From all that I have read, it is clear that ETG is dose dependent, I.e. The more alcohol consumed, the more ETG produced. Detection of ETG is also more dependent on time than actual consumption, although consumption as noted above, does play a role. One has been repeatedly advised to calculate ETG elimination time windows from a 0 BAC state. This all brings me to my question. Will a higher peak BAC produce more ETG? In other words, if two people drank four drinks, but one person drank four drinks over four hours with a peak BAC never going over .02 while the other drank all four quickly, would the same amount of ETG be produced? In other words, the doses are the same, 0 BAC would be reached at the same time, but peak BAC would be different. Is total ETG the same for both individuals or will the individual who drank over time pass ETG sooner? Thanks for the information.

Here's how it should be.

EtG is a product of Phase II metabolism in the liver, or so it is written.

Not all ethanol (EtOH) metabolism occurs in the liver. About 20% of the dose is metabolized in the gastrointesinal tract, primarily in the stomach by the enzyme Alcohol dehydrogenase (ADH).

It is assumed that this extra-hepatic metabolism would not produce EtG/EtS as the EtOH never enters circulation therefore never reaches the liver.

Add to this that metabolism in the stomach is influenced by the EtOH concentration of the substance. Seems most efficient at about 23%. Above that figure ADH is either reduced or overly saturated and becomes less efficient.

This would seem to point to lower production of EtG in spaced low consumption (lower peak). It would also indicate that anything retaining EtOH in the stomach, food as best example, increases extra-hepatic metabolism thereby reducing hepatic involvement.

The phenomena outlined is well tested in relation to EtOH metabolism but has not been tested in relation to EtG synthesis. As example, there has never been a study comparing EtG production in a fasted state as compared to a fed state, while many such studies have been conducted on EtOH.

It could be that there is a missing link here. Perhaps EtG synthesis is not exclusive to the liver, rather an intra-cellular process. I believe that is a possibility based on studies involving endogenous EtOH production and metabolism.

Therefore, lower peak should result in lower EtG based on the assumption (current science) that EtOH never reaches the point where EtG is synthesized.

Don't take that to the bank. There are too many variables that have not been investigated. Probably never will be.

Are you asking as a medical professional and want your diagnosis confirmed?