If we’re honest with ourselves, we know if a relationship isn’t working, if it is abusive or hurtful, or if it has run it’s course. We can ask trusted family and friends for their opinion if we’re confused or unsure.

Well, hello and good morning, afternoon, and evening readers. I truly hope you’re swimming in the pleasantries of life rather than keeping your head above water in the unpleasant swamp. HOPE = Hold On Pain Ends. And there’s generally a learning or personal growth that comes after the storm of every painful experience, even if it’s simply greater empathy and compassion for others.

Today’s the day to learn or remember the fallacies of the human mind. I am not as smart as I look, haha. Have you heard of heuristics before? In cognitive psychology, a heuristic is a mental “shortcut” that allows people to solve problems and make judgments quickly and efficiently. They can be very helpful in many situations, but they can also lead to cognitive biases, errors in thinking, and even perhaps without the mental shortcut, our thinking is often filled to the brim with cognitive distortions, assumptions and fallacies (faults). Awareness raising is probably the first step to identify our own cognitive traps and also identify them in others. Cognitive errors are natural – we all have them. Below are some cognitive distortions/errors to be aware of when we reflect on our interactions with people, during personal reflection, and when making meaningful decisions or judgements.

• ALL-OR-NOTHING THINKING (aka. POLARISED THINKING, SPLITTING, and BLACK-AND-WHITE THINKING: is extreme thinking i.e., the error in a person’s thinking to bring together the dichotomy of both positive and negative qualities of the self and others into a cohesive, realistic whole. It is a common defense mechanism. Before you think “I must have really shitty thinking because I do this ALL the time”, give yourself a break. If you’re thinking in black and white, you probably internalised this from social media, television and movies, your family of origin and the broader society. Be mindful of using extreme, dichotomist terms, such as “failure”, “success”, “best”, “worst”, “freezing”, “boiling”, “everything”, and “nothing”. If you think “I’m a terrible person”, that is bullshit and inaccurate. You may have behaved terribly for a period of time towards yourself, to someone else, or towards some “thing”, but we cannot discount all the NON-terrible qualities about you. We must THINK in DIALECTICS i.e., the ability to view issues from multiple perspectives with reason and wisdom or in other words being able to have two contradictory viewpoints, where a greater truth emerges from their interplay. The truth is, if you think you’re a terrible person, there’s also virtuous person in there too.

• OVERGENERALISTION: The words “always”, “every” and “never” come into play here, and you have an unshakable “rule” or “conviction” about yourself, something, or someone, based on one or two incidences. Overgeneralising is “a cognitive distortion in which an individual views a single event as an invariable RULE, so that, for example, failure at accomplishing one task will predict an endless pattern of defeat in all tasks.” Coming into the present moment and being specific can be helpful if you are someone who overgeneralises. You may also want to ask yourself if what your saying is the really the truth. Is it really accurate or correct. There’s an assumption that because something has happened once or a few times that it’s like going to happen every time. Remember, the words “always”, “every”, and “never” frequently appear in this cognitive “trap”. I encourage you to look at the big picture and ask yourself if what you’re saying or thinking is accurate. Overgeneralisations tend to be vague and board statements e.g., “I always get every red light”. Perhaps this is part of our evolutionary negativity bias. We tend to notice the so-called “bad” and overlook the so-called “good”. If you find yourself using overgeneralisations that suggest a future prediction (e.g., “I’ll never get a partner) … use some humour – you may have big balls but neither one of them are crystal – VEEP. If there is some truth to unusually frequent and specific situations that are making your life unpleasant, validate them, talk to someone, and brainstorm some solutions. We humans have plenty of blind spots that others can see sometimes.

• MENTAL FILTER: is considered to be the opposite to OVERGENERALISATION the mental filter takes one small event and focuses on it exclusively, filtering out anything else that’s relevant. Filtering out the positive and focusing on the negative can have a detrimental impact on your mental well-being. Filtering out the so-called “negative” can also make one a bit hubris (excessive pride or self-confidence), arrogant, vain and conceited – and then you’re just a stone’s throw away from narcissism.

• PERSONALISATION AND BLAME: Personalization and blame is a cognitive distortion whereby you entirely blame yourself, or someone else, for a situation that in reality involved many factors that were out of your control. I think this is a symptom of our wounded ego, or simply just the ego. As human’s we are egocentric, like children, and we often think that circumstances in our environment are solely because of our influence. For example, your friend isn’t behaving like they usually do, so it must be because you have done something.

Again, personalisation is an egocentric error in cognition. “Of course it has to do with me”, we think. It makes sense that we personalise things. We are the star of our own show, our own narrative. If you personalise something, it means we’ve directly influenced it – we are the primary cause. This may elicit internal pain, shame or guilt, so what’s the pay-off? Personalisation is a cognitive error that offers us the illusion of control e.g., “If we caused it then we will learn how to not cause it again, and maybe even undo what we have caused”. If you think about it, personalising something is something children do. Remember, there are infinite variables in any situation to take full credit of the outcome. That being said, it is responsible and mature to reflect objectively on the influence of our behaviour and what we can learn about our shortcomings.

Blame deserves it’s own blog post but in short, it can be defined as a defence mechanism to protect the self from feeling some unwanted emotion or thinking something unacceptable in relation to the “self”. Blaming provides a way of devaluing others, an the pay-off or reinforcement the blamer receives is a sense of superiority. It protects our ego from feeling responsible for something, and protects us from feeling guilt or shame. Perfectionists are very good at blaming others, and themselves. Even if you genuinely think faulting someone or something is valid, remember that no one is perfect. Recognise that you are human and others are fallible humans. As they say in recovery, “there is a bit of bad in the best of us and a bit of good in the worst of us“. We may have internalised from society and culture that we couldn’t make mistakes (because we receive “punishment” for making mistakes) but we must move beyond that now. As adults, we need to get real. Validate your experience because it may be very disappointing when we don’t meet others or our own expectations. We must nurture and care for the wounded child. Lets attend and befriend to our shortcomings and accept we are not superhuman. Learn to expect you will make mistakes. Failure is kind of an illusion, isn’t it? Or maybe a social construct? “Failure” is really learning – replace ‘failure’ with the word ‘feedback’. Would a cat or dog blame them self for a “mistake”? In the minds of animals, there’s no such concept as failure or a mistake.

Here’s a link to website “simplypsychology” that discusses a theory called Attribution Theory, an idea about how people explain the causes of behaviour and events: Attribution Theory – Situational vs Dispositional | Simply Psychology

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.