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

[haidut]

Why don't clearly antiserotonergic drugs like caffeine, amphetamine or cocaine have psychadelic effects?

Some of them do. See my response above discussing methysergide.

 

[haidut]

I think @debored13 has also mentioned this discrepancy elsewhere regarding LSD and serotonin. I’m curious as well regarding the relationship.

The full mechanism of action of LSD is not known. Not by a long shot. Its overall effects are anti-serotonin and pro-dopamine, even though at individual 5-HT receptors things get rather complicated. Also, keep in mind that even if assume reductionist medicine is correct with all of its "receptors" we currently know of at least 7 5-HT receptor types, and there likely many more. The effects of LSD on these is unknown, and even on the known ones it has only been studied (sparsely) on 5-Ht1 and 5-HT2.

 

[Regina]

Peat wrote a few times on the brain's innate need to dream and how anti-serotonin chemicals like LSD removes the barriers on consciousness imposed by an authoritarian culture. He said that the ability to dream in an awake state is an indication of high metabolic rate and that is a testament to serotonin's negative effect on metabolism - a serotonin antagonist like LSD intensifies greatly a biomarker (awake dreaming) of high metabolism. He has also spoken about the high metabolic rate of young children and their ability to quickly heal from trauma or overcome disease much more easily than adults.
http://orthomolecular.org/library/jom/1975/pdf/1975-v04n03-p189.pdf
"...LSD works the other way, stimulating intense dreams even when awake, but causing a few dreamless nights when its direct effect wears off. (Para-chloro-phenylalanine, which blocks serotonin synthesis, not only interferes with sleep — especially R.E.M. sleep —but it causes rats to reject alcohol, and to become hypersexual, Campbell, 1970). The dream process involves greater conductivity through the head, whether it happens during sleep or when awake (my unpublished observations). This suggests that it corresponds to a high efficiency "resting" state."

Serotonin: Effects in disease, aging and inflammation
"...Some recent reviews have discussed the evidence supporting the serotonin system as primarily inhibitory and protective (Anne Frederickson, 1998, Neil Goodman, 2002). Goodman describes the serotonergic system as one of our "diffuse neuroregulatory systems," and suggests that drugs such as LSD weaken its inhibitory, filtering effect. (Jacobs, 1983, 1987: by changes in the effects of serotonin in the brain, produced by things that affect its synthesis, release, catabolism, or receptor action.) LSD depresses the rate of firing of serotonergic nerves in the raphe nuclei (Trulson and Jacobs, 1979) causing arousal similar to stimulation of the reticular formation, as if by facilitating sensory input into the reticular formation (Bowman and Rand, 1980)."

In confirmation of this statements, the study below discovered that the brains of awake babies have very similar activity to adult brains while in state of dreaming and the brains of animals given LSD. Blake thought that the doors on perception are artificially kept semi-closed for cultural reasons - i.e. the ability to focus and do work for the enrichment of the powers that be. While Blake is not known to have used LSD, he stated several times that the child-like state of open/full perception can be restored by increasing exposure to novel situations and avoiding authoritarian (I think he called them "stiff") minds. Aside from LSD, other anti-serotonin chemicals also have similar effects. In my experience, while serotonin antagonists like cyproheptadine are not hallucinogenic, they also have quite a liberating effect on openness to new experiences and creative thought. Less sedating alternatives like ondansetron have also been reported in animal studies to increase cognitive ability and creative problem solving.

For Babies, Life May Be a Trip
"...But recently, neuroscientists have started to explore other states of consciousness. In research published in Nature in 2017, Giulio Tononi of the University of Wisconsin and colleagues looked at what happens when we dream. They measured brain activity as people slept, waking them up at regular intervals to ask whether they had been dreaming. Then the scientists looked at what the brain had been doing just before the sleepers woke up. When people reported dreaming, parts of the back of the brain were much more active—like the areas that are active in babies. The prefrontal area, on the other hand, shuts down during sleep."

