The Connection Between Chronic Fatigue Syndrome, Lupus, Fibromyalgia, Autoimmune Disease and Chronic Lyme DiseaseBy ENVITA MEDICAL CENTER
Idiopathic disease, one that presents without any definitive causes, can have recognizable signs and symptoms. It remains the causality, however, that troubles medical schools, private practices and hospitals. Only pharmaceutical companies benefit from ongoing symptom treatments ordered for CFS, Lupus, Autoimmune disease and Fibromyalgia. These can total in the billions every year.
Proposed Non-Idiopathic Causes for Chronic Fatigue Syndrome and Fibromyalgia
- Brain abnormalities
- Genetic factors (HPA axis)
- A hyper-reactive immune system
- Viral or other infectious agents like (chronic Lyme disease complex)
- Psychiatric or emotional conditions
Fibromyalgia and CFS - Are Genetics to Blame?
CFS and fibromyalgia have been linked with genes involved in the hypothalamic-pituitary-adrenal (HPA) axis as well as the sympathetic nervous system. These genes regulate response to trauma, injury and other stressful events. After ten years of ongoing clinical experience, Envita is confident that while such traumas could play a role in these diseases' etiology, they are likely not the causes.
What is the HPA (Hypothalamic-Pituitary-Adrenal Axis)?
HPA comprises a complex set of direct influences and feedback interactions among the hypothalamus, the pituitary gland (a pea-shaped structure located below the hypothalamus), and the adrenal, also called "suprarenal" glands, small, conical organs atop of the kidneys.
The interactions among these organs constitute the HPA axis, a major part of the neuroendocrine system that controls reactions to stress and regulates many body processes including digestion, the immune system, mood and emotions, sexuality, as well as energy storage and expenditure. Infectious disease, such as chronic Lyme disease complex, impacts the HPA-axis via neurotoxins that compete for the same receptor sites used by the HPA-axis.
In fact, such infections can bring about identical symptoms of some idiopathic disease and many of the symptoms associated therewith. This should alert us that a complex of infections such as Lyme disease complex (that is composed of a number of infections and neurotoxins) bring about all the same symptoms and more.
Does the HPA Effect Fibromyalgia or CFS?
Abnormal levels of certain chemicals regulated by the hypothalamus-pituitary-adrenal (HPA) axis have been proposed as a potential cause of Chronic Fatigue Syndrome. It has also been cited as being related to fibromyalgia. This HPA system controls important functions including sleep, stress response and depression. Of particular interest to researchers are the following chemicals and other factors controlled by the HPA axis as it pertains to the neurobiology of mood disorders and functional illnesses:
- Anxiety disorder
- Bipolar disorder
- Post-traumatic stress disorder
- Borderline personality disorder
- Major depressive disorder
- Borderline personality disorder
- Irritable bowel syndrome
Antidepressants, which are routinely prescribed for many of these illnesses, serve to regulate HPA axis function. All of these conditions and their symptoms are commonly seen in chronic Lyme disease patients that contain a host of infections and neurotoxins.
Can Chronic Lyme Disease Complex or Infectious Disease Effect HPA?
In the etiology of chronic infectious disease, the traumatic event is a trigger but not the cause of autoimmune disease, Chronic Fatigue Syndrome or fibromyalgia. Nevertheless, treating these triggers is critically important to patient care. It seems that infection, rather than genetic defects, is the progenitor of HPA axis disruption, psychiatric or emotional conditions.
Major Impact of Epigenetic Changes Gene Involvement
Studies show that gene alterations are caused by infections involving immune function, intercellular communication, and energy transfer.
Researchers have identified many different genes in patients with Chronic Fatigue Syndrome that relate to blood disease, immune system function, and infection. Despite these identifications, however, there is no clear pattern to them and it is quite possible that infection alone that is altering these genes. In the same vein, they are likely responsible for impacting mental and emotional health as well. It is very possible that infections can alter these genes that impact both mental and emotional health as well.
Important Neurotransmitters Changed by Neurotoxins Competing for Receptor Sites
Some patients with Chronic Fatigue Syndrome have abnormally high levels of serotonin – a neurotransmitter (chemical messenger in the brain), and also show deficiencies in dopamine – an important neurotransmitter associated with feelings of reward. In some cases there is also a demonstrable imbalance between norepinephrine and dopamine.
A number of studies on Chronic Fatigue Syndrome have shown patients with lower cortisol levels, a stress hormone produced by the adrenal glands. It has been suggested that such cortisol deficiencies are responsible for Chronic Fatigue Syndrome patients having impaired or weakened responses to psychological or physical stresses like worry, infection, or exercise. However, administering replacement cortisol improves symptoms only in some patients. Why? Infection and their toxins (neurotoxins) must be cleared before hormone replacement can begin to be effective in these patients clinically.
Idiopathic Diseases at the Root of Many Psychological Disorders
Evidence suggests that some idiopathic disease patients experience disturbances in their circadian rhythms (disorder of the sleep-wake cycle), which is regulated by the so-called circadian clock, a nerve cluster in the HPA axis. These are commonly seen in Lyme disease complex among a number of other neurological symptoms.
