Deep Nutrition: Why Your Genes Need Traditional Food by Catherine Shanahan M.D.
The concept of gene health is simple: genes work fine until disturbed. External forces that disturb the normal ebb and flow of genetic function can be broken into two broad categories: toxins and nutrient imbalances.
But you do have control over what may be the most powerful class of gene-regulating factors: food.
But medicine is different from other sciences because, more than being a science, it is first and foremost a business.
Thanks to the plasticity of genetic response we can all improve the health of our genes and rebuild our genetic wealth.
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.
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.
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.”
epigenetic tagging occurs in response to chemicals that form as a result of nearly everything we eat, drink, breathe, think, and do.25
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.
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.
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.
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.
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
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.
good nutrition can compel the epigenetic adaptation system to reprise an earlier strategy appropriate for a more optimal nutrition environment.
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.
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.
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 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.”
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
There was a clear pattern: the native diets had ten or more times the fat-soluble vitamins and one-and-a-half to fifty times more minerals than the diets of people in the United States.63
Percentage of Americans aged 100 in 1830: 0.020 Percentage of Americans aged 100 in 1990: 0.015 Percentage of people living today expected to live to 100: 0.001
And we continue to neglect the nutrition-development equation when our patients develop scoliosis, joint malformations, aneurysms, autism, schizophrenia, and so on later in life. If doctors and nutritionists were as willing as other professionals to use their basic senses, every child would have a better chance to grow up healthy.
suboptimal architecture impairs development of normal geometry, leading to imperfectly formed facial features, be it the eyes or ears or nose or jaw and throat. For example, narrow nasal passages irritate the mucosa, increasing the chances of rhinitis and allergies.88, 89 When the airway in the back of the throat is improperly formed, a child may suffer from sleep apnea, which starves the brain of the oxygen needed to develop normal intelligence.90
1.618033988. This is the golden ratio, used by the Greeks and Egyptians to design perfectly balanced works of structural art that mystify architects even today. The golden ratio is symbolized by the Greek letter phi: Ö (pronounced fie, rhymes with pie). The Egyptians and Greeks worshipped phi
In his pursuit of the perfect face, Dr. Marquardt discovered that the golden ratio is uniquely capable of generating a special kind of symmetry called dynamic symmetry. According to the theory of perception, there are two ways to create harmonic balance within an object or space. One is to divide it into equal parts, creating the symmetry of balance. Biradial symmetry is an example of this kind of symmetry. (See illustrations on pages 61 and 62). The other is a division based on the golden section, creating the perfect form of asymmetry—perfect because the ratio of the lesser part to the greater part is the same as the ratio of the greater part to the whole. (See illustration below.) This is dynamic symmetry. Interestingly, dynamic symmetry characterizes the growth of living matter, while the symmetry of balance characterizes the growth of crystals.
Beautiful people exist not because of luck, but because all DNA is naturally driven to create dynamically symmetric geometry as it’s generating tissue growth.
This is a benefit of a phenomenon called phyllotaxis, which describes the spiraling growth of stems, petals, roots, and other plant organs in 90 percent of plants throughout the world.102 The angle of phyllotaxis is 137.5 degrees, or 1/phi2 x 360 degrees. We can see the same pattern of branching, twisting—so-called dendritic growth—when we look at nerve cells in the brain. All these instances of patterned growth are directed not by DNA but by the rules of math and physics which act on living tissue automatically to create pattern.
WHY ATTRACTIVE PEOPLE ENTRANCE US We presume we are entranced by beautiful faces because we are sexually attracted, but it may be that we are attracted to their patterns. When animal researchers show rats checkerboard patterns, the resulting brain waves demonstrate rhythmic spikes (upper right panel), which are said to reflect a state of “attentive immobility.” While staring at the checkered image, blood flow to the pleasure center of the brain is increased, suggesting the rat enjoys looking at the pattern. Researchers believe this kind of brain activity allows for the “optimization of sensory integration within the corticothalmic neural pathways,” which helps the rat “learn” the pattern.
When looking for that perfect man or woman, research shows that facial features deviating from Marquardt’s geometric blueprint even slightly make a surprisingly large impression—or lack of impression.110
“If you put the mask over the population, you’ll see that many people are not that far off from a perfect fit, though we wouldn’t regard them as highly attractive.” The variability we do have, he believes, stems from the fact that “we’ve evolved past the point of efficiency.” In other words, societal safety nets allow people who aren’t perfectly healthy or functional to reproduce, whereas, in the past, they would simply have died off. Marquardt’s pragmatic
Letting Your Body Create a Perfect Baby Mom’s nutritional status before and during pregnancy influences how much facial and body symmetry her child develops. In the context of modern diet, birth order correlates with two distinct symmetry shifts away from ideal. Studies show that most women are nutritionally deficient during childbearing years. Eating sweets and fried foods during pregnancy is likely to be as detrimental as smoking and drinking, if not moreso. All evidence suggests that optimizing nutrition represents a powerful strategy for creating healthy, beautiful babies.
But unless the mother gives herself ample time (generally at least three years) and nutrients for her body to fully replenish itself, child number two may not be as healthy as his older sibling.
One study shows that overall, 74 percent of women “are falling short on nutrients from their diet.”
So to better protect baby, nature has provided a built-in safety mechanism, allocating as many resources to the placenta as it can get away with, even if it means putting mom’s health at some risk.
“The fetus is well protected against maternal malnutrition—that indeed it behaves like a parasite oblivious to the health of its host.”124
deficient in brain-building fats—as horrible as this sounds—the fats that make up the mother’s own brain will be sought out and extracted.125 Pregnancy
Studies show that maternal brains can actually shrink, primarily in the hippocampal and temporal lobe areas, which control short-term memory and emotion.
Sugar and vegetable oils act like chemical static that blocks the signals our bodies need to run our metabolisms smoothly.128
Researchers are recognizing the role of chemical interference from oxidation in disrupting the normal responsiveness of the uterus to hormones like estrogen, progesterone, and more.150, 151 As we’ll see in later chapters, two foods that most powerfully promote oxidative stress are vegetable oils and sugar.
“Performance specialists in the NBA and elsewhere are always looking for the most valid and reliable ways to assess musculoskeletal asymmetry levels. This helps give critical insight into injury susceptibility and an athlete’s ability to withstand the rigors of the sport.”
no child, not even an only child, is immune from symmetry shifts because the underlying problem is not birth order; it’s malnutrition. While a first baby grows in mother’s womb, static interference from dietary sugar and vegetable oils too often disrupts hormonal communication between placenta, uterus, and ovaries, delaying uterine development and reducing physical space for the baby while tending to blunt the child’s potential for sexual dimorphism. In a woman’s subsequent children, the cellular circuits necessary to coordinate the various baby-making stations (uterus, placenta, etc.) have already been optimized, enabling faster uterine responses (such as quicker growth and speedier deliveries), which permits greater biradial symmetry, and primes the baby’s potential for sexual differentiation. But in the context of a modern diet, the cost of going second (particularly with close birth intervals) is often relative maternal nutrient deficiencies that result in relatively less material to build bone, nerve, and so on, thinning and flattening facial features to create a worn-down look.
