LSD basics?

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Originally Posted by usedchemicals

one more thing: how long is the shelf life of LSD?

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i suggest rolling it up in tinfoil, then in a baggie, then in a paper bag.

things that degrade acid: heat, light, moisture.

ideal acid storing, - keep it DRY, in a dark spot, thats 55-60 degrees or lower.

you can keep it in room temperature but it will very slowly degrade... so just play it safe..

if you keep it in the right conditions it can be safe for years.

but be careful, depending on what state you live in, possession of LSD/acid can be a life sentence

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Originally Posted by justinsane

but be careful, depending on what state you live in, possession of LSD/acid can be a life sentence

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and what state is that?

The setting in which the treatment session is to be conducted must be comfortable
and quiet. Frequently the subject may feel like lying down. It is best to provide enough
chesterfields, cots or beds so that each person who has had the drug has a place to stretch
out comfortable.


The place should be quiet, not only as far as the general noise level is concerned
but particularly in terms of interruptions of intrusions of the outside world upon the
experience. Worries about getting home for supper or getting certain work done are
disruptive and all such interference should be reduced as much as possible. People
coming into the room can cause the subject to become upset, particularly from the second
to the eighth hour after he has taken the drug. If a group is to be used, all members
should be present when the experience begins. Other intrusions should be present when
the experience begins. Other intrusions should be kept to a minimum. This is more
difficult than it at first appears because LSD therapy usually catches the imagination and
provokes the curiosity of nearly all the staff members of the unit involved. Many people
will find excellent reasons to be in and out of the treatment room unless the policy of no
visitors is established.


The telephone too can be exceptionally disturbing. It is often the greatest
nuisance in a session. If the telephone is in the treatment room, the noise of its ringing is
a bother but no matter where it is, it is troublesome for the person called, whether or not
he has taken the drug, to completely alter his frame of reference such that he can conduct
a normal telephone conversation. As much as possible, telephone calls should be held
up.

At times, particularly in individual sessions, the subject may become extremely
restless or violent. At the height of this disturbed state he is apt to knock or throw things
about. For this reason it is wise to use fairly durable furnishings.


Washroom facilities should be relatively near by. It is often a severe strain on the
subject to have to walk through a ward or indeed to walk any distance under the effect of
the drug. Also, in subjects who become paranoid, the trip to the washroom offers
opportunity for them to attempt to get away from the session. ~LSD Handbook

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Originally Posted by tokinggreg

Um.. Schizophrenia is caused by an imbalance of seratonin in the brain. That fact has been known for decades.

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Depression is caused by that.....i thought. I was under the impression that there was something wrong with the brain makeup and that that's as much as they knew.

eurphoric states the exact truth.

just keep your first dose lower, maybe just 1 hit, but id suggest 2 for the start. then see where your comfortable.

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Originally Posted by ibreakthings

Depression is caused by that.....i thought. I was under the impression that there was something wrong with the brain makeup and that that's as much as they knew.

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actually serotonin really doesnt have much of an affect, and they still arnt sure what causes it

Genetic and environmental influences

While the reliability of the schizophrenia diagnosis introduces difficulties in measuring the relative effect of genes and environment (for example, symptoms overlap to some extent with severe bipolar disorder or major depression), there is evidence to suggest that genetic vulnerability and environmental stressors can act in combination to cause schizophrenia.

The extent to which these factors influence the likelihood of being diagnosed with schizophrenia is debated widely, and currently, controversial. Schizophrenia is likely to be a disorder of complex inheritance (analogous to diabetes or high blood pressure). Thus, it is likely that several genes interact to generate risk for schizophrenia. This, combined with disagreements over which research methods are best, or how data from genetic research should be interpreted, has led to differing estimates over genetic contribution.
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Genetic

Some researchers estimate schizophrenia to be highly heritable (some estimates are as high as 70%). However, genetic evidence for the role of the environment comes from the observation that one identical twin does not universally develop schizophrenia if the other one does. A recent review of the genetic evidence has suggested a 28% chance of one identical twin developing schizophrenia if the other already has it9 (see twin study).

