The Case Against Sugar: Book Notes
The Case Against Sugar by Gary Taubes
Sugar appears to be a substance that causes pleasure with a price that is difficult to discern immediately and paid in full only years or decades later.
- 30k Foot Summary
- Meaningful Stats
- Defining Sugar and It’s Properties
- Pathology of Sugar
- History of Sugar
- Sugar Entrepreneurs
- Medical Community & Sugar
- Sugar & Cigarettes
- Lipstick on a Pig: Sugar, the FDA, and Incentives
- Prenatal Imprinting
- How Much Sugar Should We Consume
30k Foot Summary
Gary demonstrates how sugar is toxic to the body over the long term and is responsible in the pathology of a cluster of ‘Western’ chronic diseases including: insulin resistance, metabolic syndrome, type two diabetes, fatty liver disease, obesity and gout.
His argues that sugars, such as, sucrose and high-fructose corn syrup are fundamental causes of diabetes and obesity, using the same simple concept of causality that we employ when we say smoking cigarettes causes lung cancer.
Gary takes a sound scientific approach to nutrition research while dissecting the questions against his thesis and not definitively making conclusions he isn’t able to support without strong research. It’s clear from his analysis that sugar is far more toxic than I originally thought and should be avoided unless in fruits or vegetables. Given the lack of research supporting artificial sweeteners it seems prudent to avoid them as well.
Below are select highlights from book.
Meaningful Stats
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Fifty years ago, one in eight American adults was obese; today the number is greater than one in three.
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The USDA now reports that in 2014 (the latest numbers available) the average American consumed only 67 pounds of the sucrose and HFCS out of the 114 pounds the industry made available—slightly less than 60 percent. (The USDA factors in an arbitrary error percentage to ‘account’ for food waste)
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In 2012, the latest year for which the Centers for Disease Control (CDC) have provided estimates, one in every seven to eight adults in this country had diabetes—12 to 14 percent, depending on the criteria used to diagnose it. Another 30 percent are predicted to get diabetes at some point during their lives. Almost two million Americans were diagnosed with diabetes in 2012—one case every fifteen to sixteen seconds.
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In more than one in every ten individuals diagnosed with type 2 diabetes is neither obese nor overweight).
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In 1978, Kelly West, the leading American authority on diabetes epidemiology—the study of how diseases move through populations—suggested that diabetes had already killed more people in the twentieth century than all wars combined. “Diabetes mellitus has become one of the most important of human problems,”
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The World Health Organization reports that obesity rates have doubled worldwide since 1980; in 2014, more than half a billion adults on the planet were obese, and more than forty million children under the age of five were overweight or obese. Without doubt we’ve been getting fatter, a trend that can be traced back in the United States to the nineteenth century, but the epidemic of diabetes is a more intriguing, more telling phenomenon.
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In fact, anywhere populations begin eating Western diets and living Western lifestyles—whenever and wherever they’re acculturated or urbanized, as West noted in 1978—diabetes epidemics follow.
Defining Sugar and It’s Properties
Serge Ahmed has reported, offer a rat the choice of a sweet solution or its daily cocaine fix, and the rat will switch over to the sweets within two days.
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Biochemically, the term “sugar” refers to a group of carbohydrate molecules consisting, as the word “carbohydrate” implies, of atoms of carbon, hydrogen, and oxygen. The names of these carbohydrates all end in “-ose”—glucose, galactose, dextrose, fructose, lactose, sucrose, etc. All of these sugars will dissolve in water, and they all taste sweet to us, although to a greater or lesser extent. When physicians or researchers refer to “blood sugar,” they’re talking about glucose, because it constitutes virtually all of the sugar circulating in our blood.
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These sugars are very likely unique in that they are both a nutrient and a psychoactive substance with some addictive characteristics.
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Sugar does induce the same responses in the region of the brain known as the “reward center”—technically, the nucleus accumbens—as do nicotine, cocaine, heroin, and alcohol.
