Equally obnoxious is that these surveys are blind towards receptor subtypes, all of which do very different things in the brain, as well as its bias towards amine neurotransmitters, while there are other neurotransmitters that appear to have more selective pathways.
Finally, this type of hypothesis doesn't explain the "lag" between when an antidepressant raises neurotransmitters and when it achieves therapeutic value. There are studies indicating, for instance, that patients' (lab measure) serotonin levels had nothing to do with the therapeutic value of SSRI's.
My orthomolecular psychiatrist had me get labs for catecholamine levels in the serum, and I really told him that I won't take stock of those numbers until they check my cerebrospinal fluid; besides, the labs are designed to check for excesses only, not deficiencies. They were designed to screen for pheochomocytoma (adrenal tumor). There really isn't enough science to these surveys, and I resent the notion that you can attribute symptoms like these to simply a "deficiency". Notably, why are extrapyramidal symptoms and Parkinsonian traits not on the list? What about elevated prolactin? Curiously, I have myoclonic jerks in my sleep, I have most of the psychiatric symptoms above (but not the physical ones, even though by all rights I should be anemic), and I also have elevated prolactin.
There are better ways of detecting which neurotransmitter receptor ligands/potentiators will have the most therapeutic value, and this is by the empirical evidence regarding which population subtypes respond to such agents.
I'll present the matter somewhat more articulately in a scholarly book I got called "Clinical Advances in MAOI Therapy"
The available data today suggest a revised version of the monoamine hypotheses: Depression is caused by imbalances in the activity of different neuronal systems, of which the cause is unknown. Thes imbalances can be favorably influenced in an indirect manner by activation of monoaminergic systems. This formulation assumes that changes in receptor sensitivity after antidepressant treatment reflect primarily a reaction to continuously changing transmitter concentrations in the synapse and do not bear a direct significance on the therapeutic effect. Also, it assumes that activation of monoaminergic systems by whichever mechanism represents one of several ways to acheive an antidepressant effect. It permits an understanding of the latency of onset of action because it is assumed that the therapeutic effect is not mediated directly by activation of monoaminergic systems, but rather that this causes cascade-like alterations in the activities of several other transmitter systems, which themselves subsequently evoke adaptational processes, until a new, more favorable state of equilibrium is established. It is thus easy to understand that some time is needed to reach a new stable state.