Free This Is Your Brain on Sex by Kayt Sukel Page A

epigenetic changes to gene expression are of little consequence. The important take-home message is that life experience has the power to change your genetic material at the molecular level, not by mutating your genes, but by affecting the manner in which those genes express themselves—or, more specifically, by facilitating the production of more or fewer proteins by your cells. And as we learned in chapter 3, the number of those proteins can have grand consequences in how our brain cells communicate with one another, ultimately resulting in changes to our own behaviors. “This is evolution riding on the back of software,” Jirtle told me. “These changes happen rapidly. It’s easier to change the code in the software, or the epigenome, than to mutate the genes in the hardware. And these changes can have profound effects on our behaviors.”
    It Starts with a Genetic Battle
    Want to see epigenetics work its magic? Consider a newborn baby. He is the product of both his parents, both contributing their own DNA when the sperm fertilized the egg and the cells grew into a fetus. He has not had much experience in the world yet. He sleeps, he eats, and he dirties his diapers. Maybe he has worked up to a little cooing. But despite this lack of worldliness, his genome, made up of half his mother’s DNA and half his father’s, already shows some epigenetic markers from a phenomenon called genomic imprinting.
    You inherit two copies of each gene from your respective parents. But in some cases, scientists were surprised to learn, one of those two copies is turned off. Take the gene for insulin growth factor 2 (IGF2), a hormone that plays a big role in gestational growth. Although you inherit a copy of this gene from each parent, only the copy from dear old Dad will be expressed. The maternally inherited allele is silenced. In contrast, cyclin-dependent kinase inhibitor 1C, a gene that is thought to suppress tumor growth, shows the opposite pattern of expression: Dad’s copy is turned off,Mom’s is expressed. The cases, in which you see these parent-of-origin effects, in an estimated two to four hundred genes, are called “genomic imprinting.”
    “The phenomenon is paradoxical,” explained Catherine Dulac, a Howard Hughes Medical Institute investigator studying genomic imprinting at Harvard University. “It’s a huge advantage to have two copies of each gene. But here you have something that shuts down one of the two copies of an essential gene. There must be some advantage.”
    David Haig, an evolutionary geneticist at Harvard University, hypothesizes that genomic imprinting is simply an evolutionary battle for nutrients, that is, a genetic conflict between the two sexes that helps to determine the size and growth of offspring. Going back to that cute, cuddly newborn—his mom knew he was hers from the get-go. After all, she carried him in her belly for nine months and some change. Dad, however, has no real way of knowing, short of trust and a modern DNA test, that he is the father of that baby. Given this discrepancy of knowledge over the past few million years, Haig suggests, maternally expressed genes are working to make sure all of a mother’s various offspring get the resources they need for survival, while allowing the mother to remain healthy and whole enough to have more babies in the future. The paternally expressed genes, however, are not worried about Mom or the health of any other kids that may belong to different fathers. Instead they work to demand more nutrients for that single newborn from the mother in utero and beyond so it might have a leg up on its potentially unrelated siblings.
    Take IGF2, the paternally expressed gestational growth gene I mentioned above. If the maternal copy of this gene was not silenced, moms would likely end up birthing some big ol’ babies—too big to successfully nourish without detriment to herself as well as to her other children. Haig hypothesizes that while the paternally