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Recreational drugs and nootropics


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#1 Exile

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Posted 29 December 2002 - 11:28 AM


Can any recommend nootropics that can be administered to reliably counter the negative effects of recreational drugs like:

cannabis
LSD
XTC
GHB/GBL
Psilocybin


Can any nootropics that have pleasurable/recreational/enchancing effects be recommended?


I have experimented with a variety of "research chemicals" which include:

2 C-B experiences (this chemical was once legal in the UK).

DPT (N,N-dipropyltryptamine) experiences

5-MEO-DIPT experiences

GBL experiences (gamma-butyrolactone)

GHB experiences (legal until 2003)

Zolpidem experiences (legal until 2003)

Salvia Divinorum experiences (illegal in Australia)

Melatonin experiences

Sun Opener (aka Heimia Salicifolia aka Sinicuichi)

Mushroom (Psilocybin) experiences (note, fresh mushrooms are legal in the UK, so long as they aren't dried and stored.)




The results can be found, along with further resources, here:

http://www.noumenal....iles/drugs.html



Exile

#2 LifeMirage

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Posted 29 December 2002 - 07:08 PM

cannabis
LSD
XTC
GHB/GBL
Psilocybin

Most True Nootropics will protect you (to some extend) from damage. Vasopressin will help the most with cannabis.

GHB is a natural dietary supplement it has no side effects as long as it is pure and you do not take large amounts or mix it with other drugs.

Deprenyl for me has the most /enchancing effect.

Sceletium tortuosum from http://www.sceletium.com/ I've tried with good results in the pleasurable/recreational area, but it is not a nootropic.

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#3 Guest_Guest_*

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Posted 31 December 2002 - 10:37 PM

OUt of the list of rec drugs above I think GHB/GBL by far has the worst withdrawal symptoms. Best to stay away from that stuff.

#4 LifeMirage

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Posted 01 January 2003 - 12:32 AM

Apparently you have never tried pure GHB or researched it. It has no withdrawal syptoms because it is not a drug nor is it addictive. Please do some research before posting.


GHB/ ALCOVER®

Genetika® only contains powdered Sodium Oxybate or Na-GHB. This leaflet is of the liquid Na-GHB called Alcover( which is no longer manufactured. It is presented because there is no leaflet with the Genetika® product. Please note however that 1ml of Genetika is equal to 350mg of GHB.

Chemical:
Sodium Oxybate (GHB- Gamma Hydroxybutrate)-Alcover contains 24.5 grams of SO in 140ml syrup. Alcover is a product to be taken by mouth, its main agent is sodium gamma-hydroxyl-butyrate, which is used in the treatment of alcohol withdrawal crisis. The active principal is a normal component of the central nervous system. It is found at the Brain level in concentration varying between 1.78 nM/g in rats and 4.1 nM/g in guinea pigs.

Information for the User:
Alcover is a coadjutant in the following treatments. Control of ethyl alcohol syndrome - In the primary phase of multimodal treatment of alcohol dependence - In the prolonged treatment of cases of alcohol dependence resistant to other therapeutic defenses, in which other pathologies are aggravated by the consumption of ethyl alcohol.

Contraindications:
Do not take Alcover- - If you are pregnant, or think you are pregnant, if you are nursing, or if you suffer from serious organic or mental disorders, since the short and long term effects of Alcover on such physiopathological conditions are as yet unknown. - If you suffer from epileptic disorders or epileptic related convulsions, so as to avoid a possible intensification of the sedative effect of the anti-epileptic medication. - In the case of progressive or actual drug dependence, so as to avoid the risks of voluntary overdose and of the pharmaco-toxicological synergism present in such pathological states, not compatible with the multiple consumption of psychoactive substances and the compulsion to increase the dose. - Individual hypersensitivity to the product

Side Effects:
Clinical research has shown that the only frequent side effects are a “subjective dizziness” that often accompanies the first treatment. Such sensations disappear on their own after the first 15 to 30 minutes and do not re-occur in subsequent dosages. There have also been cases in which this medication has been known to provoke nausea.


Special Precautions Regarding the Use of this Product:
Alcover is a product of the utmost reliability. Nether the less, and as with all medication, certain precautions should be taken. Above all, Alcover should only be taken under a doctor’s supervision. It should also be kept out of reach of small children. In the event that the patient suffers from mental deterioration and serious compulsion with regard to ethyl alcoholism, and thus a diminished capacity and desire to understand the situation, and is thus exposed to the risks of overdose and acute intoxication, it’s administration should be delegated to one particular person.

Directions for Use:
In the therapeutic control of ethyl alcohol abstinence syndrome and during the initial phase (the first 60 days), of the multimodal treatment of alcohol dependence, the usual dosage is 50mg per day to be taken in three separate doses- Morning- Afternoon and Evening. For the prolonged multimodal treatment of alcoholic dependence (following the first 60 days)- the most effective posology varies between a minimum of 50mg per day and a maximum of 100mg per day, to be taken also in three separate doses- Morning- Afternoon and Evening.

Length of the Therapeutic Cycle:
7 days in the control of ethyl alcohol abstinence syndrome - 60 days in the initial multimodal treatment for alcohol dependence and longer than 60 days in the case of prolonged treatment.

Medical Interactions:
Because of the possible synergetic effects when used with anti-epileptic drugs and psychoactive substances, the simultaneous use of the two substances is to be avoided.

In the Case of Overdose:
In the event of overdose, the medication essentially causes a depressive action on the central nervous system, resulting in a possible state of confusion and respiratory difficulty. Emergency treatment- Respiratory assistance and increased diuresis. Antidote, the above mentioned action is remedied by gastric lavage.

#5 LifeMirage

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Posted 01 January 2003 - 12:36 AM

Discover The Regenerative Effects of GHB, the Elixir of Life!
By James South MA

GHB (Gamma-Hydroxybutyric Acid) is a hydroxylated form of the short-chain fatty acid. GHB is also closely related to GABA (Gamma-Aminobutyric Acid), the chief inhibitory neurotransmitter of the mammalian nervous system.

GHB was first synthesised in 1960 by H. Laborit, a French physician. Laborit was interested in studying the action of GABA in the nervous system, but GABA was known to be unable to cross the blood-brain barrier. Laborit hoped that by adding a hydroxyl (OH) group to butyric acid, the resulting molecule-GHB-would be protected from being destroyed by beta-oxidation (the process by which cells 'burn' fat), would cross the blood-brain barrier, and then serve as a precursor to GABA once in the brain. (1).

However, GHB turned out to be pharmacologically distinct in many of its actions from GABA, even though later research showed that GABA and GHB are interconvertible in the brain through a common metabolite- Succinic Semialdehyde (SSA). (2,4).

Somewhat surprisingly, in 1963 Bessman and Fishbein first reported GHB to be a naturally occurring molecule in the brain, and by 1970 the work of Roth and Giarman had proven conclusively that GHB is a normal, natural brain metabolite. (3),

It is now known that 0.08% to 0.16% of whole brain GABA is normally converted to GHB each minute. (4). And in a 1992 'mini-review' of the significance of GHB in the brain, G. Tunnicliff concluded: "There is little doubt that GHB is not merely a by-product of GABA metabolism.

Clearly it has distinct neuro-physiological and pharmacological actions, many of which are undoubtedly the result of the activation of specific GHB receptors.... The evidence is fairly substantial that GHB plays a role in the functioning of the central nervous system, perhaps as an inhibitory transmitter acting on dopaminergic neurons.... The ...actions of GHB make it a viable candidate as a neurotransmitter or neuromodulator in the CNS." (5).

Also somewhat surprisingly, research has shown that GHB is naturally present in kidney, heart, skeletal muscle, and brown fat, often at levels 10 to 20 times higher than whole brain GHB levels. (2,4).

In his detailed 1989 review of GHB as an endogenous regulator of energy metabolism, pioneer GHB researcher M.Mamelak stated: "Clinical and experimental work indicate that GHB can protect both central and peripheral tissues from the damaging effects of hypoxia or excessive metabolic demand.... GHB could function naturally to regulate cell activity when metabolic energy is in short supply." (4).

