Does Alcohol Kill Brain Cells? Part Three
Part Three from the Series: Does Alcohol Kill Brain Cells?
Research on Clinical Samples
by Kenneth Anderson, MA
Stavro et al. (2013) conducted a review of clinical studies of cognitive impairments in people with alcohol use disorder (AUD) and their reversal with abstinence. IQ was found to be unaffected by AUD; there were no significant differences in IQ between people with AUD and control subjects. However, 11 other cognitive domains were moderately impaired in people with AUD: verbal fluency/language, speed of processing, working memory, attention, problem-solving/executive functions, inhibition/impulsivity, verbal learning, verbal memory, visual learning, visual memory, and visuospatial abilities. Cognitive impairments began to abate during the first month of abstinence from alcohol, and cognitive function had largely returned to normal after a year of abstinence. The bulk of the research suggests that cognitive impairment is a result of brain shrinkage, and cognitive recovery is a result of the reversal of this brain shrinkage. Sullivan et al. (2000) found that people with AUD who had greatly reduced their drinking showed similar cognitive gains to total abstainers.
Reversible brain shrinkage was first noted by Carlen et al. in a study published in 1978. Subjects were eight men with AUD; all eight were given CT scans at two different points in time. Six of the eight subjects maintained abstinence from alcohol; two relapsed. Of the six who maintained abstinence, four showed large reversals of brain shrinkage at the time of their second CT scan; two did not. Likewise, the two relapsers showed no reversal of brain shrinkage. There was no control group.
In 1988, Schroth et al. published an MRI study of nine patients with AUD before and after five weeks of abstinence from alcohol. Subjects were an average of 47 years old and consumed an average of 235 grams of alcohol (17 US standard drinks) per day. Sex was not specified. The researchers determined that the brain volume had increased by looking at the decrease in the volume occupied by cerebrospinal fluid; when the volume occupied by the brain increases the amount of cerebrospinal fluid in the head must decrease, and vice versa. The researchers found that the volume occupied by the cerebrospinal fluid had decreased 30.5% after five weeks of abstinence, a statistically significant amount.
A similar study was published by Zipursky et al. in 2009. Subjects were 10 male patients with AUD and 10 male controls. AUD subjects had consumed an average of 149 grams of alcohol (10.6 US standard drinks) per day in the past month and were an average of 37.5 years old. Subjects were all inpatients at the Palo Alto VA Medical Center on a 28-day alcohol treatment unit. The average age of controls was 35.7 years old. The initial MRI scan was taken within two weeks of alcohol withdrawal, and the second scan was taken 19 to 28 days thereafter. At the time of the first scan, subjects with AUD had significantly larger ventricles (spaces filled with cerebrospinal fluid) than controls. There was no significant difference in ventricle size between AUD subjects and controls at the time of the second scan because their brains had expanded.
Durazzo et al. (2015) conducted an MRI study of 111 subjects undergoing treatment for AUD at the San Francisco VA Medical Center or the San Francisco Kaiser Permanente Chemical Dependence Recovery outpatient treatment clinics. The study began with 82 subjects who were given an MRI after one week of abstinence. An additional 29 subjects had been detoxified at other facilities and then transferred in for additional treatment; this made a total of 111 subjects who were given an MRI after one month of abstinence. Of these 111 subjects, 36 had maintained continuous abstinence and were still available for MRI follow-up seven and a half months later; the other 75 had either relapsed, moved, or changed their cigarette smoking status. A control group was comprised of 32 subjects, although only 15 control subjects remained at follow-up. MRIs taken after one month of abstinence showed significant increases in gray matter when compared to those taken after one week of abstinence. Likewise, MRIs taken after seven and a half months of abstinence showed significant increases in gray matter when compared to those taken after one month of abstinence. Interestingly, the greatest gains in gray matter volume occurred during the first month of abstinence, after which they continued at a much slower pace. White matter showed no significant increase in volume during the first month of abstinence; however, the white matter had increased significantly after seven and a half months of abstinence, showing that the rate of increase for white matter was slower but steadier than that for gray matter. At seven and a half months of abstinence, the AUD group still had significantly less total gray matter in the neocortex than the control group, although there was no longer a significant difference between the two groups in the volume of gray matter in the frontal lobe.
