Mental Health
Alcohol and Stress: Why Drinking to Cope Makes It Worse
Alcohol feels like stress relief — and short-term, it genuinely is. It dampens your cortisol response and sedates the nervous system. The problem is what comes after. Regular stress-drinking sensitizes your HPA axis, making you more reactive to stress over time, not less. You end up needing alcohol to feel normal, and feeling worse stress without it.
AK
Dr. Ananya Krishnan, PhD
Clinical Psychologist · Reviewed September 2026
Quick Answer
Alcohol relieves stress short-term by suppressing cortisol and boosting GABA. But when it clears, cortisol surges above baseline — producing rebound stress that's often worse than before drinking. Regular stress-drinkers develop a sensitized HPA axis: they feel more stressed without alcohol and need it to feel calm. Quitting alcohol typically reduces baseline stress substantially within 4-8 weeks, once the HPA axis re-regulates. The anxiety you were drinking to relieve was partly being caused by the drinking itself.
How Alcohol Affects the Stress Response
The HPA (hypothalamic-pituitary-adrenal) axis is your body's primary stress system. When you perceive a threat or stressor, the hypothalamus signals the pituitary, which signals the adrenal glands to release cortisol — the main stress hormone.
Alcohol suppresses this axis acutely. A drink or two reduces cortisol production, dampening the physical stress response. Combined with its GABA-boosting, glutamate-suppressing effect in the brain, alcohol produces genuine short-term relief: lower heart rate, reduced muscle tension, quieter mind.
This is why drinking to cope feels like it works. It does work — briefly.
20–40%
of drinkers cite stress relief as a primary reason for drinking
14%
increase in alcohol consumption during COVID-19 pandemic
12%
increased AUD risk from job strain (meta-analysis of 333K workers)
4–8 wks
for HPA axis to re-regulate after quitting alcohol
The Cortisol Rebound Cycle
When alcohol wears off, suppressed cortisol doesn't simply return to baseline — it overshoots. The HPA axis rebounds with a cortisol surge that exceeds pre-drinking levels. This is the biology behind hangover anxiety, morning anxiety after drinking, and the "hair of the dog" craving: alcohol relieves the cortisol surge it created.
The Stress-Drinking Cycle
1
Stress triggers drinkingHPA axis activated by stressor → cortisol rises → drinking feels like relief
2
Short-term reliefAlcohol suppresses HPA axis, GABA boosts, glutamate drops → genuine short-term calm
3
Cortisol reboundAlcohol clears → HPA axis overshoots → cortisol surges above baseline → more anxious than before
4
SensitizationRepeated cycles sensitize HPA axis → baseline stress threshold rises → need alcohol to feel calm
5
More stress, more drinkingEveryday stressors feel amplified → more drinking required → cycle deepens
How Regular Stress-Drinking Changes the Brain
With repeated cycles of alcohol-induced HPA suppression and rebound, the brain recalibrates. The stress response system becomes sensitized — it fires more readily and more strongly. What felt manageable before now triggers a stronger stress response. This is why long-term stress-drinkers often report feeling more anxious, more stressed, and less able to cope than they did before they started drinking heavily.
Sleep is the other major mechanism. Alcohol disrupts sleep architecture — particularly REM sleep, which is critical for emotional regulation and stress processing. Sleep-deprived people are substantially more reactive to stress. Chronic stress-drinkers are often in a perpetual state of poor sleep, which keeps their stress reactivity elevated and their need for alcohol higher.
When Does Stress Drive Toward Alcohol Use Disorder?
Drinking to cope is one of the 11 DSM-5 criteria for alcohol use disorder. Its presence alone doesn't mean AUD — but it's an early warning sign and a strong predictor of escalation. The specific risk pathway: stress → drinking → temporary relief → more stress (rebound) → more drinking.
People at highest risk of this escalation are those with high-stress jobs or life situations, pre-existing anxiety, a history of trauma (which activates the HPA axis chronically), and environments that normalize heavy drinking as a stress response.
What Actually Works for Stress (That Isn't Alcohol)
The goal isn't to eliminate stress — it's to reduce cortisol without the rebound. These strategies have strong evidence behind them:
Exercise (20+ min)
Reduces cortisol, produces endorphins lasting 4-6 hours. Consistent exercise lowers baseline cortisol over time.