"...A number of recent studies also explore the brain activity that accompanies psychedelic experiences. A study published last month in the journal Cell by David Olson of the University of California, Davis, and colleagues looked at how mind-altering chemicals affect synapses in rats. They found that a wide range of psychedelic chemicals made the brain more plastic, leading brain cells to grow more connections. It’s as if the cells went back to their malleable, infantile state."

"...In other words, the brains of dreamers and trippers looked more like those of young children than those of focused, hard-working adults. In a way, this makes sense. When you have a dream or a psychedelic experience, it’s hard to focus your attention or control your thoughts—which is why reporting these experiences is notoriously difficult. At the same time, when you have a vivid nightmare or a mind-expanding experience, you certainly feel more conscious than you are in boring, everyday life. In the same way, an infant’s consciousness may be less focused and controlled than an adult’s but more vivid and immediate, combining perception, memory and imagination. Being a baby may be both stranger and more intense than we think."

 

[Regina]

Direct from the OP "the brains of dreamers and trippers looked more like those of young children than those of focused, hard-working adults."
LOL Turn adults into children.

The title of this thread could also read "Adults using lsd experience life as young children.

Meanwhile the CIA is emailing Peat about what to give it's armies to rule the world by fighting super hard, get amazing sleep, and have great motivation. That ain't gonna be lsd.
More like ghb or gaba med for precise sleep, testosterone/dhea, caffeine or some type of stimulant during the day... all Peat approved.

Good luck fighting against that Peat approved stack

"the men became less urgent." Some Peaters have noted feeling less urgent since Peating. Myself included. Amazingly, more gets done.

 

[Collden]

Some of them do. See my response above discussing methysergide.

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.

Just read that one of the most reliable physical indicators of LSD use is pupil dilation, which is a well-known effect of elevated dopamine levels. I also have the impression that high-thyroid people tend to have more dilated pupils in any given context than low-thyroid people. Would make sense if there is a direct link between pupil dilation and sensory gating.

 

[Collden]

This brings up the question, can one train oneself to increase the doors of perception (i.e. reduce sensory gating) and function in society with reduced sensory gating by habituating oneself to this higher state of consciousness in everyday life? It is said that reduced sensory gating is associated with certain negative mind states such as schizophrenia, paranoia and panic attacks, but are these necessary byproducts of reduced sensory gating, or only dependent on a persons attitude and perhaps lack of experience with heightened states of awareness?

I notice that when I drink too much coffee I tend to become paranoid and hyper-aware of negative mind states, at which point I freak out and again sharply reduce coffee consumption, but is it maybe possible to habituate oneself to this reduced sensory gating and transcend it to be able to enjoy the benefits of more opened doors of perception? Is increased sensory gating merely a protective mechanism that is hyper-active in people with fearful insecure minds who have not learned to tolerate experiences out of the ordinary, or is sensory gating a more general adaptive function without which we are less able to function in a highly complex and streamlined society?

 

[LUH 3417]

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.

Just read that one of the most reliable physical indicators of LSD use is pupil dilation, which is a well-known effect of elevated dopamine levels. I also have the impression that high-thyroid people tend to have more dilated pupils in any given context than low-thyroid people. Would make sense if there is a direct link between pupil dilation and sensory gating.

But don’t people with serotonin syndrome also have dilated pupils?

 

[haidut]

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.

Just read that one of the most reliable physical indicators of LSD use is pupil dilation, which is a well-known effect of elevated dopamine levels. I also have the impression that high-thyroid people tend to have more dilated pupils in any given context than low-thyroid people. Would make sense if there is a direct link between pupil dilation and sensory gating.

Caffeine is well-known to induce hallucinations, but in very high doses that are considered toxic. It also potentiates the absorption and effects of many psychoactive chemicals and this is why it is sometimes added to the formulations sold as prescription drugs.

 

[Collden]

But don’t people with serotonin syndrome also have dilated pupils?

Looking further into it I can't really make heads or tails of this one. On the one hand dopamine is known to dilate pupils, on the other hand pupils are known to dilate in any state of heightened arousal (such as a life-threatening situation like serotonin syndrome), and dopamine is supposed to reduce physiological arousal actually.

