1) Stereotype threat does factor into reported cognitive deficits, but probably does not account for the totality of the deficiency--perhaps not even the bulk
Do you mean to say that you feel stereotype threat does not account for all of YOUR observed deficiencies in memory? If so, that's what I've been trying to say from the start.

If, on the other hand, you are trying to say that stereotype threat couldn't account for all of the deficiency measured in Shilt et al's word recall test, the research I cited suggests that it clearly can bridge the gap (and then some.)
2) In the Schilt study, researchers noted that they did not believe that anxiety from priming significantly factored into their results, as users were impaired in only one of several tests of memory and cognition
I believe they may indeed have been impaired. By definition, the research subjects who became drug users during the course of the study had changed. Their lifestyle had likely changed, their sleep habits may have changed, etc. These things could certainly have been factors. I would also expect MDMA (and just about any drug) to have the potential to cause subtle alterations of brain function lasting for weeks or even months after the last exposure, based simply on changes in receptor density. I wouldn't for a moment argue that MDMA can't make you dumb or screw with your memory. However, I don't see how a convincing argument can be made, given the SERT ligand brain scan work with very heavy users, that the sort of axonal pruning seen in animal models is occurring at recreational doses in humans. (At least, in most cases. Humans are varied bunch, genetically and behaviorally.)
3) I think there is some confusion...I don't think that a 20% reduction in verbal memory capacity has caused the recurring suicidal ideations; rather it has made life more difficult and even hopeless at times, as the nature of my work depends on verbal memory and verbalization.
So, you accept that you are stressed out and depressed (which by itself can very easily and fully explain your cognitive difficulties), yet you go looking for a secondary cause. Why? 'Do not multiply entities unnecessarily' and all that, wouldn't you agree?
4) There is no evidence in support of changes cerebral blood flow after ecstasy use being either transient or permanent, but it is lasting (at least several months).
Yes, several months. My apologies if my imprecise choice of words implied something else.
5) Regarding chronology, as neurological injury is an acute effect, the subtlety of the impairment in question may have gone unnoticed while I was still using marijuana (during those 6 months). Only after a prolonged period of abstinence have I started noticing difficulties.
Possible. On the other hand, depression (perhaps formerly partially treated with marijuana) remains the much simpler answer.
SERT levels do not entail functional recovery, but recovery in synaptic plasticity; thus the brain's electrical current is preserved while the direction of the current may be compromised.
If the measurements had been simply of total SERT within the brain, I would agree with that statement. However, a very large body of animal evidence shows that MDMA neurotoxicity results in a re-distribution of serotonin axons; some regions become hyper-enervated, while others (further from the raphe nuclei) are forever de-enervated.
The brain's neuroadaptive mechanisms may very well compensate for neurotoxic insult, though if given a sufficiently demanding, these compensatory mechanisms begin to fail thus resulting in evident neuropsychological impairment.
True, true. But the return of SERT densities to normal on a per-region basis is not compatible with a theory of axonal pruning.
I should point out that my interest has always been in the gross structural injury to the serotonin system, as this was (and still is) the primary focus of interest in the field of MDMA neurotoxicity. I do not preclude the possibility of lasting harm to neurological function by other means, such as persistent changes in signaling pathways mediated by permanent changes in inter-neuron connections, gene regulation, etc. In fact, I would bet that it's possible.
from my own particularly intensive research I have concluded that even in low doses there are measurable brain differences in ecstasy users
Absolutely true. As I have always told people. If I had to boil down my position to a single sentence, I would say "At common recreational doses, MDMA won't eat holes in your brain or destroy your serotonin system, but it can seriously fuck you up (functionally and emotionally) if you over-do it." As I've said before, I've seen this drug destroy minds and lives. It's not pretty. But that's also not relevent to the question at hand, which is why somebody with a perfectly simple and obvious explanation for their problems (depression, anxiety, stress) is trying so hard to find an explanation elsewhere. At the very least, an intellectually honest person would admit to themselves that the depression had to be a major contributing factor.
Although I wish to be more optimistic about the situation, I can't help but conclude--or at the least entertain--that given sufficient intensity of experience (cognitive or emotional), my brain, after mild use, has exhibited permanent changes in function. These changes are a reflection of a deficit in capacity,
And you may even be right. As I imagine you well know, science rarely offers absolute, inviolate truth. Instead, it offers probabilities, odds, trends. The very high odds are that your problems are due to your depression.
At the very least, it's in your interest to treat the clearly known problem.