Transcript: ALS (Lou Gehrig’s Disease): Fishing for Answers
Lou Gehrig’s disease, known as amyotrophic lateral sclerosis or ALS, strikes healthy, middle-aged people seemingly at random, and, of the major neurodegenerative diseases, it has the least hope for treatment and survival. Although mental capabilities stay intact, ALS paralyzes people, often from the outside in, and most patients die within three years, when they can no longer breathe or swallow. At any given time, an estimated 30,000 are fighting for their life with it in this country. We each have about a 1 in 400 chance of developing this dreaded disease.
So ALS is more common than generally recognized, an incidence rate now close to that of multiple sclerosis. What causes it? Well, 50 years ago scientists found that the rate of ALS among the indigenous peoples on the island of Guam was 100 times that found in the rest of the world, potentially offering a clue into the cause of the disease. So instead of 1 in 400, in some villages in Guam, 1 in 3 adults died of the disease.
Cycad trees were suspected, since the powdered seeds were a dietary staple of the natives and there were reports of livestock showing neurological disease after eating them. And indeed, a new neurotoxin was found in the seeds, called BMAA. Maybe that’s what was causing such high levels of ALS, but the amount of BMAA in the seeds people ate was so small that it was calculated that people would have to eat 1,000 kilograms a day to get a toxic dose—that’s like a ton of seeds daily. So the whole cycad theory was thrown out, and the trail went cold.
But then famed neurologist Oliver Sachs and a colleague had an idea. Cycad seeds were not all the natives ate. They also ate fruit bats, stewed in coconut milk, and guess what these so-called flying foxes ate? Cycad tree seeds. So maybe this is a case of biomagnification up the food chain. Remember how you’d have to eat a ton of seeds' worth of BMAA to run into problems? Well, guess how much builds up in the flesh of flying foxes? A ton's worth of BMAA. And the natives also ate other animals that foraged on the seeds.
The final nail in the coffin was the detection of high levels of BMAA in the brains of six out of six native victims of the disease on autopsy, but not in control brains of healthy people who died. So with the final puzzle piece apparently in place, the solution to this mysterious cluster on some exotic tropical isle of ALS/PDC, so-called because the form of ALS attacking people in Guam also had signs of Parkinson’s disease and dementia, so they called it ALS parkinsonism dementia complex. So for the heck of it, when the researchers were choosing a comparison group of control brains, they threw in two cases of Alzheimer’s disease. And they had BMAA in their brains too. But these were Alzheimer’s victims in Canada, on the opposite side of the globe. So they ran more autopsies. No BMAA in the control brains, but BMAA was detected in all the Canadian Alzheimer’s victims tested.
Wait a second; Canadians don’t eat fruit bats. Well, the neurotoxin isn’t made by the bat. Yeah, it’s made by the trees, but Canadians don’t eat cycad trees either. Their flag doesn’t look like this. It turns out that cycad trees don’t make the neurotoxin either. A blue-green algae that grows in the roots of the cycad trees makes the BMAA that gets into the seeds, that gets into the bats, that gets into the people. And it’s not just this type of blue-green algae— but nearly all types of blue-green algae found all over the world produce this neurotoxin, BMAA. Up until only about a decade ago, we thought this neurotoxin was confined to this one weird tropical tree, but now we know the neurotoxin is created by algae throughout the world, from Europe to the U.S., Australia, the Middle East, everywhere.
So, if these neurotoxin-producing blue-green algae are ubiquitous throughout the world, maybe BMAA is a cause of progressive neurodegenerative diseases, including ALS, worldwide. Researchers in Miami put it to the test. Maybe the Canadians were a fluke? No, the researchers found BMAA in the brains of Floridians who died from sporadic Alzheimer’s disease and ALS, but not in the brains of those who died from a different neurodegenerative disease, called Huntington’s, which we know is caused by a genetic mutation, not some neurotoxin. Significant levels of BMAA were found in 49 out of 50 samples from 12 Alzheimer’s patients and 13 ALS patients. The results shown here for American Alzheimer’s and ALS patients from the Atlantic southeast, compared with Canadian Alzheimer’s patients from the Pacific Northwest, suggest that exposure to BMAA may be widespread. The same thing was then found in the brains of those dying from Parkinson’s disease. And you can even pick up more BMAA in the hair of live ALS patients compared to controls.
So is BMAA present in Florida seafood? All over the place, in freshwater fish and shellfish, like oysters and bass, and out in the bay. In fact some of the fish, shrimp, and crabs had levels of BMAA comparable to those found in the fruit bats of Guam. In the U.S., fish may be the fruit bats.
To see any graphs, charts, graphics, images, and quotes to which Dr. Greger may be referring, watch the above video. This is just an approximation of the audio contributed by Katie Schloer.
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