Organic certification for Alcoholic

Courtesy: Organic certification for Alcoholic

Kinetics

Absorption

Ethanol can be taken orally, by inhalation, rectally, or by injection (e.g., intravenous), though it is typically ingested simply via oral administration. The oral bioavailability of ethanol is around 80% or more. In fasting volunteers, blood levels of ethanol increase proportionally with the dose of ethanol administered. Blood alcohol concentrations may be estimated by dividing the amount of ethanol ingested by the body weight of the individual and correcting for water dilution.

Onset

Peak circulating levels of ethanol are usually reached within a range of 30 to 90 minutes of ingestion, with an average of 45 to 60 minutes. People who have fasted overnight have been found to reach peak ethanol concentrations more rapidly, at within 30 minutes of ingestion.

The onset varies depends on the type of alcoholic drink:

• Vodka/tonic: 36 ± 10 minutes
• Wine: 54 ± 14 minutes
• Beer: 62 ± 23 minutes

Also, carbonated alcoholic drinks seem to have a shorter onset compare to flat drinks in the same volume. One theory is that carbon dioxide in the bubbles somehow speeds the flow of alcohol into the intestines.

Food in the gastrointestinal system and hence gastric emptying is the most important factor that influences the absorption of orally ingested ethanol. The absorption of ethanol is much more rapid on an empty stomach than with a full one. The delay in ethanol absorption caused by food is similar regardless of whether food is consumed just before, at the same time, or just after ingestion of ethanol. The type of food, whether fat, carbohydrates, or protein, also is of little importance. Not only does food slow the absorption of ethanol, but it also reduces the bioavailability of ethanol, resulting in lower circulating concentrations.

Distribution

Upon ingestion, ethanol is rapidly distributed throughout the body. It is distributed most rapidly to tissues with the greatest blood supply. As such, ethanol primarily affects the brain, liver, and kidneys. Other tissues with lower circulation, such as bone, require more time for ethanol to distribute into. Ethanol crosses biological membranes and the blood–brain barrier easily, through a simple process of passive diffusion. The volume of distribution of ethanol is around .55 L/kg (0.53 US pt/lb). It is only weakly or not at all plasma protein bound.

Approximately 90% of the metabolism of ethanol occurs in the liver. This occurs predominantly via the enzyme alcohol dehydrogenase, which transforms ethanol into its metabolite acetaldehyde (ethanal). Acetaldehyde is subsequently metabolized by the enzyme aldehyde dehydrogenase into acetate (ethanoate), which in turn is broken down into carbon dioxide and water. Acetate also combines with coenzyme A to form acetyl-CoA, and hence may participate in metabolic pathways. Alcohol dehydrogenase and aldehyde dehydrogenase are present at their highest concentrations in the liver, but are widely expressed throughout the body, and alcohol dehydrogenase may also be present in the stomach and small intestine. Aside from alcohol dehydrogenase, the microsomal ethanol-oxidizing system (MEOS), specifically mediated by the cytochrome P450 enzyme CYP2E1, is the other major route of ethanol metabolism. CYP2E1 is inducible by ethanol, so while alcohol dehydrogenase handles acute or low concentrations of ethanol, MEOS is predominant with higher concentrations or with repeated/chronic use. A small amount of ethanol undergoes conjugation to form ethyl glucuronide and ethyl sulfate. There may also be another metabolic pathway that metabolizes as much as 25 to 35% of ethanol at typical concentrations.

At even low physiological concentrations, ethanol completely saturates alcohol dehydrogenase. This is because ethanol has high affinity for the enzyme and very high concentrations of ethanol occur when it is used as a recreational substance. For this reason, the metabolism of ethanol follows zero-order kinetics at typical physiological concentrations. That is, ethanol does not have an elimination half-life (i.e., is not metabolized at an exponential rate), and instead, is eliminated from the circulation at a constant rate. The mean elimination rates for ethanol are 15 mg/dL per hour for men and 18 mg/dL per hour for women, with a range of 10 to 34 mg/dL per hour. At very high concentrations, such as in overdose, it has been found that the rate of elimination of ethanol is increased. In addition, ethanol metabolism follows first-order kinetics at very high concentrations, with an elimination half-life of about 4 or 4.5 hours (which implies a clearance rate of approximately 6 L/hour/70 kg). This seems to be because other processes, such as the MEOS/CYP2E1, also become involved in the metabolism of ethanol at higher concentrations. However, the MEOS/CYP2E1 alone does not appear sufficient to fully explain the increase in ethanol metabolism rate.

Some individuals have less effective forms of one or both of the metabolizing enzymes of ethanol, and can experience more marked symptoms from ethanol consumption than others. However, those having acquired alcohol tolerance have a greater quantity of these enzymes, and metabolize ethanol more rapidly