The groundbreaking study, led by Kelly Huffman, a psychology professor at the University of California Riverside (UCR), was published earlier this month in the journal Cerebral Cortex.
Speaking to Science Daily, Huffman explained it was previously thought that prenatal ethanol exposure (PrEE) from maternal consumption of alcohol only affects directly exposed embryos or fetuses in the womb. New evidence, however, showed that PrEE could persist transgenerationally, meaning that it might impact not only the child who was exposed to alcohol but also that kid's offspring, for generations to come.
Previous studies conducted by Huffman and her team have demonstrated a connection between PrEE and neurological problems. They found that PrEE could impact the anatomy of the neocortex, an important part of the brain responsible for complex behavior and cognition. Additionally, PrEE could also lead to abnormal motor behavior and increased anxiety in the exposed offspring.
Together with a group of UCR students, Professor Huffman extended her research by providing strong evidence that in utero alcohol exposure causes neurobiological and behavioral effects in later generations of mice that were never exposed to alcohol.
For the study, the UCR scientists generated a mouse model of FASD and tested many aspects of brain and behavioral development across three generations. As anticipated, the offspring exposed to alcohol in the womb showed atypical gene expression, abnormal development of the neural network within the neocortex and behavioral deficits. However, to the researchers’ surprise, non-alcohol exposed mice also exhibited neurodevelopmental and behavioral problems similar to the first generation that was directly exposed to alcohol.
The authors of the study noted that body weight and brain size were significantly reduced in all generations of PrEE animals when compared to controls. Furthermore, all generations of PrEE mice showed increased anxiety- and depressive-like behavior and sensory-motor deficits.
In conclusion, the study authors wrote that their research demonstrated strong transgenerational effects of PrEE in a mouse model, suggesting that FASD may be a heritable condition in humans. Since it is unethical to expose a human fetus to potentially harmful substances, the UCR researcher cannot study the effects of PrEE in humans. But Professor Huffman explained that the brain pattern of a mouse is nearly identical to a human's, so they make a very good substitute.
In an interview with Romper, Professor Huffman noted that the team’s results clearly show evidence that PrEE causes something called epigenetic modification. Though nothing can change your gene sequence, certain compounds have been found to change the way genes are expressed.
To explain epigenetic modification, she compared our genes with a set of LEGO blocks. Imagine you have five red square bricks, three yellow rectangles, and so on, that represent your genes. With these building blocks also comes a manual showing you how to build different things, like a race car or a robot. Just as our genes are the instruction book to build a brain, an arm, or a toenail.
In the case of PrEE, the manual for the cerebral cortex can lose a few pages, meaning your body must guess and the result comes out a little differently than it should have. This is what they call epigenetic modification.
Though Huffman hopes her research will uncover a way to reverse the damage done by PrEE, the best she can do right now is increasing awareness for prevention.
"The only way we know that alcohol won't affect your baby is if you don't drink it,” she added.
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