Parkinson Disease

Red Meat, Vitamin B2 Deficiency, and Parkinson Disease

Recently, someone in my family got a diagnosis of Parkinson disease, which is the same disease that Michael J. Fox has. So naturally I searched the medical literature to see if there was a dietary angle to the disease. There is, and it’s very exciting! Removing red meat from the diet and correcting a vitamin B2 deficiency might prevent Parkinson disease, and it might even help reverse some of the effects of the disease. This would actually change the course of the disease, whereas all doctors can do at present is treat its symptoms.

How I Searched the Medical Literature

I went to and clicked on MeSH Database. Then I typedParkinson disease in the search box and clicked onGo. One of the results was Parkinson disease. I clicked on that and selected the subheading “diet therapy” and added that to the search box. Then I clicked on Search PubMed.

What I Found

One of the articles that I found pointed out that Parkinson disease is far more common in elderly people in Europe and North America than it is in elderly sub-Saharan Black African, rural Chinese, and Japanese people. In other words, it’s far more common in people who eat a lot of meat than in people who eat a heavily plant-based diet.

Another interesting article suggested that Parkinson disease might result from two separate problems related to diet and nutrition (High doses of riboflavin and the elimination of dietary red meat promote the recovery of some motor functions in Parkinson’s disease patients. C.G. Coimbra and V.B.C. Junqueira. Brazilian Journal of Medical and Biological Research, 36: 1409-1417, 2003). The first problem is an overload of iron from eating too much red meat. The second is some problem in the way the body handles riboflavin (vitamin B2). To put these ideas to the test, the researchers tested 31 consecutive Parkinson disease patients who entered their clinic. Every single one of them had abnormally low levels of vitamin B2 in their bloodstream, even though they were eating food that should have provided enough vitamin B2. In comparison, only 3 out of 10 patients with other neurodegenerative diseases had a vitamin B2 deficiency. The Parkinson patients were also big red meat eaters. The researchers told the Parkinson disease patients to stop eating red meat and to take 30 mg of riboflavin three times a day. The patients who followed this advice regained some of their lost motor skills. Mildly afflicted patients became completely asymptomatic, and even some of the more severely afflicted patients improved a lot. These findings were dramatic and exciting, and this article should have lit a fire under the researchers who are studying Parkinson disease. Here was a simple, cheap, and safe dietary modification that addressed the actual cause of the disease, and could even reverse some of its effects.

Unfortunately, people tend to discard the results of dietary studies out of hand, partly because these studies can’t follow the same format as a drug trial. For example, you can’t “blind” people to what they’re eating, so there’s never a “placebo control.” Also, some people become totally unhinged if they hear that the foods they like aren’t good for them. Predictably, someone wrote in a truly idiotic critique of the study (Comments of H.B. Ferraz et al. ) The authors’ responsewas withering. They said things like “By searching the current medical literature, Ferraz and associates might readily become familiar with countless preliminary studies which have been subsequently confirmed by larger and better controlled research” and “The citations made by Ferraz and associates demonstrate that they have completely missed our point, even though it was clearly emphasized even in the title of our study.” What a smack-down!

Ferraz and coworkers were worried that if people stopped eating red meat, they might end up with a protein deficiency. Well, where do gorillas get their protein? If a diet without red meat provides enough protein for a 500-pound silverback male gorilla, it should provide enough for a human being. And what would be the harm in testing Parkinson disease patients for riboflavin deficiency? Why aren’t Ferraz and coworkers worried about the possibility that we’re missing an opportunity to stop Parkinson disease in its tracks?


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