Cloudscape

Hypomimia, or lack of mimic, is not specific to mental conditions such as schizophrenia or autism, but rather is a defense mechanism all of us have to some extent, which we may use instinctively against people we do not trust, in which case it is safer not to show our emotions. Because people such as schizophrenics often hardly trust anyone, it is therefore obvious that they seem to lack mimic altogether.

 

It is because of the irresponsibility of the illicit drug black market that drugs have been made illicit; but in doing so, the government has refused to take on responsibility for these drugs, and left it to the masses. In this, they only gave the illegal drug industry an advantage, whereas if they took drug industry in their own hands in a responsible way, illicit drug industry would cease to be attractive to users. Since users would therefore be better informed and guided about their drugs, this would probably result in an actual decrease in the abuse of illicit drugs, so that drug use would lead to less addictions, overdoses, and side-effects such as brain damage.

All use of drugs should therefore be monitored by a psychiatrist, unless or until the subject is deemed sufficiently responsible to use them independently; in this case, the subject could receive a license, the allocation of which would be based on the psychiatrist's assessment of the individual's prudence and knowledge. Without this license, the use of the drug should be prohibited. Police officers could take action if they see that someone uses a drug in an irresponsible way, as they can in the case of alcohol. Whenever they know that someone has used a drug they can ask their license, even if the drug is alcohol (in the case of alcohol, however, this would only be done in obviously high dosages, as alcohol is otherwise used far too frequently). In doing so, it is important that, should they have used hallucinogens, they do not do this in an aggressive way.

If someone is caught using a drug without license, the penalty depends on the nature of the drug. If, by taking the drug without license, they might cause harm to others, they are penalized for that risk. Such risk to others would usually be seen in the case of addiction, such as to cocaine or alcohol. If they cause no significant risk to others in taking the drug, for instance in the case of marijuana, they receive no penalty for this. However, they are encouraged, in either case, to see a psychiatrist to guide their use of the drug. In the case of drug addiction, they could even get reduction in costs as any other mental patient (that is, in countries where such reductions occur), since DSM-IV recognizes drug addiction as a mental illness.

However, they could receive a penalty for buying their drugs from the black market, as they thereby support their dealers and so indirectly harm others by encouraging them to further deal drugs; not only do they thereby encourage their dealers to continue dealing, but they might also encourage others to buy from them. The subject is promptly interrogated (as soon as the drug has worn off, of course) about where he got the drugs, and if he can remember his dealer's face, this may also prove useful in finding him.

The foremost role of the psychiatrist would be to educate the subject about the substance, not to decide whether or not they should use it; if they educate them correctly, the subject will be able to decide for themselves whether they should use it or not. The only exception is that in their use of the substance, they do not harm anyone else, as they cannot decide for the others they might pose a danger to. Disorders such as schizophrenia and psychopathy are therefore possible contraindications.

Legal conditions of use should be a responsible set and setting: if usage results in dangerous psychotic behavior which may be harmful to themselves or others, this is a sign that they have not made responsible use of it, either because they have used it without a license or because the psychiatrist has misjudged their responsibility. Dangerous behavior while under influence of a substance will result in a retraction of their permit for the particular class of that substance, just as dangerous driving may result in a retraction of one's driving license.

The police officers may, if qualified to do so, administer an antipsychotic to sedate someone under influence if they are using it in an irresponsible way (something which can also be useful in other cases of dangerously psychotic behavior). Usually, punishment will be unnecessary because the negative experience will be the most efficient way of discouraging anyone from using the drug in an unpremeditated way; rather, the abuser should be incited to see a psychiatrist; an exception is when the user is driving or handling a mechanical device. Since this need not be associated with a negative experience, it is best to impose a sanction on the user either how, upon which the user should be escorted back home.

In doing so, however, the police officer must be warned to be as respectful and careful as possible, lest the sanction itself will lead to a negative experience. In the case of psychedelic, this can be a traumatizing experience, so it is quite out of place to do cause a negative experience as a punishment; to do this, as well, should be punishable, whether the person who caused the negative experience is a police officer or anyone else. It can be very difficult to judge, however, if the negative experience was in effect caused by the person in question, as this can be very subtle. This can be a conundrum for trials, but the same is true for bullying, which in some countries is nonetheless punishable.

