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Mainely Tipping Points 29: A Cultural Studies Answer

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Tipping Points 29

A CULTURAL STUDIES ANSWER

In WHY WE GET FAT (2011), Gary Taubes asks a scientific question.  His answer deploys scientific data from respected scientists working with the relationship of food to human body chemistry.  To recap, overweight people develop a hormonal disorder which is caused by eating carbohydrates, especially the easily digestible, highly processed carbohydrates (white flour, sugars, grains, starchy and/or sweet vegetables, and fructose from fruits bred to be big and sweet).  This disorder causes human bodies either to trap and store food energy in fat cells, no matter the energy needs of the body, or to funnel food energy to the muscles, which makes for a lean body with lots of energy that must be exercised away.

Taubes addresses some of why the inaccurate calorie in/calorie out, or “energy,” paradigm has persisted despite a decided lack of supporting science and the existence of a growing body of contrary evidence stretching back at least sixty years.  My own discipline, Cultural Studies, would begin where Taubes often leaves off by asking who is benefitting and what structural and cultural forces are being deployed for support.   

Cultural belief systems are probably the most powerful organizing forces man has ever devised.  Taubes describes a particularly insidious cultural belief that supports the energy paradigm.  By arbitrarily deciding that obesity is not a dysfunction of the body, a path opens which allows the belief that obesity is caused by the brain —which has been culturally interpreted to be about behavior, about character, about gluttony and sloth (80-86).    

Taubes’ identifies Louis Newburgh, a professor of medicine at the University of Michigan, as one originator of the “head case,” or psychological, explanation for obesity.    In the 1920s, Newburgh became a nationally recognized expert on obesity, and he posited that either obese people were taught to overeat by their parents or they had a “`combination of weak will and a pleasure seeking outlook upon life’” (83). 

“Newburgh,” Taubes notes, “was preaching to a medical establishment that had been taught to revere authority figures, not question their pronouncements” (83).  Newburgh, I’d say, lived in a time when most fat people were poor people.  He was a patriarch who was preaching something that most people of his own class understood to be true:  there’s something wrong with people who are poor, and the fat ones, well, they have “perverted appetites” (82).   

Wrapped up in this psychological explanation are the intersections of class, race, and gender.  Taubes points out that the poorer one is, the fatter one is likely to be since the calories available to the poor derive from cheap carbohydrates (18).  Taubes lists many worldwide studies of poor fat populations who are, with one exception, people of color.  (The exception is Naples, Italy, right after World War II ended, when Naples was destitute.)   Within these studies, the fattest of the fat, by large percentages, are women, who, Taubes infers, are giving the best food to their families (17-32). 

Taubes demonstrates that these poor people are not lazy, that they work hard, physical jobs.  And, like the investigating scientists, Taubes concludes that both malnutrition and subnutrition coexist in these populations because traditional patterns of living have been displaced and available food is mostly highly processed carbohydrates (17-32). 

The medical community, Taubes explains, uniformly swerved in the “head case” direction until well after World War II (84).  Historically, we know that post World War II America is when industry began providing more and more processed food, particularly the highly processed vegetable oils and margarines that replaced animal fats like butter, lard, and tallow.  And, we know that obesity, diabetes, heart disease, and cancer rates all increased.

In the 1970s, Taubes relates, the practice of “behavioral medicine” emerged and the term “eating disorder” became the preferred label, but the “head case” tenants are still intact.  The psychological eating dictates are with us today:  slow down your eating and eat only in the kitchen or at the dining room table (84).  I’d add this one:  we eat when we’re emotionally disturbed in order to nourish ourselves—rather than understanding when we’re emotionally upset, we have more trouble controlling an unsatisfying diet.  Anyway, Taubes notes that today “many, if not most, of the leading authorities on obesity are psychologists and psychiatrists, people whose expertise is meant to be in the ways of the mind, not of the body”—an outcome that ignores the chemical connections between obesity and diabetes (84). 