GHB has been the subject of hundreds of published scientific papers since 1960 (see the bibliographies in references 4 and 6). GHB is a legal drug in various European countries, including France and Italy, where it has been in clinical use since the early 1960's. It has been widely used as an anaesthetic- Laborit summarized the anaesthetic benefits of GHB in 1964, based on 6000 (!) case-reports. (1). GHB is also used to treat alcoholism, alcohol withdrawal syndrome, opiate addiction and opiate withdrawal syndrome. (7,27-29).

GHB has also proved useful in obstetrics. (8). GHB is also used in Europe to treat narcolepsy, a serious and disabling sleep disorder, as well as insomnia. (7). Yet in spite of the mere 40-year history of safe clinical and experimental use of GHB, in November 1990 the U.S. Food and Drug Administration (FDA) declared-through a press release-that GHB was an 'illegally marketed drug', and claimed that it was a danger to public health.

Since the U.S. Dietary Supplement Health and Education Act of 1994 (DSHEA) in effect classified GHB as a dietary supplement, not to be regulated only as a drug, and because the FDA had not bothered to legally classify GHB as a drug before DSHEA, the FDA has now backed off its claims that GHB is illegal at the federal level in the U.S. Instead, the FDA has orchestrated a campaign to get the various U.S. states to declare GHB an illegal drug, since DSHEA does not operate at the state level.

The FDA's smear-and-fear, disinformation and demonization campaign has been based in significant part on a brief 1992 paper by California medical bureaucrats Chin, Kreutzer and Dyer that claimed "The drug GHB is a substance with documented clinical actions consistent with severe neurotoxicity."

It is therefore necessary to look closely at the clinical and experimental record of GHB to ascertain if there is any documented evidence or general consensus of GHB as a "severe neurotoxin."

When scientists wish to determine the relative safety of a drug or nutrient, they perform experiments to establish a substance LD50. This is the amount of the substance (lethal dose) necessary to kill 50% of the test animals. The LD100 is the lethal dose that kills 100% of the test animals.

In his 1964 GHB review, Laborit reported: " In rat, the LD50 is 1.70gm/kg [of animal bodyweight]; the LD100, 2 gm/kg. The cause of death is respiratory depression, and under artificial respiration, rabbits can tolerate up to 7gm/kg. The dog is less sensitive.... In the rat no significant differences are observed between controls and the group injected daily with a 1/10th of the LD50, particularly with respect to weight, bone marrow, liver and kidneys [where toxic effects frequently show up]."(1)

In his 1969 review on GHB, anaesthesiologist M. Vickers wrote: "In acute experiments in animals, the LD50 has been 5 to 15 times the dose necessary to produce coma. Death was probably due to sodium intoxication rather than to any effect of the active drug.... No deaths have been reported in man attributable to acute toxicity.

The author [Vickers] has used doses of 20g to 30 g. [28,4 g = 1 oz] per 24 hours for several days without ill effect.... No toxic effect on the liver or kidney have been reported.... Its low acute toxicity may make it a safer sedative drug to prescribe when suicide is a possibility." (8)

While extrapolation from animal LD50 studies is at best an approximation of a drug's toxicity for humans, the rat LD50 of 1.7 g/kg of bodyweight would translate into 85 g (3 ounces) for a 50 kg (110 pound) person. This would equate to roughly 10 to 15 heaping teaspoons of GHB - rather more than anyone is likely to ingest at one time.

It should also be noted that Laborit's LD50 was based on injecting the GHB, rather than taking it orally, as humans normally do. Injecting GHB at least doubles its effect, as Laborit noted. (1) Thus a 50 kg/110 pound person would really need 170g (6 ounces) or 20 - 30 heaped teaspoons of GHB taken orally, to equal the rat LD50.

Another estimate of the human lethal dose is provided by the official package insert for the legal French GHB drug (Gamma - OH), where the human LD50 is stated as 4.28 g/kg. This would equate to an oral lethal dose in excess of 200g (7 ounces) for a 50 kg/110 pound person.

A perusal of the published GHB literature attests to the safety and low toxicity of GHB. In a 1977 report measuring the effect of 2.5g intravenous GHB given to 6 healthy young men, Takahara et al reported: "All volunteers except one fell asleep ... after GHB injection and slept for 30 to 150 min.

As side effects, one volunteer complained of nausea and another volunteer had orthostatic hypotension [dizziness upon arising] after test." (9) In a 1979 report on the use of GHB to treat 16 narcolepsy patients Mamelak and Broughton stated: "There have been very few adverse clinical effects with [GHB] treatment [3.75 to 6.25 gm, divided into 2 or 3 oral doses] and no abnormal laboratory findings.

Minor side effects of GHB have been seen for the first few days in a number of patients which consisted of a 'thick head', ocular discomfort, and other apparent hangover effects, but these were rare after one week.... The main disadvantage at present is its [GHB] short duration of action." (10) (Hardly a sign of "severe neurotoxicity a la chin and colleagues!)

In a 1985 report on treatin g 30 patients with narcolepsy, Scharf and co-workers specifically emphasize the toxicity and side effects of standard drugs used to treat narcolepsy (amphetamines, Ritalin, and tricyclic anti-depressants) .

They note that in contrast Our results confirm those of previous clinical studies of GHB, namely, that it is a safe, non-toxic substance...." (11). And in a 1986 review of 48 patients who took GHB for 6 months to 9 years as a narcolepsy treatment, Mamelak, Scharf and Woods report that: "Few adverse effects have been observed. All patients have been followed with serial liver, renal, and blood studies, periodic chest X-rays, and electrocardiograms; no abnormalities have been noted.

On the first few nights of treatment with GHB, two patients had enuresis [bed-wetting].... Patients who resist the sleep-inducing properties of the drug may become confused and emotionally [upset]...." (12).

In their 1989 double-blind study on GHB to treat narcolepsy, Scrima et al note: "The total number of adverse reactions [primarily upset stomach, muscle weakness, urinary urgency and dizziness] reported during GHB treatment was less than during the placebo treatment [!].... No patient discontinued participation in the study because of side effects. The blood test results... indicated that GHB did not cause hypokalemia [low blood potassium] or other marked changes in blood chemistry." (13).

And in their 1990 paper on GHB use with narcoleptics, Scrima et al remark: "GHB is a more appealing treatment for narcolepsy patients than other alternative treatments.... GHB has been found to cause only minor side effects that usually occur only during the first few days of treatment." (14).

In this remarkable paper integrating masses of GHB study data, Mamelak makes observations that clearly cast doubt on any claim that GHB is a 'severe neurotoxin'. "In man, oral or intravenous doses greater than 50mg/kg [=3.5g for a 70kg/154 pound person] produce anaesthesia.... The drug is rapidly metabolized and the central [nervous system] effects of an intravenous dose of 60-70mg/kg run their course in about 2 hours.... In the rat... 600mg/kg [=42g for a 70kg person]... produces a reversible continuum of EEG changes... Complete recovery occurs about 2 hours after the drug has been given.... As much as 1000mg/kg [=70g for a 70kg person] have been given to monkeys without harmful effects.... As has been demonstrated in other circumstances, GHB appears to promote survival under hypoxic [low oxygen] conditions." (4). Does that sound like any 'severe neurotoxins' you know?

Mamelak has also noted the unique ability of GHB to reduce brain glucose consumption, without toxic effect. Thus, he states: "An intravenous dose of 600mg/kg of [GBL, which is converted to GHB by an enzyme in the blood], for example, reduces glucose utilization in grey matter by 68% compared with 44% in white matter [of the brain]. Similar results have been reported with GHB. It is remarkable that in spite of these extraordinary degrees of metabolic depression full tissue recovery can take place.

Other [CNS] depressants such as the barbiturates also produce comparable effects on... energy metabolism, but doses of barbiturates which would be necessary to inhibit cerebral glucose utilization as much as that observed with [GBL] and GHB would likely be lethal." (4). By now it should be evident that (to put it politely) Chin et al may have exaggerated when they suggested (only by implication, if you read their statement carefully) that GHB might be a 'severe neurotoxin'.

And ironically comments made by Chin et al in their paper seem to contradict the implication that GHB might be a 'severe neurotoxin'. They point out that "The prognosis for those who experience GHB poisoning [sic] is quite good. There are no documented or anecdotal reports of long-term adverse effects or fatalities...." (2).

