Photo by Barbara Vallance, iStock
THE NEXT TIME Florida’s blue-green algae blooms make the news, DMV residents should not be dismissive. Maryland, especially the Chesapeake Bay area, has had its own toxic blooms. Also, high levels of the neurotoxin BMAA (B-N-Methylamino-1-alanine), which can be produced by blue-green algae blooms, have been detected in clusters of patients with Amyotrophic Lateral Sclerosis (ALS) in the Chesapeake Bay area, as well as in New Hampshire and France. ALS is a motor-neuron disease linked to the “misfolding” of proteins, also called tangles, that are also found in the brains of people with Alzheimer’s and Parkinson’s diseases.
Blue-green algae, generally found in low, harmless concentrations, are in fact bacteria, “cyanobacteria” — cyan means “blue green” — called microcystis. They were originally classified as algae because they require sunlight and warmth to grow.
In conditions combining warm temperatures with water rich in nutrients — usually from fertilizer run-off — algae can proliferate into a bloom that looks bluish, brownish or like green paint floating on water. Blue-green algae blooms can contain toxins that affect the skin, the liver and the brain. In 2014, blooms in Lake Erie caused the shut-down of Toledo’s water supply.
Perhaps due to global warming, blue-green algae blooms have increased worldwide and are on the rise in the Chesapeake Bay — up from 13/year in the 1990s to 23/year in the 2000s. Like mercury, BMAA accumulates in fish, with high levels found in shellfish and the highest in shark fins. In Florida coastal waters affected by algae blooms, high BMAA levels were found in pink shrimp and blue crabs.
Florida bottlenose dolphins with high BMAA levels appeared confused and seemed to be getting lost, swimming into fresh-water rivers and lakes, said University of Miami marine biologist Larry Brand: “just like an Alzheimer’s patient.” Miami researchers are working to replicate the Dartmouth study that found “hot spots” of ALS patients tied to high BMAA levels in New Hampshire lakes contaminated with the algae.
In studies of samples from the University of Miami’s brain bank, high levels of BMAA were found in 23 of 24 samples from Alzheimer’s patients, compared to very little from the control group. From patients with ALS, all 13 samples tested positive. Importantly, samples from patients with Huntington’s Disease — also a motor-neuron disease, but 100% genetically-based and thus not susceptible to environmental influences — contained no BMAA at all.
Paradoxically, blue-green algae is sold as a healthy supplement — a source of B-vitamins, iron and dietary protein — used for weight loss, ADHD, anxiety and PMS. Research is underway to examine beneficial effects on the immune system, inflammation and viral infections. The most popular “microalgae,” spirulina — to some, pond scum — is harvested as a “superfood.” And one compound isolated from cyanobacteria, Nostoc, might actually help combat neurodegenerative diseases.
Because the toxins affect people who either inhale or come into contact with a bloom, the advice is to avoid drinking or swimming in the water — and to wash off with fresh water after any contact. Besides skin rashes, symptoms of neurotoxin poisoning due to algae blooms include numbness, tingling and dizziness while liver poisoning may cause abdominal pain and digestive problems.
The most intriguing research into BMAA began with findings by ethnobotanist Paul Cox, at the Institute for EthnoMedicine in Jackson Hole. Among the Chamorro people of Guam, almost one-fourth of adults had some type of neurological disorder similar to ALS.
Years of observation led Cox to connect the dots between the Chamorros and high concentrations of blue-green algae in the cycad fruit eaten by flying foxes (fruit bats) — which had very high levels of BMAA in their skins, 10,000 times that found in cyanobacteria. The flying foxes were, in turn, consumed in copious amounts by the Chamorros.
Cox’s next step was such a breakthrough for tangle-disease that some researchers had tears in their eyes when it was announced he’d found the first animal model for research on neurological diseases: vervet monkeys fed fruit dosed with BMAA developed both neurofibrillary tangles and amyloid deposits, the hallmarks of these diseases.
In the brains of vervets who developed ALS-like symptoms, BMAA appeared to cause the misfolding of proteins by replacing the amino acid L-serine. When L-serine was added to the diet of these monkeys, their brains had fewer tangles — although still more than the brains of the group that received placebos.
ALS was chosen as the focus for clinical research because 90% of ALS cases have no genetic link, because the disease has no treatment and little hope for survival, and because it affects healthy, predominantly middle-aged people. Lifetime risk in the U.S. is estimated at 1 in 350 men, and 1 in 450 women. ALS paralyzes its victims, who generally die within five years of diagnosis.
ALS is problematic because it’s likely not one disease but a variable disorder. (Stephen Hawking has an ALS variant with the possibility of longer survival than most.) Research on the effects of L-serine on ALS has reached the stage of human trials — now in Phase I, to determine safety — in 20 Phoenix-area patients with advanced disease.
Cautions abound in discussions of Cox’s research and of conclusions about BMAA that can be drawn at this point. Said Cox, “Our findings show that chronic exposure to BMAA can trigger Alzheimer’s-like brain tangles and amyloid deposits,” but whether the bacteria blooms are a risk factor for the tangle diseases is “an open question.”
At this point, blue-green algae is a “candidate environmental risk factor,” making it worrisome enough to warrant attention for local blooms.
— Mary Carpenter
Mary Carpenter is the well-being editor of MyLittleBird. Her last post was “Bats in the Bedroom.”
