“Good genes” make us healthy, strong, and beautiful and represent a kind of family fortune we call genetic wealth.
We hear all the time that harmful gene mutations that cause disease are random, but the latest science suggests that’s not always true.
We don’t need to wait for technology to synthesize disease-free genes or designer babies.
Simply by giving our genes the nutrients they’ve come to expect, we can accomplish a lot, with zero risk.
Reorienting our financial priorities around healthy eating rebuilds our family’s genetic wealth and is the best investment we can make.
I remember getting caught up in the excitement when Halle Berry took the stage at the 2002 Oscars, how she stood before the audience and tearfully thanked God for her blessings. “Thank you. I’m so honored. I’m so honored. And I thank the Academy for choosing me to be the vessel for which His blessing might flow. Thank you.” A laudable Hollywood milestone, Berry was the first woman of African-American descent to be awarded the Oscar for a leading role. While so much focus was placed on what made this actor, and that evening, unique in the history of Hollywood movies, I couldn’t avoid the nagging feeling that there was something familiar about the woman in her stunning gown, something about her face that reminded me of every other woman who had, over the years, clutched the little golden statue in her hands. What was the link between Ms. Berry and all her Academy-honored sisters like Charlize Theron, Nicole Kidman, Cate Blanchett, Angelina Jolie, Julia Roberts, Kim Basinger, Jessica Lange, Elizabeth Taylor, Ingrid Bergman, and the rest? Yes, they are all talented masters of their craft. But there was something else about them, something more obvious, maybe so obvious that it was one of those things you just learn to take for granted.
Then it occurred to me: They are all breathtakingly gorgeous.
Like Halle Berry, we are all vessels—not necessarily designed to win Oscars—but made to eat, survive, and reproduce genetic material. So if you happen to win an Oscar, you could make history by extending one last note of gratitude to your extraordinary DNA. When your PR agent chastises you the next morning, just explain to her that we are all active participants in one of the oldest and most profound relationships on our planet—between our bodies and our DNA, and the food that connects both to the outside world. Halle Berry’s perfectly proportioned, fit, healthy body is evidence of a happy relationship between her genes and the natural environment, one that has remained so for several generations. As this chapter will explain, if you hope to create a more fruitful relationship with your own genes, to get healthier and improve the way you look, you need to learn to work with the intelligence embedded within your DNA.
DNA’S GIANT “BRAIN”
Every cell of your body contains a nucleus, floating within the cytoplasm like the yolk inside an egg. The nucleus holds your chromosomes, forty-six super-coiled molecules, and each one of those contains up to 300 million pairs of genetic letters, called nucleic acids. These colorless, gelatinous chemicals (visible to the naked eye only when billions of copies are reproduced artificially in the lab) constitute the genetic materials that make you who you are.
If you stretched out the DNA in one of your cells, its 2.8 billion base pairs would end up totaling nearly three meters long. The DNA from all your cells strung end to end would reach to the moon and back at least 5,000 times.19 That’s a lot of chemical information. But your genes take up only 2 percent of it. The rest of the sequence—the other 98 percent—is what scientists used to call junk. Not that they thought this remaining DNA was useless; they just didn’t know what it was for. But in the last two decades, scientists have discovered that this material has some amazing abilities.
This line of discovery emerges from a branch of genetics called epigenetics. Epigenetic researchers investigate how genes get turned on or off. This is how the body modulates genes in response to the environment, and it is how two twins with identical DNA can develop different traits.
Epigenetic researchers exploring this expansive genetic territory are finding a hidden world of ornate complexity. Unlike genes, which function as a relatively static repository of encoded data, the so-called junk DNA (more properly called non-coding DNA) seems designed for change, both over the short term—within our lifetimes—and over periods of several generations, and longer. It appears that junk DNA assists biology in making key decisions, like turning one stem cell (an undifferentiated cell that can mature into any type of cell) into part of an eye, and another stem cell with identical DNA into, say, part of your liver. These decisions seem to be made based on environmental influences. We know this because when you take a stem cell and place it into an animal’s liver, it becomes a liver cell. If you took that same stem cell and placed it into an animal’s brain, it would become a nerve cell.20 Junk DNA does all this by using the chemical information floating around it to determine which genes should get turned on when, and in what quantity.
