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Alcohol myopia
Alcohol myopia
Alcohol myopia
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Alcohol myopia is a cognitive-physiological theory on alcohol use disorder in which many of alcohol's social and stress-reducing effects, which may underlie its addictive capacity, are explained as a consequence of alcohol's narrowing of perceptual and cognitive functioning. The alcohol myopia model[1] posits that rather than disinhibit, alcohol produces a myopia effect that causes users to pay more attention to salient environmental cues and less attention to less salient cues. Therefore, alcohol's myopic effects cause intoxicated people to respond almost exclusively to their immediate environment. This "nearsightedness" limits their ability to consider future consequences of their actions as well as regulate their reactive impulses.[2]

Alcohol's ability to alter behavior and decision-making stems from its impact on synaptic transmission at GABA receptors.[2] Alcohol's effects on the synaptic level dampen the brain's processing ability and limit attentional capacity.[3]

Overall, the alcohol myopia theory proposes that intoxicated individuals will act rashly and will choose overly simple solutions to complex problems.[original research?]

Three classes of myopia

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Alcohol's myopic effects on the drinker's cognitive processes can be characterized into three classes: self-inflation, relief, and excess.

Self-inflation

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Alcohol consumption alters the drinker's self-image by "enhancing feelings of self-appraisal and even narcissism".[4] Alcohol inhibits sophisticated levels of mental processing that are necessary to recognize personal flaws. The ‘tunnel vision’ effect of alcohol myopia, which limits the attentional capacity of the drinker, causes individuals to focus on favorable and superficial characteristics of themselves. Overall, the self-inflating effect of alcohol can increase the drinker's self-confidence and therefore lead them to engage in activities or social situations that would normally make her or him nervous or uncomfortable when sober.[4]

Relief

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Alcohol can alleviate the drinker's feelings of stress or anxiety. Alcohol myopia limits those under the influence of alcohol to see the world through a nearsighted lens;[2] in other words, consumption of alcohol will lead individuals to temporarily forget about previous worries or problems, for these feelings lay outside of the restricted set of immediate cues that the drinker can respond to. By depriving the individual of the attention capacity necessary to process undesirable thoughts, alcohol myopia can bring the drinker a sense of relief.[4]

Excess

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Alcohol exaggerates the drinker's perception of the world around them. The drinker's response to this exaggerated world manifests in erratic and dramatic behaviors. Under the influence of alcohol, individuals are incapable of sufficiently processing the long-term consequences of their actions; they will respond to immediate and salient cues in the moment. In this way, drunk individuals can be described as "slaves to the present moment".[4]

Alcohol is believed to disinhibit urges normally considered socially unacceptable. The sober brain is able to utilize the frontal cortex to make executive decisions and restrain these impulses. However, the drunk brain is unable to regulate the urges for excessive behavior.[4]

By leading the brain to overreact to present cues and disregard the implications of one's actions, alcohol often provokes aggressive behavior. Alcohol consumption can result in a "Jekyll and Hyde" effect in individuals who are typically amiable when sober but are perhaps predisposed to aggressive behavior.[5] Additionally, alcohol has a dramatic connection to criminal behavior, rage, physical destruction, and sexual assault.[4]

It is important to note, however, that alcohol myopia's effects on excessive behavior do not incite aggression in all drinkers. In some intoxicated individuals, excess simply manifests itself in their becoming significantly more talkative, flirtatious, or adventurous. Additionally, in situations in which inhibitory cues are the most salient, the individual may behave in a more prudent or passive manner than they would when sober.[5]

Alcohol's effects on neurotransmission

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Alcohol is classified as a sedative hypnotic drug. Alcohol produces a sedative effect by acting on receptors of the inhibitory neurotransmitter GABA. GABA receptors contain a binding site for the chemical, GABA, a chloride ion channel, and an additional binding site for alcohol molecules.[2]

GABA produces its normal inhibitory effects on cell activity by reducing a neuron's firing rate. When a GABA molecule attaches to its binding site, it activates the receptor, resulting in an inflow of chloride ions. The increase in concentration of negative charge inside the cell hyperpolarizes the membrane. This hyperpolarization decreases the likelihood that the membrane will send an action potential to neighboring neurons; the difference of charge across the membrane has increased, while it would need to decrease in order to reach the threshold charge necessary to propagate an action potential.[2]

Alcohol acts as a positive allosteric modulator and therefore amplifies the transmitter's inhibitory effects. When alcohol molecules bind to its site on the GABA receptor, they lengthen the time that the receptor's chloride ion pore remains open, resulting in an even greater hyperpolarization of the membrane. Additionally the binding of alcohol causes the GABA transmitter to bind to its receptors more frequently, and therefore augments the transmitter's ability to inhibit cell activity.[2]

Overall, alcohol's interactions with GABA receptors decrease neuronal firing across the body and inhibit cortical activation.[6] Behavioral changes associated with alcohol myopia stem from the inhibitory effects of this reduction of firing and activation. [2]

The inhibition conflict

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One effect of alcohol myopia is that it amplifies rash responses in intoxicated individuals. Alcohol does not directly affect the emotions and actions of inebriated people, but does so indirectly via its involvement in the inhibition conflict.

Inhibition conflict is a cognitive function that arises in people and allows them to make decisions based on immediate stimuli and stimuli that require a higher level of processing. In sober individuals, situations that produce an inhibition conflict would consist of one set of salient cues (external stimuli) that stimulate a certain response and other cues (internal stimuli such as possible negative consequences or societal standards and norms) that would inhibit the salient cues and therefore prevent rash action.[7] Those influenced by alcohol myopia are unable to comprehend this second set of cues, as the condition narrows an individual's ability for higher-level cognitive functioning. Therefore, these individuals tend to act rashly without consideration for the consequences of their actions.[7]

Studies have been conducted to test the effects of alcohol on the intensity of males’ aggressive response to external stimuli, demonstrating the role of inhibition conflict on alcohol myopia. Male subjects under the influence of alcohol often ignored external cues, both in laboratory settings and in real life situations. In the lab patients who were given alcohol were more likely to respond to unpleasant tones (external stimuli) violently, despite internal cues advising them against aggression.[8] Surveys conducted also demonstrated that while intoxicated men are more likely to address the salient cue of anger with aggressive behavior towards their partners.[9] The results of these studies demonstrate men experiencing the effects of alcohol myopia were unable to process the consequences of their actions, and continued to act aggressively despite consequences. Alcohol had effectively limited their interpretation of salient cues and prevented them from interpreting cues that would inhibit aggressive action.

