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.
These days, when we look at someone who is overweight, we tend to reflexively make the connection between their body’s condition and their diet. But it’s now abundantly clear that body size is just one of many consequences of an imbalanced diet, as many metabolic disorders clear up when people eat better and restore normal weight. By the time you finish this chapter, my hope is that when you see a person suffering from depression, Alzheimer’s, or even when you encounter a child with a learning disorder, you will likewise think about diet—both as a cause and as a cure. I sincerely hope that you will come to understand why, if you care about your mental health, the single most important product to avoid is a staple so ubiquitous it goes largely unnoticed. I’m talking, of course, about vegetable oil.
In the last chapter we learned that dietary vegetable oil can transform ordinary fatty acids into a kind of atomic tornado, tearing through cellular structures and leaving molecular wreckage in its wake. We also saw that lipid scientists have been publishing papers on this topic for decades, trying to warn us that vegetable-oil-rich diets can cause dangerous oxidative stress and are an under recognized cause of heart disease and accelerated aging. But the most terrifying thing about vegetable oil is that it’s also destroying the organ most susceptible to oxidative stress, our brains. It’s no exaggeration to say that vegetable oil attacks your family legacy at both ends of the generational spectrum, robbing your children of their physiologic birthright and erasing memories from our parents’ and grandparents’ minds.
Vegetable oil is undoubtedly the most unnatural product we eat in any significant amount. Keep in mind, GMOs (genetically modified organisms) are generally the starting point in the production of vegetable oil, and things just go downhill from there. Thanks to vegetable oil’s inherent ability to inhibit life, vegetable oils are the chemicals that preserve a Twinkie for years on end. More than any other ingredient, vegetable oil is what puts the “junk” in junk food. A patient of mine on Kauai told me that the paniolos (Hawaiian cowboys) used to cure hide leather to make their saddles using cottonseed oil, but did they eat the stuff? Ho, brah, dat’s lolo (“crazy”). They didn’t eat it, and neither should you.
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.
If you’ve read Grain Brain, Cereal Killer, Sugar Crush, Sweet Poison, The Sugar Blues, Fat Chance, Sugar Nation, The Starch Solution, or any of the other excellent books delineating the relationship between excess dietary sugar and poor health, particularly mental health, then you’re well aware of the fact that sugar in any form can have toxic effects. But fructose, glucose, sucrose, starch, and other members of the sugar-sweet gang only have one weapon at their disposal, glycation, which we’ll discuss in the next chapter. Vegetable oil has multiple strategies by which it wreaks havoc in your body. Like a seasoned general, it knows your weaknesses and probes every vulnerability point for the opportunity to get into your brain and dismantle your cognitive functioning. These are: (1) attack the gut; (2) deactivate the defense systems; (3) counterintelligence; (4) cut off supplies; (5) fire bombing; (6) blow up the roads; and (7) identify theft.
Vegetable oil often initiates its attack on the brain by first attacking the gut. More and more researchers are appreciating the connection between gut and brain function. Inflammation in the gut causes heartburn, which is just the tip of the inflammation iceberg and should serve as a kind of red flag telling us that whatever we’re eating is harmful. Unfortunately, many people wrongly attribute heartburn in spicy foods to the spices, and simply ignore the warning signs. Others quiet the gastric flames with heartburn medications and antacids, but these do nothing to block the damaging effects of MegaTrans fats on the gut. As you’ll see, when these bad fats exit the stomach to make their way further down the digestive system, the impact on your microbial flora can have mind-altering effects.
Vegetable oil gets into the body via the gut. Every bite of food you swallow lands first in the stomach. The stomach releases acid and gently massages it through the food with peristaltic action, the name given to the squeezing of the intestines that serves to both help break food down and propel it forward through the digestive tract. The acid aids digestion by activating digestive enzymes and killing off pathogenic bacteria, ultimately enabling us to extract as much nutrition as possible from our diets. But in the presence of vegetable oils, stomach acid interacts with otherwise beneficial compounds in our food in such a way as to incite oxidative reactions that lead to the formation of MegaTrans fats that cause damage to the stomach lining.
In 2001, a pair of Israeli lipid scientists aware of the tendency for PUFAs to react with iron—present in high concentrations in all types of meat—wanted to evaluate whether stomach acid would accelerate or delay oxidative reactions. 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). Another group of scientists whose work appeared in the Saudi Journal of Gastroenterology wanted to compare the effects of different fats on a stressed-out gut. Using mice as subjects, they reduced the bloodflow to the stomach to simulate the effect of emotional stress on the gut. Half the mice were fed oleic acid, the predominant component of olive oil, and the other half got the same component of vegetable oil studied by Dr. Spiteller—linoleic acid. The mice who got the vegetable oil ingredient, linoleic acid, developed lesions, whereas the mice who got the olive oil did not.308 And a third group of lipid scientists309—aware that antioxidants can sometimes have the opposite of the desired effect and will, depending on the chemicals they’re surrounded by, potentially act as pro-oxidants—evaluated the antioxidant vitamin C. 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. On the other hand, adding a lot of vitamin C slowed these reactions down again, leading to less MegaTrans fat being produced than when vitamin C was absent, which is more like what you’d expect. 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.
Vegetable oil’s irritating pro-inflammatory effect on the stomach lining is just the beginning; there’s another twenty-eight feet of digestive tract to go and no shortage of evidence that vegetable oil can irritate and inflame every inch. For example, 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. It is often confused with appendicitis, and for some unlucky patients, the only effective treatment is removal of the colon. The authors of the study concluded that simply cutting down the intake of linoleic acid could immediately reduce the number of people suffering from this painful, disfiguring disorder by 30 percent.310
What you can take away from this is that if you have heartburn, gastritis or other digestive symptoms, one of the simplest things you can do as a first proactive step is to eliminate the vegetable oil in your diet. I’m not saying that vegetable oil is the only possible cause of these symptoms, but eliminating vegetable oil is certainly the most important first step to take toward reducing digestive discomfort, no matter what other factors may be involved. In my decades of clinical experience I’ve found that vegetable oil consumption, and the attendant MegaTrans-induced inflammation, makes people more susceptible to developing food sensitivities and autoimmune reactions. If you are thinking about cutting out gluten, dairy, or other common foods but haven’t yet eliminated vegetable oils, I’d recommend you consider cutting out vegetable oils first. Cutting out vegetable oil is far easier to accomplish than limiting your exposure to nearly ubiquitous toxic food contaminants, or avoiding any side effects of medications that you’re not able to discontinue, and is an essential first step toward eliminating intestinal parasites and other infections.
The downstream effects of vegetable-oil-induced stomach inflammation can potentially be quite serious. Persistent stomach inflammation might lead to gastritis, or an ulcer, or cancer. Inflammation can also reduce your ability to produce adequate stomach acid, which can in turn limit the ability of beneficial bacterial colonies to stake their claim of intestinal territory. A scarcity of do-gooder bacteria in the gut can leave you open to all manner of pathogenic invasion, which can result in bacterial diarrhea (like Salmonella, Shigella, and C-diff), blood born infections, and (particularly in the very young or very old) even septic shock. Inadequate acid production also interferes with the absorption of vitamins (including antioxidants that ameliorate the dangerous effects of vegetable oils in your bloodstream) and prevents digestive enzymes from doing their job—because many enzymes must be activated by acid. This in turn can lead not just to malnutrition but also to bacterial overgrowth and inflammation in the lower digestive tract, producing bloating, constipation, diarrhea, and intolerances to certain foods—all of which indicate inflammation somewhere in the small or large intestine, or both. Because the intestine contributes greatly to the overall function of your immune system, and houses the microbiota, which also contributes greatly to your overall health, this means that frequent heartburn is a red-flag symptom potentially indicating widespread damage to several body systems.
MOST FISH OIL SUPPLEMENTS CONTAIN MEGATRANS
You may have heard that marine oils are a good source of the essential, heart-healthy, brain-building omega-3 fatty acids, and it’s true. Unfortunately, trying to extract long-chain omega-3 fats out of living organisms while keeping their molecular structure intact is a little like trying to put lightning in a bottle. Omega-3 fats are even more prone to oxidation reactions than omega-6 because (given equal fatty acid lengths) omega-3s typically have an additional double bond.311 This extreme oxidizability mandates gentle treatment of the oil, i.e., cold-pressing and no refining or processing. Even so, after thirty days, you’d be better off saving your money for real seafood, because, as a group of lipid scientists in New Zealand investigating the safety of marine oil products explain, “Even oil stored in the dark at 4 degrees Centigrade may oxidize unacceptably within a month of storage.” The New Zealand group’s conclusion: “Consuming purchased supplements entails risk of exposure to unacceptably oxidized oil.”312
My conclusion: get your omega-3 fix from real foods, like sushi, oysters, grass-fed butter, raw nuts (especially walnuts) and seeds, and lots of green leafy vegetables. By the way, another group of researchers found that fish oils react with stomach acid to form three potent genotoxic and cytotoxic compounds: 4HNE, 4HHE, and malonaldehyde.313 Little wonder that at least half my patients tell me that fish oil supplements give them indigestion!
Severe heartburn is enough to make you miserable all by itself. It hurts. It disrupts sleep. It can make every meal feel like a game of Russian roulette. But more concerning still is the recent evidence of a link between heartburn and poor mental functioning. A 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
There are several deservedly influential books that argue that a healthy microbiota is a necessary prerequisite to normal brain health.315 Conversely, they argue, an unhealthy microbiota compromises the gut lining leading to leaky gut, which, in turn, interferes with nutrient absorption and immune function in ways that directly impair mood, cognition, and memory. These popular books have brought the general public a great deal of valuable information about the role of diet in cultivating a healthy microbiota.
