The Island of the Colorblind

John could not contain his excitement at these new thoughts and findings – everything seemed to fit together perfectly. He would phone Spencer in New York, and the two would have excited conversations for hours, sometimes nightly, discussing clinical data, and bringing out more and more ‘coincidences’ of cycads and disease in the Marianas. With his colleague Tomasa Guzman, John now embarked on reexamining the whole question of cycad distribution and use in the Marianas. They observed that while lytico-bodig was common among the Chamorros on Guam and Rota, where cycads were plentiful, there was no lytico-bodig reported on the island of Saipan (at least none in the previous seventy years – it remained uncertain whether the Saipanese Chamorros had been prone to it before this).[71] But they pointed out that the cycad forests of Saipan had been cut down by the Japanese in 1914, to clear land for sugar cane, and that the use of fadang had ceased soon after this. And that on lytico-bodig – free Tinian, where there were forests of cycads, the Chamorros had never made use of them. They proposed that the family clusters of disease found on Guam, which did not follow any known genetic distribution, could be related to differences in the way each family prepared their fadang – some family recipes involved soaking the seeds overnight, some for three weeks; some would use seawater, some fresh; some would shorten the washing process so that the flour would have a stronger taste. Steele and Guzman ended their paper with some striking accounts of people who had developed lytico-bodig as long as twenty years after a single exposure to fadang.

But many researchers felt, after the first flush of enthusiasm, that the amounts of BMAA Spencer was feeding his monkeys were completely unphysiological – more than the most devoted fadang eater could consume in a lifetime. Indeed, Gajdusek calculated, to reproduce Spencer’s experiment in a human being, the subject would have to eat a ton and a half of unprocessed cycad seeds in twelve weeks. This in itself was not an annihilating criticism – experimental toxicology often uses massive doses of materials in its initial experiments in order to increase the chance of getting results within a reasonable time. But now John, knowing how meticulously the seeds were detoxified before the production of fadang, set about measuring the amount of BMAA the flour actually contained; he started sending samples out for analysis, and was surprised to find that many of these had very low levels of BMAA, and some almost none at all. With this he turned against the cycad hypothesis, which had so exercised him for more than three years – turned against it with the vehemence with which he had once espoused it.

Gajdusek and his group, meanwhile, had also been trying to produce an animal model for lytico-bodig and had been maintaining a number of macaques on a low-calcium, high-aluminum diet. The monkeys developed no clinical symptoms in the four years of the trial, but autopsies showed many neurofibrillary tangles, as well as degenerative changes in the motor neurons, throughout the neuraxis. These changes seemed to resemble those of lytico-bodig or the presymptomatic changes described by Anderson and Chen, and it was speculated that a longer period of calcium deficiency, or higher doses of toxic metals, might have led to overt clinical disease. And though Gajdusek had told John in 1983 that he thought the lytico-bodig was dying out in Guam, he has continued to investigate it in Irian Jaya, where in 1993 he found it still had a remarkably high incidence. He and his colleagues continue to see aluminum neurotoxicity as the cause of lytico-bodig and indeed of a wide range of other conditions.

While Spencer, for his part, was greatly encouraged by his own success in inducing neurological disorders in primates with BMAA, he soon developed reservations. The disorders shown by his monkeys were dose-related, came on promptly, and were acute and nonprogressive (they resembled, in this way, the neu-rocycadism of cattle); whereas human lytico-bodig, it was abundantly clear, had a very long latency or incubation period, but once it had become symptomatic, was almost invariably progressive. Was it possible, Spencer speculated, that another factor was involved besides the BMAA, which might not predispose to overt disorder for many years? Slow viruses had been described by Gajdusek; could there not be, analogously, a slow toxin? Spencer did not have any clear idea, at this stage, of how such a toxin might work, or any way of validating the concept.