Meyerhoff and Durazzo (2020) conducted an MRI study of 54 subjects (49 men and five women) undergoing treatment for AUD at the facilities named in the previous paragraph. Subjects were an average of 47 years old and had drunk an average of about 102 US standard drinks per week (15 per day) in the year prior to entering treatment. At eight months after the start of treatment, subjects were divided into three categories: abstainers (26 subjects: 24 men and two women), light relapsers (17 subjects: 16 men and one woman), and heavy relapsers (11 subjects: nine men and two women). These three groups were then given MRIs and cognitive evaluations. Abstainers were defined as subjects who had remained totally abstinent over the eight-month period, light relapsers were defined as men who had drank less than an average of 40 grams of alcohol (2.9 US standard drinks) per day or women who had drunk less than an average of 20 grams of alcohol (1.4 US standard drinks) per day over the eight-month period, and heavy relapsers were defined as men who had drank more than an average of 40 grams of alcohol (2.9 US standard drinks) per day or women who had drunk more than an average of 20 grams of alcohol (1.4 US standard drinks) per day over the eight-month period. Abstainers and light relapsers showed significantly more total gray matter volume than heavy relapsers at the eight-month follow-up period. Likewise, abstainers and light relapsers showed significantly more matter volume than heavy relapsers in the frontal lobe and the thalamus (a deep-brain structure that acts as a neural relay station). There were no significant gray matter differences between abstainers and light relapsers: both had improved equally. There were no significant differences between light relapsers and heavy relapsers on cognitive performance; however, there was a trend for light relapsers to perform better, which may have showed significance in a larger sample. The article did not report on the cognitive performance of abstainers compared to either relapse group. The upshot is that moderation is as good as abstinence in terms of improved brain structure after treatment for AUD.
Gazdzinski et al. (2008) conducted an MRI study that compared subjects in treatment for AUD with heavy drinkers who had never sought treatment for AUD and with light drinkers. There were 35 subjects (33 males and two females) in the treatment group, 32 subjects (27 males and five females) in the heavy drinker group, and 38 subjects (30 males and eight females) in the light drinker group. All subjects in the treatment group were from the same two facilities as the previous paragraph. MRIs for the treatment group were taken about one week after starting treatment. Of the 32 heavy drinkers, 22 met DSM-IV criteria for alcohol dependence, and 10 met criteria for alcohol abuse. Prior to controlling for confounding factors, it was found that the treatment group showed significantly more shrinkage of the gray matter of the neocortex and the thalamus than the heavy drinking group. White matter was not significantly different. Even after controlling for all possible confounding variables, including differences in the quantity of alcohol consumed, it was found that the treatment group showed significantly more shrinkage (4%) in the parietal lobe than the heavy-drinking group. This is an example of why conclusions from clinical samples cannot be generalized to community samples.
So, Does Alcohol Kill Brain Cells?
In conclusion, when answering the question, “Does alcohol kill brain cells?”, it is important not to exaggerate differences in cognitive performance between drinkers and nondrinkers, and not to treat them as absolutes. Some alcohol-dependent subjects score higher on cognitive tests than some lifelong abstainers: it is the group average that is lower, not the scores of all members of the group. Likewise, not all people with AUD have larger ventricles than those without AUD; anytime you see a picture purporting to show “alcoholics” with giant holes in their brain compared to “normies,” you can be certain you are looking at a reefer-madness style propaganda lie based on cherry-picking the most extreme cases.
Unfortunately, far too many drug and alcohol counselors have jumped on small statistical differences in brain function and have erroneously told their clients that they have brain damage and are incapable of thinking for themselves and that they must therefore get a sponsor to do their thinking for them. This is not only untrue but can serve to drive away many people who wish to make positive changes in their drinking habits.
More from the Series, “Does Alcohol Kill Brain Cells?”