One of the most talked about dietary factors is grains. Lately, many physicians and researchers have shown a link between gluten and mental illnesses. In so doing they cast light on an important connection between diet and health. While I believe there is a lot to be gained by limiting refined grains and thus reducing your intake of blood-sugar-elevating empty calories, I am not yet convinced that the gluten itself is inherently toxic to the beneficial organisms living in our gut. (For more on this topic, see Chapter 14). I have, however, long suspected that vegetable oil might be directly damaging to our tiny microbial friends because of its now well-established pro-inflammatory effects that begin the moment you ingest any food containing vegetable oil. Over the past decade I’ve encountered plenty of circumstantial evidence to this effect, but I never had direct evidence showing that oxidized fats—which is principally what makes vegetable oils so unhealthy, the fact that they are oxidized—can completely reorder the power structure among microbial populations in the gut until I happened upon an article entitled “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.
It’s no fun to be fat. Of the many problems associated with obesity, the one my patients tell me bothers them most is that they feel bad about how they look, and that makes them feel hopeless and discouraged and unmotivated to sustain difficult habit change. Since 2003, researchers have found increasing evidence that the brain function of obese and normal weight people is fundamentally distinct: “Functional studies report deficits in learning, memory, and executive function in obese compared with nonobese patients.”317 Executive functioning requires being able to break down complex tasks into their individual components and gives you the ability to plan ahead. A lack of such skill is associated with anxiety and depression, which should not come as much of a surprise. After all, if you’re not great at strategizing but are being forced to do so for work or a wedding—or even to go grocery shopping for the week—it can be pretty stressful, and failing at it can get depressing. If that sounds like you or someone you know, you may be relieved to hear that scientists have discovered evidence that those elements of your personality may not be nearly as personal as you might think. They may be a complication of an unhealthy balance of microbes growing in your gut. Research shows that the health of your microbiome has a direct effect on your own ability to view your circumstances and your body in a positive light. In other words, what you see in the mirror is at least in part mediated by tiny creatures living inside you.318, 319, 320, 321, 322
This is a compelling idea, and it’s not just theoretical. One of many studies that substantiates this idea was performed with two groups of mice whose gut flora had been obliterated by large doses of antibiotics. Each group received an inoculation of microbiota isolated from either obese or normal-weight donor mice. Two weeks after the transplant, both groups underwent a battery of tests to evaluate memory and anxiety states. The mice given the obese mouse microbiota showed “significant and selective disruptions in exploratory, cognitive, and stereotypical behavior,” engaged in excessive marble burying (a measure of anxiety), spent less time exploring an open field, and failed to freeze—stop what they’re doing to listen—when a novel sound was played. They also failed other tests of memory and learning ability. The mice given normal-weight mouse microbiota, on the other hand, passed all of these tests with no problem. While the differences were subtle, they were significant and not mediated by excessive weight.323
So does this suggest that people with excess weight could benefit from what’s called fecal transplant therapy, sterilizing their guts with antibiotics and infusing a bacterial slurry extracted from a skinny friend via a nasogastric tube into their stomach? It will be years, if not decades, before scientists can recommend such a radical and potentially dangerous procedure. But there may be an easier and safer way to accomplish the same beneficial shift in your microbiota: cut vegetable oil out of your diet.
In the anxious mouse study, the authors tell us they used obese mice as donors of the microbiota which ultimately transformed the study mice into little nervous wrecks. This made me wonder what it was that made the mice obese in the first place—was it their diets or a genetic tendency? It turns out that the obese donor mice were not genetically obese, but rather they were made obese through diet.324 And what kind of diet? A very important question, since we know it was the very same diet that bred the microbes that made the experimental mice anxious and impaired their ability to learn. Well, the diets that the obese and the normal mice were fed were nearly identical except for one important factor: the amount of oxidized fats (MegaTrans) formed from the reactions between sunflower oil and lard stored for months on end in pelleted chow containing iron, copper, and ascorbate—all known to incite oxidation reactions during extended storage with PUFA and monounsaturated fats.325 This study applies to you because although you are not living off stale, rancid rat chow that has been oxidized through months of storage, in a way you kind of are, because the oxidized vegetable-oil-rich foods typical of an American diet contain the very same blends of oxidized fats. Keep in mind, these compounds not only turned calm happy rats into skittery anxious little rodents, they also made them fat. Other toxins may impact the microbiome in a similarly negative way, like chemotherapy or infection or radioactivity.
By the way, getting at the root of what was actually in the study’s food was not easy. But this is the kind of mining operation a good scientist has to do with these kinds of studies. You have to seek out with a divining rod the actual useful conclusions buried in a poorly constructed study. If you look hard enough you find out what they really did conclude; in this case, that the mice were fed not just any high-fat diet, but a high toxic–fat diet.
Thanks to research studies like this, people who never would have thought about mental health as something their diet could impact are now waking up to the potential links. And there are many surprising connections.
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.
You already know that antioxidants are vital to your health, but to understand the vital role they play in the maintenance of your brain’s health, you first need to understand a little about how the structure and function of your brain make it uniquely vulnerable to oxidative damage and, therefore, particularly dependent on antioxidant protection.
The brain runs on electricity. Keeping the grid online requires a constant supply of fuel. Although your brain represents just about 2 percent of your total weight, it uses a full 20 percent of the calories you’re burning each minute while you sit quietly at rest. Brain cells, like all cells, produce energy by oxidizing (burning) a variety of fuels in little chambers called mitochondria.
Cell physiologists have recently found that our mitochondrial reaction chambers have a nasty habit of leaking explosive material into the surrounding cellular cytoplasm.326 Called superoxide anion, this explosive material is a kind of activated oxygen molecule that escapes the boundary of the mitochondrial membrane during the transfer of electrons inside the mitochondrial electron transport chain. A little like sparks flying out of a furiously hot fireplace, superoxide anions are an unavoidable byproduct of the process of mitochondrial energy production. It seems that, just as in the outside world, the production of energy in the body comes with an inherent cost of some kind of hazardous waste.
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.
Your thoughts are made of electric impulses. As an idea is about to manifest, electricity in the brain travels down the length of a nerve until it reaches a synapse. At the synapse, it must jump from one nerve to the next, or the thought you were about to have will evaporate before it can ever form.
All communication between nerves happens through the action of compounds called neurotransmitters that a nerve ending releases into the space between it and the neighboring nerve it’s talking to, called the synaptic cleft. Here’s how they make the connection between two nerves: at the terminal end of nerve number one, neurotransmitters, including dopamine and serotonin, sit waiting inside a bunch of tiny globules, called vesicles. Upon stimulation by an electrical impulse coming from the head of the nerve, the vesicles in the tail end of nerve number one immediately fuse with the cell’s outer membrane, dumping their neurotransmitter contents into the synaptic cleft. There, the neurotransmitters can reach nerve number two and bind to a receptor that regenerates the electric impulse on the receiving end of the synaptic cleft. For this process to work, the vesicles must be flexible, like microscopic water balloons. And the only kinds of fatty acids that are capable of fusing fast enough to make this all happen—literally at the speed of thought—are those extremely fluid, flexible, and unfortunately unstable long-chain PUFAs.327
The nature of the brain’s uniquely fragile construction combined with its intense mitochondrial energy production puts your brain in a perpetually precarious state.328 This is why, more than any other type of cell, brain cells must do a near-perfect job of defending against the inevitable high-energy atomic releases from the mitochondria. And the only defense mechanism cells have at their disposal are the antioxidants. Think of antioxidants as a kind of force field that absorbs and neutralizes free radicals that would otherwise threaten the integrity of your brain. Without a constant supply of fresh antioxidants, sparks flying out of the mitochondrial chamber may ignite free radical reactions in the nerve cell membrane, damaging large sections of the cell and interfering with basic metabolic functions. When enough cells are damaged and malfunctioning all at once, we develop clinical symptoms. In the immediate term that would be something along the lines of a migraine or a seizure. But as the brain ages, much more serious problems begin to take shape.
Psychiatrists and neurologists have begun to pay more attention to the important role these oxidative reactions play in major diseases affecting their patients. A 2009 review article—an analysis and conclusion of recent relevant research written by a group of neurologic researchers in Milan, Italy—advises doctors to be aware of the harms of oxidative stresses in the nervous system. “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 And in 2014, 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 I feel we’ve reached a point in medical science where it’s clear that when depleted of antioxidants, the brain suffers a slow death by oxidative stress. This bolsters what other doctors and authors have suggested, which is: if you want to know what’s damaging the brain, look no further than oxidative stress.
On the one hand it is encouraging that so much important research is being done to show doctors and patients that something as simple as controlling oxidation reactions can help with such a vast array of otherwise not very treatable disorders. On the other hand, I find it discouraging that the authors of otherwise excellent articles such as these continue to look to antioxidant supplements or pharmaceuticals as their primary source of therapeutic solutions. We just saw in the previous section that antioxidant supplementation can produce the opposite of the desired effect, serving as a pro-oxidant, depending on the chemical milieu. So it seems to me that a safer and more productive intervention would come from, once again, looking to the scientists who specialize in lipid oxidation—the lipid scientists.
As I’ll discuss in a moment, their research has shown that 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.
Thus far, we have seen that most researchers now agree oxidative stress plays a major role in just about every brain disease you can name, and that the brain’s unique physiology makes it uniquely susceptible to oxidative stress. Now let’s take a look at how pro-oxidative vegetable oils knock out the brain’s antioxidant defense system at every stage of the process.
Polyunsaturated fats—the type of fats most common in all the vegetable oils—are uniquely prone to oxidative reactions. As I just described, this is the very same kind of molecule that makes up 30 percent of your brain by dry weight. And as we saw in Chapter 7, oxidative reactions readily transform PUFAs into dangerous free radicals that smash into molecules randomly, transforming them, zombie style, into high-energy molecules that are themselves capable of generating more free radicals in a cascading fashion. Your survival and reproduction depends on a working, functional brain, so it’s little wonder that your body has built-in defenses that try to protect it from oxidative damage. To that end, your body depends on two lines of antioxidant defense: (1) enzymatic antioxidants, produced in almost every cell in your body; and (2) diet-derived antioxidants that 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. The enzymes act a little like bouncers whose job it is to deal with drunken belligerent patrons—but with one key limitation: they can only deal with a specific class of free radical, characterized by a specific size, and a specific electron spin state. Think of them as bouncers who are only allowed to deal with customers between the ages of twenty-eight and thirty. These antioxidant enzymes must be in close proximity to the troublemaking “excited” oxygen molecule to catch it before it smashes into something else and thereby generates a secondary free radical. The enzyme “bouncers” are trying to deal with free radicals preemptively by going after the excited oxygen before it can cause more free radical trouble.
