Kurzgesagt – In a Nutshell
Kurzgesagt – In a Nutshell
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Sources – Alcohol
Sources – Alcohol
We thank the following expert for his input and critical reading:
Prof. Dr. med. Helmut K. Seitz
Professor of Internal Medicine, Gastroenterology and Alcohol Research, University of Heidelberg
- Alcohol is the most harmful substance on Earth.
Four times more people die from alcohol than psychoactive drugs (e.g. heroin, cocaine, etc.).
At first glance, nicotine seems to kill more people (7.7 million). However, if we add accidents and crimes committed under the influence of alcohol, for example, as we explain a bit further below, alcohol can be described as the most dangerous substance.
#WHO (2024): Over 3 million annual deaths due to alcohol and drug use, majority among men
Quote: “A new report from the World Health Organization (WHO) highlights that 2.6 million deaths per year were attributable to alcohol consumption, accounting for 4.7% of all deaths, and 0.6 million deaths to psychoactive drug use. Notably, 2 million of alcohol and 0.4 million of drug-attributable deaths were among men.”
#WHO (2024): Global status report on alcohol and health and treatment of substance use disorders
https://iris.who.int/bitstream/handle/10665/377960/9789240096745-eng.pdf
Quote: “According to the latest WHO estimates, psychoactive drug use resulted in almost 0.6 million deaths in 2019 with infectious diseases (viral hepatitis, HIV), drug use disorders (including drug overdose),
road traffic injuries and suicides as the causes of these deaths (Figure 1.3).”
#Lancet (2021): The global burden of tobacco
https://www.thelancet.com/infographics-do/tobacco
Quote: “The most comprehensive data on global trends in smoking highlights its enormous global health toll. The number of smokers worldwide has increased to 1.1 billion in 2019, with tobacco smoking causing 7.7 million deaths – including 1 in 5 deaths in males worldwide.”
This is a brief summary of the following paper:
#Reitsma, M. et al. (2021): Spatial, temporal, and demographic patterns in prevalence of smoking tobacco use and attributable disease burden in 204 countries and territories, 1990–2019: a systematic analysis from the Global Burden of Disease Study 2019. The Lancet, Volume 397 (10292)
The following study concerning UK assessed 20 drugs using 16 harm criteria through multicriteria decision analysis (MCDA), where experts rated each drug on a scale from 0 to 100 and applied different weightings to the criteria. Alcohol was ranked as the most harmful drug overall, followed by heroin and crack cocaine. A similar study in the EU came to comparable conclusions
#Nutt, D. et al. (2010): Drug harms in the UK: a multicriteria decision analysis. The Lancet, Vol. 376
https://www.ias.org.uk/uploads/pdf/News%20stories/dnutt-lancet-011110.pdf
Quote: “Background
Proper assessment of the harms caused by the misuse of drugs can inform policy makers in health, policing, and social care. We aimed to apply multicriteria decision analysis (MCDA) modelling to a range of drug harms in the UK.
Method
Members of the Independent Scientific Committee on Drugs, including two invited specialists, met in a 1-day interactive workshop to score 20 drugs on 16 criteria: nine related to the harms that a drug produces in the individual and seven to the harms to others. Drugs were scored out of 100 points, and the criteria were weighted to indicate their relative importance.
Findings
MCDA modelling showed that heroin, crack cocaine, and metamfetamine were the most harmful drugs to individuals (part scores 34, 37, and 32, respectively), whereas alcohol, heroin, and crack cocaine were the most harmful to others (46, 21, and 17, respectively). Overall, alcohol was the most harmful drug (overall harm score 72), with heroin (55) and crack cocaine (54) in second and third places.”
#van Amsterdam, J. et al. (2015): European rating of drug harms. Journal of Psychopharmacology, Vol. 29 (6)
The criteria show the possible spectrum of harm to others: from injuries to violence and environmental damage to economic costs.
#Nutt, D. et al. (2010): Drug harms in the UK: a multicriteria decision analysis. The Lancet, Vol. 376
https://www.ias.org.uk/uploads/pdf/News%20stories/dnutt-lancet-011110.pdf
#Gell, J. et al. (2015): Alcohol’s Harm to Others. A report for the Institute of Alcohol Studies produced by the University of Sheffield School of Health and Related Research (ScHARR).
https://www.ias.org.uk/uploads/pdf/IAS%20reports/rp18072015.pdf
Quote: “Key Points
• Surveys conducted across Western countries have identified that the prevalence of harm from another person’s drinking is high (e.g. 70% in Australia and 53% in the USA).
• Understanding of the harm caused by drinkers is better developed in some fields (e.g. child welfare, domestic violence and foetal alcohol spectrum disorders) than others.
• Socio-demographic variations in harm are reported across the international literature. For example, younger age groups are significantly more likely to experience harm across most outcomes in Australia and Ireland.
• Few studies have quantified the costs of harm to people other than the drinker, but in the UK the total cost was estimated at up to £15.4 billion in 2004, excluding the costs to family and social networks.”
- Every year it kills more people than terrorism, wars, homicides and car accidents combined.
55 million people died in 2019, 3.25% of which were war battle deaths, victims of terrorism, homicides and transport accidents. in total figures, these were 1.787.500 deaths.
These figures are from 2019, i.e. before conflicts such as the full-scale Russian invasion of Ukraine. However, given the large number of alcohol-related deaths (2.6 million or 4.7% of all deaths) compared to the above figure, the statement would still be valid.
OWID (2021): Causes of death globally: what do people die from?
- And yet, more than 2 billion people drink.
#WHO (2018): Harmful use of alcohol kills more than 3 million people each year, most of them men.
Quote: “An estimated 2.3 billion people are current drinkers. Alcohol is consumed by more than half of the population in three WHO regions – the Americas, Europe and the Western Pacific. Europe has the highest per capita consumption in the world, even though its per capita consumption has decreased by more than 10% since 2010. Current trends and projections point to an expected increase in global alcohol per capita consumption in the next 10 years, particularly in the South-East Asia and Western Pacific Regions and the Region of the Americas.”
#Griswold, M. et al. (2018): Alcohol use and burden for 195 countries and territories, 1990–2016: a systematic analysis for the Global Burden of Disease Study 2016. The Lancet, Vol. 392 (10152)
https://www.thelancet.com/action/showPdf?pii=S0140-6736%2818%2931310-2
Quote: “In 2016, 32.5% (95% uncertainty interval [UI] 30.0–35.2) of people globally were current drinkers. 25% (95% UI 23–27) of females were current drinkers, as were 39% (36–43) of males (appendix 2). These percentages corresponded to 2.4 billion (95% UI 2.2–2.6) people globally who were current drinkers, with 1.5 billion (1.4–1.6) male current drinkers and 0.9 billion (0.8–1.0) female current drinkers (appendix 2, pp 2–1994). Globally, the mean amount of alcohol consumed was 0.73 (95% UI 0.68–0.78) standard drinks daily for females and 1.7 (1.5–1.9) standard drinks daily for males.”
- With just one sip, sextillions of alcohol molecules flood your stomach and small intestine.
Let’s say, one sip of beer is 30 ml with the Alcohol content of 5%. Density of ethanol is 0.79 g/ml, the molar mass of ethanol (C₂H₅OH) = 46 g/mol. The Avogadro's number is 6×1023 molecules/mol.
The Avogadro number is a fundamental constant that represents the number of particles (atoms, molecules, or ions) in one mole of a substance while a is a unit in chemistry that represents 6.022×1023 particles of a substance.
The volume of ethanol in one sip of beer:
30 ml × 5/100 =1.5 ml
The mass (volume × density) is: 1.5 ml × 0.79 g/ml=1.185 g, converted into moles is: 1.185 g / 46 g/mol ≈ 0.02576 moles. Converted to molecules (Moles × Avogadro’s number) is 0.02576 × (6×1023) = 1.55 × 1022
- From there they head to your liver – your primary detox center - and to other organs like the brain. But your liver can only process about one sip of beer every 5 minutes. So unless you drink really slowly, it will become overwhelmed while an ever-growing swarm floods your brain.
How quickly alcohol is processed depends on a number of factors (e.g. body weight, whether you have eaten anything). As a rule of thumb, you can say that one drink is metabolized per hour, i.e. a 0,33ml beer, a small glass of wine or a shot.
If you gulp down the beer all at once, the blood alcohol level would still rise sharply, as the liver can only process the alcohol step by step. We have therefore roughly estimated how many sips you would need for a beer so that alcohol consumption and metabolization rate would theoretically be in balance.
#Cederbaum, A. (2012): Alcohol Metabolism. Clinics in Liver Disease, Vol. 16 (4)
https://pmc.ncbi.nlm.nih.gov/articles/PMC3484320/pdf/nihms-402840.pdf
Quote: “Although rates vary widely, the “average” metabolic capacity to remove alcohol is about
170 to 240 g per day for a person with a body weight of 70 kg. This would be equivalent to
an average metabolic rate of about 7 g/hr which translates to about one drink per hr.”
#Wilson, D. & Matschinsky, F. (2020): Ethanol metabolism: The good, the bad, and the ugly. Medical Hypotheses, Vol. 140
https://www.sciencedirect.com/science/article/pii/S0306987720300797
Quote: “Dettling et al. [25] measured the rate of elimination of ethanol by humans following ingestion of 0.9 g/kg body weight over a period of 2 h, an amount that resulted in maximal blood alcohol levels near 0.08 g/dl (legal limit for driving in US). After consumption stopped, ethanol disappearance, measured by decrease in blood levels, occurred at a constant rate (zero order) of about 0.016 g/dl/h for men and 0.018 g/dl/h for women.”
- Here’s where the chaos begins. The legion of intruders fills your brain and starts messing with neurotransmitters and receptors. Their sabotage is so complex that scientists aren’t fully sure yet about all their mechanisms.
#Noori, H. R. et al. (2018): Ethanol-induced conformational fluctuations of NMDA receptors. Molecular Physics, Vol. 117 (2)
https://www.tandfonline.com/doi/full/10.1080/00268976.2018.1504135#abstract
Quote: “Alcohol addiction ranks among the leading global causes of preventable death and disabilities in human population. Understanding the sites of ethanol action that mediate its acute and chronic neural and behavioural effects is critical to develop appropriate treatment options for this disorder. The N-methyl-d-asparate (NMDA) receptors are ligand-gated heterotetrameric ion channels, which are known to directly interact with alcohol in a concentration-dependent manner. Yet, the exact molecular mechanisms and conformational dynamics of this interaction are not well understood.”
#Toyama, Y. et al. (2018): Structural basis for the ethanol action on G-protein–activated inwardly rectifying potassium channel 1 revealed by NMR spectroscopy. PNAS, Vol. 115 (15)
Quote: “Ethanol exerts various functions by acting on ion channels in neural systems. Despite its biological importance, molecular mechanisms underlying the ethanol action remained unknown, due to the weak binding affinity and the dynamic nature of the interaction."
#Harris, R. A. et al. (2008): Ethanol’s Molecular Targets. Science Signaling, Vol. 1 (28)
Quote: “Ethanol produces a wide variety of behavioral and physiological effects in the body, but exactly how it acts to produce these effects is still poorly understood. Although ethanol was long believed to act nonspecifically through the disordering of lipids in cell membranes, proteins are at the core of most current theories of its mechanisms of action. Although ethanol affects various biochemical processes such as neurotransmitter release, enzyme function, and ion channel kinetics, we are only beginning to understand the specific molecular sites to which ethanol molecules bind to produce these myriad effects. For most effects of ethanol characterized thus far, it is unknown whether the protein whose function is being studied actually binds ethanol, or if alcohol is instead binding to another protein that then indirectly affects the functioning of the protein being studied.”
- But we know that alcohol numbs your neurons, makes them slower and disrupts their communication.
#Davies, M. (2003): The role of GABAA receptors in mediating the effects of alcohol in the central nervous system. Journal of psychiatry & neuroscience, Vol. 28 (4)
https://pmc.ncbi.nlm.nih.gov/articles/PMC165791/
Quote: “However, in recent years, there has been an accumulation of evidence pointing to the importance of ligand-gated ion channels (LGICs) in mediating the effects of ethanol. Of these LGICs, γ-aminobutyric acid type A (GABAA) receptors appear to occupy a central role in mediating the effects of ethanol in the CNS. GABA is the primary inhibitory neurotransmitter in the mammalian CNS, and activation of GABAA receptors by GABA tends to decrease neuronal excitability.
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Alcohol, or more specifically, ethanol, produces several effects in humans. It is a central nervous system (CNS) depressant and shares many of the effects of other CNS depressants, such as sedatives, hypnotics and anesthetic agents.”
#Enoch, M.-A. (2008): The role of GABA(A) receptors in the development of alcoholism. Pharmacology, biochemistry, and behavior, Vol. 90 (1)
https://pubmed.ncbi.nlm.nih.gov/18440057/
Quote: “GABAA receptors undergo allosteric modulation by several structurally unrelated drugs, most with their own binding sites, including ethanol, benzodiazepines (BZs), barbiturates, anesthetics and also
endogenous neurosteroids. These drugs have similar anxiolytic, sedative–hypnotic, anticonvulsant, motor-incoordinating, and cognitive impairing effects. GABAA receptors are implicated in the acute and
chronic effects of alcohol including tolerance, dependence and withdrawal, as discussed below.”
#Dharavath, R. et al. (2023): GABAergic signaling in alcohol use disorder and withdrawal: pathological involvement and therapeutic potential. Frontiers in Neural Circuits, Vol. 17
https://www.frontiersin.org/journals/neural-circuits/articles/10.3389/fncir.2023.1218737/full
Quote: “Ethanol produces a wide variety of behavioral and physiological effects in the body, but exactly how it acts to produce these effects is still poorly understood. Like most dependence-producing substances, ethanol binds and acts on multiple proteins, receptors, and signaling pathways throughout the brain (Figure 1A), including amino acids, opioids, enzymes, and ion channels (Heinz et al., 2009; Koob and Volkow, 2016). The primary targets behind ethanolinduced behavioral phenotypes (disinhibition, hyperlocomotion, and anxiolysis) are GABAA receptors. Besides modulating GABAA receptor activity, ethanol can directly bind and modulate the activity of several proteins, including ionotropic glutamatergic (NMDA) receptors, alcohol dehydrogenase (ADH), and glycine receptors (Grant and Lovinger, 2018). Further, it has been observed that ethanol is capable of indirect modulation of other neurotransmitters (dopamine, serotonin, opioid, and cholinergic), particularly in brain regions involved in the mesolimbic reward system [i.e., amygdala, hippocampus, striatum, and ventral tegmental area (VTA)] via GABAergic/glutamatergic neurons or their respective receptors present on other types of neurons (Abrahao et al., 2017).”
- It sedates you, melting away tension and stress.
#Hendler, R. et al. (2011): Stimulant and Sedative Effects of Alcohol. In: Behavioral Neurobiology of Alcohol Addiction.
https://link.springer.com/chapter/10.1007/978-3-642-28720-6_135
Quote: “Researchers know less about which brain mechanisms mediate alcohol’s sedative effects. Sedation does not seem to arise simply from the dopamine reward circuit ‘‘turning off,’’ since stimulation and sedation increase simultaneously after alcohol consumption (Conrod et al. 2001; King et al. 2002; Erblich et al. 2003; Holdstock and de Wit 1998). The pons, thalamus, and putamen are thought to play a role in anesthetic-induced sedation, which shares many similarities with sleep-induced sedation. However, it is unclear whether these same mechanisms mediate alcoholinduced sedation, and researchers in fact know relatively little even about the mechanisms that mediate sedation and anesthesia (Campagna et al. 2003; Mhuircheartaigh et al. 2010). Some researchers hypothesize that alcohol-induced sedative effects reflect a general decrease in activity throughout the cerebral cortex. PET studies, for example, have shown that consuming moderate (Wang et al. 2000) or high (de Wit et al. 1990) doses of alcohol reduces cerebral glucose metabolism throughout the entire brain. Gradual, decentralized depression of brain activity could co-occur with more dramatic but short-term stimulant effects in the ventral striatum, resulting in the pattern of effects researchers observe. Scientists have begun to localize brain inactivity related to salient sedative-like effects such as anxiolysis. Gilman et al. (2008), for example, used fMRI to show a blunting of the amygdala’s ability to distinguish threatening stimuli from neutral stimuli, which may underlie the reduction in anxiety seen following alcohol use (see Fig. 2). Researchers hypothesize that alcohol may also reduce functioning in brain regions like the cerebellum, associated with motor coordination (Hanchar et al. 2005; Volkow et al. 1988; Boecker et al. 1996), and the frontal lobe, associated with higher order cognitive abilities (Peterson et al. 1990; Zorko et al. 2004).2”
#Jia, F. et al. (2007): GABAA receptors in the thalamus: alpha4 subunit expression and alcohol sensitivity. Alcohol, Vol. 41 (3)
https://pubmed.ncbi.nlm.nih.gov/17521848/
Quote: “The inhibitory neurotransmitter g-aminobutyric acid (GABA) has long been implicated in the anxiolytic, amnesic, and sedative behavioral effects of alcohol. A large number of studies have investigated the interactions of alcohol with GABA receptors. Many investigators have reported effects of ‘‘high concentrations’’ (50-100 mM) of alcohol on GABA-mediated synaptic inhibition, but effects of the ‘‘low concentrations’’ (1-30 mM) of alcohol normally associated with mild intoxication have been elusive until recently. A novel form of ‘‘tonic inhibition’’ has been described in the central nervous system (CNS) that is generated by the persistent activation of extrasynaptic g-aminobutyric acid type A receptors (GABAA-Rs). These receptors are specific GABAA-R subtypes and distinct from the synaptic subtypes. Tonic inhibition regulates the excitability of individual neurons and the activity and rhythmicity of neural networks. Interestingly, several reports show that tonic inhibition is sensitive to low concentrations of alcohol. The thalamus is a structure that is critically important in the control of sleep and wakefulness. GABAergic inhibition in the thalamus plays a crucial role in the generation of sleep waves. Among the various GABAA-R subunits, the 𝛂1, 𝛂4, β2, and 𝛅 subunits are heavily expressed in thalamic relay nuclei. Tonic inhibition has been demonstrated in thalamocortical relay neurons, where it is mediated by 𝛂4β2𝛅 GABAA-Rs. These extrasynaptic receptors are highly sensitive to gaboxadol, a novel hypnotic, but insensitive to benzodiazepines. Tonic inhibition is absent in thalamic relay neurons from 𝛂4 knockout mice, as are the sedative and analgesic effects of gaboxadol.”
