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Probleminfected

finished off the verte last night

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I'm guessing about 24hrs??????

since the post on the 20th about trying his first real absinthe,now its gone already?

dude,....you guzzle too fast. :D

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Good ghod, that's fast! I had a friend in college who could hold his liquor when others would have either passed out or died of alcohol poisoning, but absinthe? How can you afford it? More importantly, if your liver can handle the ethanol, how about the thujone?

 

(After my first couple of glasses, I must agree that I like it better without the added sugar.)

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well i must have drank 1/3 of the bottle on friday and 1/8 on thursday. friends drank the rest

 

lets just say, i had one hell of a night, and i'm still feeling hungover haha.

 

also can't do that, that often, to much $$$

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I finally found words to respond to this.

 

 

I have been capable of doing a half a bottle in a night, but not without a hangover that could kill a horse the next day.

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I have only had a hang over from Absinthe when I made the error of mixing it with champagne.

 

I'm pretty sure it wasn't the absinthe that caused it.

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I have only had a hang over from Absinthe when I made the error of mixing it with champagne.

 

I'm pretty sure it wasn't the absinthe that caused it.

 

 

champagne was alot of wood grain alcohol, which is what causes massive hangovers.

 

also the reason why moonshine, from retarted people, will make you go blind (you'll die before this happends).

 

i get hung over easy, even though i can drink alot in one night

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well methanol is much more poisoness then ethanol.

 

and since most "not in the know" don't know that methanol starts coming out at a much lower temp (i don't remember i think its 147 or somthing), while ethanol comes out at 172. Novice shiners that don't read or get taught how, just keep/mix everything together. which will give massive hangovers, and after years and years of drinking it will kill you, liver failure.

 

somebody i know *wink*wink* toses the methonal in the grass, but some people use it as a good cleaner.

 

god i sound like a know it all, i'll stop

Edited by Probleminfected

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IIRC hangovers are generally caused by sulfites (ides?) and a lack of water. I have yet to get a hangover but the times I've been drunk from mainly absinthe, I woke up the next morning more energetic than normal.

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How hangovers work.

 

Probleminfected, I believe you will find this thread to be very informative and useful.  :devil:

 

 

wow thats was great, funny though, i have been doing some of those already, like the burnt toast, energy drink w/vitamins, fried fatty food.

 

i think i need to drink more water

 

i'll be trying this next time (i know there will be)

 

thanks

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The "moonshine contains a lot of methanol and can make you go blind" theory is a myth perpetuated by the MAN. A lot of Grappa and Whiskey producers don't even toss the heads! The cure for methanol poisoning is ethanol. Unless you're drinking pure methanol, which is unlikely due to waste and cost, you are probably not going to go blind (unless you mix swords and Absinthe.)

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The "moonshine contains a lot of methanol and can make you go blind" theory is a myth perpetuated by the MAN. A lot of Grappa and Whiskey producers don't even toss the heads! The cure for methanol poisoning is ethanol. Unless you're drinking pure methanol, which is unlikely due to waste and cost, you are probably not going to go blind (unless you mix swords and Absinthe.)

Jack! You are loosin it. Methanol is no myth and you should know better. :puke:

Maybe I should expound a little. The methanol content of a brew depends sitgnificantly on what you start with to a high defree. Lots of fructose (apples for instance are very high in fructose and consequently produce more methanol than corn). Newbies should use extreme caution drinking the heads of any distillate until they understand this!! Old moonshiners really did throw away the heads!Temperature control and knowing the various alcohols boiling points really is important.

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Methanol

Pharmacology: Methanol (methyl alcohol) is produced from the distillation of wood and is a clear, colorless, volatile liquid with a weak odor that is somewhat sweeter than ethanol. Methanol is used in the industrial production of many synthetic organic compounds and is a constituent of many commercially available solvents. Products that are available in the home that contain methanol include: windshield wiper fluids and de-icers, antifreeze, glass cleaner, canned heat, paints, varnishes, paint thinners and removers. It can also be used in gasohol, which could present problems as people try to siphon the gas by mouth and accidentally ingest some. Methanol is a natural fermentation product and its concentration may be up to 300 mg/L in wine, and even higher in other spirits.

 

Methanol is well absorbed from the gastrointestinal tract mucosa as well as through the skin and lungs. Both inhalation and transdermal exposure can result in toxicity. The exact lethal dose for a human is not known. Doses as low as 25 cc of 40% methanol have been reported as causing toxicity. In other cases doses up to 500 cc have occurred with no side effects. Most sources consider the minimal lethal dose to be around 100 cc (1 g/kg). Poisoning with methanol may be accidental or intentional. There have been epidemics of methanol toxicity in cases where illicit whiskey has been sold to large populations or when the less expensive methanol was substituted for ethanol in drinks.