How is it that certain people get to be “experts” in combating obesity?  Newburgh, for instance, was a doctor of medicine.  Yet, most medical doctors study neither nutrition nor the chemical impact of foods on the human body.  So, where are medical doctors getting their information?  Like most of us, not many medical doctors have time to sit down and figure out whom among the “experts” actually has adequate credentials, is asking the right questions, has formulated solid scientific answers in an independent arena that is not tainted by either personal belief system or corporate funding, whose work has withstood ensuing peer critique, and whose results have been duplicated. 

Today, we are struggling with pronouncements from a host of medical doctors who have written very famous diet books—and made a lot of money–but whose diets often prove ineffective or, even, unhealthy when scientifically tested.  Many of these books are predicated upon the lipid hypothesis (anti-saturated fat).  Taubes uses the 1960s turn toward the belief that animal fats are bad for us and carbohydrates “heart healthy” to describe the formation of the lipid hypothesis belief system:   “…doctors and nutritionists started attacking carbohydrate-restricted diets, because they bought into an idea about heart disease that was barely even tested at the time and would fail to be confirmed once it was….They believed it though, because people they respected believed it, and those people believed it because, well, other people they respected believed it” (160-161). 

We are struggling with information from “expert” organizations like the American Dietetic Association, whose partners and sponsors, as revealed by Zoe Harcombe in THE OBESITY EPIDEMIC,  include “Coca-Cola ($31.4 billion), PepsiCo ($44.3 billion), GlaxoSmith Kline ($45.2 billion), General Mills ($14.9 billion), SoyJoy ($9.2 billion), Mars ($30 billion) and many others” (Tim Boyd, book review of Zoe Harcombe, THE OBESITY EPIDEMIC:  WHAT CAUSED IT?  HOW CAN WE STOP IT?, in “Wise Traditions,” Winter 2010, 50-52). Corporate industry funds academic departments and specific scientists and successfully obfuscates bedrock science, just as it did with tobacco and is doing with many current drugs and toxic chemicals.       

And we are struggling with a government whose agenda and regulatory mechanisms are controlled largely by industry–a government who has, regardless of dissenting bedrock science, used its authority and our tax dollars to effect vast, damaging, and unsustainable changes in our food system since World War II.  Industry has bent our government and our legal system to its will–corporations are now people, but do not have the ethical responsibilities of people–which is a potential death knoll for what remains of our democracy.      

In 1977, when Senator George McGovern’s U.S. Senate Select Committee on Nutrition and Human Needs—a group operating out of belief, not science, decreed that saturated animal fat was dangerous, Dr. Mary Enig, then a graduate student of biochemistry at the University of Maryland, was so puzzled that she analyzed the report and reached the opposite conclusions.  Enig’s own work pointed to the highly-processed vegetable oils and trans fats as the likely culprits in increasing rates of cancer and heart disease.  She noted that the McGovern committee had “manipulated the data in inappropriate ways in order to obtain untruthful results.”  She published her findings, and the edible oils industry not only successfully silenced her and her colleagues, they prevented them from getting any further research money.  Though Enig and her colleagues continued their research, it wasn’t until the 1990s when European work on trans fats began to be published that Enig was vindicated (http://www.stop-trans-fat.com/mary-enig.html).  Nevertheless, deadly trans fats, often labeled “partially hydrogenated fats,” are still allowed in our foods.  

So, who is benefitting from the current energy paradigm?  In the end, no one.

Mainely Tipping Points 28: Why We Get Fat

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Mainely Tipping Points 28:  WHY WE GET FAT

 

In WHY WE GET FAT (2011), Gary Taubes—a highly respected science researcher and writer, drives a scientific stake into the heart of the “calories in/calories out” paradigm that began developing in the 1950s and grew to become the medical orthodoxy we experience today.  Taubes explains the proven science behind why some people get fat—a question totally lost in the wilderness of the “energy balance” paradigm and its attendant low-fat/high carbohydrate diet.  The circular logic of this paradigm holds overweight people in a vicious, unscientific, damaging, deeply cultural  polarity:   either people of low character eat too much (gluttony) or exercise too little (sloth).  

