The customer nobody speaks to

The figures are known and are nonetheless rarely thought through together. Around four per cent of the Swiss population aged fifteen and over drink at chronically risky levels, with a rising share at higher ages. An estimated 250,000 to 300,000 people are considered alcohol-dependent. Each year around 1,600 people die from the consequences of alcohol consumption, and the social costs are put at some 2.8 billion francs.[1][2] At the same time only about one in ten of those affected receives any pharmacotherapy at all, even though its effectiveness is documented.[3]

These people do not come into the pharmacy with the request “I drink too much”. They come because of sleep disturbances, heartburn, headaches, high blood pressure, diarrhoea, nervousness or a wound that will not heal. They buy ibuprofen, proton pump inhibitors, valerian, electrolyte powder. The community pharmacy is thus in fact the institution with the most contacts with this group, and at the same time the one in which it is least talked about.

Recognising without labelling

The signals are rarely dramatic. What stands out are patterns: the repeated purchase of gastric acid blockers without medical assessment, a need for sleeping aids that grows over years, frequent minor injuries, unexplained weight loss, morning tremor, alternating pharmacies for the same substance class, questions about the alcohol content of preparations. Added to this are the classic laboratory indications that sometimes appear on a report the customer brings along: raised gamma-GT, raised MCV.

As a brief instrument, the AUDIT-C has become established: three questions on frequency, quantity and binge drinking. It is validated, can be taken in two minutes and is nonetheless usually too formal for a counter conversation. The decisive step is therefore not a questionnaire but a permission: “May I ask you about something that might have to do with your stomach?”

That the effort is worthwhile is well documented. Brief interventions in low-threshold settings reduce consumption measurably; the Cochrane review by Kaner and colleagues found a mean reduction of the order of around twenty grams of alcohol per week compared with control groups.[4] That sounds modest, and at the individual level it is. At population level, extrapolated to a pharmacy’s contact numbers, it is not.

The interactions that actually count

Here lies the genuinely pharmaceutical contribution, and it is greater than the standard sentences in the package leaflet suggest.[5][6]

Paracetamol. Chronic alcohol consumption induces CYP2E1, so that more of the hepatotoxic metabolite NAPQI is formed, while at the same time glutathione reserves are exhausted through malnutrition. The dangerous constellation is not the glass of wine with the tablet, but chronically high consumption plus fasting plus dosing at the upper limit. In this situation the maximum daily dose has to be reduced and self-medication limited in time.

Non-steroidal anti-inflammatory drugs. Alcohol and NSAIDs both raise the risk of gastrointestinal bleeding, disproportionately so in combination. Where liver disease already exists, the renal component is added. This is the most frequent and at the same time most easily avoidable combination in over-the-counter sales.

Sedating substances. Benzodiazepines, Z-drugs, opioids, sedating antihistamines and antitussives add up with alcohol to a depression of respiration and vigilance. This combination lies behind a considerable share of the deaths in this group. Where risky consumption is known, every one of these dispensings should be questioned, including the supposedly harmless one.

Antidiabetics. Alcohol inhibits hepatic gluconeogenesis. Under insulin or sulfonylureas, this can turn into severe, often nocturnal and delayed hypoglycaemia, which is moreover easily misread as intoxication. With metformin, the risk of lactic acidosis rises during acute intoxication.

Anticoagulation. With vitamin K antagonists, acute alcohol consumption inhibits metabolism and drives the INR up, while chronic consumption induces it and lowers the INR. The result is fluctuating values that nobody can explain as long as nobody asks. With advanced liver disease, coagulation shifts anyway.

Disulfiram-like reactions. Metronidazole is the best-known case; the warning appears in the product information, even though the evidence base is debated in the professional literature. Further candidates are tinidazole, griseofulvin and individual cephalosporins. In practice: with these substances, abstinence from alcohol is raised actively and not left to the package insert.

And the point only a pharmacy sees: alcohol is present in medicines. Tinctures, herbal drops, some cough syrups and oral solutions contain ethanol in relevant amounts. For a person in abstinence this can be a relapse trigger, and under disulfiram even a dangerous reaction. Anyone who knows and offers an alcohol-free equivalent achieves more in thirty seconds than any factsheet.

Withdrawal is the dangerous part

Anyone who wants to stop occasionally receives the well-meant advice in the pharmacy simply to give it a try. That advice can be fatal.

In physical dependence, withdrawal symptoms typically begin six to twenty-four hours after the last drink with tremor, sweating, tachycardia, restlessness and nausea. Withdrawal seizures occur predominantly in the first two days, delirium tremens usually after forty-eight to seventy-two hours, and untreated it carries considerable mortality.[7]

Warning signs of a relevant withdrawal risk are morning drinking, drinking to avoid shaking, previous withdrawal seizures or a previous delirium, and pronounced autonomic signs. If one of these is present, the only correct advice is: do not stop abruptly, but have it medically supervised. A qualified withdrawal is possible on an outpatient or inpatient basis, but it belongs in medical hands.