Women have also exhibited the effects of alcohol myopia's ability to disrupt the inhibition conflict. Research conducted in 2002 determined that there was a positive relationship between college females’ level of sobriety and their decisions to engage in risky sexual behavior. Results showed that a majority of college aged females who had been drinking chose not to address risk topics before sexual intercourse with a partner.[10] Alcohol myopia can explain this relationship. The inebriated females’ abilities to analyze internal cues warning them of the risks of sex were inhibited by alcohol, while alcohol caused them to become more responsive to the salient cue of arousal.

Risky behavior

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Alcohol myopia has been shown to increase the likelihood that a person will engage in risky behavior. The increased risk taking brought on by alcohol myopia often ends with aversive consequences for the person acting dangerously or those influenced by the intoxicated's actions.[11] Those under the influence of alcohol myopia are often unaware of the consequences of their behavior as well as its risky nature. It has been shown that alcohol myopia causes people to function like those with maladaptive risky behaviors, often caused by behavior disorders or a personal history of substance use.[12] Dosage of alcohol intensifies these effects of myopia.[11]

People under the influence of alcohol myopia act in a risky manner because of the myopia's inhibiting effects on their ability to analyze the probable outcomes of their actions. Alcohol activates dopaminergic circuits in the midbrain that also regulate the brain's analyzation and recognition of the outcomes of an action.[13][14] It is not yet clear on exactly how alcohol effects these dopaminergic circuits. The following behaviors are influenced by risk taking when a person is experiencing the effects of alcohol myopia.

Personal goals

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Alcohol myopia has also been found to affect one's level of commitment to a personal goal. Individual commitment to a goal is dependent upon level of personal desire and feasibility of the goal. A person's ability to appropriately interpret feasibility is inhibited by alcohol myopia. This is because desire is a more salient stimulus than feasibility, causing those experiencing alcohol myopia to ignore the less salient stimulant of feasibility. Because one is less inhibited by the prospect of unfeasible goals, those under the influences of alcohol myopia tend to feel more committed to their goals than sober individuals. Studies testing the relationship between intoxication and level of commitment to goals support the theory that increased goal commitment (despite level of feasibility) is a side effect of alcohol myopia.[15][16]

Sexual arousal

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Alcohol myopia causes individuals to become increasingly aware of sexual arousal and more likely to respond rashly to the arousal stimulus. The decision about how to respond to sexual arousal involves cognitive function that synthesizes both impelling cues (those that draw attention to the benefits of an action) and inhibiting cues (those that focus on the consequences of an action). The alcohol myopia theory suggests that intoxicated individuals will be more likely to engage in risky sexual behavior. Intoxicated males subject to high levels of sexual arousal were more likely to engage in unprotected sex than sober males subject to the same levels of arousal.[17] This is because the impelling cues (sexual arousal) are often more imminent than inhibitory cues (safety precautions), and those affected by alcohol myopia are limited to cognitive processing of the more immediate cues and often ignore the inhibitory cues.

The extent of alcohol myopia's effects on one's decisions about how to react to sexual arousal is dependent upon the level of confliction one feels. The more intense the personal conflict of whether or not to use a condom, the greater effect alcohol has on the final decision to engage in risky sexual behavior. Intoxicated males who had felt heavily conflicted about condom use were least likely to use a condom. Those intoxicated men who had been less conflicted about using a condom were more likely to engage in safe sex.[17] Therefore, some intoxicated individuals can actually be less likely to engage in risky sexual behavior than their sober counterparts, given appropriate cues.[18] The effects of alcohol myopia on response to sexual arousal also depend on the level of sexual arousal. When sexual arousal levels were high, a greater percentage of men reported not using a condom than when arousal levels were low. This goes back to the importance of saliency in alcohol myopia. The more salient the external cue (in this case, higher levels of sexual arousal were more salient than lower levels) the more likely it is for alcohol to inhibit the comprehension of the consequences of an action.

Drunk driving

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The Alcohol Myopia Model proposes that intoxication increases the likelihood that an individual will decide to drive in an unsafe situation. The drinker is unable to properly weigh the future consequences of his or her decision to drive; “inhibitory cues that prohibit driving are less likely to be considered because they lack salience and immediacy."[5] Meanwhile, the intoxicated individual responds to the immediate motivations to drive. For example, he will focus on the rewards of getting home quickly and not having to pay for a cab. Therefore, under the influence of alcohol, driving becomes the simplest and most compelling option. Studies show that when questioned, intoxicated individuals reported “greater intentions to drink and drive...and fewer moral obligations against drinking and driving” than they did when sober.[5]

See also

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References

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Revisions and contributorsEdit on WikipediaRead on Wikipedia

Alcohol myopia

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from Grokipedia
Alcohol myopia is a psychological theory proposing that acute impairs cognitive processing capacity, thereby narrowing an individual's attentional focus to the most salient, proximal cues in the environment while diminishing awareness of peripheral or distal information. Formulated by Claude M. Steele and Robert A. Josephs in , the theory frames alcohol's behavioral effects—such as increased , risk-taking, and —not primarily as pharmacological disinhibition but as a consequence of this attentional constriction, which limits the mental resources available for encoding and responding to complex situational demands. Under alcohol myopia, intoxicated individuals exhibit heightened responsiveness to immediate instigatory cues (e.g., sexual temptations or aggressive provocations) at the expense of inhibitory cues (e.g., long-term risks or social norms), often resulting in maladaptive decisions like unprotected intercourse or escalated conflicts. This mechanism also accounts for alcohol's effects, as the reduced capacity to allocate to ruminative worries or stressors facilitates temporary emotional , though it may exacerbate underlying issues upon . Empirical investigations, including paradigms assessing recall after stress exposure and goal commitment tasks, have substantiated these dynamics, demonstrating that moderate-to-high doses selectively amplify focus on prominent stimuli. While the theory has influenced understandings of alcohol-related harms in domains like and sexual risk behavior, subsequent reviews have refined its scope, emphasizing that myopia's intensity varies with dose, individual differences (e.g., greater effects in males), and contextual salience of cues, rather than a uniform disinhibitory blanket. Critiques highlight limitations in generalizing from controlled settings to real-world intoxication, where factors like expectancies may interact, yet controlled attentional studies continue to affirm its core predictions over alternative models.

