Fluoroquinolone Toxicity…

  • is not Magnesium deficiency.   There are theories that magnesium levels can play a role in the precipitation of an adverse event to the FQ’s.  It is also true  that FQ’s can leach magnesium.  However, low magnesium is not floxing.  If after floxing, you can ‘cure’ yourself or find a solution to your problems with magnesium then your symptoms were caused by low magnesium, NOT FQ Toxicity.  Also, it is possible that normalizing magnesium post floxing can help alleviate some negative symptoms.     

  • is not Vitamin D deficiency.   Vitamin D is a wonderful vitamin that does many amazing things in the body.  Being low on vitamin D can cause many unpleasant symptoms including pain. If after floxing, you can ‘cure’ yourself or find a solution to your problems by normalizing vitamin ‘D’ levels then your symptoms were caused by low vitamin D, NOT FQ Toxicity.  Again,  it is possible that normalizing vitamin D levels post floxing can help alleviate some negative symptoms.     

  • is not MTHFR.  According to Dr. Ben Lynch, probably the foremost expert on MTHFR mutations, the rate of one MTHFR mutation in the standard population is a whopping 50% and the likelihood of having 2 copies is between 10% and 20%.  Those of Italian and Mexican ancestry can have a much larger rate of MTHFR mutations. Having said that, over the last five years many floxed individuals have had their DNA sequenced.  When we did an analysis several years ago, it was found that the FQ community had a representation of MTHFR mutations on par with the general population.  This would see to rule out MTHFR as the ‘sole’ cause of Fluoroquinolone Toxicity. It is true that after floxing having the mutations for MTHFR can make your adverse event symptoms much more unpleasant.      

  • is not G6PD.  G6PD deficiency is a genetic disorder that most often affects males. It happens when the body doesn’t have enough of an enzyme called glucose-6-phosphate dehydrogenase (G6PD). G6PD helps red blood cells work. It also protects them from substances in the blood that could harm them.  Without enough G6PD to protect them, the red blood cells break apart in a process called hemolysis. When many red blood cells are destroyed, a person can develop hemolytic anemia causing dizziness, and a myriad of other symptoms.  It is true that the Fluoroquinolones can trigger G6PD type symptoms and probably should never be taken by those with this genetic mutation but many doctors are not familiar with this deficiency.  However, like MTHFR, the rate of G6PD has not found not to be consistent in the Fluoroquinolone community.  I will concede that there are many genes in the G6PD spectrum, but overall there are there are individuals who in the community that do not have this mutation and who are severely floxed, ruling out G6PD being a risk factor.  

  • is not caused by Flouride or Flourine. The first medical case report of a short-term quinolone induced syndrome from a non-fluorinated quinolone was reported in the year 1972, before fluorinated fluoroquinolones were developed. It could be successfully argued that with the addition of fluorine, the subsequent metabolites produced by the Fluoroquinolone’s molecule metabolization caused an exponential increase in the ability for toxicity. The fluorine addition made a pharmaceutical that had a penchant for toxicity much worse. Bottom line, the quinolones had the capability to be toxic before the addition of fluorine but gained the ability to be super toxic after the addition of fluorine. Also read Does adding fluorine make the quinolones toxic?

  • is not caused by iodine deficiency. It has bene postulated that fluorinated quinolone  leach or shift iodine in the body in such a way as to cause symptoms.  Again, FQAD has its roots, before fluorinated quinolones were developed.   If this theory was the simple cause it could be easily corrected and it would have been. Unfortunately, research has shown the FQAD is far more complicated involving epigenetic pathogenic mtDNA damage.