Insulin Resistance and the Diabesity Epidemic

Here is a ton of information on the insulin resistance>diabesity link for those who are interested from my capstone project for my Master’s in Public Health degree.  Enjoy.  Feel free to ask me any questions you may have.

 

 The “Diabesity” Epidemic:

Is it only obesity and diabetes, are sugary drinks a primary cause, and does Occam’s Razor apply?

Robert U. Wright, Jr.
Capstone Project
MPH Candidate, Epidemiology
University of Georgia College of Public Health
Spring 2012

 

 

 

 

 

 

 

 

 

 

Table of Contents

  • Background on “Diabesity” Epidemic-pgs. 3-36
    • Diabesity trends in U.S.-pg.4
    • Diabesity =metabolic syndrome? –pg. 3-36
    • Insulin resistance/carbohydrate hypothesis of metabolic syndrome-pg. 5-36
    • Sugary drinks as primary cause of metabolic syndrome?-pg. 7-8
    • Metabolic syndrome = most chronic diseases in U.S.?-pg. 5-9
    • Failure of public health to prevent metabolic syndrome -pg.5, 10-36
    • The unintended consequences of low-fat dietary guidelines -pg. 10-17
    • Does public health impede scientific progress?-pg. 11-36
    • Food consumption trends in U.S.-pgs. 12-17
    • Implications of metabolic syndrome on our understanding of obesity treatment and prevention-pgs. 17-36
    • Why current diabesity treatments/prevention efforts fail pgs. 17-28
    • The common misinterpretation of the law of conservation of energy -pgs. 26-33
    • A calorie is not a calorie -pg. 28
    • An alternative treatment = carbohydrate restriction? -pg. 29-36
    • Occam’s Razor: can carbohydrate be considered the primary driver of diabesity?  -pg. 34-35
    • The “Fight for Fitness in Fulton” Survey –pg. 37-62
      • Problem –pg. 37
      • Objectives –pg. 37
      • Methods –pg. 37-38
      • Results -pgs. 39-54
      • Discussion –pgs. 54-58
      • Limitations –pg. 59
      • Recommendations –pg. 60
      • Future Studies –pg. 60-62
      • Definitions-pg. 63-73
      • References-pg. 74-115

 

Background on “Diabesity”:

“‘Like a malignant tumor or like the fetus, the uterus or the breasts of a pregnant woman, the abnormal lipophilic [fat] tissue seizes on foodstuffs, even in the case of undernutrition.  It maintains its stock, and may increase it independent of the requirements of the organism.  A sort of anarchy exists; the adipose tissue lives for itself and does not fit into the precisely regulated management of the whole organism.’”

-Dr. Julius Bauer, 1929, quoted by Gary Taubes in Good Calories, Bad Calories[1]

“Dysregulation of adipose tissue physiology contributes to disease…experience with human and animal lipodystrophies (abnormalities of adipose tissue quantity and distribution), indicates that the relationship between obesity and diabetes is not due to the magnitude of fat accumulation per se, but rather the functioning of the adipose organ.”

-Todd Leff and James G. Grannerman, 2010, Adipose Tissue in Health and Disease[2]

“Obesity has long been known to be a state of resistance to insulin, the preeminent metabolic hormone.” [3]

–Dr. Jeffery Flier, Dean of the Harvard Medical School, October, 2010, Cell

“Insulin resistance increases the chance of developing type 2 diabetes.”[4]

– U.S. Dept. of HHS, NIDDK, NDIC., Dec. 6, 2011, “Insulin Resistance and Prediabetes”

“The association of obesity with risk for diabetes is most notable. Women aged 30–55 years with a BMI ≥35 kg/m2 have, for instance, a more than 80-fold increase in risk, and men of this degree of obesity a more than 40-fold increase [relative to those with a normal BMI].”

-Bakker, Stephen J.L et al, Oct. 18, 2006, Nephrology Dialysis Transplantation[5]

 

“Imagine how many more dead diabetics we’d have if victims of that disease were treated by psychologists instead of physicians.  And yet diabetes and obesity are so closely linked-most type 2 diabetics are obese, and many obese people become diabetic-that some authorities have taken to calling the two disorders “diabesity,” as though they’re two sides of the same pathological coin, which they assuredly are.”[6]

–Gary Taubes, Why We Get Fat and What to Do About It, 2010

In the U.S., the prevalence of obesity[i] and type 2 diabetes, the predominate form of diabetes in the American population, have both increased dramatically over the past 40-50 years.[7],[8],[9],[10], [11]  Over this time period, the prevalence of obesity has nearly tripled in non-institutionalized adults[ii] over 20 years of age to nearly 78 million people, nearly quadrupled in adolescents between 12 and 19 years of age, and doubled in children aged 2-5 according to NHANES data (found 12.5 million youths aged 2-19 were obese in 2009-2010).[12],[13],[14],[15]  At the same time, the proportion of the U.S. population with diagnosed diabetes has increased from, according to the CDC’s NHIS survey, 0.93% in 1958 to 6.86% in 2009, with most of these cases being type 2 diabetes (other sources, such as the BRFSS, list diagnosed diabetes prevalence at 8.7%, with ethnic and racial minorities suffering at higher rates than non-Hispanic Whites).[16],[17],[18]  Another 79 million people are thought to be pre-diabetic and at risk for the eventual development of diabetes within ten years.[19],12

Given the similar population trends and hypothesized etiology of both conditions (explained in subsequent paragraphs), many researchers consider obesity and diabetes to be different sides of essentially the same epidemic, a “diabesity” epidemic, composed of the concurrently explosive incidence of both conditions within the same U.S populations.[20],[21]  Many researchers go even further by linking these conditions to a vast array of co-morbidities that compose and are consequences of a syndrome they believe has a common origin.[22],[23],[24],[25],[26],[27]  This syndrome, first known as “Syndrome X” and now “The Metabolic Syndrome,” includes and may lead to the development of such conditions as central obesity, hyperinsulemia, type 2 diabetes, hypertension, stroke, dyslipidemia, inflammation, coronary heart disease, many types of cancer, Alzheimer’s (now described as “type 3 diabetes” by certain researchers), non-alcoholic fatty liver disease (which 0.5 million UK children now have), even goutand many other conditions.[28],[29],[30],[31],[32],[33],[34],[35],[36],[37],[38]  In May of 2009, the CDC, using 2003-2006 NHANES data (which uses actual measured, not self-reported, data), estimated that over 34% of American adults had metabolic syndrome (defined in 2001 by ATP III panel of The National Cholesterol Education Program, “arbitrarily” according to the man who coined the term “the metabolic syndrome,” Dr. Gerald Reaven, as at least three of the following: abdominal obesity, high triglycerides, low HDL, high blood pressure, and high blood glucose) and that overweight and obese individuals were 6 and 32 times (for males) and 5.5 and 17 times (for females) more likely to have metabolic syndrome than normal weight individuals, respectively.[39],[40]  Therefore, whatever causes obesity may also cause all of the other conditions associated with metabolic syndrome (which may explain the consistent observation that excess body fat is associated with many other chronic diseases like type 2 diabetes, heart disease, stroke, and that up to one-half of common cancers, like breast, colorectal, endometrial, adenocarcinoma, are “account[ed]” for by excess body fat).[41],[42]

The metabolic syndrome and the conditions associated with it are thought to encompass the wide spectrum of  chronic diseases, once referred to as “diseases of civilization” and now called “diseases of Western [American] lifestyles,” as they are virtually absent in most non-Western and/or pre-modern societies and yet emerge within a few generations in these peoples after they adopt westernized-lifestyles.[43]  Therefore, it is likely that one or more variables unique to the American/Westernized-lifestyle are contributing to the metabolic syndrome disease burden within our population (and others around the world that adopt certain aspects of our American lifestyle).[44],[45]

Given that obesity and diabetes prevalence rates have approximately tripled in the past 30 years, it is clear that public health has failed in preventing this “diabesity” epidemic.  Therefore, we, as public health scientists, must be willing to question the conventional wisdom of obesity and diabetes prevention and obtain funding to test alternative hypotheses that may better explain the problem by uncovering the fundamental variables at work (even if the conduction and conclusions of such studies suggest that past recommendations were flawed and require a public admission of such mistakes).  One persuasive alternative hypothesis of metabolic syndrome and diabesity derived from much of the latest anthropological, biochemical, epidemiological, and food availability research is that the primary biological mechanism driving metabolic syndrome may be a condition called insulin[iii] resistance, a condition related to the body’s inability to regulate blood sugar and fat tissue metabolism, likely caused by the primary “necessary cause” of the chronic overconsumption of refined carbohydrates, especially sugar and high fructose corn syrup (HFCS) (both of which are roughly 50/50% glucose/fructose), as well as other low-fiber starches such as white flour foods, rice, and potatoes in the majority (~70%) of the American population who are, as Volek and Phinney describe, overweight and obese due to “carbohydrate intolerance.” [46],[47],[48],[49],[50],[51],[52],[53],[54],[55],[56],[57]

This widespread “carbohydrate intolerance” likely arose because, as Cordain et al suggest, refined carbohydrates, such as grains from agriculture and sugars like sucrose and HFCS, are a very recent addition to the evolutionary diet of man (grains coming ~10,000 years ago, and high consumption of sugar and HFCS only emerging in the U.S. roughly 100 and 30 years ago, respectively) and that humans evolved over the previous 2.4 million years to eat a relatively low carbohydrate diet (~22-40% of energy mostly from high fiber, low carbohydrate wild plants, not year-round access to very sweet fruits and refined carbohydrates like grains and sugars).[58]  Codain et al also hypothesize that most hunter-gatherer societies (73%) gathered a majority of their daily calories (45-65% of energy) from animal foods and that the carbohydrates that were consumed (again, only ~22-40% of energy) were from plants higher in fiber and lower in carbohydrate than current produce (certain pre-modern societies, such as the Inuits of Northern Canada, Native Americans of the Great Plains, and Masai tribesmen of Central Africa, consumed only animal products, meaning no carbohydrates other than the glycogen in muscle tissue, with little if any obesity, diabetes, cancer, etc.).[59],[60],[61]

Refined carbohydrates are considered the primary driver of insulin resistance and therefore metabolic syndrome/diabesity, for two reasons.  First, because they are the primary driver of insulin-the hormone responsible for putting what we eat in our fat tissue (according to Basic Medical Endocrinology, “Insulin is essential for the uptake and synthesis of the triglycerides that form the lipid droplet that is the central feature of adipocyte morphology and function”) and, when insulin levels are high, of keeping fat in our fat tissue (known as the “lipid trapping” effect of insulin); as renowned lipid researcher George Cahill has stated, “carbohydrate is driving insulin is driving fat,” (protein has a slight effect upon insulin and fat none at all).[62],[63],[64]  And secondly, because of the effects of fructose, found in large quantities in sugar and HFCS, in generating fat in the liver-making it the likely “trigger” of insulin resistance.[65],[66],[67],[68],[69],[70]  It is the quantity and speed of absorption (flux) of the fructose and glucose compounds in these foods (liquids faster than solids) that raise insulin levels (the glucose) and fatten and damage the liver (the fructose) that may, over time, generate hyperinsulemia and eventually the insulin resistance in sensitive populations that increases their risk of developing metabolic syndrome/diabesity (central obesity, type 2 diabetes, and many other chronic conditions discussed below).[71]

Though the mechanisms of metabolic syndrome are complex and numerous, they primarily involve the effects of glucose upon the body’s insulin system (the pancreas’s β-cells) and fructose’s lipogenic (“fat producing”) effects upon the liver, both of which damage the body’s hormonal regulation of blood glucose and fat tissue (and have other homeostatic-disruptive effects).[72],[73],[74],[75],[76]  High glucose consumption raises blood sugar which spikes blood insulin levels through over-stimulation of the pancreas beta-cells which, in conjunction with excess fructose’s conversion to triglycerides in the liver, leads to fat deposition, chronically elevated blood glucose levels (which generate inflammation and AGE-production), hyperinsulemia and, eventually, the development of insulin resistance (usually first in the liver and lean tissue) which begins the process of driving the metabolic syndrome conditions.[77]  Fructose, known as the most lipogenic carbohydrate, is thought to be especially harmful to the body’s regulation of insulin and triglycerides (fat) through its effect on the liver and, again, is likely the “trigger” that sparks insulin resistance.[78],[79],[80],[81],[82],[83]

Certain types of refined carbohydrate foodstuffs may play a greater role in generating metabolic syndrome than others.  Beverages sweetened with sugar/HCFS are likely the primary driver of metabolic syndrome for three reasons: one, both are roughly 50/50 glucose/fructose and this unique combination of the two is thought to be especially disruptive of insulin (pancreas), the liver, inflammation, and other homeostatic organ-systems, two, they are liquids and so are absorbed faster than solid sugars, and, three, because they comprise the highest proportion of added sugar in the American diet (average sugary drink intake for Americans increased three-fold from the late 1970’s to 2001).[84],[85],[86]  The reason why sugary drink’s liquidity is thought to be such a powerful driver of metabolic syndrome is that the sugars they contain are absorbed so much faster than solid sugars; this increased flux likely explains why sugary drinks appear to increase food intake relative to solid sugars because the faster absorption of glucose and fructose likely increases the rate of insulin secretion that blocks leptin, a satiety hormone, from registering at the hypothalamus to register satiety more quickly than the same amount of solid sugar, though both likely have more disruptive effects upon hunger/satiety signals than non-sugars. [87]

These are a few of the reasons why certain public health researchers and authorities are pushing for regulation of sugary drinks (especially in California, which is consistently on the vanguard of progressive public health initiatives). [88],[89],[90],[91]  Another is that sugar is thought to be addictive in much the same way as nicotine, heroin, and cocaine (through their action on the brain’s “pleasure centers”); this addictiveness may make effective regulatory efforts difficult to implement, however and may explain why banning sodas, but not other sugary drinks in schools, did not reduce average student sugar consumption in a recent study analyzing school sugary drink policies.[92],[93],[94]  These sugary drinks may also have greatly shortened the traditional latency period of metabolic syndrome/diabesity following exposure to sugar in the diet (~20 years): the historical latency period for the development of diabetes in a susceptible population after its exposure to sugar was thought to be potentially decades yet now, children are developing type 2 diabetes (no longer adult-onset) as well as NAFLD (Non-alcoholic fatty liver disease, a key early predictor of the incidence of insulin resistance) at tremendous incidence rates at historically unparalleled ages (~0.5 million of UK youth).[95],[96],[97],[98]

The “lipid trapping” effect of insulin also may explain the existence of carbohydrate cravings, for sugars and starches, amongst the obese and diabetic because someone with hyperinsulemia, a key marker of insulin resistance, can only burn glucose (i.e. carbohydrates) for fuel as the elevated insulin prevents stored triglycerides in adipose tissue from being released as fatty acids in the blood stream and burned for fuel (hence the term “lipid trapping”).[99],[100]  This then generates a destructive positive feedback loop where increased hyperinsulemia and insulin resistance (especially in lean tissues) drives increased carbohydrate consumption drives increased hyperinsulemia and insulin resistance; meanwhile, the person is becoming progressively more obese and suffering from other worsening complications of metabolic syndrome that include progressively elevating body weight, blood glucose, etc.[101]

Interestingly, Seneff et al hypothesize that it is the interaction of a high refined carbohydrate intake AND a low-fat, low-cholesterol diet, that is the main generator of metabolic syndrome for a few interrelated  physiological reasons: de novo lipogenesis in the liver is upregulated by a high-carbohydrate, but not high fat, diet, especially one rich in fructose, while lack of fat fails to slow digestion of carbohydrates (and so fails to slow blood glucose rise) and lack of cholesterol leads to low cholesterol in adipocyte plasma membranes which may contribute to insulin resistance (again, the liver’s de novo lipogenesis likely plays a pivotal role in insulin resistance which is why NAFLD and liver insulin resistance are reliable early indicators of the incidence of insulin resistance, according to Seneff et al).[102],[103],[104]  Seneff et al also hypothesize that high-fiber intake, in conjunction with a low-fat and low-cholesterol diet, exacerbates insulin resistance and pancreatic β cell dysfunction by blocking absorption of calcium in the gut.[105]

Metabolic syndrome includes and may lead to the development of a vast and disparate group of diseases because the overconsumption of glucose and fructose leads to the deregulation of the hormone insulin which induces hyperinsulemia and insulin resistance  which, in some way, may cause ALL of these diseases (i.e. hyperinsulemia/insulin resistance is possibly a slice of the “causal pie”-see Rothman below, of all of these conditions, and may even effect non-obese/diabetics with elements of insulin resistance, only at much lower rates than the obese).[106],[107],[108]  These metabolic syndrome/diabesity co-morbidities include, but are not limited to: fattening (insulin deposits triglycerides in insulin sensitive fat cells, many being in the abdomen and around the viscera, now that lean tissue (i.e. “muscle”) is resistant), dyslipidemia (carbohydrates lower HDL levels and elevate triglyceride, Type-B or small, dense LDL, and AGE (advanced glycolated end-product) levels), inflammation (elevated C-reactive protein), hypertension (raised insulin and/or fructose make the kidneys reabsorb salt and therefore water so blood pressure rises), and therefore, the atheriosclorosis of heart disease (dyslipidemia, along with elevated blood pressure and inflammation leads to small, dense LDL becoming oxidized and forcing its way between artery walls to cause damage that begins the foam cell process of plaque formation), hyperinsulemia and cancers[iv] (hyperinsulemia is thought to promote tumor growth as many tumors “love the [hyperinsulemic] metabolic environment of the obese” and feed off of blood glucose, insulin-like growth factor (IGF), and insulin; one researcher, in Taubes 2012, describes breast cancer cells as “addicted to [insulin]”), gout (fructose leads to uric acid buildup in the blood stream which, along with obesity, inflames joints causing arthritis), and, potentially, many other conditions.[109],[110],[111],[112],[113],[114],[115],[116],[117],[118],[119],[120],[121]

Therefore, using Rothman’s sufficient-component cause model of disease, for the vast majority of Americans suffering from obesity and related conditions, their “causal pie” model includes the “necessary cause” of refined carbohydrate overconsumption, specifically fructose, to complete the “pie” and trigger the condition of insulin resistance that drives metabolic syndrome.[122]  As discussed in regards to latency period, this causal mechanism may be accelerated in obese children, many of whom may have suffered epigenetic alterations while in the womb of their obese and diabetic mothers, which predispose them to fatten right out of the womb.[123]  According to Kim et al, there is an epidemic of obese six-month olds, and ~31% of 2-4 year olds on Women Infants Children food programs were overweight and obese in Georgia in 2009 (two times the estimated prevalence in the early-1990’s): these data are alone are enough to refute the “energy balance” hypothesis of obesity that one’s poor personal choices regarding eating and exercise behavior over years and decades are the sole variable responsible for determining obesity (i.e. that children as young as sixth months are becoming obese in record numbers is clear and irrefutable proof that obesity is a hormonal condition due to the deregulation of the fat tissue due to excess insulin secretion from carbohydrate consumption, and therefore, that obesity is not an eating disorder residing in the brain, it is a metabolic disorder residing in the body-see subsequent paragraphs below).[124],[125],[126]

It is clear that the past 32 years of nutritional recommendations by government (such as the USDA and Dept. of HHS’s “1980[-2000] Dietary Guidelines for America” and “Food Guide Pyramid”), the medical community (JAMA, The American Heart Association, etc.), and the media (see Jane Brody of the New York Times) to eat a low-fat, high carbohydrate, calorie-restricted diet plus exercise to combat heart disease and promote “energy balance,” and thereby limit weight gain, have failed to prevent obesity and heart disease given the huge simultaneous increase in prevalence in obesity and related conditions during this time period (the fact that the incidence of heart disease did not decline during this period, even with drastic reductions in smoking prevalence, suggests something, possibly metabolic syndrome/diabesity, is counteracting the effect of smoking reduction on heart disease incidence).  [127],[128],[129],[130], [131],[132],[133],[134],[135],[136],[137],[138]   This failure has likely likely occurred in part because nutritional ’distraction with dietary fat caused them to ignore the biochemical/physiological data on insulin and fructose metabolism that has suggested, since the 1960’s, that the fundamental causes of metabolic syndrome/diabesity (and, therefore, of heart disease) is refined carbohydrates and sugars (according to Dr. Walter Willet, of the Harvard School of Public Health, in a 2002 article in Obesity Reviews).[139],[140],[141],[142]

This “distraction” with the saturated fat > heart disease hypothesis (the diet-heart hypothesis) led to a complete, and necessary reversal on the obesity hypothesis, from the pre-1960’s conventional wisdom that carbohydrates were fattening and low-carbohydrate diets were the cure, to the “diet-heart hypothesis” of Ancel Keys that saturated fat causes heart disease and, because fat is nine calories/gram (more calories/gram than carb or protein), everyone over the age of two should eat a low-fat, high carbohydrate diet to prevent heart disease and lose weight/prevent weight gain (eating a low-carbohydrate diet must be high in percent fat and a low-fat diet must be high in percent carbohydrate by necessity).[143]  The traditional low-carbohydrate diets used at Stanford, Harvard, Cornel and other medical centers for obesity treatment in the 1950’s was now decried as “mass murder” by nutritionists in the New York Times (they were also described as “new,” even though they had been used by prominent American and European obesity specialists for at least 60 years).[144],[145]

It now appears that the diet-heart hypothesis may have been incorrect in hypothesizing that saturated fat caused atherogenesis and that fat was uniquely fattening as a large number of randomized controlled trials conducted in recent years comparing a low-carb, high fat diet (LCHF) versus a low-fat, high carbohydrate diet show the LCHF diet consistently leading to more weight loss and better heart health risk factors (higher HDL, lower triglycerides, larger, more buoyant LDL known as type A LDL, and lower BP) (at least in 1-2 years of follow-up, using current indicators of heart disease risk, and, in most studies, not adjusting for weight loss differences between treatments-which should NOT be done as the weight loss difference is important). [146],[147], ,[148],[149],[150],[151],[152],[153],[154],[155],[156],[157],[158],[159],[160]  However, recent studies by Phinney and Volek and by Krauss, suggests that the isocaloric replacement of refined carbohydrates with saturated fat may even improve heart disease risk factors in the absence of weight loss (at least, in Phinney’s study, over a 12 week period in obese men and women eating a LCHF diet of %carbs/%fat/%protein 12 /59 /28  compared with a higher carbohydrate diet of 56/24/20, respectively).[161],[162]

However, it is unlikely that this evidence will be discussed publically by major public health authorities (such as the Dept. of HHS, NIH, AHA, and the USDA, to name a few) as it is a direct contradiction of the past 30-50 years of nutritional guidelines and would therefore cause the public to lose faith in their credibility (and possibly lead to lawsuits) which it probably should. 

This distraction with dietary fat has also likely prevented the funding of alternative research not couched in the dietary fat-is-bad paradigm (that has, ironically, been so ineffective at preventing the accumulation and maintenance of excess body fat in ~two-thirds of adult Americans) because, according to Vanderbilt University nutrition researcher, George Mann, “To be a dissenter was to be unfunded because the peer-review system rewards conformity and excludes criticism.”[163],[164]  The “conformity” he mentions means adherence to national public health recommendation (first generated in McGovern’s 1977 “Dietary Goals for Americans” and in the 1980-2000 “USDA Dietary Guidelines for Americans”) to eat a low-fat diet to prevent heart disease and lose weight; because the authorities were espousing this blanket recommendation, to the media, citizenry, and politicians (the bankrollers of NIH research), it must be true, so researchers were funded to rubber stamp the recommendation; research that did not confirm the hypothesis was either suppressed or ignored (or biased in interpretation to show support of the recommendations) while truly objective interpretation of the data was curtailed because, according to Gary Taubes in Good Calories, Bad Calories, “Skeptics [of public health recommendations] have often been attacked or ignored, as if disloyal at time of war. Skepticism, however, cannot be removed from the scientific process. Science does not function without it.”[165],[166],[167],[168]

Such consensus may have been generated by what New York Times reporter, John Tierney, describes was an “informational cascade,” meaning, a generation of nutrition researchers believed the diet-heart hypothesis to be reality because a few influential leaders in the field believed it and that once this consensus became engrained as dogma, it was now a “reputational cascade”, meaning that one’s reputation, funding, and career were on the line if one questioned the diet-heart hypothesis.  The dire consequences of not conforming, of being “disloyal in a time of war,” as Taubes explains, , were likely so severe because the evidence supporting the hypothesis was so very weak.[169]

Here, the public health guidelines generated belief, both in the general public and many nutrition researchers, in the validity of the saturated fat>heart disease hypothesis before the science was conclusive; therefore, because the recommendations created the perception of scientific truth in the minds of many Americans, no skepticism (i.e. testing of alternative hypotheses) in research would be allowed or funded (i.e. no randomized controlled trial comparing the pre-1960’s conventional wisdom, a low-carb, high fat diet, with the new conventional wisdom, the low-fat, calorie-restricted diet).[170] Because why spend hundreds of millions of dollars to test something public health already knows to be true?  Here, public health may have been detrimental not only to the public’s health but to science itself by preventing truly objective testing and analysis of the conventional hypothesis from being funded.

The Harvard School of Public Health recently suggested that, not only did the low-fat guidelines fail to prevent obesity and heart disease incidence, they may have actually driven the obesity/diabetes epidemic because, in our efforts to cut fat from 40 to 30% of our daily calorie intake, which were successful, Americans ate more carbohydrates which have driven the insulin resistance process in many Americans that has driven the metabolic syndrome/diabesity epidemic.[171]  Dr. Frank Hu, of the Harvard School of Public Health’s Nutrition Dept., stated, in a 2010 interview in The Los Angeles Times, “The country’s big low-fat message backfired.  The overemphasis on reducing fat caused the consumption of carbohydrates and sugar in our diets to soar. That shift may be linked to the biggest health problems in America today.”[172]

If this recommendation did indeed inflict unintended net negative consequences upon the American people, it was likely due to the interaction of incorrect public health advice (due to what David Sackett, , calls the “disastrous inadequacy of lesser evidence”) with a population-wide recommendation based upon the theories of UK epidemiologist, Geoffrey Rose.[173],[174]  Rose asserts that a “population strategy” of prevention must be instituted for the “restoration of biological normality,” but this raises important questions: what is biological normality and can we actually create it through adding or removing an exposure shown, only in observational studies, to be associated, but not necessarily causally related to the outcome of interest?  And, if we “act now!” in conventional public health fashion to apply a population-wide intervention based upon inadequate evidence, might we do more harm than good?  Dr. Hu and the Harvard School of Public Health seem to think so.

They are not alone, however.  While Dr. Hu only uses “linked”-suggesting correlation, not causation, to describe this unintended societal shift, The American Journal of Preventative Medicine published an article in 2008 suggesting that low-fat recommendations may very well have caused, at least in part, our metabolic syndrome epidemic, as the majority of caloric increase was, as the recommendations desired, in carbohydrates, and carbohydrates are thought, by many researchers, to be the primary cause of metabolic syndrome as they are essentially the only nutrient that regulates insulin levels; therefore, the development of metabolic syndrome in most people with the disease may be: chronically high carbohydrate consumption (especially sugars)  > elevated insulin levels (glucose) and liver fattening (fructose) > insulin resistance in the liver which spreads over time to other organs and lean tissue> metabolic syndrome in those genetically susceptible (other exposures may also cause insulin resistance, such as trans fats, ethanol, and branched chain amino acids (soy), but fructose likely has the highest attributable proportion in the total population of these foodstuffs related to metabolic syndrome/diabesity due to its physiological effects on the liver and the degree and breadth of its exposure amongst all ages and genders in the U.S.).[175],[176],[177],[178],[179],[180],[181]  The most recent public health nutrition guidelines, The USDA’s “2010 Dietary Guidelines for Americans,” still promotes a low fat diet through reduction in animal fats and high consumption of grains (now whole grains) though certain researchers now believe that these guidelines are biased in their interpretation of the scientific evidence to support such a claim and that a neutral, third party, unrelated to the food industry (which the USDA certain is not), should review the legitimacy of the USDA’s “2010 Dietary Guidelines for Americans”.[182]

Americans have indeed eaten more carbohydrates, especially refined grains and sugars, over the past 30-40 years since the government and medical industry admonished all citizens to eat a low-fat, high carbohydrate diet.  From 1971 to 2000 according to NHANES data, proportional food consumption averages of adults older than 20 years changed as follows for men and women, respectively: fat- 36.9 to 32.8% and 36.1 to 32.8, saturated fat- 13.5 to 10.9% and 13 to 11%, carbohydrate- 42.4 to 49% and 45.4 to 51.6%).[183],[184],[185],[186],[187]  Actual, non-proportional, food consumption trends (in pounds or gallons per capita, depending on food item, based upon food availability data-see subsequent paragraphs) also suggest that carbohydrates, especially sugary drinks, comprise the majority of the excess calories Americans consumed in 1997 compared with 1970, as total caloric sweeteners were 154 pounds per capita in 1997 (fruit juices not included in estimates, however, so likely an underestimate of caloric sweetner/sugary drink consumption).[188]   Figures 4 and 9 of Putnam show trends in carbonated soda consumption and caloric sweetener, respectively (again, other sugary drinks excluded so sugary beverage consumption likely far higher):

Putnam found that average per capita consumption of meat, fruits and vegetables, grain, and vegetable fats (though not animal fats) have all increased, which explains the 27% increase in carbohydrate, 16% increase in protein (from lean meats), 3% increase in total fat with a 4 and 13% decrease in saturated fat and cholesterol consumption, respectively (again, based on per capita annual estimates).[189]  Meat consumption increased (most increase being from lower fat meats like poultry, fish, and seafood with red meat seeing a decrease), egg consumption decreased, dairy products were fairly constant (cheese saw an increase, as did ice cream, yogurt, and low-fat milk, whole milk consumption dropped sharply, butter was constant), added fats and oils increased (most increase came from salad and cooking oils, i.e. vegetable oils).[190]  Again, these trends show a greater intake in low-fat items (cheese was not stratified by fat content) such as grains, sugars, dairy, meat (again, chicken and seafood over red meat) that follow the USDA’s Dietary Guidelines from 1980 to 2000 and show a decrease in proportional fat intake (though a nearly constant absolute intake) and an increased intake in carbohydrates.[191],[192],[193]

Figures 1 and 2 below are trends in proportional daily calorie food intake taken from CDC MMWR analysis of NHANES data on self-reported food consumption data.[194]

Therefore, it would appear Americans have indeed lowered fat intake while raising sugar and refined carbohydrate intake and seen a 3-4 fold increase in obesity and diabetes prevalence among nearly all age groups (see paragraphs 1 and 2 for trends and references).  Though correlation is not necessarily causation, these trends, in conjunction with the physiological mechanisms of carbohydrate metabolism related to metabolic syndrome, suggest that refined carbohydrates may indeed have been the main driver of the U.S.’s diabesity epidemic.