One of the most fascinating, and unexpected, lessons of the Human Genome Project is the discovery that our genes are very similar to mouse genes, which are very much like other mammalian genes, which in turn are surprisingly similar to those of fish. It appears that the proteins humans produce are not particularly unique in the animal kingdom. What makes us uniquely human are the regulatory segments of our genetic material, the same regulatory segments that direct stem cell development during in-utero growth and throughout the rest of our lives. Could it be that the same mechanisms facilitating cell maturation also function over generations, enabling species to evolve? According to Arturas Petronis, head of the Krembil Family Epigenetics Laboratory at the Centre for Addiction and Mental Health in Toronto, “We really need some radical revision of key principles of the traditional genetic research program.”21 Another epigeneticist puts our misapprehension of evolution in perspective: mutation- and selection-driven evolutionary change is just the tip of the iceberg. “The bottom of the iceberg is epigenetics.”22
The more we study this mysterious 98 percent, the more we find it seems to function as a massively complicated regulatory system that serves to control our cellular activities as if it were a huge, molecular brain. A genetic lottery winner’s every cell carries DNA that regulates cell growth and activity better than your average Joe’s. Not because they’re just dumb-lucky, but because their regulatory DNA—their chromosomal “brain” located in the vast non-coding portions of their chromosomes—functions better. Just like your brain, DNA needs to be able to remember what it’s learned to function properly.
One example of what can happen when DNA “forgets” how to operate is cancer. Cancer develops in cells that have misunderstood their role as part of a cooperative enterprise and lost their ability to play nice in the body. The DNA running a cancer cell essentially becomes confused, believing its job is to instruct the cell it operates to divide and keep dividing without regard for neighboring cells until the growing mass of clones begins to kill its neighbors. This is an example of how epigenetics can work against us.
THE NUCLEUS: WHERE FOOD PROGRAMS GENES
A special chamber in every cell, called the nucleus, houses and protects all your DNA. Inside the nucleus, DNA is divided into chunks called chromosomes. Though each would measure several feet when uncoiled, all forty-six chromosomes are packed into just a few microns of space, spooled tightly around tiny structures called histones. These spooled threads of genetic information can loosen up to make a given section of DNA available for enzymes to bind to it, thus “turning on,” or enabling expression of, that particular gene or 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.
HOW CHROMOSOMES LEARN
To understand the genetic brain, how it works, and why it might sometimes forget how to function as perfectly as we may wish, let’s get a closer look at chromosomes.
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.
WHAT MAKES DNA FORGET?
Recent discoveries suggest that, just as with many of us, DNA tends to become a bit forgetful with advancing age.
One of the most well-studied risk factors for having a child with a brain-development disorder is paternal age. While every egg carried in a woman’s ovaries was created before she was even born, men continuously produce fresh batches of sperm, beginning at puberty. With the onset of puberty, spermatogonia (precursors of fully functioning sperm) begin dividing about twenty-three times each year. Each division is a critical process as not only do all three billion letters of the DNA code need to be replicated perfectly but so, too, does all the epigenetic bookmarking that will allow that DNA to “remember” which genes to turn on or off in response to nutrient and hormone signals—a set of coordinated functions that is essential for optimal growth and health throughout the future child’s life.
While numerous “proofreading” enzymes ensure near-perfect fidelity of DNA replication, this is not the case with epigenetic bookmarking.29 This suggests environmental circumstances at the time of replication have a relatively much greater impact on epigenetic fidelity than on the rate of genetic (DNA) mutation, a fact borne out in the latest research.30 In other words, if a man lacks adequate raw materials for bookmarking, then the bookmarking simply won’t go that well during the manufacturing process of that particular batch of sperm. Unfortunately, uncorrected errors tend to accumulate as a man ages. Neurological disorders like autism, bipolar disorder, and schizophrenia have been found to be more common among the children of older men who also have very high rates of abnormal bookmarking.31
But it’s not only a man’s age that can influence genomic memory. It’s also how well a man takes care of himself. I believe it’s quite possible for older men to significantly increase their odds of having perfectly healthy babies if they support their testicular sperm factories by eating well—a powerful strategy in assuring quality control on the sperm production line.
In 2014, geneticists working in conjunction with Albert Einstein College of Medicine in New York found evidence supporting the idea that low levels of certain nutrients could promote these reproduction errors. Folic acid, B12, and a number of essential amino acids are used for a type of epigenetic bookmarking called methylation; a lack of any one of these vital nutrients would result in undermethylation and critical bookmarks may be omitted. Their research showed bare patches of missing methylation occurring almost exclusively in the out-of-the-way places of the gene, where the DNA is tightly coiled and therefore harder for the methylation equipment to reach.32 If this is really the case, then it would seem that optimizing a man’s diet would effectively fortify him against these errors and the diseases they may cause.
