measuring neurotransmitters?



In our society today we can draw blood and determine what levels of certain things (vitamins or what not) people are low on, and then prescribe them things to make their levels “better”.

When it comes to mental health/mental illness, why can’t we do something similar with our brain chemicals? Like somehow draw some brain fluid or something and see that this person is low on dopamine or serotonin and then prescribe accordingly? Wouldn’t that help the mental health community immensely?

In: Biology

It’s difficult to measure neurotransmitters directly, since they are quickly metabolized. But we can measure their metabolites. For example, metanephrine is a metabolite of adrenaline, and homovanillic acid is a metabolite of dopamine. These can be measured in blood, urine and CSF (fluid drawn from the spinal cord). It is used to diagnose certain tumors.

These tests are not used in psychiatry, but I suppose they could be. You might need to know a patient’s baseline levels first though. I did a quick search and found [this study]( showing higher homovanillic acid in schizophrenic patients, and [this study]( showing higher metanephrines in ADHD patients.

Basically, it’s way too dangerous.

Spinal taps are only done when you need to. To deliver pain medication, or to draw CFS in very necessary situations. A lot can go wrong sticking a needle into a spine, so the practice would never become commonplace like drawing blood is.

In order to measure your relative neurotransmitter levels, you’d need to have a “before” level when you’re healthy. That would mean routine CFS draws for everyone. Then you could compare that to the “after” when you got sick.

So there’s a few different problems with your hypothetical tests (which would in theory yes help a lot with mental health diagnosis).

We can draw and measure many molecules in blood and cerebrospinal fluid (CSF, the liquid which fills various spaces in/around the brain and spinal cord). As someone else has pointed out, drawing CSF is an invasive procedure (google ‘spinal tap’ for more, and a great unrelated film), which isn’t done routinely unless it’s particularly useful. Blood is much easier to draw. However in both cases, there is a question mark over what the level of a molecule in the fluid tells us. For blood in particular, some molecules can pass easily between the brain and circulating blood, but even for these molecules we cannot always be sure if the level we see in the blood reflects what’s in the brain. In CSF, the ‘blood-brain barrier’ (the body’s way of protecting the brain from things circulating in the blood) is less of a problem, but as u/BobSeger1945 stated, most neurotransmitters are very quickly metabolised. In terms of neurobiology, we can make some guesses from the metabolism we see, but because the action of certain neurotransmitters in the brain is based on very rapid events and changes, CSF metabolites does not tell us so much.


That said, the real issue with your idea comes from how complex mental health issues are. For a long time, it was thought that tests like the ones you imagine would become diagnostic standards for illnesses like depression, because the ‘chemical imbalance’ theory was still the strongest we had. We now recognise that this theory isn’t really adequate to explain these diseases, in part through the failure of tests like these. While transmitters like dopamine, serotonin and noradrenaline (the main ‘monoamine’ neurotransmitters) seem to be dysfunctional in depression, it is not simply a case of less = bad, more = good. For example, we know from animal models that in some cases depressive symptoms are linked to increased levels of these transmitters in the brain tissue, but when we measure the activity at certain sites, there is less being released. This shows us why some of these potential diagnostic tests have failed to show us what we expected – the problem is not necessarily too little of a transmitter, but that there is something wrong in the complex system it is part of.


One other minor (but important) point: a big challenge in treating conditions like depression is that, from what we know, treatment doesn’t always mean normalising something like with a vitamin deficiency. The most common anti-depressant drugs increase serotonin function, but we actually think the effect doesn’t come directly from this mechanism. So this also reduces the value of taking a blood or CSF test and trying to simply raise the level of one thing or another, as this may not be the most efficient way to treat the symptoms. We still don’t have a great understanding of how anti-depressant treatments work, so while the aim is to have patient-specific diagnostic tests like you propose, we still lack the understanding of both the disease and treatment to implement these accurately.