15 hours ago, FrozenColdDonut said:

Could PQQ help I've read its suppose to protect and grow mitochondria

To be entirely honest I haven't read much on PQQ, as far as I understand though it is good for mitochondria. Niacin right now is the best I have seen for mitochondria though. Better than CoQ10 even.

https://jnnp.bmj.com/content/early/2021/07/13/jnnp-2020-325881

Localised increase in regional cerebral perfusion in patients with visual snow syndrome: a pseudo-continuous arterial spin labelling study

5 hours ago, FrozenColdDonut said:

So antioxidants will help lower oxidative stress and free radicals that seem to be the problem because they cause mitochondria to become dysfunctional?

They should help for sure, to assist in proper functioning of mitochondria, mitochondria are massively dense in synapses, and make all the work happen so they are crucial for a well function brain. Antioxidants may not make you live forever, but they do support and assist mitochondria massively, and niacin appears to be something special. So just eating healthy foods, fruits, veggies, nuts, and whole grains, will boost all these levels. Its a great place to start absolutely.

15 hours ago, FrozenColdDonut said:

Has this helped you? Have you got better by removing free radicals?

I can't really say that it has because mine got significantly better to the point where I'm not really in a position to try things out, my symptoms now are so vague it would be hard for me to tell improvement. Realistically as well any improvement would simply just mean slight improvement to 100% symptom free. The only symptoms I have anymore is if I drink too much coffee, I've also noticed an increase in heart rate after eating potatoes lol, but that could be completely unrelated, although it does seem to give me some mild anxiety. I think as well my brain doesn't regulate normal anxiolytic reactions from external sources as it should or used to. Other than that for my symptoms I can only say that sometimes I just feel like there is a certain joy missing that I used to have in life, but again that could be circumstantial and not symptomatic per say, it could also be an end result of suffering so severely for years from crushingly painful HPPD, this condition in a severe form I do believe does take a great deal of toll on the mental state of a human, as though being trapped in a tortuous prison. 

Although NMDA antagonists were once thought to reliably cause neurotoxicity in humans in the form of Olney's lesions, recent research suggests otherwise. Olney's lesions involve mass vacuolization of neurons observed in rodents.^[18][19] However, many suggest that this is not a valid model of human use, and studies conducted on primates have shown that use must be heavy and chronic to cause neurotoxicity.^[20][21] A 2009 review found no evidence of ketamine-induced neuron death in humans.^[22] However, temporary and permanent cognitive impairments have been shown to occur in long-term or heavy human users of the NMDA antagonists PCP and ketamine. A large-scale, longitudinal study found that current frequent ketamine users have modest cognitive deficits, while infrequent or former heavy users do not.^[23] Many drugs have been found that lessen the risk of neurotoxicity from NMDA receptor antagonists. Centrally acting alpha 2 agonists such as clonidine and guanfacine are thought to most directly target the etiology of NMDA neurotoxicity. Other drugs acting on various neurotransmitter systems known to inhibit NMDA antagonist neurotoxicity include: anticholinergics, diazepam, barbiturates,^[24] ethanol,^[25] 5-HT_2A serotonin receptor agonists,^[26] anticonvulsants,^[27] and muscimol.^[28]

"I was amazed to follow the discussion about vacuoles in the dorsal root ganglia neurons (Toxicol Pathol38, 554–59; 999; 39, 451–453). Vacuolation of neurons represents hydropic degeneration, which in the dorsal root ganglia may result in neuronal death and formation of nodules of Nageotte replacing the lost neurons. Obviously for some neuropathologists the only possible way neurons can die is through “apoptosis.” But this is not true. In our studies with toxicity of extremely high doses of pyridoxine (vitamin B6), we have demonstrated that cytoplasmic vacuoles can easily be produced experimentally and that they are harbingers of neuronal death (Krinke et al. 1981; Krinke et al. 1985; Krinke 1988). Neuronal vacuoles can appear spontaneously, especially in aging animals. They are unspecific, that is, not related to the chemical structure of the toxicant, and they can also be produced by trauma. In the context of “mad cow disease,” or bovine spongiform encephalopathy, the attention of European pathologists was focused on the occurrence of vacuolated neurons in the bovine brain. Examination of 378 bovine brains revealed that in 11.5% of the animals, there were large neuronal vacuoles in the brain stem, especially the red nucleus, that were nonspecific and spontaneous (Guarda and Fatzer 1995). More research into neuronal cytoplasmic vacuolation and its role as an alternative to apoptosis is needed."

