Immunity Blog

Chronic Fatigue Syndrome 

Would you like to know about my approach for Chronic Fatigue Syndrome?

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What is Chronic Fatigue Syndrome (CFS), also known as Myalgic Encephalomyelitis (ME)?

  • a new onset fatigue which leads to a substantial reduction or impairment in pre-illness levels of activity.

  • it persists for more than 6 months

  • it is not the result of ongoing excessive exertion and is not substantially alleviated by rest; sleep is unrefreshing

  • even minor physical or mental exertion causes post-exertional malaise

  • there is cognitive impairment (memory, concentration) and / or postural orthostatic intolerance (POTS)

  • there may be sore throat, lymphadenopathy, muscle pain, headaches

There are many other types of chronic fatigue.  I often work with clients suffering from adrenal or metabolic fatigue, as well as thyroid fatigue and sleep disorders.  If you are interested in herbal medicine for any type of fatigue, please call me for more details.

 

The energy deficit explained

ME / CFS symptoms are manifestations of physiological effects mostly directed from the brain.  Here are some of the mechanisms that produce the severe energy deficit of CFS:

  • Brain inflammation 

    ME / CFS patients can present with neuroinflammation and brain lesions on MRI, reduced blood flow (cerebral, brainstem and cortex), reduced cerebral glucose metabolism, and lower brain glutathione.

  • Postural orthostatic tachycardia syndrome (POTS) 

    ME / CFS patients display high rates of POTS, orthostatic intolerance and blood pressure variability.  Impaired reciprocal connectivity between the vasomotor centre, midbrain, and hypothalamus regions impact blood pressure; the reticular formation of the brainstem is affected in ME / CFS and acts as a cardio-depressant.

  • Hypothalamic Pituitary Adrenal axis (HPA)

    HPA dysfunction originates in the brain (hypothalamus and pituitary) and affects release of cortisol by the adrenals, the small glands that produce the hormones cortisol, adrenaline, noradrenaline, aldosterone and DHEA.  ME / CFS patients suffer from low cortisol and attenuated diurnal cortisol variation. Cortisol has two major functions: on the one hand its diurnal rhythm regulates the body’s chronobiology that gets us up in the morning as it peaks, and helps us go to sleep in the evening as it wanes.  Compounding the problem, Cortisol is a major anti-inflammatory hormone and a deficiency suppresses immunity.  

  • Mitochondria

    Mitochondria are cell organelles that produce ATP, the energy currency of the body, through oxygen dependent (aerobic) metabolism.  There is evidence of oxidative stress-induced damage, low plasma coenzyme Q10 and low serum ATP.

  • Acidosis

    Lactic acid-producing bacteria can over-colonise the gut of ME / CFS patients and cause acidosis of the muscles, causing pain; if they affect the blood they can contribute to neurocognitive issues.

 

What are the potential causes of ME / CFS? 

Often the trigger is identified as a viral infection; there is a complex relationship between the immune and neuroendocrine systems that involves the brain, the hormonal axes originating in the brain and the hormonal feedback loops, relaying information back to the brain.  

Any factor that puts the body under extreme physical, mental or emotional stress is interpreted by the body as a stressor.  If the stressor is overwhelming, it can create, in susceptible individuals, excess demand for energy production, ineffective hormonal adaptation and immune hyperactivity.  ME / CFS can often overlap with diverse conditions like irritable bowel syndrome, chronic pelvic pain, fibromyalgia, and multiple chemical sensitivities.      

Some of these factors / stressors have been identified by ME / CFS patients as extreme stress, accident/injury / surgery, pregnancy and childbirth; infections: Epstein-Barre virus / glandular fever / tonsillitis / throat infection / lower respiratory tract infections / flu- or cold-like illnesses / gastrointestinal problems / infections and tropical infectious diseases.

Different infections may act as triggers but this blog post concentrates on the potential role of the Epstein-Barre Virus (EBV).

 

What about the role of Epstein-Barre virus in ME / CFS?

A virus known to reactivate from latency is Epstein Barre Virus or EBV, related to CMV, HHV-6 and VZV, all of the Herpes family; EBV causes infectious mononucleosis (glandular fever).  Most individuals are infected with EBV as children without complications.  A number of ME / CFS patients report an adult-onset EBV infection as a trigger; however, it is likely that this is not a new infection but a reactivation of latent EBV.  

EBV can induce autoreactivity in susceptible individuals which makes it difficult to clear persistent infections or reactivations

  • EBV codes for antigens with highly repetitive structure which can elicit an autoimmune response in the body through biological mimicry.

  • A peptide of the viral protein EBNA6 shares a high sequence homology with the human enzymes lactoperoxidase and thyroid peroxidase. 

  • EBV induces ‘EBV virus-induced gene 3’ (EBI3) which has immune effects through interleukin IL-27.

When a viral antigen mimics a self-antigen it can ‘lock’ the adaptive immune system in an active state of hyperregulation.

Sufferers of ME / CFS may have autoimmunity in the family and comorbidities like Irritable Bowel Syndrome, hypothyroidism or fibromyalgia.  Several autoantibodies have been found in ME/CFS as well as associated comorbidities.

 

EBV can infect immune cells and cause immune dysregulation in susceptible individuals

Although some patients report a viral or flu-like disease before the onset of ME / CFS it is important to recognise that EBV can remain latent in the body and that patients may be suffering from reactivation (not a new infection).  It is possible that reactivation is enabled by the presence of other viruses, as it is also possible that susceptible individuals cannot clear multiple infectious agents due to induced immune dysfunction.  Patients with ME / CFS report frequent infections suggesting an ongoing immune dysregulation.

  •  Efficient interactions between cells of the adaptive immunity (T-cells, B-cells and antigen-presenting cells) take place at the secondary lymphoid organs e.g. tonsils, lymph nodes; these are tissues often affected in ME / CFS patients.

  • Dysregulation of adaptive immune cells can inhibit antibody production and antibody maturation leaving the door open to viral persistence or reactivation, through immune suppression.  

  •  Dysregulation of immune cells also affects their energy metabolism. Patients with ME / CFS can have reduced mitochondrial membrane potential (CD8+ T cells) and reduced glycolysis at rest (CD4+ and CD8+ T cells) and following activation (CD8+ T cells).

 

Conclusion

ME / CFS is a chronic condition characterised by post-exertional malaise, fatigue which is not alleviated by rest, POTS, cognition problems and muscle pain. The debilitating energy deficit of ME / CFS has sources in the brain and the HPA axis, the mitochondria and potentially the intestinal biome.

In susceptible individuals viral infection or reactivation of Epstein-Barre Virus can contribute to development of ME / CFS.  EBV can induce autoreactivity and hyperregulation which play a role in the maintenance of the ME / CFS condition.  At the same time, EBV can also cause immune suppression through dysregulation of the adaptive immunity.

 

My approach for ME / CFS is addressing all aspects of the condition.

Any treatment approach for ME / CFS must take into account all aspects of the condition so that there can be a positive effect on the energy deficit.  I use herbal medicine to: 

  • address chronic infections

  • support the immune system to redress immune dysregulation and autoreactivity,

  • improve hormonal function, especially of the HPA axis,

  • tackle inflammation

I develop an approach that is adapted and personalised to your needs; this takes into account your individual medical history and any comorbidities that may be contributing to a state of autoreactivity and immune dysregulation.

If you are interested in finding out more about my approach and how it would apply to your individual profile, please contact me for a -free- exploratory discussion of your situation.