But it is still about the microbiome
After 4 decades dealing with Chronic Fatigue patients, I came to the conclusion that patients so affected have a poor immune-detox system, most of which is found in the gut and liver. In other words, those with a poor microbiome are more likely to experience a wide gamut of chronic symptoms and signs after a viral infection, particularly after COVID. Throw in stress with an overburdened Hypothalamus-Pituitary-Adrenal axis, and you have the perfect storm for CFS (now dubbed Myalgic Encephalomyelitis/Chronic Fatigue Syndrome) to develop. Most of these patients have some degree of Serotonin issues, be it synthesizing, or detoxifying it. Noting that 95% of Serotonin is in the intestines also points to the Brain-Gut connection. This is likely why many CFS and Long COVID patients have symptoms that point to the Vagus Nerve. Its anatomy is quite telling: 2/3 of its fibers ascend from the Gut to the Brain.
By now you can guess what you could do to lower the risk of ending up in the 10% of people who develop Long COVID or CS after a viral infection: improve your Microbiome. In short. Eat a ton of veggies and get off sugar. Taking Pre and Probiotics also helps.
References
Predictors of fibromyalgia, chronic fatigue in patients with IBS
HCP Live (10/31, Brooks) reports, “Findings from a recent study are calling attention to an increased prevalence of somatic comorbidities among patients with irritable bowel syndrome (IBS), highlighting increased odds of having fibromyalgia and chronic fatigue syndrome among this group.” Investigators “identified several factors including increasing age, female sex, white race, obesity, smoking, and hyperlipidemia as predictors for having a co-diagnosis of both fibromyalgia and chronic fatigue syndrome in patients with IBS.” The findings were published in Biomedicines.
Study traces long COVID symptoms to SARS-CoV-2 infection in gut
Healio Minute, October 19, 2023
Viral persistence and low depleted serotonin levels may be the cause of some Long COVID symptoms. SSRIs may effectively treat some patients with long COVID.
A new study links some neurocognitive symptoms of long COVID to persistent SARS-CoV-2 infection in the gut, which triggers a series of reactions that lowers serotonin levels. The finding suggests that selective serotonin reuptake inhibitors (SSRIs) may reduce a patient’s risk for post-COVID-19 conditions. A study linked low serotonin levels to some neurocognitive symptoms of long COVID, suggesting SSRIs may be an effective treatment. According to the CDC, nearly one in five adults in the United States with a previous case of COVID-19 experience symptoms of long COVID.
The long COVID symptoms brain fog, fatigue and memory loss appear to be linked to reduced circulating levels of serotonin, Andrea C. Wong, PhD, and colleagues at the University of Pennsylvania Perelman School of Medicine, and colleagues wrote in the study, published this week in Cell.
The Relationship between COVID-19 and Hypothalamic–Pituitary–Adrenal Axis: A Large Spectrum from Glucocorticoid Insufficiency to Excess
Int. J. Mol. Sci. 2022, 23(13), 7326
Coronavirus disease 2019 (COVID-19) is a highly heterogeneous disease regarding severity, vulnerability to infection due to comorbidities, and treatment approaches. The hypothalamic–pituitary–adrenal (HPA) axis has been identified as one of the most critical endocrine targets of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that might significantly impact outcomes after infection. Herein we review the rationale for glucocorticoid use in the setting of COVID-19 and emphasize the need to have a low index of suspicion for glucocorticoid-induced adrenal insufficiency, adjusting for the glucocorticoid formulation used, dose, treatment duration, and underlying health problems. We also address several additional mechanisms that may cause HPA axis dysfunction, including critical illness-related corticosteroid insufficiency, the direct cytopathic impacts of SARS-CoV-2 infection on the adrenals, pituitary, and hypothalamus, immune-mediated inflammations, small vessel vasculitis, microthrombotic events, the resistance of cortisol receptors, and impaired post-receptor signaling, as well as the dissociation of ACTH and cortisol regulation. We also discuss the increased risk of infection and more severe illness in COVID-19 patients with pre-existing disorders of the HPA axis, from insufficiency to excess. These insights into the complex regulation of the HPA axis reveal how well the body performs in its adaptive survival mechanism during a severe infection, such as SARS-CoV-2, and how many parameters might disbalance the outcomes of this adaptation.
Impaired Vagal Activity in Long-COVID-19 Patients
J. Viruses 2022, 14(5), 1035
Abstract
Long-COVID-19 refers to the signs and symptoms that continue or develop after the “acute COVID-19” phase. These patients have an increased risk of multiorgan dysfunction, readmission, and mortality. In Long-COVID-19 patients, it is possible to detect a persistent increase in D-Dimer, NT-ProBNP, and autonomic nervous system dysfunction. To verify the dysautonomia hypothesis in Long-COVID-19 patients, we studied heart rate variability using 12-lead 24-h ECG monitoring in 30 Long-COVID-19 patients and 20 No-COVID patients. Power spectral analysis of heart rate variability was lower in Long-COVID-19 patients both for total power (7.46 ± 0.5 vs. 8.08 ± 0.6; p < 0.0001; Cohens-d = 1.12) and for the VLF (6.84 ± 0.8 vs. 7.66 ± 0.6; p < 0.0001; Cohens-d = 1.16) and HF (4.65 ± 0.9 vs. 5.33 ± 0.9; p = 0.015; Cohens-d = 0.76) components. The LF/HF ratio was significantly higher in Long-COVID-19 patients (1.46 ± 0.27 vs. 1.23 ± 0.13; p = 0.001; Cohens-d = 1.09). On multivariable analysis, Long-COVID-19 is significantly correlated with D-dimer (standardized β-coefficient = 0.259), NT-ProBNP (standardized β-coefficient = 0.281), HF component of spectral analysis (standardized β-coefficient = 0.696), and LF/HF ratio (standardized β-coefficient = 0.820). Dysautonomia may explain the persistent symptoms in Long COVID-19 patients. The persistence of a procoagulative state and an elevated myocardial strain could explain vagal impairment in these patients. In Long-COVID-19 patients, impaired vagal activity, persistent increases of NT-ProBNP, and a prothrombotic state require careful monitoring and appropriate intervention.