Other studies show that prenatal vitamin pills don’t solve many nutritional problems. The following are just a few examples: Vitamin D Deficiency: In studies in which over 90 percent of participants took prenatal vitamins, 56 percent of white babies and 46 percent of black babies were vitamin D insufficient. Insufficiency in early life increases the risk of schizophrenia, diabetes, and skeletal disease.156 Long Chain Essential Fatty Acids: As of the date of this writing, there is no recommendation about how much of these to consume, and most people who don’t supplement get almost none. But supplementing with cod liver oil during pregnancy has protective and lasting effects on the baby’s intelligence.157 Choline: Gestational deficiency of choline is associated with lifelong learning deficits.158 One survey showed 86 percent of college-age women were lacking adequate dietary choline.159 Choline is not part of any prenatal vitamin supplement commonly marketed in the United States.
Another report comparing mineral levels of twenty-seven fruits and vegetables from 1930 and 1980 found modern produce to be depleted by an average of 20 percent, with calcium dropping 46 percent, magnesium 23 percent, iron 27 percent, and zinc 59 percent.176 Meat and dairy, which ultimately depend on healthy soil, have declined commensurately in quality between 1930 and 2002, with iron content in meat falling an average of 47 percent, 60 percent in milk, and lesser declines in calcium, copper, and magnesium.177, 178 When plants and animals are reared on mineral-deficient soil, not only are they missing nutrients, they’re not as healthy. And their cells are, in turn, less able to manufacture the
SIX WAYS NUTRITION CAN OPTIMIZE YOUR CHILD’S GROWTH 1. Height. Pour more milk. A meta analysis concluded that for each additional 100 milliliters of milk (roughly 3.3 ounces) consumed daily, children grew an extra 0.2 centimeters (roughly 1/8 inch) per year.181 Children in the study were aged two to twenty and the study duration ranged from a few months to two years. The study’s authors noted that the growth effect was especially powerful in teens. It is not known if higher and sustained milk supplementation would have additive effects. But if avid milk drinker and NBA player Jeremy Lin is any example, at six-foot-three with five-foot-six parents, then perhaps it may. 2. Vision. Look for lots of variety. In a study of children between ages seven and ten, children who developed nearsightedness compared to children who did not consumed significantly less of a wide variety of nutrients: protein, fat, cholesterol, vitamin B1, vitamin B2, vitamin C, phosphorus, and iron.182 Of note, although the myopic children ate roughly 300 fewer calories, there was no difference between the two groups in several anatomic metrics: height, weight, or head circumference. This suggests that while normal height, weight, and head circumference are indications of sufficient nutritional intake they are not definitive indicators of optimal nutrition. It also suggests that the children with normal vision may have been more physically active. 3. Cognitive development. Skip starchy snacks. Nutrients shown to correlate most strongly with high IQ include vitamin E, omega-3, and iodine. Studies have shown that the higher a child’s vitamin E, the better their language and social skills.183 Similarly, the higher a newborn’s omega-3 (as measured in maternal umbilical cord blood) the higher that child’s IQ later in childhood.184 Additionally, cognition has been shown to be impaired by a “snacky pattern” of eating high-carb foods “characterized by foods that require minimum preparation such as potatoes and other starchy roots, salty snacks, sugar, preserves, and confectionery.”185 Presumably this effect is mediated through reduced nutrition-to-calorie ratio. 4. Life span. Beget big babies. Larger children, born to non-diabetic moms, have greater muscle mass, a higher resistance to diabetes and obesity, and longer telomeres (the part of the DNA that determines how many more divisions a cell can undergo, thus influencing cellular lifespan)—all known to be associated with longer life expectancy.186, 187 How to grow a big baby without developing gestational diabetes? Aside from being tall and well fed during your own childhood, we don’t know much about specific interventions to produce bigger babies. But we do know something about how to avoid having a too-small baby: don’t smoke, don’t conceive while you’re undernourished or underweight, and don’t restrict protein (i.e. if you’re vegan, you may need to supplement). 5. Immune system. Maximize microbes and micronutrients. Researchers at…
You can get off the sugar and vegetable oils that would block your child’s genetic potential. That means cutting out processed food, fast food, junk food, and soda. And you should give yourself at least three, preferably four, years between pregnancies and make every effort to fortify your body with vitamin-rich foods (or if you can’t, at least use prenatal vitamins) before conception. Those who want to do everything possible to have a healthy baby will find additional instruction throughout this book. But this discussion opens up a new question: If I do everything right, how beautiful and healthy can I expect my child to be?
What’s most striking about Price’s visit to Peru is that when he left the desert mummies to study modern city dwellers, he found the people’s structural symmetry and balanced growth patterns had melted away, replaced by what he described as “a sad wreckage in physique and often character.”
This ability to adjust stature to better match a given nutritional context lends more support to the idea of an intelligent, responsive genome (as the operating mechanism) than to the suggestion that physiologic change depends solely on random mutation. If evolutionary change were dependent on random mutation, then it would be exceedingly unlikely that responses to nutritional change would be so consistent and quick to appear. If, however, an intelligent genome had recorded in its epigenomic library which physiologic adjustments were most appropriate in any given nutritional context, then the epigenomic librarian (see Chapter 2) could simply read the instructions on what to do next. And this is why we see that “throughout the course of human evolution, features of robusticity like supraorbital and occipital tori [boney ridges] have been acquired, lost, or changed in different groups.”212
Disproportionality impairs the body’s ability to function.
