JaimeS
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Hello, all! I am curating a small collection of the best / most interesting ME/CFS studies to make an informative packet regarding what we know about ME/CFS. Each will have a small commentary, so consider poorly-performed studies that have had an impact on the ME/CFS landscape, such as PACE.
From the quick article / intro to ME/CFS I wrote as a blog post awhile back:
FLUGE AND MELLA 2016; ARMSTRONG ET AL, 2016; ARMSTRONG ET Al, 2015
Recent research from Fluge and Mella in Norway, and Christopher Armstrong of Australia have identified errors in cellular energy metabolism in ME patients that differs from sedentary controls. Reduced glyolysis, accompanying high blood glucose, and metabolites that demonstrate a marked uptick in mitochondrial activity in response have been documented. Other energy-producing reactions’ metabolites were elevated, which may indicate compensatory energy metabolic mechanisms in people with ME. Women’s amino acid stores in particular are being utilized in place of glucose, and are decreased in comparison to that of healthy controls. Women’s diet showed no difference in protein intake than in controls.
Further analysis by Fluge and Mella impicated PDH inhibitors as a mechanism for decreased glycolysis.
Finally, bathing culture-grown cells in ME patients’ serum caused them to exhibit the same metabolic abormalities as patients’ cells.
HANSEN ET AL., 2016
Hansen of Cornell as well as researchers from the University of Melbourne have confirmed an older study’s results showing that ME patients have gut bacteria that is not just different from controls, but different in a predictable manner, with Firmicutes and Bacterioides off. Using a machine-learning approach, the Melbourne team was able to identify the right patient utilizing a sample of their gut bacteria over 80% of the time.
HORNIG ET AL, 2015:
Mady Hornig and her team at Columbia University discovered a pattern of upregulated inflammatory and anti-inflammatory markers in early ME (first three years after onset) all of which were inverted in late ME (over three years after onset). Long-term patients’ immune markers were lower even than those of controls.
Dysregulated immune markers included IL-12p40, IL-12p70, IFN-gamma, TNF-alpha, and GM-CSF (CSF2). The marked involvement of interferon-gamma points to an initial infective trigger, as it is the product of activated T-cells, natural killer cells, and macrophages.
Hornig’s study, besides pointing to a future blood test for ME, is the first to identify a two-stage illness, with an acute phase and a chronic phase.
NEWTON ET AL, 2015:
Julie Newton and her team discovered that muscle cells of patients with ME had increased myogenin expression but decreased IL-6 secretion in comparison to controls and, when an electrical pulse was sent through the tissue to simulate exercise, muscle cells of ME patients demonstrated impaired AMPK activation and impaired uptake of glucose. Cells responded normally to insulin.
FLUGE AND MELLA:
Fluge and Mella found that the anti-cancer drug Rituximab caused complete remission in a significant percentage of ME patients.
Other suggestions?
[Edit: changed first Fluge and Mella citation to 2016 -- it came out in December of 2016. I had it as a 2017 article.]
From the quick article / intro to ME/CFS I wrote as a blog post awhile back:
FLUGE AND MELLA 2016; ARMSTRONG ET AL, 2016; ARMSTRONG ET Al, 2015
Recent research from Fluge and Mella in Norway, and Christopher Armstrong of Australia have identified errors in cellular energy metabolism in ME patients that differs from sedentary controls. Reduced glyolysis, accompanying high blood glucose, and metabolites that demonstrate a marked uptick in mitochondrial activity in response have been documented. Other energy-producing reactions’ metabolites were elevated, which may indicate compensatory energy metabolic mechanisms in people with ME. Women’s amino acid stores in particular are being utilized in place of glucose, and are decreased in comparison to that of healthy controls. Women’s diet showed no difference in protein intake than in controls.
Further analysis by Fluge and Mella impicated PDH inhibitors as a mechanism for decreased glycolysis.
Finally, bathing culture-grown cells in ME patients’ serum caused them to exhibit the same metabolic abormalities as patients’ cells.
HANSEN ET AL., 2016
Hansen of Cornell as well as researchers from the University of Melbourne have confirmed an older study’s results showing that ME patients have gut bacteria that is not just different from controls, but different in a predictable manner, with Firmicutes and Bacterioides off. Using a machine-learning approach, the Melbourne team was able to identify the right patient utilizing a sample of their gut bacteria over 80% of the time.
HORNIG ET AL, 2015:
Mady Hornig and her team at Columbia University discovered a pattern of upregulated inflammatory and anti-inflammatory markers in early ME (first three years after onset) all of which were inverted in late ME (over three years after onset). Long-term patients’ immune markers were lower even than those of controls.
Dysregulated immune markers included IL-12p40, IL-12p70, IFN-gamma, TNF-alpha, and GM-CSF (CSF2). The marked involvement of interferon-gamma points to an initial infective trigger, as it is the product of activated T-cells, natural killer cells, and macrophages.
Hornig’s study, besides pointing to a future blood test for ME, is the first to identify a two-stage illness, with an acute phase and a chronic phase.
NEWTON ET AL, 2015:
Julie Newton and her team discovered that muscle cells of patients with ME had increased myogenin expression but decreased IL-6 secretion in comparison to controls and, when an electrical pulse was sent through the tissue to simulate exercise, muscle cells of ME patients demonstrated impaired AMPK activation and impaired uptake of glucose. Cells responded normally to insulin.
FLUGE AND MELLA:
Fluge and Mella found that the anti-cancer drug Rituximab caused complete remission in a significant percentage of ME patients.
Other suggestions?
[Edit: changed first Fluge and Mella citation to 2016 -- it came out in December of 2016. I had it as a 2017 article.]
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