Q7. How would you respond to Dr. Ronald Davis’s recent statement: “What is important to note is that in the absence of evidence of an active infection, it is plausible that the long-term antimicrobial treatments often used for ME/CFS patients are doing more harm than good.”
I am in complete agreement. Many antibiotics like tetracyclines, erythromycin, and the fluoroquinolones (eg, Cipro), and antivirals like acyclovir, fialuridine, AZT, and ddC also inhibit mitochondrial functions when used chronically (usually for more than about 3 weeks). Because mitochondria are descendants of free-living bacteria, their machinery for protein synthesis, RNA synthesis, and DNA replication are susceptible to many antibiotics, and for reasons unique to mitochondrial DNA synthesis, they are also sensitive to antivirals. Chronic use of these drugs can do more harm than good if there is no longer good evidence for an active infection. When mitochondrial functions are critically impacted by long-term use of certain antibiotics, a ripple effect in metabolism and gene expression is produced that can further impair energy production by mitochondria, converting an active cell danger response that occurs during active infection to a hypometabolic survival response.
In the field of mitochondrial medicine we are particularly sensitive to these issues of iatrogenic toxicity because some of the drugs that inhibit mitochondrial functions are very commonly used in patients without mitochondrial disease. For example, statins, valproate, and metformin can each produce problems in patients with pre-existing mitochondrial dysfunction. Most doctors do not think about how some antibiotics, antivirals, and other common drugs can inhibit mitochondrial function when they are used chronically. Our patients with mitochondrial disease are often the ones who educate their doctors about the mitochondrial dangers of many common drugs.
I know this is a sensitive area for many people struggling with CFS. It is important to emphasize that individual medical decisions must be governed by individual responses to treatment. Medical decisions should be informed by science, but cannot be based solely on abstract scientific concepts without also considering the clinical variables that are relevant to the care of each specific patient treated as an individual. Some patients do better on drugs that we would consider to be inhibitors of mitochondrial function. This may not have anything to do with the conventional pharmacologic classification of the drugs as antibiotics, antivirals, anticonvulsants, antidepressants, neuroleptics, or anticholesterol agents. Most drugs have metabolic effects beyond their primary action. Because the field of metabolomics is so new, these “pharmacometabolomic” effects of drugs have not yet been studied well.