Sapiens: A Brief History of Humankind.

Did you know that through a series of controversial (and incredibly sad) experiments, psychologist Harry Harlow, was able to demonstrate the importance of early attachments, affection, and emotional bonds on the course of healthy development. Harlow discovered that love and affections may be primary needs that are just as strong as or even stronger than those of hunger or thirst.

1 Think positive

This sounds easier said than done. I challenge you to intentionally consider alternatives to your habitual, default thinking pattern. We all want to be liked by others – because we want to belong to a group and to feel valued, needed and wanted. Worrying about social situations is very natural because we want to be perceived by others in a certain way. Other people’s perceptions are out of our control. So, we worry about it. We worry about things that are out of our control. We also know that we control our own behaviour, therefore, we feel responsible for behaving in ways that will mesh with others. We believe the likelihood of being liked will increase if we behave in certain ways.

Worrying can become problematic if we overthink past and future interactions, and perhaps we choose to avoid some or all interactions to protect ourselves. But then we don’t get the social connection we need.

I challenge you to think positive. Choose that instead. It will take energy because it might not be your default thinking pattern. Set your positive intention. Use mental energy. Trust that the opposite of your thinking can be true as well.

2 Forget comparison – unless you are a clone of someone else, you don’t have their genes, their life experience, their upbringing, their family history etc. It’s kind of illogical to compare yourself to someone else if you think about it, hey.

Don’t be concerned if others appear to have more or better friends than you. Quality and enjoyment matter more than quantity. Savour the moments of connection, wherever you can find them.

3 Anticipate change

Our life circumstances can leave us vulnerable to a sense of isolation. Relationships shift over time, and we may lose touch with friends who were once important. People form new relationships, move away, start families, become busier at work or start studying etc. Accepting change as normal can help you adjust to a change in your relationships. Just as we grow, evolve, and change, so will our relationships. Couples who were once in love will fall out of love. And friendships that were once enjoyed may become less enjoyable overtime.

4 Tolerate discomfort

Anxiety may cause you to avoid socialising. Understand that feeling awkward or embarrassed in social situations does not mean you are doing anything “wrong”. I remember a period I went through growing up. I noticed people around me starting to use for sophisticated language. I thought I had nothing of value to say, or nothing of interest. I would struggle to form sentences in my head. I was becoming so anxious that my social cognition was compromised. Learning to be comfortable with myself, relaxing into conversations, and listening more deeply to the other person helped me. I remember going on dates thinking I have absolutely nothing to say to this person. That cognition, that thought, wasn’t true. It was part of a larger story that I was creating in my mind.

Reach out to others and your skills will improve with time.

5 Listen well

Practice listening. Ask questions and really listen to the answers, rather than just waiting for your turn to talk, or worrying about how you will respond. If you’re curious about what someone is saying, your mind will naturally form a question or recall a similar experience that you can share.

Respond warmly to people’s experiences through your posture, facial expressions and words. Put the mobile phone away and be present.

6 Rehearse

Out of practice with small talk? Spend some time thinking about questions you can use when conversation stalls. You might ask if the other person has been overseas or travelled, what music do they like, or what movies they like to see at the cinema. A natural question to ask is what did you get up to today? What do you have planned for the weekend?

I once attended a training for work. The facilitator shared her experience of often finding herself in similar situations, and she decided to formulate a “go-to” script for when she became tense, and a conversation stalled. Rather than panic, she had a mental go-to script to bridge the gap until the conversation returned to a natural flow. Sometimes it’s nice to allow for a silence, scan your environment and discuss something happening around you.

7 Go offline

Social media helps many people, but it can also increase disconnection, depression, loneliness, anxiety, and headaches. Ensure you have a healthy offline life. Perhaps invite trusted online friends to an offline meeting to build your relationship.

8 Help and service

Helping someone gives a feel-good rush. Oxytocin and dopamine neurotransmitters have been shown to be involved in human bonding. These chemicals can make us feel pleasure. Create a bond with someone by offering help or asking for it. If we’re not someone who asks for help often, the people who know us well will likely feel closer to you because you need them for something, nourishing the bond you have. Have you noticed that strangers in the street are often very willing to help someone with directions? It makes people feel good to help others and be helped in return. Something as little as assistance with a bag or holding a lift can help people feel seen and cared for.

9 Get involved

I know this one may make some people go “Eeeeek” and cringe. However, evolutionary and developmental psychology … and all psychology, has suggested time and time again, that feeling part of a larger community and getting involved makes us feel alive and part-of. Joining in connects you to other people, unites you in a shared activity, and provides an easy way to get to know people better.

Have you ever watched a group of people in the street having a laugh, or watched people playing a sports game, or doing an activity together – while you’re sitting alone on the outside. You might mock them to yourself to make yourself feel superior or protected. We’d rather be part of. It’s just the truth.

10 Manage stress

Everybody has some social situations they dread. Practice simple stress management techniques, such as breathing deeply and slowly, to help keep your stress in check through awkward moments.

We need stress to perform optimally. Befriend your stress. When it becomes overwhelming, recognise that it’s happening, allow it to be there, investigate where it’s living in your body, and nurture that part of yourself. Talk to a trusted friend in times of excessive or toxic stress. Do whatever you need to come back home to yourself. Rest. Drink water. Eat nutritious food. Shower or bathe. Spend time outdoors in nature. Watch something on tv. Listen to music. Come home to your true self, recharge the batteries, and then jump back in. You’re allowed to switch off for a while.

11. Practice, practice, practice

Relationship skills can be learnt. Don’t be discouraged. Remember that social connections are good for you. If you feel like you need support to build better connections skills, a counsellor or therapist can help.

We learn from new experiences. They create, wire, and strengthen, neural pathways in the brain. You can be silent and listen during social interactions. Get curious about the other person. Ask questions. Share some of your story and ideas. And breath. Practice makes progress – not perfection.

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.