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Dietary Consumption of Excess Free Fructose is Linked to Asthma, Chronic Bronchitis, COPD, Auto-immune Disease.

What is Cheap Sweet Sick?

It is the PLAIN LANGUAGE TRANSFORMATION of a scientific research project elucidating what is known about fructose, high fructose corn syrup (HFCS) and the link to hypertension, metabolic syndrome, diabetes, obesity, abdominal weight gain, auto-immune reactivity, lung disease, and asthma. While laboratory studies have linked HFCS to diabetes and hypertension, the links to chronic lung, and auto-immune reactivity remain medically unrecognized. The book explores the science of how consumption of a high fructose diet, and HFCS may be able to trigger incidence of chronic bronchitis, asthma, and auto-immune reactivity by modifying dietary proteins. The easy-to-read book by L.R.D. Christopher, MS Biochemistry & Molecular Biology represents the culmination of several years of study and research on the topic of a high fructose diet and HFCS as an immunogen. It's also the personal story of parents who learn of the link after experimenting with a rigorous HFCS elimination diet in their 3 year old more than 15 years ago. Driven by the goal to shatter conventional wisdom that fructose and HFCS is not associated with auto-immune reactivity, and chronic lung disease, the author (and parent) embarks on a journey transforming from business executive and technologist to biochemist and molecular biologist.

Who Should Read This Book?

The book is a must read for anyone suffering from idiopathic (arising from an unknown cause) asthma, chronic lung, or auto-immune disease. It is of particular relevance for parents of kids with these conditions. The book is a must read for anyone interested in being able to separate fact from fiction about this ubiquitous sweetener. What has been pouring out of the scientific community about the adverse effects of high fructose corn syrup on health is the focus of this book and it is nothing short of startling.

Excerpts From the Upcoming Book

... Compelling case reports link high dietary fructose and HFCS to cough associated chronic bronchitis and asthma.[3] These reports are alarming when considered in the context of the significant and parallel increases in HFCS consumption and escalating asthma rates occurring in the US. They in fact point to the possibility of a national health crisis that has remained off the medical and scientific radar.

... The numbers relating to both trends are staggering. Asthma, which has been steadily increasing in prevalence in the United States since 1980 affects an estimated 25.7 million people, including approximately 7.1 million children.[39] This dramatic rise in asthma coincides with US HFCS consumption, a trend not typically discussed in the context of rising rates of asthma and auto-immune disease. In fact when both trends are over laid as can be seen in the table below, they track in parallel.

... According to USDA reports, in 1980, annual per capita consumption of HFCS was 16.9 pounds; by 1999 it had grown to 56.7 pounds - a dramatic rise from 1980 levels. By 1999 Americans were consuming more than a dry pound per week of HFCS. While current levels are off slightly, likely due to scientific research linking HFCS to obesity and diabetes related metabolic syndrome, the rise in average per capita consumption of this highly processed sweetener is stunning.

... As large as these numbers are, they may be dwarfed as similar data relating to auto-immune diseases are considered.

Connecting the Dots

... Since HFCS has been ubiquitous in the food supply since the early 1980's, why hasn't its immunogenicity been identified and characterized in the scientific literature to date?

... A number of reasons may be contributing to this lack of awareness and why this link has remained below the medical community's radar for so long. The first and foremost reason is the general consensus that most often proteins are implicated as food "allergens" or "immunogens", not sugars. What's been overlooked is the potential for modification of dietary proteins by high fructose levels in the digestive tract of fructose malabsorbers. Once modified by fructose, these digestion resistant fragments are thought to become absorbed into the body and elicit the immune responses observed.[3]

... to assess a child's sensitivity to a food requires its elimination from the child's diet. This is extremely challenging to do in the case of CS/ HFCS due to its ubiquitous presence in the U.S. food supply over the past 20 to 30 years. It is not just present in “snack” foods like cookies, candy and soda, which would make the elimination task more “family friendly”, rather, it is a staple additive in an overwhelming number of foods that parents would otherwise consider nutritious and wholesome, including a majority of breads, and breakfast cereals. Elimination of CS/ HFCS relegates families to very limited choices in entire food categories.