However, the estimates of heritability of schizophrenia from twin studies varies a great deal, with some notable studies10 11 showing rates as low as 11.0%â??13.8% among monozygotic twins, and 1.8%â??4.1% among dizygotic twins.

A recent review of linkage studies listed seven genes as likely to be involved in the inheritance of schizophrenia or the risk of developing the disease12. Evidence comes from research suggesting multiple chromosomal regions are transmitted to people who are later diagnosed as having schizophrenia. Some genetic association studies have demonstrated a relationship to a gene known as COMT that is involved in encoding the dopamine catabolic enzyme catechol-O-methyl transferase13. This is particularly interesting because of the known link between dopamine function, psychosis, and schizophrenia.
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Environmental

There is also considerable evidence indicating that stress may trigger episodes of schizophrenia psychosis. For example, emotionally turbulent families14 and stressful life events15 have been shown to be risk factors for relapses or triggers for episodes of schizophrenia. In common with other forms of mental illness, abuse as a child and early traumatic experience have also been suggested to be a risk factor for developing schizophrenia later in life16 17 18, although the "bad parenting" theory of causation is now largely held in disrepute on the grounds that it overlooks the likelihood that the parental incompetences may have been a result of schizophrenia in the parents, and the disorder itself in the offspring was actually transmitted genetically from the parents.

Factors such as poverty and discrimination may also be involved in increasing the risk of having a schizophrenic episode due to the high levels of stress that these lifestyles harbor. This may explain why minority communities have much higher rates of schizophrenia than when members of the same ethnic groups are resident in their home country. On the other hand, the "social drift hypothesis" suggests that people affected by schizophrenia may be less able to hold steady or demanding, higher-paying jobs, consigning them to lower incomes thereby increasing stress levels and leaving them susceptible to lapsing into a schizophrenic episode.

One particularly stable and replicable finding has been the association between living in an urban environment and risk of developing schizophrenia, even after factors such as drug use, ethnic group and size of social group have been controlled for19. A recent study of 4.4 million men and women in Sweden found a 68%â??77% increased risk of psychosis for people living in the most urbanized environments, a significant proportion of which is likely to be accounted for by schizophrenia20.

One curious finding is that people diagnosed with schizophrenia are more likely to have been born in winter or spring21 (at least in the northern hemisphere). However, the effect is not large and it is still not clear why this may occur.
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Neurobiological influences
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Early neurodevelopment

It is also thought that processes in early neurodevelopment are important, particularly during pregnancy. For example, women who were pregnant during the Dutch famine of 1944, where many people were close to starvation, had a higher chance of having a child who would later develop schizophrenia22. Similarly, studies of Finnish mothers who were pregnant when they found out that their husbands had been killed during the Winter War of 1939â??1940 have shown that their children were much more likely to develop schizophrenia when compared with mothers who found out about their husbands' death after pregnancy23, suggesting that even psychological trauma in the mother may have an effect.

Some researchers have proposed that environmental influences during childhood also interact with neurobiological risk factors to influence the likelihood of developing schizophrenia later in life. The neurological development of children is considered sensitive to features of dysfunctional social settings, such as trauma, violence, lack of warmth in personal relationships and hostility. These have all been found to be risk factors for the later development of schizophrenia. It is thought that the effects of the childhood environment, favorable or unfavorable, interact with genetics and the processes of neurodevelopment, with long-term consequences for brain function. This is thought to influence the underlying vulnerability for psychosis later in life, particularly during the adult years.24
Data from a PET study25 suggests the less the frontal lobes activated (red) during a working memory task, the greater the increase in abnormal dopamine activity in the striatum (green), thought to be related to the neurocognitive deficits in schizophrenia.
Data from a PET study25 suggests the less the frontal lobes activated (red) during a working memory task, the greater the increase in abnormal dopamine activity in the striatum (green), thought to be related to the neurocognitive deficits in schizophrenia.
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Role of dopamine

In adult life, particular importance has been placed upon the function (or malfunction) of dopamine in the mesolimbic pathway in the brain. This theory, known as the dopamine hypothesis of schizophrenia, largely resulted from the accidental finding that a drug group which blocks dopamine function, known as the phenothiazines, reduced psychotic symptoms. These drugs have now been developed further and antipsychotic medication is commonly used as a first line treatment.

