u/Anxious-Traffic-9548

Hello everyone,

I've been taking 5mg methylfolate daily for the past week for depression. So far it's been working well, I feel more emotionally stable and my mood is better overall too. However, I've noticed since starting that text now has a sort of "psychedelia" to it akin to reading while, well, tripping. It's subtle but noticeable, especially in the first couple seconds after I move to a new line of text. For example, Os will at first appear with a low-opacity ring overlayed around it. Aside from this I have no other side effects and my sleep is fine (to clarify that I'm not hypomanic).

It doesn't bother me too much, but I'm minding it in case it's an indicator for something else I should be concerned about, or if it gets worse as to affect my reading.

Is this at all similar to HPPD symptomology? Should I consider stopping, will monitoring it be okay?

I intend this question within the bounds of usual differences in adult lifestyles. Mild alcohol and other drug use vs abstinence, good vs poor diet, mental health issues vs good mental health, etc. Do these typical lifestyle differences at all meaningfully affect IQ scores in adulthood?

Some research suggests that even light alcohol consumption can accelerate subclinical cognitive decline. The testing that has established is not based on IQ from what I gather, but I wonder if it could generalize to greater drop in raw IQ score with age, which would translate a drop in IQ relative to the same-aged peers.

Relevant research is appreciated. To anyone who will try to reason the answer because CAIT told them 145, please don't reply.

Hey everyone,

I wanted to share my experience with apolactoferrin after having been unable to tolerate even the "GI friendly" iron supplements, in case it's of help to anyone else. I tried ferrous sulfate (terrible GI sides), iron bisglycinate, and then succinylate. Succinylate was the best of the 3 but the amount of capsules I'd need to take made it both very expensive and inconvenient. After 3 months of daily supplementation, I my ferritin only increased from 14 to 30.

So for a while I just gave up and my ferritin stayed steady. Eventually I had enough of my RLS (ferritin-related) and decided to give apolactoferrin a try. I took 250mg for 6 weeks and my ferritin went from 30 to 60 with 0 GI sides. In fact, I think my baselines GI symptoms have gotten better (I may have had IBS, not sure) and my stools no longer take the wind out of me nearly as much as they did before. Most importantly, my RLS is gone! I don't even get it when I take melatonin now. I'll continue taking the lactoferrin until I get my ferritin near 100, since I have other issues that may benefit from a higher ferritin level.

Hope this can help anyone else.

Curious if anyone has had other providers pull their controlled substances list and question or refuse to continue care due to an at-home ketamine treatment.

Something to address: I'm very disorganized when it comes to titrating meds. Unfortunately, while my doctors are cooperative and recognize my disorder, they aren't really knowleadgeable enough to titrate things themselves. So often times I'm being written a script for an intermediate dose and have to do the titration alone.

My provider prescribed 1.5mg LDN and let me at it. I knew this was probably too high a dose for me, so I tried .5mg, nightly. I had no problems sleeping through the night and experienced dreams that, although vivid, were not bothersome. However, during the day I feel generally poisoned. I've come to understand that this may be due to the dose being too high. What really sucks is that none of the clinical trials comment on titration. "Patients were given x mg of naltrexone for 4 weeks and then POOF, here's data from only the end timepoint". Are people really just being thrown into 4.5mg no problem? Maybe I am confusing PEM with LDN side effects. Who knows, I don't!

That's just to say that I'm feeling a bit dissuaded. I can't really afford to have days below my already low baseline due to work demands, so the idea of starting up again and experiencing similar symptoms is daunting. At the same time, i want to give LDN a fair shot, especially knowing how bad I am with properly evaluating meds before moving on.

Any words of encouragement or recounts of similar experiences are appreciated. Have as good a day as you can today.

Pre-illness I used to find subclinical doses of stimulants highly effective. They'd entirely cut through whatever fog I had and give me 3-4 hours of uninterrupted focus and calm (ritalin). Now, and especially during PEM, I feel as though stimulants are "blocked" by my brain. They have more side effects at the same doses, and require greater doses to reach a vaguely comparable level of efficacy. I'm certain this isn't due to tolerance formation as this has been the case even after long breaks.

I really miss how stimulants used to work for me :(

Favorite stimulant "landing gear"? As in, a hypnotic/sedative that counteracts the post-stimulant insomnia one can get from longer-acting stimulants. There is a similar post over on the drugs subreddit, but the culture there is a bit more haphazard in their compound selection. Curious to hear people's takes on here with neuroprotection in mind.

