2023-11-21 13:30:12
New marker of mental disorders
One of the popular trends in modern psychiatry is the search for markers of psychopathology using blood tests or other laboratory tests. Neuroimaging methods identify changes in brain function in patients with mental disorders, but their cost is too high for routine diagnosis. A simple and accessible “analysis for psychopathology” does not yet exist, but the relationship between laboratory markers of inflammation and mental state has been proven.
The most reliable and studied marker of inflammation is c-reactive protein (CRP), synthesized in the liver. Its production is activated by pro-inflammatory cytokines. Increased CRP concentration observed for acute inflammation, as well as for many chronic diseases, including arterial hypertension, metabolic syndrome, type 2 diabetes. It is also found in people with psychopathologies, including depression and PTSD.
Among the symptoms of long COVID is in the lead post-Covid depression leading to chronic fatigue and pain syndromes. Its severity correlates with the level of CRP and other proinflammatory markers. Elevated c-reactive protein associated with a decrease in mental abilities both in healthy people and patients with psychopathologies.
Monitoring CRP levels and maintaining them within normal limits reduces the risk of developing mental disorders and cognitive impairment.
Triggers of inflammatory depression
Study involving more than 85 thousand subjects demonstratedthat C-reactive protein levels are elevated in patients with depression. But since overproduction of CRP is revealed not all patients with depression, it is assumed that there is a special inflammatory form of the disease, which should be distinguished from others.
Triggers of inflammatory depression include dysbiosis of the gut microbiome and disruption of the gut-brain axis. With dysbiosis, the intestinal epithelium becomes “leaky”, and through it lipopolysaccharides of intestinal pathogens penetrate into the bloodstream, causing the synthesis of cytokines. In turn, cytokines circulating in the blood send a signal to the brain through the vagus nerve or penetrate into it through the blood-brain barrier (BBB). In both the first and second cases, neuroinflammation and activation of neuroglia occur, which underlie inflammatory depression.
Another mechanism that has been associated with increased cytokine synthesis and subsequent development of depression is adherence to a Western diet, which is high in omega-6 and low in omega-3 polyunsaturated fatty acids. The former trigger inflammatory processes in the body, the latter suppress.
Risk factors for inflammatory depression are obesity, type 2 diabetes, physical inactivity, and smoking. All of this contributes to systemic inflammation.
Obesity disrupts the functioning of many immunocompetent cells, including macrophages. In a healthy body, they serve as the main fighters of the innate immune system. With obesity, macrophages “hide” in adipose tissue and begin to actively synthesize cytokines, provoking inflammation. The more body fat you have, the more inflammation you have and the higher your risk of inflammatory depression.
The key symptoms of inflammatory depression are fatigue, psychomotor retardation, and motivational anhedonia, which is associated with the influence of inflammation on dopamine signaling in the central nervous system. In people with inflammatory depression, increased levels of CRP in the blood correlate with decreased activity in the reward system, which is responsible for motivation.
An urgent problem in the treatment of depression is the low effectiveness of modern antidepressants. Less than a third of patients with depression react When initially prescribed antidepressants, more than 35% do not respond to two or more courses of treatment. The ineffectiveness of prescribed medications contributes to the progression of depressive symptoms and increases the risk of suicide. The existence of inflammatory depression may explain the tolerance of many patients to antidepressant therapy. Selective serotonin reuptake inhibitors (SSRIs) are most commonly used to treat depression. For inflammatory depression, SSRI monotherapy does not work.
In addition to CRP, the proinflammatory cytokine IL-17 may become a new biomarker for the selection of antidepressants. Patients with low levels of this cytokine respond well to SSRIs, while those with high levels require combined antidepressant treatment.
The ability of anticytokine therapy to combat inflammatory depression is being studied. In particular, the use of monoclonal antibodies once morest IL-17 alleviated depressive symptoms in patients with elevated levels of this cytokine.
Inflammation and post-Covid mental disorders
Common symptoms of post-Covid syndrome relate depression, pathological anxiety, distress, insomnia, cognitive impairment. Depression and anxiety disorders occur in 20-40% of COVID-19 survivors. And while anxiety disorder caused by coronavirus can go away on its own, post-Covid depression and cognitive impairment tend to become chronic.
Long-term post-Covid mental disorders are provocateurs of decreased quality of life and social activity, increased morbidity, and disability.
The most powerful mental consequence of coronavirus is depression, which causes other complications, including pain syndromes, decreased mental abilities, and shortness of breath. It is recognized as the most reliable predictor of the development of chronic fatigue syndrome.
The development of post-Covid depression may be due to direct damage to the brain by the coronavirus, as well as neuroinflammation following recovery from Covid. In people who have had coronavirus, the permeability of the BBB may be impaired. Then the cytokines circulating in the blood easily penetrate the brain and cause an inflammatory process in it, which is clinically manifested by depression.
