Final Thoughts

When I attended the first class, and found out we had to do the talks every other week, I’m not going to lie, I contemplated dropping the course. The thought of speaking in front of others used to scare the heck out of me. However, I decided to stick it out and I’m glad that I did. This course has helped me to interact with my peers, something that was previously out of my comfort zone. I feel like the whole point of university is to get us to experience new things that we wouldn’t normally do.

This course has allowed me to view so many different topics, by having to research many aspects of social cognition and then writing about it. Not only did I learn a lot when doing my own research and writing, but also by reading the blogs of my peers and having to make constructive comments related to their given topics. The talks were also something that I actually quite enjoyed. It brings new insight listening to other people talk about subjects that they are interested in. Many times over the course of the semester I found myself doing further research related to someone else’s talk just to learn more about it.

My advice to any one considering taking this course would be to do it! The whole no exams thing was awesome. I feel that the structure of this class allowed the students to interact with each other in a way where socialization was happening at the same time learning was occurring. It was refreshing walking into class knowing that I wouldn’t be sitting in the same spot for an hour and fifteen minutes with a prof standing at the front giving a lecture, while everyone takes notes. I feel that this style of teaching was very effective for learning, I actually learned a lot from my peers, which is something that I’ve never really experienced during my time in university.

Overall this course was by far one of my favourites, and I will definitely recommend it to everyone. It’s nice when the marks are spread out over the course of a semester rather than having three exams that make up your whole grade. Other professors should take note of this style of teaching, I mean it’s great for hands on learning and the prof gets to sit back while the students do all the talking!


Social Physique Anxiety

In my previous blog post I talked about social anxiety and the ways it can affect an individual. In this blog post, I will be talking about Social Physique Anxiety (SPA). SPA is characterized as a category of social anxiety. It is defined as the inclination to experience fear or worry in response to the aspect or expectation of unfavourable physique evaluation (Focht, & Hausenblas, 2004). Individuals with SPA will often avoid public gyms due to fear of having their physiques judged by other people. SPA is often a result of other peoples’ evaluations regarding one’s body. This can cause self-criticism, anxiety, and low self esteem. SPA is found to be more prevalent in women than in men, although the rates for men are rising as well. Often times, individuals will go to great lengths to change their image, and they may start working out for the wrong reasons, which can result in negative consequences if they aren’t taking the right precautions. SPA is found to be comorbid with body dysmorphic disorder, which is characterized by excessively checking self in the mirror, excessive use of makeup, or other attempts to cover up (Mohammadi, 2015). Both of these disorders result in educational deficits, and low social performance on every-day tasks. Many of the individuals who have SPA have different ways of coping with it, there are behaviours such as changing their appearance. There are also cognitive measures used in attempt to cope with SPA, for example hoping to be accepted by others, wishful thinking, or the person may have complete cognitive avoidance in order to avoid coping, this can be seen as a protective measure used in attempt to protect oneself from shame or embarrassment (Atalay, & Gençöz, 2008). One study that researched SPA came up with themes related to women’s experiences with SPA. The themes were:

Web of emotion: Women described their experience of SPA as an underlying web of emotion rather than one concrete emotion, related to how they felt about their bodies, whether it was positive or negative. Although most times individuals with SPA will have negative body images.

Uncertainty: The women within the study explained how they felt others viewed their bodies, and many said that they felt uncertain about how (they perceived) others evaluated them which left them feeling nervous and anxious.

Beyond Physique: Participants often included their hair and makeup or clothing when talking about overall appearance. They also focused on specific parts of their bodies, for example talking about how they would like to enhance their lips, or how they wished they were thinner, prettier etc (McHugh et al., 2008).


Atalay, A., & Gençöz, T. (2008). Critical Factors of Social Physique Anxiety: Exercising and Body Image Satisfaction. Behaviour Change, 25(03), 178-188.

FOCHT, B., & HAUSENBLAS, H. (2004). Perceived Evaluative Threat and State Anxiety During Exercise in Women with Social Physique Anxiety. Journal Of Applied Sport Psychology, 16(4), 361-368.

McHugh, T., Kowalski, K., Mack, D., Crocker, P., Junkin, S., Lejbak, L., & Martin, S. (2008). Young Women’s Experiences of Social Physique Anxiety. Feminism & Psychology, 18(2), 231-252.

