“It is not the man who has little, but the man who craves more, that is poor” – Seneca

Integrated into our everyday lives are ideas of how we can 6a00e554eecbdf88330120a7ad5e67970b-500wiachieve happiness – buy the next best car, gain a huge promotion, find your ideal partner… We are rarely made to feel content in our own skin and current state. Sadly, we have become accustomed to this; we see it everywhere and many of us recognise how such messages, particularly those in the media, buy into our feelings of dissatisfaction and insecurity. Living in such an environment, how can we ever believe enough is enough? 

Psychologists Brickman and Campbell first coined the term ‘hedonic adaptation’ in 1971. They suggest each person has a ‘set point’ of happiness18nat_married which remains constant until we experience sudden highs or downfalls. For instance, when receiving an exam grade, one might initially feel intense happiness or disappointment that will eventually return to that set point. The same goes in the context of a romantic relationship: we fall in love ecstatically, and over time reach a state of equilibrium that makes us think, “is this it?” – a thought which characterises many break-ups.

demandeuphoria_6642Positive Psychology research has looked into the idea of a ‘hedonic treadmill’ – a permanent cycle of desire fuelled by dissatisfaction. Particularly in an environment where things like money and success are highly valued, once you’re on that treadmill, you don’t want to simply feel content. You want all your hard work to pay off with feelings of ecstasy and triumph; you sacrifice the present moment in the hope that it will bring you greater satisfaction in the future. In this way, many people obtain motivation as it serves a path for ambitions. However, it can lead to anxious or depressive states in cases where people devote themselves to unattainable goals or feel a lack of appreciation for what is already within their reach.

To help combat this negative cycle, a great body of recent research points to the value of mindfulness – focusing awareness on the present moment and all its encompassing sensations. In doing so, we can free ourselves from our attachment to the past and the future and find satisfaction in the present. Mindfulness has been found to significantly improve symptoms of mental disorders like anxiety, depression and ADHD. There are some excellent blog articles that write more in depth on mindfulness techniques, such as here, here and here.

On the other hand, research has shown that our happiness levels are not always determined by the environment we are in; they are 50% heritable in our genes. In addition to this, it is found that not everyone is hedonically neutral – we all have differing set points meaning we feel pleasure differently. For example, people with depression can experience anhedonia – a total inability to feel pleasure. Some research suggests that hedonic set points can be raised using new antidepressant compounds that are currently being investigated.

Psychological research has thrown light on how our desires can lead to dissatisfaction, and provides interventions that can be used to reframe negative mind-sets. If you have any experience with subjects I have mentioned or have any ideas or questions, please comment or send me a message.


Works Cited

Brickman, P., & Campbell, D. T. (1971). Hedonic relativism and planning the good society. Adaptation-level theory, 287-305.

Eysenck, H. J., & Eysenck, M. W. (1994). Happiness: Facts and myths. Psychology Press.



An efficacious attitude works as a driving force – an individual with a strong sense of efficacy is more likely to become self-motivated, committed and assured in the face of a challenge. With high self-efficacy, one can attempt goals and conquer stress more readily, and as a result, experience better wellbeing. On the contrary, those who have doubts about their own abilities ruminate on personal flaws, slacken efforts and lose faith in the face of failure – a mind-set that in the long run can act as a brake on one’s ambitions and increase proneness to mental illness. But how does one develop self-efficacy? Is it ever as simple as telling yourself, “I can do this” when faced with a challenge? Is self-efficacy something that can be moulded and strengthened to the level we want it to be? Is anyone ever totally self-confident, and if so, is that always a good thing?

Efficacy beliefs shape the course of our lives – what goals we choose to pursue, how much we commit to those goals and how much effort we put into given endeavours. Our everyday realities are filled with obstacles, frustrations and limitations. However, it is not the difficulties we face that influence our strength and wellbeing, but the beliefs we hold about them. Our beliefs determine how much stress we experience when confronting challenges, and how long it takes before we give up altogether. We must, therefore, develop a robust sense of self-worth to sustain the enduring effort needed to flourish.


