Can We Get Off
the Superhighway?
Most of our neurohormonal superhighways are formed before age seven and fortified during adolescence, when the brain works overtime to make sense of the world around us while being bathed in the sudden onslaught of sex hormones. If our existing highways make sense, they are cemented. If not, we struggle to form new ones, which is harder than in childhood. This is why puberty is so challenging!
If you think deeply about your emotional responses to situations, you’ll find that they are quite similar to how you reacted in your childhood or adolescence. Your language may be more sophisticated and your reasoning may be more complex, but the fundamental emotional response is the same. Language and reasoning arise in the prefrontal cortex, which has made its connections over time, but your limbic system, where emotions are registered, was hard-wired much earlier in life. This is why kids who were bullies in high school grow up to be dominating and aggressive adults. Whether it is aggression or meek submission, the trait was cultivated because the limbic system registered it as being essential for survival.
Neuroplasticity
Even though our superhighways have been laid out from our repetitive behavior over years, it is indeed possible to change their courses. This is the trait that differentiates us from other animals. We have the ability to apply ourselves in such a way that we create new synapses and superhighways that take us from stress to joy. This remarkable ability of the brain to change course is known as neuroplasticity.
It is neuroplasticity that makes us learn new information throughout our lives and consciously make choices that are better for us. While superhighways are formed quite rapidly in childhood, it is a slower process in adulthood. This is why it takes us longer to learn a new skill or language compared to when we were younger. Remember that superhighways are formed through repetition. Compared to children, it takes us many more repetitions to change the course of our superhighways, but the good news is that neuroplasticity continues well into old age. We can keep changing our responses to suit our ever-changing circumstances.
Just as we are not stuck with the superhighways that we innocently built in childhood, we are also not bound by the genes we inherited from our parents. The recently emerging science of epigenetics is beginning to show us the shocking implications of this revelation.
Freedom from Determinism
Jenny was fifty-six years old when she came to my office for a second opinion. She had had her first heart attack at age fifty and told me with a bit of pride that she had seven stents. She became increasingly agitated as I interviewed her about her lifestyle and habits, stating that she was a “solid Midwestern ‘meat and potatoes’ type of girl” and that she had no time to exercise. She lived a sedentary but stressful life and was on a dozen pills for heart disease, high blood pressure, diabetes, high cholesterol, and anxiety. She asked me if I could prescribe another medicine for the occasional muscular pain she had in her chest. Reassuring her that she didn’t need another medication, I reiterated the importance of lifestyle changes to prevent another heart attack.
She looked at me in disbelief and asked me if there was not enough evidence that her disease was genetic considering that both her parents and her three siblings had heart disease at an early age. When I asked her to review her family’s lifestyle, she responded that all of them were severely overweight, smoked, never exercised, and were also “meat and potatoes” sorts of folks. She seemed unhappy to discover that we don’t inherit just our parents’ genes, but also their impressions—the way they live, act, think, and feel. As we explored in The Stress Cauldron, mirror neurons help us learn from others, particularly our primary caregivers. Our upbringing is reinforced by our caregivers’ lifestyles and mindsets that we innocently adopt as our own. We don’t have to rely on neuroscience to see if this is true. Instead, we can take a peek into the structure of genes to see if they really determine our fate.
Do Our Genes Determine Our Fate?
In the early part of the twentieth century, scientists discovered that hereditary information passed from one generation to the next was contained in chromosomes. These are threadlike structures in the nucleus of the cell that become most obvious just before a cell divides. When chromosomes were further dissected, they were found to contain two types of molecules—deoxyribonucleic acid (DNA) and protein. A quarter century later, DNA emerged as the sole carrier of genetic information. In 1953, based on the extensive work of scientists who had discovered its components, Watson and Crick proposed the double-helix model of DNA molecules that are made up of four nitrogen-containing “bases” (adenine, thymine, guanine, and cytosine, abbreviated as A, T, G, and C). A always pairs with T, and G with C. The sequence of the bases determines the amino acids (building blocks) of a particular protein.
The two strands of DNA are held together by hydrogen and are mirror images of each other. Thus, when the two strands separate, each contains the information to produce an exact replica of itself. The intermediary between DNA and life-sustaining protein is ribonucleic acid (RNA), which is a temporary copy of DNA that encodes various proteins based on the patterns of the bases.
