Webb Therapy Uncategorized Predicting behaviour: Social Psychological Models of Behaviour

Predicting behaviour: Social Psychological Models of Behaviour

Social psychological models of behaviour attempt to explain why individuals act the way they do in various social contexts. These models integrate individual, interpersonal, and societal factors to provide insights into behaviour. Here’s an overview of some key models:

1. Theory of Planned Behaviour (TPB) proposes that behaviour is influenced by:

– Attitudes toward the behaviour

– Subjective norms (perceptions of others’ approval)

– Perceived behavioural control (i.e., confidence in one’s ability to perform the behaviour [self-efficacy])

2. Social Cognitive Theory (SCT) suggests that behaviour is the result of:

– Reciprocal interaction between personal factors (beliefs, attitudes), environmental factors (social norms), and behaviour itself

– Concepts like self-efficacy (belief in one’s ability) play a major role.

3. Health Belief Model (HBM), designed to predict health-related behaviours. Behaviour is driven by factors such as perceived:

– Susceptibility (risk of harm)

– Severity (consequences of harm)

– Benefits (advantages of action)

– Barriers (obstacles to action)

4. Cognitive Dissonance Theory explains how people strive for consistency between their beliefs, attitudes, and behaviours. When inconsistency arises, they feel dissonance (mental discomfort) and are motivated to reduce it by changing their attitudes or actions.

5. Social Identity Theory examines how individuals define themselves within social groups. Behaviour is influenced by group membership, including in-group favouritism and out-group bias.

6. Attribution Theory focuses on how people explain their own and others’ behaviours. Explains behaviour as being attributed either to internal (dispositional) or external (situational) factors. For example, it is common for people to attribute negative outcomes in their life to external factors rather than internal factors.

7. Elaboration Likelihood Model (ELM) explains how people process persuasive messages and what determines whether those messages will change attitudes or behaviour. It’s often applied in areas like marketing, communication, and public health campaigns. The ELM identifies two primary routes through which persuasion can occur:

– Central Route; this route involves deep, thoughtful consideration of the content and logic of a message. People are more likely to take the central route when they are motivated to process the message (e.g., the topic is personally relevant or important to them) and they can understand and evaluate the arguments (e.g., they aren’t distracted, and they have enough knowledge about the subject). Persuasion through the central route tends to result in long-lasting attitude change that is resistant to counterarguments. Example: A person researching the pros and cons of electric cars before deciding to buy one.

– Peripheral Route, which relies on superficial cues or heuristics (mental shortcuts) rather than the message’s content. People are more likely to take the peripheral route when they are not highly motivated or lack the ability to process the message deeply, and when they focus on external factors like the attractiveness or credibility of the speaker, emotional appeals, or catchy slogans. Persuasion through this route tends to result in temporary attitude change that is less resistant to counterarguments. Example: A person choosing a product because their favourite celebrity endorsed it.

8. Self-Determination Theory (SDT) emphasizes intrinsic and extrinsic motivation. It emphasizes the role of intrinsic motivation—doing something for its inherent satisfaction—over extrinsic motivation, which is driven by external rewards or pressures. It suggests that behaviour is influenced by the need for:

– Autonomy (control over one’s actions); When people perceive they have a choice and are acting in alignment with their values, their motivation and satisfaction increase.

– Competence; Refers to the need to feel effective, capable, and successful in achieving desired outcomes. People are motivated when tasks challenge them at an appropriate level and provide opportunities for growth and mastery. Example: A gamer progressing through increasingly difficult levels, gaining skills and confidence along the way.

– Relatedness; Refers to the need to feel connected to others and experience a sense of belonging. Supportive relationships and positive social interactions enhance motivation and well-being. Example: Employees feeling a bond with their colleagues in a collaborative work environment.

9. Social Learning Theory proposes that behaviour is learned through observation and imitation. Role models and reinforcement play a key role in shaping actions.

10. Transtheoretical Model (Stages of Change) explains behaviour change as a process occurring in stages: precontemplation, contemplation (ambivalence), preparation, action, and maintenance

These models provide frameworks to understand behaviours in contexts like health, decision-making, group dynamics, and social influence.

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What is love and how do I know if I’m in love?What is love and how do I know if I’m in love?

Love isn’t a single chemical but it does involve powerful chemicals in your body. When people say “love is just chemicals,” that’s oversimplified. Love is a complex emotional and psychological experience, but it’s strongly influenced by brain chemistry.

Here are the main chemicals involved:

1. Dopamine — the reward chemical

This is linked to pleasure, motivation, and craving. When you’re attracted to someone, dopamine spikes, which is why love can feel exciting, addictive, and energising.