History and Origins

Development of the Theory

The alcohol myopia theory originated as a cognitive framework to address empirical inconsistencies in alcohol's behavioral effects, which prior disinhibition hypotheses—positing alcohol as a general remover of cognitive restraints—could not consistently explain, as alcohol sometimes facilitated prosocial behaviors and at other times exacerbated antisocial ones depending on situational cues rather than dosage alone. Traditional models emphasized direct pharmacological disruption of inhibition or expectancy-driven effects, yet studies revealed irregular outcomes, such as the same intoxicated individual displaying on one occasion and sociability on another, underscoring the role of contextual variability over fixed impairment. Building on earlier explorations of alcohol's attentional impacts in contexts, Claude M. Steele and Robert A. Josephs formulated the theory in their seminal 1990 Psychological Bulletin article, "Alcohol Myopia: Its Prized and Dangerous Effects," which shifted emphasis from broad to alcohol-induced narrowing of perceptual and cognitive focus, drawing on cognitive psychology's attentional models. This integration posited that intoxication creates a "myopic" state by taxing limited attentional capacity, prioritizing salient, immediate cues (e.g., instigatory social prompts) while de-emphasizing distal or inhibitory ones, thereby explaining divergent effects without relying solely on metabolic or learned anticipation mechanisms. The formulation extended prior work, including Steele's 1985 conceptualization of myopia in response conflict during aggressive scenarios, to encompass wider social and emotional domains. Empirical motivations stemmed from laboratory and observational data predating , which demonstrated alcohol's amplification of dominant response tendencies under cue-salient conditions—for instance, heightening to strong social pressures while blunting awareness of weaker countervailing influences—thus resolving paradoxes in how alcohol could enhance adaptive self-perception in supportive settings yet precipitate maladaptive extremes in provocative ones. This context-dependent lens challenged simplistic linear models by highlighting alcohol's interaction with environmental affordances, laying groundwork for subsequent tests of attentional in behavioral outcomes.

Key Proponents and Initial Formulation

Claude M. Steele and Robert A. Josephs, psychologists at the , originated the alcohol myopia theory in their 1990 article published in the American Psychologist. Building on prior observations of alcohol's impairment of perception and thought, they conceptualized alcohol's effects as arising from a pharmacological reduction in attentional resources, which narrows cognitive focus to prominent, immediate cues while diminishing processing of less salient or complex information. This manifests as "a state of shortsightedness in which superficially understood, immediate aspects of experience have a disproportionate influence on and ," treating as a finite capacity overloaded by alcohol, thereby prioritizing central incentives over peripheral inhibitions or long-term considerations. Steele's earlier work on self-affirmation theory, which examines how individuals preserve self-integrity by selectively attending to affirming values amid discrepancies between ideal and actual self-views, provided a foundational basis for understanding how selectively amplifies positive self-evaluations by blocking access to self-critical cues.60229-4) The theory hypothesizes three core outcome classes from this attentional narrowing: self-inflation, enhancing evaluations of personally valued traits; relief, alleviating anxiety or depression by restricting rumination on stressors when paired with engaging distractions; and excess, promoting impulsive actions like heightened or prosocial extremes by failing to resolve inhibitory conflicts between salient impulses and restraining factors. These predictions drew initial support from paradigms assessing social behaviors, such as increased shock delivery in tasks under intoxication due to overlooked inhibitory contingencies and amplified helping responses amid strong interpersonal appeals at blood alcohol levels around 0.04%.

Theoretical Foundations

Attentional Narrowing and Cognitive Mechanisms

Alcohol consumption induces attentional narrowing by diminishing the brain's capacity to process a broad array of information, thereby concentrating focus on the most salient or proximal stimuli while peripheral cues receive reduced attention. This mechanism, central to alcohol myopia theory as articulated by Steele and Josephs in 1990, stems from alcohol's disruption of cognitive resources, creating a state of overload that filters out distal or less immediate information in favor of compelling instigators or goals. The underlying causal process parallels limited-capacity models of , where intoxication elevates cognitive demands akin to those in sober multitasking overload, diverting finite resources to primary focal points and impairing the integration of secondary inputs. Alcohol specifically compromises functions, which orchestrate executive control over allocation, resulting in prioritized processing of immediate environmental demands over reflective or inhibitory signals. Behavioral experiments corroborate this, revealing that intoxicated participants exhibit delayed detection and responses to peripheral stimuli compared to sober controls, evidencing a literal narrowing of attentional scope. In contrast to disinhibition models, which imply a general erosion of internal restraints leading to unchecked impulses, alcohol myopia highlights selective amplification: responses intensify based on what captures narrowed attention, potentially bolstering inhibition if restraint cues dominate salience or exacerbating when provocations do. This distinction underscores that alcohol enhances rather than indiscriminately releases attended tendencies, resolving empirical inconsistencies where intoxication sometimes curbs rather than provokes behavior.