4 hours ago, Onemorestep said:

Hppd made me gain weight. This doesn’t seem to happen to everyone but some people gain weight. It could be stress eating for some but wasn’t for me. 
 

when I first got hppd I lost a lot of vocabulary and I would stop talking mid sentence. It was like I couldn’t find the words. I knew what I wanted to say meaning wise, but it was as if I had lost language. 
 

I had a huge amount of anxiety about people thinking I was weird or whatever. Most people didn’t even notice. 
 

and lastly—- these things went away. I don’t have pausing issues with speech and the weight went away. Give it some time  

 

focus on helping yourself feel more safe around people. Their just people—most are obsessed with what’s going on with them and pay you very little attention  

 

unless you’re hot. In which case you can walk funny and talk weird. They’ll notice then but more because they’re watching how hot you are. No one cares when you’re hot. So just focus on getting hot and then nothing matters. You could get a muscle suit like in arrested development but that’s lame. Fly to Korea and plasticize yourself. Take Chinese steroids. DO WHATEVER IT TAKES TO MAKE YOURSELF THE ADONIS THAT DISTRACTS FROM THE GOOP THAT IS OUR BRAINS. 
 

Make a show about it. Become the YouTube. You have some speech issues but You’ll get follows because guess what—I’m not listening anyway I’m just staring at you and imaging the ocean because you’re giving Jason Momoa a run for it. 

 

 

ignore all of this.

 

Lmao.... its true.

Interesting that he eventually develops seizures. You see kids, doctors are fucking stupid, case in point. Now hes on topiramate, Im not sure about that one specifically but  most anti seizure meds long term cause neuronal loss, and after about 20 years most patients so significant signs of reduced brain size.

But as I have said I do believe that HPPD, migraines, and seizures are closely related.

On 7/11/2021 at 4:57 PM, Brattymaddy said:

Yes I'm sure, But that doesn't mean others have little to no issues. I have 0 idea why this could be the case but it is?

Before I even got HPPD I tried vaping nicotine and I had averse reactions to it then too. It was nauseating, I was sweating and clammy. and was overall uneasy, borderline anxious.

If I don't get any legitimate answers within the next few days for hemp flower I might just be a guinea pig my self and go for it tbh, sadly that's the only true way to find out if it's "safe".

I realized I only ever had problems with it after combining the 2.

Its your choice, I just don't understand exactly why you would though. I don't particularly understand a lot of peoples choices though.

Can you give at least a brief description of your symptoms, its not entirely common for HPPD to progress in symptoms after about a month of getting it.

5 hours ago, Brattymaddy said:

It was just tobacco and hemp but I had a negative reaction to it, which I thought was odd too lol.

The hemp it self never really caused any problems, atleast that I could see short term.

The problem here is I don't know which one did it and caused the relapse. That's why I'm wondering if others had a negative reaction to it.

I smoke a cigar every now and again, with little to no issues.

"Took me another year to get back to my semi normal state."

Pretty much answered your own question.

Edit: Im a little confused as to what was in the "blunt" though.

if it was just tobacco thats a little strange. 

4 hours ago, Lucas said:

I'd be willing to try Niacin and keep a journal if the results interest you Fawkinchit.

Vitamin B3 sounds pretty safe... right ?

Definitely!

Its extremely safe, nothing more safe than vitamins, other than water and air lol.

Just be sure to do a minimum of 500mg per day, max 1000mg should do the trick. And make sure to read up on niacin flush so it doesn't freak you out. Based on what I have read no flush is not as effective as normal niacin.

