Could this, Whiting and Kurland wondered, be a model for lytico? The idea was intriguing: fadang had been a common food before the war and, during the Japanese occupation, was used in much larger quantities, as other crops were requisitioned or destroyed. After the war, fadang consumption declined sharply because of the greater availability of imported wheat and corn flour – this, it seemed to them, could provide a very plausible scenario for the disease, why it had peaked immediately following the war, and steadily declined thereafter, an incidence which ran parallel to the use of fadang.
But the cycad theory was problematic on several grounds. First, there were no other known examples, outside Guam, of a chronic human illness ascribable to the use of cycads, despite their very wide and long use throughout the world. It was, of course, possible that there was something special about the Guam cycad, or some special vulnerability to it among the Chamorros. Second, the period of decades which might elapse between exposure to the cycads and the onset of lytico-bodig, if indeed the two were connected, was something which had no precedent in poisonings of the nervous system. All known neurotoxins acted immediately or within a few weeks, the time needed to accumulate to toxic levels in the body or for neurological damage to reach critical, symptomatic levels – this was so with heavy metal poisoning, as had occurred in the notorious Minamata Bay paralysis, with the neurolathyrism in India caused by eating the toxic chickling pea, and with the neurocy-cadism in cattle.[56] But these seemed quite different from a poison which, while causing no immediate effects, might lead to a progressive degeneration of particular nerve cells starting many years later. No such delayed toxic effect had ever been described – the very concept strained belief.
We set off again, to return to Umatac; John had more patients he wanted me to meet. He loved showing me patients, he said, taking me on house calls with him – I also loved this, seeing his energy, his neurological skill, and, even more, the delicate feeling, the caring, he showed for his patients. It took me back to my own growing up, when I would go out on house calls with my father, a general practitioner – I had always been fascinated by his technical skills, his elicitation of subtle symptoms and signs, his knack for making diagnoses, but also by the warm feeling which manifestly flowed between him and his patients. It was similar, I felt, with John; he too is a sort of GP – a neurological GP, an island GP – for his hundreds of patients with lytico-bodig. He is not just a physician to a group of individuals, but physician to a whole community – the community of the afflicted Chamorros and their relatives who live in Umatac, Me-rizo, Yona, Talofofo, Agat, Dededo, in the nineteen villages which are scattered over Guam.
Juan, another of John’s patients, has a very unusual form of the disease, John had told me. ‘Not like ALS, not like parkinsonism, not like any of the typical forms of lytico-bodig. What he does have is a peculiar tremor which I have never seen before in lytico-bodig – but I am sure this is the beginning of the disease in him.’ Juan was fifty-eight, very powerfully built, deeply sunburned, looked much younger than his years. His own symptoms had come on a couple of years ago, and he noticed them first when he was writing a letter. The act of writing brought on a shaking, and within a year it was no longer possible to write, at least with his right hand. But he had no other symptoms at all.
I examined him and was puzzled by the tremor. It looked nothing like the resting (‘pill-rolling’) tremor one usually sees in parkinsonism, for it came on with action or intention (which suppress the resting tremor). Nor did it resemble the ‘intention tremor’ which one may see (with incoordination and other cerebellar signs) if there is damage in the cerebellum or its connections. It resembled instead what neurologists gaily call essential or benign tremor. ‘Essential’ because it seems to arise without any demonstrable lesion in the brain, and ‘benign’ because it is usually self-limiting, responds well to medication, and does not interfere with life too much.
Usually this is the case. But there are a certain number of people who go on from such a ‘benign’ tremor to develop fullblown parkinsonism or other neurodegenerative disease. I thought of one patient of mine, an elderly woman in New York, who, when she developed such a tremor, in her seventies, was severely incommoded by it. She burst into tremor whatever she did, and could only prevent this by sitting stock-still. ‘They call it benign,’ she said, ‘what’s so benign about it?’ In her case, it was intensely malignant, not only in the way it interfered with her life, but in the fact that it proved to be the first symptom of a rare corticobasal degeneration, going on to rigidity, spasticity, and dementia, and, within two years, death.
There was no reason to suppose that Juan had anything like this. What he probably had, John felt – and I trusted his intuition – was an extremely mild form of bodig, so mild that he would probably be able to work and live independently for the rest of his life. Progressive and disabling as the lytico-bodig usually is, there are some, like Juan, who are only touched by it lightly, and who, after a sometimes rapid development of symptoms over a year or two, seem to show little further advance of the disease (though I have recently heard from John that Juan has developed some parkinsonian rigidity now).[57]
Had I let him, John would have driven straight on to the next patient, and the next. He was eager to show me everything in the few days I would be on Guam, and his energy and enthusiasm seemed to know no limits. But I had had enough for one day, and needed a break, needed a swim. ‘Yes, you’re right, Oliver,’ said John. ‘Let’s take a break – let’s go snorkelling with Alma!’
Alma van der Velde has a charming, sloping house, covered by vines, perhaps held together by them, surrounded by ferns and cycads, right by the water’s edge in Merizo. She herself is a water creature, who spends half her days swimming in the reef – badly arthritic, she moves painfully on land, but she is a graceful, strong, and tireless swimmer. She came to Micronesia as a young woman, fell in love with it, has never left. She has swum among these reefs daily for thirty years; she knows where to find the best chitons, cowries, and top shells, she knows the caves where octopuses hide, the underhangs of the reef where the rarest corals are found. When she is not swimming, she sits on her verandah, painting the sea, the clouds, the rocky out-croppings by the reef – or reading, or writing, completely self-sufficient. She and John are close friends, so close they hardly need to talk when they are together; they sit, they watch the waves thundering on the reef, and John is able, briefly, to forget the lytico-bodig.