Alcoholism and Cognition: The damage of drinking
It will not come as a surprise that alcohol has a detrimental impact on our cognitive processes. These involve such core functions as perceiving the world, forming memories, using and understanding language, and solving problems and decisions.[1] Over time, with repeated and excessive alcohol exposure, these deficits in normal functioning become engrained and persistent – leading to what we might crudely call brain damage. Problematic alcohol usage is understood as continuing to drink despite knowing the negative consequences. However recent studies show the neuroplasticity of the brain, with just two weeks of abstinence already showing notable strides in the recovery of one’s cognition. We will consider these deficits and neuroplasticity in more detail, along with those cognitive impairments that remain chronic for problematic alcohol users. This review is split into two parts: this is Part I: The damage of drinking.
To understand some of the neurology underlying cognitive damage, we first will take a look at the mechanisms causing it. When we drink alcohol, it enters our system and acts to block our neuronal connections.[2] It does this through the ethanol in alcohol, which inhibits our excitatory glutamate receptors and excites our inhibitory GABA receptors.[3] In other words, inhibiting the usual channels of communication between our brain cells. This interruption of normal brain communication means that very visible behaviours, such as our speech, motor control and decision making, can be impaired. Also because of this, an abrupt stop to drinking can cause withdrawal symptoms like hallucinations, tremors, seizures, and general cognitive instability. Over time, a prolonged and repetitive blockage of those connections through alcohol overconsumption means that the brain itself responds and changes, and increases the release of neurotransmitters to compensate for the blockage. This results in what is known as neurotoxicity – essentially, death of brain cells or brain damage. This is a direct result of the over-exposure of our brain cells to this increased neurotransmitter production, which causes a kind of ‘burn out’. Neurotoxicity results in both shrinkage of grey matter (cell bodies) and white matter (cell connections). In this way, the ethanal found in alcohol is considered to be a neurotoxin.[4] One area particularly receptive to this kind of brain damage is our frontal lobe, which deals with so called “higher functions”. These involve such cognitive processes as problem-solving, working memory (keeping things in your head whilst working on another problem), impulse control, decision making and more.[5] Adolescents in particular are even more affected by this long-term, given that their frontal lobe is not fully developed and will not be until the age of twenty-five. This is a brief overview of how long-term alcohol overconsumption can lead to brain cell death and cognitive deficits as a result.
With those with problematic alcohol use (PAU), these kind of cognitive deficits can also interact with vitamin B deficiency, which acts to makes them worse. This deficiency is common in alcoholics, as alcohol slows the absorption of vitamin B1 (thiamine) in particular. One study investigated whether if one “took thiamine deficiency and combined it with chronic alcohol intake, would you then create a situation that would produce a more severe impairment of cognition and memory than you would with either [factor] alone.”[6] Having found an increased detrimental impact when the two factors were combined – due to the fact that thiamine is involved in the metabolism and function of brain cells – this study concluded that, yes, the individual’s cognition is damaged even more. This particularly affects memory and language function, which in extreme cases can develop into Wernicke-Korsakaff Syndrome, a brain disorder.[7] Therefore other medical conditions exacerbated by alcoholism can also act to make cognitive symptoms more severe.
Another notable dynamic is how the impact alcohol has on cognition actually works as a feedback mechanism for alcoholism.[8] For example, the resulting cognitive deficits such as increasing distractibility, impairing decision making, and reducing self-control – all of these traits only perpetuate the kind of decisions which keep an individual in the addiction cycle. Thus, one’s personal decisions and neurobiology enter an amplifying relationship, making it even harder for an individual to stop drinking. Researchers identify this state in alcoholics as “learned helplessness”, meaning the individual finds it incredibly difficult to motivate oneself to tackle their alcoholism.[9] They feel very much at the mercy of their condition. Indeed, the specific cognitive impairments caused by alcoholism in themselves also increase the likelihood of relapse in abstaining alcoholics.[10] It is not a case of blame, but rather of understanding the personal circumstances and concurrent factors which make some people struggle to tackle their problematic alcohol use.
Follow through to Part II: The brain bounces back.
References
[1] Evert DL, Oscar-Berman M. (1995) Alcohol-Related Cognitive Impairments: An Overview of How Alcoholism May Affect the Workings of the Brain. Alcohol Health Res World. 19(2):89-96.
[2] Brust, J. C. M. (2010). Ethanol and cognition: Indirect effects, neurotoxicity and neuroprotection: A review. International Journal of Environmental Research and Public Health. 7, 1540–1557.
[3] Davis KM, Wu J-Y. (2001) Role of glutamatergic and GABAergic systems in alcoholism. J. Biomed. Sci. 8:7–19.
[4] Brust, J. C. M. (2010). Ethanol and cognition: Indirect effects, neurotoxicity and neuroprotection: A review. International Journal of Environmental Research and Public Health. 7, 1540–1557.
[5] Rogers, B. P., Parks, M. H., Nickel, M. K., Katwal, S. B., & Martin, P. R. (2012). Reduced fronto-cerebellar functional connectivity in chronic alcoholic patients. Alcoholism: Clinical and Experimental Research. 36(2), 294–301.
[6] Langlais PJ. (1995) Alcohol-Related Thiamine Deficiency: Impact on Cognitive and Memory Functioning. Alcohol Health Res World. 19(2):113-121.
[7] Butler Centre for Research (2015) Alcohol's Effects on the Brain and Cognitive Improvement in Recovery. Hazelden Betty Ford. Available at: https://www.hazeldenbettyford.org/education/bcr/addiction-research/alcohol-effects-brain-ru-515
[8] Sullivan EV, Harris RA, Pfefferbaum A. (2010) Alcohol's effects on brain and behavior. Alcohol Res Health. 33(1-2):127-43.
[9] Butler Centre for Research (2015) Alcohol's Effects on the Brain and Cognitive Improvement in Recovery. Hazelden Betty Ford. Available at: https://www.hazeldenbettyford.org/education/bcr/addiction-research/alcohol-effects-brain-ru-515
[10] Rolland B, D’Hondt F, Montegue S, et al. (2019) A patient-tailored evidence-based approach for developing early neuropsychological training programs in addiction settings. Neuropsychol Rev. 29(1):103–115.