Babies Experience Life As An LSD Trip, As A Result Of Their High Metabolism

zewe

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Born again with K2 + ketotifen. :lol:

Too funny!

Sheds new light on JC's words, "I tell you the truth, unless you change and become like little children, you will never enter the kingdom of heaven."

I always wondered what he was doin' during those lost years!
 
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Yes Regina, it is strange. Some people are dumber than wood nowadays.

I've got alot of theories on that. Kids have most things done for them. Like no use for scissors when there's perforated cutouts.

No glueing and painting of models; just snap together and press on decals.....I believe this and the above taught us patience too.

Entertainment is mostly passive, today.

When a young one asks me the time and I say, "Quater to 4," I get a blank stare. So then I say, "3 semicolon 45 flash flash!"

Not many readers of books. Look up an article from around 2008, in the Atlantic magazine, "Is Google Making Us Stupid?"

Not to mention adulterated food and water supplies.....and the air we breathe.

Not many will read the following book if I give it to them, "Four Arguments For The Elimination Of TV." Older but very enlightening.

I'm totally hijacking this interesting thread...sorry.

One more thing, Regina, is that a wolf in your picture?! Lucky you!

Air pollution is reducing IQ significantly.
 
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I do this often, say I have a crush on a girl, I can create a dream of me and her walking through a garden as vividly as dreaming or life while I’m just sitting awake in the day, eyes open and everything else dissolves away.

Oh day dreaming. I thought that was a high serotonin escapist activity. A form of self soothing.
 
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It gets hardened thru chemicals, pharma drugs, EMFs, fluoride....(all keep the masses from awakening, ugh, the PTBs!)

The load increases as we age. Hence, babies start with a fairly clean slate.

And yes, authoritarian cultures dump their own load of toxic debris.

Not everyone has a soul nowadays. Some people are born without functioning pineal glands. The great work is complete. They have created Goyem.
 

Regina

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Air pollution is reducing IQ significantly.
I think it is the high serotonin on display when full grown adults walk into a room and not know how it can be used unless given explicit and specific cues (daresay permission). Breathtaking lack of creativity. Similarly, there is hostility toward anyone suggesting anything different than what has been signified by authorities. The reactions I have received when I have stupidly mentioned vitamin K or the heretical progesterone (gasp) belong in a sci-fi movie.
 

Travis

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I wonder if use of such antiserotonergic substances like caffeine that, while not being psychedelic in themselves, can nevertheless facilitate and potentiate psychedelic experiences and altered states of consciousness. I'll just note that some of the most visionary and surreal artists such as David Lynch are very heavy coffee consumers.

The effects of coffee are quite dissimilar to those from green tea or Coca-Cola™. For those reasons, and also a few more,⁽¹⁻⁴⁾ I nominate caffeoyl quinide as being responsible for most of coffee's unique effects. Formed upon roasting from chlorogenic acid, this μ-opioid receptor antagonist is as powerful as naloxone. Mu-opioid receptors are expressed in the human digestive tract where coffee's caffeoyl quinide likely accounts for its laxative effects. But it doesn't stop there: this opiate antagonist has been detected in the plasma after coffee consumption—twice.

The true de-stupifyer in coffee could be caffeoyl quinide, a molecule that distinguishes it from the lesser caffeinated beverages.

[1] Whittle, Robin. "Beyond Caffeine: Coffee Contains Opioid Antagonists." Journal of Caffeine Research (2015)
[2] De Paulis, Tomas. "4-Caffeoyl-1, 5-quinide in roasted coffee [³H]-naloxone binding and reverses anti-nociceptive effects of morphine in mice." Psychopharmacology (2004)
[3] Farah, Adriana. "Effect of roasting on the formation of chlorogenic acid lactones in coffee." Journal of Agricultural and Food Chemistry (2005)
[4] Bennat, Carolin.."HPLC Analysis of chlorogenic acid lactones in roasted coffee." Zeitschrift für Lebensmittel-Untersuchung und Forschung (1994)
 
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Travis

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Histadelia, a condition characterized by excessive levels of histamine in the blood, is usually an inherited trait, according to Canadian psychiatrist Abram Hoffer, author of “Common Questions About Schizophrenia and Their Answers.” He explains that the condition usually manifests itself when patients are about 20 years old, and because high levels of histamine speed up metabolism, patients are most often thin. Symptoms of histadelia include increased production of saliva and mucus, compulsive behavior, hyperactivity, sparse body hair, easy sexual orgasm, light sleep and depression. Hoffer says that histadelics make up roughly 20 percent of all schizophrenics and are “the problem patients at psychiatric clinics and hospitals.”

