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.

To answer that question, I’ll need to explain a part of the brain called the Limbic System.

Within the brain there is a set of structures called the limbic system. There are several important structures within the limbic system: the amygdala, hippocampus, thalamus, hypothalamus, basal ganglia, and cingulate gyrus. The limbic system is among the oldest parts of the brain in evolutionary terms. It’s not just found in humans and other mammals, but also fish, amphibians, and reptiles.

The limbic system is the part of the brain involved in our behavioural and emotional responses, especially when it comes to behaviours we need for survival: feeding, reproduction and caring for our young, and fight or flight responses (https://qbi.uq.edu.au/brain/brain-anatomy/limbic-system).

The limbic system contains the brain’s reward circuit or pathway. The reward circuit links together several brain structures that control and regulate our ability to feel pleasure (or “reward”). The sensation of pleasure or reward motivates us to repeat behaviours. When the reward circuit is activated, each individual neuron (nerve cell) in the circuit relays electrical and chemical signals.

In a healthy world without addictive manufactured drugs, humans survive and thrive when they are rewarded for certain behaviours (cleaning, hard work, sex, eating, achieving goals etc), hence evolution has provided us with this feel-good chemical so that we will repeat pleasurable behaviours.

There is a gap between neurons called the synapse. Neurons communicate with each other by sending an electro-chemical signal from one neuron (pre-synaptic neuron) to the next (post-synaptic neuron). In the reward circuit, neurons release several neurotransmitters (chemical messengers). One of these is called dopamine. Released dopamine molecules travel across the synapse and link up with proteins called dopamine receptors on the surface of the post-synaptic neuron (the receiving nerve cell). When the dopamine binds to the dopamine receptor, it causes proteins attached to the interior part of the post-synaptic neuron to carry the signal onward within the cell. Some dopamine will re-enter the pre-synaptic nerve cell via dopamine transporters, and it can be re-released.

When a reward is encountered, the pre-synaptic nerve cell (neuron) releases a large amount of dopamine in a rapid burst. Dopamine transporters will remove “excessive” amounts of dopamine naturally within the limbic system. Dopamine surges like this help the brain to learn and adapt to a complex social and physical world.

Drugs like methamphetamine (a stimulant drug) are able to “hijack” this process contributing to behaviours which can be considered unnatural or potentially dysfunctional. A range of consequences can follow.

When someone uses methamphetamine, the drug quickly enters the brain, depending on how the drug is administered. Nevertheless, meth or ice is quick acting. Meth blocks the re-entry of dopamine back into the pre-synaptic neuron – which is not what happens naturally. This is also what cocaine does to the brain. However, unlike cocaine, higher doses of meth increase the release of dopamine from the presynaptic neuron leading to a significantly greater amount of dopamine within the synapse. Higher doses of cocaine will not release “more dopamine” from the pre-synaptic neuron like meth does. This is why after about 30 minutes or so, people who use cocaine will need more to maintain the high.

Dopamine gets trapped in the synapse (space between nerve cells) because the meth (like cocaine) prevents “transporters” from removing it back into the cell it came from. The postsynaptic cell is activated to dangerously high levels as it absorbs so much dopamine over a long period of time. The person using meth experiences powerful feelings of euphoria, increased energy, wakefulness, physical activity, and a decreased appetite.

When an unnatural amount of dopamine floods the limbic system like this over a long period of time, without reabsorption, then our brain is not replenished with dopamine, hence people who use meth often (even on a single occasion) may feel unmotivated, depressed, joyless, and/or pointlessness when they stop using. Figuratively speaking, the brain is “empty” or low on dopamine fuel, and it will take time to for dopamine to return to baseline levels and replenish itself. This may motivate the user to seek more methamphetamine to return to “normal”.