While the oxygen-derived free radicals are limited in possible shapes and sizes, technically called spin states and energy levels, the secondary free radicals generated by the excited oxygen can assume any one of a great number of possible shapes and sizes. To defend against these 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. Since the 1922 discovery of vitamin E, a fat-soluble antioxidant, we’ve codified thousands of other compounds with antioxidant properties, including familiar vitamins A, C, and E, and less familiar plant phytochemicals like allicin (from garlic), cinnamic acid (from cinnamon), and cocoa and chocolate flavonoids. There are quite possibly millions of molecules with potentially useful antioxidant capabilities. And that’s good news, because collectively, they can step in and calm down just about any kind of free radical that might form. On a whole-foods diet rich in flavor-intense vegetables, herbs, and spices, you can be assured your body is flush with all manner of antioxidants—those we know and those we have yet to discover.
So now you understand not only why antioxidants are so vitally important to the health and function of your brain, but also why a whole class of antioxidants that are not produced by the brain must be ingested through diet. Once absorbed they have to be delivered to your brain so they can join in the fight against oxidative stress. And here we have yet another point of vulnerability, because the same lipoproteins your body uses to deliver fat-soluble antioxidants and other lipid nutrients to the brain (and other body tissues) will also, on a bad diet, deliver more ammunition to the enemy, feeding the oxidative cascades that put your brain at risk.
You might be wondering, If vegetable oils and other harmful distorted fats are so bad for us, particularly for our brains, why doesn’t the body just reject them or deal with them somehow? Can’t the body recognize how harmful these substances are and somehow detoxify them before they reach the brain to do their damage?
This is a great question. And the answer is that, much like asbestos or mercury, the human body has not adequately adapted to deal with high levels of what is in evolutionary terms a very novel toxin. For millions of years, when lipoproteins delivered their goods, they would be delivering only the naturally occurring, healthy versions of fats. Only in the past century or so have we had the industrial technology now used to extract fragile PUFA fats from the seeds that created them. 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).
When these distorted MegaTrans fats hitch a ride inside your lipoproteins they don’t just sit quietly, like stowaways. They necessarily interact with whatever antioxidants are also present in the lipoprotein332, 333 (which would have had to come from your diet). Through this interaction the antioxidants are able to mitigate some of the damaging effects of the distorted MegaTrans fat. But the price they pay for this interaction is their lives. Like bees guarding the nest, the non-enzyme antioxidants can only sting an intruder once. After that, they’re permanently out of commission. So by the time the lipoprotein vehicle arrives in the brain to deliver its cargo, many of the antioxidants that should be part of the delivery are conspicuously absent.334 What the brain gets instead is a truck full of what it takes to be natural fat—remember that these distorted fats are so novel the brain has no mechanism for rejecting them—so it must accept the delivery.
While the method by which lipoproteins cross the blood-brain barrier is still being studied, we already know that when the arriving lipoproteins are devoid of antioxidants they can cause oxidative stress and inflammation in the central nervous system. In 2015, researchers at the Linus Pauling Institute in Corvallis, Oregon, investigated this problem using a zebrafish model.336 (Zebrafish have a similar antioxidant requirement to humans, and unusually large nervous systems for their size.) They discovered that inadequate brain antioxidant supply (the focus of this study was vitamin E) translates to damage of the essential DHA, an omega-3 fatty acid that composes roughly 15 percent of the dry weight of a human brain. When the deficiency occurs during brain development, growth of the nervous system is disrupted and, in this fish model, leads to abnormal motor responses to light. And since we now know that the human brain demonstrates what neurologists call neuroplasticity (the brain’s ability to grow and change) well into old age,337 it makes sense that oxidative insult that impairs development in youth would likewise impair basic nervous system function and other aspects of neuroregeneration as we age.
CAN VEGETABLE OILS LEAD TO “EMOTIONAL EATING”?
You’ve probably heard that sugar is addicting, which is one of the reasons people have such a hard time weaning themselves off junk food. But what if junk food contained a major ingredient that could lower your self-esteem, make you feel hopeless, and make you far more critical of your body every time you looked in the mirror—a perfect recipe for emotional eating?
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 female psychology students, investigated the possible correlation between each participant’s antioxidant enzyme activity and parameters of emotional intelligence.
What the researchers found was that the women showing the highest antioxidant enzyme activity scored significantly higher in six variables: optimism, self-regard, reality-testing, stress tolerance, happiness, and impulse control.
In the next chapter, I’ll discuss in detail how vegetable oil and sugar work together to predispose you to weight gain and metabolic syndrome. This study shows how the combination of sugar and vegetable oil form a perfect, biochemical weapon of addiction—reminiscent of “impact boosting” used by cigarette manufacturers—to turn junk foods, and other processed foods, into effective delivery systems of metabolic disease.
So far, I’ve been talking about processed vegetable oils that were not used for griddle frying or subjected to extended heat. When you turn the heat on these fragile fats, the percentage of distorted fats contained in the vegetable oil you consume grows dramatically. This translates to a higher percentage of distorted fats in your lipoproteins, and an ever greater reduction in the antioxidants available for your brain.338
If your head is spinning from all this chemistry, the take-home is quite simple: since for every instance of vegetable oil use there’s a far better and tastier alternative, why not just go with a healthier, tastier fat? Switch out the canola oil dressing for an olive oil alternative. If you can’t find one, make one yourself (see recipes in Chapter 13). Instead of the usual brand-name mayo, have a taste of Primal Kitchen’s new mayo product, which I can tell you is pretty good. At your local restaurant, where they no doubt fry the fish in a vegetable oil or “blended oil,” ask if they can cook yours using butter. If you want to make yourself a batch of home-fries, make sure it’s either peanut oil or (if you can afford it) duck fat, and that you change the oil after every couple uses.
The other takeaway from all this is that since flavor-intense vegetables tend to be great sources of antioxidants and cooking diminishes antioxidant content, just about everyone could benefit by having more fresh, raw veggies in their diet. Studies show that most flavor-imparting phytonutrient compounds also have antioxidant capacity that protects fragile PUFA fats against oxidative damage.339 Of course, leaders of the vegan community like David Wolfe, Dr. Caldwell Esselstyn and his son Rip, Dr. Michael Greger, and Gene Stone have been telling us this for years. Given the almost unavoidable presence of vegetable oil in restaurants and supermarkets, making sure that your diet is consistently plant strong is a great way to defend yourself against the brain killers that may sneak their way onto your plate.
It’s impossible not to notice the popularity of gluten-free diets these days—now that some supermarkets have entire aisles stocked only with gluten-free products. The argument behind these diets is that, in its most basic form, modern-day wheat bears little resemblance to its distant ancestor, the wheat cultivated ten thousand years ago. Proponents argue that modern wheat triggers inflammation, an overactive immune response, and plays a role in nearly every disease you can name, including brain diseases like Alzheimer’s, Parkinson’s, schizophrenia, depression, and more. As the gluten-is-bad-for-you idea has caught on—between 20340 and 30 percent341 of Americans are making a conscious effort to avoid products containing gluten—so too has the idea that gluten may not be good for your brain.
I agree with the idea that gluten is a real problem for a substantial number of American consumers: the statistics that claim 1 to 2 percent of us suffer from celiac disease342 and that another 4 to 6 percent343 have some level of gluten sensitivity seem reasonable. Where I disagree with the leaders of the anti-gluten phenomenon is with the cause-and-effect relationship.
The anti-gluten folks tell a simple story: gluten is the underlying cause of a substantial portion of modern disease. You know my argument: pro-inflammatory fat found in vegetable oil is public health enemy number one. I don’t see the body’s reaction to gluten as the underlying problem; I see it as a symptom. Gluten intolerance is a serious condition. But as a doctor, I think of it very much the same way as I think of other allergies.
That’s why, when I see a child allergic to cats, I don’t say, “Well, cats are just dangerous and we should probably all be avoiding them.” The same applies when I see a child allergic to bees or peanuts or shellfish or eggs or soy or grasses or dust mites or newspaper ink or shoe leather glue or any of the hundreds of allergens doctors like me encounter on a regular basis. When I see anyone with an allergy of any kind, my first thought is that something has gone awry with my patient’s immune system. Their immune system has developed a hyper-reactivity to a common protein. I don’t use their allergic reaction as evidence that there is something inherently dangerous about bees or peanuts or shellfish or eggs or soy or grasses or dust mites or newspaper ink or shoe leather glue—or anything else. A recent CDC report344 shows that all these allergies, not just gluten, are on the rise. Have these proteins all changed or has something changed about our reaction to them?
I think it’s the latter. The immune system in the gut sees more foreign substances in a day—from food, bacteria, and viruses—than the systemic immune system sees in its lifetime. (Substances that the immune system treats as dangerous are called antigens.) The most important thing the gut immune system needs to do is be able to ignore most of them. The ability of the immune system to ignore non-threatening agents is called immune tolerance. And lately, our immune systems—especially those of our children—have become increasingly intolerant. Why would that be?
