The 3 Most Important Biological Theories Of Anxiety

A summary of the biological theories of anxiety that put the brain under scrutiny.

Biological theories of anxiety

Anxiety has become a true epidemic in the 21st century. There are many people who suffer from this problem in their day to day 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? Are we equally vulnerable to feeling 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 is not at all overlooked. Here we are going to see biological theories of anxiety and what are its mechanisms involved.

Biological bases of anxiety

Since experiencing anxiety is a practically universal phenomenon, its definition is not difficult to understand. Anxiety is understood to be the emotional response caused by being exposed to a problem or situation that may involve a risk, either emotionally, physically or psychologically. Thus, the situations that generate it can be very varied and, depending on how the person experiences them, they will manifest a greater or lesser degree of anxiety.

But not only individual differences are responsible for people manifesting varying degrees of anxiety. The use of certain substances also mediates this response, which shows its biological basis.

Certain medications such as decongestants and psychoactive substances such as caffeine have been shown to increase this emotion. Also medical diseases, such as acute myocardial infarction, make the patient more vulnerable to suffering an episode of anxiety.

Predisposition towards anxiety disorders

As we were already saying, there is a different predisposition to suffer anxiety and, consequently, to suffer disorders associated with it. Research has tried to see to what extent biological factors may be involved in a person displaying excessively exaggerated behavior when faced with a stimulus that, perhaps, is not as dangerous as perceived.

According to work by Svenn Torgensen (1983), who evaluated the genetic risks of manifesting an anxiety disorder, hereditary factors seem to play a not inconsiderable role. He found that about 34% of monozygotic twins and 17% of dizygotic twins shared the diagnosis of an anxiety disorder.

Components of anxiety

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

1. Cognitive

Anxiety arises from threatening anticipations or overly exaggerated evaluations of the potential risk of a certain stimulus.

Negative automated thoughts may also be involved, which are triggered when the seemingly threatening situation appears.

2. Physiological

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

3. Movers and behavior

The person can carry out various types of behavior when exposed to the threatening stimulus. Mainly, when faced with a dangerous element, one of the following two behaviors is carried out: or fight or flight (fight or flight).

However, other behaviors are possible, such as submission to the individual who poses a threat or trying to de-stress the environment. These behaviors are neither considered fighting nor fleeing, and are common in social animals.

These three aspects involved in the anxiety experience and response can involve very different levels of intensity. However, when the intensity is very high and, in addition, there is no correlation between the anxiety stimulus and the anxious response, we speak of an anxiety disorder. In these cases, the degree of suffering is very high, as well as being a 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 anxiety response have been studied. The central nervous system, characterized by being 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 what are the structures that make up the central nervous system: spinal cord, medulla oblongata, pons, midbrain, diencephalon, cerebellum and both brain hemispheres..

The 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, it sends signals to the parts of the body to carry out an appropriate response.

Stimuli from the outside are processed by different brain structures. First, the stimulus passes through the primary association areas, and then through the secondary areas, in which they are combined with information from other stimuli. For example, visual information first passes through the occipital visual area, which is a primary area, but so that what is seen can be seen with what is being heard (for example, the song of a canary that we are seeing and hearing) 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 brain, and it also works as a filter for it. In this way, you avoid sending too much information to the brain, which could be a true oversaturation.

Two pathways emerge from the thalamus, responsible for responding to stimuli: the direct thalamic pathway and the indirect thalamic pathway. If the thalamus presents some type of dysfunction, such as not being able to prevent certain information from passing at the brain level, 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 in the face of the potentially harmful element, such as fleeing from it or dealing with it. Then we have the autonomic expression, such as the increase in the heart beat and the increase in respiration and, finally, the changes at the endocrine level, such as the secretion of certain hormones.

All the explanations that follow are biological theories of anxiety, which, although they do not have a specific name, have tried to demonstrate how the body responds, at a neurological level, to a determining anxiety stimulus, in addition to trying to explain the process . Let’s take a closer look at them.

