Popping pills for depression is not always the right way to go about it and not even ignoring the symptoms help. One needs to know the right treatment for it. There is a new way of testing where with the help of blood test one can identify the most effective antidepressant treatment.
Researchers in the US have recognized a biological marker that could help doctors recommend the most effective medications for depression by means of a simple blood test. The findings bring hope to patients who don’t find relief from the most commonly prescribed antidepressants.
Research from the University of Texas Southwestern Medical Center suggests that levels of C-reactive protein (CRP) in the blood can determine whether an antidepressant treatment can improve symptoms. Levels of C-reactive protein (CRP) in the blood increase in response to inflammation or bacterial infection. The researchers gave 100 depressed patients two types of antidepressants: escitalopram and bupropion. The patients were prescribed either escitalopram alone or escitalopram plus bupropion.
For patients whose CRP levels were less than 1 milligram per litre, escitalopram alone was more effective, with a 57% remission rate compared to less than 30% when combined with the other drug. For patients with higher CRP levels, escitalopram plus bupropion was more likely to work, with a 51% remission rate compared to 33% on escitalopram alone.
It isn’t always easy to find the right drug for treating depression, which can take different forms and has a diverse range of side effects (weight gain, sexual dysfunction, etc.). Patients sometimes need to change medication or doses in order to find an effective treatment.
In recent years, studies have investigated an inflammatory origin of depression, establishing a correlation between the immune system and depression symptoms. CRP was identified as a potential marker for depression treatments because it has been an effective measure of inflammation for other disorders.
While previous research to establish CRP as an antidepressant marker relied on levels three to five times higher than the latest study, Dr. Madhukar Trivedi, who led the research, suggests that “you don’t need that high of an inflammation to experience the sickness of depression. Even a little inflammation may be sufficient for the patients to experience some of these symptoms of depression.”
In the future, testing depressed patients for signs of low-level inflammation could become routine practice in psychiatric medicine. The next step for the researchers is to undertake larger studies to verify CRP’s role with other antidepressants and find alternative markers where CRP does not prove effective.