Research by Prof. Doron Lancet, research student Idan Menashe, and colleagues, published in this month's PLoS Biology, shows that this difference is at least partly genetic.

Our sense of smell often takes a back seat to our other senses, but humans can perceive up to 10,000 different odors. Like mice, which boast a highly developed sense of smell, we have about 1000 different genes for the smell-detecting receptors in our olfactory retinas. In humans, however, over half of these genes have become defunct in the last few million years. Some of these genes are broken in all people, while others still function in some of the population.

Lancet and his coauthors, from several institutions in Israel and Florida, had their experimental volunteers sniff varying concentrations of compounds that smelled like banana, eucalyptus, spearmint, or sweat. They compared their ability to detect each odor with their patterns of receptor gene loss. The team found that one gene (OR11H7P) appeared to be associated with the capacity of smelling sweat. When participants had two genes with disrupting mutations, they were likely to be impervious to the offending odor, while those that were hypersensitive to the smell had at least one intact gene.

The scientists noted, however, that while having at least one intact OR11H7P gene might determine if you can smell whether your loved one has just come from the gym, this is not the entire story. Women were generally slightly more sensitive to many smells than men, and some individuals of both sexes were better or worse in across-the-board acuity to all odorants. Furthermore, as is always the case, not all variation was caused by genetic differences; environmental factors were seen to play an important role as well.

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In their study, Becker's group used information collected from 1983 to 2006 as part of a larger study known as the Sibling and Family Heart Study, which involves risk-factor monitoring in 800 siblings between the ages of 30 and 60. Study participants come from nearly 350 families in the Baltimore region and were generally healthy, but all had at least one sibling with premature coronary heart disease that had required hospitalization. Half of the participants were women; 20 percent were black.

Blood tests and physical exams were conducted at the beginning of the study to assess each individual's risk factors.

Earlier findings by the team in 2005 showed that people who have a family history of heart disease needed to keep their weight down. In these families, the Hopkins team found that siblings who were obese or overweight had a 60 percent increased risk of suffering a serious heart ailment, such as a heart attack, before the age of 60.

As follow-up to their latest findings, Becker says she and her colleagues have done a genome-wide scan at deCode Genetics in Reykjavik, Iceland, a company known for its rapid genetic study of that country's genetically isolated inhabitants to hunt for the genes linked to sibling risk.

If we can crack this code, then we hope to develop a blood test for identifying families at risk long before any symptoms manifest themselves, she says.

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