But it would be great for even just a few people to try this, just to see if it works or not.

If I remember correctly there was even a study on rat neurons that showed only 2 weeks of niacin therapy relegated all age related cellular conditions, so basically the cells in older rats became again as though they were young. If this condition is caused by neuronal dysfunction, as opposed to neuronal loss, then niacin will be the best treatment there is for HPPD, hands down.

Honestly if thats the only symptom you have consider yourself lucky as fuck. Dont do drugs ever again and enjoy your life.

Dude! Thank you so much for trying this, I talk about this in my thread, I think it may be one of the better if not possibly the best treatments for this, but I have found no one willing to try it as of yet. So thank you so much. Please keep updating, I would love to see how this turns out and I really hope the best.

I have taken Niacin myself and I feel like it helped me feel better all around in general, but by the time I learned about it most of my symptoms have receded, so its great to see someone with more apparent symptoms trying it.

If it doesn't help or work then so be it, but I feel it has enough potential that it should be tried. So thank you!

This is my thread for anyone wondering.

5 minutes ago, cosmiccharlie said:

Hi, 

I have made the mistake of tripping on mushrooms and smoking DMT plus periods of heavy weed use after developing HPPD.  For me, the weed always brings it back and when I get off of it, the symptoms usually recede within a few months.  Everyone's different, mine is primarily from heavy LSD use when I was 18-20.  I am now 32 and still have fairly strong visuals. My advice is to really evaluate why you want to still use drugs and also appreciate that if you contracted HPPD from one time acid use, you are probably sensitive to this condition.  I contracted it from heavy doses upwards of 10 hits of good acid on multiple occasions.  The disorder can be debilitating so it really is best not to tempt fate.  For me, I had to get burned enough times until I learned how to be happy without drugs or alcohol.  It's not to say that I don't sometimes miss being high or drunk but it's become a matter of overall gain.  My life is better this way so I choose to live this way.  I hope this helps. 

Take Care,

Nick 

Had no idea you were 32

@Löken Honestly, IMO, why mess with it all. I will drink sometimes but thats it. Some HPPDers cant even do that.

11 hours ago, iwasnineteen2 said:

ya, i "got over it" and started feeling super normal after 1.5 years of hppd, but recently something crazy happened and i was insanly high stress for 2 months straight, and now idk if my hppd symptoms are back or it's ptsd from what was happening to me. but every min is hell. i was so good and so happy for so long!

 

Yah that sounds really difficult, especially after such a long interim. Its really hard to say what it could be, but large amounts of stress and emotion can definitely be hard on the neurons themselves, exhibiting like symptoms or causing reoccurrence thereof. That's one of the things about HPPD, is that normal life becomes much more difficult to deal with when things are hectic, its really a struggle for sure.

Damn 10 year later lmao

On 4/18/2021 at 2:31 AM, Hall89 said:

If you have no visual disturbances you don't have HPPD, which you should feel very thankful for! A tip is that you stay away from all drugs that are known to cause it for the rest of your life, which are all hallucinogens (including cannabis), but even MDMA has been proven to cause HPPD. I've also talked to people that have gotten visual snow from cocain. So the best thing is just to stay away from all drugs.

This may not be entirely accurate, I do believe there are rare cases that do not present much for visual disturbances. For myself in fact I didn't develop visual snow for a couple weeks, and eventually the visual snow went away, however other symptoms remained.

It does however seem like something is going on, I agree it may not be HPPD, but it does seem like something neurological is going on, and given the series of events a form of HPPD is probable. To be honest though, what you're reporting Lucas is rather mild in comparison to what I have seen in other sufferers. 

