Boredom, Depression, and Degenerative Brain Diseases

Is Boredom a Psychological Disorder?


Colleen Merrifield and James Danckert have conducted extensive research concerning characterization of boredom in their article “Characterizing the Psychophysiological Signature of Boredom” (

They purpose of their study was to explore the signature of the subjective experience of boredom. They exposed 72 healthy undergraduates to standardized video clips that were selected to induce boredom, sadness, and a neutral state. Cortisol levels were measured at the arrows in Figure 1 (below).


Their experimental design tested skin conductance, heart rate, and cortisol levels while the undergraduates were watching each video. They hypothesized from previous studies that there was a directional fractionation of autonomic response to boredom that could be measured though heart rate (HR) and skin conductance level (SCL). More specifically, HR and SCL should decrease when attention is focused externally, but HR should increase and SCL should decrease if attention is focused internally. From several of these complex variations between HR and SCL with attention and focus, Merrifield and Danckert determined that one might expect to see an increase in HR and decrease in SCL if boredom is connected with inattention and internal focus; however, both HR and SCL should decrease is boredom is associated with external focus.

The results of their study indicated that boredom yields a “dynamic psychophysiological [response]” that differed significantly from other emotional states. The signature of boredom relative to sadness “was characterized by rising HR, decreased SCL, and increased cortisol levels.” These findings may help resolve differing conceptualizations of boredom in present literature and ultimately enhance the treatment and understanding of clinical maladies in which self-reported boredom is a prominent aspect.

As reported in Table 2 (below), participants’ responses during the boring, sad, and interesting videos were associated with lower HRs, cortisol levels, and higher SCL when compared to the baseline, as well as increased arousal. Although boredom and sadness are two different psychophysiological states, we may still be able to use boredom as a tool to overcome depression because it is a prominent and integral symptom of depression. However, since sadness is a “basic” emotion, and depression is comprised of a variety of affective, behavioral, and cognitive aspects, it is not guaranteed that it will be able to completely “cure” individuals of their depression. It may provide important progress into the insight of what makes up depression, and non-medicated options in which to treat it, as well as other psychophysiological disorders.


Additionally, a practical understanding of how boredom may be related to, or differ from, similar emotional states would greatly expand research on human emotion, which is relatively unexplored. It may also aid our understanding of clinical syndromes that are difficult to treat, and in which boredom is a typical symptom (i.e. depression, bipolar disorder, generalized anxiety disorder).

What Causes Depression?


It is evident that depression is caused by a combination of malfunctions with the structures of the brain, deficiencies/excesses of certain neurotransmitters, as well as individual history.

So, how do neurotransmitters transmit information in the brain, and how could they cause depression or other manic disorders? These particles travel between synapses in the brain, which cause different parts of the brain to release chemicals, hormones, etc. Brain cells produce a certain amount of neurotransmitters that keep movement, mood, learning, and senses at a “normal” level. In individuals who are manic or extremely depressed, this system malfunctions; for example, the receptors may be inaccessible or oversensitive to certain neurotransmitters, which causes their response to its release to be abnormal.


The thalamus receives vast amounts of sensory information, and relays it to the cerebral cortex. The cerebral cortex directs speech, movement, learning, thinking, and other high-level functions. Some studies indicate that bipolar disorder may branch from malfunctions in the thalamus, which would cause defects in the link between sensory input to unpleasant and pleasant feelings.

The hippocampus has an integral role in processing long-term memory and recollection. Interchange between the amygdala and hippocampus is thought to account for our ability to learn from past experiences. In some depressed individuals, the hippocampus can be 9-13% smaller; ongoing exposure to stress hormone impairs the growth of nerve cells in the hippocampus, further preventing recovery.

The amygdala is associated with emotions such as pleasure, anger, sorrow, sexual arousal, and fear. It is activated when an individual recalls emotionally charged memories; amygdala activity is higher when a person is clinically depressed or sad. This elevated activity often continues after recovery from depression.

