Hello friends, I’ve posted about this topic before but it’s been almost a year and I need some updated guidance. I’m 19 months into my hppd recovery and my visuals have improved significantly. The only symptoms that remain are slight (but mostly benign) screen sensitivity, flickering of vision in low light conditions, and tinnitus (by far the most annoying symptom).

I was hoping after this amount of time I would have returned to my baseline but I’m quite discouraged this is not the case. The tinnitus is quite pervasive and is tied to my mood and stress levels. It’s extremely distressing when it flares and often makes me suicidal. I often try to ignore it/tune it out but that’s been difficult as it’s really in your face. At this point in time do I just accept that this is part of my new life. Was really hoping of being capable of experiencing silence again but I’m losing more and more hope as the months go on. Thanks!

I abused Benzos heavily since I was 15 I am 19 now and am recovering, one of the many, many, long term side effects is visual distortions. Im curious as to why recovered Benzo, Heroin, Meth addicts ect are able to go on interviews and have a positive outlook on life despite having undoubtable permanent brain damage, meanwhile people on this sub are still figuring out IF THEY EVEN HAVE brain damage from psychedelics. I know I have permanent brain damage from benzos and accepted it. Why can’t psychedelic users accept the permanent changes that come with altering your perception?

Just found out that I’ve had HPPD for years and didn’t even notice. Im in early recovery and I actually enjoy the visuals. I do see how this could be distracting once I have more responsibilities to take care of, cuz if I pay attention to it I can dissociate pretty hard into the experience.

Music also makes things so much more intense and certain songs make me physically feel like im tripping not just the visuals. Crazy.

i never realized it wasnt normal until a couple days ago when someone said “when you look at the wall do you see static?” And i was like, “you dont?”

I have really bad struggles with mental health so the visuals are kind of a welcome distraction, and the more I read I see that mental health struggles are somewhat a part of this as well…I just never connected the two. Anyway thanks.🙏

hello, i thought about writing this for quite a long time. i’m a 21 year old Male. I took mushrooms on weekends consecutively for two months and the last time i took them i took the most i ever had. that was in december 2025 from then on, i had mild dprd and very mild visual snow. it was almost non existent as well as no anxiety or depression. after a while i felt myself recovering. i had not drank alcohol since that happened and i havent smoked weed in over 3 years so that never effected me. then fast forward to april this year i had an extreme shutdown mode where i had completely debilitating anxiety and depression, visual snow and dprd. it was so horrible and the worst thing ive ever been through. i could not sleep at my own house for 3 weeks and had to live at my moms house. i was extremely depressed. i’ve experienced depression in the past but i had recovered and found purpose in my life. that day it came back like a truck was the day i thought for sure i would end my life. thanks to my family and friends and god that didn’t happen. anyways, since then ive slowly started recovering (or just getting used to it over time i can’t tell). i still do not drink and i would not dare to touch any kind of drugs ever again. i don’t go to the movies or large events with stages as it bugs my symptoms very badly. i am now on 10g of lexapro everyday, which has helped me tons. i also refuse to eat normal mushrooms now. i know its stupid but i won’t even eat any normal mushrooms that are included in food it’s just a thing i have. i go to therapy every two weeks to help cope with symptoms. but for the most part what helped me was just keep moving forward in my life with my career and social life. it irritates me that everyone i talk to about this can’t grasp what i go through. but yeah thats my story and i try hard to take care of myself. i never knew how important sleep was until this happened to me. to everyone that goes through this i love you all and hope we all recover and get over this one way or another. :)

I really never have used drugs much. But from august to february i had shrooms three times and mdma once. The last time i had a bad trip consisting on a panic attack and the thought of being stuck like that forever. Since then i have had some problems with anxiety but until last month i really didnt put the focus on my vision. I really don't think i fit the classis symptoms such as afterimages and dense static. I really only have the feeling of being sensitive to light; when looking to the sky or a wall my eyes hurt and see like a black fog i rlly couldnt describe (wich could be only static, but i cant rlly tell); when looking at patterns they sometimes very lightly move like when looking at an optical illusion; and sometimes i feel like colours are more intense (but this could only because my obsession over it).

Idk, it sometimes feels like i have hppd and im going to be like this forever and sometimes like its just regular vision things that seem new beacuse of my hypervigilance. Hope that somebody can clarify this a little

The Unifying Model (the framework from which the research frontiers emerge)
If you line up Hallucinogen Persisting Perception Disorder (HPPD), Visual Snow Syndrome (VSS), tinnitus, migraine with aura, depersonalization/derealization, and even Parkinson’s disease psychosis, a common axis emerges: an excitation/inhibition (E/I) imbalance, thalamocortical dysrhythmia, and failure of the top-down “noise-cancelling” filtering system. In VSS, this is measurable: increased gamma activity in the primary visual cortex together with reduced alpha–gamma phase-amplitude coupling (PAC), reflecting both an E/I imbalance and a breakdown of the brain’s intrinsic noise-suppression mechanism.
But there is a deeper layer that is almost never connected to HPPD, and it may explain why the disorder is so treatment-resistant. Neurodegenerative psychosis provides the blueprint: hyperactivation of pyramidal neurons in the visual cortex generates visual hallucinations within a context of dysregulated serotonergic, GABAergic, glutamatergic, and dopaminergic signaling. More importantly, recent psychedelic neurobiology shows that 5-HT2A receptor activation does far more than simply “turn perception on.” It induces metaplasticity through remodeling of the extracellular matrix (ECM) and perineuronal nets (PNNs), structures that normally function as molecular “brakes,” stabilizing neural circuits after critical periods close.
This leads to a reformulation that changes the entire perspective:
Refractory HPPD is not best understood as “brain damage.” It may instead represent a pathological perceptual circuit that has consolidated into a stable attractor state, with the PNNs effectively locking the brain into the wrong configuration.
This also explains why symptom suppression with benzodiazepines or antipsychotics rarely produces recovery: they dampen the symptoms without altering the consolidated pathological circuit.
From this perspective, the research frontiers naturally organize into several mechanistic layers.

Layer 1 — Rhythm: Precision Neuromodulation Rather Than Conventional rTMS
Conventional fixed-frequency rTMS has already been explored. However, if the underlying problem is an individual’s specific oscillatory dysrhythmia, then the true frontier becomes biomarker-guided closed-loop transcranial alternating current stimulation (tACS).
Closed-loop EEG-guided tACS protocols already exist that synchronize stimulation with the phase of ongoing alpha oscillations while modulating their amplitude over visual cortex. Even more specifically, studies have demonstrated that:
tACS can rhythmically suppress visually induced gamma oscillations;
gamma bursts can be locked to alpha troughs;
alpha–gamma coupling can be selectively reconstructed within occipital cortex.
Now connect this with VSS:
VSS consistently demonstrates
elevated gamma activity,
reduced alpha–gamma PAC.
This creates an almost lock-and-key therapeutic hypothesis:
Suppress pathological V1 gamma activity while rebuilding normal alpha–gamma coupling.
To date, this approach has not been meaningfully applied to HPPD.
Rather than simply “stimulate and hope,” the logical strategy would be:
phenotype each patient’s oscillatory signature using EEG or MEG;
identify individual alpha slowing, gamma excess, and PAC abnormalities;
design individualized stimulation waveforms.
The cognitive risk profile would likely remain minimal and reversible—precisely the type of intervention desirable in HPPD.

Layer 2 — Inhibition: Tonic Rather Than Phasic GABAergic Control
This represents perhaps the most elegant pharmacological gap.
Benzodiazepines primarily enhance synaptic (phasic) GABA-A receptors, and tolerance inevitably develops.
However, the baseline gain control of cortical networks—the mechanism determining how excitable cortex remains at rest—is governed largely by extrasynaptic δ-subunit-containing GABA-A receptors, which mediate tonic inhibition.
These receptors:
are essentially insensitive to benzodiazepines,
are highly sensitive to neurosteroids.
Neurosteroids such as
allopregnanolone,
THDOC,
and δ-selective agonists such as gaboxadol (THIP) selectively enhance tonic conductance, producing shunting inhibition that regulates overall network excitability and seizure threshold.
A patient who failed cl*****am has generally never engaged this system.
One particularly interesting candidate is ganaxolone, a synthetic neurosteroid already approved for a rare epilepsy syndrome, whose pharmacological profile avoids many of the tolerance issues associated with benzodiazepines.
There is, however, an important paradox.
At sufficiently high concentrations, neurosteroids may initially suppress inhibitory interneurons—which are themselves highly sensitive—producing transient disinhibition rather than inhibition.
The effect is therefore biphasic.
Dose becomes everything, requiring careful titration under clinical supervision.
Even so, the anticipated cognitive risk remains relatively low.

Layer 3 — Resolving the Serotonergic Paradox
Perhaps the most targeted frontier lies here.
5-HT2A activation appears central to initiating HPPD.
Serotonergic drugs often worsen symptoms.
Conventional D2-blocking antipsychotics—including olanzapine and lurasidone—may worsen cognition or even exacerbate symptoms.
The missing piece is remarkably simple:
A selective 5-HT2A inverse agonist with essentially no dopaminergic receptor affinity.
Such a drug already exists:
Pimavanserin.
Pimavanserin is the first antipsychotic approved without meaningful dopamine receptor affinity.
Instead, it acts as a highly selective 5-HT2A inverse agonist, and was specifically developed for Parkinson’s disease psychosis because it preserves both motor and cognitive function.
Mechanistically it targets precisely the receptor believed to trigger HPPD while avoiding the D2 blockade responsible for many problems associated with conventional antipsychotics.
Even more intriguing, pharmacological literature explicitly notes that, based on its 5-HT2A inverse agonism, pimavanserin may have therapeutic potential for symptoms associated with hallucinogen exposure.
Its signaling profile is unusually precise:
inverse agonist at the Gαi1 pathway, believed to mediate hallucinogenic signaling;
neutral antagonist at the canonical Gαq/11 pathway.
To the best of my knowledge, it has essentially never been systematically investigated for HPPD.
Mechanistically, it may represent one of the cleanest pharmacological candidates currently available.

