Webb Therapy Uncategorized AIPC (2021). Busting Common Myths About Anger. Issue 355 // Institute Inbrief. Retrieved June 17, 2021.

AIPC (2021). Busting Common Myths About Anger. Issue 355 // Institute Inbrief. Retrieved June 17, 2021.

All human beings experience anger at least occasionally. It’s a natural emotion helping us recognise that we or someone or something we care about has been violated or treated badly. When we feel threatened or our goals are thwarted, anger is a coping mechanism that enables us to act decisively, especially in situations where there is little time to reason things out. It can motivate problem-solving, goal-achievement, and the removing of threats. It serves a protective function and is not always a problem (Lowth, 2018; Stosny, 2020; Zega, 2009).

But anger is a complex emotion, and all too often manifests maladaptively in clients’ lives, when they perceive excessive need for protection, protect the “wrong” things, or use anger to thwart their longer-term best interests. The result is problem anger.

Perhaps because it is so multi-faceted, misperceptions about anger abound, and the question arises: how shall we regard anger? How do we advise the client to think about it? Folk wisdom often would say that the best thing to do is just let it all out, but is it? Clients complain that they cannot control it, that the tendency to be easily angered is inherited, but again, is there evidence for that? Here are common myths people tend to hold about anger, and factual statements following them that you can use to clarify for the client why learning to deal with problem anger is time well spent.

Myth 1: “Anger is inherited.”

This is the client that may try to claim that their father was short-tempered and they have inherited that trait from him, so there is nothing they can do. Such a stance implies an attitude that the expression of anger is a fixed, unalterable set of behaviours. Research shows, however, that expression of anger is learned, so if we have – say, through exposure to aggressive influential others, such as parents – learned to be violent in our expressions, we can also learn healthier, more appropriate, pro-social ways of dealing with it.

Myth 2: “Anger and aggression are the same thing.”

Fact: Nope. Anger is a felt emotional state. Aggression is a behaviour, sometimes carried out in response to anger, but not the same as it. A person can be angry, yet use healthy methods of expression without resorting to violence, threats, or other aggression. Anger does not always lead to aggression. In fact, some experts claim that most daily anger is not followed by aggression. When it does result in aggression the “I3 Model” (pronounced “I cubed”) is deemed responsible. This suggests that aggression emerges as a function of three interacting factors, which all begin with “I”:

Instigation, an event which instils an urge to aggress as a result of, say, being addressed rudely or learning that one’s partner has had an affair (or a relatively “minor” event, such as being cut off in traffic);

Impellance, meaning a force that increases the urge to act in response to an instigating stimulus. These could be strong hormonal releases or a belief system which says that the instigating event should not be tolerated, or even a sociocultural norm which demands that instigating stimuli be responded to immediately and harshly (such as punching back someone who has hit you);

Inhibition, referring to forces that typically work to counter aggression, such as cultural norms, awareness of negative consequences, or perspective-taking or empathy (Kassinove & Tafrate, 2019).

Myth 3: “Other people make me angry.”

Fact: How often in common parlance do we say things like, “He made me so angry!” or “You make me so mad I could kill you!”? Even though we may occasionally speak about people causing emotions other than anger, it is far more frequent to hear such statements in regard to anger. We can choose whether or not we let someone else’s behaviour make us happy, sad, or something else, but we often think and talk about it as if anger is caused directly by others. With the undiscerning listener, an angry person thus gets to use anger as an excuse for unacceptable behaviour. Ultimately, it is not the other person’s behaviour that causes our anger, and in fact, it’s not even their intention, though that may influence our behaviour. Being precise, we must acknowledge that it is our interpretation of their intention, expressed in their behaviour/language, which is causative.

Myth 4: “I shouldn’t hold anger in; it’s better to let it out” (either by venting or catharsis).

Fact: If by “holding it in” someone means that they suppress anger, it’s true; ignoring it won’t make it go away and squashing it down is not a healthy choice. Neither, however, is venting. Blowing up in an aggressive tirade only fuels the fire, reinforcing the problem anger. Ditto the use of pillow-punching or other means of catharsis; this may come as a surprise to therapists trained a few years ago, when catharsis was an anger management technique in good standing. Now researchers have found that, even though we feel better in the moment after hitting something, our brain notices, subtly changing its wiring. Then the next time we are angry it softly whispers, “Hit something; you’ll feel better”. The time after that, the wiring is stronger in the brain towards a hitting catharsis, and the angry-brain-voice speaks a little louder. Continuing in this vein means that eventually, we could decide to hit something more alive than a pillow. Rather than either angry venting or catharsis is the use of skills to manage the angry impulse.

