The 3 most important biological theories of anxiety.
A summary of the biological theories of anxiety that put the brain under scrutiny.
Anxiety has become a real epidemic in the 21st century. Many people suffer from this problem on a daily basis and, in many cases, at a pathological level.
We know how to define it, we have felt it, some of us suffer from it right now, but... Do we know where it comes from? Do we know where it comes from? Are we equally vulnerable to feel it?
Of course, anxiety has a psychological part, which can be a great impediment to day-to-day life, but it also has a biological part that cannot be ignored. Here we are going to see biological theories of the anxiety and which are their implied mechanisms..
Biological bases of anxiety
Since experiencing anxiety is a practically universal phenomenon, its definition is not difficult to understand. Anxiety is understood as the emotional response caused by being exposed to a problem or situation that may involve a risk, whether emotional, physical or psychological.either at an emotional, physical or psychological level. Thus, the situations that generate anxiety can be very varied and, depending on how the person experiences them, he or she will show a greater or lesser degree of anxiety.
But it is not only individual differences that are responsible for the varying degrees of anxiety in people. The consumption of certain substances also mediates this response, which demonstrates its biological basis.
It has been seen that certain medications such as decongestants and psychoactive substances such as caffeine increase this emotion.. Also medical illnesses, such as acute myocardial infarction, make the patient more vulnerable to suffer an episode of anxiety.
Predisposition towards anxiety disorders
As we were saying, there is a different predisposition to suffer from anxiety and, consequently, to suffer from disorders associated with it. Research has tried to see to what extent biological factors may be involved in a person's overly exaggerated behavior in the face of a stimulus that, perhaps, is not as dangerous as he or she perceives it to be.
According to work done by Svenn Torgensen (1983), who assessed the genetic risks of manifesting an anxiety disorder, hereditary factors appear to play a not insignificant role. He found that about 34% of monozygotic twins and 17% of dizygotic twins shared the diagnosis of an anxiety disorder..
Components of anxiety
In order to understand anxiety a little better and to relate it to the biological theories that try to explain it, it is necessary to review the three aspects involved in the experience of this type of emotion.
1. Cognitive
Anxiety arises in the face of threatening anticipations or overly exaggerated evaluations of the potential risk of a given of a given stimulus.
Automated thoughts that are negative, which are triggered when the apparently threatening situation appears, may also be involved.
2. Physiological
The autonomic nervous system is activated, involving changes at the level of circulation and respiration, which contributes to the perception of the risk as even more dangerous..
3. Motor and behavioral
The person can carry out various types of behavior when exposed to the threatening stimulus. Mainly, in the presence of a dangerous element, one of the following two behaviors is carried out: fight or flight..
However, other behaviors are also possible, such as submission to the threatening individual or trying to defuse the environment. These behaviors are not considered either fight or flight, and are common in social animals.
These three aspects involved in the anxiogenic experience and response can involve widely varying levels of intensity. However, when the intensity is very high and, in addition, there is no correlation between the anxiogenic stimulus and the anxious response, we speak of an anxiety disorder.In these cases, the degree of suffering is very high. In these cases the degree of suffering is very high, in addition to involving great incapacitation for the person and damage both physically, mentally and emotionally.
How is the anxious response mediated?
The neurological mechanisms that produce and mediate the anxious response have been studied. The central nervous system, characterized as a complex, dynamic and open system, is the structure involved in this process..
Before going into detail regarding how the anxiety response occurs at the organic level, it is necessary to mention the structures that make up the central nervous system: spinal cord, medulla oblongata, pons, midbrain, diencephalon, cerebellum and the two cerebral hemispheres.
Signals from the outside are picked up by the sense organs, which send signals to the peripheral nervous system and subsequently reach the central nervous system. Once they have been processed in the central system, the central system sends signals to the parts of the organism to carry out an appropriate response.