- It stuns your prefrontal cortex, your center for decision-making and self-control, making you more disinhibited and prone to say or do things that you normally wouldn’t.
#Abernathy, K. et al. (2010): Alcohol and the prefrontal cortex. International review of neurobiology, Vol. 91
https://pmc.ncbi.nlm.nih.gov/articles/PMC3593065/pdf/nihms447130.pdf
Quote: “The PFC normally exerts “top-down” (e.g., information derived from prior experience) inhibitory control over internal and external sensory-driven compulsive behaviors. Increasing evidence suggests that continued drug exposure leads to attenuation of the ability of the PFC to monitor and inhibit these behaviors, with eventual loss of inhibitory control over drinking.
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It is clear from the above discussion that exposure to alcohol, either acutely or chronically,
has significant effects on the functional and structural status of the prefrontal cortex. Given
the key role that this brain region plays in the integration, manipulation, and evaluation of
incoming sensory and cognitive information, it is not surprising that alcoholics display
deficits in executive control, decision making, and risk management.”
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Acute ethanol administration in humans has been shown to cause deficits in executive activities that are thought to require the PFC. For example, performance in a spatial recognition task and a planning task was decreased in social drinkers while inebriated (Weissenborn and Duka, 2003) and acute EtOH has been shown to cause poorer decision making using a gambling task to assess PFC function (George et al., 2005). Working memory (WM) tasks are also commonly used to test executive function given the role that the PFC has been shown to play in mediating this activity. However, the effects of acute EtOH on working memory performance in humans are mixed.”
#Li, M. et al. (2021): Alcohol reduces the activity of somatostatin interneurons in the mouse prefrontal cortex: A neural basis for its disinhibitory effect? Neuropharmacology, Vol. 188
https://www.sciencedirect.com/science/article/abs/pii/S0028390821000551?via%3Dihub
Quote: “The prefrontal cortex (PFC) is involved in executive (“top-down”) control of behavior and its function is especially susceptible to the effects of alcohol, leading to behavioral disinhibition that is associated with alterations in decision making, response inhibition, social anxiety and working memory. The circuitry of the PFC involves a complex interplay between pyramidal neurons (PNs) and several subclasses of inhibitory interneurons (INs), including somatostatin (SST)-expressing INs. Using in vivo calcium imaging, we showed that alcohol dosedependently altered network activity in layers 2/3 of the prelimbic subregion of the mouse PFC. Low doses of alcohol (1 g/kg, intraperitoneal, i.p.) caused moderate activation of SST INs and weak inhibition of PNs. At moderate to high doses, alcohol (2–3 g/kg) strongly inhibited the activity of SST INs in vivo, and this effect may result in disinhibition, as the activity of a subpopulation of PNs was simultaneously enhanced. In contrast, recordings in brain slices using ex vivo electrophysiology revealed no direct effect of alcohol on the excitability of either SST INs or PNs over a range of concentrations (20 and 50 mM) consistent with the blood alcohol levels reached in the in vivo experiments. This dose-dependent effect of alcohol on SST INs in vivo may reveal a neural basis for the disinhibitory effect of alcohol in the PFC mediated by other neurons within or external to the PFC circuitry.”
#Chikritzhs. T. et al. (2024): Alcohol and the Brain. Alcohol and Society 2024.
Quote: “Alcohol affects the brain through multiple mechanisms. Some of them are acute, meaning that there is immediate impairment (i.e. brain dysfunction). Impairment refers to reduced ability to perform certain tasks and functions. Acute alcohol-related impairment has multiple dimensions in the form of altered mood (e.g. dysphoria, increased sociability) and decrements in judgment, impulse control, cognition and physical performance. Sometimes these acute effects can combine to cause problems. For example, alcohol-related car crashes are generally caused by the acute effects of alcohol. But what contributes to the event might include reduced executive functioning (e.g. impaired driver fails to notice it might not be a good idea to drive a car, or that it’s a good idea to wear a seatbelt), loss of impulse control that could lead to faster driving speed, plus slower reaction time to apply the brakes or otherwise avoid crashing. Similarly, in the case of an alcohol-caused drowning, impaired swimming performance might be accompanied by loss of executive functioning and misjudgement of swimming conditions or one’s swimming ability.”
#Choi, K. W. et al. (2018): Alcohol-induced disinhibition is associated with impulsivity, depression, and suicide attempt: A nationwide community sample of Korean adults. Journal of affective disorders, Vol. 227
https://www.sciencedirect.com/science/article/abs/pii/S0165032717313137
Quote: “A total of 9,461 adults who had a history of drinking completed a face-to-face interview using the Korean version of Composite International Diagnostic Interview (K-CIDI) with the Suicide Module, and Barratt Impulsiveness Scale 11 (BIS-11). In this study, we defined the AID group as those who had been involved with the two antisocial behaviors, including fights, being arrested or dangerous driving, according to the K-CIDI. Results Among 9,461 subjects, 564 were classified as the AID group (5.96%). The AID group had a significantly higher number of lifetime suicidal ideation, plan, attempt, and multiple attempts, and higher BIS-11 scores than non-AID group. The total scores of BIS-11 of the AID group reported the highest score compared with other psychiatric disorders. The AID group experienced more frequently three types of alcohol withdrawal symptoms, including nervousness, heart beating fast, and feeling weak. Compared with subjects without both AID and MDD, subjects with both AID and MDD showed significant association with a lifetime suicide attempt (AOR= 6.86, p< 0.001) and showed stronger association with multiple attempts (AOR= 10.38, p< 0.001). Conclusion AID was associated with suicide attempt and impulsivity, and the both AID and MDD showed much stronger association with lifetime suicide attempt and multiple attempts.
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There is evidence to support alcohol as a disinhibiting agent in terms of central mechanisms of control (Fillmore, 2003). Alcohol is known to have a disinhibitory quality, i.e. reduced inhibitory control of behavior, as opposed to impulsivity or impaired prefrontal brain function. Previous studies supported that alcohol could induce disinhibition, which means a decrease in the ability to inhibit impulses (Jentsch and Taylor, 1999; Lyvers, 2000; Goldstein and Volkow, 2002; Fillmore, 2003).”
- And it releases endorphins – “feel good” molecules deeply tied to human connection.
Endorphins are naturally occurring opioid-like neuropeptides that block pain perception and are associated with feelings of pleasure and euphoria. They function both as neurotransmitters in the central nervous system (CNS) and as hormones in the bloodstream. β-endorphins play a key role, particularly in phenomena like the "runner’s high." Endorphins bind to opioid receptors, especially mu-receptors, inhibiting pain signals and increasing dopamine release. They are also linked to mental conditions like depression, as well as activities such as laughter and exercise.
#Chaudhry, S. R. & Gossman, W. (2023): Biochemistry, Endorphin
https://www.ncbi.nlm.nih.gov/books/NBK470306/
Quote: “Endogenous morphine, coined by the morphing of the two descriptive terms into endorphins, are opioid neuropeptides that are naturally produced in the body that serve a primary function as an agent blocking the perception of pain and, additionally, present in cases of pleasure. Historically, morphine receptors were discovered in the nervous system before the discovery and understanding of endorphins. This natural receptor spoke to the possibility of the existence and effect of endorphins that was later confirmed.
Endorphins were discovered to not only display functions as neurotransmitters in the central nervous system but additionally as peptide hormones released into the circulatory system by the pituitary gland. Endorphins have been linked clinically to cases of mental issues, including autism, depression, and depersonalization disorder, as well as to activities such as laughter and vigorous aerobic exercise.[1][2][3]
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The function of endorphins can be stated in general terms as well as broken down specifically and observed per each endorphin type. In general, the release of endorphins is understood to be associated with the body’s response to pain. The pain relief experienced as a result of the release of endorphins has been determined to be greater than that of morphine. β-endorphin (an endogenous opioid) is one of the neurochemicals involved with exercise-induced euphoria (runner's high). Additionally, endorphins have been found to be associated with states of pleasure, including such emotions brought upon by laughter, love, sex, and even appetizing food. Of the three endorphin types, beta-endorphins have been the most studied and prevalent, accounting for the majority of the functional properties of endorphins as generalized and understood as a whole. Research is ongoing on each type to further understand the full functional potential of each, along with how they can be used in a medically beneficial manner. Endorphins express functional duality as they fall into the category of either neurotransmitters or neuromodulators in the central nervous system (CNS) and hormones in the pituitary gland.[7][8]
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The mechanism of endorphins can be viewed through two different lenses through activity in the peripheral nervous system (PNS) and the CNS. In the PNS, the perception of pain relief is produced beta-endorphins bind to opioid receptors. Opioid receptors are broken down into four primary classes of G protein-coupled receptors: mu-receptors, delta-receptors, kappa-receptors, and nociceptin receptors. The greatest binding potential exists between the beta-endorphins and the mu-receptors. Mu-receptors can be found throughout the nerves of the PNS. When this beta-endorphin to mu-receptor binding occurs on nerve terminals (happening pre-synaptically or post-synaptically), analgesic effects are realized. The effects are realized as the aforementioned binding results in triggering of chemical events preventing the release of substance P, amongst other tachykinins, which is an instrumental undecapeptide in the conveyance of pain. Just as beta-endorphin to mu-opioid binding occurs in the peripheral nervous system, it also occurs in the central nervous system. There is a difference, though, as the mechanism triggered by the binding opposes the release of the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) as opposed to substance P. With this suppression of GABA, the result is an increase in production and action of dopamine, the pleasure, and reward-associated neurotransmitter.”
#Pilozzi, A. et al. (2021): Roles of β-Endorphin in Stress, Behavior, Neuroinflammation, and Brain Energy Metabolism. International Journal of Molecular Sciences, Vol. 22 (1)
https://www.mdpi.com/1422-0067/22/1/338
Quote: “β-Endorphins are peptides that exert a wide variety of effects throughout the body. Produced through the cleavage pro-opiomelanocortin (POMC), β-endorphins are the primarily agonist of mu opioid receptors, which can be found throughout the body, brain, and cells of the immune system that regulate a diverse set of systems. As an agonist of the body’s opioid receptors, β-endorphins are most noted for their potent analgesic effects, but they also have their involvement in reward-centric and homeostasis-restoring behaviors, among other effects.
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Alcohol consumption appears to stimulate the release of β-endorphin, but habitual consumption ultimately results in a reduction in β-endorphin levels [148]. Those with genetic deficiencies in β-endorphin levels are more likely to become alcoholics [148], and excessive alcohol consumption in rats can be curbed through the use of opiate antagonists [149], further cementing the peptide’s role in the development of alcoholism. β-endorphin has also been suggested to be related to the phenomenon of exercise addiction; increases in plasma levels of the peptide is often observed in strenuous exercise, and is associated with feelings of well-being and euphoria similar to that observed in drug addiction [150,151].”
#Mitchell, J. M. et al. (2012): Alcohol Consumption Induces Endogenous Opioid Release in the Human Orbitofrontal Cortex and Nucleus Accumbens. Science Translational Medicine, Vol. 11 (4)
https://www.science.org/doi/abs/10.1126/scitranslmed.3002902
Quote: “Excessive consumption of alcohol is among the leading causes of preventable death worldwide. Although ethanol modulates a variety of molecular targets, including several neurotransmitter receptors, the neural mechanisms that underlie its rewarding actions and lead to excessive consumption are unknown. Studies in animals suggest that release of endogenous opioids by ethanol promotes further consumption. To examine this issue in humans and to determine where in the brain endogenous opioids act to promote alcohol consumption, we measured displacement of a radiolabeled μ opioid receptor agonist, [11C]carfentanil, before and immediately after alcohol consumption in both heavy drinkers and control subjects. Drinking alcohol induced opioid release in the nucleus accumbens and orbitofrontal cortex, areas of the brain implicated in reward valuation. Opioid release in the orbitofrontal cortex and nucleus accumbens was significantly positively correlated. Furthermore, changes in orbitofrontal cortex binding correlated significantly with problem alcohol use and subjective high in heavy drinkers, suggesting that differences in endogenous opioid function in these regions contribute to excessive alcohol consumption. These results also suggest a possible mechanism by which opioid antagonists such as naltrexone act to treat alcohol abuse.”
#Jarjour, S. et al. (2009): Effect of Acute Ethanol Administration on the Release of Opioid Peptides From the Midbrain Including the Ventral Tegmental Area. Alcoholism, clinical and experimental research, Vol. 33 (6)
https://onlinelibrary.wiley.com/doi/10.1111/j.1530-0277.2009.00924.x
Quote: “The present findings suggest that the ethanol-induced increase of 𝛃-endorphin release at the level of midbrain ⁄ VTA may influence alcohol reinforcement.
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The increased release of 𝛃-endorphin in response to moderate doses of ethanol at the level of midbrain/VTA observed in the present investigation is in agreement with previous reports demonstrating increased content of b-endorphin peptides in tissue extracts of the VTA and NAcb at 30 minutes following intragastric ethanol administration (Rasmussen et al., 1998).”
- Conversations flow easier, smiles last a little longer, and strangers can become friends or lovers more easily.
#Sayette, M. A. et al. (2012): Alcohol and Group Formation: A Multimodal Investigation of the
Effects of Alcohol on Emotion and Social Bonding. Psychological science, Vol. 23 (8)
https://pubmed.ncbi.nlm.nih.gov/22760882/
Quote: “Main effects of beverage condition on individual-level responses
Facial expressions—During the interaction, participants drinking alcohol displayed
Duchenne smiles for significantly longer3 amounts of time and expressed negative affect (as
assessed by the composite negative-affect index) for significantly shorter amounts of time
than did participants drinking nonalcoholic beverages (see Table 2). AUs 9 and 14/15
occurred significantly less often in the alcoholic-beverage condition than in the two other
beverage conditions. (AU 20 was the only negative AU not significantly affected by alcohol,
a result that may have been due to its rare occurrence in our study.) Placebo-beverage
participants tended to spend less time displaying Duchenne smiles than control-beverage
participants did (p = .07), but there were no differences between the placebo-beverage and
control-beverage conditions in the time spent displaying negative AUs.
Speech behaviors—Participants who drank alcohol spent significantly more time talking
than did participants who did not drink alcohol (see Table 2). There were no differences
between placebo- and control-beverage participants in the amount of time spent talking.
Self-reported social bonding—Participants in the alcoholic-beverage condition had
significantly higher PGRS scores than did participants who did not consume alcohol, and
control-beverage participants had significantly higher PGRS scores than placebo-beverage
participants did (see Table 2). Follow-up contrast analyses showed that alcoholic-beverage
participants’ PGRS scores (M = 7.22) were higher than those of placebo-beverage
participants (M = 6.74), p < .001, but PGRS scores did not differ significantly between
alcoholic-beverage and control-beverage (M = 7.07) participants (p = .27).
(...)
Main effects of beverage condition on group-level responses
Facial expressions—Groups drinking alcohol spent more time engaging in triadic Duchenne smiling than did groups not drinking alcohol (i.e., groups consuming placebo or control beverages; see Table 3). There were no differences between the placebo-beverage and control-beverage participants in this measure.
Speech behaviors—As Table 3 shows, groups that drank alcohol had significantly more triadic sequential-speech events than did groups that did not drink alcohol. (Each instance in which 3 different speakers spoke in succession was counted as a new triadic speech event.) There were no differences between the placebo- and control-beverage conditions in the frequency of triadic sequential-speech events.”
#Goodman, F. et al. (2018): Social Anxiety and the Quality of Everyday Social Interactions: The Moderating Influence of Alcohol Consumption. Behavior Therapy, Vol. 49 (3)
https://www.sciencedirect.com/science/article/abs/pii/S0005789417301156
Quote: “In one laboratory study of individuals high in social anxiety, participants who consumed alcohol during a social interaction spent more time speaking to interaction partners compared with participants who did not consume alcohol (Battista, MacDonald, & Stewart, 2012). Alcohol consumption may temporarily alleviate interpersonal fears and allow individuals high in social anxiety to more comfortably and successfully engage with others. However, no research to date has tested this framework in the context of a person’s everyday social interactions.
(...)
Nonetheless, short-term benefits of alcohol consumption (e.g., improvement in social
interaction quality) often occur at the expense of long-term problems and impairment (e.g.,
Lazareck et al., 2012; Robinson et al., 2011). To illustrate, a person may begin using alcohol
primarily as means to experience pleasure and positive social experiences (e.g., Boden, Heinz, & Kashdan, 2017). When they drink in social settings, they experience a reduction in social anxiety and obtain social rewards (e.g., strengthening friendships, feeling more self-assured). When they enter a social interaction in the future, they anticipate that similar to their prior interactions, consuming alcohol will yield higher quality interactions (i.e., positive reinforcement). Over time, they may become increasingly dependent on alcohol to socialize because they lack confidence they can effectively regulate their emotions without drinking.”
- And when your body breaks it down, it transforms into acetaldehyde – a chemical that is even more toxic than alcohol itself and that wreaks havoc in your tissues, cells and DNA.
#Peana, A. et al. (2017): Mystic Acetaldehyde: The Never-Ending Story on Alcoholism. Frontiers in Behavioral Neuroscience, Vol. 11
https://www.frontiersin.org/journals/behavioral-neuroscience/articles/10.3389/fnbeh.2017.00081/full
Quote: “In addition to the above, acetaldehyde has multiple tissue damage effects and these also should be appreciated as a feature of another never-ending story. In fact, humans are frequently exposed to acetaldehyde from various sources including alcoholic beverages, tobacco smoke and foods and even microbes are responsible for the bulk of acetaldehyde production from ethanol both in saliva and in the Helicobacter pylori-infected and achlorhydric stomach (Salaspuro, 2011). Moreover, acetaldehyde is also usually used as a food additive and aroma agent. Unfortunately, acetaldehyde is mutagenic and carcinogenic being responsible of DNA damage and of several cancer-promoting effects (Dellarco, 1988; Seitz and Stickel, 2010). Accordingly, acetaldehyde and ethanol are two of the compounds for which the most comprehensive evidence on epidemiology and mechanisms of carcinogenesis is accessible. In the relationship between alcohol consumption and development of different forms of cancer, the impact of the risk of developing this pathology mostly depends on alcohol consumption (Shield et al., 2013) and even a moderate drinking has been shown to cause cancer (Bagnardi et al., 2013). Different hypothesis have been proposed to explain how ethanol and acetaldehyde may cause or contribute to carcinogenesis, the main mechanism being attributable to the metabolism of ethanol into the carcinogenic, and DNA binding, acetaldehyde (Seitz and Stickel, 2007).”