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The more we use these substances, the less dopamine we produce naturally in the brain, and the more habituated our brain cells become to the dopamine that is produced—the number of “dopamine receptors” declines. The result is a phenomenon known as dopamine down-regulation: we need more of the drug to get the same pleasurable response, while natural pleasures, such as sex and eating, please us less and less.
Pathology of Sugar
“Rises and falls in sugar consumption are followed with fair regularity…by similar rises and falls in the death rates from diabetes.”
1924 - Haven Emerson and Louise Larimore
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When blood-sugar (glucose) levels rise, the pancreas secretes insulin in response, which then signals the muscle cells to take up and burn more glucose. Insulin also signals the fat cells to take up fat and hold on to it. Only when the rising tide of blood sugar begins to ebb will insulin levels ebb as well, at which point the fat cells will release their stored fuel into the circulation (in the form of fatty acids); the cells of muscles and organs now burn this fat rather than glucose. Blood sugar is controlled within a healthy range, and fat flows in and out of fat cells as needed. The one biological factor necessary to get fat out of fat cells and have it used for fuel, as Yalow and Berson noted in 1965, is “the negative stimulus of insulin deficiency.”
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The glucose we consume—in starch or flour, or as half of a sugar molecule—will be used directly for fuel by muscle cells, the brain, and other tissues, and can be stored in muscles or the liver (as a compound called glycogen), but the fructose component of sugar has a much different fate. Most of it never makes it into the circulation; it is metabolized in the liver. The metabolic pathways through which glucose passes when it is being used for fuel—in both liver and muscle cells—involve a feedback mechanism to redirect it toward storage as glycogen when necessary. This is the case with fructose, too. But the metabolism of fructose in the liver is “unfettered by the cellular controls,” as biochemists later put it, that work to prevent its conversion to fat. One result is the increased production of triglycerides, and thus the abnormally elevated triglyceride levels that were observed in many research subjects, though not all, when they ate sugar-rich diets.
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The more refined or processed a carbohydrate, and the less fat and fiber accompanying it to slow its digestion, the greater the blood-sugar response, and thus the more insulin required to metabolize it; or, as Cleave might have phrased it, the greater the strain on the pancreas.
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Here’s another way to think about the idea that a cluster of chronic Western diseases associate with insulin resistance, metabolic syndrome, obesity, and diabetes and hence sugar consumption: Diabetes, though a discrete diagnosis by our doctors, is not a discrete phenomenon in which bad things suddenly start happening that didn’t happen before. It’s part of a continuum from health to disease that is defined in large part by the worsening of the metabolic abnormalities—the homeostatic disruption in regulatory systems—that we’ve been discussing and that are associated with insulin resistance, if not caused by it, and so part and parcel of metabolic syndrome.
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As we become ever more insulin-resistant and glucose-intolerant, as our blood sugar gets higher along with our insulin levels, as our blood pressure elevates and we get ever fatter, we are more likely to be diagnosed as diabetic and manifest the diseases and conditions that associate with diabetes. These include not just heart disease, gout, cancer, Alzheimer’s, and the cluster of Western diseases that Burkitt and Trowell included in their provisional list, but all the conditions typically perceived as complications of diabetes: blood-vessel (vascular) complications that lead to strokes, dementia, and kidney disease; retinopathy (blindness) and cataracts; neuropathies (nerve disorders); plaque deposits in the arteries of the heart (leading to heart attacks) or the legs and feet (leading to amputations); accumulation of advanced glycation end products, AGEs, in the collagen of our skin that can make diabetics look prematurely old, and that in joints, arteries, and the heart and lungs can cause the loss of elasticity as we age. It’s this premature aging of the skin, arteries, and joints that has led some diabetes researchers to think of the disease as a form of accelerated aging.
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But increasing our risk of contracting all these other chronic conditions means we’re also likely to get these ailments at ever-younger ages and thus, effectively, age faster.
