im a forst year neuroscience student, have studied psychology an pharmacology in in uni(dropped out) before, and im wondering what it takes for me to become a psychopharmaologist or neuropsychologist? is it worth it? im also severely mentally ill het aiming to get a PhD… I just want to study the effects of psychoactive drugs on the human brain and experiment on it, goal is to minimize the side effects and move treatments of mental disorders towards a less chemically based, and more efficient (such as neurofeedback, rTMS, psilocybin/ketamine/mdma based therapy, etc.) which are known to be more effective yet are not getting the attention they deserve. I dont know which branch would suit the goals the best, especially since i want to put my overwhelmingly high knowledge about all treatments for mental illnesses to use (im a bit autistic and its been my special interest since i remember) and I feel alive while im at a lab experimenting on anything basically, and i basically RARELY feel any joy (not trying to sound edgy im just severely depressed and on a bunch of meds that dont work) sorry for the long rant, just wanted to give a semi-complete context for this since its my future you know.

TLDR; im a severely mentally ill student (got a disability pass at uni as well) trying to find a job that helps me study the effects of psychoactive medications on the brain and aim to reduce the side effects of them and shine more light into less harmful ways of treating mental illness such as neurofeedback rtms psilocybin therapy etc. and basically anything related to mental illness + psychoactive substances. thank you 🙏

What would be the pharmacology behind this medication cocktail? Does it counteract the dopamine blockage will the antipsychotic only be working on serotonin then? I’m interested in this also with partial agonists like abilify and atypicals with full blockage.

I was wondering if you amazing drug nerds could give me a neurochemical reason as to why theobromine in chocolate and coffee causes and/or increases avolition symptoms in people with bipolar, ADHD and schizophrenia. I know that high altitude training, Erythropoietin and heavy weightlifting reduce avolition symptoms since all three patient groups have low red blood cell counts. What else exactly is going on in the brain?

Thank you in advance.

Can anyone please explain to me why there are different FDA approved maximum doses for venlafaxine extended release (max 225)versus the immediate release (max 375) formulation? Thanks!

Does such a drug/substance exist? Or something that poorly crosses and has mostly peripheral effects?

Side question: do the common SSRIs differ in their propensity to cross the BBB?

A few years ago I was talking to a psychiatrist who had been working since the 70s. In a conversation about quetiapine he told me that a small dose (more likely smaller than 25mg) could make a patient who is down and apathetic more energetic. He emphasized that the dose has to be really small, but never specified what that would be.

I’m a nursing student now and from the pharmacology course (that also didn’t go deep in psychiatric meds) I understood that it works by blocking D2 receptors, also helps negative symptoms.

Could someone explain how this would work, if it even can or could that be placebo?

I am sorry if this sort of thing is asked a lot, I've been trying to find information and it seems like it's really hard to find what I am looking for.

Are there any pre-doctoral psychopharm degrees? Most of the ones that I find are post-doctoral, and I really don't want to have to get a whole other degree to pursue this learning. ):

I would really prefer to have an online degree, as I need to continue working while going to school and I don't have money to move anywhere. I don't really mind which career path I take, I mainly just want to learn more about psychopharm. I have a BA in Psychology with a minor in Neuroscience. I am currently a social worker.

I've found some options, but people rate the schools really badly, I may just take one of these options though, because it may be better than not pursuing the degree at all

thank you for your help, i really appreciate it

Someone asked an interesting question, and I can’t readily come up with an answer. Per Stahl’s Essential Psychopharmacology (p. 556), acamprosate interacts with both the glutamate system to inhibit it, and with the GABA system to enhance it, a bit like a form of “artificial alcohol.” If I am interpreting Figure 13-17 correctly, it appears to show benefits for alcohol withdrawal by reducing glutamate release and causing downstream effects on dopaminergic neurons in the VTA. Also, Ademar et al. (2023) state that acamprosate increases mesolimbic dopamine.