 

Once methanol is absorbed it is rapidly distributed in the body water with peak blood levels occurring in about 30 to 90 minutes after exposure. If ethanol is not present 2-5% of the methanol is excreted unchanged by the kidneys and a small amount is eliminated by the lungs. At low blood levels the half-life of methanol is 2-3 hours. Once the blood levels rise above 300 mg/dl, the enzymes that metabolize methanol become saturated and the elimination half-life increases to 27 hours. When this happens a greater amount of the methanol is eliminated unchanged by the lungs and the kidneys. During therapy with ethanol the half-life of methanol becomes 30-52 hours.

 

Methanol itself may cause inebriation but by itself is almost completely non-toxic. The methanol is metabolized by alcohol dehydrogenase to formaldehyde and then to formic acid. Clinical findings correlate better with formic acid levels than with methanol levels. It is these two metabolites that cause toxicity with formic acid being more responsible. It is the formic acid that causes the profound metabolic acidosis that is typical of methanol poisoning. The overall mortality of methanol poisoning is approximately 20% and among survivors the rate of permanent visual impairment is 20-25%.

 

Clinical Presentation: The presentation within the first 1-2 hours may be similar to ethanol intoxication in that the patient may have drowsiness, vertigo, and uninhibited behavior. There is typically a delay of the toxic symptoms anywhere from six-30 hours and longer if ethanol has been co-ingested. In cases of methanol ingestion a lack of symptoms early on does not mean that the patient has not ingested a toxic amount of methanol.

 

Aside from the symptoms of intoxication patients may also present with gastrointestinal symptoms due to acute gastritis or pancreatitis. The gastritis may be severe and is occasionally hemorrhagic. Symptoms include anorexia, severe abdominal pain, vomiting, diarrhea, increased transaminases or increased amylase. Early visual disturbances are the classic findings that are associated with methanol intoxication and include decreased vision or blurred vision. Patients may complain of a 'snowstorm' in front of the eyes or photophobia. The pupils may be fixed and dilated with the funduscopic exam revealing retinal edema with hyperemia of the optic disc. In severe cases there may be papilledema and engorged retinal vessels. Other complications of severe methanol intoxication include coma, seizures, blindness, oliguric renal failure, cardiac failure, and pulmonary edema. Death may be rapid or may occur several hours after coma. Death is associated with inspiratory apnea, terminal opisthotonos and convulsions.

Diagnosis: Patients who present early in their course with knowledge that they accidentally or intentionally ingested methanol present little difficulty. Those that cannot or will not provide an complete history as to their possible ingestion are clearly more difficult. The symptoms and physical signs are non-specific. The patient may have a faint odor of methanol on the breath but this can easily be missed. Ocular findings are the most specific physical findings and are important diagnostically. The ocular physical findings or complaints in addition to a severe metabolic acidosis as well as a high osmolar gap can justify a presumptive diagnosis of methanol poisoning. The literature does contain cases where severe methanol intoxication has been present but no anion gap metabolic acidosis was found (Palmisano et al. 1987). The majority of patients reviewed had high ethanol levels which appeared to limited the formation of formic acid. Thus, it is important to be aware that a patient who presents with methanol exposure may have delayed clinical and laboratory findings even if there was a large ingestion of methanol.

 

Treatment: As with any poisoned patient the initial management includes close attention to adequate airway, ventilation, and perfusion. If the patient is seen early , gastric lavage to remove any residual gastric methanol should be done. If there is exposure to the skin, then decontamination should be done. Syrup of ipecac is not recommended as the mental status may rapidly deteriorate and there is a significant risk of aspiration. Activated charcoal has not been proven to absorb ethanol to any extent and these studies have been presumed to apply to methanol. Also, because alcohols tend to be consumed in large amounts and are rapidly absorbed there does not appear to be any benefit. Therefore, if there is no concern of coingestion with other toxic substances there is probably little indication for charcoal.

 

Labs should be sent immediately for CBC, chem 7, LFT's, amylase, U/A, serum osmolarity, and methanol level. Therapy should not be withheld pending the results of methanol level if there is a high suspicion of methanol intoxication. It may be appropriate to send ethanol and ethylene glycol levels.

 

Ultimately, when treating methanol intoxication there are three major modalities to use:

 

(1) decrease the metabolic degradation of the methanol to its toxic degradation products

 

(2) dialysis to increase the removal of both the methanol and the toxic intermediates

 

(3) alkalinization to counteract the severe metabolic acidosis.

