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- Title
Oxytocin, the panacea for long-COVID? a review.
- Authors
Diep, Phuoc-Tan; Chaudry, Mohammed; Dixon, Adam; Chaudry, Faisal; Kasabri, Violet
- Abstract
In this hypothesis paper we explore the underlying mechanisms for long-COVID and how the oxytocinergic neurones could be infected by SARS-CoV-2 leading to a reduction in plasma oxytocin (OXT). Furthermore, we aim to review the relevance of OXT and hypothalamic function in recovery from long-COVID symptoms and pathology, through exploring the pro-health effects of the OXT neuropeptide. A review of published literature was surveyed using Google Scholar and PubMed. Numerous experimental data can be shown to correlate with OXT and long-COVID symptoms and conditions, thus providing strong circumstantial evidence to support our hypothesis. It is postulated that the reduction in plasma OXT due to acute and post-viral damage to the hypothalamus and oxytocinergic neurones contributes to the variable multi-system, remitting and relapsing nature of long-COVID. The intranasal route of OXT application was determined to be most appropriate and clinically relevant for the restoration of oxytocinergic function post COVID-19 infection. We believe it is imperative to further investigate whether OXT alleviates the prolonged suffering of patients with long-COVID. Succinctly, OXT may be the much-needed post-pandemic panacea. – A comparison of long-COVID pathology with OXT therapeutic mechanisms was performed – Following advances in neuroendocrinology and proposed use of OXT as an acute antiviral for COVID-19; we elaborate OXT mechanisms in treating long-COVID, via therapeutic relevance and methods of administration. – Further demonstration of OXT levels for different demographic and susceptibility groups, acute levels in COVID-19 patients and periodic monitoring of OXT levels is warranted.
- Subjects
POST-acute COVID-19 syndrome; COVID-19; OXYTOCIN; HYPOTHALAMUS; PATIENT monitoring
- Publication
Hormone Molecular Biology & Clinical Investigation, 2022, Vol 43, Issue 3, p363
- ISSN
1868-1883
- Publication type
Article
- DOI
10.1515/hmbci-2021-0034