People living with obsessive-compulsive disorder are encouraged to follow three general tips for effective self-management. They are: challenge the obsessive thoughts and compulsive behaviours (this includes use of distraction skills, and resisting the compulsion), maintain high self-care (you may need to put your needs first a lot – this is NOT selfishness or self-centredness), and reaching out for support. I want to clarify that I am not trained or qualified in OCD treatment – this is an extract from an article posted on the Australian Institute of Professional Counselling website.

The following information has been retrieved from AIPC Article Library | Self-help Strategies for OCD and OCPD. I think it’s also important to reinforce that if you have been living with OCD for years, you’re probably the expert on what is already most effective for you, and some of the following suggestions may make you roll your eyes. It can be very helpful/useful to talk to other people who live with OCD. They may understand your experience better than health workers, and this can be comforting, validating and healing.

Challenge the obsessive thoughts and compulsive behaviours. In addition to refocusing, the OCD client can learn to recognise and reduce stress. Some of the strategies here are counter-intuitive. You can urge clients to “go with the flow” by writing down obsessive thoughts, anticipating OCD urges, and creating “legitimate” worry periods. Tell them to:

Write down your obsessive thoughts or worries. Keep a pen and pad, laptop, tablet, or smartphone nearby. When the obsessive thoughts come, simply write them down. Keep writing as the urges continue, even if all you are doing is repeating the same phrases over and over. Writing helps you see how repetitive the obsessions are and also causes them to lose their power. As writing is harder than thinking, the obsessive thoughts will disappear sooner.

Anticipate OCD urges. You can help ease compulsive urges before they arise by anticipating them. For example, if you are a “checker” subtype, you can pay extra attention the first time you lock the window or turn off the jug, combining the action with creating a solid mental picture of yourself doing the action, and simultaneously telling yourself, “I can see that the window is now locked.” Later urges to check can then be more easily re-labelled as “just an obsessive thought”.

Create an OCD worry period. Rather than suppressing obsessions or compulsions, reschedule them. Give yourself one or two 10-minute “worry periods” each day, times you are allowed to freely devote to obsessing. During the periods, you are to focus only on negative thoughts or urges, without correcting them. At the end of the period, let the obsessive thoughts go and return to normal activities. The rest of the day is to be free of obsessions and compulsions. When the urges come during non-worry periods, write them down and agree to postpone dealing with them until the worry period. During the worry time, read the list and assess whether you still want to obsess on the items in it or not.

Create a tape of your OCD obsessions. Choose a specific worry or obsession and record it into a voice recorder, laptop or smartphone, recounting it exactly as it comes into your mind. Play the recording back to yourself over and over for a 45-minute period each day, until listening to it no longer causes you to feel highly distressed. This continuous confrontation of the obsession helps you to gradually become less anxious. When the anxiety of one worry has decreased significantly, you can repeat the exercise for a different obsession (Robinson et al, 2013).

Maintain good self-care. A healthy, balanced lifestyle plays an important role in managing OCD and the attendant anxiety (generally present with OCD, even though the disorder is no longer classified as an “anxiety disorder” per se), so the helpfulness of the following practices – truly not rocket science – cannot be underscored. Encourage OCD clients to:

• Practice relaxation techniques, for at least 30 minutes a day, to avoid triggering symptoms.
• Adopt healthy eating habits, beginning with a good breakfast followed by frequent small meals – with much whole grain, fruit and vegetable – throughout the day to avoid blood sugar lows and to boost serotonin.
• Exercise regularly; it’s a natural anti-anxiety treatment. Get 30 minutes plus of aerobic activity most days.
• Avoid alcohol and nicotine, as these increase anxiety after the initial effects wear off.
• Get enough sleep; a lack of it exacerbates anxious thoughts and feelings (Robinson et al, 2013).

Reach out for support. Staying connected to family and friends is the best defense an OCD client can muster against intrusive obsessions and compulsive urges, because social isolation exacerbates symptoms. Talking about worries and urges makes them seem less threatening. Also, involving others in one’s treatment can help maintain motivation and guard against setbacks. To help remind the client that s/he is not alone in the struggle with OCD, ask him or her to consider joining a support group, where personal experiences are shared and attendees also learn from others facing similar problems.

OCPD: Self-help strategies for survival

For both the person diagnosed with OCPD and also for his family and friends, dealing with this disorder requires patience, compassion, and fortitude. To start with, the ego-syntonic nature of OCPD means that the person does not necessarily agree that he has anything wrong at all. For those who staunchly continue to insist that their relational problems arise because of others’ faults, treatment is complicated. Given the OCPD’s general world view of “I am correct; you are wrong”, the prognosis for change is often poor. Transformation is likely to occur only when the OCPD’s relational skills and outlook are shifted. This is not a job for medication (at least not for long and not alone), and yet psychotherapy is not always available. When it is, the OCPD is not always willing to avail himself of it.

Regardless of this less-than-ideal context for managing OCPD, there are some things that the client himself and also friends and family can do to alleviate some of the tension and conflict that goes with living with the disorder. As a therapist, you can encourage the client and those around him to utilise some of these strategies.

Bibliotherapy. It’s a good idea to read up on OCPD, not only in order to know what to expect, but also for tips in dealing with it. Your client may also come upon writings that link some behaviours and lifestyle choices to the disorder in ways not understood before. When comprehension deepens, so, too, does the prospect of compassion.

Gentle confrontation (agreed beforehand). While we agree that OCPD clients have a mammoth need to be right, those clients who truly seek to feel better may be willing to make agreements with family and friends in which OCPD behaviours, when noticed, are gently challenged; the operative word here is gently.

Self-insight through journalling or tape-recording. We noted above that many OCPD clients are intelligent, sensitive people. Thus, keeping a diary or making voice recordings to note anything upsetting, anxiety-provoking, overwhelming, or depressing is a step toward the self-insight that will eventually help to manage the disorder. Too, family and friends may agree to note their observations and share them in a constructive, non-confrontational manner.

Good self-care. OCPD is a disorder about exaggerated need for control, so keeping on an emotional even keel can help reduce the unconscious need to micro-manage all of life. Strategies to achieve this are listed above under Tip 2 for maintaining self-care with OCD. They revolve around the basic life efforts of practicing relaxation techniques, adopting healthy eating and exercise regimens, getting decent sleep, and avoiding excessive alcohol/drug consumption (the last is not hard for the OCPD).

Reaching out for help. OCPD individuals tend to be loners, and relationships are hard for them to build and maintain. Nevertheless, it is helpful to the ultimate reduction of OCPD-engendered tension to go for support. This can be in the form of self-help groups, informal support from partner, family, and friends, or even from joining online communities of people dealing with the disorder. Whatever the form of the support, it may be helpful for OCPD clients to own their places of dysfunction when they see others owning their imperfect humanness – and surviving (Robinson et al, 2013)!

References

• Long, P. (2011). Obsessive-Compulsive Personality Disorder. Internet mental health. Retrieved on 18 April, 2013, from: hyperlink.
• Robinson, L., Smith, M., & Segal, J. (2013). Obsessive-Compulsive Disorder: Symptoms and treatment of compulsive behaviour and obsessive thoughts. Helpguide.org. Retrieved on 24 April, 2013, from: hyperlink.

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.