I didn't know that Hoffer had considered histamine in schizophrenia etiology, and through reading his book a person could get the impression he assumed adrenochrome responsible. Based on this study below, I also had got the impression that histamine was accountable for most schizophrenia:

Prell, George D. "Histamine metabolites in cerebrospinal fluid of patients with chronic schizophrenia: their relationships to levels of other aminergic transmitters and ratings of symptoms." Schizophrenia research (1995)

schizophrenia.png click to embiggen

Everyone knows that Hoffer had used niacin, and I had started to think this could work by inhibiting brain histidine uptake—the direct precursor of histamine. Yet after reading a bit more about niacin I had also learned that it (1) reliably removes methyl groups from the body via the formation of N-methylnicotinic acid, a phenomenon observed by cardiologists also using high-dose niacin; and (2) it reliably increases serotonin by a sort-of 'reverse kynurenine pathway inhibition' effect: It has been well-established that nicotinic acid can be made from tryptophan, and also that the former's presence prevents the catabolism of the latter. Niacin would be expected to spare tryptophan, and studies on rats show this predictably leads to higher serotonin:

Tian, Yan-Jie. "Excess nicotinamide increases plasma serotonin and histamine levels." Acta Physiologica Sinica (2013)

So you have that as well, and Hoffer could have been pacifying his schizophrenic patients with their' own endogenously-produced serotonin. [I am under the impression that niacin had increased plasma histamine levels in the study above by inhibiting brain uptake and/or displacing it from binding sites.]

Niacin's inhibition of histidine brain uptake remains to be proven, yet should this occur we'd then have the following trends: (1) reduced brain histamine, (2) increased serotonin via sparing tryptophan, and (3) decreased epinephrine by removing methyl groups though the kidneys. Any one of these probably could be expected to attenuate the schizophrenic state, but niacin could be capable of doing all three simultaneously. And in a weird twist, adrenochrome could also be inhibited because this molecule comes from the oxidation of epinephrine. The methyl group of epinephrine allows it to transgress the blood–brain barrier, and the positively-charged norepinephrine is more excluded.

As it turns out: not only had Hoffer & Osmond though of the reduced methylation, but a supposed reduction in epinephrine (adrenaline) had actually been their primary justification for using niacin in the first place:

Hoffer & Osmond. "Massive niacin treatment in schizophrenia. Review of a nine-year study." Lancet (1962)

'We decided to try niacin because it might compete for methyl groups and so prevent more noradrenaline being methylated to adrenaline.' ―Hoffer

'We still do not know whether niacin reduces the methylation of noradrenaline to adrenaline in the body, which led us to use it in schizophrenia. But Udenfriend et al. (1959) have found that methoxylation of noradrenaline is significantly reduced by nicotinamide.' ―Hoffer
 

LUH 3417

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I think it is the high serotonin on display when full grown adults walk into a room and not know how it can be used unless given explicit and specific cues (daresay permission). Breathtaking lack of creativity. Similarly, there is hostility toward anyone suggesting anything different than what has been signified by authorities. The reactions I have received when I have stupidly mentioned vitamin K or the heretical progesterone (gasp) belong in a sci-fi movie.
well now i feel a lot better about myself after converting an used waste basket into a planter. thank you @Regina
 

REOSIRENS

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Many people report feeling like a kid again when taking LSD or psilocybin. It also matches what Ray said about serotonin antagonists like LSD improving learning and increasing playfulness, and cause behavioral impairment only at very high doses.
I have experienced that time ago when I took thyroid with thymus extract...my mind seemed to play around with lights and colors I felt like nothing could put me down
 

Murtaza

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Ok, I'm going to stir the pot. Bear with me, I have much to say.

Concerning RP's statement that LSD is a serotonin antagonist, this is cherry picking info from studies. Let me elaborate.