Dr. Marquardt, the plastic surgeon who discovered how phi-based growth occurs in the human species and created a mask to illustrate it, has shown us that balanced growth occurs in three dimensions, the X, Y, and Z facial planes. When that balanced phi-proportionality is lost, the resulting growth distortions lead to problems. In my own face, the loss of phi-proportionality in the horizontal (or X) dimension narrowed my skull so that my wisdom teeth didn’t fit into my head and had to be pulled, and my disproportionately sized eye sockets distorted the shape of my eyeball, forcing my lens to focus light to a point in front of (rather than on) my retinas, blurring my vision. A face that is more severely narrowed than mine may pinch the airway, causing sinus problems. When skull narrowing affects the Z-plane (visible in profile), it may foreshorten the palate, increasing the likelihood of sleep apnea, a condition in which a person’s own soft tissues collapse inward and periodically suffocate them, causing fatigue, memory problems, and heart disease. Phi seems to be the universal
Over the past 100 years, we have completed the single most comprehensive dietary shift in the history of our race. This shift, a major dietary migration over vast nutritional territory, has gone on largely unnoticed—even by the medical community—for the following reasons: The shift didn’t involve moving from one geographic point to another; only our food has changed. Except for the very well-off and the recently urbanized, few of us in America have been exposed to the products of culinary tradition and therefore don’t know what we’re missing. Since the migration from real to fake food has occurred over five generations, even our parents were likely born into an environment bereft of culinary tradition. Cheap and convenient products catch on quick, and we tend not to ask where they were made or what they were made of, so the easier and cheaper our food gets, the less we think about it. The merging of business and science into one corporate body means that medical science can no longer countenance advice incompatible with the interests of commerce. A constant stream of new technologic fixes continues to buttress our collapsing physiologic infrastructure, which has so far masked what would otherwise be obvious maladaptive consequences of that collapse.
Lies, damn lies, and statistics. Keys blamed natural fat consumption for heart attacks. But the United States, England, Canada, and Australia had the highest levels of margarine consumption. Keys never mentions margarine in his famous “Six-Countries Study” and the deception was never exposed. Keys is still considered to be a hero of modern medicine.
Scientists had pointed out Dr. Keys’s misleading use of scientific terms. In public, he fingered animal fat as the culprit behind the rising rates of heart attacks. But in his laboratory and human experiments, he didn’t use animal fat.234 His subjects were fed margarine made from partially hydrogenated vegetable oil. And what was in the margarine? Trans fat—a full 48 percent!
Dr. Spiteller, who, in his 2000 article, “Oxidation of Linoleic Acid in Low-Density Lipoprotein: An Important Event in Atherogenesis,” definitively points us in the right direction.239 In this meticulously researched article, Dr. Spiteller makes the case that it is processed polyunsaturated fats, not saturated fat or cholesterol, that deserve the blame for the stiffening of arteries throughout the body.
Over the past century, as butter consumption dropped to less than one quarter of what it was (from eighteen pounds per person per year to four), vegetable oil consumption went up five-fold (from eleven pounds per person per year to fifty-nine).242, 243 In 1900, heart disease was rare.244 By 1950, heart problems were killing more men than any other disease.245 Now, at the dawn of the second millennium, heart disease is the number-one cause of death in both men and women.246
In the late 1800s, Emperor Napoleon III offered a prize for a butter substitute to feed his army and “the lower classes.”247 The goal was a product that cost very little and wouldn’t rot on extended sea voyages. After some experimentation, a chemist named Hippolyte Mege-Mourie found that squeezing slabs of tallow under pressure extracted oily elements that fused into a solid when churned together with skim milk. The dull gray material had a pearly sheen and so Mege-Mourie called it margarine, after the Greek margarites, meaning “pearl.” It didn’t taste good, but it was cheap.
By the turn of the century, chemists had found a way to reinvent the reinvented butter by starting with material nearer the bottom of the food chain: cottonseeds. There were sacks and sacks of them lying around without much use. In fact, the tiny black seeds were hard to store because, if left alone, they would ferment and make a terrible stink. Chemists recognized that odoriferous volatiles meant the oil was reacting with oxygen, and they smelled opportunity. The reactive nature of the oil meant that it had the potential to be chemically modified for a variety of purposes and, soon enough, they found a way to spin this worthless byproduct of the textile industry into solid gold.
They engineered a transformation of the fatty acids in the oil, ironing them almost flat with heat, pressure, hydrogen gas, and a nickel catalyst. The key to making the product appear edible was the catalyst, which prevented the molecules from tangling up into plastic. When the oils get squashed flat in this process, their double bonds change from the natural bent and flexible configuration to something stiffer. And thus, trans fat was born.
PARTIAL HYDROGENATION SQUASHES FATS FLAT The chemical process of partially hydrogenating an unsaturated fatty acid may turn cis-shaped fatty acids into trans or convert the unsaturated bond into a saturated bond. Either outcome leads to a flatter shaped molecule with less fluid characteristics than the original cis-configuration, unsaturated fatty acid. Food manufacturers exploit this to make butter substitutes.
Naturally occurring fatty acids contain bonds in a cis configuration. In this configuration, fatty acids are highly flexible, which prevents crystallization (solidification), and so the molecules behave as liquids. Partial hydrogenation does two things: it irons some cis-configuration bonds completely flat (by saturating the bond with hydrogen) and switches others around to trans. Converting a cis fatty acid to saturated or trans makes it a stiffer and more stackable molecule. This is why partially hydrogenated vegetable oils solidify like butter (which contains naturally stiff and stackable saturated fats).
Processing distorts the fatty acids in vegetable oil so they can no longer assume the typical five- or six-sided geometry. Like Chinese finger traps, our enzymes pick up these distorted fatty acids and then can’t let them go, which hampers cellular function so profoundly it can kill your cells. And if you eat enough trans fats, cellular dysfunction will impair so many cells in so many tissues that the cumulative effects will disrupt basic functions (like blood circulation or your body’s ability to fight infection) and eventually kill you. Vegetable oils rarely kill children, but they can disrupt normal metabolism so profoundly that a child’s dynamic symmetry is lost, and their skeletal proportions become imbalanced.
Vegetable oils contain mostly heat-sensitive polyunsaturated fats. When heated, these fragile fats turn into toxic compounds including trans fat.258 The heat sensitivity issue means that all processed vegetable oils, and all products that contain vegetable oil, necessarily contain trans fat. Canola oil degrades so rapidly that a testing company, needing to find the purest canola oil to use as a standard against which other oils could be compared, couldn’t locate any canola oil even from pharmaceutical-grade manufacturers with a trans fat content lower than 1.2 percent.259 This means that vegetable oil, and products made from vegetable oil, contain trans fat—even when the label seems to guarantee them trans free.
Biology makes use of this reactivity. Enzymes in plants and animals fuse oxygen to polyunsaturated fats on purpose to change them from one shape to another. For example, fish oil isn’t anti-inflammatory per se. Enzymes in the human body oxidize the PUFAs in fish oil to convert them into specific compounds that turn off pro-inflammatory enzymes. But this mutability also means polyunsaturated fats are more capable of being accidentally altered, and thus heat is a threat to their utility.
