Watson vs Venter: the loser is race-based medicine


By Ewen Callaway When they weren’t competing to map the human genome, it often seemed like James Watson and Craig Venter were vying for the title of world’s most candid scientist. Now their genomes are doing battle, and the loser seems to be the biological concept of race. A new comparison of the scientists’ publicly available genome sequences indicates that, although Watson and Venter are both white men, they will react to some drugs quite differently. Watson’s genome hosts a mutation in a drug-metabolising gene rarely found in Caucasians. “It shows that James Watson has some Korean blood in him, or some Asian blood anyway,” says Howard McLeod, a pharmacologist at the University of North Carolina in Chapel Hill. “He wouldn’t get good pain relief from codeine.” Nor much effect from antipsychotic drugs, some antidepressants and a drug commonly used to treat breast cancer, say Venter and Pauline Ng, of the J. Craig Venter Institute in Rockville, Maryland, who compared the scientists’ genomes. Venter used the analysis to make a simple point: “Race-based medicine doesn’t have any real basis in science,” he told New Scientist. “You can look at somebody’s skin colour, but it doesn’t necessarily tell you much about the rest of their genome or how they’ll respond to drugs or which drugs they’ll respond to.” Last year, Watson quit his job as head of Cold Spring Harbor Laboratory in New York after a British newspaper quoted him making disparaging remarks about the intelligence of people from Africa. He later apologised and noted: “There is no scientific basis for such a belief.” The latest analysis supports the conclusion that skin colour doesn’t convey as much medically useful information as knowledge of individual genomes. “That became a consensus view back in the pre-Cambrian, or perhaps a tad earlier,” says David Goldstein, a geneticist at Duke University in Durham, North Carolina. Yet the availability of cheap genetic testing – and soon complete individual genome sequencing – means that such personalised information will become increasingly important in developing, testing and prescribing medicines. Although the concept of a drug for every genome is more fiction than fact, our genes will help customise drug treatments by grouping people into categories for specific diseases, Venter says. One set of genes may dictate a particular treatment for hypertension, whereas another set will influence which drugs are prescribed for cancer. Many of those connections remain weak and medically useless for now. By contrast, scientists have made big strides in understanding how the body breaks down drugs, a key criterion that determines dosing. For instance, a blood-thinning drug called warfarin breaks down slowly in patients with a certain gene mutation, putting them at risk of haemorrhaging. Knowing the sequence of a gene called CYP2C9 before prescribing warfarin can cut down on haemorrhaging and save lives. Watson and Venter have different mutations in CYP2C9, but this difference doesn�t seem to affect how they break down warfarin. But other drug-metabolism genes vary between the two genetic pioneers. Most notably, Watson has two copies of a mutation in the gene CYP2D6 that affects the break down of some heart drugs, as well as antipsychotics and antidepressants. Ng and Venter note that 3% of Caucasians have this mutation, which is far more common among East Asians. And although Venter seems to have the same drug metabolism as the average white male, genes that influence other traits will tell another story, McLeod, says. Journal reference: Clinical Pharmacology and Therapeutics (DOI:
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