Brain Damage from Vitamin Deficiency in Alcoholics: An Often Overlooked Danger

Brain damage in people with alcohol use disorder often develops gradually—and frequently stems from a simple, overlooked vitamin deficiency. If it goes unrecognized, a relatively easy-to-correct deficit can turn into a permanent, severe brain disease. The tragedy is that some of this damage could be prevented—if the warning signs were spotted early and treated properly.

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By Bernd Guzek, MD, PhD

It rarely starts dramatically. Usually, there’s just a person who begins to change. They occasionally seem confused, forget simple things, stand up unsteadily, or walk with a wide-based, swaying gait. Sometimes they stumble even on flat ground. Relatives may attribute it to intoxication, withdrawal, or exhaustion. Often, they wait and see.

That’s where the danger lies.

Early symptoms often appear in the eyes

Changes in the eyes are also common—unsettling but hard to interpret. The eyes may jerk back and forth, especially when looking sideways. One eye sometimes lags behind the other, as if it’s too slow. Affected individuals complain of double vision or close one eye to see clearly.

One eyelid may droop noticeably, as if the person is exhausted. Some become unusually sensitive to light; in others, the pupils are unequal or react sluggishly. It all looks strange—but often not alarming enough to suggest an emergency.

What can develop here is Wernicke encephalopathy. It is not a rare curiosity but an acute condition that is alarmingly often missed in people with prolonged heavy alcohol use. The classic triad is mental confusion, unsteady gait, and eye movement abnormalities. Crucially, these signs do not always appear together. Even isolated symptoms can indicate serious brain dysfunction.

Timely treatment can still save the brain

Wernicke encephalopathy is a turning point. If recognized and treated promptly, the brain can recover fully or at least partially. If it is missed or mistaken for intoxication, withdrawal, or psychiatric oddity, it can progress to a chronic condition: Korsakoff syndrome.

People with Korsakoff syndrome often appear remarkably alert from the outside. They speak fluently, answer questions, and may even seem calm. Yet their memory is profoundly impaired. New information doesn’t stick; conversations are forgotten within minutes. Events are misremembered or unconsciously embellished to fill gaps. Orientation to time is lost. For relatives, this is especially distressing because the personality seems intact while memory no longer functions.

Korsakoff syndrome is not an independent fate or typical alcohol-related dementia. In most cases, it is the consequence of an untreated or inadequately treated Wernicke encephalopathy. What could have been stopped relatively easily in the acute phase becomes permanent. What was preventable becomes irreversible.

Korsakoff: The point of no return for memory

The reason lies in deep brain structures. Regions responsible for storing new memories suffer prolonged energy deprivation. Nerve cells in these areas die or permanently lose their connections. Once this infrastructure is destroyed, it cannot be fully restored even with later treatment.

To understand this, it helps to look at a disease that was once widespread but is now rare in Western countries: beriberi. It also causes nerve, brain, and heart damage—triggered by a dietary lack of vitamin B1 (thiamine). The symptoms strikingly resemble those of Wernicke encephalopathy. This shows that the core problem is not alcohol itself, but thiamine deficiency.

Thiamine is an everyday substance—but it must never be missing

Thiamine is not exotic. It is found in ordinary foods such as whole grains, legumes, meat, nuts, yeast, and egg yolk. Alcohol, however, interferes in multiple ways: it displaces nutrient-rich food, impairs thiamine absorption in the gut, and disrupts its utilization in the body. The brain quietly falls into an energy crisis.

Thiamine is essential for nerve cells’ energy metabolism. Without it, they can no longer efficiently use glucose. Brain regions responsible for orientation, balance, memory, and eye movements are particularly vulnerable. This explains why these functions fail early. One could say: the brain receives fuel but can no longer burn it. The result: vital cells die—irreversibly.

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Important reminder for relatives

Wernicke encephalopathy rarely presents with a single symptom; it typically involves a characteristic combination. Be especially alert if several of the following changes occur together:

Increasing confusion, disorientation, or unusual memory gaps
Unsteady gait, staggering, frequent stumbling, or wide-based stance
Eye abnormalities such as double vision, jerky eye movements, drooping eyelid, or misaligned gaze
Unusual fatigue, apathy, or marked lack of drive

If several of these changes appear simultaneously, it is not a harmless state or “normal drunkenness.” Waiting is not advisable.

In emergency medicine, thiamine therefore has special priority. During alcohol withdrawal—especially in delirium tremens—administering vitamin B1 is one of the very first measures, before other therapies begin, when done correctly. The reason is straightforward: the brain depends almost entirely on glucose for energy.

Emergency treatment in withdrawal: Give thiamine before glucose

The background lies in cerebral glucose metabolism. Although glucose is the main energy source for nerve cells, it cannot be burned directly. It must pass through several biochemical steps. One critical step depends on thiamine.

Without vitamin B1, glucose processing stalls halfway. The sugar is present but cannot be further metabolized. Nerve cells enter an energetic dead end: fuel is available, yet the machinery stands still.

If glucose is given in this situation without first correcting the thiamine deficiency, the impaired metabolism is further stimulated. Nerve cells take up more glucose and attempt to process it—but fail at the very step that requires thiamine.

Instead of producing energy, metabolic intermediates accumulate and further burden the cells. The energy deficit is not relieved but worsened. That is why thiamine comes first: it removes the blockage in glucose metabolism.