GOOD NUTRITION CAN HELP REVERSE SOME EPIGENETIC MISTAKES
I just showed you evidence supporting the idea that a good diet can help prevent epigenetic mistakes that lead to permanent mutation. But can diet fix past mistakes before they rise to the level of mutation? In other words, can good nutrition enable your genes to return to an earlier, more adaptive strategy, thus averting the possibility that this strategy may be added to the permanent genetic record in the form of a mutation?
The following two studies demonstrate how a strategy involving a predisposition to being overweight can be toggled on or off by modulating nutrition in utero.
A 2010 study looking into how poor maternal nutrition and obesity affects subsequent generations concluded, “Poor in utero nutrition may be a major contributor to the current cycle of obesity.”33 The article shows that children born to overweight mothers are epigenetically programmed to build adipose tissue in unhealthy amounts. This suggests that millions of malnourished moms are, unbeknownst to them, programming their children for a lifetime of being overweight, and that this predisposition for putting on the pounds can be passed down to that child’s children as well.
Did one mom without access to proper nutrition doom all the subsequent generations to be overweight? Here’s where the good news comes in. As much as bad nutrition can lead to undesirable traits, good nutrition can compel the epigenetic adaptation system to reprise an earlier strategy appropriate for a more optimal nutrition environment.
Some of the classic epigenetic research suggests that forgotten strategies may be recalled, at least in some circumstances, when genes are given improved nutritional support. And this is why I believe we all have the potential to be—or at least give birth to—genetic lottery winners, because a forgetful genome can potentially be retrained.
This second study shows how optimizing in utero nutrition can have the opposite effect, by convincing the epigenome to abandon the weight-gain strategy and opt for one geared toward optimal body composition. Dr. Randy Jirtle, at Duke University in Durham, North Carolina, studied the effects of nutrient fortification on a breed of mice called agouti, known for their yellow color and predisposition for developing severe obesity and subsequent diabetes. Starting with a female agouti raised on ordinary mouse chow, he fed her super-fortified pellets enriched with vitamin B12, folic acid, choline, and betaine and mated her to an agouti male. Instead of exclusively bearing the kind of overweight, unhealthy yellow-coat babies she’d previously given birth to, her new litter now also included a few healthy brown mice that developed normally.34 You could interpret this study as follows: the agouti breed has regulatory DNA that’s essentially been brain damaged by some past traumas in the history of the lineage. As a result, agouti chromosomes, unlike those of other mice, are typically incapable of building healthy, normal offspring. In this study, researchers were able to rehabilitate the agouti’s genome by blasting the sleepy genes with enough nutrients to wake them up, reprogramming their genes for better function.
This has enormous implications for us, as researchers are finding abnormal regulatory scars all over our genes. These scars act as records of our ancestors’ experiences—their diets, even what the weather was like during their lives. For example, toward the end of World War II, an unusually harsh winter combined with a German-imposed food embargo led to death by starvation of some 30,000 people. Those who survived suffered from a range of developmental and adult disorders, including low birth weight, diabetes, obesity, coronary heart disease, and breast and other cancers. A group of Dutch researchers has associated this exposure with the birth of smaller-than-normal grandchildren.35
This finding is remarkable, as it suggests the effects of a pregnant woman’s diet can ripple, at the least, into the next two generations. Unlike the agouti mice, which required massive doses of vitamins, these people would possibly respond well to normal or only slightly above normal levels of nutrients as their genes have been affected only for a short while—just a generation or two (unlike the mice)—meaning it might not take quite so much extra nutrition to wake them up.
Some epigenetic reactions are not merely passed on but magnified. In a study of the effects of maternal smoking on a child’s risk of developing asthma, doctors at the Keck School of Medicine in Los Angeles discovered that children whose mothers smoked while pregnant were 1.5 times more likely to develop asthma than those born to non-smoking mothers. If grandma smoked, the child was 1.8 times more likely to develop asthma—even if mom never touched a cigarette! Those children whose mothers and grandmothers both smoked while pregnant had their risk elevated by 2.6 times.36 Why would DNA react this way? If you look for the logic in this decision, you might see it like this: by smoking during pregnancy, you are telling the embryo that the air is full of toxins and that breathing is sometimes dangerous. The developing lungs would do well to be able to react quickly to any inhaled irritants. Asthmatic lungs are over-reactive. They cough and spit at the slightest whiff of foreign aerosols. Still, I believe even a genome as abused as this can be reminded of normal function.