A permit for substances is especially important for hallucinogens. Because different classes of substances will have different levels of risks, such permits should, obviously, be subdivided into several classes. The endowment of such permits should not be taken lightly, as they enable a person to make use of a substance without any supervision by a psychiatrist at all. This requires the person to have a profound knowledge of the possible risks or side effects of the drugs and the dosages at which these may occur, as well as a proper judgment of these facts: for instance, people who are suffering from mania, dissociative identity disorder or orbitofrontal dementia, should not be given such a license. For some substances, such permits would be exceedingly rare, and might even require an extensive course on the substance in question. Importantly, such a license might be temporary, or otherwise provide further specifications about the place, time, or other circumstances in which the substance in question should be used.

Some licenses would be easier to obtain than others, based on the possible dangers associated with them. Some substances, like tobacco, would require no license at all, and the user would be trusted to be courteous in when to use it or not. If there would be one, a license to alcohol would require only limited assessment or more likely none at all, but it could be taken from them, for instance, in the case of binge drinking, alcoholism or drunk violence. In the case of drunk driving, it makes more sense not only to take the driver's driving license but also their drinking license. Since people will be forced to drive back home anyhow after they've drunk alcohol, it's better to just forbid them drinking alcohol.

If such law was indeed introduced for alcohol, it would be best to distribute the licenses for alcohol freely at first, lest no one would pay heed to it; later, they might be issued with one's passport. What is most important is that the license can be taken from people who engage in dangerous behavior whilst drunk, much like a driving license.

The problem with the use of drugs is not that the user might harm themselves, but that they might not be aware that they are doing this. As long as they are aware of the damage they might be causing themselves, they are free to do so if they deem the experience of the substance to be worth it. After all, if they will harm themselves, they will already be punished, and if the risk of harming themselves will not be enough to discourage them from irresponsible use, then neither will the risk of punishment.

As long as one does something only to oneself and one knows what one is doing and really wants it, one should be free to proceed. The greatest danger is that a user might underestimate the addictive nature of some substances. However, if all drugs would be legal, after all, drug addiction could be much easier to treat, since drugs such as ibogaine and other psychedelics have proven to be effective in the treatment of drug addiction. Moreover, people who are addicted to an illicit drug will be unlikely to seek help for their addiction, either because they would not trust their doctor to keep it secret, or because others might find out why they see their doctor. If the drug is licit, not only does treatment of addiction become far more evident, but so does social support.

If even the most dangerous and addictive drugs are made legal under psychiatric supervision, they automatically become less dangerous: they are less likely to be contaminated with other, sometimes toxic substances; they are less likely to be administered with unsterile needles, which may transmit disease; they are less likely to lead to addiction, and when addiction occurs, it will be less likely to remain untreated; most important of all, the user will be fully aware of the dangers.

If one can use a drug safely and legally by simply regularly consulting a psychiatrist, one will be very likely to do so rather than to resort to an unsafe and illegal black market. What the individual needs is guidance, not enforcement; as we know from experience, enforcement seldom works.

While the dangers of drugs must be dealt with, it is also important that the benefits of drugs are exploited. Doing so can save many lives from various conditions. It is known that many psychoactives could have invaluable applications in medicine, psychiatry, psychotherapy and even the self-development of the healthy individual. Some psychedelic drugs, in a

can offer a dramatically effective treatment for depression, anxiety disorders, obsessive-compulsive disorder, alcoholism, drug addiction, cluster headaches, and even schizophrenia, where any other kind of therapy has failed. It is therefore inhumane to forbid the medical use of these substances. Doing so condemns millions of innocent people to unnecessary suffering and even suicide, and it can therefore not be represented as anything less than murder.

It is, moreover, especially important for the use of psychedelics to be legitimized under psychiatric supervision so that they would not be used without. The greatest danger associated with psychedelics are caused by the irresponsible way they are used. If they were used only under the supervision of a psychiatrist, this danger would be dealt with decisively. Psychiatrists know the effects of the drugs, which dosage is best administered, and what mindset their subject has; most important of all, they are armed with anxiolytics and antipsychotics in case the subject would react adversely to the drug, such as by a panic attack.

This is especially important, of course, for people who would use psychedelics as a treatment for mental illness, as this is an extremely delicate matter best left to a psychiatrist. A psychiatric setting would offer complete safety for the subject, as the notorious "bad trips" would never have to occur. People have had severe psychological damage from bad trips which would otherwise not have occurred had they been supervised by a psychiatrist, similar to post-traumatic stress disorder. Users of some heavier psychedelics such as DMT have reported having had panic attacks for several years after a negative experience, and some were even hospitalized with psychosis (though this usually lasted only a few days). Moreover, some people have killed or injured themselves during a negative experience, both accidentally and intentionally; if nurses are nearby which can administer an injection of thorazine or benzodiazepine, or in the worst (highly unlikely) case, use a straitjacket, this cannot happen.

