Motivation and emotion/Book/2015/Lövheim cube of emotion

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Lövheim's cube of emotion:
What is the Lövheim cube of emotion?


Overview[edit]

This chapter examines the Lövheim cube of emotion (2012), how it was developed, and how it can be applied to better understand and improve our emotional lives. This theory was developed in 2012, so should be viewed critically, as it has not been specifically tested for its accuracy. Some of Lövheim's (2012) research into the neurotransmitters and their interaction with emotion is based on general assumptions, as well as limited available knowledge and theory. Despite the lack of focused research into the accuracy and reliability of the model, it still has the potential to improve our emotional lives, especially in the area of mental health.

What is it?[edit]

Figure 1. Diagram of Lövheim's cube of emotion.

[Provide more detail]

The Cube of Emotion[edit]

Lövheim's cube of emotion (2012), is a theoretical model that focuses on the interactions of monoamine neurotransmitters and the emotions we feel. A diagram of this model is shown in Figure 1. The model was created combining neurotransmitter system research and theories of 'basic' emotions, to examine how different levels of these neurotransmitters (dopamine, noradrenaline (norepinephrine), and serotonin) are linked with previously defined 'basic' emotional states (Lövheim, 2012). While the axes in this model appear to be somewhat unrelated, these neurotransmitters should not be considered independent, as there are likely to be a number of complex biological and cognitive systems involved in emotion (Lövheim, 2012). It is important to note that these neurotransmitters and their receptors do not have ultimate control over emotion. They may, however, create the pathway for emotional information to be delivered to larger brain areas, such as the cerebral cortex (Lövheim, 2012). As can be seen in Figure 1, each corner of the cube has two emotion labels, based on Tomkins (1981) 'basic' emotions. These two labels show the high and low intensities of the emotion, with the corner being the extreme and maximum emotional intensity (Lövheim, 2012). The lower intensity of the emotion is thought to be located between the corner and the centre of the cube, which represents a neutral state.

For the purposes of this model, Lövheim (2012) stated that the serotonin axis represents self-confidence, inner strength, and satisfaction; the dopamine axis shows levels of reward, motivation, and reinforcement; while the noradrenaline axis represents activation, vigilance, and attention.

Table 1. Levels of the neurotransmitters involved in the emotions in Lövheim's cube of emotion (2012).

Emotion Serotonin Dopamine Noradrenaline
Distress/Anguish Low Low High
Anger/Rage Low High High
Fear/Terror Low High Low
Shame/Humiliation Low Low Low
Disgust/Contempt High Low Low
Joy/Enjoyment High High Low
Interest/Excitement High High High
Surprise High Low High

How was it developed?[edit]

Lövheim (2012) used research conducted on 'core' or 'basic' emotions, combined with literature on monoamine neurotransmitter activity to develop his three-dimensional model, to examine the interaction between the two.

Tomkins' Theory of Basic Emotions[edit]

A theory of these 'innate' emotions was devised by Tomkins (1981), who defined "affect" as the entirely biological component of emotion, thus 'basic' emotions are those considered inherently common. Tomkins (1981) believed there are eight basic emotions and gave each of these two labels: one for a low intensity, and one for high intensity. These labels and intensities guided how Lövheim (2012) developed and created his model of emotion.

While analysing emotions, Tomkins (1981) discusses the role of unlearned responses, and their connection to affect. He states that there are multiple circumstances that can evoke the one affect, or response (Tomkins, 1981). One example of this is innate fears, such as jumping at a loud bang or being afraid of the dark. Another example is feeling happier after a hug from a parent or friend. Especially in children, these are unlearned responses and demonstrate that neurological stimulation influences emotions, whether its an external or internal event (Tomkins, 1981). In addition to this, Tomkins (1981) discussed that any sudden event or experience causes a sharp increase in neural firing that automatically creates the affect in response. The rate of increase and the frequency, or density, of the neural firing, will determine what emotional response is caused (Tomkins, 1981). One example Tomkins (1981) uses is fear/terror and interest. If the neurons fire rapidly after an experience, terror is the affect in response. If they fire slightly slower, fear is the affect activated, and if it increases at an even slower rate, then an interest in the stimuli is sparked.

