Addictive Personality: Is It Real, and Can Those Traits Be Channeled for Good?

Posted on by Stephen Brumwell

Article Snapshot

  • “Addictive personality” is not a formal diagnosis. There is no single personality type that causes addiction.
  • Personality can still influence risk. Traits such as impulsivity, sensation seeking, reward sensitivity and all-or-nothing behaviour may make certain rewards harder to moderate for some people.
  • Being intense, ambitious or highly focused is not the same as addiction. Loss of control and continuing despite meaningful harm are much more important warning signs.
  • Some of the energy once directed towards alcohol or another addictive behaviour can sometimes be redirected into exercise, learning, creative work, business or other purposeful goals.
  • The aim is not to simply swap one compulsion for another. Healthy redirection still needs boundaries, self-awareness and the ability to stop.
  • A more useful question than “Do I have an addictive personality?” may be: Which patterns increase my risk, and which parts of my personality can I use constructively?

I’ve heard the phrase “I’ve got an addictive personality” more times than I can count.

I’ve probably used it myself.

Usually, what people mean is something along the lines of: if I get into something, I really get into it. Maybe it’s alcohol, exercise, work, gaming, food, shopping, business ideas or a hobby that somehow goes from casual interest to full-blown obsession in three days.

I can relate to that all-or-nothing mentality.

When I wrote about this years ago on my older blog, Clarity Sober, I looked at the idea that some of the traits associated with addiction can also show up in highly driven, ambitious and entrepreneurial people. I still think there is something useful in that conversation, but I would frame it differently now.

The idea of a single “addictive personality” is much too simple.

There isn’t one personality type that causes addiction, and the term itself isn’t a formal diagnosis. Addiction is influenced by a mix of biology, genetics, environment, mental health, learning, social factors and behaviour. Personality can be part of that picture, but it is only one part (National Institute on Drug Abuse).

So perhaps the better question isn’t “Do I have an addictive personality?”

Maybe it’s “What patterns do I have that make certain behaviours harder to control, and can some of those same traits be used more constructively?”

Is an Addictive Personality Actually Real?

Not really, at least not in the way the phrase is commonly used.

There is no recognised diagnosis called an addictive personality, and researchers haven’t identified one universal set of personality traits shared by everyone who develops an addiction.

That makes sense when you think about how different people with substance-use problems can be.

One person may be highly impulsive and constantly chasing stimulation. Another may be anxious, cautious and using alcohol to switch off. Someone else may be dealing with trauma, chronic pain, loneliness, depression or a social environment where heavy drinking has simply become normal.

They can arrive at a similar problem through very different pathways.

I think through general discussion, using the term “addictive personality” is okay, but jus know, addiction can be far more complicated than that.

Your Personality and Addiction

Saying there is no single addictive personality doesn’t mean personality has nothing to do with addiction.

Certain traits have been studied in relation to substance use and risky behaviour, particularly impulsivity and sensation seeking. Longitudinal research has found that differences in these traits can relate to different patterns of substance use across adolescence and early adulthood (Quinn & Harden, 2013).

Again, that does not mean someone who is impulsive or adventurous will develop an addiction.

It simply means some traits may influence how strongly a person is drawn toward reward, novelty or immediate gratification.

A few patterns people often describe when they talk about having an “addictive personality” include:

  • getting intensely interested in things very quickly
  • struggling with moderation once something feels rewarding
  • chasing novelty, excitement or stimulation
  • making decisions before fully considering the consequences
  • becoming highly focused on goals or activities
  • feeling restless or bored when there isn’t enough stimulation
  • using certain behaviours as a way to escape uncomfortable emotions
  • tending toward an all-or-nothing mindset

None of those automatically equal addiction, but if you’re ticking all of these boxes, the risks of developing an addiction could be higher.

The All-or-Nothing Personality

There are people who casually decide to take up running, and kind of stop there, right?

Then there are people who buy the shoes, download Strava, research heart-rate zones, sign up for a half marathon and somehow own a Garmin by Thursday. All-or-Nothing.

I fit very much into this category, it’s really a double-edged sword. It keeps you accountable and successful, but also makes you teter on the edge of burnout.

You probably if you fall into this category. This same person might throw themselves into the below categories.

  • Extreme fitness
  • over work
  • Entrepreneurial business
  • Music
  • Academic study
  • creative projects
  • Deep nutrition tracking
  • A new hobby
  • Personal development

This intensity though, can sometimes produce genuinely impress results (and often, build great businesses).

The problem is not necessarily that you care deeply about something or become highly motivated.

The more useful question is “Can you do all these, and choose when to stop when you say you will?”

Passion Is Not the Same as Addiction

I think we need to be careful about pathologising everything people enjoy intensely.

Working long hours during an important business launch isn’t automatically a work addiction.

Loving exercise doesn’t mean you’re addicted to exercise.

Gaming regularly doesn’t automatically mean you have a gaming disorder.

Being incredibly enthusiastic about a hobby is often completely normal.

With addiction, one of the important warning signs is that control starts to deteriorate and the behaviour continues despite meaningful harm or consequences.

It’s all about the warning signs, or what I like to call, the Hallmarks of Addiction, more here: Hallmarks of Addiction: Red Flags That a Habit Has Become Hard to Control.

Can Those Same Traits Be Redirected?

This is the part of the original idea that I still find genuinely interesting.

When someone gives up alcohol or another addictive behaviour, they often don’t suddenly become a completely different person.

They don’t suddenly become bored or unmotivated.

They often still have the intensity, but it’s redirected into challenges, novelty, competition, or highly driven achievements.

Of course, this doesn’t mean the recovery challenges, the cravings or the sobriety milestones disappear. This highly driven energy also doesn’t happen immediately.

Recovery can often create a strange gap. We use to spend some much mental energy around drinking, obtaining alcohol, recovering from alcohol or thinking about when the next drink was coming.

We must learn fill the gap, and redirect the energy in a productive way.

This could be finally establishing a health exercise routine, diving into study for personal development or growth, or even leaning into some new creative work.

There is nothing wrong with becoming deeply invested in something positive that isn’t alcohol

The important part is keeping enough awareness that you don’t simply replace one uncontrolled compulsion with another.

Channel It, Don’t Just Swap It

If someone stops drinking but then starts exercising compulsively, spending uncontrollably or working until their relationships and health fall apart, we probably haven’t solved the underlying problem.

We’ve just changed the behaviour, we’ve swapped it but kept the same issue. Healthy redirection still needs it’s own boundaries.

If you still have that intensity, and you’re channeling it into some new tasks, ask yourself:

  • Is this helping me or harming me?
  • Am I choosing this, or do I feel compelled to do it?
  • Can I take a day off without becoming distressed?
  • Is this activity improving my life overall?
  • Are my relationships, sleep and health still intact?
  • Am I avoiding something emotionally by keeping myself constantly busy?

What About Entrepreneurship and Leadership?

My original article leaned heavily into the connection between addictive personality traits, leadership and entrepreneurship.

There are certainly traits that can be useful in entrepreneurship, including achievement motivation, creativity, persistence and a willingness to tolerate uncertainty or risk. Research on entrepreneurial intentions has also examined characteristics such as risk-taking propensity and achievement motivation (Sun et al., 2020).

And yes, there can be some surface-level overlap with traits people informally associate with an “addictive personality.”

I’ve mentioned them probably already, but that’s traits such as being highly driven, competitive, willing to take tasks, or become highly motivated by achievement and reward.

These maybe “addictive personality” traits don’t create successful entrepreneurs though.

A successful entrepreneur with good leadership qualities also requires good judgement, patience, consistency and healthy emotional regulation.

The same intensity that once went into destructive behaviour may potentially become useful when it is paired with self-awareness, structure and control.

Don’t Romanticise Addiction

The final part I want to discuss is the trap of romanticising addiction.

It’s not a superpower, in fact, being able to control the addiction and stop it for good, that’s the superpower.

Addiction can damage health, relationships, careers, finances and families. For some people, it can be life-threatening.

Maybe you are naturally ambitious, maybe your personality is intense, and maybe you are competitive, curious, and highly driven.

Despite your success, do not use addiction as your motivational angle for your success, because if you do, that double-edged sword will come back to bite you.

The Takeaway

You probably don’t have an “addictive personality.”

You have a personality.

Within that are strengths, vulnerabilities, habits, experiences and behavioural patterns that may influence your risk of addiction.

Some of those patterns may need serious attention.

Others may be parts of you that can be redirected rather than eliminated.

For me, that’s a much more useful way to think about the topic than deciding someone is simply born with the personality of an addict.

Recovery and personal growth aren’t always about becoming a completely different person.

Sometimes they’re about learning to point the same engine in a better direction.

If you’re interested in the behavioural side of addiction and recovery, you may also like to read the following articles

Frequently Asked Questions (FAQs)

Is an addictive personality a real diagnosis?

No. “Addictive personality” is not a formal diagnosis, and there is no single personality profile that explains why someone develops an addiction. Addiction is influenced by a combination of biological, psychological, environmental, social and behavioural factors. Personality may contribute to risk, but it is only one part of the picture.

What personality traits are linked with addiction?

Research has commonly looked at traits such as impulsivity and sensation seeking, along with differences in reward seeking and decision-making. These traits may influence risk for some people, but having them does not mean someone will develop an addiction.

Does being obsessive or all-or-nothing mean I have an addiction?

Not necessarily. You can be highly focused, competitive or deeply interested in something without being addicted to it. A more important question is whether you are losing control and continuing despite meaningful harm. I cover this distinction further in Hallmarks of Addiction.

Can addictive tendencies be channelled into positive habits?

Sometimes. People in recovery may find it helpful to direct time, energy and intensity into exercise, study, creative work, business, volunteering or structured goals. The important part is maintaining boundaries so a positive activity does not simply become another uncontrolled compulsion.

Can you replace one addiction with another?

It can happen. Stopping alcohol or another addictive behaviour does not automatically resolve the patterns underneath it. If exercise, work, shopping, gaming or another activity starts becoming difficult to control or causes harm, it is worth looking at the behaviour rather than assuming it is healthy simply because the original addiction has stopped. For more on how reward and urges can operate, see Cravings 101.