Another possible problem with some psychedelics, including THC found in cannabis, occurs when they are used in immoderate amounts or frequency. In this case, the effect of expansion of consciousness becomes excessive. The mind becomes so expanded that it becomes difficult to concentrate it, as these are two opposites. When the mind is expanded, it experiences; when it concentrates, it thinks. When consciousness becomes so expanded that it can no longer concentrate, it becomes harder to think.

The mind needs to have a flexibility between expansion and concentration, and psychedelics can help one achieve this flexibility; nonetheless, they will also generally incline the mind to expand itself more frequently than concentrating itself. Usually, this is not an issue, as in the intervening period between two uses of psychedelics, the user will maintain its powers of concentration by training them in day-to-day activities. However, if this intervening period becomes too short, the mind will have difficulty to catch up to improve its flexibility to switch back to concentration. The result, in this case, can be that the user develops cognitive problems.

This cognitive damage is, however, usually of psychological rather than neurological nature, and it is because of this that it has been found to be temporary, in contrast with the cognitive damage caused by alcohol. Two popular psychedelics which are likely to be abused, in contrast with others, are LSD and cannabis: LSD, because it can be used in extremely high dosages, and cannabis, because it causes far less tolerance. In both cases, abusers reported cognitive damage, and in both cases, recovered abusers reported recovering from this side-effect over time.

Some people have reported to have the opposite problem with nootropics, (legal) substances which increase cognition, stating that it was harder for them to experience as their increased insights crowded in on them. If so, then perhaps nootropics can be used to remedy this problem. However, it is better to avoid that these problems ever occur by not using the drugs without moderation.

In extreme cases, this effect may further escalate to cause such symptoms as "flashbacks" or HPPD, ego death or, in some cases, psychosis. Cannabis is even thought to be linked to schizophrenia, though it is uncertain if the cannabis caused the schizophrenia or schizophrenics are more likely to use cannabis. It is likely a bit of both. That this problem appears to occur mostly with cannabis is probably because unlike most other psychedelics, it can be used frequently and so has greater abuse potential.

Everything is a question of balance, and with states of consciousness as extreme as those caused by psychedelics, this balance is particularly delicate. Because of this, it is certainly possible for psychedelics to cause mental illness. Depression, anxiety, panic attacks and even psychosis may all very well occur in the case of irresponsible use. It must be noted, however, that mental illness has been caused by other practices which are normally harmless. For instance, there have been many reports of people who developed mental symptoms because of meditation, especially following retreats. In some cases, these setbacks have been very extreme, leading to, again, depression, anxiety, panic attacks or psychosis. Anything can be dangerous. Again, everything is simply a question of balance.

Although the long-term side effects of abuse for psychedelics are temporary, it is unknown if this is also so for abuse of dissociatives, another class of hallucinogens which act mostly on the NDMA receptors. Dissociatives, such as ketamine, memantine, phencyclidine and dextromethorphan, are thought to cause Olney's lesions, although for most dissociatives, this effect has been established only in rats. Nitrous oxide is known to have this effect in humans, but, at least for nitrous oxide, this effect turned out to be temporary; being a common human anesthetic, nitrous oxide is the only dissociative which can be tested on humans. This may suggest that Olney's lesions from all dissociatives are temporary. However, some heavy users have reported their brain damage lasted for several years, though it is, of course, uncertain if this was because of the dissociatives or because of other drugs they might have used in the meantime. This damage can apparently be prevented by gaba-a receptor agonists or anticholinergics. Serotonergic psychedelics and MDMA can also prevent Olney's lesions, but because the combination of any of these drugs with dissociatives is unpredictable, caution is particularly important. To a random user, it would be pure guesswork in what dosages to combine these substances, although a psychiatrist could be able to prescribe the right specific dosages.

For several reasons, most psychedelics have very little abuse potential. One is that tolerance from psychedelics forms quickly, so that after a single usage, the drug has little effect for several days. Another is that it these psychedelics do not activate the reward centers through any direct physiological action. And most importantly, the use of psychedelics can be a quite challenging activity, much like climbing a mountain or running a marathon. Users report feeling no craving to use the hallucinogen again after the effects have worn off, although they often decide yet to do so in future.