Although Tomkins (1981) focused on external experiences and the physiological responses, he did acknowledge that internal and cognitive experiences influence emotions, by both reacting to the affect or causing it. Despite this acknowledgement, Tomkins (1981) believes that affect is the primary cause of emotion because they are shown from birth. According to Tomkins (1981), there has been a cognitive bias that influences ideas about how and when emotions begin that undermine the importance of the biological factors of emotion.

It is clear, through the labelling of emotions and their intensity, and the differences in the density of neural firing, that Lövheim's cube of emotion (2012) has been developed from a comprehensive and valid emotional theory.

Interaction between neurotransmitters and emotions[edit]

The other factor that contributed to the development of this model were monoamine neurotransmitters. Lövheim (2012) used previous literature and assumptions about the effects of these neurotransmitters to assess how they may interact with Tomkins' (1981) 'basic' emotions. This was how he developed and labelled the three-dimensional model.

Fear/Terror and Anger/Rage[edit]

It is important to note that in this model, fear/terror is not the 'fight or flight' response that is often associated with situations that instill fear (Lövheim, 2012). Instead, it should be thought of as 'cold' fear, where the heart seems to slow and almost stops (Lövheim, 2012). Fear/terror is low in serotonin, as it coincides with feelings and perceptions of threat, which is the opposite of the assumed representation of serotonin on its axis (Lövheim, 2012).

Image 1. Angry cat.

Fear/terror and anger/rage are supposedly high in dopamine and coupled to reinforcement and learning, according to Lövheim (2012), which is evident from evolutionary learning about dangerous situations, whether real or perceived, that trigger these emotions. The rewarding aspect of these emotions may also explain why people learn to seek out adrenaline rushes or fear-inducing situations, like horror movies, because it is learnt, reinforced, and considered enjoyable (Lövheim, 2012).

In this model, the 'fight or flight' response is not linked to fear/terror, but it is closely tied to the emotion of anger/rage, as it is high in noradrenaline, shown through the red face and high pulse associated with anger (Lövheim, 2012). Anger/rage has been assumed to be low in serotonin, similar to fear/terror, as an individual commonly experiences these emotions when threatened (Lövheim, 2012). Anger has also been noted as a symptom in patients with depression which, according to Lövheim (2012), warrants its low placement on the serotonin axis.

Interest/Excitement[edit]

Interest/excitement is thought to involve high levels of all three neurotransmitters (Lövheim, 2012). This means that, according to the model, this emotion requires attention, reinforcement and linked to a feeling of inner strength (Lövheim, 2012). Lövheim (2012) believes this is evident through the motivating and reinforcing effects of dopamine, the absence of anhedonia, and the high noradrenaline associated with sexual excitement and other positive experiences.

Enjoyment/Joy[edit]

Enjoyment/joy is the low-noradrenaline version of interest/excitement (Lövheim, 2012). The main difference between these two emotions is that when an individual is experiencing enjoyment/joy, they are calm and relaxed (Lövheim, 2012). In this model, enjoyment/joy is thought to be high in serotonin, but does not have supporting evidence in Lövheim's proposal (2012). Enjoyment/joy is thought to be high in dopamine yet, similar to its' high serotonin levels, has no supporting evidence (Lövheim, 2012).

Contempt/Disgust[edit]

Contempt/disgust is seen as low in noradrenaline and dopamine in this model, but high in serotonin (Lövheim, 2012). It takes this place on the model because Lövheim (2012) believes that food-related disgust is related to feelings of hunger being satisfied, in its most extreme intensity. Another factor that led Lövheim (2012) to believe that contempt/disgust has high levels of serotonin is its relationship with shame/humiliation. Lövheim (2012) describes shame/humiliation as self-contempt and contempt/disgust as contempt for an object, and that this, based on the representation of the serotonin axis, shows inner strength and self-confidence as opposed to shame/humiliation. It is also assumed that contempt/disgust is low in dopamine because it relates to repulsion and withdrawal, which is the opposite to effects seen in emotions with high dopamine (Lövheim, 2012).