On page 95, the glutamate theory of psychosis and schizophrenia proposes that the NMDA glutamate receptor is hypofunctional at critical synapses in the prefrontal cortex and results in downstream hyperdopaminergia. 

Beyond its benefits in alcohol use disorder, I was wondering about acamprosate's effects on other agents, particularly related to psychosis and various drugs (i.e., D2 antagonists, NMDA antagonists, and 5-HT2A agonists), since all of these pathways sort of collide in the mesolimbic area. All roads lead to Rome, so to speak. 

There are several gaps in my understanding of this and I can’t come to a solid conclusion on my own. Theoretically, would an agent such as acamprosate affect psychosis and antipsychotic therapy as well as agents such as ketamine or psilocybin? Thank you for any insights!

Ademar et al. (2023), but it's not entirely related: https://www.nature.com/articles/s41598-023-45167-3

Is there a way to anticipate the extent to which a particular dose of Modafinil might increase metabolism of a specific dose of Guanfacine (thereby possibly decreasing plasma concentrations below a therapeutic dose)?

Are there general rules that might apply to clinical practice in terms of offsetting this effect? For example, would ER Guanfacine (Intuniv) necessarily be superior in terms of ensuring that plasma concentrations don’t fall below a therapeutic dose? In the case of IR formulations, would splitting the dose throughout the day be a good strategy to maintain the intended plasma concentrations? Is there a basis to say that one could take X% more Guanfacine to offset increased metabolism?

Thank you!

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5809348/ (A random article I found related to the subject, which unfortunately doesn’t answer my questions).

Hey all. Hang in there with me on this one, I'm giving you context and background...

I am working on a podcast for a website called SporeSwaps, which is a mycology website that is like a brokerage for high quality vendors and customers. It's a cool concept, and is a godsend for people who are interested in mycology and/or want to "cultivate/grow their own medicine" (you'll hear that explanation a lot in the myco community).

The podcast is going to be about mycology (mushrooms - not just psychedelic ones), psychedelics used responsibly as a tool and a medicine, the human experience, and mental health... We want to be able to discuss the 'end-user' viewpoint from these things, as non-experts; but, we're also going to do a bunch of interviews with all sorts of people, including experts and people who have been in the thick of it with mental health stuff.

We're going to frame a lot of the things that are out there as tools, and hopefully give perspective to the listener they didn't have before on their possible uses, and maybe further remove the stigma that may exist on treatment options.

I'll bring this up now, because I've had some people read some of my posts and assume some things... This isn't an anti-pharma podcast, because we believe they're valid tools. A lot of "us psychedelic medicine supporters" tend lose focus that traditional medications can be viable options for people, despite some of the issues that can arise... We can be a very excitable and skeptical crew, so sorry about that 😂

But maybe the listener is a mental health advocate and wants to learn more about to help others. Maybe the listener is tired of feeling depressed, is looking for possible options and they feel it's time to try SSRI's and it sparks them to talk to their medical professional. Maybe they want to skip traditional meds and consult a Ketamine Therapy doc. Maybe they want to graduate from taking SSRI's and try to go the microdosing route (after consulting their medical professional of course).

These would be wins in our book.

So... Where am I going with this?

I was originally going to launch the podcast as 2buds1shroom; but, I think it's best to repurpose the 2buds1shroom project separate from the podcast, and keep it to be focused on being a helpful knowledge bank and community for people.

Long story short, I've been able to manage and overcome the depression I fell into by sticking it out and doing some research into some alternative treatment options. Ketamine Therapy, fixing my nutrition problem (that I didn't know I had), and (self-guided) psilocybin therapy have been a winning combination for me to put my depression into remission. I've never had the stability I've ever had in my adult life... It's taken a lot of personal work and self-awareness beyond just therapy and supplementation, though...

I've felt called to develop a bunch of knowledge-bases for people on our discord (2bud1shroom.org) , that's a bit of a 'no BS' and 'quick start' for people down their own research. For example, #vitamin-d🌞 or #psilocybin🍄 (NOTE: this link takes you to our Vitamin D Discord room). That has my story there, symptoms I was experiencing (which were many) as well as other possible symptoms, dosing methodologies, who shouldn't take it, things that should be taken with it, etc...

