It’s not so often that the research we talk about in this column becomes big news. We tend to look at the small-but-crucial experiments that expand our understanding of tiny crystals, or early primates, or something else that doesn’t have that much relevance to our daily lives. But this one is different. Everyone is talking about the arsenic in our chicken.

The study itself was brilliantly simple. Researchers from Johns Hopkins’s Center for a Livable Future and Arizona State tested for drug residue in feather meal, which — sorry, this is gross — is a byproduct of poultry production that’s also added to feed for other animals. In other words, the feathers stripped off the chickens get ground up with some other stuff and fed back to the chickens (or the fish, or the cattle, or whatever). This is a pretty common practice and not a big deal in itself. What the researchers were doing in this case was analyzing that feather meal to determine what drugs the poultry may have received before slaughter. And what they found was alarming:  caffeine, banned antibiotics, arsenic, and the active ingredient in Prozac. “We were kind of floored,” said Johns Hopkins scientist Keeve E. Nachman, a co-author of the study.  “It’s unbelievable what we found.”

The antibiotics in question (fluoroquinolones) were banned by the FDA in 2005 because of fears that their excessive use was making the bacteria become resistant. (In 2009, 80 percent of all antibiotic sales in the U.S. — humans included! — went to the poultry and livestock industries, which use them primarily to speed up the growth of animals, rather than for treating disease.) The study’s authors urged the FDA to step up its regulation of the poultry and livestock industries. “By looking into feather meal, and uncovering a drug banned nearly 6 years ago, we have very little confidence that the food animal production industry can be left to regulate itself,” said Nachman.

The debate over schizophrenia has been going on for years:  is it caused by nature or nurture? Recent research from Johns Hopkins seems to indicate that schizophrenia needs a little bit of both. If someone has the particular genetic make-up that makes him/her at risk for schizophrenia, that doesn’t necessarily mean the mental disorder is inevitable. Same thing goes for the particular early experiences that tend to correlate with schizophrenia later in life — changes in environment; routine stress — aren’t enough to guarantee that the disease will develop. Instead, it seems  that both factors need to be present.

Researchers engineered one group of mice to have reduced levels of DISC1, a protein important for brain development. Then they stressed out some of the mice by separating the newborns from their mothers for a few hours every day. Stressed mice with normal DISC1 levels had normal-looking neurons; unstressed mice with DISC1 levels were similarly unremarkable. But the mice with low DISC1 and stressful experiences had neurons that were larger, more disorganized, and with projections that “went to the wrong places in the brain.”

“Our study suggests that if people have a single genetic risk factor alone, or a traumatic environment in very early childhood alone, they may not develop mental disorders like schizophrenia,” said Johns Hopkins neurology professor Guo-li Ming. “But the findings also suggest that someone who carries the genetic risk factor and experiences certain kinds of stress early in life may be more likely to develop the disease.”