Surprise[edit]

Surprise is thought to be the non-reinforcing emotion related to excitement, and provokes an incredibly attentive and focused state, which justifies its position on the cube on the corner showing high levels of noradrenaline and serotonin (Lövheim, 2012). According to the representations of the axes, surprise could be thought of as positive or negative, as it incorporates an element of self-confidence and strength from the serotonin, and the activation, vigilance, and attention from the noradrenaline axis (Lövheim, 2012).

Distress/Anguish[edit]

Distress/anguish is believed to be the active version of shame/humiliation, and a physiological example of the extreme end of this basic emotion is a panic attack (Lövheim, 2012). The relationship between serotonin and depression, in that serotonin levels can influence mood in such a way that it may lead to depression, supports the placement of these basic emotions on the low serotonin side of the cube (Lövheim, 2012). In addition to this, the effect of Selective Serotonin Reuptake Inhibitors (SSRIs) when treating depression and anxiety justify this reasoning (Lövheim, 2012). There is also evidence to support a relationship between low dopamine activity and anxiety, further supporting the placement of distress (Lövheim, 2012).

Shame/Humiliation[edit]

The only emotion in the model that is not shown to have an influence by these neurotransmitters is shame/humiliation. According to Lövheim (2012), this emotion is where the individual feels defeated and unworthy and that this makes it clear, when remembering what each axis represents, that this is where this emotion belongs.

While these justifications of the dimensions and labelling of the model are logical and have some evidence in literature, there is still a considerable amount of research to be done to assess the theory's validity and accuracy. This is particularly crucial when considering the implications of this model, as the emotional descriptions and support for their placement within the cube are also based on Lövheim's (2012) and Tomkins' (1981) opinions and interpretations of both previous research and their personal emotional perception.

Does this theory help us understand our emotional lives?[edit]

There is a significant amount of research still to be conducted to determine the validity and reliability of this model, particularly where the interaction between the neurotransmitters and emotions are concerned (Lövheim, 2012). According to Lövheim (2012), cognitive processes are likely to play a part in emotion and, despite not being acknowledged within the model, does not discredit his theory. Extreme emotions have a complex relationship with risky and impulsive behaviour, and while biology may be a beginning factor of the extremity, cognition and attempts to regulate emotions generate well-planned action (Cyders & Smith, 2008).

Another key limitation of this theory that should be considered before it can be deemed reliable is that it only includes three neurotransmitters, when there are many more, including more interactions between these three, that could influence emotion. Other biological aspects should be studied in relation to this as well. Cyders and Smith (2008) also note that the functions of any neurotransmitters are complicated.

Lastly, there has been one major omission from the basic emotions used for the design of this model: sadness. While distress/anguish, shame/humiliation, and disgust/contempt can all be experienced as a form of sadness, they are all caused by different circumstances. If the model truly wishes to explain basic emotions, sadness should be included as its own corner. There may also be other emotions that deserve a place within this model that should also be included.

What do we already know about these neurotransmitters?[edit]

Understanding these neurotransmitters as elements outside of this model will help us to examine potential uses and applications for the future. For more in-depth descriptions of these neurotransmitters, and their relationships with emotions, see the see also section.

