Pharmaceutical interventions in CFS: A literature-based commentary, Richman, Morris, Broderick, Craddock, Klimas, Fletcher, March 11, 2019

[MeSci]

Source: Clinical Therapeutics

Preprint

Date: March 11, 2019

URL:
https://www.sciencedirect.com/science/article/abs/pii/S0149291819300712

Ref: See March 9 for Part 1

Pharmaceutical interventions in Chronic Fatigue Syndrome: A literature-based commentary
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Spencer Richman(1,2), Matthew C. Morris(1,2), Gordon Broderick (1,2,3,5,*), Travis J.A. Craddock(3,4,6), Nancy G. Klimas(3,6), Mary Ann Fletcher(3,6)

1 Gosnell School of Life Sciences, Rochester Institute of Technology, Rochester, NY, USA

2 Center for Clinical Systems Biology, Rochester General Hospital, Rochester, NY, USA

3 Institute for Neuro Immune Medicine, Nova Southeastern University, Fort Lauderdale, FL, USA

4 Departments of Psychology and Neuroscience, Computer Science, Nova Southeastern University, Fort Lauderdale, FL, USA

5 Department of Biomedical Engineering, Rochester Institute of Technology, Rochester, NY, USA

6 Department of Clinical Immunology, Nova Southeastern University, Fort Lauderdale, FL, USA

* Corresponding author

Received 23 January 2019
Accepted 11 February 2019
Available online 11 March 2019.

Abstract

Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a debilitating disorder characterized by prolonged periods of fatigue, chronic pain, depression, and a complex constellation of other symptoms.

Currently, ME/CFS has no known cause, nor are the mechanisms of illness well understood. Therefore, with few exceptions, attempts to treat ME/CFS have been directed mainly toward symptom management. These treatments include antivirals, pain relievers, antidepressants, and oncologic agents as well as other single-intervention treatments.

Results of these trials have been largely inconclusive and, in some cases, contradictory.

Contributing factors include a lack of well-designed and -executed studies and the highly heterogeneous nature of ME/CFS, which has made a single etiology difficult to define. Because
the majority of single-intervention treatments have shown little efficacy, it may instead be beneficial to explore broader-acting combination therapies in which a more focused precision-medicine approach is supported by a systems-level analysis of endocrine and immune co-regulation.

 

[Alvin]

Anyone know if they posted treatment ideas in this paper?

 

[Andy]

Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a debilitating disorder characterized by prolonged periods of fatigue, chronic pain, depression, and a complex constellation of other symptoms.

Hmm, not that impressed by that description.

Anyone know if they posted treatment ideas in this paper?

No, they basically say that not enough is known to be able to recommend anything, and that, due to the complexity of the condition, it will likely be a multi drug regime once we do know enough, probably personalized to the individual.

 

[Alvin]

No, they basically say that not enough is known to be able to recommend anything, and that, due to the complexity of the condition, it will likely be a multi drug regime once we do know enough, probably personalized to the individual.

I watched the presentation in Australia, their technique is interesting but i don't think it will do much beyond symptom control.
That said if we had a symptom control treatment we would all be doing better.

 

[Sunshine3]

@Alvin I thought they were trying to reboot homeostasis and effectively get us back to normal... Did they mention that in Australian presentation?

 

[Alvin]

@Alvin I thought they were trying to reboot homeostasis and effectively get us back to normal... Did they mention that in Australian presentation?

Thats what they are saying but ME is some type of immune mediated disease. Once we find out what it is we would target the disease and get better. What is ME is a very important question, and do we have the technology to target it yet is a very good question. Lets say its an immune signal to reduce energy production and its a molecule that signals power down. That would suggest there is a signaling mechanism that says turn this off. We find a drug that does that and we are treated
Or say we can't do that but we can denature the signal with a drug. Symptom control but works great.
Or it may be some part of the immune system thats not yet understood and when elucidated needs a new drug to be designed to affect it. That would take many years but it would be attacking the core of the disease.