Don't you wish all 'severe neurotoxins' (e.g. Cobra venom) were that benign? (For a detailed dissection and critique of the Chin paper on GHB 'poisoning', see references 7 and 26). Far from acting like a toxin or poison, GHB has shown a remarkable range of protective effects in a diverse array of experimental and clinical conditions. Laborit reported in 1973 that "we observed... that GHB possesses a definite protective action against convulsions produced by strychnine, cardiazol and isoniazide," (3). While Mamelak notes that "GHB can block seizure activity induced by a variety of agents. Those induced by Kainic acid, strychnine, isoniazide and mercaptoproprionate may be cited as examples." (4).

Mamelak also reports a wide range of tissue-protecting actions of GHB. For example "500mg/kg of intravenous GHB protected rats against the lethal effects of 30 minutes of hypoxia. Under these conditions none of the GHB-treated rats died in comparison with 45% of the untreated control rats. Even lower doses of GHB, 200mg/kg, significantly reduced the subcellular response of the brain to hypoxia in rats exposed to [low oxygen] atmospheric pressures comparable to those at 10,000 meters [32,000 feet]." (4).

Mamelak concludes his section on GHB brain tissue protection by noting that "More so than any protective agent studied, including the barbiturates with which it is so often compared, GHB retards the disappearance of oxygen from anoxic cerebral tissue, again demonstrating the potent [and highly protective] energy sparing effects of this agent." (4).

Laborit reported in 1964 the anti-convulsive effects of GHB in protecting mice exposed to pure oxygen under 3.5 times normal atmospheric pressure. In the control animals this procedure routinely produced convulsions in all the (non-GHB) animals. "A hypnotic dose of 500mg/kg [GHB] protects all animals against convulsions (10 mice). With 250mg/kg doses, a convulsion is noted in one mouse out of 10; the seizure is retarded and of short duration. In 20 mice, with 200mg/kg, there were three slight and one typical convulsion." (1).

GHB has also shown a wide range of protective effects outside the nervous system, especially in conditions of anoxia or energy insufficiency. GHB has been used to reduce the pain of angina pectoris and myocardial infarction (heart tissue death). (4). GHB has also been shown to minimize the deterioration of heart function produced by massive haemorrhage. (4). Sodium and lithium GHB have been used to prolong the viability of kidney to be used for organ transplant. (4).

A 1990 study found an amazing effectiveness of GHB in preventing the intestinal lining damage that normally occurs when blood supply to the tissue is cut off (ischemia), and then blood is allowed to return to the tissue (reperfusion). Eight groups of 6 hamsters were studied in a blind experiment.

After 30 minutes of intestinal ischemia, 3 hours of reperusion were allowed. The animals' intestines were then subject to careful histological examination. In untreated animals, 75% +/-6% of the villi (microscopic finger-like intestinal lining projections) were damaged (haemorrhage and necrosis).

In GHB-treated hamsters, only 8% +/- 3% of the villi were damaged. Administration of the GHB following ischemia but before reperfusion also provided significant protection to the controls, with 26% +/- 3% of the villi damaged. In contrast, Vitamin E failed to provide any protection against the injury, with 71% +/- 4% of villi damaged. (15).

In a 1991 report Pierrefiche, Laborit and co-workers detailed the profound protective effect of GHB against alloxan-induced diabetes. Alloxan is a substance that is routinely used experimentally to destroy the insulin-producing beta cells of the pancreas. The rapid uptake of alloxan and an exquisite sensitivity to free radicals (which alloxan produces en masse) are unique features of these cells.

The toxic effects of alloxan, namely elevated blood glucose due to beta cell destruction, are prevented by a number of anti-oxidants. Different levels of GHB, from 1.5 mmoles/kg to 4.2 mmoles/kg, provided almost complete protection from the hyperglycaemia induced in the mice which received alloxan but no GHB. Fasting blood sugar in the alloxan-but-no-GHB mice typically tripled at 48, 72 and 96 hours after alloxan treatment, compared to control mice given only saline (salt) injection, but neither GHB or alloxan.

In the GHB-plus-alloxan mice, blood sugar levels at 48, 72 and 96 hours after injection remained virtually identical to the normal fasting blood sugar levels displayed by the saline-control mice.

Since the beginning of GHB studies in the early 1960's, GHB has been shown to have a wide range of metabolic effects in animals and man.

Perhaps the most well-documented effect of GHB on brain metabolism is the increase GHB causes in brain dopamine. "Systemic administration of GHB leads to decreased dopaminergic [nerve] activity. This is probably a reflection of GHB's inhibitory action on the cell body of dopamine-releasing neurons.

In the substantia nigra [the chief dopamine brain area where damage leads to Parkinson's disease] this initially leads to a decrease in dopamine release and an accumulation of dopamine at nerve terminals. Finally, a stimulation of dopamine release occurs." (5). Because of GHB's dopaminergic actions, it has been used with limited success in treating Parkinson patients.

"Major studies were conducted in Italy. One study showed that in 9 patients out of 10 a single dose of 400mg/kg... produced some improvement... within 24 hours, resulting in a sensation of comfort and regulation with improved ideation and renewed initiative. Within 2-7 weeks following initiation of treatment,... there was an improvement in tremors, hypertonia [muscle rigidity] and in the writing test. One female patient regained normal gait [walking] after having been confined to bed.... These results were confirmed by Ferrari et al." (17). GHB has moderate or little effect (depending on dosage) on acetylcholine, noradrenanlin and serotonin activity. (4).

GHB has been shown to induce major increases in plasma growth hormone (GH) levels. In 10 patients scheduled for surgery, intravenous GHB anaesthesia (100-150mg/kg) increased plasma GH levels 6-fold, from 2.2ng/ml pre-induction, to 13.8ng/ml at 45 minutes after GHB injection. GHB induced only slight increase in plasma cortisol levels, from 14mcg/ml to 23.6mcg/ml. (18).

In a 1977 report Takahara et al injected 2.5g GHB into 6 healthy men (25-40 years old). Compared to the GH levels after saline injection in the same 6 men, plasma GH levels rose 16-fold, from about 2ng/ml to 32ng/ml by 60 minutes after GHB injection. Plasma GH levels were still 6 times normal (13ng/ml) 2 hours after GHB injection. Plasma prolactin levels rose to a maximum of 5 times base-line levels at 60 minutes. (9).

It has been known since the 1960's that slow-wave sleep (EEG sleep stages 3 and 4) induces GH-release. Thus Sassin et al reported in 1969: "Those subjects with more frequent slow-wave cycles had initial peaks [of GH release] of greater magnitude and more frequent secondary [GH] rises.... We conclude from our data that [GH] release is related not only to sleep but particularly to non-REM portions of... sleep, especially... EEG stages 3 or 4.... Release of GH in sleep suggests an anabolic function of slow-wave sleep...." (30). And as is discussed in more detail below, GHB in normal subjects speeds up onset and increases amount of slow-wave (stage 3 & 4) sleep. (19).

GHB typically induces a slight slowing of the heartbeat (bradycardia). GHB also slows and deepens breathing, but does not depress the breathing centers in the brain stem, unlike e.g. barbiturates and benzodiazepines. Even with high doses of GHB the respiratory centers in the brain do not lose their sensitivity to carbon dioxide in the blood-the normal stimulus to breathing. (17).

GHB also induces a remarkable hypotonia, or extreme relaxation of the musculature. In medical contexts where GHB is used anaesthetically, this promotes easier insertion of breathing tubes into the throat. (17). GHB also induces a mild hyperthermia, apparently due to its decrease in brain and muscular metabolic rate. (4).

Perhaps the most striking physiologic feature of GHB is its rapid induction of sleep, even when given orally. Studies done in the 1960's showed GHB sleep to be essentially identical to normal physiologic sleep. Thus Okada et al in 1967 reported their study with 19 men who received GHB intravenously.

They slept deeply, with EEG records similar to natural sleep. "Awakening took place very rapidly, 3 hours after administration, without disorientation. The authors believe that the therapeutic effect of GHB is very similar to that of physiological sleep." (17).

GHB has been used therapeutically since the 1970's to treat narcolepsy, (a severe and disabling sleep disorder), with generally excellent results. It is generally agreed that GHB seems to consolidate and make more efficient the night-time sleep of narcoleptics, so that they don't fall asleep uncontrollably in the daytime. (10-14).