The USDA/HHS nutritional guidelines were not the only factors that played a role in the increased consumption of refined carbohydrates and sugars.  Other events that led to a tremendous increase in per capita increase in caloric sweetener consumption since 1970 include, but are not limited to: the belief that the only primary negative outcome of sugar consumption was cavities, the belief that fructose (½ of sugar) was harmless for diabetics due to its low glycemic index content (and, therefore, that sugar/HFCS were healthier for diabetics than starchy, higher GI foods like potatoes), and the introduction of high-fructose corn syrup into a huge number of food products.  Because of these events, according to USDA data, per capita consumption from 1970 to 2000 of caloric sweetener consumption increased (again, without including fruit juice consumption) by ~35 lbs., sugar decreased by 25.8 lb., while HFCS increased by 44.6 lb.[195],[196],[197],[198],[199],[200]   Per capita consumption of fructose by teenagers is now estimated to be five times higher than pre-modern averages (75g on average today versus 15g/day historically, with some teens consuming over 100g/day); these data, according to Lustig, are due to sugary drink consumption and are driving the metabolic syndrome/diabesity epidemic in America.[201],[202]  Compounding these changes, is the estimation that per capita annual flour and cereal consumption increased by 62 lbs. between 1970 to 2000, according to the USDA, which would mean that most Americans are now exceeding the 6-11 grains/day recommendation of the USDA Food Guide Pyramid.[203]

However, there are limitations to the type of inferences that can be made from USDA data due to the fact that USDA data are not actual averages taken from actual individual consumption.  All USDA population estimates are actually inferences made from agricultural production and loss, called “food disappearance data,” which are per capita available, not necessarily eaten, food from food production “after subtracting measurable uses, such as farm inputs (feed and seed), exports, ending stocks, and industrial uses” and apply to the entire population; this generates two problems: one, available food might not be wholly eaten by the U.S. population – meaning, that most of the huge increase in vegetable oils, for such things as deep frying, may simply be discarded and not consumed, and two, the population-scope of this data prevent inferences to the individual eating habits of the obese from being made or the ecological fallacy will take effect.[204],[205]  However, assuming that these availability data have been measured in a consistent fashion over the past 50 years, they still show increased proportional availability of carbohydrates and, given that consumer demand drives supply, it is likely that people are indeed consuming greater amounts of carbohydrates, specifically refined grains and sugars, in 2000 than in 1970 (and that Americans are likely consuming greater quantities of vegetable oils, etc.).[206],[207]

Therefore, despite limitations in the data, these clear shifts in food availability between 1970-2000 suggest a primary role for carbohydrate in the metabolic syndrome/diabesity epidemic.  Therefore, these availability data, in conjunction with biochemical, human physiology, obesity treatment, and, according to Taubes, nearly 200 years of anecdotal evidence regarding the eating habits of the obese, suggest that carbohydrates, specifically sugar/HFCS, may be the primary cause of the increase in obesity and related insulin resistance disorders seen since the 1970’s/early-80’s.[208],[209],[210],[211],[212], [213]  The USDA themselves state, in their “Report of the Dietary Advisory Guidelines Committee on the Dietary Guidelines for Americans, 2010,” that, “Over this same time period [1970’s -2005/6] there was an increase in total energy intake, driven mostly by an increase in total carbohydrate intake. Given the onset of a national epidemic of obesity over this time period, it is unlikely that total fat alone was an important contributory factor.’[214]

However, again, it is not logical to infer individual eating habits from population-wide estimates, lest you invoke the ecological fallacy principle.[215]  The ecological fallacy may apply in regards to these carbohydrate estimates in that the heaviest consumption of refined carbohydrates and sugars may be occurring among the most obese and diabetic populations of America and that the average consumption in these populations may significantly exceed the national per capita averages.  For example, if non-overweight individuals (roughly one-third of U.S. adults) consume only, say, 50 lbs. of sugar/HFCS a year whereas the most obese (also, roughly one-third of adults) consume 250 lbs. of sugar/HFCS, then while the average consumption per person may be 150 lbs., there may be a much sharper dichotomy in consumption of sugar by body fat (though studies that show differences in consumption may simply be cross-sectional and therefore unable to assess any sort of causal relationship between sugar consumption and metabolic syndrome and studies that must be done to potentially suggest, but not prove, causation will likely cost billions of dollars and take decades as the average latency/induction period between the start of heavy sugar consumption and the development of body fatness may take a very long time to occur, not to mention the huge number of potential confounders, biases, and misclassification errors that always occur in massive, observational, longitudinal studies involving free-living human beings; the randomized-controlled trials needed will likely cost even more).[216],[217]

Because metabolic syndrome is a hormonal problem driven by hyperinsulemia and insulin resistance, because obesity is part of metabolic syndrome, and because insulin is the only hormone responsible for fattening and “lipid trapping”, it may be that obesity is not a behavior problem or an “eating disorder” at all but simply a hormonal problem caused by the deregulation of the body’s fat tissue caused by hyperinsulemia and insulin resistance.[218] This biochemical explanation seems obvious given what is known about carbohydrate metabolism driving insulin and of insulin’s roles as the fattening hormone in the body have been understood and accepted by biochemists for nearly 50 years (and European obesity specialists for nearly a 100 years), however, modern U.S. nutritional researchers seem to have ignored the fundamental biochemical explanations for excess fat accumulation in cells when deciding how to prevent excess fat accumulation in human bodies. [219]   This hormonal explanation of obesity argues against conventional wisdom that obesity is simply a problem of “energy balance,” i.e. over-eating and sedentary behavior, and argues against the notion that obesity is a problem of willpower and can be cured by self-control through psychiatry.

Though the hormonal mechanisms of insulin resistance that drive obesity can explain the common observation that the obese “over-eat” and are sedentary, the causation of these behaviors gets reversed when one views this condition through the lens of human physiology instead of the conventional viewpoint of psychiatry and physics.  As Wells et al explain, this alternative model of obesity starts with 1) a genetic sensitivity to fatten on carbohydrates due to excessive insulin response to carbohydrate 2) the overconsumption of carbohydrates leading to the 3) metabolic disturbance/hormonal deregulation of fat tissues that 4) drives fattening and, as you get fat and insulin resistant (in your lean tissues), you 5) “over-eat” and are sedentary to compensate for the loss of calories into your ever-growing fat tissue.[220]   Therefore, according to Tim Burton, a fellow obesity researcher working with University of Massachusetts biologist, George Wade, in the 1970’s, an obese individual, like an obese mouse, is not fattening because they’re overeating, “they’re overeating because they’re socking all the calories away into adipose tissue and they can’t get to those calories.  They’re not getting fat because they’re overeating; they’re overeating because they’re getting fat. It’s not a trivial difference.  The causality is quite different.”[221]  Meaning, as Lustig states, a biological (i.e. hormonal) drive to fatten, to grow, drives the biochemistry that drives eating and sedentary behavior.

One way to see obesity is as a form of horizontal growth that, like the vertical growth of a child during puberty, leads to a biological/hormonal drive to over-eat and be sedentary to conserve necessary calories for this growth; this means the behavior of over-eating and sedentary behavior are simply effects of a biological drive to grow larger.  An obese individual, like a hibernating ground squirrel, a teenager in puberty, or even a malignant tumor, is experiencing a hormonal drive to grow but, instead of the teenager, who’s growing bone, lean tissue, and facial hair, the obese person is growing fat.  Both vertical and horizontal growth are caused by hormones that lead to “overeating” and sedentary behavior to store enough calories to fuel the biological drive to grow, except, in puberty, growth hormone drives growth which drives over-eating and sedentary behavior to conserve calories for growth while in obesity, the hormone insulin drives the fat to grow which drives over-eating and sedentary behavior for the growth process (starvation stunts growth in children and fat storage in obese individuals but does not permanently stop or fix the hormonal drive to grow, whether in height or in fat mass).[222]

In Good Calories, Bad Calories, Taubes quotes the German internist, Gustav von Bergmann, an early-19th century internist, to explain the commonly held belief in pre-WWII Europe that obesity was a hormonal problem, not a behavioral problem of over-eating: “It seems just as illogical to say ‘Child, you shoot up in height because you eat too much or you exercise too little-or you have remained small because you play sports too much.  What the body needs to grow, it always finds, and what it needs to become fat, even if it’s ten times as much, the body will save for itself from the annual balance.”[223]  Therefore, the obese individual must “overeat” to gain the necessary calories to grow; if they are starved, they will indeed lose weight, but most of the weight will be from lean tissue and, when they are allowed free access to food again, the individual will likely gain more fat tissue back than baseline levels, even at a lower caloric intake than a similar human who did not experience starvation, because their body has entered a starvation mode, thereby leading to, what Ancel Keys called “post starvation obesity” or, what modern researchers call “post starvation overshoot in body fat” when regular eating habits are resumed (starvation diets may fail because they do not solve the hormonal drive to grow fat tissue, only make the fat tissue preferentially store more calories than pre-starvation levels; such over-eating, or hyperphagia, following starvation is not likely an issue of willpower-see Christian Bale’s weight regain after The Machinist, but of hormones and the fat tissue simply trying to regain what it has lost).[224],[225],[226]  Therefore, gluttony and sloth are effects found downstream of the initial hormonal disturbance triggered by genetic predisposition to fatten (i.e. overstimulation of insulin response to carbohydrates) plus high carbohydrate consumption.[227]

If you do not treat the underlying hormonal problem at work (hyperinsulemia/insulin resistance), and instead only treat the symptoms (excess body fat) and effects of the condition (by using semi-starvation and exercise to counteract the behaviors of over-eating and sedentary habits, respectively), you will not likely cure the condition.  This is likely why calorie-restricted diets, formerly known as “semi-starvation” diets, so consistently fail to engender long-term weight loss in obese subjects-they do not address the underlying metabolic disorder and the  body simply adjusts to regain the lost weight (i.e. an obese individual who loses 50 lbs. and is now 150lbs is fundamentally different, on a hormonal level, than a 150 lb. individual who never calorie-restricted themselves in the first place and that these hormonal differences will predestine the dieter to regain most, if not all, of the original body fat lost).[228]  Because such treatments do not address the hormonal disturbance, the deregulation of fat tissue, that drove the excess accumulation of fat in the first place, and may actually trigger the body’s homeostatic mechanisms to regain the weight (as MacLean et al hypothesize), they fail with amazing consistency (at least 80-90% of the time when long-term weight loss maintenance is given the definition of “intentionally losing at least 10% of initial body weight and keeping it off for at least 1 year”; this poor result likely worsens when the definition changes to include greater weight loss over a longer period of time, such as in the Women’s Health Initiative-see subsequent paragraphs and bibliography).[229],[230],[231] 

There is another intuitive, albeit not very scientific, reason pointing to the failure of conventional low-fat, calorie-restricted diets.  This is the fact that the National Weight Control Registry, a longitudinal database that registers individuals who have lost over 30 pounds and maintained the loss for at least 18 months, only has 10,000 members registered since its inception in 1994 even though, according to 1996 BRFSS estimates, between ~30-40% of American adults try to diet to lose weight each year (this means that, assuming adults compose roughly 75% of the total U.S. population of ~281 million people in 2000, around 74 million dietary attempts were made in 1996).[232],[233],[234]  This means that, using very crude math and making a lot of assumptions, since 1994, 1.33 billion dietary efforts have been made in the U.S. (74 million * 18 years) with only 10, 000 successes being registered (meaning 7.5*10^-4% of all dietary efforts from 1994-2012 were registered in the National Weight Control Registry) by this database assuming the annual proportional trend of adult dietary efforts stayed at 35% of their cohort during this time period.  We can assume that most of these efforts utilized the conventional recommendations proffered by the USDA/HHS and CDC (eat less, especially fat, move more) since these have been the centerpiece of the USDA Dietary Guidelines for Americans and the energy balance hypothesis is still pervasive amongst the most preeminent public health authorities (WHO, CDC, NIH, AHA, etc.).[235], [236],[237],[238],[239],[240],[241],[242]   Therefore,  conventional treatments for obesity simply do not work or there would be significantly more people registered in the National Weight Control Registry; this failure is obvious given the unceasing increase in obesity prevalence since 1980.

This consistent failure of simply eating less and moving more as a cure for obesity generates an intuitively obvious, novel definition for obesity, voiced by Gary Taubes in an interview for Reader’s Digest, “For the most part, you can define an obese person as someone for whom eating less didn’t work,”  because, if it did, they would not be obese as it can be assumed that virtually no one chooses to be obese, especially the 31% of WIC 2-4 year olds in Georgia who are overweight or obese and the 45% of Georgia third graders who were overweight or obese in 2010.[243],[244],[245]  The fact that President Obama appointed an overweight, possibly obese, surgeon general, who we can assume has tried dieting her entire life, also questions the effectiveness of current obesity prevention guidelines.[246]

Ultimately, the reasons for the failure of the current obesity prevention guidelines are contained in a single quote from a 2007 article by Drs. Jeffrey and Eleftheria Maratos-Flier, of Harvard Medical School and  Beth Israel Deaconess Medical Center, respectively, entitled, “What Fuels Fat,” as quoted in Gary Taubes’s Why We Get Fat and What to Do About It (as the Flier’s article was behind a paywall):
“An animal whose food is suddenly restricted tends to reduce its energy expenditure both by being less active and by slowing energy use in cells, thereby limiting weight loss.  It also experiences increased hunger so that once the restriction ends, it will eat more than its prior norm until the earlier weight is attained.”[247],[248]

Given the obvious failure of this current, physics- based explanation for obesity, it would greatly behoove public health researchers to reconsider the hormonal explanation for obesity as a useful explanation of the obesity epidemic because such a consideration may generate more effective prevention methods.  However, such a shift in paradigms would create an uncomfortable position for many very powerful entities invested in the status quo; such a shift would damage the profit margin of the food industry, the sales of US agriculture at home and abroad, and the public’s perception of the authority and competence of nearly all public health and medical organizations who have been espousing the low-fat, calorie-restricted diet for nearly 50 years that has failed so spectacularly to curb the incidence and prevalence of metabolic syndrome/diabesity.[249], [250],[251],[252],[253], [254],[255],[256],[257],[258],[259],[260],[261]

If refined carbohydrates and sugars do indeed make us fat, and we’ve been told to eat grains in huge quantities (again, 6-11 servings/day according to the USDA’s Food Pyramid Guide) for nearly 30 years and sugars have been added into everything (e.g. HFCS in ketchup) and these sugars are not just “empty calories” and cause far more than just cavities (as USDA/HHS “Dietary Guidelines for America” have suggested since 1980), than these organizations may forever lose the trust of the American public and be unable to function effectively.[262], [263], [264]  This may explain the unwillingness of public health authorities to relinquish their grip on the “energy balance” hypothesis of obesity.

This hormonal explanation for obesity necessitates a profound reinterpretation of the “energy balance” hypothesis – the conventional idea that a lack of willpower, of responsibility, of maturity even, are what drove the obese to overeat and therefore that they caused their own fate.  If an abnormal hormonal environment drives behavior, then this transfers the onus of responsibility for obesity from the obese individual to the American food supply itself (specifically its refined carbs and sugar, the main exports of American industry) which, as Lustig believes, is “toxic” not because it promotes gluttony and sloth but because it makes people hormonally abnormal (insulin resistant) which makes them gluttons and sloths.[265]  To continually insist that obese people are obese because they’re in “energy imbalance” or “lack of energy balance” from over-eating and sedentary behavior, as the WHO, NIH, CDC, The US Surgeon General, AHA, “Biggest Loser” trainer, Jillian Michaels, and many other reputable health authorities insist is true, misinterprets the law of thermodynamics (see subsequent paragraphs), removes blame from the food industry, and removes blame from the medical and exercise authorities for their patient’s failure to lose weight.[266],[267],[268],[269],[270],[271],[272]

As Susan Sontag wrote in her 1978 essay, “Illness as Metaphor,” quoted in Why We Get Fat and What to Do About It, in regards to the “‘blame the victim’ mentality”, “ ‘Theories that diseases are caused by mental states and can be cured by willpower are always an index of how much is not understood about the physical terrain of the disease,” (diseases like epilepsy, cancer, and tuberculosis were all once thought to be caused by the victim as obesity is now).[273]  Again, because this blame-the-victim mentality removes responsibility for the metabolic syndrome/diabesity epidemic from public health authorities, the medical industry, the government, and the American food industry, shifting the obesity paradigm away from the “energy balance, a calorie is a calorie” paradigm to instead focus on refined carbohydrates and sugars as the cause of obesity will likely be very difficult, as Dr. Lustig explains in his popular Youtube lecture entitled, “Sugar: The Bitter Truth.”[274]

There is another key reason, beyond the conception of obesity as a growth disorder, why many researchers now hypothesize that the chronic overconsumption of refined carbohydrates drives the biblical “gluttony and sloth;” because glucose and fructose drive insulin resistance and fattening, they drive hunger and sedentary behavior by fooling the body into thinking that it is, paradoxically, starving even while the person is fattening.  This likely occurs for multiple biochemical reasons involving chronically abnormal levels of the hormone insulin, including: 1) carbohydrates elevate insulin levels which blocks leptin (a primary satiety hormone generated by fat tissue) from signaling to the hypothalamus that the body cells are “full”, 2)  “semi-cellular starvation” or “internal starvation” in lean tissue as fat, in the presence of elevated insulin levels, literally steals ingested calories before they can be delivered to lean tissues and organs because lean tissue (muscle) becomes insulin resistant in a hyperinsulemic environment before fat tissue and therefore fuel (glucose, fatty acids) will be preferentially shunted to fat tissue before and instead of lean tissue, and 3) elevated insulin levels, experienced during hyperinsulemia, prevent the utilization of fatty acids in fat tissue for fuel by blocking the activity of HSL to release fatty acids into the blood stream (the body literally cannot “see” it’s fat tissue and so not use its stored triglycerides for fuel- called “lipid trapping”).[275],[276],[277]

Therefore, obese people have a metabolic defect in fat metabolism that prevents their cells from “receiving the full benefit of the calories they consume,” according to mid-20th century obesity researcher, Alfred Pennington, and must therefore “overeat” and achieve “positive energy balance” to fulfill the caloric needs of their starved lean tissues and organs; many obese then reach a new “energy balance” level at a weight that is clinically obese and may maintain this new plateau for decades (which highlights another key flaw in the “energy balance” hypothesis of obesity as many obese people remain in energy balance at an obese weight for decades, and therefore, are not “over-eating,” and any attempt to reduce calories leads to a homeostatic response by the body to regain weight to the previous energy balance level regardless of the efforts by the obese to semi-starve themselves permanently; semi-starvation also induces other negative effects such as an inability to exercise, which, ironically, is the main recommendation for obese people on semi-starvation diets).[278],[279]

Another key metabolic effect of chronically elevated insulin levels is that elevated insulin “traps” triglycerides in fat tissue by preventing the enzyme hormone-sensitive lipase (HSL) from mobilizing fat for fuel, thereby forcing the body to burn carbohydrates instead (again, this may explain carbohydrate cravings amongst obese individuals).[280]  This “lipid trapping” effect of insulin may explain why conventional obesity treatments so often fail; they try to reduce the amount of fat (i.e. triglycerides) in adipose tissue by keeping patients on relatively high carbohydrate reducing diets (between 55-60% of calories for LEARN and likely higher for Ornish, which is <10% fat) which keep insulin high and therefore traps fat in fat tissue  (again, the failure rate for high-carbohydrate obesity treatments in both youth and adults is estimated by the CDC, likely rather conservatively, to be between 80-90% of all efforts after a few years; other estimates claim between 50-95% failure rate for current obesity treatment efforts with very modest loss in those very few individuals who can maintain a net weight loss over the long-term).[281],[282],[283],[284],[285],[286],[287]

Therefore, telling individuals who are obese and diabetic to eat whole grains (still high in “total glycemic load” and therefore insulin-stimulating) and fruits like bananas and grapes (both of which have high fructose content) may keep them fat and diabetic even if they temporarily lose weight in the short term (this may be why the Women’s Health Initiative’s intervention diet of low-fat, calorie-restricted foods, primarily in whole grains and fruits and vegetables led the 25,000+ obese intervention subjects to, on average, gain body fat and, for the intervention subjects who were also diabetic, to have worse blood glucose levels then before they started the intervention).[288],[289]  Because conventional obesity treatments fail, a common assumption by nutritional researchers is that all diets fail and that the obese are doomed to their condition because the current treatment of calorie-restriction and exercise largely fails to cure obese people of their plight (see “the Fat Trap” in the New York Times, by Tara Parker-Pope, Dec. 28, 2011).[290]  Other researchers disagree with the logic that because one treatment does not work, no treatments will work (even those not properly tested in RCTs).[291]

The facts that diabetes and obesity are essentially “two sides of the same pathological coin [insulin resistance],” according to Taubesand that this  consumptionveauthoritiesstarkly divergentinterpretation and treatment of yhDr. , psychologist, head of  Center for Eating and Weight Disorderslargely hys (i.e. with insulin therapy)[292],[293] Since the same insulin resistance mechanism driven by excessive carbohydrate consumption?[294]  RCTs have consistently shown that carbohydrate restriction significantly improves the symptoms of diabetes (and heart disease) in obese, type 2 diabetics much better than a low-fat, calorie-restricted diet and this treatment was the primary tool for diabetes prior to the 1960’s and the emergence of the saturated fat-heart disease hypothesis. [295],[296], ,[297],[298],[299],[300],[301],[302],[303],[304],[305],[306],[307],[308],[309],[310]

Carbohydrate restriction (i.e. limiting the consumption of high-GI refined starches, grains, and sugars) isa in some, but not a majority of, diabetes treatment centers today[311] Why is this treatment not at least tested in every diabetes treatment center in the U.S.?  And why is this treatment not considered effective treatment for diabetes’s etiological cousin, obesity?

,  related to this strange dichotomy in the current understanding and treatment of diabetes and obesity

type 2 to be ,therefore, syh, whereas diabetes is considered a physiological problem to be treated by physicians]more victims of that disease were treated by psychiatrists instead of physicians. And yet diabetes and obesity are so closely linked-most type 2 diabetics are obese, and many obese people become diabetic-that some authorities have taken to calling the two disorders “diabesity,” as though they’re two sides of the same pathological coin, which they assuredly are.[312]

Because obesity is considered to be caused by human choice (over-eating and sedentary behavior), the obese patient, not the treatment itself, is blamed for their condition when the treatment of semi-starvation and forced exercise fails to cure them of their affliction.  Again, this “blame the victim” mentality is a common response by society to a disease they, even medical experts and public health authorities, fail, willfully or not, to understand and therefore cure.[313]

The main reason why the hormonal regulation of fat tissue is largely ignored by obesity prevention researchers is because of their commonly held blind faith in the central tenant of the conventional obesity hypothesis that a lack of “energy balance,” i.e. over-eating and sedentary behavior, causes obesity, which is embedded in the misinterpretation of law of the conservation of energy (even though this irrefutable law of physics has no arrow of causality within it).  This misinterpretation has been embedded in virtually all explanations for the causes and cures of obesity over the past 50 years and used to oversimplify human metabolism and  to treat all humans (whether obese and lean), all nutrients (whether fat or protein, all calories are equal), and therefore all efforts to reduce obesity identically.[314],[315]  All humans must simply consume less then they expend through daily metabolic requirements to maintain a negative “energy balance” and prevent weight gain (which is why current U.S. physical activity guidelines, by the USDA and HHS, recommend between 150-300 minutes of physical activity per week for adults to keep weight off, which the Dept. of HHS claimed in their “2008 Physical Activity Guidelines for Americans” was supported by “Strong Evidence”).[316],[317]

Sadly, this law leads to calorie-restricted diets which, in almost all cases as discussed previously, fail to cure obesity over the long-term; this failure is likely due to the fact that, because the first law of thermodynamics fails to take into account the hormonal regulation of fat tissue, it fails to address the fundamental causes of “positive energy balance,” which, is an obviously necessary effect seen in a body that is under a biologically-obligate drive to grow, whether muscle, bone and facial hair as in teenagers, or fat tissue, as with the obese.

And calorie-expenditure (exercise) has shown to be as clinically poor at promoting long-term effective weight loss in most obese individuals as caloric-restriction (eating less) even though most health organizations still refer to exercise as an irrefutably proven tool to promote weight loss (as Michelle Obama’s “Let’s Move” campaign makes explicitly evident: “Children need 60 minutes of play with moderate to vigorous activity every day to grow up to a healthy weight.”) even though, according to the AHA and American College of Sports Medicine in 2007, “data to support this hypothesis are not particularly compelling,”-this conclusion, after the hypothesis of physical activity for weight loss has been tested for nearly 100 years, likely suggests that the hypothesis is wrong (because exercise promotes hunger and eventual restocking of fat stores following exercise due to the upregulation of  LPL activity on the fat tissue following exercise).[318],[319]  Exercise simply makes fat tissue restock what it’s lost in exercise, which drives hunger, and if the hunger is not fulfilled, than the individual’s metabolism simply slows down to replete the calories necessary for the fat tissue to restock (i.e. the individual moves less when not exercising or experiences a chill as their cellular metabolism slows down to compensate for the lost calories-see Flier quote).

The reason that this population-wide belief in the weight-loss efficacy of exercise remains firmly embedded in public consciousness as fact even as the “data to support this hypothesis are not particularly compelling” and obesity prevalence continues to rise, may be the simple fact that most people confuse correlation with causation: i.e., we see a skinny person running and a fat person on the couch and assume if we just get the fat person to run then they’ll become skinny even though the evidence for this hypothesis remains weak if non-existent (a 1989 Dannish study found that overweight, sedentary men forced to train 18 months for a marathon lost only 5 pounds, on average, of body fat while women lose none, even while both attempted increased carbohydrate consumption to improve heart health); there is a correlational relationship between leanness and exercise behavior and it may simply be that lean people are more likely to exercise because they’re lean, and not the other way around.[320],[321],[322]

Panofsky’s law, as explained by Gary Taubes in a 1996  interview to Epimonitor.net, explains the current state of the physical activity hypothesis of weight control: “if you throw money at an effect and if it doesn’t get bigger it means it’s not really there.”[323]  Therefore, since we’ve spent many decades and many millions, if not billions, of dollars testing the hypothesis that exercise leads to weight loss and the effect, in a clinically significant sense, is not getting bigger (as Fogenholm et al found in their 2000 systematic review-subjects either regained 0.28 or 0.33 kg/month from diet or diet+exercise, respectively), then exercise probably does not lead to clinically-significant weight loss.[324],[325]

A more recent meta-analysis of 33 studies in the International Journal of Obesity in 2005, found that most people, ~50% of subjects, regained all lost weight after 1 year and that the average loss for the 50% of subjects successful after 1 year in either intervention was only between 9-12 pounds, a clinically insignificant amount that would not cure their obesity; also, interventions of diet and diet+exercise were compared  (from only 6 studies) and, while exercise did indeed lead to a 20% increase in weight lost compared with diet alone (body composition not mentioned), the actual average difference between the interventions was clinically insignificant-only 3 kg at 1 year (~6 lbs.) which shrunk to 2.2 kg (~4 lbs.) after two years.[326]  Therefore, diets don’t appear to work after a few years, and diet+exercise appears to be slightly more effective though equally as transient.  An analysis of the National Runner’s Health Study, also published in the IJO, found that extensive running had little effect on age-related adiposity, and that, even though leaner runners ran more than heavier runners, the leaner runners still got progressively fatter as they aged, regardless of running many thousands of miles over the study period (of note, one cannot make a causal assumption that the extra running made the leaner runners leaner compared to their heavier brethren, it is also equally invalid to state that the leaner runners ran more than the heavier runners because they’re lean).[327]

The behavioral/physics explanation for obesity becomes even more meaningless when one looks closely at what it means to say someone fattens due to “over-eating.”  In 1954, the father of the relatively recent idea (circa the 1960’s) that physical activity cures and/or prevents obesity, Jean Mayer, stated that “to explain obesity by overeating is as illuminating a statement as an ‘explanation’ of alcoholism by chronic overdrinking.”[328]  Such a statement is inanely obvious because, as the first law of thermodynamics (i.e. the law of the conservation of energy) dictates, energy within a closed system is neither created nor destroyed and, therefore, if a system’s total energy increases (i.e. a human body grows tissue, whether bone, lean tissue, or fat), then any system, even a human body, had to take in more energy than it expends.[329],[330]

This explains nothing of why the system took in any more energy, however.  Taubes uses an analogy to further explain the inanity of energy balance in his book Why We Get Fat and What to Do About It: consider a person fattening as a room becoming more full with people; using the “energy balance” paradigm, if someone asked you why the room was more full (i.e. why is a person fattening?), the response would be “because more people entered the room than left.”[331]  Such a statement is so blatantly obvious and meaningless that it is hardly worth mentioning because it explains nothing about causation.

Using the first law of thermodynamics to explain obesity (which is a tautology-see Energy Balance in definitions) generates more questions than it answers: Why are obese people considered to “overeat” while lean people are not when both consume similar amounts of food or when the obese maintain a stable, albeit obese, weight for decades?  Why do many obese people fatten on similar calorie intake as the lean?  Why do identical twins who have lived apart for decades have identical body types (fat deposition and BMI) even though it’s now stated that a positive energy balance of only 20 calories/day will transform us from lean in our twenties to obese in our forties; did genes program these obese twins to “overeat” to the exact same degree (i.e. 20 calories/day-which is impossible to accurately gauge) to fatten to the exact same degree for decades?[332]  Why are there obese people in “energy balance” who maintain one or two hundred pounds of excess fat for decades?  Why does their body establish a weight “set point” so much higher than what is biologically necessary?  Why do some people fail to maintain a set weight and gain weight constantly?[333]  After all, humans are mammals, yet, in the wild, no mammal will gain unhealthy levels of body fat, even with plentiful food (in fact, certain species of ground squirrel will fatten for winter hibernation without an abundance of food or overeating, they simply move less to conserve the calories necessary for annual hibernation, which is obviously necessary since a single bad summer harvest would have eradicated the entire species; this natural seasonal shift in fat deposition may simply be due to genetically-programed shifts in insulin levels which may explain why humans gain weight in winter and become lean in spring/summer, without changes in diet or exercise).[334][335],[336],[337]  Why do so many humans put on excess fat beyond what is physically necessary for homeostasis?[338]

The ultimate question “energy balance” fails to explain is this issue of homeostatic disruption: what disrupts the homeostatic mechanism found in ALL ORGANISMS ON EARTH that prevents unhealthy body fat accumulation in all mammals but humans?  No animal on earth will suffer from unhealthy weight gain even with plentiful food unless the animal’s genes, brain, or food supply are artificially manipulated by man to be foreign to what the animal evolved to eat (i.e. rabbits and cholesterol, rats and sugar+fat, monkeys and humans on high fructose diets).[339],[340],[341],[342]  What is the initial homeostatic disruptor that drives fattening, independent of food intake or physical exertion?

Given these glaring limitations in the “energy balance” hypothesis, it is likely that the current “energy balance” explanation for obesity is counterproductive to obesity prevention efforts because it fails to explain the biochemical/physiological mechanisms behind obesity and its co-morbidities, prevents alternative hypotheses from obtaining funding and therefore limits scientific progress, and ultimately fails as a preventative tool because the conventional treatment of “eating less and exercising more” fails to promote long-term weight loss in, according. to the CDC, at least 80-90% of these obesity-reducing efforts (see “The Women’s Health Initiative”). [343],[344],[345],[346],[347],[348]  Again, caloric-restriction and/or exercise ultimately fail to produce long-term weight loss because they engender a semi-starvation response in the body which generates hunger, depression, and, if food is curtailed, metabolic slowdown (i.e. hormonal disruptions) so that when food is consumed at pre-diet levels (which is inevitable for nearly all people), the patient usually gains more fat back then was present before dieting (again, see “The Women’s Health Initiative” as a large-scale example of this common occurrence).[349]Ultimately, th is mechanism leads to a necessary refutation of the long-held beliefs that all calories are equal, regardless of the type of food composing that calorie.  Given what is known about the effect of refined carbohydrates on the body, it is clear that, as Dr. Robert Lustig states, “isocaloric is not isometabolic” and, therefore, that equal calories of certain foods are worse than equal calories of others in terms of effecting the body’s hormonal regulation of fat tissues and blood glucose/insulin (which the USDA does not accept, as seen by the “MyPlate” statement that sugars are simply “empty calories”).[350],[351]  Therefore, it is possible that the chronic overconsumption of refined carbohydrates (primarily sugars) leads to the metabolic disturbance (hyperinsulemia/insulin resistence and fattening) that, due to “semi-cellular starvataion” and “lipid trapping”, as well as, insulin blocking leptin reception in the hypothalmus, drives fattening (an obligate weight-gain) which drives over-eating and sedentary behavior.  Therefore, in this model, the conventional “causes” of obesity, over-eating and sedentary behavior, are simply “effects” of a hormonal disturbance.  Instead of energy-in > energy-out = weight gain, the correct causal pathway may be sugar/starches> hormone disruption (insulin resistance)> drives obligate weight gain drives >energy-in and <energy-out (a reversal in interpretation, not of ignorance of, as is often claimed, the law of the conservation of energy which contains no causal information about obesity).[352]

Though the conventional weight loss efforts are successful short-term but largely fail long-term for the majority of people, a very small fraction of people do succeed at losing and keeping off excess body fat over the long-term with these diets.  Those that do succeed could be successful because they cure the metabolic derangement of insulin and fat-regulation because, in our efforts to halve our calories (say from 3000 a day to 1500), carbohydrates are the food group that gets reduced the most (especially if we were eating ~60% carb. as is currently recommended) and we cut out the worst carbohydrates (sodas, french fries, etc.) that have the most metabolically-damaging effects on us.[353]  Therefore, in some ways, a low-calorie, low-fat diet is a low carbohydrate diet (at least relative to previous nutritional habits) and could be explained as such.[354]  Nutritional changes are also usually confounded by exercise changes so when people claim they lost 60 lbs. through exercise, they likely made significant dietary changes as well.

Ultimately, these low-fat, calorie-restricted diets may fail because their underlying hypothesis of what causes obesity is simply wrong.  Obesity is not an energy balance problem of excess fat but a hormonal problem that has occurred because the fat tissue itself (a hormonally-active endocrine organ, not a “trash can” for energy as conventionally seen in America) has become deregulated. [355],[356],[357]  This deregulation may have occurred because the obese individual has over-consumed the primary foodstuffs (carbohydrates) that elevate the fat producing hormone (insulin) to put what they eat in their fat tissue and keep it there (known as the “lipid-trapping” effect of insulin).  Therefore, as renowned fat metabolism researcher George Cahill has said, “carbohydrate is driving insulin is driving fat,” so to reduce fat stores you must reduce insulin and this can only be done on a carbohydrate-restricted diet. [358],[359],[360]  The researchers who discovered ways to measure insulin in the body, Yalow and Berson, are quoted in Taube’s Why We Get Fat and What to Do About It, that “ ‘the negative stimulus of insulin deficiency’” is all that is necessary, according to Taubes, for “releasing fat from our fat tissue and burning it for energy.”[361]

The conventional treatment for obesity in pre-WWII Europe and many elite American hospitals (such as Stanford, Harvard, Cornell, etc.) was to put patients on a carbohydrate-restricted, high fat diet: specifically, an ab-libitum (eat as much as they want) diet of meat, fish, fowl, eggs, cheese, green vegetables, and fruit (except for grapes and bananas) without exercise because exercise simply made their patients hungry and reduced dietary adherence.[362]  This diet was so widely used in preeminent U.S. and European medical centers to treat obesity because these researchers believed carbohydrates, not fat, to be uniquely fattening.[363]  This treatment is the logical consequence of the idea that carbohydrates are the primary necessary cause for obesity and diabetes; remove the worst carbohydrates (refined grains, starches and sugars), and hundreds of millions of individuals across the U.S. and the globe may never have become obese in the first place (i.e. their sufficient cause mechanism, or “causal pie,” would never have been completed).