As we learned earlier in this chapter, vegetable oil causes inflammation in the gut, the very place where white blood cells of the immune system are doing their darndest to discriminate between the proteins you want to digest and absorb and proteins indicating the presence of potentially pathogenic bacteria (and other toxins). White blood cells play key roles in the military defense system of your body, patrolling your tissues twenty-four-seven in search of invading pathogens. When they find one, they launch an attack, literally engulfing bacteria and digesting them nearly completely. White blood cells that have ingested bacteria then travel back to central command (in your lymph nodes), where they present the bits and pieces of the bacterial outer protein coat to the white blood cell generals. These bits and pieces are analyzed and used as templates to generate antibodies that will be able to recognize the invader and destroy it more easily the next time. Surely the fact that these white blood cells are floating in a toxic vegetable oil broth won’t in any way impair their ability to profile suspect bacteria and weed them out before they can pass the gates of the intestinal wall, will it?
Of course it will. The white blood cells can’t see what’s in your stomach; they can’t see anything. All they can do is look for familiar patterns in amino acid and sugar molecules. They don’t know bacterial protein from pea protein from peanuts. They only know what they’ve learned from the progenitor white blood cells that handed them a description of a suspect that was seen in the area of inflammation in the past. The more often your intestine has been subject to episodes of inflammation, the more frequently your white blood cells will need to haul off different suspects into the interrogation room for questioning. Many interrogations are followed by the addition of a photo to the “most-wanted protein” scrapbook. Unlike the criminal justice system in the outside world, which only has to catch the bad guy once and his photo comes down off the wall, your immune system needs to remember his description for life, because bacteria have twins. Lots of twins. The very same pathogen can reappear time and time again. As you might imagine, the more protein profiles are compiled into the scrapbook, the more likely it is that white blood cells might misidentify a food-derived protein as matching the description of a previously booked criminal. Not an easy job for a white blood cell walking the beat of the intestine. And the job is made more complicated by the continued presence of vegetable-oil-induced inflammation.
One critical piece of evidence supporting the case that vegetable oil induces significant immune system disruption comes from a 1997 study in Taiwan entitled “Effects of Dietary Oxidized Frying Oil on Immune Responses of Spleen Cells in Rats.” Scientists fed one group of rats a diet containing 15 percent fresh soy oil, and fed another group of mice the same quantity of soy oil that had been used to make several batches of french fries—replicating the conditions in a typical restaurant. The feeding experiment lasted six weeks. Then, they evaluated the animals’ immune system function by examining the reaction of white blood cells in the spleen to a compound from bacterial cell membranes. They chose the spleen because it’s one of the locations where white blood cells congregate to exchange the latest immunological information—sort of like a briefing room for white blood cells. Their work showed that white blood cells of the rats 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
Wherever white blood cells patrol for pathogens, flooding their environment with pro-inflammatory oils is like asking these patrollers to search for bad guys in the midst of a thick fog while intoxicated. They get edgy, are quick to pull the trigger, feel confused—and the next thing you know, you have a corrupt force who has a tough time defending their choices about the innocent citizens they’ve unintentionally attacked. And when these otherwise well-meaning patrollers are forced to work in an impossible environment, they can go so far as to attack your body’s own proteins. This is the essence of all auto-immune disease. By inciting chaos, vegetable oil confuses the immune system and ultimately gets the body to turn on itself in ways that can lead to auto-immune brain disorders like multiple sclerosis, Lou Gehrig’s disease, Parkinson’s, and all the other neurodegenerative processes we now understand result at least in part from auto-immune attacks.
Once vegetable oils burn through your brain’s supply of antioxidants, antioxidant depletion can impair the ability of your brain to increase blood flow on demand, a process dependent upon normal endothelial function (the mechanism by which your body regulates blood flow, first introduced in chapter 7). 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 mental task you may be trying to accomplish, you can feel as if you’re not keeping up. What is more, as you’re about to see, vegetable oils can even put chronically overworked sections of your brain at risk for tiny strokes.
To understand how critical it is to maintain sufficient blood flow, it helps to realize that thinking hard—when learning a new task or concentrating on a complex problem, for instance—is effectively an athletic endeavor. By simply opening your eyes, you increase the blood flow to the area of your brain that processes visual input by 20 percent.346 If you sequentially tap your fingers against your thumb as fast as you can, you increase the blood flow to the motor cortex by 60 percent.347 So you might suspect that, just as you need better blood flow to support an athletic muscle, if you want to get better performance out of your brain to brighten your mood, enhance concentration, and improve cognitive abilities, blood flow is where it’s at. If you are healthy, your body can readily increase blood flow to the brain without increasing heart rate or blood pressure. How does your brain do this? Exactly the same way your muscles get more blood in times of increased need: by selectively dilating arteries in the tissues working the hardest. Arterial dilation instantaneously allows more blood to flow independent of any increased work on the part of the heart.
Just as endothelial function is essential to normal heart health and male sexual function, we now have two different lines of evidence supporting the idea that better endothelial function in your brain enables you to think more nimbly and sustain concentration for longer.
The first line of evidence comes from studies evaluating nitric oxide, the molecule (first introduced in Chapter 7) that sends a message to the muscles surrounding arteries to slacken, thus permitting dilation.348 When fuel supplies in a cluster of cells are running low, they produce nitric oxide. The nitric oxide in turn signals to nearby blood vessels that they need to dilate now in order to deliver more of the oxygen, glucose, glutamate, and other raw materials your brain cells need to maintain focus on the subject at hand.349
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
Another line of evidence supporting the direct link between blood flow and better brain power comes from studies on the antioxidant enzymes that support endothelial function by reducing oxidative stress and, in so doing, protect nitric oxide.355 Neuroscientists at University College, London, recently discovered a fascinating connection between an antioxidant enzyme system called CAT (for catalase) and several major markers of high cognitive functioning. They found “CAT activity correlated with … adaptability, stress management, [and] general mood.”356
On the heels of these discoveries linking bloodflow to cognitive function, in 2014, a collaboration of scientists led by researchers at the California Institute of Technology hypothesized that the feeling of brain fatigue you can get from trying to learn something new or thinking too hard about the same subject for too long may simply be a failure of your brain to deliver those raw materials on demand—literally, the food for thought. “We present a model of cognitive cost based on the novel idea that the brain senses and plans for longer-term allocation of metabolic resources by purposively conserving brain activity.” In other words, if there’s no fuel, there’s no thought. They continue: “We suggest that an individual’s decision of whether or not to incur cognitive costs in a given situation can be fruitfully understood as one of decision-making strategy: an agent will only commit limited resources in cases where the payoff is worth it.” In other words, reduced bloodflow to the brain reduces motivation for learning.357
This research has powerful implications for your ability to complete mentally demanding tasks. When you’ve been working on a project for a while—be it reading or doing your taxes—and get to a point where you feel you just can’t concentrate any longer, it may be a direct result of blood flow failure. Very much in the same way that an overtaxed muscle will twitch briefly before giving way, nerve cells of the cerebral cortex involved in running the task appear to be forced, by lack of fuel, to simply tap out for the moment, leaving you no choice but to take a break.
So what’s all this new research into blood flow and brain function got to do with vegetable oil? Earlier in this chapter we discussed how vegetable oil’s ability to generate oxidative stresses can often overwhelm all our antioxidant defense systems. And since antioxidants protect nitric oxide, that means they are likely to interfere with endothelial function. What’s more, you may recall that in Chapter 7 I explained how 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.358 Multiple studies report that vegetable oil consumption is followed by a kind of diet-induced arterial aging.359 While brain endothelial function after the ingestion of used frying oil has yet to be tested, there’s every reason to believe the effect would be the same. So when you feel fatigued or like you’re having a brain cramp, perhaps you literally are. Just as with a muscle cramp, when your ability to deliver nutrients and flush out waste products can’t stay apace with the biochemical demands of a muscle under exertion, the same physical limits are being imposed on your brain. On a related note, I’ve encountered athletes who make incredible performance gains in strength simply from cutting out vegetable oil. Why would that be? All athletes know that explosive bursts of muscular activity require intense concentration to sustain them. And I suspect that these anecdotal reports of massive, rapid strength gains may be made possible thanks to an improved ability to focus on physically demanding tasks.
So if you choose to load up on foods fried in vegetable oil right before you’re scheduled to take your IQ test, guess what: you got one question wrong before you even picked up the pencil. The sharpness of your mind—your thoughts, your focus, your ability to form and recall memories—all depend on adequate moment-to-moment blood flow, and, thus, vegetable oil blocks your mental flow.
In other words, when you lose the vegetable oil, you free your mind.
In the previous chapter, I explicitly warned men with erectile dysfunction (ED) to wake up to the fact that the condition is telling them something very important about their cardiovascular health. I don’t need to tell these men why Viagra can be a really good thing. But it can be a bad thing when it allows men with ED to brush aside a symptom indicative of a serious problem with their cardiovascular systems. In my perfect world, women would tell their pharmacologically ready-to-go partners, “I have a headache. And I’ll keep having a headache until you take your cardiovascular health more seriously.”
Well, ladies, I’m sorry to say it’s your turn for some bad news. If that headache you’re laying claim to is legitimate and the result of a migraine, we need to talk. Just as erectile dysfunction is a symptom to be taken seriously, if you’re a woman with a history of migraines, then you need to know about the latest research warning us that female migraine sufferers may be at significantly increased risk of stroke—no matter your age!360, 361, 362
I’m not talking about the kind of stroke your grandmother is likely to have. Those are typically associated with arteriosclerosis and very often occur in areas of the brain on the lowest rung of the blood supply pecking order, the so-called watershed areas that largely depend on diffusion for their nutrient supply. For the purposes of this discussion let’s define stroke as an event in which an area of brain is denied its requisite blood supply and is damaged to the extent that you can see it on an MRI. By that definition, young women with a history of migraines should be every bit as concerned about strokes—and what role their diet plays in their brain health—as their grandmothers.
In the previous section I described a link between impaired endothelial function in the cerebral cortex as a potential explanation for the feeling of mental burnout that makes you need to take a break. But what if you’re driving? Or taking an exam? Or your boss is breathing down your neck? Or for whatever reason, you simply can’t respond to your brain’s polite request for relief?
If 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, represented by 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 in other areas of the brain will commonly impair a person’s speech or cause weakness in half of the body.
