Targeting patients with chronic fatigue and other inflammation syndromes, and protocols and applications to reduce inflammation
I am very comfortable bringing awareness to patients about posture and positioning, proper belly versus chest breathing, nasal breathing, sleep hygiene, fat loss, movement and exercise. If we add even a few healthy practices for at home, i.e., establish better eating times, take out a possible food sensitivity, add some very gentle movement, when it comes to issues such as chronic fatigue and inflammation syndromes, patients may feel better.
I use modalities in the office that help “charge” the mitochondria, and this allows some wonderful changes in these people’s lives. Since ME/CFS is rarely identified at onset, unfortunately a diagnosis of ME/CFS can take years to receive and even more time following for it be recognized by the medical community.
The job of the nervous system (neuro) is to process information and coordinate action. The job of the immune system is to fight infections and repair damage. A properly functioning neuro-immune system creates healthy inflammation and resolves it in a timely sequence.
On a daily basis I see patients who have complaints related to ongoing low-grade inflammation … it’s this continual unresolved inflammation that may lead to, or be related to, chronic musculoskeletal aches and pain, and other illnesses such as myalgic encephalitis/chronic fatigue syndrome (ME/CFS).
Inflammation syndromes: an undiagnosed mass affliction
It is estimated there are between 836,000 and 2.5 million people afflicted with ME/CFS in the U.S. alone. An estimated 80-90% of people with ME/CFS have not yet been diagnosed, meaning the true prevalence is unknown.
Between 60-90% of ME/CFS patients have fibromyalgia, while irritable bowel disease is another frequent comorbidity. Through observations and experience with patients in my practice, similar conditions are chronic fatigue syndrome (CFS), fibromyalgia and neuropathy.
These are often related to:
The mitochondria need oxygen to create adenosine triphosphate, or ATP. ATP is the energy required for cells to carry out their specific functions. Nerve impulses, tissue repair, muscle contraction, the synthesis of biochemical agents within cells and more — all these actions require ATP.
Any movement or metabolic process needs ATP. Our mitochondria can be poisoned by environmental toxins; pesticides; chronic bacterial, viral and fungal infections; and nutritional and hormone deficiencies. A constant supply of ATP is imperative to maintain cellular processes for life. Without the mitochondria producing ATP from oxygen and the food we eat, life would cease. The mitochondria in our brain, especially the hypothalamus and pituitary, are sensitive to any malfunction and fatigue is one of the symptoms.
Thyroid and cortisol deficiencies are the most common ones.
Cortisol, the ‘fight-or-flight’ hormone triggered by stress, becomes depleted because the body is no longer able to produce sufficient amounts. Fatigue and exhaustion are a symptom.
Thyroid hormone is depleted by exposure to toxins and by malfunctions in the hypothalamus and/or pituitary. Both 3′,3,5-triiodo-L-thyronine (T3) and 3,5-diiodo-L-thyronine (T2) (iodothyronines) have been identified as effectors of the actions of thyroid hormones on energy metabolism. Both have significant effects on basal metabolic rate (BMR), but their mechanisms of action are not identical:
- T3 acts on the nucleus to influence the expression of genes involved in the regulation of cellular metabolism and mitochondria function.
- T2 acts by directly influencing the mitochondrial energy-transduction apparatus. A molecular determinant of the effects of T3 could be uncoupling protein-3 (UCP-3), while the cytochrome-c oxidase complex is a possible target for 3,5-T2. Imbalanced hormones might interfere with ATP synthesis.
There are many causes of inflammation and many messengers that play a role in healthy inflammation resolution. Yet there are patients who continue churning out inflammatory cells, signaling the body to keep going with inflammation and fueling inflammation syndromes.
In response to ongoing low-grade infection, injury or inflammation, pain receptors (nociceptors) in the body can become more sensitive to painful stimuli — a process called “peripheral” sensitization. These sensitized nociceptors go into overdrive, sending pain signals to the central nervous system (CNS), which can lead to the overstimulation of the CNS. This results in “central” sensitization, which increases the perception of pain. As such, central sensitization leads to the perpetuation of pain.
I notice palpation of the outer body soft tissues in certain areas along the back and shoulders as well as the arms, legs, feet and hands as being “clenched” — this contributes to low-grade inflammation via poor blood flow and lower oxygen to the soft tissues, with the CNS spinning out of control into chronic pain.
For my inflammation resolution program to inflammation and inflammation syndromes I utilize hands-on therapy alongside photobiomodulation light therapy, shockwave pulse therapy, pulsed electro-magnetic frequency (PEMF), fat-loss diets and lymphatic therapy.
I am using many of the cutting-edge therapies, like Winback TECAR therapy, high energy inductive therapy (HEIT), sound frequency dose therapy, local and whole-body vibration, along with nutritional therapy (diets, peptides, vitamin supplements and herbs).
In a normal response to injury or inflammation, cells at the site of pain release a variety of biochemical mediators, including the neurotrophin nerve growth factor (NGF), the cytokine TNFα, the interleukins IL-1ß and IL-6, and prostaglandin E2. These chemical mediators bind to pain receptors (nociceptors) in the periphery, leading to the sensitization of the pain pathway.
When the cause of pain continues beyond the normal expiration date, the persistent activation of the pain pathway leads to increased synthesis of glutamate and neuropeptides, such as substance P, calcitonin gene-related peptide (CGRP), and bone-derived neurotrophic factor (BDNF).
Substance P and CGRP enhance the sensitization of sensory nerves in the periphery. In the CNS, all these mediators — NGF, TNF, IL-1, IL-6, substance P, CGRP, BDNF — can be released by the primary afferent neuron, subsequently binding to receptors in the dorsal horn of the spinal cord, contributing to the activation of key intracellular pathways that initiate central sensitization.
Nerve growth factor (NGF) plays a key role in the amplification of pain signals by sensitizing neurons in the pain pathway and causing the overproduction of other pain mediators. NGF is found throughout the body. Levels of NGF increase in response to injuries or conditions associated with pain.
In the presence of some conditions associated with chronic pain like neuropathy, myalgia encephalitis, CFS, osteoarthritis, rheumatoid arthritis, gout or chronic low-back pain, there is continuous overproduction of NGF. As a result, more NGF is available to bind to peripheral sensory nerves, increasing the number of pain signals that travel from the periphery to the CNS. This contributes to the sensitization of nerves in both the peripheral and the central nervous system, amplifying and perpetuating chronic pain.
In short, what excess NGF does here changes what happens there. As a result, I sense patients are aware and feel a different “tone” in the area. I can palpate these areas in the body as bogginess, tightness or densification of the soft tissues, i.e. fascia, muscle, tendons, etc. This tight tissue contributes to overactivity and lack of oxygen at the local area. This causes further pain cycles to occur.
Part II will appear in the next issue of Chiropractic Economics.
JEFFREY TUCKER, DC, practices in West Los Angeles, Calif. He is a prominent and successful chiropractic doctor who specializes in treating conditions related to ongoing inflammation and chronic musculoskeletal diseases, including neuropathy, fibromyalgia and chronic fatigue syndrome. Tucker has over 40 years of specialized experience, has written over 100 articles for chiropractors and has lectured in the U.S. and abroad. He is the past president of the American Chiropractic Association Rehabilitation Council. Sign up for his newsletter on his website at DrJeffreyTucker.com.