How many times has it been said that “There’s no lab test for depression.” That was the case for thousands of years. Even since the beginning of the modern mental health treatment era with Freud and Kraepelin in the late 1800s, the causes of mental illness were guessed at by observations of behavior.
There are many reasons a person might be depressed, and there are many tools available to treat depression. How can a person know how to move forward with medication or talk therapy treatment? When is talk therapy most effective? What kind of medications are available to treat depression? Why would you choose one treatment over another? What is a biomarker, and why might it be useful in treatment?
One generally accepted treatment method is to use the STAR*D treatment steps. Start with Citalopram and see how that goes for 14 weeks. Why Citalopram? That medication is a selective serotonin reuptake inhibitor. That means that Citalopram helps keep serotonin in the part of a person’s brain where it can be most effective. Insurance companies tend to reimburse providers for this kind of treatment without complaint, and they’ll pay for those medications.
If you have a serotonin problem then this can be a nice solution. Women get better results from Citalopram than men. This is because women have more problems with serotonin than men do. The female reproductive system and hormone system affect serotonin more than men’s systems.
A biomarker is an objective medical status that can be accurately measured and reproduced. Here is a link to a study that uses an electroencephalograph (EEG) to locate a biomarker for depression and response to Prozac (fluoxetine), a similar SSRI medication. An EEG looks something like a swimming cap with a bunch of spark plugs stuck in it that are connected to a computer. First, the research team screens the patient for depression using the standard questionnaire, the Hamilton Rating Scale for Depression (HRSD). Here http://healthnet.umassmed.edu/mhealth/HAMD.pdf is a copy of that questionnaire. Insurance companies want PMHNPs and psychiatrists to use this form to decide whether a patient has depression and will accept it as documentation supporting that diagnosis. Then, researchers measured electrical brain activity in several areas of the brain and recorded their results.
I would like to call your attention to the difference between those two methods. The HRSD takes the patient’s verbal response to questions, and the EEG reads electrical brain activity.
Within that study, researchers found that using the EEG they could measure a patient’s response to Prozac at the end of the first week of treatment and predict how they would do at 8 weeks of treatment. They repeated the EEG at one week and calculated the difference between their first result on day 1 and their second result a week later. Using this calculation (called the Antidepressant Treatment Response Index), researchers could predict the patient’s response to treatment seven weeks in the future. By contrast, the HRSD did not offer a prediction of success. The EEG does not record the placebo effect, the change in the patient’s biomarker reflects the performance of the medication only. The HRSD assessment includes the placebo effect.
Wouldn’t it be nice to know whether you are experiencing the benefit of the medication vs the placebo effect? As a provider, this is vital information. I would not want to continue a medication that has the side effects that many antidepressants have (nausea and sexual dysfunction) when talk therapy would probably be a better option. A strong placebo effect indicates that a patient probably has hope. Hope is a wonderful thing to find in a patient seeking treatment for depression! Their depression might be event-driven, temporary, due to something that is not connected to serotonin, or otherwise resolvable.
Using the EEG in addition to the HRSD shortens the time from 14 weeks to 1 week. Isn’t that an incredible outcome? 13 weeks of medication costs money, and imagine spending 14 weeks waiting to see whether you are going to feel less depressed only to find out that it’s not ultimately going to work for you. Even if the medication seems to be working, there is still a significant chance that you feel better because of the placebo effect. Finding out that Citalopram or Fluoxetine probably isn’t going to work for you might not sound like good news, but it is. That tells us that your answer lies elsewhere. Instead of trying to find a version of serotonin that will be helpful, maybe we should look to dopamine or norepinephrine for a more likely solution.
The fact that a person can distinguish between these outcomes changes everything.
While this study is interesting and I believe very helpful, it was the follow-up to this one that converted me to a biomarker-hunter. We can look at that one next.