Diet free of meat and rich in vitamin B2 can regress Parkinson!

Dr. Cicero Galli Coimbra and Dr. Virginia Berlanga Junqueiro
Unifesp – Federal University of São Paulo, Brasil

Original portugese, presented at the 6th international congress of Alzheimer and Parkinson Disease, Sevilha, Spain (May 2003).

Abstract: Claudia Vaz, Biomedische techniek TUE
regards: Henk de Vree

A study revealed that Parkinson patients have deficiency in vitamin B2 and commonly consume high amounts of red meat.

To include vitamin B2 and exclude red meat! These were two small changes in the diet of 31 Parkinson patients, which resulted in visible benefits.
Those patients, under treatment in the Hospital do Servidor Publico Municipal, verified not only the stagnation of the disease but also its regression.
With only 3 months of treatment and diet, the patients showed an average recovery of the physical capabilities from 44 to 70%. The best results were found in patients in the first phase of the disease. However, some persons being conventionally treated for a long time also presented improvements of the physical functionalities from 15 to 90% after starting the new treatment.

Animal fat versus meat

Generally, medical information points out that the consumption of animal fat is one of the main factors contributing for the development of Parkinson. However, the neurosurgeon Cláudio Corrêa, says that this information is questionable since no studies could prove that link. On the other hand, he says that there are some studies confirming the direct link between the consumption of meat and the production of neurotoxins.
It is already known that red meat produces a substance called hemine, which is extremely toxic for the human cells, generating the production of free radicals. To be eliminated, these free radicals need a substance called glutatione, which, after being consumed, can only be recovered with vitamin B2. In fact, the lack of glutatione is the first neuro-chemical change present in the brain cells that are degenerating with Parkinson.
Therefore, with the reposition of vitamin B2, the researcher and doctor Cicero Coimbra expected to stop the progression of the disease. Nevertheless, the results were even more promising: the disease started to regress. The explanation for the phenomenon still not completely understood but it should be related with: i) the neurogenesis (process of formation of the nervous system); or ii) the recovery of nervous cells, which were not functioning but were still alive in the black substance of the encephalon (main region affected by the degeneration).
In conclusion, Dr. Coimbra believes that the lack of vitamin B2 in the organisms of the patients may result from a problem that affects 15% of the population: the malfunctioning of an enzyme called flavoquinase, responsible for the absorption of the vitamin B2.

The results of these studies were reported in the 6th International Conference of Alzheimer and Parkinson Diseases, Sevilha, Spain (May 2003).