Neurotransmitters and Other Things I’ve Screwed Up
Neurochemical Mayhem and Mitochondrial Treason: My Body as a Crime Scene
⚠️ Disclaimer: I’m not a neuroscientist. I didn’t ace Biology or Chemistry class. I’ve never looked through a microscope without getting a nose smudge on the lens. What I am is a recovering alcoholic who’s spent a hell of a lot of time trying to figure out why my brain turned into a chemical carnival—and what it takes to get it back.
This post combines what I’ve learned from reading actual science, therapy, the guy at rehab that thought I wasn’t paying attention, personal experience, and a few overly dramatic Google rabbit holes. If you want peer-reviewed perfection, consult a medical professional. If you want the gritty truth as I understand it with dark humor and a squirrel or two—welcome home.
Finally, I promise not to do this too often. You know, the whole academic-with-footnotes thing. It took way too long to try, and I don’t love doing research like this. But this is important stuff to know.
🧠 Who Let The Squirrels Into The Lab?
Alcohol doesn’t just mess with your liver. It rewires your entire brain, hijacks your body’s reward system, and convinces your cells that vodka is a valid nutritional group. And then, like a toxic ex, it leaves your nervous system wrecked, shaking in a corner, wondering what the hell just happened.
But you didn’t “just” get addicted.
You rewired.
And now you’re dealing with the aftermath.
Let’s break it down—squirrel-style.
🔬 Meet the Brain Chemicals You’ve Been Abusing
Serotonin: The One That Got Away (And Took My Sanity With It)
Serotonin is supposed to be the emotional cruise control of the brain.
It keeps your mood steady, regulates sleep, appetite, pain perception, and impulse control. When it’s working, you feel… okay. Not euphoric. Just calm, grounded, human1.
But alcohol doesn’t like calm.
It kicks in the serotonin door like a drunk ex at 2AM—spiking it briefly, then systematically wrecking the system that created it in the first place2.
Chronic drinking reduces both serotonin levels and receptor function, leaving you chemically incapable of emotional stability3. That’s why early sobriety feels like emotional whiplash: crying at insurance commercials one minute, fantasizing about smashing your toaster with a hammer the next.
And mine? Mine packed its bags somewhere in the early 2000s, flipped me off, and left me at an abandoned Waffle House outside Atlanta with my brain scattered, covered, peppered, and diced.
You’re not crazy. You’re serotonin-starved.
🧬 Let’s Talk Receptors (Because One Would Be Too Easy)
There are at least 14 known serotonin receptor subtypes—named things like 5-HT1A, 5-HT2C, and 5-HT7 because neuroscientists are sadists with label makers4.
Each receptor does something different:
5-HT1A? Mood, anxiety, and social behavior.
5-HT2C? Appetite and impulse control.
5-HT3? Gut function and nausea (hello, hangovers).
5-HT6 and 7? Memory and cognition (bye-bye, short-term memory).
Chronic alcohol exposure screws with these receptors like a toddler with a soundboard. Some get downregulated. Some go haywire. Some just disappear into the fog5.
💊 SSRIs: The Janitor Joke
If you’re lucky (or desperate) enough to be prescribed an SSRI (Selective Serotonin Reuptake Inhibitor), here’s the deal:
It doesn’t give you more serotonin.
It just blocks your brain from cleaning it up too fast, so more of it lingers in the synaptic gap. Think of it as yelling at the janitor to stop sweeping up the feel-good molecules until you’ve had time to enjoy them6.
But this only works if:
You actually make enough serotonin in the first place
Your receptors haven’t gone on strike
You wait several weeks for it to maybe kick in (which feels like emotional Russian roulette when you’re mid-meltdown)
SSRI effectiveness is often inconsistent in people with Alcohol Use Disorder, because the underlying receptor architecture is damaged7. It’s like trying to fix a foundation crack with a motivational poster…and duct tape.
I’m on Prozac now. It helps. Slowly.
But it’s not a silver bullet—it’s duct tape on a leaky raft.
Useful, but you still have to paddle.
Dopamine: The Party Promoter Who Burned Down the Venue
If serotonin is emotional cruise control, dopamine is the gas pedal—and the party planner. It’s the brain chemical behind motivation, reward, pleasure, drive, and that hit of satisfaction when something feels good8.
Eat cake? Dopamine.
Get a hug? Dopamine.
Have sex, win an argument, hear your favorite song, or even cross something off a to-do list? All dopamine.