Inhibition Conflict Model

The Inhibition Conflict Model, integrated within alcohol myopia theory, posits that alcohol's effects on behavior arise primarily in contexts involving response conflict, where instigatory cues (promoting action) compete with inhibitory cues (restraining action). In such scenarios, alcohol narrows attentional capacity, disproportionately amplifying focus on salient instigatory cues while diminishing awareness of inhibitory ones, thereby escalating the instigated response. This dynamic does not imply universal ; rather, alcohol's influence hinges on the relative salience of cues, determined by environmental factors and individual predispositions, such as preexisting motivations or cue accessibility. When cue balance favors instigatory elements— for instance, in provoked aggression where immediate threats overshadow long-term consequences— alcohol intensifies the response by sidelining distal inhibitors like social norms or self-control. Empirical evidence supports this: laboratory experiments demonstrate that alcohol elevates aggressive shocks delivered to a confederate only following provocations that create inhibitory conflict, with blood alcohol concentrations around 0.08% yielding effect sizes indicating heightened retaliation compared to placebo conditions. Conversely, absent conflict— such as unprovoked neutral interactions— alcohol yields negligible or null effects on aggression, underscoring that myopia does not inherently provoke but amplifies preexisting tensions. In imbalanced scenarios lacking sufficient inhibitory cues, alcohol may reinforce the dominant direction without escalation, as seen in studies where low-conflict incentives lead to modest behavioral amplification rather than . This context-dependence highlights causal interplay between alcohol's pharmacological narrowing of and situational cue hierarchies, rather than alcohol as an isolated causal agent; individual differences in cue , like trait , further modulate outcomes by altering baseline salience. Field and laboratory data consistently affirm that alcohol fails to induce novel conflicts, instead exploiting existing ones, with meta-analyses of over 30 studies confirming moderation by provocation levels.

Neurobiological Underpinnings

Effects on Brain Function and Neurotransmission

Alcohol acutely potentiates GABA_A receptor function, enhancing inhibitory throughout the , while inhibiting NMDA glutamate receptors, which suppresses excitatory signaling and disrupts . In the (PFC), this manifests as reduced NMDA-mediated excitatory postsynaptic currents (EPSCs) at concentrations of 22 mM or higher, shortening neuronal up-state duration and amplitude essential for maintaining persistent activity during . The resulting imbalance impairs executive control mechanisms, limiting the PFC's capacity to allocate across multiple cues and favoring a constricted focus on dominant stimuli. Neuroimaging evidence from (fMRI) corroborates these disruptions, showing diminished PFC activation during alcohol intoxication in tasks demanding and divided attention, such as stop-signal paradigms where reduced fronto-temporal responses slow detection of peripheral hazards. Similarly, visual perception studies reveal alcohol-induced hypoactivation in prefrontal regions, correlating with narrowed perceptual fields and impaired processing of non-focal visual information at blood alcohol concentrations around 0.05-0.08%. Alcohol also modulates dopaminergic neurotransmission by disinhibiting (VTA) neurons, elevating dopamine release in the to the and PFC, thereby heightening the motivational salience of immediate cues. This amplification biases neural circuits toward reward-relevant signals, fostering feedback loops that reinforce attentional tunneling by suppressing extraneous inputs via altered dopamine modulation of PFC gating functions. Such changes occur rapidly during intoxication, with dopamine surges peaking within minutes of consumption and persisting to influence cue prioritization.

Pharmacological Interactions

Alcohol's induction of exhibits a dose-dependent relationship, with attentional narrowing becoming evident at blood alcohol concentrations (BAC) exceeding 0.06%, particularly under high cognitive conflict where peripheral inhibitory cues are ignored in favor of salient instigators. Laboratory experiments targeting simultaneous central and peripheral have demonstrated restricted attentional scope at mean BAC levels around 0.068%, equivalent to moderate intoxication, supporting the theory's prediction of narrowed processing capacity. This threshold aligns with broader observations that low to moderate doses (0.05-0.10% BAC) suffice for measurable in controlled settings, though effects intensify with rising concentrations due to progressive depletion of cognitive resources. Individual variability modulates onset and intensity, influenced by pharmacokinetic factors such as absorption rate and . Tolerance from chronic exposure diminishes acute sensitivity, necessitating higher BAC for equivalent narrowing, as adaptive changes in neural processing blunt alcohol's impact on attention allocation. Genetic polymorphisms, notably *2 variants prevalent in East Asian populations, accelerate accumulation, heightening sedative and dizzying effects at lower doses and potentially amplifying by enhancing early cognitive restriction. Co-ingestion with substances like may counteract some myopic narrowing by sustaining , though empirical data specific to attentional mechanisms remains sparse. Pharmacokinetic models indicate that alcohol's peak plasma concentrations, typically 30-90 minutes post-oral intake depending on dose and gastric emptying, temporally coincide with maximal cognitive impairments observed in paradigms, underscoring the acute interplay between rising BAC and reduced peripheral cue processing. These timelines highlight how rapid ascent to threshold BAC exacerbates , with slower metabolism in variants like *2 prolonging exposure to impairing levels.

Positive Psychological Effects

Self-Inflation and Enhanced Self-Evaluations

Alcohol myopia theory posits that intoxication narrows attentional capacity, prioritizing salient central cues—such as positive self-affirmations or feedback—while peripheral inhibitory information, like self-doubts or ideal-real discrepancies, recedes from awareness. This cognitive filtering elevates immediate self-perceptions, fostering a temporary alignment between one's aspired and perceived self, often manifesting as heightened in personal traits. For instance, an might overlook skill deficiencies and emphasize innate talents under alcohol's influence, resulting in amplified positive self-evaluations. Experimental evidence demonstrates this self-inflation effect. In a controlled study, participants ingested alcohol or a and completed pre- and post-intoxication ratings of their "real self" across 35 traits, categorized by conflict level based on ideal-real gaps. Intoxicated subjects selectively improved ratings on high-conflict traits (e.g., those involving significant discrepancies), shifting perceptions closer to ideals, whereas low-conflict traits and conditions showed no such change; this pattern held after controlling for mood alterations, underscoring attentional over affective shifts. Similar findings validate self-inflation subscales in measurement tools like the Alcohol Myopia Scale, where intoxicated states correlate with enhanced self-worth and reduced discrepancy awareness in social or introspective contexts. This phenomenon yields prized social advantages, enabling bolder self-presentation and interpersonal engagement by suppressing , which may echo adaptive functions in group dynamics—such as signaling competence to foster alliances—countering views framing alcohol solely through pathological lenses. By magnifying central positive cues like affirming social feedback, alcohol facilitates temporary ego bolstering that reinforces bonding rituals across cultures, though it risks habitual reliance when peripheral realities are chronically ignored.

