Replicated blood-based biomarkers for Myalgic Encephalomyelitis not explicable by inactivity, 2024, Beentjes, Ponting et al

Jonathan Edwards said:
Wasn't the glucose profile the other way around in McGregor (low) - opposite of insulin resistance?
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I need to rewatch the video on the actual glucose response test measurement results. I did find this 2019 McGregor paper (link) which reported a 1.2-fold rise in glucose in the results section.
Glucose was increased in the ME/CFS cases (both NoPEM and PEM 1.2-fold higher versus controls).
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The paper also highlights the glucose : lactate ratio in PEM as changed.
The principal biochemical change related to the 7-day severity of PEM was the fall in the purine metabolite, hypoxanthine. This decrease correlated with alterations in the glucose:lactate ratio highly suggestive of a glycolytic anomaly.
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Jonathan Edwards said:
Wasn't the glucose profile the other way around in McGregor (low) - opposite of insulin resistance?
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I believe he said glucose went up (at least intitially) as it would in burn victims. I don't think he mentioned insulin resistance specifically... Can you have an increase in serum glucose without insulin resistance, say by increased gluconeogenesis?
 
It is confusing. Does anyone know if there was a paper published on the Don Lewis clinic glucose tolerance testing?

Slide at 11:00 showing:
* 641 of 777, 82%, ME/CFS patients from Don Lewis who had a glucose tolerance test with complete data had a truncated glucose tolerance test response. ~20% of those were hypoglycemic at 60 mins.
* 54 of 777, 7%, had a flat response and at 60 mins ~60% (32/54) of those exhibited hypoglycemia - first column on graph, purple colour.
* Only 82 of 777, 11%, had a normal response!
* Note : 1155 glucose tests. There was a large 33% excluded for not having complete data.
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I don't see if the hypoglycemia here is indicating insulin resistance. Some of these people are making too much insulin (hyperinsulinemic) and that is causing their blood sugars to drop. If they were insulin resistant I would expect hyperinsulinemia to make a normal blood sugar, not a low sugar. That's the definition of insulin resistance, yes? Huge amounts of insulin don't make your sugar go down much if at all. Here huge amounts of insulin are causing low sugars... in some.

What does a truncated response mean? The test stopped before time?
 
A truncated test is a test that just samples at one hour. I don't know what a 'truncated response' would be, if there is such a thing.
 
Jonathan Edwards said:
A truncated test is a test that just samples at one hour. I don't know what a 'truncated response' would be, if there is such a thing.
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Sorry, I was going to add this graph from 9:55 in the video to explain what they mean by truncated but I ran out of energy to post it.

This is a reduced number of patients n=41 that also had insulin data and the slide explains the characteristics of the different responses. Insulin response is stated as being normal and there appears to be low glucose absorption (utilization for energy?).

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Note that the Beentjes paper did not measure insulin resistance directly, they show that proxy markers for insulin resistance characteristics are elevated. What I'm wondering, are Beentjes et al and McGregor et al looking at the same thing but from different angles?

Do you think we can say for certain that Beentjes et al proves there is insulin resistance or could be it low glucose absorption/utilisation as written in the slide?
 
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