Stimuli from the outside are processed by different structures in the brain.. First, the stimulus passes through the primary association areas and then through the secondary association areas, where it is combined with information from other stimuli. For example, visual information first passes through the occipital visual area, which is a primary area, but in order to match what is seen with what is being heard (for example, the song of a canary that we are seeing and hearing) it will pass to the secondary association area.
One of the structures involved in this process, whose importance is key in the manifestation of anxiety, is the thalamus. The thalamus is located in the diencephalon and has two main functions: it is a kind of relay station for information before it reaches the diencephalon. for information before it reaches the encephalon and, in addition, it works as a filter for it. In this way, it avoids sending too much information to the brain, which could lead to real oversaturation.
Two pathways arise from the thalamus, responsible for responding to stimuli: the direct thalamic pathway and the indirect thalamic pathway. If the thalamus presents some kind of dysfunction, such as not being able to prevent certain information from passing to the encephalon, psychopathology may occur. This has been seen in disorders such as schizophrenia and also in anxiety disorders.
Biological theories of anxiety
The anxious response involves up to three types of expression. On the one hand we have the motor, that is, the observable behavior that the individual can carry out before the potentially harmful element, as it would be to flee from it or to face it. Then we have the autonomic expression, such as the increase of the heartbeat and the increase of respiration and, finally, the changes at the endocrine level, such as the secretion of certain hormones.
All the following explanations are biological theories of anxiety.The first is the "anxiolytic stimuli", which, although they do not have a specific name, have tried to demonstrate how the organism responds, at a neurological level, to a given anxiogenic stimulus, in addition to trying to explain the process. Let's see them in more depth.
1. Motor expression
The direct thalamic pathway is, as its name suggests, the shortest and fastest. The thalamus passes the information to the amygdaloid nuclear complex, where the motor response is orchestrated. The response in the direct thalamic pathway involves the following pathway: signal (afferent) - thalamus - amygdaloid nuclear complex - response (efferent). It involves action without thought.
For example, this circuit is the one that would be used in case we put our hand on the lid of a pot that is burning and quickly withdraw our arm, without thinking about it. The amygdaloid nuclear complex is a subcortical structure, belonging to the limbic system. The amygdala has the role of coordinating the responses linked to the expression of anxiety..
As we have already said, in most cases, the motor behavior of the individual in the face of an anxiogenic stimulus can be either to flee or to fight, with some exceptions.
The indirect thalamic pathway is longer, involving the following structures: afferent - thalamus - prefrontal cortex - amygdaloid nuclear complex - efferent (motor response). This cortical response is more elaborate, more integrated and sophisticated.. The difference between the direct and indirect thalamic pathway is that the former is about 300 milliseconds faster than the latter.
When both pathways are not well coordinated is when inappropriate and inefficient responses appear, such as being totally paralyzed in front of a dangerous stimulus. The functioning of the amygdala is controlled by the prefrontal cortex. Its more dorsal part is in charge of executive functions, while the ventral part is the one that inhibits the amygdala's functioning when necessary.
2. Autonomic expression
The autonomic expression of anxiety is dependent on the brainstem nuclei. It is in this structure where the signals of those stimuli that involve some damage, such as being pricked by a needle or feeling a burn, arrive directly. They receive information coming from the amygdala, which, as we were saying before, is in charge of coordinating anxious responses.
When the sympathetic nervous system is activated, changes occur at the organic level, preparing the organism for the dangerous situation. The organism is in a state of alert, watching how the situation is going to evolve and preparing for the worst. These changes include an increased heart rate or tachycardia, as well as an accelerated respiratory rate. Blood Pressure shoots up and the pupils are triggered.
In contrast, the activation of the parasympathetic system involves responses that would not be adaptive to a threatening situation, such as bradycardia.In contrast, the activation of the parasympathetic system involves responses that would not be adaptive to a threatening situation, such as bradycardia, decreased heart rate, and even cases in which the person suffers a syncope or faints.
