EMBARGOED FOR RELEASE UNTIL 4 PM ET, August 11, 2003
Hypothesis Linking Flying Foxes to High Incidence of ALS/PDC Gets Boost From New Study
St. Paul, Minn. -
Fifty-year-old museum specimens of the Guamanian flying fox may shed more light on why Guam’s Chamorro people once had an extremely high incidence of ALS-parkinsonism dementia complex (ALS/PDC). At the same time, the study, supported by the ALS Association, introduces the role that biomagnification of neurotoxins might play in the development of symptoms similar to those of ALS, Parkinson’s disease and Alzheimer’s disease. The Chamorro people once had an incidence rate of ALS-parkinsonism dementia complex that was 50 to 100 times higher than the rate of ALS elsewhere. The decline in the incidence of ALS/PDC among the Chamorro mirrored the decline of the population of flying foxes (a type of bat), by the 1960s and 1970s. Researchers report in the August 12 issue of Neurology that skin tissues of the flying foxes contained elevated quantities of BMAA (ß-methylamino-L-alanine), a non-protein amino acid that has shown to kill neurons in cell culture, and is believed to be a possible cause of ALS/PDC. Once readily available and consumed by the Chamorro, native flying foxes in Guam are now an endangered species. Therefore researchers Paul Alan Cox, PhD, and Sandra A. Banack, PhD, at the Institute for Ethnobotany, National Tropical Botanical Garden in Kauai, Hawaii, turned to bat skin specimens from Guam now housed at the Museum of Vertebrate Zoology at the University of California at Berkeley, to measure the concentration of BMAA. The skins contained a high concentration of BMAA – ranging from 1,287 ug/g to 7,502 ug/g. For comparison, the researchers also analyzed cycad plant seeds for their toxicity because they were an important part of the diets of both the flying foxes and the Chamorro. Although cycad seeds contain BMAA, the concentrations of the neurotoxin in processed cycad flour is believed to be too low to be toxic, and therefore their consumption was not associated with immediate ill effects. Compared to the high concentrations in bat skins, the concentration of BMAA in the unprocessed seeds averaged 9 ug/g. “The concentration of BMAA in these 50-year-old museum specimens suggests that the Chamorro people may have unwittingly ingested high doses of BMAA when they ate flying foxes,” said Cox. “This appears to be a consequence of biomagnification of the toxic substances in the food chain.” Cox and Banack were building on the research hypothesis by Cox and Oliver Sacks, MD, published in Neurology in March 2002, which theorized that the flying foxes’ penchant for cycad seeds (which are toxic only in extreme doses) is what made the flying foxes toxic to humans. Earlier epidemiologic studies had raised the suspicion that the high incidence of ALS/PDC in Guam was due to the traditional foods of the region. Cox said other neurotoxic cycad molecules should be studied to learn whether they are possible contributors to development of the disease. In a related editorial in Neurology, Carmel Armon, MD, MHS, of the Department of Neurology at Loma Linda University School of Medicine, Loma Linda, Calif., called the evidence of biomagnification of cycad-derived toxins in flying foxes “tantalizing.” He suggests it would be useful if future studies would confirm that the flying foxes in the museum are representative of the flying foxes that were consumed, adding: “The high concentration of BMAA in the museum specimens may have been the reason why these specific bats became museum exhibits.” ALS/PDC research would also benefit from a look for biomagnification of suspected toxins in current ALS/PDC patients as well as in controls.