In his article, "Serotonin: Effects in disease, aging & inflamation," that's not exactly what Anne Frederickson said:
SNIP:
Depression is an illness that also seems to have one of its causes in low serotonin levels (2,3). Many of the anti-depressants currently on the market are drugs that work by increasing serotonin levels in synapses. However, given that serotonin is an inhibitory neuron, and depression appears to be mostly a decrease in behavior and affect, one would expect that depression would be caused by an increase in serotonin levels, rather than a decrease.

However, the serotonergic system of the nervous system is a complex system that mediates so many behaviors, it may have multiple functions that the scientific community has only an inkling of. Some of these functions are revealed by the effects of LSD.

As with depression, the action of LSD is not completely understood. There is evidence, however, that serotonergic neurons are involved. LSD is structurally similar to serotonin and seems to affect many of the systems that serotonin has been implicated in (12). In addition, administration of haloperidol blocks the hallucinations associated with LSD use (7). Haloperidol has an especially strong affinity for serotonin receptors. Also, other psychedelics that have similar effects to LSD have been shown to affect serotonin producing neurons. MDMA, or ecstasy, blocks the reuptake of serotonin, thereby leaving more serotonin in the synapse and prolonging activation (6). Prolonged use of MDMA results in destruction of serotonergic neurons in the brain (4,5). Because of the similarities between ecstasy 'trips' and LSD 'trips,' it can be concluded that they must activate a similar pathway, i.e. the serotonergic pathway.

Several theories of the mechanism of LSD have been postulated. Each one presents a way in which LSD could affect behavior through activation of serotonergic neurons along with research to support it. However, each one has its weaknesses. In the end, it is difficult to determine how LSD actually alters behavior.

The first theory is that
LSD is a serotonin antagonist, specifically activating (or actually blocking) 5-HT2 receptors (12). This would prevent serotonin from having its normal effect. Support for this theory comes from studies that have shown that administration of some 5-HT2 antagonists do not decrease the effects of LSD, as you would expect if LSD was a serotonin agonist. Activation of 5-HT2 receptors seems to cause serotonin to have an excitatory effect on some neurons. LSD prevents this action, thus having an antagonistic effect on the 5-HT2 serotonin system (12). However, even within this theory there are problems. The general theory of LSD as an antagonist is consistent with how it affects behavior. LSD seems to increase sensation, heart rate, and blood pressure, all of which are excitations of the nervous system. Because serotonin is an inhibitory neurotransmitter, antagonism of serotonin would result in an increase in neural activity. However, the fact that LSD is an antagonist to 5-HT2 receptors specifically makes this conclusion problematic. Because of the special action of 5-HT2 receptors, antagonism of serotonin at those receptors would result in a decrease in neural activity which would not explain the effects of LSD. If 5-HT2 receptors are in fact excitatory, one would expect antagonism of this system to have an inhibitory effect.

The next theory postulates that LSD is in fact a 5-HT agonist rather than an antagonist (12). One researcher was able to train rats to discriminate between LSD and saline based on it psychological effects. When the rats were given certain 5-HT2 antagonists, the rats lost the ability to discriminate between the two (12). Also, LSD has been shown to have a higher affinity for 5-HT receptors over all than serotonin but has a lower potency (12). Thus, while is more likely to bind to the receptors, it is not as likely to have an effect as serotonin. Even though LSD has some activity, it does not appear to be very strong. LSD may appear to be an antagonist even though by definition it is an agonist.

The last theory partially combines the last two theories. This theory postulates that 5-HT1 and 5-HT2 have an agonist/antagonist relationship. Thus substances that are agonistic to 5-HT1 receptors are antagonistic to 5-HT2 receptors (8). This is supported by the above research. LSD operates under this mechanism by enhancing serotonin activity at 5-HT1 receptors, while also blocking 5-HT2 receptors from the more effective activation of serotonin.


