Beyond dementia

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. A LITTLE HISTORY 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-SaturatedFat 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. CARBS, DIABETES, 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