First published 17 December 2016 · substantially revised August 2026, because the science moved further than I expected it to.
From time to time people ask me a version of the same question, and it is always asked sincerely:
If God didn’t intend for us to drink alcohol, why do we have an enzyme — alcohol dehydrogenase — in our liver and other tissues, whose function is to process alcohol?
I wrote this with sincere believers in mind — people who ask themselves questions like this and want a reasonable answer rather than a slogan. I also wrote it in response to those who argue the enzyme settles the matter: if God did not intend us to use alcohol, they say, He would not have placed the machinery to process it in so many of our cells.
I have learned that questioning why God did or did not do something a certain way leads, invariably, to our discovering how little we know. This is no exception. But the biology itself is not mysterious at all, and it is where the argument comes apart.
What alcohol dehydrogenase actually does
ADHs are a family of enzymes found in most living things. They convert alcohols into aldehydes and ketones, and in doing so reduce a coenzyme, NAD+, to NADH.
Notice the plural. Their substrate is not just ethanol — the intoxicating alcohol in drinks — but a whole family of alcohols, most of which have nothing to do with making anyone drunk. Two examples matter:
- Methanol. ADH oxidises it, which is part of how the body handles a genuinely poisonous alcohol found in trace amounts in ordinary food.
- Vitamin A. Retinol is, chemically, an alcohol. ADH converts it to retinoic acid, a hormone with major roles in growth, development and vision. Without this reaction you do not have a nutritional inconvenience; you have a developmental catastrophe.
ADH enzymes are present in animals, plants, bacteria and yeast alike. The enzyme was first described in brewer’s yeast, Saccharomyces cerevisiae — where, tellingly, it runs the other way, turning sugars into ethanol rather than clearing it.
An enzyme that can process a substance is not evidence that we were built to consume it. We metabolise prescription drugs, plant toxins and industrial solvents too.
That sentence is really the whole answer, and everything below is detail. But the detail turns out to be more interesting than I realised when I first wrote this.
Endogenous ethanol: your gut makes alcohol
I used to order drug screens regularly for patients taking controlled medications. Occasionally one came back showing a small amount of alcohol in someone adamant they never touch it — and I had known some of them long enough to believe them.
They were telling the truth. Small amounts of ethanol are produced in the digestive tract by bacteria and yeast fermenting carbohydrate, and absorbed into the bloodstream along with everything else. This is endogenous alcohol, and everyone has it.
We do not wander about half-drunk after meals for two reasons. The amount is normally tiny. And every blood vessel draining the intestine passes through the liver before reaching the rest of the body — and the liver holds more ADH than anywhere else. Ethanol levels leaving the liver are roughly fifteen times lower than those arriving from the gut.
So one honest answer to the original question is simply: we need ADH because we produce ethanol ourselves, whether or not we ever drink any. The enzyme is not waiting for a glass of wine. It is doing housekeeping, every hour of every day.
What has changed since 2016
When I first wrote this I mentioned the rare cases where this system goes wrong — auto-brewery syndrome, where gut yeast overgrows and produces enough alcohol to intoxicate someone who has not been drinking. I treated it as a curiosity.
It is no longer a curiosity. In 2019 a group studying non-alcoholic fatty liver disease found strains of Klebsiella pneumoniae that generate high levels of alcohol in a large majority of their patients with the condition, against a small minority of healthy controls. Transplanting those bacteria into mice produced fatty liver disease; selectively removing the strain first prevented it.1
Why that finding is remarkable
“Non-alcoholic” fatty liver disease was named to distinguish it from liver damage caused by drinking. In at least some patients, it now appears to be caused by alcohol after all — produced internally, by their own gut bacteria, from ordinary food.
The name may turn out to be exactly wrong. That is worth sitting with before anyone gets confident about what a biological system is “for.”
Two other situations where the housekeeping fails: people with advanced liver disease cannot clear even endogenous ethanol well, and some develop mental fogginess from it; and people with diabetes can generate a similar picture after meals very high in sugar.
The enzyme that shows what the system is really for
This is the argument I did not have in 2016, and it is the strongest one.
ADH is only the first step. It converts ethanol to acetaldehyde, which is considerably more toxic than the alcohol it came from, and a recognised carcinogen. A second enzyme, aldehyde dehydrogenase 2 (ALDH2), clears the acetaldehyde promptly.
Roughly 8% of the world’s population — including a large share of people of East Asian descent — carries a variant that leaves ALDH2 barely functional. They are the people who flush, flood and feel ill after one drink. Acetaldehyde accumulates instead of being cleared.
