The human nose doesn't always know.
According to the latest research, we do not all smell the same thing when we walk through a flower-studded meadow in April or a fetid alley in August.
As neuroscientist Charles Wysocki sees it, we all live in different sensory worlds.
Some people can't smell cilantro. Some can't smell truffles. And thanks to research at the Monell Chemical Senses Center in West Philadelphia, it's been scientifically documented that some can't detect the funky odor of post-asparagus-eating urine.
The reason we're all smelling so differently tells a story about our evolution from much keener-smelling ancestors. Evolution doesn't always lead to sharper senses - it can lead to duller ones if they become less crucial for survival. The evidence for this is in the fossil record as well as in genetic fossils - dead genes lurking in our DNA.
A new paper released Friday contends that the advantage of keen smell was the major factor driving the expansion of the mammalian brain far beyond that of our reptilian ancestors.
Scientists used CT scanning to image skeletons from tiny, 190 million-year-old mammal-like creatures - animals on a transitional path toward becoming mammals.
That gave the scientists a way to approximate the brains of these creatures; what they found was that as these mammals evolved, the growth of their brains was dominated by a ballooning of the smell center, also known as the olfactory bulb.
That helps explain why many mammals today are extremely good sniffers - dogs, rodents, and even chimps can outsniff us.
We share common ancestors with those animals, but after we primates branched off, it all started going downhill smell-wise.
Now, geneticists can show how we got to this state of affairs, with everyone smelling the world differently. In the 1990s, scientists identified a family of approximately 1,000 genes that encode our smelling ability - a finding that led to the 2004 Nobel Prize in medicine and physiology.
Those genes hold the recipe for odor-catching "receptors" in our noses, each one geared to a different assortment of scent-causing molecules. Various scents activate different combinations of these receptors, making it possible to identify millions of different scents.
But soon it became apparent that in each of us, only about half of the scent receptor genes work.
The half that don't work are called pseudogenes because they carry mutations that render them completely nonfunctional.
"In a way those useless genes are a fossil record of how the genome transitions itself," said paleontologist Zhe-Xi Luo of the Carnegie Museum of Natural History.
Our ancestors had to be good sniffers, and probably benefited from having working versions of all those genes at some point. Then, as we came to depend more on vision, some of them deteriorated.
It's not that we don't need smell - we just don't apparently need all 1,000 of our smell receptors to work in order to survive and reproduce, said Doron Lancet, a geneticist at the Weizmann Institute of Science in Israel. Many dangerous odors have multiple components, so even with all our olfactory blind spots, most people still think a rotting fish stinks - it just stinks differently.
Genetic analysis of other animals shows that mice have lost only about 15 percent of their working smell receptor genes, and chimps have lost 35 percent of theirs.
We've lost a lot of them just in the last six some-odd million years since our lineages split off.
We're not the only mammal with a degenerating sense of smell. Some other primates are full of broken olfactory genes, as are dolphins and platypuses.
In the last couple of years, scientists have been able to get genetic information from large groups of people, thus allowing them to tie specific mutations to smell deficits.
The first such connection was discovered in 2007 by geneticist Andreas Keller and colleagues at Rockefeller University. He studied people's ability to smell a pig pheromone called androsterone, which is a very sexy smell if you're a female pig. For humans it's either odorless, slightly floral, or it smells like a male pig in heat.
Keller was able to find a specific genetic variation that determined which of those you'd experience.
A similar study out of Monell focused on the infamous smell of asparagus urine. Thanks to that study, this spring represents the first asparagus season in which there's an answer to that long-standing question of whether people who claim not to notice this aren't producing the odor, aren't smelling it, or aren't telling the truth.
(Philadelphia has a double claim to fame over this phenomenon, since Ben Franklin wrote about his own experience with asparagus and smelly urine.)
The Monell researchers recruited 38 subjects, treated them to roasted asparagus, and then sampled their urine. At some point the brave subjects had to sniff other people's pre- and post-asparagus urine as well.
The conclusion: Eight percent of them didn't produce the smell and 6 percent couldn't smell it. Most of us, like Ben Franklin, make it and smell it. By taking a DNA sample from each subject, the researchers also connected a specific genetic mutation to the inability to smell it.
In a wider-ranging study, Rockefeller's Keller along with collaborators at Duke University got a hint at our variability by testing 500 subjects for the ability to detect 66 different odors. He found that for most of the odors, the responses ranged from weak to strong, pleasant to stinky.
He is now working on a larger study, connecting a whole slew of genetic variants with different smelling abilities. "We recruit people from Craigslist and have them smell things and take blood samples," he said.
What he hopes to find is a window into the ongoing process of human evolution. Many human genes have complicated multiple functions, but odor receptor genes do something very specific, making them good candidates for study. "It's a pretty straightforward connection to an evolutionary relevant behavior," he said.