Long COVID is Not Psychosomatic
This post is part of a new blog series focusing on long COVID. See parts 1, 2, 3, and 4.
Long COVID is a complex chronic illness. Its symptoms can be highly inconsistent, and with no diagnostic tests for the disease, it can be difficult to identify and treat.1,2 The lack of measurable indicators for long COVID, combined with its unpredictable nature, can also make it difficult for people to understand the disease. As a result, false claims that long COVID is a psychosomatic illness – an illness caused by mental factors rather than physical ones – are all too common.
According to one study, 82% of long-haulers have experienced psychologization of their illness – having their illness explained by psychological factors such as stress or poor mental health.3 You can also look at long COVID groups on social media to see countless personal stories of individuals being psychologized by healthcare providers, family and friends, and the general public. Long-haulers are often told that it’s our mental health causing our illness, with our long COVID symptoms commonly misdiagnosed and misinterpreted as depression or anxiety. Many of us have heard, “it’s all in your head.”
The truth, however, is that long COVID is not psychosomatic.
Research on long COVID increasingly points to physical factors as the root causes of the disease. Theories on the underlying mechanisms of long COVID are complex, and while I can’t describe them all in one post, I have summarized a few. These theories include:
- Viral persistence. The SARS-CoV-2 virus or its remnants may linger in the body long after acute COVID-19 infection.4,5 This viral persistence may trigger chronic pro-inflammatory responses throughout the body, resulting in long COVID symptoms.
- Viral reactivation. COVID-19 may reduce immune defenses, allowing latent viruses (e.g., human herpesviruses and Epstein Barr virus) to reactivate.6,7 The reemergence of these viruses may result in long COVID symptoms such as fatigue.
- Nervous system dysfunction. COVID-19 may trigger pro-inflammatory and autoimmune responses against the nervous system, with long COVID linked to several autoantibodies that target the brain and its receptors.8 This may cause brain damage and disruption to neurological processes, resulting in long COVID symptoms such as fatigue, brain fog, and dysautonomia.
- Mitochondrial abnormalities. COVID-19 may damage mitochondria, cellular organelles responsible for producing energy.9,10 In long COVID, both the number of mitochondria and the rate of mitochondrial energy production may be affected, resulting in symptoms such as fatigue and muscle weakness.
- Endocrine dysfunction. COVID-19 may disrupt endocrine processes, with evidence of pro-inflammatory and autoimmune responses against the pituitary, adrenal, and thyroid glands in long COVID.11 This may result in a variety of symptoms, depending on which gland is affected and how.
- Vascular dysfunction. COVID-19 may damage the endothelium (the layer of cells that lines the insides of blood vessels), as well as promote microclotting.12,13 This may impair blood flow to tissues and reduce oxygen saturation, resulting in long COVID symptoms.
As you can see, there is plenty of evidence indicating that long COVID is caused by physical factors. To be clear, we still don’t know how to determine which mechanisms of disease apply to which patients, with no identified biomarkers that consistently apply to the entire spectrum of long-haulers.1,2 More research is needed to fully understand long COVID. However, enough progress has been made to definitively state that long COVID is not psychosomatic.
And while it is true that chronic illnesses are associated with increased risk of mental health issues like depression and anxiety,14 it’s often the chronic illness that causes the mental health issue – not the other way around. With mental functioning tied to physical brain function, depression and anxiety in long COVID may be the direct result of COVID-19’s effects on the brain.8 Moreover, chronic illness is stressful, especially when it comes to complex diseases like long COVID. Struggling with this kind of illness will naturally result in some level of depression and anxiety in many people. This does not make them mentally ill – it makes them human.
Additionally, if long COVID were truly psychosomatic, we would expect standard psychological and psychiatric treatments to alleviate long COVID symptoms. While these treatments can help long-haulers cope with the mental burden of chronic illness, they will not erase their physical symptoms. For example, I struggle with gastroparesis (stomach paralysis) as a complication of long COVID, and it’s depressing when I can’t eat properly. Yet, there is no amount of therapy or antidepressants that will cure my stomach and make me feel better after I eat, because the gastroparesis isn’t caused by depression – depression is a result of the gastroparesis.