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The great proportion of this tidal wave of diabetics—perhaps 95 percent—have what is now known as type 2 diabetes, the form of the disease, as Sushruta would have said over two thousand years ago, that associates with overweight and obesity.
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Those afflicted with diabetes will die at greatly increased rates from heart disease or stroke, from kidney disease—the disease is now considered the cause of more than 40 percent of cases of kidney failure—and diabetic coma. Without appropriate treatment (and occasionally even with), their eyesight will deteriorate (often a first symptom); they’ll suffer nerve damage; their teeth will decay and fall out; they’ll get foot ulcers and gangrene; and they’ll lose limbs to amputation. Six in every ten lower-limb amputations in adults are due to diabetes—some seventy-three thousand of them in 2010 alone.
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Insulin disturbs what is technically known as “electrolyte balance” or “electrolyte physiology” (sodium is an electrolyte) in such a way that the kidneys retain both sodium and water, rather than excrete them in the urine (just as insulin signals the kidneys to retain uric acid, and so plays a role in gout).
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If sugar causes insulin resistance and chronically elevates levels of insulin, then these are among the mechanisms through which it would be expected to cause hypertension.
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This, regrettably, links fructose and sugar not just to hypertension but to the kidney disease that is considered one of the “vascular complications” of diabetes, making it also a Western disease (albeit not mentioned in Burkitt and Trowell’s provisional list). If Johnson’s work and its implications are correct, simply raising uric acid levels is enough to cause insulin resistance and thus, perhaps, type 2 diabetes and obesity, independent of these other effects on insulin and insulin resistance.
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Isolated populations—including Swiss mountain villages, pastoral populations in Central Africa, the Inuit and First Nations people of North America, South Pacific Islanders—had nearly cavity-free teeth and retained their teeth for life, as long as they consumed their traditional diets and avoided the sugar and white flour that had come to dominate diets in the United States and Europe.
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Diabetes had an incubation period similar, for example, to the time it took lung cancer to appear in cigarette smokers. From the medical histories he had taken in his clinic, Campbell noted “a remarkably constant period in years of exposure to town life”—eighteen to twenty-two years—before diabetes appeared.
History of Sugar
By the 1830s, when the British emancipationists finally put an end to the slave trade, some twelve and a half million Africans had been shipped off as slaves to the New World; two-thirds of them worked and died growing and refining sugar.
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Hindu physicians had diagnosed diabetes back in the sixth century and even then had noticed the honey urine—“ants flock” around it—while observing that this was a disease “which the rich principally suffer from, and is brought on by their overindulgence in rice, flour, and sugar.”
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Honey was consumed throughout Europe and Asia before sugar displaced it, and when European colonists arrived in the New World and found no honey, they introduced honeybees, which Native Americans took to calling the “English Man’s Fly.”
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The Physiology of Taste, perhaps the most famous book ever written about food, that obesity was caused by the consumption of starches and bread (“fecula” or “farinaceous foods,” he called them) and that this fattening process occurs “more quickly and surely” when such foods are consumed with sugar.
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When cultivated with the instruments of modern technology, sugarcane can produce (as the sugar industry and nutritionists would state in its defense repeatedly in the twentieth century) more calories per acre to feed a population than any other animal or plant.
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As such, inexpensive sugar made possible the revolution in jams and jellies that began in the mid-nineteenth century (one of many revolutions in sugar-rich foods that began at the same time, as we’ll discuss shortly). It inhibits mold and bacteria in condensed milk and other liquids by increasing what’s called the osmotic pressure of the liquid. It reduces the harshness of the salt that’s used for curing and preserving meat (and the salt increases the sweetness of the sugar). Sugar is an ideal fuel for yeast, and thus the rising and leavening of bread. The caramelization of sugar provides the light-brown colors in the crust of bread. Dissolve sugar in water and it adds not only sweetness but viscosity, and thus creates the body and what food scientists call the “mouth feel” of a soda or juice. As a seasoning or a spice, it enhances flavors already present in the food, decreases bitterness, and improves texture.