Box breathing
4 counts in, 4 hold, 4 out, 4 hold. Activates parasympathetic system within minutes. Measurably reduces cortisol.
Social connection
Talking to a trusted person releases oxytocin, which directly lowers cortisol. One of the fastest biological stress relievers.
Cold water
Cold water on face or wrists triggers the mammalian dive reflex — heart rate slows rapidly, cortisol drops.
Progressive muscle relaxation
Tensing and releasing muscle groups systematically reduces physical stress tension and lowers cortisol measurably.
Address the source
Alcohol numbs the stress without changing what's causing it. Addressing the underlying problem (workload, relationship, finances) removes the stressor.
How Long Until Stress Improves After Quitting Alcohol?
The first 1-2 weeks of sobriety are often harder stress-wise — the GABA/glutamate system is rebalancing, and the HPA axis is still sensitized. This is the period most likely to feel worse before it gets better.
By weeks 3-4, the cortisol rebound cycles have stopped and the HPA axis begins to normalize. By 6 weeks, most former drinkers report significantly lower baseline stress reactivity than during their drinking period. By 3-6 months, many describe a fundamental shift — everyday stressors feel more manageable, and the coping capacity that alcohol was substituting for begins to rebuild.
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Frequently Asked Questions
Does alcohol relieve stress?
Short-term, yes — it suppresses cortisol and boosts GABA. But when alcohol clears, cortisol surges above baseline (rebound), producing more stress than before. Regular drinkers develop a sensitized stress response, requiring alcohol to feel calm.
Why does drinking to cope make stress worse over time?
Repeated cortisol rebound cycles sensitize the HPA axis — the brain recalibrates its baseline stress threshold upward. What felt manageable before now triggers stronger stress responses without alcohol. Combined with alcohol's sleep disruption (sleep deprivation worsens stress reactivity), chronic stress-drinkers end up more stressed, not less.
What percentage of people drink to cope with stress?
Studies find 20-40% of drinkers cite stress relief as a primary reason. Among heavy drinkers, approximately 60-70% report drinking primarily to cope. Alcohol consumption increased 14% during the COVID-19 pandemic, with stress being the most cited reason.
How long until stress improves after quitting alcohol?
Stress and anxiety may worsen for 1-2 weeks as the HPA axis normalizes. By weeks 3-6, most people report significantly lower baseline stress. The HPA axis takes 4-8 weeks to fully re-regulate. Most former drinkers find everyday stressors feel more manageable within 2 months.
What are healthy ways to cope with stress instead of drinking?
Exercise (reduces cortisol, lasts hours), box breathing (activates parasympathetic system within minutes), social connection (releases oxytocin, lowers cortisol), cold water on face or wrists (triggers dive reflex, slows heart rate), progressive muscle relaxation, and addressing the source of stress directly.
Is drinking to cope with stress a sign of alcohol use disorder?
It's one of the 11 DSM-5 AUD criteria. Its presence alone doesn't indicate AUD, but it's an early warning sign and predictor of escalation — especially in people with high stress, pre-existing anxiety, or trauma histories.
Can alcohol cause stress and anxiety?
Yes, directly. Regular drinking sensitizes the HPA axis and dysregulates GABA/glutamate, producing morning anxiety, increased stress reactivity, and heightened baseline anxiety. Many people's "stress" that they're drinking to relieve is being actively worsened by the alcohol itself.
What is the relationship between work stress and drinking?
A meta-analysis of 61 studies covering 333,000 workers found job strain associated with a 12% increased AUD risk. High-demand, low-control jobs show the strongest effect. After-work drinking cultures in corporate, legal, and healthcare environments normalize patterns that gradually become problematic.
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Why do people drink alcohol when stressed?