In a 1990 double-blind study, Lapierre and colleagues reported that GHB induced normal sleep in their subjects, but with an increase in the restorative (and GH-release promoting) slow-wave sleep (stages 3&4), and a more efficient REM (rapid eye movement) sleep, as well, while lessening time in the shallow initial stage of sleep (EEG stage 1). (19).

GHB is not a foreign substance which must be detoxified through the liver's detoxification system, unlike most other psychoactive drugs (e.g. barbiturates, benzodiazepines, SSRI's like Prozac, phenothiazines, etc.). As Vickers notes, "[GHB] represents a unique development in the pharmacology of anaesthesia.

It is the first compound to exert a pharmacological action which is at the same time fully metabolized as an energy-producing substrate." (8). When GHB is catabolized (broken down), it is first converted into Succinic Semialdehyde (SSA). SSA is then converted to Succinic Acid, a Krebs cycle metabolite. The Succinic Acid is then oxidized through the Krebs cycle in the ATP-producing mitochondria, eventually becoming water and carbon dioxide, as has been experimentally verified following radioactively-labelled GHB administration. (17).

Thus, GHB leaves no 'toxic residue' in the body, unlike virtually all other drugs. GHB is rapidly metabolized in the human body, with a half-life of only 35-40 minutes. (7). Because it is so rapidly metabolized, its acute effects typically last only 2-3 hours.

The pioneering work of H. Laborit on GHB over several decades has led him to elaborate on extremely detailed explanation of the homeostatic normalizing, restorative, regenerative effects of GHB. (1,3,17). Laborit discovered that in effect, GHB serves as a switching agent to cycle brain/muscle activity from its high-energy output, "yang", daytime activities to a "yin," restorative/recuperative repair and rebuilding (anabolic) phase during night-time sleep.

Virtually all of the known properties of GHB, including its slowing of heartbeat and respiration, mild hypothermia, muscle relaxation, lowered brain and muscle energy consumption, increasing of the deep and restorative sleep phases (stage 3 & 4 slow-wave sleep), increasing growth hormone output, to name just a few, are involved in this integrated 'regeneration reflex'. At the center of Laborit's explanation of the therapeutic nature of GHB-induced sleep is what he terms the 'neuron-neuroglia as a metabolic and functional pair'. (3)

The human brain is generally 'guesstimated' to contain 10-100 billion neurons. Yet it also contains roughly 10 times as many glial or neuroglial cells, also called 'astrocytes'. The astrocytes completely surround neurons, and in effect comprise the second half of the blood-brain barrier.

Astrocytes completely surround blood vessels feeding the brain, and play a role in distributing at least some blood-borne nutrients to the neurons, as well as having key roles in disposing of some neuronal metabolite wastes. (20). Astrocyte neuroglia also secrete a number of growth factors for neurons. Some, like nerve growth factor, may stimulate the neuron as a whole, while others may increase growth of axons. (20). Neurons are the electrically active signalling cells in the brain, transmitting billions of electrical impulses between each other every second.

Neurons have the highest metabolic rate of any cells in the body, and are furious 'burners' of glucose (blood sugar) in the glycolytic-mitochondrial energy cycles to generate the massive ATP energy supplies they run on. Glial cells are metabolically more passive, 'burning' sugar primarily through the glycolytic and pentose shunt pathways. (3).

Drawing upon his own laboratory's research as well as the published research of hundreds of other scientists, Laborit discovered that GHB reverses the normal daytime pattern of energetic activity in the brain.

When we're awake, the glial cells are relatively quiescent, while the billions of neurons are intensely metabolically and electrically active. During normal sleep, and even more so during GHB sleep, the electrical-metabolic activity of neurons quiet down (especially during slow-wave sleep) and glial cells become more active. (metabolizing glucose through the pentose shunt, a non-oxygen using pathway).

The pentose shunt generates two key substances that are critically important for neurons to regenerate themselves during sleep, when they must restore their ion balances (sodium/potassium) and neurotransmitter stores, as well as engage in new protein synthesis.

The pentose pathway generates the 5-carbon sugar, ribose, which is the base of RNA. RNA in turn, as messenger, transfer, and ribosomal RNA, is the key to new protein synthesis. During sleep, neurons must repair the damage to their protein structures (e.g. the antenna-like neurotransmitter receptors on their cell membrane surfaces, microtubules, etc.) as well as elaborate new protein involved in memory consolidation.

The pentose pathway also generates NADPH, the chief 'reducing equivalent' of cells. (25). It is NADPH that ultimately allows neurons to repair the free radical damage created by the combination of their high daytime oxygen-using metabolic activity and the high polyunsaturated fat content of brain mitochondrial and cell membranes.

In the course of mitochondrial ATP bioenergy metabolism, neurons inevitably generate masses of hydrogen peroxide (H2O2). (22). Neurons are particularly vulnerable to damage by H2O2. (21,22). The main detoxifier of H2O2 is an enzyme called 'glutathione peroxidase' (GSH-Px). (21). GSH-Px in turn requires reduced glutathione (GSH) to dispose of H2O2 and the lipid peroxides ('rancid fats') that H2O2 creates in brain cell and mitochondrial membranes. (21).

GSH is also involved in protecting against/repairing oxidized proteins. (21). Unfortunately, neurons are unable to create GSH by themselves, and must depend upon glial cells to provide them with it. (24). When the neurons use GSH to detoxify H2O2, lipid peroxides, oxidized proteins, etc., the reduced glutathione (GSH) is 'burned up' and becomes oxidized glutathione (GSSG). And this is where the neuroglia 'come to the rescue'.

When GHB stimulates glial pentose pathway metabolism, this produces NADPH. The NADPH then combines with the oxidized glutathione (GSSG), regenerating it back to the free radical-quenching reduced glutathione (GSH). GSH is also essential for regenerating vitamin E and vitamin C after they have 'sacrificed' themselves to quench various types of free radicals. (21).

Thus, because GHB is such a powerful and effective stimulator of glial pentose pathway metabolism, (1,3,4,16,17,23). and because GHB simultaneously slows down the free-radical producing mitochondrial energy metabolism in neurons, (3,4). GHB, far from being a 'severe neurotoxin', in effect becomes the anabolic agent to promote healing and restoration of neurons during sleep!

GHB: Other Uses

Given the space limitations of this article, it is impossible to present an in-depth summary of the many uses of GHB reported in the scientific literature. From a life extension/enhancement perspective, the unique ability of GHB to promote brain structure/function regeneration during sleep must surely be its most important general use. Laborit details other uses for it, including psychotherapy, (17) anti-depressive and anti-anxiety therapy, (17) and sexual disorders. (17)

With regard to sexual disorders he notes: "Since GHB causes disruption of neocortical pathways, it suppresses inhibition and creates a special condition relaxing neurotic controls and defences. Greater emotional liability may thus develop and produce readiness for stronger affectivity [feelings].

This 'relaxing' effect has been used very efficiently in certain sexual inhibitions that produce anxiety syndromes or real infirmities (premature ejaculation, frigidity). This effect is not aphrodisiac, but rather an effective or libidinal action-stimulating relationship, associated with an objective... sensitivity which produces stronger [clitoral] and vaginal sensitivity in women and marked delay of ejaculation in men."

GHB: Cautions!

The published literature on GHB stretching almost 40 years has consistently shown it to be a safe and non-toxic substance, rapidly metabolized, usually within 2 or 3 hours. However, because of its powerful sleep inducing and muscle relaxant effects, it must be used with care and caution! In addition, GHB may potentate the neuro-depressive effects of other agents (e.g. alcohol, opiates, benzodiazepines, barbiturates, etc.), all of which can by themselves severely depress-or even stop!-breathing.

Thus the following cautions must be observed to ensure safe and responsible GHB use.

1) Do not EVER mix GHB with central nervous system depressants including but not limited to: benzodiazepines- 'minor tranquillisers' such as Valium, Librium, Xanax, or Halcion; 'major tranquillisers' such as Thorazine, Haldol or Stellazine; opiates-such as codeine, morphine, heroin, opium, or Vicodin; barbiturates such as phenobarbital; alcohol; or even various non-prescription allergy and sleep remedies.

2) Do not drive or operate dangerous devices or machinery (e.g. chainsaws, guns, power tools, construction machinery, etc.) while under the influence of GHB.

