W. French Anderson 
to insert a gene to make more of one product might adversely affect 
numerous other biochemical pathways. 
We possess insufficient information at present to understand the 
effects of attempts to alter the genetic machinery of a human. Is it 
wise, safe, or ethical for parents to give, for example, growth hor- 
mone (now that it is available in large amounts) to their normal sons 
in order to produce very large football or basketball players? Un- 
fortunately, this practice now takes place in this country. But even 
worse, why would anyone want to insert a growth hormone gene 
into a normal child? Once it is in, there is no way to get it back out. 
The child’s reflexes, coordination, and balance might all be grossly 
affected. In addition, even more serious questions can be asked: 
might one alter the regulatory pathways of cells, inadvertently affect- 
ing cell division or other properties? In short, we know too little 
about the human body to chance inserting a gene designed for 
‘improvement’ into a normal healthy person. 
An Acceptable Use 
There is, however, a set of circumstances under which enhancement 
genetic engineering may be ethical. This is when it could be justified 
on grounds of preventive medicine. For example, it is well established 
that heart attacks and stroke are a direct result of atherosclerosis (i.e., 
hardening of the arteries). The rate of development of atherosclerosis 
appears to correlate directly with elevated levels of cholesterol in 
the blood. The level of blood cholesterol is regulated, at least in part, 
by its rate of clearance from the blood by the low density lipoprotein 
(LDL) receptors on body cells (Goldstein and Brown, 1983). LDL is 
the major cholesterol-transport protein in human plasma, if further 
research should verify that an increased number of LDL receptors on 
cells would result in lower blood cholesterol levels and, consequently, 
in a decreased incidence of heart attacks and strokes, then the inser- 
tion of an additional LDL receptor gene in ‘normal’ individuals could 
significantly decrease the morbidity and mortality caused by athero- 
sclerosis. In this type of situation, the purpose of the intervention 
would be the prevention of disease, not simply the personal desire 
of an individual for an altered characteristic. The concerns expressed 
above about disrupting the regulatory pathways in the body still 
should be considered, of course. However, since there is a range for 
the number of receptors on a cell’s surface, shifting a person with a 
“low normal” number of receptors to a “high normal” number may 
not be disruptive to other physiological or biochemical pathways. 
Recombinant DNA Research, Volume 12 
[331] 