Drinking when stressed is one of the most common patterns of alcohol use, and understanding why it happens is essential for developing alternatives. The pharmacological reason: alcohol is a GABA-enhancing central nervous system depressant; GABA activity suppresses the fight-or-flight stress response; and drinking produces a rapid reduction in physiological stress markers (cortisol, heart rate, blood pressure, muscle tension). The psychological conditioning: every time someone drinks in response to stress and experiences relief, the association between stress and drinking is reinforced; this classical and operant conditioning builds over time; and the association becomes so strong that stress itself becomes a trigger for craving alcohol. The neurobiological overlap: the brain's stress and reward systems are anatomically and functionally interconnected; CRF (corticotropin-releasing factor), the key stress signaling molecule, directly activates dopamine reward circuits; and this anatomical connection means stress reliably triggers the desire for rewarding substances including alcohol. Social factors: stress-related drinking is often socially normalized ('I need a drink after that day'); colleagues and friends may model drinking as a stress response; and the social reinforcement of this behavior makes it both more likely and harder to recognize as problematic. Why it's counterproductive: while alcohol reduces stress acutely, it produces a rebound elevation in cortisol as it wears off; chronic heavy drinkers have chronically elevated cortisol even when not drinking; and the stress system becomes more reactive, not less, with chronic alcohol use, meaning stress eventually feels more overwhelming rather than less.
Does alcohol relieve stress?
Alcohol appears to relieve stress in the short term, but a more complete understanding reveals that this relief is temporary, self-reinforcing, and ultimately counterproductive. The evidence for short-term stress relief: controlled laboratory studies show that moderate alcohol doses reduce subjective feelings of stress; physiological stress markers (cortisol, heart rate) are reduced by moderate alcohol; and this stress relief is real, not imagined. The conditions that limit stress relief: higher doses of alcohol can paradoxically increase negative emotions and aggression; people who are stress-reactive and drink specifically to manage stress develop tolerance faster; and the stress-relieving effect diminishes significantly with regular use. The rebound effect: as blood alcohol drops, cortisol rebounds above baseline levels; this 'stress rebound' is why the hangover feels more stressful than normal; and chronically, this rebound means each drinking occasion adds to the overall stress burden rather than reducing it. The neuroadaptive problem: the brain's stress system adapts to chronic alcohol exposure; CRF (the stress molecule) increases in the extended amygdala with chronic alcohol use; and withdrawal from alcohol produces a highly stressed neurological state driven by this CRF elevation. The research conclusion: multiple longitudinal studies show that people who drink to manage stress are more likely to develop alcohol use disorder; and controlled studies of stress response in heavy drinkers show greater stress reactivity, not less, compared to light drinkers. The practical implication: alcohol is an effective acute stress reliever that worsens chronic stress reactivity, making it a poor long-term stress management strategy.
How does chronic stress lead to alcohol use disorder?
The pathway from chronic stress to alcohol use disorder involves identifiable neurobiological and behavioral mechanisms that explain why stress is the primary risk factor for developing problematic drinking. Allostatic load: chronic stress creates 'allostatic load' - a state of chronic dysregulation of the stress system; the HPA axis (stress response system) becomes chronically activated; and people with chronic stress seek repeated stress relief, including alcohol. Negative reinforcement learning: when alcohol repeatedly relieves stress, this relief is one of the most powerful reinforcers of behavior; negative reinforcement (removing something unpleasant - stress - through drinking) is more powerful than positive reinforcement (getting something pleasant); and the behavior (drinking) is maintained and intensified because it reliably removes stress. Neurological sensitization: chronic stress sensitizes the brain's CRF system; CRF is both a stress signaling molecule and directly activates alcohol craving through its action on the extended amygdala; and the sensitized CRF system means that stress produces stronger alcohol craving over time. The escalation pattern: drinking to manage stress begins with occasional use; tolerance develops, requiring more alcohol for the same stress relief; use escalates to maintain the effect; and the pattern of drinking to manage stress gradually meets criteria for alcohol use disorder. Individual vulnerability: genetic factors affect stress responsivity and alcohol metabolism; people with high stress reactivity are at highest risk; and people with childhood adversity (which produces lasting HPA axis dysregulation) are particularly vulnerable to stress-related alcohol escalation.
What are better ways to manage stress than drinking?