3) GHB has a rapid, but variable, onset of action when taken orally, and taking GHB after food may delay its action. Therefore it is unwise to delay going to bed after taking GHB. You may literally pass out on the couch, at the dinner table, going upstairs, etc. if you delay after taking GHB. Indeed, in most GHB sleep studies, subjects are advised to take GHB once they're already in bed. It is also best NOT to take GHB right after a meal (wait 2-4 hours, depending on meal size) as this may cause nausea or even vomiting in some individuals.

4) If you choose to 'cancel' your choice after taking GHB, a large cup of strong caffeinated coffee may counteract the GHB, depending on the dose of GHB taken. (4). This is not recommended as a 'standard practice', though.

GHB: Side Effects

GHB is generally considered to be without serious side effects. However, depending on unique individual health, emotional, metabolic, psychoactive drug history and liver status effects, GHB can have various 'side effects'. These may include fatigue and drowsiness, dizziness and 'light-headedness', nausea, diarrhoea, and occasionally, vomiting. Ataxia (clumsiness, poor co-ordination) may occur. Myoclonias (spasming or jerking of muscles, especially of limbs or face) may occur during the onset of GHB sleep. On rare occasions bed-wetting, confusion and sleepwalking may occur-although sleepwalking has only been reported in narcoleptics. These effects are temporary, and will usually dissipate with 4-24 hours after a GHB dose.

GHB: Contraindications

"There are only very few contraindications: severe alcoholics and epileptics..., patients with eclampsia, severe arterial hypertension, or bradycardia caused by conduction modifications. It should be noted that all hypolipemias with diarrhoea, vomiting, Cushing's syndrome, and renal duct lesions caused by chronic corticoid [cortisol, prednisone, etc.] treatment must first be thoroughly diagnosed and have potassium chloride prescribed before GHB treatment." (17).

GHB: Dosage

Sleep studies have typically used 1.5 to 3gms GHB at bedtime, with possibly a second or third (1-2.5gm) dose if subject awakens during night and can't return to sleep. Many people who use GHB as a sleep aid/restorative find their sleep need decreases 1/2 to 2 hours/night, yet they feel more rested than usual. Thus only those who demand their 'full 8 hours' of 'coma' before arising would be likely to need a third dose during the night.

For use as a sexual aid, probably only 1/2gm is needed (even slightly more, and sleep may ensue-that's usually not a 'sexual aid'!).

Some people have reported 1/2gm, used occasionally, is effective as an anti-anxiety aid, or to restore emotional equilibrium after an intense shock or emotional 'blow up'.

REFERENCES

1. H. Laborit (1964) 'Sodium 4 - Hydroxybutyrate' Int J Neuropharmacol 3, 433-52.
2. M.-Y. Chin et al (1992) 'Acute Poisoning from Gamma-Hydroxybutyrate in California' 156, 380-84.
3. H. Laborit (1973) 'Gamma-Hydroxybutyrate, Succinic Semialdehyde and Sleep' Prog Neurobiol 1, 255-74.
4. M. Mamelak (1989) 'Gammahydroxybutyrate: An Endogenous Regulator of Energy Metabolism' Neurosci & Biobehav Rev 13, 187-98.
5. G. Tunnicliff (1992) 'Significance of Gamma-Hydroxybutyric Acid in the Brain' Gen Pharmacol 23, 1027-34.
6. C. Cash (1994) 'Gammahydroxybutyrate: An Overview of the Pros and Cons for it Being a Neurotransmitter and/or a Useful Therapeutic Agent' Neurosci & Biobehav Rev 18, 291-304.
7. W. Dean et al, GHB - The Natural Mood Enhancer', Petaluma, CA: Smart Pub., 1998.
8. M. Vickers (1969) 'Gammahydroxybutyric Acid' Int Anaesthesia Clin 7, 75-89.
9. J. Takahara et al (1977) 'Stimulatory Effects of [GHB] on Growth Hormone and Prolactin Release in Humans' J Clin Endocrinol Metab 44, 1014-17.
10. R. Broughton & M. Mamelak 'The Treatment of Narcolepsy-Cataplexy with Nocturnal Gamma-Hydroxybutyrate' Can J Neurol Sci 6, 1-6.
11. M. Scharf et al (1985) 'The Effects and Effectiveness of Gamma-Hydroxybutyrate in Patients with Narcolepsy' J Clin Psychiatry 46, 222-25.
12. M. Mamelak et al (1986) 'Treatment of Narcolepsy with Gamma-Hydroxybutyrate. A Review of Clinical and Sleep Laboratory Findings' Sleep 9, 285-89.
13. L. Scrima et al (1989) 'Efficacy of Gamma-Hydroxybutyrate versus Placebo in Treating Narcolepsy-Cataplexy: Double-Blind Subjective Measures' Biol Psychiatry 26, 331-43.
14. L. Scrima et al (1990) 'The Effects of Gamma-Hydroxybutyrate on the Sleep of Narcolepsy Patients' Sleep 13, 479-90.
15. A. Boyd et al (1990) 'The Protective Effect of Gamma-Hydroxybutyrate in Regional Intestinal Ischemia in the Hamster' Gastroenterol 99, 860-62.
16. G. Pierrefiche et al (1991) 'Protective Effects of Gamma-Hydroxybutyrate on Alloxan Induced Diabetes in Mice' Res Comm Chem Path Pharmacol 71, 309-19.
17. J. Muyard & H. Laborit (1977) "Gammahydroxybutyrate' in Psychotherapeutic Drugs, Vol. 2, part 2, E. Usdin & I. Forrest, eds., 1339-75. N.Y: Marcel Dekker.
18. T. Oyama & M. Takiguchi (1970) 'Effects of Gamma-Hydroxybutyrate and Surgery on Plasma Human Growth Hormone and Insulin Levels' Aggressologie II, 289-98.
19. O. Lapierre et al (1990) 'The Effect of Gamma-Hydroxybutyrate on Nocturnal and Diurnal Sleep of Normal Subjects' Sleep 13, 24-30.
20. H. Kimelberg and M. Norenberg (1989) 'Astrocytes' Sci Am 260, 66-76.
21. S. Levine & P. Kidd, Antioxidant Adaptation, S.F. : Biocurrents Pub., 1985.
22. R. Bradford & H. Allen, Oxidology, Chula Vista, CA: R.W. Bradford Foundation, 1997.
23. P. Taberner et al (1972) 'The Action of Gamma-Hydroxybutyric Acid on Cerebral Glucose Metabolism' J Neurochem 19, 245-54.
24. J. Sagara et al (1993) 'Maintenance of Neuronal Glutathione by Glial Cells' J. Neurochem 61, 1672-76.
25. D. Reed (1986) 'Regulation of Reductive Processes by Glutathione' Biochem Pharmacol 35, 7-13.
26. J. Morgenthaler & D. Joy, Better Sex Through Chemistry, Petaluma, CA: Smart Pub. 1995.
27. L. Gallimberti et al (1989) '[GHB] for Treatment of Alcohol Withdrawal Syndrome' Lancet, 9-30-89, 787-89.
28. L. Gallimberti et al (1993) 'Gamma-Hydroxybutyric Acid for Treatment of Opiate Withdrawal Syndrome' Neuropsychopharmacol 9, 77-81.
29. L. Gallimberti et al (1994) 'Gamma-Hydroxybutyric Acid in Treatment of Opiate Withdrawal' Eur Arch Psychiatr Clin Neurosci 244, 113-14.
30. J. Sassin et al (1969) 'Human Growth Hormone Release: Relation to Slow-Wave Sleep and Sleep-Walking Cycles' Science #3892, 513-15.

www.antiaging-systems.com
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#6 LifeMirage

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Posted 01 January 2003 - 12:42 AM

The FDA’s “Date-Rape” of the American People
Issue Date: January 2000


by Paul Anacker, J.D.

The FDA is a rogue, out-of-control bureaucracy. In the past, in its war against dietary supplements, it has threatened people with criminal prosecution for claiming that anti-oxidants prevent disease. It has made giant food companies take words as innocuous as “ask your doctor” off cereal boxes. It has instigated guns-drawn, Gestapo-like raids on 80-year old health food storeowners.

The American people might have thought they finally put an end to that absurd oppression and won the war with the Dietary Supplement Health & Education Act (DSHEA). But, for the FDA that was only a challenge to find new ways to sub-vert the will of the American people.

