Grain Brain: The Surprising Truth about Wheat, Carbs, and Sugar--Your Brain's Silent Killers




Attention, Carboholics and Fat Phobics

Surprising Truths About Your Brain’s Real Enemies and Lovers

No diet will remove all the fat from your body because the brain is entirely fat. Without a brain, you might look good, but all you could do is run for public office.


SOME OF MY MOST REMARKABLE CASE STUDIES involve people transforming their lives and health through the total elimination of gluten from their diets and a new appreciation for fats instead of carbs. I’ve watched this single dietary shift lift depression, relieve chronic fatigue, reverse type 2 diabetes, extinguish obsessive-compulsive behavior, and cure many neurological challenges, from brain fog to bipolar disorder.

But apart from gluten, there’s much more to the story of carbohydrates in general and their impact on brain health. Gluten isn’t the only villain. To shift your body’s biochemistry to one that burns fat (including the kind that “never goes away”), tames inflammation, and prevents illness and mental dysfunction, you need to factor in another big piece of the equation: carbs versus fats. In this chapter, I’ll take you on a tour of why an extremely low-carb and high-fat diet is what your body fundamentally craves and needs. I’ll also explain why consuming excess carbohydrates—even those that don’t contain gluten—can be just as harmful as eating a gluten-laden diet.

Ironically, ever since we “scientized” nutrition, the state of our health has declined. Decisions about what to eat and drink have gone from habits of culture and heritage to calculated choices based on shortsighted nutritional theories, with little consideration of how human beings reached modernity in the first place. And we can’t forget about all the commercial interest out there. Do you think the makers of high-carbohydrate breakfast cereals (read: the entire aisle in your grocery store devoted to boxed cereals) truly have your health in mind?

One of the most profitable businesses for food manufacturers is cereal. It’s one of the only industries that can turn an inexpensive ingredient (i.e., processed grains) into a pricey commodity. The R&D department for General Mills, called the Institute of Cereal Technology and located in Minneapolis, is home to hundreds of scientists whose sole purpose is to design new and tasty cereals that can command a high price and last for a long time on the shelves.1

Consider what you’ve experienced in just the past few decades. You’ve witnessed an untold number of ideas on what you should consume to fuel your metabolism, only to learn the opposite could be true. Take eggs, for instance. Eggs were thought to be good for you; then they were deemed to be bad for you because of their saturated fat content; and then you were exceedingly confused by messages implying that “More evidence is needed to determine the health effect of eggs.” It’s unfair, I know. With all of this white noise, it’s no wonder that people feel endlessly frustrated.

This chapter should make you rejoice. I’m going to rescue you from a lifetime of trying to avoid eating fat and cholesterol and prove how these delicious ingredients preserve the highest functioning of your brain. We’ve developed a taste for fat for good reason: It’s our brain’s secret love. But in the last several decades it’s been demonized as an unhealthy nutritional source, and we’ve regrettably become a fat-phobic, carb-addicted society (and it doesn’t help that we automatically lower our intake of healthy fat when we eat lots of carbs). Advertisements, weight-loss companies, grocery stores, and popular books are touting the idea that we should be on a low-fat or as close to a no-fat, low-cholesterol diet as humanly possible. True, there are certain types of fat that are associated with health issues, and no one can deny the health threat linked squarely with commercially modified fats and oils. There is compelling scientific support that “trans fats” are toxic and are clearly linked to any number of chronic diseases. But the missing message is simple: Our bodies thrive when given “good fats,” and cholesterol is one of these. And we don’t do so well with copious amounts of carbohydrates, even if those carbs are gluten-free, whole grain, and high in fiber.

Interestingly, the human dietary requirement for carbohydrate is virtually zero; we can survive on a minimal amount of carbohydrate, which can be furnished by the liver as needed. But we can’t go long without fat. Unfortunately, most of us equate the idea of eating fat to being fat, when in reality, obesity—and its metabolic consequences—has almost nothing to do with dietary fat consumption and everything to do with our addiction to carbs. The same is true about cholesterol: Eating high-cholesterol foods has no impact on our actual cholesterol levels, and the alleged correlation between higher cholesterol and higher cardiac risk is an absolute fallacy.


Of all the lessons in this book, the one I hope you take seriously is the following: Respect your genome. Fat—not carbohydrate—is the preferred fuel of human metabolism and has been for all of human evolution. We have consumed a high-fat diet for the past two million years, and it is only since the advent of agriculture about ten thousand years ago that carbohydrates have become abundant in our food supply. We still have a hunter-gatherer genome; it’s thrifty in the sense that it’s programmed to make us fat during times of abundance. The thrifty gene hypothesis was first described by geneticist James Neel in 1962 to help explain why type 2 diabetes has such a strong genetic basis and results in such negative effects favored by natural selection. According to the theory, the genes that predispose someone to diabetes—“thrifty genes”—were historically advantageous. They helped one fatten up quickly when food was available, since long stretches of food scarcity were inevitable. But once modern society changed our access to food, the thrifty genes were no longer needed but were still active—essentially preparing us for a famine that never comes. It is believed that our thrifty genes are responsible for the obesity epidemic, too, which is closely tied to diabetes.

Unfortunately, it takes forty thousand to seventy thousand years for any significant changes to take place in the genome that might allow us to adapt to such a drastic change in our diet and for our thrifty genes to even think about ignoring the instructions that say “store fat.” While some of us like to believe we’re plagued with genes that promote fat growth and retention, thus making weight loss and maintenance hard, the truth is we all carry the “fat gene.” It’s part of our human constitution and, for the majority of our existence on the planet, has kept us alive.

Our forebears could not have had any meaningful exposure to carbohydrates, except perhaps in the late summer when fruit ripened. Interestingly, this type of carbohydrate would have tended to increase fat creation and deposition so we could get through the winter when food and calories were less available. Now, however, we signal our bodies to store fat 365 days a year. And through science we are learning about the consequences.

The Framingham Heart Study referenced in the first chapter, which identified a linear association between total cholesterol and cognitive performance, is just the tip of the iceberg. In the fall of 2012, a report in the Journal of Alzheimer’s Disease published research from the Mayo Clinic revealing that older people who fill their plates with carbohydrates have nearly four times the risk of developing mild cognitive impairment (MCI), generally considered a precursor to Alzheimer’s disease. Signs of MCI include problems with memory, language, thinking, and judgment. This particular study found that those whose diets were highest in healthy fats were 42 percent less likely to experience cognitive impairment; people who had the highest intake of protein from healthy sources like chicken, meat, and fish enjoyed a reduced risk of 21 percent.2

Earlier studies examining patterns in diet and risk for dementia unveiled similar findings. One of the first studies to really compare the difference in fat content between an Alzheimer’s brain and a healthy brain was published in 1998.3 In this post-mortem study, researchers in the Netherlands found that the Alzheimer’s patients had significantly reduced amounts of fats, notably cholesterol and free fatty acids, in their cerebrospinal fluid than did the controls. This was true regardless of whether the Alzheimer’s patients had the defective gene—known as APoE ε4—that predisposes people to the disease.

