Fear and anxiety

Historical Context

Historically, mental illness and addiction have been misunderstood and stigmatized. For much of history, these conditions were seen as moral failings or character flaws rather than medical issues. This has led to a persistent stigma that continues to influence societal attitudes.

Lack of Awareness and Education

There is still a significant lack of awareness and education about mental health and addiction. Many people do not understand that these conditions are medical issues that require treatment, just like physical illnesses. This lack of understanding contributes to negative attitudes and discrimination.

Media Representation

Media often portrays mental illness and addiction in a negative light, reinforcing stereotypes and misconceptions. These portrayals can shape public perception and contribute to the stigma surrounding these conditions.

Criminalization

Addiction, in particular, has been heavily criminalised. This has led to a perception of addiction as a criminal issue rather than a health issue, further entrenching stigma and discrimination.

Internalised Stigma

Individuals with mental illness or addiction often internalise the stigma they experience, leading to feelings of shame and low self-worth. This can prevent them from seeking help and support, perpetuating the cycle of stigma and discrimination.

Healthcare System

Even within the healthcare system, biases and stigma can affect the quality of care provided to individuals with mental illness or addiction. This can lead to inadequate treatment and support, further exacerbating the issue.

Social and Cultural Factors

Social and cultural factors also play a role in how mental illness and addiction are perceived. Different cultures have varying attitudes towards these conditions, which can influence how they are treated and supported.

The differential treatment of treatment-resistant substance use disorder (SUD) and treatment-resistant cancer by society can be attributed to several factors:

1. Perception of Control

Substance use disorders are often perceived as a result of personal choices or moral failings, whereas cancer is seen as an uncontrollable disease. This perception leads to stigma and blame towards individuals with SUD, while those with cancer are more likely to receive sympathy and support.

2. Historical Stigma

Historically, substance use has been stigmatised and criminalised, leading to a societal view that addiction is a choice rather than a medical condition. In contrast, cancer has been recognized as a medical condition requiring treatment and compassion.

3. Media Representation

Media often portrays substance use in a negative light, emphasising criminality and moral failure. Cancer, on the other hand, is often depicted with empathy and urgency, highlighting the need for medical intervention and support.

4. Healthcare System

The healthcare system has historically been more equipped to handle cancer treatment, with extensive research, funding, and specialized care. SUD treatment has lagged behind, with fewer resources and less comprehensive care options.

5. Complexity of Treatment

Treatment-resistant SUD involves complex psychological, social, and biological factors, making it challenging to treat effectively. Cancer treatment resistance, while also complex, has seen significant advancements in research and technology, leading to more effective treatments.

6. Social and Cultural Factors

Cultural attitudes towards substance use and addiction vary widely, with some societies viewing it as a personal failing. Cancer is generally viewed more universally as a disease that requires medical intervention.

REFERENCES

Substance Use Disorder and Stigma

Australian Government Department of Health and Aged Care. (2024). Initiatives and programs. Retrieved from https://www.health.gov.au/about-us/what-we-do/initiatives-and-programs

Morrison, A. P., Birchwood, M., Pyle, M., Flach, C., Stewart, S. L. K., Byrne, R., Patterson, P., Jones, P. B., Fowler, D., & Gumley, A. I. (2013). Impact of cognitive therapy on internalised stigma in people with at-risk mental states. The British Journal of Psychiatry, 203(2), 140-145. https://doi.org/10.1192/bjp.bp.112.112110

Wood, L., Byrne, R., Burke, E., Enache, G., & Morrison, A. P. (2017). The impact of stigma on emotional distress and recovery from psychosis: The mediatory role of internalised shame and self-esteem. Retrieved from https://repository.essex.ac.uk/21927/1/woodpr2017.pdf

Cancer Treatment and Stigma

American Cancer Society. (2023). Cancer treatment and survivorship. Retrieved from https://www.cancer.org/treatment/treatments-and-side-effects.html

National Cancer Institute. (2022). Cancer treatment (PDQ)–Patient version. Retrieved from https://www.cancer.gov/types/treatment-pdq/patient/cancer-treatment-pdq

World Health Organization. (2021). Cancer treatment and palliative care. Retrieved from https://www.who.int/cancer/prevention/diagnosis-screening/cancer-treatment-palliative-care/en/

Hello readers. I hope you are well. I imagine some of you are struggling and some of you are flourishing. Life consists of both. As humans, we relish pleasurable feelings and experiences and we tend to dislike uncomfortable emotions and experiences. I get it. I am just like you. We share this. I hope that provides some comfort.

