Dietary exposure to an environmental toxin triggers neurofibrillary tangles and amyloid deposits in the brain

This study indicates that chronic exposure to BMAA can trigger neurodegenerative illness such as ALS/PDC (amyotrophic lateral sclerosis/parkinsonism dementia complex) or more commonly known as Lou Gehrig’s disease. Click here to read the full study or an excerpt below.

 

(e) BMAA exposures beyond Guam

Diverse taxa of cyanobacteria produce BMAA [23,24], which is biomagnified in some marine ecosystems, accumulating in sharks, bottom-dwelling fish and shellfish. BMAA also occurs in cyanobacterial soil crusts [25]. BMAA exposure through inhalation of desert dust has been suggested as triggering the increased incidence of ALS a decade subsequent to the deployment of military personnel in Operation Desert Storm [26]. Similarly, inhalation of aerosolized BMAA from wave break has been proposed to explain the increased risk of ALS in individuals who live near lakes with persistent cyanobacterial blooms [18,19]. Exposure through ingestion of drinking water has not been ruled out [27]. Maternal exposures to BMAA may also increase the risk of ALS in neonates later in their life [20,21].

In conclusion, Koch’s postulates [38] have been satisfied with respect to establishing chronic dietary exposure to BMAA as a cause of a neurodegenerative illness: (i) BMAA has been identified in post-mortem brain tissue from ALS/PDC patients from Guam who consume a BMAA-rich diet but not in control patients who have not been exposed to the traditional Chamorro diet, (ii) vervets fed BMAA over 140 days developed NFT and β-amyloid deposits, and (iii) BMAA was isolated and identified in BMAA-fed vervets that had NFT and β-amyloid deposits in their brains. This study indicates that chronic exposure to BMAA can trigger neurodegenerative illness and that adding L-serine to the diet can reduce the risk of disease.

 

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