Psychologist Albert Bandura, known primarily for his research on behavioural modelling, suggests we can improve our self-efficacy, ironically, through failure. After all, if people only experience straightforward successes, it becomes an expectation that makes them far more vulnerable when things don’t go as planned. Therefore, if one comes to realise their self-worth and capability through sustained effort in overcoming adversity, they can emerge with more resilience rather than disheartenment. He discovered this during his research on fear arousal, where he saw the mediating effect that strong self-efficacy had on phobics, war veterans and hurricane survivors in overcoming incapacitating trauma.


A second way in which Bandura suggests we can shape our efficacy beliefs is through second-hand experiences provided by social role models. When we see people similar to ourselves accomplish goals, we can foster our own beliefs that we too have it in us to master similar challenges. With this in mind, we can see others’ achievements not as unattainable comparisons, but as an inspirational framework to guide our own aspirations and plans of action we set ourselves. So, instead of becoming envious and measuring our success through triumphs over others, we can do so through focusing on our own self-improvement and sharing encouragement.

Finally, because our self-efficacy can vary as a function of our physical and mental state, it can be difficult to approach a task that arouses a sense of debility or anxiety. Some people experience a nervous state as an added driving force to their motivation, whereas others view it as a sign to remove themselves from the situation as quickly as possible. This can be a particularly tough thought pattern to eradicate in the moment, but through a structured process of identifying, eliminating and replacing maladaptive or irrational thoughts and behaviours (such as through cognitive behavioural therapy), we can transform what holds us back into a force that pushes us forward. For example, we can break down large challenges into smaller, more manageable steps.

Demetri-Martin_tumblr_lo9k5j8SE31qhtggqo1_500.jpgBandura offers some extremely useful suggestions for how we can manage our own levels of self-efficacy – a skill that can motivate us to change ineffective attitudes and behaviours that might be holding us back. However, these are not limited to themselves – there are a range of other methods to be explored if these do not fit for you or every aspect of life. If you have any ideas or have had personal experience trying the above strategies or any others, please comment or message me with your thoughts and suggestions.



Bandura, A. (1994). Self‐efficacy. John Wiley & Sons, Inc..

Bandura, A., & Adams, N. E. (1977). Analysis of self-efficacy theory of behavioral change. Cognitive therapy and research, 1(4), 287-310.

Bandura, A. (2005). The primacy of self‐regulation in health promotion. Applied Psychology, 54(2), 245-254.

Benight, C.C. & Bandura, A. (2004). Social cognitive theory of post-traumatic recovery: The role of perceived self-efficacy. Behaviour Research and Therapy, 42 (10), 1129–1148


In this article, I use illustrations taken from the website of Bryan Charnley, an artist who suffered with schizophrenia and very tragically took his own life soon after these self-portraits were completed. Each painting was created as an experiment to come “face-to-face” with his illness. I felt it would be appropriate to use them here as they demonstrate, far more poignantly than can be done with words, what schizophrenic symptoms can feel like.

Psychiatrist Eugen Bleuler first coined the term ‘schizophrenia’, originating from the Greek “schizo” meaning to tear or split, and “phren” meaning intellect. This could explain the common contemporary myth about the illness involving a split personality. In reality, schizophrenia comprises a range of distressing symptoms including delusions, hallucinations, incoherent thoughts and speech, catatonic behaviour, affective flattening, alogia and avolition. The varied nature of the illness makes it challenging to diagnose using a single modality. However, it is one of the most debilitating of mental illnesses, with more than 24 million sufferers worldwide, which compels scientists in a variety of fields to continue in their search. Psychological and biological accounts present quite distinct determinist perspectives, unless combined within the ‘diathesis-stress’ model – a more holistic explanation that is now the leading approach in providing aetiology for the illness.