Mohammadi, M. (2015). Social Physique Anxiety and its Relation with Body Dysmorphic Disorder. The European Journal Of Social And Behavioural Sciences, 13(2), 1736-1746.

Social Anxiety Disorder

Social anxiety disorder (SAD) is defined as being an increased amount of fear in various social situations, in which the individual becomes extremely distressed and has a lack of ability to function properly (The Social Anxiety Association, 2017). Social anxiety can be a repercussion of adverse childhood experiences, and the onset might not be seen until adult life. The brain develops social anxiety over time, after it is primed over and over again, it learns what to be afraid of. Repeating certain behaviours overtime, will allow those behaviours to become automatic, this is important when thinking about social anxiety. People who have social anxiety display an increased fear response within social settings (Boehme et al., 2013).

Often times, individuals with SAD will over estimate and over analyze a social situation thinking that they will judged. On the other hand, they also underestimate their ability to handle certain situations, by believing that they will say or do something stupid. Another characterization of this would be thinking that situations will always turn out negative, for example believing that people will think less of you.

Due to these beliefs that individuals with SAD have, they will often to go above and beyond to avoid socialization. People with SAD are likely to remember a social situation worse than it actually was, and use that as a cue to enforce their fears (Andrew Kukes Foundation For Social Anxiety, 2017).

The cause of social anxiety is unknown, but early research suggests that it arises from a sequence of nature (genetics), and nurture (environment). There is also evidence to suggest that an imbalance in the hormone serotonin may add to the onset of SAD. Serotonin is the hormone responsible for mood regulation, and an imbalance of this hormone along with an overactive amygdala can also be indicative of causation.


Boehme, Stephanie et al. “Brain Activation During Anticipatory Anxiety In Social Anxiety Disorder”. Social Cognitive and Affective Neuroscience 9.9 (2013): 1413-1418.

The Cognitive Theory of Social Anxiety – Andrew Kukes Foundation for Social Anxiety. (2017). Andrew Kukes Foundation for Social Anxiety. Retrieved 24 March 2017, from

Social Anxiety Fact Sheet | Social Anxiety Association. (2017). Retrieved 24 March 2017, from

How Does Anxiety Affect Cognition?

Anxiety is a reality for many individuals, with the prevalence being approximately one in four Canadians (Anxiety Disorders Association of Canada, 2003). The definition of anxiety as defined by the DSM-V is an excessive amount of worrying, that occurs for more days than not and lasts at least six months (American Psychiatric Association, 2013). The anxiety can be triggered by certain events or situations such as school/sports performance or work/family life. Looking through an evolutionary lens, anxiety can be seen as a tool that our brains use to let us know when we are in dangerous situations. This can be helpful to let us know whether we should be in fight or flight mode. However, in today’s society there are many individuals who suffer from anxiety disorders without being in stressful situations. Anxiety can now be treated with medication, cognitive behavioural therapy or relaxation therapy. Treatment doesn’t necessarily cure an individual from their anxiety, however it does help with the symptoms.

This got me to thinking, what goes on in the brain during an anxiety attack? In this post I will attempt to answer this question. First of all I will add that anxiety is a natural and normal response to potential threats and can trigger a heightened level of alertness when present during an appropriate situation. When an individual becomes anxious, it evokes the same fight or flight response as when one’s stressed. Which can cause a lot of chemical changes in the brain, including an increase in cortisol levels which can lead to increased heart rate, reflexes and circulation.

The amygdala and hippocampus play a compelling role in almost all anxiety disorders. The amygdala is thought to be a communicator that serves as a processor and interpreter for incoming sensory signals. It can inform the rest of the brain, and relay a message if there is a possible threat. Which will then cause an individual to feel fear, worry, or uncertainty which is the epitome of anxiety. The amygdala is also responsible for storing emotional memories that can potentially bring about anxiety disorders associated with specific fears. For example, if a person was bit by a dog in the past, they may experience anxiety when they are around dogs due to that fearful memory. The hippocampus is responsible for encoding fearful or threatening situations or events into memories that are stored in the amygdala(National Institute of Mental Health, 2016). In my next post, I will be going into more detail on how anxiety affects self efficacy. Stay tuned, thanks for reading!