For people who have been managing stress with alcohol, developing effective alternatives is essential both for reducing alcohol use and for genuine long-term stress reduction. Aerobic exercise: the most evidence-supported stress management intervention; reduces cortisol; increases endorphins and BDNF; and as little as 30 minutes of moderate exercise produces acute stress reduction comparable to the acute effect of moderate alcohol. Mindfulness-based stress reduction (MBSR): the gold-standard mindfulness intervention for stress; 8-week programs produce measurable reductions in cortisol and subjective stress; and unlike alcohol, the effects compound over time rather than diminishing. Deep breathing/diaphragmatic breathing: activates the parasympathetic nervous system; reduces heart rate and cortisol; can be deployed immediately in stressful situations; and is a direct alternative to the immediate stress relief that alcohol provides. Social support: talking with supportive friends and family about stressors is one of the most effective stress management strategies; social connection activates the oxytocin system, which directly reduces CRF (the stress molecule); and building and maintaining social support is a core stress management strategy. Time in nature: exposure to natural environments reduces cortisol; even brief (20-minute) exposure to green spaces produces measurable stress reduction; and this is accessible and requires no special training. Sleep: the relationship between sleep and stress is bidirectional; adequate sleep reduces cortisol and improves stress reactivity; and protecting sleep quality is a foundational stress management strategy. Cognitive reappraisal: the way a stressor is interpreted affects the magnitude of the stress response; CBT teaches reappraisal - viewing stressors in less catastrophic ways; and this cognitive skill reduces the subjective and physiological stress response.
What is the stress-alcohol cycle?
The stress-alcohol cycle is a self-reinforcing pattern where stress drives drinking, and drinking worsens the stress system over time, creating escalating alcohol use. The cycle: stress occurs; the person drinks to relieve the stress; alcohol temporarily reduces stress; but as alcohol wears off, cortisol rebounds above baseline; the next stressful event feels more stressful due to the sensitized stress system; more alcohol is consumed to manage this increased stress sensitivity; and the cycle escalates. The neurobiological underpinning: CRF in the extended amygdala increases with chronic alcohol use; CRF is the primary driver of alcohol craving during stress; and the elevated CRF from drinking means that stress triggers stronger alcohol craving over time, making the cycle self-reinforcing. Timeline of cycle development: occasional stress-drinking begins the cycle; within months of regular drinking, tolerance develops; within a year or more of heavy drinking, the stress system is significantly dysregulated; and the alcohol craving triggered by stress becomes intense and automatic. Breaking the cycle: recognizing the cycle is the first step; developing alternative stress management strategies replaces alcohol; therapeutic support (CBT, mindfulness) addresses both the stress management deficit and the alcohol use; and medications can help during the most challenging phases of breaking the cycle. The recovery process: when alcohol is stopped, the CRF system takes months to normalize; stress triggers intense craving during early recovery because of the sensitized CRF system; and this is why stress management skills are a core component of addiction recovery programs.
How does work stress contribute to alcohol use?
Work stress is one of the most commonly cited triggers for alcohol use, with specific features of modern work environments creating particular vulnerability to stress-related drinking. The work stress mechanisms: job demands (high workload, time pressure, role ambiguity) activate the HPA stress axis; lack of control over work demands amplifies the stress response; and the effort-reward imbalance (high effort, low reward) is a particularly potent stress model linked to alcohol use. The 'after-work drink' culture: many workplaces and professional cultures normalize after-work drinking as the primary stress management strategy; this social reinforcement makes stress-driven drinking feel appropriate and expected; and the workplace drinking culture affects the individuals within it, increasing overall consumption. The types of workers at highest risk: professionals with high-demand, high-status jobs (physicians, lawyers, executives) have elevated rates of alcohol use disorder; workers in service industries with high emotional labor demands; and workers with unpredictable or irregular schedules that disrupt sleep and routine. Remote work effects: remote work has blurred the boundaries between work and personal time; the 'end of the work day' drinking occasion has become less well-defined; and some research suggests increased alcohol use in remote workers partly for this reason. The occupational health approach: employee assistance programs (EAPs) provide confidential counseling; workplace stress management programs reduce the occupational drivers of drinking; and organizational interventions (job redesign, management training) that reduce work stress can reduce alcohol use at the population level.
What is cortisol and how does alcohol affect it?