There’s a reason these oils are particularly temperature sensitive. Seeds stay dormant over the cold winter. But come spring thaw, the heat-sensitive PUFAs wake up in response to warming, facilitating germination.260 To protect the PUFAs from damage as the ground warms and the sun’s rays beat down on them, the plant has loaded its seeds with antioxidants. Unfortunately, refining these oils ultimately destroys both healthy PUFAs and their complementary antioxidants, converting them into distorted, unhealthy molecules. So what was once healthy in the seed isn’t healthy in the bottle.
American Heart Association plays right along. They claim that canola oil is rich in anti-inflammatory omega-3 essential fats. And there’s a grain—I should say seed—of truth to that claim. There’s just one problem: omega-3 is a PUFA, which means it is easily distorted when exposed to heat. And since the omega-3 in canola seeds has three places for oxygen to react, it’s really, really reactive. Canola oil still in the seed may indeed be full of omega-3, but factory-processed canola oil, even organic-expeller-pressed, contains mutated, oxidized, heat-damaged versions of once-healthy fats.
In fact, one of the initial steps in making vegetable oil involves the use of hexane, a component of gasoline.
Using free radicals (defined in the next section), mutated PUFAs convert normal fatty acids into fellow ghouls at the rate of billions per second.265
HOW FREE RADICALS DAMAGE MEMBRANES This is a closeup view of a cell membrane under attack. This particular section of membrane is composed of PUFAs. (The insert in the upper right is a cross-section of the same membrane.) Once the radical strips an electron from one of the PUFAs, it initiates a cascade reaction across the membrane, releasing more damaging unpaired electrons. In addition to mangling and distortion membrane PUFAs, the cascade reaction can damage hormone receptors, nutrient channels, and other proteins in the membrane, disrupting membrane function and putting the entire cell at risk.
WHY MEN GET HEART ATTACKS BEFORE WOMEN Men get heart attacks ten to fifteen years on average before women. Why would that be? The only explanation cardiologists offer is that “women are just more perfect organisms.”266 While I tend to agree, I also believe there’s more to the story. The real reason is that men have more testosterone, which makes them produce more red blood cells, so that men also have more iron in their blood.267 Iron acts as an accelerant, activating oxygen in ways that make it more likely to damage the linoleic acid and other fragile PUFAs traveling in lipoproteins right alongside iron-rich red blood cells.268 Does this mean men are doomed to get heart attacks? Of course not! Aside from cutting vegetable oil, eating plenty of antioxidant-rich fresh vegetables will slow the reaction between iron and PUFA fats, rendering them less explosive and preventing the process of lipid deposition inside a person’s arteries.269, 270
Free radicals can fry your cell membranes, damaging your arteries and, as I suggested earlier, eating foods fried in vegetable oil may very well precipitate a heart attack. But something happens before you have a full-blown heart attack: your arteries stop responding to normal body stresses. It’s called abnormal endothelial function. And there’s a test for it.
They planned to feed subjects french fries and then test them to see if their blood vessels were still able to regulate blood flow normally (this ability is called endothelial function). The test is performed by slipping the patient’s arm into a blood pressure cuff, then squeezing it to cut off the blood flow for a few minutes. Normally, on releasing the cuff again, the oxygen-starved arteries open wider so blood can come rushing back in, just like you would suck in more air after holding your breath for a while. This dilation response depends on the endothelial cells lining the blood vessels which have to be healthy enough to generate the nitric oxide that makes arteries dilate. If endothelial cells can’t make nitric oxide, or if the nitric oxide they make gets destroyed too soon, a person’s circulatory system can’t work correctly. Male sexual function depends on healthy endothelial function, for reasons that pertain to arterial dilation and the obvious tissue expansion facilitated by such dilation. What may be less obvious is, if a person has erectile dysfunction (ED), they (most likely) have endothelial dysfunction, meaning their health problems extend beyond the bedroom. Specialized centers can perform an endothelial function test on anyone. This easy test tells your doctor how healthy your arteries are and how readily they can deliver blood in response to exercise or other activities.
The scientists in New Zealand acquired week-old frying oil (rich in MegaTrans) from a typical restaurant and made a batch of fries. Four hours after study subjects ate the fries, they slipped their arms into blood pressure cuffs to test their endothelial function. The effect of the oil was unmistakable. Before the fries, the subjects’ arteries had dilated normally, opening 7 percent wider. Afterward, there was almost no dilation—barely one percent.272
What this test tells us is that after eating food fried in vegetable oil, your blood vessels won’t work right. You may feel lethargic. Men may suffer from temporary ED. As the authors point out, exercising after a fast food meal will also stress your heart.274 Why? MegaTrans free radicals attack the nitric oxide signal that arteries send when they sense oxygen levels are low. Without that signal, your muscles don’t get the oxygen they need. The most active muscles will be the most affected—and your heart is always active. Men with ED have sick endothelial cells that can’t generate normal amounts of nitric oxide. Viagra works by helping sick endothelial cells in the penile arteries generate nitric oxide as if they were healthy. Nasty frying oil temporarily inhibits that ability. You could call it anti-Viagra. But listen up, boys: if you keep eating foods made with vegetable oil (especially if you also eat too much sugar), you’ll damage those endothelial cells so much that even Viagra won’t work anymore.
After reading the study, I started asking patients admitted to the hospital for heart attacks what they’d eaten last. So far, everyone has told me they ate something fried in vegetable oil. One
One is to have your doctor check your fasting blood sugar level. If it’s 89 or higher, you may have prediabetes, a condition in which your cell membranes have become too rigid to take in glucose as fast as they normally could. (This often leads to insulin resistance and full-blown diabetes.) And what makes cell membranes stiff? MegaTrans-instigated free radical damage, nutrient deficiency, and sugar. It’s also not a bad idea to check your blood pressure. Normal levels range from 80 to 120 over 50 to 75. Higher than 130/80 (while relaxed) can indicate abnormal endothelial function. You can also get a test of your liver enzymes. Elevated liver enzymes occur when MegaTrans explosions damage liver cells. Finally, you can get a cholesterol test. But ordering the right test and then interpreting the test correctly requires some knowledge of the way fats circulate through your body, a physiologic function I call the lipid cycle.
Lipoproteins made in the intestine are called chylomicrons. They contain some cholesterol, but mostly they contain triglycerides, other fatty nutrients (like lecithin, choline, omega-3 and omega-6, and phospholipids), varying amounts of fat-soluble vitamins, and antioxidants.
After the packaged lipoprotein leaves an intestinal cell, it travels through the bloodstream for several hours, completing many circuits. As it floats along, it deposits its fatty nutrients into the tissues that need them most. Hungry tissues get fed by signaling endothelial cells lining their smallest blood vessels to place special proteins on their surface, which act like tiny fishing rods set to snag lipoproteins as they float by. Once snagged, the particle may unload some of its payload into the endothelial cell or, alternatively, the endothelial cell may open up a tunnel-like structure right through its center to allow the lipoprotein to pass from the bloodstream, through the endothelial cell, and directly into the hungry tissues.