Why do I have so much faith in the restorative power of good epigenetic care? Because contrary to the old ways of thinking, we now know that most diseases are not attributable to permanent mutation but rather to misdirected genetic expression.37 As we’ve seen, environmentally derived chemicals mark the long molecule with tags that change its behavior. Such a system, according to the author of the seminal agouti mouse study, Randy Jirtle, seems to exist to provide a “rapid mechanism by which [an organism] can respond to the environment without having to change its hardware.”38 This way, any physiologic tweak or modification can be recalled based on its apparent success or failure. Call it test marketing for a proposed “mutation.” That may seem a rather sophisticated operation for a molecule to pull off, but remember we’re talking about a molecule that has been in development ever since life on Earth began. With this new understanding of how DNA works, we can now appreciate how easily nutrient deficiencies or exposure to toxins might lead to chronic disease—and how readily these diseases might respond to eliminating toxins and improving nutrition.
At Yale’s Center for Excellence in Genomic Science, Dr. Dov S. Greenbaum shares my faith in the intellect behind the design of our genetic apparatus. In describing how junk DNA functions to guide evolution, he writes, “The movement of transposable junk results in a dynamic system of gene activation, which allows for the organism to adapt to its environment.”39 He describes the function very much like Jirtle, adding that this transposition system “allows for the organism to adapt to its environment without redesigning its hardware.”40 To further the analogy, it’s conceivable that genetic modifications are introduced under a protocol similar to that used by software designers: test for bugs, then run concurrent with other software on a provisional basis (the beta version of the program), then integrate into the operating system, and finally—when proved to be indispensable—build it into the hardware.
This might have been exactly what happened with the human gene for making vitamin C. After generations of nonuse (due to abundance of vitamin C in our food), the gene would have grown very “sleepy.” Eventually, when epigenetic “test marketing” had demonstrated that we could live without being able to make our own vitamin C, a mutation within the gene permanently deactivated it. How, exactly, might this test marketing work? Certain markers increase the error rate during reproduction, and thus a temporary epigenetic change can set up the gene to be permanently altered by a base pair mutation.41 Genes are like tiny protein-producing machines that create different products. If a factory worker (think epigenetic tagging) shuts off one machine and everything in the cell continues to run smoothly over the ensuing generations, then that particular machine (gene) can be refashioned to produce something else, or turned off altogether. The more we learn about epigenetics, the more it seems that genetic change—both the development of disease and even evolution itself—is as tightly controlled and subject to feedback as every other biologic process from cell development to breathing to reproduction, and, therefore, isn’t so random after all.
What helps regulate all these cellular events? Food, mostly. After all, food is the primary way we interact with our environment. But here’s what’s really remarkable: those tags that get placed on the genes to control how they work and help drive the course of evolution are made out of simple nutrients, like minerals, vitamins, and fatty acids, or are influenced by the presence of these nutrients. In other words, there’s essentially no middleman between the food you eat and what your genes are being told to do, enacting changes that can ultimately become permanent and inheritable. If food can alter genetic information in the space of a single generation, then this powerful and immediate relationship between diet and DNA should place nutritional shifts at center stage in the continuing drama of human evolution.
GUIDED EVOLUTION?
In 2007, a consortium of geneticists investigating autism boldly announced that the disease was not genetic in the typical sense of the word, meaning that you inherit a gene for autism from one or both of your parents. New gene sequencing technologies had revealed that many children with autism had new gene mutations, never before expressed in their family line.
An article published in the prestigious journal Proceedings of the National Academy of Sciences states, “The majority of autisms are a result of de novo mutations, occurring first in the parental germ line.”42 The reasons behind this will be discussed in Chapter 9.