Bryan Charnley: Self-Portrait (1991) “My mind seemed to be thought broadcasting very severely and it was beyond my will to do anything about it. I summed this up by painting my brain as an enormous mouth, acting independently of me… I feel I am always divided against my self by myself… the nail in the mouth expresses my social ineptitude and an inability to socialise which makes me a target…”

A genetic susceptibility for psychotic symptoms is problematic to trace back to a particular genetic locus or even a small amount of genes. Therefore, a range of methods provide evidence for the involvement of numerous specific genes and rare mutations within them. Findings strongly indicate a heritable aspect to the disease, such as the fact that those with a first-degree relative with schizophrenia are ten times more likely to develop symptoms than those without. Moreover, twin studies reveal an overall heritability estimate of 80%. These discoveries highlight schizophrenia to be one of the most heritable of mental disorders. However, it can be difficult for researchers to discriminate between findings that are due to one’s environment as opposed to genetic makeup. To overcome this issue, adoption studies have been conducted using adoptees with and without schizophrenic family members. One early study found that 16.6% of adopted children with schizophrenic mothers developed the illness while none did within the control group. These findings were supported by a more recent study, where adopted children with psychotic symptoms had a 21.4% chance of having biological relatives with schizophrenia, compared to 5.4% in those who did not.

The leading biochemical theory of schizophrenia is the dopamine hypothesis, which maintains that symptoms like hallucinations, thought disorder and behavioural problems are significantly correlated to excess activity of the neurotransmitter dopamine. Antipsychotic drugs such as phenothiazines act on symptoms of psychosis by blocking the brain’s dopamine receptor sites, lowering dopamine activity. While these drugs attenuate many symptoms of schizophrenia, they have side effects such as tremors similar to those shown in Parkinson’s Disease, which is known to be caused in part by low dopamine levels. This effect is interestingly reversed when Parkinson’s patients are administered L-dopa – a drug that raises dopamine levels – resulting in the display of psychotic symptoms. Post-mortem studies have also revealed increased levels of dopamine and a considerably greater number of dopamine receptors in the brains of deceased schizophrenia patients.

Cognitive theories of schizophrenia centre on attributional and interpretational biases regarding anomalous experiences. For instance, auditory hallucinations are typically experienced by around 10 to 15% of healthy individuals, but may be interpreted in a way that makes them believe they are becoming insane, or that they ought to listen to and adhere to what the voices say in order to avoid negative consequences. Such biases are associated with deficits in cognitive functioning, again linked to excess dopamine activity, resulting in a slow decline in abilities such as early stages of sensory information processing. As a result, some sufferers experience affective flattening – a symptom rendering them socially isolated with a lack of emotions – meaning schizophrenic patients who have developed paranoid beliefs are not in the presence of others who can disconfirm their ideas, leading to a spiralling self-fulfilling prophecy.


The double-bind hypothesis suggests that schizophrenic symptoms result from a pattern of contradictory, hostile and blameful treatment from family members. For instance, families with high expressed emotion (EE) tend to place blame on the sufferer for their circumstances, and express this through shouting rather than talking through. Prior to these findings, it was advised that schizophrenic patients should go home to their families from their institution, however it has now been established that the median relapse rate in a high-EE environment is 48% compared to 21% in a low-EE environment, and that interventions to control EE in families is a more effective approach to improving symptoms. This assumption is associated with the diathesis-stress hypothesis, which intends to merge biological and psychological approaches. For instance, an individual who is genetically liable to schizophrenia may not develop symptoms of psychosis until they encounter certain life stressors that can transpire during early development, in dysfunctional family relationships or in adolescence.

The above approaches are similar in their use of empirical methods, problems with defining cause and effect and investigation into family influences. They also coincide in their discussion of the influence of dopamine, which in turn affects cognitions and the attribution of symptoms to external factors. However, they differ in that the biological approach looks at inherent traits such as genetics and biochemical composition and uses pharmacological treatments, whereas the psychological approach focuses on upbringing and cognitive processes, and family therapeutic or cognitive behavioural treatments. Overall, they work in harmony within the diathesis-stress approach, which claims a genetic predisposition to schizophrenia will only result in symptoms when activated by life stressors.