Myth 5: “Anger, aggression, and intimidation help me to earn respect and get what I want.”

Fact: People may be afraid of a bully, but they don’t respect those who cannot control themselves or deal with opposing viewpoints. Communicating respectfully is a far superior way to get (most) people to listen and accommodate one’s needs. While the momentary power that comes with successful intimidation may feel heady in the moment, it does not help build the healthy relationships that most people coming to counselling yearn to have.

Myth 6: Anger affects only a certain category of people.

Fact: Anger is a universal emotion that affects everyone. It does not discriminate against people of any particular age, nationality, race, ethnicity, socioeconomic status, education, or religion. It is tempting for some people in the educated middle classes to believe that anger is more prevalent among the poor, or those who are less educated or lacking in social skills. Reality does not bear this out, although the expressions of anger do vary among different social groups. Remember, anger is just an emotion, one which does not make people “good” or “bad” for having it.

Myth 7: “I can’t help myself. Anger isn’t something you can control.”

We don’t always get to control the situations of our lives, and some of them may trigger our anger. In fact, it’s also agreed by experts that we don’t (in the short-term) control whether we have angry feelings or not; they just come – although there are longer-term ways to work with clients that see them less easily provoked, and therefore less prone to have the experience of anger. What we do have the short-term choice to control is how we express that anger. Continuing in sessions with you (the therapist) for the purpose of learning how to better handle anger means having more choices of response, even in highly provocative situations.

Myth 8: “When I’m angry I will say what I really mean.”

Fact: This is rarely true. Uncontrolled angry expressions are more about gaining control of or hurting others, not saying what a person’s deepest truth is. 

Myth 9: “By not saying what I’m thinking in the moment, I’m being dishonest and will be even angrier later.”

Fact: There is a strong pull to “speak our mind” when angry. But it is at this time that a person’s judgment is most severely flawed. To speak from anger is to allow the impulsive part of the brain to overrule the rational part. Better for relationships, career, and pretty much everything else to wait until that reasoning part can regain control.

Myth 10: “Men are angrier than women.”

Fact: The sexes experience the same amount of anger, says research; they just express it differently. Men often use aggressive tactics and expressions, whereas women (often constrained culturally) more frequently choose indirect means of expression, such as found in passive-aggressive tactics. This could mean getting back at someone by talking negatively about them or cutting them out of their lives (categories adapted from: Therapist Aid LLC, 2016; Segal & Smith, 2018; Morin, 2015; Morrow, n.d.; Better Relationships, 2021; Gallagher, 2001).

Thought for reflection

Anger has many facets to it, and we have introduced some information here that may seem either startling or counterintuitive. As you think back over the myths we just debunked, which aspect has surprised you the most? Do you have any sense of why that might be? One woman, for example, was very surprised to hear that “men are angrier than women” was only considered a myth; it turned out that in her family, women “never got angry” (we hypothesise that perhaps they were socialised to not show anger), and the men got angry all the time (perhaps more allowed in that woman’s family/culture). In what ways, if at all, might your views about anger have shaped how you behave? How you respond to others? 

And here’s the ultimate question if you share this material with a client: what are their responses to the above questions? How might hearing these myths help them seek more adaptive ways to deal with problem anger? 

The upcoming Mental Health Academy course, “Helping Clients Deal with Problem Anger” draws from numerous therapies and neuroscience to help clinicians and clients collaboratively create a program to address each client’s unique challenges with this universal human emotion.

References:

  1. Better Relationships. (2021). Common myths about anger. Anglicare Southern Queensland. Retrieved on 13 April, 2021, from: Website.
  2. Gallagher, E. (2001). Anger. eddiegallagher.com.au. Retrieved on 13 April, 2021, from: Website.
  3. Kassinove, H., & Tafrate, R.C. (2019). The practitioner’s guide to anger management: Customizable interventions, treatments, and tools for clients with problem anger. Oakland, CA: New Harbinger Publications, Inc. 
  4. Lowth, M. (2018). Anger management. Patient. Retrieved on 7 April, 2021, from: Website.
  5. Morin, A. (2015). 7 myths about anger and why they’re wrong. Psychology Today. Retrieved on 13 April, 2021, from: Website.
  6. Morrow, A. (n.d.). Anger myths. Stress and Anger Management Institute. Retrieved on 13 April, 2021, from: Website.
  7. Segal, J., & Smith, M. (2018). Anger management: Tips and techniques for getting anger under control. Helpguide.org. Retrieved on 9 April, 2021, from: Website.    
  8. Stosny, S. (2020). Beyond anger management. Psychology Today. Retrieved on 9 April, 2021, from: Website.
  9. Therapist Aid, LLC. (2016). Anger warning signs. Therapist Aid LLC. Retrieved on 7 April, 2021, from: Website.
  10. Zega, K. (2009). Holistic Psychotherapy (159). Retrieved on 7 April, 2021, from: Website.

