"Too Long; Didn't Read" Version:
Has anyone else noticed that the effects of amphetamine seem to change or transform over time?
What do you think causes this?
Is it permanent?
Will this "shift in mental processes" overlap into normal-everyday life, even when sober?
Does this "change in effects" indicate other, more-serious, matters -- such as brain damage?
Do anxiety and other mental health disorders resulting from amphetamine use correspond with amphetamine's changing effects? If so, could we preemptively halt the onset of such disorders by identifying their corresponding indicators via amphetamine's changing effects?
The LONG version -- Advanced discussion for Psychonauts:
Those who use amphetamine (or similar stimulants) more than occasionally may have noticed that amphetamine's effects quite literally "change" as use progresses.
I am not talking about during a single session of use (where the effects are well-known to change from something like phases of a "Rush", a subsequent "High", and finally a "comedown"/"crash"), I am referring to prolonged use - over the course of weeks, months, and years.
As with most people who enjoy amphetamine (or consider it their drug of choice), the first few times are the most pleasant. The euphoria is the strongest during these periods.
The first (or second) is often the most euphoric, with a noticeable decrease in euphoria with the second or third use (especially if the second/third dose is within a day or two after the first). During this period, amphetamine will still be strongly euphoric, but eventually the "feeling" changes, or "shifts", into something "different".
It is hard to describe such a topic (which, by its very nature, is almost metaphysical -- akin to describing the qualia of "color" to a blind man), but psychonauts (or those who otherwise consider chemical experimentation a hobby) should identify with these terms for the most part.
The initial euphoria of amphetamine use could be described as "lovey", "empathetic", extremely pleasurable. There is a strong physical sensation of euphoria and pleasure. Some may even consider it to be "overwhelming".
The second phase (usually beginning at around the second, third, or fourth session of use) seems to be characterized by a decline in the "empathetic" feelings - as well as the intensity of the euphoria. The euphoria of the second phase seems to be more of mental and emotional nature, and less of a physical one.
The third phase could be described as being "raw stimulation" - the euphoria (although still present to some extent) transforms into something like an "uppity feeling", and not so much pleasurable.
Then there are subsequent phases, most of which progress differently for each person (depending presumably on factors such as frequency of use, weight, gender, dosages, diet, nutrition, metabolism, time of day being taken, amount of sleep, etc)..
The main point I wish to acknowledge is that amphetamine's effects will distinctly change, and sometimes irreversibly.
The increased sense of awareness and introspection (called "metacognition") allows for the user to easily take note of his/her changing mental statuses when using amphetamine.
Now, the point of this thread is that I believe there are several important questions that are provoked by this "shifting of effects" -- we are now presented with a unique opportunity to gain insight into the foundation of our mind: How they work, the processes involved, etc..
The purpose for answering these questions is derived solely out of the curiosity of those who asked them, as the answers likely do not have much practical use in the fields of psychology and medicine.
Here are the questions I have proposed:
1. I undoubtedly believe that a fluctuaion of neurotransmitter levels is responsible for amphetamine's "transformation of effects". The question then arises:
A) Does this indicate a transition of cognitive operations themselves, or only amphetamine's effects?
B) Is this transition irreversible? If it indicates a transition in cognition, is it permanent?
C) Perhaps the answer is not quite concrete, and there is actually a variety of variables at play that we are not quite aware of. Could it be that this transition's impact on cognition is partially temporary and partially permanent?
2. In continuation of my proposal in problem 1, I think it is possible for us to actually make connections between specific occurrences in amphetamine's "transformation of effects" and their corresponding neurotransmitters (or neurotransmitter systems) responsible for the transformation.
What are some postulated neurotransmitter systems that correspond with amphetamine's shifting effects?
3. We could posit that amphetamine's limited affinity for serotonergic pathways is what is responsible for amphetamine's initial effect "lovey" feelings and empathy, as well as the intensity of the resulting euphoria. This is connection is speculated due to its similarities with the MDMA's effects; the effects of MDMA arise largely from serotonergic activity. MDMA is also quite similar in molecular structure to amphetamine, and is theorized to have a similar mechanism of action within the brain (albeit a different region of the brain).
We could consider this to be a reasonable conclusion. However, more questions arise.
When amphetamine's "lovey" and "empathetic" effects begin to fade with continued usage, does this indicate a decline in serotonergic functioning? It can be noted by many amphetamine users that it is quite difficult to replicate the intense euphoria that they had experienced from their first few sessions of use, even if they raise the dose considerably. Even with prolonged cessation of use, it is very difficult to re-obtain the intensity of the initial euphoria. What could this indicate? Some possibilities are:
- A tolerance has developed specifically for the serotonergic effects of amphetamine.
- Nerve-tissue damage in serotonergic pathways. This hypothesis could be tested, as serotonergic nerve damage would cause the effects of MDMA to also be mitigated. If an individual were to use amphetamine until the initial euphoria of the aforementioned "Phase 1" had diminished, then try a subsequent dose of MDMA a while later (perhaps a few hours or maybe a day or two), we would be able to confirm or dismiss this hypothesis. If MDMA's effects are unimpeded, then no nerve-damage has taken place. Of course, all variables would have to be eliminated to rule out other possibilities; the individual would have to get adequate sleep and nutrition (to rule out sleep deprivation and malnutrition) before taking the subsequent dose of MDMA.
