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For some people, fava beans can be deadly. What is it about this little legume that makes it so?

Hosted by: Hank Green
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Image Sources:
https://commons.wikimedia.org/wiki/File:Broad-beans-after-cooking.jpg
https://commons.wikimedia.org/wiki/File:G6PD_-_3D_structure_-_PDB1qki.png
https://commons.wikimedia.org/wiki/File:Tuinboon_voor_zaad.jpg
https://commons.wikimedia.org/wiki/File:Malaria.jpg

Sources:
https://ghr.nlm.nih.gov/condition/glucose-6-phosphate-dehydrogenase-deficiency
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2749581/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2398001/pdf/postmedj00048-0016.pdf
https://www.researchgate.net/publication/5672089_Cappellini_MD_Fiorelli_G_Glucose-6-phosphate_dehydrogenase_deficiency_Lancet_371_64-74
http://www.bloodjournal.org/content/92/7/2527
(SciShow Intro)

Hank Green: Beans, beans, the magical fruit. They're known for being packed with protein and other nutrients and of course, causing lots of gas. But for some reason, eating beans can result in more than just bloating and flatulence.

Fava beans, also known as broad beans, can cause some people to experience a sudden rapid breakdown of their red blood cells, a condition known as hemolytic anemia. With fewer red blood cells to deliver oxygen to your organs, hemolytic anemia can cause fatigue, shortness of breath, gallstones, and jaundice, and also occasionally, in severe cases, death.

And the weird and scary thing is you don't even have to eat fava beans for this to happen. Some people can get a reaction just by inhaling the pollen of the fava bean plant. This extreme response to fava bean is called favism and it's associated with low levels of an enzyme called glucose-6-phosphate dehydrogenase or G6PD.

There are many factors that contribute to favism, including how many of the offending beans you've eaten, the severity of your G6PD defficiency, and other things relating to your personal heath and your environment.

But favism, really, is just one flavor of G6PD deficiency. Worldwide, there are about 400 million people who have lower-than-normal levels of the enzyme. And as it happens, most of them are biologically male. That’s because the gene that’s responsible for making G6PD is on the X chromosome.

Females have two X’s, so they usually need mutations in both copies to have a deficiency – a pretty rare event. Males, on the other hand, only have one X, so all it takes is one bad copy. And a lack of G6PD can be dangerous, because the enzyme protects your red blood cells from molecules called reactive oxygen species.

These molecules are a natural part of life -- they’re made when cells produce energy, for instance, which our bodies definitely need to keep us alive. But they can also wreak havoc because they steal electrons from other molecules. This loss of electrons is what’s called oxidation. If it goes unchecked, it can be really bad news, destroying proteins and tearing apart cells.

Fortunately, G6PD is normally there to neutralize these oxidizing molecules. But mutations in the G6PD gene can cause your body to produce less of the enzyme, or it can change the enzyme itself, so that it can’t do its job.

That means that those oxidizing molecules can build up to dangerously high levels and damage your cells. And your red blood cells are especially at risk, because -- unlike most of your other cells -- they don’t have any back-up plan for fending off those hazardous molecules. G6PD is all they have.

So yes, what does that have to do with fava beans? Fava beans contain compounds that when digested, boost the production of reactive oxygen species. So there are even more of these threatening molecules in your body, and without their bodyguard enzyme to protect them, your red blood cells end up sustaining a lot of damage -- and prompting hemolytic anemia.

There’s no treatment for G6PD deficiency, even though it’s the most common enzyme defect that humans have. But most people can avoid complications by getting vaccinated and by avoiding triggers, like fava beans. Coincidentally, it was actually a drug-induced complication that led to the discovery of G6PD deficiency in the first place.

Back in the 1950s, researchers found that some patients who received primaquine -- an anti-malarial drug -- developed hemolytic anemia and had lower levels of G6PD in their blood. Which leads to an interesting theory involving G6PD deficiency and malaria...

Most people who are deficient in this enzyme live in Africa, the Middle East, Southern Europe, and Southeast Asia -- areas where malaria is -- or until recently, was -- common. Researchers think that G6PD mutations may have stuck around in ethnic populations from these areas because the mutations might help protect people from malaria.

Malaria parasites don’t seem to fare as well in red blood cells when less of the enzyme is around. That’s probably because, where there’s less of the enzyme, there are more of those oxidizing molecules. And all of those oxidizers might harm the parasites, or injure infected cells just enough that they’re gobbled up by the immune system -- before the most dangerous forms of the parasite develop. So, while people with the G6PD deficiency might have to give up fava beans at the dinner table, they might be a little safer when the mosquitoes come out to bite.

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