Chronic Fatigue Syndrome 

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Chronic Fatigue Syndrome


Jan 2018: 13 Trials found for: cfs | Recruiting, Not yet recruiting, Available Studies | "Fatigue"

Jan 2018: 57 Trials found for: cfs | Available, Active, not recruiting, Completed Studies | "Fatigue"

  • RESULTS: Duloxetine po 60-120 mg/day for 12 weeks. Pain Severity Score: Duloxetine: -1.6,    Placebo: -0.8 ---
    Patient Global Impression of Improvement: Duloxetine: 3.2 , Placebo: 3.3
  • RESULTS: Viagra Change in Fatigue Impact Scale at 6 Weeks. Viagra: -32.6 Placebo: -1.5
  • RESULTS: Effect of Carnosine Supplementation on Chronic Fatigue Syndrome Severity. Carnosine -3.8, Placebo: -2.0

Jan 2018: 240 Studies found for: Recruiting, Not yet recruiting, Available Studies | "Fatigue"


Dec 27, 2016 Fuel Shortage: Norwegian Study Expands on Energy Problem in Chronic Fatigue Syndrome (ME/CFS)

Scientists reveal new avenue for drug treatment in neuropathic pain

Symposium highlights new chronic fatigue syndrome research

" a disease of things that are low" there's a metabolic problem going on.'s a hypometabolic disease ---molecules necessary for energy production... were "very, very low,"

The citric acid cycle is needed to burn glucose, which provides energy. These very low numbers suggest that a patient cannot generate energy or another key molecule used for energy, Adenosine triphosphate (ATP), very well.

"ATP is the gasoline of the body. The molecule allows energy to be consumed in your body," he said, noting it is necessary for movements such as muscle contractions.

Something in ME/CFS patients appears to shut down these necessary processes, he said. It appears that the pathway leading up to the citric acid cycle is somehow shut.

"Scientists have some theories about why the metabolic sequence in a ME/CFS patient might turn off. ....... the switch-off mechanism could be a "danger response." ME/CFS is a metabolic state designed to protect the body during a viral infection, for example, but for some reason it doesn't get turned back on after the infection has gone away.


Fibromyalgia and Male Physiology: Why It's Different A 2008 study published in Neuroimage showed that men have fewer serotonin receptors (brain cells that respond to it) than women. However, the process of reuptake—which is essentially "recycling" so the neurotransmitter can be used again—may be more efficient in men.

Drugs that slow reuptake are commonly prescribed for fibromyalgia. They're called SSRIs (selective serotonin reuptake inhibitors) or SNRIs (serotonin-norepinephrine reuptake inhibitors. Two of the three drugs approved for this condition are SNRIs: Cymbalta (duloxetine) and Savella (milnacipran).

the vagus nerve’s neurotransmitter, how it communicates with the body, is acetylcholine, which is inhibited by various meds regularly prescribed to many of us, including: Benadryl, Xanax and various other psych and stomach meds (Google acetylcholine inhibitors for a full list).

.If you're taking vitamin D, you're probably taking too much.   Two vitamin D capsules a day (at 2000 international units each) adds up to 4000 IU—the daily limit. If you’re taking in any vitamin D at all otherwise (and you almost certainly are), you’re already over the safe dosage.  There’s no solid evidence that taking multi- or any other kind of vitamin is beneficial to your health unless you’re vitamin-deficient.
t’s not uncommon to have a deficiency in it. Studies can’t agree on an exact number, but around 30-40 percent of U.S. adults don’t get enough of the D from their diet and sunlight. Only a few foods contain it at all and those that do, like fatty fish or egg yolks or cheese, may be hard to eat enough of to actually get the benefit. That’s why the U.S. dairy industry started fortifying milk with it. And the trouble with sunlight (which doesn't give you vitamin D, but does trigger your body's production of it) is that it’s harmful to get too much of it. It’s better to cover up and avoid skin cancer than it is to go unprotected in an effort to get enough vitamins. Plus, the darker your skin is, the fewer UVB rays get through to produce vitamin D in the first place.
High doses have the potential to cause nausea, vomiting, constipation, and weakness.  And since too much vitamin D can lead to too much calcium, you can also wind up with kidney stones and abnormal heart rhythms.
Unless you’re getting almost no vitamin D, you’re probably fine. 

Albrecht et al:- "excessive sensory nerve fibers around specialized blood vessel structures located in the palms of the hands,” . “This discovery provides concrete evidence of a fibromyalgia-specific pathology"

Are Peripheral Pain Generators Important in Fibromyalgia and Chronic Widespread Pain?

Fibromyalgia (FM) is a chronic widespread pain syndrome (CWPS) that is generally considered to be the result of a dysfunctional central pain modulating system. It is thought to importantly involve the descending pain inhibitory system.