References

Cravings 101: Understanding the Fundamentals of Why We Crave

Posted on by Stephen Brumwell

What to Know

  • Cravings are learned responses involving reward, stress, memory, habit and the environment.
  • A trigger is the cue, a craving is the urge, and withdrawal is the body’s response to reducing or stopping alcohol after physical dependence.
  • Heavy alcohol use can affect dopamine, GABA, glutamate, stress and opioid systems, but cravings are not caused by one simple neurotransmitter imbalance.
  • Cravings can feel relentless, but they often rise, peak and change. The immediate aim is to create time, distance and support before acting.
  • Recognising your common triggers helps you plan for the moments when judgement and impulse control may be under pressure.
  • If you drink heavily, drink daily or have had withdrawal symptoms, seek medical advice before stopping suddenly.

As I drove home on a Friday evening, travelling down my usual route, I noticed a familiar sensation as I passed the bottle shop.

An intense craving.

My mind started creating reasons to pull in:

Come on, you’ve done so well.

You’ve got it this time.

One night will be fine.

For someone trying to stay sober, these thoughts can sound convincing. They can also reopen a pattern that took months of work to interrupt.

Cravings are one of the major roadblocks in recovery from alcohol or other substance use. They can make us vulnerable and may increase the risk of relapse.

The truth is that even when a craving feels relentless, painful and seemingly endless, the intensity can change.

Understanding what is happening gives us more places to intervene.

Cravings Are Old Wiring

A craving is old wiring: a learned connection between a cue, an expected effect and a familiar response. The pathway may have been useful for escaping discomfort in the short term, but it no longer serves the life you are trying to build.

I used to describe it as the body’s old “source code”.

The brain relies heavily on patterns. If alcohol repeatedly follows stress, finishing work, social anxiety, Friday afternoon or a particular route home, those cues can begin to activate the expectation of drinking.

The pattern can look like this:

  1. Cue: a place, time, person, emotion or thought.
  2. Expectation: alcohol will provide relief, reward, confidence or escape.
  3. Craving: attention narrows and the urge becomes stronger.
  4. Response: drinking, buying alcohol or moving closer to the opportunity.
  5. Short-term outcome: the expected state change arrives.
  6. Learning: the brain strengthens the connection between the cue and the response.

This mechanism can trick us into believing alcohol is the only way to get through a situation.

But it is not.

Once we begin to recognise substance cues, or “triggers” as I prefer to call them, we can understand where cravings come from and build a different response.

For many people, cravings become less frequent or less intense with time, new routines and support. They can still return unexpectedly, so the aim is not to prove that you will never have another urge. It is to know what to do when one appears.

Cravings Are Painful, and Your Brain Can Bargain With You

Cravings often narrow attention towards the expected benefit of drinking while pushing previous consequences into the background. That is why the inner argument can sound so reasonable in the moment.

Before you say, “Getting over cravings is not that easy,” I get it.

Cravings can be freakin’ nasty.

There were many times in my own sober journey when I gave in to an intense craving and ended up in a rough patch.

I completed long stints away from alcohol, only for the pattern to return after one apparently harmless thought:

Maybe I have it under control now.

After six months, the mind might say:

You have proven you do not have a drinking problem.

This is a classic priming scenario. The urgency around the original problem fades, the difficult memories feel less immediate, and the idea of drinking again begins to look safer than it is.

That does not mean the brain is deliberately trying to sabotage you. It means reward, memory, stress and habit systems can place enormous weight on the expected short-term effect while the reflective part of the mind is trying to remember the bigger picture.

Craving is clinically important, but it is not a perfect prediction of what happens next. A person can experience a strong urge without drinking, while relapse can also happen with little conscious craving (Tiffany & Wray, 2012).

A craving is an experience. It is not a command.

Cravings on a Biochemical Level

Alcohol cravings involve several interacting brain systems, including reward learning, stress, memory, motivation and executive control. They cannot be reduced to one chemical being simply “high” or “low”.

Heavy or prolonged alcohol use can affect neurological pathways involving dopamine, glutamate, GABA, stress hormones and endogenous opioid systems.

Dopamine is often called a pleasure chemical, but its role is broader. It helps the brain learn which cues deserve attention and motivates us to pursue expected rewards.

If alcohol repeatedly follows a particular cue, the cue itself can become important.

The drive home. The sound of ice in a glass. A difficult meeting. The first quiet moment after the children go to bed.

Glutamate and GABA are also relevant. GABA has inhibitory effects in the nervous system, while glutamate is a major excitatory neurotransmitter. Repeated heavy alcohol exposure can disrupt the balance and adaptation of these systems, which is particularly important in alcohol withdrawal.

The National Institute on Alcohol Abuse and Alcoholism describes addiction as involving changes across reward, stress, memory and executive-control systems. Alcohol-related cues can become powerful because the brain has learned to associate them with alcohol’s effects (NIAAA, 2025).

For a fuller explanation, read Substance Abuse and Neurotransmitters: Understanding the Neurochemistry Behind Addiction and Sobriety.

Our brain chemistry is only part of the picture.

Poor sleep, missed meals, isolation, ongoing stress and a lack of routine can make emotional regulation harder and leave us more exposed when the usual cue appears. These factors do not cause every craving, and fixing them is not a treatment for alcohol dependence. They are part of the foundation that can either support or strain recovery.

Cravings, Triggers and Withdrawal Are Different

A trigger is the cue, a craving is the urge, and withdrawal is the body’s response to reducing or stopping alcohol after physical dependence has developed. They can overlap, but they are not interchangeable.

Withdrawal may include anxiety, sweating, tremor, nausea, agitation, disrupted sleep and an increased heart rate. Severe alcohol withdrawal can involve seizures or delirium and may be life-threatening.

A person in withdrawal may crave alcohol because drinking can temporarily relieve the symptoms.

If you drink heavily, drink daily, have experienced withdrawal before or are unsure about your risk, speak with a GP or alcohol and other drug service before stopping suddenly. The Australian Government advises that some people need medical support to reduce or quit safely (Australian Government Department of Health, Disability and Ageing, 2024).

For more detail, read Alcohol Withdrawal: The Seesaw Effect of Glutamate and GABA.

Substance Cues or “Triggers”

Triggers are situations, thoughts, emotions and environmental cues that can activate a craving or move us closer to drinking. Learning your patterns makes it easier to plan before impulse and judgement come under pressure.

One thing I noticed across longer periods of sobriety, and while writing about recovery, was that certain scenarios repeatedly intensified cravings.

If we can identify those scenarios, we can improve stress adaptation, change the environment and develop different coping responses.

Research on alcohol cue reactivity has found relationships between responses to alcohol-related cues, subjective craving and relapse-related outcomes, although the strength of these relationships varies between people and studies (Witteman et al., 2015).

The triggers I kept seeing fell into four useful categories.

1. Perceived Opportunity Triggers

Perceived opportunity triggers happen when the body senses that alcohol is available or easy to access.

This might be passing a bottle shop or bar, being home alone, having alcohol in the house, receiving a message from someone you used to drink with, or reaching a particular time of day.

Friday evening was a major example for me. The route, the time and the bottle shop formed a familiar sequence.

Early in recovery, there is no prize for testing yourself unnecessarily. Change the route. Remove alcohol from the house. Plan where you will be during the high-risk period. Make the safer response easier to begin.

2. Attention-Allocating Triggers

Attention-allocating triggers occur when alcohol begins taking up more mental space, which can intensify craving and wear down self-control.

You might replay old drinking experiences, focus on what you think you are missing, plan a possible return to drinking or spend hours arguing with the urge.

The aim is not to force every thought away. It is to notice where attention has gone and redirect it deliberately.

A practical activity, conversation, walk, meal, meeting or change of environment can interrupt the mental loop.

3. Stress Triggers

Stress triggers occur when pressure, conflict, fatigue or emotional discomfort activates the old expectation that alcohol will provide relief.

Stress may come from work, family, finances, poor sleep, loneliness, anxiety or the accumulated load of too many demands.

When alcohol has been used as a coping response for a long time, the brain can continue to reach for that option under pressure. Stress-related craving can involve changes in both reward and stress systems, particularly after repeated heavy use (Sinha, 2013).

This is why stress management is not a fluffy extra in recovery. It is part of relapse prevention.

4. Priming Triggers

Priming triggers appear when someone starts believing they can safely control drinking again, often after a longer period of sobriety.

This is the one where the mind loves to bargain:

It has been six months.

I am different now.

I will only drink occasionally.

For some people with a history of alcohol dependence, returning to alcohol can reactivate craving and old patterns quickly.

If this thought appears, bring another person into the decision before acting. Revisit why you stopped, what alcohol was costing you and what happened the last time controlled drinking was attempted.

I explore these four categories in more depth in Identifying Triggers: How to Recognise and Manage the Cues That Lead to Drinking.

What to Do When a Craving Hits

When a craving arrives, focus on the next safe action. Create time, move away from alcohol and contact support before the urge becomes a plan.

Name It

Say: “This is a craving. It is uncomfortable, but I do not have to act on it.”

You can rate the intensity from 0 to 10 and check again after a few minutes. The purpose is to observe change, not to achieve a perfect score.

Delay the Next Action

Do not try to solve the rest of your life while the craving is loud.

Delay the next action. Set a short timer. Shower. Walk. Prepare food. Start a task that occupies your hands. Call someone.

You are creating room for the intensity to shift.

Change the Environment

Leave the bottle shop car park. Take a different route. Go somewhere alcohol-free. Remove access to money or alcohol if that is appropriate and safe.

You do not need to prove your willpower by sitting beside the trigger.

Surf the Urge

Urge surfing treats the craving like a wave.

Notice where you feel it in the body: tightness, restlessness, heat, salivation or a hollow feeling in the stomach.

Observe the sensations as they build and change without feeding them or trying to force them away.

Mindfulness-based relapse prevention has shown promise as one component of treatment for substance use disorders, although it is not a stand-alone solution for everyone (Bowen et al., 2014).

Check the Basics

Ask whether you are hungry, angry or overwhelmed, lonely or tired.

Eat if you have missed a meal. Drink water. Rest if you can. Contact someone if you are isolated.

Basic care does not replace addiction treatment, but it can reduce extra strain in the moment.

Contact Someone

Choose the person before you need them.

A message can be simple:

I am having a strong craving and need to talk for ten minutes.

This might be a friend, sponsor, family member, counsellor, peer worker, GP or alcohol and other drug service.

