Transcript: Diet and Amyotrophic Lateral Sclerosis (ALS)
These data on BMAA neurotoxin concentrations in animals in South Florida waters indicate that the situation in Guam is not unique. Looks like BMAA could be found in high concentrations in aquatic animals in many areas of the world.
This could explain ALS clustering around lakes in New Hampshire: up to 25 times the expected rate of ALS with some families eating fish several times a week. Or in New Hampshire, where the most significant ALS risk factor was the past consumption of fish out of Lake Michigan. Or clustering in Finland’s Lakeland district, or maybe seafood eaters in France, or around the Baltic Sea, building up particularly in fish, mussels and oysters.
When I think of algae blooms, I think of the Chesapeake Bay near where I live, which gets choked off thanks in part to the poultry industry pollution. And indeed there was a recent report linking BMAA exposure to ALS in Maryland. The ALS victims living within a half mile of each other raised some eyebrows at the Hopkins ALS center, all of whom ate Chesapeake Bay blue crabs every week. And so they tested a few, and two out of three crabs tested positive for BMAA, indicating that the neurotoxin is present in the aquatic food chain of the Chesapeake Bay, and a potential route for human exposure.
To bring the story full circle, things in Guam are looking up. The ALS epidemic there may have been triggered by their acquisition of guns. But now, the epidemic appears to be over, thanks to near extinction of the fruit bats due to over-hunting. But while the rates decline in Guam, neurodegenerative diseases like ALS around the rest of the world are on the rise.
It’s plausible that humans have been exposed to some level of BMAA throughout their evolutionary history. But the increase in algae blooms as a result of human activities is probably increasing this exposure.
There is a general consensus that harmful algal blooms are increasing worldwide thanks in part to industrialized agriculture. More people means more sewage, fertilizer, and manure, which may mean more algae, which may mean more exposure to this neurotoxin, leading to a possible increased incidence of neurodegenerative diseases such as Alzheimer’s, Parkinson’s, and ALS. BMAA is a strong contender as the cause of, or at least a major contributor to the cause, of both endemic and sporadic ALS and Alzheimer’s disease, and possibly conferring risk for Parkinson’s disease as well. The ramifications of this discovery are enormous.
With substantial and ever growing evidence that BMAA does play a role in the onset and progression of neurodegenerative diseases, the most important question is, what mode of activity does BMAA exert? What? No it’s not. The most important question is how do we reduce our risk.
We know that the presence of BMAA in aquatic food chains could be a significant human health hazard. There may even be a synergistic toxicity between mercury and BMAA, making certain fish even riskier. Until more is known about the possible link of BMAA to Alzheimer’s and ALS, it may be prudent to limit exposure of BMAA in the human diet.
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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