In 2007, the journal Neurology published a study that looked at more than eight thousand participants who were sixty-five years or older and had totally normal brain function. The study followed them for up to four years, during which some 280 people developed a form of dementia (most of the 280 were diagnosed with Alzheimer’s).4 The researchers aimed to identify patterns in their dietary habits, homing in on their consumption of fish, which contains lots of brain- and heart-healthy omega-3 fats. For people who never consumed fish, the risk of dementia and Alzheimer’s disease during the four-year follow-up period was increased by 37 percent. In those individuals who consumed fish on a daily basis, risk for these diseases was reduced by 44 percent. Regular users of butter had no significant change in their risk for dementia or Alzheimer’s, but people who regularly consumed omega-3-rich oils, such as olive, flaxseed, and walnut oil, were 60 percent less likely to develop dementia than those who did not regularly consume such oils. The researchers also found that people who regularly ate omega-6-rich oils—typical in the American diet—but not omega-3-rich oils or fish were twice as likely to develop dementia as people who didn’t eat omega-6-rich oils. (See the sidebar below for a more in-depth explanation of these fats.)

Interestingly, the report showed that consumption of omega-3 oils actually counterbalanced the detrimental effect of the omega-6 oils, and cautioned against eating omega-6 oils in the absence of omega-3. I find results like these to be quite stunning, and informative.


We hear so much these days about omega-3 and omega-6 fats. Overall, omega-6 fats fall under the “bad fat” category; they are somewhat pro-inflammatory, and there is evidence that higher consumption of these fats is related to brain disorders. Unfortunately, the American diet is extremely high in omega-6 fats, which are found in many vegetable oils, including safflower oil, corn oil, canola oil, sunflower oil, and soybean oil; vegetable oil represents the number one source of fat in the American diet. According to anthropological research, our hunter-gatherer ancestors consumed omega-6 and omega-3 fats in a ratio of roughly 1:1.5 Today we consume ten to twenty-five times more omega-6 fats than evolutionary norms, and we’ve dramatically reduced our intake of healthy, brain-boosting omega-3 fats (some experts believe our increased consumption of brain-healthy omega-3 fatty acids was responsible for the threefold increase in the size of the human brain). The following chart lists the omega-6 and omega-3 content of various vegetable oils.


Omega-6 Content

Omega-3 Content


































Seafood is a wonderful source of omega-3 fatty acids, and even wild meat like beef, lamb, venison, and buffalo contain this fab fat. But a caveat to consider: If animals are fed grains (usually corn and soybeans), then they will not have adequate omega-3 in their diets and their meat will be deficient in these vital nutrients. Hence the call for consuming grass-fed beef and wild fish.

Beyond dementia, other neurological issues have been associated with low fat intake and cholesterol levels in particular. In a recent report published by the National Institutes of Health, researchers compared memory function in elderly individuals to cholesterol levels. They found that the people who did not suffer from dementia had much better memory function if they had higher levels of cholesterol. The conclusion of the report crisply stated: “High cholesterol is associated with better memory function.” In the discussion that followed, the researchers indicated: “It is possible that individuals who survived beyond age eighty-five, especially those with high cholesterol, may be more robust.”6

Parkinson’s disease is also strongly related to lower levels of cholesterol. Researchers in the Netherlands writing in the American Journal of Epidemiology published a report in 2006 demonstrating that “higher serum levels of total cholesterol were associated with a significantly decreased risk of Parkinson’s disease with evidence of a dose effect relation.”7 In fact, more recent research in 2008 published in the journal Movement Disorders showed that people with the lowest LDL cholesterol (the so-called bad cholesterol) were at increased risk for Parkinson’s disease by approximately 350 percent!8

To understand how this could possibly be true, it helps to recall what I hinted at in the first chapter about LDL being a carrier protein that’s not necessarily bad. The fundamental role of LDL in the brain is to capture life-giving cholesterol and transport it to the neuron where it performs critically important functions. As we have now seen, when cholesterol levels are low, the brain simply doesn’t work well, and individuals are at a significantly increased risk for neurological problems as a consequence. But a caveat: Once free radicals damage the LDL molecule, it’s rendered much less capable of delivering cholesterol to the brain. In addition to oxidation destroying the LDL’s function, sugar can also render it dysfunctional by binding to it and accelerating oxidation. And when that happens, LDL is no longer able to enter the astrocyte, a cell charged with nourishing neurons. In the last ten years new research has shown that oxidized LDL is a key factor in the development of atherosclerosis. Hence, we should do everything we can to reduce the risk of LDL oxidation—not necessarily levels of LDL itself. A principal player in that risk of oxidation is higher levels of glucose; LDL is far more likely to become oxidized in the presence of sugar molecules that will bind to it and change its shape. Glycosylated proteins, which are the products of these reactions between proteins and sugar molecules, are associated with a fiftyfold increase in free radical formation as compared to non-glycosylated proteins. LDL is not the enemy. The problems occur when a higher-carbohydrate diet yields oxidized LDL and an increased risk of atherosclerosis. In addition, if and when LDL becomes a glycosylated molecule, it cannot present cholesterol to brain cells, and brain function suffers.