Dr. Walter Willet, a renowned nutritional researcher and head of the Harvard School of Public Health’s Nutrition Department, echoed this refined carbohydrate>diabesity hypothesis in The LA Times in 2010 when he said:

“Fat is not the problem.  If Americans could eliminate sugary beverages, potatoes, white bread, pasta, white rice and sugary snacks [i.e. refined carbohydrates], we would wipe out almost all the problems we have with weight and diabetes and other metabolic diseases.”[364]

Low-carb, high-fat (LCHF)  diets do seem to be uniquely effective in reducing body fat in the obese and improving metabolic syndrome conditions (atherogenic blood lipid levels) independent of calories consumed (though questions about adherence to the diet, as with any diet, remain important).[365],[366]  One early 20th-century researcher, Blake Donaldson, treated over 17,000 obese patients with this diet from the early 1920’s to 1960’s and claimed great success with the regime.[367]  Current use of a low-carb, high-fat (LCHF) reducing diet is increasing in popularity in weight loss centers (such as the Duke University Medical Center) as many randomized controlled trials run by independent (i.e. non-Atkin’s aligned) researchers show that a LCHF diet consistently beats LFCR (low-fat, calorie-restriction) diets in weight and body fat loss and heart disease risk factors (even potentially when, according to Volek et al and Gardner, et al, caloric consumption is higher in LCHF than LFCR-see discussion below) (these references, taken from a webpage run by Swedish obesity specialist, Dr. Andreas Eenfeldt, (from dietdoctor.com) do not represent the totality of all RCTs of diet comparisons but they are numerous and from sources such as Stanford, Oxford, Duke, The University of Cincinnati, The University of Connecticut and many other prestigious research and medical universities and institutions again, except for Yancy et al and Westman et al, who were not aligned with the Atkins Corporation) (though plenty of research gets funded by the U.S. government that is considered free from influence that may not be…).[368],[369], ,[370],[371],[372],[373],[374],[375],[376],[377],[378],[379],[380],[381],[382]

Another consistent observation of high fat, carbohydrate-restriction treatment is that patients did not exhibit common symptoms of semi-starvation as did people consuming a higher carbohydrate, more “balanced” diet of identical caloric intake; the lack of semi-starvation means that hunger was minimal if non-existent and depression was absent, even when weight loss was very pronounced.[383]   This consistent observation can be explained by two biological changes that occur during a LCHF diet: the body’s shift from utilizing glucose for fuel to ketone bodies (from fat stores) during ketosis, and, because, it is hypothesized, those on the low-carbohydrate have lowered their insulin levels enough so that their body can now “see” their fat stores and therefore burn the previously-stored fatty acids, as “ketone bodies,” for fuel, whereas those on a higher-carb., higher insulin, diet cannot use their fat stores for fuel due to insulin’s “lipid trapping” effect. [384],[385],[386], ,[387],[388],[389],[390],[391],[392],[393],[394],[395],[396],[397],[398],[399],[400]  Ultimately, this means that someone on a LCHF diet of 1,500 calories/day will lose more weight than someone on a low-fat, higher carbohydrate diet of 1,500 calories/day, not because of misclassification of intake or boredom (common explanations for these observations), but because the LCHF literally reregulates the fat tissue to dump fatty acids into the blood stream for fuel and so lessen the amount of body fat stored in the body.[401]

This seems like a violation of the law of the conservation of energy but can again be explained by the physiological differences experienced by patients on a low-carbohydrate, high fat diet (LCHF) versus a low-fat, higher carbohydrate calorie-restricted diet (LFCR) (though many physicians still believe that isocaloric diets of different carbohydrate proportion must lead to equal weight loss, because, a “calorie is a calorie,” and therefore that the A to Z Study’s LCHF group, who claimed to have eaten similar levels of calories as other interventions yet lost ~ twice as much weight, either all LCHF overestimated or lied about calories consumed or all other interventions underestimated calories consumed, or, in the case of the Women’s Health Initiative, that intervention subjects, who only lost an average of 2 lbs. of weight yet claimed to have eaten a few hundred calories less than the comparison group, must have also underestimated calorie consumption (and that the comparison group also did not): this assumption, still widely held by many researchers, may not be true).[402],[403],[404]

When someone eats 1500 calories on a LCHF diet, the low insulin levels could allow for the freeing of, say, 1000 calories a day of fat deposits for fuel and, because the body does not distinguish between exogenous (eaten) and indogenous (internally-generated) fuels, this means they’re burning 2500 calories a day, not 1500, which results in a higher basal metabolic rate, absence of semi-starvation symptoms, and significantly higher loss of fat tissue than those on a calorically-identical LFCR diet (which may explain the seemingly-impossible situation where a MD named Peter Attia went from eating a higher-carb 3000 calories/day diet (whole grains, fruit, etc.) with ~20% body fat to eating 4500 calories/day of ~80% fat (mostly saturated), and lost nearly 25 pounds of pure body fat (mainly abdominal-gauged according to DXA, or dual energy X-ray absorptiometry, scans) while drastically raising his HDL and lowering his triglyceride levels (fat in the blood) with NO change in physical activity; this is from a self-experiment with a sample size of one but it is theoretically explained by the biochemistry of a low-insulin ketogenic state that many human populations, like Inuit in Canada, Native Americans in the Great Plains, and Masai tribes in parts of Africa, may have evolved to live in).[405],[406],[407],[408]

The profound implications of the effects of a LCHF diet is that if you lower insulin levels far enough, the body will burn its own fat tissue for fuel which directly attacks the problem of obesity, which is excess body fat (NOT a “positive energy balance” problem).  If you stay on a 1500 calorie, higher-carbohydrate diet, your insulin levels will be higher than on an isocaloric LCHF diet, and your fat will be trapped in your fat tissue and your body will have to subsist on 1500 calories when your basal metabolism wants 2500 calories/day.  Therefore, you will enter semi-starvation (experience hunger, lethargy, depression, and low libido) while the other test subject eating a 1500 cal. LCHF diet is actually providing there basal metabolism with the desired 2500 calories/day, only 1000 of these are from the now-liberated fat tissue (again, the body does not care whether the fuel comes from external sources, food, or internal sources, fat tissue).  This explains the high body fat loss and lack of semi-starvation with a LCHF diet and the perceived increase in basal metabolism in these diets (again, see Attia video).  A recent 10-week clinical trial of humans found that high fructose consumption actually reduced basal metabolism, possibly due to reduced fat oxidation due to greater levels of hyperinsulemia/insulin resistance, compared with glucose alone.[409]

Ironically, heart disease risk factors improve on LCHF diets as the decrease in carbohydrate and increase in saturated fat consumption will actually decrease fat (i.e . triglyceride) levels in the blood while raising HDL which will, according to current understanding of heart disease risk, improve heart health (this heart-health improvement observation is seen repeatedly in randomized clinical trials of the LCHF diets versus low-fat, calorie-restricted diets).  This could explain how obese women eating a high saturated fat diet in the “A to Z Diet Study” run by Stanford, had lower levels of blood triglycerides and higher HDL than the obese women randomized to the very low saturated fat Ornish diet.[410]  This “eat more fat, have less fat in adipose tissue and blood” is counter-intuitive to common sense and anathema to conventional dietary recommendations yet it appears repeatedly in RCTs thereby meeting one key criteria of causality: repetition of observed results.[411],[412], [413],[414],[415], ,[416],[417],[418],[419],[420],[421],[422],[423],[424],[425],[426],[427],[428],[429]  Krauss et al found that a LCHF diet improved blood lipid levels even after controlling for weight loss when compared to a low-fat, calorie-restricted diet.[430],[431]

Despite the mounting evidence that a LCHF diet may be ideal for weight loss and heart health, these diets are still considered “fad diets” due to their high animal fat consumption and promises of weight loss even with unrestricted consumption of food; health researchers think that this promise is impossible, and therefore “quackery,” as it violates the law of thermodynamics (how can one lose weight without restricting calories?) and will give patients heart disease (which explains Jean Mayer’s labeling of these diets as “mass murder”).[432],[433]  Because researchers are stuck in this physics paradigm of obesity (based on misinterpreting the law of conservation of energy) and believe that a “perverted appetite” (coined by an American MD named Louis Newbergh in the early 20th century) and sloth drive obesity, carbohydrate essentially gets a free pass because public health authorities fail to consider the biochemistry and human physiology of carbohydrate and fat metabolism to be important, even with regards to the condition of obesity that is, at its core, a problem of excess body fats in humans likely driven by the “carbohydrate intolerance” of insulin resistance.[434],[435],[436]

A surreal situation now exists in public health nutrition where the accepted biochemical mechanisms of carbohydrate metabolism, fat metabolism, and insulin resistance, and the necessary extensions of these mechanisms and the results of multiple RCTS of LCHF diets, are largely ignored by health authorities in their efforts to educate the public on the cause and prevention of insulin resistance-the likely cause of most obesity and diabetes in the U.S.  Essentially, the United States is experiencing an epidemic of excess body fat and public health authorities do not care what regulates body fat; if they did, the NIH’s NIDDK page on insulin resistance would mention carbohydrates as a primary cause of hyperinsulemia/insulin resistance because they are, given the known biochemistry carbohydrate metabolism and fat regulation regarding insulin.[437]  Yet, the NIH’s site on insulin resistance mentions nothing about how carbohydrate metabolism likely drives the condition due to its effect on insulin-why not?[438]  The site mentions how scientists are discovering genes related to the condition and how “excess weight and physical inactivity” “contribute” to insulin resistance and how losing weight and physical activity, along with “wise food choices,” may reverse the condition yet no mention of what constitutes a “wise food choice” is discussed.[439]

How can these researchers assign causal blame to a likely effect of the condition, “excess weight and physical inactivity,” and ignore the blatantly obvious possibility that the foods that raise insulin (carbohydrates) are the likely cause of the condition, and that restricting the foods that drive the biochemical condition causing the syndrome might be a good idea?  Researchers are also pushing epidemiology beyond its capabilities by assigning causal criteria to a condition when the available observational epidemiological evidence can only show association and, yet, at the same time, are ignoring the proven biochemistry/physiology on insulin regulation which we know is primarily controlled through the quality and quantity of carbohydrates consumed in the diet.  Therefore, it appears that public health has become, at least in terms of nutritional recommendations, anti-science.

This field-wide foray into the side-streets of genetic research appears similar to hydrogen fuel cell research for cars being funded by oil companies in that both may simply be a tool of distraction, a smokescreen, to cover the obvious solution to the problem (i.e. reduce emissions by producing electric cars, which can already be made, or reduce defects in carbohydrate metabolism by promoting carbohydrate-restriction, which has been used for over a century to effectively treat obesity and diabetes) that prevents recommendations from actually incorporating obvious physiological facts that may actually prevent and/or cure the condition.[440]  Another reason for this genetic research may also be because, if researchers say refined carbohydrates are the primary cause of metabolic syndrome, then they’ll be admitting that the past 40 years of admonishment to reduce calories, fat, and to exercise more were likely wrong, and, potentially, harmful due to the previously outlined unintended consequences of such recommendations.  The AHA recently took a small step in the direction of, as Lustig says, “righting the ship” of nutritional guidelines by advocating a shift in recommended daily sugar consumption in adults from 22 teaspoons/person/day to less than 9 a day for men and 6 for women.[441]  But it is clear, given the NIDDK’s insulin resistance website, that the field still has a huge amount of work left to extricate itself from the poorly constructed science of decades past, and to actually solve the problem of metabolic syndrome.

Can this problem really be so simple?  Are carbohydrates really the primary driver of metabolic syndrome, not fat?  Therefore, does Occam’s Razor (i.e. do not use a complex hypothesis when a simpler one will do) apply to our metabolic woes? [442]  Again, many prominent researchers, including Dr. Walter Willet of Harvard, seem to think it does.[443]  Because obesity and diabetes are linked to all other insulin resistance co-morbidities (cancer, hypertension, heart disease, gout, Alzheimer’s), what Dr. Willet is suggesting is that the removal of the fattening refined carbohydrate may indeed prevent, to some degree, due to its effects on insulin and IGF levels, all of these conditions: therefore, if this is true, the principles of Occam’s Razor are valid in explaining the diabesity/metabolic syndrome epidemic in light of increased refined carbohydrate consumption.  Willet’s logic ultimately suggests that, because metabolic syndrome consists of most of the conditions associated with a “Westernized” lifestyle, and refined carbohydrates, specifically sugars, are thought to be the primary cause of diabesity and metabolic syndrome, the primary cause of these chronic diseases may very well be sugar/HFCS along with other refined carbohydrates as the consumption of these items has increased dramatically over the past 50 years.[444],[445]   Another interesting observation by Taubes is that, while the physics community is eagerly pursuing a unified theory of everthing (Einstein and Hawking are a few of these trail-blazers), the nutritional research community sees a unifed theory of chronic diseases to be simplistic, stupid, and likely a waste of time because it is impossible that only one nutrient item could possibly cause so many conditions.[446]

What Dr. Willet is suggesting is that “Occum’s Razor” may apply in regards to metabolic syndrome because a single food group, refined carbohydrates/sugars, are hypothesized to be the primary necessary cause that may trigger all of the conditions associated with metabolic syndrome when consumed in large enough quantities over time.[447]   Though past nutritional researchers have been mocked for suggesting that a single nutrient may be a primary cause of all chronic diseases (contrary to physics where such luminaries as Einstein and Hawking actively sought a single unified theory of everything (Einstein’s “unified field theory” or Hawking’s “M-theory”) for a large portion of their careers), the underlying reality may indeed be that refined carbohydrates, again, with sucrose/HFCS being the worst), are a primary cause of all of these related metabolic disorders that crop up in modern/Westernized-populations who start consuming a high sugar/refined carbohydrate diet.[448],[449],[450]

Willet’s point is that refined carbohydrates are to metabolic syndrome what tobacco smoking is to lung cancer, i.e., even though only roughly 1 in 6 to 1 in 9 lifetime smokers get lung cancer, 90% of these lung cancer cases can be attributed to smoking (assuming Canadian risk experiences from 1987-1989 are similar to the U.S.).[451],[452],[453]  In the same vein, though many people can eat copious sugar and potato chips and not fatten, for the majority of metabolic syndrome cases (~34% of US adults) and the 35.6% of U.S. adults now obese (2010 NHANES), refined carbohydrates were the likely cause of their disease (though there is some evidence that lean people still suffer from refined carbohydrate-generated insulin resistance as certain conditions of metabolic syndrome, namely, high levels of C-reactive protein of cardiovascular inflammation (associated with CHD risk), can occur independently of obesity in these individuals).[454],[455]  Also, the slow development of insulin resistance in lean tissue (and therefore caloric deposition in the insulin sensitive fat tissue) over decades due to chronic carbohydrate consumption may explain the creeping weight gain experienced by many Americans, say 1-2 pounds a year of body fat, over a 20 year period, that will transform a lean 20 year old into an obese 40 year old.[456]  If insulin and insulin-like growth factor are also involved in cancer cell growth, then carbohydrates may be a primary risk factor for cancer even in non-obese/diabetic individuals (though obese/diabetics still have a higher relative risk of getting cancer then lean individuals).[457]

Metabolic syndrome leaves a person with a body that, due to the deregulation of its fat tissue and chronically elevated insulin, can only burn carbohydrates, which, sugars primarily, are known to be addictive in the same way as nicotine, heroin, and cocaine due to its effect on the brain; refined carbohydrates are also the cheapest and most available foods (in terms of cost per calorie).[458],[459]  Given these biochemical and economic realities, it is no wonder that America is suffering from an epidemic of metabolic syndrome, especially amongst poorer populations who, sadly, due to economic hardship and “food deserts,” can only afford the very foods that make them sick and addicted, and, due to the epigenetic effects of insulin resistance (a type of intrauterine “metabolic memory”), will likely have children and grandchildren at higher risk (then higher SES populations) for becoming sick and addicted to refined carbohydrates.[460],[461]

This epigene-gene-environment effect will likely lead to the perpetuation of an ever higher prevalence of metabolic syndrome through future generations of impoverished Americans if the food environment is not fundamentally altered.[462]  These individuals then suffer the dual insults of poverty (and all the associated “risk clustering” of having a low SES) and obesity/diabetes, are told to exercise/eat less (which won’t work), take insulin (which they can barely afford and which promotes further fattening and cancer genesis), and produce babies who (due to the damaging epigenetic effects of hyperinsulemia on the fetus) are genetically and environmentally predisposed to acquire metabolic syndrome themselves at much earlier ages.[463][464]  The poverty>metabolic syndrome link may explain why the number of overweight and obese children on WIC in Georgia has doubled in the past ~20 years, with a full 15% of two to four year olds on WIC now obese (likely due to the epigenetic-carbohydrate interaction).[465],[466]  There is also now an epidemic of obese six month olds on WIC because, it’s hypothesized, government subsides for orange juice leads to the overconsumption of fructose by these babies.[467]

Given what we know about metabolic syndrome, its causes, and its prevalence, it is tragic and inexcusable for public health to continue to promote ineffective recommendations based upon antiquated and ambiguous, if not incorrect, science. Given what we know about metabolic syndrome, its causes, and its prevalence, it is tragic and inexcusable for policy makers to not regulate the very food companies (Coca-cola, Pepsi, Kraft, Nabisco, Frito-Lay) that produce and distribute these addictive and fattening foods to schools, hospitals, work places, and poor areas that likely have caused and will continue to fuel this epidemic.  Given what we know about the biochemical effects of refined carbohydrates, specifically sugar/HFCS, and the trends in consumption and metabolic syndrome, it is imperative that we reduce our populations’ consumption of refined carbohydrates.  Given that sugar/HFCS are the worst forms of these molecules and provide the most sugar to our fellow citizens, sugary drinks (SD) are probably the best first target of prevention efforts.

We also know that Georgia suffers from extremely high childhood obesity rates (#2 in the nation in terms of prevalence with 45% of 3rd graders and 27% of high school students either overweight/obese in 2010) and that obese children make obese adults (~80% of the time) who are at risk acquiring metabolic syndrome.[468], [469],[470],[471]  Therefore, to reduce youth sugary drink (SD) consumption we must first obtain an accurate assessment of the amount of SDs youths consume and where youths acquire them.  My project, “Fight Fitness in Fulton,” will attempt to assess these important nutritional habits, along with physical activity behavior, in 9-12 grade high school students so that, if the survey is implemented annually at the county-level, public health researchers, teachers, parents, and policy-makers can finally have data with which to implement new and effective policies to reduce SD consumption amongst Georgia adolescents.  These prevention efforts will be a first step towards preventing future generations of Georgians from developing metabolic syndrome.

 

POSSIBLE FUTURE STUDIES:

Though cross-sectional surveys like the FFF survey have many problems with assessing true associations between variables of interest, large prospective studies also have many problems.  THE main problem with using large, prolonged observational longitudinal studies to assess nutritional exposures and disease risk among free-living human beings are the huge number of biases and confounders that are introduced into the study over the follow-up period that cannot be controlled away, even with randomized selection of subjects as found in RCTs, and that may prevent the accurate assessment of the true association between exposure and disease.[472], [473],[474],[475]    These studies are then misinterpreted, largely by the press, as showing cause and effect when they can only show associations between factors, and the possible limitations in regards to biases and confounders are ignored.[476]

A recent example of this was the hormone-replacement therapy (HRT) controversy: the Nurse’s Health Study (NHS), a long-term uncontrolled prospective longitudinal study run by the Harvard School of Public Health, found a protective association between HRT and chronic heart disease, breast cancer, and death because nurses on HRT were less likely to get heart disease and breast cancer and die than women not on HRT.[477],[478]  A later, better controlled RCT, The Women’s Health Initiative, found that HRT potentially caused these diseases.[479]  It may be that the NHS subjects who self-selected to take HRT also engaged in other associated healthy activities, such as drinking less, smoking less, exercising, etc. and were of a higher SES (more educated, etc.) than those who did not use HRT; this self-selection bias (“the healthy user effect”) may have led to confounding differences between the two groups that could not be totally controlled for (“residual confounding” possibly by “life course socioeconomic position,” not just SES itself-as evidenced by HRT being as protective against accidental and violent death as CHD-Lawlor et al) and may have masked the potentially harmful effect of HRT on disease risk (therefore, healthy activities associated with HRT masked the true effect of HRT on disease risk and biased the association qualitatively “across the null” and made HRT appear healthful).[480],[481],[482],[483]

Another recent potentially confounded association found in the NHS was the slightly increased risk of death (RR=1.13) with high red meat consumption versus low red meat consumption; this may be another example of the healthy user effect at work, only relative to low red meat consumption, not HRT use.[484] Given that red meat has been considered unhealthy for decades, it is likely that those who ate high levels of red meat were less healthy in other ways that put them at a slightly increased risk of death over the 28 years of follow-up.  Indeed, researchers found that those who ate more red meat were also more overweight, drank more, smoked more, exercised less, etc.[485]  Though they claimed to have controlled for these potential confounders, there may be residual confounding that distorts the relationship between red meat and mortality risk because free-living human beings, as the study subjects were, engage in and experience thousands if not millions of different exposures over a 28 year period that are not controlled for.[486]  A recent meta-analysis, also out of Harvard, found no correlation between red meat consumption and CHD and diabetes, though overall mortality was not assessed.[487]

Therefore, the main problem with observational studies, even prospective RCTs with free-living humans, is free-living human beings.  Free-living humans are too complicated, they do too many things, are exposed to too many things over decades that are not recorded or controlled for, and therefore, we cannot truly assess the relationship between a single nutrient or exposure and an outcome using the available epidemiologic tools.  To truly assess the causal relationship between food and health over a lifetime in humans, researchers will need to treat humans like lab rats, such as occurs in a metabolic ward or in prison.  Only then can researchers tease apart the relationship between individual nutrients and diseases, like metabolic syndrome and type 2 diabetes, that millions of Americans currently suffer from.

Given the tremendously negative impact that obesity, metabolic syndrome, and type 2 diabetes have upon the human and financial health of the American population, it would greatly behoove the U.S. government to spend the money to actually determine what is really causing this diabesity epidemic.  It would be well worth spending a few billion dollars on a exceptionally well-run study to figure out the cause of a condition, diabesity and metabolic syndrome, that costs the U.S. government approximately $150 billion a year.[488]

A study worth a few billions dollars would be a 50 year, multi-armed randomized controlled trial that assesses metabolic syndrome incidence among prisoners of all genders, ages 20-75, condemned to life imprisonment without parole. 100-200 prisoners would be randomized onto a low-carbohydrate, high fat diet, a low-fat, calorie-restricted diet, a two-soda a day diet, and a control group consuming average prison fare.  Baseline measurements would be taken using DXA scans that include, but are not limited to: amount and location of body fat, waist circumference, blood pressure, blood lipids (TG, type B LDL, HDL), A1C, fasting glucose, etc.) and the actual meals consumed would be recorded (and videotaped to make sure that they consume the food given to them).  Body measurements would be taken every two weeks.  An interesting outcome to assess is the incidence of insulin resistance between groups: the carbohydrate/fructose hypothesis of diabesity would predict that the soda group would have a higher incidence of insulin resistance/metabolic syndrome than other groups after a few years.

The use of prisoners would be controversial but it would not be unethical.  These subjects are imprisoned and forced to eat certain foods prior to the survey anyway and would therefore not be under coercion because they would have to give voluntary and informed consent to take part in the survey.  There would be no unknown or residual confounders or biases between groups that could not be controlled away.  There would also be no loss to follow up and potential for bias as they’re imprisoned, cannot be lost to follow-up, and would be under constant video-surveillance.

These human guinea pigs could finally give this nation (and planet) a concrete, highly confident idea of what causes diabesity so that humanity can prevent and possibly cure the deadly and costly spectrum of diseases associated with insulin resistance.

 

 

 

DEFINITIONS:

Adipose (Fat) Tissue:

 

Definition:

“Dysregulation of adipose tissue physiology contributes to disease…experience with human and animal lipodystrophies (abnormalities of adipose tissue quantity and distribution), indicates that the relationship between obesity and diabetes is not due to the magnitude of fat accumulation per se, but rather the functioning of the adipose organ.”

-Todd Leff and James G. Grannerman, “Adipose Tissue in Health and Disease,” 2010.[489]

“‘Like a malignant tumor or like the fetus, the uterus or the breasts of a pregnant woman, the abnormal lipophilic [fat] tissue seizes on foodstuffs, even in the case of undernutrition.  It maintains its stock, and may increase it independent of the requirements of the organism.  A sort of anarchy exists; the adipose tissue lives for itself and does not fit into the precisely regulated management of the whole organism.’”

-Dr. Julius Bauer, 1929, quoted by Gary Taubes in “Good Calories, Bad Calories”[490]

An independently-active, regulated endocrine organ (not a passive energy silo as previously thought) responsible for regulating energy storage.[491],[492],[493] Like an ATM machine or a wallet, used for daily energy storage needs by releasing or storing fatty acids as triglycerides (three fatty acids bound to a glycerol molecule).[494]  LPL on fat tissue, in the presence of insulin, uptakes fatty acids and keeps them locked into the fat tissue.  With low insulin levels, HSL will dump fatty acids into the bloodstream for fuel (nearly all other hormones, like adrenaline, cause adipose tissue to release fatty acids as well, such as during the “flight-or-flight” stimulus).

High insulin levels keep fatty acids trapped in the fat tissue which, for all intensive purposes, makes the fat invisible to the body (like a Swiss bank account hiding bullion from the IRS).[495]  Therefore, hyperinsulemia both places and keeps fat in fat tissue (thereby keeping the individual fat).  Ironically, nicotine’s effect on the hormonal regulation of fat tissue may explain its success in causing fat loss amongst smokers and that appetite suppression is simply a down-stream effect of the action of nicotine on the hormonal regulation of adipose tissue.[496]

Triglycerides are stored along with some cholesterol in adipose tissue which may explain why the accelerated fat loss of carbohydrate restriction diets (relative to high-carbohydrate diets) may lead to temporarily elevated cholesterol levels (known as “transient hypercholesterolemia”).[497]

 

 

 

Carbohydrates

 

          Definition

 

A set of cyclical hydrocarbon molecules with oxygen molecules that end in the suffix “-ose.”[498]  These molecules including glucose-based isomer monosaccharides, 6 carbon ring molecules like glucose, galactose, which compose larger di- and poly-saccharides like sucrose (“table sugar”), lactose (“milk sugar”), maltose (“malt”) , and starch (long glucose chains connected by 1-4 α bonds that compose many foods like potatoes, rice, and many grains);  all of these carbohydrates are metabolized to “blood sugar” which raises insulin in the blood.[499]  Fructose, a 5-membered ring, travels straight to the liver and is converted, at nearly 100%, to triglycerides (which may be the reason why high chronic sugar and HFCS, both ~50% fructose, are the necessary cause for insulin resistance for many individuals and that this insulin resistance starts in the liver (see “Fructose” in Definitions).[500]  Starches (i.e. long chains of glucose molecules with 1-4α bonds) are detrimental to insulin levels and aid in this insulin resistant process when consumed at high enough levels but fructose is likely the worst offender and the primary cause of this metabolic derangement (without excess sugar/HFCS to trigger insulin resistance, lower calorie consumption of starches may be inadequate to generate insulin resistance/obesity as seen by high-carbohydrate, low-obesity/diabetes populations, like the Japanese and Kitavins, who eat virtually no sugar/HFCS, but high dietary proportions of starchy vegetables).[501],[502],[503],[504]

Glucose and fructose may even produce adipocity in different areas of the body.[505]

 

 

Dietary Fats

 

          Defintion:

 

A complex assortment of fatty acid molecules that are composed of chains of carbons and hydrogens that are hydrophobic; the type of fat and its properties are determined by the saturation level and types of bonds present in its constituent fatty acids (i.e. the amount of hydrogens on each carbon atom in the chain; the higher the level of hydrogens, the more “saturated” the molecule, the higher the melting point of the lipid-which is why saturated fatty acids, SFAs, are solid at room temperature which leads many people to then naively assume that these fats are also solid in the bloodstream (though the body is ~98.6 F, not 70 F of a common room)).[506]

There are three main types of fats all with multiple subclasses that all effect blood lipid levels differently:

  • Saturated Fatty Acids (SFA): raise total blood cholesterol by raising both HDL (the “good” lipoprotein) and LDL (the “bad” lipoprotein) but increase the size of LDL (to form “buoyant” or type-A LDL, now thought to be harmless in regards to heart disease risk) which negates any potentially harmful effect from the molecule (acc. to Dr. Ronald Krauss).[507],[508]  This may explain the 2010 meta-analysis by Krauss and others that found that there was no correlation between saturated fat and heart disease risk.[509]
  • Monounsaturated Fatty Acids (MUFA): now universally lauded as the healthiest types of fat, these molecules both raise HDL and lower LDL (commonly found in olive oil and nuts of various types to various degrees).[510],[511]  Ironically, ~50% of beef is monounsaturated and another 20% of the saturated portion is steric acid (the fat now claimed to make chocolate heart healthy) which means ~70% of fatty beef and lard are heart healthy and the other 30% of SFA is heart risk neutral (as it raises LDL but decreases its density while simultaneously raising HDL).[512]
  • Polyunsaturated Fatty Acids (PUFA): raises HDL and no effect on LDL (the mirror opposite of SFA) and so are therefore heart neutral according to current understanding.[513]  There is some evidence that this type of fat may cause cancer due to its immunosuppressive effects following its oxidation and generation of free-radicals in the bloodstream; though human consumption of polyunsaturated fats has increased since the 1950’s to evoluntionarily-novel levels, primarily due to the higher consumption of vegetable oils, certain researchers question the PUFA>cancer hypothesis.[514]  Some evidence is emerging that even the most minute of molecular chemistry (such as the placement of a C=H bond within a fatty acid chain) affects the health effects of these molecules, thereby making the science of fat>heart health that much more complicated.[515]   Omega-3 fatty acids, a type of PUFA containing the ALA compound, and largely found in fish and grass-fed animals, are now considered heart healthy due to possible anti-inflammatory effects while their Omega-6 kin, found in corn-fed animals, are considered detrimental to heart health.[516]

 

“Energy-balance” hypothesis of Obesity:

 

          Defintion:

The globally prevailing hypothesis of obesity is that it simply a problem of “energy balance” (calories-in > calories-out = weight gain) and that if people simply consumed less food and exercise more than they would lose weight. [517],[518],[519],[520],[521],[522],[523]    However, systematic reviews and meta-analyses (not to mention the fact that >95% of calorie-restriction/exercise diets fail) have shown that this dietary regimen does not work to promote long-term weight loss. [524],[525],[526]  For much of the past 40 years in America, the main calorie-restriction diet advocated by the government and allied-medical organizations was a  low-fat diet as many researchers believed, starting in the 1960’s, that fat, specifically animal fats, caused heart disease, though evidence to support this hypothesis was ambiguous if not non-existant; current researchers question this hypothesis.[527][528],[529][530] While heterogeneity in fats is now generally accepted (i.e trans fats are worse than monounsaturated fats), the government’s nutritional recommendations for weight maintenance (see “MyPlate”) are still low-fat, calorie-restricted recommendations.[531]  Given what researchers now know about refined carbohydrates and metabolic syndrome, the inadequacy of low-fat/calorie-restricted diets, and the effectiveness of carbohydrate-restriction diets in promoting weight loss and improving blood lipids (<Trigs/small, dense LDL, >HDL) without hunger, it is time for carbohydrate-restricted diets to be accepted as viable methods to prevent and reduce obesity. …).[532],[533], ,[534],[535],[536],[537],[538],[539],[540],[541],[542],[543],[544],[545],[546]

 

This hypothesis is also a tautology-a specious, circular logic that makes the necessary effects of a condition also its cause; such as “because a system that accumulates more energy (i.e. gets bigger), such as a fat cell getting fatter, must take in more energy than it expends to accumulate more energy (as law of conservation of energy dictates must be true), the accumulation of energy is what causes it to accumulate energy-this explanation does not give any causal information as to why the system accumulates more energy than it expends, however.[547]

Definition:

Fructose is the carbohydrate responsible for endowing fruit with its sweet taste.[548]  Considered by biochemists to be the most lipogenic carbohydrate, fructose is also considered by many researchers to be the primary “trigger” for insulin resistance primarily due to fructose-induced lipogenesis in the liver which, among many other consequences, blocks the liver’s ability to metabolize glucose, thereby causing insulin upregulation by the pancreas and the further development of hyperinsulemia and insulin resistance (there are numerous other hypothesized negative effects of fructose that may generate insulin resistance-see Fig. 1 of Dekker et al and Fig. 1 of Seneff et al). [549],[550],[551],[552],[553],[554],[555],[556],[557]  It is now consumed in quantities far beyond mankind’s evolutionary daily consumption levels year-round (as opposed to the hypothesized evolutionary levels of 15g/day only during the few months a year when fruit is in season).