The orexin-2 agonist Oveporexton was recently approved for the treatment of narcolepsy type 1. OX-2 agonists are of interest to the nootropic space because they've been shown to improve wakefulness in healthy controls and are likely to bestow some cognitive benefit akin to stimulants, but in a potentially more discrete and selective way.

However, oveporexton's approval means that it will soon be scheduled by the DEA. Based on the available clinical research, it will likely be schedule IV. This will mean that, in uncertain legal clauses which loom but are only selectively policed, that all unapproved OX-2 agonists will become risky to sell as RCs. Even if they are structurally dissimilar "abuse potential" will be mechanistically implied. This will inevitably mean that their vendors, if any, will be of lower quality and integrity than those that stick to solely to less legally ambiguous RCs. This is an unfortunate consequence of drug scheduling as it is currently implemented.

Why no vendors picked up OX2 agonists before now is surprising to me, but the door is closing, and once it has, people should be cautious of whatever actors take the risk.

The new update seems to have dramatically reduced my deep sleep estimates while virtually eliminating my intranight wake (replacing it with “restlessness” it seems). Anyone else’s experience the same?

Prior to the update, I used to get ~1:35 a night.

The general dynamics of sleep disorders are such that a single night of non-disordered sleep results in MARKED improvement almost immediately. I feel that this very underappreciated sleep disordered sleep communities. We know from extreme sleep deprivation in non-sleep disordered people (60+ hours, often pharmacologically assisted) that a single night of unrestricted recovery sleep restores cognitive function to baseline. There is no basis for "needing to repay your sleep debt" before you feel better. I suspect that much of the lag that is observed with CPAP relates to tolerating the machine before the sleep actually improves, at which point the improvement to wakefulness is clear.

There are long-term consequences of disrupted sleep and sleep apnea specifically which may take longer to resolve with proper treatment (brain atrophy, metabolic issues, etc.), but these do not immediately mediate the day-to-day feeling of "I'm awake" vs "I'm awake but asleep". They may exert negative effects on sleep themselves, which would manifest as a lag before they are resolved, but this is not due to "repaying your sleep debt".

Believing that you are "repaying your sleep debt" as you continue to struggle during the day is potentially harmful because it promotes delaying care and correction when something isn't working. CPAP takes time, but probably not because you are paying debt before it begins working.

ISI and SCI scores improved significantly (both p < .001). Actigraphy confirmed longer total sleep time, higher sleep efficiency, and shorter sleep onset latency; after correction, ISI/SCI improvement and longer total sleep time remained significant. Clinically, 62.5% achieved meaningful improvement (≥7-point ISI reduction), 25% partial-to-minimal, and 12.5% no change or worsening; nearly two-thirds reached non-clinical insomnia levels. CPT-3 revealed enhanced sustained attention and response consistency, with further gains in selective attention and reduced impulsivity among responders. BAARS-IV showed overall improvement, with the sluggish cognitive tempo subscale reaching significance. Mood and anxiety improved, and the SDQ appetite/weight subscale decreased significantly even after correction, suggesting reduced perceived appetite or weight. Daridorexant was well tolerated; two participants reported daytime sleepiness or sedation, and one discontinued due to persistent sedation.

Starting this thread to document my experience with Sunosi (solriamfetol) from the perspective of depression with hypersomnolence and vague auto-immune issues triggered by excessive exertion (CFS/ME) in case it's of help to anyone else. Most of the anecdotes online are for its primary indications or ADHD. For those unaware, it is a DNRI that may be more biased in its dopaminergic effects than bupropion while lacking active metabolites and being comparably shorter acting at steady state (bupropion is effectively a 24/7 drug at SS). It also has some activity at TAAR1 which is unusual for a clinically utilized NDRI and an activity it shares with dexamphetamine.

Day 1 75mg:

Today I took 75mg after an overnight fast. I did not "feel" it kick in because I was busy throughout the morning, but I did notice the effects once it was near its peak (~2 hours post). The wakefulness and generally feeling it provides is not unlike what I have experienced pre-morbidly. It feels like a context-appropriate excitement/interest without forceful stimulation.

There was an anxiolytic component not unlike a low dose of amphetamine, but without the "body high" effect one gets when starting. For me, amphetamine anxiolysis feels like I've gone for a morning run and is unlike sedative/hypnotic anxiolysis which feels more blunting by comparison. I wonder if the TAAR1 activity plays any role in this, since I do not experience the same for methylphenidate or modafinil. The effect on motivation also feels quite natural and in the background. It is most noticeable after starting tasks, rather than at rest, unlike amphetamine. Peripherally I noticed no side effects aside from increased perspiration.

