Clinical studies show that 10% or less of CFS patients make a full recovery. Despite the seriousness of the illness, a few thousand people around the world have fully recovered from ME / CFS. Considering the fact that approximately 90 million people around the world have ME / CFS, this means only a very small percentage have fully recovered. High-tech diagnostic equipment and tests followed by special medical treatments have played a significant part in these recoveries. There is a medical and clinical pattern in these recoveries, this fact offers hope to all of those currently suffering from CFS. In this section we will analyse this medical and clinical pattern and the recovery process.

Actual Recovery Process  -  what are we dealing with ?
Scientific research and medical evidence has shown and is continuing to show us that Chronic Fatigue Syndrome is a multi-factor illness. CFS also has three distinct stages as outlined by Dr. Paul Cheney. Dr. Paul Cheney runs a specialist CFS clinic in the USA and has treated 5,000 CFS patients over a 15 year period. He has helped hundreds of patients recover from CFS. What has he learned about CFS - click here to view his lecture on CFS. 
The findings of Dr. Paul Cheney and researchers and scientists around the world show that CFS progresses in three stages over time. This accounts for it's multi-factor nature and it's complexity.

Phase 1     RnaseL abnormality

• Some biochemical or biological event leads to the following:
  (i) cleavage of the 80 kDa form of RnaseL into 37 kDa RnaseL. An accompanying high  LMW RnaseL (37 kDa)  to  HMW RnaseL (80 kDa) ratios found in CFS patients
  (ii) cleavage of STAT1-alpha protein, and accompanying STAT1-alpha deficiencies
  (iii) cleavage of p53 protein, and p53 deficiencies
  (iv) abnormal caspase activity and disrupted cell apoptic process
  (v) cleavage of RnaseL leads to  the presence of RnaseL fragments. 3 RnaseL fragments have been found to be significant: 
  Fragment 1, an ankyrin binding repeat domain which is known to interact with various transport proteins. It is is capable of NF-kappaB mimicry ; 
  Fragment 2,  the 2-5A binding fragment that has catalytic activity and thus is able to degrade RNA ; 
  Fragment 3, shares homology with chain A of Cdk6 (Cyclin dependent kinase). It  of Cdk6 chain A mimicry ;
  Research article:   Total Exposure: Expanded Model for RNase L Fragmentation in CFS Uncovered; The National CFIDS Foundation Announces the Use of Elastase Inhibitors as a Potential Treatment for CFS Patients (2003)
  (vi) Cell Apoptosis (cell death) increases initially in CFS and then is inhibited when the levels of Rnase L related fragments reach a certain point
  (vii) cleavage of Actin ;
  
  All of the above factors (i) to (vii) above interfere with the 2-5A synthetase / RNaseL pathway which is part of the anti-viral and anti-mycoplasma defense mechanism in cells. RnaseL destroys both viral messenger RNA and human messenger RNA. An over-active RnaseL destroys human messenger RNA preventing synthesis of essential human proteins and putting cells into significant dysfunction. Research by Suhadolnik, De Meirleir  and De Becker show that the abnormal RnaseL in CFS is over ten times as destructive as normal Rnase L, and this destructive phase continues indefinitely for years.
  
  The drug Ampligen effective in many cases, because it treats the RnaseL abnormality
  
  

• Effects of Rnase L (37 kDa RnaseL) :
  RnaseL destroys both viral messenger RNA and human messenger RNA. An over-active RnaseL destroys human messenger RNA preventing protein synthesis within cells and putting cells into significant dysfunction. Research by Suhadolnik, De Meirleir and De Becker show that the abnormal Rnase L (37 kDa RnaseL) in CFS is over ten times as destructive as normal Rnase L, and this destructive phase continues indefinitely for years. 
  Abnormal Rnase L (37 kDa RnaseL) and RnaseL fragments disrupt human messenger RNA, protein synthesis within cells and other cell functions, mitochondria function, the liver, the immune system, the kidneys, HPA glands, growth hormone production, muscles, brain and nervous system.
  