Ironically, fructose’s non-stimulation of insulin prompted the medical community to recommend high fructose consumption for type 2 diabetics in the late-1980’s in America (and for sucrose to be considered safe for diabetics due to the low glycemic index of fructose in the sugar); this recommendation most likely severely damaged their health as fructose is an extremely strong contributor to triglyceride production, insulin resistance, and AGE production, and therefore would exacerbate the negative effects from diabetes even further (AGEs are thought to cause the premature aging found in diabetics and, along with blood triglycerides, cause cardiovascular disease).[558],[559],[560],[561]  A state of depleted glycogen will spur the conversion of ingested fructose into glucose and glycogen, however, this glycogen depleted state is only present after extreme physical stress (such as in elite athletes after competition) or in starvation victims (see Mayes-66% of fructose was converted to glucose in starvation patients).[562]  Therefore, the overconsumption of fructose by children may lead to NAFLD (Non-alcoholic fatty liver disease); Britain is experiencing an epidemic of NAFLD in children (estimated at 0.5 million children), it’s thought, because of excessive fructose consumption by youth.[563]

/Glycemic load

Defintion:

The G is an index that compares the  thedifferent  when compared with a certain amount of pure glucose as a comparison (set at 100)ohyrdrates, or “simple” carbohydrates,such aswhite, y foods like white bread, potatoes, and rice, even sucrose/HFCS,[564],[565]  Glycemic load allows for analysis of the glycemic index and quantity of carbohydrates consumed (and may therefore be a better measure of the effect of foods on blood sugar/insulin for an entire meal, not just a single nutrient).[566]

 

Glucose:

         

          The primary molecule in carbohydrates responsible for raising blood glucose and, therefore, insulin levels (because glucose is toxic to the blood stream and must be removed from the bloodstream quickly, insulin acts to transform glucose to glycogen before handling any other food molecule, possibly leading to the faulty assumption by most nutritional researchers that glucose is the primary, preferred fuel for the body simply because it is burned first due to its toxicity).[567]  Also, the fact that the brain and central nervous system will run on approximately 125g of glucose per day, is used as evidence to support this assumption though the fact that brain will also run on ketones (see “Ketosis” definition-a state of running on byproducts of fat and protein metabolism) is often omitted as is the fact that all of the 125g of  glucose can be obtained from converting amino acids in proteins into glucose through gluconeogenesis in the liver meaning no carbohydrate intake is actually needed.[568]  Many physicians (even researchers at NIH) also confuse the natural and healthy state of ketosis (the utilization of ketones from fatty acids and amino acids as fuel normally utilized after a prolonged fast, such as after waking up from sleep) with ketoacidosis, a harmful and damaging side effect of uncontrolled diabetes (where ketone levels are ~20 times greater than those found during ketosis).[569],[570]  A ketogenic diet is also used to great success to prevent seizures in epileptic children and routinely performs better than anti-seizure drugs.[571],[572]

 

 

High Fructose Corn Syrup (aka, “HFCS” or “HFCS 55”): see “Sucrose” below.

 

Ketosis

“When I interviewed ketosis experts, however, they universally sided with Atkins, and suggested that maybe the medical community and the media confuse ketosis with ketoacidosis, a variant of ketosis that occurs in untreated diabetics and can be fatal. ”Doctors are scared of ketosis,” says Richard Veech, an N.I.H. researcher who studied medicine at Harvard and then got his doctorate at Oxford University with the Nobel Laureate Hans Krebs. ”They’re always worried about diabetic ketoacidosis. But ketosis is a normal physiologic state. I would argue it is the normal state of man. It’s not normal to have McDonald’s and a delicatessen around every corner. It’s normal to starve.”

Simply put, ketosis is evolution’s answer to the thrifty gene. We may have evolved to efficiently store fat for times of famine, says Veech, but we also evolved ketosis to efficiently live off that fat when necessary. Rather than being poison, which is how the press often refers to ketones, they make the body run more efficiently and provide a backup fuel source for the brain. Veech calls ketones ”magic” and has shown that both the heart and brain run 25 percent more efficiently on ketones than on blood sugar.”

-Gary Taubes, “What if It’s all Been a Big Fat Lie?,” New York Times, 2002[573]

A natural state of body metabolism where all cells run on byproducts of fat and protein metabolism.[574], [575]  Many physicians also confuse the natural and healthy state of ketosis (the utilization of ketones from fatty acids and amino acids as fuel normally utilized after a prolonged fast, such as after waking up from sleep) with ketoacidosis, a harmful and damaging side effect of uncontrolled diabetes (where ketone levels are ~20 times greater than those found during ketosis). [576]  A ketogenic diet is also used to great success to prevent seizures in epileptic children and routinely performs better than anti-seizure drugs. [577],[578]

Carbohydrate consumption must be kept very low (~<50g/day at least for most individuals) to stay in this metabolic state or the body will return to a state of burning glucose (from carbohydrates and/or glycogen) for fuel as glucose, but NOT fatty acids, is toxic to the blood stream. [579],[580],[581]

 

 

Insulin:

 

Definition:

“Since the 1960’s, four facts had been established beyond reasonable doubt: (1) carbohydrates are singularly responsible for prompting insulin secretion; (2) insulin is singularly responsible for inducing fat accumulation; (3) dietary carbohydrates are required for excess fat accumulation; and (4) both Type 2 diabetics and the obese have abnormally elevated insulin response to carbohydrates in the diet…the obvious implication is that obesity and Type 2 diabetes are two sides of the same physiological coin…of the same underlying defects-hyperinsulemia and insulin resistance.” –Gary Taubes, Good Calories, Bad Calories, pg. 394.

 

THE hormone responsible for putting what we eat into our fat tissue and for keeping what we eat in our fat tissue.[582], [583],[584],[585]  Considered an “excellent fattening tool,” by German doctors in the early 20th century, insulin injections were repeatedly used to fatten anorexic dogs, humans, and undernourished children to great success.[586]  Type 1 diabetics lack insulin (likely due to the auto-immune destruction of their pancreatic β-cells which produce insulin) and so cannot gain any weight, even when consuming over 10,000 calories a day as many often do.[587]  When put on insulin therapy, they fatten quickly.  Type 2 diabetics are primarily insulin resistant on their lean tissue and remain sensitive on their fat tissue, especially in their abdomen; this would explain the generation of visceral fattening during insulin resistance and of the “semi-cellular starvation” experienced by insulin resistant lean tissue during this state.  Because centralized adipose tissue is insulin sensitive and lean tissue is not, this fat tissue preferentially siphons off calories consumed.  More and more calories, and insulin, must be consumed to then force enough fuel into lean tissues to satisfy their demand for energy for metabolism.  This deregulation of the fat tissue than leads to the observation that overweight and obese people “overeat” when compared with lean people because the obese metabolism must overcome the parasitic effects of adipose tissue found in such a deranged fat regulation system (as Jean Mayer explains regarding obesity in animals predetermined to become obese, such as Zucker rats, “These mice will make fat out of their food under the most unlikely circumstances…even when half starved”).[588]  The fat tissue in mice with VMH lesions in the hypothalamus leads to the conservation of calories in fat tissue at 6 times the rate of mice without VMH lesions; this would explain the expansion of adipose tissue at the expense of lean tissues in animals genetically predisposed to fatten.[589]

Insulin also works to keep triglycerides trapped in adipose tissue so that hyperinsulemia, a trademark concurrent state with insulin resistance of metabolic syndrome, keeps individuals from accessing the triglycerides in their adipose tissue for fuel (known as “lipid trapping” effect of insulin). [590],[591],[592]  This may explain why obese, type 2 diabetics gain even further weight on insulin therapy, thereby exacerbating their metabolic syndrome further, without losing adipose fat, even on reduced calorie diets.[593]  The same is seen in obese mice played on starvation diets; their muscles, organs, and even brains will be burned for fuel before much of their fat tissue.

The main driver of insulin production is carbohydrate (protein has a slight effect upon insulin but much less so than carbohydrates).  The more refined the carbohydrate (i.e. the greater the glycemic index of the food), the greater the insulin response.  Fructose is a unique case in that it does not generate an insulin response and is metabolized directly by the liver; it essentially “clogs” the liver from metabolizing glucose which may explain why it is the primary factor considered to trigger insulin resistance in most metabolic syndrome cases.[594] Ironically, fructose’s lack of a high GI prompted the medical community to recommend high fructose consumption for type 2 diabetics in the late-1980’s in America; this recommendation most likely severely damaged their health as fructose is an extremely strong contributor to triglyceride production, insulin resistance, and AGE production, and therefore would exacerbate the negative effects from diabetes even further (AGEs are thought to cause the premature aging found in diabetics and, along with blood triglycerides, cause cardiovascular disease). [595],[596],[597],[598],[599],[600],[601],[602],[603]

 

The Metabolic Syndrome:

         

Defintion:

Formerly called “Syndrome X,” the metabolic syndrome, or insulin resistance syndrome, is characterized by the body’s inability to correctly use insulin due to the development of insulin resistance on various tissues (with the liver and lean tissue usually becoming resistant first).[604], [605],[606],[607],[608],[609],[610],[611],[612],[613],[614]  The overconsumption of glucose (which elevates blood insulin levels) and fructose especially are thought to cause this condition.[615]

 

Measurement:

 

According to the US. Dept. of HHS, people are considered to have metabolic syndrome if they exhibit at least 3 of the following conditions (as listed above, the overweight and obese are much more likely to have metabolic syndrome but non-obese can still suffer certain conditions as well) (certain researchers, such as Dr. Gerald Reaven, who found “Syndrome X,” believe these catagories to be rather arbitrary): [616], [617],[618]

  • waist measurement of 40 inches or more for men and 35 inches or more for women
  • triglyceride levels of 150 milligrams per deciliter (mg/dL) or above, or taking medication for elevated triglyceride levels
  • HDL, or “good,” cholesterol level below 40 mg/dL for men and below 50 mg/dL for women, or taking medication for low HDL levels
  • blood pressure levels of 130/85 or above, or taking medication for elevated blood pressure levels
  • fasting blood glucose levels of 100 mg/dL or above, or taking medication for elevated blood glucose levels

 

Obesity:

Definition:

 

Obesity is a disorder of the accumulation of unhealthy levels of excess body fat.[619]  Modern researchers consider it a problem caused by a lack of “energy balance” (i.e. consuming more calories than we expend-see Energy balance above) while, according to science journliast Gary Taubes, pre-WWII European researchers considered it a growth disorder where the fat tissue, much like a tumor or a teenage boy during puberty, is driven to grow by hormones that make it abnormally accumulate excess calories; the former hypothesis, couched in physics and the law of the conservation of energy, believes that over-eating and sedentary behavior are causes of obesity (which is a tautology-a specious, circular logic that makes the necessary effects of a condition also its cause; such as “because a system that accumulates more energy (i.e. gets bigger), such as a fat cell getting fatter, must take in more energy than it expends to accumulate more energy, the accumulation of energy is what causes it to accumulate energy-this explanation does not give any causal information as to why the system accumulates more energy than it expends, however) while the latter sees obesity and other forms of growth as simply effects of hormonal conditions where the fat tissue is deregulated and driven to grow and that it is the growth itself, again, as with tumors and puberty, that than drives these behaviors (gluttony and sloth). [620],[621],[622],[623],[624],[625],[626],[627],[628]

 

Measurement:

Obesity is conventionally measured by most medical and public health authorities in America and around the world (though not in certain Asian countries) as having a BMI, or body mass index (kg/m2), of >30.[629]  While the BMI tool is not perfect (having problems with specificity due to its inability to distinguish between lean tissue, muscle, and fat tissue (“adipocytes”)-the primary problem of obesity; therefore muscular athletes may end up as false positives and elderly people, especially women, with muscular atrophy but unhealthy body fat levels may be false negatives), BMI is generally considered an effective and efficient tool for assessing obesity as most individuals with too much body fat (i.e. obesity) will fall above the BMI >30 cutoff. This means that the BMI tool is ultimately a useful tool because it has high sensitivity and will rarely “miss” an obese individual and also have a high PPV+ given the much greater prevalence of body fatness in the U.S. population relative to muscular fitness.[630], [631],[632] 

 

Recent research by Braverman et al, which compared a nationally representative sample of adults and compared BMI estimates with DXA scans, found that BMI misclassified 25% of men and 48% of women as non-obese when they were in fact obese, judging from body fat percentages gleaned from DXA scans; this fault of BMI may lead to a large underestimation of the national adult obesity prevalence and a lack of awareness and education of obesity’s co-morbidities in the millions of adults who may be “false negatives” for obesity.[633],[634]  Therefore, they recommend a reclassification of “obese” as a BMI of 24 for adult women and 28 for adult men, respectively to limit the number of missed obese cases.[635]

*Childhood obesity is measured in a unique way.  A youth’s (anyone under 18 or 20?) weight and height is taken and their BMI is then compared to a standard frequency distribution created by the CDC that compares the youth’s BMI to other youths of the same age and gender.  If the youth is above the 95th percentile for BMI of their age/gender, they are classified as obese.[636]

 

Pre-diabetes:

 

[637]

 

Sucrose/HFCS:

Definition:

Both molecules are roughly 50/50% glucose and fructose and it may be that this unique, evolutionarily-unnatural mix of carbohydrates are a perfect synergistic storm for developing insulin resistance by “offer[ing] the worst of both sugars,” according to Taubes in that the simultaneous effects of glucose on the pancreas and fructose on the liver are significantly greater than either molecule by itself, and that this unnatural mixture may, over time, generate insulin resistance and metabolic syndrome in susceptible populations.[638]  The reasons the metabolic interaction between both is so effective at generating insulin resistance is that fructose’s lipogenic effect in the liver blocks glucose metabolism which then causes the pancreas to upregulate insulin, which generates greater triglyceride production by the liver (though few studies have tested such an interaction).[639],[640],[641]

Type 2 Diabetes Definition and Measurement:

 

Formerly known as “Adult-onset diabetes,” this condition is characterized by the inability of the body to shift blood glucose into tissues due to the development of insulin resistance in certain tissues (usually lean tissue before adipocytes (“fat cells”) which promotes fatteningand) and the eventual failure of the pancreatic β-cells to produce insulin.  , known as “glycosuria”[642],[643]The current epidemic of childhood obesity and the concurrent incidence of TII diabetes in children has led to a shift in the usage of “Adult-onset diabetes” to “Type II Diabetes.”[644] 

A person is considered diabetic if positiveg  Though not universally recommended for use to diagnosis diabetes, the glycated hemoglobin (Hba1c) test is a useful tool for assessing the average blood sugar levels of an individual over a 2-3 month period and is not subject to short-term blood glucose fluctuations or the need to prep the patient with fasting or a glucose infusion (a score >6.5 is considered diabetic).[645]

References


[i] Please refer to the Definitions section for definitions of all terms.

[ii] Adult obesity estimates, particularly in older women with muscular atrophy and elevated leptin (a satiety hormone produced by fat tissue), may be underestimated by as much as 40%, according to Braverman et al, due to the specificity limitations of the BMI measurement tool leading to huge numbers of “false negatives” when compared with DXA scans of body fat percentage (see “Obesity” in Definitions section).  Reanalyzing NHANES data with BMI>24 reclassified as “obese” for adult women, 64.1% of U.S. adult women would be considered obese “Obesity” in Definitions section)!

[iii] See “Insulin” in Definition’s section.

[iv] Interestingly, many researchers now believe the primary effect of environmental factors in tumor growth is not from mutating DNA but from enhancing the reproductive rate of tumor cells and their ability to evade immune defenses (something which blood glucose, and insulin and IGF especially, all do well for many types of “insulin-dependent” cancers, including breast, colorectal, etc.; the elevated blood glucose, insulin, and IGF levels in obese pre-diabetics/type 2 diabetics may explain why they suffer from cancer at greater incidence rates than non-obese/diabetic individuals). The enhanced tumor growth seen in a hyperinsulemic environment (relative to a semi-starved, low-insulin/IGF environment in which tumor growth is severely restricted) may be explained by the fact that many types of prostate, breast, and colorectal cancer cells express high numbers of insulin and 2-3 times the number of IGF receptors as normal tissue cells which enables greater uptake of glucose for cellular mitosis (through the inefficient aerobic glycolysis of the “Warburg effect”) which leads to greater reproductive rates in these tumor cells.  Insulin and IGF are also thought to enhance the P13 Kinase enzymatic pathway in tumor cells which enhances their sensitivity to insulin and IGF which increases glucose uptake and enhances replication (this suggests that elevated insulin/IGF inhibit the PTEN P13K suppressor which leads to enhanced P13K >insulin/IGF sensitivity >increased glucose uptake> enhanced growth and insulin/IGF receptor proliferation>glucose>growth>metastisis, etc.; this suggests that, according to the president of the Memorial Sloan-Kettering Cancer Center of New York, that  elevated insulin/IGF, perhaps from high refined carbohydrate intake, may initiate the cellular changes in endocrine cells which sparks cancerous development by initiating the Warburg effect and increased P13K signaling which then leads to a 10-20 fold increase in glucose consumption which drives reactive oxygen species (“free radicals”) which lead to genetic mutations and increased glucose uptake and more genetic damage (a “feed-forward acceleration of tumor growth”) (critics instead argue that insulin/IGF promote tumor growth not by generating the Warburg effect and free radical/DNA damage, but, instead, by inhibiting cell apoptosis, a primary defense mechanism to destroy oncogenic cells).  Might insulin do both?  Many researchers have started dividing tumors into either insulin-dependent (in which insulin/IGF disrupt PTEN and generate P13K signaling) and insulin-nondependent (in which mutations disrupt normal PTEN functioning) (Taubes, 2012,Science, “Unraveling the Obesity-Cancer Connection.”-see Ref. 119 for more information).


[1] Taubes, Gary, “Good Calories, Bad Calories,” 2007. New York: Knopf Publishing.pg. 362.

[2] Leff, Todd, & James. G. Grannerman. (). “Adipose Tissue in Health and Disease.” Wiley Publishers: , pg. xix-xixi, 98, 143-152.

[3] Flier, Jeffery. (Oct., 2010). “Lasker Lauds Leptin.” Cell, Volume 143, Issue 1, pgs. 9–12. Retrieved from: http://www.sciencedirect.com/science/article/pii/S009286741001069X.

 

[4] U.S. Dept. of Health and Human Services, NIDDK, NDIC. (Dec. 6, 2011). “Insulin Resistance and Prediabetes.” Retrieved from: http://diabetes.niddk.nih.gov/dm/pubs/insulinresistance/#risk.

[5] Bakker, Stephen J.L., et al. (Oct. 18, 2006). “Metabolic syndrome: a fata morgana?”

Nephrology Dialysis Transplantation, Vol. 22 (1), pgs. 15-20.doi: 10.1093/ndt/gfl581.  Retrieved from: http://ndt.oxfordjournals.org/content/22/1/15.full.

[6] Taubes, Gary. (2010). “Why We Get Fat, and What to Do About It.” New York: Anchor Books. Pg. 84.

[7] Ogden, Cynthia, & Margaret Carrol (2010). The Centers for Disease Control and Prevention NCHS Health E-Stat: Prevalence of Obesity Among Children and Adolescents: United States, Trends 1963-1965 Through 2007-2008. Division of Health and Nutrition Examination Surveys. Retrieved from http://www.cdc.gov/nchs/data/hestat/obesity_child_07_08/obesity_child_07_08.htm#figure1

[8] The Centers for Disease Control and Prevention. (2011). NCHS Health E-Stat

Prevalence of Overweight, Obesity, and Extreme Obesity Among Adults: United States, Trends 1960–1962 Through 2007–2008. Retrieved from:http://www.cdc.gov/nchs/data/hestat/obesity_adult_07_08/obesity_adult_07_08.htm

[9] The Centers for Disease Control and Prevention. (2011). Diabetes: Successes and Opportunities for Population-Based Prevention Control: At a Glance, 2011. Retrieved from: http://www.cdc.gov/chronicdisease/resources/publications/AAG/ddt.htm

[10] The Centers for Disease Control and Prevention. (2011). Diabetes Public Health Resource: National Prevalence of Diagnosed Diabetes. Retrieved from: http://www.cdc.gov/diabetes/statistics/ .

[11] Ogden, Cynthia L., Carroll, Margaret DKit, ., Brian K., and Katherine M. Flegal, The Centers for Disease Control and Prevention (January 2012). “Prevalence of Obesity in the United States, 2009–2010.” NCHS Data Brief, Number 82. Atlanta, GA. Retrieved from: http://www.cdc.gov/nchs/data/databriefs/db82.htm .

[12] Ogden, Cynthia, & Margaret Carrol (2010). The Centers for Disease Control and Prevention NCHS Health E-Stat: Prevalence of Obesity Among Children and Adolescents: United States, Trends 1963-1965 Through 2007-2008. Division of Health and Nutrition Examination Surveys. Retrieved from http://www.cdc.gov/nchs/data/hestat/obesity_child_07_08/obesity_child_07_08.htm#figure1

[13] The Centers for Disease Control and Prevention. (2011). NCHS Health E-Stat

Prevalence of Overweight, Obesity, and Extreme Obesity Among Adults: United States, Trends 1960–1962 Through 2007–2008. Retrieved from: http://www.cdc.gov/nchs/data/hestat/obesity_adult_07_08/obesity_adult_07_08.htm

[14] Ogden, Cynthia L., Carroll, Margaret DKit, ., Brian K., and Katherine M. Flegal, The Centers for Disease Control and Prevention (January 2012). “Prevalence of Obesity in the United States, 2009–2010.” NCHS Data Brief, Number 82. Atlanta, GA. Retrieved from: http://www.cdc.gov/nchs/data/databriefs/db82.htm .

[15] The Centers for Disease Control and Prevention, NHANES. (June 2011). “Specifying Weighting Parameters.” Atlanta, GA. Retrieved from: http://www.cdc.gov/nchs/tutorials/nhanes/surveydesign/Weighting/intro.htm .

[16] The Centers for Disease Control and Prevention, Division of Diabetes Translation (October 2010). Long-term Trends in Diabetes. Retrieved from: www.cdc.gov/diabetes/statistics/slides/long_term_trends.pdf.

[17] The Centers for Disease Control and Prevention, Behavioral Risk Factor Surveillance System. “Prevalence and Trends Data –Diabetes, 2010, Nationwide (States, DC, and Territories).” Atlanta, GA. Retrieved from: http://apps.nccd.cdc.gov/brfss/list.asp?cat=DB&yr=2010&qkey=1363&state=All .

[18] The Centers for Disease Control and Prevention, Behavioral Risk Factor Surveillance System. “Prevalence and Trends Data –Diabetes, 2010, Nationwide (States, DC, and Territories), by Race.” Atlanta, GA. Retrived from: http://apps.nccd.cdc.gov/brfss/race.asp?cat=DB&yr=2010&qkey=1363&state=US .

[19] The Centers for Disease Control and Prevention, National Center for Chronic Disease Prevention and Health Promotion, Division of Diabetes Translation. “National Diabetes Fact Sheet, 2011.” Atlanta, GA. Retrieved from: http://www.cdc.gov/diabetes/pubs/pdf/ndfs_2011.pdf .

[20] Schmidt, MI, and BB Duncan. (September 2003). “Diabesity: an inflammatory metabolic condition.” Clinical Chemistry and Laboratory Medicine, 41(9):1120-30. Retrived from: http://www.ncbi.nlm.nih.gov/pubmed/14598860 .

[21] Taubes, Gary. (2010). “Why We Get Fat, and What to Do About It.” New York: Anchor Books. Pg. 84.

[22] Lustig, Robert H. (2009). “Sugar: The Bitter Truth,” Youtube. Retrieved from http://www.youtube.com/watch?v=dBnniua6-oM

[23] Taubes, Gary. (2011, April 13). “Is Sugar Toxic?” The New York Times. Retrieved from http://www.nytimes.com/2011/04/17/magazine/mag-17Sugar-t.html?scp=1&sq=is%20sugar%20toxic?&st=cse

[24] Collino, Massimo. (2011). High dietary fructose intake: Sweet or bitter life? World Journal of Diabetes.  Obtained from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3158875/pdf/WJD-2-77.pdf

[25] Oda, E. (July 2011). Metabolic Syndrome: its history, mechanisms, and limitations. Acta Diabetologica, Epub: July 1st. Retrived from: http://www.ncbi.nlm.nih.gov/pubmed/21720880 .

[26] Taubes, Gary. (2007) “Good Calories, Bad Calories,” New York: Knopf Publishing. Pg. 180-183.

[27] Taubes, Gary. (2010). “Why We Get Fat, and What to Do About It.” New York: Anchor Books. Pg. 195-197.

[28] Ibid.

[29] Lustig, Robert H. (2009). “Sugar: The Bitter Truth,” Youtube. Retrieved from http://www.youtube.com/watch?v=dBnniua6-oM

[30] Taubes, Gary. (2007) “Good Calories, Bad Calories,” New York: Knopf Publishing. Pg. 180-183.

[31] Taubes, Gary. (2011, April 13). “Is Sugar Toxic?” The New York Times. Retrieved from http://www.nytimes.com/2011/04/17/magazine/mag-17Sugar-t.html?scp=1&sq=is%20sugar%20toxic?&st=cse

[32] Wells, JC, & Siervo M. (2011). Obesity and energy balance: is the tail wagging the dog? European Journal Clinical Nutrition.  Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/21772313 doi: 10.1038/ejcn.2011.132

[33] Kroner, Z. (December 2009). “The relationship between Alzheimer’s disease and diabetes: Type III diabetes?”Alternative Medicine Review, 14(4):373-9. Retrived from: http://www.ncbi.nlm.nih.gov/pubmed/20030463 .

[34] De la Monte, SM, and JR Wands. (November 2008). “Alzheimer’s disease is type-III diabetes-evidence reviewed.” Journal of Diabetes Science and Technology, 2(6):1101-13. Retrieved from: http://www.ncbi.nlm.nih.gov/pubmed/19885299 .

[35] Taubes, Gary. (2010). “Why We Get Fat, and What to Do About It.” New York: Anchor Books. Pg. 195-200.

[36] Braun, Sandra, Bitten-Worms, Keren, and Derek LeRoith. (August 2011). “The Link between the Metabolic Syndrome and Cancer.” International Journal of Biological Sciences, 7(7):1003-15. Haifa, Israel. Retrived from: http://www.ncbi.nlm.nih.gov/pubmed/21912508 .

[37] The Telegraph. (July 3, 2011). “Obesity Crisis: Half a Million Chidren have Liver Disease.” United Kingdom.  Retrived from: http://www.telegraph.co.uk/health/healthnews/8612881/Obesity-crisis-Half-a-million-children-have-liver-disease.html .

[38] Taubes, Gary. (January 2012). “Unraveling the Obesity-Cancer Connection.” Science, Vol. 335 no. 6064 pp. 28-32. Retrieved from: http://www.sciencemag.org/content/335/6064/28 .

[39] Ervin, R. Bethene. The Centers for Disease Control and Prevention, National Health Statistics Report. (May 5, 2009). “Prevalence of Metabolic Syndrome Among Adults 20 Years of Age and Over, by Sex, Age, Race and Ethnicity, and Body Mass Index: United States, 2003–2006.”  Number 13. Retrived from: http://www.cdc.gov/nchs/data/nhsr/nhsr013.pdf .

[40] Reaven, G.M. (June, 2005). “The Metabolic Syndrome: Requiscat in Pace.” Clinical Chemistry, Vol. 51 no. 6, pgs. 931-938. Retrieved from: http://www.clinchem.org/content/51/6/931.full.

[41] National Cancer Institute. “Obesity and Cancer Risk.” Retrieved from:http://www.cancer.gov/cancertopics/factsheet/Risk/obesity.

[42] Taubes, Gary. (January 2012). “Unraveling the Obesity-Cancer Connection.” Science, Vol. 335 no. 6064 pp. 28-32. Retrieved from: http://www.sciencemag.org/content/335/6064/28 .

[43] Taubes, Gary, “Good Calories, Bad Calories,” 2007. New York: Knopf Publishing. Pg. 91, 112.

[44] Taubes, Gary. (2011, April 13). “Is Sugar Toxic?” The New York Times. Retrieved from http://www.nytimes.com/2011/04/17/magazine/mag-17Sugar-t.html?scp=1&sq=is%20sugar%20toxic?&st=cse

[45] Taubes, Gary, “Good Calories, Bad Calories,” 2007. New York: Knopf Publishing. Pg. 91, 112.

[46] Collino, Massimo. (2011). High dietary fructose intake: Sweet or bitter life? World Journal of Diabetes.  Obtained from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3158875/pdf/WJD-2-77.pdf

[47] Lustig, Robert H. (2009). “Sugar: The Bitter Truth,” Youtube. Retrieved from http://www.youtube.com/watch?v=dBnniua6-oM

[48] Taubes, Gary, “Good Calories, Bad Calories,” 2007. New York: Knopf Publishing. Pg. xxiii, 152, 180-183, 394-397.

[49] Taubes, Gary. (2011, April 13). “Is Sugar Toxic?” The New York Times. Retrieved from http://www.nytimes.com/2011/04/17/magazine/mag-17Sugar-t.html?scp=1&sq=is%20sugar%20toxic?&st=cse

[50] Wells, JC, & Siervo M. (2011). Obesity and energy balance: is the tail wagging the dog? European Journal of Clinical Nutrition.  Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/21772313 doi: 10.1038/ejcn.2011.132

[51] Aschengrau, Ann, and George R. Seage III. (2008). “Essentials of Epidemiology in Public Health: Second Edition.” Sudbury, MA: Jones and Bartlett Publishers. Pg. 400.

[52] Malik, et al Circulation. (2010). Sugar-Sweetened Beverages, Obesity, Type 2 Diabetes Mellitus, and Cardiovascular Disease Risk.” Circulation, Vol. 121, pgs. 1356-1364.  Retrived from: http://circ.ahajournals.org/content/121/11/1356.full.pdf+html .

[53] The Los Angeles Times. (Dec. 20, 2010). “A Reversal on Carbs.” Retrieved from: http://articles.latimes.com/2010/dec/20/health/la-he-carbs-20101220 .

[54] Aschengrau, Ann, and George R. Seage III. (2008). “Essentials of Epidemiology in Public Health: Second Edition.” Sudbury, MA: Jones and Bartlett Publishers.

[55] Seneff, Stephanie, Wainwright, Glyn, & Luca Mascitelli. (Feb. 7, 2011). “Is the metabolic syndrome caused by a high fructose, and relatively low fat, low cholesterol diet?” Archives of Medical Science, Vol. 7(1), pgs. 8-20. Retrieved from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3258689/pdf/AMS-7-1-8.pdf

[56] Cordain, Loren, et al. (2000). “Plant-animal subsistence ratios and macronutrient energy estimations in worldwide hunter-gatherer diets.” American  Journal of  Clinical  Nutrition, Vol. 71, pgs. 682–92.Retrieved from: http://www.ajcn.org/content/71/3/682.long.

[57] Volek, Jeff S., and Stephen D. Phinney (May 19, 2011). “The Art and Science of Low Carbohydrate Living.”  Chapter 1: Overview of Low Carbohydrate and Ketogenic Diet. Beyond Obesity LLC.

[58] Cordain, Loren, et al. (2000). “Plant-animal subsistence ratios and macronutrient energy estimations in worldwide hunter-gatherer diets.” American  Journal of  Clinical  Nutrition, Vol. 71, pgs. 682–92.Retrieved from: http://www.ajcn.org/content/71/3/682.long.

[59] Ibid.

[60] Volek, Jeff S., and Stephen D. Phinney (May 19, 2011). “The Art and Science of Low Carbohydrate Living.”  Chapter 1: Overview of Low Carbohydrate and Ketogenic Diet. Beyond Obesity LLC.

[61] Taubes, Gary, “Good Calories, Bad Calories,” 2007. New York: Knopf Publishing. Pgs. 91-97.

[62] Taubes, Gary, “Good Calories, Bad Calories,” 2007. New York: Knopf Publishing. pg. 393-395.

[63] Taubes, Gary. (2010). “Why We Get Fat, and What to Do About It.” New York: Anchor Books. Pg. 118-121.

[64] Goodman, H. Maurice. (2009). “Basic Medical Endocrinology: Adipogenesis.” Academic Press, Fourth Edition.  Pg. 165. Retrieved from: http://books.google.com/books?id=gjpi2MYVKGAC&pg=PA165&dq=insulin+AND+adipocyte&hl=en&sa=X&ei=CVtJT7XVIsWatwent7TyAg&ved=0CEkQ6AEwAg#v=onepage&q=insulin%20AND%20adipocyte&f=false.

[65] Lustig, Robert H. (2009). “Sugar: The Bitter Truth,” Youtube. Retrieved from http://www.youtube.com/watch?v=dBnniua6-oM

[66] Taubes, Gary, “Good Calories, Bad Calories,” 2007. New York: Knopf Publishing. Pg. 200-201.

[67] [67] Malik, et al Circulation. (2010). Sugar-Sweetened Beverages, Obesity, Type 2 Diabetes Mellitus, and Cardiovascular Disease Risk.” Circulation, Vol. 121, pgs. 1356-1364.  Retrived from: http://circ.ahajournals.org/content/121/11/1356.full.pdf+html .

[68] Seneff, Stephanie, Wainwright, Glyn, & Luca Mascitelli. (Feb. 7, 2011). “Is the metabolic syndrome caused by a high fructose, and relatively low fat, low cholesterol diet?” Archives of Medical Science, Vol. 7(1), pgs. 8-20. Retrieved from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3258689/pdf/AMS-7-1-8.pdf

[69] Stanhope, Kimber L., et al. (May, 2009). “Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans.” The Journal of Clinical Investigation, Vol. 119, Number 5, pgs. 1322- . Retrieved from: http://www.jci.org/articles/view/37385.