Edit

5 hours ago, kmt1993 said:

I spent quite a bit of time on google looking specifically for a study on a microdosing regimen and it’s link to hppd to no avail, that’s how I wound up here. Not to say I didn’t find anything about potential negatives. The study you just showed me is actually the first one I’ve seen like that. However I think that even most of the anecdotal data available here is probably more useful than that study is for a couple of reasons. The first being that a proper microdose schedule (at least the one I adhered/may continue to adhere to after taking a lot of time to learn as much as possible) is spaced out every 3 days rather than continuously dosed every day for 7 days. the second reason being that 80 micrograms over 7 days is more than 10 micrograms a day, which I understand is easily a microdose for a human but let’s think about the fact that you are giving a 180 lb human microdose to a <5lb rat. I can’t consider that a low dose relative to the specific animal in question. I would like to see studies done on humans taking properly spaced out micro doses/threshold doses more than anything. 

Those are valid points. However its unarguable that microdosing causes HPPD, there are numerous people to attest to the fact that thats how they got it.

Just going to randomly throw this article in here lmao... wtf

A woman took 550 times the usual dose of LSD, with surprisingly positive consequences

https://www.cnn.com/2020/02/27/health/lsd-overdoses-case-studies-wellness/index.html

https://pubmed.ncbi.nlm.nih.gov/2780790/ This shows aggressive long term affects from microdosing. And there are plenty of people that have reported HPPD from microdosing. @NRFAdmin knows more examples of people than I do however. @Jay1 Also can probably attest to the fact that a good amount of people that post here got it from microdosing. Also a google or reddit search will probably help as well.

Microdosing can definitely cause HPPD, has, and may even have a higher potential than normal recreational use for causing it if the the microdosing is consistent. Studies have shown this.

Just posting this for further reading

Ion channels have key functions in the nervous system, including the generation, repression and propagation of action potentials. The opening of Na⁺ channels depolarizes neurons, while the opening of K⁺ channels will lead to hyperpolarization. The situation is more complex with Cl⁻ channels, because the cytoplasmic chloride concentration depends upon the cell type, and changes during development. Thus, an opening of Cl⁻ channels may lead to a hyperpolarization (as in most neurons of the adult CNS) or to a depolarization (as in early development). Given the very large transmembrane gradient of Ca²⁺, Ca²⁺ currents will always be depolarizing. However, the role of Ca²⁺ as a second messenger is more important under most circumstances.

Taking these considerations into account, loss-of-function mutations in neuronal K⁺ or Cl⁻ channels, or gain-of-function mutations in neuronal Na⁺ channels, should give rise to hyperexcitability and perhaps epilepsy. While this indeed turns out to be true in some cases, it should be borne in mind that the systemic effect depends on the particular neuronal circuitry that is affected. For instance, ion channel mutations leading to a selective hyperexcitability of inhibitory interneurons are expected to rather decrease CNS excitability.

Although K⁺ channel defects were long suspected to underlie some forms of epilepsy, this was proven only in 1998, when it was shown that mutations in KCNQ2 and KCNQ3 underlie benign familial neonatal convulsions, a generalized epilepsy of the newborn (21,22,51). KCNQ2 and KCNQ3 are neuron-specific K⁺ channels that are broadly expressed in the CNS, where they assemble to heteromeric channels (11,52). KCNQ2/KCNQ3 heteromers are a molecular correlate of the M current (53). This current was first described in sympathetic neurons as a non-inactivating K⁺ current that could be inhibited by muscarinic stimulation (hence its name ‘M current’) (54). M currents are involved in regulating the subthreshold excitability of neurons and their responsiveness to synaptic inputs. This physiological, extremely sensitive regulation of neuronal excitability probably explains why a small loss of M currents suffices to cause epilepsy (55). From in vitro studies, it was concluded that mutations found in BFNC reduce current amplitudes by merely 25% (11). Interestingly, the homozygous knockout of KCNQ2 in mice is lethal, and heterozygous animals have a reduced seizure threshold (56). Recently, a particular mutation in the voltage sensor of KCNQ2 was shown to lead to neonatal epilepsy with myokymia (involuntarily contractions of skeletal muscles), pointing to a role of M currents in motor neuron control (57). A dominant form of episodic ataxia that is accompanied by myokymia was previously shown to be caused by mutations in the Kv1.1 K⁺ channel (encoded by KCNA1) (58). This K⁺ channel is strongly expressed in myelinated peripheral nerves and cerebellar interneurons, where it contributes to the repolarization of action potentials.

