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Thursday, September 15, 2011

Humans Are Starch Eaters



Here’s an interesting talk by Nathaniel Dominy, PhD, an Associate Professor of Anthropology at Dartmouth University. He explains the central role of diet in the amazing worldwide success of the human species. If you can’t find enough to eat, you can’t do any of the other things that you would need to do to help your species survive, such as bear and rear children.

He makes several important points. One is that human beings are behaviorally “plastic.” He uses the term “plastic” in the scientific sense, meaning that something can take any shape. Our behavior is “plastic” because it can easily be reshaped. As he pointed out, human beings can adapt to many different climates because we have learned to make and wear clothes. We can also learn to eat lots of different foods.

One type of food that is available everywhere except the Artic is starchy foods. All of the energy in our diet comes from sunlight, which green plants use to make glucose out of carbon dioxide and water. Plants then store a lot of this glucose in the form of starch, often in their roots or tubers and in their seeds. Unfortunately, starch is hard to digest. To digest it, we use amylase, an enzyme that converts the starch back to glucose.

Dominy suspects that our ancestors’ ability to recognize and use tuber-forming plants opened up a food source unknown to other primates. “It’s kind of a gold mine. All you have to do is dig it up.” 

Dominy points out that, when compared with other primates, human beings have extra copies of the gene for the starch-digesting enzyme amylase. As a result, we have a lot more amylase in our saliva than gorillas or chimpanzees do. People from societies that depend heavily on starchy diets have several more extra copies of the amylase gene and therefore produce a lot more amylase in their saliva. In other words, they have become genetically more efficient at digesting starches. This kind of change can be seen in genetically related populations that have been adapting to different diets for only a few thousand years.

Although humans can and do eat practically anything (we are behaviorally plastic), that doesn’t mean that we are well adapted to a meat-based diet. As he puts it, “Anatomically, we’re not adapted to meat at all…. We simply don’t have the adaptations that you would need to chew meat efficiently. Anyone can look at the teeth of their dog or cat and see what your teeth should look like if you’re going to eat meat. Our teeth don’t match.” Dominy concludes, “The fundamental component of the human diet is a mix of plant foods, with a large amount of starch coming from tubers and seeds.”

In this context, I’d point out that the adaptations to a meaty diet go far beyond the shape of the teeth. Even though dogs often eat a fatty, meaty diet, they generally don’t get high cholesterol or atherosclerosis unless they also have a thyroid disorder that upsets their cholesterol metabolism. In contrast, human beings that eat a fatty, meaty diet are much more susceptible than dogs are to high cholesterol and atherosclerosis. That explains why atherosclerosis is the leading cause of death in the United States but practically nonexistent in societies where people eat a low-fat, plant-based diet.

Friday, September 2, 2011

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

 
Illustration of Parkinson's disease by William Richard Gowers, which was first published in A Manual of Diseases of the Nervous System (1886)

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.