#NIAAA (2022): Alcohol Metabolism
https://www.niaaa.nih.gov/publications/alcohol-metabolism
Quote: “Alcohol is metabolized by several processes or pathways. The most common of these pathways involves two enzymes—alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH). These enzymes help break apart the alcohol molecule, making it possible to eliminate it from the body. First, ADH metabolizes alcohol to acetaldehyde, a highly toxic substance and known carcinogen.1 Then, acetaldehyde is further metabolized down to another, less active byproduct called acetate,1 which then is broken down into water and carbon dioxide for easy elimination.2
(...)
Much of the research on alcohol metabolism has focused on an intermediate byproduct that occurs early in the breakdown process—acetaldehyde. Although acetaldehyde is short-lived, usually existing in the body only for a brief time before it is further broken down into acetate, it has the potential to cause significant damage. This is particularly evident in the liver, where the bulk of alcohol metabolism takes place.4 Some alcohol metabolism also occurs in other tissues, including the pancreas3 and the brain, causing damage to cells and tissues.1 Additionally, small amounts of alcohol are metabolized to acetaldehyde in the gastrointestinal tract, exposing these tissues to acetaldehyde’s damaging effects.5
In addition to acetaldehyde’s toxic effects, some researchers believe that it may be responsible for some of the behavioral and physiological effects previously attributed to alcohol.6 For example, when acetaldehyde is administered to lab animals, it leads to incoordination, memory impairment, and sleepiness, effects often associated with alcohol.7
On the other hand, other researchers report that acetaldehyde concentrations in the brain are not high enough to produce these effects.7 This is because the brain has a unique barrier of cells (the blood–brain barrier) that help to protect it from toxic products circulating in the bloodstream. It is possible, however, that acetaldehyde may be produced in the brain itself when alcohol is metabolized by the enzymes catalase8,9 and CYP2E1.10”
#Molina, P. & Nelson, S. (2018): Binge Drinking’s Effects on the Body. Alcohol Research, Vol. 39 (1)
https://pmc.ncbi.nlm.nih.gov/articles/PMC6104963/pdf/arcr-39-1-e1_a12.pdf
- In your brain, this shrinks your neurons and severs their connections, making it harder for different parts of your brain to communicate.
In general, alcohol doesn’t directly “kill” neurons but primarily damages their connections and support structures. It leads to the degeneration of white or grey matter, loss of myelin, and shrinkage of neuronal cell bodies, impairing communication between brain regions. While prolonged alcohol abuse can result in neuron loss due to axonal degeneration and synaptic disconnection, many of these damages are partially reversible with abstinence. The idea that alcohol directly kills brain cells is a rather some kind of misconception. Instead, it disrupts their function and connectivity.
According to the following paper, alcohol causes important connections between nerve cells (synapses) to disappear, especially in a brain region (prefrontal cortex) that controls thinking and behavior. This happens because the brain's immune cells (microglia) become overactive and remove too many synapses.
#Socodato, R. et al. (2020): Daily alcohol intake triggers aberrant synaptic pruning leading to synapse loss and anxiety-like behavior. Science Signaling, Vol. 13
https://pubmed.ncbi.nlm.nih.gov/32963013/
Quote: “Here, we show that alcohol intake over ten consecutive days resulted in substantial loss of excitatory synapse in the prefrontal cortex, a consequence of aberrant synaptic pruning, which led to increased anxiety-like behavior. Mechanistically, these effects of alcohol intake were mediated by a detrimental increase of microglia engulfment capacity via Src dependent activation of NFkB and consequent TNF production. Accordingly, pharmacological blockade of Src activation or TNF production by microglia, genetic ablation of TNF, or diphtheria toxin-mediated conditional ablation of microglia attenuated aberrant synaptic pruning preventing excitatory synapse loss and anxiety like behavior.
(...)
The severity of Purkinje cell loss increases with alcohol dose and duration. For example, 20–30 years of regular alcohol consumption (41–80 g/day) produces a 15 % reduction in the Purkinje cell population, whereas consumption of 81–180 g/day produces a 33.4 % loss of Purkinje cells. Purkinje cell degeneration and white matter loss in the vermis correlate with ataxia, whereas Purkinje cell loss in the lateral lobes correlates with cognitive dysfunction [11]. The causes of cerebellar atrophy and degeneration in alcoholics are still debated with regard to the roles of alcohol neurotoxicity and thiamine deficiency. Experimental data support the concept that alcohol exposure is sufficient to cause cerebellar degeneration [30], but in humans, thiamine deficiency could be either a cofactor or possibly a pathogenic agent.”
#Yang, X. et al. (2016): Cortical and subcortical gray matter shrinkage in alcohol-use
disorders: a voxel-based meta-analysis. Neuroscience and Biobehavioral Reviews, Vol. 66
https://www.sciencedirect.com/science/article/abs/pii/S0149763415302451?via%3Dihub
Quote: “Although gray matter (GM) damages caused by long term and excessive alcohol consumption have long been reported,the structural neuroimaging findings on alcohol-use disorders (AUD) are inconsistent. The aim of this study was to conduct a meta-analysis, using a novel voxel-based meta-analytic method effectsize signed differential mapping (ES-SDM), to characterize GM changes in AUD patients. Twelve studies including 433 AUD patients and 498 healthy controls (HCs) were retrieved. The AUD group demonstrated significant GM reductions in the corticostriatal-limbic circuits, including bilateral insula, superior temporal gyrus, striatum, dorsal lateral prefrontal cortex (DLPFC), precentral gyrus, anterior cingulate cortex (ACC), left thalamus and right hippocampus compared to HCs. GM reduction in the right striatum is significantly negatively related to duration of alcohol dependence, while GM shrinkage of the left superior, middle frontal gyrus, and left thalamus is related to lifetime alcohol consumption. The findings demonstrate that the GM abnormalities caused by AUD are in corticostriatal-limbic circuits whose dysfunctions may involve in craving and observed functional deficits.
(...)
Lifetime alcohol consumption is significantly associated with volume decreases in the left middle frontal gyrus and leftthalamus, indicating that heavier alcohol consumption is more toxic to the brain. Prior studies have identified that heavy alcohol drinkers tend to have brain atrophy, the severity of which is related to the level of alcohol consumption, and this is largely attributed to GM loss (Cardenas et al., 2007;Kril et al., 1997). For example,the frontal lobe volume was inversely related to measures of alcohol consumption (Cardenas et al., 2007), and significant brain damage does occur as a result of alcohol abuse; also, damage is regionally specific with the frontal lobes being particularly affected (Kril and Halliday, 1999). Smaller frontal and thalamic GM was found in patients with alcohol dependence compared with light drinkers (Mon et al., 2014). Kril and colleges also found that the thalamic volume was negatively correlated with maximum daily alcohol consumption (Kril et al., 1997). As a result, structural differences in the frontal cortex and thalamus may contribute to the effect of alcohol consumption in patients with AUD.”
#Chikritzhs. T. et al. (2024): Alcohol and the Brain. Alcohol and Society 2024.
Quote: “However, high levels of consumption for shorter time periods that result in very high blood alcohol concentrations can also cause lasting damage and subsequent cognitive difficulties. Alcohol consumption can over time lead to chronic structural changes in the CNS including generalized cortical and cerebellar atrophy.3 Studies using Magnetic Resonance Imageing (MRI) to measure changes from alcohol consumption in the brain typically find loss of brain volume, with greater loss at higher levels of consumption.
(...)
Several physiological mechanisms that can lead to cognitive impairment have been identified. Alcohol (as ethanol) readily crosses over the blood brain barrier where it is toxic to brain cells (i.e. alcohol is a neurotoxin) potentially resulting in short- and long-term tissue damage. Long-term heavy alcohol use can also lead to acute thiamine deficiency with profound potential impacts on learning and memory abilities e.g. Wernicke’s encephalopathy and Korsakoff Syndrome.4
(...)
Dannenhoffer et al (2021)1 provide a comprehensive review of the kinds of cognitive deficits alcohol use may cause across different phases of the life course and the extent to which these can be reversed variously through avoiding alcohol or other treatments e.g. nutritional supplements. They conclude that “cognitive flexibility” as indicated by the ability to change behaviours in response to different cues is impacted by alcohol exposure at every stage of life. Further, although the ability to recover cognitive flexibility (learn new habits, unlearn old) can be substantial at young ages it increasingly deteriorates with advancing age.”
- As your brain withers, your memories fade, your thinking slows down and your risk of dementia increases.
#Chikritzhs. T. et al. (2024): Alcohol and the Brain. Alcohol and Society 2024.
Quote: “Several plausible biological mechanisms may explain alcohol’s role in raising dementia risk. Cumulative direct effects such as brain cell death brought about by exposure to neurotoxic effects of alcohol metabolites such as acetaldehyde or activation of inflammatory processes that compromise brain structure and function are probable. In addition to or alternatively, more indirect effects such as alcohol’s role in promoting thiamine deficiency4 or in elevating blood pressure in connection with vascular dementia160 may play a key role. Some forms of dementia specifically involve diagnosis of an underlying alcohol use disorder and may be broadly referred to as “alcohol-related dementia” (e.g. alcoholic dementia, Korsakoff’s psychosis).161 For these conditions, diagnoses directly establish that the patient’s brain has been injured by longterm heavy alcohol use, however, in terms of disease expression, alcohol-related dementia is not easily distinguished from Alzheimer’s disease.
(...)
Notably, for all types of dementia, heavy alcohol use has been identified as the strongest modifiable risk factor for disease onset (especially early onset, i.e. <65yrs) and is associated with all other independent risk factors.162,163 An important Swedish study conducted on men conscripted for mandatory military service found that a history of being treated in hospital for alcohol intoxication during adolescence was the most important risk factor for vascular, unspecified and alcoholic dementia diagnosed before the age of 65 (early onset).44 Most, but not all (e.g. 164), recent reviews and meta-analyses of observational studies agree that heavy alcohol use increases risk of dementia, including early onset dementia.162,165-170 However, many of these same meta-analyses have also found that at lower doses, alcohol use appears to reduce dementia risk. For example, drawing on data from seven European studies Kilian et al (2023)166 found that compared to non-drinkers, heavy drinkers (i.e. at least 24g of pure alcohol per day) had higher risk of mild cognitive impairment and dementia, whereas low to moderate level drinkers (i.e. <= 24g per day) had lower risk of dementia compared to current abstainers. There are many reasons to suspect that findings of protection from dementia associated with low-dose alcohol consumption (i.e. J-shaped or U-shaped curves) are spurious.”
#Rehm, J. et al. (2019): Alcohol use and dementia: a systematic scoping review. Alzheimer's Research & Therapy, Vol. 11 (1)
https://alzres.biomedcentral.com/articles/10.1186/s13195-018-0453-0#Sec12
Quote: “Overall, 28 systematic reviews were identified: 20 on the associations between the level of alcohol use and the incidence of cognitive impairment/dementia, six on the associations between dimensions of alcohol use and specific brain functions, and two on induced dementias. Although causality could not be established, light to moderate alcohol use in middle to late adulthood was associated with a decreased risk of cognitive impairment and dementia. Heavy alcohol use was associated with changes in brain structures, cognitive impairments, and an increased risk of all types of dementia.
(...)
Light to moderate alcohol use in middle to late adulthood was associated with a decreased risk of cognitive impairment and dementia in numerous observational studies; however, there were contradictory findings, and owing to a number of methodological weaknesses (listed in the Results section), causality of this association could not be established. Heavy alcohol use was associated with changes in brain structures as well as with cognitive and executive impairments in observational and imaging studies. Heavy alcohol use and AUDs were also associated with an increased risk for all types of dementia. Furthermore, an alcohol consumption threshold above which cognition would be impaired (reversibly or irreversibly) may exist but has not yet been identified.”
#Xu, W. e al. (2019): Alcohol consumption and dementia risk: a dose–response meta-analysis of prospective studies. European Journal of Epidemiology, Vol. 32
https://link.springer.com/article/10.1007/s10654-017-0225-3
Quote: “Modest alcohol consumption (≤12.5 g/day) is associated with a reduced risk of dementia with 6 g/day of alcohol conferring a lower risk than other levels while excessive drinking (≥38 g/day) may instead elevate the risk.”
#Jeon, K. H. et al. (2023): Changes in Alcohol Consumption and Risk of Dementia in a Nationwide Cohort in South Korea. JAMA network open, Vol. 6 (2)
https://pubmed.ncbi.nlm.nih.gov/36745453/
Quote: “In this cohort study of 3 933 382 individuals in Korea, maintaining mild to moderate alcohol consumption was associated with a decreased risk of dementia compared with sustained nondrinking, whereas sustained heavy drinking of alcohol was associated with an increased risk of dementia. Reduction of drinking from a heavy to a moderate level and initiation of mild drinking were associated with a decreased risk of dementia compared with a sustained level of drinking.
(...)
Alcohol consumption level was categorized into none (0 g per day), mild (<15 g per
day), moderate (15-29.9 g per day), and heavy (30 g per day) drinking. On the basis of changes in
alcohol consumption level from 2009 to 2011, participants were categorized into the following
groups: nondrinker, quitter, reducer, sustainer, and increaser.”
#Chikritzhs. T. et al. (2024): Alcohol and the Brain. Alcohol and Society 2024.
Quote: “Experimental lab and neuroimaging studies (e.g. MRI) concur that alcohol impairs specific brain centres and CNS processes. Extensive reviews, some of over 200 experimental studies (e.g. 27) conducted on alcohol’s acute effects on the brain and CNS have confirmed impairments for visuo-motor control (i.e. eye-hand-foot coordination), divided and focused attention, reaction time, response inhibition and threat detection, motivation and reward-seeking, spatial learning and working memory.25 These findings are consistently supported by high resolution neuroimaging studies that detect alcohol-induced changes in brain metabolism (i.e. shift from glucose to acetate metabolism) and structure, even at low doses. These changes are centred in brain regions thought to be critical to behavioural/performance skills including the cerebellum, hippocampus, occipital cortex, striatum and amygdala (e.g. 28,29).
(...)
Several physiological mechanisms that can lead to cognitive impairment have been identified. Alcohol (as ethanol) readily crosses over the blood brain barrier where it is toxic to brain cells (i.e. alcohol is a neurotoxin) potentially resulting in short- and long-term tissue damage. Long-term heavy alcohol use can also lead to acute thiamine deficiency with profound potential impacts on learning and memory abilities e.g. Wernicke’s encephalopathy and Korsakoff Syndrome.4
(...)
Finally, recent large-scale neuroimaging studies (i.e. MRI) of general populations consistently show that alcohol use and brain structure have a negative linear association (i.e. more lifetime alcohol consumption, less brain). At any level of consumption, reductions in grey and white matter volume and in white matter cortical thickness and microstructure are widely apparent throughout the brain4 and particularly the hippocampus (an area of the brain associated with memory).178”
#Bernadin, F. et al. (2014): Cognitive impairments in alcohol-dependent subjects. Frontiers in Psychiatry, Vol. 5
https://pmc.ncbi.nlm.nih.gov/articles/PMC4099962/pdf/fpsyt-05-00078.pdf
Quote: “The characteristic profile of alteration of episodic memory in alcohol-dependent patients comprises limited learning capacities, impairments of encoding, and recollection processes, difficulties recalling the temporospatial context and deficits of autonoetic consciousness, while information storage is preserved (25, 30). Alteration of executive functions, particularly disorders of inhibition, flexibility, or dual-task coordination also constitute predictive factors of memory impairment (25, 30). In contrast, apart from obvious deficits (i.e., related to dysexecutive syndrome), there is also probably a genuine impairment of episodic memory likely due to the hippocampal atrophy observed in these patients (25). Finally, visuospatial functions are also predominantly affected, as several studies have demonstrated impaired performances on visuospatial processing, memory and visual learning, visuospatial organization, and visuoconstruction tasks (31, 32).”
- When and how you drink matters – the younger you are, the wider the damage; and the more you drink in one go, the worse you’ll make it.
#Chikritzhs. T. et al. (2024): Alcohol and the Brain. Alcohol and Society 2024.
Quote: “Significant brain development continues throughout adolescence and young adulthood with key brain regions highly susceptible to adverse effects of alcohol, particularly “binge drinking” (drinking to the point of intoxication, with high blood alcohol concentrations [BACs]). High BACs increase impulsivity and the risk of injuries in violence; in the case of traumatic brain injury the damage is permanent and the effects lifelong. Binge drinking among adolescents is also a major risk factor for dementia later in life.
(...)
Tapert (2022)111 has summarized the scientific research on alcohol’s impact on adolescent and young adult brains as follows:
• Adolescent binge drinking is linked to a greater risk of more prominent grey matter reductions during adolescence.
• Drinking onset is associated with, and appears to precede, disrupted white matter integrity.
• Initiation of moderate to heavy alcohol use and incurring hangovers during adolescence may adversely influence neurocognitive functioning.
• Pronounced alcohol cue reactivity in heavy drinking teens, particularly in reaction to alcohol advertising materials.”
#Spear, L. (2018): Effects of adolescent alcohol consumption on the brain and behaviour. Nature reviews. Neuroscience, Vol. 19 (4)
http://pubmed.ncbi.nlm.nih.gov/29467469/
Quote: “Adolescents also typically differ from adults in showing greater enhancement of GABAA receptor-meditated tonic inhibition upon acute administration of alcohol. Given that enhancing tonic inhibition typically disrupts learning and memory206, these findings are thought to contribute to the greater sensitivity of adolescents than adults to the memory-disrupting effects of acute alcohol challenges119. This greater enhancement of tonic inhibition following alcohol challenge is likewise maintained into adulthood after repeated adolescent alcohol exposure206.
(...)