Now the FDA has falsely taken the role of protector of date-rape victims in a cold and calculated strategy to use the basic human revulsion for a despicable crime of violence in order to further its agenda. It has been waging a campaign of lies and misinformation to create emo­tional hysteria in order to get Con­gress to do politically what it can’t do legally – classify a dietary supplement, gamma-hydroxybutyrate (GHB), curiously both as Schedule I (meaning it has no medical use) and Schedule III (requires a prescription), in a “Date-Rape Drug Act.”

You can fool some of the people…

The FDA has fooled the media with cleverly worded press releases about GHB and its related products, gamma-butyrolactone (GBL) and 1,4-butanediol (BDO). It has fooled most members of 21 state legislatures by making sure only its “experts” presented testimony at hearings. Now it’s trying to fool Congress by making sure the only information members receive is from FDA-invited “experts.”

But the FDA has not fooled everyone. In a series of FDA lawsuit losses, federal courts have lambasted the FDA’s reasoning; calling it “absurd” and “almost frivolous.”1 The Government Accounting Office (GAO) has questioned FDA regulations because of the “limitations and uncertainties associated with the agency’s scientific and economic analyses.” 2 The Honorable F. James Sensenbrenner, Jr. (R-WI), Chairman of the House Science Committee, recently stated, “I am concerned about the apparent lack of scientific data behind the FDA’s actions.”

Chairman Sensenbrenner further stated, “(T)o use such poor science for a dietary supplement raises warning flags for the other products the agency regulates.” 3

GHB is a product for which the warning flags should be raised about FDA “science.” Here are some FDA lies about GHB.

FDA Lie – GHB is a drug

GHB is a simple carbohydrate found naturally in every cell of the human body. GHB is both a metabolite of and precursor to an amino acid consumed daily by millions of Americans – gamma aminobutyric acid (GABA). DSHEA clearly states that metabolites of amino acids are dietary supplements.

The FDA’s label of GHB as a “drug” is a lie. The language it uses, to lead the media to label GHB as a “synthetic designer” or “date-rape” drug, is gross misinformation.

FDA Lie – GHB has no medical uses

The FDA “experts” know they’re telling a lie when they state GHB has no medical uses. In 1974, the FDA approved an Investigational New Drug (IND) application for GHB that discussed 15 medical uses. GHB has been used safely to treat cataplexy, insomnia, narcolepsy, depression, alcoholism, and opiate addiction, and to stimulate natural growth hormone release, to name a few.

FDA Lie – GHB is hazardous

Patients in the IND trials are handed large containers of GHB; told to take doses of 2 to 8 grams; and to come back when they need more. Something the FDA would NOT allow if it truly believed GHB was “hazardous.”

The comparative safety of GHB is shown in the table above. The data (from Medline research) is from scientists doing primary research; unlike FDA “experts” who give opinions based merely on anecdotal reports. The data shows sodium-GHB (NaGHB) is far safer than acetaminophen (Tylenol) or alcohol (EtOH).

National Toxicology Program reports4 contradict FDA “science” on the safety of the GHB-related substances GBL and BDO.

Even the FDA contradicts the FDA. It has released a number of “Talking Papers” stating it has received reports of adverse events and deaths “associated” with GHB, GBL and BDO. When Freedom of Information Act (FOIA) re-quests have been made for copies of those reports, the FDA’s FOIA office has written that the FDA has no such reports.5

FDA Lie – GHB is highly addicting

The 30 years of primary research reports prior to 1990 and the IND reports all state GHB is non-addicting. In the FDA-supervised studies on narcolepsy, no patient has ever become addicted to GHB. The scientific record is clear: When GHB is used responsibly it’s not addicting. In fact, it is used to treat addiction to alcohol and narcotics.

FDA Lie – GHB is a “date-rape” drug

Date rape is a very serious subject. So, it’s important to use science and reason when discussing it. However, it’s such a traumatic topic that most people are more influenced by emotional hysteria than reason. The FDA knows this and plays upon that hysteria.

The use of any substance to facilitate date rape should be a crime. And that’s already the law in many states.

GHB and many other substances the FDA has approved for insomnia can be (but rarely have been)6 used to facilitate date rape since they can cause a deep sleep. But that’s no reason to label GHB a “date-rape” drug any more than Nytol, Tylenol PM, or Benadryl.

There are a few substances which truly should be labeled as “date-rape” drugs. They enable a perpetrator to keep a victim conscious, but easily compelled to engage in sex. They cause a victim to forget what happened while under their influence. And they clear from the body fairly quickly, making their detection difficult.

The only attribute GHB has in common with those substances is it clears from the body quickly (and safely), as carbon dioxide and water. But, GHB does NOT cause a person to remain conscious, be sexually violated, and then not remember what happened.

The FDA’s constant and repetitive linking of GHB together with those substances diverts attention from counseling people on the real dangers of the substance used most often to facilitate date rape, alcohol. The FDA’s single-minded focus on GHB demeans victims by ignoring far more serious and more wide-spread risks. It is tokenism the FDA uses in a very base manner to further its agenda.

FDA synthetic designer “science”

In the 1980s, GHB was available in health food stores. GHB containers had labels with dosage instructions and warnings. People were using it safely for many health purposes.

In 1990, a private-sector pharmacist made an “amazing” discovery. Just 3 years after finishing her residency, Ms. Jo Ellen Dyer “discovered” what world-class scientists had “missed” for 30 years – “GHB poisoning!”

What she really “discovered” was alcohol poisoning. Alcohol and GHB are metabolized in the body by the same enzyme, alcohol dehydrogenase. If GHB and alcohol are co-ingested, the toxic effects of alcohol are increased. Alcohol poisoning, NOT “GHB poisoning” (sic) causes coma and seizure.

[State prosecutors pay Ms. Dyer up to $9,000 (taxpayer dollars) as a fee for an hour of testimony about her “discovery.” Not much incentive to want the truth known about GHB.]

Without holding hearings to ascertain the validity of this “discovery,” the FDA simply issued a press release “ban” of GHB on Nov. 8, 1990. Fearing FDA Gestapo-like raids, health food storeowners took it off their shelves.

Unable to obtain GHB in health food stores, people obtained “street” GHB. It didn’t come with labels. Without the benefit of the labels, more people unwittingly took high doses of GHB with excessive amounts of alcohol and ended up in hospital emergency rooms.

Doctors, “educated” by the FDA about GHB symptoms, made reports of “GHB poisoning” that were more “politically correct” than scientifically accurate. The FDA used those reports and its press release “ban” as the basis of briefings for state legislatures and law enforcement personnel. It made sure non-scientific people got the “right” picture. And the FDA hit upon its unsavory strategy of “associating” GHB with “date-rape” drugs.

Suggested Congressional action
[b]
A rush to schedule a dietary supplement, under the guise of a “date-rape” bill, without scientific debate, is a poor basis for public policy. Before depriving millions of Americans of dietary supplements sold in hundreds of health food stores, Congress should take the time to listen to testimony from experts knowledgeable about the full scientific record on GHB. The requests of those experts to be heard have been ignored by the FDA.

If Congress doesn’t take the time, the FDA will have succeeded in manipulating Congress into doing politically what the FDA couldn’t do scientifically. This will make a mockery of DSHEA and all the work the American people put into getting it passed.

[b]References:


1 see, e.g., Pearson v. Shalala 164 F3d 650.

2 “Dietary Supplements: Uncertainties in Analyses Underlying FDA’s Proposed Rule on Ephedrine Alkaloids” (available at gao.gov).

3 Press Release 106-71, 1999 Aug 4.

4 Toxicology Reports TR-406 and TOX-54 (at http://ntp-server.niehs.nih.gov).

5 Private correspondence of Ward Dean, M.D.

6 “Prevalence of drugs used in cases of alleged sexual assault” J. Anal. Toxicol. 1999 23(3), 141-146. Preston Publications.

Paul Anacker, J.D. (anacker@email.com), is a private attorney. He is a former Chairman of Lawyers in Mensa International (1979-1991). He has been a consultant to several dozen MDs and JDs on the medical and legal aspects of GHB and related substances. He’s received no payment from anyone for writing this message (except contributions to subsidize the cost to place it).
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#7 PaulH

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Posted 01 January 2003 - 03:31 AM

Hi LifeMirage,

I couldn't agree with you more about GHB. I used it for years right after it first came out and up until they made both it and its analogues, Renewtrient and SomatoPro, illegal. This is a tragic shame, as these nutrients did wonders for me, my family and friends in countless ways. I personally found it very powerful as a boost to exercise, a fantastic sleep enhancer, a sexual enhancer, and most importantly an effective tool in resolving permanently negative emotional armouring.