When the world discovered how DNA works, it attained the superior status as the unchangeable principle that controlled our fates since the quality of an organism is defined by the natures of its proteins, and the proteins are birthed by DNA. This implied that the path from DNA to protein was a one-way event. Until recently, it was believed that our life experiences were determined by our genes but not the other way around.
Epigenetics
In the last decade, the science of epigenetics has begun to challenge the model that genes control our destiny in a one-sided fashion. Epigenetics is the study of environmental factors that turn genes on or off without altering the underlying DNA sequence. Studies show us that life influences such as stress, emotions, and nutrition can modify gene behavior. Not only do these changes affect the way our own genes work, but such traits can be passed on to future generations. Thus, the trauma your parents experienced not only could have altered their health, but if the modifications in their genes were passed on to you, you may experience the same kinds of health issues and also react to certain stimuli the way they did, even though you have no personal history with those stimuli. This is why we have aversions and attractions to things that we never experienced in our lives. Exactly how does the environment influence the behavior of DNA?
Remember that chromosomes contain two components: DNA and protein. The proteins were ignored for decades in the excitement of the discovery of DNA. It turns out that these proteins act as switches for DNA behavior by forming a sort of sleeve over it. If the proteins bind tightly around the DNA (via a process known as methylation), its genetic information cannot be expressed. Thus, you may have inherited a gene for breast cancer, but as long as the protein encases the gene, it is not expressed. An environmental signal is needed for the protein to change its shape and bare the DNA underneath, where it can be expressed. Thus, while DNA contains information, proteins control what information is actually expressed or switched on. The switch, in turn, is influenced by our lifestyles, habits, and how we think, feel, and act. Thanks to epigenetics, we now know that less than 5 percent of heart disease and cancer are attributed directly to heredity.
In one classic study in recent years, Dr. Dean Ornish and his team demonstrated that the activity of more than 500 genes can be changed through diet and lifestyle changes among men with prostate cancer. More recently they demonstrated that diet changes, a moderate exercise program, and stress reduction resulted in an increase in telomere length.27 Telomeres are protective caps at the end of chromosomes. Recall that for a cell to divide, the DNA must first unwind so that each strand can duplicate itself. The duplication process is performed by an enzyme known as DNA polymerase, which travels down the strand to assemble the mirror-image strand. When it reaches the end of the strand, it stops because it cannot duplicate the part of the strand it sits on. Thus, every time a DNA strand is replicated, it is slightly shorter than the “parent” strand, and eventually the polymerase will begin cutting off essential information at the ends of the strands.
Telomeres provide a length of noncoding DNA whose loss will not affect the information contained in the gene. The length of the telomerase determines how fast we age as well as our susceptibility to illnesses such as cancer, stroke, heart disease, diabetes, osteoporosis, obesity, and dementia. Until recently we were under the impression that telomere length could not be changed. Epigenetic studies like the one above show us that this is not true and that our lifestyle influences the behavior of our genes. We can finally let go of the kind of paralyzing thinking that we saw in Jenny and be empowered by the fact that we can indeed rebuild our neuronal superhighways, which have a direct effect on our genes.
Rebuild Your Superhighways
to Change Your Life
By now we know that our circumstances are far from being static. No matter how hard we try to control our lives, we never seem to succeed all the time. Sometimes we have what we want and at other times what we don’t want. We constantly try to manipulate our life situations to find happiness. Driven by our dopamine-powered neural pathways, we seek the ideal education, partner, and job, never at peace with what we already have. Our neurohormonal system just doesn’t let up and keeps us on the path of seeking throughout our lives. Once we have breathed a sigh of relief that our children are reasonably well-educated and have gone off to college, we feel the familiar nagging of seeking where we now want for them everything that we wanted for ourselves (and more). Worries about their relationships and jobs keep us up at night. Just as soon as our retirement party ends, we are faced with concerns about our grandchildren and whether they are being raised right. Then, as the wrinkles and grays proliferate, we are nagged by the greatest anxiety of all: our impending death.
