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.
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