Layer 4 — Consolidation: The Deepest Frontier (and the Greatest Paradox)
If HPPD represents a pathological circuit locked in place by PNNs, then genuine treatment would not consist merely of suppressing symptoms.
It would require:
reopening plasticity → retraining the circuit → reclosing plasticity around the correct configuration.
This is the central paradox of the entire disorder.
The same 5-HT2A receptor that may contribute to HPPD also serves as the gateway through which psychedelics reopen critical periods by remodeling the extracellular matrix.
In theory, reopening that critical period could allow normal perception to be relearned.
In practice, administering psychedelics to someone already suffering from HPPD may be among the most dangerous interventions imaginable, potentially reinforcing the pathological attractor permanently.
The key that could unlock the prison is forged from the very material that built it.
Therefore, the safer frontier would be to decouple plasticity reopening from 5-HT2A activation.
Three conceptual approaches emerge.
First: induce metaplasticity without engaging 5-HT2A.
Research from Dölen, Nardou, and colleagues suggests that reopening critical periods converges upon extracellular matrix remodeling and may be achievable through pathways independent of 5-HT2A signaling.
The true target may therefore be the ECM itself rather than the receptor upstream.
Second: directly manipulate ECM or PNN biology.
Rather than using psychoactive drugs, interventions could transiently loosen the molecular brakes imposed by PNNs.
This framework is increasingly discussed for disorders characterized by rigid maladaptive circuit dynamics.
Third: couple any reopened plasticity window with intensive perceptual learning together with Layer 1 rhythm restoration.
The objective would be for the circuit to reconsolidate into a healthy attractor state.
Conceptually, this represents the only approach aimed at actual recovery rather than symptom suppression.
At present, however, it remains highly experimental and largely confined to animal models and translational neuroscience.

The Meta-Frontier: Phenotype First, Combine Second
This also explains why virtually every previous intervention has failed.
Almost every pharmacological trial has treated HPPD as though it were a single-layer disorder, testing monotherapies sequentially without physiological biomarkers.
But a multilayer disorder involving
abnormal oscillatory rhythms,
impaired tonic inhibition,
pathological circuit consolidation,
is unlikely to respond to isolated interventions.
Instead, a coherent frontier protocol—while remaining within the constraint of preserving cognition—might conceptually resemble:
EEG/MEG phenotyping;
restoration of tonic inhibitory tone using a δ-selective neurosteroid;
selective silencing of the trigger receptor with pimavanserin rather than dopamine-blocking antipsychotics;
individualized closed-loop tACS designed to suppress pathological V1 gamma activity while reconstructing alpha–gamma coupling;
ultimately, a non-psychedelic plasticity window coupled to intensive perceptual retraining.
The emphasis shifts from a sequence of isolated treatment attempts to an integrated systems-level intervention.

Low-Risk Adjunctive Strategies Worth Considering
Several additional interventions deserve attention because they may influence the same physiological framework while carrying relatively low cognitive risk:
a ketogenic diet, which shifts the E/I balance toward inhibition and possesses anticonvulsant properties;
transcutaneous vagus nerve stimulation (tVNS), already explored in tinnitus research for modulation of cortical excitability;
careful investigation of the retino-thalamo-cortical pathway, including the possibility of abnormal peripheral or lateral geniculate nucleus (LGN) generators contributing to pathological signaling.

Two Essential Caveats
Two points must be emphasized, because omitting them would be scientifically irresponsible.
First, these concepts represent research frontiers and mechanistic hypotheses rather than established clinical protocols. To the best of current knowledge, pimavanserin, ganaxolone, and individualized closed-loop tACS have not been evaluated in controlled clinical trials specifically for HPPD. Their use would therefore ideally occur within research settings or, where appropriate, through carefully documented off-label treatment under specialists familiar with the emerging literature.
Second, any intervention involving psychedelic-mediated reopening of plasticity should presently be regarded as a major theoretical hazard rather than a therapeutic option. It is discussed here solely because it represents one of the most important scientific paradoxes underlying HPPD—not because it constitutes a clinically appropriate strategy today.

We are a group of researchers from Humboldt University of Berlin and we look forward to your participation in our study! The survey is completely anonymous.

Have you ever taken a psychedelic substance?
Share your opinion and possibly experiences you have had with psychedelic experiences without (immediate) previous use of psychedelics with us!

https://psychedelicflashbacksurvey.info  

We would like to learn more about who has these experiences, what they look like in concrete terms, which factors contribute to the associated effects and how they can be dealt with.

https://pmc.ncbi.nlm.nih.gov/articles/PMC10521293/

"A conclusion is valid if the inferences follow from the evidence presented. There are two tiers of challenges here. First, authors in the psychedelic literature have regularly drawn conclusions that are either misleading or clearly contrast with the data. Four examples follow to showcase that this problem is common practice. Abbar et al. ²⁷ found in a randomized controlled trial (RCT) comparing ketamine against placebo that there was no persistent benefit of ketamine over placebo at the exit timepoint of the trial in week 6, but concluded in the abstract that ‘ketamine [. . .] has persistent benefits for acute care in suicidal patients’. Ionescu et al. ²⁸ found in an open-label ketamine study that only 2 of 14 patients show sustained improvement at 3-month follow-up (which may well be due to the placebo effect or other factors), but the title of the paper reads ‘Rapid and Sustained Reductions in Current Suicidal Ideation’ (our highlight). Palhano-Fontes et al. ²⁹ **concluded in their ayahuasca study (**n = 14 treatment, n = 15 placebo) that ‘blindness was adequately preserved’, when all participants in the treatment group said they believed they had received ayahuasca, but less than half of participants in the placebo group said so. And Daws et al. ³⁰ compared two treatment arms, including one using psilocybin-assisted psychotherapy, against each other, concluding that one treatment outperformed the other despite the lack of a statistically significant interaction term between the treatments. Journals, reviewers, funders, and scientific institutions need to hold authors accountable for such inferences.

The second tier of challenges is when questionable research practices – that usually go hand in hand with a lack of transparency – raise doubts about the validity of conclusions.^31 –33 One common practice concerns flexibility regarding the analysis of primary outcome measures, which is common in psychedelic science. A recent phase II trial ³⁴ administering psilocybin for treatment-resistant depression funded by a pharmaceutical company registered their primary outcome on clinicaltrials.gov for the time frame ‘up to 12 weeks’, which allows for degrees of freedom in obtaining statistically significant results and severely threatens valid inferences. Another study, using ketamine to treat depression ³⁵ switched a secondary to a primary outcome a year after data collection started, and the publication contains no results at the time point of 2 weeks that can be found in the clinicaltrials.gov registration (https://osf.io/uhdrp). Yet another psilocybin trial for depression ³⁰ analyzed a different outcome than registered on clinicaltrials.gov. ³⁶ In all these cases, doubts remain whether equally positive results had occurred if stricter procedures would have been in place.

Another concern is related to multiple testing. Psychedelic studies often contain a flurry of different outcomes, including physiological, neural, cognitive, and self-report measures. This dramatically increases the chances of false positive findings when not dealt with appropriately. For instance, a recent paper on the efficacy of psychedelic therapy concluded that several secondary outcomes clearly favored psilocybin over escitalopram, but the lack of correction for multiple testing raises doubts about the validity of these findings. ¹ In our own research on psilocybin microdosing, we included six different tasks, with multiple subcomponents and measures per task, ³⁷ totaling the number of dependent measures to more than 20. We found effects of psilocybin microdosing on two outcomes. But because we had all outcomes preregistered transparently, and these two findings did not survive correcting for multiple testing, they likely reflected chance findings."

"There are further problems, such as selectively removing outliers that result in significant findings, interpreting nonsignificant p**-values in small samples as ‘trends toward significance’ (but not interpreting barely significant** p**-values as trends toward nonsignificance), and using one-sided tests over two-sided tests to obtain desired results,** ³⁰ discussed in Love. ^38"

^" For instance, an analysis of 397 clinical trials in psychiatry has shown that studies reporting a COI were five times more likely to report positive results. ⁴⁸ COIs are also pronounced in the psychedelic literature: a recent opinion paper on ketamine for treatment-resistant depression featured a COI section nearly five times as long as the paper’s introduction section ⁴⁹ : of 25 authors, 19 declared COIs, including patents for treating depression with ketamine. We are not convinced that the research community always takes best COI practices sufficiently seriously. For example, while the organizers for the psychedelic science 2023 conference (with over 300 speakers) originally followed recommended disclosure protocols, ⁵⁰ by asking speakers to declare COIs in a dedicated presentation slide, slides were removed by the organizers before the talks and moved to the conference mobile app." [??????????]

"Sufficient information on potential risks, dangers, and adverse events is missing to draw conclusions that psychedelics are safe to use in the context of mental health treatments. For example, although esketamine (in the form of a nasal spray) was approved by the FDA for treatment-resistant depression in 2019, there is evidence that the approval process overlooked red flags, ¹⁴ and a meta-analysis from 2021 concluded that there was insufficient data regarding the long-term safety of ketamine. ⁵⁴ A recent analysis found a systematic underreporting of serious adverse events studies on the safety and efficacy of esketamine in depression ⁵⁵ : 41.5% of serious adverse advents that were found on clinicaltrials.gov were not reported in published articles, and nearly all of them (88 out of 94) occurred in esketamine treatment arms, not placebo arms."

"We see similar issues for other drugs now. Adverse events for therapy with MDMA and classical serotonergic hallucinogens are not systematically assessed and reported. ⁵⁶ A straightforward definition of an adverse event in psychedelic research is missing, and standardized measurements and transparent reporting of adverse events are lacking. Most studies rely only on spontaneous reporting by patients or therapists, which in turn require a careful process of interpretation to assess whether the adverse event can be attributed to the psychedelic therapy specifically."

"And adverse events do occur. ⁵⁷ A recent clinical trial using psychedelic therapy ³⁴ reported increased suicidal ideation and intentional self-injury in the 10 and 25 mg psilocybin group, whereas the control group who received 1 mg of psilocybin remained unaffected. In the same study, suicidal behaviors were observed in three patients, but authors concluded in a media report that ‘these cases were probably random events and unrelated to the dose of psilocybin, which would have been fully cleared from the patients’ bodies’. ⁵⁸ This is not the most careful interpretation of the data, and we note that the opposite rationale is applied to successful treatments: people get better despite the drug being fully cleared from the patients’ bodies. Sometimes, conclusions are radically opposed to presented evidence. In a placebo-controlled study using ayahuasca as an intervention for depression, 4 of 15 participants in the experimental group (i.e. ~27%) had to be hospitalized for 1 week ‘due to presenting a more delicate condition’. ²⁹ Nonetheless, authors concluded that the ‘study brings new evidence supporting the safety and therapeutic value of psychedelics’ (our highlight)."