Multiple studies have shown that repeated exposure to alcohol during adolescence reduces the number of neurons showing immunoreactivity to choline O-acetyltransferase (ChAT; the enzyme responsible for acetylcholine synthesis) in the basal forebrain76,88,91,99,189,190, an effect that was associated with decreases in the level of acetylcholine efflux190 and that was not evident after comparable alcohol exposure in adulthood88. This decline in ChAT immunoreactivity was correlated with greater disinhibitory behaviour91, an increase in risky-choice behaviour99 and decreased performance on a set-shifting task190, suggesting that adolescent exposure to alcohol leads to loss of cholinergic tone, which in turn has lasting functional consequences.”
#Kuntsche, E. et al. (2017): Binge drinking: Health impact, prevalence, correlates and interventions. Psychology & Health
https://escholarship.org/content/qt5vf3k21b/qt5vf3k21b.pdf?t=oqtrok
Quote: “Binge drinking among adolescents and young adults commonly occurs on weekends, with moderate or no drinking on most other weekdays (Kuntsche & Gmel, 2013). This drinking pattern is widely associated with an increased risk of acute consequences, including long-lasting effects, e.g. irreversible disabilities due to injury or death (Anderson, 2007; Courtney & Polich, 2009; Dawson et al., 2008; Gmel et al., 2003; Ham & Hope, 2003; Plant & Plant, 2006). This also includes consequences directly related to the state of intoxication, such as hangovers, blackouts, memory loss, nausea and vomiting. High doses can lead to alcohol poisoning, with occasional fatalities. Among young people, binge drinking is associated with academic or educational impairment owing to missed classes, falling behind on work and lower grades. These consequences become more pronounced as the frequency of binge drinking increases. Binge drinking may also lead to unintended and unprotected sexual activity (Perkins, 2002).
(...)
Due to its cognitive and psychomotor effects on reaction time, cognitive processing, and coordination (Gmel et al., 2003), alcohol use is a major contributory factor in the incidence of injuries, motor vehicle accidents and other trauma, particularly among younger age groups. For alcohol-related injuries, binge drinking has been found to be a major factor (Taylor, Shield, & Rehm, 2011).
(...)
Overall, it has been estimated that acute conditions, which are often related to binge drinking, may be responsible for over 50% of the alcohol-related deaths with an even higher proportion for years of life lost (Centers for Disease Control and Prevention, 2004).
(...)
Moreover, some studies investigated the typical pattern of binge drinking with heavy alcohol intake during certain episodes (weekend) coupled with abstinence or low consumption on most other days, and compared individuals with a binge pattern to those with the same overall alcohol intake, but who drank more frequently and did not binge. These studies suggest that the specific consumption pattern of alternating alcohol intoxications and abstinent episodes, which is linked to excitotoxic cell death during withdrawal, may be particularly deleterious for the brain (e.g. Maurage et al., 2012; Petit et al., 2014).
#Molina, P. & Nelson, S. (2018): Binge Drinking’s Effects on the Body. Alcohol Research, Vol. 39 (1)
https://pmc.ncbi.nlm.nih.gov/articles/PMC6104963/pdf/arcr-39-1-e1_a12.pdf
Quote: “Of all tissues affected by binge-like alcohol consumption, the gastrointestinal tract bears the greatest burden due to its direct exposure to high tissue concentrations of alcohol following ingestion (Figure 3). Binge drinking often occurs apart from meals, which may also contribute to its deleterious effects on organs. Food consumed at the time of alcohol consumption influences not only the alcohol absorption rate and blood alcohol concentration, but also the direct effect of alcohol on the gastrointestinal mucosa.”
- The human brain isn’t fully wired until your mid 20s, so drinking before that age is like smashing wet cement before it has set.
The idea that there is a hard cut-off point, such as age 25, when the brain is “fully developed” is more or less a myth. Brain development and maturing is a complex, gradual process, and while we’ve had to simplify a lot here, it’s generally considered that maturation slows down over the course of the twenties.
#Chikritzhs. T. et al. (2024): Alcohol and the Brain. Alcohol and Society 2024.
Quote: “Following birth, the brain continues to develop and mature, and is generally considered fully developed in the mid to late 20s. The prefrontal cortex, responsible for planning, prioritizing and decision making is the last part of the brain to mature. Adolescence is the phase of life between late childhood and early adulthood. In this life phase (sometimes defined as between 12–20 years of age) an adolescent experiences major changes in physical maturation including reaching maximum height and alterations in their brain and CNS.
(...)
The human brain is fully grown relatively soon after birth and the cerebral cortex soon reaches its maximum. However, structural imaging studies have shown107-109 that grey matter matures from back to front such that maximum brain density is first reached by the grey matter, primarily the sensorimotor cortex where sensation and motor tasks reside. The higher functioning areas such as the dorsolateral prefrontal cortex, the inferior parietal gyrus, and the superior temporal gyrus are fully developed last, which includes higher cognitive functions such as behavioural control, planning, and assessing the risk of decisions. Autopsy findings suggest that these grey matter changes are due to synaptic pruning. Many synapses are formed in childhood that are later removed in adolescence109, condensing the amount of synapses and increasing the effectivity. Brain synapses that survive are likely the ones most being used. Even as the grey matter decreases in volume, the white matter which conducts neural information rapidly increases continually from childhood into early adulthood.110 In short, the natural development and state of the brain during adolescence is one in which risk desirability and sensation seeking behaviour are often paramount.”
#Bonnie, R.J. & Backes, E. P. (eds. 2019): The Promise of Adolescence. Realizing Opportunity for All Youth. https://nap.nationalacademies.org/catalog/25388/the-promise-of-adolescence-realizing-opportunity-for-all-youth
Quote: “Adolescence is a period of significant development that begins with the onset of puberty1 and ends in the mid-20s.”
#Kuntsche, E. et al. (2017): Binge drinking: Health impact, prevalence, correlates and interventions. Psychology & Health
https://escholarship.org/content/qt5vf3k21b/qt5vf3k21b.pdf?t=oqtrok
Quote: “It appears that adolescence is a critical period for brain development. It is during these extensive neuromaturational processes that significant restructuring of the brain takes place. Consequently, the adolescent brain is particularly sensitive to alcohol, and binge drinking may therefore result in long-term changes in general brain functioning.”
#O’Rourke, S. et al. (2020): The development of cognitive and emotional maturity in adolescents and its relevance in judicial contexts. The Scottish Sentencing Council
Quote: “Thus, the nature of adolescent cognitive development is not a process that allows us to specify an exact age at which cognitive maturity is definitively reached at an individual level. While we do not therefore recommend the use of stringent age ranges in sentencing guidelines, it is however recommended that the brain’s continued growth, until as late as 25-30 years of age, and the resulting cognitive immaturity, is considered during judicial processes involving adolescents and young people.
(...)
This loss of grey matter, through processes such as synaptic pruning (considered to coincide with increased efficiency), is reported to increase from age 11 years in girls and age 12 years in boys and found to continue up until the age of 25-30 years. Specifically, the prefrontal cortex (PFC) only reaches full biological maturity at ~25 years or older, after significant periods of ‘rewiring’ (5,9,23), and with a degree of individual variation (24).
(...)
Maturational changes can be observed to continue in some brain regions until as late as 25-30 years, but these trajectories of development are typically not linear, and vary from brain region to region, and from person to person. We have yet to fully understand the considerable inter-individual variation in brain maturation as a field, but this will have critical implications in terms of judicial and clinical decision making and guidelines.”
#Lebel, C. et al. (2007): Microstructural maturation of the human brain from childhood to adulthood. Neuroimage, Vol. 40(3)
https://pubmed.ncbi.nlm.nih.gov/18295509/
Quote: "Brain maturation is a complex process that continues well beyond infancy, and adolescence is thought to be a key period of brain rewiring. To assess structural brain maturation from childhood to adulthood, we charted brain development in subjects aged 5 to 30 years using diffusion tensor magnetic resonance imaging, a novel brain imaging technique that is sensitive to axonal packing and myelination and is particularly adept at virtually extracting white matter connections. Age-related changes were seen in major white matter tracts, deep gray matter, and subcortical white matter, in our large (n= 202), age-distributed sample. These diffusion changes followed an exponential pattern of maturation with considerable regional variation. Differences observed in developmental timing suggest a pattern of maturation in which areas with fronto-temporal connections develop more slowly than other regions. These in vivo results expand upon previous postmortem and imaging studies and provide quantitative measures indicative of the progression and magnitude of regional human brain maturation."
- In 20-year-olds, blackout drinking episodes have been found to cause mental struggles during the year later – forgetting why you entered a room or problems learning new things.
#Linden-Carmichael, A. et al. (2023): Associations Between Blackout Drinking and Self-Reported Everyday Cognition among Young Adults. Addictive behaviors, Vol. 141
https://pmc.ncbi.nlm.nih.gov/articles/PMC10001203/pdf/nihms-1875264.pdf
Quote: “3.2 Associations Between Typical Alcohol Use and Everyday Cognitive Functioning
After including demographic covariates in the models, heavier alcohol consumption during a typical episode (Table 3a) and more frequent alcohol use (Table 3b) was significantly related to more memory lapses (d=0.31 and d=0.39, respectively) and more non-memory cognitive difficulties (d=0.36 and d=0.52, respectively). More frequent alcohol consumption was related to cognitive concerns (d=0.38), although greater amounts of alcohol consumption was not (p=.29).
3.3. Associations Between Blackout Experiences and Everyday Cognitive Functioning
More frequent blackout experiences were significantly related to more memory lapses (b=.40, SE=.08, p<.001), more non-memory cognitive difficulties (b=0.48, SE=0.06, p<.001), and more cognitive concerns (b=−0.74, SE=0.07, p<.001) after controlling for demographic covariates as well as typical alcohol use and cognitive abilities in the model (see Models 1a, 2a, and 3a in Tables 4a and 4b for full results). Effect sizes were medium to large at Cohen’s d=0.48 for memory lapses, Cohen’s d=0.55 for cognitive difficulties, and Cohen’s d=0.75 for cognitive concerns.
The current study aimed to examine the unique association between frequency of engaging
in blackout drinking and everyday cognitive functioning while accounting for typical
drinking behavior. Moreover, we also examined the role of gender and simultaneous use
on the relationship between blackout drinking frequency and everyday cognitive functioning.
Importantly, we found that more frequent blackout drinking was associated with more
memory lapses and non-memory cognitive difficulties, as well as greater cognitive concerns,
even after controlling for typical drinking behavior (i.e., frequency or quantity of alcohol use
per drinking occasion). This finding adds to the growing body of literature supporting the
potentially hazardous effects of blackout drinking on numerous negative outcomes including
physical injury, sexual assault, and overdose (Hingson et al., 2016).”
- Binge drinking in late adolescence is also one of the highest risk factors for early dementia.
#Nordström, P. et al. (2013): Risk Factors in Late Adolescence for Young-Onset Dementia in Men: A Nationwide Cohort Study. JAMA Internal Medicine, Vol. 173 (17)
https://jamanetwork.com/journals/jamainternalmedicine/fullarticle/1726998
Quote: “Nine independent risk factors for YOD (n = 487) were identified (Table 2), including alcohol intoxication (hazard ratio [HR], 4.82 [95% CI, 3.83-6.05]; PAR, 0.28), stroke (2.96 [2.02-4.35]; PAR, 0.04), use of antipsychotic drugs (2.75 [2.09-3.60]; PAR, 0.12), depression (1.89 [1.53-2.34]; PAR, 0.28), father’s dementia (1.65 [1.22-2.24]; PAR, 0.04), drug intoxication other than alcohol (1.54 [1.06-2.24]; PAR, 0.03), low cognitive function at conscription (1.26 per 1-SD decrease [1.14-1.40]; PAR, 0.29), high systolic blood pressure at conscription (0.90 per 1-SD decrease [0.82-0.99]; PAR, 0.06), and low height at conscription (1.16 per 1-SD decrease [1.04-1.29]; PAR, 0.16). The PAR associated with these 9 independent risk factors was 68% (95% CI, 39%-85%). Independent risk factors for the subtypes of YOD are presented in the Supplement (eTable 2). The risk of alcohol intoxication during follow-up was strongly associated with subjects’ drinking habits at conscription in a subcohort of 23 696 men (eg, 6-fold higher in men who drank beer daily than in men who never drank beer) (Table 3). In the same subcohort, smoking at conscription was higher (74.6% vs 59.4% [P = .01]) in those later diagnosed with YOD (n = 59).
#Barnett, A. et al. (2022): Adolescent Binge Alcohol Enhances Early Alzheimer's Disease Pathology in Adulthood Through Proinflammatory Neuroimmune Activation. Frontiers in pharmacology, Vol. 13 https://pubmed.ncbi.nlm.nih.gov/35559229/
Quote: “In fact, adolescent binge ethanol promotes progressive neurodegeneration of adult cholinergic neurons that are lost in Alzheimer’s disease (AD) (Coleman et al., 2011; Crews et al., 2019). Epidemiological studies support that heavy ethanol use increases risk for Alzheimer’s disease (AD) (Mukamal et al., 2003; Koch et al., 2019) with additional work finding that heavy use earlier in life increases risk for AD in late adulthood (Langballe et al., 2015). Further, heavy alcohol use was the number one modifiable risk factor for AD and all-cause dementia in a French study that assessed over a million patients (Schwarzinger et al., 2018). A recent preclinical study similarly found that adolescent binge ethanol increased AD pathology in an amyloid-expressing transgenic mouse model (Ledesma et al., 2021). Thus, binge alcohol use during adolescence is emerging as a key risk factor for AD.”
- Then there is cancer. Just as smoking hits your lungs, alcohol causes 8 types of cancer – basically everywhere from mouth to bowel, plus breast in women.
#Office of the U.S. Surgeon General (2025): Alcohol and Cancer Risk 2025 - The U.S. Surgeon General’s Advisory
https://www.hhs.gov/sites/default/files/oash-alcohol-cancer-risk.pdf
Quote: “Extensive research has demonstrated specific biological mechanisms by which alcohol causes cancer as well. For example, multiple studies have shown that giving rats and mice drinking water with ethanol (the same type of pure alcohol in alcohol-containing beverages) or its primary metabolic breakdown product, acetaldehyde, results in increased tumor numbers at multiple places in the body.7 At high levels such as those that occur with consumption of alcohol, acetaldehyde is highly toxic and cancer-causing.23-27
Further, the data in humans on alcohol and health show a strong association between drinking alcohol and increased cancer risk, regardless of the type of alcohol (e.g., beer, wine, and spirits).6,28 Cumulatively, rigorous research, across observational, biological, and genetic studies, has shown that alcohol consumption increases the risk of cancer for at least seven sites: breast (in women), colorectum, esophagus, liver, mouth (oral cavity), throat (pharynx), and voice box (larynx) (Figure 3).6,7”
#Rumgay, H. et al. (2021): Alcohol and Cancer: Epidemiology and Biological Mechanisms. Nutrients, Vol. 13 (9)
- Here risks start at an average consumption of less than 1 glass of wine per day.
#Anderson, B. et a. (2023): Health and cancer risks associated with low levels of alcohol consumption. The Lancet Public Health, Vol. 8 (1)
https://www.thelancet.com/journals/lanpub/article/PIIS2468-2667(22)00317-6/fulltext
Quote: “In the EU, light to moderate alcohol consumption (<20 g of pure alcohol per day, which is equivalent to consumption of approximately <1·5 L of wine [12% alcohol by volume; ABV], <3·5 L of beer [5% ABV], or <450 mL of spirits [40% ABV] per week) was associated with almost 23000 new cancer cases in 2017, accounting for 13·3% of all alcohol-attributable cancers and for 2·3% of all cases of the seven alcohol-related cancer types.4 Almost half of these cancers (approximately 11000 cases) were female breast cancers. Also, more than a third of the cancer cases attributed to light to moderate drinking (approximately 8500 cases) were associated with a light drinking level (<10 g per day).4
(...)
No studies have shown that the potential existence of a protective effect for cardiovascular diseases or type 2 diabetes also reduces the risk of cancer for an individual consumer. Evidence does not indicate the existence of a particular threshold at which the carcinogenic effects of alcohol start to manifest in the human body. As such, no safe amount of alcohol consumption for cancers and health can be established. Alcohol consumers should be objectively informed about the risks of cancer and other health conditions associated with alcohol consumption.”
In a study that examined cases caused by cancer, it was shown that several thousand new cases of cancer resulted from just one glass of wine a day (approx. 10g ethanol). At up to twice this amount (10g to 20g per day), there were almost twice as many new cases.
#Rovira, P. & Rehm, J. (2020): Estimation of cancers caused by light to moderate alcohol consumption in the European Union. European Journal of Public Health, Vol. 31 (3)
https://academic.oup.com/eurpub/article/31/3/591/6041768?login=false
- Worldwide, alcohol causes around 740,000 new cancer cases per year, leading to 400,000 deaths.
#Rumgay, H. et al. (2021): Global burden of cancer in 2020 attributable to alcohol consumption: a population-based study. The Lancet Oncology, Vol. 22 (8)
https://www.thelancet.com/journals/lanonc/article/PIIS1470-2045(21)00279-5/fulltext
The cancer cases are listed here under “malignant neoplasms”.
#WHO (2024): Global status report on alcohol and health and treatment of substance use disorders
https://iris.who.int/bitstream/handle/10665/377960/9789240096745-eng.pdf?sequence=1
- Another victim is your liver. Alcohol disrupts fat metabolism, causing fat to build up in your liver cells. But this often has no symptoms, so you may go on drinking as your liver slowly turns to fat, swells with inflammation and starts to fail.
Alcoholic liver disease (ALD) progresses in different stages. An early stage is alcoholic fatty liver. This is followed by alcoholic steatohepatitis. This is a chronic inflammation with fibrosis formation, i.e. basically scar tissue. This can progress to the final stage of alcoholic cirrhosis, an irreversible destruction of the liver tissue that can lead to liver failure and cancer.
#Patel, R. & Mueller, M. (2023): Alcohol-Associated Liver Disease
https://www.ncbi.nlm.nih.gov/books/NBK546632/
Quote: “The alcoholic liver disease covers a spectrum of disorders beginning from the fatty liver, progressing at times to alcoholic hepatitis and culminating in alcoholic cirrhosis, which is the most advanced and irreversible form of liver injury related to the consumption of alcohol.
(...)