Booze?
Dopamine, but turbocharged.
Alcohol doesn’t just activate the reward system—it drowns it in fireworks. It floods the brain with far more dopamine than it’s naturally equipped to handle9, and your poor little neurons do not know what hit them.
Picture this:
You give a squirrel a Costco-sized crate of Skittles and a machine gun.
Now the squirrel thinks this is normal.
Take the Skittles away, and what do you get?
Squirrel riot.
That’s your dopamine system post-addiction.
Over time, the brain tries to protect itself from this overwhelming chemical chaos. So it downregulates dopamine production and starts shutting down receptors—your brain’s way of saying, “Whoa, we were not designed for this level of awesome.”10
The result?
When you stop drinking, even the good stuff doesn’t feel good anymore.
Sunshine doesn’t work.
Music sounds flat.
Puppies? Meh.
You’re chemically joyless and spiritually constipated.
This is part of what’s known as a hypodopaminergic state—meaning your reward system is underactive, understaffed, and probably on strike11.
Worse yet, dopamine is anticipatory. It doesn’t just reward you for pleasure—it motivates you toward pleasure12. So in early recovery, you can’t even get excited about things that might feel good, because the chemical “go-get-it” signal is offline.
And the fix?
There isn’t a magic dopamine pill.
You have to earn it back, slowly:
Movement
Nature
Human connection
Accomplishing tiny goals
Letting your brain relearn what real rewards feel like
Which is hard to do when you don’t want to do anything, because… no dopamine.
Early sobriety is the chemical equivalent of trying to train a pack of depressed puppies to herd cats.
But eventually, one of those puppies will wag its tail.
And then another.
And one day—maybe when you least expect it—you’ll laugh at something that isn’t cruel.
That’s dopamine, coming home.
Leave the door open.
Norepinephrine: The One Who Brought a Bazooka to a Panic Attack
Norepinephrine (aka noradrenaline) is your brain’s fight-or-flight fuel.
It sharpens focus, raises heart rate, and keeps you alert in emergencies. It’s the chemical that says:
“Shit’s going down. Move!”
Under normal conditions, it kicks in when you dodge a car, cram for a final, or almost drop your phone in the toilet. Then it simmers down and lets your brain return to Earth.
But with chronic alcohol use?
Norepinephrine gets stuck in the “ON” position like a smoke alarm that won’t shut up even though nothing’s on fire13.
And when you finally stop drinking?
Your brain—no longer numbed—unleashes a norepinephrine tsunami that turns you into a shaky, sweating, wide-eyed anxiety burrito14. You wake up in early sobriety with your heart trying to moonwalk out of your chest because someone coughed.
💥 Imagine…
A squirrel on Adderall with a flamethrower.
A raccoon in a meth lab who just realized you’re watching him.
Hearing your dog make that pre-puke noise at 2AM.
That’s what it feels like when your norepinephrine system has no chill.
📉 How Booze Breaks the Switch
Chronic alcohol disrupts the locus coeruleus, the brain’s main norepinephrine factory15. Over time, it desensitizes the system and hijacks the feedback loop that normally shuts it off16. So when you quit drinking, it doesn’t ease off the gas—it floors it.
This is why withdrawal comes with:
Shaky hands
Racing thoughts
Rapid heart rate
Cold sweats
That charming sense of impending doom you can’t explain
And insomnia that makes you believe God has personally banned you from sleep
It also explains why alcohol feels like it “helps anxiety”—because it temporarily shuts this system down. But the more you drink, the worse your baseline gets.
So what’s the fix?
🧠 Recovery Tips (That aren’t Just ‘Meditate More’)
Unfortunately, there’s no instant off-switch for a norepinephrine system in overdrive.
But:
Beta-blockers like propranolol can help during detox and post-acute withdrawal by slowing heart rate and reducing physical symptoms17.
Regular movement (even gentle walks) actually helps recalibrate norepinephrine levels. Think of it as draining the battery without punching walls.
Grounding exercises and controlled breathing can convince your brain you’re not being hunted, even if your body’s unconvinced.
And time—yep, that same annoying friend who helps with everything in recovery—does eventually help the brain reestablish healthy response patterns18.
But early on? It’s gonna be loud in your head. Like Chinese New Year loud.
You’ll overreact to everything. You’ll feel like the world is ending because you dropped a spoon. You’ll vibrate like a tuning fork during a thunderstorm.
