Good day, friends! Today, I begin the presentation of the latest research on Chronic Fatigue Syndrome. In this part of the series, I will present how an overabundance of a specific protein interferes with energy production. Let me begin by reintroducing CFS. Let’s jump in, shall we?

More than 2 million people suffer from Chronic Fatigue Syndrome nationwide. Many people present with symptoms after a viral infection, although the causes of CFS are still not clearly understood, making diagnosis and finding treatments difficult. However, one discovery is an overabundance of a protein called WASF3.

A team of doctors led by Drs. Paul Hwang, Avindra Nath, and Brain Walitt from the National Institutes of Health or NIH, studied a woman who took days to recover from physical exertion as well as some of her family members at the NIH Clinic Center. Tests performed during exercise revealed a very slow recovery in energy production with in the cell. Muscle cells were taken from her and examined in the lab, which showed oxygen usage was reduced in the mitochondria, which is where energy molecules are produced in the cells. Upon further studies, a protein called WASF3 was discovered. WASF3, it was discovered, interferes with muscle cell function at high levels. High levels of WASF3 interfered with production of mitochondrial proteins into molecular complexes supporting normal energy. WASF3 in turn, was boosted in response to cellular stress, disrupting the cells’ energy production. The blocking of WASF3 allowed the mitochondria to produce energy at normal levels.

The team then compared muscle tissue samples taken from 14 volunteers with ME/CFS to samples from ten volunteers who did not have CFS. There were significantly higher levels of WASF3 in most volunteers with CFS.

The increase in WASF3 seemed to be linked to impairment of a signaling pathway in the cells called the ER(Endoplasmic Reticulum)stress pathway. The endoplasmic reticulum is a structure inside the cell of which the main function is to produce proteins and lipids and transport them throughout the cell. ER stress is defined as the accumulation of proteins in the Endoplasmic Reticulum, causing disease progression in such diseases as metabolic diseases, neurodegradation(destruction of cells in the brain and spinal cord) rheumatic diseases, as well as cancer. When the team of doctors treated the muscle cells with a substance known to increase ER stress, there was an increase in WASF3.

The good(or bad) news is this; mitochondrial dysfunction has been found in other conditions of which fatigue is a symptom, including Long Covid. Of course, more studies are necessary before researchers know whether or not targeting ER stress would be a feasable approach for treatment of these other conditions.

Based on all of this information, it looks like we are on our way to some kind of treatment. Yes, there is still much to be done, but we will get there one day. Five years ago we weren’t nearly as far as we are today.

Tune in next week to see what is next in the journey to finding a treatment for ME/CFS!

Have a great week!

Beckie.

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