The interesting point of this theory is its implications for the actual effects of those two serotonergic systems. Agonization of the 5-HT1 receptors by LSD indicate that they might be involved in the production of moods. If low serotonin produces a decrease in positive moods, as in depression, then agonization of serotonin levels should produce a more positive mood state. LSD agonization would be consistent with the production of euphoria and mood changes that are associated with LSD use. The 5-HT2 receptors might then be responsible for the control of sensation and possibly autonomic nervous system control. Under the control of LSD, sensation appears uninhibited. Users report enhanced sensations, synesthesia, and distortions of sensations. All of this would seem to be a result of over activation of the sensory system. In addition, LSD produces an increase in heart rate, blood pressure, and body temperature, all of which are a result of activation of the sympathetic nervous system. Because it has been shown that LSD limits serotonin's activation of the 5-HT2 receptors, it can be concluded that these receptors must be involved in the inhibition of sensation and the sympathetic branch of the autonomic nervous system under normal conditions. The only problem with this theory is that it fails to reconcile the theory that 5-HT2 receptors are actually excitatory.

Once again, the nervous system proves to be too mysterious for explanation. As with most alterations of behavior, researchers can explain what happens but not how it happens. Our postulated theories of LSD action only allow us a glimpse at the whole picture, and it is a rather incomplete, confusing glimpse at that. We can guess how LSD affects serotonin levels, but there will always be evidence that contradicts the theories. There will always be a part of the brain that uses serotonin in a different way than the other parts, a receptor that activates neurons differently. The only way that we can get at the truth is to approach the problem from different angles. One approach to the problem of LSD action would be to investigate where the different 5-HT receptors are located in the brain. Location may shed light on the actual purpose of these receptors. Based on the theories and experiments described above, one might assume that 5-HT1 would be located in areas of the brain responsible for the production of mood. Such areas might include the frontal cortex and the hypothalamus. 5-HT2 receptors might appear in the lower regions of the brain that are devoted to the production of basic physiological functions as well as in areas devoted to sensation and the interpretation of sensation. An interesting point is the fact that in the end, LSD does not seem to have an inhibitory effect on the areas involved with the I-function (where ever they may be). LSD users are always aware that the hallucinations and euphoria are a product of the substance; the awareness is called insight (7). This may be the most important implication for the serotonergic system. Because LSD is unable to produce alterations in the I-function, serotonin appears not to be involved in the production of the sense of self, an interesting point considering the fact that it effects almost every other facet of behavior.

Full article:
Mechanisms of LSD: a Glimpse into the Serotonergic System

The following is not about this thread's LSD topic but it is about serotonin.

Here's where some might get exasperated with me, because I speak so much about histamine. Again, bear with me. I can see all of what I want to say in my mind's eye, but it is difficult and lengthy to explain.

Brain monoamines (serotonin, norepinephrine, dopamine, and histamine) play an important role in emotions, cognition, and pathophysiology and treatment of mental disorders. The interactions between serotonin, norepinephrine, and dopamine were studied in numerous works; the histamine system received less attention. However, when it was studied,
it was concluded that histamine stimulates serotonin, norepinephrine, and dopamine transmission in the brain

Abnormally high blood levels of histamine -- a condition known as histadelia -- can significantly increase your risk for depression, a relationship first studied extensively by pharmacologist Carl C. Pfeiffer, founder of the Princeton Brain Bio Center. Because its origins differ from other forms of the mood disorder, high histamine depression may not respond well to conventional modes of treatment for depression.

Histadelia, a condition characterized by excessive levels of histamine in the blood, is usually an inherited trait, according to Canadian psychiatrist Abram Hoffer, author of “Common Questions About Schizophrenia and Their Answers.” He explains that the condition usually manifests itself when patients are about 20 years old, and because high levels of histamine speed up metabolism, patients are most often thin. Symptoms of histadelia include increased production of saliva and mucus, compulsive behavior, hyperactivity, sparse body hair, easy sexual orgasm, light sleep and depression. Hoffer says that histadelics make up roughly 20 percent of all schizophrenics and are “the problem patients at psychiatric clinics and hospitals.”

Histamine and estrogen also have a symbiotic relationship. Histamines release estrogen, and estrogen releases histamines. Estrogen also drives serotonin production. So now you're in a thyroid-suppressive feedback cycle with elevated serotonin levels.

Here's more. Both estrogen and serotonin increase histamine production and the release of estrogen from mast cells. Estrogen also prevents the clearing of histamine, which further allows the buildup of histamine.

