously when used with levodopa, M. pruriens or synthetic, without a decarboxylase inhibitor, carbidopa/benserizide. P5P will speed the conversion of levodopa into dopamine in the body and decrease its effectiveness.

Dec 37, 1971

Pyridoxine Antagonism of Levodopa in Parkinsonism

"Since the decarboxylation of dopa to form dopamine is dependent upon pyridoxal phosphate, Duvoison and co-workers1 hypothesized that pyridoxine might enhance the therapeutic effects of levodopa. Accordingly, they administered pyridoxine hydrochloride to patients with parkinsonism who were receiving maintenance doses of levodopa. They found that large doses of pyridoxine completely eliminated the clinical effects of levodopa, while smaller doses reduced or abolished its therapeutic activity or only dyskinetic side effects. This was associated with a reduced rise in plasma dopa levels following levodopa administration. Other workers have also reported reduced clinical activity of levodopa following pyridoxine.2-3 The purpose of the present study was to correlate the effects of pyridoxine on the therapeutic activity of levodopa with its effects on absorption and metabolism."


Hinz et al, used P5P at 65 mg/day because of prior use of carbidopa by the patient. "Since the decarboxylation of dopa to form dopamine is dependent upon pyridoxal phosphate..." and carbidopa binds to P5P thus preventing decarboxylation in the body; but P5P also passes the blood brain barrier and is required in the brain for decarboxylation of levodopa into dopamine. Hence the high dose use of P5P by Hinz to replete P5P in the brain (caused by carbidopa-induced deficiency).

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High amount of vitamin B6 can contribute to Neuropathy which in many cases irreversible.

I think that’s too much B6.


I was just looking at that per Silvestrov's post. Per the research he linked to, the neuropathy was reversible. In any case it turns out that half of the B6 I am taking is in the P5P form. Also keep in mind that Sinemet will destroy some of the B6. If neuropathy starts up I will know what to blame!


“Vitamin B6 toxic effects – sensory & motor neuropathies, some not reversible”



The cited study can be found here: ncbi.nlm.nih.gov/pubmed/250...

"High dose pyridoxine is neurotoxic. Previous case reports were sparse and little is known about the clinical and electrodiagnostic findings. Three patients with pyridoxine-induced sensory ataxic neuropathy were studied and a review of the involved literature was performed. Three patients, aged 80, 83 and 83 years old, presented with sensory ataxia for 3-8 months. Examination showed signs of polyneuropathy and sensory ataxia. Six hundred milligrams of pyridoxine was consumed each day for 3-10 years, in the form of vitamin B1-6-12 combination tablet. Investigations for other causes of neuropathy were unremarkable."

600 mg is a huge overdose. I am not so worried taking 50 mg of pyridoxine + 50 mg of P5P

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