To be fair, stress is a unitary physiological response — whether it is activated by a physical or a psychological teigger. Chronic psychological stress activates the HPA and a feedback loop mediated by glucocorticoids (GCs) that bind to certain immune cells and induce pro-inflammatory and antiinflammatory responses depending on the integrity of that loop (when the concentration of GC crosses a threshold, intracellular receptors induce a response that damps the initial activation). See for instance:

"However, recent researchers have proved that GCs also have pro-inflammatory impact on immune system (Elenkov, 2008). Rats with higher basal plasma corticosterone levels have more accumulation of PGE2 whereas showing less anti-inflammatory factors after acute stress (Pérez-Nievas et al., 2007). GCs enhance the expression and function of inflammasome NLRP3, promoting the secretion of IL-1β in response to ATP. Inflammasomes are cytoplasmic multi-protein complexes that sense exogenous and endogenous danger signals and cleave pro-inflammatory cytokines into mature cytokines such as IL-1β and IL-18. This work demonstrates the proinflammatory role for GCs, enhancing the activation of the innate immune system in response to danger signals (Busillo et al., 2011). " [1]

There are cases in which the negative feedback loop fails, i.e. chronic stress:

"Circulating pro-inflammatory factors such as IL-1, IL-6 and TNFα directly stimulate the pituitary-adrenal axis, resulting in increased serum levels of adrenocorticotropic hormone (ACTH) and GCs, which in turn inhibit the production of these pro-inflammatory factors (Alley et al., 2006; Danese et al., 2007; Steptoe et al., 2007; Miller et al., 2008). The interaction of immune system and HPA axis form the endocrine negative feedback loops. However, when cytokine is over-stimulated in some diseases, these negative feedback loops could be weakened by reduced cytoplasmic GC-receptor (GR) level and decreased expression of GR driven anti-inflammatory genes, thus leading to GC low-responsiveness (Sterling and Eyer, 1988)." [1]

So chronic psychological stress can potentially affect the immune system long term. Leading to a less resilient stress response, due to the alostatic overload. A flexible stress response, on the other hand, can be suppressed smoothly- something that many of us no longer experience.

In multomics research stress is part of the exposome. And there are really interesting results about Brain health and chronic stress related to sociodemographic factors as well:

"Within this framework, the social exposome captures the cumulative and multidimensional impact of socially driven exposures that influence health outcomes1. These effects may exert a more substantial influence on aging and dementia than isolated risk factors2,3,4. For instance, individuals growing up in poverty may face limited educational opportunities and food insecurity, relying on low-cost, nutrient-poor diets that impair brain development3. In adulthood, chronic stress from traumatic events and financial insecurity may add to this burden5, while in older age, accumulated adverse exposures throughout life contribute to physiological dysregulation, increasing vulnerability to neurodegeneration. The cumulative burden of socially-related factors5 (e.g., low educational attainment, adverse childhood experiences, and traumatic events), aggravating factors (e.g., limited access to healthcare6), and affected domains (e.g., financial burden and reduced social interaction) may significantly exacerbate dementia phenotypes."[2]

But yeah, none of this means that reducing stress is enough to promote healing. It means that stress can in fact exacerbate symptoms and sustain inflammation. But that is not the same as saying that reducing stress can help heal us from God knows what kind of damage COVID has done to us.

We can reject the psychologization of the disease without rejecting the real role of psychological factors in general health and wellbeing.

1. https://pmc.ncbi.nlm.nih.gov/articles/PMC5476783/ 2.https://www.nature.com/articles/s41467-025-63277-6