**"**Psychedelic experiences can have short- and long-term adverse consequences. Short-term risks include the destabilizing effects that psychedelics can have through the experiences they can trigger, which can be difficult to handle both for the person and their therapist ⁵⁹ – experiences that can result to everything from increased acute agitation to prolonged emotional dysregulation. ⁶⁰ Many people also report adverse after-effects including recurrent hallucinations, increased anxiety, and physiological discomfort. ⁶¹ In the long term, such experiences can also cause ontological shocks, resulting in a dramatic shift in one’s religious and spiritual worldviews. ⁶² In a recent article, a patient who had participated in a psilocybin study described their state of confusion, anxiety, and distress, ⁶⁰ resulting in a long and desperate search including the use of spiritual practices, meditation techniques, and theology. This illustrates the dramatic effects that psychedelic therapy may have on some patients, and the need for careful spiritual, existential, religious, and theological support, ⁶³ long after psychedelic sessions. ^64"

^{These were the easy problems of that study. They follow up moderate and hard problems afterwards as well.}

https://pubmed.ncbi.nlm.nih.gov/36001741/

"A recent paper in Nature Medicine found that psilocybin therapy in patients with depression decreased brain network modularity (measured with task-free functional magnetic resonance imaging), an effect supposedly not found with the selective serotonin reuptake inhibitor S**-citalopram. This decrease in network modularity also correlated with depression. Here, we raise several issues with this paper, including inconsistencies in reports of the primary clinical outcome, statistical flaws including a one-tailed test, nonsignificant interaction, and regression to the mean, the ambiguity and overinterpretation of "resting state" data, and a missing reference for a conceptually similar study that exemplifies why a one-tailed test cannot be justified. Together, these issues make us question the uniqueness and impact of these findings, as well as the unwarranted media hype that they generated."

( https://pubmed.ncbi.nlm.nih.gov/35411074/ )

i'm dealing with what seems like a pretty mild case of hppd after doing shrooms for the first time a few days ago (light sensitivity, increased eye floaters/similar visual effect, very subtle pattern over parts of my vision even with closed eyes), and right now i am feeling pretty sad about the idea of having to go completely sober. obviously i am willing to do it if the alternative is staying like this forever, but what happens if i am able to make a full recovery? does it ever get to a point where i can enjoy weed/alcohol again? alternatively, if i'm able to come to terms with the symptoms i experience is it safe to use weed/alcohol in moderation or will that make the symptoms even worse? i think i could make peace with the symptoms i'm currently experiencing but i would not want them to get worse.

https://doctorsonly.co.il/wp-content/uploads/2015/01/13_Flashbacks-and-HPPD.pdf

"Hallucinogens encompass a group of naturally occurring and synthetic substances (1) which may trigger a transient and generally reversible state of intoxication characterized by perceptual disturbances primarily visual in nature, often referred to as “trips” (2, 3)."

"LSD is the prototype of synthetic hallucinogenic substances and it is probably the most investigated hallucinogen associated with the etiology of this condition. Other substances that have been associated with the development of this condition include: psilocybin (Magic Mushrooms or Shrooms) (4), mescaline (San Pedro and Peyote Hallucinogenic Cacti) (5), cannabis (6), 5-MeO-DiPT (Synthetic Hallucinogen) (7), Ecstasy (MDMA) (8), Phencyclidine (PCP) (9, 10), dextromethorphan (11) and ketamine (12). Datura, salvia divinorum, ayahuasca, ibogaine, synthetic cannabis and inhalants also appeared to be implicated (13). Recurrent visual disturbances attributed to this syndrome are geometric hallucinations, false perception of movement in the peripheral visual fields, flashes of colors, intensified colors, trails of images of moving objects, positive afterimages, halos around objects, macropsia and micropsia (9). A variety of distinct visual disturbances that are reminiscent of those generated by the previous use of substances have been widely reported and described by patients."

"The basic mechanism underlying this syndrome appears to affect vulnerable LSD users who develop chronic disinhibition of visual processors and consequent dysfunction in CNS function (3,15-17). This disinhibition might be associated with an LSD-generated intense current (18) that led to the destruction or dysfunction of cortical serotonergic inhibitory interneurons with GABA-nergic outputs mechanisms which are involved with sensory filtering process of unnecessary stimuli in certain brain areas (16, 18)."

"Investigations of HPPD patients with qEEG mapping indicate that the disorder is represented by disinhibition in the cerebral cortex (15). Thus, an unsuccessful defective sensory gating mechanism may be involved in the pathogenesis of this syndrome (19), facilitating the continuation of the central process of visual imagery after the image has been removed from the visual field (20)"

"HPPD is still poorly understood due to great variability of recurrent perceptual disturbances and different subtypes associated with various psychotropic substances, and may suggest that multiple mechanisms are involved in the etiology (22, 23)."

"It is a typically chronic, recurrent, trigger-precipitated or spontaneous, slowly reversible or irreversible and highly distressing visually pervasive experience (22-24). It is a radically different condition in which the re-experiencing of one or more perceptual symptoms may produce significant distress or impairment in individual, familial, social, occupational or other important areas of functioning. Users are certainly aware of these severe, intruding and disabling consequences of substance consumption and generally actively seek psychiatric help (22-24)"

"HPPD II appears to be an underreported, misdiagnosed or under-diagnosed disruptive side effect (22-24). Additional factors that may contribute to this lack of accurate reports and diagnoses may include patient guilt, relatively ineffective treatments and poor awareness of the disorder in the medical community. HPPD II may be more common and frequent than generally considered."

"Pharmacologically treated HPPD II, despite administered treatment, tends sometimes to be chronic in nature. Inexplicably, sometimes disturbing HPPD II may slowly transform into innocuous HPPD I (22-24). HPPD I and II appear to be part of an abundant large spectrum of nonpsychopathological and psychopathological experiences reported by users (23)."

Stable quantitative EEG difference in post-LSD visual disorder by split-half analysis: evidence for disinhibition

"In 1994 the lifetime prevalence rate of LSD use among high school seniors was 10.5%. Evidence suggests some subjects may suffer long-term consequences from LSD use. Prolonged visual disturbances in certain individuals following LSD have been described for nearly 40 years (Cooper, 1955; Hollister, 1962; Rosenthal, 1964; Robbins et al., 1967; Horowitz, 1969; Holsten, 1976)."

"Thus there appears to be a similarity between acute and chronic LSD- induced neurophysiologic change in humans much as there is between acute and chronic positive hallucinatory symptoms. While it is not es- tablished if the mechanisms behind acute and chronic LSD effects are identical, it appears that the subjective reports of LSD effects acutely, and after the fact (which share common features) have similar electrophysiological findings."

Brain changes not going back to normal.

"One possible explanation for the apparently permanent nature of HPPD in certain individuals is that LSD may be neurotoxic to inhibitory neurons, which then leads to chronic visual disinhibition."

Even though not all qualify for HPPD: Findings still suggest altercations through usage:

https://www.henryabrahammd.com/the

"Controlling for visual acuity and ambient light, I found that subjects with LSD related HPPD needed to get closest to see “white.” See below. Better were LSD users without visual disturbances. Performing the best were LSD abstinent subjects. HPPD, it appeared, was something more than simply the madness of crowds. (5)"

"And third, there was increased coherence of brain waves, a measure of connectivity between brain regions in LSD users, most commonly found in the occipital and temporal cortices. (7, 8)"

"A study of qEEG coherence in a 24-year-old HPPD patient. The nose is symbolized by a triangle at the top of the brain map. The white and red notations show abnormally increased connections in the occipital and temporal parts of the brain, which deal with visual perception.

Thus, qEEG showed that HPPD involves the cerebral cortex, especially the posterior regions of the brain, and that disinhibition appears to occur there."

"There is no known treatment which results in the total remission of HPPD. Symptoms can be vexatious to treat, and not uncommonly are permanent. "

https://pmc.ncbi.nlm.nih.gov/articles/PMC10615149/

"Individuals tend to experience mild symptoms that do not affect their normal functioning. Its prognosis is usually good compared to type II. In contrast, HPPD type II is irreversible and causes long-term, persistent hallucinations. These symptoms are chronic and distressful, and the duration of the recurrent hallucinations might extend for months to years, “waxing and waning” in severity. The prognosis is worse for type II [2, 3]."

https://pmc.ncbi.nlm.nih.gov/articles/PMC8385145/

"Moreover, EEG patterns in acute intoxication states—as well as in HPPD patients not under the influence of substances—show faster alpha frequencies and shorter visually-evoked response times, both indicative of cortical disinhibition and thus of neurophysiological changes in the central nervous system (CNS; Abraham and Duffy, 1996, 2001)."

"These changes may well be partly or fully due to serotonergic effects. With hallucinogens partially agonizing 5-HT2A receptors throughout the brain, chronic cortical disinhibition resulting from damage to inhibitory interneurons is believed to play an important role in the mediation of HPPD (Abraham and Aldridge, 1993)."

"Specifically, the 5HT2 hypothesis suggests the involvement of chronic cortical disinhibition and a dysfunctioning of visual tracts in the thalamus through the destruction of serotonergic inhibitory neurons (Martinotti et al., 2018). This hypothesis is mainly based on the working mechanisms of LSD and other hallucinogens, which achieve their effects through the activation of the 5-HT2A receptor."

"Time distortions, in turn, would seem to be mainly associated with dopaminergic dysfunction (Rammsayer, 2009; Jones and Jahanshahi, 2011; Blom et al., 2021)."

