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GBL/GHB, dosage, duration, withdrawals

Brain fade on the K-chlorate, I meant to type CITRATE. (Sometimes I'm a dangerous moron!) Sorry bout that one, just a bad error I didn't catch. I use it a great deal and cannot justify the error, so I'm glad you caught that one.

About the acidosis caused by GBL --

This is an effect that I have personally experienced and verified via blood tests. I can understand the instruction to do research before posting, but rest assured that when it comes to GBL/GHB I have done research as well as used for twelve years, and I promise that GBL will acidify your blood if used too frequently. The explanation that I proposed is not comprehensive, but it is not "just plain wrong" either. I have spoken with my doctor about this very phenomenon, and as we witnessed a specific correlation between dosage and rate of potassium depletion I can give testimony to the fact that it is a direct result of GBL consumption. To suggest that this will not occur seems to me to be a much more dangerous position.

I understand that the goal is harm reduction. I will take your reprimand and instruction in that spirit...the chlorate thing probably means I deserve the added condescention for good measure...but I must say that it is not my most serious error about GHB. That one would have to be the time I carelessly typed Sodium Oxylate instead of Oxybate.

That one would be deadly. So its good to have an educated set of eyes on me, and I am glad to learn here.

Either way, I am curious as to your explanation for the acidification that I and several colleagues experienced, verified and ameliorated via the methods outlined above for years on end without incident.
 
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Call me stupid, but I missed the logic part. Maybe you can cut and paste it for me?

Again I ask -- what caused the MEDICALLY OBSERVED AND DOCUMENTED ACIDOSIS that I experience regularly when I use GBL for extended periods of time and do not supplement with an alkalyzing agent? This has happened three times, the last two were specifically done on purpose to see if the effect was directly related to GBL consumption. I can post blood tests and results if that would help...

The udeniable fac t is that acidosis occurs. That is not in question, as it has been documented. Even the head of the GBL/GHB research team in Utah verified the fact on the phone for me when I asked about this effect. So my question is: WHY?

The explanation that I proposed is reasonable: The use of a hydroxide ion from the blood. Yes, GBL is hygroscopic, but the hydroxide ion is lost forever, isn't it? Some of the water is recycled, all of the CO2 is expelled, yes?

Forgive my thickeheadedness, but my personal experience and medical supervision have verified the acidosis -- it is NOT a myth.
 
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^ It's more likely to have something to do with the effects of GHB/GBL on the endocrine system (hormones eg HGH etc) rather than a direct acidosis, as on its own, GBL does not contribute a hydrogen ion to the body, either directly, or by removing hydroxyl ions
 
Interesting. I will pursue the matter with some empirical data in the near future. Dr. Ward seems to side with the theory of a hydroxide ion from the blood, but he could be wrong I suppose. I did not major in chemistry, but my colleague who also sides with this theory did -- he is a chemical engineer now. I cannot speak with authority on this, only from personal experience, and I do not represent myself as a chemical expert. I am only repeating what those with knowledge have said to me. This includes, as I mentioned, the local head of the GHB project and several chemists. I will pass your words on to them and give you their feedback as soon as possible, as I wish to have an accurate understanding of this process.

For those on the fence, I would opoint out that the ingestion of an alklyzing agent such as potassium citrate (or even dietary agents like watermelon and lemons) will ameliorate the acidosis, a fact which further supports the hypothesis (proven in my mind) that GBL consumption (in sufficient quantities and at a sufficient rate) directly causes acidosis.

In any event, it is a good idea to eat alkalyzing foods regardless, as most viruses and bacteria have a more difficult time surviving in a slightly alkaline environment. As a side not, if you are slightly alkaline your muscle recruitment will be better and your strength will be noticably increased -- this is why some athletes ingest potassium citrate prior to competitions -- endurance and strength are increased dramatically (yes I have tried this too).

Fastand bulbous -- thanks for your input. I'm not sure I agree with everything, but as I said before, I will research the matter more diligently and find a solid conclusion to present to the board for consideration.

Anyone who would like to see my blood tests with notes can email me and I will gladly provide them.
 