1. Motor expression

The direct thalamic route is, as its name suggests, the shortest and fastest. The thalamus passes the information to the amygdala nuclear complex, in which the motor response will be orchestrated. The response in the direct thalamic pathway involves the following path: signal (afference) – thalamus – amygdalin nuclear complex – response (efference). 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 burned and we quickly withdraw our arm, without thinking. The amygdala nuclear complex is a subcortical structure, belonging to the limbic system. The amygdala has the role of coordinating responses related to the expression of anxiety.

As we have already said, in most cases, the individual’s motor behavior in the face of an anxiogenic stimulus can be either flee or fight, with few exceptions.

The indirect thalamic pathway is longer, involving the following structures: afference – thalamus – prefrontal cortex – amygdalin nuclear complex – efference (motor response). This cortical response is more elaborate, more integrated, and sophisticated. The difference between the direct and indirect thalamic pathways 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 when faced with a dangerous stimulus. The functioning of the amygdala is controlled by the prefrontal cortex. Its most dorsal part is responsible for executive functions, while the ventral part is what inhibits the functioning of the amygdala when necessary.

2. Autonomic expression

The autonomic expression of anxiety depends on the nuclei of the brainstem. It is in this structure where the signals of those stimuli that involve some damage arrive, directly, such as being pricked with a needle or feeling a burn. They receive information from the amygdala, which, as we were already saying, is responsible for coordinating anxious responses.

When the sympathetic nervous system is activated, changes occur at the organic level, preparing the organism for the dangerous situation. The body is in a state of alert, monitoring how the situation will evolve and preparing for the worst. These changes include an increase in heart rate or tachycardia, in addition to having an accelerated respiratory rate. Blood pressure skyrockets and pupils skyrocket.

In contrast, the activation of the parasympathetic system supposes responses that would not be adaptive to a threatening situation, such as bradycardia, a decrease in heart rate, reaching cases in which the person suffers 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 body.

The hypothalamus releases a substance, adrenocorticotropic hormone releasing hormone (CRH), which impacts on the pituitary gland and both structures will impact the entire body through the release of adrenocorticotropin (ACTH).

Among all the glands that the hormone ACTH will bathe, the adrenal cortex, which produces corticosteroids, stands out. Corticosteroids vary based on the time of day. Normally, the maximum amount of this substance is secreted in the morning and they are related to cortisol, the stress hormone.

When a stressful stimulus occurs, 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 greater performance, an increase in energy, a higher pain threshold, a decrease in the inflammatory response and promotes the reserve of calories.

It also causes an increase in carbohydrate intake, especially sugars. It is for this reason that in stressful situations people tend to binge on sweet foods, such as ice cream, candy or chocolate.

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

As soon as the anxiety stimulus disappears, cortisol is diminished, the number of receptors in the hippocampus recovers, and episodic memory returns to a normal state. However, and in situations in which stress is too prolonged, there is a suppression of cortisol production, something that has been seen in depression.

Cortisol in large amounts and long-term, produces a damaging effect on neurons in the hippocampus. It causes the number of dendrites to be decreased, in addition to making them smaller.

But not only cortisol is a substance involved in the anxiety response. In anxiety states 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 various 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 maintains that a manipulation of the serotonergic system affects the noradrenergic tone. When there is an alteration in the balance of serotonergic neurotransmission, it contributes to the appearance of psychopathology, being anxiety when there is too much and depression when there is an absence.

Jeffrey Allan Gray argues that anxiety is generated from the stimulation of the behavioral inhibition system, which is located in the structures of the limbic system and connects with the brain stem and subcortical regions. This system can be stimulated by indicators of punishment or signals of no reward, and innate stimuli of fear.

Joseph Ledoux attaches importance to the direct thalamic pathway, which connects directly to the amygdala. This pathway is highly involved in emotional reactions. According to Ledoux, emotional responses start in this structure, even before being aware of the stimulus that causes them to react anxiously or even without identifying it.

Bibliographic references:

  • Stahl, S. (2011) Stahl’s Essential Psychopharmacology. Volume II. Editorial Aula Médica. Madrid.
  • Bauleo, A. – Alvano, AS (2004). Clinic avatars. Medicine. 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 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.

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