The following link ( helps to realistically visualize how another brain disease, Alzheimer’s, destroys certain aspects of brain function. It also breaks down which specific parts of the brain do what, in much greater detail than outlined above.

Tramautic brain injury, boredom, and depression

Yael Goldberg and James Danckert’s research, “Traumatic Brain Injury, Boredom, and Depression” ( explores the relationship between boredom and depression in a group of individuals with moderate-to-severe traumatic brain injury (TBI), mild TBI, and healthy controls. Their results suggest that the connection between boredom and depression is strongest with moderate-severe TBI individuals, as well as a strong connection between boredom and depression (across all 3 groups), as shown in Figure 1.

Goldberg and Danckert also discovered that the need for stimulation from the external environment was the integral driver in the relation between boredom and depression (which was again strongest in the moderate-severe TBI group). Their results indicated that a failure to satisfy the need for external stimulation was a common factor underlying boredom and depression; this disconnect was most strongly represented in moderate-severe TBI individuals.


Goldberg indicates that the findings might have propositions for the treatment of generalized depression and brain injury. One proposed therapeutic approach is “behavioural activation therapy”, which entails engaging the patient with self-generated goals with positive reinforcement given for achievement of said goals.

Although their research was extremely thorough, Goldberg and Danckert say that there are important steps in the future of this research, which could include following the development of each “affective state” over time in individuals with varying degrees of TBI. Another step is utilizing structural and practical neuroimaging techniques (such as Diffusion Tensor Imaging) to determine the fundamental bases of boredom and depression in the population they monitored.

Boredom: Clue to Alzheimer’s


Scientists at MIT may have found a way to stimulate an individual’s ability to recover long-term memory. Their new research suggests that expelling boredom may aid memory recovery in patients with degenerative brain diseases, such as Alzheimer’s (

Dr Li-Huei Tsai’s experiment consisted of observing mice with artificially stimulated Alzheimer’s-like ailments when placed in “an enriched environment”. They were given things such as “an exercise treadmill, an array of colourful toys with various shapes and textures that were changed daily, and the companionship of other mice.” When subjected to memory tests, the stimulated mice were more efficient than those who were placed in bare cages. The mice in stimulated environments also had the ability to recover their long-term memories, even after weeks of training. Although their tests were conducted on mice, there is evidence that environmental stimulation also recovers long-term memories in humans.

An unfortunate fact of elderly individuals is that they are often placed in nursing homes, and they are not interacted with as people; their caretakers just view them as helpless children who can’t do anything on their own, and have no independent thought. In environments like these, those with Alzheimer’s often retreat to their own minds and enter a comatose state. The study previously mentioned that there is a strong correlation between stimulation and long-term memory recovery, but they have only tested this in mice. 

In the following video it is evident that audio stimulation helped this man, Henry, emerge from his comatose state (, he is very quiet and doesn’t interact with those around him; Dr. Oliver Sacks, a neurologist describes Henry as an individual with possible depression and Alzheimer’s. After Henry hears the music he is very willing to answer questions and is quite articulate. It appears as though he has the capability of recovering his long-term memory when he is asked questions about his favorite songs, and his past. Henry’s case provides hope and evidence that external stimulation has the ability to draw people out of their mental diseases, and aid in long-term memory recovery in humans.



As seen through much clinical research, it is evident that there is a way to connect boredom and other brain diseases, psychological maladies, and traumatic brain damage. Perhaps complex neurological issues such as Alzheimer’s and depression have an aspect of boredom layered with their other symptoms; if we find a way to combat boredom in these, and other, degenerative brain diseases/injuries.

Since the field human emotion is relatively unexplored, it is quite possible to discover emotional links (or defects in these links) in mental disorders which could lead to non-medicinal treatments for a plethora of diseases. Overall, it seems that stimulation and genuine interaction with individuals has the capability of returning their long-term memory recovery, pushing away some degenerative brain diseases, and aiding in a plethora of other degenerative brain disorders.




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