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Fructositis Disease
In 2011 L.R. Christopher coined the term "Fructositis" and describes it in a scientific paper titled, “Consumption of Fructose and High Fructose Corn Syrup: Is Fructositis triggered bronchitis, asthma, & auto-immune reactivity merely a side bar in the Etiology of Metabolic Syndrome II (to be defined)? – Evidence and a Hypothesis.”. (Where is this published???) Christopher cites incidence of chronic bronchitis and asthma associated with consumption of HFCS and a high fructose diet by fructose malabsorbers. The link was originally discovered after a comprehensive and rigorous food elimination diet in a chronically ill three year old. The paper elucidates a viable hypothesis and biochemical mechanism to explain the association between high dietary fructose, HFCS, and incidence of respiratory mucus hypersecretion, chronic bronchitis, asthma, and auto-immune reactivity.

When aberrant food proteins bind RAGE, they may trigger a cascade of symptoms including mucus hypersecretion, cough, fever, inflamed tonsils, and airway hyper-reactivity that often leads to chronic bronchitis, allergic rhinitis, ear infections and, most notably, asthma.

Among individuals who inadequately absorb high levels of dietary fructose, a biochemical pathway is thought to occur that gives rise to the formation of biomolecules, known as Fru-AGE, from the interaction of food proteins with fructose inside the digestive tract. Similar biomelecules known as Advanced Glycation End-products (AGE) have been studied extensively in the context of high glucose levels, diabetes, aging, and a variety of disease states. However, no research has been done to date that explains the link between consumption of a high fructose diet, HFCS and asthma. The chemical reaction thought to occur in the intestines of fructose malabsorbers structurally changes the food proteins, causes them to resist breakdown by digestive enzymes, and alters normal patterns of digestion. No longer able to be broken down and absorbed as typical nutrients, it is thought that these biomolecules gain access to the lymphatics and circulation of those at risk. A receptor for these chemically altered proteins is known to exist in high concentration in the human lung, where it has been implicated in lung tissue inflammation. When the abberant food proteins bind the receptor, they may trigger a cascade of pro-inflammatory symptoms including mucus hypersecretion, cough, fever, inflamed tonsils, and airway hyper-reactivity that often leads to chronic bronchitis, allergic rhinitis, ear infections and, most notably, asthma.

The Link to Malabsorption
Fructose Malabsorption is believed to be at the root of Fructositis disease. Scientific research available to date indicates that 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%.

Research regarding the difference in intestinal transport routes taken by fructose when consumed in equal amounts to glucose versus excess free fructose as occurs with HFCS offers a link to how fructose malabsorption and fructositis disease may be related. Findings by researchers that GLUT2 is the co-transporter of equal amounts of glucose and fructose, whereas GLUT5 is the transporter of excess "free" fructose   is significant because it provides a possible explanation and mechanism as to why consumption of high fructose elicits symptoms of fructose malabsorption and fructositis disease whereas consumption of sucrose does not. While GLUT5 deficiencies may contribute to fructose malabsorption and possibly fructositis disease, the exact mechanisms of both remain unknown.

The fructositis hypothesis links the dramatic increases in rates of asthma amongst school aged, preschool and specifically black children since 1980 (Asthma and Allergy Foundation of America (AAFA)), , to the concomitant shift from sugar to HFCS. While the link between aero-allergens and asthma has been studied extensively and is well characterized, such is not the case with the association between food allergy and asthma. Mechanisms that relate the two are not well understood. Yet according to the CDC, in 2007, 29% of children who had a food allergy also had asthma. These rates continue to climb despite significant and steady improvements in air quality.

Allergy or Autoimmune?
The cell receptor believed to be implicated in Fructositis disease is also known to be elevated in many autoimmune diseases. The receptor known as RAGE (an acronym for Receptor [for] Advanced Glycation End-products) is not only known to be elevated in pulmonary disorders including neutrophilic asthma and Chronic Obstructive Pulmonary Disease COPD, lung cancer and fibrosis , it is also elevated in a host of auto-immune diseases including Lupus Erythematosus (SLE) , Rheumatoid Arthritis (RA) , Irritable Bowel Syndrome (IBS), Inflammatory Bowel Disease (IBD) , Atherosclerosis , ulcerative colitis and Crohn's , Psoriasis and other auto-immune disorders.