American Psychiatric Association (2013) ‘Substance-related and addictive disorders’, in Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition. Arlington, VA: American Psychiatric Publishing, .

“Anxiety In Your Brain: What Happens When Anxiety Attacks?”. N.p., 2017. Web.

“Anxiety Disorders”. The National Institute of Mental Health. N.p., 2016. Web. 17 Mar. 2017.

When Does Worry Become Too Much?


Many individuals have experienced the feeling of anxiety at some point in their life. Especially university students having to write exams and papers under strict deadlines. However when the anxiety is persistent and constantly interfering with daily activities then individuals are usually given a general anxiety disorder (GAD) diagnosis. Anxiety disorders are mental disorders that inflict with feelings of worry, uneasiness, fear, etc. on one’s life and in turn, affect various, if not all aspects of their life. Generalized anxiety disorder is a common disorder in which a person has unfocused worry that is not related to recent stressful events, although it can be brought on by certain situations. GAD is twice as common in women than in men and it is characterized by feelings of threat, restlessness, irritability, sleep disturbance and tension. There are also physical symptoms that individuals will experience such as: dry mouth, sweating, tachycardia and tremors. Many people who are diagnosed with GAD may never completely escape their symptoms, however there are short term treatments that can help with the ease of the symptoms. Some of the treatments that can help with GAD are, cognitive behavioural therapy, psychological treatments, and pharmacological treatments, most commonly serotonin re-uptake inhibitors (Tyrer and Baldwin, 2006).

Since the period of the DSM-III, GAD has had a series of changes made specifically in the classification areas. The revisions were made due to the poor inter-rater reliability as well as concerns that it was lacking diagnostic criteria. One of the main implementations in the DSM-V was adding the symptom of ‘worry’. Worry is classified as being a troubled state of mind arising from the frets and cares of life. The feeling of worry is a cognitive component and it is distinct from the physiological symptoms of anxiety. Researchers have found that worry is an avoidant coping strategy that is negatively enforced by reduction in patient’s worry. This causes the reduction in emotional reactivity in the short-term. Due to the issue that patients’ with GAD are not able to process their distresses in a normative manner, they are bound to experiencing continued distress and worry as a means of reducing their particular distress (Andrews et al., 2010).

Generalized anxiety disorder is highly comorbid with specific phobias, panic disorder, obsessive-compulsive disorder and personality disorders. Depressive and bipolar disorders are also comorbid with separation anxiety disorder in older adults. Anxiety disorders differ from developmentally normative fear or anxiety because the fear is excessive and persistent beyond developmentally appropriate periods and usually lasting six months or more. Many anxiety disorders develop in childhood and tend to persist into adulthood (American Psychiatric Association, 2013).



American Psychiatric Association (2013) ‘Substance-related and addictive disorders’, in Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition. Arlington, VA: American Psychiatric Publishing, .

Andrews, G., Hobbs, M. J., Borkovec, T. D., Beesdo, K., Craske, M. G., Heimberg, R. G., Rapee, R. M., Ruscio, A. M. and Stanley, M. A. (2010), Generalized worry disorder: a review of DSM-IV generalized anxiety disorder and options for DSM-V. Depress. Anxiety, 27: 134–147. doi:10.1002/da.20658

Tyrer, P. and Baldwin, D. (2006) ‘General Anxiety Disorder’, The Lancet, 368(9553), pp. 2156-2166. doi: S0140-6736(06)69865-6.

Child Resiliency

Childhood is a very critical period for brain development, during this time the brain is in an extremely sensitive state and undergoes a series of changes. In the midst of these changes, many children will experience adversities in their lives due to several reasons, one example is poverty. Adverse childhood experiences can negatively impact the brain development of a child, and can cause health problems later in life. However despite the negative impacts these experiences can have on an individual, many children have an ability to overcome them. This phenomena is often referred to as child resilience, which means the ability to successfully adapt to life tasks in the face of social disadvantage or highly adverse conditions.

