The unsolved mystery resurfaced in the PNAS cyanobacteria bloom study, which provides the first evidence for BMAA biomagnification in an aquatic food chain. After measuring BMAA levels in cyanobacteria blooms in the Baltic Sea and in the plankton, fish and mussels that feed on them, researchers from Stockholm University in Sweden concluded that, BMAA levels were six times higher in plankton and up to 200 times higher in some fish than in the blooms.
But unlike Guam, the coastal regions surrounding the Baltic Sea are "not a hot spot for ALS or any neurodegenerative disease," says study lead author Sara Jonasson. And it's unknown whether the brains of fish analyzed, which reportedly contained BMAA levels up to 82 times higher than the fishes' muscles, showed evidence of neuronal damage. Jonasson says the elevated levels of BMAA found in fish from the Baltic Sea were still very low, and people should not be worried about eating seafood.
Neurologist Elijah Stommel of Dartmouth–Hitchcock Medical Center has been investigating the link between cyanobacteria-produced BMAA and neurodegenerative disease from an epidemiological angle. "We've seen a number of ALS patients that seem to be living near water bodies that have known present or historical cyanobacteria blooms," he says. In a preliminary analysis published November 2009 in the journal Amyotrophic Lateral Sclerosis, living near a bloom or the site of a former bloom more than doubled the risk of ALS.
Steele worries such studies will set off a great deal of needless public concern. "We need to reevaluate the whole hypothesis starting right back at the fruit bats of Guam," he says. He's calling for a consortium—a team of experts, including chemists skilled at detecting and quantifying BMAA, drawn from both camps—to settle the debate for good. "Guam is terribly important. If we can solve the puzzle on Guam, we might be able to better understand the cause and cure of neurodegenerative disease elsewhere."