And that’s okay. That’s healing.
Your body is slowly shutting off the alarm it thought it needed to survive.
You’re not broken. You’re coming down from code red.
GABA: The One Who Held the Leash on the Squirrels (and Then Quit)
GABA (gamma-aminobutyric acid, because why use one word when six syllables will do?) is your brain’s main inhibitory neurotransmitter19. It’s the chemical responsible for calm, stillness, quiet. When GABA is flowing, your thoughts slow down, your heart rate levels out, and the squirrels in your head finally take a nap.
In healthy brains, GABA is the chill friend who rubs your shoulders, puts on lo-fi beats, and says, “It’s okay, buddy. You’re not dying. Let’s just breathe.”
Now enter alcohol.
Booze mimics GABA—so well, in fact, that your brain eventually stops bothering to make its own. Why keep producing calm when you’re delivering it 750ml at a time20? It’s like outsourcing your serenity to a drunk clown with a flamethrower.
Over time, your GABA receptors get lazy and your natural GABA production plummets. So when you remove alcohol?
It’s not just that you’re sober—it’s that you’re now catastrophically low on the brain’s only built-in anti-anxiety system.
Symptoms of a GABA Crash:
Full-body anxiety that makes coffee nervous
Restless limbs
Insomnia so bad you consider punching the moon
Panic attacks that come out of nowhere
Irritability so intense even your pet goldfish avoids you
Seizures (yes, really—that’s why detox should be medical)
Basically: GABA is the tranquilizer dart to your inner chaos.
Without it, the squirrels are not only awake—they’ve joined a militia and taken meth.
Why You Can’t “Just Relax” in Early Sobriety
Because your GABA system is broken.
It’s like trying to play jazz on a piano that’s missing half the keys and occasionally bursts into flames.
This is also why you may feel more anxious, not less, after quitting alcohol—especially in the first few weeks. You’re not just coming down. You’re chemically naked.
You’ll hear people say, “It gets better.” And that’s true.
But at first, it gets weirder. Your brain doesn’t know how to GABA anymore. And that’s not a you problem—it’s a neurological one.
Can You Fix It?
Yes. But slowly.
Benzodiazepines (like Ativan or Librium) are sometimes used during detox to prevent seizures and regulate GABA activity21.
Do NOT self-prescribe. These are addictive, too, and only used short-term.Gabapentin and baclofen are sometimes prescribed post-detox to help stabilize GABA systems in early recovery22.
Meditation, sleep hygiene, exercise, nutrition, and time all help your brain start making its own GABA again23.
But nothing speeds it up like… not drinking.
Sorry. That’s the magic secret. Let your brain do what it forgot how to do. Eventually, the squirrels get drowsy again.
You might not feel like you’re healing.
But even in the quiet moments of “why the hell am I still shaking,” your brain is working its ass off to rebuild the bridge to calm.
GABA isn’t gone forever.
It’s just in witness protection—waiting to see if you’re serious this time.
Glutamate: The Overcaffeinated Gremlin in Your Brain
If GABA is your brain’s brake pedal, glutamate is the gas.
It’s the most abundant excitatory neurotransmitter in the human brain—responsible for keeping you alert, helping you think, learn, remember, and move through the world without drooling on yourself24. In proper balance, it’s a critical part of what makes you, well… function.
But in early sobriety? That gremlin doesn’t just sip espresso—it freebases Red Bull and plays Metallica on your neurons at 3am.
What Glutamate Does (When It’s Behaving):
Helps form memories
Encourages neuroplasticity (your brain’s ability to learn and adapt)
Regulates cognition, attention, learning, and sleep-wake cycles
Fuels excitement and motivation
Keeps your neurons communicating like a well-run call center
Basically, glutamate is what gets your mental hamster on the wheel.
Too little? You’re foggy.
Too much? You’re insane.
What Alcohol Does to Glutamate (Spoiler: It's Bad)
Alcohol is a CNS depressant—it dulls your central nervous system by suppressing glutamate activity25. That’s part of why it feels relaxing. Less glutamate means less neuronal firing, less anxiety, and less ability to care when you’ve just dropped your burrito open-end-down on the carpet.
But when you drink chronically, your brain fights back.
It upregulates glutamate production and supercharges your glutamate receptors (especially the NMDA subtype)26, trying to restore balance. It’s like turning up the stereo because someone keeps wrapping the speakers in squirrels.