"Although these issues are all in need of further study, for now we consider it more likely that multiple receptor systems are involved in the pathophysiology of HPPD rather than the serotonergic system alone."

https://pmc.ncbi.nlm.nih.gov/articles/PMC5870365/#B38-brainsci-08-00047

"The main neurobiological hypothesis is that LSD consumers might develop chronic disinhibition of visual processors and dysfunction in the function of the central nervous system (CNS) [4,34,35,36]. This disinhibition may be linked to an LSD-generated intense current [37] that may determine the destruction or dysfunction [18] of cortical serotonergic inhibitory interneurons with gamma-Aminobutyric acid (GABAergic) outputs, implicated in sensory filtering mechanisms of unnecessary stimuli [34,35,36,38]."

"The main consideration that has to be done with respect to HPPD is its rare and unpredictable nature [16]: current prevalence estimates are unknown, but DSM-5 suggests 4.2% [88]."

Problems with side effects of drugs:
-Spiritual people, might see side effects as a benefit. Altering consciousness and perception as something desirable, not reporting it adequatly, it not being registered.
-Lack of self reflection, drugs dampen the ability to extract own behavior changes accurately, making it harder to self report

An online survey, probably again with a probe of people who anyways wanted to trip and who are interested in tripping showed this:

https://ouci.dntb.gov.ua/en/works/9jzMvLN9/

"In adolescents, visual symptoms related to “hallucinogen persisting perceptual disorder” (HPPD) were reported at a higher prevalence than in adults (73.5% vs. 34.2%, p < .001) but were reported as distressing by only one adolescent participant."

73,5 percent of younger people reported visual altercations afterwards.

What is missing for me, is studies done regarding, first time users and frequent users, to see if frequency has an impact.

There seems to be a discrepance in HPPD and clinical HPPD.

Adverse effects of psychedelics (unwanted, negative, distressing experiences), that occur during or after the acute psychedelic experience, are generally poorly defined in the field and may be underreported [9, 10].

"De Laportalière et al. conducted a systematic review of adverse events reported in clinical trials of esketamine (a form of ketamine) for depression [11]. They found that 41.5% of serious adverse events and 39% of non-serious adverse events went unreported in publications of study findings. McNamee et al. raised concerns about the lack of research on psychedelic harms and call for further research, including phenomenological studies on adverse outcomes, to address the issues around informed consent [12]."

Other adverse effects of psychedelics:

https://www.mendeley.com/catalogue/474f2c8f-d1e5-32c8-886a-e474a3a5032f/

"Results revealed that social disconnection (72%), anxiety and panic attacks (68%), and existential struggle (65%) were the most prevalent difficulties."

The psychology of downplaying bad trips and adverse emotionally challenging effects:

https://www.akjournals.com/view/journals/2054/5/2/article-p114.xml

"Both in interviews and in the survey, respondents reported a broader range of characteristics for challenging psychedelic experiences than what has previously been recognized in the research literature. Despite the often dramatic narratives, they were convinced that the experience had positive long-term consequences."

"I felt the presence of emotionless entities with a mechanical quality about them. They wanted to show me something. I'm still not sure what it was, but my interpretation was that they were trying to show me how our reality is “constructed”. There is another reality “behind” ours, and they began to show it to me by “deconstructing” my reality. What I saw shocked me. I was not prepared to see how things worked. My illusions about reality were shattered. And I was still fully “me”, so I didn't have the security blanket that ego-loss often provides. As I was witnessing these things, I thought “Having seen what I've seen, there's no way I'll ever be able to return without going completely insane.” I was convinced that I had gone too far, and that I wouldn't be going back. (ID01)"

The topics of bad trips describes usually resolve around:
Life issues, Social paranoia, troubling visions, mental and senory overload, ego death, time distortions

These all indicate a severe overstimulation of certain brain regions and psychatrists know of phenomena that these events, can alter perception in individuals long term. That users don't report them as "bad", doesn't change the fact, that there might be a followable pathology behind this process, in altered brain chemistry or destructive activity in certain brain areas.

LSD was originally used as a drug to create "experimental psychosis".

"I was shown a frightening entity and within its tentacles was my human self. Not only me but many others as well. It was unreal. It was as if it were feeding on our souls. I was enveloped within its tentacles as if it were absorbing me and the others in its grip."

"Generally speaking, LSD at relatively high doses produces a state of transient psychotic-like state, but in some vulnerable subjects can produce a psychosis." https://pmc.ncbi.nlm.nih.gov/articles/PMC5133947/

HPPD can come with first time consumption, as there is no guaranteed correlation between frequency of usage and onset of symptoms. Although worse symptoms are linked with frequent usage. Frequent use can worsen the condition, but also definetly triggers other adverse effects!

"The condition is more often diagnosed in individuals with a history of previous psychological issues or substance misuse [56], but it can arise in anyone, even after a single exposure (mostly to LSD, but it has also been reported after use of other psychedelics) [89]." [1]

Abnormal visual experiences in individuals with histories of hallucinogen use: a Web-based questionnaire

"Most (60.6%) of the remaining 2455 participants reported having experienced drug-free visual experiences that resembled hallucinogen effects. Probability of experiencing constant or near-constant symptoms was predicted by greater past exposure to specific hallucinogens, including lysergic acid diethylamide (LSD). Although symptoms were common, few (104, or 4.2% of the sample) found them distressing or impairing enough to consider seeking treatment. Visual changes in hallucinogen users may be more common than previously suspected and are worthy of further study."

https://pmc.ncbi.nlm.nih.gov/articles/PMC10597511/

"In Carbonaro’s study of psilocybin mushrooms’ adverse effects, 24% of the participants reported experiencing one or more symptoms (anxiety, paranoia, depression, fear), that lasted a week or longer after the psychedelic session, and which they attributed to the psilocybin experience [15]. 10% reported psychological symptom(s) lasting more than a year after the challenging psychedelic experience, with 7.6% seeking professional treatment for the symptom(s)."

"In Simonsson and colleagues’ analysis of challenging, difficult, or distressing experiences using classic psychedelics, 6.7% of participants reported thoughts or attempts of hurting themselves or others, 4.6% disclosed thoughts of hurting oneself; 2.6% reported thoughts of hurting others; 1.5% admitted to attempts to self-harm; and 2.6% sought medical, psychiatric, or psychological assistance in the days/weeks following their most distressing psychedelic experience [16]. In findings from the Global Ayahuasca survey, 12% reported lasting adverse effects for which they sought professional support [17]. In the 2020 Global Drug Survey of LSD and psilocybin, 22.5% of the total sample reported at least one negative outcome, with the most common being “mental confusion, memory problems, or racing thoughts”. 6% of the total sample reported difficulties lasting longer than one month. 0.9% of the total sample sought medical help following self-treatment with LSD or psilocybin [18]."

"Transient visual distortions experienced after taking a psychedelic substance have been reported by 40–60% of users [19, 20]. "

"Bremler et al. interviewed individuals experiencing long-term negative effects from psychedelic use and found that 80% reported experiencing a sense of similarity or connection to an unpleasant psychedelic experience [27]. Some referred to this re-experiencing as ‘flashbacks’ or ‘emotional flashbacks’ and some reported re-experiencing physical symptoms such as nausea they had experienced during the original psychedelic trip. Almost half of the interviewed participants (46.7%) described feelings of disconnection and isolation [27]. The same number of participants described derealization experiences, including feeling out-of-body and an altered sense of reality around them, sometimes described as ‘losing connection with reality’."

"However, McNamee et al. [12] point to evidence from trials using MDMA and psilocybin [22] showing increases of suicidal ideation and self-injury in over 7% of participants."

Regarding bad trips:

"Bremler and colleagues, based on their interview reports, highlight adverse contextual conditions and/or special psychological vulnerability (young age or psychiatric history) [27]."

"Our findings supports the results of Simonsson et al., who found that anxiety was the most common enduring difficulty, based on quantitative questionnaire data [16] and Bouso et al’s study of the Global Ayahuasca Survey, in which ‘feeling nervous, anxious or on edge’ was the second most common adverse mental health effect [17]. Our findings also suggest that a Sense of disconnection from others was within the top five most prevalent themes, as did the studies by Simonsson et al. [16] and Bouso et al. [17]. Some extended adverse effects that were quite common in other studies weren’t so common in our data set–for example, feeling a harmful connection to the spirit world was reported by 14% of respondents to the Global Ayahuasca Survey but by less than 4% of our data set, which may suggest some forms of difficulty are particularly associated with certain psychedelic substances and/or their associated cultures [17]."

" 8% of our respondents experienced extended difficulties after taking part in a clinical trial or psychedelic therapy session. Thus, our data suggests that taking psychedelics in a clinical setting is not risk-free [45]."

"In the current study, 40% of the sample stated that they thought a childhood trauma was implicated in experiencing the post-psychedelic difficulties. This has similar theoretical connotations to the Simonsson et al. finding that a major life event prior to the experience was predictive of degree of enduring difficulty, in terms of antecedent life events being formative to psychedelic outcomes [16]. Previous research has identified a strong link between childhood trauma and developing dissociative symptoms following classic psychedelic use [46] as well as increased vulnerability to the development of psychiatric disorders [47]."

"As previous work has cautioned, re-triggering trauma with psychedelics can augment maladaptive processes and associated defense mechanisms, especially in individuals with increased vulnerability due to childhood trauma [47]."

"Also, 67% participants in the Johnstad (2021) study reported long-term consequences of their worst psychedelic experience to be positive, while only 4% reported negative consequences [13]. Bouso et al. found that 55% of respondents to the Global Ayahuasca Survey reported adverse mental health effects, but 88% thought such effects were ‘part of a positive process of growth or integration’ [17]."

Just like with HPPD, bad things are talked as good. Why is this?
1. Justifying further drug usage
2. Effect of the drug is admired anyways, emotional numbness decreases good and bad, bad is not so bad anymore
3. Social aspect of the pro drug cult, drugs as the ritual, makes them blend out negativity for the social safety

"Providing some support for these previous findings, in the current study, 55% continue to take psychedelics to the present day, and 90% agreed that psychedelics can be helpful and are worth the risks if taken in supportive settings. Nonetheless, almost half no longer take psychedelic drugs, and in some instances, respondents reported feeling significantly harmed by their psychedelic experience and expressed regret over ever trying these substances."

