Depression and gout

Metabolic disorders are common in patients with depressive disorders. The link between depression and gout has been the subject of research by various scientists.

With gout, the risk of depression increases in women, in men with hypertension, the risk of stroke, and coronary insufficiency. Also, the patient’s age plays a role in the development of depression.

With the use of non-steroidal anti-inflammatory drugs and hormonal drugs, the risk of developing depression decreases. Metabolic syndrome, manifested by an increase in body mass index, hyperlipidemia , hyperglycemia, obesity, hyperuricemia, is associated with mood disorders. The data has been tested on a large population of people. Uric acid is the end product of purine metabolism. Its precursor is adenosine. The purinergic system is also associated with ATP, a neurotransmitter and neuromodulator adenosine. These mediators promote the activity of the cerebral cortex, basal ganglia, and the limbic system. Neuronal plasticity and synapse formation are also dependent on ATP and adenosine.

    Metabolic disorders, including increased body mass index (BMI), central obesity, hyperlipidemia , hyperglycemia, and hyperuricemia , are closely associated with common mental disorders. In addition, the prevalence of metabolic syndrome in patients with mood disorders is higher than in the general population, with a significant impact on the quality of life of depression. Hyperuricemia is associated with obesity, insulin resistance, hypertension, and metabolic syndrome. 

The purinergic system affects the exchange of serotonin, dopamine, GABA. This means one thing that it can disrupt the activity of these neurotransmitter systems and cause inflammation. That is, defects in uric acid metabolism can affect sleep, mood, impulsivity, and physical activity.

    In addition, this system interacts with other neurotransmitter systems , including those associated with serotonin, dopamine, and gamma-aminobutyric acid. This means that purinergic signaling dysfunction can disrupt other neurotransmitter systems and cause neuroinflammation . Thus, the purinergic system can be involved in the regulation of mood, sleep, impulsivity, and motor activity.

Disorders in the purinergic system have been studied at the level of genetic markers and neuroimaging studies. (V. Sperlagh et al, 2012). The researcher looked at the effect of the P2rx7 purine receptor on mood. And found that its activation affects mood through the release of glutamate and changes in neuronal plasticity in depression. Nonsteroidal anti-inflammatory drugs and gout can contribute to depression. Immune inflammatory reactions, in particular the activation of pro-inflammatory cytokines, leads to the development of depression. The hypothesis about the influence of cytokines on the pathogenesis of depression is confirmed by their influence on the level of serotonin, microglia activity , “stress axis” and neuroplasticity .

 Similar effects are seen in bipolar disorder.

The above data suggest that depression is a disease involving multiple molecular mechanisms, and it is inappropriate to consider it from a clinical point of view only.

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