The ‘Triune Brain’ theory by Neuroscientist Paul MacLean — an evolutionary perspective

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)

The phrase “Say what you mean, but don’t say it mean” is all about the balance between honesty and kindness in communication.

Here’s what it means:

• “Say what you mean”:
  Be clear and truthful. Express your real thoughts and feelings. Don’t beat around the bush or pretend to agree when you don’t.
• “But don’t say it mean”:
  Speak with kindness and respect. Even when you’re being honest or giving criticism, there’s no need to be rude, hurtful, or aggressive.

Why it matters:

This phrase promotes healthy communication. It’s a reminder that:

• You can be honest without being harsh.
• Tone and delivery matter just as much as the words.
• Empathy and respect should guide your conversations—even when it’s hard.

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.