Wherever it occurs, the electric disturbance results from severe, prolonged endothelial dysfunction reducing blood flow to the point that it forces nerve cell metabolism to slow so much that energy production drops.365 If those energy levels drop below a critical threshold, the neurons can essentially go into spasm, like a docked fish flopping around as it fights for air, biochemically overexciting themselves almost to death.
In the 1990s neuroscientists used PET scanners on migraine patients during the aura just preceding a migraine to better understand the pathophysiology of an attack. They discovered that the aura phase of a migraine is associated with a dramatic reduction of blood flow in the affected area of the cerebral cortex.366, 367 While the triggers for migraines are variable and often unpredictable—MSG, red wine, dehydration, hormone fluctuations, stress—the duration of the aura is remarkably consistent: ten to thirty minutes.
The aura begins with a reduction of cerebral blood flow in a small segment of gray matter, and the phenomenon quickly spreads. The initially impacted section soon grows electrochemically unstable, and suffers abnormally prolonged electric pulses. In response, the blood vessels in this localized area constrict, reducing blood flow even further—perhaps in a kind of last-ditch attempt to shut down abnormal nerve activity in this defined area before it either triggers a seizure or kills the affected neurons. This constriction, however, means that nearby areas will now lack adequate blood as well, causing these surrounding sections to be similarly affected. This, in turn, expands the area of disturbance to the next adjacent brain region, and the next, and the next, and so on. (Hence the “spreading” in cortical spreading depression.) The disturbance expands across the brain at a rate of one to two millimeters per minute over the course of ten to thirty minutes until an entire lobe has been affected. At this point, for unknown reasons (perhaps because the muscles contracting the arteries have run out of the calcium or other fuel required to sustain the constriction), the blood vessels suddenly dilate. This dilation opens the floodgates, allowing blood to come rushing back in, arresting the spreading depression. It also coincides precisely with the point in time that many patients in the studies report developing pain and other common migraine symptoms such as nausea, light and sound sensitivity, and fatigue.
The dilation and restoration of blood flow successfully halts the spreading depression phenomenon, but this desperate attempt by the nervous system to quash the electrical storm takes its toll. The nerves deprived of oxygen were barely getting blood for ten to thirty minutes, and now are badly damaged. While cut off from their energy supply, numerous cellular activities had to grind to a screeching halt, causing buildup of intracellular toxins and the increased membrane permeability that permits leakage of valuable supplies. The affected nerves then release inflammation-promoting chemicals called cytokines to signal emergency repair crews. While cytokines are necessary for the damaged nerves to get the attention they require, the inflammation diffuses to delicate nerve endings in the lining of the brain (called the meninges), sensitizing them. This, neuroscientists believe, is why migraine pain is usually accompanied by hyper-responsiveness to light, sound, and other sensory input—even including the pulsations of the brain’s own blood vessels.368
It makes sense that the symptoms attendant to this spreading depression event sound a lot like the symptoms of a stroke. Both result from diminished blood flow. Given this, neurologists in multiple academic centers began to wonder about a link between migraine and abnormal brain MRI findings they’d been attributing to atherosclerotic stroke, called deep white matter hyper-intensities. These are bright areas that appear on MRI images of the brain to look like shining craters on the surface of the moon. The question of a possible link between migraine and stroke occurred to these scientists because many white matter hyper-intensities showed up in women without any of the typical risk factors for stroke: smoking, diabetes, hypertension, and atherosclerosis. What they did share was a history of migraine.
To investigate the possibility that these abnormalities could develop as a direct result of migraines in the absence of other risk factors, they designed a nine-year study following two groups of people, both men and women, 203 with migraines and 83 without (to serve as a control group). The study, published in JAMA in 2012, showed no obvious link in the men. The women, however, told quite a different story.369
Thirty percent of the women who had a history of migraines developed ten or more lesions within the nine-year span of the study. Of those without a history of migraine, only 9 percent developed as many lesions. Among the women with migraine, white matter hyper-intensities were also more diffusely distributed than among controls, which were generally localized to the watershed areas of the brain, just as you’d expect with atherosclerotic strokes. The younger the subject with globally dispersed lesions, the more likely it was that she had the diffuse lesions. The authors theorized it might be a matter of different strokes for different folks. While members of the younger group were developing mini strokes as a complication of their migraines, those in the older group were more likely developing silent embolic strokes due to atherosclerosis.370
So what are we to take from all this?
Although failure to achieve an erection may mean that you’re simply not in the mood, and although a migraine might be nothing more than the natural consequence of stress or hormone fluctuation, in the context of a modern diet where vegetable oil is so ubiquitous it’s difficult to avoid, migraines, just like ED, should serve as a reminder that it’s always the right time to get vegetable oils out of your diet. At least as much as you can.
A brain whose supply of antioxidants has been cut off is like a forest during a drought, cut off from its supply of rejuvenating rain, a tinderbox vulnerable to the smallest spark of lighting. One thing that can spark off a firestorm of neurologic damage is a concussive injury; even a mild concussion can instigate damaging inflammation and oxidation. But continuing research now indicates that a diet rich in vegetable oils may, in a very literal way, also add fuel to the slow-burning fire of oxidative stress associated with chronic progressive diseases, including Alzheimer’s.
Hollywood loves blowing things up. How many times have you watched the scenes where the movie’s hero is walking toward the camera, triumphantly, while the background expands in a brilliant orange ball of fire as a building or a car or a bridge or what-have-you explodes, usually in super slo-mo. On the other hand, how many times have you watched the scene where the hero walks toward the camera while in the background a large metal object quietly grows covered in rust, or a heap of bananas develop brown spots indicating ripeness, or a fallen tree gradually rots. My guess is you’ve never seen such a scene. But though a rotting pile of bananas doesn’t make for a thrilling action movie trailer, chemically, these imperceptibly slow reactions represent the same process that drives an explosion: oxidation. The major difference between an explosion and the other oxidative processes is time. Explosions happen in the blink of an eye. Ripening, rotting, and rusting occur over days or months or years.
Oxidation reactions are ongoing in our bodies all the time. We breathe oxygen because, thanks to mitochondrial enzymes, we can harness the power of oxygen to turn fat and sugar into chemical energy with a high degree of efficiency. But nothing in this universe is 100 percent efficient. So sometimes oxygen goes about its business in our bodies without enzymatic supervision, generating random reactions that our bodies do not want. It’s these random oxidation reactions that rust and rot us slowly from the inside out, playing a primary role in the natural aging of the body. 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.)
I’d like to tell you that the Human Diet can completely halt oxidation and its effects on your body, allowing you to live for hundreds of years, if not indefinitely. But that wouldn’t be true. What is true is that a vegetable-oil-free/high-antioxidant diet, along with plenty of restorative sleep and exercise, is the best strategy to slow the oxidation in your brain so you can remain sharp and independent, ideally, until the day you die.
The two factors most powerfully impacting whether you spend your final decades living your life as you’d have it or lose yourself in the devastation of moderate or severe Alzheimer’s are: (1) the rate at which your brain is exposed to oxidative damage; and (2) your brain’s ability to control oxidative damage.371 Every day of your life, your brain is engaged in a battle for control over oxidation, and the rate at which your brain ages depends largely on the daily balance of that battle. If oxidation wins the day, your brain is moved a little further toward premature aging. If oxidation is kept in check—and you keep oxidation in check day by day and year by year—then you get to keep your wits and your memory and your sense of self, ideally, for the rest of your life.
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.
Back in the 1990s, I noticed that my patients who’d gone to the emergency room after mild head trauma, and then been cleared to safely go home based on normal CT or MRI brain scans, would sometimes come to my office still impaired and not sure why. One patient, a nurse who had hit her head on an open kitchen cabinet at home a few days earlier, found herself staring blankly at a bottle of lidocaine she was supposed to prepare for the doctor she was assisting, her memory of the details of a procedure she’d performed thousands of times completely blanked out. Another, a secretary in the local university English department, had been struck while crossing the street by a slow-moving car that, in his words, “barely knocked my head” but came to me weeks later wondering if there was a connection between that minor accident and the sudden onset of headaches, dizziness, and attention deficits that had made it impossible to keep up with the usual routines of his job and were worrisome enough that he began to question his sanity.
At that time, the only explanation I could offer was based on what an attending neurosurgeon told me while on call with the hospital’s trauma team back in medical school. It was after midnight in a dimly lit hospital radiology reading room as we were waiting for a victim of a New Jersey Turnpike motorcycle accident to finish his forty-minute run through the CAT scanner. The neurosurgeon explained that even with a normal scan—done primarily to catch life-threatening bleeding—the patient’s brain might be seriously impaired. Such radiographically invisible forms of damage result not so much from the initial physical impact, which causes compression, but from the secondary rebound and expansion as the soft, fragile brain sloshes back and forth inside the skull, stretching the long, slender axons that conduct electricity from one nerve cell body to one another.
Later that same night, because it turned out the patient’s brain was bleeding and the mounting pressure could kill him, the surgeon instructed me on how to drill a hole in the skull to help release the buildup of fluid. It’s a straightforward procedure: just drill through a certain spot like you’d drill through drywall, while being extremely careful to avoid poking too far through the other side. What I remember most was when he encouraged me to “appreciate the texture” of the man’s living brain by reaching my pinky finger through the little burr hole. It was terrifyingly soft, exactly like the bowl of oatmeal I had eaten for breakfast that morning in the hospital cafeteria. After experiencing the delicate structure of the brain, literally firsthand, it was easy for me to appreciate how even a mild knock like bumping your head on a cabinet could stretch, or even tear, axons.
As with any insult to body tissue, a brain injury precipitates an inflammatory reaction that can persist for days, weeks, or even months. This post-trauma inflammation can give rise to any number of post-concussive symptoms, even following a seemingly minor bump to the head. Happily, as the inflammation subdues, the cognitive deficits diminish and finally disappear.