Somehow we have been led to believe that dietary fat will raise our cholesterol, which will in turn increase our risk for heart attacks and strokes. This notion continues to prevail despite research from nineteen years ago that proved otherwise. In 1994, the Journal of the American Medical Association published a trial that compared older adults with high cholesterol (levels above 240 mg/dl) to those with normal levels (below 200 mg/dl).9 Over the course of four years, researchers at Yale University measured total cholesterol and high-density lipoprotein (HDL) in almost one thousand participants; they also tracked hospitalizations for heart attack and unstable angina and the rates of death from heart disease and from any other cause. No differences were found between the two groups. People with low total cholesterol had as many heart attacks and died just as frequently as those with high total cholesterol. And reviews of multiple large studies have routinely failed to find correlation between cholesterol levels and heart disease.10 Mounting research like this has prompted Dr. George Mann, a researcher with the Framingham Heart Study, to go on record stating:

The diet heart hypothesis that suggests that a high intake of fat or cholesterol causes heart disease has been repeatedly shown to be wrong, and yet, for complicated reasons of pride, profit, and prejudice, the hypothesis continues to be exploited by scientists, fund-raising enterprise, food companies, and even governmental agencies. The public is being deceived by the greatest health scam of the century.11

Nothing could be further from the truth than the myth that if we lower our cholesterol levels we might have a greater chance of living longer and healthier lives. In a recent report appearing in the prestigious medical journal the Lancet, researchers from the Netherlands studied 724 elderly individuals whose average age was eighty-nine years and followed them for ten years.12 What they found was truly extraordinary. During the study, 642 participants died. Each thirty-nine-point increase in total cholesterol corresponded to a 15 percent decrease in mortality risk. In the study, there was absolutely no difference in the risk of dying from coronary artery disease between the high-versus low-cholesterol groups, which is incredible when you consider the number of elderly folks who are taking powerful cholesterol-lowering drugs. Other common causes of death in the elderly were found to be dramatically associated with lower cholesterol. The authors reported: “Mortality from cancer and infection was significantly lower among the participants in the highest total cholesterol category than in the other categories, which largely explains the lower all-cause mortality in this category.” In other words, people with the highest total cholesterol were less likely to die from cancer and infections—common fatal illnesses in older folks—than those with the lowest cholesterol levels. In fact, when you compare the lowest- and highest-cholesterol groups, the risk of dying during the study was reduced by a breathtaking 48 percent in those who had the highest cholesterol. High cholesterol can extend longevity.

Perhaps one of the most extraordinary studies performed on the positive impact of cholesterol on the entire neurological system is a 2008 report published in the journal Neurology, which describes high cholesterol as a protective factor in amyotrophic lateral sclerosis (ALS, also known as Lou Gehrig’s disease).13 There is no meaningful treatment for ALS, a devastating disease that I deal with in my medical practice on a daily basis. ALS is a chronic degenerative disorder of the body’s motor neurons that leads to death within two to five years of onset. The FDA has approved one medication, Rilutek, that may extend life by approximately three months, at best. But it’s very expensive and toxic to the liver; most patients refuse to take it. In this study from French investigators, however, it was shown that those individuals with considerably higher cholesterol ratios lived, on average, one year longer than patients with lower levels, when compared with normal controls. As the authors stated: “Hyperlipidemia (high levels of cholesterol) is a significant prognostic factor for survival of patients with amyotrophic lateral sclerosis. This finding highlights the importance of nutritional intervention strategies on disease progression and claims our attention when treating these patients with lipid lowering drugs.”

As the infomercials say, “But wait, there’s more!” We can’t limit our talk about fat to just brain health. Volumes have been written in the scientific literature about fat and heart health as well—but not in the context I know you’re thinking about. In 2010, the American Journal of Clinical Nutrition published an astonishing study that revealed the truth behind urban legends about fat, especially the saturated kind, and heart disease.14 The study was a retrospective evaluation of twenty-one previous medical reports involving more than three hundred forty thousand subjects followed from periods of five to twenty-three years. It concluded that “intake of saturated fat was not associated with an increased risk of coronary heart disease, stroke, or cardiovascular disease.” In comparing the lowest to the highest consumption of saturated fat, the actual risk for coronary heart disease was 19 percent lower in the group consuming the highest amount of saturated fat. The authors also stated: “Our results suggested a publication bias, such that studies with significant associations tended to be received more favorably for publication.” What the authors are implying is that when other studies presented conclusions that were more familiar to the mainstream (i.e., fat causes heart disease), not to mention more attractive to Big Pharma, they were more likely to get published. The truth is we thrive on saturated fats. In the words of Michael Gurr, PhD, author of Lipid Biochemistry: An Introduction, “Whatever causes coronary heart disease, it is not primarily a high intake of saturated fatty acids.”15

In a subsequent report from the American Journal of Clinical Nutrition, a panel of leading researchers in the field of nutrition from around the globe clearly stated: “At present there is no clear relation of saturated fatty acid intake to these outcomes [of obesity, cardiovascular disease, incidence of cancer and osteoporosis].” The researchers went on to say that research should be directed at “biological interactions between insulin resistance, reflected by obesity and physical inactivity, and carbohydrate quality and quantity.”16

Before we look at more studies showing the benefits of fat, especially cholesterol-rich foods, let’s consider how we got to the point where we reject the very foods that can feed our healthy brains and keep us supercharged for a long, vibrant life. This will require a short detour to the relationship between dietary fat and heart health, but the story ties directly into brain health.


If you’re like most Americans, at some time in your life you’ve eaten more margarine than butter, felt like you were splurging when you polished off a plate of red meat, eggs, and cheese, and gravitated toward products that said “low-fat,” “non-fat,” or “cholesterol-free.” I don’t blame you for making these choices. We are all members of the same society that relies on “experts” to tell us what’s good and, conversely, bad for us. We’ve lived through historic events in our understanding of human health over the past several generations, as well as momentous discoveries about what makes us sick and prone to disease. In fact, the turn of the twentieth century marked the very beginning of a huge shift in American life due to advances in technology and medicine. Within the span of a few decades, we had widespread access to antibiotics, vaccines, and public health services. Common childhood illnesses that once gravely lowered the average life span were vanishing, or at least coming under better control. More people moved into cities and left their agrarian lifestyles behind. We became more educated, better informed, and ever more sophisticated. But in a lot of ways, we also became more easily tantalized and deceived by information that wasn’t fully deciphered and proven yet. You might not remember the days when doctors endorsed smoking cigarettes, for instance, but this same kind of ignorance has happened on a much subtler scale in the world of dieting. And sadly, much of it continues today.

In 1900, the typical city dweller consumed about 2,900 calories per day, with 40 percent of these calories coming from equal parts saturated and unsaturated fat. (Rural families living and working on farms probably ate more calories.) Theirs was a diet filled with butter, eggs, meats, grains, and seasonable fruits and vegetables. Few Americans were overweight, and the three most common causes of death were pneumonia, tuberculosis, and diarrhea and enteritis.