The liver tolerates mild alcohol consumption, but as the consumption of alcohol increases, it leads to disorders of the metabolic functioning of the liver. The initial stage involves the accumulation of fat in the liver cells, commonly known as fatty liver or steatosis. If the consumption of alcohol does not stop at this stage, it sometimes leads to alcoholic hepatitis. With continued alcohol consumption, the alcoholic liver disease progresses to severe damage to liver cells known as "alcoholic cirrhosis." Alcoholic cirrhosis is the stage described by progressive hepatic fibrosis and nodules.
(...)
Alcohol metabolism by the liver is primarily via two enzymes:
Alcohol dehydrogenase
Aldehyde dehydrogenase
Alcohol dehydrogenase converts alcohol into acetaldehyde, and aldehyde dehydrogenase converts acetaldehyde into acetate. The metabolism of alcohol increases the production of NADH by reducing NAD in the body. This shifting of metabolic balance toward the production of NADH leads to the formation of glycerol phosphate, which combines with the fatty acids and becomes triglycerides, which accumulate within the liver. When lipid oxidation (lipolysis) stops due to alcohol consumption, fats accumulate in the liver and lead to "fatty liver disease." Continued alcohol consumption brings the immune system into play. Interleukins with the help of neutrophils attack the hepatocytes, and swelling of the hepatocytes known as the "alcoholic hepatitis" takes place. Ongoing liver injury leads to irreversible liver damage, the cirrhosis of the liver.”
#Seitz, H. et al. (2018): Alcoholic liver disease. Nature Reviews Disease Primers, Vol. 4 (16)
Quote: “ALD follows a well-recognized pattern of disease progression (Fig. 1; Box 1). The spectrum of ALD begins with alcoholic fatty liver (AFL), which is characterized by hepatic steatosis (an accumulation of triglycerides in hepatocytes). Some individuals will progress and develop hepatic inflammation, hepatocyte injury and ballooning, which is histologically defined as alcoholic steatohepatitis (ASH). ASH may progress slowly, with continual chronic liver injury and inflammation eventually leading to progressive fibrosis and cirrhosis, which ultimately may drive the development of hepatocellular carcinoma (HCC).”
(...)
An early pathophysiological response to chronic alcohol consumption is the accumulation of fat (mainly triglycerides, phospholipids and cholesterol esters) in hepatocytes (hepatic steatosis), which can lead to AFL. Alcohol and its metabolite acetaldehyde do not directly contribute to fatty acid synthesis, whereas acetate, the metabolite of acetaldehyde (Fig. 3), can be converted to acetyl-CoA, which does contribute to fatty acid synthesis. However, acetate generated from alcohol metabolism in hepatocytes is rapidly secreted into the circulation. Thus, acetate may have a minimal direct contribution to fatty acid synthesis in AFL. Alcohol consumption can induce fat accumulation in the liver via alterations to fat metabolism by several mechanisms72. First, alcohol consumption elevates the ratio of reduced NAD/oxidized NAD (NADH/NAD+) in hepatocytes, which interrupts mitochondrial β-oxidation of fatty acids and results in steatosis73. Second, alcohol consumption can upregulate hepatic expression of SREBP1c, a transcription factor that stimulates expression of lipogenic genes74, which results in increased fatty acid synthesis. Third, alcohol inactivates peroxisome proliferator-activated receptor-α (PPARα), a nuclear hormone receptor that upregulates expression of many genes involved in free fatty acid transport and oxidation75. Evidence suggests that alcohol is able to directly alter transcription of SREBF1 (encoding SREBP1c) and PPARA (encoding PPARα) via the metabolite acetaldehyde or indirectly control the expression of these genes via the regulation of multiple factors (for example, bacterial translocation of pathogenassociated molecular patterns (PAMPs) such as lipopolysaccharide (LPS), 2-arachidonoylglycerol, complement activation, ER stress, increases in adenosine, decreases in adiponectin, decreased signal transducer and activator of transcription 3 (STAT3) activation and dysregulated zinc homeostasis) that affect their expression and activation72 (Figs 3,4). Fourth, alcohol can inhibit 5ʹ-AMP-activated protein kinase (AMPK) and subsequently inhibit fatty acid synthesis but promote fatty acid oxidation via the dysregulation of acetyl-CoA carboxylase (ACC), carnitine O-palmitoyltransferase 1, liver isoform (CPT1) and SREBP76. In addition to alteration of fat metabolism, alcohol consumption can affect fatty acid mobilization and clearance. Alcohol consumption induces lipolysis (the breakdown of fats into fatty acids and other products) and adipocyte death, resulting in elevation of circulating fatty acids and their subsequent hepatic accumulation77–79. Alcohol consumption can also increase the supply of lipids to the liver from the small intestine73. Notably, autophagy has a critical role in clearing lipid droplets in hepatocytes, and chronic alcohol consumption inhibits autophagy, thereby reducing lipid clearance80. By contrast, acute alcohol intake may activate autophagy, which may play a compensatory role in preventing the development of AFL during the early stages of alcoholic liver injury81.
(...)
Before patients with ALD undergo laboratory or sonographical evaluation, a clinical diagnosis is needed, which includes the search for signs of AUD. A major problem exists in the clinical diagnosis of ALD, which is that patients often appear asymptomatic until they develop serious and advanced disease.
(...)
Patients with early ALD, such as AFL, or low to moderate ASH (Box 1) may not show any clinical symptoms, and ALD may be detected during a routine follow-up.”
#Crabb, D. et al. (2020): Diagnosis and Treatment of Alcohol-Associated Liver Diseases: 2019 Practice Guidance From the American Association for the Study of Liver Diseases. Hepatology, Vol. 71 (1)
https://pubmed.ncbi.nlm.nih.gov/31314133/
Quote: “Accurate assessment of the full spectrum of ALD prevalence is challenging, particularly given the difficulty with identifying earlier, asymptomatic stages of ALD, such as alcohol-related steatosis or moderate AH, challenges that may be overcome with broader use of noninvasive steatosis and fibrosis assessment tools and increased awareness for the need to diagnose early stage disease.”
- The final stage is cirrhosis – your liver is full of scars and barely functioning. This might take over 10 years, but once it appears it's largely irreversible.
We are referring here to the final stage of alcoholic liver disease, but also other diseases can result: about 2% develop liver cancer.
#Romanelli, R. & Stasi, C. (2016): Recent Advancements in Diagnosis and Therapy of Liver Cirrhosis. Drug Targets, Vol. 17 (999)
Quote: “Necro-inflammatory-regenerative processes through intermediately active hepatic inflammation leads to cirrhosis in a period of time ranging from 10 to 30 years.”
#Hazeldine, S. et al. (2015): Alcoholic liver disease - the extent of the problem and what you can do about it. Clinical medicine, Vol. 15 (2)
https://pmc.ncbi.nlm.nih.gov/articles/PMC4953739/
Quote: “It takes upwards of ten years for alcohol-related liver disease to progress from fatty liver through fibrosis to cirrhosis to acute on chronic liver failure. This process is silent and symptom free and can easily be missed in primary care, usually presenting with advanced cirrhosis.”
- Every year, 600,000 people die from an alcohol-destroyed liver.
In the following source, “digestive diseases” refers to diseases of the liver. Although this group also includes diseases of the pancreas, most of them relate to the liver.
#WHO (2024): Global status report on alcohol and health and treatment of substance use disorders
https://iris.who.int/bitstream/handle/10665/377960/9789240096745-eng.pdf
It is not entirely clear how many people died from liver cirrhosis. There are various figures. In 2019, there were 1,472,011 deaths from liver cirrhosis and other chronic liver diseases, while other sources from report 1.2 million deaths due to liver cirrhosis. According to the WHO, 42% of liver cirrhosis is attributable to alcohol, which would be between 488,000 and 618,000 deaths per year according to our sources.
#WHO (2024): Global status report on alcohol and health and treatment of substance use disorders
https://iris.who.int/bitstream/handle/10665/377960/9789240096745-eng.pdf
#Wu, X. N. et al. (2024): Global burden of liver cirrhosis and other chronic liver diseases caused by specific etiologies from 1990 to 2019. BMC Public Health, Vol. 24 (363)
https://bmcpublichealth.biomedcentral.com/articles/10.1186/s12889-024-17948-6
Quote: “In 2019, there were a total of 1,472,011 deaths (95% UI 1,374,608-1,578,731) caused by liver cirrhosis and other chronic liver diseases worldwide.”
#Huang, D. et al. (2023): Global epidemiology of cirrhosis - aetiology, trends and predictions. Nature reviews. Gastroenterology & hepatology, Vol. 20 (6)
https://pmc.ncbi.nlm.nih.gov/articles/PMC10043867/
Quote: “Cirrhosis is an important cause of morbidity and mortality among patients with chronic liver disease1. Cirrhosis can lead to hepatocellular carcinoma (HCC) and hepatic decompensation, including ascites, hepatic encephalopathy and variceal bleeding1–7, and is a leading cause of death worldwide — it was associated with 2.4% of global deaths in 2019 (ref. 8). The major aetiologies of cirrhosis are hepatitis B virus (HBV) and hepatitis C virus (HCV) infection, alcohol-associated liver disease and non-alcoholic fatty liver disease (NAFLD)9,10. However, the past decade has seen major changes in the aetiology and burden of liver disease11–16.”
- Drinking also weakens your heart, raises blood pressure and increases the risk of stroke and thrombosis – leading to another 500,000 deaths from cardiovascular diseases every year.
We can't go into detail here, but the popular belief that small amounts of alcohol are good for heart health has been disputed for a number of years and is outdated. The first two sources provide an overview of this topic.
#Arora, M. et al. (2022): The Impact of Alcohol Consumption on Cardiovascular Health: Myths and Measures. Global Heart, Vol. 17 (1)
https://world-heart-federation.org/wp-content/uploads/WHF-Policy-Brief-Alcohol.pdf
Quote: “There are multiple reasons that the belief that alcohol is good for cardiovascular health is no longer acceptable: • Such evidence has been mostly based on observational studies • Comparisons to people who do not use alcohol are often confounded by social, cultural, religious, and medical reasons to not drink • Studies have been conducted in predominantly older (>55 years of age) and Caucasian populations • Some studies that show positive effects are funded by the alcohol industry(21) • Alcohol use is often associated with other heart disease risk factors including tobacco use, access to health care, and other social determinants of health • No randomized controlled trials (RCTs) have confirmed health benefits of alcohol.
Alcohol increases the risk for hypertensive heart disease, cardiomyopathy, atrial fibrillation, flutter and strokes. Alcohol consumption (100gm/ week) is linearly associated with a higher risk of stroke, heart failure, fatal hypertensive disease and fatal aortic aneurysm, and has a borderline elevation in the risk of coronary heart disease, as compared to those consuming between 0-25g/ week.*(22) It has been argued that people with moderate consumption and no binge episodes may appear to have a slightly lower risk of ischaemic heart disease (IHD), but the protective effect of moderate alcohol consumption for CVD has been challenged(23).
#Naimi, T. et al. (2017): Selection biases in observational studies affect associations between 'moderate' alcohol consumption and mortality. Addiction, Vol. 112 (2)
https://pubmed.ncbi.nlm.nih.gov/27316346/
Quote: “Selection biases may lead to systematic overestimate of protective effects from ‘moderate’ alcohol consumption. Overall, most sources of selection bias favor low-volume drinkers in relation to non-drinkers. Studies that attempt to address these types of bias generally find attenuated or non-significant relationships between low-volume alcohol consumption and cardiovascular disease, which is the major source of possible protective effects on mortality from low-volume consumption. Furthermore, observed mortality effects among established low-volume consumers are of limited relevance to health-related decisions about whether to initiate consumption or to continue drinking purposefully into old age. Short of randomized trials with mortality end-points, there are a number of approaches that can minimize selection bias involving low-volume alcohol consumption.”
#Larsson, S. et al. (2020): Alcohol Consumption and Cardiovascular Disease: A Mendelian Randomization Study. Circulation: Genomic and Precision Medicine, Vol. 13 (3)
https://www.ahajournals.org/doi/10.1161/CIRCGEN.119.002814
Quote: “Heavy alcohol consumption is an important cause of death and disability,1 but the association between moderate drinking and cardiovascular disease (CVD) is complex. On a population level, given its widespread nature, it is important to disentangle any risks or benefits of alcohol consumption. Observational studies have generally shown that alcohol consumption is positively associated with risk of atrial fibrillation,2 heart failure,3 and hemorrhagic stroke,4 whereas moderate drinking is associated with lower risk of coronary heart disease and ischemic stroke.3–6 Data from observational studies on alcohol consumption in relation to other CVDs, including venous thromboembolism,7,8 peripheral artery disease,9 aortic valve stenosis,10 and abdominal aortic aneurysm,9,11,12 are limited or inconsistent. Observational studies are unable to fully account for confounding and reverse causation bias, and, therefore, causality in the associations of alcohol consumption with different CVDs remains uncertain. Furthermore, self-reported alcohol consumption may be underestimated, leading to measurement error in the assessment of alcohol consumption, which may result in attenuated categorical risk estimates. Mendelian randomization (MR) is an epidemiological technique that utilizes genetic variants that are reliably associated with a potentially modifiable risk factor to determine its causal role for disease risk.13 MR studies are less vulnerable to bias from confounding, reverse causation, and measurement error compared with conventional observational studies.
(...)
This MR study provides evidence that higher alcohol consumption may be causally associated with increased risk of stroke and peripheral artery disease. There was also suggestive evidence for positive associations of genetically predicted alcohol consumption with coronary artery disease, atrial fibrillation, and abdominal aortic aneurysm, but the associations were attenuated after adjustment for smoking. Alcohol consumption instrumented by the full set of variants was additionally associated with higher blood pressure and high-density lipoprotein cholesterol levels and with lower triglyceride levels.”
#Day, E. et al. (2019): Alcohol use disorders and the heart. Addiction, Vol. 114
https://onlinelibrary.wiley.com/doi/pdfdirect/10.1111/add.14703
Quote: “When considering the heart and cardiovascular system, high doses of alcohol can have both acute (depression of cardiac contractility, cardiac rhythm disturbances, arterial hypertension, sudden death) and chronic effects (ventricular dysfunction, atrial dysfunction, arrhythmia, alcoholic cardiomyopathy and heart failure) [11]. In addition, chronic high doses of alcohol are associated with the development of hypertension, coronary and peripheral atherosclerosis, changes in lipid profile and an increased risk of all forms of stroke. Heavy use of alcohol is often accompanied by the use of other harmful drugs such as tobacco and cocaine, with synergistic deleterious effects [18,19].”
#WHO (2024): Global status report on alcohol and health and treatment of substance use disorders
https://iris.who.int/bitstream/handle/10665/377960/9789240096745-eng.pdf
- On a more vain side, alcohol damages cells around your body, including your skin which looks older, sooner.
Acetaldehyde adducts (AA adducts) are formed when acetaldehyde, a toxic byproduct of alcohol metabolism, reacts with specific amino acids like lysine, cysteine, and aromatic amino acids in proteins. However, not all proteins react equally, and some are more likely to form these adducts. Commonly affected proteins include red blood cell membrane proteins, which are important for oxygen transport, hemoglobin, which carries oxygen in the blood, tubulin, which helps maintain cell structure, lipoproteins, which transport fats, albumin, which plays a key role in blood function, and collagen, which provides strength and structure to connective tissues.
#Rungratanawanich, W. et al. (2021): Advanced glycation end products (AGEs) and other adducts in aging-related diseases and alcohol-mediated tissue injury. Experimental & Molecular Medicine, Vol. 53
https://www.nature.com/articles/s12276-021-00561-7
Quote: “Acetaldehyde adducts (AA adducts) are formed by the interaction of acetaldehyde, a direct metabolite of ethanol oxidation and a human carcinogen, with certain amino acids, including lysine, cysteine, and aromatic amino acids. However, these amino acids in different proteins may exert an unequal preference for AA adduct formation. The proteins commonly bound to acetaldehyde to produce AA adducts include membrane proteins of the red blood cells (erythrocytes), hemoglobin (oxygen transport), tubulin (cellular structure), lipoproteins (lipid transport), albumin (blood), and collagen (connective tissue)167,169,180. In addition, some of these AA adducts are produced in a CYP2E1-dependent manner137,181.”
#Goodman, G. et al. (2019): Impact of Smoking and Alcohol Use on Facial Aging in Women: Results of a Large Multinational, Multiracial, Cross-sectional Survey. The Journal of clinical and aesthetic dermatology, Vol. 12 (8)
https://pmc.ncbi.nlm.nih.gov/articles/PMC6715121/pdf/jcad_12_8_28.pdf
Quote: “Alcohol consumption impairs the skin’s antioxidant defense system by decreasing dermal carotenoid concentrations.10 Alcohol also causes peripheral vasodilation,11,12 which can lead to dilated facial capillaries. Social perceptions and value judgments are often based on appearance. Wrinkles; undereye puffiness; uneven skin tone; and volume loss around the eyes, midface, and lips add to the perception of increased age.5,13
Previous studies have shown varying associations exist between tobacco or alcohol use and skin photoaging,5,14 wrinkling,6,15–18 or facial aging in general.13,19 However, these studies were generally conducted in single countries and involved relatively small study populations (i.e., a few hundred participants or fewer).
(...)
Measurements: Using a mirror, participants determined their own aging severity on photonumeric rating scales for 11 facial characteristics. Linear regressions were used to assess associations between each feature’s severity and smoking status (never vs. current and former smoker); smoking pack years (0 versus 1–10, 11–20, and >20 years); alcohol use (none vs. moderate and heavy); and alcoholic beverage type, after controlling for body mass index, country, age, and race.
Results: Smoking was associated with an increased severity of forehead, crow’s feet, and glabellar lines; undereye puffiness; tear-trough hollowing; nasolabial folds; oral commissures; perioral lines; and reduced lip fullness (p≤0.025) but not midface volume loss or visible blood vessels. Heavy alcohol use (≥8 drinks/week) was associated with increased upper facial lines, undereye pu ness, oral commissures, midface volume loss, and blood vessels (p≤0.042).
Conclusion: Smoking and alcohol consumption signi cantly but di erentially impact skin and volume-related facial aging.”
- And not only does alcohol contain a lot of calories by itself, it also makes many people very hungry.