Except, that is, when they don’t. Sometimes problems continue to wax and wane for years, never allowing the head-injured person to return to full capacity at home or work. Sometimes symptoms will even worsen over time. This begs the question: Why do some people with seemingly minor impacts develop significant and worsening problems while others with more serious trauma fully recover? I think the difference lies in part in the post-concussive conditions that either facilitate or disrupt the dynamic processes of healing in the hours, days, weeks, and months following the initial injury.
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
In those cases where a person walks away from major head trauma without suffering cognitive problems, it’s likely because their membranes were preloaded with antioxidants that helped to contain the free radical reactions, inhibiting oxidative reactions and “cooling” the inflammation thought to be responsible for the “injury after the injury” catalyzed by the initial concussive event. The brain armed with a rich supply of antioxidants and free of pro-oxidative MegaTrans is poised to defend itself against the ravages of oxidative stress and can more quickly get to the business of repairing damaged tissues. Mechanical engineers design helmets to protect the skull from an initial concussive event; an anti-oxidative/anti-inflammatory diet is designed—as just one of its many benefits—to protect the concussed brain itself, and help it heal.
Emergency room staff know the phrase well: time is brain. They’re talking about time between the onset of stroke symptoms and the threading of a catheter into the internal carotid artery to release clot-busting drugs. But the phrase applies aptly to a head-injured person’s need to control oxidation reactions. 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.
In 2002 a brilliant humble Nigerian-born pathologist named Bennet Omalu showed the world what OTD looked like. In examining a thin section of a deceased NFL player’s brain, he found something very surprising: brown comma-like splotches reminiscent of bats hanging from cave ceilings—tau proteins. Tau proteins had long been recognized as a hallmark of Alzheimer’s.374 And though the football player had died at forty-five, Omalu had found tau protein concentrations consistent with “a ninety-year-old brain with advanced Alzheimer’s.”375
When he published his paper describing his findings, the now infamous initial reaction from the NFL was one of denial. Dr. Omalu’s conclusion couldn’t possibly be true. So years went by, and nothing changed. Only after more NFL players and their families stepped forward to share their tragic stories—of memory loss, depression, anxiety, aggression, and even suicide—did the league finally take any action.
A critical part of that action was to change the guidelines that athletic trainers follow when dealing with players who have had their “bells rung.” Since that change, concussed football players are now examined carefully before they’re allowed to re-enter the game, as a secondary head trauma of an already concussed player can have multiplier effect on the player’s already wounded brain, diminishing his chances of a positive recovery outcome. My hope is that as more team doctors and other medical professionals understand the important role oxidative stress plays in traumatic brain injury (TBI) recovery, more steps will be taken to coddle the post-concussive brain with a combination of stress reduction, plenty of restorative sleep, and dietary intervention to give the player every possible chance of complete recovery.
It’s important that you fully understand how the healthy brain formula can help you to make the best real-world choices. And to do that, it’s crucial to understand the relationship between your brain (particularly the PUFA fatty acids in your brain), the highly pro-inflammatory MegaTrans delivered to your brain through the consumption of vegetable oils, and the arsenal of protective, diet-derived antioxidants whose beneficent function is to protect plant and animal tissues, including the tissues of your brain, from oxidative damage.
Think of a healthy brain as a forest that gets plenty of rainfall. Everywhere you look, there are lush, verdant leaves, babbling creeks, ponds or marshes—the kind of forest that relaxes and restores the senses. The forest’s health is a direct result of receiving all the moisture that its ecology has, over millennia, come to depend on and expect. The water—from rain, the water table, the moisture sustaining the soil where fungus recycles organic matter—is like antioxidants in the brain, an especially fitting metaphorical element, as moisture does in fact act as an antioxidant in the prevention of the wildly oxidative event of a forest fire. Now imagine lightning striking this healthy forest: this is a concussion. In our healthy, moist forest, a single lightning strike is unlikely to start a fire. And if it does, it probably won’t be a major fire; it’ll likely burn for a little while in a contained area and then burn itself out.
If a lush, moist forest is like a healthy brain, a brain without a rich complement of antioxidants is like a forest in a drought. The creeks that used to flow have been reduced to a trickle or, worse, a ribbon of cracked, dry mud. Brittle leaves and pine needles crunch underfoot. And the earthy scent of mushroom and loam is absent—just the smell of dust is in the air. It’s as if the trees themselves sense what you sense, that this once verdant wonderland has been reduced to a tinderbox ready to go up in flames with the first spark. And that’s exactly what happens when a single finger of heat lightning flickers down to touch the ground.
As long as we’re in this forest, let’s add one more metaphoric element: an abandoned meth lab in the middle of the drought-dry woods. Much like the MegaTrans fat in vegetable oil, a meth lab is something even drought-stressed forests have not had to deal with until very recently. You see, this drug lab is a real hazard, littered as it is with cans of accelerant—paint thinners, gasoline, and other dangerous flammables that, when the heat rises from the fire, are ready to explode.
Keep this metaphor in mind, because it’s shorthand for understanding how, in the discussion of creating the best possible healing environment for a concussed brain, we must take into consideration not just vegetable oil or antioxidants alone but rather the two together. So now it should be easy to see that the best-case healing environment is a diet rich in antioxidants (fresh vegetables, herbs, and spices) and free of vegetable oils. A suboptimal environment is one in which the diet is either rich in vegetable oils and rich in antioxidants or absent of vegetable oils and low in antioxidants. And the worst possible dietary scenario is a diet absent in antioxidants but rich in vegetable oil—this creates the metaphorical dessicated forest with a meth lab right in the middle of it.
I’ll be taking on sugar and its effects in the next chapter, but for now I should at least mention that MegaTrans fat and sugar, taken together, create a particularly volatile combination—let’s say that two cans of two different chemicals in the meth lab are wildly explosive when combined. You’ll learn more about why this combination is so deadly a little later on, and why reducing sugar while reducing vegetable oil consumption and increasing dietary intake of antioxidant-rich veggies during concussion recovery is a simple, low-cost, no-risk strategy to rebuilding the healthy rainforest of the brain.
Certainly, more research and more funding need to be focused on the very important question of how much we can improve TBI outcomes with diet. Until that happens, and until those findings are applied in a clinical setting, this physician will continue to cringe whenever I consider typical hospital food: the trays of canola-grilled overcooked meats, the canola or soy or cottonseed salad dressing, the whipped margarine on toast, the uninspiring tasteless vegetables, and the fruit punch and tapioca pudding topped with a dollop of hydrogenated vegetable oil. My antidote for this thought is the hopeful image of a future mixed martial arts superstar one day publicly attributing his or her speedy and full recovery to the caring and talented hospital chef who was allowed to cook for his patients as if food really were medicine.
As you now understand, PUFAs are particularly prone to chemical degradation, which is why factory refining of PUFA-rich vegetable oils generates highly toxic compounds. The most toxic of these many compounds are present only in trace amounts in bottles off the shelf, but because of the zombie effect (discussed in Chapter 7), they multiply when reheated, and continue to multiply in your body even after you’ve consumed them. What makes these compounds so toxic to your brain? In addition to the mechanisms already discussed, they also cause the breakdown of the subcellular highways essential for normal nerve function, giving rise to delays in learning in early life, or, as we age, even dementia.
The idea that vegetable oil is a brain killer rests on the reality that it’s swirling with toxic compounds. One of the worst is called 4-hydroxy-2-nonenal, or 4-HNE. Like many of the toxic fats produced by refining vegetable oils, 4HNE is derived from an omega-6 essential fatty acid our bodies require for optimal function, called linoleic acid. The processing steps (discussed in Chapter 7) squeeze the seeds too hard, distort their fragile fats, and lead to production of 4-HNE, along with other mutated versions of once-healthy PUFA fats. Present in trace amounts in bottles straight off the shelf, when the oils are used to cook your dinner, 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. In a 2002 study conducted by researchers in Osaka, Japan, rats were given an anti-gout drug called colchicine to prevent the formation of new microtubules. These rats were unable to learn their way through a maze.378
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. The job of tau protein is to stabilize the cellular microtubule highways similar to the way steel girders support the concrete and asphalt of an elevated roadway. Take away the girder, and the elevated roadway goes crashing to the ground. Take away tau protein, and the microtubule structure dismantles itself. As researchers in Rome described it in 2012, “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 What they don’t have is the ability to make new synaptic connections. It turns out intact microtubules allow for the steady delivery of supplies essential for the development of new synapses, which are, in turn, essential for the development of new memories. This is why the common findings of MCI include things like repeatedly asking questions, making the same comments, or forgetting an important event—say, a big meeting or a friend’s birthday, when that’s something you wouldn’t have done before.
If you’re getting the feeling that I’ve declared war on vegetable oil, you’re exactly right. But it’s not for nothing. Now that you’ve seen up close the specific mechanisms by which vegetable oil robs your brain of the ability to form new memories, I hope that you feel like picking up a weapon and joining the fight. Nothing takes away your identity the way Alzheimer’s does, with one possible exception: when the effects of vegetable oil reach past the individual and rearrange the genes that will help define the identity of your children, as in the case of Autism.
