Case reports have linked consumption of a high fructose diet, high fructose corn syrup (HFCS), and fructose malabsorption, with auto-immune reactivity, respiratory mucus hypersecretion, chronic bronchitis, and asthma.
When fructose modified food proteins bind RAGE, they may trigger a cascade of auto-immune reactions including mucus hypersecretion, cough unassociated with a cold or flu, fever, inflamed tonsils, and airway hyper-reactivity that often leads to chronic bronchitis, allergic rhinitis, ear infections and, most notably, asthma.In 2011 L.R.D. Christopher coined the term "Fructositis" and describes it in a 2012 scientific paper titled, “...HFCS [and] the Etiology of Metabolic Syndrome II...– Evidence and a Hypothesis”. The paper elucidates a viable hypothesis and biochemical mechanism to explain the association between high dietary fructose, HFCS, and auto-immune reactivity. In 2012, faculty researchers at New York Medical College in biochemistry and immunology confirmed the scientific merits of the hypothesis. Symptoms associated with the disease include a peculiar cough that often lasts through the night and is not associated with a cold or flu; mucus hypersecretion of the airways; airway hyper-reactivity; chronic bronchitis; asthma; eustachian tube dysfunction; otitis media; chronically enlarged and inflamed tonsils; and gastrointestinal distress, gas and abdominal discomfort.
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 and 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 food proteins. Once modified, dietary proteins are thought to resist breakdown by digestive enzymes. Normal patterns of digestion are thereby altered.
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 lungs, where it has been implicated in lung tissue inflammation and atypical pneumonitis.. When these abberant food proteins bind this receptor, 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.
One mission of Fructositis.org is to raise awareness of this high fructose triggered auto-immune disease and to raise funds for scientific research. At the present time, the disease is not recognized by the medical community. The published case history and case report and other known cases provide evidence of immune reactivity to HFCS. Aside from an early onset dry cough, the symptoms do not follow patterns most often associated with food borne allergies. The symptoms observed are more often associated with aero-allergens as described, including bronchial mucus hyper-secretion, low grade fever, airway hyper-reactivity, bronchitis triggered asthma, chronic bronchitis, wheezing, allergic rhinitis, eustachian tube dysfunction and inner ear infections. Factors contributing to why HFCS has remained an unknown “immunogen” to date include
Food elimination is a recognized scientific method in food immunogen diagnosis. Given the ubiquitous presence of HFCS in the food supply, elimination is difficult to achieve.
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 (as exists in HFCS) is significant because it provides a possible explanation and mechanism as to why consumption of high fructose [and HFCS] elicit symptoms of fructose malabsorption and fructositis disease whereas consumption of sucrose [regular sugar] does not. While GLUT5 deficiencies may contribute to fructose malabsorption and possibly fructositis disease, the exact mechanisms of both remain unknown.
Given the high rates of fructose malabsorption, and the lack of information available on HFCS immunogenicity, research into fructositis disease is long overdue.
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.
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. Research is clearly needed. Learn about our different awareness campaigns and how you can help support Fructositis disease research.