A mentally or physically stressful event may disrupt these natural circadian rhythms. A patient whose body is unable to reset these rhythms could fall into a perpetual cycle of sleep disturbances. Some medications that improve sleep can be very helpful, but until the infections are cleared and neurotransmitters are rebalanced, long-term improvement is unlikely.
Psychological, personality, and social factors are strongly associated with Chronic Fatigue Syndrome, fibromyalgia, and autoimmune disease like Lupus. There is a decidedly complex relationship between physical and emotional factors.
What Specific Infections are Responsible
Because many CFS features resemble those of a lingering viral illness, many researchers have openly considered the possibility that a virus or some other infectious agent causes the syndrome in some cases.
In such circumstances, Envita has clinically determined that these patients usually have a group of viral, bacterial, parasitic, and fungal infections that make up what we call Lyme disease complex. Some patients may or may not have actual Lyme disease but they may have other tick-borne illness and their coinfections that have catalyzed immunological, hormonal, and neuroendocrine changes. This is where we see the hyper-immune response in the patient.
Still, not all Chronic Fatigue Syndrome patients show signs of infection. And although experts have long been divided on whether infections play any role in this disorder at all, it does seem clear that subtypes of both viral and non-viral Chronic Fatigue Syndrome exist. That being said, researchers have seemingly overlooked the complexity of muti-infections, multi-toxins, and heavy metal components that complicate these conditions making them extremely difficult to diagnose on a case to case basis.
When a complex of infections exists they can affect the activation and replication of each other via biofilm communities. To be certain most patients are never tested thoroughly and correctly for all the infections that make up, chronic Lyme disease complex.
Infections Looking More Like the Cause
Chronic Fatigue Syndrome having a viral cause is not based on hard evidence, rather, on an ever-growing series of observations that suggest this association. CFS as well as fibromyalgia and autoimmune disease patients are often found with elevated antibody levels for a variety of organisms that cause fatigue and other symptoms. These organisms include those that cause Lyme disease, Candida ("yeast infection"), herpes virus type 6 (HHV-6), human T cell lymph tropic virus (HTLV), Epstein-Barr, measles, coxsackie B, cytomegalovirus, or parvovirus.
Many of these infectious agents are very common, however, and none has emerged as a definitive cause of CFS. Well-designed studies of patients who met strict criteria for CFS without any known cause have not found an increased incidence of any specific infection(s). However, is it a combination of these infections, toxins and other insults. Then, the answer clinically is yes.
In up to 80% of cases, CFS starts suddenly with a flu-like condition. In the U.S., there have been reports of cluster outbreaks of CFS occurring within the same household, workplace, and community (but most have not been confirmed by the Center for Disease Control and Prevention). However, most cases of CFS occur sporadically in individuals, and do not appear to be contagious. These all have the pattern of infections and more importantly community of infections taking over the patient's immune system, which is clearly seen in the depressed CD57 markers found in almost all of this population.
Immune System Abnormalities and Immunocompromised States
CFS is referred to as "chronic fatigue immune dysfunction syndrome" by some, and oftentimes studies have detected myriad immune system irregularities. In some cases, these are over-reactive, while others appear are often under-reactive, but no consistent picture has emerged to explain CFS as an immune disease.
Some studies report that many CFS patients also have allergies to foods, pollen, metals (such as nickel or mercury), or other substances. One theory is that allergens, like viral infections, may trigger a cascade of immune abnormalities leading to CFS. That being said, most allergic people are not CFS sufferers. The risk profile for CFS is similar to those for a number of autoimmune diseases. Nevertheless, studies are inconsistent in reporting the presence of autoantibodies (antibodies that attack the body's own tissues). The disease is unlikely to be due to autoimmunity, making it more likely connected to infectious disease.
Autoimmunity Overlaps with Conditions
Envita Medical Center continue to lead the way in comprehensive, personalized patient care. Contact us today for more information. At Envita you can find the help you need to improve the quality of your life.
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 Annals of Tropical Medicine and Parasitology, Volume 92, (citation)
 Hunfeld, K.P., Hildebrandt, A., Gray, J.S. Babesiosis: Recent insights into an ancient disease. Int. J. Parasitol. 2008 Mar 20 (Epub).
 Welc-Faleciak, R., Behnke, J.M., Sinski, E. Effects of host diversity and the community composition of hard ticks (Ixodidae) on Babesia microti infection. Int. J. Med. Microbiol. 2008 Feb. 6 (Epub).
 Skotarczak, B. Babesiosis of human and domestic dog; etiology, pathogenesis, diagnostics. Wiad. Parazytol. 2007; 53(4): 271-80.
 Parasite Immunology Volume 22, Dehua Chen, D. Bruce Copeman,, Jim Burnell, , Gareth W. Hutchinson (citation)
 Infectious Diseases Division, Massachusetts General Hospital, Boston (citation)
 Dr. Victor Jimenez, HSC T15-080, State University of New York at Stony Brook, Stony Brook, NY (citation)