Serotonin[edit]

  • Regulates mood, appetite and impulse control (Blaszczynski, Tait, & Mattick, 2014)
  • Low serotonin is associated with risky behaviour, impulsivity, aggression and increased emotion-based engagement with irrational behaviour (Cyders & Smith, 2008; Kalat, 2012)
  • Activity relevant to depressed mood and symptoms (Kalat, 2012; Thagard, 2008)
  • Relevant to alleviating distress systems (Pringle, McCabe, Cowen, & Harmer, 2013)
  • Serotonin release is increased by alcohol consumption, which may contribute to aggression and violence in social drinking situations (Chastain, 2006)
  • Interrupts REM sleep (Kalat, 2012)

Dopamine[edit]

  • High dopamine associated with three dimensions of Borderline Personality Disorder: emotional dysregulation, impulsivity, and cognitive perception impairment. (Cyders & Smith, 2008)
  • Thought to influence behaviour seen in Attention Deficit Hyperactive Disorder, and behavioural disinhibition (Cyders & Smith, 2008)
  • Key factor in biological models of schizophrenia (see External Links) (Blaszczynski, Tait, & Mattick, 2014; Kalat, 2012; Thagard, 2008)
  • Associated with reward sensitivity, cravings and memory (Blaszczynski, Tait, & Mattick, 2014)
  • Regulates emotional and motivational changes in individuals suffering from general withdrawal (Blaszczynski, Tait, & Mattick, 2014)

Noradrenaline[edit]

  • Regulates mood (Blaszczynski, Tait, & Mattick, 2014)
  • Plays a crucial role in arousal and excitement (Blaszczynski, Tait, & Mattick, 2014; Goddard et al., 2010)
  • Drugs that act on the noradrenaline system effectively reduce symptoms related to anhedonia in depression, when compared with serotonin (Pringle, McCabe, Cowen, & Harmer, 2013)
  • Helps us adapt to stressors, both internal and external, to maintain an equilibrium to prevent persistent arousal of the noradrenaline system (Goddard et al., 2010)
  • Increased arousal and firing of noradrenaline can cause damage to this system, and its homeostasis, and generate chronic stress, even leading to mental illnesses like depression or anxiety (Goddard et al., 2010)

Interactions[edit]

Serotonin and dopamine have been shown to influence decision-making: while dopamine encourages impulsive behaviour and desire to act, serotonin appears to reduce this urge, so the individual can consider options and consequences which leads to significantly reduced impulsivity (Cyders & Smith, 2008)

How could this model help us improve our emotional lives?[edit]

Despite the infancy of this theory, there are still a number of ways that we could apply this model and what we already know about neurotransmitters to improving our emotional lives.

Understanding mental illness[edit]

Knowing more about the neurological and experiential causes of mental illness can increase the accuracy of diagnosis and improve both psychotherapy and psychopharmacology treatment outcomes.

Treating Mental Illness[edit]

This model has the potential to assist the understanding and treatment of mental illness through the neurotransmitter interactions that occur in drug treatments (Lövheim, 2012). As everyone is unique in their illness and reactions to drug therapy, there are no 'right' ways or 'cures' for mental illnesses (Pringle, McCabe, Cowen, & Harmer, 2013). Being able to give all patients a tailored treatment, especially when using medication as a treatment option, has the potential to drastically improve the patient outcomes (Pringle, McCabe, Cowen, & Harmer, 2013).

Selective serotonin reuptake inhibitors (SSRIs) are one example of an antidepressant medication that holds serotonin in the synapse to regulate its levels and the individuals' mood (Szabó, 2014). While this medication is often prescribed to patients with depression, and sometimes anxiety, they are not always effective, particularly in the long term (Szabó, 2014). Drug treatments like this can be beneficial, but are most effective in circumstances where they are taken for shorter periods of time, as they are not a cost-effective option and individuals can become sensitised as they continue to take the medication (Szabó, 2014). SSRIs do have milder side effects than a number of other medicated treatment options, such as tricyclic antidepressants which effect dopamine and noradrenaline levels and block histamine, causing drowsiness (Kalat, 2012). Side effects are another example of why this treatment is not always an appropriate option, especially if the individual is not participating in therapy sessions (Szabó, 2014).