3. Endocrine expression
When the amygdala transmits stimuli to the hypothalamus, an important endocrine system, the hypothalamic-pituitary-adrenal axis, is activated. The hypothalamus is a structure that is responsible for the control of the other glands of the organism.
The hypothalamus releases a substance, adrenocorticotropic hormone-releasing hormone (CRH), which impacts the pituitary gland and both structures will impact the whole organism by releasing adrenocorticotrophin (ACTH).
Among all the glands that the ACTH hormone will bathe is the adrenal cortex, which produces corticosteroids.. Corticosteroids vary depending on the time of day. Normally the maximum amount of this substance is secreted in the morning and is related to the stress hormone cortisol.
When a stressful stimulus is presented, the hypothalamic-pituitary-adrenal axis is activated and the amount of cortisol in the blood increases. Cortisol implies changes at the organic level, such as increased performance, increased energy, increased pain threshold, decreased inflammatory response and promotes caloric reserve.
It also causes an increased intake of carbohydrates, especially sugars, and an increase in the. It is for this reason that in stressful situations people tend to binge on sweet foods, such as ice cream, candy or chocolate.
When plasma cortisol concentrations are high, the number of receptors for this substance in the hippocampus decreases. This affects a cognitive process such as episodic or biographical memory.
When the anxiogenic stimulus disappears, cortisol decreases, the number of receptors for this substance in the hippocampus recovers.The number of receptors in the hippocampus recovers and episodic memory returns to a normal state. However, and in situations where stress is too prolonged, there is a suppression of cortisol production, something that has been seen in depression.
Cortisol in large quantities and in the long term, produces a damaging effect on the neurons of the hippocampus.. It causes the number of dendrites to decrease, as well as dwarfing them.
But not only cortisol is a substance involved in the anxiogenic response. In states of anxiety there is also an increase in the secretion of thyroxine, catecholamines, prolactin, vasopressin and growth hormone.
What do the experts say?
Having seen the biological bases of anxiety, the time has come to mention the main explanations that several scientists have tried to give to the phenomenon.
Michael S. Eison considers that a disturbance of the dynamic interactions between catecholaminergic and serotonergic neurotransmitters occurs in both anxiety and depression. In fact, he argues that a manipulation of the serotonergic system affects noradrenergic tone. When there is a disturbance in the balance of serotonergic neurotransmission, it contributes to the onset of psychopathology, being anxiety when there is too much and depression when there is an absence..
Jeffrey Allan Gray argues that anxiety is generated by stimulation of the behavioral inhibition system, which is located in the limbic system structures and connects with the brainstem and subcortical regions. This system can be stimulated by punishment cues or non-reward signals, and innate fear stimuli.
Joseph Ledoux gives importance to the direct thalamic pathway, which connects directly to the brain stem and subcortical regions.which connects directly with the amygdala. This pathway is heavily involved in emotional reactions. According to Ledoux, emotional responses start in this structure, even before we are aware of the stimulus that makes us react in an anxiogenic way or even without identifying it.
Bibliographical references:
- Stahl, S. (2011) Stahl's Essential Psychopharmacology. Volume II. Editorial Aula Médica. Madrid.
- Bauleo, A. - Alvano, A. S. (2004). Avatars of the clinic. Mediciencia. Buenos Aires.
- Fratícola, G. (2008) Neuroanatomy in psychiatry.
- Baeza Villarroel, J. C. (2008). Clinical Anxiety. Psychologists specializing in the treatment of anxiety. Madrid and Barcelona
- Torgensen, S (1983). Genetic factors in anxiety disorders. Archives of General Psychiatry. 40(10), 1085 - 1089.
- Lebowitz, M. et al. (2014). Biological Explanations of Generalized Anxiety Disorder: Effects on Beliefs About Prognosis and Responsibility. Psychiatric Services 65(4). 498 - 503.
(Updated at Apr 14 / 2024)