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As sugar diffused through Europe, it did so primarily as a medicine—as would tea, coffee, tobacco, and chocolate centuries later—a decorative, a spice, and a preservative.
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Modern equivalent in CBD, THC or probiotics.
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As the price of sugar slowly dropped, its use as a sweetener and a food went up. It moved from the shops of apothecaries, “who kept it exclusively for invalids,” to being devoured “out of gluttony.”
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Sugar and slavery went hand in hand from the earliest times.
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From the seventeenth through the nineteenth centuries, sugar was the equivalent, economically and politically, of oil in the twentieth. It was the stuff over which wars were fought, empires built, and fortunes made and lost.
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Both the British and U.S. governments came to be vigorous promoters of the sugar industry because of the revenues they could garner by taxing it. Sugar was an ideal target of taxation: production was localized to tropical colonies, so its import could be controlled, and it was in universal demand but not (yet) considered a necessity of life.
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Many of the wealthiest New York families would make their fortunes initially as sugar refiners, as confectioners, and as middlemen in the triangular slave trade that hauled sugar and molasses north to New York, sent rum to Africa, and brought slaves back to the Caribbean, while also supplying the sugar islands in the Caribbean directly with the food and naval stores “without which the West Indian plantations couldn’t survive.”
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“I know not why we should blush to confess that molasses was an essential ingredient in American independence,” wrote John Adams in 1775. (“To scientific ability he did not unite business acumen,” wrote Noël Deerr in The History of Sugar about the first of these German beet-sugar entrepreneurs.)
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Napoleon allotted eighty thousand acres for growing sugar beets and established technical centers to teach the art and business of beet-sugar production. Within three years, over three hundred factories were producing beet sugar in France alone.
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By 1880, beet sugar had surpassed cane sugar, and the total amount of all sugar being refined and apparently consumed worldwide had increased over fivefold in forty years.
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When the U.S. Department of Agriculture was founded in 1862, its impetus, as much as anything, was to encourage sugar-beet production.
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The second factor in the transformation of sugar into a dietary staple—one of life’s necessities—was technology.
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By the 1920s, sugar refineries were producing as much sugar in a single day—millions of pounds—as would have taken refineries in the 1820s an entire decade.
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Here was a disease of carbohydrate metabolism that was becoming increasingly common as populations began consuming sugar—a kind of carbohydrate—at levels that were virtually unimaginable a century before; in some cases, just twenty or thirty years before.
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As sugar consumption exploded in the United States and the United Kingdom with the industrial revolution; with the birth of the confectionary, cereal, and soft-drink industries; and with the increasing availability of chocolate bars and ice-cream treats, so did diabetes begin its inexorable climb. When sugar and sugar-rich products spread around the globe, so did diabetes.
Sugar Entrepreneurs
By 1903, The New York Times was estimating yearly candy industry sales at $150 million in the United States alone, up from “almost nothing” a quarter century earlier.
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The chocolate bar also dates to the 1840s, when Swiss confectioners—the Lindt brothers—figured out the trick of solidifying chocolate powder into a bar that could be mass-produced, packaged, and shipped. Until then, chocolate had been consumed as a hot beverage; only high-end French confectioners had known the secret of making edible chocolate in solid form.
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A remarkable proportion of the chocolate staples of the twentieth century and today were first created and mass-produced between 1886 (the Clark bar) and the early 1930s—Tootsie Rolls (1896), Hershey’s Milk Chocolate bar (1900), Hershey’s Kisses (1906), Toblerone (1908), the Heath bar (1914), Oh Henry! (1920), Baby Ruth (1921), Mounds and Milky Way (1923), Mr. Goodbar (1925), Milk Duds (1926), Reese’s Peanut Butter Cups (1928), Snickers (1930), Tootsie Roll Pops (1931), and the Mars and 3 Musketeers bars (1932).
