The therapy with thiamine if administrated at the right doses improves both motor and non-motor symptoms of Parkinson Disease (PD). Since often the non-motor symptoms are less intense than the motor ones, the former may regress completely even if the high dose thiamine is the only therapy the patients take. To date, no therapy has demonstrated to be effective against the non-motor symptoms. As for motor symptoms, the high dose thiamine alone is not capable of leading to the complete regressions of these unless the disease has had a very recent onset (rare cases we observed). This may be due to the fact that even though thiamine restores survived cells and seems to stop the development of the disease, the cells left untouched by the aggression of the disease are in limited number and are not capable to substitute all functional systems that depend upon a healthy substantia nigra. We observed that the right dose of thiamine can lead to an improvement of the symptoms between 50 and 80-90%, but in order to push towards the complete regression of the symptoms the correct dose of l-dopa should be coupled to power the dopaminergic motor circuits. L-dopa then shall no longer lead to dyskinesia if used together with the high dose thiamine. The treatment is based upon the hypothesis that the disease leads to the death of neurons blocking through its interaction with the intracellular metabolism of thiamine. This action can be blocked by the administration of high doses of thiamine. The neurons, once no longer burdened by the primary cause of the disease, restart their activity and this leads to the improvement of most symptoms. Continuing the therapy, the neurons might stay healthy regardless of the existence of PD. Thus, in addition to a rapid improvement of the symptoms, we observe also a freezing of the evolution of the disease. However, the primary cause of the disease is not directly affected by the therapy. High dose thiamine does not eliminate the primary cause of the disease but blocks all damages inflicted by the disease. Therefore, the high dose thiamine is a pathogenetic therapy. The therapy thus limits the degeneration of the nervous system which continues to work efficiently when freed from the limitations posed by the disease. When the high dose thiamine is suspended after a cycle of treatments of three months, the beneficial effects do not cease right away but start to diminish within the next two months. We believe that this happens because the mechanisms of action of the disease have a certain buffer effect which in turn requires a couple of months before getting back to the status of the symptoms before the use of high dose thiamine.
The correct dose varies on the basis of:
- Duration of the disease (the longer is the duration of the disease, the higher will be in general the doses);
- The severity of the symptoms and rate of progression of the disease;
- Weight and physical characteristics of the patient;
- Sensitivity/responsiveness to the treatment.
In order to determine the right dose we usually stick to the following protocol:
First of all, we learned that if the initial dose of thiamine is too high for the patient, this will experience a worsening of the symptoms after a few days characterized by an initial improvement. In this case, we invite the patient to halt the treatment with high dose thiamine for a week or so, and when the worsening regresses we restart the therapy with lower doses, often half the original dose. In our experience, the correct dose should not lead to collateral effects, but only to benefits for the patient. This includes an improvement of UPDRS symptoms by at least 50%, and normalize the pull test. The improvement of the results of the pull test is only observed with the treatment with high dose thiamine. A normal person received the pull-back stays either steady or takes one single step back to avoid falling.
However, if a patient with PD is pulled strongly backward him/her will take two or three steps before recovering, or requires support to avoid falling back. This symptom is improved only with the use of the high dose thiamine protocol as we have never observed its improvement with other treatments. Usually, we obtain the normalization of the performance of the pull test within a month from the beginning of the therapy, in rare cases, it is necessary to adjust the dosage and for this reason it may take up to three months in total to appreciate the improvements of the pull test.
The correct high dose thiamine therapy reduces greatly the symptoms. What remains (particularly the tremor is especially tough and resists to most of the therapies) is responds readily to the use of l-dopa.
In case of recent onset of the disease in patients whose weight is comprised between 50 to 65 kg (110 – 145 lbs), we begin the therapy with two grams of thiamine per day, before and after lunch. In case the patient weighs more, the dose can be three grams per day, always divided into two administrations. Oral thiamine should not be taken with juices or any sour beverage, water only. The equivalent Intramuscular administration of thiamine would be:
For 2 grams/day orally → 1 x 100mg injectable solution per week;
For 3 grams/day orally → 2 x 75mg injectable solution per week;
For 4 grams/day orally → 2 x 100 mg injectable solution per week.
In order to obtain the same effects of the intramuscular dose, the oral dosage should be around 140 times higher. For instance, 100 mg injected once a week have the same therapeutic effect that 2 grams per day x 7 days (total 14,000 mg, thus 140 times 100 mg) have if administrated orally.
Before starting the therapy with thiamine it is necessary that the patient records him/herself. In the video, the facial mimic, the speaking, the walking, and possibly a pull test should all be performed and recorded. These items should be repeated periodically to notice changes in the performances.
Even though in our experience thiamine is well effective alone, it is possible to add other group B vitamins, including folic acid. However, we do not begin the therapy with high dose thiamine in addition to multivitamin compounds, especially if these contain vitamin B6. This because vitamin B6 is a facilitator of the peripheral decarboxylase and in PwP may interfere with the amount of L-dopa that reaches the brain and thus worsen the symptoms. Usually the L-dopa compounds contain inhibitors of such action, however since this interference may occur even in presence of inhibitors, we would not be able to detect whether the effectiveness of the high dose thiamine is maximized or if it could be further fostered.
It could also be useful to take a tablet of magnesium longlife 375 twice a week.
Some supplements on the market contain high shares of magnesium or other elements. These should be avoided because the patients who do the high dose thiamine do not benefit from the relatively high doses of the other supplements. For instance, some thiamine tablets contain 500 mg of thiamine HCL and 100 mg of magnesium. Given the high number of tablets that a patient is supposed to take throughout the day and the week, and lifelong for that matter, the risk of hyper-concentration of magnesium is high.
When we start the treatment with high dose thiamine we usually do not suspend nor modify the original drugs regime that the patient is on since we have learned from our clinical experience that thiamine improves the efficacy of traditional PD medicines.
Thiamine is highly safe for the patient and it can be taken together with whatever other supplement or drug. When it is administrated through intramuscular injections it could lead to allergic reactions (we observed 4 cases in 2,500+). Mainly there are dermatological rushes and allergic phenomena.
It is not suggested to use IM high dose thiamine for patients under treatment with anticoagulants (e.g. Coumadin; Sintrom) since the injection may cause a hematoma in the location of the shot. The several thousands of patients we follow have never reported major collateral effects or problems with the therapy, neither for the clinical nor concerning the blood tests and the monitoring of their general vital functions, we have observed unfavorable conditions.
It is clear though that the best therapeutic results with the high dose thiamine are obtained by expert practitioners and after an accurate initial clinical evaluation of the status of the patient, the video recordings etc. The cure must be followed forever but it is possible to make short interruptions of the thiamin (even one or two months) without any worsening of the symptoms. this happens because the condition needs time to start damaging the neurons again. We have several patients who started the therapy in 2012-2013 and that nowadays are still in good overall physical and mental conditions, without showing evident signs of progression of the disease.
Summarizing, out of the 2,500+ patients we have treated we found the following:
- Relevant improvement of motor and non-motor symptoms;
- The disease does not seem to progress;
- An absence of insurgence of complications due to long-term use of L-dopa;
- No collateral effects or alterations of the results of blood tests.