The 3 most important biological theories of anxiety

Anxiety has become a real epidemic in the 21st century. Many people suffer from this problem in their daily life and in many cases at a pathological level.

We know how to define it, we’ve heard it, some of us are suffering from it right now, but … do we know where it came from? Are we also vulnerable to hearing it?

Of course, anxiety has a psychological part, which can be a big obstacle in everyday life, but it also has a biological part that is by no means overlooked. Here we will examine the biological theories of anxiety and what are their mechanisms involved..

    Biological basis of anxiety

    Since anxiety is a virtually universal phenomenon, its definition is not difficult to understand. It is understood by anxiety the emotional response caused by exposure to a problem or a potentially risky situation, Whether on an emotional, physical or psychological level. Thus, the situations that generate it can be very varied and, depending on how the person experiences them, it will manifest a more or less degree of anxiety.

    But it’s not just individual differences that are responsible for people exhibiting varying degrees of anxiety. The consumption of certain substances is also on average in this response, demonstrating their biological basis.

    It has been seen that certain drugs such as decongestants and psychoactive substances such as caffeine they imply an increase in this emotion. Medical conditions, such as acute myocardial infarction, also make the patient more vulnerable to an episode of anxiety.

    Predisposition to anxiety disorders

    As we said, there is another predisposition to suffer from anxiety and, therefore, to suffer from disorders associated with it. Research has sought to see to what extent biological factors may be involved in a person exhibiting overly exaggerated behavior in the face of a stimulus that may not be as dangerous as they perceive it to be.

    According to the work of Svenn Torgensen (1983), who evaluated the genetic risks of manifestation of an anxiety disorder, hereditary factors seem to play a significant role. saw that about 34% of monozygotic twins and 17% of dicygotic twins shared the diagnosis of an anxiety disorder.

    Components of anxiety

    To better understand anxiety and relate it to the biological theories that attempt to explain it, it is necessary to review the three aspects involved in experiencing this type of emotion.

    1. Cognitive

    Anxiety pops up in the face threatening expectations or overly exaggerated assessments of potential risks of a given stimulus.

    Negative automated thoughts, triggered when the seemingly threatening situation arises, may also be involved.

    2. Physiological

    The autonomic nervous system is activated, causing changes in circulation and respiration, which contributes to the perception of risk as something even more dangerous.

    3. Engines and behavior

    A person can behave in a variety of ways when exposed to the threatening stimulus. Mainly in the face of a dangerous element, one of the following two behaviors is performed: or fight or flight (fight or flight).

    However, other behaviors are possible, such as submission to the individual who poses a threat or the attempt to relax the environment. These behaviors are not considered fighting or fleeing and are common in social animals.

    These three aspects involved in the anxiety experience and response can involve very varied levels of intensity. However, when the intensity is very high and, in addition, no correlation is given between the anxious stimulus and the anxious responseWe are talking about an anxiety disorder. In these cases, the degree of suffering is very high, besides causing great disability to the person and damage both physically, mentally and emotionally.

    How did the anxious response come about?

    The neurological mechanisms that produce and mediate the anxiety response have been studied. The central nervous system, characterized in that it is a complex, dynamic and open system, is the structure involved in this process..

    Before going into detail on how the anxiety response occurs at the organic level, it is necessary to mention what are the structures that make up the central nervous system: spinal cord, medulla oblongata, bulge, midbrain, diencephalon, cerebellum and both cerebral. hemispheres.

    External signals are picked up by the sense organs, which send signals to the peripheral nervous system and then reach the central nervous system. Once they have been processed in the central system, it sends signals to parts of the body to effect an appropriate response.

    External stimuli are processed by different brain structures. First, the stimulus passes through the primary association areas, and then through the secondary areas, where they are combined with information from other stimuli. For example, visual information first passes through the occipital visual area, which is a main area, but so that it can be seen with what is heard (for example, the song of a canary that we see and hear ) will move to the secondary association area.

    One of the structures involved in this process, the importance of which is essential 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 rescue station for information before it reaches the brain and also functions as a filter for it. This avoids sending too much information to the brain, which could lead to true oversaturation.

    Two pathways emerge from the thalamus, responsible for the response to stimuli: the direct thalamic pathway and the indirect thalamic pathway. If the thalamus exhibits some type of dysfunction, such as the inability to prevent certain information from passing to the brain, psychopathology may occur. This has been observed 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 to say the observable behavior that the individual can lead in the face of the potentially harmful element, such as running away from it or treating it. Then we have autonomic expression, such as increased heart rate and increased respiration, and finally changes at the endocrine level, such as the secretion of certain hormones.

    All of the following explanations are biological theories of anxiety, Which, although they do not have a specific name, have attempted to show how the body responds, at the neurological level, to a determining anxiety stimulus, as well as to try to explain the process. Let’s take a closer look.

    1. Motor expression

    The direct thalamic route is, as the name suggests, the shortest and fastest. The thalamus transmits information to the nuclear complex of the amygdala, in which the motor response will be orchestrated. The response to the direct thalamic pathway involves the following pathway: signal (afference) – thalamus – amygdala nuclear complex – response (efference). It involves thoughtless action.