Some people here as well, still support drugs, even though they literally state, that they are scared to try certain psychedelics. They would still suggest them to others? How does that make sense? They want others to become a part of the drug cult, because it is their social circle and the growth of said social circle benefits themselves. The drug exposure is not needed anymore, the individual is permanently tripping basically. Some people with HPPD, apparently never stopped doing drugs, seen like that, and apparently, they also don't want to stop it. They don't really want recovery. When conversing here, drugs are almost treated like a religious entitiy you are not allowed to harm or talk harshly to. It is almost like certain individuals fear, that with such harsh talk, their "religion" is weakening and they don't want people to turn away from pro-drug thought, which at that point, somehow already become religious doctrine, hence I call parts of this sub cult! I think the main culprit is not even the drug, or HPPD, but the delusional thinking, that acts like a bonding between people. When being aggressive towards anything regarding contra drug, they don't fear or care about drugs or HPPD, they care about the social construct around it being destroyed. I think like this, you just become ignorant to life's problems. HPPD is a non-factor in facing life. Like no hallucinogenics, or no or less caffeine or alcohol would make a life worth living or not. It is all in the head basically. But realistically speaking and how I was introduced into it by professionals, it is a pre state to psychosis, just like hallucinogenics are known to induce psychotic like states, that then can persist in a lower intensity.

https://pmc.ncbi.nlm.nih.gov/articles/PMC5701998/

"However, limited publications suggested that chronic visual disturbances may be relatively common among hallucinogens’ users. It has often been assumed that HPPD may be a severe clinical manifestation of the drug-induced visual changes (3–5). While the probability of flashbacks occurring in the wake of hallucinogen use may vary from 5 to 50% among hallucinogens’ users (6, 7), the probability of an HPPD being manifested is lower (3)."

Reagrding pro-usage of psychedelics:

https://pubmed.ncbi.nlm.nih.gov/37766730/

"Research in the last decade has expressed considerable optimism about the clinical potential of psychedelics for the treatment of mental disorders. This optimism is reflected in an increase in research papers, investments by pharmaceutical companies, patents, media coverage, as well as political and legislative changes. However, psychedelic science is facing serious challenges that threaten the validity of core findings and raise doubt regarding clinical efficacy and safety. In this paper, we introduce the 10 most pressing challenges, grouped into easy, moderate, and hard problems. We show how these problems threaten internal validity (treatment effects are due to factors unrelated to the treatment), external validity (lack of generalizability), construct validity (unclear working mechanism), or statistical conclusion validity (conclusions do not follow from the data and methods). These problems tend to co-occur in psychedelic studies, limiting conclusions that can be drawn about the safety and efficacy of psychedelic therapy."

"NIH recently developed guidelines for funding psychedelic research, concluding that studies that lack ‘basic quality controls and methodological rigor’ should be considered as ‘low priority’. ¹³¹ In our reading, this renders nearly all work in this field as ‘low priority’."

"Given the current state of research, strong caution is warranted regarding the hype around psychedelics as treatments: there is not enough robust evidence to draw any firm conclusions about the safety and efficacy of psychedelic therapy. "

"To be hopeful and optimistic about psychedelic drugs and their potential is one thing; to be messianic is another. Both the present and the future of psychedelic research already have been grievously injured by a messianism that is as unwarranted as it has proved undesirable. ^132"

"In psychedelic studies, internal validity is commonly threatened by the lack of control groups, the breaking blind problem, and placebo effects. The main sources of threats to external validity are low-powered studies and a strong selection bias in the inclusion of participants. Threats to construct validity include measurement problems as well as the lack of long-term treatment effects and mechanisms of action. Statistical conclusion validity is threatened by the multiple comparisons problem, conflicts of interest (COIs), outcome switching, and other questionable research practices. Of note, these validity threats are well-understood, ²¹ and it is therefore surprising that psychedelic science appears to ignore many of the lessons learned from decades of research. Much of the recent work is history repeating itself."

https://pmc.ncbi.nlm.nih.gov/articles/PMC9548934/

^"AEs are poorly defined in the context of psychedelic treatments and are probably underreported in the literature due to study design (lack of systematic assessment of AEs) and sample selection. "

Looking for a general consensus on if being sick makes your HPPD worse. Much harder to focus and things are constantly waving, the last time I did psychedelics was 5 months ago and the HPPD eases up months ago.

You tell others to take psychedelics, you are frequently tirpping on shrooms.

You say HPPD is "If it is hppd, it's very chill. You could freak out and stop everyting forever, but it would probably make more sense to take it slow with them to see if your symptoms worsen at all."

How great you yourself perceive HPPD:
"I feel you on feeling like your old self is dead and gone :( wouldn’t wish it on anyone"
You speak of sleep deprivation and this "I’ve had heart palpitations, head pressure and fatigue all constantly since getting HPPD."

Your own addiction to drugs, on the basis you are confronting me without any arguments, how you expose yourself here:
"They just amplify the visual snow that I already have and make everything shift with the snow subtly. Makes the head pressure worse but gives me some energy which is usually nice because a main symptom is fatigue. I can pretty much only feel the body high anymore. Even some of the cool auditory stuff seems to be gone as well. I like shrooms for dancing and have had some pretty deep spiritual experiences since hppd, but it’s like 1/100th the experience it used to be. If I take too much my body starts to overheat as well which can be pretty scary. I just can’t imagine my life without feeling that beautiful oneness every once in a while, even if it’s just a little bit. I’m in a pretty long sober period but it’s hard once festival season creeps around."
"I take shrooms occasionally. Feels weird. I barely get visuals, just kind of amplifies the weird slow movement that I already get from hppd. Makes the head pressure a little worse too. "

So you advise for drugs, as being such a beautiful and mind opening experience, but yourself having bad symptoms off it, saying that it doesn't make anything better, as well as you have adverse reactions to cannabis and you are also to scared to take LSD. Yet, you advise others to take LSD? "Haven’t been brave enough to try acid. Weed is not worth it, gives me hot flashes now ? Wtf."

What is this? What is wrong with you? Are these people here your test subjects? When people ask if they shall trip, you tell them to do it, because it is so beautiful, but yourself is to scared to try it? You want others to try it? Huh? So if you advise others to trip, you only talk about shrooms? Because other things you are to scared to try?

"I live a somewhat normal life. Actually a much more incredible and beautiful life than most people without hppd. I have a lot to be grateful for. But the parts of myself that are gone and altered are an incredible weight on my being and will always cause me infinite grief and rage. I think some things happen for no good reason. Maybe from a higher perspective. But in this reality bad stuff just happens and we have to learn to deal with it. I’m tired of being resilient. I do not wish this for anyone."

Yet, you tell people to trip, bringing them at risk.

Your symptoms include:

"Bounding Pulse

Head Pressure (dominantly on right side)

Pulsatile and Normal Tinnitus

Fatigue

Hypnagogic Hallucinations

Visual Snow + BFEP (flickering points of red, blue, etc) (sky vortex) (tunnel vision) (double vision) (visible pulse) (asymetrical dilation in line with right side pressure)

and more!"

You further describe it as:

"Well I have one of the worst cases I’ve heard of. Dxm overdose. Visual snow, the blue field phenomenon you talk about, double vision sometimes, extreme head pressure, fatigue, bounding pulse, dpdr"

You stated to me: "I’m not suppressed. Perfectly capable of feeling my emotions over here. "

Based on your previous descriptions, trips do not do anything better for you at all and even have adverse effects, as well as an hallucinogenic got you "the worst condition" you could imagine. This LSD, shrooms etc. also had for other ones:

"The risks are incredibly low. We represent like 0.001 of the population that trips. The experiences are amazing and life changing. I would always reccomend safe doses to people even though I have HPPD"

These things you still spread? Why? No, the likelyhood is not 0,001, if you would look at questionnaires, even from "pro-psychedelic" industries, then you would see, that visual disturbances occur in a lot of short time and long time users, up to 40 percent report these chronic visual disturbances. Academics and authors even suggest, that visual disturbances are fairly common with drug usage, but only a handful manifest in a way of a clinical syndrome, called HPPD. We are considered the 4-4,5 percent of the worst cases. ~4,2 percent, NOT, 0,001. This is so incredibly harmful shit you are spreading in the internet... But, importantly, perceptional issues, are oftenly claimed, but not seen as "disturbing" enough. But that is highly subjective, since tripping does in fact lower prefontal cortex and amygdala activity, so one has to see, that this will decrease the subjective threat recognition and one will easierly downplay such conditions. The important thing is, that visual disturbances happen, and also quite a lot, and even more often they can be chronic, than was thought. But consumers won't report it as HPPD, but will remain silent, accept it etc.

"I’m not suppressed. Perfectly capable of feeling my emotions over here. I’m sorry you feel so strongly that you know me and feel so many judgements. I’m okay with that. I hope you find peace"

Well, you say that, but then you say: "I've found I can still be in romantic relationships and love my family even though I simultaneously feel disconnected and dissociated from life itself."

You know what this is a sign for? Dissociating, is exactly a severe symptom of amygdala dampening my friend... And even though the motivation of empathy is there, it doesn't say something about the quality. And since dissociating (look it up) makes self reflection worse, you are not neccesarily aware of subjective shift bias in your emotions!

Regarding recovery of type 2, that you have now since 3 years with other adding psychatric symptoms, you say:

"But let’s be real, 9.9/10 any improvement is because someone has HPPD type 1 as another commenter here said."

So, even though yourself doesn't believe in a recovery at all, you still act like, type 2 would just recover, even though also the literature suggest otherwise. Filtered HPPD through type 2, the prognosis becomes bad.

"I am not one of the lucky ones dude my symptoms are 20x worse than most people here"

"no one here is going to advise you to take a research chemical or classic psychedelic soon or anytime in the future, since you do indeed have hppd."

Well, you do! 🤣

"I also feel like I’ve failed my self and my friends and the world and my life is ruined, but you just gotta go day by day."

Wow, what a ground to be pro-psychedelic today!

"3 years ago, a chapter of deep psychedelic exploration ended when I accidentally mixed the wrong supplements and gave myself serotonin syndrome, which gave way to hppd and dysautonomia symptoms."

"I have tried against the warnings of the hppd community to take shrooms many times since, with no apparent permanent worsening. But they definitely increase my head pressure and destabilize temperature regulation sometimes to a very scary extent. I also don’t get visuals from them anymore…"

Go for trips, boys!