If you would like to know more about schizophrenia and learn about treatments available, there are many websites to refer to and helplines and services to contact. I have listed some below:


American Psychiatric Association. (2003). Diagnostic and Statistical Manual of Mental Disorders:: DSM-5. ManMag.

Anderson, C. M., Reiss, D. J., & Hogarty, G. E. (1986). Schizophrenia and the family: A practitioner's guide to psychoeducation and management. Guilford Press.

Andreasen, N. C. (1982). Negative symptoms in schizophrenia: definition and reliability. Archives of General Psychiatry39(7), 784-788.

Andreasen, N. C., Flashman, L., Flaum, M., Arndt, S., Swayze, V., O'Leary, D. S., ... & Yuh, W. T. (1994). Regional brain abnormalities in schizophrenia measured with magnetic resonance imaging. Jama272(22), 1763-1769.

Angrist, B., Lee, H.K. & Gershon, S. (1974). Antagonism of amphetamine-induced symptomatology by a neuroleptic. American Journal of Psychiatry, 131(7), 817- 819.

Baker, C. A., & Morrison, A. P. (1998). Cognitive processes in auditory hallucinations: attributional biases and metacognition. Psychological Medicine,28(05), 1199-1208.

Bateson, G. (1978). The double-bind theory – misunderstood? Psychiatric News, April, 40.

Berry, N., Jobanputra, V., & Pal, H. (2003). Molecular genetics of schizophrenia: a critical review. Journal of Psychiatry and Neuroscience28(6), 415–429.

Bleuler, Eugen Dementia praecox or the group of schizophrenias. Oxford, England: International Universities Press Dementia praecox or the group of schizophrenias. (1950). 548 pp.

Cardno, A.G. & Gottesman, I.I. (2000). Twin studies of schizophrenia: From bowand-arrow concordances to star wars Mx and functional genomics. American Journal of Medical Genetics, 97, 12–17.

Davey, Graham C. (2008) Psychopathology: Research, Assessment and Treatment in Clinical Psychology, 235-255 John Wiley & Sons.

Davis, J.O. & Phelps, J.A. (1995). Twins with schizophrenia: Genes or germs. Schizophrenia Bulletin, 21(1), 13–18

Davis, K. L., & Kahn, R. S. (1991). Dopamine in schizophrenia: a review and reconceptualization. The American journal of psychiatry148(11), 1474.

Dickerson, F. B., Tenhula, W. N., & Green-Paden, L. D. (2005). The token economy for schizophrenia: review of the literature and recommendations for future research. Schizophrenia Research75(2), 405-416.

Freeman, D., Garety, P. A., Kuipers, E., Fowler, D., & Bebbington, P. E. (2002). A cognitive model of persecutory delusions. British Journal of Clinical Psychology41(4), 331-347.

Gejman, P.V., Sanders, A.R. & Kendler, K.S. (2011). Genetics of schizophrenia: New findings and challenges. Annual Review of Genomics and Human Genetics, 12, 121–144.

Gottesman, I.I., McGuffin, P. & Farmer, A.E. (1987). Clinical genetics as clues to the real genetics of schizophrenia (a decade of modest gains while playing for time). Schizophrenia, 13(1), 23-47.

Gottesman, I.I. & Bertelsen, A. (1989). Confirming unexpressed genotypes for schizophrenia: Risks in the offspring of Fischer’s Danish identical and fraternal discordant twins. Archives of General Psychiatry, 46(10), 867–872.

Grilly, D.M. (2002). Drugs and human behaviour (4th edn). Boston: Allyn & Bacon.

Harrop, C. & Trower, P. (2001). Why does schizophrenia develop at late adolescence? Clinical Psychology Review, 21, 241–266.

Heston, L.L. (1966). Psychiatric disorders in foster home reared children of schizophrenic mothers. British Journal of Psychiatry, 112(489), 819–825

Jablensky, A., Sartorius, N., Ernberg, G., Anker, M., Korten, A., Cooper, J. E., ... & Bertelsen, A. (1992). Schizophrenia: manifestations, incidence and course in different cultures A World Health Organization Ten-Country Study.Psychological medicine. Monograph supplement20, 1-97.