Methamphetamine can also cause a variety of cardiovascular problems, including rapid heart rate, irregular heartbeat, and increased blood pressure. Hyperthermia (elevated body temperature) and convulsions may occur with methamphetamine overdose, and if not treated immediately, can result in death (What are the immediate (short-term) effects of methamphetamine misuse? | National Institute on Drug Abuse (NIDA) (nih.gov))

SIGNS OF SUBSTANCE MISUSE OR ADDICTION

• Finding it difficult to meet responsibilities.
• Withdrawing from activities or not enjoying activities that used to provide satisfaction e.g. work, family, hobbies, sports, socialising.
• Taking part in more dangerous or risky behaviours e.g., drink driving, unprotected sex, using dirty needles, criminal behaviour.
• Behaviour changes e.g., stealing, exhibiting violence behaviour toward others.
• Conflict with partner/family/friends, losing friends.
• Experiencing signs of depression, anxiety, paranoia, or psychosis.
• Needing more substance to experience the same effects
• Cravings and urges to use the substance and symptoms of withdrawal when not using the substance.
• Having difficulty reducing or stopping substance use.
• Regretting behaviours while under the influence and continuing to use again.

(Substance abuse, misuse and addiction | Lifeline Australia | 13 11 14)

Abstract

Addiction is a complex, multifaceted phenomenon that has been described variously as a disease, disorder, syndrome, obsessive-compulsive behaviour, learned behaviour, or spiritual malady. Modern scientific understanding emphasises addiction as a chronic brain disorder shaped by neurobiological changes, learning, and social context. This article examines each conceptualisation and presents an integrated definition that aligns with current neuroscience, psychological, and public health evidence.

Conceptualising Addiction: Labels and Their Accuracy

No single label fully captures addiction’s complexity; each highlights certain truths while overlooking others.

Disease

From a medical perspective, disease is the closest match. Addiction involves persistent neurobiological changes in reward, stress, and self-control circuits, increases relapse risk over years, and shows substantial genetic vulnerability (~50–60%) (NIDA, 2018; Heilig et al., 2021). Treatments improve outcomes but rarely “cure” the condition. This framing is used by the American Society of Addiction Medicine (ASAM), NIDA, WHO ICD-11, and DSM-5-TR (as “Substance Use Disorder”) (NIDA, 2018).

Disorder

Disorder is also scientifically accurate and slightly less medicalised. DSM-5’s “Substance Use Disorder” captures behavioural, psychological, and biological criteria and recognises functioning and harm rather than framing addiction strictly as a lifelong disease (Heather, n.d.; Heilig et al., 2021).

Syndrome

Addiction may be described as a syndrome because it is a cluster of symptoms with behavioural and physiological manifestations, without a single causative factor. However, the term is too generic for practical use outside clinical texts (Blithikioti et al., 2025).

Obsessive and Compulsive Learned Behaviour

Addiction involves learning, habit formation, and compulsion through reinforcement of rewarding behaviours (Hyman, 2005; Hausotter, 2013). Yet describing it solely as learned behaviour ignores genetic predisposition, neuroadaptation, withdrawal, and social factors.

Spiritual Malady

Some mutual-aid traditions characterise addiction as a spiritual malady. While this may be meaningful for individuals, it is not scientifically explanatory: addiction can be adequately explained via biological, psychological, and social mechanisms (Lewis, 2017).

Modern Integrative Definition

The most accurate contemporary description of addiction is:
“A chronic, relapsing disorder of brain circuits involved in reward, stress, and self-control, shaped by learning, environment, and social context”.

This definition encompasses:

• Disease/disorder: medical accuracy
• Learned behaviour and compulsion: neuroscience and behavioural accuracy
• Social determinants: public health relevance
• Flexibility for personal or spiritual interpretations

In short, addiction is best understood as a bio-psycho-social condition that is treatable and sometimes reversible, rather than a deterministic, lifelong curse.

Neurobiology: Why Addiction Is Considered a Brain Disorder

Repeated substance use alters structural and functional brain circuits involved in reward, stress, motivation, memory, and self-control (Nwonu et al., 2022; NIDA, 2018). These changes can persist long after use stops, explaining why addiction is more than a matter of “bad habits” or weak will (NIDA, 2025).

Chronicity and Relapse

Addiction is often chronic and relapsing. Even after long periods of abstinence, cues and stressors can trigger relapse (Meurk et al., 2014; SAMHSA, 2023). Key regions implicated include the basal ganglia (habit formation), extended amygdala (stress), and prefrontal cortex (decision-making) (Kirby et al., 2024). Nevertheless, many individuals achieve stable remission, highlighting heterogeneity in clinical outcomes (Heilig et al., 2021).

Learning, Memory, and Habit Formation

Addiction exploits neural mechanisms of learning and memory: rewarding behaviours are repeated and consolidated into habits, with cues triggering compulsive responses even when the substance’s reward diminishes (Hausotter, 2013; Lewis, 2017). This intertwines biological disorder and learned behaviour.