A much more simpler way would be to look at the self-given reports of others -- perhaps it has been previously reported that former methamphetamine or amphetamine addicts are unable to achieve a euphoria from MDMA, or the euphoria is dampened significantly.
- Perhaps the intensity of amphetamine's initial euphoria (perceived as "lovey" and empathetic) is a state of mind that can only be achieved when the brain is functioning at its maximum potential, and it is not solely caused by serotonergic activity. Possibly after several sessions of amphetamine, a long-term impairment results in the brain, causing the brain to be unable to achieve this state of bliss until after an extended period of sobriety. If this is true, then an individual experiencing this would be unable to reach a state of blissful euphoria with any drug, and not just amphetamine. I do not think this is true, however, as I personally am still able to experience intense euphoria with the use of opiates and other drugs, and this feeling is very similar to the unique feeling of an initial dose of amphetamine. I have been able to get an intense euphoria from opiates, even though hours earlier I had been unable to achieve any euphoria at all from a standard dose of amphetamine. This suggests that the solution is one of the two possibilities above.
4. It has been noted by many amphetamine users that the negative effects of use will last for days, weeks, months, and even years into sobriety. This is noted more often with methamphetamine, supporting the serotonin hypothesis mentioned above (since methamphetamine has more of a serotonergic affinity); however, the increased reports of anxiety from methamphetamine use may simply be the result of anti-meth propaganda, hysteria, and placebo effects reported from individuals influenced by those things. This is merely speculation, however.
A) What could we attribute long-term amphetamine-induced anxiety to? If serotonergic damage is indeed the cause, then perhaps serotonergic damage is long-term (or even permanent) as suggested above.
B) What could we attribute amphetamine psychosis (particularly the long-term incidences of psychosis) to? It is often theorized that increased dopaminergic activity is responsible for amphetamine psychosis (as well as schizophrenia and other classic psychoses). However, perhaps "psychosis" is actually just a vague categorization for non-specific symptoms. Amphetamine-induced memory impairment, anxiety, sleep-deprivation, agitation, malnutrition, akathisia, skeletal muscle deterioration, hyperthermia, and high blood-pressure could all collectively lead to the extreme state of mind that health-professionals recognize as "psychosis". It becomes a series of questions concerning "cause and effect". For example, short-term memory impairment (often caused by prolonged usage of amphetamine) can cause states of mind identical to psychosis. However, short-term memory impairment might actually just be an indicator of declining functionality within the cognition, as it is often accompanied by confusion, cognitive dissonance, "ego death", and delusions.
5A). Does the increased level of introspection into one's own mental process (called "Meta-Cognition") have any practical application? Perhaps merely even for curiosity? Perhaps there is still discoveries left to be made in the field of psychology (regarding the abstract concepts of cognitive processing and the like), and amphetamine could be a useful application here? Although, any information obtained would be limited in its real-life usefulness, other than perhaps a better understanding of the mind itself.
5B). Is information gained during this "state of awareness" reliable/accurate, or flawed? It almost seems to be a cliche stigma in entertainment that drug users will have epiphanies, feel enlightened, think they have discovered the meaning of life, or otherwise think they have come to important philosophical conclusions, when actually whatever they are saying is just gibberish to another person, or common sense that lacks any significance. "Woah dude.. I think I just found the meaning of life... The meaning of life is to love other people, man... I think I've become one with God..." This is more notable on psychedelics (acid and mushrooms notoriously), but is noted to occur with amphetamine as well. Amphetamine is often regarded to be a much more "psychedelic" stimulant (props to its relatives with similar phenethylamine structures such as mescaline or the 2C-? family).. but perhaps due to the given clarity and vividness during this amphetamine-induced state of "enlightenment", discoveries and epiphanies reached during such a state might actually be useful - perhaps this "high-functioning" state of meta-cognition could even be exploited.
6. Memory impairment is often experienced after using amphetamine frequently, or if the amphetamine habit has been going on for a long time. The memory impairment can sometimes be long-lasting, even after extended periods of sobriety. What causes this memory impairment? Some possibilities are:
- Anti-cholinergic activity that comes from higher doses of amphetamine
- Prolonged sleep deprivation
- The brain does not have enough resources to supply for an individuals mental demands; an individual may feel compelled to work non-stop or "keep going", when his/her brain (and likely the body as well) lack the resources needed to continue. As a result, memory is impaired - the mind is working faster than the short-term memory allows.
- Neural damage of a specific neurotransmitter pathway, such as dopamine or serotonin.
- non-specific brain damage (perhaps irreversible) that may have occurred from malnutrition, hyperthermia, sleep deprivation, or simply because of prolonged sessions of high-level activity within the brain.
-disproportionate neurotransmission; the dopamine pathways in certain regions of the frontal lobe may not have yet run out of neurotransmitter reserves, and their high level of activity urges the individual's cognition to "keep going" -- but, other regions of the frontal lobe (or other dopamine pathways) might have exhausted their supply of dopamine, and are simply unable to function. This could also explain amphetamine psychosis, and the distinct obsessive behavior often resulting from amphetamine use.
![:\](https://bluelight.org/xf/BL_Images/Orig_Emoji/wrygrin.gif "wry grin :\")
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