[70] Mayes, Peter. (1993). “Intermediary metabolism of fructose.” American Journal of Clinical Nutrition, Vol. 58 (5), pgs. 7545-7655. Retrieved from: http://www.ajcn.org/content/58/5/754S.full.pdf.

[71] Ibid of references 36-52.

[72] Taubes, Gary, “Good Calories, Bad Calories,” 2007. New York: Knopf Publishing. Pg. 197-201.

[73] US. Dept. of Health and Human Services, NIDDK, National Diabetes Information Clearinghouse (Dec. 6, 2011). “Insulin Resistance and Prediabetes.” Retrieved from: http://diabetes.niddk.nih.gov/dm/pubs/insulinresistance/ .

[74] Lustig, Robert H. (2009). “Sugar: The Bitter Truth,” Youtube. Retrieved from http://www.youtube.com/watch?v=dBnniua6-oM

[75] Seneff, Stephanie, Wainwright, Glyn, & Luca Mascitelli. (Feb. 7, 2011). “Is the metabolic syndrome caused by a high fructose, and relatively low fat, low cholesterol diet?” Archives of Medical Science, Vol. 7(1), pgs. 8-20. Retrieved from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3258689/pdf/AMS-7-1-8.pdf

[76] Dekker, Mark J., et al. (May 10, 2010). “Fructose: a highly lipogenic nutrient implicated in insulin resistance, hepatic steatosis, and the metabolic syndrome.” American Journal of Physiology, Vol. 299 (5), pgs. 685-694. Retrieved from: http://ajpendo.physiology.org/content/299/5/E685.long#ref-94. Figure 1: http://ajpendo.physiology.org/content/299/5/E685/F1.expansion.html.

[77] US. Dept. of Health and Human Services, NIDDK, National Diabetes Information Clearinghouse (Dec. 6, 2011). “Insulin Resistance and Prediabetes.” Retrieved from: http://diabetes.niddk.nih.gov/dm/pubs/insulinresistance/ .

[78] Lustig, Robert H. (2009). “Sugar: The Bitter Truth,” Youtube. Retrieved from http://www.youtube.com/watch?v=dBnniua6-oM

[79] Taubes, Gary, “Good Calories, Bad Calories,” 2007. New York: Knopf Publishing. Pg. 200-201.

[80] [80] Malik, et al Circulation. (2010). Sugar-Sweetened Beverages, Obesity, Type 2 Diabetes Mellitus, and Cardiovascular Disease Risk.” Circulation, Vol. 121, pgs. 1356-1364.  Retrived from: http://circ.ahajournals.org/content/121/11/1356.full.pdf+html .

[81] Seneff, Stephanie, Wainwright, Glyn, & Luca Mascitelli. (Feb. 7, 2011). “Is the metabolic syndrome caused by a high fructose, and relatively low fat, low cholesterol diet?” Archives of Medical Science, Vol. 7(1), pgs. 8-20. Retrieved from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3258689/pdf/AMS-7-1-8.pdf

[82] Stanhope, Kimber L., et al. (May, 2009). “Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans.” The Journal of Clinical Investigation, Vol. 119, Number 5, pgs. 1322- . Retrieved from: http://www.jci.org/articles/view/37385.

[83] Mayes, Peter. (1993). “Intermediary metabolism of fructose.” American Journal of Clinical Nutrition, Vol. 58 (5), pgs. 7545-7655. Retrieved from: http://www.ajcn.org/content/58/5/754S.full.pdf.

[84] Taubes, Gary, “Good Calories, Bad Calories,” 2007. New York: Knopf Publishing. Pg. 201.

[85] Seneff, Stephanie, Wainwright, Glyn, & Luca Mascitelli. (Feb. 7, 2011). “Is the metabolic syndrome caused by a high fructose, and relatively low fat, low cholesterol diet?” Archives of Medical Science, Vol. 7(1), pgs. 8-20. Retrieved from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3258689/pdf/AMS-7-1-8.pdf

[86] [86] Malik, et al Circulation. (2010). Sugar-Sweetened Beverages, Obesity, Type 2 Diabetes Mellitus, and Cardiovascular Disease Risk.” Circulation, Vol. 121, pgs. 1356-1364.  Retrived from: http://circ.ahajournals.org/content/121/11/1356.full.pdf+html .

[87] Ibid.

[88] Ibid.

[89] Pomeranz, Jennifer L. (2011). “Advanced policy options to regulate sugar-sweetened beverages to support public health.” Journal of Public Health Policy,1-14. Retrieved from: http://www.yaleruddcenter.org/resources/upload/docs/what/law/PolicyOptionsSSBs_JPHP_8.11.pdf.

[90] Brownell et al. (Oct. 15, 2009). “The Public Health and Economic Benefits of Taxing Sugar-Sweetened Beverages.” The New England Journal of Medicine. Retrieved from: http://www.nejm.org/doi/full/10.1056/NEJMhpr0905723

[91] Lustig, Robert H, Schmidt, Laura A. & Claire D. Brindis. (February 2, 2012). “Public health: The toxic truth about sugar.” Nature, Vol. 482, pgs. 27-29. Retrieved from: http://www.nature.com/nature/journal/v482/n7383/full/482027a.html

[92] Garber, AK & Lustig RH. (Sept. 2011). “Is fast food addictive?” Current Drug Abuse Reviews, 4(3), 146-62. Retrieved from: http://www.ncbi.nlm.nih.gov/pubmed/21999689.

[93] Taber DR, Chriqui JF, Powell LM, & FJ Chaloupka. (Nov. 7 2011). “Banning All Sugar-Sweetened Beverages in Middle Schools: Reduction of In-School Access and Purchasing but Not Overall Consumption.” Archives of Pediatrics & Adolescent Medicine, Epub. Retrieved from: http://www.ncbi.nlm.nih.gov/pubmed?term=Banning%20All%20Sugar-Sweetened%20Beverages%20in%20Middle%20Schools

[94] Ogden, Cynthia L., et al. (August 2011). “Consumption of Sugar Drinks in the United States, 2005-2008.” HHS, CDC, NCHS Data Brief, No. 71. Retrieved from: http://www.cdc.gov/nchs/data/databriefs/db71.pdf.

[95] Taubes, Gary. (2007) “Good Calories, Bad Calories,” New York: Knopf Publishing. Pgs. 103, 129.

[96] Seneff, Stephanie, Wainwright, Glyn, & Luca Mascitelli. (Feb. 7, 2011). “Is the metabolic syndrome caused by a high fructose, and relatively low fat, low cholesterol diet?” Archives of Medical Science, Vol. 7(1), pgs. 8-20. Retrieved from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3258689/pdf/AMS-7-1-8.pdf

[97] The Telegraph. (July 3, 2011). “Obesity Crisis: Half a Million Chidren have Liver Disease.” United Kingdom.  Retrived from: http://www.telegraph.co.uk/health/healthnews/8612881/Obesity-crisis-Half-a-million-children-have-liver-disease.html

[98] Curtis, Michael. (2004). “The Obesity Epidemic in the Pacific Islands.” Journal of Development and Social Transformation, Vol.1(No.1), pgs. 37-42. Retrieved from: http://www.maxwell.syr.edu/uploadedFiles/moynihan/dst/curtis5.pdf?n=3228.

[99] Taubes, Gary. (2007) “Good Calories, Bad Calories,” New York: Knopf Publishing. Pgs. 393.

[100] Taubes, Gary. (2010). “Why We Get Fat, and What to Do About It.” New York: Anchor Books. Pgs. 126.

[101] Taubes, Gary. (2010). “Why We Get Fat, and What to Do About It.” New York: Anchor Books. Pgs. 130-133.

[102] Seneff, Stephanie, Wainwright, Glyn, & Luca Mascitelli. (Feb. 7, 2011). “Is the metabolic syndrome caused by a high fructose, and relatively low fat, low cholesterol diet?” Archives of Medical Science, Vol. 7(1), pgs. 8-20. Retrieved from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3258689/pdf/AMS-7-1-8.pdf

[103] Vance, Dennis E. (April 28, 2008). “Biochemistry of Lipids, Lipoproteins, and Membranes.” Elsevier. Pg. 171. Retrieved from: http://books.google.com/books?id=LZprTsjcvIMC&pg=PA171&dq=regulation+of+fat+tissue&hl=en&sa=X&ei=CFpJT4DpIMbItgeUjL3uAg&ved=0CEoQ6AEwBA#v=onepage&q=regulation%20of%20fat%20tissue&f=false.

[104] Mayes, Peter. (1993). “Intermediary metabolism of fructose.” American Journal of Clinical Nutrition, Vol. 58 (5), pgs. 7545-7655. Retrieved from: http://www.ajcn.org/content/58/5/754S.full.pdf.

[105] Seneff, Stephanie, Wainwright, Glyn, & Luca Mascitelli. (Feb. 7, 2011). “Is the metabolic syndrome caused by a high fructose, and relatively low fat, low cholesterol diet?” Archives of Medical Science, Vol. 7(1), pgs. 8-20. Retrieved from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3258689/pdf/AMS-7-1-8.pdf

[106] Ibid

[107] Steiner, G, & M Vranic. (1982). “Hyperinsulemia and hypertriglyceridemia, a vicious cycle with atherogenic potential.” International Journal of Obesity, Vol. 6, Suppl 1, pgs. 117-24. Retrieved from: http://www.ncbi.nlm.nih.gov/pubmed/6749716.

[108] Aschengrau, Ann, and George R. Seage III. (2008). “Essentials of Epidemiology in Public Health: Second Edition.” Sudbury, MA: Jones and Bartlett Publishers. Pg. 400.

[109] Lustig, Robert H. (2009). “Sugar: The Bitter Truth,” Youtube. Retrieved from http://www.youtube.com/watch?v=dBnniua6-oM

[110] Taubes, Gary. (2007) “Good Calories, Bad Calories,” New York: Knopf Publishing. 393-395.

[111] Taubes, Gary. (2011, April 13). “Is Sugar Toxic?” The New York Times. Retrieved from http://www.nytimes.com/2011/04/17/magazine/mag-17Sugar-t.html?scp=1&sq=is%20sugar%20toxic?&st=cse

[112] Wells, JC, & Siervo M. (2011). Obesity and energy balance: is the tail wagging the dog? European Journal Clinical Nutrition.  Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/21772313 doi: 10.1038/ejcn.2011.132

[113] Kroner, Z. (December 2009). “The relationship between Alzheimer’s disease and diabetes: Type III diabetes?”Alternative Medicine Review, 14(4):373-9. Retrived from: http://www.ncbi.nlm.nih.gov/pubmed/20030463 .

[114] De la Monte, SM, and JR Wands. (November 2008). “Alzheimer’s disease is type-III diabetes-evidence reviewed.” Journal of Diabetes Science and Technology, 2(6):1101-13. Retrieved from: http://www.ncbi.nlm.nih.gov/pubmed/19885299 .

[115] Taubes, Gary. (2010). “Why We Get Fat, and What to Do About It.” New York: Anchor Books. Pgs. 129-133.

[116] Braun, Sandra, Bitten-Worms, Keren, and Derek LeRoith. (August 2011). “The Link between the Metabolic Syndrome and Cancer.” International Journal of Biological Sciences, 7(7):1003-15. Haifa, Israel. Retrived from: http://www.ncbi.nlm.nih.gov/pubmed/21912508 .

[117] The Telegraph. (July 3, 2011). “Obesity Crisis: Half a Million Chidren have Liver Disease.” United Kingdom.  Retrived from: http://www.telegraph.co.uk/health/healthnews/8612881/Obesity-crisis-Half-a-million-children-have-liver-disease.html .

[118] Taubes, Gary. (January 2012). “Unraveling the Obesity-Cancer Connection.” Science, Vol. 335 no. 6064 pp. 28-32. Retrieved from: http://www.sciencemag.org/content/335/6064/28 .

[119] Ibid.

[120] Seneff, Stephanie, Wainwright, Glyn, & Luca Mascitelli. (Feb. 7, 2011). “Is the metabolic syndrome caused by a high fructose, and relatively low fat, low cholesterol diet?” Archives of Medical Science, Vol. 7(1), pgs. 8-20. Retrieved from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3258689/.

[121] Ibid.

[122] Aschengrau, Ann, and George R. Seage III. (2008). “Essentials of Epidemiology in Public Health: Second Edition.” Sudbury, MA: Jones and Bartlett Publishers. Pg. 400.

[123] Haemer MA, Huang TT, Daniels SR. The effect of neurohormonal factors, epigenetic factors, and gut microbiota on risk of obesity. Prev Chronic Dis 2009;6(3):A96. Retrieved from: http://www.cdc.gov/pcd/issues/2009/
jul/09_0011.htm
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[125] Neilsen, Chad D. (July 2011). “2011 Update: Overweight, Obesity and Physical Activity in the State of Georgia.” Georgia Dept. of Public Health. Atlanta, GA.

[126] Kim, Juhee, et al. (July 2006). “Trends in Overweight from 1980 through 2001 among Preschool-Aged Children Enrolled in a Health Maintenance Organization.” Obesity, Vol. 14(7), pgs. 1107-1112. Retrieved from: http://www.nature.com.proxy-remote.galib.uga.edu/oby/journal/v14/n7/pdf/oby2006126a.pdf.

[127] Marantz PR, Bird E, Alderman MH. “A call for higher standards of evidence

for dietary guidelines.” American Journal of Preventative Medicine, Vol. 34, pgs. 234 – 40. Retrieved from: http://www.sciencedirect.com/science/article/pii/S0749379707007398

[128] Taubes, Gary, “Good Calories, Bad Calories,” 2007. New York: Knopf Publishing. Pgs. XX, 258-259, 292-293.

[129] USDA/HHS. (2000). “Dietary Guidelines for America.” Retrived from: http://www.cnpp.usda.gov/Publications/DietaryGuidelines/2000/2000DGConsumerBrochure.pdf.

[130] USDA/HHS. (1980). “Dietary Guidelines for America.” Retrived from: http://www.cnpp.usda.gov/Publications/DietaryGuidelines/1980/DG1980pub.pdf .

[132] USDA. (2011). “MyPlate-What is Dairy?.” Retrived from: http://www.choosemyplate.gov/food-groups/dairy.html

[133] USDA. “The Food Guide Pyramid.” Retrived from: http://www.nal.usda.gov/fnic/Fpyr/pmap.htm .

[134] Brody, Jane. (1985). “Jane Brody’s Good Food Book: Living the High-Carbohydrate Way.” W.W. Norton & Company. New York. Retrived from: http://books.google.com/books/about/Jane_Brody_s_Good_food_book.html?id=It6ySlOx8b8C .

[135] The Centers for Disease Control and Prevention. (Feb. 6, 2004). “Trends in Intake of Energy and Macronutrients-United States, 1971-2000.” MMWR, 53(04);80-82. Retrieved from: http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5304a3.htm .

[136] Marantz, Paul R. (2010). “Rethinking Dietary Guidelines.” Critical Reviews in Food Science and Nutrition, 50:17–18 (2010). Retrieved from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3024813/pdf/bfsn50-17.pdf .

[137] National Heart Lung and Blood Institute, National Institutes of Health. (2012). “Balance Food and Activity: What is Energy Balance?” Retrieved from: http://www.nhlbi.nih.gov/health/public/heart/obesity/wecan/healthy-weight-basics/balance.htm

[138] USDA. (2010). “Dietary Guidelines for America, 2010.” Retrieved from: http://www.cnpp.usda.gov/Publications/DietaryGuidelines/2010/PolicyDoc/PolicyDoc.pdf.

[139] Willet, Walter C. (April 23, 2002). “Dietary fat plays a major role in obesity: no.” Obesity Reviews, Vol 3(2), pgs. 59-68. Retrieved from: http://onlinelibrary.wiley.com/doi/10.1046/j.1467-789X.2002.00060.x/abstract.

[140] Taubes, Gary. (2010). “Why We Get Fat, and What to Do About It.” New York: Anchor Books. Pgs. 24, 48, 55, 59.

[141] Seneff, Stephanie, Wainwright, Glyn, & Luca Mascitelli. (Feb. 7, 2011). “Is the metabolic syndrome caused by a high fructose, and relatively low fat, low cholesterol diet?” Archives of Medical Science, Vol. 7(1), pgs. 8-20. Retrieved from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3258689/.

[142] Seneff, Stephanie, Wainwright, Glyn, & Luca Mascitelli. (Feb. 7, 2011). “Is the metabolic syndrome caused by a high fructose, and relatively low fat, low cholesterol diet?” Archives of Medical Science, Vol. 7(1), pgs. 8-20. Retrieved from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3258689/pdf/AMS-7-1-8.pdf

[143] Taubes, Gary, “Good Calories, Bad Calories,” 2007. New York: Knopf Publishing. Pgs. viv-85.

[144] Borders, William (July 7, 1965). “New Diet Decried by Nutritionists: Dangers Are Seen in Low Carbohydrate Intake.” The New York Times. Retrieved from: http://select.nytimes.com/gst/abstract.html?res=FB0D1FFA3D5A157A93C5A9178CD85F418685F9&scp=1&sq=new%20diet%20decried%20as%20dangerous&st=cse.

[145] Taubes, Gary. (2010). “Why We Get Fat, and What to Do About It.” New York: Anchor Books. Pgs. 161.

[146] Dyson PA, et al.(Dec. 2007).  “A low-carbohydrate diet is more effective in reducing body weight than healthy eating in both diabetic and non-diabetic subjects.” Diabetic Medicine;24(12). Pgs. 1430-5. Retrieved from: http://www.ncbi.nlm.nih.gov/pubmed/17971178 .

[147] Krebs NF, et al. (August, 2010). “Efficacy and Safety of a High Protein, Low Carbohydrate Diet for Weight Loss in Severely Obese Adolescents.” Journal of Pediatrics Vol. 157,  pgs. 252-8. Retrieved from: http://www.jpeds.com/article/S0022-3476(10)00120-4/abstract .

[148] Brehm BJ, et al. (2003). “A Randomized Trial Comparing a Very Low Carbohydrate Diet and a Calorie-Restricted Low Fat Diet on Body Weight and Cardiovascular Risk Factors in Healthy Women. The Journal of Clinical Endocrinology and  Metabolism , Vol. 88, pgs.1617–1623. Retrieved from: http://jcem.endojournals.org/content/88/4/1617.long.

[149] Samaha FF, et al. (2003). “A Low-Carbohydrate as Compared with a Low-Fat Diet in Severe Obesity.” The New England Journal of Medicine, Vol. 348, pgs. 2074–81. Retrieved from: http://www.nejm.org/doi/full/10.1056/NEJMoa022637.

[150] Sondike SB, et al. (March 2003). “Effects of a low-carbohydrate diet on weight loss and cardiovascular risk factor in overweight adolescents.” The Journal of Pediatrics. Vol. 142(3), pgs. 253–8. Retrieved from: http://www.jpeds.com/article/S0022-3476(02)40206-5/abstract.

[151] Aude YW, et al. (2004). “The National Cholesterol Education Program Diet vs a Diet Lower in Carbohydrates and Higher in Protein and Monounsaturated Fat. A Randomized Trial.” Archives of Internal Medicine, Pgs. 164:2141–2146. Retrieved from: http://archinte.ama-assn.org/cgi/content/full/164/19/2141.

[152] Volek JS, et al. (2004). “Comparison of energy-restricted very low-carbohydrate and low-fat diets on weight loss and body composition in overweight men and women.” Nutrition & Metabolism, Vol. 1, pg. 13. Retrieved from: http://www.nutritionandmetabolism.com/content/1/1/13.

[153] Yancy WS Jr, et al. (2004). “A Low-Carbohydrate, Ketogenic Diet versus a Low-Fat Diet To Treat Obesity and Hyperlipidemia. A Randomized, Controlled Trial.” Archives of Internal Medicine, pgs. 140:769–777. Retrieved from: http://www.annals.org/content/140/10/769.long

[154] Nichols-Richardsson SM, et al. “Perceived Hunger Is Lower and Weight Loss Is Greater in Overweight Premenopausal Women Consuming a Low-Carbohydrate/High- Protein vs High-Carbohydrate/Low-Fat Diet.” Journal of the American Dietetic Association, Vol. 105, pgs. 1433–1437. Retrieved from: http://www.ncbi.nlm.nih.gov/pubmed?term=Perceived%20Hunger%20Is%20Lower%20and%20Weight%20Loss%20Is%20Greater%20in%20Overweight%20Premenopausal

[155] Gardner CD, et al. (2007). “Comparison of the Atkins, Zone, Ornish, and learn Diets for Change in Weight and Related Risk Factors Among Overweight Premenopausal Women. The a to z Weight Loss Study: A Randomized Trial.” Journal of the American Medical Association, Vol. 297, pgs. 969–977. Retrieved from: http://jama.ama-assn.org/content/297/9/969.long

[156] Shai I, et al. (2008). “Weight loss with a low-carbohydrate, mediterranean, or low-fat diet.” The New England Journal of Medicine, Vol. 359(3), pgs. 229–41. Retrieved from: http://www.nejm.org/doi/full/10.1056/NEJMoa0708681.

[157] Summer SS, et al. (Mar 31, 2011). “Adiponectin Changes in Relation to the Macronutrient Composition of a Weight-Loss Diet.” Obesity (Silver Spring). [Epub ahead of print] Retrieved from: http://www.nature.com/oby/journal/v19/n11/full/oby201160a.html.

[158] Daly ME, et al. (Jan 23, 2006). “Short-term effects of severe dietary carbohydrate-restriction advice in Type 2 diabetes–a randomized controlled trial.” Diabetic Medicine, Vol. 23(1), pgs. 15–20. Retrieved from: http://onlinelibrary.wiley.com/doi/10.1111/j.1464-5491.2005.01760.x/abstract;jsessionid=F2FCA81A7A0BD31D425BCDD7291C4D9E.d03t01?systemMessage=Wiley+Online+Library+will+be+disrupted+2+July+from+10-12+BST+for+monthly+maintenance.

[159] Westman EC, et al. (2008). “The effect of a low-carbohydrate, ketogenic diet versus a low- glycemic index diet on glycemic control in type 2 diabetes mellitus.” Nutritional Metabolism (Lond.), Vol. 19, pgs. 5-36. Retrieved from: http://www.nutritionandmetabolism.com/content/5/1/36.

[160] Taubes, Gary, “Good Calories, Bad Calories,” 2007. New York: Knopf Publishing. 51-52.

[161] Volek, Jeff, et al. (Oct. 6, 2008). “Carbohydrate Restriction has a More Favorable Impact

on the Metabolic Syndrome than a Low Fat Diet.” Lipids, DOI 10.1007/s11745-008-3274-2. Retrieved from: http://www.cnpp.usda.gov/Publications/DietaryGuidelines/2010/Meeting2/CommentAttachments/Feinman-Volek2009-170.pdf.

 

[162] Krauss, RM, et al. (May 2006). “Separate effects of reduced carbohydrate intake and weight loss on atherogenic dyslipidemia.” American Journal of Clinical Nutrition, Vol. 83, No. 5, 1025-1031Retrieved from: http://www.ajcn.org/content/83/5/1025.long

[163] Taubes, Gary, “Good Calories, Bad Calories,” 2007. New York: Knopf Publishing. 52.

[164] Mann GV. Diet-heart: end of an era. New England Journal of Medicine 1977;297:644-650. Retrieved from: http://www.nejm.org/doi/pdf/10.1056/NEJM197709222971206.

[165] Select Committee on Nutrition and Human Needs of the United States Senate. (1977). “Dietary goals for the United States.” (2nd ed.). US Government Printing Office, Washington, DC.

[166] Taubes, Gary, “Good Calories, Bad Calories,” 2007. New York: Knopf Publishing. Pgs. xxi.

[167] USDA/HHS. (1980). “Dietary Guidelines for America.” Retrived from: http://www.cnpp.usda.gov/Publications/DietaryGuidelines/1980/DG1980pub.pdf .

[168] USDA. (2000). “Dietary Guidelines for America, 2000.” Retrieved from: http://www.cnpp.usda.gov/Publications/DietaryGuidelines/2000/2000DGConsumerBrochure.pdf.

[169] Tierney, John. (Oct. 9, 2007). “Diet and Fat: A Severe Case of Mistaken Consensus.” The New York Times. Retrieved from: http://www.nytimes.com/2007/10/09/science/09tier.html?pagewanted=1&_r=1&sq=gary%20taubes&st=cse&scp=13.

[170] Ibid.

[171] The Los Angeles Times. (Dec. 20, 2010). “A Reversal on Carbs.” Retrieved from: http://articles.latimes.com/2010/dec/20/health/la-he-carbs-20101220 .

[172] Ibid.

[173] Sackett, David L. (2002). “The arrogance of preventative medicine.” Canadian Medical Association, Vol. 167 (4), 363-364. Retrieved from: http://www.cmaj.ca/content/167/4/363.full.pdf.

[174] Rose, Geoffrey. (1985). “Sick Individuals and Sick Populations.” International Journal of Epidemiology, Vol. 14(1), pgs. 32-38. Retrieved from: http://ije.oxfordjournals.org/content/14/1/32.full.pdf+html.

[175] Marantz, Paul R. (2010). “Rethinking Dietary Guidelines.” Critical Reviews in Food Science and Nutrition, 50:17–18 (2010). Retrieved from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3024813/pdf/bfsn50-17.pdf

[176] US. Dept. of Health and Human Services, NIDDK, National Diabetes Information Clearinghouse (Dec. 6, 2011). “Insulin Resistance and Prediabetes.” Retrieved from: http://diabetes.niddk.nih.gov/dm/pubs/insulinresistance/ .

[177] Lustig, Robert H. (2009). “Sugar: The Bitter Truth,” Youtube. Retrieved from http://www.youtube.com/watch?v=dBnniua6-oM

[178] Taubes, Gary. (2010). “Why We Get Fat, and What to Do About It.” New York: Anchor Books. Pgs. 129-133.

[179] Seneff, S., Wainwright G., and L. Mascitelli. (Feb. 7, 2011). “Is the metabolic syndrome caused by a high fructose, and relatively low fat, low cholesterol diet?” Archives of Medical Science, Vol. 7(1), pgs. 8-20. Retrieved from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3258689/pdf/AMS-7-1-8.pdf

[180] Bremer, AA, et al. (Feb. 20, 2012). “Toward a Unifying Hypothesis of Metabolic Syndrome.” Pediatrics, Epub. Retrieved from: http://www.ncbi.nlm.nih.gov/pubmed/22351884.

[181] Aschengrau, Ann, and George R. Seage III. (2008). “Essentials of Epidemiology in Public Health: Second Edition.” Sudbury, MA: Jones and Bartlett Publishers. Pg. 66.

[182] USDA. (2010). “Dietary Guidelines for America, 2010.” Retrieved from: http://www.cnpp.usda.gov/Publications/DietaryGuidelines/2010/PolicyDoc/PolicyDoc.pdf.

[183] The Centers for Disease Control and Prevention. (2011). US Obesity Trends. Retrieved from http://www.cdc.gov/obesity/data/trends.html#National

[184] Kraja, Aidi T. et al (2006). Longitudinal and age trends of metabolic syndrome and its risk factors: The Family Heart Study. Nutrition & Metabolism 2006, 3:41. Retreived from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1697811/pdf/1743-7075-3-41.pdf

[185] The Centers for Disease Control and Prevention, National Center for Health Statistics. (2011, March). NCHS Data on Obesity. Retrieved from http://www.cdc.gov/nchs/data/factsheets/factsheet_obesity.pdf

[186] Wright JD, Wang, C-Y. “Trends in intake of energy and macronutrients in adults from 1999-2000 through 2007-2008”. Hyattsville, MD: National Center for Health Statistics; 2010. Retrieved from: http://www.cdc.gov/nchs/data/databriefs/db49.htm

[187] The Centers for Disease Control and Prevention (Feb. 6, 2004). “Trends in Intake of Energy and Macronutrients — United States, 1971—2000.” Atlanta, GA. Retrieved from: http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5304a3.htm .

[188] Putnam, Judy, & Shirley Gerrior. “Trends in the U.S. Food Supply, 1970-97.” Retrieved from: http://162.79.45.195/publications/aib750/aib750g.pdf.

[189] Ibid.

[190] Ibid.

[191] USDA/HHS. (1980). “Dietary Guidelines for America.” Retrived from: http://www.cnpp.usda.gov/Publications/DietaryGuidelines/1980/DG1980pub.pdf .

[192] USDA/HHS. (2000). “Dietary Guidelines for America.” Retrived from: http://www.cnpp.usda.gov/Publications/DietaryGuidelines/2000/2000DGConsumerBrochure.pdf.

[194] The Centers for Disease Control and Prevention (Feb. 6, 2004). “Trends in Intake of Energy and Macronutrients — United States, 1971—2000.” Atlanta, GA. Retrieved from: http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5304a3.htm .

[195] Lustig, Robert H. (2009). “Sugar: The Bitter Truth,” Youtube. Retrieved from http://www.youtube.com/watch?v=dBnniua6-oM

[196] Brownell et al. (Oct. 15, 2009). “The Public Health and Economic Benefits of Taxing Sugar-Sweetened Beverages.” The New England Journal of Medicine. Retrieved from: http://www.nejm.org/doi/full/10.1056/NEJMhpr0905723

[197] USDA, Economic Research Service. “Sugar and Sweeteners: Recommended Data-Tables 50-53.” Retrieved from: http://www.ers.usda.gov/Briefing/Sugar/Data.htm .

[198] USDA. Economic Research Service. “Sugar and Sweeteners: Background.” Retrieved from: http://www.ers.usda.gov/briefing/sugar/background.htm .

[199] USDA/HHS. (1980). “Dietary Guidelines for America.” Retrived from: http://www.cnpp.usda.gov/Publications/DietaryGuidelines/1980/DG1980pub.pdf .

[200] Lustig, Robert. (2011). “JumpstartMD: Dr. Robert Lustig, “Sugar is a Toxin” – Part 2.” Retrieved from: http://www.youtube.com/watch?feature=endscreen&NR=1&v=aQMWxIORUiY .

[201] Ibid.

[202] [202] Malik, et al Circulation. (2010). Sugar-Sweetened Beverages, Obesity, Type 2 Diabetes Mellitus, and Cardiovascular Disease Risk.” Circulation, Vol. 121, pgs. 1356-1364.  Retrived from: http://circ.ahajournals.org/content/121/11/1356.full.pdf+html .

[203] USDA. “Profiling Food Consumption in America: Chapter 2.” Retrieved from: http://www.usda.gov/factbook/chapter2.pdf .

[204] USDA. Economic Research Service. “Food Availability: Documentation.” Retrieved from: http://www.ers.usda.gov/data/foodconsumption/FoodAvailDoc.htm .

[205] Aschengrau, Ann, and George R. Seage III. (2008). “Essentials of Epidemiology in Public Health: Second Edition.” Sudbury, MA: Jones and Bartlett Publishers. Pg. 162-164.

[206] USDA. Economic Research Service. “Sugar and Sweeteners: Background.” Retrieved from: http://www.ers.usda.gov/briefing/sugar/background.htm .

[207] USDA. “Profiling Food Consumption in America: Chapter 2.” Retrieved from: http://www.usda.gov/factbook/chapter2.pdf .

[208] Taubes, Gary, “Good Calories, Bad Calories,” 2007. New York: Knopf Publishing. 393-395.

[209] Ogden, Cynthia, & Margaret Carrol (2010). The Centers for Disease Control and Prevention NCHS Health E-Stat: Prevalence of Obesity Among Children and Adolescents: United States, Trends 1963-1965 Through 2007-2008. Division of Health and Nutrition Examination Surveys. Retrieved from http://www.cdc.gov/nchs/data/hestat/obesity_child_07_08/obesity_child_07_08.htm#figure1

[210] The Centers for Disease Control and Prevention. (2011). NCHS Health E-Stat

Prevalence of Overweight, Obesity, and Extreme Obesity Among Adults: United States, Trends 1960–1962 Through 2007–2008. Retrieved from:http://www.cdc.gov/nchs/data/hestat/obesity_adult_07_08/obesity_adult_07_08.htm

[211] Ogden, Cynthia L., Carroll, Margaret DKit, ., Brian K., and Katherine M. Flegal, The Centers for Disease Control and Prevention (January 2012). “Prevalence of Obesity in the United States, 2009–2010.” NCHS Data Brief, Number 82. Atlanta, GA. Retrieved from: http://www.cdc.gov/nchs/data/databriefs/db82.htm .

[212] The Centers for Disease Control and Prevention. (2011). Diabetes: Successes and Opportunities for Population-Based Prevention Control: At a Glance, 2011. Retrieved from: http://www.cdc.gov/chronicdisease/resources/publications/AAG/ddt.htm

[213] Cordain, Loren, et al. (2000). “Plant-animal subsistence ratios and macronutrient energy estimations in worldwide hunter-gatherer diets.” American  Journal of  Clinical  Nutrition, Vol. 71, pgs. 682–92.Retrieved from: http://www.ajcn.org/content/71/3/682.long.