What is human development?

Human development can be described as “systematic changes and continuities in the individual that occur between conception and death, or from “womb to tomb”” (Sigelman, De George, Cunial, & Rider, 2019, p. 3).

Human development involves the continuities (i.e., what remains consistent across time) and the systematic changes (i.e., patterns of change that are expected to come in order across time) that one experiences throughout the lifespan. Based on my education, there are three domains of continuity and change: 1. The physical and biological, 2. Cognitive (i.e., mind processes/thinking), and 3. Psychosocial and emotional. Let’s open these one at a time.

Physical development includes:

• Physical and biological processes (e.g., genetic inheritance).
• Growth of the body and its organs.
• Functioning of physiological systems (e.g., brain).
• Health and wellness.
• Physical signs of ageing and changes in motor abilities.

Cognitive development includes:

Perception: the sensing of stimuli in our environment (internal and external), sending that information to the brain to be identified and interpreted in order to represent and understand our experience of the world and give it meaning. All perception involves signals that go through the nervous system.

Attention: the ability to actively (and often, involuntarily) process specific information in the environment while tuning out other details. Attention is a very interesting cognitive process because when we bring mindfulness to our thoughts we become open to the direction and attention of our mind. Remember this: where attention goes, energy flows.

Language: very broadly, Language is a communication system that involves using words (i.e., sounds arranged together) and systematic rules to organise those words into sentences and meaning, to transmit information from one individual to another. I was never very interested in language when I was studying at university however that has changed. We used language and concepts to talk to ourselves, about other people, and it is open to misinterpretation, error, and oftentimes language can be used as a means to hurt people or … bring us closer together.

Learning: very broadly defined as a relatively permanent change in behaviour, thinking, and understanding as a result of experience. Experience is everything from formal education to unique personal experience. We learn from each other, the world around us, books, movies, self-reflection and education etc. All of which are experiences.

Memory: Memory refers to the processes that are used to gather, organise, store, retain, and later retrieve information. I’m sure you’ve all seen a tv show or read a book about a person with Amnesia or Alzheimer’s disease. Imagine what your life would be like if you didn’t have the function of memory. I wouldn’t be able to type this very well, I don’t think. I wouldn’t remember my loved ones or what was dangerous in my environment. I know we all have unpleasant memories too and that may feel like a negative evolutionary by-product – however it is actually designed to protect us. Memory is finite – we actually forget a lot of stuff, or perhaps more accurately, we do not have the capacity to store and recall everything we experience.

Intelligence: I would like to reframe intelligence from what might be a common belief. Intelligence does not mean academically gifted as is considered valuable in Western society. I think Olympians and caregivers/parents have an intelligence that I do not because I haven’t learned their skills. Intelligence involves the ability to learn (i.e., sport, academics, the arts, swimming, survival, interpersonal skills), emotional knowledge, creativity, and adaptation to meet the demands of the environment effectively

Creativity: I consider creativity to be an evolutionary gift of our imagination, providing humans with the ability to generate and recognize ideas, consider alternatives, think of possibilities that may be useful in solving problems, communicating with others, and entertaining ourselves and others. Creativity can be stunted when we are struggling or caught in reactivity to external pressures or perceived stress.

Problem solving: is a process – yes, a cognitive one but also a behavioural process. It is the act of defining a problem; determining the cause of the problem; identifying, prioritizing, and selecting alternatives for a solution; and implementing a solution. Problem solving can be both creative or stress driven. I like to say whenever I am solving a problem I am also making a decision. A decision of mine is a choice. At university, our problem solving lessons were coincided with decision making which is why I think of it that way.

Psychosocial development involves:

Aspects of the self (i.e., your identity – which may change over time), and social and interpersonal interactions which include motives, emotions, personality traits, morality, social skills, and relationships, and roles played in the family and in the larger society. This is a huge area to be explored. I will endeavour to elaborate on our psychosocial development in later blogs.

In the late 1950’s, a German-American developmental psychologist named Erik Erikson created a theory for human psychosocial development across the lifespan. His theory suggests that human personality develops in a predetermined order through 8 stages of psychosocial development. See the table below:

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.