What Causes Cystic Fibrosis?

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Marvin Whiteley is a professor of molecular biosciences at The University of Texas at Austin. I don’t know Dr Whiteley, but I admire his passion when trying to figure out the cause of Cystic Fibrosis (CF). In 2015, an article referring to Dr. Whiteley’s CF work, appearing on Science Daily, caught my attention. CF, it stated, is a genetic disease that causes recurrent lung infections. 


These lung infections are treated with antibiotics in an effort to kill bacterium that has been isolated from the mucous in the lungs of CF patients, called P. aeruginosa. The problem is that the bacteria are now resistant to the antibiotics used to treat it. So Dr Whiteley’s suggested that researchers might find a way to manipulate genes, by turning them off in CF sufferers. Perhaps I may assist his research.

“Fungal mycotoxins are well-studied and documented as inducing DNA mutations”

First, what led to the DNA mutation that led to the CF diagnosis? Fungal mycotoxins are well-studied and documented as inducing DNA mutations. 
Recent research has made a relevant discovery. These bacterial colonies of P. aeruginosa grow in biofilms (think of scotch tape). Few doctors know that fungal biofilms also exist, so fungal biofilm diseases are likely often treated with antibiotics. 

I’ve long believed that treating fungal infections with antibiotics, (penicillium is the fungus and the mycotoxin it makes is called penicillin), creates antifungal resistant strains of fungus and since the infective agent is not bacteria, leads to antibiotic resistance as well.

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As it turns out, a protein made by these P. aeruginosa bacteria called “Pyocyanin” might have proven my point. Pyocyanin is known to inhibit the growth of P. aeruginosa, but it has a property that doctors are likely unaware of. Pyocyanin is an antifungal agent.

Might fungal infections be causing CF? Some CF patients suffer from a concomitant lung fungal condition known as allergic bronchopulmonary aspergillosis, or ABPA. In 2010, the International Journal of Pediatrics discovered that in 6 of 7 study children with ABPA, 6 were relieved of CF, without the use of cortisone for over a year, when they used the antifungal agent, Amphoterecin B, twice weekly. Since CF patients live on steroids for extended periods of time, this represents a breakthrough in treatment, and perhaps in diagnosis also.


Recall that ABPA is an allergic reaction to Aspergillus mold, but this mold has far reaching toxicological ramifications over and above causing simple allergic reactions. Aspergillus makes several byproducts, including both carcinogenic and immunosuppressive mycotoxins. Allergy is the very least of an ABPA CF sufferer’s problem. If this mold can suppress immunity and cause cancer, you can bet it can fill the lungs with mucous in mysterious ways that would lead to a complicated diagnosis! Treatment, consisting of antifungal agents like pyocyanin and amphotericin B seem to be working better than steroids and antibiotics. Couple this with dietary changes and more benefit might be observed.

Given that diet is of questionable benefit, it would be fascinating to place CF patients on a diet that would reduce carbohydrates in all forms. Such diets assist in literally starving fungus. A differential diagnosis is recommended in CF patients. Offering a presenting CF patient antifungal agents and a changed diet for 14 days would have the physician better understanding the etiology of the chronic lung mucous.

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