I am writing this at T+7 hours and will report back on my sleep. Amphetamines and modafinil cause me a fair bit of onset and late insomnia, even when taken in the morning, so I'm hoping solriamfetol fairs better given its shorter half-life.

At T+7 hours I continue to feel the background effects on motivation, fatigue, and wakefulness. I noticed that I didn't crash like usual after eating my first meal of the day at T+6 hours.

Day 1 TL:DR
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Last week I took 15mg of methylfolate and got a runny nose and some physical anxiety. However, mentally I was basically teleported back to my pre-morbid state. This lasted for a few days after. I then a couple days ago I tried again at 5mg and felt great, but am experiencing terrible insomnia ever since. Strangely, I am very energized during the day and have read the same from many others. I do not find this energy to hypomanic in the slightest aside from the greatly reduced need for sleep. I'm not entirely sure how reduced my sleep is because I have taken steps to pharmacologically ensure some at least 5 hours as I wait for this to pass. I'm thoroughly impressed if not a bit overwhelmed by how effective this has been otherwise, though. Next time I'll trial 500mcg and work my way up in weekly increments.

Thought I'd share in case others have had similar experiences or have thoughts to share.

Last week I took 15mg of methylfolate and got a runny nose and some physical anxiety. However, mentally I was basically teleported back to my pre-morbid state. This lasted for a few days after. I then a couple days ago I tried again at 5mg and felt great, but am experiencing terrible insomnia ever since. Strangely, I am very energized during the day and have read the same from many others. I do not find this energy to hypomanic in the slightest aside from the greatly reduced need for sleep. I'm not entirely sure how reduced my sleep is because I have taken steps to pharmacologically ensure some at least 5 hours as I wait for this to pass. I'm thoroughly impressed if not a bit overwhelmed by how effective this has been otherwise, though. Next time I'll trial 500mcg and work my way up in weekly increments.

Thought I'd share in case others have had similar experiences or have thoughts to share.

Has anyone else noticed that psych NPs tend to have "prescribing boundaries" in a different way than most Psychiatrists? It tends to be a statement of "I wont prescribe you stimulants" rather than the usual "make appointments for med switches and f/u every X months for control refills". I've always found this strange, because in the case of properly diagnosed ADHD, stimulants are the recommended and most effective first line treatment. I've noticed that many ADHD patients managed by psych NPs are started on atomoxetine or bupropion and never actually trialed stimulants.

If you are not comfortable prescribing the most evidence based treatment for a given condition, should you really be treating it?

I understand that many patients can be demanding of stimulants with largely unsubstantiated family GP or NP "diagnoses". These patients should be directed to proper neuropsychological testing or other means of establishing a proper diagnosis, and then treated in the most evidence-based way possible. I don't believe starting everyone on objectively inferior, second line medications should be the reaction to this influx of demanding patients.

Thoughts?

Over the past year there has been an influx of “looksmaxxers” on this sub. At a glance the mindset may appear aligned in its pursuit of self-improvement, but the culture that has come to define it is extremely toxic and close-minded. “Adderall mogs”, “larp”, “holy dopamine”, are all examples of this insufferable way of communicating. You can quite literally feel the seething hatred of users part of this culture from these braindead comments alone.

This sub’s original culture should be careful to not merge with that of looksmaxxing culture. Thats all.

Over the past few years I’ve scaled back my exercise a tonne to avoid PEM. Occasionally, I have days where I feel okay and exercise. This always ends up triggering PEM the next day. I know this, but I help myself in the moment because it’s the only thing that makes me feel fully like myself before. That post workout mood used to take away my stresses and even pulled me out of some bad places mentally in the past. But now, the mood is followed by PEM lasting a few days. My condition is mild, but I feel that losing the ability to exercise has made me vulnerable to the mental health issues that plague me now, which are certainly not mild.

Sharing to vent. I hate this.

Compared to oral selegiline, buccal selegiline appears to generate a similar concentration of metabolites but results in ~8 fold greater selegiline concentrations (when dose is not adjusted for potency). Interestingly, the half-life of selegiline absorbed through buccal routes appears to be more than twice as long as oral, which may be relevant to its effects given its MAO-B independent CAE action.

When adjusted for potency, an equivalent buccal dose generates ~8 fold fewer metabolites than oral selegiline. I couldn't get a clear answer on this last part when browsing discussions already posted to reddit, so I decided to dig for myself and post here.

Source Page 6, 1st table.