There's many resources already out there, but bringing them together IS the project.
The other challenge is making them relatable and digestible.

Is this knowledge-base perfect? Well... No; but, I've tried to be as grounded in science and link my references the best as possible, while giving my own anecdotal evidence and mentioning when it's exactly that...

I'm basically looking for:

• fact checkers to double-check my quality work
• when I'm inaccurate on something, help correct me
• when there's necessary information needed, let me know
• when there are better resources out there, let me know
• people who want to contribute on a topic they personally love or have first hand experiences with... To name a few Examples: Antidepressants, LSD, MDMA, Ibogaine Therapy, Ayahuasca, Sleep, THC & CBD, Alcohol, Nicotine (which is apparently a treatment for ADHD), mescaline, omega fatty acids, Food Fasting, Keto...

I've been hitting Vitamin D, Magnesium, Ketamine Therapy, and Psilocybin research pretty hard because I have first hand experience with it... I could easily do DMT, LSD, and MDMA do write-ups on those; but, I respect psychedelics used as medicines so much that I don't want to take these drugs merely to take them... Plus, there's inherent risk when you use ANY of these tools and I realllllly don't want to set a bad example or mess up my achieved ascent from depression.

I know there are online resources already exist; but, I'm looking for volunteers who want to contribute to a project they have a say in**.** Maybe it can become something you'd be proud enough to put on an application or resume.

I'm looking for some passionate hobbyists (like myself), med or sci students, or professionals who want to pick a topic to dive deep into and help someone out... I'm spread too thin between doing this and the podcast, and I'd appreciate any help for someone who is hot on a topic!

You'd be surprised about some of the people go come through out Discord looking for options... It feels good to help people, or at least give them hope.

Thoughts on where I could go to find people like this? .... oh god, should I go from subreddit to subreddit? 💀

Hi, ive been reading alot about Shulgins work, and just reread pihkal for the second time. Is what he was doing similiar to whats done in psychopharmocology today? Apart from the self administration of the drugs he created.

Hello. I'm currently a second year BSc Chemistry student in London, on the way to specialising in organic chemistry. I've decided that I absolutely want to go into the field of pharmaceuticals, specifically psychopharmacology (Hamilton Morris may or may not have played a role in my interest in chemistry). However, I am a little concerned with the potential lack of routes for me to take. Due to Chemistry's status as a physical science, a lot of the masters programs offered which seem closest to psychopharmacology are not an option to me. The closest I can get is a few programs in general drug discovery and development. Does psychopharmacology as a field require university level biological knowledge? I have not studied biology since secondary school, and the modules offered at my university that cover synaptic/receptor research and research on the CNS are only available to people from a life science background. Basically, am I a little screwed or is this still achievable for me?

Immunotherapy and Cannabis: A Harmful Drug Interaction or Reefer Madness?

Prior observational research, cited in clinical practice guidelines, found marijuana decreases the efficacy of nivolumab. Reanalysis found that <5% of their statistics could be verified. There were errors in calculating percentages too!

Summary

Two Israeli studies about medical marijuana potentially interfering with immunotherapies like nivolumab for cancer treatment have received substantial attention. However, there have been anonymous but detailed concerns about these reports on PubPeer. This team attempted to verify the data analysis and statistics of these two reports and the published correction. Many findings, including some that could impact the statistical conclusions, could not be verified. Of 22 statistical in the prospective report, 4 could not be repeated using the same statistics or with the provided N. The p-value on 17 corresponded with that of a different statistical test than was listed in the methods. Re-analysis also identified some previously unreported significant differences (e.g., age) between cannabis users and non-users at baseline. Further study of the safety of immunotherapy and cannabis combination may be warranted using patient groups that have been matched on key demographic and medical variables.