It was also around the turn of the twentieth century that the Department of Agriculture began to keep track of food trends, noting a change in the consumption of the kind of fats Americans were eating. People were beginning to use vegetable oils instead of butter, which prompted food manufacturers to create hardened oils through the hydrogenated process so they resembled butter. By 1950 we had gone from eating about eighteen pounds of butter and a little under three pounds of vegetable oil each year to just over ten pounds of butter and more than ten pounds of vegetable oil. Margarine was rapidly gaining ground in our diets, too; at the turn of the century people consumed only two pounds per person per year, but by midcentury, people were eating around eight pounds.

Although the so-called lipid hypothesis had been around since the mid-nineteenth century, it wasn’t until the mid-twentieth century that scientists tried to correlate a fatty diet to fatty arteries, as deaths from coronary artery disease (CAD) began to climb. According to the hypothesis, saturated animal fat raises blood cholesterol levels and leads to the deposition of cholesterol and other fats as plaques in the arteries. To bolster this theory, a University of Minnesota public health researcher named Ancel Keys showed a nearly direct correlation between calories from fat in the diet and deaths from heart disease among populations across seven countries. (He ignored countries that didn’t fit this pattern, including many where people eat a lot of fat but don’t get heart disease and others where the diets are low in fat yet their populations have a high incidence of fatal heart attacks.) The Japanese, whose diets have only 10 percent of calories coming from fat, showed the lowest CAD mortality—less than 1 in 1,000. The United States, on the other hand, had the highest CAD mortality—7 in 1,000—with 40 percent of its calories coming from fat.17 On the surface, it would seem that these patterns point directly to the idea that fat is bad, and that fat causes heart disease. Little did scientists know then that these numbers weren’t telling the whole story.

This erroneous thinking persisted, however, for the next several decades as researchers looked for more proof, which included the Framingham Heart Study, which found that people with higher cholesterol were more likely to be diagnosed with CAD and die from it. In 1956, the American Heart Association began pushing the “prudent diet,” which called for replacing butter, lard, eggs, and beef with margarine, corn oil, chicken, and cold cereal. By the 1970s, the lipid hypothesis had become well established. At the heart of this hypothesis was the unyielding claim that cholesterol caused coronary artery disease.

This naturally motivated the government to do something, which led to the release of “Dietary Goals for the United States” by the Senate’s Select Committee on Nutrition and Human Needs in 1977. As you can imagine, the goals aimed to lower fat intake and avoid foods high in cholesterol. “Artery-clogging” saturated fats were deemed especially bad. So down went meat, milk, eggs, butter, cheese, and tropical oils such as coconut and palm oil. This perspective also paved the way for the billion-dollar drug industry’s focus on lipid-lowering medications. At the same time, health authorities began to advise people to replace these now-bad fats with carbohydrates and processed polyunsaturated vegetable oils, including soybean, corn, cottonseed, canola, peanut, safflower, and sunflower oils. Fast-food restaurants followed suit in the mid-1980s, switching from beef fat and palm oil to partially hydrogenated (trans fat) vegetable oil to fry their foods. Even though the U.S. Department of Agriculture (USDA) has since converted its food guide from a pyramid to a plate, it still communicates the idea that “fat is bad” and “carbs are good.” In fact, the new “My Plate” doesn’t feature fats at all, making it very confusing for consumers to know how fats fit into a healthy diet, and which kind.18

Dr. Donald W. Miller, cardiac surgeon and professor of surgery at the University of Washington, stated it perfectly in his 2010 essay entitled “Health Benefits of a Low-Carbohydrate, High-Saturated-Fat Diet”:19 “The sixty-year reign of the low-fat, high-carbohydrate diet will end. This will happen when the health-destroying effects of excess carbohydrates in the diet become more widely recognized and the health benefits of saturated fats are better appreciated.” The lipid hypothesis has dominated cardiovascular circles for decades despite the fact that the number of contradictory studies exceeds those that are supportive. There hasn’t been a published study in the last thirty years that has unequivocally demonstrated that lowering serum cholesterol by eating a “low-fat, low-cholesterol diet” prevents or reduces heart attack or death rate. And as Dr. Miller points out, population studies from around the world do not support the lipid hypothesis. We can even go as far back as 1968 to find studies that flatly dispel the notion of a low-fat diet as ideal. That year, the International Atherosclerosis Project examined twenty-two thousand corpses from fourteen nations and found that it didn’t matter whether people ate large amounts of fatty animal products or followed a mostly vegetarian diet—the prevalence of arterial plaque was the same in all parts of the world, both in those with high rates of heart disease and in populations with little to no heart disease.20 Which means that the thickening of the arterial wall could just be an unavoidable process of aging that doesn’t necessarily correlate with clinical heart disease.

So if eating saturated fat doesn’t cause heart disease, then what does? Now let’s look at these circumstances from the perspective of the brain, and then we’ll circle back to matters of the heart. You’ll soon be able to understand the root cause of both obesity and brain disease.


As I’ve already detailed, one of the ways in which grains and carbs set fire to the brain is through surges in blood sugar; this has direct negative effects on the brain that in turn start the inflammatory cascade. The science really comes down to your body’s neurotransmitters. Neurotransmitters are your main mood and brain regulators, and when your blood sugar increases, there’s an immediate depletion of the neurotransmitters serotonin, epinephrine, norepinephrine, GABA, and dopamine. At the same time, B-complex vitamins, which are needed to make those neurotransmitters (and a few hundred other things), get used up. Magnesium levels also diminish, and this handicaps both your nervous system and liver. In addition, high blood sugar triggers a reaction called “glycation,” which we’ll explore in detail in the next chapter. In simplest terms, glycation is the biological process whereby glucose, proteins, and certain fats become tangled together, causing tissues and cells to become stiff and inflexible, including those in the brain. More specifically, sugar molecules and brain proteins combine to create deadly new structures that contribute more than any other factor to the degeneration of the brain and its functioning. The brain is tremendously vulnerable to the glycating ravages of glucose, and this is made worse when powerful antigens like gluten accelerate the damage. In neurological terms, glycation can contribute to the shrinking of critical brain tissue.

Aside from sweetened beverages, grain-based foods are responsible for the bulk of carbohydrate calories in the American diet. Whether from pasta, cookies, cakes, bagels, or the seemingly healthful “whole-grain bread,” the carbohydrate load induced by our food choices ultimately doesn’t serve us well when trying to optimize brain health and function. When you add to this list the potpourri of other high-carbohydrate foods like potatoes, corn, fruit, and rice, it’s no wonder that Americans are now rightly called “carboholics.” It’s also not surprising that we have an epidemic of metabolic dysfunction and diabetes in our culture.