  

• Infections by one or more of the following:
  Viruses: HHV-6a virus, EBV, CMV, Coxsackie viruses, Stealth virus (from a subclass of retroviruses called "spumaviruses"), JHK virus,  Parvovirus B-19 infections, Enteroviruses in spinal fluids, blood, brain, nerve tissues, muscles
  Mycoplasmas: M. fermentans, M. penumoniae, M. hominis, M. penetrans, M. pirum,  M. incognito. in spinal fluids, blood, brain, nerve tissues, muscles
  Chlamydia:  Chlamydia pneumonia in spinal fluids, blood, brain, nerve tissues, muscles
  
  

Phase 2    Cellular toxicity due to xenobiotics

• RnaseL (37 kDa RnaseL) by destroying messenger RNA and blocking protein synthesis disrupts the production of liver enzymes and leads to impaired Liver detoxification. This leads on to a build-up of toxicity in the body which forms Phase 2 of CFS. The body is poisoned both from metabolising food and from toxins within and outside the body. Mercury fillings in particular will worsen this toxicity, as it interferes with glutathione. This increased level of toxicity damages the brain, in particular the hypothalmus and subcortex, leading to cognitive dysfunction, "brain fog" and constant exhaustion. The injury to the hypothalmus leads to a HPA axis dysfunction and a deficiency of key hormones - growth hormone,  cortisol, female sex hormone, and anti-diuretic hormone. The damage to the subcortex affects balance, thinking, memory and concentration. This toxicity is increased by infections due to a depleted immune system, the toxins produced by microbes worsen the patient's condition further. This toxic build-up can last from two years to ten years or more. 
  There is an abnormally high build-up of lactic acid in the cells of CFS patients. Scientists already know that if mitochondria can't function properly, pyruvate is converted to lactate acid and other organic acids. This explain the intracellular acidosis and extracellular alkalosis found in CFS. Alkaline blood in CFS inhibits oxygen transport to the mitochondria. Glutathione reduction in CFS induces an increase in citrate levels, which can inhibit 2,3 DPG. A deficiency of 2,3 DPG leads to a reduction of oxygen to the mitochondria.
  The mitochondria dysfunction is a key factor in CFS as it leads to a serious depletion of energy throughout the entire body in CFS patients.

Phase 3     Dynamic injury phase

• The build-up of toxicity in the body becomes cumulative over time, damaging the brain, mainly the subcortex and hypothalamus in the brain, the pituitary gland and adrenal gland, the immune system, muscles, cell functions, mitochondria & ATP production, and nervous system. This ongoing damage has a particularly devastating effect on CFS patients, causing severe fatigue. Thus patients remain in a state of sickness over many years. This toxicity leaves people highly susceptible to premature deaths from cancers, opportunistic infections and heart attacks.
  

These phases are a general guide. Some patients may have symptoms from two phases, though one phase will be dominant. Not all patients will share all of the same symptoms even if they are in the same phase of the illness. This may be due to genetic differences, different environmental and toxic exposures, different exposures to infectious agents, different diets and lifestyles, etc.. The multiple dysfunctions and abnormalities involved in each CFS patient must be identified.

The Multiple dysfunctions and abnormalities involved in CFS 

As the illness progresses from one stage to another, one dysfunction will lead onto further dysfunctions and so on. Patients will typically have three or more of the following Core abnormalities and dysfunctions and three or more of the Secondary abnormalities and dysfunctions at any given time :

Core abnormalities and dysfunctions in CFS

1. Immune System dysfunction
   Primary Immune system dysfunction : RnaseL abnormality  -  high LMW RnaseL to  HMW RnaseL ratio,  abnormal caspase activity and accompanying STAT1-alpha and p53 deficiencies.  
   Secondary Immune system dysfunctions : increased  neutrophil  apoptosis, over-activation of the TH2 cytokines, and under-activation of TH1 cytokines, low NK cell numbers and activity, weakened cell mediated immunity.

2. Chronic virus and / or mycoplasma infection co-existing with RnaseL abnormality

3. Single and Multiple virus infections  -  HHV6a virus, EBV, CMV, Coxsackie virus, stealth virus (from a subclass of retroviruses called "spumaviruses"), JHK virus, Parvovirus B-19, Enteroviruses mainly Cocksackie B virus infections of the  spinal fluid, brain, blood, nerve tissues and muscle tissues.  