2. Oxytocin — the bonding hormone

Often called the “love hormone.” It’s released during physical touch, cuddling, sex, and even deep conversation. It helps create feelings of trust, attachment, and emotional closeness.

3. Vasopressin — attachment chemical

Plays a role in long-term bonding and pair attachment, especially in committed relationships.

4. Serotonin — mood regulator (also influences sleep, appetite, digestion and cognition)

Serotonin activity (or “signalling”) can shift during early romantic attraction, which may explain why you obsessively think about someone in the early stages.

5. Adrenaline & norepinephrine

These create the physical symptoms: racing heart, sweaty palms, butterflies.


Love isn’t just chemistry — but chemistry is part of how your brain creates the feeling. Think of it like this:

  • Chemicals are the mechanism.
  • Love is the experience.

Being “in love” isn’t always a big, dramatic lightning-bolt moment. It’s usually a mix of feelings, attachment, and a steady choice to be with someone. Here are some signs that often point to real love rather than just attraction or a crush:

1. You care about who they are, not just how they make you feel

You genuinely admire their character, values and quirks — even their flaws. You’re not just chasing the excitement; you actually like them as a person.

2. Their happiness matters to you

You want good things for them, even when it doesn’t directly benefit you. When they’re struggling, it affects you too.

3. You feel safe being yourself

You don’t feel like you have to put on an act. You can be honest, vulnerable and imperfect, and still feel accepted.

4. You naturally think long-term

When you picture the future, they’re in it — not because you’re forcing it, but because it just feels right.

5. It’s not only intense — it’s steady

A crush can feel all butterflies and nerves.
Love often feels calmer underneath it all — grounded, warm and secure.

6. You choose them

Even on the ordinary days. Even when they annoy you a bit. Love isn’t just a feeling; it’s a consistent decision to stay connected. A couple of questions you might ask yourself:

  • If the excitement settled down, would I still want them around?
  • Do I respect them?
  • Do I feel more like myself with them — or less?

Love doesn’t always feel dramatic. Sometimes it’s quiet and steady — and that can be just as real.

Anxiety, Anxiety Attacks, and Prolonged AnxietyAnxiety, Anxiety Attacks, and Prolonged Anxiety

I want to preface this post by stating that the concepts and suggestions I’ve made below are my own thoughts, opinions, and suggestions based on my own experience working in the mental health sector and lived experience. There may also be numerous grammatical and logical errors. I know that you’re intuitive enough to understand what I’m attempting to describe and explain. Therefore, there will be no references section at the end. This is merely an expression of thoughts, a stream of consciousness (William James coined the term Stream of Consciousness).

Episodic, acute, and chronic anxiety can be miserable and debilitating. Individuals living with anxiety have generally experimented with many techniques to cope with anxiety symptoms, and they have often been practicing these techniques for months, years, or decades. Anxiety is life changing. Current treatment can be efficacious at reducing the intensity or frequency of symptoms for the vast majority of people living with anxiety, but only at best. I, myself, have tried the deep breathing technique commonly advised by mental health professionals, and it can be about as useful as taking a sugar pill. There is credible science that supports deep breathing exercises can improve symptoms and recovery rates for stress, anxiety and depression levels – but what about for an anxiety attack or a panic attack or intense chronic symptoms of anxiety?

Sometimes nothing is effective enough for immediate relief. It is my contention that building a relationship with a trained psychiatrist, specialised in this domain, is an essential first step. Your treating specialist(s) will need to have extensive experience and a comprehensive understanding of the debilitating impacts of anxiety, anxiety attacks, and/or panic attacks. I recommend psychiatry because you will need someone who can prescribe short-term medication, schedule 4 or greater, to alleviate the pain rapidly. All symptoms a person may experience from any condition in the anxiety family present a risk for searching for any immediate relief. This is true for you or me or anyone. Without prompt and effective medical care readily available, many people who do not have a plan for managing anxiety will potentially search for an unhealthy substitute to acquire relief.

These substitutes are often unhelpful long term but effective short term. We all know what they are: alcohol and other drugs, sexual promiscuity or sex addiction, love addiction, gambling, excessive or unhealthy eating habits, self-injury, addictive forms of gaming, impulse spending, co-dependent or dependent behaviours on people, people pleasing, running away (avoiding reality), raging, reckless driving and other criminal behaviour, and relying on pharmaceuticals (legally prescribes or otherwise) that will have long-term unhealthy side effects. People know how to “doctor shop”, and although this area of medicine is becoming much more regulated, it still occurs. Unfortunately, there are people who do require certain types of legal drugs, in a timely manner, to find relief as a means of not engaging in any of the previously mentioned behaviours.