Cortisol is the primary stress hormone in the body, and alcohol's effects on cortisol are central to understanding both alcohol's short-term stress relief and its long-term stress-worsening effects. What cortisol does: cortisol is released by the adrenal glands in response to stress, glucose regulation needs, and circadian rhythm; it mobilizes energy; increases blood glucose; suppresses non-essential functions (immune response, digestion, reproduction); and at appropriate levels, it is essential for healthy functioning. Cortisol and the HPA axis: the hypothalamic-pituitary-adrenal (HPA) axis is the primary regulatory system for cortisol; the hypothalamus releases CRH, which stimulates the pituitary to release ACTH, which stimulates the adrenals to release cortisol; and alcohol affects multiple points in this axis. Acute alcohol effects on cortisol: moderate to heavy drinking acutely elevates cortisol; this is part of why some people feel alert and energized initially when drinking, before the sedating effects dominate; and the cortisol elevation from drinking contributes to disrupted sleep. The hangover cortisol surge: cortisol levels are significantly elevated during hangovers; this contributes to the anxious, jittery feeling of a hangover; and the physiological stress of a hangover is partly a cortisol-mediated stress response. Chronic effects: regular heavy drinking leads to HPA axis dysregulation; baseline cortisol is chronically elevated; the stress response is exaggerated; and adrenal glands may become enlarged from chronic overstimulation. Recovery of cortisol regulation: HPA axis normalization takes months of sobriety; cortisol levels progressively normalize with sustained abstinence; and the improved stress resilience that many people in recovery report reflects this HPA normalization.
Does alcohol increase or decrease cortisol?
The relationship between alcohol and cortisol is dose-dependent and changes over time with regular use, making the answer to this question more nuanced than it first appears. Acute effects of low-moderate doses: low doses of alcohol (1-2 drinks) may produce modest cortisol reductions through a GABAergic relaxation mechanism; this is the physiological basis of alcohol's stress-relieving effect at moderate doses; and it is why moderate drinking feels calming. Acute effects of higher doses: higher alcohol doses (3+ drinks) reliably increase cortisol; the HPA axis is activated; and the cortisol elevation at higher doses contributes to the arousal and emotional dysregulation that can occur at higher blood alcohol levels. The hangover cortisol peak: cortisol surges significantly during hangovers; this is mediated by the HPA axis activation from alcohol metabolism and dehydration; and the elevated hangover cortisol contributes to the anxiety and discomfort of the post-drinking period. Chronic heavy use: with regular heavy drinking, the HPA axis becomes dysregulated; baseline cortisol is elevated; cortisol rhythms are disrupted (the normal morning peak is diminished and evening cortisol remains elevated); and this chronic cortisol elevation produces the stress system sensitization that worsens stress reactivity over time. Recovery: stopping alcohol allows HPA axis recovery; cortisol gradually normalizes over weeks to months; and the improved stress resilience that people in recovery report is partly explained by this cortisol normalization. The practical message: alcohol's short-term cortisol-reducing effect (at low doses) is real but temporary and is outweighed by the cortisol-elevating effects of higher doses, hangovers, and chronic use.
How does alcohol affect emotional regulation?
Emotional regulation - the ability to manage and respond to emotional experiences appropriately - is profoundly affected by alcohol use, with consequences for both immediate behavior and long-term emotional health. How alcohol impairs emotional regulation: alcohol reduces prefrontal cortex activity, which normally provides top-down regulation of the emotional limbic system; this reduces the brain's ability to modulate emotional responses; and the result is more intense emotional reactions, reduced ability to think through emotional situations, and impaired decision-making during emotional states. The disinhibition effect: alcohol's emotional disinhibition is sometimes viewed positively (releasing inhibitions), but the same mechanism produces more intense anger, sadness, and anxiety alongside more intense positive emotions; and the disinhibited emotional states under alcohol often lead to regretted behaviors. Long-term effects on emotional regulation: chronic alcohol use impairs the prefrontal cortex through direct neurotoxicity; the emotion regulation capacity is reduced even when sober; and chronic heavy drinkers typically show impaired emotional regulation during sobriety as well as during drinking. The recovery process: emotional regulation capacity improves with sobriety; the prefrontal cortex function recovers over months; and learning emotion regulation skills during sobriety (through DBT, mindfulness, or CBT) accelerates this recovery and builds lasting capacity. Stress and emotion regulation: poor stress management depletes the emotional regulatory resources; chronic stress reduces prefrontal cortex function; and this is another pathway through which stress drives more drinking - reduced emotional regulation capacity produces less ability to manage the emotional drivers of drinking.
What is stress eating vs stress drinking?