So deer friends, look at who is advising you to take drugs:

"It’s probably not the best idea to take Ayahuasca, but I am also at my wits end. My symptoms have caused me to give up on so many dreams and I still grieve so much the person I used to be and the states I used to be able to access, to the extent that I am willing to take any risk to heal myself. It has been a crazy healing journey, I have spent most of my money and made little progress, but that’s a story for another post."

Wow, you should definetly listen to him when talking about how great drugs are and how mind opening, and this person is also definetly not deluded! 🤡❤️ He is so comfortable with the side effects, that he is even scared to trip, but you, he will suggest it to you!

"I am truly 50/50 with this decision. And I know many say wait for a calling or a clear yes, but in my current state there will never be a clear yes, I will always be deeply terrified of how prolonged dmt exposure could exacerbate my symptoms, I feel it could potentially even be life threatening, but I have survived many mushroom experiences and kambo experiences since."

"If your only symptom is visual snow that’s a very good sign. The reality is everybody is different. Tripping again is the only way to find out if it’s just going to be snow or if it will get much… much worse."

Tripping is the only way to find out boys, and then again, and then try again! The message is clear, it will never get worse, if you don't trip again! How deeply moving these words are! Also, it is remarkable how the side effects of shrooms he mentioned earlier, are not mentioned in this post, where he also then proceeds to talk about taking shrooms, and them not making a difference. "I’ve taken shrooms many times since hppd after taking a long enough period of sobriety I was fully certain there would be no improvement, and it hasn’t made anything worse, though tripping is wildly different, like 10% the experience it used to be."

What we learn from this, never listen to a tripper, who you have no carefully examinated! "If it is HPPD it is very chill", to, "I hate everything and my life". HPPD seems to be both for him! He will decide which version he tells on the basis of his argumentation.

It is a common side effect of emotional dampening, that these people downplay side effects, but when you read through what they actually say, then it becomes very clear. That is the case especially with psychedelic users.

This sub is no place for advising drugs and if you want to make it such, you will get problems with me. Thank you!

"You are a loser. Can’t believe I am entertaining you. [Always nice, to see the psychedelic empathy playing out! 🤣 It is always gone the moment you critizise them... almost a little hypocritical? Hm?]

“The frequency of HPPD among psychedelic users overall would thus be estimated at < 1%, which is at least four times lower than the estimate provided by the DSM-V.”

“ This refers to clinically significant/distressing HPPD (the impairing form that meets diagnostic criteria, generally corresponding to Type 2), not mild/transient symptoms. The study found ~32% reported some visual effects, but only <1% overall found them distressing “

From conexiant dot com

So actually yes there was a study done where It was BELOW one percent LOL"

https://academic.oup.com/pnasnexus/article/4/4/pgae560/8111338?login=false

So the guy here, typed in Ai, got a wrong source, acted like it was true, which it wasn't, then linked another article, where 1/3 have HPPD like symptoms after psychedelic usage. The study says, that only <1 percent have trouble with it, and acts like that would mean, that only <1 percent have HPPD. This is an incredible showcase of low EQ and context understanding. No, just because someone finds it disturbing or not, doesn't matter in the diagnosis of HPPD. It is imo no HPPD diagnosis criteria, if you find it disturbing or not. It is about the symptoms and the perceptional damage caused. Subjective questionnaires of wether someone finds it disturbing is heavily biased due to the subjective shift bias and the emotional dampening effects of the drugs in empathy and self reflection (seeing lower frequency in amygdala and prefontal cortex). One has to remember, that there is literally a sub called HPPD positivity, where people with HPPD talk about how great it is, neither is that the norm, nor don't these people have HPPD, just because they act like liking it. The brain telling you to like it, is just a justification to further take the drug and run from problems.

No wonder that this study is financed by private donors of university clubs.

The donators of the pro-psychedelic studies, are certain donors, with potential interest conflicts due to business connections. Some studies supported by them:

Enhanced meaning in life following psychedelic use

"In consideration of the possibility that psychedelic substance-assisted treatments may soon be integrated into mental health practice, alongside an ongoing rise in psychedelic use in the general population (21–24), it becomes increasingly pertinent to explore the potential for any long-term, adverse effects of psychedelic use."

This is the cheap style, they try to downplay side effects. By subjective questionnaires!

No, just because of 1/3 who reported visual disturbances, only <1 percent found it disturbing, doesn't say anything about HPPD being diagnosed or not. In any case, these numbers suggest the likelyhood of a way higher number. 4 to 4,5 percent, how the literature based on all the available ressources suggest, seems therefore more likely. If anything, this study supports that. Anyone having HPPD type 2 knows, that it comes with severe extra stress and sensitivity and it is not easy.

But if finding HPPD distressing is for some academics a criteria, then let's see what the study here linked itself says about that:

"In comparison, cross-sectional survey studies of naturalistic psychedelic users have found incidences of visual abnormalities lingering post-psychedelic use ranging from 11% (2) to as high as 60%, although far fewer (4%) experienced these symptoms as distressing, a necessary criterion for diagnosing HPPD (56)."

The number 2 study linked states this:

"LSD produced robust psychological effects; including heightened mood but also high scores on the PSI, an index of psychosis-like symptoms."

Hightened mood is very subjective, as well increased trait openness and optimism are subjective symptoms and how I explained in an earlier post, don't deny any of the side effects happening.

This then again plays along with the current findings of quantified studies. This study differs in weak methodology though:

"Data were collected through a specially designed prospective online survey recruiting individuals who were planning to take a psychedelic through their own initiative. Measures were recorded at multiple time points before and after the psychedelic experience."

So, they recruit people, who anyways want to trip. How many of those will then report that they are subjectively disturbed by it? These people are active trippers. They are addicted to it.

This study was also partly done, to confront the beliefs, that psychedelics induce delusional thinking, which if you think about amygdala dampening effects, the amygdala being responsible for reflectivity and emotional context, the same as with the dampening of the prefontal cortex, it is not hard to believe that it would induce delusional thinking, especially given the fact, that something like LSD is believed to induce acute psychosis like states, or resembles similar pathways and domains. The authors state themselves:

"Early work with psychedelics recognized their ability to produce transient psychological effects mimicking some important domains of psychosis (38–40), including perceptual changes, bizarre ideation, thought-disorder, and sometimes paranoid or delusional thinking (41)."

Given that the study authors seem to have an interest in the future market of psychedelics, they now need to downplay that, for errants like here to cheaply quote, because doctor xy now said so! 🤣

"Just over a third of the cohort were “novice” users (five or fewer psychedelic experiences, ⁠, 38.2%) with the remaining two-thirds “experienced” (six or more past experiences, ⁠, 61.8%). Nearly, a third reported having ever been diagnosed with at least one psychiatric condition (33.0%). Just over half the cohort reported taking LSD/1P-LSD (⁠⁠, 54.0%) during the acute experience, followed by Psilocybin/magic mushrooms/truffles (⁠⁠, 40.8%) (Table 2). Only a minority of the cohort had an acute experience in a retreat setting (⁠⁠, 17.7%) (Table 2)."

Findings like this suggest (https://www.scienceopen.com/document_file/70b465bd-3d7f-42ea-a9f0-81118fc4aee2/PubMedCentral/70b465bd-3d7f-42ea-a9f0-81118fc4aee2.pdf#3#3) that symptoms like Flashbacks occur in 9,2 percent of cases after one time use in healthy participants, but unlikely HPPD type 2. This is only aggravated with dosage and reoccuring consumption. But without prior mental health problems diagnosed, the likelyhood of type 2 seems to fade.

While in the study here, there are trippers used, 60 percent frequent trippers, there is a high prevalance of visual disturbances (1/3 occurence of visual disturbances and unknown how many of these fit type 2 criteria). This is also due to the high prevalance of drug users having genetic prevalances to mental health problems, or general mental health problems or other psychosocial factors. This seems to directly be an amplifier for more severe symptoms.

This study proves, that frequent trippers or people who intend to trip by themselves and already did (who are also shown to be likelier prone to psychological problems) have more visual disturbances up to 30 percent, but are also likelier to talk down the severity of their condition and act like they are fine with it in subjective questionnaire.

This plays along with my personal findings, of psychedelic people advocating for their drug, but leaving out their bad trips and only after some time revealing (acting like they wouldn't have left that out on purpose ;)) that they frequently have them and that that would be a "learning experience" one would have to go through. This for me is a sign for emotional dampening, as the effect is talked down. In what world are visual disturbances not bad? The antidepressive effect of the drug is so admired, that the side effects are talked down.

That more than 1 percent, even if they say they are not bothered, have HPPD in that sample, is for me clear and I think the numbers of 4 to 4,5 percent, that are officially used and were concluded out of all the quantified data are close to reality.

I think, that people who trip and have visual disturbances, should be only asked after 2 months of drug abstinence, if they are fine with it, to get a more sober and emotionally more normal mind, to give the appropriate answer.

I remember that even the bald head youtube guy who takes drugs all the time, many here will know who I talk about, reports visual altercations in his daily life. These people have these visual altercations, but don't mention them. He never talkes about this in his videos? Isn't that kinda crazy? He has perceptional changes after the drugs, that are seemingly always there, but he doesn't mention it all the time to warn others?

This is exactly what I mean and why people like me who got HPPD don't get a chance. People have symptoms, side effects whatever, but they don't talk about it, because they subjectively have no problem with it.

It is like, yeah I have a bullet in my knee, but I don't care. So also point that pistol to your knee and see what happens. I don't mind it, so you surely also won't. That is not empathic at all. It is disgusting and sickening!

Where are we in a world, where people claim that perceptional damage wouldn't bother them and on that basis downplay drug usage? And why are people who are to scared to take drugs again because of this, are still supportive of exactly these individuals, because they have a social connection to them? They profit from them talking the condition down, so they can also downplay it themselves. I think it should be warned properly. Someone suffering depression won't fucking care about you not caring about your own symptoms. He will care a lot about his symptoms LOL. Sad, that one even has to point it out... 🤣

To important questions like this (also the delusional ideation), there should be more than subjective online questionnaires of frequent trippers, who all want to trip again... lol

"Slightly less than a quarter (23.8%) of participants showed increased delusional ideation at the 4-week endpoint, with a mean change of 1.8 points. A logistic regression model to investigate persistent increases in delusional ideation at 4 weeks did not find any significant predictors (SI appendix Table S1). However, the odds for reporting increased magical ideation, which occurred in 28.1% of participants was found to increase by 6.0% (95% CI [0.98, 1.03], ⁠) for a one-unit increment in baseline personality trait absorption (Table 3)."