Anxiety and Stress Relief

Alcohol consumption induces attentional narrowing that diminishes rumination on chronic stressors by prioritizing salient, immediate environmental cues over distal threats, thereby providing short-term relief from anxiety. This mechanism, central to alcohol myopia theory, facilitates adaptive disengagement from persistent worries, akin to voluntary distraction techniques used in , but pharmacologically driven. Experimental evidence demonstrates that moderate doses (e.g., 0.03-0.08% blood alcohol concentration) reliably lower self-reported anxiety levels post-consumption, particularly when paired with engaging activities that further constrain attentional capacity. Physiological corroboration includes attenuated responses to stressors following acute alcohol intake, reflecting dampened hypothalamic-pituitary-adrenal axis activation under myopic conditions. In laboratory paradigms inducing , such as anticipation of or evaluative tasks, participants administered alcohol exhibited reduced and subjective tension compared to controls, mediated by impaired processing of threat-related information. These effects hold across diverse samples, including non-dependent drinkers, underscoring myopia's role in transient emotional regulation rather than pathological reinforcement. Unlike chronic use fostering dependency, acute serves as a resilience tool by interrupting maladaptive to non-imminent concerns, with benefits most pronounced in low-to-moderate intoxication states before inhibitory overload occurs. Longitudinal data indicate that such episodic relief does not inherently escalate to habitual when decoupled from high-risk contexts, distinguishing it from pathways. However, individual differences in baseline anxiety and expectancy biases can modulate efficacy, with heavier drinkers showing less consistent attenuation due to tolerance.

Risky and Dysfunctional Behaviors

and Excess in Decision-Making

Alcohol myopia fosters and excess in decision-making by constraining cognitive resources, thereby prioritizing salient immediate cues—such as short-term rewards or impulses—over peripheral inhibitory factors like potential long-term costs or risks. This attentional narrowing impairs comprehensive cost-benefit analysis, leading individuals to overcommit to dominant impulses without restraint, as peripheral deterrents receive insufficient processing. For instance, when immediate gratification cues are prominent, intoxicated decision-makers exhibit heightened acceptance of options favoring proximal gains, even when those entail disproportionate risks relative to sober evaluations. Empirical evidence from experimental paradigms demonstrates this mechanism in controlled decision tasks. In studies manipulating cue salience, alcohol-intoxicated participants showed elevated risk-taking in scenarios where rewards were centrally emphasized, with blood alcohol levels correlating positively with choices ignoring probabilistic losses. This pattern aligns with causal dynamics wherein reduced attentional capacity equates to truncated deliberation, amplifying commitment to heuristically appealing but excessive actions, such as unrestrained pursuit of salient pleasures. Conversely, when inhibitory cues are rendered central, alcohol can mitigate certain impulsive tendencies, underscoring the context-dependent nature of myopia-driven excess. Such effects manifest in real-world analogs, including disproportionate financial or temporal overcommitment during intoxication, where elevates responses to immediate incentives like spending sprees triggered by environmental prompts. Laboratory validations, including those assessing goal commitment under alcohol, confirm that disproportionate focus on proximal elements erodes balanced evaluation, favoring unmoderated in impulses. These findings highlight alcohol's role in escalating decision excess through selective perceptual bias, independent of broader behavioral domains like .

Aggression and Social Responses

Alcohol myopia contributes to heightened during interpersonal conflicts by selectively narrowing toward salient provocative cues—such as insults or threats—while diminishing of peripheral inhibitory cues, including potential retaliation or social sanctions. This attentional distortion intensifies inhibition conflicts inherent in aggressive impulses, where immediate instigations gain disproportionate influence over deliberative restraints. Experimental paradigms, like provoked shock administration tasks, reveal that intoxicated individuals deliver nearly three times more aversive shocks than sober participants, as myopia restricts processing of consequence-related information. Laboratory investigations from the , including those simulating bar-like social provocations, corroborated this mechanism through controlled manipulations of cue prominence. Moderate intoxication consistently escalated aggressive outputs under high-provocation conditions, with inhibitory cues (e.g., verbal warnings of consequences) significantly attenuating responses when attended. A of such conflict scenarios found alcohol to produce a 1.06 standard deviation elevation in extreme behaviors, accounting for 20-30% of variance in attributable to myopic cue prioritization. Another across 49 studies confirmed that weak inhibitory cues amplify alcohol's aggressive effects, with moderation by provocation levels and dosage. This framework does not posit alcohol as a sole or inevitable aggressor trigger, as comparable attentional narrowing arises in sober states amid acute or trait-driven , underscoring the role of individual differences like low or hostile rumination. Contextual moderators, including and trait aggressivity, further qualify myopia's influence, emphasizing that intoxication facilitates rather than originates aggressive escalation in predisposed scenarios.