Taubes traces the history of when research in nutrition and obesity “lost its way” and observes that these fields have “resisted all attempts” at correction.  Much understanding, Taubes writes, was lost after World War II with “the evaporation of the European community of scientists and physicians [particularly the Germans] that did the pioneering work” (ix).  Since that time, writes Taubes, “individuals involved in this research have not only wasted decades of time, effort, and money but have done incalculable damage….Their beliefs have remained impervious to an ever-growing body of evidence that refutes them while being embraced by public-health authorities and translated into precisely the wrong advice about what to eat and, more important, what not to eat if we want to maintain a healthy weight and live a long and healthy life” (ix). 

Taube’s earlier book GOOD CALORIES, BAD CALORIES (2008) is an extended, densely researched book written to start a conversation with “the experts.”  Taubes believes that it might take another lifetime to change this paradigm, but, meanwhile, he sees that the disease burden (obesity, diabetes, heart disease, and cancer) being created by eating the wrong foods is “overwhelming not only hundreds of millions of individuals but our health-care systems…” (x).  Taubes wrote WHY WE GET FAT so the lay person could understand what’s wrong and have the courage to take personal charge of his/her health rather than relying on “some of the misconceptions that pass for public-health and medical advice in this country” (xi).

So, why do some people get fat?  All real food, as compared to some of the chemical brews passed off as food today, is composed of fats, proteins, and/or carbohydrates.  In a nutshell, people have genetic tendencies toward fatness or thinness that combines with a hormonal chemical disorder caused by eating too many carbohydrates—which throws off the body’s ability to regulate fat accumulation appropriately in both fat and thin people. 

Here’s a gross simplification of Taube’s main explanation:  Fat accumulation is regulated by hormones, and the most important hormone is insulin.  Ideally, when our insulin levels are elevated, we accumulate fat in our fat tissue.  When insulin levels fall, fat is liberated from fat tissue and is burned for fuel.  However, easily digestible carbohydrates, like highly processed sugars and grains and starchy vegetables, make the body produce more insulin.  And, this insulin works to trap fat inside fat cells; it does not release them to burn for energy.  Thus, obesity is a hormonal imbalance, not a caloric imbalance.  Worse, this hormonal imbalance makes an overweight person hungrier because the body is growing larger, and it makes that person sedentary because all the food energy is being stored, not burned.  Gluttony and sloth are effects of this hormonal imbalance, not causes (10). 

Insulin, Taubes writes, works also with other hormones, like the sex hormones, and countless enzymes to partition fuel around the body.  This chemical process decides what food energy is burned, what is stored, and in which tissues it is stored (fat, muscle, liver).  An insulin disorder can partition a disproportionate amount of consumed calories into storage as fat, rather than having them used for energy by the muscles.  In lean people, the factors work to burn as fuel a disproportionate share of the consumed calories, which creates high energy levels (128).   

Some people, Taubes explains, develop insulin resistance, which means the body has to secrete higher and higher insulin levels in order to perform the same tasks—a “vicious cycle” intensified by eating easily digestible carbohydrates.  Next, these people start to manifest the precursor to heart disease, metabolic syndrome.  Body fat accumulates, especially around the waist; blood pressure rises; triglycerides levels rise; LDL cholesterol particles become small and dense; HDL cholesterol levels fall; and blood sugar becomes erratic (glucose intolerance).  Diabetes occurs when the pancreas can no longer secrete enough insulin to keep the body balanced.  And Alzheimer’s and most cancers are “associated with metabolic syndrome, obesity and diabetes” (195-198). 

Taubes’ subject is why we get fat, so he does not address the health effects on the lean, energetic person whose leanness is created by this hormonal disorder, which is, in turn, caused by eating too many of the wrong kinds of carbohydrates.  He does note that that as we age, our muscles become increasingly resistant to insulin and more energy gets partitioned into fat (130-131).   

There are generational components to these disorders.  Taubes notes that worldwide studies demonstrate that children born to a mother with hormonal imbalances that have created obesity are likely, also, to struggle with obesity.  The nutrients the mother’s body supplies to her baby affects his/her levels of glucose, which, in turn, affects the pancreas so that it develops more insulin-secreting cells, which, in turn, makes the baby fatter at birth.  These babies have a tendency both to oversecrete insulin and to become insulin-resistant (132).            

