Is CFIDS/ME a mitochondrial disease? Yes and no. Mitochondrial diseases are mainly thought to affect the mitochondria and science has long postulated that this is the case with CFIDS/ME. More recently, that become a proven scientific fact (Hokama et al*) but what that research team found was that the ciguatera epitope is found in all autoimmune diseeases and that the epitope, which is very much like ciguatera, targets the mitochondria along with other areas of the body.

The mitochondria are like little energy factories in every cell of the body. There are hundreds of mitochondria in each cell, zillions in the body, and they take in oxygen and glucose and they put out carbon dioxide and adenosine triphosphate (APT). APT is the essential form of stored energy of the body. Think of it as your own "energizer" battery. ATP is 3 phosphates which are converted to ADP which is 2 phosphates. In a helathy person, the ATP recylces about every ten seconds but slower cycling is a hallmark of CFIDS/ME. The oxidative phosphorylationn (oc-phos) are a very complex transportation chain of electrons that do the major work. This is an essential part for every organ system in the body.

But mitochondrial diseases are thought of by most medical practitioners as diseases that are quickly fatal and that strike the very young. While CFIDS/ME certainly strikes the young (the youngest diagnosed patient in the US was just two), it is not quickly fatal. Yet the symptoms of mitochondrial diseases include neurological symptoms including ataxia which is a loss of coordination, myoclonis which is involuntary jerking of the muscle, encephalitis which is a disease of the brain, exercise intolerance, constipation and a sensitivity to anesthesia. That is a description of CFIDS/ME! In fact, the sensitivity to anesthesia has been proven to be when the same pathway to the body is used for anesthesia that the ciguatera epitope uses. The National CFIDS Foundation, in fact, funded research to find the exact part of the sodium channel** being used that must be avoided by all CFID/ME patients and, it seems more than apparent, all those with mitochondrial diseases that are, in fact, autoimmune diseases.

When medical practitioners, however, diagnose a mitochondrial disease, they usually require muscle biopsies and ox-phos testing yet oxphos are usually found to be normal in CFIDS/ME! Most physicians think of diseases as organ specific and the mitochondria affect every organ in the body. The main problem patients have for their reason for disability is that they cannot sustain any level of activity. That is because the recyling process is far too slow with CFIDS/ME and the patient who tries to push themselves find themselves in what they term a "crash". The problem with the mitochondria has been found by many researchers. Even Dr. Walter Tarello found it in animals who had CFIDS/ME***. Yet Plioplys and Ploiplys tested the mitochondria with electron microscopy and found no differences in the structure although they admitted the dysfunction could be functional. Years before their own paper was published, it had been scientifically proven that part of CFIDS/ME was apoptosis (cell death). The mitochondria, it should be noted, play an important role in the regulation of cell death.

An insufficient supply of ATP molecules means the patient has insufficient energy which is called "chronic fatigue". "Chronic fatigue" is a symptom of insufficient molecular energy and, of course, our Centers for Disease Control and Prevention (CDC), in it's infinite wisdom, called this state of accelerated oxidative molecular injury "chronic fatigue syndrome".

Dr. Alan Krensky, a deputy director of the National Institutes of Health where mitochondrial research is one of the six priority areas of new funding over the next five years, said, "All these diseases --- diabetes, cancer, atherosclerosis --- the major diseases of mankind, appear to have major mitochondrial components." In 2003, researchers found genes involved in the mitochondira were less active, for instance, in Type 2 diabetes. Other researchers, who bred rats with little capacity for aerobic exercise, found evidence of impaired mitochondria function while other studies linked cancer, Parkinson's and Alzheimer's to the mitochondria. One pharmacuetical giant, GlaxoSmithKline, through Sirtris Pharmaceuticals, is working on drugs that can increase the number of mitochondria as well as boosting their function including one based on resveratrol.

The main problem of calling CFIDS/ME a mitochondrial disease is that science has yet to catch up. Last fall, researchers at the Roswell Park Cancer Institute (Cancer Biol and Ther, Singh, Smiraglia) found dysfunction of the mitochondria were alterations that are linked to cancer. Mitochondria contain their own DNA and changes are associated with the development of cancer. Didn't the National CFIDS Foundation (NCF) point that out already? Do you remember the headline of the first article in the last edition about the NCF already funding a study on leukemia? Our medical committee is thankful that the NCF is not waiting for science to play catch-up! We need more answers today and their research direction is not just pointing the way but leapfrogging the staid and slow movement of most research endeavors.

*"Acute Phase Phospholipids Related to the Cardiolipin of Mitochondria in the Sera of Patients with Chronic Fatigue Syndrome (CFS), Chronic Ciguatera Fish Poisoning (CCFP), and Other Diseases Attributed to Chemicals, Gulf War, and Marine Toxins," J Clin Lab Anal, 22:99-105, 2008.

**"Biological Activity of the Functional Epitope of Ciguatoxin Fragment AB on the Neuroblastoma Sodium Channel in Tissue Culture," J Clin Lab Anal, 20:126-132, 2006.

***"Chronic Fatigue Syndrome (CFS) in a Family of Dogs,", Vet On-Line, August 2000.