To this belongs a second point that is regularly forgotten. Chronic alcohol consumption leads to thiamine deficiency, and a thiamine deficiency can result in Wernicke’s encephalopathy. Administering carbohydrates or glucose without prior thiamine can trigger it.[8] Anyone encountering someone in this situation in the pharmacy should have thiamine in mind – and before the well-meant dextrose.

The group that stands out least

Chronically risky consumption is not the domain of the young. Its share rises with age and is highest among those over sixty-five.[1] That is the group that appears most frequently in the pharmacy, obtains the most medicines and about which someone asks least often.

Pharmacologically, each of the points above becomes more acute in old age. The proportion of body water falls, so the same amount of alcohol produces a higher blood concentration. Hepatic metabolism slows. Polymedication multiplies the number of possible interactions, and sedation meets an already increased risk of falls. At the same time, the symptoms are systematically misinterpreted: forgetfulness counts as incipient dementia, unsteady gait as a sign of ageing, insomnia as normal, tremor as a side effect.

The sentence “at that age it doesn’t matter any more” is, in this constellation, not benevolent but wrong. It is also epidemiologically outdated: since 2023 the World Health Organization has held that there is no safe level of alcohol consumption for health, particularly with regard to cancer risk.[10]

What is possible pharmacologically

In Switzerland, acamprosate, naltrexone and nalmefene are available for relapse prevention; disulfiram is also on the market and is listed in the product information as a second-line option after naltrexone or acamprosate.[9]

The evidence is solid but unspectacular. The large meta-analysis by Jonas and colleagues in JAMA calculated for acamprosate a number needed to treat of twelve to prevent a return to any drinking, and for naltrexone at the 50-milligram dose an NNT of twenty for preventing heavy drinking days.[3] These are magnitudes familiar from cardiovascular prevention, where they are accepted as a matter of course.

Four things matter for dispensing. Under naltrexone, opioids are ineffective or dangerous; those affected should carry a note, because emergency analgesia otherwise becomes a problem. Acamprosate is dosed by weight, at over sixty kilograms three times daily two tablets, which represents an adherence hurdle and brings diarrhoea as the most frequent side effect. Nalmefene is taken as needed, ideally one to two hours before the expected drinking situation, and explicitly targets reduction of consumption rather than abstinence. Disulfiram presupposes complete abstinence, including hidden sources of alcohol, and only makes sense if the person concerned expressly wants it.

The last point deserves a remark of its own, because it changes the consultation. The treatment goal need not be abstinence. Reduction of consumption is a recognised, evidence-based goal, and for many people it is the only one they are willing to talk about at all. Anyone who counts only complete abstinence as success in the conversation loses the person before anything has begun.

How the conversation actually works

Research on motivational interviewing is unambiguous on one point: confrontation generates resistance, not change. What works is unspectacular.

Ask permission before raising the topic. Stay within your own field, that is with the medicine and its tolerability, rather than with character. Ask an open question, for instance how much someone drinks on an ordinary day, without judgement in the voice. Let the answer stand, even if it is evidently understated. And at the end name a concrete, low-threshold follow-up option, rather than making a diagnosis.

In Switzerland these include the cantonal addiction counselling centres, the anonymous online counselling of safezone.ch, the services of Addiction Switzerland and the Blue Cross, and for one’s own professional research the platform praxis-suchtmedizin.ch, which holds procedural schemes for every substance group.

One sentence that has proved itself: “If you ever want to talk about it, there are options, and I can tell you where.” It demands nothing, it insinuates nothing, and it stays in the mind.

Relatives

Often it is not the person concerned who asks, but the wife, the son, the neighbour. They come with a hidden question: whether one could give them something for the father, whether there is something one could mix into his food, whether one could force him.

These conversations deserve time, and they need three clear statements. First: covert medication is defensible neither legally nor pharmacologically, and under disulfiram it would be dangerous. Second: abrupt withdrawal without medical supervision is risky in physical dependence, which is why the well-meant suggestion of disposing of all the bottles can come to nothing. Third, and this is the real contribution: relatives have their own entitlement to counselling, regardless of whether the person concerned ever does anything. The cantonal addiction counselling centres and the services for relatives of Addiction Switzerland and the Blue Cross are open to them. Anyone who gives this pointer relieves a person who has often been alone with it for years.

What remains

Alcohol dependence is the country’s most frequent addictive disorder, it is treatable, and it still predominantly goes untreated. The pharmacy will not close this gap. But it can do two things that nobody else does.

It can prevent someone from dying of a combination they put together themselves, because they did not know that sleeping tablets and an evening beer together depress respiration. And it can be the place where the subject is spoken aloud for the first time without reproach.

Neither costs any prescribing authority. It costs a question.