Exercise, Taubes demonstrates effectively, will not make one lose weight.  Indeed, for weight loss, exercise is counterproductive because it creates hunger (40-56).  And, undereating  does not work.  At some point one must return to eating normally, and the weight returns.  Taubes reports that the eight-year, billion-dollar National Institutes of Health initiative, the Women’s Health Initiative (WHI) of the 1990s, showed that a low-fat diet did not result in weight loss and “did not prevent heart disease, cancer, or anything else” (33-39). 

Taubes looks at many current studies, among them the 2007, two million dollar, government-funded A TO Z Weight Loss Study from Stanford University which compared four diets:  Atkins (low carbohydrate), LEARN (a traditional diet with 55-60 percent carbohydrates), Ornish (low fat), and the Zone diet.  The Atkins diet won, substantially and significantly, across the measured categories (weight loss, dropping triglyceride levels, dropping blood pressures, and improved cholesterol conditions)—prompting lead researcher Christopher Gardner, a twenty-five year vegetarian, to note that the results were, for him, a “`bitter pill to swallow’” (191-192). 

Taubes notes that Atkins diet participants were allowed to eat as much red meat and meat fat as they wanted (191-192).  And, that “since the 1960s, when it was first argued that animal products could be bad for our health because they contains saturated fat, nutritionists have typically refrained from pointing out that meat contains all the amino acids necessary for life, all the essential fats, and twelve of the thirteen essential vitamins in surprisingly large quantities.”  Meat, writes Taubes, “is a particularly concentrated source of vitamins A and E, and the entire complex of B vitamins.”  Indeed, “vitamins B12 and D are found only in animal products….”(176).

Vitamin C is the “one vitamin that is relatively scarce in animal products.”  But, “the more fattening carbohydrates we consume, the more of these vitamins we need.  We use B vitamins to metabolize glucose in our cells.  So, the more carbohydrates we consume, the more glucose we burn (instead of fatty acids), and the more B vitamins we need from our diets.”  When we eat carbohydrates, we “excrete vitamin C with our urine rather than retaining it” (176). 

Without carbohydrates in the diet, Taubes notes, “there’s every indication that we would get all the vitamin C we ever needed from animal products.”  Thus, Taubes concludes, “Carbohydrates are not required in a healthy human diet.”  And, “another way to say this (as proponents of carbohydrate restriction have) is that there is no such thing as an essential carbohydrate” (176).             

The solution to both obesity and leanness accompanied by excessive energy is actually pretty simple:  stop eating carbohydrates, especially the easily digestible ones, like, bread, pasta, potatoes, sweets, beer, fruit  juices, and sodas.  (I’d add cold breakfast cereals to this list.)  Taubes notes that before the 1960s, conventional wisdom recognized that these foods were “uniquely fattening.”  And, he notes that this message has been at the heart of an “unending string of often best-selling diet books” (11).  He also notes that “when physicians stopped believing it, a process that began in the 1960s and concluded in the late 1970s,” their change coincided “with the beginning of the current epidemics of obesity and diabetes” (150).     

Taubes does note that if the obesity has gone on too long, the body may not be able to reset its own chemistry (205).  And, that if one is taking medications to lower blood sugar or blood pressure, one should work closely with a doctor because following a low-carbohydrate diet lowers both so that a dangerous “double whammy” effect can occur (216). 

Taubes reproduces the Atkins-version diet used by Dr. Eric Westman of the Lifestyle Medicine Clinic at the Duke University Medical Center.  Westman has been working with this diet since 1998 (202).  And, Taubes points to four other doctors with similar clinical practices across the country (202).   

My only critique of this diet is that it allows artificial sweeteners and does not distinguish well between good fats and bad fats.  But, you can read Tipping Points 14 to understand how to sort those fats out for yourself.