The simple reason it was made illegal was because of massive payoffs from the pharmaceutical industry to both the media (to initally create the false hysteria) and the goverment to act on this falsity and legislate it to Schedue 1. The pharmaceutical giants did this because wide-spread use of GHB would have threatened whole sections of their product line, from anti-depressants and sleep agents to sexual enhancers. They stood to loose $billions in lost revenue to a cheaper, safer, non-propietary and natural alternative called GHB.

May you enjoy this happy new year!

Paul Hughes
Planet P Blog - Liberty with Technology.
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#8 Exile

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Posted 05 January 2003 - 01:35 PM

Excellent info. LifeMirage! But do you have this kind of detail on GBL? Is GBL just as good for you? Also, do you have any resources for GHB/GBL? My source: http://www.ghb-sales.com/ dried up at the end of last year under threat of this http://www.homeoffic...oicd/letter.htm legislation. A GBL supplier should allow one to make GHB so long as one uses Sodium Hydroxide in mixing. Is Xyrem worth looking into? Is it the same as GHB?

Many thanks! :-)

#9 Exile

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Posted 05 January 2003 - 01:38 PM

You may not have had GHB withdrawals, but the GBL withdrawals I experienced after a years daily use were significant. They involved sleeplessness for several nights, a fuzzy head for a few days, and a mild desire for more. However, after almost a week, I felt normal again.

#10 LifeMirage

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Posted 06 January 2003 - 01:58 AM

Hi Exile

I have never tried GBL despite the fact it converts into GHB, I believe GHB is far safer and moer effective.

Xyrem is great, I strongly recommend it (with a prescription for it's approved use of course).

#11 av8kyl

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Posted 28 January 2003 - 05:24 PM

LifeMirage,
what is Vasopressin? (I haven't heard about it, but I'll search the forums and web after I post this. You say it will be the best in overcoming the harmful effects of cannabis? I am interested, what effects are these? I have done extensive scouring of resources and have not found any reliable information pertaining to harmful effects of cannabis, other than some short term memory loss for the duration of the intoxication. Is this what you are refering to? Or are you talking about the effects of breathing combusted plant matter? As I said I haven't read anything yet about vasopressin, but will due so immediatly. If you are referring to the lung damage, it should be noted to the thread starter that obviously the best way to counterract this damage is to use a vaporizer to retrieve that active compounds rather than breath the smoke...

Exile,
I have found www.erowid.org to be an extremely useful site when it comes to recreational drug information. They stay up to date on all harm-reduction research, including which anti-oxidants or other chemicals work best in reducing damage caused by use of said drugs.

Edited by av8kyl, 28 January 2003 - 05:27 PM.


#12 LifeMirage

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Posted 29 January 2003 - 08:14 PM

what is Vasopressin?
Vasopressin is a peptide that occurs in the brain that is involved in memory and learning, when you smoke cannabis your brain uses it up very fast making you depleted in it, resulting in memory & learning problems for some. But taking vasopressin brings your cognitive abilites back up to normal for most.

You say it will be the best in overcoming the harmful effects of cannabis?
No, but it will help reverse 1 specfic factor of the damage caused by smoking cannabis.

I am interested, what effects are these?
Mainly an increase in memory and learning.

I have done extensive scouring of resources and have not found any reliable information pertaining to harmful effects of cannabis, other than some short term memory loss for the duration of the intoxication.

Is this what you are refering to?
Yes.

Or are you talking about the effects of breathing combusted plant matter?
No.

As I said I haven't read anything yet about vasopressin, but will due so immediatly. If you are referring to the lung damage, it should be noted to the thread starter that obviously the best way to counterract this damage is to use a vaporizer to retrieve that active compounds rather than breath the smoke...
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#13 KidCharlemagne

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Posted 07 July 2003 - 08:24 AM

Can I recommend a better recreational drug? Is that kosher on this message board? If you've found your way to this website then you're probably of a mind that would find Ketamine to be, well, completely ineffable. My first experience with it was during plastic surgery when I had to have a broken nose reset. The drug is classified as a dissociative (as in dissociating your mind from your body). During surgery I heard the bones of my nose break under the force of a metal rod and said "Wow cool." Recreational doses (roughly 1/5 - 1/20 of the dose I got that day) are completely different in character - you wouldn't classify the feeling as dissociated; you wouldn't classify it as a "feeling" at all. Nor would you say it was a "trip" (unless you get a dose that I got in the operating room). Words completely and utterly fail to describe it so I'm gonna stop using them.

#14 kevin

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Posted 07 July 2003 - 10:25 PM

Addiction seems to be an issue with Ketamine use.. Here's an abstract from a recent study. People should weigh the pros and cons of any drug use and most importantly, educate themselves as to what they are.

Singapore Med J. 2003 Jan;44(1):31-4. Related Articles, Links


Ketamine associated psychedelic effects and dependence.

Lim DK.

Department of Adult Psychiatry Unit 3, Woodbridge Hospital, Singapore 539747. dominic.lim@chmeds.ac.nz

Ketamine, a dissociative anaesthetic in use since 1970, produces prominent psychoactive effects in humans. Its non-medical use has raised concerns in many countries, including Singapore. This paper narrates the psychedelic and psychotic effects of ketamine in two ketamine dependent patients who have presented to the psychiatric service. These effects were dose-related and comprised multimodal hallucinatory experiences, a sense of slowing, paranoid ideation and enhancement of sexual, musical and sensory enjoyment. In both ketamine users the psychotic symptoms resolved quickly with symptom-targeted treatment. However, breaking the ongoing addiction cycle seemed more difficult. The neuro-pharmacological mechanisms of these phenomena are largely due to its complex multi-receptors actions, notably through the excitatory amino acids through mainly the N-methy-D-aspartate (NMDA) receptors. The detection of ketamine abuse requires a high index of suspicion and needs to be considered when there is an acute presentation with multi-modal hallucinations and psychosis.

PMID: 12762561 [PubMed - indexed for MEDLINE]

#15 KidCharlemagne

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Posted 12 July 2003 - 08:30 PM

My guess is you googled "ketamine addiction" because addiction is not typically associated with ketamine. As a matter of fact some people use it to kick heroin. If it is addictive it is probably more akin to the escapist addiction that some people have to weed. But yes, people should most definately do there own research before trying anything - especially processed foods. ;)

#16 kevin

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Posted 12 July 2003 - 10:07 PM

You guessed wrong... I went to pubmed and searched on ketamine and this was one that had direct bearing on human use. To be sure, there is probably a genetic basis to predisposing individuals to addiction to any chemical and the psychological profile of the person is important as well... I just wanted to point out that addiction was a possibility...

But I totally agree with you on processed foods, which perhaps over the long haul are more destructive than occasional use of a substance like ketamine! ;)

Edited by kperrott, 12 July 2003 - 10:11 PM.


#17 hughbristic

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Posted 13 July 2003 - 02:04 PM

Sceletium tortuosum from http://www.sceletium.com/ I've tried with good results in the pleasurable/recreational area, but it is not a nootropic.


Could you give more detail on this? How unambiguous are its effects? Is there a chance it is placebo, in your opinion? What other substances is it similar too?

Thanks,
Hugh

#18 LifeMirage

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Posted 14 July 2003 - 12:46 AM

Could you give more detail on this?
It's been a while since I've taken it and only for a few days, so not really.

How unambiguous are its effects?
Various.

Is there a chance it is placebo, in your opinion?
No. It has known neuroactive chemicals. The DEA is reviewing it.

What other substances is it similar too?
THC in effects.

Edited by LifeMirage, 14 July 2003 - 12:47 AM.


#19 staz

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Posted 29 October 2003 - 02:44 AM

As far as I know, Selegiline in high doses can interact badly with MDMA/ecstasy..