The data confirming the relationship between high carbohydrate consumption and diabetes is clear and profound, and it’s compelling to note that in 1994, when the American Diabetes Association recommended that Americans should consume 60 to 70 percent of their calories from carbohydrates, rates of diabetes exploded. In fact, the number of cases of diabetes in this country actually doubled between 1997 and 2007.21 Take a look at the rapid upward slope from 1980 through 2011, during which the number of Americans diagnosed with diabetes more than tripled:


In 1992, the U.S. government endorsed a high-carb, low-fat diet. The American Diabetes Association and the American Heart Association followed suit with similar recommendations in 1994. Notice the sharp incline thereafter as more people became diabetic (and obese).

This is significant since, as you already know, becoming a diabetic doubles your risk of Alzheimer’s disease. Even being “pre-diabetic,” when blood sugar issues are just beginning, is associated with a decline in brain function and shrinkage of the brain’s memory center; it is also an independent risk factor for full-blown Alzheimer’s disease.

It’s hard to believe that we couldn’t have known about this connection between diabetes and dementia sooner, but it’s taken us a long time to connect the dots and conduct the kind of longitudinal studies that such a conclusion requires. It’s also taken us time to figure out the obvious question that stems from this link: How does diabetes contribute to dementia? First, if you’re insulin resistant, your body may not be able to break down a protein (amyloid) that forms brain plaques associated with brain disease. Second, high blood sugar provokes menacing biological reactions that injure the body, by producing certain oxygen-containing molecules that damage cells and causing inflammation that can result in hardening and narrowing of the arteries in the brain (not to mention elsewhere in the body). This condition, known as atherosclerosis, can lead to vascular dementia, which occurs when blockages and strokes kill brain tissue. We tend to think about atherosclerosis in terms of the heart, but the brain can be equally affected by changes in its arteries’ walls. Back in 2004, Australian researchers boldly stated in a review paper that “there is now a consensus that atherosclerosis represents a state of heightened oxidative stress characterized by lipid and protein oxidation in the vascular wall.”22 They also pointed out that such oxidation is a response to inflammation.

A most disturbing finding was made by Japanese researchers in 2011 when they looked at 1,000 men and women over age sixty and found that “people with diabetes were twice as likely as the other study participants to develop Alzheimer’s disease within fifteen years. They were also 1.75 times more likely to develop dementia of any kind.”23 This link remained true even after they took into account several factors associated with both diabetes and dementia risk, such as age, sex, blood pressure, and body mass index. Now they and other researchers are documenting how controlling blood sugar and reducing risk factors for type 2 diabetes also reduces dementia risk.


To fully grasp the bane of carbs and the benefits of fats, it helps to understand some basic biology. In the body, dietary carbohydrates, including sugars and starches, are converted to glucose, which you know by now tells the pancreas to release insulin into the blood. Insulin shuffles glucose into cells and stores glucose as glycogen in the liver and muscles. It’s also the body’s chief fat-building catalyst, converting glucose to body fat when the liver and muscles have no more room for glycogen. Carbohydrates—not dietary fats—are the primary cause of weight gain. (Think about it: Many farmers fatten animals destined for the butcher block with carbohydrates like corn and grain, not fats and proteins. You can see the difference just by comparing, for example, a cut of grain-fed New York strip steak and a grass-fed one: the grain-fed cut will contain a lot more fat.) This partly explains why one of the major health effects of a low-carbohydrate diet is weight loss. Moreover, a low-carb diet decreases blood sugar in diabetics and improves insulin sensitivity. In fact, replacing carbohydrates with fat is increasingly becoming the preferred method for treating type 2 diabetes.

When your diet is continuously rich in carbohydrates, which in effect keep your insulin pumps on, you severely limit (if not completely halt) the breakdown of your body fat for fuel. Your body gets addicted to that glucose. You may even use up your glucose but still suffer from a lockdown of available fat for fuel due to high volumes of insulin. In essence, the body becomes physically starved due to your carb-based diet. This is why many obese individuals cannot lose weight while continuing to eat carbs. Their insulin levels hold those fat stores hostage.

Now let’s turn to dietary fat. Fat is and always has been a fundamental pillar of our nutrition. Beyond the fact that the human brain consists of more than 70 percent fat, fat plays a pivotal role in regulating the immune system. Simply stated, good fats like omega-3s and monounsaturated fats reduce inflammation, while modified hydrogenated fats, so common in commercially prepared foods, dramatically increase inflammation. Certain vitamins, notably A, D, E, and K, require fat to get absorbed properly in the body, which is why dietary fat is necessary to transport these “fat-soluble” vitamins. Because these vitamins do not dissolve in water, they can only be absorbed from your small intestine in combination with fat. Deficiencies due to incomplete absorption of these vitally important vitamins are always serious, and any such deficiency can be linked to brain illness, among many other conditions. Without enough vitamin K, for instance, you won’t be able to form blood clots upon injury and can even suffer from spontaneous bleeding (imagine that problem in the brain). Vitamin K also contributes to both brain and eye health, helping reduce the risk of age-related dementia and macular degeneration (and dietary fat is good for macular degeneration). Without adequate vitamin A, your brain won’t develop properly; you will go blind and become exceptionally vulnerable to infections. A lack of vitamin D is known to be associated with increased susceptibility to several chronic diseases, including schizophrenia, Alzheimer’s, Parkinson’s, depression, seasonal affective disorders, and a number of autoimmune diseases such as type 1 diabetes.

If you follow today’s conventional wisdom, you know that you’re supposed to limit your total fat intake to no more than 20 percent of your calories (and when it comes to saturated fat, that percentage goes down to less than 10). You also know that this is difficult to achieve. (You can breathe a sigh of relief: It’s misguided advice, and on my program you won’t have to worry about counting fat grams or overall percentages.) However, while the synthetic trans fats found in margarine and processed foods are poisonous, we know now that monounsaturated fats—such as the fat found in avocados, olives, and nuts—are healthy. We also know that the polyunsaturated omega-3 fatty acids in cold-water fish (e.g., salmon) and some plants (e.g., flaxseed oil) are deemed “good.” But what about natural saturated fats such as those found in meat, egg yolks, cheese, and butter? As I’ve been detailing, saturated fat has gotten a bad rap. Most of us don’t even question why these particular fats are unhealthy anymore; we just assume that the purported science is true. Or we erroneously place these fats in the same category as trans fats. But we need saturated fat, and our body has long been designed to handle the consumption of natural sources of it—even in high amounts.