Through all this, rarely do we stop to wonder if this dissatisfaction is our destiny. We look around, see that everyone is more or less in the same boat, and conclude that this constant dissatisfaction with what is must be normal. We live our lives constantly at war with whatever is going on around us since it never meets our definition of “ideal.” It is not only the world that does not conform to our unique definitions of good and bad; even our bodies begin to let us down. We fall sick and develop disease despite the limbic system’s protest that this is a bad thing. If we are not fighting the world, we are fighting our bodies and minds. Through it all, the neurohormonal pathways continue to do their thing, revving up the stress pathways that cause internal havoc.
At any given time we are ruminating about the past or the future. Pause for a moment and answer these questions. How many times did you have to re-read sections of this book because you were “somewhere else” when you first read them? How many times have you driven from point A to B only to realize you don’t remember getting there? When in a conversation, how many times do you find that you’ve missed parts of what the other person is saying because you were not paying attention?
Now consider this: What were your thoughts about when you were not present in an activity? What is the constant mind chatter about?
Default Mode Network: The I-Maker
It turns out that only 5 percent of the brain’s total energy consumption is for focused tasks such as reading or working on a project. Most of the brain’s energy is consumed in the ongoing personal narrative that weaves together the various experiences of our lives into one coherent story. In other words, the brain uses most of its energy ensuring that you remain the protagonist in the story of your life. For this, you can thank your default mode network (DMN).
The DMN is a network of various brain centers that light up simultaneously when focused attention is not required. Consisting of three arms, it is the network that brain activity defaults to. The first arm is responsible for the personal autobiographical storytelling, or the I-making that is self-referencing (thoughts that revolve around why you like or don’t like something and how these choices define you) and validates your own emotional state. Any time you are retelling your story in your mind, this network is active. The second arm of the DMN is associated with assuming what someone else knows or doesn’t know, understanding someone else’s emotional state, moral justification, assessing right and wrong, and evaluating the social standing of your family, group, or tribe. The third arm of the DMN is associated with recalling the past, imagining the future, and the ability to connect the two into a story.
The DMN keeps the I alive and well. The curious thing about the I is that it consists of fragments of information such as your likes and dislikes, your ancestry, and how you feel about your nose, body, job, spouse, children, or race. The I isn’t one thing but a whole box of ideas about who you think you are. You collected these ideas over the course of your life and then built your identity upon them, and you’ve collected them because each came with a distinct emotional high or low that created particular neurohormonal superhighways.
We collect most of the ideas about who we are before the age of seven. The younger we were when an emotional signature arose, the more surely was a superhighway created. This is when we started believing things like “I’m cute,” “My nose is too big,” “I’ll never be good at sports,” or “I’m a good musician.” In adolescence our superhighways were reinforced as we added on to our existing beliefs, strengthened them, and added new ideas based on more complex concepts like religion and politics. Unlike in childhood, stories around our ideas become more complex in adolescence. As young adults we embellish our beliefs with more elaborate and sophisticated stories. The I is created through the self-referencing part of the DMN, which is cemented by our beliefs and tying them all together.
However, even though our nerves fire in certain ways that seem to point to our identity, the I doesn’t live in the brain.
Try this exercise right now.
Notice that when you refer to your body parts, you use prepositions like “mine” that denote they belong to you. Even in daily language, you are assuming that there is an I that owns the body and the mind. Your day-to-day language gives away the fact that you don’t really think that you are your body or your mind.
Even though we don’t really think we are our body-mind, we continue to identify deeply with it, which causes us to maintain our learned behaviors and fixed ways of thinking and feeling. Patterns of thinking and feeling create specific neurohormonal superhighways, ensuring that we continue to think and act in the same habitual ways. Like hamsters on wheels, we get stuck in our body-mind-I loops. If the body suffers, I suffer. If the mind is shaken up, I become discombobulated. The I is essentially based on fear of suffering and desperate wanting to be free of fear and suffering. And because this cannot be guaranteed, the fragile I fights to keep itself alive.
An ancient definition of health includes being saturated with bliss. We cannot be saturated with bliss if our sense of I is being constantly threatened! The path to bliss requires us to question the very basis of our existence, which we will do when we examine the bliss model in detail in the next chapter.
Summary
27. D. Ornish, J. Lin, J. M. Chan, et al., “Effect of comprehensive lifestyle changes on telomerase activity and telomere length in men with biopsy-proven low-risk prostate cancer: 5-year follow-up of a descriptive pilot study,” Lancet Oncol 14 (2013): 1112–20.