Charlie Hillier

@charliehillier.bsky.social

Science, Molecular Biology, Myalgic Encephalomyelitis/Chronic Fatigue Syndrome

1/7 Excited to share our new paper co-produced with @simonmcg.bsky.social. We found that previous reports of ME having two age peaks in Norway replicates in two different datasets and across 7/10 European countries we examined, suggesting this is a generalisable- and distinctive- feature of ME.

Three onset age distributions for ME/CFS, one for Norway, one for the combined 9 other countries, and one for a DecodeME subcohort, with fitted splines.

Read our paper with @simonmcg.bsky.social @aryback.bsky.social here! We report that ME/CFS has a bimodal age onset pattern with peaks in adolescence and early middle age. It is unusual for a disease to have more than one onset peak, a feature that may provide a clue into the causes of the illness.

Tom Kindlon@tomkindlon.bsky.social · 5mo ago

Incidence age is bimodal for Myalgic Encephalomyelitis/Chronic Fatigue Syndrome, with higher severity burden for early onset disease by @simonmcg.bsky.social et al academic.oup.com/ooim/advance... "early onset peak with a mean of 16.0 years old...& a late onset peak at 36.6 years old" #MEcfs #PwME

Abstract
Myalgic Encephalomyelitis, or Chronic Fatigue Syndrome (ME/CFS), is a disease of uncertain origin. Studies of Norwegian health records have suggested that ME/CFS incidence across age groups is bimodal–a characteristic that could provide insight into the aetiology of the disease. Here, we analysed survey data from over 9,000 respondents with ME/CFS from 10 European countries, and observe an early onset peak with a mean of 16.0 years old (standard deviation [sd]: 4.3) and a late onset peak at 36.6 years old (sd: 10.5). Statistical support for multimodal onset age was evident in 7 of the 10 countries examined. Infection as a trigger for ME/CFS is 10 percentage points higher among early compared to late onset disease (P = 2.1 × 10−13). Early onset ME/CFS was associated with greater odds of being severely or very severely affected (OR = 2.15, 95% CI [1.84—2.51], p < 2 × 10−16). Those with first degree relatives with ME/CFS had greater odds of early than late onset ME/CFS (OR = 1.43, 95% CI [1.25—1.63], P = 4.4 × 10−07). We further validated our findings in a UK dataset where we replicated bimodal onset age and observed significantly greater odds of glandular fever/infectious mononucleosis as a trigger in early onset cases (OR = 2.32, 95% CI [1.99—2.71], P = 2.4 × 10−24). Our findings suggest that incidence of ME/CFS peaks in adolescence and in early middle-age and that early onset ME/CFS is more common in those with affected relatives, more often triggered by infection, and associated with more severe disease.

1/2 New pre-print: We performed a large-scale replication testing the effect of serum from 67 pwME and 53 healthy donors on muscle cell mitochondria, revealing no significant differences. This suggests earlier results may not be true for people with ME in general. doi.org/10.1101/2025...

Indistinguishable mitochondrial phenotypes after exposure of healthy myoblasts to myalgic encephalomyelitis or control serum

Myalgic Encephalomyelitis (ME)/Chronic Fatigue Syndrome is a disease of uncertain aetiology that affects up to 400,000 individuals in the UK. Exposure of cultured cells to the sera of people with ME has been proposed to cause phenotypic changes in these cells in vitro when compared to sera from healthy controls. ME serum factors causing these changes could inform the development of diagnostic tests. In this study, we performed a large-scale, pre-registered replication of an experiment from Fluge et al (2016) that reported an increase in maximal respiratory capacity in healthy myoblasts after treatment with serum from people with ME compared to serum from healthy controls. We replicated the original experiment with a larger sample size, using sera from 67 people with ME and 53 controls to treat healthy cultured myoblasts, and generated results from over 1,700 mitochondrial stress tests performed with a Seahorse Bioanalyser. We observed no significant differences between treatment with ME or healthy control sera for our primary outcome of interest, oxygen consumption rate at maximal respiratory capacity. Results from our study provide strong evidence against the hypothesis that ME blood factors differentially affect healthy myoblast mitochondrial phenotypes in vitro. ### Competing Interest Statement The authors have declared no competing interest. Action for ME, https://ror.org/0569v7v35, Clare Francis Research Fellowship

doi.org

@actionforme.bsky.social are running their Big Give campaign this week to raise money for ME and ME research, with matched donations up to Monday! AfME have been supporting Audrey Ryback's important research on blood factors in ME. Do consider donating and sharing! donate.biggive.org/campaign/a05...

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