WHY THE AUTISTIC BRAIN IS UNIQUELY UNIQUE
The brains of autistic children can exhibit every manner of growth anomaly. They can be overly large due to a failure of non-contributing nerve cells to undergo the natural process of cell death that allows for normal structural development of the brain. 384 Children with autism can have unusually high numbers of local cellular connections and fewer long-distance connections.385 They can have completely novel connections between two areas of the brain, or between an area of the brain and some other part of the body,386 disrupting movement. Differences can be seen even at the cellular level, such as smaller cell bodies, or atypically low connectivity between nerves (called synapses).387 The layers of the brain may not develop completely, so that the six distinct layers of gray matter are dimpled with interruptions where no differentiation is present.388
What does all this mean for the autistic child’s day-to-day experiences? This is one of the most troubling mysteries for the parent of an autistic child, and one for which there is no easy answer. To help guide us, we can listen to, and learn from, children affected by autism who have the language to express themselves, who describe profoundly uncomfortable sensory reactions to input that most of us take for granted. When asked why autistic children perform repetitive behaviors, Carly, a young woman affected by autism who cannot speak but is eloquent on a computer keyboard, explains, “You don’t know what it feels like to be me. When you can’t sit still because your legs feel like they’re on fire. It’s a way for us to drown out all sensory input that overloads us all at once. We create output to block input.”389
Autistic children tend not to make eye contact. Some have attributed this avoidance, perhaps wrongly, to a lack of interest in other people. Carly’s story, and her continuing contribution to the autism discussion, tells us that sometimes this behavior may stem not from a lack of ability, but from a capability so acute that it leads to distraction. “Our brains are wired differently…. I see over a thousand pictures of a person’s face when I look at them. That’s why I have a hard time looking at people.”390
Could Carly’s sensory processing disturbances arise from one or more of the structural brain anomalies associated with autism? My sense is absolutely yes. And because, as with all autistic children, Carly’s brain is unique—more so, by far, than those of non-autistic kids—each child’s sensory experiences, capabilities, and impairments are their own.
There was a patient I got to know during the years I was in Hawaii who I’ll never forget because she almost always spent the entire office visit in tears. For good reason: her life was a mess. Once a successful realtor and part-time model, after having a son followed by a set of twin boys one year later, it seemed like nothing could go right for her. The first son was diagnosed with a learning disorder and Attention Deficit Disorder (ADD), and her twins were both on the autism spectrum. She lost her job, got divorced, gained 150 pounds, and though she tried to put a bright face on things, she did not seem like a happy woman.
I met her as the twins were entering puberty, their bodies flush with testosterone and not dealing with it well at all. In spite of the fact that the state provided her with four full-time in-home staff to cover twenty-four-seven care, bursts of unexpected violence were part of daily household routines. Lamps shattered. Tables upturned. On several occasions she came in with bite wounds to her hands requiring antibiotics. Once, she pulled out of her purse a clump of hair attached to a tiny section of her own scalp—torn off in the prior day’s scuffle. She loved her children. She didn’t blame the twins for their behavior. But she was devastated to a breaking point by the lack of normal human connection.
Many times she’d look me in the eyes and say “I know they’re in there,” and then she’d break down. I couldn’t begin to grasp the depth of her loneliness, until one day she managed to follow the thought with “because they only act out at me. They never hurt the staff.” That their anger had a consistent trajectory was her singular indication that she had any particular significance to her twins at all. She hung on to it like a lifeline.
I’d like to tell you that she implemented the Human Diet in her household and suddenly everyone got along, but she couldn’t change the family’s diet—even though she desperately wanted to; her life was too chaotic. This story has no happy ending. I don’t retell it here because I believe that children on the spectrum cannot be as wonderful and loving as typical children. Most children on the spectrum are doing leaps and bounds better than my patient’s twins in Hawaii. I tell the story of this woman’s unending trial to make a very important point: there are some disorders that take your children away from you and you can never get them back. I want to stop that from happening.
And I believe we can.
The very first diagnostic manual for psychiatric disorders published in 1954 described autism simply as: “schizophrenic reaction, childhood type.”391 The next manual, released in 1980, listed more specific criteria, including “pervasive lack of responsiveness to other people” and “if speech is present, peculiar speech patterns such as immediate and delayed echolalia, metaphorical language, pronominal reversal (using you when meaning me, for instance).”392 Of course, the terse language of a diagnostic manual can never convey the real experience of living with a child on the spectrum, or living on the spectrum yourself.
When I graduated from medical school, autism was so rarely diagnosed that none of my psychiatry exams even covered it and I and my classmates were made aware of autism more from watching the movie Rain Man than from studying course material. The question of whether autism (now commonly referred to as ASD) is more common now than it was then or whether we are simply recognizing it more often is still controversial. Some literature suggests that it is a diagnostic issue, and that language disorders are being diagnosed less often as autism is being diagnosed more. However, according to new CDC statistics, it appears that autism rates have risen 30 percent between 2008 and 2012. Considering that diagnostic criteria had been stable by that point in time for over a decade, increased diagnosis is unlikely to be a major factor in this 30 percent figure.393
Given these chilling statistics, it’s little wonder that so many research dollars have been dedicated to exploring possible connections between exposure to various environmental factors and development of the disorder. Investigators have received grants to look into a possible link between autism and vaccines,394 smoking,395 maternal drug use (prescription and illicit),396, 397, 398 organophosphates,399 and other pesticides,400 BPA,401 lead,402 mercury,403 cell phones, 404 IVF and infertility treatments,405 induced labor,406 high-powered electric wires,407 flame retardants,408 ultrasound,409—and just about any other environmental factor you can name. You might be wondering if they’ve also looked into diet. But of course: alcohol,410 cow’s milk,411 milk protein,412 soy formula,413 gluten,414 and food colorings415 have all been investigated. Guess what they’ve never dedicated a single study to investigating? Here’s a hint: it’s known to be pro-oxidative and pro-inflammatory and contains 4-HNE, 4-HHE, and MDA, along with a number of other equally potent mutagens.416 Still haven’t guessed? Okay, one last hint: it’s so ubiquitous in our food supply that for many Americans it makes up as much as 60 percent of their daily caloric intake,417 a consumption rate that has increased in parallel with rising rates of autism.
Of course, I’m talking about vegetable oil. In Chapter 2, I discussed in some detail how and why gene transcription, maintenance, and expression are necessarily imperiled in the context of a pro-inflammatory, pro-oxidative environment, so I won’t go further into that here. 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.
First, let’s revisit 4-HNE (4-hydroxynonanol), which you may recall meeting in the above section on firebombing the highways. This is perhaps the most notorious of all the toxic fats derived from oxidation of omega-6 fatty acids, whose diversity of toxic effects requires that entire chemistry journals be devoted to 4-HNE alone. When the mutagenicity (ability to mutate DNA) of 4-HNE was first described in 1985, the cytotoxicity (ability to kill cells) had already been established for decades. The authors of a 2009 review article explain that the reason it had taken so long to recognize that HNE was such an effective carcinogen was largely due to the fact that “the cytotoxicity [cell-killing ability] of 4-HNE masked its genotoxicity [DNA-mutating effect].”419 In other words, it kills cells so readily that they don’t have a chance to divide and mutate. How potently does 4-HNE damage human DNA? 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!
THE ECONOMICS OF GENETIC WEALTH
“I am autistic. But that’s not who I am.” This is how Carly, the autistic girl I mentioned earlier, describes the struggle between her autism and what she considers to be her true identity. I suspect many autistic kids would relate to that experience. While some people with autism are extremely capable, live independently, and contribute to the betterment of our world, most never really break out of their isolation.
And given that the lifetime cost of care for each child has recently been estimated at $1.2 to $2.4 million, I think it’s safe to say that if we, as a society, have the option of giving each child a better chance at typical health by reducing the rate of autism, we would benefit economically.418
And it does boil down to economics. Autism is, in my estimation, just another complication of the industrial diet, together with obesity, diabetes, sleep apnea, hypertension, Alzheimer’s, and cancer. All these stem from the decision to ignore nutritional practices that fortified our ancestors with genetic wealth. This decision was economically driven. If what we want is cheap food, and the marketplace has spoken loud and clear in saying yes, we want cheap food, then that means we get industrial seed oils instead of grass-fed butter or extra virgin unrefined olive oil, or any of the other traditional fats that cost more to make.
How much more does healthy fat cost, compared to toxic fats? When I asked my friend, Chef Debbie Lee, a restaurant consultant, she estimated the cost of using olive oil in place of one of the vegetable oils would come out to roughly fifty cents a plate. We understand financial economics because you can hold a dollar in your hand. My hope is that we will some day see more value in the economics of genetic wealth and come to appreciate the immeasurable value of the gifts of a healthy body and mind.
Second, 4-HHE (4-hydroxy-hexanal), which is very much like 4-HNE, his more notorious bigger brother derived from omega-6, but 4-HHE is derived instead from omega-3. If bad guys had sidekicks, 4-NHE’s would be 4-HHE. Because 4-HHE does many of the same things to DNA as 4-HNE, but has only been discovered recently.422 You see, when omega-6 reacts with oxygen, it breaks apart into two major end products, whereas omega-3, being more explosive, flies apart into four different molecules. This means each one is present in smaller amounts, and that makes them a little more difficult to study. But it doesn’t make 4-HHE any less dangerous. 4-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
Finally, there is malonaldehyde (MDA), proven to be a mutagen in 1984, but presumed to only come from consumption of cooked and cured meats.426 Only in the past few decades have we had the technology to determine that MDA can be generated in our bodies as well.427 And unlike the previous two chemicals, MDA is generated by oxidation of both omega-3 and omega-6. It may be the most common endogenously derived oxidation product. Dr. J. L. Marnett, who directs a cancer research lab at Vanderbuit University School of Medicine, Nashville, Tennessee, and who has published over 400 articles on the subject of DNA mutation, summarized his final article on 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
There’s one more thing I need to add about vegetable-oil-derived toxic breakdown products, particularly given the long list of toxins now being investigated as potential causes of autism spectrum disorders. Not only do they directly mutate DNA, they also make DNA more susceptible to mutations induced by other environmental pollutants.429, 430 This means that if you start reading labels and taking vegetable oil out of your diet, your body will more readily deal with the thousands of contaminating toxins not listed on the labels which are nearly impossible to avoid.
