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.