Record the Pattern

After the craving changes, write down:

  • what happened beforehand
  • where you were
  • what you felt
  • how strong the urge became
  • what you did
  • what helped

This turns a painful moment into information for the next plan.

When Cravings Keep Returning

Frequent, intense or worsening cravings are a reason to strengthen support, not evidence that recovery is impossible.

A GP, addiction medicine specialist or alcohol and other drug clinician can assess:

  • alcohol intake and withdrawal risk
  • mental health
  • sleep and nutrition
  • medications and other substance use
  • social support
  • relapse patterns
  • whether counselling, peer support or medication may help

Medications such as naltrexone and acamprosate may be considered for some people with alcohol dependence as part of a broader treatment plan. They require individual medical assessment and are not suitable for everyone. The Australian Guidelines for the Treatment of Alcohol Problems provide evidence-based guidance on withdrawal, psychosocial care and relapse-prevention treatment.

A return to drinking is serious, but it does not erase everything you learned. Look at what happened, seek support early and strengthen the plan around the point where it broke down.

The Takeaway

There is no hiding it: when we are trying to get sober, cravings suck.

But they are understandable.

Cravings can involve old wiring, learned cues, reward and stress systems, memory, habit, withdrawal and the body’s current state.

If we remind ourselves that the intensity can change, reduce unnecessary exposure to triggers and practise a different response, we can gradually weaken the old pattern.

Start with the next safe action:

Name the craving. Create distance. Change the environment. Contact someone. Let the intensity move.

Then look beyond the immediate moment. Build routines, plan for the four trigger categories and get the level of support that matches the seriousness of the pattern.

If cravings are frequent, intense or connected with withdrawal symptoms, speak with a GP or alcohol and other drug service. In Australia, the National Alcohol and Other Drug Hotline offers free and confidential information, counselling and referrals on 1800 250 015 (Australian Government Department of Health, Disability and Ageing, 2025).

FAQ

How long does an alcohol craving last?

An alcohol craving has no fixed duration. Some urges rise and fall over minutes, while others return in waves or remain in the background for longer. Focus on whether the intensity is changing and what will help you avoid acting on it.

Why do I crave alcohol at the same time every day?

Craving alcohol at the same time each day often reflects a learned routine. The brain may associate that time with reward, transition or relief, such as drinking after work. Changing the environment and planning another activity before the usual time can interrupt the sequence.

Does craving alcohol mean I am addicted?

Craving is one feature considered in alcohol use disorder, but craving alone does not establish a diagnosis. Assessment also considers loss of control, consequences, tolerance, withdrawal, time spent drinking and the role alcohol plays in your life.

Can alcohol cravings happen after months of sobriety?

Alcohol cravings can occur after months of sobriety when a cue, memory, stressor or familiar environment activates an old learned association. A later craving does not erase recovery progress, but it is worth responding to early and reviewing the trigger.

Can medication reduce alcohol cravings?

Medication may reduce cravings or relapse risk for some people with alcohol dependence. Options such as naltrexone or acamprosate require assessment by a doctor because suitability depends on medical history, current alcohol use, other medications and treatment goals.

Is it safe to stop drinking when cravings are strong?

Strong cravings alone do not determine withdrawal risk. If you drink heavily, drink daily, have had withdrawal symptoms or seizures before, or are unsure about your risk, seek medical advice before stopping suddenly because alcohol withdrawal can be dangerous.

References

Australian Government Department of Health, Disability and Ageing. (2024). How can you reduce or quit alcohol? https://www.health.gov.au/topics/alcohol/about-alcohol/how-can-you-reduce-or-quit-alcohol

Australian Government Department of Health, Disability and Ageing. (2025). National Alcohol and Other Drug Hotline. https://www.health.gov.au/contacts/national-alcohol-and-other-drug-hotline

Australian Guidelines for the Treatment of Alcohol Problems. (2026). Guidelines for the treatment of alcohol problems. https://alcoholtreatmentguidelines.com.au/

Bowen, S., Witkiewitz, K., Clifasefi, S. L., et al. (2014). Relative efficacy of mindfulness-based relapse prevention, standard relapse prevention, and treatment as usual for substance use disorders. JAMA Psychiatry, 71(5), 547–556. https://doi.org/10.1001/jamapsychiatry.2013.4546

National Institute on Alcohol Abuse and Alcoholism. (2025). Neuroscience: The brain in addiction and recovery. https://www.niaaa.nih.gov/health-professionals-communities/core-resource-on-alcohol/neuroscience-brain-addiction-and-recovery

Sinha, R. (2013). The clinical neurobiology of drug craving. Current Opinion in Neurobiology, 23(4), 649–654. https://pubmed.ncbi.nlm.nih.gov/23764204/

Tiffany, S. T., & Wray, J. M. (2012). The clinical significance of drug craving. Annals of the New York Academy of Sciences, 1248, 1–17. https://pubmed.ncbi.nlm.nih.gov/22172057/

Witteman, J., Post, H., Tarvainen, M., et al. (2015). Cue reactivity and its relation to craving and relapse in alcohol dependence: A combined laboratory and field study. Psychopharmacology, 232, 3685–3696. https://pubmed.ncbi.nlm.nih.gov/25439993/

Alcohol Withdrawal: The Seesaw Effect of Glutamate and GABA

Posted on by Stephen Brumwell

Article Snapshot (AI Generated)

  • Chronic alcohol use can create what I like to call the seesaw effect of glutamate and GABA.
  • The more heavily and regularly alcohol is used, the harder the brain may have to work to keep things balanced.
  • When alcohol is suddenly reduced or removed, the opposite effect can happen: the nervous system can become overstimulated.
  • This is one reason alcohol withdrawal can involve anxiety, shaking, sweating, insomnia, agitation and, in more serious cases, seizures or delirium.
  • Alcohol withdrawal can be medically serious. If you have been drinking heavily or for a long time, speak with a medical professional before stopping suddenly.

Chronic alcohol use creates what I like to call the seesaw effect of glutamate and GABA, and the more alcohol is used, the larger the swing can become.

When we wake up the next day, depending on the amount of alcohol consumed, we can often see the opposite of alcohol’s sedating effect.

Instead of relaxed, we feel anxious. Instead of sleepy, we feel wired.

Instead of calm, the nervous system feels like it has been turned up too high.

In this article, I’ll help you understand what alcohol withdrawal actually is, and unpack what’s known as the seesaw effect of glutamate and GABA.

Understanding Alcohol Withdrawal Symptoms

Alcohol withdrawal can happen when someone who has been drinking heavily or regularly suddenly stops drinking or significantly cuts down.

This is not the same as a standard hangover. A hangover is unpleasant, but alcohol withdrawal involves a nervous system that has adapted to alcohol and is now trying to function without it.

Common alcohol withdrawal symptoms may include:

  • anxiety
  • sweating
  • shaking or tremors
  • nausea or vomiting
  • poor appetite
  • poor sleep
  • increased heart rate
  • agitation or irritability
  • sensitivity to light, sound or stress
  • difficulty concentrating

More severe alcohol withdrawal can include seizures, hallucinations, severe confusion or delirium tremens. These symptoms require urgent medical care.

Alcohol withdrawal can also present as a potentially serious syndrome that can occur after abrupt cessation or reduction of heavy, sustained alcohol intake, with symptoms ranging from autonomic hyperactivity and tremor through to seizures and delirium in more severe cases (Jesse et al., 2017).

If you or someone else has severe confusion, seizures, hallucinations, chest pain, severe dehydration or looks seriously unwell, seek urgent medical help. In Australia, call 000 in an emergency. For non-emergency alcohol and drug support, the National Alcohol and Other Drug Hotline is 1800 250 015.

GABA and Glutamate

GABA and glutamate are two important neurotransmitters in the brain, and neurotransmitters are chemical messengers that help our nerve cells communicate.

GABA is generally inhibitory. It slows things down. It is associated with calm, relaxation, sleep and reduced nervous system activity.

Glutamate is generally excitatory. It speeds things up. It is involved in alertness, learning, memory and normal brain activation.

We need a tightly regulated balance of both, otherwise we may feel too sedated or hyper stimulated. Our body is always trying to maintain this balance.

This is where the seesaw analogy will come into play, we’ll discuss a bit more on this soon.

When both sides are balanced, the nervous system can respond appropriately. When one side is pushed too far, the body tries to compensate.

How Alcohol Affects GABA and Glutamate

Alcohol is a central nervous system depressant.

This means it can slow brain and nervous system activity. Part of this effect happens through GABA and glutamate.

Alcohol can increase GABA activity, which is one reason it may initially feel calming, sedating or relaxing. At the same time, alcohol can reduce glutamate activity, which further slows things down.

So, in simple terms:

  • GABA goes up
  • glutamate goes down
  • the nervous system becomes more sedated
  • We generally, feel pretty good!

The downside? Our brain doesn’t like being pushed out of balance.

When alcohol is used repeatedly, the brain starts compensating. It may reduce some GABA-related activity and increase glutamate-related activity to try to keep the nervous system functioning.

Chronic alcohol consumption creates neuroadaptive changes, including downregulation of GABA receptors and increased NMDA receptor expression, which is part of glutamate signaling (Haber & Lintzeris, 2021).

This is the body trying to restore that balance, and when we drink chronically, it’s almost a never ending cycle that worsens over time..

The Seesaw Effect

Think of alcohol as pushing down on one side of the seesaw. We first, experience the lovely, pleasant, sedating effects that come with it – Queue GABA.

When alcohol is removed after a good nights sleep, the sedating effect begins to dissipate.

The brains compensatory mechanics begin to kick in, and some level of anxiety, stimulation or uncomfortable…ness arises – Queue Glutamate.

This is why alcohol withdrawal can feel like the opposite of alcohol intoxication. Alcohol makes us feel relaxed, numb, sometimes sleepy. When we wake up the morning after, we start to feel more anxious, shaky, jittery, and wired..

StatPearls describes alcohol withdrawal as involving a relative reduction in GABA signaling alongside excess glutamate activity, contributing to the hyperactive state seen in withdrawal (Newman & Duby, 2024).

This does not mean every person will have severe withdrawal. It depends on the person’s drinking history, health, previous withdrawal episodes, medications, nutrition status and other factors.

The more we chronically indulge in repeated episodes of drinking though, the larger our seesaw swings, and the worse the symptoms become.

Why Alcohol Withdrawal Can Feel So Uncomfortable

When the nervous system is overstimulated, the symptoms can feel physical, mental and emotional, all at the same time.