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And then there was soda pop. Dr Pepper, Coca-Cola, and Pepsi were all launched in the 1880s. A late-twentieth-century Coca-Cola CEO would describe the latter two as “the magnificent competitors,” dominating the industry and competing in the dissemination of their products—flavored, caffeinated sugar water—to every last backwater in the world. Soft
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Vin Mariani — was originally a Bordoux wine with Kola nuts and Cocoa leaves. The ethanol in the wine broke down Cocoa leaves into a solution of ~7% cocaine. Eventually became Coca-Cola.
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In 1891, Pemberton sold the Coca-Cola rights for twenty-three hundred dollars to Asa Candler, a former drugstore clerk and another maker of patent medicines, who set about creating a distribution network that within four years would have the product available in soda fountains in every state in the country and, within another two, in Canada and Mexico.
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Just as diabetes was an exceedingly rare disease (or at least diagnosis) prior to the industrial revolution and the steep rise in sugar consumption that followed, lung cancer was an exceedingly rare disease until cigarettes surged in popularity and transformed an uncommon disease eventually into a scourge.
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By the 1960s, children’s breakfasts had been reshaped into a morning variation on the theme of candy bars or dessert—perhaps lower in fat content, but richer than ever in sugar. Companies would offer all sorts of rationalizations for the creation of cereals that in some cases were over 50 percent sugar, and they would market them relentlessly to children.
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Kellogg’s, in 1950, released Sugar Corn Pops, even though most of the company stock was still held by the W. K. Kellogg Foundation, “a charitable organization established to promote children’s health and education.”
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As the University of California, Berkeley, authority Michael Pollan has so memorably put it, we should “eat food. Not too much. Mostly plants.” If we do this, we will get as close as we reasonably can to a healthy diet.
Medical Community on Sugar
When Isaac Newton said, “We are to admit no more causes of natural things than such as are both true and sufficient to explain their appearances,” he was saying the same thing that Albert Einstein, three centuries later, said (or was paraphrased as saying): “Everything should be made as simple as possible, but no simpler.”
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The purpose of a hypothesis in science is to offer an explanation for what we observe, and, as such, its value is determined by how much it can explain or predict.
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One of the common themes in the history of medical research is that a small number of influential authorities, often only a single individual, can sway an entire field of thought.
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The medical research community came to recognize that insulin resistance and a condition now known as “metabolic syndrome” is a major, if not the major, risk factor for heart disease and diabetes. Before we get either heart disease or diabetes, we first manifest metabolic syndrome.
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As soon as we think we are right about something,” the New Yorker writer Kathryn Schulz noted in her 2010 book Being Wrong, “we narrow our focus, attending only to details that support our belief, or ceasing to listen altogether.”)
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“The method of science is the method of bold conjectures and ingenious and severe attempts to refute them.”
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The simplest hypothesis—as encapsulated in Occam’s Razor—is always the most likely.
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Nutrition hypotheses are particularly challenging because they’re often about how foods or constituents of foods or dietary patterns influence our pursuit of a long and healthy life.
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The Nutritional Fads often have little evidence to support them from a science basis especially long term.
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Often in science, repeated tests of a hypothesis result not in its disproof but in less and less reason to believe it’s true.
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At the core of all nutrition controversies is a simple fact: the requirements of public-health policy and the requirements of good science can be mutually exclusive.
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One danger here, of course, is that once we insist or pretend that we know the answer based on premature or incomplete evidence (even if we’re pushed against our will to take such stands), we’re likely to continue to insist we’re right, even when evidence accumulates to the contrary. This is a risk in any human endeavor.
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Without rigorous tests, as many as necessary, beliefs and preconceptions will persevere because it’s always easier to believe that a single test has been flawed, or even a few of them, than it is to accept that our belief had been incorrect.
Sugars Role in Cancer, Alzheimers.
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Diabetes, heart disease, cancer, stroke, and Alzheimer’s account for five of the top ten causes of death in the U.S. A conservative estimate is that they cost the medical system and our society, in lost work and productivity, one trillion dollars a year.