4. Single and Multiple mycoplasma infections. 6 pathogenic mycoplasmas have been found in CFS :   M. fermentans, M. penumoniae, M. hominis, M. penetrans, M. pirum,  M. incognito. Co-exising with a virus infection in a  minority of cases.

5. Chronic Chlamydia pneumonia infection in spinal fluid, brain, blood, nerve tissues and muscle tissues

6. Adrenal gland abnormalities  -  symptoms of adrenal burn-out, many of the symptoms found in Addison's disease etc.

7. Thyroid gland abnormalities  -  detected by special TRH tests

8. Hypothlamus and Pituitary gland abnormalities  -  HPA axis dysfunction

9. Chronic Ciguatera poisoning

10. Brain hypo-perfusion and lesions on the brain  -  causing brain fog, mental confusion, inability to concentrate, etc..

11. Damage to the subcortex in the brain. Subcortex dysfunction.

12. Chronic insomnia caused by neurotransmitter depletion in the brain and nervous system and /or lack of neurotransmitter precursors in the diet. There is excess NMDA activity in the brain and depleted GABA activity and Serotonin and Melatonin activity, resulting in insomnia and sleep deprivation.

13. Significant proteolytic cleavage of IGFBP-3 by elastase.  IGFBP-3 / IGF-1  ratio greater than 3.5 indicates an IGF-1 deficiency. Also, depleted growth hormone levels

14. A unique urinary marker contained N-methylpyrrolidine has been found in a significant number of CFS patients. This is associated with  amyloid formation and protein misfolding.

15. Excessive stress and anxiety over a prolonged period of time, leading to adrenal burn-out, nervous exhaustion and accompanying immune system weaknesses.

16. Genetic factors which make one susceptible to CFS  or  an interaction of genetic factors with environmental factors which make one susceptible to CFS. Gene tracking is showing up abnormal gene activity in CFS patients.

17. Glutathione depletion and deficiency

18. Mercury toxicity from mercury fillings and / or mercury in one's food and environment   -   mercury has destructive effects on the brain, nervous system, DNA, hypothalmus and pituitary glands, immune system and endocrine system

19. Poor oxygen transport to the tissues

20. Undiagnosed Lyme disease

21. Excess Toxicity in the body from air pollutants, pesticides and herbicides in food and water, and exposure to chemicals in one's environment

22. Damaged mitochondria and defective ATP production throughout the body, particularly in muscle tissues  -  this accounts for the muscular pains and intolerance to exercise. 

Secondary abnormalities and dysfunctions in CFS

1. Increased oxidative stress in bones, muscles and tissues

2. Serious vascular disorders  -  inflammation in the blood vessels, failure to metabolise acetylcholine, heart beat irregularities, increased risk of sudden heart attack.

3. Orthostatic Intolerance and Low blood volume. Related to over-alkaline blood.

4. High levels of citrate in the urine

5. Vestibular Dysfunction related to subcortical injury

6. High Beta 2 micro-globulin levels

7. High levels of quinolinic acid. A serious neurotoxin

8. Lymphodynia (tender lymph nodes)

9. Parasitic infection of the intestines and / or overgrowth of Candida Albicans in the intestines

10. Bacteria overgrowth in the intestines, as indicated by the presence of CFSUM 1 in urine

11. Liver abnormalities and seriously impaired detoxification  -  many CFS patients have swollen livers and fatty livers

12. Toxicity in the intestines  -  build-up of undigested matter over many years, with toxins and poisons being re-absorbed into the blood system etc..

13. Underlying allergies and leaky gut syndrome

14. Excessive use of antibiotics resulting in depletion of beneficial bacteria in the intestines. Accompanying digestive difficulties, irritable bowel syndrome. 

15. Low systolic blood pressure ; 50% are below 100

16. Abnormal red blood cell structure

17. Substance P is elevated in CFS / ME patients

18. High levels of circulating plasma RNAs

19. High serum ACE levels

20. Raised levels of urinary toxins  -  Beta-alanine, CFSUM 1, Tartaric Acid and Arabinose

21. Coagulation abnormalities revealed by  Prothrombin Time (PT),  Activated Partial Thromboplastin Time (PTT) by photo-optical method,  Fibrinogen by nephelometry method. 