Stress eating and stress drinking are both forms of emotional eating/drinking, but they have meaningfully different mechanisms, consequences, and intervention approaches. The similarity: both are attempts to use food or alcohol to manage emotional distress; both are reinforced by the temporary relief they provide; and both tend to escalate over time as tolerance develops and the behavior becomes more automatic. The neurobiological difference: stress eating primarily involves the endocannabinoid system and opioid receptors, activated by palatable foods; stress drinking primarily involves GABA receptors, alcohol's primary mechanism; and the reinforcement mechanisms and addiction potential differ between food and alcohol. The addiction potential difference: alcohol use disorder is characterized by physical dependence and potentially dangerous withdrawal; food addiction, while real, does not produce the same severity of withdrawal; and the medical and social consequences of severe alcohol use disorder are generally more acute than those of overeating. The co-occurrence: stress eating and stress drinking frequently co-occur; people who use food to manage stress are more likely to also use alcohol for this purpose; and the same underlying emotion regulation deficit drives both behaviors. Treatment differences: addiction treatment programs address alcohol; behavioral health and nutrition counseling address stress eating; and when both are present, integrated treatment addressing the underlying emotion regulation skills is most effective. The common element: developing genuine stress management skills (exercise, mindfulness, social support, cognitive reappraisal) addresses the underlying emotion regulation deficit that drives both stress eating and stress drinking.
How can you manage stress in alcohol recovery?
Managing stress in alcohol recovery is particularly challenging because the brain's stress system is dysregulated, the person's primary stress coping mechanism is no longer available, and early sobriety brings its own stressors. The neurobiological challenge: the CRF system is sensitized by chronic alcohol use; stress triggers more intense craving during early recovery than during active drinking; and the first year of sobriety is when stress-related relapse risk is highest. Building a stress management toolkit: no single alternative is as immediately effective as alcohol for acute stress relief, so multiple strategies are needed; the combination of exercise, mindfulness, social support, and cognitive coping skills provides broader coverage than any single approach; and building the toolkit before stress occurs, rather than improvising when stressed, is more effective. Exercise as the cornerstone: regular aerobic exercise produces durable changes in the stress response system; it reduces baseline cortisol; it increases the brain's natural stress buffering capacity; and starting an exercise routine in early sobriety provides both stress management and structure. Mindfulness and meditation: recovery-specific mindfulness programs (like Mindfulness-Based Relapse Prevention, MBRP) are specifically designed for people in recovery; they develop awareness of the stress-craving connection; and they build tolerance for stressful emotions without acting on them. Social support as buffer: having people to call when stressed reduces the stress burden and provides the alternative to drinking; 12-step programs provide both social support and stress management guidance; and building genuine friendships in recovery reduces the social isolation that amplifies stress. Anticipating high-stress periods: knowing that certain situations (holidays, work deadlines, relationship stress) are high-risk periods allows advance preparation; having a specific plan for managing these stressors reduces the likelihood of alcohol as a stress response.
What supplements reduce stress naturally?
For people managing stress during alcohol recovery or using natural stress relief alternatives to alcohol, several supplements have meaningful evidence for reducing stress and supporting the stress response system. Ashwagandha (KSM-66 extract): among the best-evidenced adaptogenic herbs; multiple placebo-controlled trials show significant cortisol reduction; reduces both subjective stress and physiological stress markers; and 300-600mg daily is the evidence-based dose. Magnesium: alcohol significantly depletes magnesium; magnesium deficiency worsens anxiety and stress reactivity; and supplementation (200-400mg magnesium glycinate) reduces the physiological stress response. L-theanine: an amino acid from green tea; produces calm alertness without sedation; reduces cortisol response to stress in controlled studies; and can be combined with caffeine to reduce caffeine-induced anxiety. Rhodiola rosea: an adaptogenic herb with good evidence for fatigue and stress reduction; reduces cortisol during acute stress; and is particularly useful for work-related stress and burnout. Phosphatidylserine: blunts cortisol response to exercise and psychological stress; some evidence for reducing ADHD and cognitive stress-related symptoms; and is found in high concentrations in the brain. B vitamins: B vitamins are essential cofactors for neurotransmitter synthesis and energy metabolism; stress depletes B vitamins; and alcohol depletes them further; so a B-complex supplement addresses a genuine deficiency that worsens stress. Omega-3 fatty acids: reduce neuroinflammation; some evidence for reducing anxiety and stress reactivity; and EPA has more mood-related evidence than DHA. Important caveat: supplements are not substitutes for evidence-based stress management practices, and their effects are modest compared to exercise and mindfulness.