MY RESPONSE: Landmark study or red herring? Study of 23 patients with Fibromyalgia (FM) & small fiber neuropathy(SFN; found in FM & diabetics) showed elevated HgbA1c levels & pain reduction with use of Metformin.
The authors point out the obvious: people with Fibromyalgia are often sedentary due to pain. Sedentary people ➡️ obese. Obesity ➡️ Diabetes, which ➡️ small fiber neuropathy.
No one knows if chronic peripheral pain independently ➡️ small fiber neuropathy. Darwinian evolution might postulate such an adaptive neurological compensation to reduce nociceptive pain.
Metformin reduction of pain has been previously known. Pain reduction is not a known function of lower glucose levels or regional density of small fiber neuropathy. No one knows metformin mechanism of analgesia; might be centralized in brain.
Dynamic overlooked by etiologic hypothesis of authors is predominance of Fibromyalgia in women. Clearly femaleness is not genetically coupled to diabetes or even to predisposition to diabetes.
I have studied hundreds of Fibromyalgia (FM) patients for over a decade. Fibromyalgia is a disorder that is multifactorial and which, because of progressive musculoskeletal disorders d/t lifestyles, begets itself.
Understanding Fibromyalgia requires linear observations of sufferers for months & years, historical knowledge of mechanisms of injury, & recognition of co-morbidities common to FM sufferers.
Inciting injury seems: bio-mechanical low back/pelvis injury or severely incapacitating illness (e.g. viral illness).
Bedrest & a sedentary existence leads to global musculoskeletal weakness, additionally excessive bedrest, lack of sun, & low Vitamin D.
Poor nutrition & depression seem to attend pain-interfered sleep & locomotor inabilities to shop for & to prepare nutrient dense foods.
The timeline for evolution of Fibromyalgia is measured in months and years. It takes this time for chronic widespread pain to evolve as result of global myofascial/muscle weakness & consequent compensatory soft tissue spasms.
Perhaps greatest clue to etiology of Fibromyalgia is association of FM & Hypermobility Spectrum Disorder (HSD). Persons with HSD are predisposed to chronic joint ligament injuries ➡️ chronic pain generators.
Hypermobility Spectrum Disorder is genetically linked to femaleness; explaining predominance of Fibromyalgia in women. Childbirth is associated with increased laxity/pain of pelvic girdle; especially in women with HSD.
Chronic low back pain is a sine qua non for Fibromyalgia. Chronic pelvic girdle instability leads, over months & years, to functional scoliosis, shoulder girdle asymmetry, & crossed-muscle syndromes in neck & shoulders.
Consequences of upper body tower musculoskeletal asymmetries are Cervicalgia, Arm-Hand Syndrome, TOS, Migraine, & Dysautonomias (Vagus n. impingement) of POTS & Gastroparesis.
There is a timeline for evolution of these phenomenon, but it is long (months & years), & serial evolution of these disorders/symptoms needs to be observed/documented in dozens of people for etiology to be appreciated.
In October 2019, I presented (on line) eight papers which captured the timelines for various symptoms & disorders attendant with Fibromyalgia; at the 10th Interdisciplinary World Congress on Low Back & Pelvic Pain in Antwerp.
Fibromyalgia is real. The cause is officially determined to be “unknown”. One reason for this circumstance is that Fibromyalgia has multifactorial causations.
Finally, phenomenon of recovery from Fibromyalgia is known. Survivors’ stories are video-reviewed @cfsunravelled. Survivors focused their healing journeys on reversal of the multiple factors described above.
The insights and clinical impressions herein are of my own inventions and gained via an iterative evidence based method of medical discovery. They are not intended for medical advice.
ASSOCIATION OF hEDS & RHEUMATOLOGICAL DISORDERS; AN OPINION (1/7/2020):
Either there is genetic linkage between these disparate Syndromes or there is not. I searched for physiologic relationship, but I find no ready theories of associations between these diseases & tissue disorders.
The environmental dynamics that explain these relationships (associations) are sedentary lifestyles that beget weak bodies & chronic pain that forestalls ongoing pursuit of daily locomotor confrontations with the ambient gravitational field.
EDS: I include EDS in the estimated 15% of women I encounter in my medical practice and who have manifest hypermobility. My view is that Mother Nature gave women genes for ligaments rendered more lax, via the hormone Relaxin, to ease the bio-mechanical assaults of childbirth.
The genes for female Hypermobility are sex linked because men are not well served, in their pursuits of war & hunting, by delicate joints of knees, spine, & pelvis.
My encounters with the common expression of Hypermobility amongst Hmong, Mexican, & Hawaiian cultures, recently evolved from a long history of agrarian-subsistence existence, led me to a theory about why hypermobility genes are so highly conserved.
ARTHRITIS PREDICTS WEATHER? In previous posts (in my threadreader library) I have explained this phenomenon. The cause and effect is related to barometric pressure.
The body is like a sausage, with contained hard & soft tissues. Bones are connected by ligaments, which are highly imbued with pain fibers intended to keep us from injuring & stretching joint ligaments; to protect against being pulled asunder. Remember “Rack” of Inquisition fame.
When ligaments are lax from chronic wear, serial acute injuries, or from one serious joint injury, these injuries predispose joints to excessive range of joint motion & painful stretch of ligaments that tether these loose joints. Those with flexible joints potentiated for injury.
BOTOX: A PRINCIPLE OF MEDICAL DIAGNOSIS & THERAPY? Several insidious medical disorders encompass similar pathophysiology seeming amenable to #Botox therapy: #Migraine, #TMJ, chronic neck pain (#cervicalgia), & Thoracic Outlet Syndrome (#TOS).
The pathophysiology found within all these disorders is the phenomenon of “crossed muscle” syndromes. Dr. Victor Janda is possibly first to describe this curious syndrome, which is easily discovered by simple physical examinations.
When the body musculoskeletal tower is asymmetric (tilted) within the ambient gravitational field, muscle pairs symmetric from side to side or which oppose in individual body part functions, become dissimilar in dynamic action; one muscle stronger & hypertrophic. The other weak.
Botox yes! In TOS 1 Superior trapezius usually spastic/hyperdynamic; inducing same-side Pectoralis minor muscle to be spastic/hyperdynamic. These muscles control directional shift of distal clavicle; which, as drawn inferior, closes Thoracic Outlet (1 cm vs. clavicle & 1st rib).
The physical exam should note shoulder asymmetry; one shoulder lower with head usually tilted toward lower shoulder. The tilted 10# head often induces spasm & hypertrophy of Superior trapezius associated with opposite & higher shoulder.
Superior trapezius hyperdynamic function then induces spasm/hypertrophy within same-side opposing (shoulder lift & draw-down are complementary functions) Pectoralis minor (PM) muscle. It is PM hyperdynamic function that draws distal clavicle excessively inferior in TOS disorder.
LONG COVID: etiology of long-COVID, CFS, Fibromyalgia, etc. evolves from acute injury to musculoskeletal tower. Two weeks of intense bedrest, from injury to skeletal tower or viral illness, causes severe soft tissue deconditioning, loss of tissue mass, & weakened body tower...
Greatest force threatening weakened organism is ambient gravitational field: all body parts falling to earth at 32’/sec/sec. As body tower attempts upright station, widespread painful muscle spasms ensue to stiffen tower. Upright posture & even walking become difficult.
A natural response is to lay down & rest. Exercise becomes exhausting. Additional rest magnifies the pathology. As the weakened body tower encounters ground force of sleep/resting site, painful spastic muscles beget REM disruption & non-restorative sleep➡️depression/fatigue.