I do believe people with high thyroid levels generally have higher sympathetic nervous system activity (since thyroid stimulates SNS), so high thyroid likely correlates with elevated basal arousal levels.

 

[zewe]

What is awake dreaming?

Nobody answered this question. Are you talking about lucid dreaming or expanded consciousness?

 

[Regina]

Nobody answered this question. Are you talking about lucid dreaming or expanded consciousness?

I'm not sure what is meant but I am often flabbergasted by how uncreative a large majority of humans are these days. I sometimes work with helping staging people's condos for sale. Everything has to be shown. You have to put a desk there (w a fake computer on it) in the second bedroom to show you can bring your laptop there. Nothing whatsoever can be left to the imagination. It's weird.

 

[zewe]

I'm not sure what is meant but I am often flabbergasted by how uncreative a large majority of humans are these days. I sometimes work with helping staging people's condos for sale. Everything has to be shown. You have to put a desk there (w a fake computer on it) in the second bedroom to show you can bring your laptop there. Nothing whatsoever can be left to the imagination. It's weird.

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!

 

[Regina]

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!

"no use for scissors when there's perforated cutouts" ggggg
Yes, it is a wolf. I got to do an intensive workshop inside the enclosure at a Wolf Park. So, only semi-wild wolves and this one was known to be a very sweet female wolf (named Ayla).

 

[Douglas Ek]

I think most drugs even if their serotonergic, dopamine or gaba agonists or a mix just primarily affects the brain patters of different states. Cocaine enhances the ego. Amphetamine slightly different probably affects motivation more than cocaine. Mdma increases how easy youll like someone. Lsd brain pattern is probably very similair to a kids because the effects is quite similair. You start thinking differently, seeing vividly etc. All of the drugs i mentioned increases both dopamine and serotonin but in different brain areas.

 

[Douglas Ek]

Looking further into it I can't really make heads or tails of this one. On the one hand dopamine is known to dilate pupils, on the other hand pupils are known to dilate in any state of heightened arousal (such as a life-threatening situation like serotonin syndrome), and dopamine is supposed to reduce physiological arousal actually.

I do believe people with high thyroid levels generally have higher sympathetic nervous system activity (since thyroid stimulates SNS), so high thyroid likely correlates with elevated basal arousal levels.

Dude mdma is supposed to be serotonergic and people who take it get the most dilated pupils ever. No drug does it like mdma.
Cocaine on the other hand doesnt even change the pupils. Even if your aroused.
Cocaine is more focus and talkative. Mdma is just a 6 hour long orgasm

 

[Herbie]

What is awake dreaming?

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.

 

[zewe]

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.

 

[lollipop]

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.

Interesting post @zewe. I appreciate how you pulled across multiple disciplines to create food for thought; especially the pineal gland connection. Will reread this post a few times. Got me thinking.

 

[zewe]

Interesting post @zewe. I appreciate how you pulled across multiple disciplines to create food for thought; especially the pineal gland connection. Will reread this post a few times. Got me thinking.

Been up all night pulling that together. My brain's smokin' and I'm not sleepy. Histamine is a waking
neuro transmitter.

My son and I are both histadelics [sic?] AND psychic. I've given that a lot of thought!

We're from the original 1% There are positives to it like type A personality, driven, perfectionist good when channeled toward worthwhile pursuits.

Sex was always great too. WAS. The dirtbags that hurt me took the steam out of that....BUT with the supplements I'm taking and work on rewiring my brain, I'm getting those feelings back.

 

[lampofred]

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.

Peat has said 5HT1 receptors are autoreceptors, meaning agonizing them actually reduces the release of serotonin. So I think the article you posted actually fully supports Peat's assertion that LSD is a serotonin antagonist, since it says that LSD agonizes 5HT1 receptors and antagonizes 5HT2 receptors. LSD also strongly increases dopamine which can explain its stimulant properties. Haloperidol can block these stimulant properties because it is a dopamine antagonist.

Not saying anything for sure, this is just an guess as to how LSD can be a serotonin antagonist like Peat says