Hours after a meal, the amount of fat in circulation drops as lipoproteins either exit circulation or give up their fat and shrink (gradually decreasing in size and increasing in density as they travel). Eventually, the liver picks up the shrunken, high-density remnants and sorts through the contents to recycle anything useful while discarding any waste. Unwanted or damaged fats exit by way of the liver’s bile system back into the intestinal tract for disposal.
One loop of the lipid cycle starts in the intestine and distributes lipids you just ate. Another starts in the liver and distributes lipoproteins your liver made. And a third loop starts in the periphery—that is, the rest of the body—and distributes lipoproteins made by the skin, brain, and other organs. Each of the three sources (intestine, liver, and periphery) manufactures its own brand of lipoproteins complete with its own proprietary labels.
As efficient as this system is, it has one important vulnerability. The APO E lacks the ability to distinguish good fats from bad. So if a person’s diet is loaded with MegaTrans fat, their lipoproteins will be too—and that’s what Fred will get delivered to him, whether he likes it or not.
What are those cycle-disrupting foods? You guessed it: foods rich in vegetable oils (and sugary foods as well). These foods disrupt the lipid cycle by damaging the very fragile proteins on their surfaces, the apolipoproteins, which serve to help direct the particles during their journey through the lipid cycle.
HOW DYSFUNCTIONAL LIPOPROTEINS CAUSE ATHEROSCLEROSIS The endothelial cell on the right is worried because naked oxidized fats from degraded lipoproteins are landing on him and oxidizing his membrane PUFAs. PUFA oxidation can disrupt cell metabolism or even kill the cell (see “How Free Radicals Damage Cell Membranes”). When this kind of damage affects many endothelial cells, it can lead to the first state of atherosclerosis, called “The Fatty Streak.”
What damages lipoprotein labels? One of the most important factors appears to be vegetable oil. Since 1977, lipid scientists have been writing about linoleic acid oxidation in lipoproteins. Citing articles published that year and in the 1980s by himself and by others, Dr. Spiteller, the Austrian lipid scientist, writes, “Oxidatively modified LDL is no longer recognized by the LDL receptor.”277 And how does LDL get oxidatively modified? MegaTrans fat generates free radicals that char the lipoprotein’s surface, rendering it unrecognizable by the LDL receptor. The more MegaTrans-rich vegetable oil you eat, and the worse your diet in general—low in antioxidants and particularly low in naturally occurring vitamin E—the faster the LDL label (the apoprotein coat by which each LDL particle is identified) gets oxidized.278, 279
problem. In 1988, researchers working in Lyon, France, discovered that when the labels on HDL particles got jammed up with sugar, they simply fell off.
1990, another experiment investigated just that. This time, the labels didn’t fall off, but rather became so deranged as to be illegible and unrecognizable to hungry cells.281 As a result, these sugar-encrusted (glycated) LDL particles stayed in circulation too long, which would explain why some diabetics have high LDL levels: with so many undeliverable LDL packages floating around, they just start adding up.282, 283 (When LDL levels are high because of glycation, then high LDL is a problem, as we’ll see.)
Triglycerides are carried in both LDL and HDL particles. But the vast majority of triglyceride is carried by chylomicrons (the lipoprotein particles your gut makes right after a meal) and very low-density lipoproteins (VLDL), which your liver makes from recycled fats. These plump nutrient carriers want to deliver their cargo into your hungry cells. But, like all lipoproteins, they can’t do the job all alone. They need a special enzyme—think of it as a dock worker—to pick the fatty acids up and carry them into the cell. A study done in 1990 showed that sugar interferes with the function of this enzyme.284 So if you have high blood sugar, that sugar may shred the lipoprotein coats beyond recognition, or simply rip them off the particles’ backs. If the particles ever do make it to a cellular dock, sugar keeps them from completing the delivery. With so many barriers to getting nutrition into hungry cells, it’s no wonder people with diabetes feel hungry all the time.
Dr. Spiteller focused his investigation on the most prevalent PUFA in all vegetable oils—linoleic acid, a kind of omega-6.294 His interest in linoleic acid was piqued because, as a lipid scientist, he understood how easily linoleic acid oxidizes and how damaging it can be. His research suggests that the total amount of LDL in a person’s bloodstream is practically irrelevant. What matters to our health, and particularly to our risk of heart attack, is how much oxidized linoleic acid is present in LDL.
I’ve also learned that the best indicator of oxidized linoleic acid is low HDL and high particle counts. (For more on particle counts see “The Best Cholesterol Test”.)
But what happens when the liver can’t recognize the smaller, partially empty lipoprotein (what lipidologists call a “remnant” particle) because the particle’s protein coat (which displays vital information identifying the particle and it’s cargo) has been damaged by oxidation? These smaller, orphan particles are now forced to wander through the bloodstream looking for a home until the same oxidative process that damaged their coats forces them to precipitate out of circulation and onto the delicate surfaces of your arterial walls. A regular cholesterol test can’t tell you how many of these little, wayward particles are floating around destined to cause damage, but a particle-size test can! (See Chapter 14 to learn how to talk to your doctor about ordering one of these tests.)
Large swaths of the cell membrane are scorched as “zombie” fats spawn and free radicals propagate across the surface, incinerating everything they touch—ion channels, sugar transporters, hormone receptors (see illustration). This disables, and ultimately destroys, functional cells. This is how free radicals fry arteries. Over the years, the damage can become so advanced that during open heart surgery it is visible to the naked eye. It looks a lot like fried chicken skin. And it’s about as crispy and weak as fried chicken skin, too, and tears more easily than the unfried version. Free radical chain reactions weaken the underlying collagen scaffolding and fuse molecules together, polymerizing the arterial walls into a kind of crunchy protein plastic. Now the artery can easily rupture and bleed.296 If blood ever contacts collagen directly it will clot, plugging up the artery. And that’s how you get a heart attack or a stroke. So it’s a blood clot, not fat, that shuts off the flow of blood. That’s why ER doctors treat heart attacks and strokes with clot busters, not fat busters.
Your body tries to patch these badly damaged sections with matrices of protein, calcium, and cholesterol. Most of these patches do just fine, holding the arterial section together for the rest of your life. These sturdy, calcium-reinforced plaques are called stable plaques.
In reality, however, that’s almost never what causes a heart attack or stroke. In fact, if the arterial plaques that the body has built to repair damaged arterial surfaces were perfect—permanent fixes that would remain forever stable—they would pose little threat at all.