Since post-Covid depression is caused by inflammation, people who have recovered from coronavirus definitely need to monitor their CRP level – and, if it is elevated, bring it back to normal. More than half of patients who have had a mild form of Covid have levels of c-reactive protein exceeds 10 mg/l. The prevalence of this indicator following a severe form of infection is 81.5%.
C-reactive protein levels and cognitive function
Many patients with mental disorders observed deficits of attention, short-term and long-term memory, decreased speech fluency, vocabulary, psychomotor speed, problems with planning. The biological processes underlying these disorders include changes in neurotransmission at the synapse, malfunction of the hypothalamic-pituitary-adrenal axis, and systemic inflammation.
In patients with schizophrenia and bipolar disorder, CRP and cytokine levels correlate with declines in abstract thinking, learning, attention, mental flexibility, and processing speed. The relationship between CRP and cognitive impairment is observed in patients with depression, anxiety, dissociative, and somatoform disorders. It can also be observed in people without psychopathologies.
Elevated CRP levels are often found in people with obesity and metabolic syndrome, and they correlate with decreased mental performance.
Chronic inflammation associated with obesity quadruples the risk of executive function deficits.
Obese people have particular problems with cognitive processes such as decision making, attention, and speed of information processing.
In obesity, adipose tissue starts produce many pro-inflammatory adipokines. The level of anti-inflammatory adipokines, on the contrary, decreases. In particular, the production of adiponectin, which affects brain function, decreases. Adiponectin receptors are located in the hypothalamus, brain stem, hippocampus, their activation promotes neurogenesis, normal functioning of synapses, and maintenance of cognitive processes. Adiponectin deficiency in obese individuals is associated with cognitive dysfunction and Alzheimer’s dementia.
Prevention of inflammation and mental disorders
Since inflammation underlies many psychopathologies, eliminating it is an effective prevention of mental disorders. You can suppress inflammation with medications, but they have many side effects. Safer remedies include normalizing weight, eliminating vitamin and mineral deficiencies, modifying diet, and improving the intestinal microbiome.
The best way to reduce inflammation in an obese body is to lose weight. Losing body weight by more than 5 kg in three months reduces CRP level almost 3 times. Physical exercise, which is accompanied by a decrease in BMI, significantly improve c-reactive protein indicators.
Exists link between magnesium deficiency and low-level inflammation. Magnesium deficiency provokes an imbalance of calcium homeostasis, oxidative stress, and activation of cytokines. All these processes are provocateurs of inflammation.
A meta-analysis involving almost 33 thousand patients revealed a correlation between magnesium deficiency and C-reactive protein levels. Normalizing magnesium status reduces CRP levels and suppresses inflammation in the body.
Low-level inflammation and increased CRP levels is revealed with a lack of vitamin D, which is recognized as a complete hormone that affects many functions of the body. Its anti-inflammatory effect is mediated by hormonal effects on immune cells (monocytes, B cells, T cells) and the ability to suppress the synthesis of proinflammatory cytokines. Eliminating the deficiency of this nutrient reduces CRP levels, the risk of inflammatory diseases, and mitigates complications caused by obesity.
Anti-inflammatory diet (such as Mediterranean) prevents the occurrence of depression. Products with betaine (spinach, wheat, beets, asparagus) and whole grain products have the ability to suppress the level of cytokines. Powerful anti-inflammatory effect provide flavonoids, which are abundant in apples, grapes, citrus fruits, olive oil, red wine. Walnuts also resist neuroinflammation. A diet rich in them improves cognitive functions, reduces the risk of depression, dementia, Parkinson’s disease.
Anti-inflammatory properties have omega-3. Omega-3 supplements reduce C-reactive protein even in severe diseases such as sepsis and coronavirus. International nutritional associations recommend omega-3-rich treatments to boost the immune response in COVID-19 patients. Appears There is growing evidence regarding the ability of these polyunsaturated acids to counteract post-Covid mental disorders.
Omega 3 improve course of depression associated with inflammation. The most well-known omega-3s include docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA). The second has a more powerful antidepressant effect.
12 Week Omega-3 Supplement reduces weight and abdominal fat percentage in obese people, and also helps improve their cognitive function.
Meta-analysis of 20 studies demonstrated the ability of probiotics to significantly reduce the levels of CRP and pro-inflammatory cytokines. Probiotics suppress inflammation through several mechanisms:
Restore the integrity of the intestinal epithelium, preventing lipopolysaccharides from entering the blood. Increases the production of short-chain fatty acids by the intestinal microbiome, which have anti-inflammatory properties. Strengthen the synthesis of antimicrobial peptides.
The effect of probiotics on the course of psychopathologies is being studied. Lactobacillus supplementation improved mental status and reduced hospitalizations in patients with bipolar disorder and systemic inflammation. An 8-week supplementation with Lactobacillus acidophilus, Lactobacillus casei and Bifidobacterium bifidum alleviated depressive symptoms and CRP levels in untreated depressed patients.
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