Few people understand that saturated fat plays a pivotal role in a lot of biochemical equations that keep us healthy. If you were breast-fed as a baby, then saturated fats were your staple, as they make up 54 percent of the fat in breast milk. Every cell in your body requires saturated fats; they comprise 50 percent of the cellular membrane. They also contribute to the structure and function of your lungs, heart, bones, liver, and immune system. In your lungs, one particular saturated fat—16-palmitic acid—creates lung surfactant, reducing surface tension so that your alveoli—the tiny air sacs that capture oxygen from your inhalations and allow it to be absorbed into your bloodstream—are able to expand. Without surfactant, you would not be able to breathe because the wet surfaces of your lungs’ alveoli would stick together and prevent your lungs from expanding. Having healthy lung surfactant prevents asthma and other breathing disorders.

Heart muscle cells prefer a type of saturated fat for nourishment, and bones require saturated fats to assimilate calcium effectively. With the help of saturated fats, your liver clears out fat and protects you from the adverse effects of toxins, including alcohol and compounds in medications. The white blood cells of your immune system partly owe their ability to recognize and destroy invading germs, as well as to fight tumors, to the fats found in butter and coconut oil. Even your endocrine system relies on saturated fatty acids to communicate the need to manufacture certain hormones, including insulin. And they help tell your brain when you are full so you can pull away from the table. I don’t expect you to remember all this biology. I mention it as a way of emphatically expressing to you the biological necessity of saturated fat. For a complete list of where these good fats can be found (and where the bad fats lurk), here.


If you’ve had your cholesterol levels tested, you’ve probably lumped HDL (high-density lipoprotein) and LDL (low-density lipoprotein) into two different categories—one “good” and one “bad.” I’ve already mentioned these two labels for cholesterol in passing. But contrary to what you might think, they are not two different kinds of cholesterol. HDL and LDL reflect two different containers for cholesterol and fats, each of which serves a different role in the body. Several other lipoproteins also exist, such as VLDL (very low) and IDL (intermediate). And as I’ve already begun to outline, cholesterol—no matter which “kind”—is not as terrible as you’ve been taught to believe. Some of the most remarkable studies of late on the biological value of cholesterol—and for brain health in particular—clue us in on how the pieces to this puzzle fit together and tell a coherent story. As we’ve seen, science is only recently discovering that both fat and cholesterol are severely deficient in diseased brains and that high total cholesterol levels in late life are associated with increased longevity.24 The brain holds only 2 percent of the body’s mass but contains 25 percent of the total cholesterol, which supports brain function and development. One-fifth of the brain by weight is cholesterol!

Cholesterol forms membranes surrounding cells, keeps cell membranes permeable, and maintains cellular “waterproofing” so different chemical reactions can take place inside and outside the cell. We’ve actually determined that the ability to grow new synapses in the brain depends on the availability of cholesterol, which latches cell membranes together so that signals can easily jump across the synapse. It’s also a crucial component in the myelin coating around the neuron, allowing quick transmission of information. A neuron that can’t transmit messages is useless, and it only makes sense to cast it aside like junk—the debris of which is the hallmark of brain disease. In essence, cholesterol acts as a facilitator for the brain to communicate and function properly.

Moreover, cholesterol in the brain serves as a powerful antioxidant. It protects the brain against the damaging effects of free radicals. Cholesterol is a precursor for the steroid hormones like estrogen and the androgens, as well as for vitamin D, a critically important fat-soluble antioxidant. Vitamin D is also a powerful anti-inflammatory, helping to rid the body of infectious agents that can lead to life-threatening diseases. Vitamin D is not really a vitamin; it acts more like a steroid in the body or a hormone. Given that vitamin D is directly formed from cholesterol, you won’t be surprised to hear that vitamin D levels are low in people with a variety of neurodegenerative diseases like Parkinson’s, Alzheimer’s, and multiple sclerosis. As we age, natural cholesterol levels generally increase in the body. This is good because as we age our production of free radicals increases. Cholesterol can offer a level of protection against these free radicals.

And beyond the brain, cholesterol plays other vital roles in human health and physiology. The bile salts secreted by the gallbladder, which are needed for the digestion of fat and, therefore, the absorption of fat-soluble vitamins like A, D, and K, are made of cholesterol. Having a low cholesterol level in the body would therefore compromise a person’s ability to digest fat. It would also jeopardize your body’s electrolyte balance since cholesterol helps manage that delicate equilibrium. In fact, cholesterol is regarded by the body as such an important collaborator that every cell has a way to make its own supply.

So what does this mean for dietary recommendations? For years we have been told to focus on “low-cholesterol” foods, but foods rich in cholesterol, such as eggs, are very helpful and should be considered “brain food.” We have eaten cholesterol-rich foods for more than two million years. As you now know, the real culprits when it comes to decreased brain function and health are foods that are high on the glycemic index—basically, high in carbohydrate.

One of the most pervasive myths I’m constantly debunking is the notion that the brain prefers glucose for fuel. This also couldn’t be further from the truth. The brain uses fat exceptionally well; it is considered a brain “superfuel.” This is why we use a fat-based diet as therapy for all manner of neurodegenerative diseases (in chapter 7, I describe in detail how the brain accesses fat for fuel and what this means for health and for tailoring the perfect diet).

Part of the reason I am focusing on fats, and cholesterol in particular, is not only because these ingredients have everything to do with brain health, but also because we live in a society that continues to demonize them, and the huge pharmaceutical industry preys on the public’s misinformation and perpetuates falsehoods, many of which could physically destroy us. To really understand where I’m going with this, let’s look at one problematic area: the statin epidemic.


Our understanding of how cholesterol is critical for brain health has brought me and many others in my field to believe that statins—the blockbuster drugs prescribed to millions of Americans to lower cholesterol—may cause or exacerbate brain disorders and disease.

Memory dysfunction is a known side effect of statins. Dr. Duane Graveline, a former doctor to NASA astronauts who earned the nickname “Spacedoc,” has been a strong opponent of statins. Ever since he experienced total memory loss that he believed was caused by the statins he was taking at the time, he has been collecting evidence of their side effects from people around the world. Today he has written three books on the matter, the most famous of which is Lipitor, Thief of Memory.25

In February 2012, the FDA released a statement indicating that statin drugs could cause cognitive side effects such as memory lapses and confusion. One recent study performed by the American Medical Association and published in the Archives of Internal Medicine in January 2012 demonstrated an astounding 48 percent increased risk of diabetes among women taking statin medications.26


Risk of type 2 diabetes in women using statin drugs

This study involved big numbers—more than one hundred sixty thousand postmenopausal women—making it hard to ignore its significance and gravity. Recognizing that type 2 diabetes is a powerful risk factor for Alzheimer’s disease, a relationship between statin drugs and cognitive decline or cognitive dysfunction is certainly understandable.