In 2012, a group investigating these new, spontaneous mutations discovered evidence that randomness was not the sole driving force behind them. Their study, published in the journal Cell, revealed an unexpected pattern of mutations occurring 100 times more often in specific “hotspots,” regions of the human genome where the DNA strand is tightly coiled around organizing proteins called histones that function much like spools in a sewing kit, which organize different colors and types of threads.43
The consequences of these mutations seem specifically designed to toggle up or down specific character traits. Jonathan Sebat, lead author on the 2012 article, suggests that the hotspots are engineered to “mutate in ways that will influence human traits” by toggling up or down the development of specific behaviors. For example, when a certain gene located at a hotspot on chromosome 7 is duplicated, children develop autism, a developmental delay characterized by near total lack of interest in social interaction. When the same chromosome is deleted, children develop Williams Syndrome, a developmental delay characterized by an exuberant gregariousness, where children talk a lot, and talk with pretty much anyone. The phenomenon wherein specific traits are toggled up and down by variations in gene expression has recently been recognized as a result of the built-in architecture of DNA and dubbed “active adaptive evolution.”44
As further evidence of an underlying logic driving the development of these new autism-related mutations, it appears that epigenetic factors activate the hotspot, particularly a kind of epigenetic tagging called methylation.45 In the absence of adequate B vitamins, specific areas of the gene lose these methylation tags, exposing sections of DNA to the factors that generate new mutations. In other words, factors missing from a parent’s diet trigger the genome to respond in ways that will hopefully enable the offspring to cope with the new nutritional environment. It doesn’t always work out, of course, but that seems to be the intent.
You could almost see it as the attempt to adjust character traits in a way that will engineer different kinds of creative minds, so that hopefully one will give us a new capacity to adapt.
Evidence for Language in DNA
We have no clear idea how nature keeps track of which programming codes work best for what, or how the many environmental inputs—minerals, vitamins, toxins, and so on—might be translated into a new epigenetic strategy, but some intriguing research offers support to the idea that DNA can indeed take notes.
In 1994, mathematicians observed that junk DNA contained patterns reminiscent of natural language, since it follows, among other things, Zipf’s Law (a hierarchical word distribution pattern found in all languages).46, 47, 48, 49 ‘Some geneticists disagree with this assessment, while others think this added layer of complexity might eventually help explain many of DNA’s hidden mysteries. But everyone agrees there’s plenty of space in junk DNA for all kinds of data storage. Junk DNA is a large enough repository of information to function as a kind of chemical software programmed to, for want of a better term, recognize something about the dietary conditions provided it and then include this updated information when it reproduces itself. Some molecular biologists feel that this capability to orchestrate a measured response to environmental change demands that we consider the language encoded in junk DNA as “important for … the evolution process” implying the existence of an “independent mechanism for the gradual regulation of gene expression.” This suggests that evolution involves more than the previously accepted mechanisms of selection and random mutation. The field of evolutionary study that explores how all three of these mechanisms guide evolution is called adaptive evolution.
One example of the logic underlying DNA’s behavior can be found by observing the effects of vitamin A deficiency. In the late 1930s, Professor Fred Hale, of the Texas Agricultural Experiment Station at College Station, was able to deprive pigs of vitamin A before conception in such a way that mothers would reliably produce a litter without any eyeballs.50 When these mothers were fed vitamin A, the next litters developed normal eyeballs, suggesting that eyeball growth was not switched off due to (permanent) mutation, but to a temporary epigenetic modification. Vitamin A is derived from retinoids, which come from plants, which in turn depend on sunlight. So in responding to the absence of vitamin A by turning off the genes to grow eyes, it is as if DNA interpreted the lack of vitamin A as a lack of light, or a lightless environment in which eyes would be of no use. The eyeless pigs had lids, very much like blind cave salamanders. It’s possible that these and other blind cave dwellers have undergone a similar epigenetic modification of the genes controlling eye growth in response to low levels of vitamin A in a lightless, plantless cave environment.
Taken together, all epigenetic evidence paints DNA as a far more dynamic and intelligent mechanism of adaptation than has been generally appreciated. In effect, DNA seems capable of collecting information—through the language of food—about changing conditions in the outside world, enacting alteration based on that information, and documenting both the collected data and its response for the benefit of subsequent generations. Junk DNA is full of genetic treasure. It may function as a kind of ever-expanding library, complete with its own insightful librarian capable of researching previously written volumes of successful and unsuccessful genetic adaptation strategies. It follows that more complex organisms, with larger cells—whose genomes represent a more complex evolutionary history—would carry relatively more substantial libraries filled with more junk DNA. And we do.51
The intelligent librarian stands in direct opposition to the placement of selection and random mutation as the sole mechanisms of genetic change and the development of new species. Given the highly competitive world of survival, it seems obvious that those genetic codes capable of listening to the outside world and using that information to guide decisions would enjoy a marked advantage compared to those stumbling in the dark, completely dependent on luck. This understanding may give rise to an entirely new perspective on how we came to be, placing a new spin on “intelligent design.” DNA’s ability to respond intelligently to changes in its nutritional environment enables it to take advantage of the shifting cornucopia, exploiting rich nutritional contexts, much the way an interior decorator would make use of a surprise shipment of high-quality silk upholstery fabric. Our genes may help us survive periods of famine and stress by way of experiment, and take advantage of any nutritional glut to experiment further—not blindly, not with random mutations, but with memory and purpose, guided by past experiences encoded within its own structure.