I replied this in the Rectal GBL thread as well, but I'm wondering if the water hydrolysis indeed occurs when taking pure GBL.

As stated, GBL to GHB conversion is done in labs using xOH because it goes a hell of a lot quicker. Besides, it is my understanding that the water hydrolysis conversion is a balanced one (meaning: two way), so taking everything into account and add the fact that GBL for me comes on in about 15 minutes, it at least suggests something else than just the water conversion.

Does that imply that the xOH salt conversion also takes place in the body? If so, it could account for both the acidosis and the potassium depletion...
 
My understanding is that it does exactly that. As I said before, I am not a chemist or a doctor, but I have extensive experience with GBL/GHB/BDO and the evidence seems to strongly support this hypothesis.
 
It doesn't leave behind a hydrogen ion, and it is converted from GBL to GHB in the body. I am a biochemist & my wife is an NHS toxicologist; she agrees with me that any percieved metabolic changes will be due to the effect on the endocrine system, and not directly as a result of hydrolysis. There are NO H+ or OH- ions left behind...
 
Well, I'm an neither a biochemist, nor a toxicologist (wow, what a beautiful combination!), so I still have two questions...

Why does the GBL buzz come on so fast when apparently in the laboratory it only works so fast using the xOH method?

Isn't the GBL - GHB hydrolysis a balanced one? Meaning it is GBL <-> GHB instead of GBL -> GHB. If that is indeed the case, how (and why) does the total conversion occur then?

BTW I was thinking something else too...

When on a constant GBL rhythm, one seems to have less hours of sleep than when not on it. It is often said that it causes deep, refreshing sleep, albeit a somewhat unnatural one.

Normally I sleep for about ten hours, but on GBL I can easily do with six.
Could the withdrawal symptoms perhaps be a sign for fatigue, over-tiredness if you will? The result from a long time doing with a little too less sleep per night?
 
GBL is rather non-polar and probably absorbed for the stomach more quickly than GHB.

The equilibrium GBL <-> GHB is dependant on the pH, at low pH it's shifted towards GBL, at high pH towards GHB. The pH of bodily systems is such that it wouldn't cause a ring opening of the GBL fast enough that it could explain the rapid onset of action after the ingestion of GBL.

GBL can also be seen as an ester, and the body contains enzymes called esterases which, as the name suggests, split esters into alcohols and acids. My guess is that these esterases catalyze the rapid ring opening of GBL.
 
^ What the man says. GBL crosses membranes faster than GHB as it's less polar & plasma pseudoesterases (they also are responsible for the metabolism of cocaine by causing ester hydrolysis) will open the lactone ring in the blink of an eye
 
hmmm... ok :)

It was a wise man that said "every answer starts a new question"...

So if the equilibrium is shifted towards GBL, does that then mean that there must be some other system other than the regular water hydrolysis?

You suggest that it is enzymes at work, which could very well be the case.
I'm suggesting, and so is Synchrojet, that it seems to be an xOH reaction because acidosis has been observed and K-depletion was reported.

I would love to find out which it is, because it might be important in the case of battling the results.
I am by no means questioning your expertise, it's just that the reported acidosis and K-depletion are a bit terrifying (potentially life-threatening too!) and suggesting enzymes and/or the endocrine system instead of the xOH conversion seems to go against Ogham's razor.
 
Hydrolysis from GBL to GHB requires an OH- and an H+ so there is no ion imbalance, and the K depletion is associated with lage doses of the GHB sodium salt
 
I think the following might lend some insights...the first is from Dr. Ward's letters:

Despite the illogic of Matthew’s presentation, there may be some wisdom in his advice. There

is certainly a lot we do not know about exactly how we might adapt to long-term use of

butyrolactone in different circumstances. I have two concerns. The first is acidosis. Every

molecule of GBL that is hydrolyzed by lactonase generates one molecule of GHB-acid