And those people, when they drink regularly, have a markedly higher risk of oesophageal cancer than people with fully working ALDH2.2
Consider what that demonstrates. If the ADH system existed so that we could enjoy alcohol, a partial failure of it would be a mild inconvenience. Instead a partial failure produces cancer. That is the signature of a detoxification pathway, not a digestion pathway. The body treats ethanol the way it treats a poison, because that is what ethanol is.
A mitigating mercy?
Here I want to speculate, and to label it as speculation.
From the perspective of an omniscient God, it is not difficult to imagine ADH functioning as a protection — foreseeing that human beings would develop a taste for ethanol, or meet it by accident, and providing the means to survive the encounter.
We know how toxic ethanol is when the liver is overwhelmed; acute intoxication kills people every week. We know that women, who have lower levels of gastric and hepatic ADH, reach higher blood levels from the same drink. So do people with liver disease.
We have a habit of building a straw God in our minds and then telling him what he may and may not do. Some reason that because God gave them ADH, he meant them to drink. I would suggest the opposite reading is at least as available: that the enzyme is a mercy extended to people He knew would drink anyway.
It would not be the first time. Scripture records God tolerating and working with people who practised polygamy and divorce without ever presenting either as His intention. He has been willing to forgive a great deal, and to redeem people most of us would have written off. Much of what readers find repellent in the Old Testament is exactly this: we fix on what the human characters did, and miss that the point of the story is a God who goes to considerable lengths for people who have made a mess of things.
This mitigating purpose is speculative and I will leave it there. The three biological reasons below are not.
What the evidence now says about drinking
I should be straightforward that this section did not exist in the original article, because in 2016 the picture was genuinely less clear. The received wisdom then included a protective effect of moderate drinking on the heart, and I did not want to overstate a case.
That position has weakened badly.
- The Global Burden of Disease analysis, covering 195 countries, concluded that the level of consumption minimising overall harm is zero. Whatever cardiovascular benefit exists is outweighed by cancer and other causes.3
- The 2025 US Surgeon General’s advisory describes a causal link between alcohol and at least seven cancers — breast, colorectal, oesophageal, liver, mouth, throat and larynx — with breast cancer risk rising from around one drink a day, and calls for cancer warning labels.4
- Much of the older “moderate drinkers live longer” literature compared drinkers against an abstainer group that included people who had stopped because they were ill. Correct for that and the benefit shrinks toward nothing.
I mention this without triumph. I have watched alcohol do a great deal of damage to people I was trying to help, and I have also watched clinicians dismiss patients’ concerns about a couple of glasses a night on the strength of evidence that has since been revised. Both are failures.
Concluding thoughts
There are at least three reasons we carry ADH enzymes, none of which is “so that we can drink”:
- To process alcohols other than ethanol — methanol, and vitamin A on its way to becoming a hormone.
- To clear the endogenous ethanol our gut flora, and possibly our own cells, produce continuously.
- Possibly as mitigation against accidental or intentional intoxication.
And the question illustrates three things worth carrying away:
- Reality is more complicated than our first guess. One enzyme, several substrates, an entire second enzyme downstream, and a gut flora capable of brewing alcohol without our knowledge.
- Watch the logic. Applied consistently, the original argument says we should freely consume every substance we possess an enzyme to metabolise. That list includes methanol and a good deal of the pharmacy.
- Be careful ascribing motives to God. Especially from a single biochemical observation, and most especially when the conclusion happens to be the one we wanted.
None of this is medical advice about your own drinking, and it is not a verdict on anyone’s conscience. If you are worried about how much you drink, that is worth raising with your own doctor, who can ask the questions an article cannot.
References
Every claim above traces to one of these. The 2016 original carried none, which is a fair criticism of it.
- Yuan J, Chen C, Cui J, et al. Fatty liver disease caused by high-alcohol-producing Klebsiella pneumoniae. Cell Metabolism. 2019;30(4):675–688. https://doi.org/10.1016/j.cmet.2019.08.018
- Brooks PJ, Enoch MA, Goldman D, Li TK, Yokoyama A. The alcohol flushing response: an unrecognized risk factor for esophageal cancer from alcohol consumption. PLoS Medicine. 2009;6(3):e1000050. https://doi.org/10.1371/journal.pmed.1000050
- GBD 2016 Alcohol Collaborators. Alcohol use and burden for 195 countries and territories, 1990–2016: a systematic analysis for the Global Burden of Disease Study 2016. The Lancet. 2018;392(10152):1015–1035. https://doi.org/10.1016/S0140-6736(18)31310-2
- Office of the Surgeon General. Alcohol and Cancer Risk: The U.S. Surgeon General’s Advisory. Washington, DC: US Department of Health and Human Services; January 2025. hhs.gov