[214] USDA. (January 11, 2011). “Report of the Dietary Guidelines Advisory Committee on the Dietary Guidelines for Americans, 2010.” Retrieved from: http://www.cnpp.usda.gov/Publications/DietaryGuidelines/2010/DGAC/Report/2010DGACReport-camera-ready-Jan11-11.pdf.

[215] Aschengrau, Ann, and George R. Seage III. (2008). “Essentials of Epidemiology in Public Health: Second Edition.” Sudbury, MA: Jones and Bartlett Publishers. Pg. 162-164.

[216] Ibid.

[217] Aschengrau, Ann, and George R. Seage III. (2008). “Essentials of Epidemiology in Public Health: Second Edition.” Sudbury, MA: Jones and Bartlett Publishers. Pg. 147, 162-164, 261-302.

[218] Taubes, Gary, “Good Calories, Bad Calories,” 2007. New York: Knopf Publishing. Pg. 393-395.

[219] Taubes, Gary. (2010). “Why We Get Fat, and What to Do About It.” New York: Anchor Books. Pgs. 121-126.

[220] Wells, JC, & Siervo M. (2011). Obesity and energy balance: is the tail wagging the dog? European Journal Clinical Nutrition.  Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/21772313 doi: 10.1038/ejcn.2011.132

[221] Taubes, Gary, “Good Calories, Bad Calories,” 2007. New York: Knopf Publishing. Pg. 373.

[222] Taubes, Gary. (2010). “Why We Get Fat, and What to Do About It.” New York: Anchor Books. Pgs. 97-105.

[223] Taubes, Gary, “Good Calories, Bad Calories,” 2007. New York: Knopf Publishing. Pg. 360.

[224] Johnstone, A.M. (May, 2007). “Fasting-the ultimate diet?” Obesity Reviews, Volume 8Issue 3pages 211–222. Retrieved from: http://onlinelibrary.wiley.com/doi/10.1111/j.1467-789X.2006.00266.x/full.

[225] Dullo, AG, et al. (Mar. 1997). “Poststarvation hyperphagia and body fat overshooting in humans: a role for feedback signals from lean and fat tissues.” The American Journal of Clinical Nutrition, 65(3):717-23. Retrieved from: http://www.ajcn.org/content/65/3/717.long.

[226] The Sydney Morning Herald (June 15, 2005). “Bale turns to fatman.” Retrieved from: http://www.smh.com.au/news/Film/Bale-turns-to-fatman/2005/06/15/1118645854498.html.

[227] Lustig, Robert H. (2009). “Sugar: The Bitter Truth,” Youtube. Retrieved from http://www.youtube.com/watch?v=dBnniua6-oM

[228]MacLean, Paul S., et al. (Sept., 2011). “Biology’s response to dieting: the impetus for weight regain.” American Journal of Physiology-Regulatory, Integrative, and Comparative Physiology, Vol. 301no. 3, pgs. R581-R600  Retrieved from: http://ajpregu.physiology.org/content/301/3/R581.long.

[229] Ibid.

[230] Wing RR, Hill JO. (2001). “Successful weight loss maintenance.” Annual Review of Nutrition, 21:323-41. Retrieved from: http://www.ncbi.nlm.nih.gov/pubmed/11375440

[231] Howard et al. (2006).  “Low-Fat Dietary Pattern and Weight Change over 7 Years.” JAMA: 2006;295(1):39-49. doi:10.1001/jama.295.1.39. Retrieved from: http://jama.ama-assn.org/content/295/1/39.full.

[232] The National Weight Control Registry. Retrieved from: http://www.nwcr.ws/default.htm.

[233] Serdula, Mary K. et al. (Oct. 13, 1999). “Prevalence of Attempting Weight Lossand Strategies for Controlling Weight.” Journal of the American Medical Association, Vol 282, No. 14. Retrieved from: http://jama.ama-assn.org/content/282/14/1353.full.pdf

[234] The US Census Bureau. (Jan. 17, 2012). “State & County QuickFactsL USA.” Retrieved from: http://quickfacts.census.gov/qfd/states/00000.html

[235] USDA. (2010). “Dietary Guidelines for Americans, 2010: Chapter 2: Balancing Calories to Manage Weight.” Retrieved from: http://www.fns.usda.gov/tn/Resources/DGA/Chapter2.pdf.

[236] WHO. (2011). “Media centre: Obesity and overweight.” Retrieved from: http://www.who.int/mediacentre/factsheets/fs311/en/.

[237] The Centers for Disease Control and Prevention (2011). Overweight and Obesity: Defining Overweight and Obesity. Retrieved from: http://www.cdc.gov/obesity/causes/index.html

[238] American Heart Association. (May 5, 2011). “Obesity Information.” Retrieved from: http://www.heart.org/HEARTORG/GettingHealthy/WeightManagement/Obesity/Obesity-Information_UCM_307908_Article.jsp#.T0e_ZPF5F8E.

[239] Larry King Live. (Oct. 19, 2007). “2 of 2 Gary Taubes on Larry King Live 10/19/2007.” Youtube. Retrieved from: http://www.youtube.com/watch?v=5LNH0RPXI0M.

[240] NIH, NHBLI. (Nov. 1, 2010). “What Causes Overweight and Obesity?” Retrieved from: http://www.nhlbi.nih.gov/health/health-topics/topics/obe/causes.html.

[241] US Dept of HHS, US Public Health Service. (2010). “The Surgeon General’s Vision for a Healthy and Fit Nation.” Retrieved from: http://www.surgeongeneral.gov/library/obesityvision/obesityvision2010.pdf.

[242] National Heart Lung and Blood Institute, National Institutes of Health. (2012). “Balance Food and Activity: What is Energy Balance?” Retrieved from: http://www.nhlbi.nih.gov/health/public/heart/obesity/wecan/healthy-weight-basics/balance.htm

[243] Davis, Lisa. (Feb. 11, 2011). “Is this Any Way to Lose Weight?” Reader’s Digest, Pg. 110-119. Retrieved from: http://garytaubes.com/wp-content/uploads/2012/02/WWGF-Readers-Digest-feature-Feb-2011.pdf.

[245] Georgia Dept. of Public Health. “2010 Georgia Data Summary: Obesity in Children and Youth.” Atlanta, GA. Retrieved from: http://health.state.ga.us/pdfs/epi/cdiee/DPH.Epi.7-20-11.pdf.

[246] US Dept of HHS, US Public Health Service. (2010). “The Surgeon General’s Vision for a Healthy and Fit Nation.” Retrieved from: http://www.surgeongeneral.gov/library/obesityvision/obesityvision2010.pdf.

[247] Flier, Jeffrey, et al. (Aug. 19, 2007). “What Fuels Fat.” Scientific American. Retrieved from: http://www.scientificamerican.com/article.cfm?id=what-fuels-fat.

[248] Taubes, Gary. (2010). “Why We Get Fat, and What to Do About It.” New York: Anchor Books. Pgs. 78.

[249] Lustig, Robert H. (2009). “Sugar: The Bitter Truth,” Youtube. Retrieved from http://www.youtube.com/watch?v=dBnniua6-oM

[250] Marantz PR, Bird E, Alderman MH. A call for higher standards of evidence

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[251] Taubes, Gary, “Good Calories, Bad Calories,” 2007. New York: Knopf Publishing. Pgs. XX, 258-259, 292-293.

[252] USDA/HHS. (2000). “Dietary Guidelines for America.” Retrived from: http://www.cnpp.usda.gov/Publications/DietaryGuidelines/2000/2000DGConsumerBrochure.pdf.

[253] USDA/HHS. (1980). “Dietary Guidelines for America.” Retrived from: http://www.cnpp.usda.gov/Publications/DietaryGuidelines/1980/DG1980pub.pdf .

[255] USDA. (2011). “MyPlate-What is Dairy?.” Retrived from: http://www.choosemyplate.gov/food-groups/dairy.html

[256] USDA. “The Food Guide Pyramid.” Retrived from: http://www.nal.usda.gov/fnic/Fpyr/pmap.htm .

[257] Brody, Jane. (1985). “Jane Brody’s Good Food Book: Living the High-Carbohydrate Way.” W.W. Norton & Company. New York. Retrived from: http://books.google.com/books/about/Jane_Brody_s_Good_food_book.html?id=It6ySlOx8b8C .

[258] The Centers for Disease Control and Prevention. (Feb. 6, 2004). “Trends in Intake of Energy and Macronutrients-United States, 1971-2000.” MMWR, 53(04);80-82. Retrieved from: http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5304a3.htm .

[259] Marantz, Paul R. (2010). “Rethinking Dietary Guidelines.” Critical Reviews in Food Science and Nutrition, 50:17–18 (2010). Retrieved from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3024813/pdf/bfsn50-17.pdf .

[260] National Heart Lung and Blood Institute, National Institutes of Health. (2012). “Balance Food and Activity: What is Energy Balance?” Retrieved from: http://www.nhlbi.nih.gov/health/public/heart/obesity/wecan/healthy-weight-basics/balance.htm

[261] USDA. (2010). “Dietary Guidelines for America, 2010.” Retrieved from: http://www.cnpp.usda.gov/Publications/DietaryGuidelines/2010/PolicyDoc/PolicyDoc.pdf.

[262] USDA. (2010). “Dietary Guidelines for America, 2010.” Retrieved from: http://www.cnpp.usda.gov/Publications/DietaryGuidelines/2010/PolicyDoc/PolicyDoc.pdf.

[263] USDA/HHS. (1980). “Dietary Guidelines for America.” Retrived from: http://www.cnpp.usda.gov/Publications/DietaryGuidelines/1980/DG1980pub.pdf .

[265] Lustig, Robert H. (2009). “Sugar: The Bitter Truth,” Youtube. Retrieved from http://www.youtube.com/watch?v=dBnniua6-oM

[266] WHO. (2011). “Media centre: Obesity and overweight.” Retrieved from: http://www.who.int/mediacentre/factsheets/fs311/en/.

[267] The Centers for Disease Control and Prevention (2011). Overweight and Obesity: Defining Overweight and Obesity. Retrieved from: http://www.cdc.gov/obesity/causes/index.html

[268] American Heart Association. (May 5, 2011). “Obesity Information.” Retrieved from: http://www.heart.org/HEARTORG/GettingHealthy/WeightManagement/Obesity/Obesity-Information_UCM_307908_Article.jsp#.T0e_ZPF5F8E.

[269] Larry King Live. (Oct. 19, 2007). “2 of 2 Gary Taubes on Larry King Live 10/19/2007.” Youtube. Retrieved from: http://www.youtube.com/watch?v=5LNH0RPXI0M.

[270] NIH, NHBLI. (Nov. 1, 2010). “What Causes Overweight and Obesity?” Retrieved from: http://www.nhlbi.nih.gov/health/health-topics/topics/obe/causes.html.

[271] US Dept of HHS, US Public Health Service. (2010). “The Surgeon General’s Vision for a Healthy and Fit Nation.” Retrieved from: http://www.surgeongeneral.gov/library/obesityvision/obesityvision2010.pdf.

[272] National Heart Lung and Blood Institute, National Institutes of Health. (2012). “Balance Food and Activity: What is Energy Balance?” Retrieved from: http://www.nhlbi.nih.gov/health/public/heart/obesity/wecan/healthy-weight-basics/balance.htm

[273] Taubes, Gary. (2010). “Why We Get Fat, and What to Do About It.” New York: Anchor Books.pg.85.

[274] Lustig, Robert H. (2009). “Sugar: The Bitter Truth,” Youtube. Retrieved from http://www.youtube.com/watch?v=dBnniua6-oM

[275] Lustig, Robert H. (2009). “Sugar: The Bitter Truth,” Youtube. Retrieved from http://www.youtube.com/watch?v=dBnniua6-oM

[276] Taubes, Gary, “Good Calories, Bad Calories,” 2007. New York: Knopf Publishing.pg. 356-57

[277] Taubes, Gary. (2010). “Why We Get Fat, and What to Do About It.” New York: Anchor Books.pg. 109-111.

[278] Taubes, Gary, “Good Calories, Bad Calories,” 2007. New York: Knopf Publishing. pg. 349-354

[279] Sumithran, Priya, et al. (Oct. 27, 2011). “Long-Term Persistence of Hormonal Adaptations to Weight Loss.” New England Journal of Medicine, Vol. 365, pgs. 1597-1604. Retrieved from: http://www.nejm.org/doi/full/10.1056/NEJMoa1105816.

[280] Taubes, Gary. (2010). “Why We Get Fat, and What to Do About It.” New York: Anchor Books.pg. 90-92, 118-121.

[281] Gardner, Christopher D, et al. (2007). “Comparison of the Atkins, Ornish, Zone, and LEARN Diets for Change in Weight and Related Risk Factors Among Overweight and Premenopausal Women.” Journal of the American Medical Association, 297(9):969-977. doi:10.1001/jama.297.9.969. Retrieved from: http://jama.ama-assn.org/content/297/9/969.full.pdf+html  .

[282] Haemer MA, Huang TT, Daniels SR. The effect of neurohormonal factors, epigenetic factors, and gut microbiota on risk of obesity. Prev Chronic Dis 2009;6(3):A96. Retrieved from: http://www.cdc.gov/pcd/issues/2009/
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[283] Taubes, Gary. (2010). “Why We Get Fat, and What to Do About It.” New York: Anchor Books.pg. 90-92, 118-121.

[284] Stice, Eric, et al. (Sept. 2006). “A Meta-Analytic Review of Obesity Prevention Programs for Children and Adolescents: The Skinny on Interventions that Work.” Psychological Bulletin, Vol 132(5), pgs. 667-691. doi: 10.1037/0033-2909.132.5.667 Retrieved from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1876697/.

[285] Curioni, CC, et al. (May 31, 2005). “Long-term weight loss after diet and exercise: a systematic review.”International Journal of Obesity, Vol. 29, pgs. 1168–1174. doi:10.1038/sj.ijo.0803015. Retrieved from: http://www.nature.com/ijo/journal/v29/n10/full/0803015a.html.

[286] Witham, Miles D., et al. (Jan. 18, 2010). “Interventions to achieve long-term weight loss in obese older people.

A systematic review and meta-analysis.” Age and Ageing, Vol. 39, pgs. 176–184

doi: 10.1093/ageing/afp251. Retrieved from: http://ageing.oxfordjournals.org/content/39/2/176.full.

[287] Sumithran, Priya, et al. (Oct. 27, 2011). “Long-Term Persistence of Hormonal Adaptations to Weight Loss.” New England Journal of Medicine, Vol. 365, pgs. 1597-1604. Retrieved from: http://www.nejm.org/doi/full/10.1056/NEJMoa1105816.

[288] Shikany, James M, et al. (2010). “Effects of a low-fat dietary intervention on glucose, insulin, and insulin resistance in the Women’s Health Initiative (WHI) Dietary Modification trial.” American Society for Nutrition, May 11, 2011, doi: 10.3945/ajcn.110.010843. Retrieved from: http://www.ajcn.org/content/early/2011/05/11/ajcn.110.010843.abstract .

[289] Harvard Medical School. “Glycemic index and glycemic load for 100+ foods.” Retrieved from: http://www.health.harvard.edu/newsweek/Glycemic_index_and_glycemic_load_for_100_foods.htm.

[290] Parker-Pope, Tara. (Dec. 28, 2011). “The Fat Trap.” The New York Times. Retrieved from: http://www.nytimes.com/2012/01/01/magazine/tara-parker-pope-fat-trap.html?pagewanted=all .

[291] Taubes, Gary, and Peter Attia. (Jan. 20, 2012). “Reply to ‘The Fat Trap’.” The New York Times. Retrieved from: http://www.nytimes.com/2012/01/22/magazine/reply-all-fat-trap.html.

[292] Taubes, Gary. (2010). “Why We Get Fat, and What to Do About It.” New York: Anchor Books. 84.

[293] UC Berkeley Graduate School of Journalism. (2008). “The Politics of Obesity: Our National Eating Disorder.” Retrieved from:

http://www.youtube.com/watch?v=r3MSUji85zs.

[294] Ibid.

[295] Dyson PA, et al.(Dec. 2007).  “A low-carbohydrate diet is more effective in reducing body weight than healthy eating in both diabetic and non-diabetic subjects.” Diabetic Medicine;24(12). Pgs. 1430-5. Retrieved from: http://www.ncbi.nlm.nih.gov/pubmed/17971178 .

[296] Krebs NF, et al. (August, 2010). “Efficacy and Safety of a High Protein, Low Carbohydrate Diet for Weight Loss in Severely Obese Adolescents.” Journal of Pediatrics Vol. 157,  pgs. 252-8. Retrieved from: http://www.jpeds.com/article/S0022-3476(10)00120-4/abstract .

[297] Brehm BJ, et al. (2003). “A Randomized Trial Comparing a Very Low Carbohydrate Diet and a Calorie-Restricted Low Fat Diet on Body Weight and Cardiovascular Risk Factors in Healthy Women. The Journal of Clinical Endocrinology and  Metabolism , Vol. 88, pgs.1617–1623. Retrieved from: http://jcem.endojournals.org/content/88/4/1617.long.

[298] Samaha FF, et al. (2003). “A Low-Carbohydrate as Compared with a Low-Fat Diet in Severe Obesity.” The New England Journal of Medicine, Vol. 348, pgs. 2074–81. Retrieved from: http://www.nejm.org/doi/full/10.1056/NEJMoa022637.

[299] Sondike SB, et al. (March 2003). “Effects of a low-carbohydrate diet on weight loss and cardiovascular risk factor in overweight adolescents.” The Journal of Pediatrics. Vol. 142(3), pgs. 253–8. Retrieved from: http://www.jpeds.com/article/S0022-3476(02)40206-5/abstract.

[300] Aude YW, et al. (2004). “The National Cholesterol Education Program Diet vs a Diet Lower in Carbohydrates and Higher in Protein and Monounsaturated Fat. A Randomized Trial.” Archives of Internal Medicine, Pgs. 164:2141–2146. Retrieved from: http://archinte.ama-assn.org/cgi/content/full/164/19/2141.

[301] Volek JS, et al. (2004). “Comparison of energy-restricted very low-carbohydrate and low-fat diets on weight loss and body composition in overweight men and women.” Nutrition & Metabolism, Vol. 1, pg. 13. Retrieved from: http://www.nutritionandmetabolism.com/content/1/1/13.

[302] Yancy WS Jr, et al. (2004). “A Low-Carbohydrate, Ketogenic Diet versus a Low-Fat Diet To Treat Obesity and Hyperlipidemia. A Randomized, Controlled Trial.” Archives of Internal Medicine, pgs. 140:769–777. Retrieved from: http://www.annals.org/content/140/10/769.long

[303] Nichols-Richardsson SM, et al. “Perceived Hunger Is Lower and Weight Loss Is Greater in Overweight Premenopausal Women Consuming a Low-Carbohydrate/High- Protein vs High-Carbohydrate/Low-Fat Diet.” Journal of the American Dietetic Association, Vol. 105, pgs. 1433–1437. Retrieved from: http://www.ncbi.nlm.nih.gov/pubmed?term=Perceived%20Hunger%20Is%20Lower%20and%20Weight%20Loss%20Is%20Greater%20in%20Overweight%20Premenopausal

[304] Gardner CD, et al. (2007). “Comparison of the Atkins, Zone, Ornish, and learn Diets for Change in Weight and Related Risk Factors Among Overweight Premenopausal Women. The a to z Weight Loss Study: A Randomized Trial.” Journal of the American Medical Association, Vol. 297, pgs. 969–977. Retrieved from: http://jama.ama-assn.org/content/297/9/969.long

[305] Shai I, et al. (2008). “Weight loss with a low-carbohydrate, mediterranean, or low-fat diet.” The New England Journal of Medicine, Vol. 359(3), pgs. 229–41. Retrieved from: http://www.nejm.org/doi/full/10.1056/NEJMoa0708681.

[306] Summer SS, et al. (Mar 31, 2011). “Adiponectin Changes in Relation to the Macronutrient Composition of a Weight-Loss Diet.” Obesity (Silver Spring). [Epub ahead of print] Retrieved from: http://www.nature.com/oby/journal/v19/n11/full/oby201160a.html.

[307] Daly ME, et al. (Jan 23, 2006). “Short-term effects of severe dietary carbohydrate-restriction advice in Type 2 diabetes–a randomized controlled trial.” Diabetic Medicine, Vol. 23(1), pgs. 15–20. Retrieved from: http://onlinelibrary.wiley.com/doi/10.1111/j.1464-5491.2005.01760.x/abstract;jsessionid=F2FCA81A7A0BD31D425BCDD7291C4D9E.d03t01?systemMessage=Wiley+Online+Library+will+be+disrupted+2+July+from+10-12+BST+for+monthly+maintenance.

[308] Westman EC, et al. (2008). “The effect of a low-carbohydrate, ketogenic diet versus a low- glycemic index diet on glycemic control in type 2 diabetes mellitus.” Nutritional Metabolism (Lond.), Vol. 19, pgs. 5-36. Retrieved from: http://www.nutritionandmetabolism.com/content/5/1/36.

[309] Taubes, Gary, “Good Calories, Bad Calories,” 2007. New York: Knopf Publishing. pg. 50-53.

[310] Taubes, Gary, “Good Calories, Bad Calories,” 2007. New York: Knopf Publishing. pg. 327-354.

[311] Duke University Medical Center, Lifestyle Medicine Clinic. “Low Carbohydrate Diet: Low-carb Menu Planning.” Retrieved from: http://www.nmsociety.org/docs/Consumer/Low_Carb_Menu_Planning.pdf.

[312] Taubes, Gary. (2010). “Why We Get Fat, and What to Do About It.” New York: Anchor Books.pg. 84.

[313] Ibid.

[314] National Heart Lung and Blood Institute, National Institutes of Health. (2012). “Balance Food and Activity: What is Energy Balance?” Retrieved from: http://www.nhlbi.nih.gov/health/public/heart/obesity/wecan/healthy-weight-basics/balance.htm

[315] The Centers for Disease Control and Prevention. (May 2011). “Overweight and Obesity: Causes and Consequences.” Atlanta, GA. Retrieved from: http://www.cdc.gov/obesity/causes/index.html .

[316] USDA. (2010). “Dietary Guidelines for Americans, 2010: Chapter 2: Balancing Calories to Manage Weight.” Retrieved from: http://www.fns.usda.gov/tn/Resources/DGA/Chapter2.pdf.

[317] US Dept. of HHS. (2008). “2008 Physical Activity Guidelines for Americas: At-A-Glance: A Fact Sheet for Professoinals.” Retrieved from: http://health.gov/paguidelines/pdf/fs_prof.pdf.

[318] Haskell et al (2007). “Physical Activity and Public Health: Updated Recommendations for Adults from the American College of Sports Medicine and the American Heart Association.” Circulation, Vol. 116, pgs. 1081-1093. Retrieved from http://circ.ahajournals.org/content/116/9/1081.long

[319] First Lady Michele Obama. “Let’s Move! Get Active!” Retrieved from: http://www.letsmove.gov/learn-facts/epidemic-childhood-obesity.

[320] Taubes, Gary. (2010). “Why We Get Fat, and What to Do About It.” New York: Anchor Books.pg. 46.

[321] Haskell et al (2007). “Physical Activity and Public Health: Updated Recommendations for Adults from the American College of Sports Medicine and the American Heart Association.” Circulation, Vol. 116, pgs. 1081-1093. Retrieved from http://circ.ahajournals.org/content/116/9/1081.long

[322] Janssen, GM, et al. (1989). “Food Intake and Body Composition in Novice Athletes During a Training Period to Run a Marathon.” International Journal of Sports Medicine, Vol. 10, pgs. S17-S21. DOI: 10.1055/s-2007-1024949 Retrieved from: https://www.thieme-connect.com/DOI/DOI?10.1055/s-2007-1024949.

[323] Taubes, Gary. (July 14, 1995). “Epidemiology Faces Its Limits.” Science, Vol. 269, pgs. 164-169. Retrieved from: http://geography.ssc.uwo.ca/faculty/baxter/readings/Taubes_limits_epidemiology_Science_1995.pdf

[325] Curioni, CC & PM Lourenco. (May 31, 2005). “Long-term weight loss after diet and exercise: a systematic review.” International Journal of Obesity, Vol. 29, 1168–1174. doi:10.1038/sj.ijo.0803015. Retrieved from: http://www.nature.com/ijo/journal/v29/n10/full/0803015a.html.

[326] Ibid.

[327] Williams, PT, & PD Wood. (March 2006). “The effects of changing exercise levels on weight and age-related weight gain.” Int J Obes (Long). Vol. 30(3): 543–551. doi:10.1038/sj.ijo.0803172. Retrieved from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2864590/pdf/nihms176949.pdf.

[328] Taubes, Gary, “Good Calories, Bad Calories,” 2007. New York: Knopf Publishing.

[329] Wells, JC, & Siervo M. (2011). Obesity and energy balance: is the tail wagging the dog? European Journal Clinical Nutrition.  Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/21772313 doi: 10.1038/ejcn.2011.132

[330] Purdue University, Bodner Research Web. “Energy, Enthalpy, and the First Law of Thermodynamics.” Retrieved from: http://chemed.chem.purdue.edu/genchem/topicreview/bp/ch21/chemical.php .

[331] Taubes, Gary. (2010). “Why We Get Fat, and What to Do About It.” New York: Anchor Books. 75.

[331] Biology online. (2008). “Homeostasis.” Retrieved from: http://www.biology-online.org/dictionary/Homeostasis .

[331] Haskell et al (2007). “Physical Activity and Public Health: Updated Recommendations for Adults from the American College of Sports Medicine and the American Heart Association.” Circulation, Vol. 116, pgs. 1081-1093. Retrieved from http://circ.ahajournals.org/content/116/9/1081.long

[332] Taubes, Gary. (2010). “Why We Get Fat, and What to Do About It.” New York: Anchor Books. Pgs. 57-61, 63-66.

[333] Wells, JC, & Siervo M. (2011). Obesity and energy balance: is the tail wagging the dog? European Journal Clinical Nutrition.  Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/21772313 doi: 10.1038/ejcn.2011.132

[334] Taubes, Gary, “Good Calories, Bad Calories,” 2007. New York: Knopf Publishing. Pg. 372-373.

[335] Taubes, Gary. (2010). “Why We Get Fat, and What to Do About It.” New York: Anchor Books. Pg. 94-96.

[336] Wade, George N. (January 2004). “Regulation of Body Fat Content?” American Journal of Physiology: Regulator, Integrative and Comparative Physiology, vol. 286 no. 1. Retrieved from: http://ajpregu.physiology.org/content/286/1/R14.long .

 

[337] Taubes, Gary. (2010). “Why We Get Fat, and What to Do About It.” New York: Anchor Books. Pg. 94-96.

[338] Biology online. (2008). “Homeostasis.” Retrieved from: http://www.biology-online.org/dictionary/Homeostasis .

[339] Ozaki, MR, et al. (2011). “Evolution and involution of atherosclerosis and its relationship with vascular reactivity in hypercholesterolemic rabbits.” Experimental and Toxicologic Pathology, Epub. Retrieved from: http://www.ncbi.nlm.nih.gov/pubmed/22024507.

[340] Chung, YM, et al. (Feb. 2012). “Dietary d-Psicose Reduced Visceral Fat Mass in High-Fat Diet-Induced Obese Rats.”Journal of Food Science, Vol. 77(2), pgs. H53-8. doi: 10.1111/j.1750-3841.2011.02571.x.

Retrieved from: http://www.ncbi.nlm.nih.gov/pubmed/22339545.

[341] Bremer, AA, et al. (Aug. 2011). “Fructose-fed rhesus monkeys: a nonhuman primate model of insulin resistance, metabolic syndrome, and type 2 diabetes.” Clinical and Translational Science, Vol. 4(4):243-52. doi: 10.1111/j.1752-8062.2011.00298.x. Retrieved from: http://www.ncbi.nlm.nih.gov/pubmed/21884510.

 

[342] Stanhope, Kimber L., et al. (May, 2009). “Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans.” The Journal of Clinical Investigation, Vol. 119, Number 5, pgs. 1322- . Retrieved from: http://www.jci.org/articles/view/37385.

[343] Haskell et al (2007). “Physical Activity and Public Health: Updated Recommendations for Adults from the American College of Sports Medicine and the American Heart Association.” Circulation, Vol. 116, pgs. 1081-1093. Retrieved from http://circ.ahajournals.org/content/116/9/1081.long

[344] Howard et al (2006). “Low-Fat Dietary Pattern and Risk of CVD in WHI Diet RCT.” JAMA:2006;295(6):655-666. doi:10.1001/jama.295.6.655 http://jama.ama-assn.org/content/295/6/655.full.pdf+html

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[345] Howard et al. (2006).  “Low-Fat Dietary Pattern and Weight Change over 7 Years.” JAMA: 2006;295(1):39-49. doi:10.1001/jama.295.1.39. Retrieved from: http://jama.ama-assn.org/content/295/1/39.full.

[346] The Cochrane Collaboration. (Jan. 21, 2009). “Long-term non-pharmacological weight loss interventions for adults with type 2 diabetes mellitus.” Retrived from: http://summaries.cochrane.org/CD004095/long-term-non-pharmacological-weight-loss-interventions-for-adults-with-type-2-diabetes-mellitus .

[347] Taubes, Gary, “Good Calories, Bad Calories,” 2007. New York: Knopf Publishing. Pg. 258.

[348] Haemer MA, Huang TT, Daniels SR. The effect of neurohormonal factors, epigenetic factors, and gut microbiota on risk of obesity. Prev Chronic Dis 2009;6(3):A96. Retrieved from: http://www.cdc.gov/pcd/issues/2009/
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[349] MacLean, Paul S., et al. (Sept., 2011). “Biology’s response to dieting: the impetus for weight regain.” American Journal of Physiology-Regulatory, Integrative, and Comparative Physiology, Vol. 301no. 3, pgs. R581-R600  Retrieved from: http://ajpregu.physiology.org/content/301/3/R581.long.

[350] Lustig, Robert H. (2009). “Sugar: The Bitter Truth,” Youtube. Retrieved from http://www.youtube.com/watch?v=dBnniua6-oM

[351] USDA. (2011). “MyPlate-What are Empty Calories?.” Retrived from: http://www.choosemyplate.gov/weight-management-calories/calories/empty-calories.html

[352] Wells, JC, & Siervo M. (2011). Obesity and energy balance: is the tail wagging the dog? European Journal of Clinical Nutrition.  Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/21772313 doi: 10.1038/ejcn.2011.132

[353] Taubes, Gary. (2010). “Why We Get Fat, and What to Do About It.” New York: Anchor Books. Pg. 144-147.

[354] Ibid.

[355] Taubes, Gary. (2010). “Why We Get Fat, and What to Do About It.” New York: Anchor Books. Pg. 106-126.

[356] Bjorntorp, P. (April 20, 1996). “The regulation of adipose tissue in humans.” International Journal of Obesity and Related Metabolic Disorders, Vol. 20(4), pg. 291-302. Retrieved from: http://www.ncbi.nlm.nih.gov/pubmed/8680455.

[357] Leff, Todd, & James. G. Grannerman. “Adipose Tissue in Health and Disease.” Wiley Publishers: , pg. xix-xixi, 98, 143-152.

[358] Taubes, Gary, “Good Calories, Bad Calories,” 2007. New York: Knopf Publishing. pg. 393-395.

[359] Taubes, Gary. (2010). “Why We Get Fat, and What to Do About It.” New York: Anchor Books. Pg. 118-121.

[360] Goodman, H. Maurice. (2009). “Basic Medical Endocrinology: Adipogenesis.” Academic Press, Fourth Edition.  Pg. 165. Retrieved from: http://books.google.com/books?id=gjpi2MYVKGAC&pg=PA165&dq=insulin+AND+adipocyte&hl=en&sa=X&ei=CVtJT7XVIsWatwent7TyAg&ved=0CEkQ6AEwAg#v=onepage&q=insulin%20AND%20adipocyte&f=false.

[361] Taubes, Gary. (2010). “Why We Get Fat, and What to Do About It.” New York: Anchor Books. Pgs. 125.

[362] Taubes, Gary, “Good Calories, Bad Calories,” 2007. New York: Knopf Publishing. Pg. 327-354.

[363] Taubes, Gary, “Good Calories, Bad Calories,” 2007. New York: Knopf Publishing. Pg. viv-xv.

[364] The Los Angeles Times. (Dec. 20, 2010). “A Reversal on Carbs.” Retrieved from: http://articles.latimes.com/2010/dec/20/health/la-he-carbs-20101220 .

[365] Hite, Adele H. (June, 2011). “Low-Carbohydrate Diet Review: Shifting the Paradigm.” Nutrition in Clinical Practice, Vol. 26(3), pgs. 300-308. Retrieved from: http://www.nmsociety.org/docs/LowCarbDiet/Nutrition-in-Clinical-Practice-2011.pdf

[366] Alhassan, S. (Jun. 2008). “Dietary adherence and weight loss success among overweight women: results from the A TO Z weight loss study.” International Journal of Obesity, Vol. 32(6), pgs. 985-91. Retrieved from: http://www.ncbi.nlm.nih.gov/pubmed?term=%20Dietary%20Adherance%20and%20Weight%20Loss%20Success%20Among%20Overweight%20Women%3A%20Results%20from%20A%20to%20Z%20Weight%20Loss%20Study.

[367] Taubes, Gary, “Good Calories, Bad Calories,” 2007. New York: Knopf Publishing. Pg. 329.