#Caton, S. J. et al. (2004): Dose-dependent effects of alcohol on appetite and food intake. Physiology & Behavior, Vol. 81 (1)
https://www.sciencedirect.com/science/article/abs/pii/S0031938404000332?via%3Dihub
Quote: “Intake at lunch (excluding energy from the preload) was significantly higher following 4 UA (5786 ± 991 kJ) compared to 1 UA (4928 F 1245 kJ). Participants consumed more high-fat salty food items at lunch following 4 UA compared to the other preloads. Hunger was rated higher following 4 UA across the day in comparison to the other preloads, but fullness ratings failed to reflect any difference by condition. Energy intake at dinner was similar in all conditions and total energy intake across the day was significantly higher after 4 UA (14,615 ± 1540 kJ) than after 1 UA (13,204 ± 2156 kJ). In conclusion, above a certain threshold, alcohol appears to stimulate appetite in part, due to elevated levels of subjective hunger. When this occurs, energy intake is not reduced at subsequent meals. Thus, alcohol may contribute to positive energy balance via its additive effects to total energy intake and by short-term appetite stimulation.
(...)
Alcohol is a macronutrient with an energy density of around 29 kJ (7 kcal) per gram and an estimated average alcohol intake in Western countries constitutes 8– 10% of total daily energy intake [1].”
#Kwok A, et al. (2019): Effect of alcohol consumption on food energy intake: a systematic review and meta-analysis. British Journal of Nutrition, Vol. 21(5) https://www.cambridge.org/core/journals/british-journal-of-nutrition/article/effect-of-alcohol-consumption-on-food-energy-intake-a-systematic-review-and-metaanalysis/2F9AB5C64A86329EB9E817ADAEC3D88C
Quote: “Studies consistently demonstrated no compensation for alcoholic beverage energy intake, with dietary energy intake not decreasing due to alcoholic beverage ingestion. Meta-analyses using the random-effects model were conducted on twelve studies and demonstrated that alcoholic beverage consumption significantly increased food energy intake and total energy intake compared with a non-alcoholic comparator by weighted mean differences of 343 (95 % CI 161, 525) and 1072 (95 % CI 820, 1323) kJ, respectively. Generalisability is limited to younger adults (18–37 years), and meta-analyses for some outcomes had substantial statistical heterogeneity or evidence of small-study effects. This review suggests that adults do not compensate appropriately for alcohol energy by eating less, and a relatively modest alcohol dose may lead to an increase in food consumption.
(...)
Alcohol consumption has been suggested to stimulate appetite and potentially increase food intake. Although the mechanisms are unclear, it has been postulated that ingestion of alcohol appears to bypass the satiety mechanisms that modulate short term food intake(9) . Alcohol has been proposed to support an overall increase in food intake in two different pathways: (1) binding to type-A gamma-aminobutyric acid (GABAA) receptors and stimulating the release of opioid and (2) decreasing the serotonin response, a hunger suppresser (3, 9) . Alcoholic beverages may contribute to passive overconsumption of energy from foods. The relatively high energy density of alcoholic beverages may be additive to food energy intake, meaning it may be easier to unintentionally consume excess dietary energy(9, 10).”
- Drinking is a huge source of weight gain and increases the risk of obesity, opening the door to a cascade of other health problems.
Even if there are different results, which also depend on the methodology (cohort study vs. cross-sectional study), for example, there are some indications that alcohol consumption and obesity are linked.
#Fazzino, T. et al. (2017): Heavy Drinking in Young Adulthood Increases Risk of Transitioning to Obesity. American Journal of Preventive Medicine, Vol. 53 (2)
https://www.sciencedirect.com/science/article/abs/pii/S074937971730140X
Quote: “Results: Heavy episodic drinking was associated with 41% higher risk of transitioning from normal weight to overweight (relative risk ratio, 1.41; 95% CI=1.13, 1.74; p=0.002) and 36% higher risk of transitioning from overweight to obese by Wave IV (relative risk ratio, 1.36; 95% CI=1.09, 1.71; p=0.008), compared with individuals not drinking heavily, while accounting for covariates. Heavy episodic drinking was associated with 35% higher risk of maintaining obesity (relative risk ratio, 1.35; CI=1.06, 1.72; p=0.016) and gaining excess weight (OR=1.20, 95% CI=1.03, 1.39, p=0.02).
Conclusions: Regular heavy episodic drinking in young adulthood is associated with higher risk of gaining excess weight and transitioning to overweight/obesity. Obesity prevention efforts should address heavy drinking as it relates to caloric content and risk of transitioning to an unhealthy weight class.”
#Agarwal, K. et al. (2021): Relationship between BMI and alcohol consumption levels in decision making. International Journal of Obesity, Vol. 45
https://www.nature.com/articles/s41366-021-00919-x
Quote: “Heavy drinking is associated with a greater waist-hip ratio in mid-life even when taking other influences into account such as having overweight parents, maternal smoking in pregnancy, and physical inactivity [1, 2]. Further, regular and/or heavy episodic drinking in young adults increases the risk of being overweight or obese [3]. On the other hand, some cross-sectional studies have shown an inverse relationship between moderate alcohol consumption and high waist circumference [4] and the prevalence of metabolic syndrome [5]. A systematic review of large cross-sectional and long-term prospective cohort studies found no conclusive evidence for a positive association between alcohol consumption and weight gain [6]. Moderate to hazardous levels of alcohol consumption have been linked with lower BMI in females due to decreased carbohydrate intake from other sources (for example sucrose) [7]. Reduced energy intake from food or non-alcoholic beverages in heavy alcohol drinkers (both males and females) has been reported through the National Health and Nutrition Examination Survey (NHANES) by various groups [8,9,10]. However, there are inconsistent reports on the effect of alcohol as a major energy source contributing to the BMI of drinkers. Colditz et al. reported an inverse association between alcohol consumption and BMI, particularly in women, which could be related to alcohol calories being less efficiently utilized [7]. In contrast, higher total energy was associated with higher BMI in male heavy drinkers as compared to those consuming lower quantities of alcohol on days when drinking occurred [10]. Furthermore, some epidemiological studies have reported that energy intake from alcohol beverage type and drinking pattern (i.e., high intensity/volume, high frequency) contribute to total energy intake and are associated with excess body weight amongst young adults [3, 11, 12]. Higher consumption of energy-dense alcoholic beverages was associated with lower diet quality scores in males and females [9]. One of the major adverse effects of higher calorie intake among drinkers is the lower nutrient densities of protein, fat, carbohydrate, and some minerals and vitamins [13].”
#Kim, B. Y. et al. (2021): Association between alcohol consumption status and obesity-related comorbidities in men: data from the 2016 Korean community health survey. BMC Public Health, Vol. 21 (733)
https://bmcpublichealth.biomedcentral.com/articles/10.1186/s12889-021-10776-y
Quote: “Our results revealed alcohol drinkers, especially heavy alcohol drinkers, had increased odds of overweight, overweight/obesity, and abdominal obesity than non-alcohol drinkers or light alcohol drinkers among cross-sectional studies but not cohort studies.”
#AlKalbani, S. R., & Murrin, C. (2023): The association between alcohol intake and obesity in a sample of the Irish adult population, a cross-sectional study. BMC public health, Vol. 23 (1)
https://pmc.ncbi.nlm.nih.gov/articles/PMC10594818/
Quote: “Harmful alcohol consumption was associated with obesity (high BMI, large WC) after controlling for possible confounders. Frequent binge drinkers were more likely to have a large WC, while frequent alcohol consumers were less likely to have obesity. Further longitudinal studies to examine the exact association between alcohol consumption and obesity are warranted.”
- When scientists crunch these numbers, what they see is that health problems can start at about 1 beer a day, and that the chances of premature death start rising significantly at around 3 beers a day for men, and less than 2 for women.
#Rovira, P. & Rehm (2020): Estimation of cancers caused by light to moderate alcohol consumption in the European Union, European Journal of Public Health, Volume 31, Issue 3
https://academic.oup.com/eurpub/article/31/3/591/6041768?login=false
Quote: “The causal relationship between alcohol use and various cancer subcategories has been established based on epidemiological evidence, animal bioassays, mechanistic and other relevant data.7–10 Based on these considerations, the International Agency for Research on Cancer deemed the following cancer types to have sufficient evidence for carcinogenicity in humans7,8:
Lip and oral cavity cancer (ICD-10 codes: C00–08)
Other pharyngeal cancers (mainly oropharyngeal cancers; ICD-10 codes: C09–10, C12–14)
Oesophagus cancer (ICD-10 codes: C15)
Colon and rectum cancers (ICD-10 codes: C18–21)
Liver cancer (ICD-10 codes: C22)
Breast cancer (ICD-10 codes: C50)
Larynx cancer (ICD-10 codes: C32)
In the following, the above-noted cancer types will be grouped together and referred to as alcohol-related cancers. All of these cancers have shown dose–response relationships between the level of alcohol consumption and the probability of developing cancer with no lower threshold of alcohol use identified.7,9 In other words: even for alcohol use with less of one standard drink per day, significantly elevated risks for cancer were detected (e.g. References11,12; Reference7 for the general concept).
(...)
Light to moderate drinking was defined here as consumption of <20 g of pure alcohol per day, ≤2 standard drinks in most European countries.23 As such, a standard drink is equivalent to a small can or bottle of beer (about 300 ml), one decilitre of wine, or one shot of spirits. Please note that, our definition of light to moderate drinking is restrictive; other authors have defined drinking of more than 20 g of pure alcohol per day as a moderate drinking level (e.g. Reference24) However, to avoid overclaiming harm, we elected to be conservative by selecting a relatively low threshold.”
(...)
Dividing the category of light to moderate drinking into two subcategories based on drinking of 0–10 g/day and 10–20 g/day, shows that 37% of the 23 000 alcohol-attributable cancer cases arose as a result of the lower drinking level subcategory (0–10 g/day). For women, the percentage caused by the lower of the two light to moderate drinking categories was 40%, and for men it was 32% (see Supplementary appendix for details on each of the alcohol-related cancer categories in tables S10 and S11).”
#Zhao J. et al. (2023): Association Between Daily Alcohol Intake and Risk of All-Cause Mortality: A Systematic Review and Meta-analyses. JAMA Network Open, Vol. 6 (3)
https://jamanetwork.com/journals/jamanetworkopen/fullarticle/2802963
In this table you see that, for men, the risk of premature mortality (RR > 1) starts being statistically significant (P value < 0.05) at what they call "High volume", which is above 45 grams of ethanol per day. 45 grams of ethanol are around 3.4 beers. For women, you see that the risk of premature mortality becomes statistically significant at "Medium volume" i.e. more than 25 grams ethanol per day. 25 grams are around 1.9 beers.
- If this sounds like a lot to you, maybe look around. In the EU, the average man drinks the equivalent of almost 3 beers a day. The average woman, almost 1.
17.4 liters of pure alcohol is around 0.047 liters of pure ethanol per day. That is roughly the amount contained in three 0.3 liter beers. At 4.9 liters, this is about 13 ml per day, which is roughly equivalent to one beer
#WHO (2024): Alcohol, health and policy response in the European Union
Quote: “In 2019, the average adult in the European Union (EU) drank 11.0 litres of pure alcohol, higher than the WHO European Region average. Men consumed 3.6 times more alcohol (17.4 litres) than women (4.9 litres). In the same year, there were more than 289 million drinkers in the EU, with an average of almost four out of every five (77%) adults consuming alcohol. Drinking was more common among men (84.2%) than women (69.4%). Among current drinkers only, excluding lifetime abstainers and former drinkers, the average consumption per adult was 14.3 litres of
pure alcohol, with men consuming 20.7 litres and women 7.1 litres.”
- Similar figures apply to much of the world, especially the West.
This source below is an interactive chart. There you can view different countries or regions (e.g. Europe) individually.
#OWID (2024): Alcohol consumption per capita in men and women, 2019
https://ourworldindata.org/grapher/alcohol-consumption-per-capita-men-women
Data based on: World Health Organization via UN SDG Indicators Database (https://unstats.un.org/sdgs/dataportal), UN Department of Economic and Social Affairs (accessed 2024). More information available at: https://unstats.un.org/sdgs/metadata/files/Metadata-03-05-02.pdf.
- There is no other drug we consume that gets so close to the harmful edge.
The following study evaluates the risks of alcohol, tobacco, cannabis, and other drugs using the Margin of Exposure (MOE) method, which compares how much of a substance people typically consume to how toxic it is. A lower MOE means higher risk, while a higher MOE means lower risk.
Every substance has a certain “toxic dose”: the one at which its harmful effects start becoming apparent. The paper below estimated the toxic dose of all kind of drugs. It is what they call "BMDL10 values". In a nutshell, you take all the e.g. cannabis consumed in the world and divide by the number of adults. This gives you the average daily intake of cannabis for the whole population. Now you do the same for heroin, alcohol, etc.
#Lachenmeier, D. & Rehm, J. (2015): Comparative risk assessment of alcohol, tobacco, cannabis and other illicit drugs using the margin of exposure approach. Nature Scientific Reports, Vol. 5 (8126)
https://www.nature.com/articles/srep08126
Quote: “A comparative risk assessment of drugs including alcohol and tobacco using the margin of exposure (MOE) approach was conducted. The MOE is defined as ratio between toxicological threshold (benchmark dose) and estimated human intake. Median lethal dose values from animal experiments were used to derive the benchmark dose. The human intake was calculated for individual scenarios and population-based scenarios. The MOE was calculated using probabilistic Monte Carlo simulations. The benchmark dose values ranged from 2 mg/kg bodyweight for heroin to 531 mg/kg bodyweight for alcohol (ethanol). For individual exposure the four substances alcohol, nicotine, cocaine and heroin fall into the “high risk” category with MOE < 10, the rest of the compounds except THC fall into the “risk” category with MOE < 100. On a population scale, only alcohol would fall into the “high risk” category and cigarette smoking would fall into the “risk” category, while all other agents (opiates, cocaine, amphetamine-type stimulants, ecstasy and benzodiazepines) had MOEs > 100 and cannabis had a MOE > 10,000. The toxicological MOE approach validates epidemiological and social science-based drug ranking approaches especially in regard to the positions of alcohol and tobacco (high risk) and cannabis (low risk).”
The results are in figure 2. There you can see that the average daily intake of cannabis of the whole population is 0.006% the toxic dose of cannabis. For cocaine, the average intake is 0.06% of the corresponding toxic dose of heroin. For tobacco, it's almost 4%. But for alcohol, the average person takes about 50% of the toxic dose.
- Alcohol is unique for another reason: its unmatched ability to destroy others.
- Alcohol is unique for another reason: its unmatched ability to destroy others.
The following study concerning UK assessed 20 drugs using 16 harm criteria through multicriteria decision analysis (MCDA), where experts rated each drug on a scale from 0 to 100 and applied different weightings to the criteria. Alcohol was ranked as the most harmful drug overall, followed by heroin and crack cocaine. A similar study in the EU came to comparable conclusions
#Nutt, D. et al. (2010): Drug harms in the UK: a multicriteria decision analysis. The Lancet, Vol. 376
https://www.ias.org.uk/uploads/pdf/News%20stories/dnutt-lancet-011110.pdf
Quote: “Background
Proper assessment of the harms caused by the misuse of drugs can inform policy makers in health, policing, and social care. We aimed to apply multicriteria decision analysis (MCDA) modelling to a range of drug harms in the UK.
Method
Members of the Independent Scientific Committee on Drugs, including two invited specialists, met in a 1-day interactive workshop to score 20 drugs on 16 criteria: nine related to the harms that a drug produces in the individual and seven to the harms to others. Drugs were scored out of 100 points, and the criteria were weighted to indicate their relative importance.
Findings
MCDA modelling showed that heroin, crack cocaine, and metamfetamine were the most harmful drugs to individuals (part scores 34, 37, and 32, respectively), whereas alcohol, heroin, and crack cocaine were the most harmful to others (46, 21, and 17, respectively). Overall, alcohol was the most harmful drug (overall harm score 72), with heroin (55) and crack cocaine (54) in second and third places.”
#van Amsterdam, J. et al. (2015): European rating of drug harms. Journal of Psychopharmacology, Vol. 29 (6)
The criteria show the possible spectrum of harm to others: from injuries to violence and environmental damage to economic costs.
#Nutt, D. et al. (2010): Drug harms in the UK: a multicriteria decision analysis. The Lancet, Vol. 376
https://www.ias.org.uk/uploads/pdf/News%20stories/dnutt-lancet-011110.pdf
#Gell, J. et al. (2015): Alcohol’s Harm to Others. A report for the Institute of Alcohol Studies produced by the University of Sheffield School of Health and Related Research (ScHARR).
https://www.ias.org.uk/uploads/pdf/IAS%20reports/rp18072015.pdf
Quote: “Key Points
• Surveys conducted across Western countries have identified that the prevalence of harm from another person’s drinking is high (e.g. 70% in Australia and 53% in the USA).
• Understanding of the harm caused by drinkers is better developed in some fields (e.g. child welfare, domestic violence and foetal alcohol spectrum disorders) than others.
• Socio-demographic variations in harm are reported across the international literature. For example, younger age groups are significantly more likely to experience harm across most outcomes in Australia and Ireland.
• Few studies have quantified the costs of harm to people other than the drinker, but in the UK the total cost was estimated at up to £15.4 billion in 2004, excluding the costs to family and social networks.”
- Every year, alcohol-fueled accidents kill 500,000 people; 300,000 of them in car accidents.
#WHO (2024): Global status report on alcohol and health and treatment of substance use disorders
https://iris.who.int/bitstream/handle/10665/377960/9789240096745-eng.pdf
23% of all traffic fatalities worldwide are attributed to alcohol. With 1.3 million deaths in transport accidents worldwide, that's 299,000.
#OWID (2021): Causes of death globally: what do people die from?
#Wegman, F. (2017): The future of road safety: A worldwide perspective. IATSS Research, Vol. 40 (2)
https://www.sciencedirect.com/science/article/pii/S0386111216300103?via%3Dihub
Quote: “Estimates by the World Health Organization suggest that, on a yearly basis, road crashes kill 1.25 million people—nearly 3400 road fatalities per day—and injure up to 50 million.”
- But more than half of the people who died in those crashes didn't drink. They just died because someone else did.