There are few drugs which are known to be completely safe, but the possibility of side-effects must not be dramatized: many drugs have been used by millions of people, and any side effects associated with them, though not scientifically established, are therefore generally known to them. Usually, the knowledge among them of the possible side effects can be relied upon, as they are based on past experiences of people, although not everyone among them has that knowledge, and not everyone among them believes it to be true.

Long-term side-effects of drugs are generally caused by a buildup of short-term side-effects, so that one may notice them as they start to appear. There is no way that after causing no short-term damage, a drug would suddenly magically start causing damage after several years, long after it has left the body, at least, not damage of a physiological nature. Therefore, if the use is supervised by a psychiatrist, he or she may decrease, suspend or discontinue use when noticing that long-term side effects are starting to build up to form actual long-term side effects. Usually, like the short-term side effects, these long-term side-effects will usually wear off in time, though they will obviously take longer to do so than the short-term side effects — unless, that is, the side-effects are of a psychological nature, but as discussed before, these could already be prevented by psychiatric supervision.

It is usually hard to research the long-term side effects of illegal drugs, because of two reasons. The first is that most people who use one illegal drug will often use another, especially if the drug in question is a hard drug. The second is that many people who use illegal drugs are already mentally unstable before using the drugs. Especially, there is an obvious inclination among people with schizoid personality disorder, schizotypal personality disorder and schizophrenia to drugs. Moreover, some people with other mental illnesses will use drugs, especially psychedelics, as a self-medication.

However, there are some drugs which can be researched without these stumbling blocks, because in certain cultures, they are both seen as normal and used separate from other drugs. These are the alkaloids used in some ancient tribes, mostly in Africa and North- and South-America: three prominent examples are ayahuasca, san pedro and peyote. Peyote is likely one of the only so-called hard drugs of which there is conclusive and compelling evidence that it is safe: comparing a group of 79 Navajos who used no alcohol or other drugs with a group of 61 Navajo members of the Native American Church who regularly used peyote, Dr. John Halpern et al. found no short- or long-term cognitive, emotional or perceptual damage among the group who used peyote, and that in fact they emotionally scored better. That they scored better emotionally may be partly because they were religious, but it also seems likely to be partly because of their peyote experiences themselves.

San pedro is very similar to Peyote, and since the primary active substance in both cacti is mescaline, it is also highly probable that mescaline itself is physiologically harmless. It must be noted, however, that psychological damage might still likely follow from these substances. The reason why no psychological damage had been found among the members of the Native American Church is because this group had learned to make use of the Peyote in a responsible way. Notably, there is a convention among them never to use it alone. The experience is normally always shared by the entire group, and is preceded by extensive ritual preparations.

In theory, almost any psychoactive can have applications in psychiatry in subjects who miss just that which the psychoactive brings about. The problem with some of these psychoactives is, of course, that they can have side effects, most notably addiction. However, if those particular psychoactives are used only rarely, this need not be a problem. Heroin, for instance, is routinely used in hospitals, where it is known as diacetylmorphine or diamorphine, to alleviate pain — as is morphine itself.

Though most therapeutic value lies in psychedelics and empathogens, in rare cases other drugs might similarly be of value. Cocaine or other stimulants could perhaps be used in the case of chronic catatonia, though this is quite speculative. Some people remain in catatonia for weeks or even months (in some cases, as in encephalitis lethargica, even years or decades). This may lead to severe complications such as thrombosis, joint symptoms and bedsores, the latter being the primary iatrogenic cause of death. Obviously, in this state, these patients are unresponsive to any form of psychotherapy, but should they first be given cocaine or other stimulants to take them out of their catatonic state, they might temporarily be more responsive to reality; ensuing treatment can then lead to long-term recovery.

In these patients, the reward centers are usually hypoactive, so that addiction is hardly an issue. Nonetheless, tolerance could eventually cause a relapse into catatonia unless the patient has been successfully treated by then. One must be very careful with these cases, however, as in many of these patients, a too-high dosage might trigger psychosis or cause an aggravation of already extant psychotic symptoms. There are, on the other hand, many non-psychotic cases of catatonic schizophrenia in which cocaine might speculatively have some use. Extra caution should be paid if the catatonic patient has had made past attempts to kill or injure him- or herself or someone else, in which case the cocaine might elicit renewed attempts. However, as such cases of chronic catatonia are mostly found in mental hospitals, this would be relatively easy to control. Catatonia also occurs in some other mental illnesses, however, such as depression or autism, which is less severe and in which such treatment would not be necessary or advisory.