Abstract

A retrospective (N = 140) and a prospective (N = 102) observational Israeli study by Bar-Sela and colleagues about cannabis potentially adversely impacting the response to immunotherapy have together been cited 202 times, including by clinical practice guidelines. There have also been concerns on PubPeer outlining irregularities and unverifiable information in their statistics and numerous errors in calculating percentages. This reanalysis attempted to verify the data analysis while including non-parametric statistics. The corrected prospective report contained 22 p-values, but only one (4.5%) could be verified despite the authors being transparent about the N and statistics employed. Cannabis users were significantly (p < 0.0025) younger than non-users, but this was not reported in the retrospective report. There were also errors in percentage calculations (e.g., 13/34 reported as 22.0% instead of 38.2%). Overall, these observational investigations, and especially the prospective, appear to contain gross inaccuracies which could impact the statistical decisions (i.e., significant findings reported as non-significant or vice-versa). Although it is mechanistically plausible that cannabis could have immunosuppressive effects which inhibit the response to immunotherapy, these two reports should be viewed cautiously. Larger prospective studies of this purported drug interaction that account for potential confounds (e.g., greater nicotine smoking among cannabis users) may be warranted.

Overall, the two prior studies, and especially the prospective one, were riddled with errors.

Thoughts?

Here's the link to the free full-text too:

https://www.mdpi.com/2072-6694/16/7/1245

What happens if someone is deprescribed something like risperidone, but is left on an SNRI like duloxetine simulatneously?

I'm not finding very many papers on antipsychotic withdrawal, and even less (like zero) on what happens if someone remains on an SNRI while undergoing withdrawal, so any links would be appreciated if you have them.

hey guys, hope this is a good place to ask.

I'm writing a review on schizophrenia for my assignment, and I came across something that I had missed some time ago. Atypical antipsychotics act as inhibitors on the excitatory 5-HT2a, but agonists on autoinhibitory 5-HT1a. How does this work to neutralise negative symptoms? Depression is generally regarded to be caused by reduced serotonin signalling, hence SSRIs to increase 5-HT in the synapse to keep signalling. How come in this case inhibition of serotonergic signalling reduces depressive symptoms? I just can't find papers that properly explain this mechanistically.

Thank you for anyone answering!

Hi, wondering if anyone has examples of oral depot (a drug being used less frequently than once daily when "normal" dosing is once daily or more frequent) regimens for psych drugs.

I am aware of the now discontinued version of Prozac weekly, whereby 90mg weekly was equivalent to 20mg daily dose. I've also heard whisperings of aripiprazole being used 3 times weekly but am curious what else might be out there. Thanks in advance!

As psychiatry resident I'm approaching a very variegated population: an interesting case of woman in a moderate depressive episode but also affected by primary hyperaldosteronism made me wondering which drug could I administrate her without make her suffering excessive electrolytes unbalancing and/or blood pressure. Any suggestions to go over a classic SSRI/mood stabilizer approach? Thanks for any idea will come ☺️

Corydalis seems to impact the opioid receptors without creating addiction related to dopamine. This study seems to indicate that most of the alkaloids in it interact with opioid receptors and are affected by the administration of narcan. Thoughts on the validity of whether it constitutes as an opioid or not?

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8704877/

I know that stimulants work via reuptake of dopamine, so are the cognitive enhancing effects due to dopamine binding to receptor subtypes other than D1 and D2?

Forgive my bad knowledge of neuroanatomy, but are other subtypes also expressed as abundantly in areas of the basal ganglia and frontal lobes?

Does 5ht2a antagonism have anything to do with this?

I know plenty of people with commorbid mood disorders/ personality-disorders and ADHD that take stimulants and antipsychotics effectively.

I'd appreciate any insight, thanks in advance.

This question has been on my mind for a while, but I haven't yet found the answers I'm looking for. I work a lot with both direct and indirect sympathomimetics, as well as anticholinergic drugs (in intensive care and anesthesia). It is well known that directly acting sympathomimetics have dose-dependent effects on various receptors, like adrenaline, for example. I am aware that ephedrine, especially in subtherapeutic doses, can have paradoxical effects due to compensatory counter-regulation, although this is individual. It's known with atropine (an anticholinergic) – half an ampoule can make a patient who is already bradycardic in an emergency even more bradycardic.