On the issue of selegiline with serotonergic drugs (legal and otherwise). Selegiline (apparently, when administered orally, for they've found that when it is administered trans-dermally it 'behaves' differently) loses its MAOI-B selectivity in doses over 10 mg/day. When a substance ends up inhibiting MAO-A, then serotonin is not MAO-ed. The risk is then for serotonin syndrome which is quite dangerous. So, as there is really no need to exceed 10 mg of selegiline per day, and to the extent that one is meticulous about taking anything, pre- and post-loading with selegiline is the royal road to neuroprotection.


LifeMirage (or others), would you consider any nootropic possibly interacting with a drug in such a way that it could/would increase the damage caused by a drug? (I.e. increasing possible MDMA neurotoxicity) Due to the increased blood flow provided, or perhaps other effects. I also wonder if the increased brain blood flow would mean that in many cases a drugs effects would last for a shorter amount of time while acting more intense.

edit: about ghb:
http://www.qhi.co.uk...es/feat_003.asp
good read.

Edited by staz, 02 November 2003 - 04:46 AM.


#20 jpars82

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Posted 04 November 2003 - 02:10 AM

GBL sources: http://www.khemical..../chemistry.html

Also, Tranquili-G's a GHB analogue that's still legal. I was told on the psycho-babble forums it works too. http://www.anphealth.../tranquili.html

#21 bradcure

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Posted 14 December 2003 - 09:08 PM

If you abuse GHB - the BEST thing for G withdrawals is L-Theanine. Use it every time you feel anxious/depressed from not being on G.

#22 staz

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Posted 15 December 2003 - 11:59 PM

Tranquili seems interesting.. I never tried GHB/GBL though, so don't really know what they're like from a 1st person pov.. In what ways is tranq different from GHB, in your personal experience?

#23 jpars82

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Posted 16 December 2003 - 12:58 AM

http://www.dr-bob.or...sgs/212566.html

#24 staz

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Posted 16 December 2003 - 04:43 PM

http://www.smartbody...quil-g-text.htm

Hmm

Q: Could one mix Tranquili-G with Alcohol?

A: Yes, and as such, a given amount of Tranquili-G would lessen the amount of Alcohol needed to produce a given subjective state.


Doesn't sound like the standard doctors recommendation. Is tranquili not a powerful CNS depressant such as GHB? skyrocketing the risks of serious adverse effects if mixed?

Funny too how on the same page they say:

Do not take this product:

Before or while driving motorized vehicles
With anti-depressants or other dangerous prescription drugs (prescription drugs kill 100,000+ people each year in The USA according to The Journal of the American Medical Association)
With alcohol or other CNS depressants
By anyone under 21 years of age
In excess of label recommendations
If you have a pre-existing medical condition


cheaper source here: http://www.renewtrie.../tranquili.html
that site seems to sell loads of 'miracle' products by the way.. would be funny to hear what really has effect and works in most of the cases..
just check the other products in their 'mood enchance/relaxation' section.. http://www.oneononen...ore/page16.html - and what's this thing with having different URL's for the same site? I never understood that.

Edited by staz, 16 December 2003 - 05:06 PM.


#25 cygnus

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Posted 23 January 2004 - 03:42 AM

As far as I know, Selegiline in high doses can interact badly with MDMA/ecstasy..



LifeMirage (or others), would you consider any nootropic possibly interacting with a drug in such a way that it could/would increase the damage caused by a drug? (I.e. increasing possible MDMA neurotoxicity) Due to the increased blood flow provided, or perhaps other effects. I also wonder if the increased brain blood flow would mean that in many cases a drugs effects would last for a shorter amount of time while acting more intense.

edit: about ghb:
http://www.qhi.co.uk...es/feat_003.asp
good read.

Considering that most of the suggested neurotoxicity from MDMA/MDA usage stems from MA0-B metabolizing dopamine and thereby increasing the levels of free radicals.Using selegiline if anything would decrease the neurotoxicity. Althougth I don't anymore, I regularly used MDMA/MDA 2-3 times a month for a period of over years. During this time I was regularly taking selegiline. In comparison to my peers who were not taking any supplements, I faired very well. I had already been taking selegiline before I started experiementing with MDMA/MDA, and only discovered the neuroprotective effects of it in regards to MDMA afterwards.

However in my experience, selegiline has a potentiating effect on LSD, and 2C-B. Both in length of experiences and strength. Be extremely careful with that combination. 2C-B is known as a relative short lived (3-4 hours) psychedelic with a pleasent MDMA-like body high. 5mg of selegiline taken 24 hours prior to the 2C-B, resulted in a extremely intense 12 hour trip that I would never want to have again (not bad- but took some time to get used to normal space).

Edited by cygnus, 23 January 2004 - 11:18 AM.


#26 staz

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Posted 23 January 2004 - 01:54 PM

Yes, but in higher doses selegiline loses it's MAO-B selectivity, and it is when it starts inhibiting MAO-A that the trouble can occur. I don't know exactly wat what doses the selectivity is lost, but it probably differs between persons, I've heard above 10mg doses.

#27 abolitionist

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Posted 31 May 2004 - 01:58 PM

Can any recommend nootropics that can be administered to reliably counter the negative effects of recreational drugs like:

cannabis
LSD
XTC
GHB/GBL
Psilocybin

Can any nootropics that have pleasurable/recreational/enchancing effects be recommended?

I have experimented with a variety of "research chemicals" which include:

2 C-B experiences (this chemical was once legal in the UK).

DPT (N,N-dipropyltryptamine) experiences

5-MEO-DIPT experiences

GBL experiences (gamma-butyrolactone)

GHB experiences (legal until 2003)

Zolpidem experiences (legal until 2003)

Salvia Divinorum experiences (illegal in Australia)

Melatonin experiences

Sun Opener (aka Heimia Salicifolia aka Sinicuichi)

Mushroom (Psilocybin) experiences (note, fresh mushrooms are legal in the UK, so long as they aren't dried and stored.)

Exile


MDMA can be enhanced by preloading with 5-htp and taking additional amounts about 3-4 hours after MDMA ingestion will help greatly with comedown. Strong doses of anti-oxidants: R-ALA, Selenium, E, C, A, etc.. will guard against toxicity and tolerance.

Some report enhanced LSD experiences with Piracetam.

I would take large doses of anti-oxidants and picamilon/L-theanine when taking any phenethylamines, tryptamines, amphetamines or other hallucinogens to prevent toxicity and promote a calm and relaxed state of mind.

All the best,
Sean

www.abolitionist-society.com

Edited by abolitionist, 03 June 2004 - 01:02 AM.


#28 bradcure

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Posted 04 June 2004 - 03:46 AM

My current website is still not up. But I do have many interesting substances in offer.
The ones hardly obtainable:
- Pharmaceutical GHB powder
- Pramiracetam
- Nooglutyl

Cheaper than at any smart drug web sites:
- Deprenyl
- Piracetam
- L-Theanine
- Picamilon
- Aniracetam
- Alpha Lipoic Acid
- Acetyl L-Carnitine
- R-Alpha Lipoic Acid
- Morphine XR tabs (there are studies which show its anti-oxidant effect)
- Sildenafil (Viagra)
- Cialis
- Hydrocodone
- Oxycodone
- Tramadol
- Xanax / Xanax SR
- Klonopin
- Valium
- Adderall
- Dexedrine
- Ritalin
...
well the list is not over but I offer actually anything that can/can't be obtainable.
Just send me an email, or PM, or AIM: bradcure

#29 bradcure

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Posted 04 June 2004 - 05:27 AM

Well I forgot about very important part.
Brad ICQ:309970975 AIM (GAIM!!!): bradcure email:
mike34 at safe-mail dot net

Please create your PGP key and sign your emails with your public PGP.
For example free email account at www.hushmail.com does it
automatically.
Or you can use GAIM to talk. Here are the links:
http://belnet.dl.sou...m/gaim-0.75.exe
+ install this (important!) -> http://gaim-encrypti...ourceforge.net/

Have a good day.

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#30 bradcure

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Posted 04 June 2004 - 05:40 AM

Strong doses of anti-oxidants: R-ALA, Selenium, E, C, A, etc.. will guard against toxicity and tolerance.
[/quote]

There is an actual study that Alpha-Lipoic-Acid totally blocked MDMA's neurotoxicity. Since its a powerful anti-oxidant and MDMA releases lots of free radicals, destroying via it serotonin receptors - the effect was 100% success. I will dig up this study today and post.




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