In the past, LSD has effectively been used by psychiatrists to treat various mental illnesses, as well as a means of self-development, until it was forbidden in 1968. Originally, it was limited to psychiatric settings; later, it was used by the general public with little responsibility. Perhaps what the government should have done then was to forbid people to use it irresponsibly, rather than to forbid its use entirely and thereby only increase its irresponsible use.

The same goes for MDMA, more commonly known as ecstasy, which was originally used to treat post-traumatic stress disorder, and some countries are currently re-evaluating this application. MDMA has also been used, generally as a self-medication, for general anxieties, and it could likely likewise be used for more specific anxieties, such as phobia, in particular social anxieties. Many people have reported becoming more sociable after using MDMA. It is not unthinkable that it could even be used to treat autism, to those who would prefer to be treated for it.

It is known that MDMA causes damage to serotonergic axons, although the original US government-sponsored research which discovered this effect had dramatically exaggerated it, stating that a single recreational dosage could cause a decrease of up to 85% serotonin function — a decrease of which it is questionable if it could be survived at all. The same research also found a link between MDMA use and Parkinson's disease, which was later found to be because the researchers had administered methamphetamine instead of MDMA. This debacle has caused the government to lose a lot of its credibility in its attitude towards drugs and in particular MDMA.

Later researchers found a far slighter decrease of just 5%, which appeared to be temporary: the brain recovered its lost axons after a period of three months or less. However, more recent research suggests that this pattern of reinnervation is abnormal, with approximate brain areas becoming hyperinnervated and more distant brain areas remaining denervated. It is, after all, more difficult for the newly sprouted axons to reach the more distant brain areas. Because of this effect, MDMA may still, after all, cause cognitive and emotional damage over time, though it is uncertain to what extent. When used infrequently, it is doubtful that this effect is significant.

It must be noted, however, that everything, no matter what is is, has side-effects of some sort. Many prescription medications have caused thousands of deaths, including some which have not been retracted from the market. Some neuroleptics, for instance, can cause neuroleptic malignant syndrome, which can cause death in 10-20%. Others can cause tardive dysphrenia, which can trigger or worsen psychosis. If psychedelics and empathogens became the new medicines in psychiatry, then perhaps there would be far less side-effects.

Compared to long-term acting drugs such as antidepressants (which work only when used long-term), short-term acting drugs like psychedelics (which work immediately upon using once) have many advantages. The most important is probably that long-term acting drugs change the individual in a purely chemical way, short-acting drugs do so instead in a psychological way. The former force one's personality to change in a particular way that is outside one's control, while the latter encourage one to change one's personality in one's own way. People who use long-term acting drugs often complain that they do not feel themselves, as though they are becoming someone else, while people who use short-term acting drugs often claim that they have finally found themselves, as though they are, instead, becoming who they really are. Drugs such as psychedelics work by giving people insight into who they are and how they can become better people, much like psychotherapy; drugs such as antidepressants, on the other hand mask who they truly are.

While most long-term acting drugs remove some quality from the individual's personality in order to add another, short-term acting drugs usually only add qualities, rarely taking any away from the individual. Many people using medicines complain that they are becoming superficial, unfeeling uncaring or uninspired. Some lose their emotions, others their creativity, their dreams or their willpower.

Mental illness has been associated with artistic abilities. 70 percent of all artists have had some mood disorder at some point. Many great geniuses had mental illnesses of some sort of other: Einstein, Da Vinci, Edison and possibly Beethoven might have been dyslectic, Dali schizotypal, Beethoven, Lord Byron, Edgar Allan Poe, Robert Schumann, Nietzsche and Newton bipolar, Oppenheimer, Kierkegard, Van Gogh, Tchaikovsky and Tolstoy and Bohm depressive; John Nash, Van Gogh, Enduard Einstein (Einstein's son) schizophrenic, Dostoevsky and Edgar Allan Poe might have had Geschwind syndrome, Leonardo Da Vinci ADHD, and the list goes on, as I omit all but the most well-known names, as well as the more speculative diagnoses. These people all had abilities which modern medications would take away from them, and there is no telling how many people today might have lost such abilities because of them. On the other hand, psychedelics would, rather than taking away these abilities to end their suffering, learn the people who have them to be able to deal with them in such way that they do not cause them as much suffering.

