Vitamin B1 may help stem alcohol-induced cognitive decline – Austrian study

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Researchers from the Medical University of Vienna in Austria have hypothetically linked alcohol-induced vitamin B1 deficiency with iron deposits in the brain that could be key factors in cognitive decline. Administering vitamin B1 could help protect the brain, according to their study published in the journal Alzheimer’s and Dementia.

According to Medical University of Vienna material published by News Medical on 9 September 2020, a common consequence of chronically high alcohol consumption is a decline in cognitive function, which can even progress to full-blown dementia. However, it has not been fully understand yet how alcohol damages the brain.

The hypothesis that iron deposits in the brain – resulting from alcohol-induced vitamin B1 deficiency – can be regarded as key factors in cognitive decline, has been developed by a research group led by Stephan Listabarth from the Medical University of Vienna.


In Austria, around 5% of the population is alcohol dependent from the age of 15 onwards. This means that approximately 365,000 people are affected by the dangerous health consequences associated with high alcohol consumption.

One of those consequences is a decline in cognitive function, especially memory and abstraction. This is then referred to as alcohol-related dementia. However, we do not yet fully understand the exact pathomechanism, that is to say the way in which the brain is damaged by alcohol.

The hypothesis to explain alcohol-induced brain damage has been advanced by Stephan Listabarth, Daniel König and Benjamin Vyssoki from the division of social psychiatry in the Department of Psychiatry and Psychotherapy at the Medical University of Vienna, and Simon Hametner from MedUni’s division of neuropathology and neurochemistry in the Department of Neurology.

The research is important because the administration of vitamin B1 could protect the brain from the cognitive deterioration that is caused by iron deposits.

The research

We know from various neurodegenerative diseases that iron deposits in the brain are responsible for nerve tissue damage. These deposits can also be detected in specific regions of the brain (including the basal ganglia) in people who drink a lot of alcohol.

The hypothesis advanced by the study authors now also offers an explanation as to why iron deposits are so prevalent in this patient group: high alcohol consumption results in elevated iron levels in the blood and also to vitamin B1 (thiamine) deficiency, which, among other things, is important for maintaining the blood-brain barrier.

If these two situations coincide, more iron will be deposited inside the brain, ultimately leading to oxidative tissue damage.

The newly described role of vitamin B1 in this process could represent a huge step forward in our understanding of the development of alcohol-related neurological damage and, in particular, could offer a new point of attack for preventive and therapeutic approaches. It would then be conceivable to give continuous vitamin B1 substitution in future, as a preventive measure.

The researchers believe it would also be useful to evaluate the use of drugs to reduce iron levels (eg chelators), as is already done in other neurodegenerative diseases.

The authors of the research have started planning a prospective clinical study to validate the above-mentioned relationship between alcohol dependency, vitamin B1 deficiency and cerebral iron deposits and to provide a basis for further research in the field of alcohol-related dementia in the future.


Does thiamine protect the brain from iron overload and alcohol‐related dementia?

The journal Alzheimer’s & Dementia. First published on 18 August 2020.


Stephan Listabarth, Daniel Konig, Benjamin Vyssoki and Simon Hametner


Alcohol‐related dementia (ARD) is a common and severe co‐morbidity in alcohol use disorder (AUD). We propose brain iron overload (BIO) to be an important and previously neglected pathogenic process, accelerating cognitive decline in AUD.

Furthermore, we suggest thiamine, which is frequently depleted in AUD, to be a key modulator in this process: Thiamine deficiency impairs the integrity of the blood‐brain barrier, thereby enabling iron to pass through and accumulate in the brain.

This hypothesis is based on findings from animal, translational, and neuroimaging studies, discussed in this article. To validate this hypothesis, translational studies focusing on brain iron homeostasis in AUD, as well as prospective clinical studies investigating prevalence and clinical impact of BIO in AUD, should be conducted.

If proven right, this would change the understanding of ARD and may lead to novel therapeutic interventions in prevention and treatment of ARD.


Alcohol-induced vitamin B1 deficiency can be a key factor in cognitive decline


Does thiamine protect the brain from iron overload and alcohol‐related dementia?


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