Parkinson's Movement

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.

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Interesting and clearly explained thanks.

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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.


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.


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 And EGCG from green tea should be considered as adjuvant L-dopa therapy because it can 'modestly' inhibit levodopa methylation:

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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