USA: Center for Solutions for ME/CFS - news and updates from Columbia University's NIH funded center, Lipkin

[Andy]

Lipkin seems to suggest that the planned GWAS and collaboration with DecodeME was cancelled

There never was a US-based GWAS with DecodeME planned. What was planned was that Chris would lead on a US-based GWAS, which would follow the DecodeME template, and the data from that would be able have been able to be used in a meta analysis along with the DecodeME data.

 

[Sasha]

There never was a US-based GWAS with DecodeME planned. What was planned was that Chris would lead on a US-based GWAS, which would follow the DecodeME template, and the data from that would be able have been able to be used in a meta analysis along with the DecodeME data.

What were the funding plans for that? Is that not going forward? I don't remember hearing about it.

 

[Andy]

What were the funding plans for that? Is that not going forward? I don't remember hearing about it.

Details here,

W

Post in thread 'USA: Center for Solutions for ME/CFS - news and updates from Columbia University's NIH funded center, Lipkin'

Jun 5, 2025

Has this group done anything to move the needle in ME/CFS?

They have published extensively for 25 years, had close ties with the CDC via Ian Lipkin to try and influence things, and I think Ian Lipkin advocated strongly for the need for NIH Research centers with sufficient funding. They were the first to establish a biospecimen repository / biobank which NIH has now taken over. The team was planning to try and replicate DecodeME findings in a US cohort.

This is from NIH Reporter - they had one of two NIH center grants that were renewed for 5 years in 2024 but that was stopped by the...

• wigglethemouse

• 

 

[ME/CFS Science Blog]

hat were the funding plans for that? Is that not going forward? I don't remember hearing about it.

More info about it here:

RePORT 〉 RePORTER

reporter.nih.gov

SUMMARY The epidemiology of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) indicates a significant relationship in the population for both close (first or second cousins) and distant (third cousins) relatives. Our objective is to identify DNA differences that distinguish people with ME/CFS from healthy controls. We will use a well-established, well-powered, genome-wide association study (GWAS) design that has a demonstrated ability to identify genes, as well as novel molecular and cellular pathways, contributing to susceptibility for other complex diseases. GWAS have shown that about 10-times more cases will be needed to be well-powered. We will obtain saliva DNA from a minimum of 5,000 individuals meeting Institute of Medicine/National Academy of Medicine (IOM/NAM) and/or Canadian Consensus Criteria (CCC) for ME/CFS. ME/CFS subjects will be recruited via a questionnaire created by the Solve ME/CFS Initiative (Solve ME) and will utilize a smartphone application designed by Care Evolution. Genotyping data from these US-based ME/CFS cases will be compared to data from 400,000 healthy controls genotyped by the Kaiser Permanente Research Bank (KPRB) using the Axiom Precision Medicine Diversity v2 Plus Array. Once data from US-based cases is obtained (Solve ME and KPRB), it will be used in a US case-control GWAS, before being trans-ancestry meta-analyzed with UK cohort data from the DecodeME Study and the UK Biobank (UKB). The two cohorts are complementary by providing opportunities for replicating associated loci and for using diverse genetic ancestries to enhance predictive power. We anticipate that genetic associations will provide the evidence base necessary to improve the perception of ME/CFS among health care professionals and the general public and yield insights into risk and pathogenesis that have the potential to result in interventions.

 

[bobbler]

In this interview with David Tuller, Lipkin seems to suggest that the planned GWAS and collaboration with DecodeME was cancelled. Instead they seem to have set up a different genetics study. They will look at genes of families where more than one person is affected, in collaboration with the University of Utah and the Bateman Horne Center

I like the taking measures for good day vs bad days in a broad sense getting tackled

But I think this in itself presents all sorts of questions. Given PEM is after but something is also ‘accumulating’ when eg I think back to when I was working and had to work out new ridiculous levels to push my body to ‘turn up’ (it’s not pushing thru when you set your alarm 4hrs early to drag it up or go to work in one hours sleep so many days a week - I need to stop having that under stated by how I talk about it, what I went thru was ridiculous snd then the behaviour you have to do and live in to make those others happy gets held against you).

Anyway I’m starting to think one issue is researchers thinking they need to ‘manufacture bad days’ as the issue when really find a truly good day would be the hard bit. Everyone having a quiet 10dayd mostly in bed might do it but then you end up still not having their body for no reason just going into not sleeping well or pain (so what is happening there and when did it start and with what and then which things show on a test and when).