Related Post

Neurobiological Mechanisms of AddictionNeurobiological Mechanisms of Addiction

Addiction is a chronic, relapsing disorder involving changes in brain reward, motivation, learning, stress and executive control systems. While different substances (and behaviours) act through distinct primary mechanisms, they converge on common neurobiological pathways — particularly the mesocorticolimbic dopamine system.

Below is an overview in Australian English of the core mechanisms and then substance-specific and behavioural addiction processes.


Core Neurobiological Pathways in Addiction

1. The Mesocorticolimbic Dopamine System

The central pathway implicated in addiction is the mesocorticolimbic circuit, involving:

  • Ventral tegmental area (VTA)
  • Nucleus accumbens (NAc)
  • Prefrontal cortex (PFC)
  • Amygdala
  • Hippocampus

All addictive drugs increase dopamine transmission in the nucleus accumbens, either directly or indirectly. Dopamine does not simply produce pleasure — it encodes reward prediction, salience and learning. With repeated exposure:

  • Drug-related cues gain exaggerated salience
  • Natural rewards become less reinforcing
  • Behaviour becomes increasingly habitual and compulsive

2. Neuroadaptation and Allostasis

Repeated substance exposure produces:

Tolerance — Reduced response due to receptor downregulation or neurotransmitter depletion.

Dependence — Neuroadaptations that produce withdrawal when the substance is removed.

Allostatic shift — The brain’s reward set point shifts downward, mediated by stress systems (e.g. corticotropin-releasing factor), resulting in dysphoria during abstinence.

3. Habit Formation and Loss of Control

With repeated use:

  • Control shifts from ventral striatum (goal-directed) to dorsal striatum (habit-based)
  • Prefrontal cortex regulation weakens
  • Impulsivity and compulsivity increase

Substance-Specific Mechanisms

Alcohol

Alcohol acts on multiple neurotransmitter systems:

  • Enhances GABA-A receptor function (inhibitory)
  • Inhibits NMDA glutamate receptors (excitatory)
  • Increases dopamine release in nucleus accumbens
  • Affects endogenous opioid systems

Chronic exposure leads to:

  • GABA downregulation
  • NMDA upregulation
  • Hyperexcitable state during withdrawal (risk of seizures, delirium tremens)

Alcohol dependence also involves stress system activation and impaired frontal cortical control.

Methamphetamine

Methamphetamine is a potent psychostimulant that:

  • Enters presynaptic terminals
  • Reverses the dopamine transporter (DAT), causing carrier-mediated dopamine efflux
  • Inhibits vesicular monoamine transporter 2 (VMAT2), releasing dopamine from synaptic vesicles into the cytoplasm
  • Causes massive dopamine release into the synapse

It also increases noradrenaline and serotonin.

Chronic use causes:

  • Dopamine neurotoxicity (particularly to dopaminergic terminals)
  • Reduced dopamine transporter availability
  • Structural changes in striatum and PFC
  • Persistent cognitive deficits

Methamphetamine produces particularly strong sensitisation of cue-driven craving.

Cocaine

Cocaine:

  • Blocks the dopamine transporter (DAT), preventing reuptake
  • Increases synaptic dopamine concentration

Unlike methamphetamine, cocaine acts by blocking DAT rather than reversing it, and does not cause large presynaptic vesicular release — the elevation in synaptic dopamine arises from impaired clearance.

Repeated use leads to:

  • Dopamine receptor downregulation
  • Enhanced cue reactivity
  • Rapid cycling between intoxication and crash
  • Strong psychological dependence

Opioids (e.g. heroin, morphine, oxycodone)

Opioids act primarily at mu-opioid receptors (MORs), which are expressed throughout the brain, including in the VTA. Their dopaminergic effects arise through multiple mechanisms:

  • MORs on GABAergic interneurons in the VTA suppress inhibitory tone, thereby disinhibiting dopamine neurons (the classical disinhibition mechanism)
  • MORs are also expressed on VTA dopamine neurons and projection targets directly, contributing additional excitatory drive beyond the disinhibition pathway

They also act in brainstem respiratory centres, which underlies the risk of respiratory depression in overdose.

