Plant-Based Diet and Vitamin B2 Might Help in Managing Parkinson Disease

Back in Novem­ber 2009, I wrote a blog post about a study that sug­gest­ed that a hered­i­tary prob­lem in the metab­o­lism of riboflavin (vit­a­min B2) and the heavy con­sump­tion of red meat could both con­tribute to the cause of Parkin­son dis­ease. The researchers did blood tests for riboflavin for 31 con­sec­u­tive Parkin­son patients who entered their clin­ic. Every sin­gle one of them had abnor­mal­ly low blood lev­els of riboflavin. In com­par­i­son, only a few of the patients with oth­er neu­ro­log­ic dis­eases had low riboflavin lev­els. The Parkin­son patients also tend­ed to be heavy con­sumers of red meat. After the riboflavin defi­cien­cy was cor­rect­ed and the Parkin­son patients stopped eat­ing red meat, their motor skills improved dra­mat­i­cal­ly.

I thought that this study was impor­tant. It sug­gest­ed that cheap and gen­er­al­ly ben­e­fi­cial inter­ven­tions could pro­vide sig­nif­i­cant ben­e­fits for peo­ple with Parkin­son dis­ease. It should have been fol­lowed up with larg­er stud­ies. Keep in mind that Parkin­son dis­ease is a major cause of dis­abil­i­ty among elder­ly Amer­i­cans and ranks 14th among caus­es of death in the Unit­ed States.

Since then, I’ve seen a few stud­ies in which inves­ti­ga­tors assess riboflavin sta­tus by ask­ing peo­ple what they’ve been eat­ing, instead of doing a blood test! This is a big mis­take because the Parkin­son patients in the 2003 study had riboflavin defi­cien­cy even though they were eat­ing nor­mal amounts of riboflavin. Their bod­ies just weren’t han­dling the riboflavin effi­cient­ly. We need more research to show whether Parkin­son patients should rou­tine­ly be screened for riboflavin defi­cien­cy. Of course, if you or a loved one has Parkin­son dis­ease, you can just ask for the riboflavin lev­el to be test­ed. If a patient has a vit­a­min defi­cien­cy, it should be cor­rect­ed, shouldn’t it?

Anoth­er study, pub­lished in Jan­u­ary of 2011, found that Parkin­son patients improved when they switched to a plant-based diet. This came as no sur­prise to me because sim­ply eat­ing less pro­tein, espe­cial­ly dur­ing the day­time, can dra­mat­i­cal­ly improve the patient’s response to L-dopa, which is the drug of choice for treat­ing Parkin­son dis­ease.

Don’t Eat Fruit Bats, and Avoid Algae Blooms!

The peo­ple with the world’s high­est risk of Lou Gehrig’s dis­ease were the Chamor­ro peo­ple, who were the native peo­ple of Guam. These peo­ple also had a high risk of Alzheimer-like demen­tia and dis­or­ders like parkin­son­ism. The prob­lem didn’t seem to be genet­ic or con­ta­gious, and the dis­eases became less com­mon when the pop­u­la­tion became more Amer­i­can­ized after World War II. These facts sug­gest­ed that the prob­lem result­ed from some­thing that the peo­ple had been eat­ing.

The prime sus­pect in this case is a neu­ro­tox­in called BMAA (beta-methy­lamino-L-ala­nine). It’s sim­i­lar to the amino acid ala­nine that your body uses in mak­ing pro­tein. When BMAA was giv­en to rhe­sus macaques, the result­ing dam­age to the ner­vous sys­tem was sim­i­lar to what was hap­pen­ing to the afflict­ed peo­ple on Guam.

The BMAA orig­i­nal­ly came from cyanobac­te­ria. The cyanobac­te­ria are true bac­te­ria, although they are some­times called blue-green algae. The cycad plant, which was an impor­tant food source for the Chamor­ro peo­ple, has a part­ner­ship (sym­bi­ot­ic rela­tion­ship) with cyanobac­te­ria of the genus Nos­toc. The cycads give some sug­ar to the Nos­toc liv­ing on their roots. In return, the Nos­toc con­vert some of the nitro­gen from the atmos­phere into ammo­nia, which the cycad can use as fer­til­iz­er.

Unfor­tu­nate­ly, the Nos­toc also make some BMAA, which is also absorbed by the cycad. The Chamor­ro peo­ple then were exposed to BMAA when they ate seeds from the cycad plant. They got an even big­ger dose of BMAA when they ate fruit bats, because the BMAA had become con­cen­trat­ed in the bats’ bod­ies. This process of con­cen­tra­tion is called bioac­cu­mu­la­tion.

There are two take-home lessons from this sto­ry. The first is that we may need to be care­ful about human expo­sure to cyanobac­te­ria. All types of cyanobac­te­ria but only cyanobac­te­ria pro­duce BMAA. Human beings could be exposed to BMAA as a result of the tox­ic algae blooms that are becom­ing increas­ing­ly com­mon because of fer­til­iz­er runoff. Peo­ple could become exposed to BMAA by drink­ing or swim­ming in con­t­a­m­i­nat­ed water, such as the water in ponds and reser­voirs. They could also be exposed to BMAA through cyanobac­te­ria in foods or sup­ple­ments made from algae.

The sec­ond les­son is that BMAA, like many oth­er tox­ins, becomes more con­cen­trat­ed as you move up the food chain. Fruit bats con­tained more BMAA than the cycad seeds did. Oth­er tox­ins, such as diox­in and mer­cury, also con­cen­trate as you go up the food chain. It’s anoth­er rea­son why it’s bet­ter for us to eat plants, not ani­mals.

Pho­to by Tam­bako the Jaguar