... It is easy to understand that the symptoms associated with “fructositis” can be masked, and misdiagnosed as frequent colds, and recurrent flu, bronchitis and unrelated aero-allergen triggered asthma.

... A diet free of CS/ HFCS is not only difficult to achieve, it can be considerably more expensive given the higher prices for CS/ HFCS free packaged foods now available in specialty grocers. These choices are often unaffordable and therefore less accessible to lower income families.

... Entrenched financial interests are often difficult to overturn.... According to senior analyst Moskow from Credit Suisse, industry revenue from HFCS has been steady at $3 billion to $4 billion a year. The five HFCS manufacturers in the U.S are Archer Daniels Midland Inc., Corn Products International, Cargill, Roquette America, and Tate & Lyle.

... While we enjoy lower food prices in part due to US subsidies to corn growers and because less fructose is needed to achieve the same sweetness as regular sugar, we are paying more in healthcare. According to EPA estimates, the current annual direct health care cost of asthma is estimated at $50.1 billion. That translates into expenditures of about $30 per person [with asthma] per week for asthma related care.

... Even so, the steps to undo our systemic use of HFCS, America's premiere sweetener, may be more difficult than meets the eye. Its ubiquitous use continues despite the controversy that already surrounds it due to it's conclusive link to diabetes and metabolic syndrome.[41] [42] [43] It has already and will likely continue to test our corporate and legislative moral conscience. In fact, the American story of the adverse affects on health due to consumption of high levels of fructose may be just beginning.

The Link To Fructose Malabsorption

....Fructose Malabsorption is believed to be at the root of Fructositis disease.[3] This is concerning given that scientific research available to date indicates that conservatively 12% to 30% or higher of “healthy” adults are fructose malabsorbers, but scant research has been done in children. What research is available suggests children are at significantly higher risk of being fructose malabsorbers, with rates in children potentially as high as 44% [20] [9] [10]

... A review of the studies that have been done suggest many of us malabsorb fructose when its consumed in excess of glucose as occurs with HFCS. As we will see in more depth in the following pages, research conducted during the 1980’s and 1990’s by various research groups, including the venerable University of California at Berkely, indicates that more than 30% of “healthy” adults are fructose malabsorbers when consuming fructose in excess of glucose [20] at rates reflective of the western diet (60 grams – 100 grams daily) [27].

You need to eat 8 to 10 apples daily to equal the 100 grams of HFCS per capita consumption in the US

... In order to understand the meaning of these experiments it is important to gain a sense of the relative rates of fructose versus glucose in the average American daily diet and to be able to calculate “excess-free-fructose” and the ratio of daily fructose to glucose monomers consumed. The significance of knowing these numbers becomes clearer during the review of mechanisms of sugar transport in the pages ahead.

... Most UNPROCESSED, natural foods that are high in fructose are also known to have equivalent amounts of glucose. Only a few foods that might make it onto the daily short list of staples stand out as exceptions. These include apples, and watermelons [33].

... At approximately 4 grams of “excess-free-fructose” per average sized apple, the average consumer would need to eat 8 - 10 apples per day to consume the amount of excess-free-fructose in the 100 daily grams of HFCS presently being taken in primarily from processed foods mostly in the form of HFCS. How likely is that? Not likely...

... that there is a significant relationship between fructose malabsorption and fructose dose. Of importance to note is that these studies suggest that fructose when consumed in equal proportion to glucose, triggers little to no malabsorption. On the other hand, when fructose is consumed in proportions that are greater than glucose, as occurs during consumption of HFCS, researchers report that 10% to 30% of healthy adults experience fructose malabsorption as measured by the hydrogen breath test. In some test groups rates were as high as 70%.[5][20][21][22]

HFCS, The "Corn Sugar", is Not "Just Like Table Sugar".

Claims by the Corn Refiners Association that HFCS, ... "Like table sugar,... is roughly half glucose and half fructose and is metabolized by the body in the same way as regular table sugar", is misleading and fails to consider absorption, or more specifically - excess-free-fructose malabsorption.