So when you suddenly stop drinking?
BOOM. Glutamate storm.
Your brain is now overstimulated AF—because the booze is gone, but the cranked-up glutamate is still there, running naked through your neurons with a blowtorch and a bullhorn.
The Fallout: Glutamate Toxicity and Withdrawal Hell
Anxiety that makes caffeine look like chamomile
Insomnia so violent your dreams file HR complaints
Hyperarousal (startling at everything—lights, sounds, your own heartbeat)
Seizures and hallucinations in severe cases
Brain fog followed by random brain explosions
Excess glutamate is literally neurotoxic in large doses—it can kill brain cells through a process called excitotoxicity27. This is why alcohol withdrawal isn’t just unpleasant—it can be fatal.
Long-Term Recovery = Rebalancing Glutamate
Once you quit drinking, your brain slowly reduces the glutamate overdrive—but it takes time.
Sleep will suck at first. That’s the glutamate.
Anxiety spikes at random? Also glutamate.
Feeling like your skull is a beehive? Yep. That’s our guy.
But this is also where healing begins. Neuroplasticity—the brain’s ability to rewire itself—is deeply tied to glutamate. Once it calms down, it becomes one of your greatest allies28.
That terrifying tornado in your head?
It’s also the raw material of your recovery.
Final Thought: The Gremlin Can Be Tamed
You can’t punch glutamate into submission. But you can outlast it.
Meditation, nutrition, exercise, therapy—these things teach your brain to stop yelling.
Slowly, the storm calms. The overcaffeinated gremlin takes a nap.
And one day, the only buzz in your head is the sound of peace.
It’s Not Just Your Brain
🧬 Mitochondrial Mayhem: How My Cells Got Drunk and Quit Their Day Job
We tend to talk a lot about brain chemistry in addiction recovery—dopamine, serotonin, GABA, blah blah blah. But alcohol doesn’t just trash your neurotransmitters. It hits every cell in your body, right down to the mitochondria. You remember those guys, right?
The mitochondria are the powerhouse of the cell.
—Every biology teacher, ever
What they don’t tell you is:
Alcohol turns that powerhouse into a dive bar.
🧪 Mitochondria 101 (Don’t Worry, No Quiz)
Mitochondria are responsible for converting the food you eat—glucose, fats, amino acids—into ATP, which is basically the energy currency of your body29. Every time you move, think, breathe, or blink? That’s ATP keeping the lights on.
Under normal circumstances, mitochondria pull from a balanced mix of nutrients to keep your cells running smoothly. But when you flood your body with booze, everything changes.
🍻 Alcohol: The Ultimate Cheat Code (Until It’s Not)
Here’s the twisted part: your body can metabolize alcohol into energy. Ethanol gets broken down in the liver into acetaldehyde (a toxic mess) and then into acetate, which your cells can use as fuel30.
It’s easy. It’s fast. It’s dirty.
And your mitochondria go, “Sweet! This is so much easier than dealing with proteins and carbs!”
So they start prioritizing alcohol over everything else.
Over time, your cellular metabolism reprograms itself. Your mitochondria become acetate junkies, bypassing normal energy pathways in favor of the quick-hit rocket fuel of alcohol31.
🚨 The Downside? Everything Else Gets Ignored
Once your cells are getting most of their energy from alcohol:
Fat metabolism slows → You gain weight
Glucose regulation goes haywire → Hello blood sugar crashes
Muscle breakdown accelerates → Weakness, fatigue, injury risk
Brain cells stop firing efficiently → Foggy thinking, memory loss
Liver mitochondria get overloaded → Steatohepatitis and cirrhosis, anyone?
Your body starts to forget how to power itself normally. It's like switching from a well-balanced meal to an all-energy-drink diet. Sure, you’re awake—but you’re shaking, malnourished, and one Monster away from a cardiac event.
🔄 Early Sobriety = Mitochondrial Withdrawal
When you stop drinking, your mitochondria go into a kind of cellular panic.
They’re still wired to run on acetate. But you’re no longer providing the goods. So now:
Energy crashes
Extreme fatigue
Sluggish metabolism
Muscle pain
Mood swings
Increased oxidative stress (yay, more inflammation!)
This is why even weeks into sobriety, you can still feel like garbage. Your cells are trying to relearn how to eat breakfast. Literally.