During times of stress, the brain actually undergoes physical structural changes which can then affect things such as mood, decision making and planning to name a few. So how does our brain adapt to stress? Well we are constantly being bombarded with stimuli, and responding to that stimuli can sometimes be a challenge. However after experiencing stressful events our brain goes through a process called allostasis which is essentially the brain trying to regain homeostasis (McEwan, Gray, and Nasca, 2015). This process involves several complex systems such as the autonomic nervous system, cortisol, and neuromodulators in the brain. This system is responsible for how our brains adapt to stressful events. However this system will only work efficiently if there it is being turned on and off at the right time. Too much or too little cortisol (stress hormone) can result in impairment of this system which is called allostatic load or overload (McEwan, 1998). This system could aid us in understanding how children adapt to their stressful environments.

Another factor that influences resilience and could help in explaining the phenomena is epigenetics, which is the study of changes caused by modification of gene expression. In one study, researchers found that the acetylating agent L-acetylcarnitine (LAC), which is a naturally occurring substance acts like an antidepressant. LAC was shown to cause a rapid long-lasting antidepressant effect in rats and mice who were exposed to chronic unpredictable stress. This finding offers a suggestion that LAC is critical for stress resilience (Dantzer et al., 2008).

There is a substantial amount of research done on this topic and I have merely grazed the surface. These are just a few of the ways our brains can adapt to adverse experiences and can help us understand why some children are resilient and are able to overcome such experiences and why some cannot.


McEwen, B.S., Gray, J.D. and Nasca, C. (2015) ‘Recognizing resilience: Learning from the effects of stress on the brain’, Neurobiology of Stress, 1, pp. 1–11. doi: 10.1016/j.ynstr.2014.09.001.

R. Dantzer, J.C. O’Connor, G.G. Freund, R.W. Johnson, K.W. Kelley

From inflammation to sickness and depression: when the immune system subjugates the brain

Nature., 9 (2008), pp. 46–57

B.S. McEwen

Protective and damaging effects of stress mediators

N. Engl. J. Med., 338 (1998), pp. 171–179

The Aging Brain

The Aging Brain

The human brain is constantly adapting as people age and gain more life experience. However there are declines that come with age, such as the speed of processing, working memory, inhibitory functioning, and long-term memory. The overall size of the brain and it’s white matter also decrease. In the midst of these decreases, functional imaging studies have shown fairly remarkable, positive increases in prefrontal activation. Although there are decreases in certain areas, other areas are protected such as implicit memory and knowledge storage. (Park & Reuter-Lorenz, 2009). The brain is a complex organism that seeks to maintain homeostatic cognitive function. With age, the amount of dopaminergic receptors declines and several brain structures show volumetric shrinkage. The brains of even very highly functioning individuals are frequently characterized by destructive neurofibrillary plaques and triangles (Park & Reuter-Lorenz, 2009).

The brain areas that undergo the greatest shrinkage across the lifespan occur in the caudate, cerebellum, hippocampus, and prefrontal areas. There is minimal shrinkage in entorhinal cortex, and the visual cortex volume remains stable across the lifespan (Raz, 2000). Evidence suggests that age-related changes in the volume of specific brain structures have direct consequences for cognitive functioning. For example, shrinkage of entorhinal cortex over a five-year period in a sample of older adults predicted poor memory performance. This suggests that memory performance is related to hippocampal and entorhinal volume (Rosen et al., 2003).

One theory that explores the relationship of the brain and aging, is the scaffolding theory of aging and cognition (STAC). The STAC model integrates the impact of biological aging and experience to account for the neural reorganization of function that occurs in late adulthood. This theory describes how existing strengths can be harnessed to build new skills or recover and sustain capabilities that have been threatened by challenge. STAC establishes the relationship between neurocognitive aging within the context of both plasticity and challenge. In doing so, this theory ties a potentially important comparison between the brain’s response to aging, early development, new skill acquisition, and both transient and chronic states of disorder that include, sleep deprivation, neurological lesions, and other stressors (Park & Reuter-Lorenz, 2009).


Park, D. C., & Reuter-Lorenz, P. (2009). The Adaptive Brain: Aging and Neurocognitive Scaffolding. Annual Review of Psychology, 60, 173–196.

Raz N. Aging of the brain and its impact on cognitive performance: integration of structural and functional findings. In: Craik F, Salthouse TA, editors. The Handbook of Aging and Cognition. Hillsdale, NJ: Erlbaum; 2000. pp. 1–90

Differential associations between entorhinal and hippocampal volumes and memory performance in older adults.

