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 researches it has been possible to know some of the consequences of consuming in excess chemical compounds such as ethanol.

Since then , the belief that alcohol kills brain cells has become very popular . How true is this? Let’s see it in the following text.

How do neurons die?

To begin we will briefly recall the life cycle of neurons and what we understand by “neuronal death”. As with the various cell populations that make up our bodies, nerve cells (neurons) act by a proliferation mechanism that includes cell loss, cell renewal and cell differentiation.

The death of a cell is defined as the arrest of its biological processes by irreversible morphological, functional and biochemical modifications that prevent it from performing 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, preventing the ability to function . And the latter does not necessarily correspond to a decrease in the volume of cells within the affected areas. Let us 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 the neuron’s functions due to the influence of external factors. In this process the cells are not always phagocytes (that is, they do not completely disintegrate within the organism, which can bring about other medical complications), but they are considered dead because they lose the capacity to be activated and to produce connections between themselves.

Having said that, we will see what is the toxic mechanism that produces the consumption of alcohol 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 (the recreational alcohol) vary according to the specific brain region in which they act. Also vary according to age or stage of development, dose, and duration of exposures .

When it comes to the mature brain, chronic or intense exposure to ethanol can cause various diseases of both the central and peripheral nervous systems, as well as skeletal muscle (de la Monte and Kril, 2014).

The consequence is that, in the long term, excessive alcohol consumption significantly impairs executive functions. In other words, alcohol can lead to degenerative activity of the nervous system, as it gradually deteriorates the function of neurons, including the ability of neurons to survive, cell migration and glial cell structures. While the latter does not mean that the neurons necessarily disintegrate, it does imply the definitive loss of their functions, which falls within 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 the special memory and increases perseverative behaviour. Likewise, some of the long-term consequences include the loss of functions necessary for plasticity and neuronal survival.

Peri- and post-natal alcohol exposure

There is a large body of scientific literature reporting several of the consequences of frequent exposure to alcohol, both in the late perinatal period and in the first years of life (the period in which the human brain is formed).

It is during the early stages of postnatal development when an explosion of synaptogenesis occurs, the formation of synapses or connections between neurons. Several studies agree that ethanol (which has antagonistic properties to glutamate receptors – the main excitatory neurotransmitter in the brain), triggers a harmful and widespread process of apoptosis . This is because this antagonistic activity favours excitotoxic neurodegeneration and abnormal inhibition of neuronal activity.

In other words, ethanol blocks the passage of glutamate, which in turn inhibits the formation of synapses, encouraging an unnecessary process of programmed neuronal death. This has been accepted as one of the possible explanations for the reduction of brain mass and human fetal alcohol syndrome in newborns.

It is worth mentioning that the neuronal immaturity, characteristic of the first years of human development, is especially sensitive to different environmental agents that can generate harmful modifications in the synaptic connections. Among these agents is ethanol, but it is not the only one, and furthermore, it can come from different emitters, often external to the pregnancy itself or the child.

Some Harmful Effects of Alcohol on Februle

According to Suzanne M. de la Monte and Jillian J. Kril (2014), the causes of brain degeneration and atrophy in people with alcoholism are continuously debated in the scientific community .

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In their review on Alcohol-Related Human Neuropathology, 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 white matter fibers. We will briefly explain what this consists of.

1. Decrease in white matter

The most visible and studied harmful reaction of the brain of people who have consumed alcohol excessively is the decrease of white matter. The clinical manifestations that derive from this range from subtle or undetectable impairment to cognitive decline with significant deficits in executive functions . The scientific findings suggest that cortical atrophy resulting from excessive alcohol consumption is associated with a definite loss of synapses or with significant impairment in their functions.

2. Granular cells and purkinje cells

Granular cells are the smallest cells in the brain. They are found in different parts of the cerebellum, bordering on the purkinje cells, which are a type of neuron known as GABAergic. The latter are some of the largest neurons that have been located so far.

Among other things, they regulate sensitive and motor functions. A regular consumption of alcohol that lasts between 20 and 30 years produces a 15% reduction in Purkinje cells, while high consumption during the same years produces 33.4% (de la Monte and Kril, 2014). The degeneration of these cells in the vermis (the space that divides the two brain hemispheres) correlates with the development of ataxia; while their loss in the side lobes has been associated with cognitive impairment.

In summary

In summary, we can say that alcohol can generate both a momentary and permanent deterioration in the activity of nerve cells, as a result of important modifications in the structure of these cells and their ability to establish communication.

To a large extent the severity of the impairment depends on the length of exposure to alcohol, 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 during the perinatal period and in organisms with few years of life has been studied.

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 over many years, as well as very early contact with that substance, can result in the death of neurons, among other harmful consequences for health.

Bibliographic references:

  • De la Monte, S. & Kril, J. (2014). Human alcohol-related neuropathology. Acta Neuropathologica, 127: 71-90.
  • Creeley, C. & Olney, J. (2013). Drug-Induced Apoptosis: Mechanism by which Alcohol and Many Other Drugs Can Disrupt Brain Development. Brain Sciences, 3: 1153-1181.
  • Tokuda, K., Izumi, Y., Zorumski, CF. (2011). Ethanol enhances neurosteroidogenesis in hippocampal pyramidal neurons by paradoxical NMDA receptor activation. Journal of Neuroscience, 31(27): 1660-11.
  • Feldstein, A. & Gores, G. (2005). Apoptosis in alcoholic and nonalcoholic steatohepatitis. Frontiers in Bioscience, 10: 3093-3099.
  • He, J., Nixon, K., Shetty, A. & Crews, F. (2005). Chronic alcohol exposure reduces hippocampal neurogenesis and dendritic growth of newborn neurons. European Journal of Neuroscience, 21(10): 2711-2720.
  • Olney, J. (2002). New Insights and New Issues in Developmental Neurotoxicology. NeuroToxicology, 23(6): 659-668.
  • Goodlett, C. & Horn, K. (2001). Mechanisms of Alcohol-Induced Damage to the Developing Nervous System. Alcohol Research and Health. 25(3): 175-184.
  • Sánchez, V. (2001). Regulatory mechanisms of non necrotic cell death. Revista Cubana de Investigaciones Biomédicas, 20(4): 266-274.