22. Crimson crescents in the back of the mouth or throat

23. Poor quality nutrition over a prolonged period of time (junk foods and trans-fatty acids ) leading to increased damage from free radicals and to immune system weaknesses and nervous system dysfunction.

24. Enzyme deficiencies and accompanying poor digestion and absorption of nutrients

Patients will vary in the number of the above abnormalities they possess, some will have two of the Core abnormalities and dysfunctions and three of the Secondary abnormalities,  some will have five of the Core abnormalities and dysfunctions and seven of the Secondary abnormalities, others will have eight of the Core abnormalities and dysfunctions and ten of the Secondary abnormalities. This has led to a number of sub-groups within the heading "Chronic Fatigue Syndrome" . 

Examples of Sub-groups

Patients in a particular sub-group may share 6-10 abnormalities and dysfunctions but they are very different to those in other sub-groups who may have less or more abnormalities  -  yet they all have CFS. Thus the symptoms and ' Diagnostic markers ' will vary from one group of patients to another and indeed vary from one patient to another in sufficiently small groups or samples of the patient population. 

The Domino Effect in CFS
These abnormalities do not exist in isolation, as one abnormality will create, contribute to, or worsen another abnormality and so on, increasing the overall burden on the body. One example is glandular abnormalities which contribute to immune system abnormalities and vice versa, these immune system abnormalities lead on to chronic infections in various parts of the body and to further dysfunctions and abnormalities. Another example is mitochondria abnormalities which lead onto immune system abnormalities, muscular abnormalities and endocrine abnormalities, and these in turn lead onto further abnormalities, and so on. In fact the mitochondria abnormalities found in CFS affect the entire body as mitochondria are the body's "energy factories". Another is neuro-endocrine abnormalities which consist of neurological and endocrine abnormalities which in turn can lead to immune system abnormalities. The body is a series of complex interacting systems, where one or more abnormalities can create or contribute to other abnormalities.  

Diagnostic markers
The long awaited single Diagnostic marker for CFS has not been found by researchers and scientists because there are sub-groups even within the small groups of patients researchers have examined. Researchers will typically find a Diagnostic marker among 40 - 70% of their patient population, and wonder why this Diagnostic marker cannot be found in the other 30 - 60% of the patient population. These findings appear contradictory and confusing to researchers, unless one accepts the existence of sub-groups within CFS. Once one accepts this, one can progress towards more effective research methods, and more effective diagnosis and treatment. This will mean very comprehensive, thorough and sensitive tests of all CFS patients to establish the specific abnormalities and dysfunctions in each individual case, and then dividing patients into relevant sub-groups according to their diagnostic markers. Thus each sub-group will consist of people with very similar symptoms and identical diagnostic markers and they will be given particular treatment plans aimed at alleviating their specific abnormalities and dysfunctions. This route to recovery has been successfully applied by several American doctors, and most patients have made full recoveries. This is outlined in the Patient and Doctor Recovery Databases on this web-site. This is the only viable option open  to CFS patients at present.

Your recovery 

Your recovery will depend on the number of abnormalities and dysfunctions that you have and  which sub-group you belong to. Thorough and accurate scientific and medical tests are required to establish which set of abnormalities and dysfunctions you have, and then medical, scientific, nutritional, herbal and alternative medicine techniques can be deployed to remedy these abnormalities and dysfunctions. This must be done under the supervision of a medical doctor.

However there is one major problem, most research equipment and clinical diagnostic equipment is ten or more years out of date in Ireland, Britain and most European Union countries. The existing labs and equipment cannot test for the above medical abnormalities found in CFS : 

Thus seriously ill patients cannot get an accurate diagnosis of their condition, if the diagnosis cannot be made then an effective treatment plan cannot be put in place. Thus patients and their doctors are left in a limbo, with no proper treatment and the patient's condition deteriorating over time, leading to further health complications such as opportunistic infections, accelerated liver degeneration and build-up of toxicity in the body, brain and organ damage, constant exhaustion and weakness, accelerated immune system degeneration, cancers, a worsening heart condition and a high risk of sudden heart attack. CFS can and has led to premature deaths. There is also a high rate of suicide among CFS patients, this being brought about by frustration, desperation for some cure, social isolation, lack of support, constant pain, exhaustion and weakness, and financial hardships.