In 2009, Stephanie Seneff, a senior research scientist in the Computer Science and Artificial Intelligence Laboratory at MIT who recently became interested in the effects of drugs and diet on health and nutrition, wrote a compelling essay explaining why low-fat diets and statins may cause Alzheimer’s.27 In it, she chronicles our knowledge of statins’ side effects and paints a stunning portrait of how the brain suffers in their presence. She also synthesizes the latest science and input from other experts in the field. As Dr. Seneff explains, one of the main reasons statins promote brain disorder is that they handicap the liver’s ability to make cholesterol. Consequently, the level of LDL in the blood drops significantly. As I’ve just detailed, cholesterol plays a vital role in the brain, enabling communication between neurons and encouraging the growth of new brain cells. In an ironic twist, the statin industry advertises its products by saying that they interfere with cholesterol production in the brain as well as in the liver.

Professor of Biophysics at Iowa State University Dr. Yeon-Kyun Shin is a noted authority on how cholesterol functions within neural networks to transmit messages. He put it bluntly in an interview for aScienceDaily reporter:28

If you deprive cholesterol from the brain, then you directly affect the machinery that triggers the release of neurotransmitters. Neurotransmitters affect the data-processing and memory functions. In other words—how smart you are and how well you remember things. If you try to lower the cholesterol by taking medication that is attacking the machinery of cholesterol synthesis in the liver, that medicine goes to the brain too. And then it reduces the synthesis of cholesterol, which is necessary in the brain. Our study shows there is a direct link between cholesterol and the neurotransmitter release, and we know exactly the molecular mechanics of what happens in the cells. Cholesterol changes the shape of the proteins to stimulate thinking and memory.

In 2009, an updated review of two major studies completed in 2001 of statin medications used by more than twenty-six thousand individuals at risk for dementia and Alzheimer’s disease showed that statins are not protective against Alzheimer’s, which contradicted previous thinking. The lead author of the study, Bernadette McGuinness, was quoted by ScienceDaily as saying, “From these trials, which contained very large numbers and were the gold standard—it appears that statins given in late life to individuals at risk of vascular disease do not prevent against dementia.”29 When asked to comment on the results, UCLA researcher Beatrice Golomb said, “Regarding statins as preventive medicines, there are a number of individual cases in case reports and case series where cognition is clearly and reproducibly adversely affected by statins.”30 Golomb further added that various studies have demonstrated that statins either negatively affected cognition or were neutral, and that no trial has ever shown a positive outcome.

Besides statins’ direct impact on cholesterol, they have an indirect effect on the supply of fatty acids and antioxidants. They not only reduce the amount of cholesterol contained in LDL particles, but also diminish the actual number of LDL particles. So in addition to depleting cholesterol, they limit the stash available to the brain of both fatty acids and antioxidants, which are also carried in the LDL particles. Proper brain functioning depends on all three of these substances31 (and later on, you’ll read about the importance of boosting the body’s own natural production of antioxidants).

Another way in which statins may contribute to Alzheimer’s, beautifully described by Dr. Seneff,32 is by paralyzing cells’ ability to make coenzyme Q10, a vitamin-like substance found throughout the body, where it serves an important role as an antioxidant and in producing energy for cells. Because coenzyme Q10 shares the same metabolic pathway as cholesterol, its synthesis is disrupted by statins, and the body and brain are deprived of it. Some of the side effects listed for statins, such as fatigue, shortness of breath, problems with mobility and balance, and muscular pain, weakness, and atrophy, are related to the loss of coQ10 in muscles and a reduced capacity for energy production. At the extreme, people who experience severe reactions to statins suffer from serious damage to their skeletal muscles. A deficiency in coQ10 also has been linked to heart failure, hypertension, and Parkinson’s disease. Given all these effects, it’s logical to see why coQ10 has been proposed as an actual treatment for Alzheimer’s disease.

Finally, statins could have an indirect effect on vitamin D. The body makes vitamin D from cholesterol in the skin upon exposure to UV rays from the sun. If you were to look at the chemical formula for vitamin D, you’d have a hard time distinguishing it from cholesterol’s formula; they look virtually identical. “If LDL levels are kept artificially low,” writes Dr. Seneff, “then the body will be unable to resupply adequate amounts of cholesterol to replenish the stores in the skin once they have been depleted. This would lead to vitamin D deficiency, which is a widespread problem in America.”33 Vitamin D deficiency is not just about an increased risk for weak, soft bones and, at the extreme end, rickets; it’s associated with many conditions that heighten one’s risk for dementia, such as diabetes, depression, and cardiovascular disease. If the brain didn’t demand vitamin D for proper development and function, then it wouldn’t have widespread receptors for it.

The benefits of statins are questionable, and major studies have failed to show how they protect the body from illness. Although numerous studies do point to the positive effects statins have on reducing mortality rates in people with coronary artery disease, new research reveals that these outcomes have little to do with the cholesterol-lowering activity of these drugs and more likely reflect the fact that they reduce inflammation, a mainspring of the disease. But that doesn’t mean that the trade-offs for taking a statin merit their seal of approval. For some, the risk of negative side effects is just too great. People with a low risk of heart disease but a high risk for other ailments would be putting themselves in harm’s way if they chose to take a statin.

Studies dating back to the mid-1990s reveal a link between statin use and an increased risk of certain cancers, not to mention a long list of side effects from digestive challenges to asthma, impotence, inflammation of the pancreas, and liver damage.34 A trial published in January 2010 in the American Journal of Cardiology found that statin medications actually increased the risk of death. Researchers in Israel followed nearly 300 adults diagnosed with heart failure for an average of 3.7 years, and in some cases up to 11.5 years. Those who were taking statin drugs and had the lowest levels of low-density lipoprotein (LDL) were found to have the highest rates of mortality. Conversely, people with higher levels of cholesterol had a lower risk of death.35


If you can limit carb intake to a range that is absolutely necessary (the details of which are in chapter 10) and make up the difference with delicious fats and protein, you can literally reprogram your genes back to the factory setting you had at birth. This is the setting that affords you the ability to be a mentally sharp, fat-burning machine.