🍽️ Rebuilding: Fuel, Rest, and Time
The good news? Mitochondria are resilient. They’re high-maintenance drama queens, but with the right care, they bounce back.
Ways to support mitochondrial recovery:
Whole foods: Nutrients like CoQ10, B-vitamins, magnesium, and antioxidants all support cellular repair32
Exercise: Especially cardio, which increases mitochondrial biogenesis (they make more of themselves!)
Sleep: Deep, consistent rest is when a lot of repair happens
Time: There’s no hack. It’s a long game.
🧟♂️ When You Feel Like a Zombie… You’re Healing
That early sobriety fatigue? The one that makes you take a nap between coffee refills? That’s not laziness—it’s rebooting. Every cell in your body is waking up, trying to remember how to work without booze as its boss.
So be gentle. With your brain, with your body, with the mitochondria that are trying to stop shaking and get back on task.
🛠️ So Now What? (Or: How to Rebuild Yourself Without the Instruction Manual)
If you’ve made it this far—first of all, congratulations. You’ve just read the biochemical equivalent of a David Lynch movie narrated by a squirrel on a Red Bull drip.
So what the hell are you supposed to do now?
Honestly? Not much.
At least not all at once.
Your brain and body are rebuilding themselves on a cellular level, whether you're aware of it or not. This isn't just a spiritual awakening—it’s a mitochondrial uprising. And those little bastards are unionized, exhausted, and demanding overtime pay.
So here’s the real advice:
Stop expecting to feel better right away.
You broke some things. They take time to mend. That doesn't mean you're doing it wrong—it means you're healing.Eat like a grown-up.
Protein. Veggies. Actual food. Doritos are not a food group, and caffeine is not a personality trait.Move.
Walk. Stretch. Do weird yoga. Dance terribly in your kitchen. Get your blood moving. You’re not dead anymore—act like it.Sleep (or try).
Even if your squirrel-brain insists on throwing 2am dance parties with strobe lights and a megaphone.Laugh at it all.
This shit is ridiculous. You survived it. You’re still surviving it. Might as well own the absurdity.Ask for help.
From humans. From doctors. From squirrels in business suits who may or may not be hallucinations. It all counts.And above all: Don’t drink.
Even if your ass falls off. Especially if your ass falls off. (Call me—I’ve got Ass Glue.)
🎯 Final Words from the Biochemical Crime Scene
This isn’t just a brain problem. It’s a body-wide biochemical mutiny.
And recovery isn’t about getting better—it’s about rebuilding from scratch.
So when your brain says:
“Why am I still anxious after three months?”
“Why does music still suck?”
“Why do I feel nothing while everyone else is out there hugging trees and writing gratitude lists?”
Remind yourself:
This is the science behind the storm.
You’re not lazy.
You’re not broken.
You’re not crazy.
You’re healing.
Every meeting, every snack that isn’t a donut, every awkward connection, every nap between cups of coffee—it all counts. You’re doing the work. Even if it doesn’t feel like it.
You're not resetting.
You're rebooting.
And one day—probably when you're not even looking—your body, your brain, and even your twitchy-ass squirrel council will thank you…the cuddly little bastards.
Footnotes
Young, S. N. (2007). How to increase serotonin in the human brain without drugs. Journal of Psychiatry & Neuroscience, 32(6), 394–399.
Lovinger, D. M. (1997). Serotonin’s role in alcohol’s effects on the brain. Alcohol Health and Research World, 21(2), 114–120.
Heinz, A., et al. (1998). Reduced central serotonin transporters in alcoholism. American Journal of Psychiatry, 155(11), 1544–1549. https://doi.org/10.1176/ajp.155.11.1544
Hoyer, D., et al. (2002). International Union of Pharmacology classification of receptors for 5-hydroxytryptamine (Serotonin). Pharmacological Reviews, 54(2), 203–229
LeMarquand, D., et al. (1994). Serotonin and alcohol intake, abuse, and dependence: Clinical evidence. Biological Psychiatry, 36(5), 326–337
Wong, D. T., et al. (1995). A new selective inhibitor of serotonin uptake: pharmacology and clinical trials. Journal of Clinical Psychiatry, 56(Suppl 2), 7–12.
Pettinati, H. M., et al. (2001). Sertraline treatment for alcohol dependence: interactive effects of medication and alcohol subtype. Alcoholism: Clinical and Experimental Research, 25(6), 1041–1049.