Some key withdrawal symptoms you may see (or familiar with) include:

  • shaking hands
  • sweating
  • racing heart
  • nausea
  • poor sleep
  • anxiety
  • irritability
  • agitation
  • panic-like feelings
  • strong cravings

Most of these symptoms are our nervous system trying to recalibrate.

For some people, this process is uncomfortable but manageable with appropriate support. For others, it can become dangerous.

In individuals with severe alcohol withdrawal, this glutamate/GABA ratio gap can widen significantly (Brousse et al., 2012). If alcohol has been used heavily, daily, or for a long time, get medical advice before stopping suddenly.

That is why also to not guess your own risk level from just a simple blog post alone (Yes, even this one).

The Kindling Effect

Another important concept is kindling.

Kindling refers to the way repeated withdrawal episodes may make the nervous system more sensitive over time.

In practical terms, this means repeated cycles of heavy drinking, stopping, withdrawing and drinking again can sometimes make future withdrawal episodes more severe.

Repeated withdrawal experiences can progressively intensify withdrawal symptoms, and this includes an increased risk of seizure vulnerability (Becker, 2014).

It’s one reason why the stop-start cycle becomes so difficult. The swing is so great that we swing ourselves back to alcohol for comfort. We also just try do it alone, which when it comes to quitting alcohol, you should always get help.

For more on the wider neurochemistry involved in alcohol use and recovery, see Substance Abuse and Neurotransmitters: Understanding the Neurochemistry Behind Addiction and Sobriety.

Best Approaches for Alcohol Withdrawal

If you are drinking heavily or think you may be physically dependent on alcohol, the safest first step is to make it known to others.

This can be your loved one, friends, or other related family. You then need to get medical support; speak to your GP or related health professional before stopping suddenly.

This caveat is important here, because if you have been drinking for a long time, you can experience seizures and your life can be at risk.

Once you have spoken with a health professional for medical assessment/monitoring (and medication where appropriate) you can then look at habits, foundational nutrition, and ongoing peer support.

I would recommend looking at the articles below as well to support cravings and getting your foundations on track.

If you’re still unsure, please reach out or book a discovery call.

The Takeaway

Alcohol withdrawal is not simply a rough hangover. It can be the nervous system rebounding after adapting to regular or heavy alcohol use.

GABA and glutamate are only part of the picture, but they give us a useful way to understand why withdrawal can feel shaky, anxious, wired and physically intense.

The brain has been trying to keep the seesaw balanced. When alcohol is suddenly removed, the swing back can be uncomfortable and, for some people, dangerous.

If you are planning to reduce or stop heavy alcohol use, get medical guidance first. With the right support, withdrawal can be managed more safely, and the next stage of recovery can begin from a steadier place.

FAQ

Is alcohol withdrawal the same as a hangover?

No. A hangover usually follows a drinking episode and may include headache, nausea, fatigue and dehydration. Alcohol withdrawal occurs when someone who is physically dependent on alcohol reduces or stops drinking. It can involve nervous system overactivity and may become medically serious.

Why does alcohol withdrawal cause anxiety?

Alcohol can temporarily increase calming GABA-related activity and reduce excitatory glutamate-related activity. With repeated heavy use, the brain adapts. When alcohol is removed, the nervous system can rebound toward overactivity, which may feel like anxiety, agitation, poor sleep or internal restlessness.

Can alcohol withdrawal cause seizures?

Yes. Alcohol withdrawal can cause seizures in some people, especially when there is heavy long-term alcohol use, previous withdrawal seizures or other risk factors. This is one reason medical advice is important before stopping suddenly.

What is delirium tremens?

Delirium tremens, also called alcohol withdrawal delirium, is a severe form of alcohol withdrawal. It can involve confusion, agitation, hallucinations, tremor, unstable blood pressure and other serious symptoms. It is a medical emergency.

What should I do if I want to stop drinking?

Speak with a GP, addiction medicine clinician or alcohol and other drug service before stopping suddenly, especially if you drink heavily or daily. In Australia, you can call the National Alcohol and Other Drug Hotline on 1800 250 015. In an emergency, call 000.

References

Becker, H. C. (2014). Neurochemical mechanisms of alcohol withdrawal. Handbook of Clinical Neurology, 125, 133-156. https://pmc.ncbi.nlm.nih.gov/articles/PMC6943828/

Brousse, G., Arnaud, B., Vorspan, F., Richard, D., Dissard, A., Dubois, M., Pic, D., Geneste, J., Xavier, L., Authier, N., Sapin, V., Llorca, P.-M., De Chazeron, I., Minet-Quinard, R., & Schmidt, J. (2012). Alteration of glutamate/GABA balance during acute alcohol withdrawal in emergency department: A prospective analysis. Alcohol and Alcoholism, 47(5), 501-508. https://doi.org/10.1093/alcalc/ags078

Haber, P. S., & Lintzeris, N. (2021). Alcohol withdrawal. In P. S. Haber & B. C. Riordan (Eds.), Guidelines for the Treatment of Alcohol Problems (4th ed.). Specialty of Addiction Medicine, University of Sydney. https://alcoholtreatmentguidelines.com.au/chapter-8-alcohol-withdrawal

Jesse, S., Brathen, G., Ferrara, M., Keindl, M., Ben-Menachem, E., Tanasescu, R., Brodtkorb, E., Hillbom, M., Leone, M. A., & Ludolph, A. C. (2017). Alcohol withdrawal syndrome: Mechanisms, manifestations, and management. Acta Neurologica Scandinavica, 135(1), 4-16. https://pmc.ncbi.nlm.nih.gov/articles/PMC6084325/

Newman, R. K., & Duby, J. J. (2024). Alcohol withdrawal syndrome. StatPearls. https://www.ncbi.nlm.nih.gov/books/NBK441882/

Alcohol and Nutrition: Does Chronic Drinking Cause Nutrient Deficiency?

Posted on by Stephen Brumwell

What To Know (AI Summary)

  • Alcohol can contribute to micronutrient deficiency. Chronic exposure to alcohol may affect micronutrient status, including vitamin A, vitamin D, zinc, iron and several B vitamins involved in energy production.
  • Zinc and magnesium deserve attention. Alcohol may increase urinary zinc losses and affect zinc transport in the body, while magnesium issues are commonly discussed in chronic drinking because of poor intake, electrolyte disturbance and broader metabolic stress (Sun et al., 2014; Poikolainen & Alho, 2008).
  • Testing beats guessing. If you are worried about nutrient deficiency after heavy drinking, it is worth checking your levels with a qualified practitioner rather than throwing random supplements at the problem.

When it comes to alcohol and nutrition, the two generally do not mix well once drinking starts moving into chronic territory.

Besides alcohol taking up a large portion of a heavy drinker’s diet, it can also cause us to neglect the basic dietary requirements we need to remain healthy.

On top of this, even if we try to eat well, chronic alcohol consumption may affect our ability to properly absorb, use and store certain nutrients. Over time, that can contribute to deficiency.

Although we may not be too concerned about this while drinking, understanding alcohol’s impact on nutrition can be a useful starting point for getting sober, rebuilding health and feeling better in the process. If you want the bigger brain-chemistry picture behind this, the related article on substance abuse and neurotransmitters is worth reading alongside this one.

Alcohol and Nutrition: Its Impact In A Nutshell

Chronic alcohol intake can contribute to nutrient problems through impaired absorption, altered metabolism, poor utilisation and, frankly, lower-quality food choices while intoxicated.

A few key areas are worth understanding.

Alcohol inhibits fat mobilisation. Drinking has been shown to reduce lipid oxidation, or fat burning, in healthy subjects, which may be one reason alcohol can make weight loss harder for some people (Suter et al., 1992). Mind you, this was not a study in people with chronic alcohol dependence, so it should be interpreted with that context.

Alcohol can affect blood sugar control. Alcohol can influence glucose regulation, which is relevant for energy, cravings, weight gain and metabolic health. In treatment-seeking alcohol dependence, blood glucose has also been studied in relation to heavy drinking and craving patterns (Leggio et al., 2009).

Alcohol affects protein metabolism. Alcohol can interfere with post-meal hepatic protein metabolism and broader protein turnover, which matters because amino acids are the small building blocks we use to repair tissue, maintain muscle and support many biological processes (De Feo et al., 1995; Preedy et al., 1999). For more on the practical side of protein intake, see Protein Intake for Exercise.

Alcohol can contribute to micronutrient deficiency. Chronic exposure to alcohol may affect the status of several vitamins and minerals, including B vitamins, vitamin A, zinc, magnesium, iron and other nutrients involved in energy production, immune function and nervous system health.

Let’s look a little deeper at the micronutrients alcohol can impact, and why this could become a problem.

Alcohol and Micronutrient Deficiency

Chronic drinking can have a big impact on micronutrient status. This may happen through impaired absorption of vitamins, increased urinary excretion of minerals, altered liver metabolism and poor dietary intake.

Micronutrient deficiency can also rise simply because food choices tend to suffer during heavy drinking. If alcohol is replacing proper meals, the body has fewer raw materials to work with.

Below is a non-comprehensive list of nutrients that can be affected by chronic exposure to excessive alcohol intake.

B1 (Thiamine) Deficiency

Exposure to alcohol can impair the utilisation and absorption of thiamine, an important B vitamin involved in energy metabolism, nervous system function and cellular brain processes (Butterworth, 1995).

This is one of the big ones. Thiamine deficiency is not something to brush off, especially in the context of heavy alcohol use, because severe deficiency can affect the brain and nervous system.

B9 (Folate) Deficiency

Alcohol can impair folate absorption, increase urinary losses and reduce uptake and storage. Folate is critical for the formation of red and white blood cells and helps with DNA production in the body (Halsted et al., 2002).

In practical terms, this means folate status can matter for energy, blood health, cell repair and overall recovery.

B12 (Cyanocobalamin) Deficiency

Chronic alcohol consumption may also affect B12 status. B12 is required for red blood cell formation, DNA production, brain health and nerve cell function. One retrospective study found functional B12 deficiency to be an important consideration in alcoholic patients with megaloblastic anaemia (Fragasso et al., 2010).

B12 issues can be tricky because symptoms may overlap with fatigue, low mood, brain fog or nerve-related complaints. Testing is useful here.