It’s important to understand that when you have a blood cholesterol test, the number that is represented is actually 75 to 80 percent derived from what your body manufactures and not necessarily what you’ve eaten. In fact, foods that are high in cholesterol actually decrease the body’s production of cholesterol. We all make up to 2,000 grams of cholesterol every day because we desperately need it, and this is several times the amount found in our diets. But despite this amazing ability, it’s critical to obtain cholesterol from dietary sources. Our bodies much prefer that we “spoon-feed” our cholesterol from the foods we eat rather than manufacture it internally, which is a complex multistep biological process that taxes the liver. Dietary cholesterol is so important that your body absorbs as much as it can for use.

So what happens if you restrict your cholesterol intake, as so many people do today? The body sends out an alarm that indicates crisis (famine). Your liver senses this signal and begins to produce an enzyme called HMG-CoA reductase, which helps make up for the deficit by using carbohydrates in the diet to produce an excess supply of cholesterol. (This is the same enzyme that statins target.) As you can likely predict, it’s a Molotov cocktail in the works: As you eat excessive carbohydrates while lowering your cholesterol intake, you incite a steady and punishing overproduction of cholesterol in the body. The only way to stop this internal pathway run amok is to consume an adequate amount of dietary cholesterol and back way off on carbs. Which explains why my “high-cholesterol” patients who go on my diet can safely return their levels to normal without drugs while enjoying cholesterol-rich foods.


Cholesterol is at most a minor player in coronary heart disease and represents an extremely poor predictor of heart attack risk. Over half of all patients hospitalized with a heart attack have cholesterol levels in the “normal” range. The idea that aggressively lowering cholesterol levels will somehow magically and dramatically reduce heart attack risk has now been fully and categorically refuted. The most important modifiable risk factors related to heart attack risk include smoking, excess alcohol consumption, lack of aerobic exercise, overweight, and a diet high in carbohydrates.

So when I see patients with cholesterol levels of, say, 240 mg/dl or higher, it’s almost a given that they will have received a prescription for a cholesterol-lowering medication from their general practitioners. This is wrong in thought and action. As discussed, cholesterol is one of the most critical chemicals in human physiology, especially as it relates to brain health. The best lab report to refer to in determining one’s health status is hemoglobin A1C, not cholesterol levels. It is rarely, if ever, appropriate to consider high cholesterol alone to be a significant threat to health.

A good question: Who suffers from high cholesterol? Thirty years ago, the answer was anyone whose cholesterol level was more than 240 and who had other risk factors, such as being overweight and smoking. The definition changed after the Cholesterol Consensus Conference in 1984; then it became anyone with a cholesterol level over 200, regardless of other risk factors. Today, the threshold is down to 180. And if you’ve had a heart attack, you’re in a totally different category: No matter how low your cholesterol level is, you’ll likely be prescribed a cholesterol-lowering medicine and told to maintain a low-fat diet.


Okay. So cholesterol is a good thing. But it’s not just about your brain’s wit, physical health, and future longevity. It’s also about a very important part of your lifestyle that typically gets shoved under the carpet in serious health books. I’m talking about your sex life. How sparky is it?

Although I’m a neurologist, I treat a fair share of people who suffer from sexual dysfunction and are either impotent and avoid sex altogether or who hoard bottles of pills to help them out. You know about these pills—the ones that get advertised like candy on the evening news and promise to transform your sex life. My patients with sexual health woes obviously don’t come to me for that specifically, but it’s a noted problem when I ask them about that part of their life in addition to any neurological issues I am addressing.

A quick anecdote. A seventy-five-year-old retired engineer came to see me with a variety of complaints, including insomnia and depression. He had been taking sleeping pills for the past forty years, and his depression had worsened in the two to three months prior to his appointment. At the time I saw him, he was actually taking a few drugs: an antidepressant, a medication for anxiety, and Viagra for erectile dysfunction. I first checked him for gluten sensitivity and discovered, to his surprise, a positive panel. He agreed to adopt a gluten-free, high-fat diet, and we next communicated by telephone after about one month. That’s when he had magnificent news: His depression had improved, and he no longer needed to take Viagra in order to have sex with his wife. He thanked me very much.

Most everyone can agree that sex has everything to do with what’s going on in the brain. It’s an act that’s deeply tied to emotions, impulses, and thoughts. But it’s also inexorably connected to hormones and blood chemistry. Without question, if you’re depressed and not sleeping well, like my engineer patient, sex is the last thing on your mind. But one of the most common reasons for impotence is actually neither of these two conditions. It’s what I’ve been talking about through much of this chapter: abysmally low cholesterol levels. And the studies to date have achieved proof of concept: Unless you have healthy testosterone levels (this goes for both men and women), you’re not going to have a hot sex life, if any at all. And what makes testosterone? Cholesterol. What are millions of Americans doing today? Lowering their cholesterol levels through diet and/or taking statins. In the meanwhile, they are lowering their libido and ability to perform. Is it any wonder there’s an epidemic of erectile dysfunction (ED) and demand for ED drugs today, not to mention (perhaps ironically) testosterone replacement therapy?

Plenty of studies have confirmed these connections.36 Decreased libido is one of the most common complaints among those taking statins, and lab reports have repeatedly demonstrated low testosterone in statin consumers.37 Those on statins are twice as likely to have low testosterone levels. Luckily, this condition is reversible by stopping the statin and increasing cholesterol intake. There are actually two ways that statins can lower testosterone. The first is by directly lowering levels of cholesterol. The second is by interfering with the enzymes that create active testosterone.

One study that came out in the United Kingdom in 2010 looked at 930 men with coronary heart disease and measured their testosterone levels.38 Low testosterone was found in 24 percent of the patients, and the risk of dying was 12 percent in those with normal testosterone but 21 percent in those with low testosterone. The conclusion was staring them in the face: If you have coronary disease and low testosterone, you’re at much greater risk of dying. So again we are giving statin medications to lower cholesterol, which lowers testosterone… and lower testosterone increases the risk of dying. Is this crazy or what?

I rest my case.


I’ve covered a lot of ground in this chapter, mostly dealing with the role of fats on the brain. But we now have to ask ourselves the following: What happens when you inundate the brain with sugar instead? I started this chapter by addressing the ills of carbohydrates on our bodies, but I’ve saved the conversation about this particularly devastating carbohydrate for its own chapter. Unfortunately, this is a subject area that’s gotten remarkably little attention in the press. We increasingly hear about the relationship between sugar and “diabesity,” sugar and heart disease, sugar and fatty livers, sugar and metabolic syndrome, sugar and risk for cancer, etc…. but sugar and brain dysfunction? It’s time you got up close and personal with your brain on sugar.