Exercise as a Moderator of Persistent Neuroendocrine Symptoms of COVID-19, 2023, Rebello, Candida et al

[Mij]

KEY POINTS

• Postacute COVID-19 hyperglycemia likely results from lingering inflammation or chronic psychological stress that is compounded by β-cell dysfunction.
• Chronic psychological stress produces a dysregulated and overactive hypothalamic-pituitary-adrenal axis that drives sympathetic nervous system activation and an exaggerated immune response, which promotes insulin resistance and β-cell dysfunction.
• High local concentrations of interleukin-1β (IL-1β) in the β-cell microenvironment inhibit insulin secretion, trigger β-cell dysfunction and apoptosis, increase levels of glucose, and prompt IL-1β autostimulation.
• Regular exercise plays a key role in protecting against psychologic and metabolic aspects of stress to alleviate insulin resistance and symptoms of depression.
• We hypothesize that exercise will attenuate β-cell dysfunction and the long-term neuroendocrine effects of COVID-19 by moderating the inflammatory response, supporting brain homeostasis, and promoting insulin sensitivity.

Abstract
Precipitated by chronic psychological stress, immune system dysregulation, and a hyperinflammatory state, the sequelae of postacute COVID-19 (long COVID) include depression and new-onset diabetes. We hypothesize that exercise counters the neuropsychiatric and endocrine sequelae of long COVID by inducing the release of circulating factors that mediate the anti-inflammatory response, support brain homeostasis, and increase insulin sensitivity.

https://journals.lww.com/acsm-essr/Fulltext/2022/04000/Exercise_as_a_Moderator_of_Persistent.2.aspx

 

[Andy]

• 
  
  • We hypothesize that exercise will attenuate β-cell dysfunction and the long-term neuroendocrine effects of COVID-19 by moderating the inflammatory response, supporting brain homeostasis, and promoting insulin sensitivity.

I hypothesize that the authors are wrong.

 

[rvallee]

Postacute COVID-19 hyperglycemia likely results from lingering inflammation or chronic psychological stress

Uh huh. Sure. Psychogenic hyperglycemia. Why not? Let's just make stuff up, who cares?!

Zero attempt at making sense. Psychogenic hyperglycemia, treated by exercise? Come on. At this point, it's not really possible in EBM to do the thing with submitting joke papers to test if they get accepted, clearly anything can as long as it has the proper cultural and political slant.

And, yeah, I wasn't sure but they're saying it's not COVID, it's stress. How is this any different from HIV denial? Most HIV denial models were psychosocial, not a coincidence.

 

[rvallee]

Something about some PACE-like trial buried in there:

Program ACTIVE (Adults Coming Together to Increase Vital Exercise) was a pilot and feasibility study to assess the effect of an intervention that combined community-based aerobic exercise and CBT in patients with type 2 diabetes and depression. The program demonstrated feasibility of the intervention, and participants experienced improvements in depressive symptoms and glycemic control, which were sustained 3 months after the intervention. Participants also reported a host of improvements in psychosocial outcomes assessed in the study (23).

Program ACTIVE II was a multicenter study that used a community-engaged research approach to parse out the effects of exercise and CBT (24). Program ACTIVE II demonstrated that exercise alone, CBT alone, and the combination were comparable in improving depressive symptoms. There was no effect of the interventions on HbA1C compared with usual care. However, in an exploratory analysis that included patients with baseline elevated HbA1C (>7%), combination therapy showed a clinically significant reduction of 0.74%. Importantly, the improvements in psychosocial outcomes were consistent with Program ACTIVE (24).​

This is peak pseudoscience. Absurd. Medicine has lost connection with reality.