Vitamin A Deficiency

Chronic exposure to alcohol can disrupt vitamin A metabolism. Vitamin A is important for vision, immune function, growth, development and healthy tissues. Alcohol-related effects on vitamin A metabolism have been discussed in the context of liver function, storage and transport (Clugston & Blaner, 2012).

This is also a nutrient where more is not automatically better. Vitamin A can be toxic in high supplemental doses, so it should be approached carefully.

Zinc Deficiency

Alcohol may increase urinary excretion of zinc and affect zinc transport in the body. Research has also explored altered hepatic zinc transporters in alcohol-related liver disease models (Sun et al., 2014).

A deficiency in zinc can affect immune function, skin health, wound healing, taste and many enzyme-driven processes in the body.

For a deeper look at this mineral, see Zinc: Why It Matters for Immunity, Recovery and Overall Health.

Magnesium Deficiency

Lower magnesium status in chronic drinkers is commonly discussed because of poor intake, malnutrition and disturbances in electrolyte balance. Magnesium is involved in energy production, nerve signalling, muscle function and relaxation.

Low magnesium can contribute to fatigue, weakness and nervous system irritability. Magnesium treatment has also been studied in people with alcohol dependence, though supplement decisions should still be individualised (Poikolainen & Alho, 2008).

For more detail, see Magnesium: Why This Mineral Matters for Energy, Stress, Sleep and the Nervous System.

As mentioned earlier, this list is not comprehensive. The range of potential micronutrient issues is long when it comes to chronic alcohol abuse.

Other nutrients to consider include B6, vitamin D, calcium, iron and potassium. If iron status is part of the picture, the related article Beyond Iron: Why This Mineral Matters for More Than Energy and Fatigue may also be useful.

Restoring Micronutrient Deficiency

Firstly, if you have not already stopped drinking, or you are strongly thinking about it, reducing or quitting alcohol is the first and most important step.

This is not about perfection. It is about removing the thing that keeps making the problem harder to fix. If you are trying to understand whether drinking has moved into a more serious pattern, read Hallmarks of Addiction: The Red Flags of Addictive Behaviour.

The second step is to get your nutrient levels assessed through a qualified health professional, such as a GP, nutritionist, naturopath or dietitian.

It is important to understand what you are actually deficient in so you know what needs attention. Although the “shotgun” approach can sometimes help, throwing down supplements you may not need can waste money and, in some cases, create other problems.

Testing may include markers such as:

  • B12
  • Folate
  • Iron studies
  • Vitamin D
  • Magnesium or related electrolyte markers
  • Zinc where appropriate
  • Liver enzymes
  • Blood glucose markers
  • Full blood count

The third step is to manage cravings and stabilise the basics. This can often be the tough part in early sobriety, especially if certain cues keep pulling you back into old patterns. The article on identifying triggers pairs well with this section.

Useful foundations include:

  • Eating regular meals
  • Including protein at each main meal
  • Adding colourful plant foods daily
  • Drinking enough water
  • Prioritising sleep, including the basics covered in Sleep Hygiene and Morning Sun and Circadian Rhythm
  • Reducing long gaps between meals
  • Getting professional support if withdrawal, cravings or mood symptoms are difficult to manage

Following this kind of process can help get you on the right track: reduce the alcohol load, identify what needs replenishing, and then support the body with food, targeted supplementation where appropriate and better daily habits.

Food First, Supplements Second

Supplements can be useful, but they should not become the whole strategy.

A good recovery nutrition plan usually starts with food:

  • Protein for muscle repair, neurotransmitter production and appetite control
  • Vegetables and fruit for vitamins, minerals, fibre and antioxidants
  • Wholegrains and legumes for B vitamins, minerals and steady energy
  • Nuts and seeds for magnesium, zinc and healthy fats
  • Eggs, seafood, dairy, meat or plant-based alternatives depending on the person’s diet

From there, supplementation can be more targeted.

For example, thiamine may be clinically important in people with heavy alcohol use, but that is exactly why it should be handled properly rather than casually guessed. If there are neurological symptoms, confusion, poor coordination or significant withdrawal symptoms, medical advice is essential.

Related Reading

If you want to keep building out the recovery picture, these articles connect naturally with this topic:

Final Thoughts

Alcohol and nutrition do not play nicely together once drinking becomes heavy or chronic.

Alcohol can affect fat metabolism, blood sugar, protein metabolism and micronutrient status. It can also make it harder to eat well, absorb nutrients properly and maintain the daily habits that keep the body functioning well.

The good news is that the body often responds well when the basics are put back in place.

Get the alcohol load down. Test rather than guess. Rebuild food quality. Use supplements strategically. And if symptoms are significant, get proper support early.

Nutrition will not fix everything on its own, but it can be a powerful part of feeling human again after alcohol.

FAQs

Can alcohol cause nutrient deficiency?

Yes, heavy or chronic alcohol use can contribute to nutrient deficiency through poor intake, impaired absorption, altered metabolism and increased losses of some nutrients. B vitamins, zinc, magnesium and vitamin A are commonly discussed in relation to alcohol and nutrition.

What vitamin deficiency is most associated with alcohol?

Thiamine, or vitamin B1, is one of the most important deficiencies associated with heavy alcohol use. Severe deficiency can affect the brain and nervous system, so it should be taken seriously.

Should I take a B complex after quitting alcohol?

A B complex may be useful for some people, but it is better to assess your diet, symptoms and blood markers first. If drinking has been heavy, professional advice is especially important because thiamine needs can be clinically significant.

Can alcohol affect zinc and magnesium?

Yes, alcohol may affect zinc and magnesium status through poor intake, increased losses, altered transport and broader metabolic stress. Food quality and testing can help guide whether supplementation is needed.

Is it better to test nutrient levels before supplementing?

In most cases, yes. Testing helps identify what is actually low and avoids wasting money on supplements you may not need. It also helps catch issues that require medical attention.

References

  • Butterworth, R. F. (1995). Pathophysiology of alcoholic brain damage: Synergistic effects of ethanol, thiamine deficiency and alcoholic liver disease. Metabolic Brain Disease, 10(1), 1-8. https://doi.org/10.1007/BF01991777
  • Clugston, R. D., & Blaner, W. S. (2012). The adverse effects of alcohol on vitamin A metabolism. Nutrients, 4(5), 356-371. https://doi.org/10.3390/nu4050356
  • De Feo, P., Volpi, E., Lucidi, P., Cruciani, G., Monacchia, F., Reboldi, G., Santeusanio, F., Bolli, G. B., & Brunetti, P. (1995). Ethanol impairs post-prandial hepatic protein metabolism. Journal of Clinical Investigation, 95(4), 1472-1479. https://doi.org/10.1172/JCI117818
  • Fragasso, A., Mannarella, C., Ciancio, A., & Sacco, A. (2010). Functional vitamin B12 deficiency in alcoholics: An intriguing finding in a retrospective study of megaloblastic anemic patients. European Journal of Internal Medicine, 21(2), 97-100. https://doi.org/10.1016/j.ejim.2009.11.012
  • Halsted, C. H., Villanueva, J. A., & Devlin, A. M. (2002). Folate deficiency, methionine metabolism, and alcoholic liver disease. Alcohol, 27(3), 169-172. https://doi.org/10.1016/S0741-8329(02)00225-2
  • Leggio, L., Ray, L. A., Kenna, G. A., & Swift, R. M. (2009). Blood glucose level, alcohol heavy drinking, and alcohol craving during treatment for alcohol dependence: Results from the combined pharmacotherapies and behavioral interventions for alcohol dependence study. Alcoholism: Clinical and Experimental Research, 33(9), 1539-1544. https://doi.org/10.1111/j.1530-0277.2009.00982.x
  • Poikolainen, K., & Alho, H. (2008). Magnesium treatment in alcoholics: A randomized clinical trial. Substance Abuse Treatment, Prevention, and Policy, 3, Article 1. https://doi.org/10.1186/1747-597X-3-1
  • Preedy, V. R., Reilly, M. E., Patel, V. B., Richardson, P. J., & Peters, T. J. (1999). Protein metabolism in alcoholism: Effects on specific tissues and the whole body. Nutrition, 15(7-8), 604-608. https://doi.org/10.1016/S0899-9007(99)00096-9
  • Sun, Q., Li, Q., Zhong, W., Zhang, J., Sun, X., Tan, X., Yin, X., Sun, X., Zhang, X., & Zhou, Z. (2014). Dysregulation of hepatic zinc transporters in a mouse model of alcoholic liver disease. American Journal of Physiology-Gastrointestinal and Liver Physiology, 307(3), G313-G322. https://doi.org/10.1152/ajpgi.00081.2014
  • Suter, P. M., Schutz, Y., & Jequier, E. (1992). The effect of ethanol on fat storage in healthy subjects. New England Journal of Medicine, 326(15), 983-987. https://doi.org/10.1056/NEJM199204093261503

Neurotransmitters: Understanding the Neurochemistry Behind Addiction and Sobriety

Posted on by Stephen Brumwell

I think since the day I started my nutrition degree, I had always been fascinated by the brain, but I never really knew why.

This all changed when I was introduced to the world of antidepressants, something that came into regular use as I tried to cope with alcohol addiction.

See, I never knew much about antidepressants at that point, and the extent of my knowledge of neurotransmitters was pretty basic.

Fast forward to late 2017, I came across a fantastic little book called Brain in Balance: Understanding the Genetics and Neurochemistry Behind Addiction and Sobriety. That book was a gold mine for simplifying the science of neurochemistry and how it relates to addiction. It got me deep in the weeds of how substance abuse can impact our neurochemical state.

Neurotransmitters can sound like a very technical subject, but they are really just chemical messengers that help your brain and nervous system communicate. They influence mood, motivation, sleep, appetite, stress response, focus, pain, cravings, pleasure, memory and the way you respond to everyday life.

That is why they matter so much in addiction recovery, alcohol recovery, substance abuse and sobriety.

When someone has been drinking heavily, using substances, sleeping poorly, under-eating, living under long-term stress or running on inconsistent routines, brain chemistry can feel out of balance. This does not mean every low mood, craving or poor sleep pattern can be neatly blamed on one neurotransmitter. The brain is far more complex than that.

But it does mean neurotransmitters are worth understanding.