There is another advantage to psychedelic therapy above pharmaceutical therapy, and it is the decreased incidence of toxicity. Using a substance foreign to the body every day is likely to cause adverse reactions, but using such a substance once every few weeks, or every month or year, is highly unlikely to cause long-term adverse reactions. Most substances only damage the body after regular use. It is nonsensical to fear damage from substances which are would have to be used only rarely in therapy while many prescribed substances regularly cause damage the body, causing a wide range of symptoms both physical and, more importantly, mental.

By forbidding drugs, the government cannot shirk their responsibility over them; damage due to the drugs still occurs, and it is their duty to do something about it. Forbidding all use of these drugs is no help at all, as this only shoves the illegal drugs aside to the black market.

The reason why drug use is not licensed in psychiatric settings, though it could solve the greater part of the problems caused by drugs, is that the drug law isn't meant to protect the individual but to enforce norms. Drugs are forbidden because they are taboo, not because they can be dangerous. Society demonizes anything that does not conform to it, and it is therefore not surprising that they punish it.

In schizophrenia, severe chronic stress resulted in the failure of the individual's coping mechanisms; she or he loses courage to face his difficulties and therefore to care for her- or himself. In other words, the ego dissolves. Practical thought becomes reduced because the individual has lost the will to concern her- or himself with it. Not finding safety in reality, the individual is then forced to flee into unreality, leading to psychosis.
What remains is simple experience, be it of a sensory nature (i.e. sensations) or abstract (i.e. imagination). No longer having the will to filter perceptions of practical value from those without, perceptions that are normally filtered at once become more prominent. This is referred to as decreased latent inhibition. Perceptions that are normally unconscious encroach upon the conscious, while normally conscious (practical) perceptions become unconscious.
Because the individual's awareness is partly transferred from the practical thought which usually accounts for a large part of our mental processes to experience, this may lead to a state of expanded consciousness. While this may be experienced as pleasant at times, as the illness progresses it becomes so inescapable that it becomes horrifying.

A. A Comparison between Schizophrenia and Autism

Although there is some similarity in the symptoms between schizophrenia and autism, there is also a dichotomy in their causes: schizophrenics are thought to have a lack of glutamate function, while autistics are thought to have an excess. Glutamate is implicated in latent inhibition, the blocking of seemingly irrelevant stimuli. Autistics will only assimilate stimuli which are most relevant to them, while schizophrenics will be flooded by an overflow of irrelevant stimuli.
Obviously, latent inhibition impairs concentration, but it also enhances abstract thought. This is why autistics can’t think abstractly, while psychotics think too abstractly, so that they both have trouble communicating with others. In autistics, high latent inhibition may also lead to fear of novelty, obsessive-compulsive behavior, and lack of imagination, while in schizophrenics, low latent inhibition may also lead to delusions, paranoia, and thought disorder.
Glutamate decreases serotonin, modulates dopamine (increases dopamine in some areas and decreases it in others), increases acetylcholine, decreases noradrenaline, and decreases melatonin - these changes are all found in autism except for increased acetylcholine, which is decreased - in schizophrenia, the exact opposite of the effects of glutamate are seen except for increased melatonin. Autism and schizophrenia may be considered to have opposite chemical causes, even though many of their symptoms seem similar. Autism could potentially be treated by glutamate antagonists, just like schizophrenics are treated by glutamate agonists (atypical antipsychotics).

B. More on Schizophrenia

Psychotic depression, a relative of schizophrenia, has a neurological pathology which is very similar to that of schizophrenia, but in a milder version . Psychotic depression, like schizophrenia, is characterized by delusions, paranoia, and often hallucinations. Both schizophrenic and psychotically depressed people often hear voices, which will either judge them or order them. In psychotic depression, these will always be persecutory, while in schizophrenia, they may sometimes seem benevolent. In both, these may criticize the patient or tell him or her to commit suicide.
Both syndromes are caused primarily by a combination of stress and diathesis, although the diathesis (the genetic and neurological susceptibility to suffer from a condition) is usually more pronounced in schizophrenia than in psychotic depression. Both syndromes are caused primarily by a combination of stress and diathesis, although the diathesis (the genetic and neurological susceptibility to suffer from a condition) is usually more pronounced in schizophrenia than in psychotic depression. Schizophrenia can therefore be interpreted as a severe form of psychotic depression. The hallucinations and delusions that characterize is are either a manifestation of stress (eg thinking that the entire world is against the patient, or hearing voices which criticize the patient or encourage him or her to commit suicide) or, conversely, as a defense mechanism against it (eg thinking that one is sent for a mission or an imagined friend).
All symptoms of schizophrenia are a manifestation of stress, even though stress that induces schizophrenia in one person needn’t do so in all people. However, all people have susceptibility to schizophrenia, each having a different threshold of stress needed to cause it. This threshold may or may not be altered by other factors such as substance, but it is inherently there in each of us.
Research has shown that chronic stress leads to an increase of serotonin and noradrenaline and a decrease in glutamate, which are all seen in schizophrenia. Thus, one could say that anyone who suffers for a long time will become slightly schizotypal, although this is usually in such a mild form that it is not psychotic. Psychosis is still so common not only because evolution has preserved it, but also because it is not fully evolutionary.

