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The Consequences of Undiagnosed Fructose Malabsorption:

A Hypothesis

Case report evidence and existing epidemiology studies have linked fructose malabsorption and consumption of excess free fructose (EFF) and HFCS, with auto-immune reactivity, respiratory mucus hypersecretion, chronic bronchitis, and asthma.

In 2011 L.R.DeChristopher 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 EFF, HFCS, and auto-immune reactivity.[3] 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 not associated with a cold or flu that often persists through the night; mucus hypersecretion of the airways; airway hyper-reactivity; chronic bronchitis; asthma; eustachian tube dysfunction; frequent ear infections; and chronically enlarged and inflamed tonsils. Gastrointestinal distress, gas and abdominal discomfort sometimes precede these symptoms.

The Body:

An Interactive Diagram

img:Fructositis/body intestines stomach smallintestine liver

A Possible Biochemical Mechanism for Fructositis

Among individuals who inadequately absorb excess free fructose, a biochemical pathway is thought to occur that gives rise to the formation of biomolecules, known as FruAGE, from the interaction of food proteins with unabsorbed 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 other disease conditions.[38][41-42]However, no research has been done to date that explains the link between consumption of EFF, HFCS and asthma/ chronic bronchitis/ auto-immune reactivity. 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 normally broken down, these biomolecules are thought to become absorbed into the blood stream of those at risk. A receptor for these fructose modified dietary proteins is known to exist in high concentration in the lungs, where it has been implicated in lung tissue inflammation and atypical pneumonitis.[18]. When these abberant food proteins bind this receptor, they may trigger a cascade of symptoms including airway mucus hypersecretion, cough, fever, inflamed tonsils, and airway hyper-reactivity that often leads to chronic bronchitis, allergic rhinitis, ear infections and, most notably, asthma.[40]

Raising Awareness

One mission of is to raise awareness of excess free fructose associated lung and auto-immune disease and to raise funds for scientific research. The published case history and case reports 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, 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.

The Hidden Immunogenicity of EFF and HFCS

  • The medical community predominantly focuses on native proteins in food allergens
    including peanut, tree nuts, crustacean shellfish, cow's milk, hen's egg, wheat and soy
  • Aggressive advertising by the corn refining industry
    promotes the claim that HFCS is "just like sugar"
  • Factors contributing to why EFF and HFCS are not recognized as immunogens
  • Conventional wisdom is that aero-allergens trigger respiratory symptomology
    not foods, and particularly not sugars
  • The ubiquitous presence of a food such as HFCS
    makes adherence to a food elimination diet difficult, and makes its discovery as an immunogen improbable

The Link to Malabsorption

Why HFCS is not "just like sugar"

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 greater risk of being fructose malabsorbers.[9-10][20][54-55]

Food elimination is a recognized scientific method in food immunogen diagnosis. Given the ubiquitous presence of HFCS in the food supply, dietary elimination is difficult to achieve.

There are differences in how excess free fructose is absorbed as compared with fructose that has been consumed as sucrose or in equal proportion to glucose. This body of research offers a possible explanation for how fructose malabsorption, excess free fructose, HFCS 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 occurs in HFCS and apple juice products)[8][13-15][47] is significant because it provides a possible explanation and mechanism as to why consumption of EFF and HFCS elicit symptoms of fructose malabsorption and fructositis disease whereas consumption of sucrose [aka table sugar] does not.

Existing research indicates fructose malabsorption is under-recognized and under-diagnosed. This suggests individuals and families are left to try to make sense of their symptoms by themselves. Recent epidemiology studies show their is a strong statistical association between EFF consumption and asthma. Research of EFF's and HFCS' immunogenicity is long overdue.


The fructositis hypothesis links the dramatic increases in rates of asthma amongst school aged, preschool and non-Hispanic black and Puerto Rican children since 1980 (Asthma and Allergy Foundation of America (AAFA)),[1][4][34] to the concomitant shift from sugar to HFCS.[35]

Low income is also significantly associated with the epidemic rise in childhood asthma rates. This is of no surprise since value driven meals often contain high levels of HFCS. Notably, asthma rates continue to climb despite significant and steady improvements in air quality.

The Systemic Impact of Fructositis

Lung Immunogen, Broader Autoimmune Antigen or Both?

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 [of] Advanced Glycation End-products) is not only known to be elevated in pulmonary disorders[18] including neutrophilic asthma and Chronic Obstructive Pulmonary Disease COPD,[29] lung cancer and fibrosis,[2] it is also elevated in a host of auto-immune diseases including Lupus Erythematosus (SLE),[26] Rheumatoid Arthritis (RA),[7] Irritable Bowel Syndrome (IBS), Inflammatory Bowel Disease (IBD),[6] Chronic Fatigue Syndrome, Atherosclerosis,[30] [16] Ulcerative Colitis and Crohn's,[31] Psoriasis [28] and other auto-immune disorders. Learn about our different awareness campaigns and how you can help support Fructositis disease research.