On ADxS.org, in the dosing guide, it is recommended to start with a significantly smaller dose than the approved initial dose of Vyvanse – an initial dose of 5 mg (or 10 mg) and increase by 5 mg every 5-7 days.

https://www.adxs.org/en/page/232/medication-dosage-for-adhd#content-1241-elvanse-lisdexamfetamine

However, I keep reading here that especially the very low doses of Elvanse can lead to unpleasant effects - it was the same for me. That's why I'm increasingly skeptical of the justification that you can't go wrong with particularly small doses. I would like to understand it better - maybe someone here has more expertise in this area than I do?

Is there a pharmacological explanation for why a very small dosage of Vyvanse can cause unpleasant side effects, which one does not have with a higher dose?

Hi! I read about Prozac's blockage of 5HT2C serotonin receptors. I wonder if it is enough to make it stimulating by indirectly increasing dopamine and norepinephrine and if, therefore, it might be recommended for depression with lack of energy and excessive tiredness.

Thanks!

Hello! I am trying to find information specifically on the effects of combined alcohol and stimulant* use, specifically concerta (methylphenidate ER).

*ideally I want information about individuals taking stimulants as prescribed, but other info is also useful.

Some specific questions I have:

• How does alcohol use impact the effects of concerta? / Can alcohol use inhibit the (therapeutic) effects of concerta? /
• If yes, is this inhibition temporary or can it have long term consequences?
• What are the long term vs short term effects of combined use?
• Can alcohol increase tolerance of concerta? (again, would be great if there’s information on people taking concerta as prescribed)

Anything helps, thank you!

Hello,

Ive recently read multiple studies showing that the combination of psychotherapy and psychotropic medication is more effective than either one is alone. Is there a specific type of psychotherapy that especially compliments psychotropic medication? I know that historically, psychoanalysis/psychoanalytic therapy has gone hand in hand with psychopharmacology in the field of psychiatry. Does it matter at all?

A search of this subreddit shows that there has been no discussion of this relatively new ADHD medication. What are your opinions? Have you have clinical experience with it?

Is it essential for 5-HT activating small molecules to cross the BBB? Considering there are 5-HT receptors located throughout the body in places other than the brain, is crossing the BBB necessary for their MOA? Is activating 5-HT receptors within the brain responsible for the more well-known psychedelic effects?

Suppose a 5-HT regulating molecule were to be modified so that it could not pass the BBB yet retain its 5-HT receptor affinity. Could this eliminate certain psychedelic/hallucinogenic effects while retaining neuroplasticity, anti-inflammatory, etc. effects? If this is the case how do we remove BBB permeability yet retain 5-HT affinity?

Hi, hopefully this should be a good sub to ask this in. I currently have a BSc in Compsci which I doubt I can use to get a postgrad degree in something like psychopharmacology or drug discovery so I've been considering a second degree in either chemistry or biochem and just wanted to check here to see if anyone has any perspective on whether it matters much between the two with the intent of going into these postgrad studies. Unfortunately my nearby uni doesn't offer a degree in medicinal chemistry cause I'm sure then that would be the clear choice.
thanks!

Hi there-

Bit of background - did an undergrad degree in psychology, realizing in my senior year that I actually did have an interest in research and not purely clinical practice. Currently in a master's program in applied clinical neuropsychology, and very unsure what path to take from here.

I still strongly desire to go into clinical practice, but I have taken a keen interest in psychopharmacology. The question is, do I pursue Psychiatry, allowing me to practice therapy as well as prescribe and research psychopharmacology? While I could certainly see myself strongly enjoying prescribing/med management, I think the research is slightly more important to me - so I am also considering non-medical routes. Would a clinical psych phd even allow me to perform psychopharm. research as well as therapy?

Any advice welcome -

Thank you!