Stable plaques only cause problems when continued inflammation weakens the plaque material so that, within the stable plaque, small patches develop that are more prone to spontaneous rupture. These weakened areas are called unstable plaque. Unstable plaques can also form over broad areas of an artery but are not as thick or as hard; cardiologists call them buttery plaque. Whether the unstable areas are large or small, they are dangerous because they can burst open, bleed, and clot. Plaque can
In 2006, when researchers tested the blood of mothers whose babies were born with congenital spinal and heart defects, they found evidence of oxidative stress,299, 300 exactly what you would expect to find in someone eating lots of vegetable oil.
So if you are pregnant or plan on getting pregnant, banish vegetable oil and foods containing vegetable oil from your kitchen, and get the stuff out of your life.
A PLAY-BY-PLAY PICTORIAL OF A HEART ATTACK (OR STROKE) The story of a heart attack, illustrated here, begins with degraded lipoproteins dropping out of circulation, landing on the lining of your blood vessels, where they attract a cleanup crew of white blood cells. But sometimes, during the cleanup procedure, oxygen ignites a free radical reaction so large that the underlying collagen is exposed to flowing blood. Whenever collagen contacts blood, clots form. If the clot is large enough to disrupt arterial flow, it may cause a heart attack, stroke, or venous thrombosis (a blood clot in your leg).
I’ve said, I like to see LDL less than three times the HDL value. If it’s higher, you may have prediabetes and fat-encrusted arteries. Keep in mind the really important number is your fasting blood sugar level—and we’ll learn more about that in the next chapter.
Why Vegetable Oil Is Your Brain’s Worst Enemy Vegetable oils attack the brain at seven distinct vulnerability points using seven distinct strategies. All seven strategies are at work in causing autism and other childhood neurologic disorders. Vegetable oils make your brain more susceptible to damage by sugar. Eliminating these oils will enable symptoms of all sorts of brain disorders to improve, from autism to Alzheimer’s. There are five specific kinds of foods you should eat to optimize brain health.
Vegetable oil, the perfect brain-eating toxin, promotes brain disorders both directly and indirectly by impacting these systems: 1. Gut. Inflammatory reactions in the gut influence brain health by way of the microbiota, the immune system, and leaky gut. 2. Lipoproteins. These serve as Trojan horses distributing the toxins to the brain and other target organs. 3. Arteries. Vegetable oil disrupts the regulation of blood flow through the brain. 4. White blood cells. Vegetable oil turns our immune system against us, causing food and infectious diseases to trigger nerve degenerating reactions. 5. Nerve cellular architecture. Vegetable oils cause an overload of oxidative reactions inside the cell, leading to the accumulation of intra-cellular trash. When this affects our white matter, we lose our mobility. When it affects our gray matter, we lose our personalities, and our connections to the world. 6. Gene replication. Vegetable oils impair brain development through direct mutagenic effects on DNA and altered epigenetic expression.
In a study entitled “The Stomach as Bioreactor”307 they combined turkey meat with soy oil, the most commonly used vegetable oil worldwide, and varying amounts of acid. What they discovered was disturbing. They found that acid levels similar to those in the human stomach accelerated the reaction between soy oil and the iron in turkey meat, rapidly transforming the linoleic acid in soy oil into harmful MegaTrans fat (lipid peroxidation products).
The mice who got the vegetable oil ingredient, linoleic acid, developed lesions, whereas the mice who got the olive oil did not.308
Using a model stomach, they tested how various levels of vitamin C would affect the chemical reactions between iron (in meat) and linoleic acid. Surprisingly they found that adding just a little vitamin C to the mixture accelerated iron’s ability to react with linoleic acid and led to more MegaTrans fat being formed than when they added no vitamin C at all.
Taken together, these three articles suggest that cooking iron-containing foods in vegetable oil could be an important cause of inflammation-related gastrointestinal disorders including heartburn, gastritis (stomach lining inflammation), and ulcers. Throw the other variables into the mix, like vitamin C in certain concentrations, or stress, and you might be throwing gasoline on a fire.
a 2009 article published in the journal Gut showed a powerful connection between linoleic acid consumption and a serious colon disorder called ulcerative colitis, which affects nearly a million Americans and which can cause bouts of bloody diarrhea.
2016 study published in JAMA Neurology reported that older men using antacids to control their digestive symptoms had a 78 percent greater risk of dementia. The authors open the door to the possibility that these cognitive effects may be due to the medication. I find this explanation less compelling than the possibility that heartburn is the tip of the iceberg, indicating widespread inflammation resulting from the long-standing conflict between the human body and the pro-oxidative effects of vegetable oil.314
“Obese-Type Gut Microbiota Induce Neurobehavioral Changes in the Absence of Obesity” and did some digging into the diet the researchers studied.316 What I found was that by feeding mice oxidized, damaged fats, researchers so profoundly altered the gut flora of the mice that it significantly altered their emotional state of mind.
The second way vegetable oil attacks your brain is by disarming its antioxidant defense system. Of all the organs in your body, the brain is most dependent on a steady stream of fresh antioxidants to defend against oxidative stress. But because vegetable oils can deplete your brain of its antioxidants, they can also compromise this most important brain-defense mechanism, leaving your delicate nerve cells subject to destructive free radical reactions and potentially devastating inflammation.
Because of the nature of its construction, superoxide anion leakage in a brain cell creates a particularly troubling scenario. Thirty percent of the dry weight of your brain is composed of very long-chain PUFAs, some of the most highly combustible materials in the living world. DHA and AA (docosahexanoic acid and arachidonic acid, both PUFAs) are so reactive that the body uses them to respond quickly to emergencies like blood vessel breach and bacterial invasion. The brain needs them for entirely different reasons, however. These long and jointed fats are also extremely fluid and flexible, making them the perfect material for use in the connection points between nerves, called synapses.
“Oxidative stress (OS) leading to free radical attack on neural cells contributes calamitous role [sic] to neuro-degeneration” leading to “loss of cognitive function in AD [Alzheimer’s], PD [Parkinson’s], MS [multiple sclerosis] and ALS [amyotropic lateral sclerosis, a.k.a Lou Gherig’s disease].”329
from the field of psychiatry, an article entitled “Oxidative Stress and Psychological Disorders” echoed the same idea, concluding that “accumulating evidence implicates free radical-mediated pathology, altered antioxidant capacity, neurotoxicity, and inflammation in neuropsychiatric disorders.”330
when your diet is high in vegetable oils, no matter how many antioxidants you get from your food or supplements, they may not even reach the brain to aid in the constant battle of protecting its tissues from the ravages of oxidative stress.
you must get from the foods you eat. Antioxidant enzymes that directly catch and neutralize reactive oxygen molecules are your body’s first line of defense against oxidative stress. They use metals like zinc, copper, iron, or a sulfur-containing amino acid to trap high-energy, so-called excited oxygen molecules, handing off some of those oxygen molecules’ energy to other molecules, effectively calming them down.
secondary free radicals, the body is armed with a second line of defense—the non-enzymatic radical scavenging antioxidants. This defense team is composed of a much more varied set of molecules than the first line of defense, to deal with the fact that the enemy whose spin states and energy levels it must match takes so many myriad forms. Like the dangerous molecules they must be prepared to stop, they come in water-soluble and fat-soluble forms.