Deeper understanding of neural mechanisms responsible for normal functioning, especially where mental health and emotions are concerned, will allow both diagnosis and treatment to be more accurate and effective (Thagard, 2008). It is important that when treating and helping individuals living with mental illness that there is an element of psychotherapy in addition to drug therapy, particularly as more is found out about the drugs and their side effects (Thagard, 2008). Using this model, and further research that stems from this theory, can improve the diagnosis and treatment of mental illnesses, as more becomes known about how neurotransmitters interact and influence emotions, and courses of medications can be redesigned and, therefore, better tailored to the individual and their needs. Understanding more about neurotransmitters could improve the crafting of these drugs, potentially increasing their effectiveness and reducing the negative side effects.

Understanding everyday emotions[edit]

[Provide more detail]

Stress[edit]

Noradrenaline is the main neurotransmitter involved in stress, as shown in this model as distress/anguish. If there is too much noradrenaline in the system, there could be a persistent dysregulation that alters the homeostasis within the system (Goddard et al., 2010). This alteration can contribute to chronic stress, or vice versa, and ultimately increase the likelihood of anxiety disorders (Goddard et al., 2010). Using this knowledge and the model created by Lövheim (2012), we can improve our emotional lives by identifying situations that could help in calming physiological symptoms of stress and anxiety, like meditation, and work on using these techniques in times of stress, whether chronic or acute. Another way we can improve stress based on this model is increasing the presence of other neurotransmitters involved, such as increasing serotonin and noradrenaline through exercise, to evoke other emotions.

Sleep[edit]

While there are innumerable factors at play during and related to sleep, particularly from a physiological perspective, it has been shown that there is a strong link between sleep and emotional processing (Deliens, Gilson, & Peigneux, 2014). As mentioned in previous sections, serotonin has been shown to interrupt REM sleep (Kalat, 2012). This could induce a lack of sleep, or create a perception of sleep deprivation, which can significantly impair a number of cognitive processes. For example, a lack of sleep lowers emotional intelligence, reduces emotion regulation abilities by increasing irritability, and decreases overall mood (Deliens, Gilson, & Peigneux, 2014). A loss of sleep also increases self-reported feelings of depression, anger, and anxiety, and exacerbates reactions to and perceptions of stress (Deliens, Gilson, & Peigneux, 2014). In addition to this, it reduces the ability to cope with stress, perhaps as a result of increased irritability (Deliens, Gilson, & Peigneux, 2014). Lack of sleep also reduces our ability to cognitively reframe emotional events, and recognise the facial expressions of others (Deliens, Gilson, & Peigneux, 2014)

Clearly, sleep plays an important role in emotion, along with other biological and cognitive functions. While we don't need Lövheim's cube of emotion (2012) to tell us that we need to get enough sleep, investigating the relationship between sleep and each neurotransmitter would effectively inform us about their true relationship with emotion and assess the accuracy of this theory.

Conclusion[edit]

There has been no published research specifically related to Lövheim's cube of emotion (2012), aside from his proposal of the model. This means that there needs to be a significant amount of research into the interactions between the three neurotransmitters and basic emotions before this model can be appropriately assessed as a theory. Physiology can evoke emotions, like stress or a panic attack, however this is not always the case (Kalat, 2012). This theory does acknowledge that cognition and perception play a part in emotion, yet does not incorporate this, producing a major limitation in its applicability (Lövheim, 2012). After further research is conducted, particularly on the functions of each neurotransmitter, there could be an increase in uses for this model to help us understand and improve our emotional lives. The main application for this model is its applicability to the literature regarding psychopharmacological treatments and the potential improvements that can be made in this area as a result of future research on this model.

Lövheim's cube of emotion (2012) is a new concept that has a lot of potential as an explanation of how neurotransmitters contribute to emotions. With further research and an increased understanding of both neurotransmitters and emotions, this three-dimensional model could be capable of improving our emotional lives in significant and countless ways.

Quick Quiz[edit]

1

Which of these neurotransmitters is NOT one that Lövheim used to develop his model?