Mutations in pore-forming α and accessory β subunits of voltage-gated Na⁺ channels of the CNS were found to underlie other forms of epilepsy (59–61). Mutations in the SCN1A α subunit (59) and in the SCN1B β subunit (60) cause generalized epilepsy with febrile seizures (GEFS+), while mutations in another α-subunit isoform (SCN2A) (61) yield a somewhat different clinical picture (generalized epilepsy with febrile and afebrile seizures). Similar to previous findings with skeletal muscle Na⁺ channel mutations, for example in periodic paralysis (12), the mutant channels do not inactivate properly (15). Mutations in the Ca²⁺ channel gene CACNA1A (encoding Ca_v2.1) can cause ataxia and migraine (62,63), and this gene may also be associated with epilepsy (64). Mutations in another channel type whose opening leads to depolarization, namely two different subunits of the nicotinic acetylcholine receptor, have also been shown to be associated with epilepsy (65,66). Although the mutants have been studied in heterologous expression systems, the mechanism by which they lead to autosomal dominant nocturnal frontal lobe epilepsy (ADNFLE) is incompletely understood (67).

Rather surprisingly, no unambiguous association with human genetic disease has been established so far for the major class of CNS excitatory neurotransmitter receptors, the glutamate receptors. The main inhibitory neurotransmitters, GABA and glycine, exert their fast inhibitory effect through ligand-gated Cl⁻ channels: the GABA_A and glycine receptors. Because intracellular Cl⁻ is usually below its electrochemical equilibrium in adult neurons, opening of these receptors leads to a hyperpolarizing Cl⁻ influx. The sedative and anxiolytic effects of benzodiazepines depend on a modulatory upregulation of GABA_A receptor activity. Only recently, two GABA_A receptor subunit genes were found to be affected in epilepsy. Mutations in the γ₂ subunit of the GABA_A receptor (GABRG2) were identified in childhood absence epilepsy and febrile seizures (68), as well as in generalized epilepsy with febrile seizures (GEFS+) (69). A mutation of GABRA1, which encodes the α₁ subunit of the GABA_A receptor, was recently associated with an autosomal dominant form of juvenile myoclonus epilepsy (70).

Mutations of the α₁ glycine receptor cause autosomal dominant hyperekplexia (startle disease) (71), which is characterized by marked muscular hypertonia in infancy and a grossly exaggerated response to unexpected stimuli. As the electrophysiological effect of GABA and glycine depends on the intracellular Cl⁻ concentration, one may speculate that mutations in transporters involved in intracellular Cl⁻ concentration regulation may also affect neuronal excitability. In fact, a locus for rolandic and idiopathic generalized epilepsy maps close to KCC3, a K–Cl co-transporter that is expressed in the CNS. Like other KCCs, it is expected to contribute to postsynaptic inhibition by lowering [Cl⁻]_i. However, no mutations were found in SLC12A6, the gene encoding KCC3, in the linked families (72). In contrast, the disruption in mice of the neuronal-specific isoform KCC2 caused severe motor deficits due to defective GABA- and glycine-mediated synaptic inhibition, and led to early postnatal death (73). Mice with an incomplete gene disruption survived for a couple of weeks and displayed severe seizures (74).

16 hours ago, A_Star said:

Alright, I definitely won't be touching any drugs again. Also, I'm getting some foot and leg mild buzzing vibrations, is this common?

No not at all, not for HPPD, sounds more like a peripheral neurology issue(if it is anything), if it gets worse or doesn't go away typically its cause by various vitamin deficiencies.

Sounds pretty mild to be honest. Just give it time and definitely never touch hallucinogens again or you'll end up back here. Typically when you have HPPD you KNOW you have HPPD. Cause its a nightmare. The symptoms are synonymous with HPPD though, but again, sound very mild.