#WHO (2024): Global status report on alcohol and health and treatment of substance use disorders
https://iris.who.int/bitstream/handle/10665/377960/9789240096745-eng.pdf
Quote: “Alcohol consumption had a substantial impact on the harm caused to others, particularly through
road injuries. In 2019, a total of 156 000 deaths and 10.0 million DALYs were attributable to alcoholrelated road injuries caused by someone else’s drinking.”
- Figures differ by country, but essentially 50% of all violent crime and sexual assault is committed by drunk offenders.
#Markowitz, S. (2005): Alcohol, Drugs and Violent Crime. International Review of Law and Economics, Vol. 25
https://www.sciencedirect.com/science/article/abs/pii/S0144818805000207
Quote: “For example, the Bureau of Justice Statistics (BJS,1998) reports that 41% of violent male inmates in local jails admit to drinking at the time of the offense as compared to 35% of property crime inmates. Similar results are found in other studies comparing violent and non-violent criminals (Myers, 1986; Roslund & Larson 1979). Rapists are highly likely to have used alcohol prior to their crimes, with rates of use by offenders ranging from 50% to 65% (Barnard, Holzer, & Vera, 1979; Rada, 1975). A similar observation is made for people who commit murders and assaults (Tinklenberg & Ochberg, 1981; Wolfgang & Strohm 1956).
#Kuhns, J. B. et al. (2013): The Prevalence of Alcohol-Involved Homicide Offending: A Meta-Analytic Review. Homicide Studies, Vol. 18 (3)
https://journals.sagepub.com/doi/abs/10.1177/1088767913493629
Quote: This study meta-analyzes 23 independent studies that included information from 28,265 homicide offenders across nine countries. On average, 48% of homicide offenders were reportedly under the influence of alcohol at the time of the offense and 37% were intoxicated. We found no demographic variations across age, gender, or race, although the proportion testing positive within the United States appears to be decreasing over time. Further, the proportion of offenders who were under the influence of alcohol was lower among those who committed the homicide with a firearm. Communities that have high homicide rates should work to reduce alcohol consumption rates.
#Pillmann F. et al. (2000): Acute effects of alcohol and chronic alcoholism as causes of violent crime. Der Nervenarzt, Vol. 71 (9)
https://europepmc.org/article/med/11042866
Quote: “To study the influence of alcohol and psychosocial variables on delinquent behavior, we coded data from the psychiatric evaluation of 254 defendants using a standardized score sheet, analyzing correlations between acute intoxication at the time of the crime (ICD 10:F10.0), diagnosis of alcohol dependency according to ICD 10 (F10.2), psycho-biographical variables, criminal history, and parameters relating to the index offence. We found that 64.6% of all defendants studied were intoxicated when committing the crime and 25.6% suffered from alcohol dependency. Alcohol intoxication correlated to occurrence of violent crime, cruelty in committing the index offence, and earlier convictions. Logistic regression, with demographic and psychosocial variables entered as covariables, revealed acute alcohol intoxication but not alcohol dependency as a predictor of violent crime (odds ratio 2.3, P = 0.02). Alcohol intoxication and dependency were also independent predictors of earlier convictions (intoxication, odds ratio 4.4, P = 0.0001; dependency, odds ratio 3.6, P = 0.003). Our findings support the hypothesis that acute alcohol intoxication, not dependency, influences violent crime in a direct manner. However, alcohol dependency predicts criminal recidivism.”
#Landberg, J. & Norström, T. (2011): Alcohol and homicide in Russia and the United States: a comparative analysis. Journal of studies on alcohol and drugs, Vol. 72 (5)
https://pubmed.ncbi.nlm.nih.gov/21906499/
Quote: “First, the reported proportion of offenders who had been drinking before the crime is higher for Russia than for the United States. For Russia, the estimates are in the 70%–80% range (Chervyakov et al., 2002; Pridemore, 2002, 2006). The corresponding estimates for the United States, however, seem to be markedly lower. According to a review by Pernanen and Brochu (1997), the most representative U.S. studies report proportions of about 50%–60%. Greenfeld (1998) and Greenfeld and Henneberg (2001) report somewhat lower figures (40%–45%), based on data from the Bureau of Justice Statistics.”
#Abbey, A. (2011): Alcohol’s role in sexual violence perpetration: Theoretical explanations, existing evidence and future directions. Drug and Alcohol Review, Vol. 30
https://pmc.ncbi.nlm.nih.gov/articles/PMC3177166/
Quote: “Sexual assault is frequently called a hidden crime because most incidents do not fit the stranger rape prototype and are never reported to the authorities [1,2]. Approximately half of all reported and unreported sexual assaults involve alcohol consumption by the perpetrator, victim, or both (see [3–5] for reviews of this literature). Typically, if the victim consumes alcohol, the perpetrator does as well, with estimates of perpetrators’ intoxication during the incident ranging from 30% to 75%.”
- Each year, alcohol-fueled crime kills around 100,000 people. That's a city like Pisa being massacred every year by a drunk mob.
#WHO (2018): Global status report on alcohol and health 2018
https://iris.who.int/bitstream/handle/10665/274603/9789241565639-eng.pdf?sequence=1
Quote: “Globally an estimated 0.9 million injury deaths were attributable to alcohol, including around 370 000 deaths due to road injuries, 150 000 due to self-harm and around 90 000 due to interpersonal violence.”
- And then you have all the non-lethal victims. Only in England, 500,000 adults get injured every year in accidents caused by drunk people. Another 800,000 get hurt in violent attacks by drunk offenders.
In the following study, people aged 16 and older were asked whether and what kind of “alcohol-related harm to others” had happened in the previous 12 months to them. 1.1% reported having been physically injured by accidents, 1.9% reported injuries from assaults.
#Beynon C. et al. (2019): Alcohol-related harm to others in England: a cross-sectional analysis of national survey data. BMJ Open, Vol. 9
https://bmjopen.bmj.com/content/bmjopen/9/5/e021046.full.pdf
82,5% of the population in England (and Wales) are 15 years or older while the total population is 59,6 million. That means 49,170,000 people in England (and Wales) are 15 years or older
In relation to the 1.1% of people in England who reported having been physically injured by accidents and the 1.9% who reported injuries from assaults, that is approximately 500,000 people or 800,000. The study focuses on people aged 16 and over and also included England only, so the figures are slightly lower.
- The most innocent bystanders are the 600,000 babies born every year with fetal alcohol spectrum disorder, a devastating lifelong condition caused by drinking during pregnancy.
#Lange, S. et al. (2017): Global Prevalence of Fetal Alcohol Spectrum Disorder Among Children and Youth: A Systematic Review and Meta-analysis. JAMA pediatrics, Vol. 171 (10)
https://pmc.ncbi.nlm.nih.gov/articles/PMC5710622/
Quote: “Alcohol consumption during pregnancy may cause a wide range of adverse health effects to the developing fetus, including but not limited to cognitive, behavioral, emotional, and adaptive functioning deficits, as well as congenital anomalies. The health effects of prenatal exposure to ethyl alcohol have been subsumed under the umbrella term fetal alcohol spectrum disorder (FASD), which consists of as many as 4 diagnostic entities, including fetal alcohol syndrome (FAS), partial FAS, alcohol-related neurodevelopmental disorder, and depending on the diagnostic guideline, alcohol-related birth defects. Alcohol can affect any organ or system in the developing fetus, and as such, individuals with FASD may experience a broad array of comorbid conditions. A recent study identified 428 comorbid conditions in individuals with FASD, with diagnoses from 18 of 22 chapters of the International Statistical Classification of Diseases and Related Health Problems, 10th Revision (ICD-10). Thus, clinicians from all specialties and other health service professionals will likely encounter cases of FASD.
(...)
This study identified several important public health issues. First, based on the existing data, 1 of every 13 pregnant women who consumed alcohol during pregnancy is estimated to have had a child with FASD. Second, this finding leads to an estimate that more than 1700 infants with FASD are born every day (630 000 every year) globally.”
#NIAAA (2023): Understanding Fetal Alcohol Spectrum Disorders
Quote: “What Are the Symptoms of Fetal Alcohol Spectrum Disorders?
Individuals with FASD experience day-to-day challenges, which may include cognitive and behavioral impairments as well as secondary disabilities including medical, educational, mental health, and social challenges, throughout their life. They are also subject to stigmatization for their disorder. People with FASD may have difficulty in the following areas:8,9,10
Learning and memory
Understanding and following directions
Switching attention between tasks
Controlling emotions and impulsivity
Communicating and developing social skills
Experiencing depression and anxiety
Performing daily life skills, including feeding, bathing, counting money, telling time, and minding personal safety”
- When your drinking escalates to a point that it causes real harm to yourself or others, you’ve crossed the invisible line of alcoholism.
The 11th revision of the International Statistical Classification of Diseases and Related Health Problems (ICD-11) by the WHO serves as the official system for classifying diagnoses.
The term technically used for the disorder described here is "Disorders due to use of alcohol”. While the word "alcoholism" is no longer used in medical settings and lacks a single official definition, it remains widely understood in everyday language.
#WHO (2024): ICD-11 for Mortality and Morbidity Statistics
https://icd.who.int/browse/2024-01/mms/en#1676588433
Quote: 6C40 Disorders due to use of alcohol
“Disorders due to use of alcohol are characterised by the pattern and consequences of alcohol use. Alcohol—more specifically termed ethyl alcohol or ethanol—is an intoxicating compound produced by fermentation of sugars usually in agricultural products such as fruits, cereals, and vegetables with or without subsequent distillation. There are a wide variety of alcoholic drinks, with alcohol concentrations typically ranging from 1.5% to 60%. Alcohol is predominantly a central nervous system depressant. In addition to ability to produce Alcohol Intoxication, alcohol has dependence-producing properties, resulting in Alcohol Dependence in some people and Alcohol Withdrawal when alcohol use is reduced or discontinued. Unlike most other substances, elimination of alcohol from the body occurs at a constant rate, such that its clearance follows a linear rather than a logarithmic course. Alcohol is implicated in a wide range of harms affecting most organs and systems of the body (e.g., cirrhosis of the liver, gastrointestinal cancers, pancreatitis). Harm to others resulting from behaviour during Alcohol Intoxication is well recognized and is included in the definitions of harmful use of alcohol (i.e., Episode of Harmful Use of Alcohol and Harmful Pattern of Use of Alcohol). Several alcohol-induced mental disorders (e.g., Alcohol-Induced Psychotic Disorder) and alcohol-related forms of neurocognitive impairment (e.g., Dementia Due to Use of Alcohol) are recognized.”
#NIAAA (2025): Understanding Alcohol Use Disorder
https://www.niaaa.nih.gov/publications/brochures-and-fact-sheets/understanding-alcohol-use-disorder
Quote: “Alcohol use disorder (AUD) is a medical condition characterized by an impaired ability to stop or control alcohol use despite adverse social, occupational, or health consequences. It encompasses the conditions that some people refer to as alcohol abuse, alcohol dependence, alcohol addiction, and the colloquial term, alcoholism. Considered a brain disorder, AUD can be mild, moderate, or severe. Lasting changes in the brain caused by alcohol misuse perpetuate AUD and make individuals vulnerable to relapse. The good news is that no matter how severe the problem may seem, evidence-based treatment with behavioral therapies, mutual-support groups, and/or medications can help people with AUD achieve and maintain recovery. National surveys show that millions of Americans have AUD.”
- An estimated 400 million people, 1 in 14 adults, are in this territory.
In the following surce, the adult population is defined as individuals aged 15 years and older. However, this definition differs from legal or social definitions of adulthood, which vary by country. In many regions, the legal drinking age is set at 18 years or higher, meaning that while individuals aged 15-17 are included in statistical calculations, they may not legally be considered adults in other contexts.
#WHO (2024): Global status report on alcohol and health and treatment of substance use disorders
https://iris.who.int/bitstream/handle/10665/377960/9789240096745-eng.pdf
Quote: “According to WHO nomenclature, AUDs include two diagnostic categories of ICD-11: alcohol dependence and harmful pattern of alcohol use. The estimates presented in this section are based on the data available for prevalence of “harmful use of alcohol”, as defined in ICD-10. In 2019, an estimated 400 million people aged 15 years and older had an AUD (representing 7.0% of adults), and 209 million people aged 15 years and older lived with alcohol dependence (representing 3.7% of all people aged 15+ years). The past 12-month prevalence of AUDs and alcohol dependence varied globally (see Figure 2.29) and by WHO region (Figure 2.30), with the prevalence of AUDs being highest in the European Region (10.7% of people aged 15+ years) and in the Region of the Americas (10.2%), and the prevalence of AUDs being lowest in the Eastern Mediterranean Region (0.5% of people aged 15+ years). Prevalence of alcohol dependence also varied by WHO region, being most prevalent in the European Region (5.8%) and the Region of the Americas (5.3%), and least prevalent in the Eastern Mediterranean Region (0.3%).”
- The line is very fuzzy and varies from person to person. But if you consistently drink 8 beers per week as a woman, 15 as a man, or 5 on the same day, you’ve either crossed the line or are dangerously walking towards it.
There are official guidelines for alcohol consumption, but they vary significantly from country to country. A universal, consistent definition is difficult to establish, as the boundaries are individual and often hard to determine. However, the thresholds mentioned here align with what is generally considered relevant in terms of health risks and premature mortality.
The National Institute in Alcohol Abuse and Alcoholism (NIAAA) sees alcohol abuse, which includes binge drinking and heavy alcohol use, as an increased risk of developing an alcohol use disorder.
#NIAAA (2025): Alcohol's Effects on Health. Research-based information on drinking and its impact.
https://www.niaaa.nih.gov/alcohols-effects-health/alcohol-drinking-patterns
Quote: “Alcohol misuse—which includes binge drinking and heavy alcohol use—over time increases the risk of alcohol use disorder (AUD). Additional factors also increase the risk of AUD.”
#NIAAA (2025): Alcohol's Effects on Health. Research-based information on drinking and its impact.
https://www.niaaa.nih.gov/alcohols-effects-health/alcohol-drinking-patterns
Quote: “NIAAA defines heavy drinking as follows:
For men, consuming five or more drinks on any day or 15 or more per week
For women, consuming four or more on any day or eight or more drinks per week
SAMHSA defines heavy alcohol use as binge drinking on five or more days in the past month.2”
- From those 400 million, more than half have fallen into an even deeper trap – dependence. When alcohol has become something that you physically or psychologically need.
#WHO (2024): Global status report on alcohol and health and treatment of substance use disorders
https://iris.who.int/bitstream/handle/10665/377960/9789240096745-eng.pdf
Quote: “Globally, an estimated 400 million people, or 7% of the world’s population aged 15 years and older, live with alcohol use disorders, and an estimated 209 million (3.7% of the adult world population) live with alcohol dependence, with substantial differences in the numbers of people affected in different WHO regions.”
#WHO (2024): ICD-11 for Mortality and Morbidity Statistics
https://icd.who.int/browse/2024-01/mms/en#1676588433
Quote: “6C40.2 Alcohol dependence
Alcohol dependence is a disorder of regulation of alcohol use arising from repeated or continuous use of alcohol. The characteristic feature is a strong internal drive to use alcohol, which is manifested by impaired ability to control use, increasing priority given to use over other activities and persistence of use despite harm or negative consequences. These experiences are often accompanied by a subjective sensation of urge or craving to use alcohol. Physiological features of dependence may also be present, including tolerance to the effects of alcohol, withdrawal symptoms following cessation or reduction in use of alcohol, or repeated use of alcohol or pharmacologically similar substances to prevent or alleviate withdrawal symptoms. The features of dependence are usually evident over a period of at least 12 months but the diagnosis may be made if alcohol use is continuous (daily or almost daily) for at least 3 months.”
(...)
“Diagnostic Requirements
Essential (Required) Features:
A pattern of recurrent episodic or continuous use of alcohol with evidence of impaired regulation of alcohol use that is manifested by two or more of the following:
Impaired control over alcohol use (i.e., onset, frequency, intensity, duration, termination, context);
Increasing precedence of alcohol use over other aspects of life, including maintenance of health, and daily activities and responsibilities, such that alcohol use continues or escalates despite the occurrence of harm or negative consequences (e.g., repeated relationship disruption, occupational or scholastic consequences, negative impact on health);
Physiological features indicative of neuroadaptation to the substance, including: 1) tolerance to the effects of alcohol or a need to use increasing amounts of alcohol to achieve the same effect; 2) withdrawal symptoms following cessation or reduction in use of alcohol (see Alcohol Withdrawal), or 3) repeated use of alcohol or pharmacologically similar substances to prevent or alleviate withdrawal symptoms.
The features of dependence are usually evident over a period of at least 12 months but the diagnosis may be made if use is continuous (daily or almost daily) for at least 3 months.”
- In Europe and the the Americas, 1 in 20 adults are caught in this web.
In the following WHO document, the adult population is defined as individuals aged 15 years and older. However, this definition differs from legal or social definitions of adulthood, which vary by country. In many regions, the legal drinking age is set at 18 years or higher, meaning that while individuals aged 15-17 are included in statistical calculations, they may not legally be considered adults in other contexts.
#WHO (2024): Alcohol, health and policy response in the European Union
#WHO (2024): Global status report on alcohol and health and treatment of substance use disorders
https://iris.who.int/bitstream/handle/10665/377960/9789240096745-eng.pdf
Quote: “Prevalence of alcohol dependence also varied by WHO region, being most prevalent in the European Region (5.8%) and the Region of the Americas (5.3%), and least prevalent in the Eastern Mediterranean Region (0.3%).”
- A US study found that up to 50% of all alcoholics may fly under the radar. They come in two main groups: unproblematic young adults, and middle-aged professionals with successful careers and families. As one of them you’ll show no antisocial behaviors. You’ll fulfill your obligations. You’ll probably have no diagnosed health conditions.
Here, individuals with similar characteristics were grouped into five clusters. Our description of these clusters is a simplified summary. Statistically speaking, there are, of course, individuals with health problems within each cluster, but these occur at a lower rate compared to the rest.