Administering glucose without thiamine does not produce an energy boost; it intensifies the brain’s deficiency. Nerve cells come under even greater stress, and already damaged regions may sustain further injury. This is precisely why thiamine takes priority: it is the prerequisite for the brain to once again utilize available glucose effectively.

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Why benfotiamine often works better than regular vitamin B1

Standard vitamin B1 (thiamine) is water-soluble and only partially absorbed in the intestine. Some is lost during passage through the gut, and more is quickly excreted. In people with alcohol problems or impaired gut function, too little thiamine may reach the body despite supplementation.

Benfotiamine is a fat-soluble precursor of vitamin B1. This property allows it to cross the intestinal wall much more easily. In the body, benfotiamine is then converted into active thiamine.

The practical advantage: benfotiamine achieves more stable and higher thiamine levels in tissues—especially in the nervous system. It is therefore commonly used when a severe deficiency exists or reliable supply must be ensured.

Important: In acute emergencies, such as suspected Wernicke encephalopathy, a dietary supplement does not replace professional medical treatment. High-dose thiamine belongs in medical hands.

The tragedy of Wernicke and Korsakoff is not only the severity of the brain damage. It is above all that some of it was preventable—not through willpower or appeals, but through timely recognition and straightforward action.

Vitamin B1 deficiency is one of the few nutritional deficits in alcoholism that has made it into textbooks because of its dramatic clinical consequences. Not because it is the only problem, but because its effects are so obvious. Understanding this helps us see alcohol dependence not just as a behavioral issue, but as what it truly is: a serious metabolic disorder with tangible biological consequences.

Frequently Asked Questions about Wernicke or Korsakoff Syndrome (FAQ)

What is the difference between Wernicke and Korsakoff?

Wernicke encephalopathy is an acute condition caused by severe vitamin B1 deficiency. It may present with confusion, gait instability, and eye abnormalities and is partially reversible with prompt treatment. Korsakoff syndrome is usually the sequel of untreated or inadequately treated Wernicke encephalopathy and involves permanent memory impairment.

Is Korsakoff syndrome a form of dementia?

No. Korsakoff is not a classic dementia nor a normal aging process. The cause is targeted damage to specific memory structures in the brain due to prolonged vitamin B1 deficiency. Attention and speech may remain intact for a long time while memory is severely affected.

Why is vitamin B1 so important for the brain?

The brain derives its energy almost exclusively from glucose. Vitamin B1 is required for the brain to metabolize this glucose. Without thiamine, glucose metabolism is blocked, and nerve cells fall into severe energy deprivation.

Why must vitamin B1 be given before glucose during alcohol withdrawal?

Without sufficient vitamin B1, the brain cannot process glucose further. Supplying glucose before correcting the thiamine deficiency worsens the metabolic blockage in the brain. Therefore, vitamin B1 is the first step in acute treatment.

Can non-alcoholics also develop Wernicke or Korsakoff?

Yes. The underlying cause is severe vitamin B1 deficiency, which can also occur with malnutrition, eating disorders, serious illnesses, or extremely restricted diets. Alcohol is a common but not the only trigger.

Why is benfotiamine often recommended instead of regular vitamin B1?

Benfotiamine is a fat-soluble precursor of vitamin B1 and is absorbed better in the gut than water-soluble thiamine. This achieves more stable thiamine levels in the body, especially in the nervous system. In acute emergencies, however, it does not replace medical treatment.

Brief overview of studies on Wernicke or Korsakoff syndrome in alcoholism

The following review articles, guidelines, and specialist papers provide deeper insight into Wernicke encephalopathy, Korsakoff syndrome, and the role of vitamin B1. They are primarily aimed at medical professionals but are partly accessible to interested lay readers.

Sechi G, Serra A.
Wernicke’s encephalopathy: new clinical settings and recent advances in diagnosis and management.
The Lancet Neurology, 2007.
Arts NJM, Walvoort SJW, Kessels RPC.
Korsakoff’s syndrome: a critical review.
Neuropsychiatric Disease and Treatment, 2017.
Cook CC, Hallwood PM, Thomson AD.
B-vitamin deficiency and neuropsychiatric syndromes in alcohol misuse.
Alcohol and Alcoholism, 1998.
Thomson AD, Marshall EJ.
The natural history and pathophysiology of Wernicke’s encephalopathy and Korsakoff’s psychosis.
Alcohol and Alcoholism, 2006.
Isenberg-Grzeda E, Kutner HE, Nicolson SE.
Wernicke–Korsakoff syndrome: under-recognized and under-treated.
Psychosomatics, 2012.
Victor M, Adams RD, Collins GH.
The Wernicke–Korsakoff Syndrome and Related Neurologic Disorders Due to Alcoholism and Malnutrition.
FA Davis Company, classic standard work.
WHO – World Health Organization.
Thiamine deficiency and its prevention and control in major emergencies.
Technical report, also addressing the link to beriberi.

Note: The selection focuses on review articles and foundational presentations. Individual studies on specific topics such as imaging or molecular mechanisms are intentionally omitted here.

Bernd Guzek, MD, PhD

Physician, author, family member & co-founder of Bye-Bye-Booze

Has been working for many years on the biochemical foundations of addiction and brain metabolism disorders as well as their modulation by nutrients.