... Claims by the Corn Refiners Association that HFCS, ... "Like table sugar,... is roughly half glucose and half fructose and is metabolized by the body in the same way as regular table sugar", is misleading. These claims neglect to consider scientific research that is in conflict with this assertion. First, excess free fructose as occurs in HFCS has been shown to transport differently than sucrose.[8][13][14][15]Think customized tunnels from the inside of your gut to the other side, one for fructose and glucose as partners, and one for excess-free-fructose. Second, fructose malabsorption occurs at high rates when fructose is consumed in high proportion relative to glucose as is the case with HFCS. No malabsorption of fructose occurs in adults when it is consumed in equal proportion to glucose as happens with consumption of table sugar (sucrose).[20][21][22][5] The exception to this rule is observed in children who exhibit symptoms of malabsorption even when consuming fructose and glucose in equal proportion.[9][10] The exact reasons why some people are fructose malabsorbers and others are not remains unknown. Third, food elimination methods have linked high fructose and HFCS, not sugar, to chronic bronchitis and asthma.[3]

... The Annual American Society for Nutrition Public Information Committee Symposium for 2007... neglected to consider research which clarifies how these two sweeteners are absorbed and taken up within the Gastrointestinal Tract (Fulgoni 2008). Despite their apparent similarity, these two sweeteners are transported differently in the small intestine[8][13][14][15]. This physiological distinction is the key to understanding why consumption of sucrose, a disaccharide of fructose and glucose, does not elicit the same adverse reaction as does fructose when consumed in excess of glucose.

...At approximately 4 grams of “excess-free-fructose” per average sized apple, the average consumer would need to eat 8 - 10 apples per day to consume the 100 grams estimate in the 65% fructose formula that independent labs have measured in HFCS containing foods they tested. How likely is that? Not likely...

... Findings indicate that there are separate and distinct pathways for absorption of fructose consumed in excess of glucose versus fructose consumed in equal proportion to glucose as would occur during consumption of sucrose (a disaccharide with digestion products of equal amounts of glucose and fructose). Any excess fructose is absorbed via GLUT5, whereas co-transport of fructose and glucose occurs via GLUT2.[8][13][14][15]

Aergy Or Auto-Immune?

...During the past five or six years there has been a significant amount of human diseases related research involving a pro-inflammatory cell receptor associated with inflammation known as RAGE (acronym for Receptor [for] Advanced Glycation End-products).

...Research shows that the lungs, ears and heart are the human tissues known to have the highest concentrations of RAGE [2] In 2011, researchers provided definitive proof that the same digestion resistant protein fragments believed to be modified by fructose and formed in the digestive tract of malabsorbers bind RAGE.[40]

... When bound, RAGE signaling is associated with inflammation, mucus hypersecretion, airway hyperreactivity, and chronic lung diseases.[18]

... ... These receptors, A.K.A. RAGE are not only thought to be elevated and play a significant role in the pathology of Fructositis disease, they are known to be elevated in pulmonary disorders [18]; including neutrophilic asthma and Chronic Obstructive Pulmonary Disease COPD[29], lung cancer and fibrosis.[2]They are also elevated in systemic Lupus Erythematosus also known as(SLE) or Lupus[26]; Rheumatoid Arthritis (RA)[7][16][30]; Irritable Bowel Syndrome (IBS), Inflammatory Bowel Disease (IBD)[6]; Atherosclerosis, heart disease, and congestive heart failure; peripheral vascular diseases, also known as PVD[30][16]; ulcerative colitis and Crohn's[31]; Psoriasis [28]; Alzheimer's disease [11][16][30]; diabetic retinopathy, neurophathy, and nephropathy [16][30], and others. The question that arises from these observations is whether Fructositis disease is merely a side bar in the Etiology of a man-made Metabolic Syndrome II.

... A common observation between diabetics and fructose malabsorbers is the increased concentrations of reactive sugars. Yet, the environment and physiological conditions that set the stage for the reaction that structually modifies proteins differs markedly in fructose malabsorbers versus long-term diabetics and advanced renal disease patients. In fact, GI conditions appear more conducive to the reaction. This dictates the need for new strategies in research.[38]