However, this theory is now thought to be overly simplistic as a complete explanation, partly because newer antipsychotic medication (called atypical antipsychotic medication) is equally effective as older medication (called typical antipsychotic medication), but also affects serotonin function and may have slightly less of a dopamine blocking effect. Psychiatrist David Healy has also argued that pharmaceutical companies have promoted certain oversimplified biological theories of mental illness to promote their own sales of biological treatments.26
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Role of glutamate and the NMDA receptor

Interest has also focused on the neurotransmitter glutamate and the reduced function of the NMDA glutamate receptor in the development of schizophrenia. This theory has largely been suggested by abnormally low levels of glutamate receptors found in postmortem brains of people previously diagnosed with schizophrenia27 and the discovery that the glumatate blocking drugs such as phencyclidine and ketamine can mimic the symptoms and cognitive problems of associated with the condition.59 The fact that reduced glutamate function is linked to poor performance on tests requiring frontal lobe and hippocampal function and that glutamate can effect dopamine function, all of which have been implicated in schizophrenia, have suggested the glutamate hypothesis of schizophrenia as an increasingly popular explanation.28 Further support of this theory has come from trials showing the efficacy of molecules, which are coagonists at the NMDA receptor complex, in reducing schizophrenic symptoms. The precurosrs D-serine, glycine, and D-cycloserine all enhance NMDA function through the glycine modulatory site. Several placebo controlled trials have shown a reduction mainly in negative symptoms with high dose therapy.60 Currently type 1 glycine transporter inhibitors are in late-state preclinical for the treatment of schizophrenia. They increase glycine concentrations in the brain thus causing increased NMDA receptor activation and a reduction in symptoms.61
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Anatomy and Physiology of the brain

Much recent research has focused on differences in structure or function in certain brain areas in people diagnosed with schizophrenia.

Early evidence for differences in the neural structure came from the discovery of ventricular enlargement in people diagnosed with schizophrenia, for whom negative symptoms were most prominent29. However, this finding has not proved particularly reliable on the level of the individual person, with considerable variation between patients.

More recent studies have shown a large number of differences in brain structure between people with and without diagnoses of schizophrenia.30 However, as with earlier studies, many of these differences are only reliably detected when comparing groups of people, and are unlikely to predict any differences in brain structure of an individual person with schizophrenia.

Studies using neuropsychological tests and brain imaging technologies such as fMRI and PET to examine functional differences in brain activity have shown that differences seem to most commonly occur in the frontal lobes, hippocampus, and temporal lobes31. These differences are heavily linked to the neurocognitive deficits which often occur with schizophrenia, particularly in areas of memory, attention, problem solving, executive function and social cognition.

Electroencephalograph (EEG) recordings of persons with schizophrenia performing perception oriented tasks showed an absence of gamma band activity in the brain, indicating weak integration of critical neural networks in the brain.32 Those who experienced intense hallucinations, delusions and disorganized thinking showed the lowest frequency synchronization. None of the drugs taken by the persons scanned had moved neural synchrony back into the gamma frequency range. Gamma band and working memory alterations may be related to alterations in interneurons that produced the neurotransmitter GABA. Alterations in a subclass of GABAergic interneurons which produce the calcium binding protein parvalbumin have been shown to exist in the DLPFC in schizophrenia. 33
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Incidence and prevalence

Schizophrenia is typically diagnosed in late adolescence or early adulthood. It is found approximately equally in men and women, though the onset tends to be later in women, who also tend to have a better course and outcome.

The lifetime prevalence of schizophrenia is commonly given at 1%; however, a recent review of studies from around the world estimated it to be 0.55%34. The same study also found that prevalence may vary greatly from country to country, despite the received wisdom that schizophrenia occurs at the same rate throughout the world. It is worth noting however, that this may be in part due to differences in the way schizophrenia is diagnosed. The incidence of schizophrenia was given as a range of between 7.5 and 16.3 cases per year per 100,000 population.

Schizophrenia is also a major cause of disability. In a recent 14-country study35, active psychosis was ranked the third most disabling condition after quadriplegia and dementia and before paraplegia and blindness.