It gets worse. Histamine further increases estrogen levels; creating yet another thyroid-suppressive feedback cycle.

Is anyone beginning to see the real root of the problem?

In the past, about 1% of the population had histadelia due to genetics. Histamine intolerance is on the rise. I believe this is mostly induced by our pharmaceutical maddness. Many drugs raise histamine and all psych meds do this.

In RP's article:

"Migraine headaches are also increasing in incidence. By the end of the 195s, it was widely accepted that migrain headaches and associated symptoms including nausea and visual disturbances were caused by an excess of serotonin......"
These are all symptoms of high histamine!

He mentions:
"
Some fruits, including bananas, pineapples, and tomatoes contain enough serotoin to produce physiological symptoms in susceptible people."
These are all high histamine foods!

The concluding paragraph:
"Hypothyroidism is a very common cause of increased serotonin...."
I've discussed how it's not that simple.

And finally, here's my take on comparing babies' brains to the effects of "the magical mystery tour" on expanded consciousness:

I liked the inclusion of Wm. Blake's view on perception. Blake was a mystic and we mystics generally concur that the pineal gland (responsible for producing melatonin, a derivative of serotonin) is the seat of the soul. (Descartes coined this; associated with psychic ability, intuition, and expanded consciousness) And, calcification of it is the reason behind loss of our natural abilities...which babies have.

It gets hardened thru chemicals, pharma drugs, EMFs, fluoride....(all keep the masses from awakening, ugh, the PTBs!)

The load increases as we age. Hence, babies start with a fairly clean slate.

And yes, authoritarian cultures dump their own load of toxic debris.
All the more reason to take cypro?
 

zewe

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I didn't know that Hoffer had considered histamine in schizophrenia etiology, and through reading his book a person could get the impression he assumed adrenochrome responsible. Based on this study below, I also had got the impression that histamine was accountable for most schizophrenia:


Everyone knows that Hoffer had used niacin, and I had started to think this could work by inhibiting brain histidine uptake—the direct precursor of histamine. Yet after reading a bit more about niacin I had also learned that it (1) reliably removes methyl groups from the body via the formation of N-methylnicotinic acid, a phenomenon observed by cardiologists also using high-dose niacin; and (2) it reliably increases serotonin by a sort-of 'reverse kynurenine pathway inhibition' effect: It has been well-established that nicotinic acid can be made from tryptophan, and also that the former's presence prevents the catabolism of the latter. Niacin would be expected to spare tryptophan, and studies on rats show this predictably leads to higher serotonin:

Tian, Yan-Jie. "Excess nicotinamide increases plasma serotonin and histamine levels." Acta Physiologica Sinica (2013)

So you have that as well, and Hoffer could have been pacifying his schizophrenic patients with their' own endogenously-produced serotonin. [I am under the impression that niacin had increased plasma histamine levels in the study above by inhibiting brain uptake and/or displacing it from binding sites.]

Niacin's inhibition of histidine brain uptake remains to be proven, yet should this occur we'd then have the following trends: (1) reduced brain histamine, (2) increased serotonin via sparing tryptophan, and (3) decreased epinephrine by removing methyl groups though the kidneys. Any one of these probably could be expected to attenuate the schizophrenic state, but niacin could be capable of doing all three simultaneously. And in a weird twist, adrenochrome could also be inhibited because this molecule comes from the oxidation of epinephrine. The methyl group of epinephrine allows it to transgress the blood–brain barrier, and the positively-charged norepinephrine is more excluded.

As it turns out: not only had Hoffer & Osmond though of the reduced methylation, but a supposed reduction in epinephrine (adrenaline) had actually been their primary justification for using niacin in the first place:

Hoffer & Osmond. "Massive niacin treatment in schizophrenia. Review of a nine-year study." Lancet (1962)

'We decided to try niacin because it might compete for methyl groups and so prevent more noradrenaline being methylated to adrenaline.' ―Hoffer

'We still do not know whether niacin reduces the methylation of noradrenaline to adrenaline in the body, which led us to use it in schizophrenia. But Udenfriend et al. (1959) have found that methoxylation of noradrenaline is significantly reduced by nicotinamide.' ―Hoffer

Travis, Hoffer stated that roughly 20% of all schizophrenics are histadelics and are "the problem patients at psychiatric clinics and hospitals."