This industrial processing strips out many of the antioxidants nature intended to accompany them. As I discussed in Chapter 7, it also mutates a small but significant portion of the fragile PUFAs into MegaTrans fat,331 molecules that are known to initiate free radical cascades (i.e., known to cause oxidative stress).
According to a recent study appearing in the Public Library of Science, oxidative stress (an inevitable consequence of a high-vegetable-oil diet) correlates with lower “emotional IQ.”335 The study, conducted on a sample of fifty
exposed to oxidized oil overreacted significantly, and the authors concluded that “dietary oxidized frying oil may increase spontaneous spleen cell proliferation and B cell activation, which may have significance in the development of altered immunological functions.” They go on to suggest a potential link between such environmentally induced immune dysfunction and the recent “rapid increase in prevalence of certain immunological diseases such as allergic diseases and auto-immune disease.”345
By disrupting endothelial function and limiting blood flow, vegetable oil cuts off supplies to the most active regions of your brain. This necessarily means that, whatever
Studies show that nitric oxide signaling, and the blood flow increases it stimulates, play a central role in nerve cell maintenance, growth, and repair. 350, 351, 352 Most pertinent to anyone looking to enhance their aptitude for learning, nitric-oxide-induced blood flow also makes forming new memories physically possible as it plays a key role in what neurologists call long-term potentiation, a process required for assembling and reinforcing new synaptic connections throughout the entire cerebral cortex, striatum, and hippocampus.353, 354
New Zealand researchers demonstrated that a single meal of fries cooked in week-old vegetable oil can cause endothelial dysfunction lasting up to twenty-four hours, disrupting the ability of muscles to get the oxygen they need on demand.
you’ve developed a migraine enduring a prolonged stressful situation, it may have been a result of vegetable oil intake forcing endothelial dysfunction to graduate to the next level, manifested as a bioelectric phenomenon called cortical spreading depression.363 This isn’t depression as in feeling the blues; it refers to a marked reduction in normal brain electrical activity. When this disturbance occurs in the gray matter—the thinking, feeling, and dreaming part of your brain—it interferes with information processing in the affected area, often producing what’s called an aura—a sensory aberration that manifests in different ways depending on location. For many migraine sufferers the location is the part of the brain at the back of the skull that processes vision, called the occipital cortex.364 This is where you get flashing lights (called scotoma) or tunnel vision. If the brain area malfunctioning is the somatosensory cortex, a tactile aura will occur, often beginning as a tingling in the arm or the face and tongue. Auras
Wrinkles, stiffness, presbyopia (the loss of near vision resulting from a stiffening of the lens of the eye)—all the drawbacks of getting older—come at least in part from the accumulated damage of decades of oxidation reactions. (The two most important age-promoting reactions are called lipid peroxidation and protein-lipid glycation.)
A blow to the head, even a small one, can trigger nerve cell injury. The injury exposes extremely oxidizable membrane PUFA fats to pro-oxidative compounds, rapidly oxidizing vast quantities of PUFAs and potentially overloading the antioxidant capacity of the brain. Because of the uniquely volatile nature of the brain’s biochemistry, a relatively mild force can quickly cause massive cellular destruction. This interaction between oxidation-vulnerable PUFA structures of the brain and novel pro-oxidative distorted PUFAs from our diet is, I believe, what’s behind many of the life-changing personality and mood alterations some people develop after a concussion.
Many concussive injuries compromise cell integrity. When this happens, enzymes whose function it is to oxidize PUFA fats within the cell in a highly controlled beneficial manner escape from their confined location within the cell. Once released, these enzymes can now interact with PUFA fats in the nerve cell membranes where their pro-oxidative properties are not at all beneficial and are, in fact, quite harmful. Because 30 percent of the brain’s weight is comprised of these PUFAs, this enzymatic activation accelerates the normal low-grade pitter-patter of oxidative stress and rouses it into a full-blown storm of oxidative reactions.372
Seconds count, as every second that goes by, every single free radical initiates a chain reaction capable of oxidizing billions of fragile membrane PUFAs.373 You can express the problem as a formula. The quantity of oxidative damage a damaged brain experiences would be called oxidative stress (OS). The amount of time before OS is controlled would be called time (T). Multiply the two together and the product becomes the total amount of oxidative type damage (OTD) an injured brain will suffer. The formula would look like this: OS x T = OTD. Let’s call this the healthy brain formula. After a concussion, a brain with a lower OTD score will heal more quickly and more completely than a brain with a higher OTD score, no matter how old the patient, how severe the impact, or how long they’re knocked out.
continued oxidation of the parent linoleic acid increases the concentration of 4-HNE by a factor of ten or more.376 4-HNE disrupts cellular function in so many ways and is implicated in so many diseases that entire journals have been devoted to describing its toxic effects.377 One of the most dramatic ways 4-HNE terrorizes our cells relates to the demolition of nerve cell highways, called microtubules. Without microtubules, it’s difficult to form new memories.
The microtubules, in turn, depend on a protein called tau. As I mentioned in the previous section, a hallmark pathologic finding in brains of people who have died with either Alzheimer’s or the accelerated form of Alzheimer’s induced by concussions (called chronic traumatic encephalopathy, or CTE) are comma-shaped brown blotches pathologists call tau protein tangles.
“Upon HNE modification, α- tubulin [a component of the microtubule] is structurally altered, and microtubules depolymerize. Therefore, cargo cannot reach its destination and the cytoskeleton is altered.”379
But 4HNE doesn’t just take away the tau girders stabilizing the neural highways, it also does something worse. It causes oxidative stresses that lead to modification of tau by phosphate groups. That modification changes tau protein’s shape, making it less capable of stabilizing the microtubules, and prone to tangling and sticking to itself.380 This leads to the development of neurofibrillary tangles, glommed up microtubules that not only fail to function as effective cellular roadways, but physically stick to other microtubules and block the flow of traffic.381 When enough have become entangled with one another, the protein mass grows large enough to be seen under a microscope, in the form of those hanging bat-like structures. This particular form of cellular disruption appears to play a role in causing the earliest objectively measured stage of Alzheimer’s, called mild cognitive impairment (MCI).382 While Alzheimer’s is usually very obvious on an MRI because it causes gray matter losses and brain shrinkage, people with MCI often have normal brain volume.383
But I do want to better acquaint you with the three PUFA-derived mutagens I just named because when they make it to the part of your cell that houses DNA, they can bind to DNA and create new, “de novo,” mutations. DNA mutations affecting a woman’s ovaries, a man’s sperm, or a fertilized embryo can have a devastating impact on subsequent generations.