In schizophrenia, imagination and reality merge. It is as if their dreams impinge on their waking days, which is why schizophrenics have less dream recall. This may be attributed to a disruption in the circadian biorhythm: normally, we can only distinguish imagination from reality when awake, but not in our sleep. One could say that all of us are schizophrenic, but our schizophrenic episodes are all restricted to our sleep. This could be why chronic insomnia can lead to psychosis, something sometimes seen in the manic episode of bipolar disorder. And while mania is associated with elevated glutamate, manic psychosis as well as schizophrenia are associated with reduced glutamate.
Glutamate is a neurotransmitter which enables us to distinguish imagination from reality, but schizophrenics have a deficit of this neurotransmitter. Normally, glutamate cycles from day to night, but in schizophrenics, this cycle is disrupted. The glutamate is one of the neurochemicals involved in the day-night cycle, its rhythms not only caused by but also causing it , which is why administration of glutamate may increase both wakefulness and sleep . During sleep, glutamate is normally counteracted by adenosine , which triggers, so to say, healthy nighttime psychosis.
We are all somewhat mad, but our madness usually occurs only in sleep: our insanity is usually safely relegated to our dreams. Although dreams have many more functions, they can also be said to be a deposition of psychosis. Arthur Schopenhauer said that "Dreams are brief madness and madness a long dreams.” Actually, it may be that dreams and madness have the same duration, but occur respectively during night and day - in psychosis, the order is reversed.
The involvement of adenosine in the day-night cycle also explains why adenosine agonists can alleviate the symptoms of schizophrenia and why caffeine, an adenosine antagonist, worsens positive symptoms of schizophrenia . Although an acute administration of adenosine will cause a short-term decrease in glutamate, more chronic administration will cause an amplification of the glutamate rhythms. This is so because the adenosine agonist will have more effect if more adenosine is present. This principle applies to for every neurotransmitter: any neurotransmitter agonist will have more effect if it has more of the neurotransmitter to act upon.
Possibly, schizophrenia may largely be attributed to anomalies in circadian rhythms. In schizophrenia, this cycle is disrupted, so that restoring this cycle might reduce the symptoms of schizophrenia. Ironically, by by treating its nighttime symptoms, we may also be able to treat the daytime symptoms of schizophrenia. This is also one reason why melatonin has proven useful in the treatment of schizophrenia: melatonin is one of the most important chemicals involved in the biological clock. Melatonin is dubbed the “sleep hormone,” and low levels have been observed in schizophrenia as well as in depression. In addition to the voices, this is also a reason why schizophrenia have trouble sleeping. Furthermore, there is evidence that melatonin potentiates glutamate transmission.
An insufficiency of glutamate could cause both positive and negative symptoms, which are respectively delusions, paranoia, hallucinations, and thought disorder, and apathy, blunted affect, anhedonia (lack of pleasure) avolition (lack of will), alogia (saying little), and hypomimia (lacking mimic). The cooccurrence of these symptoms seems paradoxical because positive symptoms are caused by an excess of dopamine, and negative symptoms are caused by a shortage of dopamine. This apparent contradiction is resolved by the fact that glutamate is self-modulatory, meaning that the increase of glutamate in one brain area will cause a decrease of glutamate in another. As glutamate increases dopamine levels, this will likewise affect dopamine throughout the brain. This is clearly illustrated in how increased dopamine is found in the striatum and MPOA in schizophrenia, which is an effect caused by increased glutamate. The dichotomy of positive and negative symptoms in schizophrenia is proportional to the imbalance of glutamate.
The lack of dopamine in some brain areas which ensues from lack of glutamate can set in motion a vicious circle consisting of two separate cycles, together leading to the positive and negative symptoms of schizophrenia. These cycles may occur as follows. (Mentioned symptoms may or may not be present, according to severity and type of schizophrenia.)