Alcohol and other substances can affect several major neurotransmitter systems, including dopamine, GABA, glutamate, serotonin, opioid peptides, noradrenaline, acetylcholine and the endocannabinoid system. These systems help explain why early recovery can involve low motivation, anxiety-like symptoms, irritability, poor sleep, emotional sensitivity, cravings and that flat feeling where normal life does not feel rewarding yet (NIAAA, 2024; Yang et al., 2022).

The goal of this article is not to diagnose neurotransmitter deficiencies. It is to give you a clearer, practical understanding of how these systems work, why recovery can feel the way it does, and what kinds of foundations can support healthy brain chemistry over time.

What To Know (Article Snapshot)

  • Neurotransmitters are chemical messengers used by the brain and nervous system.
  • Serotonin has multiple receptor types throughout the body, often referred to as 5-HT receptors, and I like to describe these receptors as switches on a switchboard.
  • Alcohol and substance abuse affect multiple neurotransmitter systems, not just dopamine.
  • Dopamine is involved in reward, motivation, learning and habit formation.
  • GABA and glutamate help regulate the balance between calm and excitement in the nervous system.
  • Serotonin is involved in mood, appetite, sleep, pain sensitivity and emotional regulation.
  • Opioid peptides and endorphins are involved in pleasure, pain relief and reward reinforcement.
  • Noradrenaline is tied to alertness, stress response, arousal, focus and fight-or-flight physiology.
  • The endocannabinoid system helps regulate appetite, mood, pain, stress and neurotransmitter release.
  • Acetylcholine supports attention, memory, learning, REM sleep and parasympathetic nervous system activity.
  • In recovery, neurotransmitter systems can improve over time, but timelines vary. Some brain and cognitive changes may improve over months of abstinence, especially with consistent support (NIAAA, 2024; Powell et al., 2024).
  • Symptoms alone are not enough to diagnose a neurotransmitter problem. Diet, sleep, stress, alcohol history, medications, mental health, pathology and professional assessment all matter.

What Are Neurotransmitters?

Neurotransmitters are chemical signals used by our nervous system to transmit messages between neurons, or nerve cells.

We have billions of these neurons. The body could almost be considered a big battery, using neurons to send electrochemical signals across the brain and body.

These neurotransmitters are often grouped into different systems that you may have heard of before, including serotonin, dopamine, GABA and glutamate.

Some neurotransmitters are more excitatory. They help switch the system on, increase alertness, support learning and drive action. Others are more inhibitory. They help slow the system down, support calm, regulate sleep and stop the brain from running too hot.

Most of them are not simply good or bad. Dopamine is not just pleasure. Serotonin is not just happiness. GABA is not just calm. Glutamate is not just stress. Each one has multiple roles depending on the receptor, brain region, timing, context and the rest of the body.

In alcohol recovery, the useful way to think about neurotransmitters is this: repeated alcohol exposure can train the brain toward reward, relief and habit loops. When alcohol is removed, the brain has to recalibrate. That recalibration can affect mood, motivation, sleep, cravings, stress tolerance and emotional regulation.

Serotonin

Serotonin is one of the most well-known neurotransmitters, usually discussed in relation to mood.

But serotonin does much more than mood. It is involved in appetite, pain perception, sleep, arousal, gut function, sensory processing, impulse control and emotional regulation. Genetic variability in serotonin-related systems has also been studied in relation to behaviour and psychiatric disorders (Nordquist & Oreland, 2010).

Serotonin acts through many receptor types, often referred to as 5-HT receptors. I like to think of these receptors like switches on a switchboard. Some switches may increase activity in one pathway, while others may reduce activity somewhere else. That is one reason serotonin is not as simple as “more serotonin equals better mood.”

Alcohol can interact with serotonin systems and the wider reward circuitry of the brain. Serotonin also interacts with dopamine and GABA, which means it can influence reward, inhibition, mood and alcohol-related behaviour in complex ways (Lovinger, 1997; Marcinkiewcz, 2015).

Serotonin primary functions

  • Mood regulation
  • Appetite and satiety
  • Sleep and arousal rhythm
  • Pain sensitivity
  • Gut motility
  • Impulse control
  • Sensory processing
  • Emotional flexibility

Serotonin deficiency

Possible serotonin-related patterns may include low mood that feels worse during winter, anxiety or social anxiety patterns, aggression, OCD-type tendencies, carbohydrate cravings, constipation, low pain tolerance, poor dream recall, insomnia, impulsive tendencies or low self-esteem.

These patterns do not prove low serotonin. Similar symptoms can come from poor sleep, low protein intake, low iron, thyroid issues, trauma, medication changes, chronic stress, blood sugar instability or mental health conditions.

Serotonin excess

Possible serotonin excess can be more serious and may involve confusion, agitation, sweating, diarrhoea, nausea, muscle twitching or tremor. This is especially important if medications or supplements that affect serotonin are involved. Seek medical advice if symptoms are sudden, severe or medication-related.

If you have low serotonin production

A sensible serotonin-supportive foundation starts with the basics: regular meals, enough protein, daylight exposure, movement, sleep consistency and stress support.

Vitamin D status may also be worth considering, especially if mood feels worse in winter or sunlight exposure is low.

Tryptophan, an amino acid found in protein-containing foods, is a precursor for serotonin. But the answer is not to chase one amino acid in isolation. It is usually more useful to build consistent meals that contain quality protein, colourful plants, fibre and enough overall energy.

Dopamine

Dopamine is often described as the pleasure chemical, but that is only part of the story.

Dopamine is deeply involved in motivation, reward learning, drive, anticipation, habit formation, movement, attention and goal-directed behaviour.

In addiction and alcohol use disorder, dopamine is important because it helps the brain learn that alcohol and alcohol-related cues are rewarding. People, places, times of day, stress states, music, social settings or even certain emotions can become linked with drinking.

The National Institute on Alcohol Abuse and Alcoholism describes dopamine as critical for learning to associate alcohol and related cues with rewarding effects. Over time, repeated drinking can strengthen these reward and habit pathways, making cravings feel automatic rather than purely conscious (NIAAA, 2024; Volkow et al., 2010).

This is one reason early recovery can feel flat. If the brain has been trained to expect a large dopamine-related reward from alcohol, normal rewards like exercise, food, work, hobbies, sunlight, music and connection may take time to feel satisfying again.

Dopamine primary functions

  • Motivation and drive
  • Reward learning
  • Pleasure and anticipation
  • Habit formation
  • Focus and goal-directed behaviour
  • Movement control
  • Reinforcement of cues and routines

Dopamine deficiency

Possible dopamine-related patterns may include addictive tendencies, tremors or restless legs, low libido, lacking motivation, depression, mental exhaustion, dull or boring dreams, forgetfulness, low reward, cravings or impulsive behaviour.

Again, this is not a diagnosis. It is a pattern to understand, especially in early sobriety when normal rewards may feel muted.

Dopamine excess

Possible dopamine excess or overactivation may be associated with agitation, aggression, impulsivity, risk-taking, insomnia or, in more complex clinical states, psychosis-like symptoms. Schizophrenia is sometimes discussed in relation to dopamine pathways, but it is a clinical diagnosis and not something to self-diagnose from a blog post.

If you have low dopamine production

Dopamine recovery is not about forcing constant stimulation. In fact, chasing stronger stimulation can keep the reward system stuck in the same loop.

Better foundations include consistent sleep, morning light, exercise, enough protein, meaningful goals, structured routines, small wins, reduced alcohol exposure, social connection and time away from high-intensity reward triggers.

Tyrosine is an amino acid involved in catecholamine production, including dopamine and noradrenaline. It may be worth considering in some cases, but supplements should be treated carefully, especially with medications, anxiety, blood pressure issues or mental health conditions. Food and routine come first.

GABA

GABA, or gamma-aminobutyric acid, is the calming force that resides in the body, and one of the main inhibitory neurotransmitters in the brain. GABA modulation is one pathway discussed in anxiety and nervous-system regulation research (Gauthier & Nuss, 2015).

In practical terms, GABA helps slow neuronal activity. It creates calm, relaxation, supports the part of the nervous system that allows us to rest and digest, and helps balance the more agitating neurotransmitters such as glutamate and noradrenaline.

Alcohol has a strong relationship with GABA. One of alcohol’s short-term effects is that it can enhance inhibitory GABA activity while also reducing excitatory glutamate activity. This is part of why alcohol can initially feel relaxing, sedating or anxiety-reducing.

The problem is what happens with repeated exposure. The brain adapts. Over time, the nervous system may compensate for alcohol’s sedating effect. When alcohol is removed, that adapted system can feel overexcited, anxious, shaky, irritable or unable to sleep. In some people, alcohol withdrawal can become dangerous and requires medical supervision (NIAAA, 2024; Dharavath et al., 2023).

GABA primary functions

  • Main inhibitory neurotransmitters
  • Calm and relaxation
  • Sleep support
  • Sleep maintenance
  • Stress regulation
  • Balancing excitatory neurotransmission
  • Reducing excessive neuronal firing

GABA deficiency

Possible GABA-related patterns may include feeling wired, moving fast, talking rapidly, feeling overstimulated, anxiety-like symptoms, panic attacks, alcohol cravings, insomnia or dwelling over stressful situations.

But symptoms like anxiety and insomnia can have many causes. They should not be treated as proof that someone needs a GABA supplement.

GABA excess

True GABA excess is not usually something people identify from symptoms alone. Too much sedative activity from alcohol, medications or other substances may cause drowsiness, poor coordination, slowed thinking or excessive sedation, which needs appropriate medical context.

If you have low GABA production

Foundational support includes alcohol reduction or abstinence where appropriate, consistent sleep timing, magnesium-rich foods, adequate protein, breathwork, gentle evening routines, less late caffeine, light exposure management, movement and nervous-system regulation practices.

Magnesium is still one of the first nutrients I think about here because it supports normal nerve and muscle function and is involved in nervous-system regulation. That does not make magnesium a direct cure for anxiety or withdrawal, but it can be part of the bigger picture. If alcohol withdrawal symptoms are significant, medical support matters.

Glutamate

Glutamate is almost the opposite of GABA. It is one of the main excitatory neurotransmitters in the body.

It is essential for attention, learning, memory, focus, cognition, sensory processing and normal brain function. You do not want no glutamate. You want glutamate activity to be properly regulated, because chronic glutamate toxicity and excitotoxicity have been discussed in neurodegenerative and neuronal-injury research (Lewerenz & Maher, 2015; Prentice et al., 2015).

