I learned to walk early enough, but I stumbled and fell more easily than other children. My parents began to worry that something was wrong, that my muscles were weaker than they should be. Eventually, at the age of three, I was diagnosed with a form of spinal muscular atrophy (SMA).
In the 1980s, the precise mechanics were not yet understood, but the condition was known to be hereditary, probably linked to a recessive gene. It was also known to be progressive. As I aged, my muscles would not keep pace.
At eight, I began to use a wheelchair for longer distances. By the time I was 18, I rarely walked outdoors any more. It is hard to be young and to know that you are growing weaker rather than stronger.
I had all the same aspirations that my nondisabled friends did, but I lived in fear of the future in a way they did not. I spent a lot of time thinking about what my life would have been like if I didn’t have SMA. The images in my head were of something like a double: myself, only rid of this one deficit, imprecisely defined, but encoded somewhere in my body.
In the 1990s, the human genome began to be mapped. Medical genetics grew ever more precise. I was vaguely aware of this, of the fact that genetic conditions such as mine were being better understood with every year.
With that understanding came the possibility, however faint, that there might be some form of treatment for me beyond the interminable hours of painful, barely-worth-it physical therapy I took after school. At some point, it did strike me that before medical genetics could even begin to pursue a treatment, an SMA gene would be identifiable in embryos. My other self might be me, cured.
Extract — continue reading at the source.
