Somatostatin Analogs and Growth Hormone Suppressors

D

DHagen

Senior Member (Voting Rights)
Based upon some of the recent discussion concerning the hypothalamus and the potential involvement of growth hormone (GH), I was curious about whether any pwME had reported experiences with agents acting upon GH. Both dopamine agonists (already a topic of great interest) and somatostatin analogs appear to be possibilities in this regard. I am just starting to look into this, but thought I would start a thread in case anyone has any thoughts or (as is almost always the case), better research skills than I.

Or if someone wants to explain why the whole idea is just nonsense, that's good too.

So far I am coming up short on ME/CFS experiences or trials, but it does appear that at least Octreotide has been used for POTS, with some positive reports and some nasty side effects, although one 2015 case report suggests that using a pump rather than intermittent injections can alleviate the worst of these.
 

Treatment of Refractory Postural Tachycardia Syndrome with Subcutaneous Octreotide Delivered Using an Insulin Pump​

Case Reports in Medicine 2015
Muhammad Khan, Jing Ouyang, Karen Perkins, John Somauroo, Franklin Joseph
https://doi.org/10.1155/2015/545029

Abstract​

Postural Tachycardia Syndrome (PoTS) represents a disorder of the autonomic nervous system that results in symptoms of orthostatic intolerance. Despite having a severe impact on the patient’s quality of life, the current treatment options for PoTS are based on limited evidence. Subsequently, this results in clinicians having to utilise a variety of treatment regimens in the hope of successfully providing symptomatic relief. However, the options available for PoTS are not without significant side effects that can worsen an already debilitating condition. Our cases provide a further novel treatment option for clinicians to consider in PoTS refractory to established treatments.

https://onlinelibrary.wiley.com/doi/10.1155/2015/545029
 
(From the Thread for Members to Request a Paper to be Posted):

In light of the recent discussion concerning GH - does anyone have access to this paper, which appears to suggest that IFN-α can induce "low-grade chronic fatigue syndrome" (however that was defined in 1996) and that the addition of octreotide (a somatostatin analog that could suppress GH) alleviated or eliminated this side effect?

lnterferon-α versus Somatostatin or the Combination of Both in Gastro-Enteropancreatic Tumours​

Kjell Öberg

Digestion (1996) 57 (Suppl. 1): 81–83.
https://doi.org/10.1159/000201403

Abstract:
Interferon-α (IFN-α) has a direct anti-tumour effect and is an immunomodulator. Somatostatin analogues, by contrast, when used to treat neuroendocrine tumours, control the secretion and peripheral effects of hormones, although at high doses they induce apoptosis. We have used IFN-α to treat > 350 patients with neuroendocrine tumours, and combining our and published data gives a median 44% biochemical response rate and 11% tumour response rate. Side-effects are mainly flu-like symptoms, then low-grade chronic fatigue syndrome. 15% may develop autoimmune reactions. The side-effects profile of somatostatin analogues is better but patients must take frequent injections and may have bile problems. We combined IFN-α and octreotide treatment in 24 patients with malignant carcinoid tumours who did not respond biochemically to high-dose (300 μg/day) octreotide alone. Biochemical response occurred in 77% but no significant anti-tumour effect was noted besides disease stabilisation in 4 cases. The combination therapy had an effect on clinical symptoms rather than tumour mass. Interferon was better tolerated when in the combination.
 
Thank you for starting this thread! This is something I'm interested in.
DHagen said:
In light of the recent discussion concerning GH - does anyone have access to this paper, which appears to suggest that IFN-α can induce "low-grade chronic fatigue syndrome" (however that was defined in 1996) and that the addition of octreotide (a somatostatin analog that could suppress GH) alleviated or eliminated this side effect?
Click to expand...
Unfortunately, my university does not have access to this paper. It's quite rare that that happens! Hopefully someone else can help you get the full thing.
 
There is also pegvisomant that's used in acromegaly, it blocks growth hormone receptors, is used subcutaneous and seems to be better tolerated than somatostatin analogues.

https://link.springer.com/article/10.1007/s11154-025-10002-9

It seems to have positive effects in acromegaly not only on growth but also on vascular health and insuline metabolism.

Overall, though, I do wonder if we wouldn't also have to show other symptoms of acromegaly if growth hormone is so crucial. Or maybe this wouldn't be the case, if the hypophysis is healthy and all receptors besides those in the hypothalamus are also behaving normally.
 
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The paper below (thread here, did not attract much attention) noted elevated Growth Hormone Releasing Hormone (GHRH) in pwLC suffering from neurological symptoms (+25% vs controls).

"Proteins IFNλ1 and GHRH that in combination with C5a and gliomedin diagnostic biomarkers differentiated Neuro-PASC subjects from healthy subjects with 100 % specificity"
Click to expand...

Blood diagnostic biomarkers for neurologic manifestations of long COVID​

AS Padhye, IJ Koralnik, BA Hanson, L Visvabharathy, RK DeLisle, G Tachas
Brain Behavior and Immunity Health (Sept. 2025)
doi: 10.1016/j.bbih.2025.101110

https://pmc.ncbi.nlm.nih.gov/articles/PMC12554056/
 
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