Rosen AC, Prull MW, Gabrieli JD, Stoub T, O’Hara R, Friedman L, Yesavage JA, deToledo-Morrell L

Behav Neurosci. 2003 Dec; 117(6):1150-60.

Do you really want that drink?

Many of us will admit to having a drink every now and then whether it’s coping with stress, hanging with friends, or going for a night out. A little alcohol never hurt anyone right? However when does it become a problem? In this post I will be discussing the criteria for diagnosing alcohol use disorders (AUDs), as well as the affect alcohol has on our brain and cognition.

Alcohol use disorder (AUD) can be defined as a chronic disease in which the body and mind become dependant on alcohol. The prevalence of alcohol use disorder is 3-9% in Canada, and is usually seen more within the population of 18-25 year old men. The DSM-V criteria states that in order to be diagnosed with an AUD and individual must meet at least two of eleven symptoms. The symptoms include: drinking longer than intended, failing to quit or cut down on drinking, spending a lot of time drinking, wanting to drink so badly that you couldn’t think of anything else, having home, family or job/school troubles due to drinking and continuing to drink even though it was making you feel depressed or anxious or adding another health problem. These are just a few of the eleven symptoms stated in the DSM-V and the severity of AUD is defined in the amount of symptoms that are present. For example, mild AUD is the presence of 2-3 symptoms whereas severe is the presence of 6 or more, with moderate being somewhere in between (American Psychiatric Association, 2013).

The experience of alcohol use can be thought of as a spectrum of increased alcohol levels depending on the size and tolerance of a person. For example, after one or two drinks an individual may start to feel more outgoing which is a sign of decreased inhibition that is attributed to the impact ethanol has on GABA. GABA is the primary inhibitory neurotransmitter in the mammalian central nervous system. It is a chemical messenger that is widely distributed in the brain and its natural function is to reduce the activity of the neurons to which it binds. When an individual is under the influence, it is believed that the alcohol mimics GABAs effect in the brain and binds to GABA receptors which in turn inhibits neuronal signalling, causing a person to be more social and outgoing. (Davies, 2003). Which is the reason you might drunk dial or text someone a risky message, or feel more inclined to talk to a person you wouldn’t normally talk to.

Alcohol consumption is widely accepted in today’s society, and is used in different ways for different reasons. The reasons can be due to social interactions, coping mechanisms, pain relief or stress relief as I mentioned earlier.  It’s also an easy-access drug that can be purchased at liquor stores, restaurants, and bars, as well as casinos. However many people lack the knowledge of the effects that alcohol has on the human body. Chronic drinking can have a very negative impact on our brain, because consumption is associated with positive reinforcement. Drinking alcohol inhibits the major excitatory neurotransmitter, glutamate and releases other inhibitors such as dopamine which activates the reward pathway in the mesolimbic system and provides reinforcement. This can partially explain the reason that alcohol can be so addicting. Another inhibitor that is released is called serotonin, which effects mood, sleeping and eating, it can also cause cravings during times when alcohol is not present in the body (The Scripps Research Institute, 2002).

So next time you’re out with friends or feeling the weight of student stress, and decide to have a drink, know your limit. Although you may feel more inclined to do something risky, it’s probably just the alcohol and you will most likely regret whatever it is the following day.

– Cheers!




American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition. Arlington, VA, American Psychiatric Association, 2013.

Davies, M. (2003) ‘The role of GABA(A) receptors in mediating the effects of alcohol in the central nervous system’, Journal of Psychiatry & Neuroscience, 28(4), pp. 263–74.

The Scripps research institute (2002) ‘The Effects of Alcohol on the Brain’, News and Views, 2(6).

Stressed out!

As university students we often find ourselves cramming for the next exam, or staying up late finishing that ten page paper, or trying to put together a presentation for an upcoming deadline, all the while juggling other things in life. The point is that because of all the chaos in our lives we are bound to get stressed out at some point. However there are ways to cope. In the remainder of this post, I will be talking about how stress affects us throughout our lives and what we can do to manage it.

In today’s society, many people are developing chronic stress issues related to emotional pressure that is suffered for a prolonged period of time. An individual usually has no control over the stress he/she is experiencing, and the onset can be caused at any point in time. The effect stress has on the human brain varies with each individual, depending on the age of the person and the environment that they are in.