 

** Ethanol is used to decrease the metabolism of methanol. Alcohol dehydrogenase acts within the liver to break down both ethanol and methanol, and is the rate limiting step in the metabolism of both these alcohols. The enzyme, alcohol dehydrogenase, has a greater affinity for ethanol than it does for methanol. Therefore, in the presence of ethanol, the metabolism of methanol to its toxic metabolites is greatly slowed. If there is a high clinical suspicion that a patient has ingested methanol it is appropriate to begin an ethanol drip while awaiting blood levels of methanol. Ethanol drips are also indicated if the blood methanol level returns and is 20 mg/dl or above. The target ethanol level is 100-150 mg/dl since this is the level that will saturate alcohol dehydrogenase. The recommendations for loading doses and maintenance drips are seen on table 2 below. This table assumes a typical volume of distribution and elimination. Clearly, ethanol levels must be frequently checked to assure an adequate ethanol level. Chronic drinkers need a higher rate of ethanol administration. :D

The intravenous route of administration needs to be done through a central line because 10% ethanol has high osmolarity.

 

Table 2: Standard ethanol dosing in a typical adult:

 

(one ml of absolute ethanol contains 790 mg of ethanol (specific gravity 0.79) so a 10% ethanol solution has 79g/dl and an 86-proof alcoholic beverage has 34 grams per dl)

 

** Forced diuresis has little effect on methanol elimination, however, dialysis is very effective in the removal of both methanol and formic acid from the body. Hemodialysis is preferred over peritoneal dialysis because it offers a more rapid mechanism of clearance. Hemoperfusion should not be used because the columns may quickly become saturated with the methanol and then become ineffective. Hemodialysis also has the advantage of being able to correct the metabolic acidosis or fluid and electrolyte disturbances that may be present. Indications for dialysis include ocular manifestations of toxicity, all cases in which the patient may have underlying renal impairment, and a peak methanol level greater than 50 mg/dl. It is important to remember that levels below 50 mg/dl may still have significant toxicity because the majority of the measured methanol has already been converted into its toxic metabolites. Thus, the most important consideration in dialysis in the presence of clinical manifestations and a severe metabolic acidosis. If dialysis is initiated the ethanol drip must be increased. Dialysis should be continued until the methanol level falls below 20 mg/dl. The patient must be followed closely after dialysis as a 'rebound' phenomenon has been well documented with the methanol levels increasing as much as 20 mg/dl over the 72 hour period following dialysis.

 

** Additional therapeutic intervention for methanol poisoning includes controlling the degree of metabolic acidosis. This is accomplished by administering sodium bicarbonate to the patient. This should be considered in acidotic patients with a bicarb. less than 15 mEq/L. The patient's sodium, pH, and potassium must be monitored. Some reports suggest that such therapy may ameliorate the ocular manifestations and possibly reduce the mortality.

 

** A final consideration in the treatment of methanol intoxication is the addition of folate acid to the patients treatment regimen. The enzymes that metabolize formic acid into CO2 in humans are folic acid dependent. Clearly, folic acid deficiency could decrease the rate of metabolism of formic acid. Whether folic acid is beneficial in a person who does not have folic acid deficiency is not clear but it is probably prudent to administer this agent.

 

 

--------------------------------------------------------------------------------

 

On the Horizon: Pyrazole is known to be a potent competitive inhibitor of alcohol dehydrogenase. 4-Methyl pyrazole is an even more specific inhibitor of this enzyme and has less side effects than the former agent. This compound has been shown to inhibit the production of formic acid from methanol in experimental models. This agent has also been shown to be beneficial in ethylene glycol intoxication. Unfortunately, this medication is still not approved for use in the U.S.

 

Pediatric Considerations: Children tolerate the severe metabolic acidosis less well than do adults and it must be carefully managed. Ethanol is still the antidote of choice and levels of greater than 100 mg/dl are desired. This is accomplished with an IV infusion of 600 mg/kg bolus followed by 110 mg/kg/hr. The ethanol must be administered in a large volume of fluid which can become a problem in children. At times the ethanol must be given orally to prevent fluid overload in the pediatric population. As with adults, blood levels of greater than 50 mg/dl of methanol require hemodialysis.

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...Newbies should use extreme caution drinking the heads of any distillate until they understand this...

 

I agree! Don't drink heads!!!

 

My point being that in a full run, you will never cut off the hearts soon enough to cause blindness or death.

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