The Neuropathology of Alcohol-Related Brain Damage

“Excessive alcohol use can cause structural and functional abnormalities of the brain and this has significant health, social and economic implications for most countries in the world. Even heavy social drinkers who have no specific neurological or hepatic problems show signs of regional brain damage and cognitive dysfunction. Changes are more severe and other brain regions are damaged in patients who have additional vitamin B1 (thiamine) deficiency (Wernicke–Korsakoff syndrome). Quantitative studies and improvements in neuroimaging have contributed significantly to the documentation of these changes but mechanisms underlying the damage are not understood.”

From the abstract of this paper. Some more stuff from the paper:

“It has long been accepted that excessive alcohol use can cause structural and functional abnormalities of the brain and other organs (Courville, 1955; Victor et al., 1959; Dreyfus and Victor, 1961). In the brain, this has been demonstrated clinically, with imaging techniques and pathologically. Many alcoholics can also develop cirrhosis of the liver that can impact on brain structure and function and others develop nutritional deficiency states (vitamin B1 deficiency) that can cause severe brain damage and dysfunction. These latter two groups of alcoholic cases are often defined as ‘complicated alcoholics’ to differentiate them from those who do not have liver disease or nutritional deficiency states (uncomplicated alcoholics). Nevertheless, ‘uncomplicated alcoholics’ who are cognitively impaired have abnormalities (Pfefferbaum et al., 1997). The risks of ‘moderate’ alcohol consumption are more difficult to assess. Ding and colleagues showed that the more alcohol consumed, the larger the cerebrospinal fluid-filled spaces of the brain became (Ding et al., 2004). This data correspond with a neuropathological study that showed an increase in the cerebrospinal fluid-filled spaces covering the brain (pericerebral space) in men drinking more than eight standard drinks per day and a similar distinctive trend in those drinking five to eight standard drinks per day (Harper et al., 1988). [...]

The first quantitative neuropathological study on brain weights in alcoholics (Harper and Blumbergs, 1982) was inspired by the various reports of ‘brain shrinkage’ seen on CT scans in alcoholics (Cala et al., 1978; Ron et al., 1980). Alcoholics have a reduced brain weight compared to controls and the degree of brain atrophy has been shown to correlate with the rate and amount of alcohol consumed over a lifetime (Harding et al., 1996). [...]

As noted above, the mechanism for alcoholism-related white matter loss, restoration with alcohol abstinence and disruption of micro structural integrity still remains unclear but probably involves changes in both myelination and axonal integrity. This has been inferred from in vivo human and experimental MR diffusion tensor imaging studies (Pfefferbaum et al., 2006b, 2007) and may explain why tissue volume recovery appears incomplete with abstinence. Thus, alcoholic brain pathology may have two components, one reflecting permanent change and one a transient change. Regarding permanent effects, alcohol-related neuronal loss has been documented in specific regions of the cerebral cortex (superior frontal association cortex), hypothalamus and cerebellum (Harper, 1998). Such loss will result in axonal (Wallerian) degeneration and a permanent reduction in white matter volume. Structural changes in myelin, however, could explain the reversible white matter shrinkage that has been documented with serial MRI studies following periods of abstinence from alcohol (Shear et al., 1994; Pfefferbaum et al., 1995; Gazdzinski et al., 2005). [...]

Analysis of the types of neurons lost from the frontal cortex revealed that they were the larger ones with a somal area >90 μm (Harper and Kril, 1989). This population of neurons is also more vulnerable in both Alzheimer’s disease (Terry et al., 1981) and normal aging (Terry and Hansen, 1987). There does not appear to be any link between alcohol-related brain damage and Alzheimer’s disease (Morikawa et al., 1999), although there is some work that suggests a relationship between alcohol and aging (Harper et al., 1998a).”

Alcohol consumption, a few numbers

Two great graphs, from gnxp (there’s more at the link):

The ‘wordsum’ variable above is a vocabulary test; a higher score indicates that an individual has a more extensive vocabulary.

This report (pdf) concludes that in Denmark, “there’s no (/significant? /clear? /obvious?) connection between average alcohol-consumption and length of education.”

(“Der er ingen tydelig sammenhæng mellem gennemsnitligt alkoholforbrug og
uddannelseslængde, men umiddelbart har skoleelever det højeste gennemsnitlige forbrug.”)

I’m not sure that’s the right conclusion to draw and they make no attempt to justify it, they just state it as if it was a fact without any further comments. Here’s a graph of the results:

I have excluded from the graph the two variables ‘skoleelev’ and ‘anden skoleuddannelse’ because I have no clue precisely what those varibles mean and who they include (both relate to people somewhere in the educational system, but that’s all I know). Does a high school student belong to the ‘skoleelev’ or the ‘anden skoleuddannelse’ segment? When is something a ‘skoleuddannelse’? I have no idea. Stuff like that can just really make me mad – the communication here is so damn poor that I’d rather throw away the results than post them here. Anyway, I was surprised that people with the shortest education drink (much) less than average and less surprised that people with a long education drink more than average. I’d assumed that the relationsship between education and alcohol consumption was v-shaped. Maybe selection bias is at work here, I don’t know, but these data certainly do not support the hypothesis of a v-shaped relationsship. The reason why I believe their conclusion (‘no connection btw…’) is incorrect is that there do seem to be a relationsship between education and alcohol consumption; it looks like people without much schooling drink much less than average and that people with a relatively long education drink more than average. No, you can’t draw a straight line, but who says the ‘relationsship’ should necessarily be a straight line? The fact that alcohol consumption varies widely across education levels is a clear sign that the two variables are in fact connected, even if we don’t know precisely how they are connected. Note that these numbers are not age-adjusted and that I’ve taken out people from the educational system. There are a lot more 20-30 year old plumbers who’re no longer in the educational system than there are people with phd’s. That’s another way to say that the group of people with long educations should actually be drinking less than the other groups, all else equal, because they’re on average a few years older (and ‘older’ here means ‘drink less’ for the relevant age demographic).

The report has a lot more data. Some of the results are quite surprising. Here’s one bit that took me by surprise: ’41,9 % of the participants think that it is ok to drink alcohol in order to become inebriated. 58,1 % do not think it is ok.’ (41,9% af deltagerne i denne undersøgelse mener, at det er i orden at drikke alkohol for at blive beruset. Tilsvarende mener 58,1% at det ikke er i orden.). Ok – so more than half don’t think it’s ok to drink alcohol in order to get drunk? Seriously?