Sexual Risk-Taking

Alcohol myopia theory posits that intoxication narrows attentional capacity, prioritizing central cues like immediate over peripheral inhibitory signals, such as the potential for sexually transmitted infections (STIs), , or ambiguous cues. This selective focus can override precautionary decision-making, leading to elevated intentions for unprotected intercourse, particularly in high-arousal contexts where impelling cues dominate. Empirical tests, including alcohol administration paradigms, have shown dose-dependent effects: moderate intoxication (blood alcohol concentration around 0.04-0.08%) amplifies arousal-driven responses, while higher levels further impair appraisal. Laboratory experiments provide direct evidence of these mechanisms. In a 1996 study involving male participants, those administered alcohol (target BAC 0.05%) in a simulated scenario reported significantly more positive intentions toward condomless and endorsed more justifications for non-use (e.g., prioritizing over ) compared to sober controls, with effects mediated by heightened focus on cues. Similarly, a 2000 experiment with young men found that intoxicated individuals (BAC ≈0.06%) under sexual arousal conditions showed reduced intentions to use condoms, as alcohol myopia diminished attention to inhibitory risks, though this was less pronounced in low-arousal setups. Field-corroborative data from surveys of students indicate that self-reported heavy episodes correlate with 20-30% higher rates of regretted unprotected , aligning with myopia's in real-time cue prioritization. Consent misperceptions also arise under alcohol myopia, as intoxication impairs detection of subtle rejection signals while amplifying perceived mutual interest. A 2025 study on perpetration risks demonstrated that acutely intoxicated men (BAC >0.05%) overestimated female partners' sexual willingness in ambiguous vignettes, increasing non-consensual advance intentions by up to 25%, attributable to narrowed processing of peripheral rather than baseline aggression. However, in mutually low-conflict scenarios with clear affirmative cues, alcohol may reduce anxiety-driven hesitation, potentially facilitating consensual engagement without elevating risks, though aggregate evidence underscores net harm via unprotected acts and impaired . These findings emphasize individual agency amid cognitive constraints, with myopia explaining elevated risks without excusing accountability.

Impaired Driving and Hazard Perception

Alcohol myopia manifests in impaired driving through a constriction of attentional scope, whereby intoxicated individuals prioritize central roadway cues—such as the immediate forward path—while neglecting peripheral elements like road signs, mirrors, and lateral threats. This narrowing reduces visual scanning behaviors essential for perception, as evidenced by simulator studies showing decreased glances to off-road instruments and mirrors under acute alcohol influence. For instance, drivers with blood alcohol concentrations (BAC) around 0.05% exhibit diminished peripheral allocation, leading to overlooked environmental cues that sober drivers routinely monitor. Empirical data from simulators corroborate this effect, demonstrating BAC-correlated declines in detection latency and vigilance. At moderate BAC levels (e.g., 0.05%), participants take longer to identify hazards and respond more abruptly, with increased standard deviation in lateral position (SDLP) indicating unstable vehicle control due to unperceived peripheral deviations. Vigilance tasks reveal error rates rising proportionally with BAC, such as a 4.06 cm SDLP increase at 0.07% BAC, underscoring myopia's role in amplifying crash risks beyond mere motor impairment. These findings explain disproportionate involvement of alcohol in fatal crashes, where impaired peripheral contributes to in detecting side intrusions or . While alcohol myopia directly erodes perception, its effects interact with factors like and traits, rather than serving as an isolated causal agent. Extended wakefulness combined with low-dose alcohol (0.03% BAC) exacerbates vigilance lapses in simulators, preventing compensatory strategies such as increased headway maintenance. Personality-driven risk tolerance may further modulate this, as high-sensation seekers show amplified myopia under intoxication, prioritizing immediate driving flow over broader threat scanning. This interplay highlights that alcohol does not unilaterally excuse impaired performance but compounds preexisting vulnerabilities in .

Empirical Support and Evidence

Foundational Studies from the 1990s

Steele and Josephs (1990) introduced alcohol myopia theory, positing that intoxication narrows attentional capacity, prioritizing salient cues over distal or inhibitory ones, thereby explaining alcohol's role in amplifying both prosocial and antisocial extremes. Their integrated experimental showing that this attentional restriction, akin to , facilitates disinhibited responses when internal conflicts—such as between instigatory impulses and restraining norms—are present. Effects were pronounced at blood alcohol levels exceeding 0.06%, with behavioral outcomes correlating to the degree of attentional narrowing measured via distraction paradigms. Experiments on social extremity under intoxication demonstrated heightened response polarization in high-inhibition-conflict scenarios. A of 34 studies encompassing 121 alcohol-placebo comparisons revealed that alcohol increased behavioral extremity by 1.06 standard deviations when strong instigatory and inhibitory cues conflicted, versus negligible effects (0.14 SD) in low-conflict conditions, validating myopia's selective facilitation of extreme actions by blocking access to peripheral restraints. Similarly, self-rating tasks under alcohol load showed inflated evaluations on high-conflict traits—those with large ideal-self discrepancies—where sober participants tempered positivity due to negative cues, but intoxicated ones focused narrowly on affirming aspects, yielding systematically biased upward shifts. Inhibition conflict tests further corroborated conditional aggression facilitation. Aggression paradigms, such as shock-retaliation tasks, found intoxicated participants delivering approximately three times more intense shocks under provocation-conflict conditions compared to sober controls, with outcomes tied to impaired processing of inhibitory social norms amid salient aggressive cues. These findings emphasized replicable metrics, including attention task performances (e.g., distraction-induced load mimicking intoxication), which predicted variance in behavioral disinhibition across social, self-evaluative, and aggressive domains. Josephs and Steele's concurrent 1990 experiments on attentional of stress provided direct validation through two studies. In Study 1, intoxicated participants (target blood alcohol level ~0.05%) exhibited reduced cardiovascular reactivity to an impromptu speech stressor when performing a concurrent distracting task (e.g., rating slides), but heightened reactivity without distraction, demonstrating alcohol's dual anxiolytic-anxiogenic effects dependent on attentional focus. Study 2 replicated this, substituting sober for alcohol and achieving parallel stress modulation, confirming that attentional allocation—quantified via task performance interference—mediated alcohol's impact rather than direct , with correlations between load-induced and physiological outcomes supporting the theory's core mechanism.