To reiterate, long COVID is a complex chronic illness of physical origin. It isn’t caused by mental health issues like depression or anxiety, and mental health treatments won’t cure its physical symptoms. Now, we must stop treating long-haulers as if their mental health is responsible for their illness. Long-haulers’ physical health concerns are too often dismissed as psychological, and we need better support. It’s crucial to understand that long COVID is not psychosomatic.
References
1. National Academies of Sciences, Engineering, and Medicine. A long COVID definition: a chronic, systemic disease state with profound consequences. Published 2024. Accessed September 22, 2025. https://nap.nationalacademies.org/read/27768/chapter/4
2. National Institutes of Health. Routine lab tests are not a reliable way to diagnose long COVID. NIH.gov. Published August 12, 2024. https://www.nih.gov/news-events/news-releases/routine-lab-tests-are-not-reliable-way-diagnose-long-covid
3. Buchner R, Sander C, Schindler S, Walter M, Scheibenbogen C, Schomerus G. “Have you considered that it could be burnout?”—psychologization and stigmatization of self-reported long COVID or post-COVID-19 vaccination syndrome. BMC Med. 2025;23(488). doi:10.1186/s12916-025-04335-0
4. Chen B, July B, Mohands S, Bradfute SB. Viral persistence, reactivation, and mechanisms of long COVID. eLife. 2023;12:e86015. doi:10.7554/eLife.86015
5. Scoullar MJ, Khoury G, Majumdar SS, Tippett E, Crabb BS. Towards a cure for long COVID: the strengthening case for persistently replicating SARS-CoV-2 as a driver of post-acute sequelae of COVID-19. Med J Aust. 2024;221(11):587-590. doi:10.5694/mja2.52517
6. Ruiz-Pablos M, Paiva B, Zabaleta A. Epstein-Barr virus‑acquired immunodeficiency in myalgic encephalomyelitis—is it present in long COVID? J Transl Med. 2023;21(1):663-692. doi:10.1186/s12967-023-04515-7
7. Vojdani A, Vojdani E, Saidara E, Maes M. Persistent SARS-CoV-2 infection, EBV, HHV-6 and other factors may contribute to inflammation and autoimmunity in long COVID. Viruses. 2023;15(2):400-429. doi:10.3390/v15020400
8. Almulla AF, Maes M, Zhou B, Al-Hakeim, HK, Vojdani A. Brain-targeted autoimmunity is strongly associated with Long COVID and its chronic fatigue syndrome as well as its affective symptoms. J Adv Res. 2024:1-13. doi:10.1016/j.jare.2024.11.011
9. Appleman B, Charlton BT, Goulding RP, et al. Muscle abnormalities worsen after post-exertional malaise in long COVID. Nat Commun. 2023;15(17):1-15. doi:10.1038/s41467-023-44432-3
10. Molnar T, Lehoczki A, Fekete M, et al. Mitochondrial dysfunction in long COVID: mechanisms, consequences, and potential therapeutic approaches. GeroScience. 2024;46(5):5267–5286. doi:10.1007/s11357-024-01165-5
11. Bansal R, Gubbi S, Kock CA. COVID-19 and chronic fatigue syndrome: an endocrine perspective. J Clin Transl Endocrinol. 2022;27:1-6. doi:10.1016/j.jcte.2021.100284
12. Haffke M, Freitag H, Rudolf G, et al. Endothelial dysfunction and altered endothelial biomarkers in patients with post‑COVID‑19 syndrome and chronic fatigue syndrome (ME/CFS). J Transl Med. 2022;20(138):1-11. doi:10.1186/s12967-022-03346-2
13. Kell DB, Laubscher GJ, Pretorius E. A central role for amyloid fibrin microclots in long COVID/PASC: origins and therapeutic implications. Biochem J. 2022;479:537-559. doi:10.1042/BCJ20220016
14. Swathi M, Manjusha S, Isatrin JV, Gururaj A. Prevalence and correlates of stress, anxiety, and depression in patients with chronic diseases: a cross-sectional study. MECPsych. 2023;30(66). doi:10.1186/s43045-023-00340-2