Why all this focus on genes when we’re talking about autism? Nearly every day a new study comes out that further consolidates the consensus among scientists that autism is commonly a genetic disorder. The latest research is focusing on de novo mutations, meaning mutations neither parent had themselves but that arose spontaneously in their egg, sperm, or during fertilization. These mutations may affect single genes, or they may manifest as copy number variations, in which entire stretches of DNA containing multiple genes are deleted or duplicated. Geneticists have already identified a staggering number of genes that appear to be associated with autism. In one report summarizing results of examining 900 children, scientists identified 1,000 potential genes: “exome sequencing of over 900 individuals provided an estimate of nearly 1,000 contributing genes.”431
All of these 1,000 genes are involved with proper development of the part of the brain most identified with the human intellect: our cortical gray matter. This is the stuff that enables us to master human skills: the spoken language, reading, writing, dancing, playing music, and, most important, the social interaction that drives the desire to do all of the above. One need only have a few of these 1,000 genes involved in building a brain get miscopied, or in some cases just one, in order for altered brain development to lead to one’s inclusion in the ASD spectrum.
So just a few troublemaker genes can obstruct the entire brain development program. But for things to go right, all the genes for brain development need to be fully functional.
Given that humans are thought to have only around 20,000 genes, and already 1,000 are known to be essential for building brain, that means geneticists have already labeled 5 percent of the totality of our genetic database as crucial to the development of a healthy brain—and we’ve just started looking. At what point does it become a foolish enterprise to continue to look for genes that, when mutated, are associated with autism? When we’ve identified 5,000? Or 10,000? The entire human genome? At what point do we stop focusing myopically only on those genes thought to play a role in autism?
I’ll tell you when: when you learn that the average autistic child’s genome carries de novo mutations not just in genes thought to be associated with autism, but across the board, throughout the entirety of the chromosomal landscape. Because once you’ve learned this, you can’t help but consider that autism might be better characterized as a symptom of a larger disease—a disease that results in an overall increase in de novo mutations.
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 An international working group on autism pronounced this startling finding in a 2013 article entitled: “Global Increases in Both Common and Rare Copy Number Load Associated With Autism.”433 (Copy number load refers to mutations wherein large segments of genes are duplicated too often.) What the article says is that yes, children with autism have a larger number of de novo mutations, but the majority of their new mutations are not statistically associated with autism because other kids have them, too. The typically developing kids just don’t have nearly as many.
These new mutations are not only affecting genes associated with brain development. They are affecting all genes seemingly universally. What is more, there is a dose response relationship between the total number of de novo mutations and the severity of autism such that the more gene mutations a child has (the bigger the dose of mutation), the worse their autism (the larger the response). And it doesn’t matter where the mutations are located—even in genes that have no obvious connection to the brain.434 This finding suggests that autism does not originate in the brain, as has been assumed. The real problem—at least for many children—may actually be coming from the genes. If this is so, then when we look at a child with autism, what we’re seeing is a child manifesting a global genetic breakdown. Among the many possible outcomes of this genetic breakdown, autism may simply be the most conspicuous, as the cognitive and social hallmarks of autism are easy to recognize.
As the authors of the 2013 article state, “Given the large genetic target of neurodevelopmental disorders, estimated in the hundreds or even thousands of genomic loci, it stands to reason that anything that increases genomic instability could contribute to the genesis of these disorders.”435 Genomic instability—now they’re on to something. Because framing the problem this way helps us to ask the more fundamental question, What is behind the “genomic instability” that’s causing all these new gene mutations?
In the section titled “What Makes DNA Forget” in Chapter 2, I touched upon the idea that an optimal nutritional environment is required to ensure the accurate transcription of genetic material and communication of epigenetic bookmarking, and how a pro-oxidative, pro-inflammatory diet can sabotage this delicate operation in ways that can lead to mutation and alter normal growth. There I focused on mistakes made in epigenetic programming, what you could call de novo epigenetic abnormalities. The same prerequisites that support proper epigenetic data communication, I submit, apply equally to the proper transcription of genetic data.
A FOUR-STEP PATH TO UNDERSTANDING AND PREVENTING AUTISM
1. Acknowledge that autism is not an isolated disease, but rather one of a number of possible symptoms that arise with increasing frequency from an underlying problem, a ten-fold increase in de novo mutations (those muta-tions that neither parent had but the child does). Until someone comes up with a better name, let’s call it De Novo Gene Mutation Syndrome.
2. Get to work learning how to prevent De Novo Gene Mutation Syndrome.
3. Understand that there will be no technological solution to De Novo Gene Mutation Syndrome.
4. Focus on identifying the healthy reproductive environment that has allowed DNA to produce healthy children with normally developed brains for thousands of generations.
What’s the opposite of a supportive nutritional environment? A steady intake of pro-inflammatory, pro-oxidative vegetable oil that brings with it the known mutagenic compounds of the kind I’ve just described. Furthermore, if exposure to these vegetable oil-derived mutagens causes a breakdown in the systems for accurately duplicating genes, then you might expect to find other detrimental effects from this generalized defect of gene replication. Indeed we do. Researchers in Finland have found that children anywhere on the ASD spectrum have between 1.5 and 2.7 times the risk of being born with a serious birth defect, most commonly a life-threatening heart defect or neural tube (brain and spinal cord) defect that impairs the child’s ability to walk.436 Another group, in Nova Scotia, identified a similarly increased rate of minor malformations, such as abnormally rotated ears, small feet, or closely spaced eyes.437
What I’ve laid out here is the argument that the increasing prevalence of autism is best understood as a symptom of De Novo Gene Mutation Syndrome brought on by oxidative damage, and that vegetable oil is the number-one culprit in creating these new mutations. These claims emerge from a point-by-point deduction based on the best available chemical, genetic, and physiologic science. To test the validity of this hypothesis, we need more research.
DOES DE NOVO GENE MUTATION SYNDROME AFFECT JUST THE BRAIN?
Nothing would redirect the trajectory of autism research in a more productive fashion than reframing autism as a symptom of the larger underlying disease, which we are provisionally calling de novo gene-mutation syndrome, or DiNGS. (Here’s a mnemonic: vegetable oil toxins “ding” your DNA, like hailstones pockmarking your car.)
If you accept my thesis that the expanding epidemic of autism is a symptom of an epidemic of new gene mutations, then you may wonder why the only identified syndrome of DiNGS is autism. Why don’t we see all manner of new diseases associated with gene mutations affecting organs other than the brain? We do. According to the most recent CDC report on birth defect incidence in the United States, twenty-nine of the thirty-eight organ malformations tracked have increased.438
However, these are rare events, occurring far less frequently than autism. The reason for the difference derives from the fact that the brain of a developing baby can be damaged to a greater degree than other organs can, while still allowing the pregnancy to carry to term. Though the complex nature of the brain makes it the most vulnerable in terms of being affected by mutation, this aberration of development does not make the child more vulnerable in terms of survival in utero. The fact that autism affects the most evolutionarily novel portion of the brain means that as far as viability of an embryo is concerned, it’s almost irrelevant. If the kinds of severely damaging mutations leading to autism were to occur in organs such as the heart, lungs, or kidneys, fetal survival would be imperiled, leading to spontaneous miscarriage. Since these organs begin developing as early as four to six weeks of in-utero life, failure of a pregnancy this early might occur without any symptoms other than bleeding, which might be mistaken for a heavy or late period, and before a mother has even realized she’s conceived.
If enough individuals can agree that the identity-robbing nature of ASD is something we’d like not to invite into our lives; and if we can shake loose this debilitating sense that the only action we can take against this epidemic is crossing our fingers with each pregnancy and praying that the little boy on the way will not be the one in forty-two who will be affected,439 then perhaps researchers will feel compelled to look into vegetable oil consumption as a contributing factor. And every bit as important—as research is driven by consumer behaviors as much as anything else—if enough grocery shoppers and restaurant goers indicate with their purchasing dollars that they know their reproductive health depends on an antioxidant-rich, low-toxin diet, and specifically seek out vegetable-oil-free products, then the flow of research money will, in short order, begin to be redirected toward a better understanding of the role vegetable oil plays in robbing children of their genetic birthright.
DE NOVO MUTATIONS IN MEN VERSUS WOMEN
A number of studies have shown that older fathers are more likely to have autistic children. According to a 2011 study, a fifty-year-old, when compared to a man younger than thirty, carries 2.2 times the risk of having a child with autism. 440 As I discuss in this chapter, some level of de novo mutations are inevitable, even in the context of a perfect diet. The reason children born to older fathers are more likely to develop autism is that de novo mutations accumulate in a man’s sperm-producing cells (called spermatogonia) as he ages, so that the older he gets the more mutations a given sperm will carry. But, because vegetable oils are genotoxic, it’s not that much of a leap to suggest that the more vegetable oil a man exposes himself to, the more mutations his spermatogonia produce. I would, therefore, expect that if a man is following a typical American diet, with up to 60 percent of his calories coming from vegetable oils, then his rate of de novo mutations will be much greater than a man following the Human Diet—vegetable-oil-free and packed with intense nutrition.
Remember the simple equation I put forth in my explanation of Alzheimer’s, which described how vegetable oil’s effects essentially speed up the aging process of the brain? The very same vegetable-oil-induced accelerated-aging processes occur in a man’s testes every time he loads up on vegetable-oil-rich foods. To put it bluntly, this means that the testes a man carries with him into the fast food joint will be significantly older, physiologically speaking, than the mere half-hour it took for him to scarf down his burger and fries.
Monty Python does a skit where they sing about the preciousness of every single sperm, funny in part because a man’s testes produce 1,500 sperm per second. But there is something miraculous about the accurate transcription of all the billions of lines of genetic code that will help define the physiologic identity of his children. And the more youth he can maintain in those miracle workers we call the spermatogonia, the better the odds for his child.
Until the day researchers are directed to provide us with more evidence that would-be parents are well-advised to avoid vegetable oils, we can take this simple action on our own with the certainty that it will play a beneficial role in all aspects of your baby’s development: steer clear of vegetable oils and continue to optimize your diet. By doing this, you’re not so much rejecting the idea of a technological solution, but rather tapping into what is far and away the most sophisticated and effective baby-making technology that has ever existed: Mother Nature.
Now that you know what I think about Public Enemy Number One, let me tell you what I think about its conspirator, Public Enemy Number Two—sugar.