Validation Through Experimental Paradigms

Experimental paradigms validating alcohol myopia have employed manipulations of attentional load and cue salience to demonstrate how intoxication narrows focus to central, prominent stimuli while impairing processing of peripheral or inhibitory cues. In cue manipulation designs, participants intoxicated with alcohol (typically achieving alcohol concentrations of 0.04-0.08%) exhibit heightened responsiveness to salient impelling cues (e.g., provocative or rewarding prompts) relative to sober controls, particularly when inhibitory cues are less prominent. For instance, studies manipulating environmental cue salience in tasks show that alcohol reduces attention to risk-related peripherals, leading to riskier choices only under high-salience conditions for instigatory cues. Trauma film paradigms provide direct evidence of differential memory encoding consistent with myopia. In a 2019 study, participants viewed a 12-minute trauma depicting interpersonal after consuming alcohol to reach a mean breath alcohol concentration of 0.06%; immediate revealed enhanced for central details (e.g., the assault itself) but significantly reduced recall of peripheral elements (e.g., background objects or bystander actions) compared to controls. This pattern held across 20 central and 20 peripheral recall items, with intoxicated participants scoring 15-20% lower on peripherals, supporting the theory's prediction of narrowed attentional scope during encoding. Similar findings emerge in post-encoding alcohol administration designs, where intoxication disrupts consolidation of non-central details without broadly impairing . Goal commitment experiments further validate by linking intoxication to persistent pursuit of salient goals despite evident risks. In a 2011 study, alcohol-intoxicated participants (BAC ~0.05%) showed stronger commitment to personally valued goals when success expectancies were low, mediated by implicit and explicit attentional narrowing toward goal-relevant cues; sober participants attenuated commitment under similar low-expectancy conditions. A follow-up 2014 experiment replicated this, finding that alcohol's effect on commitment was disproportionately driven by focus on impelling goal cues over peripheral deterrents, with mediation analyses confirming attentional allocation as the mechanism ( β = 0.25-0.35). These paradigms isolate myopia's role in overriding inhibitory signals, as commitment wanes without alcohol when risks are salient. Dual-task interference paradigms complement these by quantifying alcohol's impact on divided attention. Intoxicated individuals perform worse on secondary tasks requiring peripheral monitoring (e.g., detecting distractors during primary pursuit), evidencing that funnels attention centrally; for example, alcohol reduces interference from competing stimuli in simulated , allowing focus on forward cues but at the cost of detection (reaction time deficits of 100-200 ms). Collectively, these methods—spanning , commitment, and interference—converge on attentional mediation, with alcohol doses of 0.04-0.08% consistently producing without global impairment.

Development of Measurement Scales

The Alcohol Myopia Scale (AMS), a 14-item self-report instrument, was developed in 2013 to quantify the narrowing of attentional focus posited by alcohol myopia theory. Items were generated to capture three core myopic effects: restricted attention to immediate cues, diminished capacity for peripheral processing, and heightened salience of proximal stimuli during intoxication, with respondents rating agreement based on past drinking experiences. The scale was constructed through exploratory and confirmatory factor analyses on samples of alcohol users (N=1,127 and N=1,007, respectively), yielding a three-factor structure that accounted for 62% of variance and demonstrated internal consistency (Cronbach's α > .80 across factors). Validation efforts established via positive correlations between AMS scores and self-reported alcohol consumption metrics, including drinking frequency (r ≈ .25-.35), quantity per occasion (r ≈ .20-.30), and maximum drinks in a single episode (r ≈ .15-.25), serving as proxies for blood alcohol concentration (BAC) exposure. Behavioral proxies were supported by associations with outcomes like risky tendencies and reduced under intoxication, aligning with theory-driven predictions. Test-retest reliability over two weeks was moderate (r ≈ .70-.75), indicating stability for repeated assessments. The enables empirical assessment of individual differences in susceptibility, distinguishing those prone to acute attentional narrowing from others, which supports its application in longitudinal designs tracking vulnerability over time or across drinking episodes. For instance, higher baseline scores predict greater manifestation in prospective alcohol challenges, facilitating studies on trait-like predictors of impairment. This measurement approach enhances rigor by providing a standardized tool beyond ad-hoc behavioral tasks, though self-report limitations necessitate with objective BAC or performance data.

Criticisms, Limitations, and Debates

Challenges to Predictive Power

While alcohol myopia theory predicts heightened under conditions of salient instigatory cues by narrowing away from inhibitory ones, empirical observations reveal inconsistencies, particularly in low-conflict or anxiety-driven scenarios where alcohol instead attenuates aggressive responses through its properties. For instance, when internal anxiety cues predominate over external provocations, alcohol's constriction of attentional capacity can prioritize anxiety relief, effectively overriding potential conflict signals and reducing rather than amplifying . This challenges the theory's universal predictive scope, as the same myopic mechanism can yield opposing outcomes depending on cue hierarchies, limiting its beyond highly controlled, provocation-heavy contexts. Laboratory-based replications of alcohol-induced aggression have also faltered in populations with lower baseline risk, such as non-aggressive college males, where point-subtraction aggression paradigm (PSAP) responses showed no significant alcohol escalation, underscoring variability in real-world applicability. These failures highlight an overreliance on artificial lab paradigms that manipulate cue salience in isolation, often failing to account for naturalistic moderators like social context or individual traits, which dilute the theory's causal universality. Consequently, while alcohol myopia excels in post-hoc rationalization of observed excesses, its prospective predictions weaken in heterogeneous settings, demanding integration with broader pharmacological and environmental factors for robust forecasting.

Alternative Causal Explanations

Alcohol expectancy theory offers an alternative explanation for alcohol-related behaviors, attributing them primarily to learned beliefs about alcohol's effects rather than attentional narrowing. Proponents argue that individuals act in accordance with pre-existing expectancies—such as anticipating relaxation or —which can drive outcomes like increased or risk-taking even in the absence of pharmacological impairment. Experimental evidence from placebo-controlled studies supports this, showing that participants who believe they have consumed alcohol exhibit behavioral changes comparable to those intoxicated with actual alcohol, including heightened sexual errors and reduced use intentions, independent of cognitive deficits. Disinhibition models posit that alcohol broadly impairs mechanisms, releasing suppressed impulses without requiring cue-specific attentional shifts as in myopia theory. This framework predicts consistent increases in impulsive actions across contexts, contrasting with myopia's emphasis on salient environmental cues determining behavioral direction. Empirical tests reveal divergences: disinhibition fails to account for situations where inhibitory cues prevent risky behavior under intoxication, yet it better explains chronic traits like habitual in heavy drinkers, where general restraint reduction overrides situational factors. For instance, animal and human studies demonstrate alcohol's suppression of activity linked to inhibition, leading to uniform behavioral escalation rather than selective focus. Evolutionary perspectives challenge myopia's portrayal of alcohol as a primary amplifier by framing it as an adaptive social enhancer that promotes group cohesion and . Moderate consumption historically facilitated in and early humans by reducing anxiety and focusing attention on immediate affiliative cues, yielding survival benefits like enhanced alliances without inherent toward harm. and data indicate alcohol's prosocial effects—such as increased and reduced defensiveness in group settings—stem from reward pathways reinforcing social reciprocity, rather than pathological narrowing; excessive focus on negative outcomes in myopia overlooks these functional roles observed in low-dose paradigms.