Volkow, N. D., & Morales, M. (2015). The Brain on Drugs: From Reward to Addiction. Cell, 162(4), 712–725. https://doi.org/10.1016/j.cell.2015.07.046
Koob, G. F., & Le Moal, M. (2006). Neurobiology of Addiction. Academic Press.
Blum, K., et al. (2000). Reward deficiency syndrome: A biogenetic model for the diagnosis and treatment of impulsive, addictive and compulsive behaviors. Journal of Psychoactive Drugs, 32(Suppl), 1–112. https://doi.org/10.1080/02791072.2000.10400488
Goldstein, R. Z., & Volkow, N. D. (2002). Drug addiction and its underlying neurobiological basis: Neuroimaging evidence for the involvement of the frontal cortex. American Journal of Psychiatry, 159(10), 1642–1652.
Berridge, K. C., & Robinson, T. E. (1998). What is the role of dopamine in reward: Hedonic impact, reward learning, or incentive salience? Brain Research Reviews, 28(3), 309–369.
Koob, G. F. (2003). Alcoholism: allostasis and beyond. Alcoholism: Clinical and Experimental Research, 27(2), 232–243.
Becker, H. C. (2008). Alcohol dependence, withdrawal, and relapse. Alcohol Research & Health, 31(4), 348–361.
Sara, S. J. (2009). The locus coeruleus and noradrenergic modulation of cognition. Nature Reviews Neuroscience, 10(3), 211–223.
Valdez, G. R., et al. (2002). Increased ethanol self-administration and anxiety-like behavior during acute withdrawal and protracted abstinence: regulation by corticotropin-releasing factor. Alcoholism: Clinical and Experimental Research, 26(10), 1494–1501.
Kranzler, H. R., & Soyka, M. (2018). Diagnosis and pharmacotherapy of alcohol use disorder: a review. JAMA, 320(8), 815–824.
Sinha, R. (2009). Modeling stress and drug craving in the laboratory: implications for addiction treatment development. Addiction Biology, 14(1), 84–98.
Olsen, R. W., & Liang, J. (2017). Role of GABA_A receptors in alcohol use disorders suggested by chronic intermittent ethanol (CIE) rodent model. Molecular Brain, 10(1), 45
Grobin, A. C., Matthews, D. B., Devaud, L. L., & Morrow, A. L. (1998). The role of GABA_A receptors in the acute and chronic effects of ethanol. Psychopharmacology, 139(1-2), 2–19.
Kosten, T. R., & O’Connor, P. G. (2003). Management of drug and alcohol withdrawal. New England Journal of Medicine, 348(18), 1786–1795.
Mason, B. J., & Quello, S. B. (2012). Gabapentin treatment for alcohol dependence: a randomized clinical trial. JAMA Internal Medicine, 174(1), 70–77.
Volkow, N. D., & Koob, G. F. (2015). Brain disease model of addiction: why is it so controversial? The Lancet Psychiatry, 2(8), 677–679.
Platt, S. R. (2007). The role of glutamate in central nervous system health and disease. Journal of Veterinary Emergency and Critical Care, 17(1), 15–23.
Tsai, G., & Coyle, J. T. (1998). The role of glutamatergic neurotransmission in the pathophysiology of alcoholism. Annual Review of Medicine, 49(1), 173–184.
Chandler, L. J. (2003). Ethanol and brain plasticity: Receptors and molecular networks of the postsynaptic density. Journal of Physiology, 54(1–2), 805–811.
Hazell, A. S. (2007). Excitotoxic mechanisms in stroke: A potential role for zinc. Stroke, 38(2 Suppl), 769–771.
Abraham, W. C., & Bear, M. F. (1996). Metaplasticity: the plasticity of synaptic plasticity. Trends in Neurosciences, 19(4), 126–130.
Nicholls, D. G., & Ferguson, S. J. (2013). Bioenergetics 4. Academic Press.
Zakhari, S. (2006). Overview: how is alcohol metabolized by the body? Alcohol Research & Health, 29(4), 245.
Lieber, C. S. (2000). Alcohol and the liver: metabolism of alcohol and its role in hepatic and extrahepatic diseases. Mount Sinai Journal of Medicine: A Journal of Translational and Personalized Medicine, 67(1), 84–94.
Wallace, D. C. (2005). A mitochondrial paradigm of metabolic and degenerative diseases, aging, and cancer: a dawn for evolutionary medicine. Annual Review of Genetics, 39, 359–407.