Depression is largely thought to result from chemical imbalances in the brain. Brain chemicals – such as serotonin and norephinephrine – alter our mood and can cause depression when levels are too low. Yet many researchers now believe depression is far more complex, involving many other processes. Growing evidence suggests that inflammation is linked to some forms of depression, especially treatment-resistant depression.
The link between inflammation and depression
A large study published in the Journal of Clinical Psychiatry found that people with depression have 46% higher levels C-reactive protein (CRP), of a marker of inflammation, in their blood. A total of 14, 275 people were screened between 2007 and 2012. Higher levels of CRP often occur in many autoimmune diseases. Several other studies also linked depression with higher levels of CRP and non-depressed people given chemicals to induce inflammation, called cytokines, experienced depression and anxiety symptoms. How inflammation contributes to the development of depression is not fully understood.
What is Inflammation and how does it affect your brain?
Inflammation is a vital process in our body that fights infections and heals wounds. The white blood cells of the immune system use pro-inflammation chemicals, called cytokines, to kill viruses. We see inflammation as the swelling around a wound. Normally, inflammation shuts down after healing. Chronic inflammation results when the process continues. Sometimes inflammation gets out of control, attacking healthy cells, causing symptoms such as brain fog, depression and joint pain – or even serious diseases such as Alzheimer’s.
Chronic brain inflammation can be hard to detect due to the absence of pain receptors in the brain. When cytokines are out of balance, changes in mood can occur. For example, some people experience low mood after fighting a cold or flu. This could be lingering inflammation in the brain from fighting infection.
Treating inflammation can help depression symptoms
Depression is typically treated with a prescription of antidepressants. Antidepressants, such as selective serotonin reuptake inhibitors (SSRIs), work to increase levels of “feel good” chemicals in the brain. Yet nearly 30% of people see no improvement in mood when treated with traditional antidepressants.
Clinical trials show that supplementary treatment with anti-inflammatory drugs, such as ibuprofen (Advil, Motrin, and Nurofen) and celecoxib (Celebrex), improved mood in patients with elevated CRP levels. These anti-inflammatory drugs belong to a class called nonsteroidal anti-inflammatory drugs (NSAIDs).
Measuring CRP levels also predicted how patients responded to two commonly prescribed antidepressants: nortriptyline and escitalopram. Patients with elevated CRP levels responded better to treatment with nortriptyline, a tricyclic antidepressant (TCA). Patients with low levels of CRP responded better to treatment with escitalopram, a selective serotonin reuptake inhibitor (SSRI).
CRP – a common marker for inflammation – is a readily available blood test. If you suffer from treatment-resistant depression, your physician can easily assess your CRP levels and determine whether you could benefit from adding celecoxib or ibuprofen to your treatment plan.
Prolonged use of anti-inflammatory drugs (NSAIDs) carries an increased risk of gastrointestinal ulcers and bleeding, heart attack and kidney disease. People who process NSAIDs more slowly due to genetic differences in CYP2C9 – the liver enzyme responsible for removing NSAIDs from your body – are more at risk of these side effects. Pharmacogenetic testing can help assess whether the use of NSAIDs at standard doses is safe for you, and can help determine the best antidepressant for your unique genetic profile.
Pharmacogenetic testing should be considered to guide treatment of depression, anxiety, ADHD and other mental illnesses. Learn more about role of pharmacogenetics in mental health here.
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