[illustration not shown], or, equivalently, consumes one molecule of hydroxide [sidebar not

shown]. This can alter pH (acidity-alkalinity) in the blood stream. In some people, blood

acidification might be a problem. While it is true that 1-2 grams of an organic acid is not

a very large acidification effect in absolute terms, it happens in a relatively short period

of time and may have subtle effects on pH-dependent systems. For example, blood pH is

critical for regulating the binding and release of oxygen from hemoglobin. This might affect

somebody with emphysema (with deficient oxygen absorption) or diabetes (with higher risk of

lactic acidosis) more than somebody in good health. Similarly, food choices affect blood

acidity. Somebody eating an extreme diet might be more susceptible to circulatory acidosis

than somebody eating a mixed diet. Since rats and mice tolerate this acidification effect at

a ten-times greater magnitude, it is not likely to be a problem in normal, healthy people.

However, it is a general rule that the average lab rat eats a more nutritious diet than the

average person. So, this could be a problem in some people.

The GBL induced acidosis is noted even back in 1983:

1: Neurosurgery. 1983 Apr;12(4):430-4. Related Articles, Links


Effect of low dose gamma-butyrolactone therapy on forebrain neuronal ischemia in the unrestrained, awake rat.

Lavyne MH, Hariri RJ, Tankosic T, Babiak T.

Low dose gamma-butyrolactone (GBL) therapy alters the natural history of experimental forebrain ischemia in the awake rat. After 30 minutes of four-vessel ischemia, repeated hydrogen cerebral blood flow determinations in awake rats over 72 hours revealed that low dose GBL therapy prevented the development of regional cerebral hyperemia and later the prolonged cerebral hypoperfusion that was experienced by the nontreated controls. Moreover, the low dose GBL-treated group had significantly less neuronal tissue loss than that in comparable brain regions of the nontreated controls. Before the stroke studies, GBL dose-response experiments performed on normal rats indicated that high dose GBL therapy produced seizures, systemic hypertension, metabolic acidosis, hyperthermia, and death.

Some insight into the reasons might be found here:

Stroke. 1980 May-Jun;11(3):271-7. Related Articles, Links


Effects of gamma-hydroxybutrate and gamma-butyrolactone on cerebral energy metabolism during exposure and recovery from hypoxemia-oligemia.

MacMillan V.

Cerebral hypoxia-oligemia was produced by lowering of the arterial PO2 to 30 mm Hg and by right common carotid artery occlusion in rats who were pretreated with intravenous Krebs' solution, gamma-hydroxybutyrate (GHB) (500 mg/kg) or gamma-butyrolactone (GBL) (300 mg/kg). At 0.5 h exposure the right cerebral hemisphere of animals receiving Krebs', GHB or GBL showed equivalent decreases of ATP and phosphocreatine and increase of ADP, AMP and lactate which indicated that these depressant drugs had no beneficial effect on the energy metabolism of the acutely hypoxic-oligemic brain. In a second series of rats in which Krebs' solution, GHB or GBL were administered to animals during the early recovery period from 0.5 h hypoxic-oligemic exposure, the brain metabolic patterns of the right hemisphere indicated that GHB retarded the restitution of energy phosphates and the oxidation of the accumulated lactate; whereas, GBL led to a delayed metabolic deterioration. It is concluded that GHB and GBL do not beneficially alter cerebral energy metabolism during acute hypoxia-oligemia and that their administration during restitution may result in metabolic alterations which suggest an unfavorable effect.

On this last abstract -- astandbulbous might have some good feedback...
 
The first is acidosis. Every

molecule of GBL that is hydrolyzed by lactonase generates one molecule of GHB-acid

[illustration not shown], or, equivalently, consumes one molecule of hydroxide [sidebar not

shown].

Where did he get that one from? I'll attach the equation for the hydrolysis of GBL that was attached to the rectal GBL thread. Yes it produces a carboxylic acid, but not a great deal, and it's buffered by plasma bicarbonate ions. If that much carboxylic acid caused a problem, then Coca-Cola would have been withdrawn a long time ago as a health hazard as it contains citric & tartaric acid that would cause a mich larger change in plasma pH than a dose of GBL would cause (and they are much more acidic due to their dissociation constants at physiological pH).