Individual Differences and Contextual Factors

Individual differences in traits, such as and behavioral undercontrol, moderate the degree to which alcohol induces attentional , with higher-trait individuals displaying amplified narrowing of focus toward immediate, salient cues at the expense of peripheral inhibitory information. For example, those prone to show stronger alcohol-attenuated processing of long-term consequences in scenarios, as alcohol exacerbates preexisting tendencies to prioritize proximal rewards. This interaction aligns with alcohol myopia theory's emphasis on allocation, where baseline cognitive control levels determine vulnerability to alcohol's restrictive effects on information processing. Twin and behavioral genetic studies indicate moderate for traits like (estimates ranging from 30% to 50%), which in turn influence susceptibility to myopic responding under alcohol influence, though direct of alcohol myopia itself remains underexplored. These findings underscore that genetic predispositions to low self-regulation heighten the risk of maladaptive myopia, such as in or risk-taking, rather than alcohol acting in isolation. Contextual factors, including the structure and salience of environmental cues, further modulate alcohol myopia by determining which stimuli capture the narrowed attentional field. In settings where pro-inhibitory cues (e.g., clear signals or commitment prompts) dominate, alcohol can facilitate more prudent outcomes by myopically amplifying focus on those elements, as demonstrated in studies of sexual where strong relational cues led to increased use under intoxication. High-stakes environments, such as those with immediate accountability or vivid consequence cues, similarly elevate the prominence of sobriety-maintaining information, potentially offsetting myopia's typical bias toward instigatory impulses. This variability rejects uniform causal attributions of alcohol to negative behaviors, as outcomes hinge on cue hierarchies shaped by the setting rather than deterministic ; for instance, distracting or low-cue environments exacerbate myopia-driven errors, while structured contexts with heightened peripheral relevance mitigate them. Empirical paradigms confirm that alcohol's effects are not invariant but emerge from person-situation interactions, emphasizing the need to assess individual baselines and environmental configurations over generalized anti-alcohol prescriptions.

Recent Developments and Applications

Post-2010 Research Findings

In 2010, researchers revisited the alcohol myopia model to refine its explanation of , particularly , through a cue-competition framework. This update posits that alcohol narrows attentional capacity, allowing salient instigatory cues—such as immediate provocations—to dominate over peripheral inhibitory cues, like potential consequences or social norms, thereby facilitating impulsive acts without implying a direct causal effect of alcohol on . Empirical tests in settings, including competitive tasks, supported this by showing intoxicated participants prioritized provocative stimuli, leading to heightened aggressive responses when inhibitory cues were less accessible. Subsequent studies extended alcohol myopia to emotional processing, demonstrating its role in disrupting emotional inertia—the tendency for affective states to persist over time. A 2013 experiment found that moderate alcohol consumption reduced affective , enabling participants to disengage from prior negative emotions and experience greater positive affect in social interactions, consistent with myopia's emphasis on present-moment cues over historical emotional momentum. This effect mediated improved mood and social outcomes, suggesting alcohol may provide temporary relief from ruminative negative states by restricting attention to immediate, rewarding stimuli, though long-term implications for emotional regulation remain unaddressed. Research on goal commitment revealed that alcohol-induced myopia sustains pursuit of personally salient goals by amplifying focus on desirability cues while downplaying feasibility barriers. In a 2012 study, intoxicated individuals reported higher commitment to identity-relevant goals despite low success expectancies, as alcohol explicitly and implicitly narrowed to motivational incentives over obstacles. A 2014 synthesis of experiments confirmed this pattern among student participants, where alcohol bolstered toward abstract goals but increased risk of derailment by ignoring distal challenges, highlighting 's dual potential for short-term drive and long-term .

Extensions to Emotional Processing and Goal Commitment

Research using the trauma paradigm has extended alcohol myopia to emotional processing in distressing contexts. In a 2019 experiment involving 98 female social drinkers exposed to a depicting , participants administered high-dose alcohol (breath alcohol concentration of 0.11%) exhibited impaired recall of peripheral details, such as room objects, compared to and low-dose groups, while central details related to itself remained unaffected. This differential recall pattern aligns with alcohol myopia by narrowing to salient central cues amid emotional , without evidence of avoidance strategies like dissociation influencing the impairment. Such findings suggest that myopia may buffer immediate emotional distress by restricting processing of peripheral stimuli that could amplify broader threat perception or rumination. Alcohol myopia also influences commitment, particularly by enhancing focus on short-term, desirability-driven objectives. A 2014 review of experimental studies indicated that acute alcohol intake increases commitment to personally important even when success expectations are low, as intoxication shifts toward instigatory cues (e.g., appeal) and away from inhibitory ones (e.g., feasibility barriers). For instance, intoxicated individuals displayed heightened persistence toward immediate interpersonal but often failed to follow through once sober, resulting in "empty" commitments mediated by disproportionate emphasis on positive aspects. When feasibility cues were rendered salient—either explicitly or implicitly—alcohol reduced commitment, underscoring the theory's cue-dependency. These extensions imply potential therapeutic applications, where controlled could facilitate adaptive disengagement from maladaptive long-term worries or unfeasible goals, promoting short-term affect . However, the risk of subsequent upon necessitates caution, particularly in treating chronic users prone to repeated cycles of overcommitment. By prioritizing immediate cues, alcohol-induced might temporarily alleviate emotional tied to peripheral inhibitions, though empirical validation in clinical settings remains limited.

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