#Moss, H.B. et al. (2007): Subtypes of Alcohol Dependence in a Nationally Representative Sample. Drug and alcohol dependence Vol. 91 (2-3)
https://pmc.ncbi.nlm.nih.gov/articles/PMC2094392/
Quote: “Cluster 1(“Young Adult Subtype”) is the most prevalent cluster (31.5 %), and is characterized by a younger age (mean age 24.5 years), a relatively early onset of AD (mean age 19.6 years), a low probability of ASPD (<1%), and a moderate probability of AD in both first and second degree family members (~22%). Relative to other clusters, cluster members manifest lower probabilities of comorbid psychiatric disorders and legal problems, and a moderate probability of being cigarette smokers (~32%) and cannabis abusers (~25%). Cluster 1 AD individuals have an elevated probability of engaging in hazardous use of alcohol and experiencing alcohol withdrawal. Examination of demographic data suggests that Cluster 1 AD males are 2.5 times more common than Cluster 1 AD females. Given the relative youth of cluster members, it is not surprising that ~75% have never been married. Only 54% work full-time, while 36.5% are in school either full-time or part-time. They tend to drink alcohol less frequently than other cluster members (~143 drinking days in last year); however, they drink 5+ drinks on an average of 104 (73%) of these drinking days. They report drinking an average maximum of 13.8 (standard) drinks on drinking days. Only 8.7% of Cluster 1 individuals have ever sought help because of drinking. When they do seek help, it is more frequently through 12-step groups rather than through private professional or specialty treatment.
Cluster 2 (“Functional Subtype”) (19.4%) is characterized by older respondents (age ~41 years), a slightly older age of initiation to drinking (mean age 18.5 years), a later onset of AD (mean age 37 years), a low probability of ASPD (<1%), and a moderate probability of AD in both first and second degree family members (~31%). Cluster members manifest a moderate probability of major depression (~24%), and low rates of anxiety disorders. Members have a moderate probability of being regular smokers (~43%), low probabilities of other substance use disorders, and the least probability of having legal problems (<1%). Cluster 2 individuals have a moderately elevated probability of endorsing engagement in hazardous use of alcohol (~35%), and the lowest cluster probability for using alcohol despite problems (~14%). They also have the lowest probability for endorsing a reduction in activities due to alcohol (~7%), and drinking despite problems (~40%). In terms of external covariates, there is a modest over-representation of males (~60%) relative to females (~40%). Nearly 50% of Cluster 2 individuals are married, 62% work full-time, and only 3.6% are in school full-time. Nearly 26% have a college degree or higher. This cluster has the highest proportion of retired individuals (~5%). Cluster 2 mean total family income ($59,576) is the highest among the AD clusters. Cluster 2 individuals tend to drink alcohol every other day (~181 drinking days in last year), and they consume 5+ drinks on an average of almost 98 (54%) of these drinking days. They report an average of 10 drinks as being the maximum number consumed on drinking days. Seventeen percent of Cluster 2 individuals have ever sought help for their drinking. Help-seeking Cluster 2 individuals more typically participate in 12-step groups or are treated for AD by private health care professionals.”
#Benton, S. (2009): Understanding the High-Functioning Alcoholic: Professional Views and Personal Insights
https://www.bloomsburycollections.com/monograph?docid=b-9798216029908
Quote: “Understanding the High-Functioning Alcoholic represents the untold story of millions of alcoholics. The goal of this book is to allow society to see that alcoholics all suffer from the same disease, but that it may manifest in different ways. The homeless person and the high-powered executive can both be alcoholics— alcoholism does not differentiate among socioeconomic class, education level, and appearance. However, because the high-functioning alcoholic (HFA) has the ability to perform and succeed, the treatment often comes too late or not at all. Each and every alcoholic should be diagnosed and treated—because denial kills.
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It is estimated that there are about 18 million people in this country who meet the diagnostic criteria for alcohol abuse and alcohol dependence.2 A study published in May 2007 by the U.S. Department of Health and Human Services National Institute on Alcohol Abuse and Alcoholism (NIAAA) reported that only 9% of these alcoholics are chronic severe alcoholics. It is this small percentage that has created the image of “the falling down booze-hound: an older person, usually male, staggering down the street and clutching a brown paper bag. A pathetic image, hopeless and depraved.”3 It is this stereotype that has left an impression in our minds preventing so many from ever knowing the truth about alcoholism. Other findings of this research study stated that young adults comprise over 30% of alcoholics, and another 20% are “highly functional and well-educated with good incomes”4 indicating that up to 50% of alcoholics may be high functioning.”
- But on average you’ll be having 4 beers a day and will get drunk every week.
Clusters 1 and 2 drink an average of 2.48 and 2.66 fl oz per day (we used 2.5 oz for simplification).
Let's assume that a typical beer has 5% alcohol content and is 12 fl oz, then the alcohol content per beer is 12 x 0.05 = 0.6 fl oz .
At 2.5 fl oz per day, that's 2.5/06 = 4.17 beers per day.
#Moss, H. B. et al. (2007): Subtypes of alcohol dependence in a nationally representative sample. Drug and alcohol dependence, Vol, 91 (2-3)
- Studies confirm what we have known for millennia. Modest quantities of alcohol help strangers bond.
#Sayette, M. et al. (2012): Alcohol and Group Formation: A Multimodal Investigation of the
Effects of Alcohol on Emotion and Social Bonding. Psychological science, Vol. 23 (8)
https://pmc.ncbi.nlm.nih.gov/articles/PMC5462438/pdf/nihms861768.pdf
Quote: “In one of the largest alcohol-administration studies yet conducted, we employed a novel group-formation paradigm to evaluate the socioemotional effects of alcohol. Seven hundred twenty social drinkers (360 male, 360 female) were assembled into groups of 3 unacquainted persons each and given a moderate dose of an alcoholic, placebo, or control beverage, which they consumed over 36 min. These groups’ social interactions were video recorded, and the duration and sequence of interaction partners’ facial and speech behaviors were systematically coded (e.g., using the Facial Action Coding System). Alcohol consumption enhanced individual- and group-level behaviors associated with positive affect, reduced individuallevel behaviors associated with negative affect, and elevated self-reported bonding. Our results indicate that alcohol facilitates bonding during group formation. Assessing nonverbal responses in social contexts offers new directions for evaluating the effects of alcohol.”
#Gurrieri, L. et al. (2021): Alcohol narrows physical distance between strangers. Proceedings of the National Academy of Sciences of the United States of America, Vol. 118 (20)
https://www.pnas.org/doi/pdf/10.1073/pnas.2101937118
Quote: “In the current study we employed a randomized alcohol-administration design paired with computer-vision measures, analyzing over 20,000 proximity readings derived from video to examine the effect of alcohol consumption on physical distance during social interaction. Results indicated that alcohol caused individuals to draw significantly closer to an unfamiliar interaction partner during social exchange, reducing physical proximity at a rate with potentially important implications for public health. In contrast, alcohol had no effect on physical distance with a familiar interaction partner. Findings suggest that alcohol might act to overcome a natural caution people feel towards strangers and thus promote virus transmission between previously unconnected social groups.”
- And individuals who drink moderately and socially tend to have more friends, closer friendships, and higher levels of trust in others.
#Dunbar, R. et al. (2017): Functional Benefits of (Modest) Alcohol Consumption. Adaptive Human Behavior and Physiology Vol. 3
https://link.springer.com/article/10.1007/s40750-016-0058-4
Quote: “Alcohol use has a long and ubiquitous history. Despite considerable research on the misuse of alcohol, no one has ever asked why it might have become universally adopted, although the conventional view assumes that its only benefit is hedonic. In contrast, we suggest that alcohol consumption was adopted because it has social benefits that relate both to health and social bonding. We combine data from a national survey with data from more detailed behavioural and observational studies to show that social drinkers have more friends on whom they can depend for emotional and other support, and feel more engaged with, and trusting of, their local community. Alcohol is known to trigger the endorphin system, and the social consumption of alcohol may thus have the same effect as the many other social activities such as laughter, singing and dancing that we use as a means of servicing and reinforcing social bonds.”
#aan het Rot, M. et al. (2008): Alcohol in a social context: findings from event-contingent recording studies of everyday social interactions. Alcoholism, clinical and experimental research, Vol. 32 (3)
https://onlinelibrary.wiley.com/doi/abs/10.1111/j.1530-0277.2007.00590.x
- In the US, the share of 18-year-olds who have ever tried alcohol has dropped by 25% in the last decades.
#Twenge, J. & Park, H. (2019): The Decline in Adult Activities Among U.S. Adolescents, 1976-2016. Child development, Vol. 90 (2)
https://srcd.onlinelibrary.wiley.com/doi/abs/10.1111/cdev.12930
- Binge drinking in adolescents has plummeted by 50%.
#Clark Goings, T. et al (2019): Trends in binge drinking and alcohol abstention among adolescents in the US, 2002-2016. Drug and alcohol dependence, Vol. 200
https://www.sciencedirect.com/science/article/abs/pii/S0376871619301437?via%3Dihub
#Statista (2025): Binge alcohol use in the past month among persons aged 18-25 years in the U.S. from 2002 to 2023, by gender
https://www.statista.com/statistics/354280/binge-alcohol-use-in-adults-18-to-25-in-the-us-by-gender/
- And even in countries like Germany or France, where beer and wine have always been part of their cultural DNA, alcohol consumption is falling.
#Destatis (2024): Indikator 3.5.2 Alkoholkonsum pro Kopf (im Alter von 15 Jahren und älter) innerhalb eines Kalenderjahres in Litern reinen Alkohols
#OWID (2025): Alcohol consumption per person, 2000 to 2020
Data based on The World Bank (2025): World Development Indicators (WDI)
https://datacatalog.worldbank.org/search/dataset/0037712/World-Development-Indicators
- And that’s a victory. Fewer accidents. Fewer hospital beds filled. Fewer lives quietly derailed.
The following study cites various reasons for the decline in numbers of alcohol-related traffic accidents, including administrative measures such as effectiveness of screening and brief counseling or lowering legal BACs to .08%.
However, changes in consumer behavior are also mentioned.
#Hingson, R. et al. (2017): Magnitude and Trends in Heavy Episodic Drinking, Alcohol-Impaired Driving, and Alcohol-Related Mortality and Overdose Hospitalizations Among Emerging Adults of College Ages 18-24 in the United States, 1998-2014. Journal of studies on alcohol and drugs, Vol. 78 (4)
https://www.jsad.com/doi/epdf/10.15288/jsad.2017.78.540?role=tab
Quote: “Results: From 1999 to 2005, percentages of emerging adults ages 18–24 reporting past-month heavy episodic drinking rose from 37.1% to 43.1% and then declined to 38.8% in 2014. Alcohol-impaired driving rose from 24% to 25.5% and then declined to 16.0%. Alcoholrelated unintentional injury deaths increased from 4,807 in 1998 to 5,531 in 2005 and then declined to 4,105 in 2014, a reduction of 29% per 100,000 since 1998. Alcohol-related traffic deaths increased from 3,783 in 1998 to 4,114 in 2005 and then declined to 2,614 in 2014, down 43% per 100,000 since 1998. Alcohol-related overdose deaths increased from 207 in 1998 to 891 in 2014, a 254% increase per 100,000. Other types of nontraffic unintentional injury deaths declined. Alcohol-overdose hospitalizations rose 26% per 100,000 from 1998 to 2014, especially from increases in alcohol/other drug overdoses, up 61% (alcohol/opioid overdoses up 197%). Conclusions: Among emerging adults, a trend toward increased alcohol-related unintentional injury deaths, heavy episodic drinking, and alcohol-impaired driving between 1998 and 2005 was reversed by 2014. Persistent high levels of heavy episodic drinking and related problems among emerging adults underscore a need to expand individually oriented interventions, college/community collaborative programs, and evidence-supported policies to reduce their drinking and related problems. (J. Stud. Alcohol Drugs, 78, 540–548, 2017).
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Among 18- to 24-year-olds, from 1999 to 2005, the percentages of college students reporting heavy episodic drinking as well as driving under the influence proportionally increased 7%. Among noncollege respondents, the proportional increases were 10%. From 2005 to 2014, college student heavy episodic drinking declined from 45% to 37%, representing a 18% proportional decline, and driving under the influence declined from 29% to 17%, representing a 41% proportional decline. Among noncollege respondents between 1999 and 2014, heavy episodic drinking increased from 36% to 40%, representing an 11% proportional increase, whereas alcohol-impaired driving declined from 20% to 16%, representing a 20% proportional decline (SAMHSA, 2000, 2006, 2016).”
- The share of young people who see their friends almost every day has plummeted by 50%.
#Twenge, J. et al. (2019): Less in-person social interaction with peers among U.S. adolescents in the 21st century and links to loneliness. Journal of Social and Personal Relationships, Vol. 36 (6)
- Attendance at parties has fallen by 30%.
#Twenge, J. et al. (2019): Less in-person social interaction with peers among U.S. adolescents in the 21st century and links to loneliness. Journal of Social and Personal Relationships, Vol. 36 (6)
- Dating and casual sex have fallen by a similar amount.
#Twenge, J. & Park, H. (2019): The Decline in Adult Activities Among U.S. Adolescents, 1976-2016. Child development, Vol. 90 (2)
https://srcd.onlinelibrary.wiley.com/doi/abs/10.1111/cdev.12930
#South, S. & Lei, L. (2021): Why Are Fewer Young Adults Having Casual Sex? Socius, Vol. 7
https://journals.sagepub.com/doi/10.1177/2378023121996854
Quote: “The decline in casual sex is apparent for both women and men. In 2007, 31 percent of the young unpartnered women reported having sexual intercourse during the past month, but in 2017 only 22 percent did so. The percentage of men who reported engaging in casual sex dropped from 38 percent in 2007 to 24 percent in 2017. These declines in causal sexual activity are generally consistent with the decline in sexual intercourse among all young adults observed in other nationally representative surveys (e.g., Twenge et al 2017a; Ueda et al. 2020).”
- And all while loneliness and mental health issues have skyrocketed.
#Twenge, J. et al. (2019): Less in-person social interaction with peers among U.S. adolescents in the 21st century and links to loneliness. Journal of Social and Personal Relationships, Vol. 36 (6)
#Kannan, V. & Veazie, P. (2022): US trends in social isolation, social engagement, and companionship ⎯ nationally and by age, sex, race/ethnicity, family income, and work hours, 2003-2020. SSM - population health, Vol. 21
https://www.sciencedirect.com/science/article/pii/S235282732200310X
#Twenge, J. et al. (2019): Age, period, and cohort trends in mood disorder indicators and suicide-related outcomes in a nationally representative dataset, 2005-2017. Journal of abnormal psychology, Vol. 128 (3)
https://www.apa.org/pubs/journals/releases/abn-abn0000410.pdf
#Blanchflower, D. & Oswald, A. (2020): Trends in Extreme Distress in the United States, 1993-2019. American journal of public health, Vol. 110 (10)
https://www.sciencedirect.com/science/article/pii/S2950004423000135
#McGorry, P. et al. (2025): The youth mental health crisis: analysis and solutions. Frontiers in psychiatry, Vol. 15
https://www.frontiersin.org/journals/psychiatry/articles/10.3389/fpsyt.2024.1517533/full
- There are many different reasons for this, from covid to social media. But the shift in which drugs we consume is probably not totally unrelated either.
The following source provides a good and up-to-date overview. It not only addresses social media and
COVID, but also climate change and general economic concerns.
#McGorry, P. et al. (2025): The youth mental health crisis: analysis and solutions. Frontiers in psychiatry, Vol. 15
https://www.frontiersin.org/journals/psychiatry/articles/10.3389/fpsyt.2024.1517533/full
Quote: “3.2.1.1.7 Digital media/social media
The digital world offers youth avenues for connection, creativity, and support, but also carries significant risks. Smartphone usage may contribute to sleep deprivation (143), and social media addiction may further exacerbate mental health issues among young people (144). While evidence suggests a longitudinal association between social media and mental health in young people, the magnitude is likely to be small and the nature of this association is uncertain owing to bidirectional effects and the range of mediating factors (145–149). With these considerations, recent studies have suggested a link between increased social media/electronic device usage and both a decrease in psychological wellbeing and increase in depressive symptoms, occurring between 2011/2012 and 2015/2016 (63, 64). This was based on two criteria: social media/electronic device usage being correlated with higher depressive symptoms/lower wellbeing and usage significantly increasing simultaneously with depression/low wellbeing. These findings are limited by the broad categories used to measure usage (e.g., ‘almost every day’), which do not capture the variance in this variable given that the majority of young people use social media daily (150). Other studies using the same surveys analysed by Twenge et al. indicate a small correlation between social media usage and both depressive symptoms and wellbeing (150–152) and that social media explained only 4% of the increase in depressive symptoms (150). Furthermore, between 2009 and 2017, the association between social media usage and depressive symptoms was found to be weak and confined to only 2009–2010 (152).”
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3.2.1.2.2 Labour market/unemployment
The impacts of the 2008 global financial crisis on young people were substantial and included insecure employment and income (153–157).
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The COVID-19 pandemic and its associated economic crisis have exacerbated inequality among vulnerable and disadvantaged groups, including young people (173). During the pandemic, young people have experienced increased rates of educational disruption, unemployment or precarious employment, financial insecurity, and housing stress (173, 174). Young people of lower socio-economic status have experienced greater economic hardship (174). This amplification of socio-economic determinants of mental health and of inequality has likely contributed to an increase in anxiety and depression that has disproportionately affected young people (15, 68, 174–176).
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3.2.1.2.5 Climate change
There is increasing evidence of climate change impacts on young people’s mental health who are a priority population group in the context of climate change. These include anxiety, sadness, grief, hopelessness, powerlessness, depression, and existential worries about the future (177–180). A range of factors including government inaction on climate change, social media exposure, and social challenges such as housing instability, food insecurity, and increased conflict influence this relationship between climate change and young people’s mental health (177, 178, 181–183).”
- Drugs like weed have massively gained ground and in contrast to drinking, smoking weed tends to make many people less energetic and likely to do things, more socially awkward and especially if you use a lot of it, more lonely.
#Patrick M. (2025): Daily or near-daily cannabis and alcohol use by adults in the United States: A comparison across age groups. Addiction (Abingdon, England), Vol. 120 (4)
https://onlinelibrary.wiley.com/doi/full/10.1111/add.16748
#UN (2023): Narcotic Drugs - Estimated World Requirements for 2024 - Statistics for 2022
https://www.incb.org/documents/Narcotic-Drugs/Technical-Publications/2023/E_Narcotics_ebook_2023.pdf
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