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Insulin resistance is the fundamental defect present in type 2 diabetes and perhaps obesity as well.
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As sugar consumption rises and people ingest it over decades, and across generations, it causes insulin resistance and triggers the progression to obesity, diabetes, and the diseases that associate with them. Once this process starts, easily digestible, carbohydrate-rich foods aid and abet it.
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They suggest that type 2 diabetics have from one and a half to two times the risk of Alzheimer’s dementia of nondiabetics, suggesting in turn, as the Rotterdam investigators did in 1999, that “direct or indirect effects of insulin could contribute to the risk of dementia.”
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From the perspective of cancer as a metabolic disease, insulin and IGF promote the cancer process through a series of steps. First, insulin resistance and elevated levels of insulin trigger an increased uptake of blood sugar (glucose) as fuel for precancerous cells. These cells then begin producing energy through a mechanism known as aerobic glycolysis that is similar to what yeast will do in a nutrient-rich environment. (This phenomenon is known as the Warburg effect and was discovered in the 1920s by the German biochemist and later Nobel Laureate Otto Warburg, although its importance in the cancer process was not embraced until recently.) Once cancer cells make this conversion, they burn enormous amounts of glucose as fuel, providing them, apparently, with the necessary raw materials to proliferate. By metabolizing glucose at such a rapid rate, as Thompson suggests, these cancer cells generate relatively enormous amounts of compounds known technically as “reactive oxygen species” and less technically as “free radicals,” and these, in turn, have the ability to mutate the DNA in the cell nucleus. The more glucose a cell metabolizes and the faster it does so, the more free radicals are generated to damage DNA, explains Thompson. And the more DNA damage, the more mutations are generated, and the more likely it is that one of those mutations will bestow on the cells the ability to proliferate without being held in check by the cellular processes that work to prevent this pathological process in healthy cells. The result is a feed-forward acceleration of tumor growth. While this is happening, the insulin and IGF in the circulation both work to signal the cell to keep proliferating, and to inhibit the mechanism (technically known as apoptosis, or cell suicide) that would otherwise kick in to shut it down.
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IGF is secreted in response to growth hormone, rather than carbohydrate or protein consumption, as insulin is. It’s also secreted in response to insulin itself. Tumor cells appear to have two to three times the amount of IGF receptors as normal cells, and researchers believe that functioning IGF receptors are necessary for the growth of cancer cells. The consensus among researchers studying the role of insulin and IGF in cancer is that these hormones supply both the fuel necessary for tumors to divide and multiply, and provide the signals necessary to the tumors to keep doing so. The more insulin and IGF in the circulation, the more cancer cells are driven to multiply and tumors to grow.
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If the sugars we consume—sucrose and HFCS specifically—cause insulin resistance, then they are prime suspects for causing cancer as well, or at the very least promoting its growth. Even if the details of the mechanism should turn out to be wrong, the association between obesity, diabetes, and cancer, and the specific association between insulin, IGF, and cancer, suggests that whatever is causing insulin resistance is increasing the likelihood that we will get cancer. If it’s sugar that causes insulin resistance, it’s hard to avoid the conclusion that sugar causes cancer, radical as this may seem, and even though this suggestion is rarely if ever voiced publicly.
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Metformin, which works to reduce insulin resistance and therefore lower circulating levels of insulin, also had a significantly reduced risk of cancer compared with diabetics on other medications.
Sugar & Cigarettes
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As for tobacco, sugar was, and still is, a critical ingredient in the American blended-tobacco cigarette, the first of which was Camel, introduced by R. J. Reynolds in 1913.
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We have to consider the fact that cigarettes themselves would have been far less harmful and far less addictive had it not been for sugar.
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The critical factor driving both addiction and cancer is that cigarette smoke can be easily inhaled. When tobacco is drawn deep into the lungs, the nicotine can be absorbed, along with oxygen itself, over an internal surface area that has been estimated to be roughly half the size of a tennis court. (At most, 5 percent of the nicotine in tobacco smoke is absorbed in the mouth, according to Wightman Garner’s 1946 book, The Production of Tobacco.