Prenatal stress has a very negative impact on the growing fetus, and usually has an increased effect on the amount of activity that goes on in the HPA axis, which in turn modifies brain development. A retrospective study was done on children whose mothers had experienced stress during pregnancy and researchers found that stress lead to the children having long-term neurodevelopmental effects, and low birth weight. Excessive prenatal stress is also known to be correlated with non-normative behaviours and psychiatric disorders such as, attention deficit hyperactivity disorder (ADHD), drug abuse later in life, as well as anxiety and mood disorders.

Stress in adolescence can be caused by several factors, such as the pressure to succeed in school/sports, or stress within the home, or social life. Whatever the causes are, the impact is unfavourable. Adolescence is a critical period for brain development, as it reaches the stages of maturation, therefore any stress that is put on the brain can cause an impairment in the natural development. The more negative life events an adolescent experiences, the more likely they are to engage in problem behaviours. Prolonged stress in teens, is also linked to poorer cognitive performance as well as decision making.

In adulthood having to balance work/school, home, and family is a stress in and of itself. However if an individual is doing more than he/she can withstand for an extended period of time (staying in the library for 8 hours every day) it can have an emotionally draining effect on him/her. Increased stress in adulthood is known to cause dendritic atrophy in hippocampal pyramidal neurons. Although this may be the case, its not all bad news, the process can be reversed by ten days after the stressor is removed. Stress in adulthood can be better managed than having it earlier on in life. Lucky for us, unlike stress in childhood or adolescence, the effects of stress in adulthood are often reversible after a few weeks of non-stress and the damage isn’t permanent. There are ways to manage stress, such as exercising, relaxation therapy, or meditation. If a person begins to develop chronic stress, it is important to deal with it earlier rather than later (Lupien., et al., 2009). So if you are feeling stressed out, take some time for yourself, your brain will thank you!

Lupien, Sonia J., et al. “Effects of stress throughout the lifespan on the brain, behaviour and cognition.” Nature Reviews Neuroscience, vol. 10, no. 6, 2009, p. 434+. Health Reference Center Academic,


There are several fundamental changes that the human body undergoes throughout the lifespan. One of those changes is, the adjustment of one’s personality over the course of his/her life. Narrative identity is described as being an individuals’ internalized and evolving life story, integrating the reconstructed past and imagined future to provide us with some degree of unity and purpose (McAdams and McLean, 2013). In a recent study done on narrative identity, evidence has shown that life-narrators who find meaning in suffering and adverse experiences, and those who construct life stories of themselves that include themes of personal agency and exploration, tend to enjoy higher levels of mental health, well-being and maturation (McAdams and McLean, 2013). Across the lifespan, personalities are constantly evolving as an individual understands more about themselves and the world around them. However there are particular traits that remain the same in some people throughout life. There are many theories that seek to explain this phenomena for example the continuity-discontinuity controversy. This controversy is concerned with whether a particular developmental phenomena represents a smooth progression over time (continuity) or a series of abrupt shifts (discontinuity). Continuity usually focuses on the amount of a specific characteristic that someone has whereas the latter focuses more on the amount of a characteristic an individual has (Cavanaugh & Blanchard-Fields, 2014). It is important for human beings to discover themselves as unique individuals in all areas of life such as, age, gender, ethnicity, and culture. Self-understanding is the role of narrative memory and life story construction (McAdams, 1987; Singer & Salovey, 1993). For researchers to understand how individuals perceive themselves, they must first understand how individuals compose narratives from experiences, and share their experiences both internally and with others. Once life experiences are processed through a narrative viewpoint, they can be useful in ways that guide ones’ actions or influence others.


Cavanaugh, J.C. and Blanchard-Fields, F. (2014) Adult development and aging. 7th edn. Stamford, CT, United States: Wadsworth Publishing Co.

McAdams, D. P. (1987). A life-story model of identity. In R. Hogan & W. H. Jones (Eds.), Perspectives in personality (vol. 2, pp. 15–50). Greenwich, CT: JAI Press.

McAdams, D.P. and McLean, K.C. (2013) ‘Narrative Identity’, Current Directions in Psychological Science, 22(3), pp. 233–238. doi: 10.1177/0963721413475622.

Singer, J. A., & Salovey, P. (1993). The remembered self: Emotion and memory in personality. New York: The Free Press.