When Science Goes Wrong Read Free Page A

release dopamine into the striatum, and this release is vital for normal function.
    In Parkinson’s disease, the cells of the substantia nigra gradually die over a period of years or decades, and their axons die too, so the striatum is gradually starved of its supply of dopamine. Well over half of the dopamine cells have to die before the disease shows itself, however: thus, a person who experiences symptoms for the first time has actually harboured the underlying disease process for years without knowing it.
    Of course, people who develop Parkinson’s disease want to know why they got the disease rather than someone else. In most cases, the answer isn’t known. Doctors commonly describe the disorder as ‘idiopathic’, meaning that it seems to develop of its own accord without any obvious external cause. Still, there are some clues. In particular, chronic exposure to pesticides, herbicides, and other environmental pollutants raises the likelihood of developing the disease. What’s more, some people have a genetic makeup that makes it hard for the body to break these pollutants down, and this makes such people more likely to develop Parkinson’s disease if they are chronically exposed to pollutants.
    Truex might have been exposed to agricultural pollutants during his childhood, when he lived in a farming area, drank well water and ate fish caught by his father in a polluted lake. Also, as mentioned earlier, Truex was exposed to a variety of toxic agents in his adult life as a result of training and racing in highly polluted air. Still, it will never be known for sure whether these exposures were a factor in his developing Parkinson’s disease, or whether his case was truly ‘idiopathic.’
    The mainstay of treatment for Parkinson’s disease is the drug L-dopa. Once ingested, this drug enters the brain, where it is transformed into dopamine and thus makes up for the brain’s own deficient supply. It is usually taken in a proprietary form called Sinemet, in which the L-dopa is combined with another drug that protects the body from some of L-dopa’s potentially harmful side-effects. Truex did take Sinemet, and it helped him, but it did not prevent the progression of his disease. In particular, his speech began to be affected. He spoke too rapidly: when he was speaking in court, the court reporter would ask him to slow down, but somehow he couldn’t. Then his voice weakened, so that it was hard to hear him in any kind of noisy environment, and he also began to slur his words. Max’s brother Don told me that he took Max to task for ‘mumbling’ – he didn’t realise that it was a symptom of his disease. ‘I said, “Max, you earn your living talking, you’ve got to talk so that you can be heard.”’
    In spite of these problems, family life went on in a reasonably normal fashion. About six months after Max was diagnosed, their daughter, Mindy, was born. Max did as much as he could to help with the children. And he even kept on running. He now knew that his disease was likely to progress, but he focused on the hope of remaining an effective father and provider for as long as the children needed him.
    Unfortunately, within two years or so, his voice deteriorated to the point that he could no longer function effectively in court. Truex wanted to continue working by concentrating on office work, but the county thought otherwise: they retired him on a disability pension. The pension was adequate to maintain the family’s standard of living, but the sudden termination of his career was a brutal experience for an active man like Truex. He worked for a few months in the office of a colleague, then quit working entirely.
    Gradually, the disease started to close in on him. He began to have problems driving, especially when he needed to make rapid turns of the steering wheel. He had always looked forward to being an active role model to his children, taking them backpacking and skiing, teaching them athletics and so on,