Kavanagh, D. J. (1992). Recent developments in expressed emotion and schizophrenia. The British Journal of Psychiatry160(5), 601-620.

Kety, S.S. (1988). Schizophrenic illness in the families of schizophrenic adoptees: Findings from the Danish national sample. Schizophrenia Bulletin, 14(2), 217– 222.

Kety, S.S., Wender, P.H., Jacobsen, B., Ingraham, L.J. et al. (1994). Mental illness in the biological and adoptive relatives of schizophrenic adoptees: Replication of the Copenhagen study in the rest of Denmark. Archives of General Psychiatry, 51(6), 442–455.

Lotharius, J., & Brundin, P. (2002). Pathogenesis of Parkinson's disease: dopamine, vesicles and α-synuclein. Nature Reviews Neuroscience3(12), 932-942.

Morrison, A. P. (2001). The interpretation of intrusions in psychosis: an integrative cognitive approach to hallucinations and delusions. Behavioural and Cognitive Psychotherapy29(03), 257-276.

Owen, M. J., Williams, N. M., & O'Donovan, M. C. (2004). The molecular genetics of schizophrenia: new findings promise new insights. Molecular psychiatry9(1), 14-27.

Schiffman, J., Abrahamson, A., Cannon, T., LaBrie, et al. (2001). Early rearing factors in schizophrenia. International Journal of Mental Health, 30, 3–16.

Schneider, F. & Deldin, P.J. (2001). Genetics and schizophrenia. In P.B. Sutker & H.E. Adams (Eds.) Comprehensive handbook of psychopathology (3rd edn). New York: Kluwer Academic/Plenum.

Seeman, P. & Kapur, S. (2001). The dopamine receptor basis of psychosis. In A. Brier, P.V. Tran, F. Bymaster & C. Tollerfson (Eds.) Current issues in the psychopharmacology of schizophrenia. Philadelphia: Lippincott Williams & Wilkins.

Segerbäck, D., Calleman, C. J., Schroeder, J. L., Costa, L. G., & Faustman, E. M. (1995). Formation of N-7-(2-carbamoyl-2-hydroxyethyl) guanine in DNA of the mouse and the rat following intraperitoneal administration of [14C] acrylamide. Carcinogenesis16(5), 1161-1165.

Sommer, I. E., Daalman, K., Rietkerk, T., Diederen, K. M., Bakker, S., Wijkstra, J., & Boks, M. P. (2010). Healthy individuals with auditory verbal hallucinations; who are they? Psychiatric assessments of a selected sample of 103 subjects.Schizophrenia Bulletin36(3), 633-641.

Tam, G. W., Redon, R., Carter, N. P., & Grant, S. G. (2009). The role of DNA copy number variation in schizophrenia. Biological psychiatry66(11), 1005-1012.

Waters, F., Allen, P., Aleman, A., Fernyhough, C., Woodward, T. S., Badcock, J. C., ... & Larøi, F. (2012). Auditory hallucinations in schizophrenia and nonschizophrenia populations: a review and integrated model of cognitive mechanisms. Schizophrenia Bulletin38(4), 683-693.

Walker, E. F., & Diforio, D. (1997). Schizophrenia: a neural diathesis-stress model. Psychological review104(4), 667.

Weakland, J. H. (1960). The 'Double-Bind' Hypothesis of Schizophrenia and Three-Party Interaction.

Basic Books. Oxford, England.

Weisman, A. G., Nuechterlein, K. H., Goldstein, M. J., & Snyder, K. S. (2000). Controllability perceptions and reactions to symptoms of schizophrenia: a within-family comparison of relatives with high and low expressed emotion.Journal of abnormal psychology109(1), 167.

Disney Disorder

The Soapbox


Being 20 I still enjoy watching Disney Movies. Recently I came to realization that a lot of Disney movie’s protagonist characters are associated with disorders. Surprised?  I was too !

I have personally grown up watching  Cinderella story, I loved and admired the story line which had the knight in shining armor that would come riding along and sweep the princess feet and on to a happily ever after .

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