Critiques and Limitations

Some scientists caution that framing addiction strictly as a brain disease is simplistic:

• Brain changes may resemble those from other motivated behaviours (Lewis, 2017).
• Many recover without formal treatment (Heilig et al., 2021).
• Social, environmental, and psychological factors are crucial to understanding addiction (Blithikioti et al., 2025).

Thus, while the disease model is powerful, it does not fully represent addiction’s heterogeneity or socio-psychological dimensions.

Implications for Treatment

Addiction is treatable, not simply curable. Interventions combining pharmacological and behavioural approaches, alongside social support, can foster long-term recovery (Liu & Li, 2018; Heilig et al., 2021). Like other chronic conditions, management — rather than elimination — is often the realistic goal (NIDA, 2018). Neural circuits can gradually readjust, particularly when environmental and personal factors support recovery.

Conclusion

Addiction is a learned, compulsive brain disorder with chronic potential, shaped by neurobiological, psychological, social, and environmental factors. Recognising addiction as both a disorder and a behavioural learning condition avoids extremes: it is neither an unchangeable fate nor merely a moral failing. This integrated perspective supports nuanced understanding, compassionate care, and effective treatment strategies.

References

Blithikioti, C., Fried, E. I., Albanese, E., Field, M., & Cristea, I. A. (2025). Reevaluating the brain disease model of addiction. The Lancet Psychiatry, 12(6), 469–474. https://doi.org/10.1016/S2215-0366(25)00060-4

Hausotter, W. (2013). Neuroscience and understanding addiction. Addiction Technology Transfer Center (ATTC) Network. https://attcnetwork.org/neuroscience-and-understanding-addiction

Heather, N. (n.d.). What’s wrong with the brain disease model of addiction (BDMA)? Addiction Theory Network. https://addictiontheorynetwork.org/brain-disease-model-of-addiction

Heilig, M., MacKillop, J., Martinez, D., Rehm, J., Leggio, L., & Vanderschuren, L. J. M. J. (2021). Addiction as a brain disease revised: Why it still matters, and the need for consilience. Neuropsychopharmacology, 46(10), 1715–1723. https://doi.org/10.1038/s41386-020-00950-y

Hyman, S. E. (2005). Addiction: A disease of learning and memory. The American Journal of Psychiatry, 162(8), 1414–1422. https://doi.org/10.1176/appi.ajp.162.8.1414

Kirby, E. D., Glenn, M. J., Sandstrom, N. J., & Williams, C. L. (2024). Neurobiology of addiction (Section 14.5). In Introduction to Behavioral Neuroscience. OpenStax. https://socialsci.libretexts.org/…/14.05:_Neurobiology_of_Addiction

Leshner, A. I. (1997). Addiction is a brain disease, and it matters. Science, 278(5335), 45–47. https://doi.org/10.1126/science.278.5335.45

Lewis, M. (2017). Addiction and the brain: Development, not disease. Neuroethics, 10(1), 7–18. https://doi.org/10.1007/s12152-016-9293-4

Liu, J. F., & Li, J. X. (2018). Drug addiction: A curable mental disorder? Acta Pharmacologica Sinica, 39(12), 1823–1829. https://doi.org/10.1038/s41401-018-0180-x

Meurk, C., Carter, A., Partridge, B., Lucke, J., & Hall, W. (2014). How is acceptance of the brain disease model of addiction related to Australians’ attitudes towards addicted individuals and treatments for addiction? BMC Psychiatry, 14, 373. https://doi.org/10.1186/s12888-014-0373-x

National Institute on Drug Abuse. (2018). Drugs, brains, and behavior: The science of addiction (Rev. ed.). https://irp.nida.nih.gov/…/NIDA_DrugsBrainsAddiction

Nwonu, C. N. S., Nwonu, P. C., & Ude, R. A. (2022). Neurobiological underpinnings in drug addiction. West African Journal of Medicine, 39(6), 874–884. https://pubmed.ncbi.nlm.nih.gov/36063103

Substance Abuse and Mental Health Services Administration. (2023). What is substance use disorder? U.S. Department of Health and Human Services. https://www.samhsa.gov/substance-use/what-is-sud