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Consumption of Cycas micronesica seed tissue has been associated with the amyo- trophic lateral sclerosis-parkinsonism dementia complex (ALS-PDC) of the Western Pacifi c. However, failures to document vital plant and neighborhood descriptors and pronounced variability in toxin concentrations noted within and among studies obfuscate decades of research on this subject. We discuss the theoretical and experimental constraints of plant tissue sampling in relation to human disease research. Comparisons are made between this approach and methods used throughout the history of ALS-PDC research, most notably very recent reports concerning β-methyl-amino-alanine. Methods for studying possible plant neurotoxins need to be standardized and must follow rigorous criteria to be valid in principle. Our discussions reveal why these criteria are essential and highlight the impact that natural variations have on environmental toxin quantifi cation and interpretation. Past research on cycad toxins is defi cient on experimental and theoretical grounds, and interpretation of published data is dominated by ambiguities. This area of study as conventionally conceived and carried out needs transforming. We argue that future empirical studies should honor appropriate plant science standards concomitantly with medical science standards. This dual focus will ensure appropriate sampling scheme, sample size, and reporting of background plant and community factors known to infl uence phenotypic plasticity. The island of Guam claims an endemic cycad species and an unwelcome high historical incidence of neurological disease among the Chamorro residents. The fi rst written record suggesting that consumption of the cycad seed tissue was a probable cause of the neurologi- cal diseases was made by Spanish Lieutenant Colonel Felipe de la Corte in 1865 (as cited by Rogers, 1995). His opinions were ignored until the mid-20th century when the disease now known as ALS-PDC and the cycad now known as Cycas micronesica K.D. Hill fi rst received joint attention from the medical research com- munity (reviewed in Kurland, 1988; Kurland et al., 1994; Mabry, 2001). Consumption of cycad megagametophyte tissue as processed fl our was commonly practiced, and the resulting inadver- tent ingestion of cycad toxins was considered the vehicle for human exposure (Whiting, 1963). Numerous articles and review chapters on cycad toxins have been published throughout recent decades, and many of these were in pursuit of a reasonable link between exposure to cycad com- pounds and the prevalence of ALS-PDC (e.g., Kurland, 1993 and citations therein). However, no article within this sizeable body of literature adequately described fi eld sampling methods, habitat, conspecifi c and interspecifi c neighbors of sampled plants, scaling and allometric rela- tions, plant life history characteristics and events, and other factors that are known to infl uence secondary metabolism of plants. Unfortunately, this assertion holds true for the most recent publications in this fi eld (e.g., Banack and Cox, 2003; Yagi, 2004), despite the exposure of this manifest shortcoming of inadequate sampling methods by Zhang et al. (1996). The endemic C. micronesica has not been popular in Guam's horticulture industry. Al- ternatively, C. revoluta Thunb. is one of the most common landscape specimens in the commercial and residential landscape. Our recent surveys revealed that the purported link between the native cycad and the dreaded human disease is partly to blame for the lack of interest in using this handsome plant in the local horticulture industry. As a result, unanswered questions surrounding the hy- pothesis that cycad toxin exposure is causal

hortscience

Cycad Toxins and Neurological Diseases in Guam: Defining Theoretical and Experimental Standards for Correlating Human Disease with Environmental Toxins