set of genes. Nutrients from food, such as vitamins and minerals, as well as hormones and proteins your body makes play various roles in regulating this winding and unwinding, called “breathing.” The more we learn, the more we understand that our genes have a life of their own. The field of epigenetics is just beginning to scratch the surface of this dynamic gene regulation control system. One thing we do know is that chromosomal data is computed in analog terms rather than digital, enabling our DNA to store and compute far more information than previously imagined.
One of the positive functions of epigenetics is to come up with novel and creative solutions to less-t genes to make intelligent compromises.
Take the development of the eye, for example. Nested inside the retina at the back of the eye is the optic disc, which acts as the central focal point for light inputs that represent what eye doctors call central vision.
Something as simple as an inadequate supply of vitamin A during early childhood can force the genes to figure out how to build the disc as best it can under suboptimal nutritional circumstances. The result? Instead of a perfectly round disc you get an oval one, which can cause near-sightedness and astigmatism.23 Not a perfect outcome, of course, but without this ability to compromise, DNA would have to make more drastic decisions, like reabsorbing the malnourished optic disc cells entirely, leaving you blind.
The creativity of this problem-solving “intelligence” does not operate without reference. Each solution is guided by a record of every challenge your DNA, and your ancestors’ DNA, has ever faced. In other words, your DNA learns.
Each of your forty-six chromosomes is actually one very long DNA molecule containing up to 300 million pairs of genetic letters, called nucleic acids. The genetic alphabet only has four “letters,” A,G,T, and C.
All of our genetic data is encrypted in the patterns of these four letters.
Change a letter and you change the pattern, and with it the meaning.
Change the meaning, and you very well may change an organism’s growth.
Biologists had long assumed that letter substitution was the only way to generate such physiologic change. Epigenetics has taught us that more often, the reason different individuals develop different physiology stems not from permanent letter substitutions but from temporary markers—or epigenetic tags—that attach themselves to the double helix or other nuclear material and change how genes are expressed. Some of these markers are in place at birth, but throughout a person’s life, many of them detach, while others accumulate. Researchers needed to know what this tagging meant. Was it just a matter of DNA aging, or was something else—something more exciting—going on? If everyone developed the same tags during their lives, then it was simple aging. But if the tagging occurred differentially, then it would follow that different life experiences can lead to different genetic function. It also means that, in a sense, our genes can learn.
In 2005, scientists in Spain found a way to solve the mystery. They prepared chromosomes from two sets of identical twins, one set aged three and the other aged fifty. Using fluorescent green and red molecules that bind, respectively, to epigenetically modified and unmodified segments of DNA, they examined the two sets of genes. The children’s genes looked very similar, indicating that, as one would expect, twins start life with essentially identical genetic tags. In contrast, the fifty-year-old chromosomes lit up green and red like two Christmas trees with different decorations. Their life experiences had tagged their genes in ways that meant these identical twins were, in terms of their genetic function, no longer identical.24 This means the tagging is not just due to aging. It is a direct result of how we live our lives. Other studies since have shown that epigenetic tagging occurs in response to chemicals that
form as a result of nearly everything we eat, drink, breathe, think, and do.25 It seems our genes are always listening, always on the ready to respond and change. In photographing the different patterns of red and green on the two fifty-year-old chromosomes, scientists were capturing the two different “personalities” the women’s genes had developed.
This differential genetic tagging would help explain why twins with identical DNA might develop completely different medical problems. If one twin smokes, drinks, and eats nothing but junk food while the other takes care of her body, the two sets of DNA are getting entirely different chemical “lessons”—one is getting a balanced education while the other is getting schooled in the dirty streets of chemical chaos.
In a sense, our lifestyles teach our genes how to behave. In choosing between healthy or unhealthy foods and habits, we are programming our genes for either good or bad conduct. Scientists are identifying numerous techniques by which two sets of identical DNA can be coerced into functioning dissimilarly. So far, the processes identified include bookmarking, imprinting, gene silencing, X chromosome inactivation, position effect, reprogramming, transvection, maternal effects, histone modification, and paramutation. Many of these epigenetic regulatory processes involve tagging sections of DNA with markers that govern how often a gene uncoils and unzips. Once exposed, a gene is receptive to enzymes that translate it into protein. If unexposed, it remains dormant, and the protein it codes for doesn’t get expressed.
If one twin sister drinks a lot of milk and moves to Hawaii (where her skin can make vitamin D in response to the sun) while the other avoids dairy and moves to Minnesota, then one will predictably develop weaker bones than the other and will likely suffer from more hip, spine, and other osteoporosis-related fractures.26 The epigenetic twin study tells us that it’s not only their X-rays that will look different, their genes will, too. Scientists are becoming convinced that failure to attend to the proper care and feeding of our bodies doesn’t just affect us, it affects our genes—and that means it may affect our offspring. Research shows that when one sibling has osteoporosis and the other doesn’t, you’ll find the genes encoding for bone growth in the osteoporotic member have gone
to sleep, having been tagged, temporarily, to stay unexposed and dormant.27 Fortunately, they’ll wake up from their slumber if we change our habits. Unfortunately, returning to the example of the twin who smoked, she may have lost too much bone to ever catch up to her milk-drinking, vitamin D-fortified sister. What is worse, any epigenetic markings she developed before conceiving children can be (as we know from studies like the fat-mouse study described below) transmitted to her offspring—so that her avoidance of bone-building nutrients has consequences for them. Her children will inherit relatively sleepy bone-growth genes and be born epigenetically prone to osteoporosis. You could say that when it comes to remembering how to build bone, the epigenetic brain has grown a wee bit forgetful. Marcus Pembry, professor of clinical genetics at the Institute of Child Health in London, believes that “we are all guardians of our genome. The way people live and their lifestyle no longer just affects them, but may have a knockoff effect for their children and grandchildren.”28
What fascinates me most is the intelligence of the system. It seems our genes have found ways to take notes, to remind themselves what to do with the various nutrients they are fed. Here’s how. Let’s say a gene for building bone is tagged with two epigenetic markers, one that binds to vitamin D and another that binds to calcium. And let’s say that when vitamin D and calcium are both bound to their respective markers at the same time, the gene uncoils and can be expressed. If there is no calcium and no vitamin D, then the gene remains dormant and less bone is built.
The epigenetic regulatory tags are effectively serving as a kind of Post-it note: When there’s lots of vitamin D and calcium around, make a bunch of the bone-building protein encoded for right here. When they do, voilà!
You’re building stronger, longer bones! It’s truly an elegant design.
Of course, DNA doesn’t “know” what a given gene actually does. It doesn’t even know what the various nutrients it contacts are good for.
Through mechanisms not fully understood, DNA has been programmed at some point in the past by epigenetic markers that can turn certain DNA portions on or off in response to certain nutrients. The entire programming system is designed for change; these markers can,
apparently, fall off or be removed, causing the genetic brain to forget, at least temporarily, previously programmed information.