Dopamine
Serotonin
Oxytocin
Noradrenaline

2

What does the noradrenaline axis of the model represent?

Self-confidence
Attention
Motivation
Inner strength

3

How did Tomkins (1981) define "affect"?

Entirely cognitive explanation of emotion
A combination of psychopharmacological and psychotherapy treatments
A therapeutic technique
Solely biological component of emotion

4

How can we use Lövheim's cube of emotion (2012) to improve our emotional lives?

Reducing our frustration when trying to draw cubes
Increasing the accuracy of drug treatments
To identify basic emotions
We can't

5

High levels of serotonin, dopamine and noradrenaline are present in:

Distress/anguish
Enjoyment/joy
Interest/excitement
All of the above


See Also[edit]

Motivation and emotion/Book/2014/Serotonin and emotion

Motivation and emotion/Book/2013/Dopamine and emotion

Motivation and emotion/Book/2015/Norepinephrine and emotional disorders

Motivation and emotion/Book/2014/Exercise and mood

Motivation and emotion/Book/2013/Exercise and emotion

Motivation and emotion/Book/2010/Sleep and emotion

Motivation and emotion/Book/2013/Sleep and emotion

Motivation and emotion/Book/2014/Sleep deprivation and emotion

Motivation and emotion/Book/2011/Sleep and negative emotions

Dopamine Hypothesis of Schizophrenia

References[edit]

Blaszczynski, A., Tait, R., & Mattick, R. (2014). Addictive disorders. In Rieger, E. (Ed.) Abnormal Psychology (3rd Ed.). (pp 264-309). Sydney, NSW: McGraw Hill Education.

Chastain, G. (2006). Alcohol, neurotransmitter systems, and behavior. The Journal of General Psychology, 133(4), 329-335. DOI: 10.3200/GENP.133.4.329-335

Cyders, M. A., & Smith, G. T. (2008). Emotion-based dispositions to rash action: Positive and negative urgency. Psychological Bulletin, 134(6), 807-828. DOI: 10.1037/a0013341

Deliens, G., Gilson, M., & Peigneux, P. (2014). Sleep and the processing of emotions. Experimental Brain Research, 232(5), 1403-1414. DOI: 10.1007/s00221-014-3832-1

Goddard, A. W., Ball, S. G., Martinez, J., Robinson, M. J., Yang, C. R., Russell, J. M., & Shekhar, A. (2010). Current perspectives of the roles of the central norepinephrine system in anxiety and depression. Depression and Anxiety, 27(4), 339- 350. DOI: 10.1002/da.20642

Kalat, J. W. (2012). Biological psychology (11th Ed.). Belmont, CA: Thomson-Wadsworth.

Lövheim, H. (2012). A new three-dimensional model for emotions and monoamine neurotransmitters. Medical Hypotheses, 78(2), 341-348. DOI: 10.1016/j.mehy.2011.11.016

Pringle, A., McCabe, C., Cowen, P. J., & Harmer, C. J. (2013). Antidepressant treatment and emotional processing: Can we dissociate the roles of serotonin and noradrenaline? Journal of Psychopharmacology, 27(8), 719-731. DOI: 10.1177/0269881112474523

Szabó, M. (2014). Conceptual issues in abnormal psychology. In Rieger, E. (Ed) Abnormal Psychology (3rd Ed.). (pp. 2-42). Sydney, NSW: McGraw Hill Education.

Thagard, P. (2008). Mental illness from the perspective of theoretical neuroscience. Perspectives in Biology and Medicine, 51(3), 335-352. DOI: 10.1353/pbm.0.0030

Tomkins, S. S. (1981). The quest for primary motives: Biography and autobiography of an idea. Journal of Personality and Social Psychology, 41(2), 308-329. DOI: 10.1037/0022-3514.41.2.306

External Links[edit]

Quick Anxiety Quiz (mindspot.org.au)

What neurotransmitter are you? (archives.drugabuse.gov)