This month I would like to discuss a problem encountered sooner or later by physicians learning the art of detecting interference fields. The problem is this: A patient presents with a complaint that is found to be caused by an interference field. The interference field is treated with neural therapy; the symptom resolves; but the patient then returns with another complaint and another interference field.
One or two additional interference fields may simply be an example of the body "peeling the onion". i.e. allowing the less urgent problems t o manifest after the more important ones resolve. However, if interference fields continue to appear, the physician is probably dealing with a situation of generalized cell membrane instability.
If the concept of "cell membrane instability" has a familiar ring to it, ‐ yes, ‐ an interference field itself is a product of cell membrane instability, but only in a specific location. Generalized cell membrane instability refers to tissues everywhere in the body, but most noticeably of nerve and muscle. A low resting membrane potential allows an influx of sodium ions, thereby lowering the membrane potential further and encouraging more sodium entry ‐ a classical positive feedback loop. If enough sodium enters the cell, (unwanted) action potentials arise. Neural therapy prevents this by closing sodium channels, raising membrane resting potentials and stabilizing membrane electrical properties.
With generalized cell membrane instability, the threshold for action potentials in all cell membranes is lowered, although not to the degree present in a specific interference field. However, if latent interference fields are present, under these circumstances they are more likely to become active, ‐ hence multiple interference fields simultaneously or sequentially. The sketch on the cover of my book is meant to illustrate this principle; the horizontal line (the threshold potential) goes up or down depending on the level of stability of cell membranes.
What then causes generalized cell membranes instability? The list of causes is long. It includes electrolyte imbalance of the extracellular and intracellular environments, nutritional deficiencies affecting the cell membrane, and toxins that poison the biochemical machinery of the cell membrane. These causes are covered in some detail in chapters 8, 9 and 10 of my book available at http://www.neuraltherapybook.com.
In this newsletter, I would like to talk about a newly discovered neurotoxin. It is not mentioned in my book and as far as I know has not yet been connected with less-than-successful neural therapy. For several decades this substance has been known to be toxic (to some people) in the gut and in the skin, but only recently has it been identified as a common cause of peripheral neuropathy and ataxia (with cerebellar degeneration), as well as autonomic nervous system dysfunction, myopathy, episodic headaches, and various psychiatric disturbances, especially depression.
This newly discovered neurotoxin (as you may have guessed) is gluten, the protein usually identified with celiac disease. For an excellent review of the gluten‐neurological disease connection see: Hadjivassiliou et al, "Gluten sensitivity as a neurological illness" J. of Neurology, neurosurgery and psychiatry 2002;72:560-563. (You will have to register, but it is worth it) at: BMJ Journals.
What may come as a surprise to many is that 50% of these people with gluten induced neurological diseases have no gastro‐intestinal symptoms or signs. Gluten sensitivity is therefore likely to be a missed diagnosis without a high degree of suspicion. Fortunately, certain "red flags" help to raise awareness. Because gluten sensitivity is an inherited condition, osteoporosis, difficult to treat iron-deficiency anemia, depression, cancer (especially lymphoma or cancers of the gut), various skin conditions, diabetes, multiple sclerosis and autoimmune diseases in the patient or family members are reasons to be suspicious.
Gluten sensitivity used to be a difficult diagnosis to make. In the 1960's small intestinal biopsy was the only definitive method. During the following decades serum anti‐gliadin anti‐endomysium and anti‐tissue transglutaminase antibody tests were developed. These demonstrated that gluten sensitivity was much more widespread than previously thought, but it was only in the 1990's when fecal antibody tests were developed that the true extent of gluten sensitivity became apparent. Some confusion still exists in research as well as clinical circles about the nature of gluten sensitivity versus celiac disease, but the case for fecal testing is strong. See Fine's discussion of various methods of testing in https://www.enterolab.com/StaticPages/EarlyDiagnosis.htm.
Testing is now quite simple. I have my patients contact http://www.enterolab.com, have a collection kit mailed to them and have them return it with a fecal sample. A copy of the report is usually sent to my office, but otherwise everything is handled by the patient.
Multiple interference fields or poor response to neural therapy are not signs of neurological disease, but they may be looked upon as signs of cell membrane electrophysiological instability. Gluten sensitivity must now be added to the differential diagnosis of underlying causes. In my patient population I am finding gluten sensitivity far more common than I had ever realized. Identifying (and treating) gluten sensitivity can benefit a patient's health in many ways. It also makes neural therapy more effective and more rewarding.
Robert F. Kidd, MD, CM