    For example, this circuit is the one that would be used in the event that we get our hands on the lid of a burning pot and quickly withdraw our arm, without thinking about it. The nuclear complex of the amygdala is a subcortical structure, belonging to the limbic system. The role of the amygdala is to coordinate responses related to the expression of anxiety.

    As we have already said, in most cases the motor behavior of the individual in the face of an anxious stimulus can be either flight or struggle, with a few exceptions.

    The thalamic way indirect is longer, involving the following structures: afference – thalamus – prefrontal cortex – amygdala 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 the two pathways are not well coordinated, it is when inappropriate and ineffective responses arise, such as being completely paralyzed in the face of a dangerous stimulus. The functioning of the amygdala is controlled by the prefrontal cortex. Its dorsal part is in charge of executive functions, while the ventral part is the one that inhibits the functioning of the amygdala when necessary.

    2. Autonomous expression

    Autonomous expression of anxiety depends on brainstem nuclei. It is in this structure that the signals of these stimuli that involve damage arrive, in a direct way, such as a puncture with a needle or a burning sensation. They receive information from the amygdala which, as we said, is responsible for coordinating anxious responses.

    When the sympathetic nervous system is activated, changes occur at the organic level, preparing the body for the dangerous situation. The body is on alert, observing the situation and preparing for the worst. These changes include an increased heart rate or tachycardia, as well as an increased respiratory rate. Blood pressure skyrockets and the students shoot.

    By opposition, activation of the parasympathetic system involves responses that would not be appropriate to a threatening situation, Such as bradycardia, the decrease in heart rate, reaching cases where the person is fainting or fainting.

      3. Endocrine expression

      When the amygdala transmits stimuli to the hypothalamus, an important endocrine system is activated, the hypothalamic-pituitary-adrenal axis. The hypothalamus is a structure responsible for controlling the other glands in the body.

      The hypothalamus releases a substance, corticotropin releasing hormone (CRH), which affects the pituitary gland and both structures will impact the whole body by releasing adrenocorticotropin (ACTH).

      Among all the glands that the hormone ACTH will bathe activates the adrenal cortex, which produces corticosteroids. Corticosteroids vary depending on the time of day. They usually secrete the maximum amount of this substance in the morning and are linked to the stress hormone cortisol.

      When a stressful stimulus is present, the hypothalamic-pituitary-adrenal axis is activated and the amount of cortisol in the blood increases. Cortisol involves changes at the organic level, such as increased performance, increased energy, higher pain threshold, reduced inflammatory response, and increased caloric reserve.

      It also allows this to happen an increase in the consumption of carbohydrates, especially sugars. It is for this reason that in stressful situations, people tend to overeat sugary foods, such as ice cream, candy or chocolate.

      When plasma cortisol concentrations are high, the number of cortisol receptors in the hippocampus decreases. This causes a cognitive process such as episodic or biographical memory to be affected.

      By the time the anxiety-inducing stimulus disappears, cortisol decreases, The number of receptors in the hippocampus is recovered and episodic memory returns to a normal state. However, and in situations where the stress is too prolonged, there is a suppression of cortisol production, which has been observed in depression.

      Cortisol in large quantities and in the long term, has a detrimental effect on the neurons of the hippocampus. This causes the number of dendrites to be reduced, in addition to reducing them.

      But not only is cortisol a substance involved in the anxiety response. In states of anxiety, there is also an increased secretion of thyroxine, catecholamines, prolactin, vasopressin and growth hormone.

      What are the experts saying?

      After having seen the biological basis of anxiety, it is time to discuss the main explanations that several scientists have tried to give to the phenomenon.

      Michael S. Eison considers that a disruption of the dynamic interactions between catecholaminergic and serotonergic neurotransmitters occurs in both anxiety and depression. In fact, he argues that manipulation of the serotonergic system affects noradrenergic tone. When there is an alteration in the balance of serotonergic neurotransmission, it contributes to the emergence of psychopathology, feeling anxious in case of mass and depression in case of absence.

      Jeffrey Allan Gray argues that anxiety is generated by stimulation of the behavioral inhibition system, which is located within structures of the limbic system and connects to the brainstem and subcortical regions. This system can be stimulated by indicators of punishment or signs of non-reward and innate fear stimuli.

      Joseph Ledoux attaches importance to the direct thalamic way, Which connects directly to the amygdala. This path is heavily involved in emotional reactions. According to Ledoux, emotional responses initiate this structure, even before they are aware of the stimulus that makes them react with anxiety or even without identifying it.

      Bibliographical references:

      • Stahl, S. (2011) Essential psychopharmacology of Stahl. Volume II. Editorial Aula Mèdica. Madrid.
      • Bauleo, A. – Alvano, AS (2004). Clinic avatars. Drug. Buenos Aires.
      • Fratícola, G. (2008) Neuroanatomy in Psychiatry.
      • Baeza Villarroel, JC (2008). Anxiety clinic. Psychologists specializing in the treatment of anxiety. Madrid and Barcelona
      • Torgensen, S (1983). Genetic factors of anxiety disorders. Archives of general psychiatry. 40 (10), 1085-1089.
      • Lebowitz, M. et al. (2014). Biological explanations of generalized anxiety disorder: effects on beliefs on prognosis and responsibility. Psychiatric services 65 (4). 498 – 503.

      Leave a Comment