Chronic use produces:

  • Receptor desensitisation and internalisation
  • Reduced endogenous opioid production
  • Severe physical withdrawal mediated by noradrenergic rebound in the locus coeruleus
  • Strong negative reinforcement (use to avoid withdrawal)

Cannabis

Δ9-tetrahydrocannabinol (THC):

  • Activates CB1 receptors (the primary psychoactive cannabinoid receptor)
  • Modulates GABA and glutamate release at presynaptic terminals
  • Indirectly increases dopamine in NAc via disinhibitory mechanisms

Cannabis produces:

  • Altered endocannabinoid system function
  • CB1 receptor downregulation with chronic use
  • A mild to moderate withdrawal syndrome (irritability, sleep disturbance, appetite changes)
  • Effects on hippocampal memory circuits

While addiction risk is generally considered lower than for opioids or stimulants, it remains clinically significant and may be underestimated, particularly given the widespread availability of high-potency THC products (e.g. concentrates and high-THC flower), which are associated with greater dependence risk and more severe withdrawal.

MDMA (Ecstasy)

MDMA:

  • Reverses the serotonin transporter (SERT), causing massive serotonin efflux — this is its primary mechanism
  • Also increases dopamine and noradrenaline

Neurobiological consequences include:

  • Acute empathogenic and entactogenic effects driven by serotonin release
  • Post-use serotonin depletion, which may contribute to dysphoria in the days following use
  • Potential serotonergic neurotoxicity, though this evidence comes largely from high-dose or repeated animal studies; the clinical significance in typical human recreational use remains under debate and is not definitively established
  • Moderate addictive potential relative to psychostimulants, partly because dopaminergic effects are less prominent than with cocaine or methamphetamine

Prescription Psychoactive Medications

Certain prescribed medications also have addictive potential:

Benzodiazepines — Enhance GABA-A receptor activity. Cause tolerance via receptor downregulation. Dependence is primarily a GABAergic adaptation. Withdrawal can be protracted and, in cases of high-dose or long-term use, may produce seizures.

Prescription stimulants — Act via similar mechanisms to amphetamine, increasing dopamine and noradrenaline. Risk of misuse exists in susceptible individuals, though therapeutic doses in appropriately diagnosed patients are associated with substantially lower addiction risk than recreational use.


Behavioural (Process) Addictions

Gambling Disorder

Gambling disorder is recognised in DSM-5-TR as a non-substance-related addictive disorder. Although no substance is ingested, similar neurobiological mechanisms are involved.

Dopamine and reward prediction error — Near misses activate the nucleus accumbens similarly to wins. Variable ratio reinforcement schedules (as in poker machines) generate strong, unpredictable dopamine prediction error signalling that powerfully drives continued behaviour.

Cue reactivity — Gambling-related cues activate the same mesocorticolimbic circuitry as drug cues, with increased striatal activation and reduced prefrontal inhibitory control.

Habit circuitry — A shift from ventral to dorsal striatal control contributes to compulsive betting despite continued losses.

Other Emerging Behavioural Addictions

Conditions such as internet gaming disorder, compulsive sexual behaviour disorder, and problematic social media use share overlapping neurobiological features including:

  • Dopamine dysregulation and sensitisation to cue salience
  • Reduced executive control
  • Stress system activation

However, the evidence base for most of these conditions is still developing, and their classification as formal addictive disorders remains an area of active research and debate. Internet gaming disorder is currently listed in DSM-5-TR as a condition for further study.


