Excessive alcohol consumption affects the brain. They can be limited and even reversed after prolonged cessation of alcohol use, but not all regions of the brain recover in the same way.
Alcohol consumption in France has steadily declined over the past fifty years, a decline largely attributed to the decline in wine consumption. Despite everything today 10% of French adults have problems with alcohol.
Excessive alcohol consumption is not without brain damage. Numerous studies have shown that the volume of brain structures involved in cognition and learning is significantly reduced in people addicted to alcohol. This decrease is partially reversible after prolonged cessation of use, but not all regions of the brain recover in the same way. Who benefits from alcohol ban? And what are the consequences for those who do not benefit?
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Alcohol decreases brain size
Even in moderate but regular drinkers, a general reduction in brain volume was observed. However, it is not definitive: stop alcoholthere is a partial recovery of brain volume, which is accompanied by an improvement in cognitive abilities. Many factors influence this recovery: age, gender, genetic factors, having a family history of alcohol addiction, smoking, etc.
Can alcohol-related brain damage itself influence addiction-related behavior? In other words, can it increase the risk of recurrence? In order to find out, it was first determined which brain regions are most affected by these volume fluctuations among those involved in addiction. The team led by Timothy Durazzo and Dieter Meyerhoff, probably the best-known authors in the field of structural imaging in alcohol addiction, recently investigated this question.
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The researchers analyzed this using MRI the brains of 85 alcohol addicts one week, one month and seven months after stopping alcohol consumption and compared them to the cerebral images of controls who consumed very little or no alcohol, i.e. without dependence.
People who had consumed more than 204 glasses of so-called “standard” alcohol (a standard glass roughly corresponds to a “balloon” of 12 cl of wine or 10 g of ethanol) per month in the last eight years were considered dependent men and 108 drinks in the last six years for women. This difference is explained by the fact that men eliminate alcohol faster than women, and that the cerebral and organic effects are greater in the latterin equal doses.
In terms of gender differences, it is interesting to note that men born between 1891 and 1910 were three times more likely to have problem alcohol use than women born in the same period, but this ratio increased during the 20th centurye Century. So much for today boys and girls born between 1991 and 2000 no longer differ significantly.
In the study, MRIs showed that all regions examined (anterior cingulate cortex, insula, dorsolateral prefrontal cortex, orbitofrontal cortex) were altered by the time participants began their abstinence period. However, after stopping alcohol, the volume of the affected brain structures increased again over time once people stopped drinking. The effects of stopping use were actually detectable from the first week or month of stopping. However, these recoveries have varied widely between individuals, with some recovering less well than others.
Also, a structure was never retrieved: the hippocampus. However, this plays an important role in memorization, especially in the formation of new memories.
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Differences that would explain the inequality in the face of alcohol
Neurobiological abnormalities that occur in the hippocampus therefore appear to be more persistent than those that occur in the cortex. This could lead to learning difficulties, especially with regard to the new tasks of long-term abstinence management. This, coupled with the fact that gray matter plasticity observed during abstinence varies from person to person, suggests that some people may be at higher risk of relapse.
However, the study had some limitations. First, an MRI had not been performed prior to stopping alcohol. Obtaining such records is of course difficult due to technical and ethical constraints. Then, most of the subjects had failed the three consecutive recordings (one week, one month, and seven months after stopping alcohol), limiting the value of the data collected. Last but not least, no associated cognitive measurement was performed (this point should be the subject of future research). This is unfortunate as they would have been necessary to show that damage to cerebral structures has real clinical significance.
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In search of the origins of individual vulnerability
Studies of the same kind that have already been done on people addicted to alcohol have shown that they experience two types of attacks. On the one hand damage that can be described as “irritation”, both diffuse and frequent, but also reversible after stopping the alcohol. On the other hand, “fixed” damage that lasts long after you stop drinking alcohol.
In this context, many questions remain unanswered. First, even if one suspects a strong association with cognitive impairment (which is also separated into the same two types – irritant and fixed), this has not yet been properly studied, while it has obvious relevance in practice. Then it’s important to understand why certain attacks (most) are reversible, while others freeze and leave a mark, if not indelible then permanent. Finally, it is important to understand why certain individuals are more vulnerable to the fixed attacks than others.
Is it a question of dose and duration of alcohol exposure? Undoubtedly too simple. The differences observed from patient to patient can probably be explained by as yet unknown individual factors of neurobiological alcohol susceptibility. A better understanding of these determinants will be the greatest challenge for researchers in the coming years.
The original version of this article was published in The conversation.