"While the DSM-V proposes a prevalence of HPPD in 4–4.5% of psychedelic drug users (American Psychiatric Association, 2013), a questionnaire-based study on the website erowid.org found that as many as 61.7% of respondents reported having had unusual visual experiences lingering on at least one occasion after psychedelic drug use (73). In another previous online survey, which specifically assessed visual effects in response to psychedelics, 40% endorsed persistent changes in visual perception (72), closer to the present findings of 32%."

"The point to emphasize strongly, is that for most users, HPPD-related aftereffects are not considered distressing."

Your downplaying of your symptoms, is actively altering the percentage of how many people are believed to get HPPD. Although a high percentage of people get visual and perceptional damage from drugs, they don't regard it as bad, and then just claim, it is not HPPD. Then some authors, who are funded by business men in the psychedelic industry, have easy play claiming the HPPD occurence to be under <1 percent, and quickly, also the official quantitative studies are overwritten by industrialized marketing geniuses. If people then get these long lasting symptoms, it is just said, "don't take it serious, then it is not HPPD". 🤣😀

Tomorrow they will say, if you don't take cancer serious, you are healed. Thanks guys! My vision is repaired, well it isn't, but thanks guys!

The problem is clear, since people have an interest in the antidepressive and dampening effect of the drug, they will blend out the side effect. The subjective finding wether it disturbs then or not, is not adequate reflection of the severity of the syndrome/symptoms. Thus it could be a very bad case, but not registered as HPPD. Is this scientifically appropriate? Is this fair for potential victims in the future, to downplay numbers and side effects?

Imo no. Every case fewer is better. Whoever is of different opinion, is in my view, already a psychopath lol 🤣

This whole reminds me of thos errants who slur around, that cannabis induced psychosis would only happen in 1 percent of cases and then genetically. Which is false. Schizophrenia first of all, is in 80 percent of cases genetically unrelated. Then, regarding different studies and different factors, the chance can go up to 20 percent. This will give a 16 year old a greater doubt in mind, before potentially destroying his minds. Of course consumers don't want that, as it damages their reputition. Not to speak of the overall side effects, similarly amygdala dampening as well as other effects well studied by e.g. the Capris Study.

"Some participants did not complete all surveys, so there might be an inherent selection bias in the reported results. We did not collect any information about why participants decided to drop out and if it had anything to do with the experience or not. It would be an interesting question to investigate if there is a pattern identifiable in baseline information of those participants who did not complete all surveys. This is something we intend to look at in the future."

Yeah, we give you some extra to not report bad result. No, but what is this?

"Further, details about the dose that was used for the psychedelic experience were given after the experience took place. It might therefore be possible, if not likely, that participants' estimate of the dose they had taken was influenced by the intensity of the experienced drug effects, rather than on the actual dose that was administered. This is a common limitation of retrospective data collection. Beyond truly controlled research, in which precision about drug purity and dose can be ensured, one way we might consider overcoming this matter in web-based designs might be to ask for an expected dose a priori, or verification of dose by a sitter, guide or “shaman,” but such measures would likely entail practical challenges and are thus not entirely satisfactory or realistic solutions."

No placebo control.

"It should also be acknowledged that the validity and concreteness of the concept of “well-being” has been debated in psychology. "

Subjective shift bias.

https://pmc.ncbi.nlm.nih.gov/articles/PMC6225734/

"This study was advertised via online postings, including on social media and drug-related websites. Whilst this helped to enhance the study population size, it may have introduced sample biases."

"We have already determined that the sample demonstrates higher than average levels of magical ideation at baseline."

"The self-selecting and self-reporting nature of the sample and study may have caused an under-estimation of iatrogenic responses to psychedelics (e.g. as discussed by Bremler et al. (49)). "

---

"Overall, prevalence of HPPD has been generally considered low (2). However, limited publications suggested that chronic visual disturbances may be relatively common among hallucinogens’ users. It has often been assumed that HPPD may be a severe clinical manifestation of the drug-induced visual changes (3–5). While the probability of flashbacks occurring in the wake of hallucinogen use may vary from 5 to 50% among hallucinogens’ users (6, 7), the probability of an HPPD being manifested is lower (3)."

https://pmc.ncbi.nlm.nih.gov/articles/PMC5701998/

I think a great reason for HPPD not being studied in any way, is the individuals great effort, to downplay it and to attack (for example me) anyone that speaks bad of drugs or makes a harsh statement of the condition.

It seems to be that A: One profits from HPPD being seen as not so severe.

And B: Some people still addict to the drugs and/or to the social cult around it.

If HPPD is actively seen as so rare, and any visual disturbance is talked off as not as bad, the people who really have this condition, are not seen. Because no, visual disturbances are not nice. And B: many have already pre existing disorders, and for them, the drugs further destroyed a lot to the point of no return.

Just like with Cannabis, the side effect rate is actively downplayed by it's users, without any respect to the victims of them. It is almost seen like a natural selection. If you get a psychosis from it, then you are just weak, while for me it works kind of.

Seeing how one is treated when speaking about this condition in a logical and study underlying way and criticizing the behavior of others, shows, who are the real culprits in the underpresentation of this condition. 🤣

I recently wrote something under a post of someone wanting to try LSD and mentioning that HPPD can occur as a side effect. This was the easiest 20 downvotes farm of my life and the leading into the comment cited above. Yep. Psychedelic openness. Love to see it! 🤣

If you don't have arguments, you attack the person behind it.

I developed mild hppd after my last acid trip. First 2 weeks were agonising (and consequently the worst symptoms I had). I have been recovering quite well since then (visual snow is down and floaters are…just floaters). The only thing I dont like is that my verbal recall has been somewhat affected (might be due to heavy weed use but have since quit). My baseline anxiety has also increased somewhat but I try to control it using techniques my shrink taught me. I became interested in Selank and Semax sprays. Have heard anecdotal reports on various forums stating that either it was a positive experience from them or no effect (hppd.net forum). Just wanted to know if anyone had any experience with their use? Im not gonna use any prescription drugs besides propanolol or atenolol. Caffiene and nicotine dont increase my visuals

Stop all hallucinogenics

Ask your doctor to rather be low dosed, when being put on medications, refer to HPPD. Especially since SSRI can sometimes also visually make some problems, but they resolve likely.

Go outside

Challenge problems. You should remain a bit cautious due to your oversensitivity, but that can be challenged through becoming more active. Step by step.

the best way i can describe it is that i feel like my eyes are adjusting from looking at a bright light. other than that all i can say is that my vision just feels *different*. i got a lot more paranoid about it when i smoked weed earlier today but i don't know if it necessarily got worse. is it possible that this is something other than hppd? if this is hppd, do i have any hope of fully recovering eventually? can the effects get worse than this over time? lastly, do i have to stop all substances forever? (weed, alcohol, nicotine, caffeine, etc.)

I'm just wondering how it was like for people back years ago before we had access to medicine that helps me before hppd was somewhat known to the medical world, if anyone in this group was around back then and knows tell us about It, what did you do to live what did you go through with doctors, what made it better

Thanks!

Doses are per day. I may need to take Benadryl for a medical condition and wanted to hear people’s experiences.

A user here used Ai again, for his Ai psychosis (a known term, coming from Ai's inability for emotional context and logic, Ai is no credible evidence people), a good example on how bad Ai is to interprete correctly: "The amygdala is responsible for processing the data of an emotion (the accuracy), but it is notthe source of the human to care about others (the motivation). Therefore, amygdala damage does not automatically create a callous, unfeeling psychopathic personality"

This only approves what I am saying below: The amygdala is processing the quality of an emotion, you have motivation to feel empathy AND you actually also feel it. So you actually have a more profound and caring behavior, actually being able to feel with people etc. Therefore, amygdala damage does in fact, decrease empathy, but not motivation. Idk how Ai can be so dumb, but don't use it, it may approves your delusion, but it is not smart, if you don't know how to prompt and just ask randomly questions... especially since you also damage environment and humans with it. Water shortages etc.

"1. The Amygdala is not a monolith
The amygdala has multiple sub-nuclei. Severe overstimulation does not make the whole thing fire uniformly; it causes a pathological shift.

• The central nucleus (which drives anxiety and vigilance) gets locked into high gear.
• However, the basolateral complex (which processes the nuance of emotions, social cues, and contextual safety) gets overwhelmed and shuts down."

"3. The Shift from "Active Coping" to "Passive Numbing"
Chronic overstimulation forces the amygdala into a state of learned helplessness. To protect itself from frying the system, the brain actively downregulates the amygdala's receptive fields to social and emotional cues. It turns down the volume on everything except raw threat detection."

So here the criticism of such Ai views:

"Damage to the amygdala has been linked to impairments in empathy, typically documented as deficits in accurately identifying others' emotional experiences, especially fear. This has led some to theorize that amygdala dysfunction is a core feature of psychopathy. There is growing evidence, however, that motivation to empathize is distinct from empathic accuracy. Moreover, anecdotal observations in patients with amygdala lesions have noted their tendencies to approach, rather than avoid, empathic encounters with strangers, even when the patients have impairments in empathic accuracy. We conducted a novel investigation specifically examining empathy motivation in patients with amygdala damage. We used a free-choice paradigm to assess motivation to empathize. We found that damage to the amygdala was not associated with avoidance of affective or cognitive forms of empathy motivation. Patients with amygdala lesions (n = 21) exhibited similar levels of empathy motivation compared with patients with damage outside the amygdala (n = 22) and healthy individuals with no brain damage (n = 24). These findings suggest that amygdala damage does not necessarily disrupt the motivation to empathize. A potential implication of the findings is that amygdala damage or dysfunction may not be associated with traits such as callousness, apathy or lack of caring that are often linked to psychopathy." https://pubmed.ncbi.nlm.nih.gov/41822985/

"This apparent contradiction in this research highlights a critical gap in the study of empathy—much of the extant literature conflates motivation to empathize with ability to empathize."