Ant effects that it has would be due to effects on the endocrine system. If you're in contact with said doctor, ask him to justify the above statement with respect to the acidic content of a hell of a lot of soft drinks - we'd all be dropping down dead if that was the case
 
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Reactivity of Lactones and GHB Formation
J. Org. Chem. 2005, 70, 420-426

Because the kinetic experiments were carried out
under pH conditions (pH ~ 2) comparable to those
existing in the stomach, from the data in Tables 5 and 6
it can be deduced that at human body temperature the
amount of GBL converted into GHB is less than 3% after
2 h (as shown in Figure 3a, 1 week is necessary for the
equilibrium situation to be reached). This means that
when ingested (see Introduction), GBL flows into the
blood in the nonhydrolyzed, nonopened form.
Although GBL is rapidly hydrolyzed in the blood by a
ß-lactonase (with a half-life of less than 1 min),
it is more liposoluble than GHB, which helps it to pass
through the lipid layers of tissues before it can be
hydrolyzed. Such tissues may act as a GBL reservoir and
extend the duration of its action as compared to GHB.
These results would also help to explain the fact that
the oral bioavailability of GBL (the degree to which it
becomes available to target tissues) in rats is 85%, higher
than that of GHB40 and also explain why GBL has a
longer duration of action than GHB, possibly due to
differences in drug distribution.
 
The "GHB" from your reaction contains an extra methyl group.

So it does (it's actually an extra methylene - CH2 - group) - but you get the principal behind the hydrolysis - no H+ ion left behind(I'll do an updated version)
 
Going back to the original topic: Synchro, your suggestion would be to taper down to a 6hrs schedule before quitting altogether?

How long would that take and what can be expected by someone on a 24/7 regime of 2.4 ml every 2,5 - 3 hrs (4-5 hrs at night though)?

I know, I shouldn't have been on that regime in the first place but Geena has turned out to be a real smooth seductress...

I'm now in day two of my attempt to taper down.
Day one was bad, I had decreased the dose to 1.5 but still found I had to renew every 2,5 - 3,5 hrs.

This morning I had a full 6, something I had not experienced in a few months...
I redosed with 1.4 and am now into hour 5 of that schedule. Did feel a bit tough around the 2 hour mark though, but I think I can make the 6 again.

The main worry is the increase in heartrate, sometimes nearly double my normal one of 60. I guess that's due to the excess adrenaline?
 
First of all I want to say a big thank you for this thread. There is more information here than I ever found in 2-3 years of amateur searching chemistry surrounding GBL usage.
I have used GBL on and off for about 2,5 years. The last 6 months mostly on. Strange thing is that I ONLY use it at nighttime, ae after 4-5 PM.

Usually starting at 2,5-3 ml. Then a few refills at 1,5-2 ml every 1,5-2 hours.
I have no need to use it during the day, as it would f*ck up my normal work he he. I do get anxiety if I am home and not use any G during the night. Sadly it is easy to take alchol to "milder" things.

Sometimes I travel in my work, and I ALWAYS use that oppourtunity to sober up. Never bringing G with me. Perhaps having a few buds with my
collegues but never any amounts of alcohol while on the road.

Regarding withdrawel, I never really felt that much of that. Last year I went almost two months without a drop of any g. Although I do have a friend that started his day with a 10ml shot of 99,7% pure GBL. And then refills with 3-5 ml every hour or so. He did this for about a year 24/7. He sufferd MAYOR withdrawels, had him hospitalized for about 4-5 days. Mostly he got Xanor, and after those 4-5 days he never had any problems staying of G.

Another warning I want to give everyone is mixing GBL and Meth. Seems like a good idea at the time but rest assure...You will pay badly for disturbing your dopamin and seratonine at the same time. Depression will have a whole new meaning for ya. Plus the obvious risk of O.D on GBL.

Well anyways I hope I gave you a few pointers on how I deal with my usage and some tips on what to do and perhaps not to do.
When it comes to GBL, and you are not using the amounts my friend did, I think cold turkey and maybe some anti-anxiouty pills are best way out. Important to be clear about one more thing, you would not want to change your GBL abuse to a benzo-abuse...Also had another friend try that path...Not a funny story.
 
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