Alcohol and health: the risk and the importance of dose

Alcohol and ethanol: what science really says about cancer risk

Alcohol and ethanol are not synonymous: chemically ethanol is an alcohol, more specifically ethyl alcohol, the substance found in all alcoholic beverages. The International Agency for Research on Cancer (IARC) classifies it as. Group 1 carcinogen, that is, a substance for which there is strong evidence of a causal role in the development of certain cancers in humans.

Said in this way, however, the message risks being simpler than reality. The key point is one: the relationship between ethanol and health – including cancer – depends solely on the dose.

Drinking too much is bad for you, of that there is no doubt

A high or prolonged consumption of alcohol (ethanol) is clearly associated with an increased risk of several cancers, including those of the mouth, throat, esophagus, liver, colorectum and breast. On this the scientific community agrees.

In these cases, ethanol and more specifically only its metabolite, theacetaldehyde, can damage DNA and promote processes that lead to the transformation of healthy cells into cancer cells.

Moderate consumption: a more complex picture

However, when you go from drinking “too much” to drinking a little or moderately, the scenario changes and becomes more articulated.

Many observational studies show a so-called “J-shaped” between ethyl alcohol consumption and total mortality:

• Heavy drinkers are worse off,
• but even teetotalers, on average, do not always show the best outcomes,
• while those who consume small amounts of alcohol often tend to have a lower all-cause mortality.

Some research has even observed a lower incidence of some specific cancers (such as kidney or thyroid) in light drinkers, although these data should be interpreted with caution, as with all epidemiological data and not referring to the molecular mechanism.

Why the “dose” is important

From a scientific point of view, ethanol can be considered a “component” cause of cancer:

• at high doses contributes to carcinogenesis;
• At low doses, however, is not necessarily sufficient by itself to trigger the process.

In fact, the body has defense systems capable of metabolizing ethanol and repairing cellular damage. In many individuals, these mechanisms are sufficient when exposure is limited (and also appear to have protective efficacy).

We don’t all react the same way

Another key aspect is that risk is not the same for everyone. It matters a lot:

• genetics,
• sex,
• the mode of consumption (drinking little and regularly is not the same as concentrating large amounts),
• the type of alcoholic beverage (it is different whether we are talking about wine drunk in moderation during a meal or hard liquor on an empty stomach),
• The general state of health,
• Lifestyle (diet, physical activity, smoking).

For this reason, public health messages that state. “there is no safe dose of alcohol” refer specifically to to oncological risk, considered in isolation.
When, on the other hand, we evaluate all health outcomes as a whole, several studies suggest that a moderate consumption may be associated with improved overall health.

A little-cited number: the “Number Needed to Harm” (NNH)

An epidemiological concept rarely explained to the general public is that of Number Needed to Harm (NNH), i.e. The number of people who must be exposed to a risk factor for additional harm to be observed. This is a purely statistical tool, useful for distinguishing between theoretical risk e actual impact on a population.

Take the oft-cited example of the relationship between ethanol and breast cancer. To the question “Does alcohol cause breast cancer?” the scientifically correct answer is. yes: there is an increase in relative risk. However, when moving from relative risk to absolute risk, the picture changes significantly.

In women between 40 to 50 years of age, epidemiological estimates indicate that to observe one additional case of breast cancer, it would be necessary that about 1,700 abstemious women to start drinking (moderately) for ten years. In other words, for 1 more women developing cancer, for 1,699 women drinking or not drinking would have made no difference on the oncological level.

This does not mean denying the risk, but contextualize it: numbers should be interpreted, not used to generate fear. Also because, in the same female population, several studies show a reduction in cardiovascular risk associated with moderate alcohol consumption, especially when wine is taken during meals.
As is often the case in medicine, there is no one-size-fits-all answer: understanding the data allows each person to make his or her own assessments in an informed way, without oversimplification or alarmism.

How, then, should ethanol be understood?

In light of the available evidence, ethanol should be considered:

• a high-dose carcinogen,
• A risk factor embedded in complex causal pathways.,
• An element whose impact depends on quantity, duration and individual characteristics.

Simply saying that “alcohol causes cancer” without further specification risks oversimplifying a nuanced scientific reality. At the same time, ignoring its causal role (at least conservatively) in overconsumption would be equally incorrect.

Balanced communication, dose-sensitive, is essential to respect science and help people make informed choices.

The vignette used for the opening is by Yulchiboev Muzaffar, “Contract,” from the Spirito di Vino (eno)satire contest, 2018 edition, Under 35 category, organized by the Movimento Turismo del Vino Friuli Venezia Giulia.