A new Penn study casts more light on the generational effects of nicotine consumption
By Jason Langendorf
Paternal nicotine use produces heritable biological changes in children that are sex-specific and can increase risk of nicotine addiction and cognitive issues, a new study indicates.
Researchers from the University of Pennsylvania recently published a paper in Molecular Psychiatry, based on their study using rats, that tied the nicotine use of parents (and especially fathers) to a specific biomarker that may help experts better understand the risks of nicotine.
The Penn researchers found new information—including a key biomarker—that has reinforced previous findings and provided additional detail about the influence of parental nicotine use.
Previous research has suggested that “parental nicotine exposure produces behavioral, physiological and molecular changes in subsequent generations,” according to the study. But the Penn researchers found new information—including a key biomarker—that has reinforced previous findings and provided additional detail about the influence of parental nicotine use.
“There’s plenty of epidemiological data to indicate that the offspring of parents who smoke tobacco products will go on to develop or be at higher risk for developing nicotine dependence,” Heath Schmidt, PhD, a neuroscientist and associate professor of nursing and psychiatry at the University of Pennsylvania, told Penn Today. “There’s a lot to suss out in all of that.”
The Paternal Nicotine Link
The Penn researchers cite preclinical sources that indicate “parental nicotine exposure produces behavioral, physiological and molecular changes in subsequent generations.” But in the paper, they note that its heritable effects were unknown.
“Children who grew up in households where smoking is a regular part of their daily lives see it,” Schmidt said. “It’s a behavior that they may model. It’s not necessarily clear whether that’s due to a direct impact of nicotine itself on the developing embryo. The real benefit of the animal model is we can hone in on the effects of the drug itself on offspring development and physiology.”
Schmidt and his colleagues found that the male and female children of fathers who used nicotine had “enhanced nicotine-taking” and were possibly at risk of developing a nicotine use disorder.
This latest study puts experts closer to determining a reinforcer-specific link. Schmidt and his colleagues found that the male and female offspring of fathers who used nicotine had “enhanced nicotine-taking” and were possibly at risk of developing a nicotine use disorder, as well as cognitive deficits such as ADHD.
“We also saw sex-dependent effects where the male, but not female, offspring developed cognitive deficits, as well as anxiety-like behavior,” Schmidt said. “Those are consistent with the previous models, too. Cognitive deficits like this are mediated by the hippocampus, an area in the brain that regulates learning and memory, so we decided to look at genes to determine which were involved. One stood out, SATB2.”
The Role of SATB2
Schmidt cites separate recent studies indicating that the protein SATB2 plays a role in synaptic plasticity in the hippocampus, and learning and memory in the adult brain. “We thought that fit perfectly with what we were seeing,” he said.
The researchers found that the male offspring in the study with cognitive deficits had decreased levels of SATB2in the hippocampus. At that point, the researchers developed a virus that would overexpress SATB2 in that area of the brain in an effort to reverse the decrease. This reduced the cognitive deficits and normalized nicotine use in the male offspring of fathers that consumed nicotine.
“It potentially offers novel ways to look at these behaviors and how to treat them,” Schmidt said. “That’s the ultimate goal—and possibly far-reaching at this point—but I think our model and the data support that type of approach.”
Top photo: Alfonso Castro