GABA and glutamate work together like a balancing system. GABA helps slow things down. Glutamate helps activate and stimulate. The nervous system needs both.

Alcohol can suppress glutamate activity in the short term. With repeated heavy alcohol use, the brain may compensate in the opposite direction. During withdrawal, this can contribute to excessive excitatory activity, which helps explain symptoms such as agitation, poor sleep, anxiety-like feelings, tremor and, in severe withdrawal, seizure risk (NIAAA, 2024; Becker & Mulholland, 2014).

This is one of the reasons alcohol withdrawal should not be taken lightly. If someone has been drinking heavily or daily, stopping suddenly can be medically risky.

Glutamate primary functions

  • Main excitatory neurotransmitters
  • Learning and memory
  • Focus and attention
  • Motor function
  • Sensory processing
  • Executive function
  • Neuroplasticity

Glutamate deficiency

Low or disrupted glutamate signalling can affect cognition, learning, focus and memory, but glutamate deficiency is not something to casually self-diagnose.

Glutamate excess

Possible glutamate excess or excitatory overactivity may feel like agitation, irritability, overwhelming anxiety, shakiness, poor memory, poor focus, poor concentration, racing thoughts, poor sleep or sound and light sensitivity. In alcohol withdrawal, excessive excitatory activity can become medically serious.

If you have high glutamate production

The biggest support is reducing the stressors that keep the nervous system overactivated. This can include alcohol support, sleep repair, consistent meals, blood sugar stability, magnesium-rich foods, calming routines, medical care where needed and gradual rebuilding of exercise tolerance.

If withdrawal symptoms are strong, professional help is not optional. It is the safer path.

Opioid and Endorphin System

The opioid system is a less commonly discussed one, but it is known for its ability to produce chemicals in the body called endorphins.

These are the body’s natural opioid-like chemicals, which are part of why you can feel good after a long run, a big exercise session, laughter, music, connection or meaningful achievement.

Opioid receptors are found across the nervous system and gastrointestinal tract and are involved in pain, reward, mood and gut function (Feng et al., 2012).

Alcohol can activate reward pathways involving opioid peptides and dopamine. This is one reason alcohol can feel reinforcing, especially when it is tied to relief, reward, social connection or emotional escape (NIAAA, 2024).

This system also helps explain why naltrexone, an opioid receptor antagonist, is used in alcohol use disorder treatment. It can reduce the pleasurable effects of alcohol by interfering with opioid-related reward activity. That does not mean everyone needs medication, but it does show how strongly reward chemistry is involved in alcohol behaviour.

Opioid and endorphin primary functions

  • Pain modulation
  • Pleasure and reward
  • Emotional comfort
  • Reward reinforcement
  • Social bonding
  • Exercise-related feel-good effects
  • Interaction with dopamine pathways

Opioid deficiency

Possible opioid or endorphin-system patterns may include low pain tolerance, addictive tendencies, carbohydrate cravings, anxiety-like feelings and tension, low mood, dwelling over major life situations, low pleasure or a strong desire for relief.

Again, these patterns are not diagnostic. They simply help explain why recovery can involve a period where life feels emotionally dull before natural rewards start to feel stronger again.

Opioid excess

Opioid-system excess is not usually a useful self-assessment category. In the context of opioid drugs or medications, excess opioid activity can be dangerous and may involve sedation, slowed breathing, confusion or loss of consciousness. That requires urgent medical support.

If you have low opioid or endorphin production

Helpful foundations include exercise at a tolerable level, sunlight, laughter, music, social connection, meaningful work, time in nature, physical affection where appropriate, cold or heat exposure if tolerated, and building routines that create natural reward without alcohol.

Noradrenaline

Noradrenaline, also called norepinephrine, are catecholamine-like neurotransmitters responsible for the body’s fight-or-flight stress response system.

It helps the body mobilise energy, increase heart rate, sharpen attention and respond to perceived threat. In the right amount, noradrenaline helps you wake up, focus and act. In excess or poor regulation, it can feel like stress, panic, tension or hypervigilance. Noradrenaline has also been discussed in stimulant addiction research and stress-related neurobiology (Sofuoglu & Sewell, 2009; Zhang et al., 2013).

In addiction science, noradrenaline is often discussed in relation to stress systems, withdrawal, negative emotional states and relapse risk. Newer reviews continue to explore noradrenergic mechanisms in alcohol use disorder, especially around stress, emotional pain and hyperkatifeia, which is a heightened negative emotional state linked with withdrawal and relapse vulnerability (NIAAA, 2024; Haass-Koffler et al., 2018; Varodayan et al., 2025).

Noradrenaline primary functions

  • Fight-or-flight response
  • Alertness and arousal
  • Focus and attention
  • Heart rate and blood pressure response
  • Stress adaptation
  • Memory formation around emotional events
  • Interaction with dopamine and serotonin systems

Noradrenaline deficiency

Possible noradrenaline-related deficiency patterns may include chronic stress, fatigue and pain, low mood, low blood pressure tendencies, blood sugar dips, exhaustion, short attention span, low pain tolerance or poor concentration.

Context matters, because the same person may swing between low arousal and overactivation depending on sleep, alcohol, caffeine, trauma, blood sugar and stress load.

Noradrenaline excess

Possible noradrenaline excess may feel like states of panic, panic attacks, racing heart, irritability, hypervigilance, poor stress tolerance, sleep disruption, tension or difficulty calming down after conflict.

If you have low noradrenaline production

Support starts with predictable routines, blood sugar stability, sleep repair, reducing alcohol and stimulant load, gentle movement, breathwork, therapy or coaching where appropriate, and building emotional regulation skills.

Because noradrenaline is made downstream from dopamine, the dopamine foundations above also matter. For some people, trauma, chronic stress or anxiety disorders are part of this picture and deserve proper support.

Endocannabinoid System

Our next neurotransmitter system is the endocannabinoid system, and to no surprise, it is closely tied with appetite, mood, pain, stress, inflammation, memory, reward and neurotransmitter release.

This is the system that gets activated in marijuana users, and it can often result in increased hunger, also known as the munchies.

The endocannabinoid system is commonly discussed through two receptor types, CB1 and CB2. CB1 receptors are found in high concentrations in the brain, especially in areas involved in emotion, memory, mood and sensory perception. CB2 receptors are often discussed in relation to immune signalling and inflammation, though the system is more complex than a simple brain-versus-immune split.

One interesting feature of the endocannabinoid system is that it can help regulate neurotransmitter release. In simple terms, it helps the nervous system modulate other signals rather than just pushing one direction all the time (Zou & Kumar, 2018). The endocannabinoid system has also been reviewed in relation to depression, reward and pain control (Huang et al., 2016).

Alcohol research has also explored endocannabinoid signalling in brain regions involved in stress and reward, including the amygdala and related circuits (Bedse et al., 2019).

Endocannabinoid primary functions

  • Regulation of feeding behaviour
  • Appetite
  • Energy metabolism
  • Learning and memory
  • Pain and inflammation
  • Mood and emotional regulation
  • Reward and motivation
  • Regulation of neurotransmitter release

Endocannabinoid deficiency

Possible endocannabinoid-related deficiency patterns may include low pain tolerance, excessive inflammation, treatment-resistant patterns, changes in appetite, poor stress tolerance, mood changes, poor sleep or feeling less able to experience natural reward.

This does not mean cannabis is automatically the answer. Cannabis can affect the same system, but it can also create problems for some people, especially when used heavily or relied on for sleep, appetite, stress or emotional regulation.

Endocannabinoid excess

Possible endocannabinoid overactivation may be associated with excessive food intake, increased obesity risk, lower motivation, altered memory, sedation or greater reliance on cannabis or other external inputs for regulation.

If you have low endocannabinoid production

A good place to start here is a foundation that supports the body’s own endocannabinoid system: exercise, omega-3-rich foods, good sleep, stress regulation, social connection, time outdoors and reducing reliance on substances that override natural regulation.

Acetylcholine

Our last neurotransmitter is acetylcholine, which is vital for memory formation, memory recall and keeping our attention span sharp.

It is also relevant to nicotine and alcohol. Nicotine acts on nicotinic acetylcholine receptors, which are connected with dopamine reward pathways. Research has also explored how nicotinic acetylcholine receptors contribute to smoking, alcohol reward and dependence (Brunzell et al., 2015; Rahman et al., 2015; Tarren et al., 2016).

This helps explain why alcohol and smoking often become paired behaviours. The combination can amplify reward learning and make cues stronger.

Acetylcholine primary functions

  • Memory formation
  • Learning
  • Attention span
  • REM sleep
  • Parasympathetic nervous system function
  • Digestive secretions and motility
  • Muscle activation
  • Interaction with reward pathways

Acetylcholine deficiency

Possible acetylcholine-related patterns may include sympathetic dominance, short-term memory problems, age-related cognitive decline, impaired digestive function, being a light sleeper, poor sleep onset, tension in muscles, poor attention or strong nicotine-related cue patterns.

But again, those symptoms can have many causes. Sleep deprivation alone can affect memory, focus and emotional regulation.

Acetylcholine excess

Acetylcholine excess is not something to casually self-diagnose. In the wrong context, too much cholinergic activity can be associated with nausea, sweating, salivation, digestive upset, muscle twitching or other symptoms that need medical interpretation.

If you have low acetylcholine production

Choline-containing foods can support acetylcholine production. These include eggs, fish, chicken, beef, dairy, soy foods and some legumes.

Acetyl-l-carnitine is sometimes discussed in this space too, but I would still look at the bigger picture first: sleep, protein intake, nutrient density, alcohol reduction, nicotine support where needed, stress regulation and consistent routines.

What Supports Healthy Neurotransmitter Production?

It is tempting to jump straight to supplements, but neurotransmitters are not built in isolation. While the list of supporting neurotransmitters can be endless, below is a rather non-selective but good starting point. Most of these are foundational to our health and habits – I write more about Foundational Health Habits here, and how they support sobriety, recovery and resilience.

  • Enough protein intake – Sufficient protein intake is essential for healthy neurotransmitter production
  • B vitamins, Magnesium, zinc, iron and other minerals
  • Omega-3 fats help our nerves and neurons fire effectively
  • Good Sleep quality, Morning light and a balanced circadian rhythm – More on sleep hygiene here.
  • Exercise and movement
  • Stress regulation
  • Gut health
  • Reduced alcohol exposure and sustained abstinence.
  • And more.

