Hamilton NEW ZEALAND
Biomedical Therapies for Optimum Health
Hamilton NEW ZEALAND
Biomedical Therapies for Optimum Health
At this time many authoritative explanations of the CFS-FMS spectrum have been published. This may strengthen the idea that there is no single cause, at least so far discovered.
In the Workup Section you will read of possible causes such as infections, gland disorders, toxic triggers and so on.
Maybe these are still consequences of an as yet undefined fault which allows such events to go unchecked by usual defence mechanisms and thus leading to an array of multi-cell, multiple organ failures. It could well be modern toxic accumulation affecting those genetically and dietary predisposed.
So should we be tackling the 'end results' or symptoms when the actual cause is unknown? Well of course, because this is a multi-organ disorder and attacking FMS from as many fronts as possible should limit or stop its progress.
Infection Cause
It is well established that many microbial infections have been followed by CFS.
According to Prof. K. De Meirleir of Brussels (he specialises in CFS research), infectious viruses or certain other microbes, invade human cells releasing their virus DNA which triggers production of enzymes called 2-5 0AS and PKR. In turn these causes activation of a substance called RNase-L which finally destroys the infectious RNA (essential nuclear code) but also the host cell too. Both die. Fortunately this stops spreading of the infection....at a cost.
Strangely, these OAS proteins are the same as a Thyroid receptor protein and they can deactivate the receptor which may lead to intense fatigue and a hypothyroid situation (note the prevalence and similarity of hypothyroid symptoms in CSF-FMS). Hence Thyroid Receptor Resistance.
Another thing happens:
Inflammation triggered by infection, produces substances that cleave (break apart) those RNase L and OAS proteins into small fragments that cause further mayhem in the walls of organ or tissue cells where they disrupt transport of vital minerals (ions) through 'channels'.
Cell functioning goes haywire and as you can imagine, results in many abnormal symptoms such as palpitations (heart cells) sweats, hypoglycaemia, reduced pain threshold, visual-taste-smell disorder, sensitivity to chemicals, depression anxiety, feeling cold or hot and so on.
These consequences are termed 'Channelopathies'.
In addition, the immune response becomes abnormal - with lowered immunity to infections, even some which normally are relatively harmless can take hold (opportunistic infections as in AIDs).
One example infection is Mycoplasma which has been found in 69% of CFS patients.
Another cleavage fragment called ankyrin, can also increase cytotoxicity of mercury compounds such as Thimerosol (used in some vaccinations as a sterilizer) as well as dental mercury. It also may cause the pain in the muscles.
The Channelopathy theory actually explains why in the CFS-FMS syndrome there ARE multiple dysfunctions of many organ systems.
We also can explain why STRESS makes it worse, at least one reason, is that it activates virus replication - which restarts the whole process as above. Stress if prolonged, increases adrenal cortisol at first, decreases protective white cells (macrophages), reduces defences and the virus multiplies.
Predisposing factors:
Unfortunately, the infection may have long gone but left the legacy. Infections can be treated - with the exception of viruses. Though here one can increase immune defences as the best attack.
It was discovered years ago that some FMS patients got better after anti-gout treatment. This lead to a theory that phosphate build up occurred in cells especially muscles.
\A Professor of Endocrinology at Harbor-UCLA University, Paul Amand and his team have worked in FMS-CFS and their research led them to a simple compound called Guaifenesin (actually a natural product common to many cough mixtures). It appears Guaifenesin (G) increases excretion of phosphates through the kidneys. Other cell changes are found such as low ATP (the energy factor produced by mitochondria in every cell).
Professor Amand postulates a primary disorder of phosphate metabolism and he can account for many of the wide spectrum of symptoms.
More importantly, he has considerable success with treating FMS with G. However, it does have to be done long term. One month for every year of FMS.
The course must be done 100% according to the protocol. Many things can negate the outcome such as taking any form of salicylate found in aspirin, toothpaste even, and many types of foods.
refer to www.fibromyalgiatreatment.com
Many symptoms of FMS and perhaps CFS are so similar to underactive thyroid that it is absolutely necessary to assess the thyroid, and all endocrine glands for that matter.
It is not enough to just measure the TSH (thyroid stimulating hormone) as many do. It is a poor screening test when confronted with hypothyroid-like clinical picture.
Full thyroid tests including thyroid antibodies, early morning as well as tds temperature testing, and full symptom evaluation and physical checkup are required.
Some workers in the FMS field such as Dr Lowe in the US place great emphasis on the thyroid as a major cause of FMS. The channelopathy theory may explain why now.
Dr Lowe recognises thyroid resistance and treats accordingly with doses of usually T3 until symptoms are controlled. i.e. when the patient has normal thyroid function. THis may not mean normal thyroid function tests! These may be irrelevant if there is such an entity as resistance in FMS.
His website is very informative. Dr Lowe also has published a well referenced textbook.
We use this technique at our clinic.
refer to www.drlowe.com
Another 'famous' person is Dr. Wilson who coined the term Wilson's Thyroid Syndrome. He regards the major culprit to be resistance from the abnormal production, under stress, of Reverse T3 (rT3). This blocks the T3 receptor site and hence produces underactive thyroid disorder (hypothyroidism) in spite of NORMAL levels of blood T4, T3 and TSH. Hence the importance of not relying only on blood tests! rT3 can now be measured to confirm this scenario. To reduce rT3, its source needs to be stopped. This means stopping T4 production by the thyroid gland. It is accomplished by prescribing cycles of increasing doses of slow release T3. This turns off TSH and in turn reduces T4. He claims several cycles may be required to do this as seen by normalising body temperature and reversal of symptoms.
refer to www.wilsonsthyroidsyndrome.com
A recent excellent works that scientifically explains the whole CFS-FMS sequence is 'Explaining Unexplained Illnesses' by Martin L.Pall, PhD 2007. He has put up the theories from the most prominent CFS researchers and explained them with a single biochemical theory.
So, how can we treat FMS? Refer to treatment protocols.