FM is known to be associated with multimodal hypersensitivity: mechanical, thermal, visual, and auditory. It is associated with a variety of comorbid conditions including

  • irritable bowel syndrome,

  • painful bladder,

  • migraine headache, and

  • temporo-mandibular joint syndrome.

The relationship of the comorbid conditions to FM has not been clear. They can be considered to be the result of hyper-effective ascending central pain transmission resulting from deficient descending pain inhibition, or they can be considered as clinical entities in themselves, whose importance in FM lies in their acting as peripheral pain generators that enhance or initiate central sensitization, thereby contributing to chronic widespread pain.

There may, of course, be some truth in both of these concepts. The presence of peripheral pain generators that lead to central sensitization initiating or maintaining CWPS or FM remains controversial, however. This question is addressed in a masterful study by Albrecht et al. [1], published in this issue.

Albrecht et al. [1] investigated the innervation of arteriolevenule shunts (AVS) that are located deep in the dermis of hypothenar glabrous skin, an area that is often painful in FM patients. The function of these AVS, as the authors note, is to increase or decrease blood flow to glabrous skin as part of the body’s thermoregulatory mechanism.

Under thermal stress conditions, as much as 60% of the cardiac output is distributed to skin, and a high proportion of this is directed to glabrous skin. They hypothesized that FM patients may have a disorder involving the sensory and sympathetic innervation of the arterioles and AVS in glabrous skin, leading to or exacerbating the pain of FM.

They performed an immunofluorescent examination of arteriole and AVS innervation, using immunofluorescent labeling to identify unmyelinated peptidergic C fibers, lightly myelinated peptidergic Ad, and lightly myelinated non-peptidergic Ad fibers. The skin biopsies were double labeled to differentiate C fiber, Ad sensory fibers, and noradrenergic sympathetic fibers. Noradrenergic sympathetic fibers were identified by being positive for neuropeptide Y and negative for calcitonin-gene-related-peptide (CGRP). The relative proportions of sensory and sympathetic nerve innervation of arterioles and AVS and the density of innervation of arterioles and AVS were also measured.

AVS were significantly larger in the FM patients than in the controls. The increased size of the AVS correlated with increased tortuosity to some degree but more significantly to an increase in the innervation of the AVS. The overall innervation area was 4x greater in FM patient AVS than in control subjects AVS.

Peptidergic (CGRPcontaining) C-fiber sensory axons made up the largest component of the increased AVS innervation.

The CGRPcontaining vasodilatory sensory innervation was far greater in proportion to noradrenergic vasoconstrictive sympathetic innervation than the ratio of the two types of innervation was in control subjects.

In summary, the authors found that AVS in palmar glabrous skin of FM patients had increased sympathetic and sensory innervation compared to control subjects, whereas arteriole and venous innervation was normal.

This study suggests, as the authors point out that changes in blood flow and increased thermal sensitivity may each contribute to local palmar pain, a common complaint of FM patients. By so doing, they contribute to peripheral nerve sensitization which gives rise to local (peripheral) pain as well as contributing to central sensitization and central pain.

These findings contribute importantly to our concept of the nature of pain in CWPS or FM. Previous studies in this area showed that lidocaine injections into tender points in the trapezius muscle in FM patients result in decreased local tenderness, and also decreased heat hyperalgesia at points remote from the injection sites, showing that peripheral nociceptive input is important in maintaining central sensitization [2].

Myofascial trigger points were not specifically mentioned as the pain source in the trapezius muscles in that study, but subsequently, in other studies, myofascial trigger points were identified as sources of peripheral nociceptive pain that caused local tenderness [3–6].

The association and reproduction of pain in FM patients produced by stimulating peripheral nociceptive sites is suggestive, but not proof of a cause and effect relationship. It is the reduction in local and widespread pain in FM in response to treatment of the peripheral nociceptive sites that is most convincing in determining that peripheral nociceptive sites play an important role in initiating and maintaining pain [7,8]. It is unlikely that chronic changes in central pain modulation would produce the changes seen in innervation patterns of AVS.

Pain is not a simple sensation, and is rarely the result of a disorder in one system only. It is complex, involving multiple interactions. CWPS and FM cannot be considered to be solely a disorder of central pain modulation, and perhaps not even primarily so. Pain is the outcome of a complex interplay between the central modulation and peripheral pain input. That balance between inhibition and facilitation of incoming pain impulses determines the pain that we experience, as shown when descending pain modulation shifts from inhibition to facilitation following sustained isometric contraction sufficient to cause muscle nociception in FM patients [9]. The work of Albrecht et al. [1] advances our understanding of this interplay with their elegantly done study of AVS in FM patients that emphasizes the importance of peripheral pain generators in determining the clinical expression of pain. source