Mainely Tipping Points 17: High Fructose Corn Syrup

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Mainely Tipping Points 17

High Fructose Corn Syrup

 Despite the food industry’s attempt to tell us so, all food calories do not have the same impact on our bodies.  Nor are all sugars equal.  Most sweeteners are formed from three different sugars (sucrose, glucose, and fructose), and each has a different impact on the body. 

 Sugars are carbohydrates, and, according to Dr. Natasha Campbell-McBride in GUT AND PSYCHOLOGY SYNDROME (2004), all carbohydrates are made of tiny molecules, called monosaccharides, or monosugars.  Glucose and fructose are monosugars, so do not need digestion.  They enter the gut directly.  Sucrose is a disaccharides, or double sugar, and it and other double sugars (lactose from milk and maltose from starches) require “quite a bit of” digestive work in a healthy body to reduce them to absorbable monosugars.  Unhealthy bodies harbor these undigested sugars in the gut, and an unfortunate chain of disease begins as these sugars feed “pathogenic bacteria, viruses, Candida and other fungi,” which themselves begin to produce toxic substances that “damage the gut wall and poison the whole body” (79-81).        

Most sweeteners have different sugar compositions.  High Fructose Corn Syrup (HFCS) is typically 42-55 percent fructose and 45-55 percent glucose.  Honey is 50 percent fructose, 44 percent glucose, and 1 percent sucrose.  Only raw sugar is 100 percent sucrose  (“Sugar by Any Other Name,” NUTRITION ACTION HEALTH LETTER, Center for Science in the Public Interest, Jan/Feb 2010, page 4).  But, as Sally Fallon Morell and Rami Nagel explain in WISE TRADITIONS (Spring 2009), the type of fructose in HFCS is not the same as fructose from fruit and our bodies do not know how to process it into energy (“Worse Than We Thought,” 44-52).

Industry creates HFCS from corn starch, which largely comes from genetically modified corn.  For an amusing, but serious explanation of how HFCS is made, take a look at the movie KING CORN (2007).  A not-so-funny fact surfaced recently according to Morell and Nagel :  nearly 50 percent of samples of commercial HFCS contained mercury, which was found also in nearly one-third of “55 brand-name food and beverage products where HFCS is the first- or second-highest labeled ingredient” (47).

 Fructose in fruit, report Morell and Nagel, is “part of a complex that includes fiber, fatty acids, vitamins and minerals.”  The fructose in HFCS is a free, unbound fructose with an important chemical difference.  Most fruit fructose is D-fructose, or levulose, but HFCS fructose is L-fructose, an artificial compound which has “the reversed isomerization and polarity of a refined fructose molecule.”  Thus, the fructose in HFCS is “not recognized in the human Krebs cycle for primary conversion to blood glucose in any significant quantity, and therefore cannot be used for energy utilization.”  Instead, HFCS, like all refined fructose sweeteners” is “primarily converted into triglycerides and adipose tissue (body fat).”  

Indeed, report Morell and Nagel, a new study published in the “Journal of Clinical Endocrinology and Metabolism, “found that obese people who drank a fructose-sweetened beverage with a meal had triglyceride levels almost 200 percent higher than obese people who drank a glucose-sweetened beverage with a meal.”  Chronic, high triglycerides, remind Morell and Nagel, cause increased insulin resistance, inflammation, and heart disease (47).

Nancy Appleton and G. N. Jacobs, in WELL BEING JOURNAL, reported that two published studies (2010) from Princeton University demonstrated that HFCS causes obesity in rats The researchers think that HFCS is more fattening than sugar because it is not bound to anything, which, in turn, allows it to be processed in the liver into fat—substantially abdominal fat—a risk factor for high blood pressure, heart disease, diabetes, and cancer.  Sucrose is” metabolized by insulin from the pancreas and is more readily used as an energy source.”  Additionally, HFCS bypasses the body’s ability to create satiety, or feeling full (“High Fructose Corn Syrup and Obesity,” WELL BEING JOURNAL, Sept/Oct. 2010, 9-10).  Morell and Nagel note that since all fructose is metabolized in the liver, the livers of test animals “fed large amounts of fructose develop fatty deposits and cirrhosis, similar to problems that develop in the livers of alcoholics (48).”