1) In brain areas where glutamate is decreased:

- glutamate ↓
NEUROLOGICAL:
→ dopamine ↓
NEUROLOGICAL:
→ GABA ↓
→ glutamate ↓
→ serotonin ↑
PSYCHOLOGICAL:
→ anhedonia
→ motor retardation
→ acetylcholine ↓
NEUROLOGICAL:
→ serotonin ↑
→ noradrenaline ↑
→ dopamine ↓
PSYCHOLOGICAL:
→ attention / concentration ↓
→ GABA ↓
NEUROLOGICAL:
→ serotonin ↑
→ noradrenaline ↑
PSYCHOLOGICAL:
→ hallucinations
→ anxiety
→ insomnia
→ serotonin ↑
NEUROLOGICAL:
→ glutamate ↓
→ acetylcholine ↓
→ GABA ↓
→ noradrenaline ↑
PSYCHOLOGICAL:
→ blunted affect
→ noradrenaline ↑
PSYCHOLOGICAL:
→ blunted affect
→ dissociation
→ inhibition
PSYCHOLOGICAL:
→ blunted affect
→ attention / concentration ↓
→ latent inhibition ↓
→ thought disorder
→ hallucinations
→ delusions
→ avolition
→ apathy

2) In brain areas where glutamate is increased:

- glutamate ↑
NEUROLOGICAL:
→ dopamine ↑
NEUROLOGICAL:
→ melatonin ↓
→ GABA ↑
→ glutamate ↑
→ serotonin ↓
PSYCHOLOGICAL:
→ obsessive-compulsive disorder
→ latent inhibition ↓
→ thought disorder
→ hallucinations
→ delusions
→ acetylcholine ↑
NEUROLOGICAL:
→ serotonin ↓
→ noradrenaline ↓
→ dopamine ↑
PSYCHOLOGICAL:
→ blunted affect
→ ACTH ↑
PSYCHOLOGICAL:
→ anxiety
→ GABA ↑
NEUROLOGICAL:
→ serotonin ↓
→ noradrenaline ↓
PSYCHOLOGICAL:
→ auditory hallucinations
→ blunted affect
→ serotonin ↓
NEUROLOGICAL:
→ glutamate ↑
→ acetylcholine ↑
→ GABA ↑
→ noradrenaline ↓
PSYCHOLOGICAL:
→ paranoia
→ obsessive-compulsive disorder
→ anxiety
→ noradrenaline ↓
PSYCHOLOGICAL:
→ attention / concentration ↓
→ memory ↓
→ melatonin ↓
PSYCHOLOGICAL:
→ insomnia
→ anxiety
→ depression
PSYCHOLOGICAL:
→ anxiety

GABA, or gamma-aminobutyric acid, may have an important yet little recognized role in schizophrenia. GABA is implicated in the auditory pathways, and most hallucinations in schizophrenia are auditory. Also, it modulates latent inhibition : both an increase and decrease of GABA reduces it, which is why benzodiazepines, which act on the GABAA receptors, are weakly hallucinogenic. Moreover, withdrawal of Zolpidem, a benzodiazepine, may lead to both auditory and visual hallucinations. In schizophrenics as well as in people withdrawn from benzodiazepines (which can lead to delirium tremens) GABA receptors are decreased.

Psychiatry and psychology are just two ways of looking at the same phenomenon - the human mind. Emotions aren’t caused by chemicals, and those chemicals aren’t brought about by emotions, either: these chemicals were our emotions. Neurochemistry and psychology were just two facets of our emotions, not two distinct causes of our emotions.
The bidirectional causal relationship between emotions and chemical reactions has been a mistake psychologists and psychiatrists have made for many years. It’s not so that some depressions are caused by chemical imbalances and some are caused by emotional complexes - all depressions are caused by both, because one leads to the other. When one’s neurochemistry is influenced, so are one's thoughts - after all, our thought processes are neurochemistry.
Anyone can increase his levels of neurotransmitters through sheer concentration, in this way energizing oneself. In this way, one could also increase one’s motivation, although this in turn required motivation, so that this is, like all emotions, something which amplifies itself. Furthermore, increasing one's motivation makes one's life more stimulating, which increases motivation and so on - the opposite is also possible, a vicious circle which can lead to depression.