If you are in alcohol recovery, this is the important part: feeling flat, anxious, unmotivated or emotionally sensitive does not mean you are broken. It may reflect a nervous system that is recalibrating after a long period of artificial reward, sedation, stimulation or stress relief.

The Takeaway

Hopefully, this gives you a fairly succinct and overall understanding of the many neurotransmitters found in the body, and why they matter so much in substance abuse, addiction recovery and sobriety.

Alcohol and substance use can affect multiple neurotransmitter systems at once. Dopamine, serotonin, GABA, glutamate, opioid peptides, noradrenaline, acetylcholine and the endocannabinoid system all play different roles in reward, relief, withdrawal, cravings, mood and nervous-system balance.

This is why early recovery can feel so physical and emotional. It is not simply a mindset issue. The brain and body are adapting.

The good news is that the brain is plastic. It can change. Research suggests that at least some alcohol-related brain and cognitive changes can improve with abstinence and the right support, although timelines vary from person to person (NIAAA, 2024; Powell et al., 2024).

The practical path is to build foundations: food, protein, sleep, morning light, movement, stress regulation, connection, medical support where needed and consistency.

If you are unsure what is driving your symptoms, Stephen can help you look at your diet, alcohol history, sleep, stress load, pathology, habits and supplement use in context.

FAQ

What neurotransmitters are involved in alcohol recovery?

Several neurotransmitter systems are involved in alcohol recovery, including dopamine, GABA, glutamate, serotonin, opioid peptides, noradrenaline, acetylcholine and the endocannabinoid system. These systems influence reward, motivation, stress, sleep, cravings, mood and nervous-system regulation.

Can low dopamine affect motivation after quitting alcohol?

Dopamine is involved in motivation, reward learning and habit formation. After repeated alcohol use, normal everyday rewards may feel less satisfying for a while. This can contribute to low motivation or feeling flat in early recovery. It does not mean dopamine is the only factor, but it is part of the picture.

Why do I feel anxious or wired after stopping alcohol?

Alcohol can affect the balance between GABA, which is inhibitory, and glutamate, which is excitatory. After repeated heavy drinking, stopping suddenly can leave the nervous system overexcited. This may contribute to anxiety-like symptoms, poor sleep, irritability or shakiness. Heavy or daily drinkers should seek medical advice before stopping suddenly because withdrawal can be dangerous.

How long does brain chemistry take to rebalance after alcohol?

There is no single timeline. Some people notice improvements within weeks, while other changes can take months or longer. Research suggests some cognitive and brain changes related to alcohol use disorder can improve with abstinence, but recovery depends on the person, drinking history, health status, sleep, nutrition, treatment and support.

What foods support neurotransmitter production?

Protein-rich foods provide amino acids used to make neurotransmitters. Examples include eggs, fish, meat, poultry, Greek yoghurt, legumes, tofu, tempeh, nuts and seeds. Nutrient-dense whole foods also provide B vitamins, magnesium, zinc, iron, omega-3 fats and other cofactors that support normal nervous-system function.

Are neurotransmitter symptoms enough to diagnose a deficiency?

No. Symptoms are not enough to diagnose a neurotransmitter deficiency. Low mood, anxiety, cravings, poor sleep, fatigue and brain fog can have many causes. Diet, blood sugar, sleep, stress, trauma, medications, alcohol history, mental health and pathology all need to be considered.

Can supplements fix neurotransmitters?

Supplements can sometimes help when there is a clear nutritional need, but they are not a shortcut for recovery and should not replace medical care. Some supplements can interact with medications or be unsuitable for certain conditions. Food, sleep, alcohol support, movement, mental health care and proper assessment come first.

Is alcohol withdrawal dangerous?

It can be. People who drink heavily or daily should not assume they can stop suddenly without risk. Alcohol withdrawal can involve serious symptoms, including seizures in some cases. Medical support is important if there is any concern.

References

Brunzell, D. H., Stafford, A. M., & Dixon, C. I. (2015). Nicotinic receptor contributions to smoking: Insights from human studies and animal models. Current Addiction Reports, 2(1), 33-46. https://doi.org/10.1007/s40429-015-0042-2

Feng, Y., He, X., Yang, Y., Chao, D., Lazarus, L. H., & Xia, Y. (2012). Current research on opioid receptor function. Current Drug Targets, 13(2), 230-246. https://doi.org/10.2174/138945012799201612

Gauthier, I., & Nuss, P. (2015). Anxiety disorders and GABA neurotransmission: A disturbance of modulation. Neuropsychiatric Disease and Treatment, 11, 165-175. https://doi.org/10.2147/NDT.S58841

Huang, W., Chen, W., & Zhang, X. (2016). Endocannabinoid system: Role in depression, reward and pain control. Molecular Medicine Reports, 14(4), 2899-2903. https://doi.org/10.3892/mmr.2016.5585

Lewerenz, J., & Maher, P. (2015). Chronic glutamate toxicity in neurodegenerative diseases: What is the evidence? Frontiers in Neuroscience, 9, 469. https://doi.org/10.3389/fnins.2015.00469

Nordquist, N., & Oreland, L. (2010). Serotonin, genetic variability, behaviour, and psychiatric disorders: A review. Upsala Journal of Medical Sciences, 115(1), 2-10. https://doi.org/10.3109/03009730903573246

Prentice, H., Modi, J. P., & Wu, J. Y. (2015). Mechanisms of neuronal protection against excitotoxicity, endoplasmic reticulum stress, and mitochondrial dysfunction in stroke and neurodegenerative diseases. Oxidative Medicine and Cellular Longevity, 2015, 964518. https://doi.org/10.1155/2015/964518

Sofuoglu, M., & Sewell, R. A. (2009). Norepinephrine and stimulant addiction. Addiction Biology, 14(2), 119-129. https://doi.org/10.1111/j.1369-1600.2008.00138.x

Tarren, J. R., Shariff, M., Holgate, J., & Bartlett, S. E. (2016). Effects of alcohol on nicotinic acetylcholine receptors and impact on addiction. In Neuropathology of Drug Addictions and Substance Misuse (pp. 411-419). https://doi.org/10.1016/B978-0-12-800213-1.00038-9

Volkow, N. D., Wang, G. J., Fowler, J. S., Tomasi, D., Telang, F., & Baler, R. (2010). Addiction: Decreased reward sensitivity and increased expectation sensitivity conspire to overwhelm the brain’s control circuit. BioEssays, 32(9), 748-755. https://doi.org/10.1002/bies.201000042

Zhang, G., Gao, Z., Guan, S., Zhu, Y., & Wang, J. (2013). Upregulation of excitatory neurons and downregulation of inhibitory neurons in barrel cortex are associated with loss of whisker inputs. Molecular Brain, 6, 2. https://doi.org/10.1186/1756-6606-6-2

Dharavath, R. N., Pina-Leblanc, C., Tang, V. M., Sloan, M. E., Nikolova, Y. S., Pangarov, P., Ruocco, A. C., Shield, K., Voineskos, D., Blumberger, D. M., Boileau, I., Bozinoff, N., Gerretsen, P., Vieira, E., Melamed, O. C., Sibille, E., Quilty, L. C., & Prevot, T. D. (2023). GABAergic signaling in alcohol use disorder and withdrawal: Pathological involvement and therapeutic potential. Frontiers in Neural Circuits, 17, 1218737. https://www.frontiersin.org/journals/neural-circuits/articles/10.3389/fncir.2023.1218737/full

Varodayan, F. P., Erikson, C. M., Scroger, M. V., & Roberto, M. (2025). Noradrenergic mechanisms and circuitry of hyperkatifeia in alcohol use disorder. Biological Psychiatry, 97(6), 580-589. https://pmc.ncbi.nlm.nih.gov/articles/PMC11839382/

Yang, W., Singla, R., Maheshwari, O., Fontaine, C. J., & Gil-Mohapel, J. (2022). Alcohol use disorder: Neurobiology and therapeutics. Biomedicines, 10(5), 1192. https://pmc.ncbi.nlm.nih.gov/articles/PMC9139063/

Haass-Koffler, C. L., et al. (2018). Noradrenergic targets for the treatment of alcohol use disorder. Psychopharmacology. https://pubmed.ncbi.nlm.nih.gov/29460163/

Lovinger, D. M. (1997). Serotonin’s role in alcohol’s effects on the brain. Alcohol Health and Research World. https://pmc.ncbi.nlm.nih.gov/articles/PMC6826824/

Marcinkiewcz, C. A. (2015). Serotonergic neuroplasticity in alcohol addiction. ACS Chemical Neuroscience. https://pmc.ncbi.nlm.nih.gov/articles/PMC5928559/

National Institute on Alcohol Abuse and Alcoholism. (2024). Neuroscience: The brain in addiction and recovery. https://www.niaaa.nih.gov/health-professionals-communities/core-resource-on-alcohol/neuroscience-brain-addiction-and-recovery

Powell, A., Sumnall, H., Smith, J., Kuiper, R., & Montgomery, C. (2024). Recovery of neuropsychological function following abstinence from alcohol in adults diagnosed with an alcohol use disorder: Systematic review of longitudinal studies. PLOS ONE. https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0296043

Rahman, S., Engleman, E. A., & Bell, R. L. (2015). Nicotinic receptor modulation to treat alcohol and drug dependence. Frontiers in Neuroscience, 8, 426. https://pmc.ncbi.nlm.nih.gov/articles/PMC4754113/

Becker, H. C., & Mulholland, P. J. (2014). Neurochemical mechanisms of alcohol withdrawal. Handbook of Clinical Neurology, 125, 133-156. https://pmc.ncbi.nlm.nih.gov/articles/PMC6943828/

Bedse, G., Centanni, S. W., Winder, D. G., & Patel, S. (2019). Endocannabinoid signaling in the central amygdala and bed nucleus of the stria terminalis: Implications for the pathophysiology and treatment of alcohol use disorder. Alcoholism: Clinical and Experimental Research, 43(10), 2014-2027. https://pmc.ncbi.nlm.nih.gov/articles/PMC6779484/

Zou, S., & Kumar, U. (2018). Cannabinoid receptors and the endocannabinoid system: Signaling and function in the central nervous system. International Journal of Molecular Sciences, 19(3), 833. https://doi.org/10.3390/ijms19030833

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