Why does this matter to you?
The chemical intelligence encoded in your DNA and the intelligence of our distant ancestors shared the same ultimate goal: survive. Inside your ancestors’ bodies, their genomes shuffled themselves to match nutrient supply with physiologic demands while the people who carried them shared tool-making tips and rumors of food sources which—propelled by this synergy of purpose—would catapult a small group of primates from a nook of the African continent to a state of world domination.
Under the watchful eye of grandmothers and midwives, special foods and preparations proved themselves effective at creating children who could learn faster and grow stronger than the generation before. Children who, naturally, would grow to become parents themselves, able to form their own sets of observations and conclusions about the way the world works and how best to guarantee survival. One of the things that makes human beings (and their ancestors) unique is the sophistication of tool use that enabled consumption of a greater proportion of the edible world than the competition, furthering the agenda of our perpetually reincarnating, self-revising, constantly upgrading, ruthlessly selfish genes. We have managed to shepherd our own genomes through millennia, roaming from one ocean to another, over mountains and across whole continents, and into the modern age.
Those hoping to maintain the product of that achievement—beautiful, healthy human bodies—will want to acquaint themselves with the foods and preparation techniques that allowed us to get this far in the first place. By eating the foods described later in this book, you will be talking directly to your genes. Your foods will tell your epigenome to make your body stronger, more energized, healthier, and more beautiful. And your epigenome will listen.
How smart and responsive is DNA? You could think of it this way. Imagine that when studying a subject for a class, your head never got “too full,” and that you could simply add new space for more memories and more knowledge on demand. So that over your lifespan, as you learned more subjects, more languages, read more books, your mind could adapt to accommodate it all. How much stuff would you know? How many problems would you be able to solve better than you can now? Now imagine that you could pass all that learning on to your offspring, so that they started life with all your accumulated wisdom. Maybe not every last detail, but at least the pertinent parts, the details of that multigenerational story that promise to aid in survival and reproduction. And imagine that you, in turn, had inherited your parents’ knowledge, and that of their parents, and so on. For thousands of generations since the beginning of your line. Well, that’s what DNA is like.
The incredible molecules orchestrating the amazing microcosm of operations inside each and every one of your living cells right now are doing exactly that. Each cell of your body is a vessel carrying a code that has been under constant development since the moment a rudimentary cluster of genetic material ensconced itself within the protection of a lipid coat, defining itself as something different than the primordial sea-world that surrounded it.
Unblocking Your Genetic Potential
Whether you believe in the idea of genetic intelligence or not, the one thing I hope I’ve made clear in this chapter is that our genes are not written in stone. They are exquisitely sensitive to how we treat them. Like a fine painting passed down through generations, conditions that either harm or preserve are permanently recorded in the provenance of a family’s DNA. When the DNA is mistreated, like a Monet painting thrown into the corner of a damp, musty basement, the inheritance loses its value. And the losses may be devastating. Between Halle Berry and the person who carries her luggage, and between all the tall, trim, and beautiful people strutting the red carpets in Hollywood or the tennis courts in the Hamptons and the rest of us who can only watch are untold stories of nutritional starvation, of lost or distorted genetic information. This variability in our ancestors’ ability to safeguard their genetic wealth is the reason why today we have so many people wishing for better health, better looks, greater athleticism, and all the manifold benefits of healthy genes.
In Chapter 1, I introduced the idea that the genetic lottery is not random, and in this chapter we saw how genes make what seem to be intelligent decisions guided in part by chemical information in the food we eat. In the coming chapters, we’ll see that when we’ve eaten right—when we’ve consistently marinated our chromosomes in the chemical soup that enables them to do their utmost best—Homo sapiens genes can produce moving sculptures of flesh and blood. This is why beautiful people of every race share the same basic skeletal geometry, and why for the bulk of human history, Hollywood beauties were as plentiful as the stars.