[368] Dyson PA, et al.(Dec. 2007).  “A low-carbohydrate diet is more effective in reducing body weight than healthy eating in both diabetic and non-diabetic subjects.” Diabetic Medicine;24(12). Pgs. 1430-5. Retrieved from: http://www.ncbi.nlm.nih.gov/pubmed/17971178 .

[369] Krebs NF, et al. (August, 2010). “Efficacy and Safety of a High Protein, Low Carbohydrate Diet for Weight Loss in Severely Obese Adolescents.” Journal of Pediatrics Vol. 157,  pgs. 252-8. Retrieved from: http://www.jpeds.com/article/S0022-3476(10)00120-4/abstract .

[370] Brehm BJ, et al. (2003). “A Randomized Trial Comparing a Very Low Carbohydrate Diet and a Calorie-Restricted Low Fat Diet on Body Weight and Cardiovascular Risk Factors in Healthy Women. The Journal of Clinical Endocrinology and  Metabolism , Vol. 88, pgs.1617–1623. Retrieved from: http://jcem.endojournals.org/content/88/4/1617.long.

[371] Samaha FF, et al. (2003). “A Low-Carbohydrate as Compared with a Low-Fat Diet in Severe Obesity.” The New England Journal of Medicine, Vol. 348, pgs. 2074–81. Retrieved from: http://www.nejm.org/doi/full/10.1056/NEJMoa022637.

[372] Sondike SB, et al. (March 2003). “Effects of a low-carbohydrate diet on weight loss and cardiovascular risk factor in overweight adolescents.” The Journal of Pediatrics. Vol. 142(3), pgs. 253–8. Retrieved from: http://www.jpeds.com/article/S0022-3476(02)40206-5/abstract.

[373] Aude YW, et al. (2004). “The National Cholesterol Education Program Diet vs a Diet Lower in Carbohydrates and Higher in Protein and Monounsaturated Fat. A Randomized Trial.” Archives of Internal Medicine, Pgs. 164:2141–2146. Retrieved from: http://archinte.ama-assn.org/cgi/content/full/164/19/2141.

[374] Volek JS, et al. (2004). “Comparison of energy-restricted very low-carbohydrate and low-fat diets on weight loss and body composition in overweight men and women.” Nutrition & Metabolism, Vol. 1, pg. 13. Retrieved from: http://www.nutritionandmetabolism.com/content/1/1/13.

[375] Yancy WS Jr, et al. (2004). “A Low-Carbohydrate, Ketogenic Diet versus a Low-Fat Diet To Treat Obesity and Hyperlipidemia. A Randomized, Controlled Trial.” Archives of Internal Medicine, pgs. 140:769–777. Retrieved from: http://www.annals.org/content/140/10/769.long

[376] Nichols-Richardsson SM, et al. “Perceived Hunger Is Lower and Weight Loss Is Greater in Overweight Premenopausal Women Consuming a Low-Carbohydrate/High- Protein vs High-Carbohydrate/Low-Fat Diet.” Journal of the American Dietetic Association, Vol. 105, pgs. 1433–1437. Retrieved from: http://www.ncbi.nlm.nih.gov/pubmed?term=Perceived%20Hunger%20Is%20Lower%20and%20Weight%20Loss%20Is%20Greater%20in%20Overweight%20Premenopausal

[377] Gardner CD, et al. (2007). “Comparison of the Atkins, Zone, Ornish, and learn Diets for Change in Weight and Related Risk Factors Among Overweight Premenopausal Women. The a to z Weight Loss Study: A Randomized Trial.” Journal of the American Medical Association, Vol. 297, pgs. 969–977. Retrieved from: http://jama.ama-assn.org/content/297/9/969.long

[378] Shai I, et al. (2008). “Weight loss with a low-carbohydrate, mediterranean, or low-fat diet.” The New England Journal of Medicine, Vol. 359(3), pgs. 229–41. Retrieved from: http://www.nejm.org/doi/full/10.1056/NEJMoa0708681.

[379] Summer SS, et al. (Mar 31, 2011). “Adiponectin Changes in Relation to the Macronutrient Composition of a Weight-Loss Diet.” Obesity (Silver Spring). [Epub ahead of print] Retrieved from: http://www.nature.com/oby/journal/v19/n11/full/oby201160a.html.

[380] Daly ME, et al. (Jan 23, 2006). “Short-term effects of severe dietary carbohydrate-restriction advice in Type 2 diabetes–a randomized controlled trial.” Diabetic Medicine, Vol. 23(1), pgs. 15–20. Retrieved from: http://onlinelibrary.wiley.com/doi/10.1111/j.1464-5491.2005.01760.x/abstract;jsessionid=F2FCA81A7A0BD31D425BCDD7291C4D9E.d03t01?systemMessage=Wiley+Online+Library+will+be+disrupted+2+July+from+10-12+BST+for+monthly+maintenance.

[381] Westman EC, et al. (2008). “The effect of a low-carbohydrate, ketogenic diet versus a low- glycemic index diet on glycemic control in type 2 diabetes mellitus.” Nutritional Metabolism (Lond.), Vol. 19, pgs. 5-36. Retrieved from: http://www.nutritionandmetabolism.com/content/5/1/36.

[382] Taubes, Gary, “Good Calories, Bad Calories,” 2007. New York: Knopf Publishing. Pgs. 50-53.

[383] Taubes, Gary, “Good Calories, Bad Calories,” 2007. New York: Knopf Publishing. Pg. 333, 337,

[384] Volek, Jeff S., and Stephen D. Phinney (May 19, 2011). “The Art and Science of Low Carbohydrate Living.”  Chapter 1: Overview of Low Carbohydrate and Ketogenic Diet. Beyond Obesity LLC.

[385] Dyson PA, et al.(Dec. 2007).  “A low-carbohydrate diet is more effective in reducing body weight than healthy eating in both diabetic and non-diabetic subjects.” Diabetic Medicine;24(12). Pgs. 1430-5. Retrieved from: http://www.ncbi.nlm.nih.gov/pubmed/17971178 .

[386] Krebs NF, et al. (August, 2010). “Efficacy and Safety of a High Protein, Low Carbohydrate Diet for Weight Loss in Severely Obese Adolescents.” Journal of Pediatrics Vol. 157,  pgs. 252-8. Retrieved from: http://www.jpeds.com/article/S0022-3476(10)00120-4/abstract .

[387] Brehm BJ, et al. (2003). “A Randomized Trial Comparing a Very Low Carbohydrate Diet and a Calorie-Restricted Low Fat Diet on Body Weight and Cardiovascular Risk Factors in Healthy Women. The Journal of Clinical Endocrinology and  Metabolism , Vol. 88, pgs.1617–1623. Retrieved from: http://jcem.endojournals.org/content/88/4/1617.long.

[388] Samaha FF, et al. (2003). “A Low-Carbohydrate as Compared with a Low-Fat Diet in Severe Obesity.” The New England Journal of Medicine, Vol. 348, pgs. 2074–81. Retrieved from: http://www.nejm.org/doi/full/10.1056/NEJMoa022637.

[389] Sondike SB, et al. (March 2003). “Effects of a low-carbohydrate diet on weight loss and cardiovascular risk factor in overweight adolescents.” The Journal of Pediatrics. Vol. 142(3), pgs. 253–8. Retrieved from: http://www.jpeds.com/article/S0022-3476(02)40206-5/abstract.

[390] Aude YW, et al. (2004). “The National Cholesterol Education Program Diet vs a Diet Lower in Carbohydrates and Higher in Protein and Monounsaturated Fat. A Randomized Trial.” Archives of Internal Medicine, Pgs. 164:2141–2146. Retrieved from: http://archinte.ama-assn.org/cgi/content/full/164/19/2141.

[391] Volek JS, et al. (2004). “Comparison of energy-restricted very low-carbohydrate and low-fat diets on weight loss and body composition in overweight men and women.” Nutrition & Metabolism, Vol. 1, pg. 13. Retrieved from: http://www.nutritionandmetabolism.com/content/1/1/13.

[392] Yancy WS Jr, et al. (2004). “A Low-Carbohydrate, Ketogenic Diet versus a Low-Fat Diet To Treat Obesity and Hyperlipidemia. A Randomized, Controlled Trial.” Archives of Internal Medicine, pgs. 140:769–777. Retrieved from: http://www.annals.org/content/140/10/769.long

[393] Nichols-Richardsson SM, et al. “Perceived Hunger Is Lower and Weight Loss Is Greater in Overweight Premenopausal Women Consuming a Low-Carbohydrate/High- Protein vs High-Carbohydrate/Low-Fat Diet.” Journal of the American Dietetic Association, Vol. 105, pgs. 1433–1437. Retrieved from: http://www.ncbi.nlm.nih.gov/pubmed?term=Perceived%20Hunger%20Is%20Lower%20and%20Weight%20Loss%20Is%20Greater%20in%20Overweight%20Premenopausal

[394] Gardner CD, et al. (2007). “Comparison of the Atkins, Zone, Ornish, and learn Diets for Change in Weight and Related Risk Factors Among Overweight Premenopausal Women. The a to z Weight Loss Study: A Randomized Trial.” Journal of the American Medical Association, Vol. 297, pgs. 969–977. Retrieved from: http://jama.ama-assn.org/content/297/9/969.long

[395] Shai I, et al. (2008). “Weight loss with a low-carbohydrate, mediterranean, or low-fat diet.” The New England Journal of Medicine, Vol. 359(3), pgs. 229–41. Retrieved from: http://www.nejm.org/doi/full/10.1056/NEJMoa0708681.

[396] Summer SS, et al. (Mar 31, 2011). “Adiponectin Changes in Relation to the Macronutrient Composition of a Weight-Loss Diet.” Obesity (Silver Spring). [Epub ahead of print] Retrieved from: http://www.nature.com/oby/journal/v19/n11/full/oby201160a.html.

[397] Daly ME, et al. (Jan 23, 2006). “Short-term effects of severe dietary carbohydrate-restriction advice in Type 2 diabetes–a randomized controlled trial.” Diabetic Medicine, Vol. 23(1), pgs. 15–20. Retrieved from: http://onlinelibrary.wiley.com/doi/10.1111/j.1464-5491.2005.01760.x/abstract;jsessionid=F2FCA81A7A0BD31D425BCDD7291C4D9E.d03t01?systemMessage=Wiley+Online+Library+will+be+disrupted+2+July+from+10-12+BST+for+monthly+maintenance.

[398] Westman EC, et al. (2008). “The effect of a low-carbohydrate, ketogenic diet versus a low- glycemic index diet on glycemic control in type 2 diabetes mellitus.” Nutritional Metabolism (Lond.), Vol. 19, pgs. 5-36. Retrieved from: http://www.nutritionandmetabolism.com/content/5/1/36.

[399] Taubes, Gary, “Good Calories, Bad Calories,” 2007. New York: Knopf Publishing. pg. 50-53.

[400] Taubes, Gary, “Good Calories, Bad Calories,” 2007. New York: Knopf Publishing. pg. 327-354.

[401] Hite, Adele H. (June, 2011). “Low-Carbohydrate Diet Review: Shifting the Paradigm.” Nutrition in Clinical Practice, Vol. 26(3), pgs. 300-308. Retrieved from: http://www.nmsociety.org/docs/LowCarbDiet/Nutrition-in-Clinical-Practice-2011.pdf

[402] Howard et al. (2006).  “Low-Fat Dietary Pattern and Weight Change over 7 Years.” JAMA: 2006;295(1):39-49. doi:10.1001/jama.295.1.39. Retrieved from: http://jama.ama-assn.org/content/295/1/39.full.

[403] Gardner CD, et al. (2007). “Comparison of the Atkins, Zone, Ornish, and learn Diets for Change in Weight and Related Risk Factors Among Overweight Premenopausal Women. The a to z Weight Loss Study: A Randomized Trial.” Journal of the American Medical Association, Vol. 297, pgs. 969–977. Retrieved from: http://jama.ama-assn.org/content/297/9/969.long

[405] Gardner CD, et al. (2007). “Comparison of the Atkins, Zone, Ornish, and learn Diets for Change in Weight and Related Risk Factors Among Overweight Premenopausal Women. The a to z Weight Loss Study: A Randomized Trial.” Journal of the American Medical Association, Vol. 297, pgs. 969–977. Retrieved from: http://jama.ama-assn.org/content/297/9/969.long

[406] Peter Attia. (2011) “JumpstartMD presents Dr. Peter Attia on the Role of Fat in Weight Loss – Part 2.”

Youtube. Retrieved from: http://www.youtube.com/watch?v=C3E0pFl370Y .

[407] Volek, Jeff S., and Stephen D. Phinney (May 19, 2011). “The Art and Science of Low Carbohydrate Living.”  Chapter 1: Overview of Low Carbohydrate and Ketogenic Diet. Beyond Obesity LLC.

[408] St-Onge, Marrie-Pierre, et al. (2004). “Dual-Energy X-Ray Absorptiometry-Measured Lean Soft Tissue Mass: Differing Relation to Body Cell Mass Across the Adult Life Span.” Journal of Gerontology: Series A, Vol. 59 (8), pgs. B796-B800. doi: 10.1093/gerona/59.8.B796. Retrieved from: http://biomedgerontology.oxfordjournals.org/content/59/8/B796.full.

[409] Cox, CL, et al. (Feb. 2012). “Consumption of fructose-sweetened beverages for 10 weeks reduces net fat oxidation and energy expenditure in overweight/obese men and women.” European Journal of Clinical Nutrition, Vol. 66(2), pgs. 201-8, Retrieved from: http://www.ncbi.nlm.nih.gov/pubmed/21952692.

[410] Gardner CD, et al. (2007). “Comparison of the Atkins, Zone, Ornish, and learn Diets for Change in Weight and Related Risk Factors Among Overweight Premenopausal Women. The a to z Weight Loss Study: A Randomized Trial.” Journal of the American Medical Association, Vol. 297, pgs. 969–977. Retrieved from: http://jama.ama-assn.org/content/297/9/969.long

[411] Ibid.

[412] Bradford Hill, Austin. (1965). “The Environment and Disease: Association or Causation?,” Proceedings of the Royal Society of Medicine, Vol. 58, pgs. 295-300. Retrieved from: http://www.edwardtufte.com/tufte/hill.

[413] Volek, Jeff S., and Stephen D. Phinney (May 19, 2011). “The Art and Science of Low Carbohydrate Living.”  Chapter 1: Overview of Low Carbohydrate and Ketogenic Diet. Beyond Obesity LLC.

[414] Dyson PA, et al.(Dec. 2007).  “A low-carbohydrate diet is more effective in reducing body weight than healthy eating in both diabetic and non-diabetic subjects.” Diabetic Medicine;24(12). Pgs. 1430-5. Retrieved from: http://www.ncbi.nlm.nih.gov/pubmed/17971178 .

[415] Krebs NF, et al. (August, 2010). “Efficacy and Safety of a High Protein, Low Carbohydrate Diet for Weight Loss in Severely Obese Adolescents.” Journal of Pediatrics Vol. 157,  pgs. 252-8. Retrieved from: http://www.jpeds.com/article/S0022-3476(10)00120-4/abstract .

[416] Brehm BJ, et al. (2003). “A Randomized Trial Comparing a Very Low Carbohydrate Diet and a Calorie-Restricted Low Fat Diet on Body Weight and Cardiovascular Risk Factors in Healthy Women. The Journal of Clinical Endocrinology and  Metabolism , Vol. 88, pgs.1617–1623. Retrieved from: http://jcem.endojournals.org/content/88/4/1617.long.

[417] Samaha FF, et al. (2003). “A Low-Carbohydrate as Compared with a Low-Fat Diet in Severe Obesity.” The New England Journal of Medicine, Vol. 348, pgs. 2074–81. Retrieved from: http://www.nejm.org/doi/full/10.1056/NEJMoa022637.

[418] Sondike SB, et al. (March 2003). “Effects of a low-carbohydrate diet on weight loss and cardiovascular risk factor in overweight adolescents.” The Journal of Pediatrics. Vol. 142(3), pgs. 253–8. Retrieved from: http://www.jpeds.com/article/S0022-3476(02)40206-5/abstract.

[419] Aude YW, et al. (2004). “The National Cholesterol Education Program Diet vs a Diet Lower in Carbohydrates and Higher in Protein and Monounsaturated Fat. A Randomized Trial.” Archives of Internal Medicine, Pgs. 164:2141–2146. Retrieved from: http://archinte.ama-assn.org/cgi/content/full/164/19/2141.

[420] Volek JS, et al. (2004). “Comparison of energy-restricted very low-carbohydrate and low-fat diets on weight loss and body composition in overweight men and women.” Nutrition & Metabolism, Vol. 1, pg. 13. Retrieved from: http://www.nutritionandmetabolism.com/content/1/1/13.

[421] Yancy WS Jr, et al. (2004). “A Low-Carbohydrate, Ketogenic Diet versus a Low-Fat Diet To Treat Obesity and Hyperlipidemia. A Randomized, Controlled Trial.” Archives of Internal Medicine, pgs. 140:769–777. Retrieved from: http://www.annals.org/content/140/10/769.long

[422] Nichols-Richardsson SM, et al. “Perceived Hunger Is Lower and Weight Loss Is Greater in Overweight Premenopausal Women Consuming a Low-Carbohydrate/High- Protein vs High-Carbohydrate/Low-Fat Diet.” Journal of the American Dietetic Association, Vol. 105, pgs. 1433–1437. Retrieved from: http://www.ncbi.nlm.nih.gov/pubmed?term=Perceived%20Hunger%20Is%20Lower%20and%20Weight%20Loss%20Is%20Greater%20in%20Overweight%20Premenopausal

[423] Gardner CD, et al. (2007). “Comparison of the Atkins, Zone, Ornish, and learn Diets for Change in Weight and Related Risk Factors Among Overweight Premenopausal Women. The a to z Weight Loss Study: A Randomized Trial.” Journal of the American Medical Association, Vol. 297, pgs. 969–977. Retrieved from: http://jama.ama-assn.org/content/297/9/969.long

[424] Shai I, et al. (2008). “Weight loss with a low-carbohydrate, mediterranean, or low-fat diet.” The New England Journal of Medicine, Vol. 359(3), pgs. 229–41. Retrieved from: http://www.nejm.org/doi/full/10.1056/NEJMoa0708681.

[425] Summer SS, et al. (Mar 31, 2011). “Adiponectin Changes in Relation to the Macronutrient Composition of a Weight-Loss Diet.” Obesity (Silver Spring). [Epub ahead of print] Retrieved from: http://www.nature.com/oby/journal/v19/n11/full/oby201160a.html.

[426] Daly ME, et al. (Jan 23, 2006). “Short-term effects of severe dietary carbohydrate-restriction advice in Type 2 diabetes–a randomized controlled trial.” Diabetic Medicine, Vol. 23(1), pgs. 15–20. Retrieved from: http://onlinelibrary.wiley.com/doi/10.1111/j.1464-5491.2005.01760.x/abstract;jsessionid=F2FCA81A7A0BD31D425BCDD7291C4D9E.d03t01?systemMessage=Wiley+Online+Library+will+be+disrupted+2+July+from+10-12+BST+for+monthly+maintenance.

[427] Westman EC, et al. (2008). “The effect of a low-carbohydrate, ketogenic diet versus a low- glycemic index diet on glycemic control in type 2 diabetes mellitus.” Nutritional Metabolism (Lond.), Vol. 19, pgs. 5-36. Retrieved from: http://www.nutritionandmetabolism.com/content/5/1/36.

[428] Taubes, Gary, “Good Calories, Bad Calories,” 2007. New York: Knopf Publishing. pg. 50-53.

[429] Taubes, Gary, “Good Calories, Bad Calories,” 2007. New York: Knopf Publishing. pg. 327-354.

[430] Krauss, RM, et al. (May 2006). “Separate effects of reduced carbohydrate intake and weight loss on atherogenic dyslipidemia.” American Journal of Clinical Nutrition, Vol. 83, No. 5, 1025-1031Retrieved from: http://www.ajcn.org/content/83/5/1025.long.

[432] Borders, William (July 7, 1965). “New Diet Decried by Nutritionists: Dangers Are Seen in Low Carbohydrate Intake.” The New York Times. Retrieved from: http://select.nytimes.com/gst/abstract.html?res=FB0D1FFA3D5A157A93C5A9178CD85F418685F9&scp=1&sq=new%20diet%20decried%20as%20dangerous&st=cse.

[433] Larry King Live. (Oct. 19, 2007). “2 of 2 Gary Taubes on Larry King Live 10/19/2007.” Youtube. Retrieved from: http://www.youtube.com/watch?v=5LNH0RPXI0M.

[434] Volek, Jeff S., and Stephen D. Phinney (May 19, 2011). “The Art and Science of Low Carbohydrate Living.”  Chapter 1: Overview of Low Carbohydrate and Ketogenic Diet. Beyond Obesity LLC.

[435] Taubes, Gary. (2010). “Why We Get Fat, and What to Do About It.” New York: Anchor Books. Pg. 82.

[436] Taubes, Gary, “Good Calories, Bad Calories,” 2007. New York: Knopf Publishing. Pg. 281.

[437] U.S. Dept. of Health and Human Services, NIDDK, NDIC. (Dec. 6, 2011). “Insulin Resistance and Prediabetes.” Retrieved from: http://diabetes.niddk.nih.gov/dm/pubs/insulinresistance/#risk.

[438] Ibid.

[439] Ibid.

[440] Wikipedia. “Who Killed the Electric Car?”. Retrieved from: http://en.wikipedia.org/wiki/Who_Killed_the_Electric_Car%3F#Hydrogen_fuel_cell.

[441] Johnson, Rachel K., et al. (Aug. 24, 2009). “Dietary Sugars Intake and Cardiovascular Health: A Scientific Statement From the American Heart Association.” Circulation 2009, Vol. 120, pgs.1011-1020.Retrieved from: http://circ.ahajournals.org/content/120/11/1011.full.pdf.

[442] Encyclopdia Brittanica. “Ockham’s razor.” Retrieved from: http://www.britannica.com/EBchecked/topic/424706/Ockhams-razor .

[443] The Los Angeles Times. (Dec. 20, 2010). “A Reversal on Carbs.” Retrieved from: http://articles.latimes.com/2010/dec/20/health/la-he-carbs-20101220 .

[444] USDA. “Profiling Food Consumption in America: Chapter 2.” Retrieved from: http://www.usda.gov/factbook/chapter2.pdf .

[445] USDA. Economic Research Service. “Sugar and Sweeteners: Background.” Retrieved from: http://www.ers.usda.gov/briefing/sugar/background.htm .

[446] Taubes, Gary, “Good Calories, Bad Calories,” 2007. New York: Knopf Publishing. Pgs. 112-113.

[447] Encyclopdia Brittanica. “Ockham’s razor.” Retrieved from: http://www.britannica.com/EBchecked/topic/424706/Ockhams-razor .

[448] Taubes, Gary, “Good Calories, Bad Calories,” 2007. New York: Knopf Publishing. Pgs. 112-113.

[449] Greene, Brian. (Oct. 28, 2003). “A Theory of Everything?” NOVA. Retrieved from: http://www.pbs.org/wgbh/nova/physics/theory-of-everything.html.

[450] Mangels, John. (Sept. 7, 2010). “Stephen Hawking’s ‘The Grand Design’ puts M-theory to the mysteries of the universe.” The Plain Dealer. Retrieved from: http://www.cleveland.com/books/index.ssf/2010/09/stephen_hawkings_the_grand_des.html.

[451] The Centers for Disease Control and Prevention. “Lung Cancer: Risk Factors.” Atlanta, GA. Retrieved from: http://www.cdc.gov/cancer/lung/basic_info/risk_factors.htm .

[452] Villeneuve, PJ, and Mao Y. (Nov.-Dec. 1994). “Lifetime probability of developing lung cancer, by smoking status, Canada.” Canadian Journal of Public Health, 85(6):385-8. Retrieved from: http://www.ncbi.nlm.nih.gov/pubmed/7895211 .

[453]  Pg. xxiii.

[454] Ogden, Cynthia L., Carroll, Margaret DKit, ., Brian K., and Katherine M. Flegal, The Centers for Disease Control and Prevention (January 2012). “Prevalence of Obesity in the United States, 2009–2010.” NCHS Data Brief, Number 82. Atlanta, GA. Retrieved from: http://www.cdc.gov/nchs/data/databriefs/db82.htm .

[455] Ndumele, CE et al. (Aug. 31, 2011). “Hepatic steatosis, obesity, and the metabolic syndrome are independently and additively associated with increased systemic inflammation.” Arterioschlirosis, Thrombosis, and Vascular Biology, (8):1927-32. Retrieved from: http://www.ncbi.nlm.nih.gov/pubmed/21546603 .

[456] Taubes, Gary. (2010). “Why We Get Fat, and What to Do About It.” New York: Anchor Books. Pg. 58.

[457] Taubes, Gary. (January 2012). “Unraveling the Obesity-Cancer Connection.” Science, Vol. 335 no. 6064 pp. 28-32. Retrieved from: http://www.sciencemag.org/content/335/6064/28 .

[458] Garber, AK, Lustig, RH. (Sept. 2011). “Is fast food addictive?” Current Drug Abuse Reviews, Vol. 4(3), pgs. 146-62. Retrieved from: http://www.ncbi.nlm.nih.gov/pubmed/21999689.

[459] Drewnowski, Adam, et al. (April 2005). “Food Choices and Diet Costs: an Economic Analysis” The Journal of Nutrition, Vol. 135, pgs. 900-904. Retrieved from: http://jn.nutrition.org/content/135/4/900.long.

[460] Taubes, Gary. (2010). “Why We Get Fat, and What to Do About It.” New York: Anchor Books. Pgs. 131-133.

[461] Drewnowski, Adam, & SE Specter. (January 2004). “Poverty and obesity: the role of energy density and energy costs.” American Journal of Clinical Nutrition, Vol. 79(1), pgs. 6-16. Retrieved from: http://www.ajcn.org/content/79/1/6.long#R116. See Figure 1.

[463] Brunner, E.J., et al. (1997). “Social inequality in coronary risk: Central obesity and the metabolic syndrome. Evidence from the Whitehall II study.” Diabetologia, Vol. 40, pgs. 1341-1349.  Retrieved from: http://www.springerlink.com/content/hgtvcrbe7un5mry3/.

[465] Neilsen, Chad D. (July 2011). “2011 Update: Overweight, Obesity and Physical Activity in the State of Georgia.” Georgia Dept. of Public Health. Atlanta, GA.

[466] Georgia Dept. of Public Health. “2010 Georgia Data Summary: Obesity in Children and Youth.” Atlanta, GA. Retrieved from: http://health.state.ga.us/pdfs/epi/cdiee/DPH.Epi.7-20-11.pdf.

[467] Kim, Juhee, et al. (July 2006). “Trends in Overweight from 1980 through 2001 among Preschool-Aged Children Enrolled in a Health Maintenance Organization.” Obesity, Vol. 14(7), pgs. 1107-1112. Retrieved from: http://www.nature.com.proxy-remote.galib.uga.edu/oby/journal/v14/n7/pdf/oby2006126a.pdf.

[468] Georgia Dept. of Public Health. “2010 Georgia Data Summary: Obesity in Children and Youth.” Atlanta, GA. Retrieved from: http://health.state.ga.us/pdfs/epi/cdiee/DPH.Epi.7-20-11.pdf.

[469] Ervin, R. Bethene. The Centers for Disease Control and Prevention, National Health Statistics Report. (May 5, 2009). “Prevalence of Metabolic Syndrome Among Adults 20 Years of Age and Over, by Sex, Age, Race and Ethnicity, and Body Mass Index: United States, 2003–2006.”  Number 13. Retrived from: http://www.cdc.gov/nchs/data/nhsr/nhsr013.pdf .

[470] U.S. Department of Health and Human Services, Assistant Secretary for Planning and Education. “Childhood Obesity.” Retrieved from: http://aspe.hhs.gov/health/reports/child_obesity/#_ftn11.

[471] Bakker, Stephen J.L., et al. (Oct. 18, 2006). “Metabolic syndrome: a fata morgana?”

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[472] Aschengrau, Ann, and George R. Seage III. (2008). “Essentials of Epidemiology in Public Health: Second Edition.” Sudbury, MA: Jones and Bartlett Publishers. Pg. 140-149, 155-164.

[473] Lawlor, Debbie A., et al. (May 2004). “Commentary: The hormone replacement–

coronary heart disease conundrum: is this the

death of observational epidemiology?” International Journal of Epidemiology, Vol. 33, pgs. 464–467. Retrieved from: http://ije.oxfordjournals.org/content/33/3/464.full.pdf+html

[474] Taubes, Gary. (Sept. 16, 2007). “Do We Really Know What Makes Us Healthy?” New York Times. Retrieved from: http://www.nytimes.com/2007/09/16/magazine/16epidemiology-t.html?scp=8&sq=gary%20taubes&st=cse.

[475] Pai, Madhukar & Jay S Kaufman. “The B Files: Case Studies of Bias in Real Life Epidemiological Studies.” McGill University, Montreal, Canada. Retrieved from: http://www.teachepi.org/documents/courses/bfiles/The%20B%20Files_File1_HRT_Final_Complete.pdf.

[476] National Public Radio. (March 12, 2012). “Death by Bacon? Study Finds Eating Meat is Risky.” Retrieved from: http://www.npr.org/blogs/thesalt/2012/03/12/148457233/death-by-bacon-study-finds-eating-meat-is-risky.

[477] Writing Group for the Women’s Health Initiative Investigators. (July 17, 2002). “Risks and Benefits of Estrogen Plus Progestin

in Healthy Postmenopausal Women: Principal Results From the Women’s Health Initiative Randomized Controlled Trial.” Journal of the American Medical Association, Vol. 288(No.3), pgs. 321-333. Retrieved from: http://jama.ama-assn.org/content/288/3/321.full.pdf.

[478] Pai, Madhukar & Jay S Kaufman. “The B Files: Case Studies of Bias in Real Life Epidemiological Studies.” McGill University, Montreal, Canada. Retrieved from: http://www.teachepi.org/documents/courses/bfiles/The%20B%20Files_File1_HRT_Final_Complete.pdf.

[479] Writing Group for the Women’s Health Initiative Investigators. (July 17, 2002). “Risks and Benefits of Estrogen Plus Progestin

in Healthy Postmenopausal Women: Principal Results From the Women’s Health Initiative Randomized Controlled Trial.” Journal of the American Medical Association, Vol. 288(No.3), pgs. 321-333. Retrieved from: http://jama.ama-assn.org/content/288/3/321.full.pdf.

[480] Lawlor, Debbie A., et al. (May 2004). “Commentary: The hormone replacement–

coronary heart disease conundrum: is this the

death of observational epidemiology?” International Journal of Epidemiology, Vol. 33, pgs. 464–467. Retrieved from: http://ije.oxfordjournals.org/content/33/3/464.full.pdf+html

[482] Taubes, Gary. (Sept. 16, 2007). “Do We Really Know What Makes Us Healthy?” New York Times. Retrieved from: http://www.nytimes.com/2007/09/16/magazine/16epidemiology-t.html?scp=8&sq=gary%20taubes&st=cse.

[483] Pai, Madhukar & Jay S Kaufman. “The B Files: Case Studies of Bias in Real Life Epidemiological Studies.” McGill University, Montreal, Canada. Retrieved from: http://www.teachepi.org/documents/courses/bfiles/The%20B%20Files_File1_HRT_Final_Complete.pdf.

[484] Pan, A, et al. (March 2012). “Red Meat Consumption and Mortality: Results From 2 Prospective Cohort Studies.” Archives of Internal Medicine. Retrieved from: http://www.ncbi.nlm.nih.gov/pubmed/22412075.

[485] Ibid.

[486] Ibid.

[487] Micha, Renata et al. (2010). “Red and Processed Meat Consumption and Risk of Incident Coronary Heart Disease, Stroke, and Diabetes Mellitus: A Systematic Review and Meta-Analysis.” Circulation, Vol. 121, pgs. 2271-2283.Retrieved from: http://circ.ahajournals.org/content/121/21/2271.long.

[488] The Centers for Disease Control and Prevention. “Overweight and Obesity: Economic Consequences.” Retrieved from: http://www.cdc.gov/obesity/causes/economics.html.

[489] Leff, Todd, & James. G. Grannerman. “Adipose Tissue in Health and Disease.” Wiley Publishers: , pg. xix-xixi, 98, 143-152.

[490] Taubes, Gary, “Good Calories, Bad Calories,” 2007. New York: Knopf Publishing.pg. 362.

[491] Taubes, Gary. (2010). “Why We Get Fat, and What to Do About It.” New York: Anchor Books. Pg. 106-126.

[492] Bjorntorp, P. (April 20, 1996). “The regulation of adipose tissue in humans.” International Journal of Obesity and Related Metabolic Disorders, Vol. 20(4), pg. 291-302. Retrieved from: http://www.ncbi.nlm.nih.gov/pubmed/8680455.

[493] Leff, Todd, & James. G. Grannerman. (). “Adipose Tissue in Health and Disease.” Wiley Publishers: , pg. xix-xixi, 98, 143-152.

[494] Ibid of 524-527.

[495] Ibid.

[496] Taubes, Gary, “Good Calories, Bad Calories,” 2007. New York: Knopf Publishing.pg. 438.