There have been findings of cognitve empathy being impaired in e.g. LSD, but also some findings that didn't find anything. I think that this can be, due to the intellect and the emotional intellect. You can intellectually understand, what emotion someone is feeling, it is like a math game. Someone like Sheldon Cooper won't fail the MET test.

I think that there are methodical gaps in the industry. Psychedelics seem to be a million market and rising. It is not properly differentiated, if someone truly has a higher empathy in his daily actions. Tests revolve around questionnaires and subjective findings, not respecting or clearing out the response shift bias. Objective findings find lower amygdala activity. The amygdala always revolves around all emotions, not only around negative and neutral, how it is proclaimed.

If someone reacts worse to even alone negtative stimuli, for example being shown a picture of wars, how can that be counted as empathy? If the person just cares less? This is what is also reported by people around psychedelic users, or even by some psychedelic users themselves. It seems only the studies have not yet understood that. But the view in the generally public regarding hippies is clear. I talked enough here about the amygdala dampening effect and how the people become uncaring, without realizing it themselves. For me these are early signs of psychosis, but just not the severity of it, but similar pathways involved. They become resistent to logic.

In mindfulness and meditation studies, which is sometimes named in comparison to effects of psychedelics, fMRT tests have been concluded and found, that amygdala functioning and response when shown to emotionaly stimuli was dampened. There were even reports of possibly fully dampened states, with no emotional quality whatsoever. This is what I expect to be ego death. A fully overstimulated amygdala and loss of emotions!

There also have been tests made regarding the behavior around emotional situations, for example when people were shown a animal cruelty film, they responded less to it.

https://www.researchgate.net/publication/330224967_Potential_negative_consequences_of_mindfulness_in_the_moral_domain

I think there are to few qualitative studies done towards the actual playing out of empathy regarding psychedelics/hallucinogenics and I think that impairments of the amygdala like shown in LSD, are definetly a sign of overall emotional dampening and the loss emotional depth.

The confusion may also arise, from the simple fact, that people who are for example psychopathic, are often times described very helpful and "caring" individuals. They are very aware of themselves needing to be very proactive and supportive, they don't want to be disliked. They often times even donate a lot etc. The attachment to being liked by everyone, comes from the inital insecurity of not knowing what anyone thinks. Seeing how many philantropists are named in the Epstein files. Isn't that a confirmation in itself, that these things may have to be regarded in a more critical manner? When it comes to empathy...

I very well think so! People who think of being more empathic, actually can be less empathic. They loose the value of what empathy is and start calling empathy, what is actually not empathy.

Not to speak of, that some studies are done by authors with dubios connections and possible conflict of interest. Some studies fail methological issues: „We did not assess the expectancy and the success of the blinding during the study"

*"*Although the results of this study are promising, several limitations should be noted. First, the current data represent secondary outcomes of the trial, which necessitates cautious interpretation due to its exploratory nature. The sample size was relatively small and the generalizability of the findings to real-world settings is unclear. Additionally, empathy was measured after one psychological preparation session and only over a period of 2 weeks, warranting further research on the initial value of empathy and the persistence of these effects." https://pmc.ncbi.nlm.nih.gov/articles/PMC12092279/

Amygdala dampening lowers emotional quality, also that of depression. But is your subjective feeling of more empathy now because of less depression, or because you actually have empathy? Those studies don't clear that out!

"Even in drug-induced ego death, the initial event is an overstimulation of serotonin 2A receptors across the cortex. This massive global excitation disrupts the Default Mode Network, and the amygdala's reduced activity is a downstream compensatory effect of that initial overload. The dampening is still a consequence of overstimulation."

A study regarding that: https://pmc.ncbi.nlm.nih.gov/articles/PMC12501219/

Another example how it plays out in meditation induced loss emotions:

"Mindfulness training has been found to increase prefrontal control over the limbic system and amygdala, which is associated with improved emotion regulation, anxiety, depression and emotional reactivity [22,32]. However, high levels of prefrontal control of the amygdala can be associated with global emotional blunting and dissociation [33]. Indeed, meditation-induced dampening of the amygdala has been found to attenuate not just negative emotions but positive ones as well [34,35]. Multiple studies have found that mindfulness meditation training can result in reduced intensity, blunting, or complete loss of both positive and negative emotions and dissociation in some people [9,12,33,34,36]."

So, a lot of people claim recovery, but when looked into history or further asked, it plays out as being "almost" recovered or "95 percent" recovered. When the inital sensitivity is subsided, these people will still flare up, have problems with drugs, caffeine etc. but their symptoms lowered due to stress adjustments.

Yes cortisol spikes worsen perception, also with non HPPD people and mostly, when the inital panic subsided from having these symptoms, symptoms better over time, as our mind adjusts to the condition.

Then there is the risk of using different methods that might not be that healthy, to lower cortisol spikes.

One is avoidance. To avoid many things, almost like obligations and to use placebo's like natural herbs with no real effect, as a justifying system, might work for some time, but overtime, this will have a strain on the brain, as this works almost like low dose amphetamine, where the humans natural desires are suppressed and HPPD is used as an excuse to avoid outside stimuli. Going out etc.

Of course one has to be careful, cortisol spikes are difficult for the body and mind and can actually damage over time, but the same goes for general avoidance and problem avoidance.

The mind then suppresses emotions and it works like amphetamines, the dopamine stays in the brain and is not "used". Therefore no cortisol is triggered and one remains in that "safe zone". During that, perception may seem clearer. It is like a drug, where the avoidance of a potential threat acts like a dopamine kick to the brain. This so makes the brain insensitive and also emotions more dull. One might also get sleep problems as a side effect of all the suppressed stress. The worst is, when avoidance is manifested through drug usage.

https://cascadeacademy.com/2022/04/01/avoidance-as-an-addiction-yes-do-that-again-and-more-of-it/

"Avoidance can present itself through calm intellectualization and rationalization, an argument that initially sounds logical but still delays facing the fear. "

There are different avoidance strategies that give the brain a dopamine kick, this fights the stress short term, but damages the cells of the brain long term.

"Experiential avoidance, as an inhibitory emotion regulation strategy, has been linked to various mental disorders and is a focus of research related to interventions for these disorders." https://pmc.ncbi.nlm.nih.gov/articles/PMC11332439/

It affects emotion regulation, empathy and overall decision making.

One might ask, how drugs can be avoidance? Well, drugs actively blunt your emotional sphere. For example in amphetamines, one just becomes unaware of emotional behavior. They just care less about that. This enables them to "hustle" more and disregard any "emotional" distraction. They not only avoid emotionality, they also become unable to engage with it properly. This obviously has a much stronger effect, than just avoiding sober. The world seems easier, because problems are not properly seen. One looses emotional flexibility. The questions weather one goes to the friend party isn't problematic anymore, because one anyways doesn't care much about what they think anymore. One cannot be hurt if one doesn't care. I don't care about you, so you don't have to worry about me.

"People who are struggling with anxiety and depression need support to increase functioning of the dopaminergic system; and we know that dopamine is also activated when someone has “escaped” an event they believed would be unpleasant.   We can see that the brain responds to a type of avoidance with dopamine! This helps us understand avoidance as a type of addiction that signals dopamine to say, “Yes! Do that again, and more of it”.   Avoiding something we believe will be unpleasant releases dopamine."

Sometimes avoidance is justified through experimental belief systems. This then also feels the purpose of having a community and a thought ideology to share. This is also extremly important, in order to have this as a social structure, as that further strenghtens the behavior and supports ones behavior. In case you are wondering, why people even in a HPPD sub, still have dubios beliefs about drugs etc. They share a certain type of living and need people to believe in it. Showing that their way of living without the social support, would not be enough.

While I understand the need to lower cortisol and stress and find a way of living, I find it problematic that the damages it could potentially take on others, are blended out in the insensitive lifestyle these people are having. Some even still encourage others to take psychedelics, as that has cult expanding purposes. The actual occurence of things like HPPD, or overall dp/dr, psychosis or overall visual disturbances, is not very low. Even the bald head that takes all the drugs talks about increased visuals caused by his consumption. So no, these things do take a toll on the head. Also on the empathy, as they mostly are in usage, imo, for avoidance of problems. Someone happy won't take drugs, face the fact. Even with cannabis, some claim the risk to be low, with psychosis for example at 1 percent. The actual state of study looks different. Schizophrenia is in 80 percent of cases not genetically related and the overall risk for cannabis induced psychosis goes from 1 percent to potentially 20 percent depending on the factors in different studies. The same goes for other side effects, these are very present in consumers and well studied. So these downplaying numbers people sometimes throw around, lack any evidence, the actual occurence of side effects is higher than believed, but often times ignored!

When people start talking for the "neuroplasticity" of drugs, it is clear to me, that they don't understand what that term means, it is neither positive nor negative, but can be both or neutral. Somehow this whole hallucinogenic drug community, is something that relies on glorifying these drugs to some extent, since many people are profiting of it, working with it, as a million dollar industry, of course you will have biased studies etc. As well as users need to glorify it, to defend themselves properly.

I again encourage those, to find a place at positive HPPD or something, there is a sub for that. If you need to spread that bs in the potential harm of others, then do it there. Here is no place for that. Here is a place for objective discussion on HPPD and treatment options, not of glorifying drugs that are factually harmful. No one denies that!

Avoidance, in what form whatsoever, through drugs or other things/behaviors, dodges stressful stimuli, mainly through becoming insensitive to it and therefore automatically dogding these stimuli or anything coming to close to ones wellbeing, over a long time and can help living a life one feels well with living. Some people don't seem to be in better circumstances. I think it can be a self treatment option to reflect on these things and think about it differently, as such a behavior comes with many side effects and potential long lasting damage.

Luckily, such a behavior and insensitivity can be reverted to some extent, so there are many options to live life differently, for example in facing problems and giving up security for emotionality.

For some the avoidance way isn't an option anymore. Because the brain does not tolerate the suppression anymore. This usually happens when the way of living through avoidance doesn't function anymore! Then symptoms become to strong when further avoiding.

Then cortisol and stress triggers have to be differently addressed.

Of course one can still avoid, but then it would be better to be aware of it, why. HPPD needs to have some adjustment in life and one has to lower some stress. But reflection is important, imo. At least it is another option to deal with it, for the right person!