Summary: Emerging evidence indicates a strong link between infections and psychiatric complications, driven largely by the body’s inflammatory response. Conditions like sepsis and pelvic inflammatory disease can lead to long-term psychiatric issues, including anxiety and depression, even after the infection is resolved. Chronic infections and persistent inflammation play a central role in these psychiatric outcomes.
Psychiatric illnesses are difficult to diagnose, and their causes remain poorly understood. This is because psychiatric issues develop slowly over the years. These issues are most likely caused by a combination of factors like stress, genetics, and even inflammation. Moreover, there are no reliable lab tests to confirm their diagnosis, and their diagnosis is mostly clinical.
Nonetheless, science is developing better insights into the causes of psychiatric illnesses. Now, a new study suggests that inflammation might be playing a greater role than imagined earlier.
Thus, one of the new studies published in the World Journal of Psychiatry explored the association between inflammation and increased risk of psychiatric disorders.
Emerging evidence suggests a strong association between infections and psychiatric complications, particularly highlighting how systemic infections can lead to psychiatric symptoms even in the absence of direct brain infection.
The COVID-19 pandemic provided a clear example, with a notable increase in psychiatric disorders, such as anxiety, depression, and cognitive impairments, observed in those infected. These complications often persisted long after the primary infection had resolved, indicating that the body’s inflammatory response plays a critical role in driving these psychiatric outcomes.
Sepsis, a systemic infection, frequently results in sepsis-associated encephalopathy (SAE), which occurs in up to 70% of patients.
SAE is characterized by neurological symptoms, including altered consciousness, cognitive deficits, and coma. The pathophysiology of SAE involves not only the direct effects of the systemic infection but also the body’s prolonged inflammatory response. This persistent inflammation can lead to chronic low-grade inflammation and subsequent psychiatric complications, demonstrating that these outcomes are likely tied to the body’s inflammatory processes rather than the infection itself.
Pelvic inflammatory disease (PID) represents another infection that can have systemic effects, including the potential to cause psychiatric symptoms.
PID, often caused by sexually transmitted infections, can lead to severe complications such as tubo-ovarian abscess (TOA), chronic pain, and infertility. Chronic PID, in particular, can lead to cell death through pyroptosis—a form of programmed cell death linked to inflammasome activation. This process not only worsens the physical symptoms of PID but also has the potential to trigger psychiatric complications through mechanisms similar to those seen in systemic infections like sepsis.
Chronic infections have been shown to impact long-term psychiatric health significantly. Infections such as brucellosis and HIV are associated with persistent inflammation and immune dysregulation, which can lead to neuroinflammation and subsequent psychiatric symptoms.
For instance, brucellosis infection in murine models has been found to cause decreased motivation, increased anxiety, and altered neurochemical levels, including reduced dopamine and serotonin in critical brain regions such as the hippocampus and frontal cortex. These findings underscore the substantial impact that chronic infections can have on mental health, contributing to conditions like depression and anxiety, which are often challenging to treat and manage and call for interventional pain management.
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The role of the hypothalamus-pituitary-adrenal (HPA) axis in mediating the stress response during infections has also gained attention. Infections activate the HPA axis, releasing cortisol and catecholamines, which are vital for managing acute stress.
However, chronic activation of the HPA axis can result in glucocorticoid resistance, where the body’s response to cortisol diminishes, contributing to chronic inflammation and psychiatric disorders. Elevated levels of proinflammatory cytokines such as IL-1β, TNF-α, and IL-6 further exacerbate this inflammatory response, playing a role in the development of major depressive disorder (MDD) and other psychiatric conditions.
Metabolic changes induced by inflammation during infections also appear to impact psychiatric health. Inflammatory cytokines can alter the metabolism of tryptophan, a precursor to serotonin, leading to decreased serotonin production and increased kynurenine, which has been associated with neuroinflammation and cognitive dysfunction.
These metabolic changes contribute to the development of sickness behavior, characterized by symptoms such as fatigue, social withdrawal, and anhedonia, which are common in both systemic infections and psychiatric disorders.
Persistent inflammation, whether due to chronic infections, immune dysregulation, or stress, emerges as a central factor in the development of psychiatric disorders following infections.
Chronic infections, in particular, pose a significant public health challenge, not only due to the direct effects of the infections but also because of the long-term psychiatric complications they can cause. These complications can have profound socioeconomic impacts, especially in regions heavily burdened by chronic infectious diseases.
Infections that induce chronic inflammation have also been linked to target organ damage or worsening of pre-existing damage. For example, post-COVID-19 patients may experience damage to the pancreas, leading to hyperglycemia and chronic low-grade inflammation.
Similar issues are observed in patients recovering from sepsis, who may suffer from chronic immunosuppression and inflammation due to changes in T lymphocytes and hematopoiesis, alongside complications from damage to vital organs such as the kidneys and heart.
Evidence suggests that antibodies produced during infections can trigger neuropsychiatric complications through a cross-reaction where antibodies recognize both pathogens and self-antigens. This cross-reactivity can lead to conditions such as streptococcal infections triggering neuropsychiatric symptoms or COVID-19-related autoantibodies against cortisol, potentially resulting in chronic inflammation and neuropsychiatric complications. A timely intervention with a chronic pain specialist helps take care of these issues from the root.
Source:
Ferat-Osorio, E., Maldonado-García, J. L., & Pavón, L. (2024). How inflammation influences psychiatric disease. World Journal of Psychiatry, 14(3), 342–349. https://doi.org/10.5498/wjp.v14.i3.342