Some people may not have much faith in the field of psychiatry or psychology – HOWEVER – you may find yourself in a situation one day where you will need a doctor who knows your history to increase the likelihood of prescribing medication to treat anxiety when you need it most. This medication usually has addictive properties. An ethical psychiatrist will usually be unwilling to prescribe more than a single repeat of potentially addictive medication to treat their patients. This is standard, regulated medical practice in Australia.

Anyone working in the drug and alcohol sector or has regular contact with a person living with anxiety, or any form of addiction, will know that patients – people – are not being seen in a timely manner top treat anxiety before the patient starts looking elsewhere. Even once the patient has accessed some type of medical care, the length of care is not long enough for the patient to be “well enough” after discharge or ending their hourly session, to be on their own in the community safely without becoming vulnerable to their condition in a short time and looking for more relief to ease their pain and improve their well-being.

If a person or a patient cannot depend on the medical system in the way they need to feel safe and well, they will almost certainly begin to lose faith and trust in health professionals, and ‘the system’. This perpetuates their internalised stigma being reinforced, yet again.

I am not saying the patient doesn’t have a significant responsibly of their own to make valuable choices outside of medical treatment. I quote what someone once said to me, “You may not have asked for this disease, but it becomes our responsibility to stay well”. That is our duty as the person living with a health issue of any kind. There are things we certainly must do (or not do) to stay as healthy as possible. The help make not be there in a timely manner the next time we need immediate help.

It can take weeks or more to enter a detox facility. It can take months to enter a rehabilitation facility. It can take months for an available appointment to open with a psychiatrist. It becomes our responsibility to know that even when we’re feeling well and back to “normal”, we must continue those relationships with medication professionals. It becomes our responsibility to try alternative medicines if that’s something you’re interested in. Let’s face it, psychiatrists cease their practice, our professional relationship has reached it’s potential for adequate, loving care, or we want to try something new.

Start the process of finding a reliable, qualified, and credible psychiatrist today. I would recommend finding a counselling psychologist or other mental health professional that you have a productive and friendly working relationship with – and if you want to practice Buddhism, or acupuncture, or hypnotherapy, or any other complementary and alternative medicine – do it. If you want to connect with God – do it. If you want to see a naturopath – do it. Whatever it is, this may very well be a lifelong journey for you. Based on my own experience, don’t stop because you think you’re “all better now”. The previously mentioned professions or treatment options or lifestyle choices can be extremely expensive, but I would encourage you to save for it, find less expensive options. Sitting in church is free, or listening to an online guru can be the price or maintaining your mobile service bill.

I once knew of a fellow peer in treatment alongside me who said he saved money for years to travel overseas to have a procedure not available in Australia at the time for this purpose. He wanted blood transfusions and heat therapy for chronic pain that didn’t doctors could not determine had physiological origins. The peer was sure it had to, and medical investigations in Australia come up negative. The peer explained the theory behind blood transfusions and heat therapy – he believed – were supposed to improve his blood circulation and blood flow to treat the chronic pain he’d been living with for years after a workplace accident. Even this procedure overseas proved ineffective in mitigating his chronic pain. So, next he tried the wim hof method. He changed is diet. He exercised differently. He tried hypnotherapy. Finally, he turned psychology to treat stress and process childhood trauma. He was being treated for this a private facility where I was a patient at that time. I lost contact with him after I ended my own treatment episode. I don’t know if he’s still living with chronic pain or not.

The following are some very basic and well-known strategies in the Western world of psychology that you can begin to practice today, and then practice every day after that too – even for 5-20 minutes:

– learning about anxiety – your specific “causes” and the conditions more generally

– mindfulness

– relaxation techniques

– correct breathing techniques

– dietary adjustments

– exercise

– learning to be assertive

– building self-esteem

– cognitive therapy

– exposure therapy

– structured problem solving

– support groups

My firm believe is this:

Strong, healthy, quality relationships are essential to treating anxiety and other psychological illnesses. This about your life today: are you lonely (romantically or otherwise), are you a stressed individual, do you regularly feel like you job is stressful or unfulfilling, do you feel sad a lot, are you feeling pointless a lot, or feeling helpless a lot, feeling shame a lot, getting angry a lot over considerably minor things? etc. etc. etc. I would strongly encourage talking to a professional and begin exploring what options you have available to you.

Try, explore, play with a few methods of treatment. However, this must take a priority in your life. It must balance will all the many other obligations and responsibilities people encounter daily.

Type alternative medications or approaches to psychology. There are so many. It can be fun to try out a few when your finances permit. Even planning a holiday every 3-6 months is taking care of your well-being.

Many blessings friends.

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.