No doubt, but not for reasons they might think. Psych drugs are disastrous for histadelics as they raise histamine levels.

Also, niacin would not be an option for this 20% as it is a "methyl sponge." And this group of schizophrenics would have a seriously impaired methylation system. This system is full of feed-back loops that can further block one's ability to lower histamine; you can't just look at one level.

Also, since niacin is a methyl mop, it requires SAM-e for its metabolism and thereby contributes to a drop in methylation. And histadelics are notorious for being low in SAM-e.

Niacin also depletes/lowers vitamin B9 [folate]. And, depletes/lowers DAO enzyme which degrades histamine.

I'm begining to think that this subgroup aren't really schizophrenic in the true sense of the definition because, very high histamine levels can give you auditory hallucinations. Address their methylation problem and the schizophrenic symptoms may disappear.

My fascination/quest to understand the role of histamine in mental illness is personal. My entire family are histadelics. And I do have a schizophrenic brother who is a case study in tragedy due to the VA's mistreatment of his illness:
Com. v. Zewe

If the above episode isn't enough, my brother was burned very badly as a teenager in a sulfur explosion. That sulfur baked into his skin and you could hear him screaming all over the hospital as they put him in whirlbaths to extract it.

He had plastic surgery for many years as most of the front of his body was charred. I don't understand why the Navy even accepted him.

After basic training, he had a motorcycle accident where he broke is collarbone; they wired his shoulder joint together too. After a medical review, they still kept him in.

Another time, last day of a month leave, had another motorcycle accident where he ran into a backhoe w/ no helmet. 13 fractures, cerebral hemorrhage which kept him in a coma and a smashed eyesocket which had to be wired together. After another med review they STILL kept him in the Navy.

Sorry about all that background but if any read his case, I need you to understand somethings about him. He also was chosen as Salior of the Year.

Crap, this is still hard for me to talk about.
 
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Travis

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Travis, Hoffer stated that roughly 20% of all schizophrenics are histadelics and are "the problem patients at psychiatric clinics and hospitals."
I do know that now, but hadn't before yesterday.
This system is full of feed-back loops that can further block one's ability to lower histamine; you can't just look at one level.
I had also considered it's second-most reliable effect, that of sparing tryptophan. Niacin also appears to be structurally similar to histamine, and they both produce a 'flush.'
 
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zewe

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I do know that now, but hadn't before yesterday.
I had also considered it's second-most reliable effect, that of sparing tryptophan. Niacin also appears to be structurally homologous with histamine, and they both produce a 'flush.'

Actually, you can check your methylation status with niacin. Someone like me would get a very uncomfortable flush at levels of 50 mg or lower, while a good methylator would get
this reaction at levels of 100 or 200. A lot of experts on histamine intolerance have clients play around with B vitamins TMG and other sups to create SAM-e, but you can end up
over methylating where they suggest taking niacin to correct that. This seems like a lot of unnecessary trial and error when you can just take the SAM-e supplement.
 

inthedark

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Awake dreaming is a side effect of huge doses of diphenhydramine, which also cause delirium:
Diphenhydramine

"- Mixture of dreaming and reality - Perhaps the most interesting effect of diphenhydramine is that it causes people to dream while they are awake. This can be a very positive experience, but also a very negative as dreams are well known to be. Users can often have much more vivid dreams after the intoxication is over. Here is how one user described the dream-reality blending: "All of his thought patterns would turn into conversations with himself, or other people. Some conversations were actually reproductions of real conversations he had had in the past week. These thought-conversations would slowly get more and more real. Eventually, he would always feel compelled to say something out loud. He would struggle for a while, not sure if he really wanted to, but would always eventually say it. This would suddenly bring him back to reality, he would realize that there was no one in the room he was talking to, and his voice would sound foreign and distant."

Very interesting reading about the side effects of high dose Benedryl in the context of the discussion in this thread.
 

charlie

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20,818 views in 5 days. :shock:
 

Terma

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Can someone who has access to LSD tell me what it feels like to watch this while you're on it and/or coming off it:

 

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