Rats aren’t humans.  But epidemiologist Devra Davis in THE SECRET HISTORY OF THE WAR ON CANCER (2007) notes that industry has been very adept at both decrying and promoting animal studies:  “Where animal studies on the causes of cancer exist, industry faults them as not relevant to humans.  Yet when studies of almost identical design are employed to craft novel treatments and therapies, the physiological differences between animals and humans suddenly become insignificant” (xii).  So, Davis argues, dismissing animal studies is a type of reasoning that is both “morally flawed” and “ignores one simple fact:  the same basic structure of DNA is found in all mammals (8)”  Davis writes that she has witnessed in her professional life “the maturing of the science of doubt promotion,” or “the concerted and well-funded effort to identify, magnify and exaggerate doubts about what we could say that we know as a way of delaying actions to change the way the world operates” (xii).  Thus, “treating people like experimental animals in a vast and largely uncontrolled study,” while ignoring data from animal studies showing direct cause-and-effect data, is ”morally indefensible” (8).

Morell and Nagel report that HFCS entered the market in the early 1970s, but the FDA did not grant it GRAS (Generally Recognized as Safe) status until 1996, “after considerable pressure from the industry” (mainly Archer Daniels Midland and Cargill) as negative research begin to emerge.  Nevertheless, “HFCS represents the major change in the American diet over the last forty years” as it has replaced more expensive sugar in most soft drinks and is “increasingly replacing sugar in baked goods, bread, cereals, canned fruits, jams and jellies, dairy desserts and flavored yoghurts.”  This substitution is occurring despite research showing that while refined sugars have “empty, depleting, addictive calories,” HFCS is “actually worse for you” (44-45).

 The Center for Science in the Public Interest (CPSI) notes that industry has added so many sugars to processed foods that “the average American swallows 350 to 475 calories’ worth of added sugars each day,” all of which are empty calories (“Sugar Overload,” NUTRITION ACTION HEALTH LETTER, Jan/Feb 2010, 3-8).  Dr. David A. Kessler, a former FDA commissioner, in THE END OF OVEREATING (2009), focuses on how industry has added sugar, salt, and bad fats to processed foods, which is changing a pattern where “for thousands of years human body weight stayed remarkably stable” (3). 

The HFCS story gets worse.  A team of researchers at the University of California Los Angeles Jonsson Cancer Center released a study on 2 August 2010 revealing that pancreatic tumor cells use fructose to divide and proliferate.  Dr. Anthony Heaney said that tumor cells thrived on glucose, but used fructose to proliferate.  He specifically referred to Americans’ use of refined fructose consumption.  Our use of HFCS has increased 1000 percent between 1970 and 1990 (Maggie Fox, “Cancer Cells Feed on Fructose, Study Finds,” 2 Aug. 2010, Reuters).         

HFCS can cause high blood pressure.  A study from the University of Colorado Denver Health Sciences Center recorded the eating habits of over 4,500 adults to determine that amount of HFCS each was consuming.  Those consuming “more than 74 grams of HFCS (the equivalent of 2.5 servings of soft drinks) exhibited `significantly increased risk of developing hypertension.’ “  Indeed, “the study concluded that HFCS consumption can raise blood pressure in adults with no history of hypertension, independently of any other causes” (“High Fructose Corn Syrup = High Blood Pressure, WELL BEING JOURNAL, March/April 2010, 6).   

 Connections are being made between HFCS and gout.  Fructose increases uric acid, and uric acid causes gout.  A study of about 46,000 men who got “at least 12 percent of their calories from fructose” were” twice as likely to be diagnosed with gout” (“Sugar Overload,” NUTRITION ACTION HEALTH LETTER, Jan/Feb 2010, 7). 

 I found much more information showing that HFCS is a dangerous product that is causing humans significant harm.  It’s also likely that industry knows how dangerous it is, but uses it anyway because it is sweet and cheap.  Remember that industry is legally organized to behave this way.  What you can do is to eat nutrient-dense, organic, local foods to maintain your health.