On what basis? I thought that exercise generated a rise in GH normally and that prolonged inactivity blunted the GH rise in any subsequent activity.
First, with regards to GHD and this study, we are talking about four of eleven subjects/patients identified as hormonally deficient. Throw those four out and you still have a majority of severely ill subjects that were deficient for other hormones.
But why throw those four out? Of all the deficiencies, the symptom profile for GHD is probably as close to the symptom profile of severe ME/CFS as any hormone deficiency (an earlier complaint of yours – see below).
Take a look at Table 2
Group Hormone levels - GH peak (Glucagon Stim test),
1A(n = 13) Group - 2.3 (1.2) - P < .001 Statistically significant vs group 1B, 1C, and controls.
1B (n = 7) Group - 5.9 (0.7)
1C (n = 10) - 6.2 (0.7)
Normal controls (n = 25) 6.9 (2.5)
Group Hormone levels - IGF-1
1A(n = 13) Group - 160.2 (50.8
) - P < .001 Statistically significant vs group 1B, 1C, and controls.
1B (n = 7) Group - 234.3 (20.3)
1C (n = 10) - 212.9 (33.6)
Normal controls (n = 25) 225 (26.3)
In the control group, GH peak was 6.9 with a SD of 2.5. In group 1A (thirteen subjects), GH Peak in response to stimulation was 2.3 with a SD of 1.2. Only four of those 13 were determined to be GHD (GH =< 1.18). The high Ab ME/CFS group (which was also the severe symptom group) had an AVERAGE GH peak that was 33% that of the controls and very close to 30% of the other two patient groups.
There is data to suggest the need for a lower cut-off in patients who are overweight/obese adults and in those with glucose intolerance but there is no evidence to suggest the need for a lower cut-off to account for activity levels (this was not a study measuring short-term GH response to exercise as that is not the diagnostic standard).
In this study, “GHD was diagnosed by the presence of low normal basal IGF-1 AND impaired GH response (< 1.18 mcg/L) to a glucagon stimulation test.” This is the recommended standard for suspicion of GHD and subsequent Glucagon Stimulation Testing/GHD diagnosis.
Direct comparisons to the data citing concerns about obesity glucose intolerance are impaired due to laboratory differences in standardization (a recognized issue across the field).
From the current version of EndoText (https://www.endotext.org/chapter/gr...in-assessing-adult-growth-hormone-deficiency/):
“Several recent retrospective studies have questioned the diagnostic accuracy of the GST when the GH cut-point of 3mg/L is applied to overweight/obese adults (
26-29) and in those with glucose intolerance (
28,
29), while Hamrahian et al. (
30) demonstrated in a prospective study of 28 patients by comparing the GST to the ITT that a lower GH cut-point of 1 mg/L improved its diagnostic accuracy with a 92% sensitivity and 100% specificity.”
In conclusion, De Bellis, et al. write: “…our results show for the first time that the GH peak in response to glucagon was significantly lower in patients with severe ME/CFS than in controls and in those with moderate/mild disease. For this reason, we suggest that several of the main typical symptoms in severe ME/CFS, such as fatigue, myalgia, contractility, delaying muscle recovery and function, exertional malaise, neurocognitive dysfunction, and physical disability may be related to severe GHD.
This also considers the multifarious role played by GH/IGF-1 secretions and in particular the important IGF-1 role in many biological processes of neurons, including neuroprotective action, mitochondrial protection, antioxidant defense, and reduction of CNS inflammation by improving brain damage (42). In this regard, we hypothesize that autoimmune GHD may amplify the severe damage in ME/CFS determined by cytokines due to the absence of neuroprotective, antioxidant, and antineuronal functions normally exerted by IGF-1.”
Lastly, hormonal deficiencies, specifically in GH, as a response to infectious disease are not something with which De bellis is unfamiliar:
Tanriverdi, F., De Bellis, A., Teksahin, H.
et al. Prospective investigation of pituitary functions in patients with acute infectious meningitis: is acute meningitis induced pituitary dysfunction associated with autoimmunity?.
Pituitary 15, 579–588 (2012).
https://doi.org/10.1007/s11102-011-0371-7
“The risk of hypopituitarism, GH deficiency in particular, is substantially high in the acute phase, after 6 and 12 months of the acute infectious meningitis. Moreover we found that 6th month after meningitis is too early to make a decision for pituitary dysfunction and these patients should be screened for at least 12 months. In addition, the occurrence of AHA and APA positivity due to acute infectious meningitis was demonstrated for the first time.”
Remarkably similar results in a group with no history of reduced activity (presumably aside from those brought about by their current health issues).
In conclusion, at this point, no one is claiming that ME is GHD but given the results of the present study, there needs to be significantly more work to understand what is going on here.