Shared Neurobiological Themes Across Addictions

Across substances and behaviours, addiction involves:

  • Dopamine sensitisation to cues
  • Reduced sensitivity to natural rewards
  • Impaired prefrontal inhibitory control
  • Stress system overactivation (particularly corticotropin-releasing factor)
  • Habit circuitry dominance (dorsal striatum)
  • Neuroplastic changes in glutamatergic signalling

Why Some Substances Are More Addictive

Addictive potential is influenced by multiple interacting factors. The speed of dopamine rise is one of the most studied — faster onset of dopamine elevation (e.g. via smoking or intravenous administration) is associated with stronger reinforcement. This framework, developed largely through the work of Volkow and colleagues, has strong empirical support, though it represents a mechanistic model rather than an established universal law. Other important factors include:

  • Intensity of dopamine release
  • Pharmacokinetics (e.g. route of administration)
  • Withdrawal severity (which drives negative reinforcement)
  • Social and environmental context
  • Genetic vulnerability (heritability of addiction is estimated at 40–60% across substances)

Conclusion

Addiction is not simply about pleasure seeking. It reflects maladaptive neuroplasticity in reward, stress, learning and executive control circuits. While alcohol, methamphetamine, cannabis, opioids, cocaine and MDMA each act through different primary molecular mechanisms, they converge on common neural pathways that drive craving, tolerance, withdrawal and compulsive use. Behavioural addictions such as gambling engage these same circuits despite the absence of an ingested substance.

The neurobiological understanding of addiction continues to evolve, and where evidence is still emerging — particularly regarding emerging behavioural addictions and the long-term neurotoxic effects of substances like MDMA — clinical interpretation should be appropriately cautious.

Unhelpful Cognitions (thoughts) and DistortionsUnhelpful Cognitions (thoughts) and Distortions

Unhelpful Cognitions

Mental Filter: This thinking style involves a “filtering in” and “filtering out” process – a sort of “tunnel vision”, focusing on only one part of a situation and ignoring the rest. Usually this means looking at the negative parts of a situation and forgetting the positive parts, and the whole picture is coloured by what may be a single negative detail.

Jumping to Conclusions: We jump to conclusions when we assume that we know what someone else is thinking (mind reading) and when we make predictions about what is going to happen in the future (predictive thinking).

Mind reading: Is a habitual thinking pattern characterized by expecting others to know what you’re thinking without having to tell them or expecting to know what others are thinking without them telling you. This is very common, and most people can identify. Oftentimes, when we are telling someone a story about an interaction, we’ve had with someone else, we will make mind reading assumptions without actually having fact or evidence e.g., “They haven’t phoned me in two weeks so they must be angry with me for cancelling on them last week.”

Personalisation: This involves blaming yourself for everything that goes wrong or could go wrong, even when you may only be partly responsible or not responsible at all. You might be taking 100% responsibility for the occurrence of external events. It can also involve blaming someone else for something for which they have no responsibility. This can often occur when setting a boundary with someone and you take responsibility for their guilt or anger.

Catastrophising: Catastrophising occurs when we “blow things out of proportion” and we view the situation as terrible, awful, dreadful, and horrible, even though the reality is that the problem itself may be quite small.

Black & White Thinking: Also known as splitting, dichotomous thinking, and all-or-nothing thinking, involves seeing only one side or the other (the positives or the negatives, for example). You are either wrong or right, good or bad and so on. There are no in-betweens or shades of grey.

Should-ing and Must-ing: Sometimes by saying “I should…” or “I must…” you can put unreasonable demands or pressure on yourself and others. Although these statements are not always unhelpful (e.g., “I should not get drunk and drive home”), they can sometimes create unrealistic expectations.

Should-ing and must-ing can be a psychological distortion because it can “deny reality” e.g., I shouldn’t have had so much to drink last night. This is helpful in the sense that it communicates to us that we have exceeded our boundaries, however, saying “shouldn’t” about a past situation can be futile because it cannot be changed.

Overgeneralisation: When we overgeneralise, we take one instance in the past or present, and impose it on all current or future situations. If we say, “You always…” or “Everyone…”, or “I never…” then we are probably overgeneralising.

Labelling: We label ourselves and others when we make global statements based on behaviour in specific situations. We might use this label even though there are many more examples that are not consistent with that label. Labelling is a cognitive distortion whereby we take one characteristic of a person/group/situation and apply it to the whole person/group/situation. Example: “Because I failed a test, I am a failure” or “Because she is frequently late to work, she is irresponsible”.

Emotional Reasoning: This thinking style involves basing your view of situations or yourself on the way you are feeling. For example, the only evidence that something bad is going to happen is that you feel like something bad is going to happen. Emotions and feelings are real however they are not necessarily indicative of objective truth or fact.

Magnification and Minimisation: In this thinking style, you magnify the positive attributes of other people and minimise your own positive attributes. Also known as the binocular effect on thinking. Often it means that you enlarge (magnify) the positive attributes of other people and shrink (minimise) your own attributes, just like looking at the world through either end of the same pair of binoculars.

(CCI, 2008)