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When the smoke is inhaled, a much greater proportion of the nicotine is absorbed.
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When tobacco is flue-cured, the harvested tobacco leaves are suspended over iron flues that heat the surrounding air to progressively higher temperatures. The process continues for the better part of a week, during which the heat first fixes the color of the tobacco leaves and then dries them, while breaking down the enzymes in the leaves that would otherwise break down the sugars they contain. Tobacco that begins with a relatively high carbohydrate content (up to 50 percent of dry weight) but is low in sugar (3 percent) ends up as much as 22 percent sugar, sucrose specifically. The “closest parallel” to what happens in the tobacco leaves during flue curing, notes the 1950 SRF report, is “the massive conversion of starch into sucrose” that happens when bananas are harvested and allowed to ripen.
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The sugar content of the flue-cured tobacco leaves is the key to inhalation.
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The high sugar content results in tobacco smoke that is acidic rather than alkaline—chemists would say that it has a lower pH. Alkaline smoke irritates the mucous membranes and stimulates the coughing response. Acidic smoke can be inhaled without doing either.
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Most people, as German researchers noted in the 1930s, are unable to inhale the alkaline smoke from pipe and cigar tobaccos, but they can inhale the acidic smoke from the sugar-rich, flue-cured tobacco in cigarettes.
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By 1929, U.S. tobacco growers were saucing Burley tobacco with fifty million pounds of sugar a year and using it in over 120 billion cigarettes.
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The sugar balanced out the tobacco’s naturally alkaline smoke, maximizing its inhalability and delivering even more nicotine into the lungs. The sugars in the tobacco also “caramelize” as they burn (technically, during the process of pyrolysis) and the caramelization of the smoke provides a sweet flavor and an agreeable smell that made cigarettes more attractive to women smokers and to adolescents as well.
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C. W. Barron, then the owner of The Wall Street Journal, made the pithy observation that if we want to make money in the stock market, we should invest in companies that provide us with our vices. “In hard times [consumers] will give up a lot of necessities,” he said, “but the last thing they will give up is their vices.”
Lipstick on a Pig: Sugar, the FDA, and Incentives
“Whose bread I eat, his song I sing,” President Franklin Roosevelt was calling the sugar lobby, according to The New York Times, “the most powerful pressure group that had descended on the national capital during his lifetime.”
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Sugar shares a common feature with those agricultural products for which the demand and supply are relatively immune to the price—what economists call “price inelastic.”
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As the economists Stephen Marks and Keith Maskus have noted, rising prices don’t lead to less consumption in these cases; they lead to greater production and eventually greater revenues for the producers.
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The Sugar Act effectively guaranteed that producing and refining sugar in the United States would always be a profitable business. It established the price of raw sugar (typically higher, if not significantly so, than world prices), put limits on domestic production, and set quotas on imports.
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In the six years leading up to America’s entry into the Second World War, soft-drink sales in the United States nearly quadrupled—from two hundred million to 750 million cases per year.
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In fact the indulgence of sugar has exceeded every other stimulant, even including tobacco, coffee, tea and alcohol.”
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(interesting fact) As late as 1900, only a single medical school in the United States—Johns Hopkins—required that applicants have a college degree. Many schools, according to a 1910 Carnegie Foundation report on the state of American medical education, did not even require that their students have finished four years of high school. Their primary criterion for acceptance was the ability and willingness to pay tuition.
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According to this logic of energy balance, of calories-in/calories-out, the only meaningful way in which the foods we consume have an impact on our body weight and body fat is through their energy content—calories.
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By the energy-balance logic, sugar is seen as at worst harmless and perhaps, as the sugar industry would come to argue, an ideal food for losing weight.
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By the mid-1960s, these carbohydrate-restricted diets, typically high in fat, were becoming fashionable, promoted by physicians, not academics, and occasionally in the form of hugely successful diet books.
