selection? . . . The issue of genetic testing for sex selection requires further analysis ... the [Canadian] Royal Commission on New Reproductive Technologies is examining issues surrounding sex selection.

The British Medical Association (BMA, 1992) advises its physicians not to participate in sex selection in the absence of medical need. The ethics committee of the Royal College of Obstetricians has a policy statement under discussion (Choo, 1993). The Canadian Royal Commission on New Reproductive Technologies is preparing a statement on genetic testing for sex selection scheduled to be issued later in 1993.


Many diseases do not manifest clinically until adulthood and may become apparent only in middle age or later. Predictive or presymptomatic testing and screening can provide clues to which people may later develop one or more of these disorders. Often such tests will give information regarding a genetic susceptibility or predisposition, rather than providing definitive prediction. In some cases, a family history of a monogenic disorder in a close relative informs others in the family that they are at high risk for developing the disease. Appropriate testing might then resolve whether the mutant gene is present. Examples include Huntington disease and polycystic kidney disease. Sometimes a certain percentage of people with a particular disease have the genetic form. Genes have been found for familial Alzheimer disease and familial amyotrophic lateral sclerosis, two devastating, fatal, late-onset disorders. Even though the majority of those with these disorders have the nonfamilial form (e.g., Alzheimer disease), understanding the flaw in the gene that causes the familial form may lead to new treatments for all who are affected.

More frequently a disorder is multifactorial—or complex—in its causation, including both multiple genetic factors and environmental effects. Many common diseases of adulthood fall in this category, including coronary artery disease, some cancers, diabetes, high blood pressure, rheumatoid arthritis, and some psychiatric diseases (King et al., 1992). Different sets of genes can operate in different families (genetic heterogeneity), and environmental factors may interact with only one set of genes and not with another. There may also be interaction between the various genes involved, so that the effects of multiple gene action cannot be predicted by separate analyses of each of the single genes. In such cases, definitive prediction will rarely, if ever, be possible, and it will be impossible to group individuals into two distinct categories—those at no (or very low) risk and those at high risk (Risch, 1992).

On the other hand, the availability of presymptomatic and predispositional testing can provide an opportunity for physicians and patients to work toward prevention of disease. Since environmental factors are often essential for the

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