After interacting with DNA, 4-HNE forms a compound called an HNE-adduct, and that adduct prevents DNA from copying itself accurately. Every time 4-HNE binds to a guanosine (the G of the four-letter ACGT DNA alphabet), there is somewhere between a 0.5 and 5 percent chance that G will not be copied correctly, and that the enzyme trying to make a perfect copy of DNA will accidentally turn G into T.420 Without 4-HNE, the chance of error is about a millionth of a percent.421 In other words, 4-HNE increases the chances of a DNA mutation rate roughly a million times!
HHE specializes in burning through your glutathione peroxidase antioxidant defense system.423 This selenium-based antioxidant enzyme is one of the three major enzymatic antioxidant defense systems, and it may be the most important player defending your DNA against oxidative stress.424, 425
MDA with the definitive statement that MDA “appears to be a major source of endogenous DNA damage [endogenous, here, meaning due to internal, metabolic factors rather than, say, radiation] in humans that may contribute significantly to cancer and other genetic diseases.”428
Almost buried by the avalanche of journal articles on genes associated with autism is the finding that autistic children exhibit roughly ten times the number of de novo mutations compared to their typically developing siblings.432
Sickly Sweet How a Carbohydrate-Rich Diet Blocks Metabolic Function Sugar is sticky, and that’s why high blood and tissue levels can have toxic effects. The body knows sugar is toxic and releases hormones to regulate it. Eventually, too much sugar disrupts hormonal function. Too much sugar also disrupts basic cellular functions in ways that accelerate the aging process. Because grocery stores are full of foods that raise blood sugar, most people eat more sugar than they realize.
As sugar seeps into your tissues, it coats the surface of cell membranes, with life-changing consequences.
For the same reasons sugar jams hormone signals, it also clogs nutrient channels, weakening bone and muscle and slowing neural communication, which can impair mood and memory and lead to dementia. While all this is going on, sugar stiffens the collagen in your tendons, joints, and skin, causing arthritis and premature wrinkling, while interfering with the production of new collagen throughout your entire body. And because sugar changes the surface markers your white blood cells need to distinguish indigenous cells from invaders, it opens the door to cancer and infection.
Glycation: The Reason Sugar Is Bad for You
The process by which sugar sticks to stuff is called glycation. Glycation reactions are reversible, but with enough heat or time, the temporary bonds become permanent due to oxidation reactions. The products of these later oxidation reactions are called advanced glycation end products, or AGEs. And that’s a useful acronym, because AGEs make you age unnaturally fast.
These AGEs change the bread from soft, pliable, and pale, to hard, stiff, and brown because the proteins and sugars form cross-links that stiffen the bread. The same thing happens inside your body as AGEs cross-link normally mobile proteins. This hardens your cells and tissues, making them brittle and stiff. Fortunately, at normal blood sugar levels, the reactions occur so slowly that cleanup crews of white blood cells keep them under control by breaking them down. The kidney cleans these AGEs from the blood and excretes them from the body. It is principally these waste chemicals that give urine its characteristic yellow color.
Cross-links turn the semi-permeable surfaces of arteries into impervious walls, preventing nutrients from exiting the bloodstream. When trapped nutrients can’t escape your bloodstream, where do you think they end up? Lining your arteries.
When responding to the call of tissues in trouble, white blood cells must exit the bloodstream. How do they know where to go? Inflammatory chemical messages from the affected tissue seep through intercellular spaces to reach the endothelial cells lining the bloodstream. Those cells then put up little flags on their surface telling white blood cells to exit the blood vessel. The white blood cells magically transform from stiff, tumbling spheres into flowing, flat amoeba-like creatures, and wriggle through tiny spaces between endothelial cells into the troubled tissues below. All of this is basic physiology. But our knowledge of the biochemistry of sugar helps us understand how glycation reactions between sugar and protein can cross-link the endothelial cells, block those tiny spaces, and prevent white blood cells from getting to where they’re needed. And it follows that the more cross-links you have, the more your immune function is impaired.
Over the life of a red blood cell (three months or so), the protein-rich red cell sops up sugar like a sponge, growing stiff and bloated. One of the jobs of the spleen is to test the quality of red blood cells in active circulation. It does this by making them pass through a maze of gradually narrowing corridors. Any cell too puffed up with sugar gets destroyed. But when sugar levels are high all the time, the spleen can’t remove all the bloated cells quickly enough, so they wind up clogging tiny capillaries. This is why diabetics go blind and develop numbness and infections in their feet.
Too much sugar makes LDL levels rise by several mechanisms. First, sugar elevates insulin. High insulin accelerates LDL production by turning on the enzyme HMGCoA-reductase—the very same enzyme statin drugs are engineered to turn off.447 Sugar also glycates circulating LDL apoproteins, locking the affected LDL molecules in circulation by making their docking proteins unrecognizable (see Chapter 7), thus raising LDL higher. Then, over several years, sugar cross-linked capillaries grow stiff. Capillaries must remain flexible to allow the passage of LDL and other lipoproteins to underlying tissues. But once caked stiff, capillary channels cannot open fast enough, if at all; the blocked-off LDL is forced to stay in circulation longer, and LDL serum levels rise further still. Most of the cholesterol in circulation is manufactured by your body, so if your diet is high in sugar, it is nearly impossible to bring your serum cholesterol down—unless you get on a cholesterol-lowering drug.
Sugar acts as a powerful epigenetic instructor, telling your child’s genes to construct a brain with a built-in hankering for drugs.
They found that infants who got sugar in their first seven days of life suffered neurologic effects that were still measurable when the study ended, eleven weeks later. Higher number of doses of sucrose predicted lower scores on motor development and vigor, and alertness and orientation … and higher NBRS [NeuroBiological Risk Score, a reflection of processes deleterious to brain development].”451 Essentially what this study indicates is that little
One of the earliest stages of Alzheimer’s dementia involves the loss of these branches, a process called dendritic pruning.453 It’s likely that sugar-induced cross-linking gumming up brain cell membranes is at least part of the problem. As with any cell membrane, cross-links reduce hormone sensitivity.