Is It True That Alcohol Kills Neurons In The Brain?
One of the main and most recent objectives of neurology has been to study the toxic or harmful effects of psychotropic substances on the brain. Through different research it has been possible to know some of the consequences of consuming excessive chemical compounds such as ethanol.
From there The belief that alcohol kills neurons has become very popular To what extent is it true? Let’s see it in the following text.
To begin we will briefly remember the life cycle of neurons and what do we mean by “neuronal death”. As with the different cell populations that make up our body, nerve cells (neurons) act through a proliferation mechanism that includes cell loss, renewal and differentiation.
The death of a cell is defined as the arrest of its biological processes due to irreversible morphological, functional and biochemical modifications that prevent it from carrying out its vital functions (Sánchez, 2001). In this sense, neuronal death is considered to have occurred when a nerve cell loses the ability to establish adequate interstitial connections.
Two major types of neuronal death
Neuronal death is when its characteristics are significantly modified, impeding the ability to function And the latter does not necessarily correspond to a decrease in the volume of cells within the affected areas. Let’s now look at the two main types of neuronal death:
1. Apoptosis
Also known as programmed neuronal death. It has adaptive purposes, that is, it serves to maintain only the most frequently used connections and occurs especially in the early years of development
2. Necrosis
It consists of the loss of neuron functions due to the influence of external factors. In this process the cells are not always phagocytosed (that is, they do not completely disintegrate within the body, which can cause other medical complications), but they are considered dead because they lose the ability to be activated and produce connections between themselves.
Having said the above, we will see what the toxic mechanism that produces alcohol consumption is and if the latter has the capacity to generate a process of apoptosis or necrosis.
Toxic mechanism of frequent alcohol consumption
The toxic effects of ethanol (recreational alcohol) vary depending on the specific region of the brain in which they act. Also vary according to age or stage of development, dose and duration of exposure
When it comes to the mature brain, chronic or intense exposure to ethanol can cause different diseases, both of the central nervous system and the peripheral nervous system, as well as of the skeletal muscle (de la Monte and Kril, 2014).
The consequence is that, in the long term, excessive alcohol consumption significantly alters executive functions. In other words, alcohol can produce degenerative activity of the nervous system, since it gradually deteriorates the function of neurons, including the capacity for neuronal survival, cell migration and the structure of glial cells. Without the latter meaning that neurons necessarily disintegrate, it does. can imply the definitive loss of its functions, which falls into the definition of neuronal death
This is because, among many other things, excessive alcohol consumption produces a deficiency of Thiamine, which is a B complex vitamin, essential in the conduction of nerve signals and in supplying energy to the brain.
Thiamine deficiency reduces protein levels in the thalamus and also modifies neurotransmitter levels in the hippocampus and cerebral cortex. As a consequence, it produces alterations in special memory and increases perseverative behavior. Likewise, some of the long-term consequences include the loss of functions necessary for neuronal plasticity and survival.
Exposure to alcohol in the peri- and postnatal period
There is a large amount of scientific literature that reports various consequences of frequent exposure to alcohol, both in the last phases of the perinatal period and in the first years of life (period in which the human brain is formed).
It is during the early stages of postnatal development that a burst of synaptogenesis, the formation of synapses or connections between neurons, occurs. Several studies agree that ethanol (which has antagonistic properties of glutamate receptors – the main excitatory neurotransmitter in the brain), triggers a harmful and widespread process of apoptosis This is so since said antagonistic activity favors excitotoxic neurodegeneration and abnormal inhibition of neuronal activity.
To put it another way, ethanol prevents the passage of glutamate, which in turn inhibits the formation of synapses, favoring an unnecessary process of programmed neuronal death. The above has been accepted as one of the possible explanations for the reduction in brain mass and human fetal alcohol syndrome in newborns.
It is worth mentioning that neuronal immaturity, characteristic of the first years of human development, It is especially sensitive to different environmental agents that can generate harmful modifications in synaptic connections. Among these agents is ethanol, but it is not the only one, and it can also come from different emitters, often external to the pregnancy itself or the child itself.
Some harmful effects of alcohol on the brain
According to Suzanne M. de la Monte and Jillian J. Kril (2014), the causes of brain degeneration and atrophy in people with alcoholism is continually being debated in the scientific community
In their review of Human Neuropathology Related to Alcohol, published in the journal Acta Neuropathologica, they tell us that the main tissues that prolonged alcohol consumption affects in the mature brain are the following: purkinje and granular cells, and fibers of the white matter. We will briefly explain what the above consists of.
1. Decrease in white matter
The most visible and studied harmful reaction in the brain of people who have consumed alcohol excessively is the decrease in white matter. The clinical manifestations that derive from this range from a subtle or undetectable deterioration, to cognitive wear and tear with significant deficits in executive functions Scientific findings suggest that cortical atrophy resulting from excessive alcohol consumption is associated with a permanent loss of synapses or with significant damage to their functions.
Granule cells are the smallest cells in the brain. They are found in different parts of the cerebellum, adjacent to the purkinje cells, which are a type of neurons known as GABAergic. The latter are some of the largest neurons that have been located so far.
Among other things, they are responsible for regulating sensory and motor functions. Regular alcohol consumption lasting between 20 to 30 years produces a 15% reduction in Purkinje cells, while high consumption during the same years produces a 33.4% reduction (de la Monte and Kril, 2014). The degeneration of these cells in the vermis (space that divides the two cerebral hemispheres) correlates with the development of ataxia; while its loss in the lateral lobes has been related to cognitive alterations.
In summary
In short we can say that alcohol can generate both momentary and permanent deterioration in the activity of nerve cells, a product of important modifications in the structure of said cells and their ability to establish communication.
To a large extent, the severity of the impairment depends on the duration of alcohol exposure, as well as the person’s age and the specific area of the brain where the damage has occurred.
If the damage is permanent then it is neuronal death, but this has only been studied in the case of people whose ethanol consumption is not only recreational, but excessive and prolonged Likewise, the programmed loss of neuronal activity due to exposure to alcohol has been studied during the perinatal period and in organisms with a few years of life.
In the case of excessive and prolonged consumption in adulthood, it is neuronal necrosis due to excitotoxicity; while in the case of exposure during peri- and postnatal development it is non-adaptive apoptosis. In this sense, alcohol consumed in excess for many years, as well as very early contact with said substance, can result in the death of neurons, among other harmful consequences for health.