[497] Phinney, Stephen D., et al. (1991). “The transient hypercholesterolemia of major weight loss.” American Journal of Clinical Nutrition, Vol. 53, pgs. 1404-10. Retrieved from: http://www.ajcn.org/content/53/6/1404.full.pdf.

[499] Ibid.

[500] Stanhope, Kimber L., and Peter J. Havel. (2009). “Fructose Consumption: Considerations for Future Research on Its Effects on Adipose Distribution, Lipid Metabolism, and Insulin Sensitivity  in Humans.” The Journal of Nutrition, Vol. 139, pgs. 1236-1241. Retrieved from: http://jn.nutrition.org/content/139/6/1236S.full.pdf

[501] Taubes, Gary. (2010). “Why We Get Fat, and What to Do About It.” New York: Anchor Books. Pg. 138.

[502] Lindeberg, S., et al. (Oct. 1997). “Age relations of cardiovascular risk factors in a traditional Melanesian: the Kitava Study.” American Journal of Clinical Nutrition, Vol. 66 (No. 4), pgs. 845-52. Retrieved from: http://www.ajcn.org/content/66/4/845.long.

[503] Lindeberg, S., et al. (Mar. 1993). “Apparent absence of stroke and ischaemic heart disease in a traditional Melanesian island: a clinical study in Kitava.” Journal of Internal Medicine, Vol. 233 (No. 3), pgs. 269-275. Retrieved from: http://www.ncbi.nlm.nih.gov/pubmed/8450295.

[504] Curtis, Michael. (2004). “The Obesity Epidemic in the Pacific Islands.” Journal of Development and Social Transformation, Vol.1(No.1), pgs. 37-42. Retrieved from: http://www.maxwell.syr.edu/uploadedFiles/moynihan/dst/curtis5.pdf?n=3228.

 

[505] Stanhope, Kimber L., and Peter J. Havel. (2009). “Fructose Consumption: Considerations for Future Research on Its Effects on Adipose Distribution, Lipid Metabolism, and Insulin Sensitivity  in Humans.” The Journal of Nutrition, Vol. 139, pgs. 1236-1241. Retrieved from: http://jn.nutrition.org/content/139/6/1236S.full.pdf

[506] Carnegie Mellon University. (2006). “Department of Biological Sciences: Interactive Animations: Introduction to Lipids.” Retrieved from: http://telstar.ote.cmu.edu/biology/MembranePage/index2.html.

[507] Scott, Paul. (2/14/2010). “Bad cholesterol: It’s not what you think.” Retrieved from: http://www.msnbc.msn.com/id/35058896/ns/health-heart_health/t/bad-cholesterol-its-not-what-you-think/#.T3M65jHy_4A.

[509] Siri-Tarino PW, et al. (Jan. 13, 2010). “Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease.” American Journal of Clinical Nutrition, Vol. 91 ,no. 3, pgs. 535-546. Retrieved from: http://www.ajcn.org/content/91/3/535.full?sid=320bcc17-09e4-4275-a18c-89ab6a444dc7.

[510] Mensink, RP, et al. (Aug. 1992). “Effect of dietary fatty acids on serum lipids and lipoproteins. A meta-analysis of 27 trials.” Arterioschlerosis and thrombosis, Vol. 12(No. 8), pgs. 911-9. Retrieved from: http://www.ncbi.nlm.nih.gov/pubmed/1386252.

[511] Taubes, Gary. (2010). “Why We Get Fat, and What to Do About It.” New York: Anchor Books. Pg 189-190.

[512] Ibid.

[513] Ibid.

[514] Willett, Walter. (Nov. 11, 1995). “Polyunsaturated fat and the risk of cancer.” British Journal of Medicine, Vol. 311, pgs. 1239-1240. Retrieved from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2551173/pdf/bmj00618-0005.pdf.

[515] Watkins, Bruce A. “Biochemistry and Nutritional Significance of Omega-3 Fatty Acids.” Purdue University. Retrieved from: http://www.omega3learning.uconn.edu/sitefile/File/presentations/biochem-nutr-omega3.pdf .

[516] University of Maryland Medical Center. “Omega-3 fatty acids.” Retrieved from: http://www.umm.edu/altmed/articles/omega-3-000316.htm .

[517] WHO. (2011). “Media centre: Obesity and overweight.” Retrieved from: http://www.who.int/mediacentre/factsheets/fs311/en/.

[518] The Centers for Disease Control and Prevention (2011). Overweight and Obesity: Defining Overweight and Obesity. Retrieved from: http://www.cdc.gov/obesity/causes/index.html

[519] American Heart Association. (May 5, 2011). “Obesity Information.” Retrieved from: http://www.heart.org/HEARTORG/GettingHealthy/WeightManagement/Obesity/Obesity-Information_UCM_307908_Article.jsp#.T0e_ZPF5F8E.

[520] Larry King Live. (Oct. 19, 2007). “2 of 2 Gary Taubes on Larry King Live 10/19/2007.” Youtube. Retrieved from: http://www.youtube.com/watch?v=5LNH0RPXI0M.

[521] NIH, NHBLI. (Nov. 1, 2010). “What Causes Overweight and Obesity?” Retrieved from: http://www.nhlbi.nih.gov/health/health-topics/topics/obe/causes.html.

[522] US Dept of HHS, US Public Health Service. (2010). “The Surgeon General’s Vision for a Healthy and Fit Nation.” Retrieved from: http://www.surgeongeneral.gov/library/obesityvision/obesityvision2010.pdf.

[523] National Heart Lung and Blood Institute, National Institutes of Health. (2012). “Balance Food and Activity: What is Energy Balance?” Retrieved from: http://www.nhlbi.nih.gov/health/public/heart/obesity/wecan/healthy-weight-basics/balance.htm

[525] Curioni, CC & PM Lourenco. (May 31, 2005). “Long-term weight loss after diet and exercise: a systematic review.” International Journal of Obesity, Vol. 29, 1168–1174. doi:10.1038/sj.ijo.0803015. Retrieved from: http://www.nature.com/ijo/journal/v29/n10/full/0803015a.html.

[526] Schoof, Michael. (Feb. 1, 2003). “Are Low-Fat Diets Better than Other Weight-Reducing Diets in Achieving Long-Term Weight Loss?” American  Family  Physician, Vol. 67(3), pgs. 507-508. Retrieved from: http://www.aafp.org/afp/2003/0201/p507.html.

[527] Taubes, Gary, “Good Calories, Bad Calories,” 2007. New York: Knopf Publishing. Pgs. 20-21, 22-59.

[528] Andrade, Jason, et al. (March 2009). “Ancel Keys and the lipid hypothesis: From early breakthroughs to current management of dyslipidemia.” British Columbia Medical Journal, Vol. 51 (No. 2), pgs. 66-72. Retrieved from: http://www.bcmj.org/article/ancel-keys-and-lipid-hypothesis-early-breakthroughs-current-management-dyslipidemia.

[529]  Siri-Tarino PW, et al. (Jan. 13, 2010). “Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease.” American Journal of Clinical Nutrition, Vol. 91 ,no. 3, pgs. 535-546. Retrieved from: http://www.ajcn.org/content/91/3/535.full?sid=320bcc17-09e4-4275-a18c-89ab6a444dc7.

[530] Siri-Tarino, Patty W., et al. (March 2010). “Saturated fat, carbohydrate, and cardiovascular disease.” American  Journal of Clinical Nutrition, Vol. 91 (no. 3), pgs. 502-509. Retrieved from: http://www.ajcn.org/content/91/3/502.

[531] TeensHealth. “MyPlate Food Guide for Teens.” Retrieved from: http://kidshealth.org/teen/food_fitness/dieting/myplate.html.

[532] Dyson PA, et al.(Dec. 2007).  “A low-carbohydrate diet is more effective in reducing body weight than healthy eating in both diabetic and non-diabetic subjects.” Diabetic Medicine;24(12). Pgs. 1430-5. Retrieved from: http://www.ncbi.nlm.nih.gov/pubmed/17971178 .

[533] Krebs NF, et al. (August, 2010). “Efficacy and Safety of a High Protein, Low Carbohydrate Diet for Weight Loss in Severely Obese Adolescents.” Journal of Pediatrics Vol. 157,  pgs. 252-8. Retrieved from: http://www.jpeds.com/article/S0022-3476(10)00120-4/abstract .

[534] Brehm BJ, et al. (2003). “A Randomized Trial Comparing a Very Low Carbohydrate Diet and a Calorie-Restricted Low Fat Diet on Body Weight and Cardiovascular Risk Factors in Healthy Women. The Journal of Clinical Endocrinology and  Metabolism , Vol. 88, pgs.1617–1623. Retrieved from: http://jcem.endojournals.org/content/88/4/1617.long.

[535] Samaha FF, et al. (2003). “A Low-Carbohydrate as Compared with a Low-Fat Diet in Severe Obesity.” The New England Journal of Medicine, Vol. 348, pgs. 2074–81. Retrieved from: http://www.nejm.org/doi/full/10.1056/NEJMoa022637.

[536] Sondike SB, et al. (March 2003). “Effects of a low-carbohydrate diet on weight loss and cardiovascular risk factor in overweight adolescents.” The Journal of Pediatrics. Vol. 142(3), pgs. 253–8. Retrieved from: http://www.jpeds.com/article/S0022-3476(02)40206-5/abstract.

[537] Aude YW, et al. (2004). “The National Cholesterol Education Program Diet vs a Diet Lower in Carbohydrates and Higher in Protein and Monounsaturated Fat. A Randomized Trial.” Archives of Internal Medicine, Pgs. 164:2141–2146. Retrieved from: http://archinte.ama-assn.org/cgi/content/full/164/19/2141.

[538] Volek JS, et al. (2004). “Comparison of energy-restricted very low-carbohydrate and low-fat diets on weight loss and body composition in overweight men and women.” Nutrition & Metabolism, Vol. 1, pg. 13. Retrieved from: http://www.nutritionandmetabolism.com/content/1/1/13.

[539] Yancy WS Jr, et al. (2004). “A Low-Carbohydrate, Ketogenic Diet versus a Low-Fat Diet To Treat Obesity and Hyperlipidemia. A Randomized, Controlled Trial.” Archives of Internal Medicine, pgs. 140:769–777. Retrieved from: http://www.annals.org/content/140/10/769.long

[540] Nichols-Richardsson SM, et al. “Perceived Hunger Is Lower and Weight Loss Is Greater in Overweight Premenopausal Women Consuming a Low-Carbohydrate/High- Protein vs High-Carbohydrate/Low-Fat Diet.” Journal of the American Dietetic Association, Vol. 105, pgs. 1433–1437. Retrieved from: http://www.ncbi.nlm.nih.gov/pubmed?term=Perceived%20Hunger%20Is%20Lower%20and%20Weight%20Loss%20Is%20Greater%20in%20Overweight%20Premenopausal

[541] Gardner CD, et al. (2007). “Comparison of the Atkins, Zone, Ornish, and learn Diets for Change in Weight and Related Risk Factors Among Overweight Premenopausal Women. The a to z Weight Loss Study: A Randomized Trial.” Journal of the American Medical Association, Vol. 297, pgs. 969–977. Retrieved from: http://jama.ama-assn.org/content/297/9/969.long

[542] Shai I, et al. (2008). “Weight loss with a low-carbohydrate, mediterranean, or low-fat diet.” The New England Journal of Medicine, Vol. 359(3), pgs. 229–41. Retrieved from: http://www.nejm.org/doi/full/10.1056/NEJMoa0708681.

[543] Summer SS, et al. (Mar 31, 2011). “Adiponectin Changes in Relation to the Macronutrient Composition of a Weight-Loss Diet.” Obesity (Silver Spring). [Epub ahead of print] Retrieved from: http://www.nature.com/oby/journal/v19/n11/full/oby201160a.html.

[544] Daly ME, et al. (Jan 23, 2006). “Short-term effects of severe dietary carbohydrate-restriction advice in Type 2 diabetes–a randomized controlled trial.” Diabetic Medicine, Vol. 23(1), pgs. 15–20. Retrieved from: http://onlinelibrary.wiley.com/doi/10.1111/j.1464-5491.2005.01760.x/abstract;jsessionid=F2FCA81A7A0BD31D425BCDD7291C4D9E.d03t01?systemMessage=Wiley+Online+Library+will+be+disrupted+2+July+from+10-12+BST+for+monthly+maintenance.

[545] Westman EC, et al. (2008). “The effect of a low-carbohydrate, ketogenic diet versus a low- glycemic index diet on glycemic control in type 2 diabetes mellitus.” Nutritional Metabolism (Lond.), Vol. 19, pgs. 5-36. Retrieved from: http://www.nutritionandmetabolism.com/content/5/1/36.

[546] Taubes, Gary, “Good Calories, Bad Calories,” 2007. New York: Knopf Publishing. Pgs. 50-53.

[547] Wikipedia. “Tautology(logic).” Retrieved from: http://en.wikipedia.org/wiki/Tautology_%28logic%29.

[549] Lustig, Robert H. (2009). “Sugar: The Bitter Truth,” Youtube. Retrieved from http://www.youtube.com/watch?v=dBnniua6-oM

[550] Taubes, Gary, “Good Calories, Bad Calories,” 2007. New York: Knopf Publishing. Pg. 200-201.

[551] [551] Malik, et al Circulation. (2010). Sugar-Sweetened Beverages, Obesity, Type 2 Diabetes Mellitus, and Cardiovascular Disease Risk.” Circulation, Vol. 121, pgs. 1356-1364.  Retrived from: http://circ.ahajournals.org/content/121/11/1356.full.pdf+html .

[552] Seneff, Stephanie, Wainwright, Glyn, & Luca Mascitelli. (Feb. 7, 2011). “Is the metabolic syndrome caused by a high fructose, and relatively low fat, low cholesterol diet?” Archives of Medical Science, Vol. 7(1), pgs. 8-20. Retrieved from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3258689/pdf/AMS-7-1-8.pdf

[553] Stanhope, Kimber L., et al. (May, 2009). “Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans.” The Journal of Clinical Investigation, Vol. 119, Number 5, pgs. 1322- . Retrieved from: http://www.jci.org/articles/view/37385.

[554] Mayes, Peter. (1993). “Intermediary metabolism of fructose.” American Journal of Clinical Nutrition, Vol. 58 (5), pgs. 7545-7655. Retrieved from: http://www.ajcn.org/content/58/5/754S.full.pdf.

[555] Dekker, Mark J., et al. (May 10, 2010). “Fructose: a highly lipogenic nutrient implicated in insulin resistance, hepatic steatosis, and the metabolic syndrome.” American Journal of Physiology, Vol. 299 (5), pgs. 685-694. Retrieved from: http://ajpendo.physiology.org/content/299/5/E685.long#ref-94. Figure 1: http://ajpendo.physiology.org/content/299/5/E685/F1.expansion.html.

[556] Seneff, S., Wainwright G., and L. Mascitelli. (Feb. 7, 2011). “Is the metabolic syndrome caused by a high fructose, and relatively low fat, low cholesterol diet?” Archives of Medical Science, Vol. 7(1), pgs. 8-20. Retrieved from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3258689/pdf/AMS-7-1-8.pdf.  Figure 1: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3258689/figure/F1/.

[557] Taubes, Gary. (2010). “Why We Get Fat, and What to Do About It.” New York: Anchor Books. Pg. 138.

[558] Dekker, Mark J., et al. (May 10, 2010). “Fructose: a highly lipogenic nutrient implicated in insulin resistance, hepatic steatosis, and the metabolic syndrome.” American Journal of Physiology, Vol. 299 (5), pgs. 685-694. Retrieved from: http://ajpendo.physiology.org/content/299/5/E685.long#ref-94. Figure 1: http://ajpendo.physiology.org/content/299/5/E685/F1.expansion.html.

[559]  Pg. 191-193.

[560] Seneff, S., Wainwright G., and L. Mascitelli. (Feb. 7, 2011). “Is the metabolic syndrome caused by a high fructose, and relatively low fat, low cholesterol diet?” Archives of Medical Science, Vol. 7(1), pgs. 8-20. Retrieved from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3258689/pdf/AMS-7-1-8.pdf.

[561] Mayes, Peter. (1993). “Intermediary metabolism of fructose.” American Journal of Clinical Nutrition, Vol. 58 (5), pgs. 7545-7655. Retrieved from: http://www.ajcn.org/content/58/5/754S.full.pdf.

[562] Ibid.

[563] The Telegraph. (July 3, 2011). “Obesity Crisis: Half a Million Chidren have Liver Disease.” United Kingdom.  Retrived from: http://www.telegraph.co.uk/health/healthnews/8612881/Obesity-crisis-Half-a-million-children-have-liver-disease.html

[564] Harvard Medical School. “Glycemic index and glycemic load for 100+ foods.” Retrieved from: http://www.health.harvard.edu/newsweek/Glycemic_index_and_glycemic_load_for_100_foods.htm.

[565] Linus Pauling Institute, Oregon State University. (April 2010). “Glycemic Index and Glycemic Load.” Retrieved from: http://lpi.oregonstate.edu/infocenter/foods/grains/gigl.html.

[566] Ibid.

[567] Porte Jr., Daniel, et al. (May 3, 1996). “Diabetes Complications—Why Is Glucose Potentially Toxic?”

Science Vol. 272 no. 5262 p. 699  DOI: 10.1126/science.272.5262.699. Retrieved from: http://www.sciencemag.org/content/272/5262/699.

[568] Taubes, Gary. (2010). “Why We Get Fat, and What to Do About It.” New York: Anchor Books. Pg. 176-178.

[569] Ibid.

[570] U.S. National Library of Medicine, NIH. “Genetics Home Reference: Ketosis.” Retrieved from: http://ghr.nlm.nih.gov/glossary=ketosis.

[571] Hutchison, Courtney. “How Can a High-Fat Diet Treat Epilepsy? Dr. Besser Reports”. ABC News. Retrieved from: http://abcnews.go.com/Health/Wellness/ketogenic-diet-high-fat-diet-treat-seizures/story?id=13366995#.T3XWTjHy_4A.

[572] Pulford, D. Schuyler. (July 1927). “Ketogenic Diet for Epileptics.” California and Western Medicine, Vol. 1, pgs. 50–56.Retrieved from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1655541/.

[573] Taubes, Gary. (July 7, 2002). “What if It’s All Been  a Big Fat Lie?.” The New York Times.  Retrieved from: http://www.nytimes.com/2002/07/07/magazine/what-if-it-s-all-been-a-big-fat-lie.html?pagewanted=print&src=pm.

[574] Ibid.

[575] Taubes, Gary. (2010). “Why We Get Fat, and What to Do About It.” New York: Anchor Books. Pg. 176-178.

[576] U.S. National Library of Medicine, NIH. “Genetics Home Reference: Ketosis.” Retrieved from: http://ghr.nlm.nih.gov/glossary=ketosis.

[577] Hutchison, Courtney. “How Can a High-Fat Diet Treat Epilepsy? Dr. Besser Reports”. ABC News. Retrieved from: http://abcnews.go.com/Health/Wellness/ketogenic-diet-high-fat-diet-treat-seizures/story?id=13366995#.T3XWTjHy_4A.

[578] Pulford, D. Schuyler. (July 1927). “Ketogenic Diet for Epileptics.” California and Western Medicine, Vol. 1, pgs. 50–56.Retrieved from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1655541/.

[579] Ibid.

[580] Porte Jr., Daniel, et al. (May 3, 1996). “Diabetes Complications—Why Is Glucose Potentially Toxic?”

Science Vol. 272 no. 5262 p. 699  DOI: 10.1126/science.272.5262.699. Retrieved from: http://www.sciencemag.org/content/272/5262/699.

[581] Taubes, Gary. (2010). “Why We Get Fat, and What to Do About It.” New York: Anchor Books. Pg. 176-178.

[582] Leff, Todd, & James. G. Grannerman. (). “Adipose Tissue in Health and Disease.” Wiley Publishers: , pg. xix-xixi, 98, 143-152.

[583] Taubes, Gary, “Good Calories, Bad Calories,” 2007. New York: Knopf Publishing. pg. 393-395.

[584] Taubes, Gary. (2010). “Why We Get Fat, and What to Do About It.” New York: Anchor Books. Pg. 118-121.

[585] Goodman, H. Maurice. (2009). “Basic Medical Endocrinology: Adipogenesis.” Academic Press, Fourth Edition.  Pg. 165. Retrieved from: http://books.google.com/books?id=gjpi2MYVKGAC&pg=PA165&dq=insulin+AND+adipocyte&hl=en&sa=X&ei=CVtJT7XVIsWatwent7TyAg&ved=0CEkQ6AEwAg#v=onepage&q=insulin%20AND%20adipocyte&f=false.

[586]  Pg. 378-380.

[588]  Pg. 274, 362.

[589]  Pg. 372.

[590] Taubes, Gary. (2010). “Why We Get Fat, and What to Do About It.” New York: Anchor Books. Pg. 106-126.

[591] Bjorntorp, P. (April 20, 1996). “The regulation of adipose tissue in humans.” International Journal of Obesity and Related Metabolic Disorders, Vol. 20(4), pg. 291-302. Retrieved from: http://www.ncbi.nlm.nih.gov/pubmed/8680455.

[592] Leff, Todd, & James. G. Grannerman. (). “Adipose Tissue in Health and Disease.” Wiley Publishers: , pg. xix-xixi, 98, 143-152.

[593]  Pg. 378-380.

[594] Lustig, Robert H. (2009). “Sugar: The Bitter Truth,” Youtube. Retrieved from http://www.youtube.com/watch?v=dBnniua6-oM

[595] Lustig, Robert H. (2009). “Sugar: The Bitter Truth,” Youtube. Retrieved from http://www.youtube.com/watch?v=dBnniua6-oM

[596] Taubes, Gary, “Good Calories, Bad Calories,” 2007. New York: Knopf Publishing. Pg. 200-201.

[597] [597] Malik, et al Circulation. (2010). Sugar-Sweetened Beverages, Obesity, Type 2 Diabetes Mellitus, and Cardiovascular Disease Risk.” Circulation, Vol. 121, pgs. 1356-1364.  Retrived from: http://circ.ahajournals.org/content/121/11/1356.full.pdf+html .

[598] Seneff, Stephanie, Wainwright, Glyn, & Luca Mascitelli. (Feb. 7, 2011). “Is the metabolic syndrome caused by a high fructose, and relatively low fat, low cholesterol diet?” Archives of Medical Science, Vol. 7(1), pgs. 8-20. Retrieved from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3258689/pdf/AMS-7-1-8.pdf

[599] Stanhope, Kimber L., et al. (May, 2009). “Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans.” The Journal of Clinical Investigation, Vol. 119, Number 5, pgs. 1322- . Retrieved from: http://www.jci.org/articles/view/37385.

[600] Mayes, Peter. (1993). “Intermediary metabolism of fructose.” American Journal of Clinical Nutrition, Vol. 58 (5), pgs. 7545-7655. Retrieved from: http://www.ajcn.org/content/58/5/754S.full.pdf.

[601] Dekker, Mark J., et al. (May 10, 2010). “Fructose: a highly lipogenic nutrient implicated in insulin resistance, hepatic steatosis, and the metabolic syndrome.” American Journal of Physiology, Vol. 299 (5), pgs. 685-694. Retrieved from: http://ajpendo.physiology.org/content/299/5/E685.long#ref-94. Figure 1: http://ajpendo.physiology.org/content/299/5/E685/F1.expansion.html.

[602] Seneff, S., Wainwright G., and L. Mascitelli. (Feb. 7, 2011). “Is the metabolic syndrome caused by a high fructose, and relatively low fat, low cholesterol diet?” Archives of Medical Science, Vol. 7(1), pgs. 8-20. Retrieved from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3258689/pdf/AMS-7-1-8.pdf.  Figure 1: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3258689/figure/F1/.

[603] Taubes, Gary. (2010). “Why We Get Fat, and What to Do About It.” New York: Anchor Books. Pg. 138.

[604] US. Dept. of Health and Human Services, NIDDK, National Diabetes Information Clearinghouse (Dec. 6, 2011). “Insulin Resistance and Prediabetes.” Retrieved from: http://diabetes.niddk.nih.gov/dm/pubs/insulinresistance/ .

[605] Lustig, Robert H. (2009). “Sugar: The Bitter Truth,” Youtube. Retrieved from http://www.youtube.com/watch?v=dBnniua6-oM

[606] Taubes, Gary, “Good Calories, Bad Calories,” 2007. New York: Knopf Publishing. Pg. 200-201.

[607] [607] Malik, et al Circulation. (2010). Sugar-Sweetened Beverages, Obesity, Type 2 Diabetes Mellitus, and Cardiovascular Disease Risk.” Circulation, Vol. 121, pgs. 1356-1364.  Retrived from: http://circ.ahajournals.org/content/121/11/1356.full.pdf+html .

[608] Seneff, Stephanie, Wainwright, Glyn, & Luca Mascitelli. (Feb. 7, 2011). “Is the metabolic syndrome caused by a high fructose, and relatively low fat, low cholesterol diet?” Archives of Medical Science, Vol. 7(1), pgs. 8-20. Retrieved from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3258689/pdf/AMS-7-1-8.pdf

[609] Stanhope, Kimber L., et al. (May, 2009). “Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans.” The Journal of Clinical Investigation, Vol. 119, Number 5, pgs. 1322- . Retrieved from: http://www.jci.org/articles/view/37385.

[610] Mayes, Peter. (1993). “Intermediary metabolism of fructose.” American Journal of Clinical Nutrition, Vol. 58 (5), pgs. 7545-7655. Retrieved from: http://www.ajcn.org/content/58/5/754S.full.pdf.

[611] Lustig, Robert H. (2009). “Sugar: The Bitter Truth,” Youtube. Retrieved from http://www.youtube.com/watch?v=dBnniua6-oM

[612] Taubes, Gary, “Good Calories, Bad Calories,” 2007. New York: Knopf Publishing. Pg. xxiii, 152, 180-183, 394-397.

[613] Taubes, Gary. (2011, April 13). “Is Sugar Toxic?” The New York Times. Retrieved from http://www.nytimes.com/2011/04/17/magazine/mag-17Sugar-t.html?scp=1&sq=is%20sugar%20toxic?&st=cse

[614] Wells, JC, & Siervo M. (2011). Obesity and energy balance: is the tail wagging the dog? European Journal of Clinical Nutrition.  Retrieved from http://www.ncbi.nlm.nih.gov/pubmed/21772313 doi: 10.1038/ejcn.2011.132

[615] Ibid of 635-644.

[616] US. Dept. of Health and Human Services, NIDDK, National Diabetes Information Clearinghouse (Dec. 6, 2011). “Insulin Resistance and Prediabetes.” Retrieved from: http://diabetes.niddk.nih.gov/dm/pubs/insulinresistance/ .

[617] Ervin, R. Bethene. The Centers for Disease Control and Prevention, National Health Statistics Report. (May 5, 2009). “Prevalence of Metabolic Syndrome Among Adults 20 Years of Age and Over, by Sex, Age, Race and Ethnicity, and Body Mass Index: United States, 2003–2006.”  Number 13. Retrived from: http://www.cdc.gov/nchs/data/nhsr/nhsr013.pdf .

[618] Reaven, G.M. (June, 2005). “The Metabolic Syndrome: Requiscat in Pace.” Clinical Chemistry, Vol. 51 no. 6, pgs. 931-938. Retrieved from: http://www.clinchem.org/content/51/6/931.full.

[619] U.S. Dept. of HHS, National Library of Medicine, Medline Plus. (March 13, 2012). “Obesity.” Retrieved from: http://www.nlm.nih.gov/medlineplus/obesity.html.

[620] WHO. (2011). “Media centre: Obesity and overweight.” Retrieved from: http://www.who.int/mediacentre/factsheets/fs311/en/.

[621] The Centers for Disease Control and Prevention (2011). Overweight and Obesity: Defining Overweight and Obesity. Retrieved from: http://www.cdc.gov/obesity/causes/index.html

[622] American Heart Association. (May 5, 2011). “Obesity Information.” Retrieved from: http://www.heart.org/HEARTORG/GettingHealthy/WeightManagement/Obesity/Obesity-Information_UCM_307908_Article.jsp#.T0e_ZPF5F8E.

[623] Larry King Live. (Oct. 19, 2007). “2 of 2 Gary Taubes on Larry King Live 10/19/2007.” Youtube. Retrieved from: http://www.youtube.com/watch?v=5LNH0RPXI0M.

[624] NIH, NHBLI. (Nov. 1, 2010). “What Causes Overweight and Obesity?” Retrieved from: http://www.nhlbi.nih.gov/health/health-topics/topics/obe/causes.html.

[625] US Dept of HHS, US Public Health Service. (2010). “The Surgeon General’s Vision for a Healthy and Fit Nation.” Retrieved from: http://www.surgeongeneral.gov/library/obesityvision/obesityvision2010.pdf.

[626] National Heart Lung and Blood Institute, National Institutes of Health. (2012). “Balance Food and Activity: What is Energy Balance?” Retrieved from: http://www.nhlbi.nih.gov/health/public/heart/obesity/wecan/healthy-weight-basics/balance.htm

[627] Taubes, Gary. (2010). “Why We Get Fat, and What to Do About It.” New York: Anchor Books. Pg. 106-111.

[628] Wikipedia. “Tautology(logic).” Retrieved from: http://en.wikipedia.org/wiki/Tautology_%28logic%29.

[629] The Centers for Disease Control and Prevention (2011). Overweight and Obesity: Defining Overweight and Obesity. Retrieved from: http://www.cdc.gov/obesity/defining.html

[630] The World Health Organization (2011).  BMI Classification. Retrieved from: http://apps.who.int/bmi/index.jsp?introPage=intro_3.html

[631] NIH, NIDDK, Weight Control Information Network, “Understanding Adult Obesity,” November 2008. Retrieved from http://win.niddk.nih.gov/publications/understanding.htm#measured .

[632] Sommers, Andrew R. “Obesity Among Older Americans.” February 20, 2009. Congressional Research Service. Retrieved from: http://aging.senate.gov/crs/aging3.pdf

[633] Braverman, Eric R., & Nirav R. Shah. (April 2, 2012). “Measuring Adiposity in Patients: The Utility of Body Mass Index (BMI), Percent Body Fat, and Leptin.” PlosOne. Retrieved from: http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0033308.

[634] St-Onge, Marrie-Pierre, et al. (2004). “Dual-Energy X-Ray Absorptiometry-Measured Lean Soft Tissue Mass: Differing Relation to Body Cell Mass Across the Adult Life Span.” Journal of Gerontology: Series A, Vol. 59 (8), pgs. B796-B800. doi: 10.1093/gerona/59.8.B796. Retrieved from: http://biomedgerontology.oxfordjournals.org/content/59/8/B796.full.

[635] Braverman, Eric R., & Nirav R. Shah. (April 2, 2012). “Measuring Adiposity in Patients: The Utility of Body Mass Index (BMI), Percent Body Fat, and Leptin.” PlosOne. Retrieved from: http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0033308.

[636] The Centers for Disease Control and Prevention (2011). Overweight and Obesity: Basics about Childhood Obesity.” Atlanta, GA. Retrieved from: http://www.cdc.gov/obesity/childhood/basics.html.

[637] US Dept of HHS, NIH, National Institute of Diabetes and Digestive and Kidney Diseases. (October 2008). “Diagnosis of Diabetes.” Retrived from: http://diabetes.niddk.nih.gov/dm/pubs/diagnosis/#types .

[638]  201.

[639] Ibid.

[640] Dekker, Mark J., et al. (May 10, 2010). “Fructose: a highly lipogenic nutrient implicated in insulin resistance, hepatic steatosis, and the metabolic syndrome.” American Journal of Physiology, Vol. 299 (5), pgs. 685-694. Retrieved from: http://ajpendo.physiology.org/content/299/5/E685.long#ref-94. Figure 1: http://ajpendo.physiology.org/content/299/5/E685/F1.expansion.html.

[641] Stanhope, Kimber L., et al. (May 25, 2011). “Metabolic responses to prolonged consumption of glucose- and fructose-sweetened beverages are not associated with postprandial or 24-h glucose and insulin excursions“American Journal of Clinical Nutrition. doi: 10.3945/ajcn.110.002246.. Retrieved from: http://www.ajcn.org/content/early/2011/05/19/ajcn.110.002246.full.pdf.

[642] WHO. (1999). “Definition, Diagnosis and Classification of Diabetes Mellitus and its Complications.” Retrieved from: http://www.staff.ncl.ac.uk/philip.home/who_dmc.htm.

[643]  Pg. 100-101.

[644] US Dept of HHS, NIH, National Institute of Diabetes and Digestive and Kidney Diseases. (October 2008). “Diagnosis of Diabetes.” Retrived from: http://diabetes.niddk.nih.gov/dm/pubs/diagnosis/#types .

[645] WHO. (2011). “Use of Glycated Haemoglobin (HbA1c) in the Diagnosis of Diabetes Mellitus: Abbreviated Report of a WHO Consultation.”  Retrieved from: http://www.who.int/diabetes/publications/report-hba1c_2011.pdf.

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One thought on “Insulin Resistance and the Diabesity Epidemic

  1. Pingback: Shadowing a Diabetes Doctor, or, You are what your hormones decide you are – May 24, 2012 « Rob Roy's Adventures in Public Health Land!

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