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Over the next three years, the Sugar Institute placed regular advertisements in newspapers and magazines, promoting sugar as a health food—a 1930s equivalent of probiotics or multiple vitamins today.
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“We now eat in two weeks the amount of sugar our ancestors of 200 years ago ate in a whole year,”
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First, though, the Sugar Association hired the legendary Madison Avenue public relations firm Carl Byoir and Associates to design a public-health campaign that would “establish with the broadest possible audience—virtually everyone is a consumer—the safety of sugar as a food.”
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In 1960, when Stare’s nutrition department broke ground on a new five-million-dollar building, it was paid for largely by private donations, including the “lead gift,” as Stare described it, of $1.026 million from the General Foods Corporation, the maker of Kool-Aid and the Tang breakfast drink.
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How much does the funding of research by private organizations or by governmnt w inside aendas influenceth outcom of science? How can you see fthis from an investment vehical? Probiotics seems like another one of these. I wonder if you could use this fact to understand where the utcomeswould be of industries as a whole. Whats happening in the cannabis industry?
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FDA can’t really be trusted then nor now. It’s far too reactive than it is proactive. It responds after the fact. See ongoing issues with high frequency radiation.
Prenatal Imprinting
Data suggests that having high blood sugar—of being insulin-resistant and thus glucose-intolerant, of having metabolic syndrome—while pregnant are passed from mother to child in the womb.
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Today this concept is known as “perinatal metabolic programming” or “metabolic imprinting.” The conditions in the womb—in the intrauterine environment—influence the development of the fetus, so that subtly different conditions will lead, in effect, to the birth of newborns who respond differently to the environment they face outside the womb. In particular, the nutrients that the developing child receives in the womb—including the supply of glucose—pass across the placenta in proportion to the nutrient concentration in the mother’s circulation.
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Maternal obesity, as has been documented repeatedly, is a strong risk factor for childhood obesity and among the strongest predictors of metabolic syndrome and obesity in adulthood.
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Combine these observations with the research implicating high blood sugar and insulin resistance in the intrauterine environment—the influence of metabolic programming or imprinting on the generation to come—and it suggests that our consumption of sugar over the centuries may have changed the species.
How Much Sugar Should We Consume?
If it takes years or decades, or even generations, for us to get to the point where we manifest symptoms of metabolic syndrome, it’s quite possible that even these apparently moderate amounts of sugar will turn out to be too much to reverse the situation and return us to health.
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If these Western diseases are associated with obesity, diabetes, insulin resistance, and metabolic syndrome, which many of them are, then whatever causes insulin resistance and metabolic syndrome is likely to be the necessary dietary trigger for the diseases, or at least a key player in the causal pathway.
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In the second half of the nineteenth century in Western populations, and far more recently in others, obesity and type 2 diabetes emerged, eventually to become the dominant diseases of modern times. Insulin resistance characterizes both these disorders. And those who are insulin-resistant, who suffer from obesity and type 2 diabetes, are at higher risk of a host of other chronic diseases—the Western diseases, as Burkitt and Trowell described them—and these diseases, too, are associated with insulin resistance. How do we explain these observations? What has changed that could cause the emergence of these diseases worldwide and the insulin resistance that is associated with so many of them? What changes in our diets and our lifestyles can explain these changes in disease patterns? Is a simple hypothesis sufficient to do it? Is it that we’re all simply eating too much and exercising too little, which is the one simple answer that the nutritional establishment will embrace in the face of so much evidence to the contrary? Another simple answer, and a more likely one, is sugar. *
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The traditional response to the how-little-is-too-much question is that we should eat sugar in moderation—not eat too much of it. But this is a tautology.
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The same logic may also apply to sugar. If it takes twenty years of either smoking cigarettes or consuming sugar for the consequences to appear, how can we know whether we’ve smoked or consumed too much before it’s too late? Isn’t it more reasonable to decide early in life (or early in parenting) that not too much is as little as possible?