Research Papers / Antidepressants: A physiological, behavioural, theoretical, and clinical review [5]

Abstract

Antidepressants have become the most widely prescribed psychotropic medication in North America and are used to treat a wide range of mental disorders, including depression, anxiety, ADHD, OCD, and alcoholism. This paper explores several topics related to antidepressants and their use in the treatment of psychiatric conditions, specifically Major Depressive Disorder. The three main classes of antidepressants-Selective Serotonin Reuptake Inhibitors (SSRIs), Monamineoxidase Inhibitors (MAOIs), and Tricyclics (TCAs)-are discussed in detail, with an emphasis on their history, pharmacokinetics, mechanisms of action, and side effects. The paper ends by evaluating the overall effectiveness of antidepressants in treating depression.

Antidepressants are the most commonly prescribed psychotropic medication. To say that the list of mental disorders for which antidepressants are prescribed is long would be an understatement. Some of these disorders include Major Depressive, Bipolar, Social Phobia, Obsessive-Compulsive, Attention-Deficit-Hyperactivity, Substance Use, and Generalized Anxiety Disorder, among others. As a result, few psychopharmacological drugs have received as much research attention as antidepressants and the present paper reviews but a fraction of this literature. But before discussing such issues as mechanisms of action and treatment efficacy, a brief review of the history of antidepressants is called for.

History of Antidepressants

The first antidepressant to be discovered was the MAOI, Iproniazid, in the 1950's. The antidepressant effects of the drug were actually discovered fortuitously. Researchers originally developed the drug to treat tuberculosis, but soon discovered that the drug alleviated depression and improved patient's moods. After the drug's antidepressant effects were publicized, several new MAOIs were developed and released on the market to treat depression. The success of the first-generation MAOIs was short lived, however, as media reports that the drug was ineffective and caused liver damage surfaced soon after its release. Although these reports were mostly unfounded and eventually refuted by subsequent research, the removal of Iproniazid from the market did inspire researchers to develop newer MAOIs that were more specific in their action and that had reversible effects.

In the late 1950's, the first TCA antidepressant, Imipramine, was also discovered by an accident. Scientists were trying to develop a drug to treat the psychotic symptoms of schizophrenia. Although it wasn't successful in treating schizophrenia, Imipramine did appear to relieve the symptoms of depression and, as a result, it was subsequently used to treat major depression. However, similar to first generation MAOIs, earlier TCAs had severe side effects. Today, many second generation TCAs have been developed which are just as effective as earlier TCAs in treating depression but which have fewer negative side effects.

Fluoxetine, or as it commonly referred to as, Prozac, was introduced to the public in 1987 as the first SSRI. Unlike its predecessors, the MAOIs and TCAs, SSRIs targeted only a specific neurotransmitter, called serotonin. Many have likened the analogy of SSRIs as North America's "happy" pills which are believed to cure all of lives problems. Today, SSRIs are the most widely prescribed antidepressant for treating depression as well as many other mental disorders, such as OCD and anxiety. In 2007 alone, there were more than 30 million prescriptions filled for Zoloft in the United States (Advanstar Communications, 2008).

Pharmacokinetics

The pharmacokinetics of a drug can be defined as the movement of the drug throughout the body, which includes the drug's method of administration; the absorption of the drug into the blood stream; the distribution of the drug to the site of action; and the removal of the drug from the body.

Antidepressants are absorbed in similar ways. They are taken orally as a pill and pass through the digestive tract, where they are absorbed into the blood through the blood vessels lining the stomach. However, before the drug enters the blood stream and reaches the brain, most of it is actually destroyed by the digestive tract and the liver, a process known as "First-pass metabolism"(McKim, 2007). Alcohol inhibits this process in all antidepressants with the exception of SSRIs, which are often prescribed to alcoholics. As a result, if someone consumes alcohol while taking certain antidepressants, toxic levels of the drug can accumulate in the blood. TCAs are absorbed quickly whereas for absorption for MAOIs and SSRIs is much slower. Antidepressants are able to cross the blood-brain and placental barrier with relative ease. The drug tends to concentrate in the liver, lungs, kidneys, and the brain (McKim, 2007), and high levels of the drug have been found in breast milk (Kim et al., 2005).

The Excretion of a drug is measured by the half life of the drug, which is the time period required for the body to eliminate half of the blood level of the drug (McKim, 2007). MAOIs have a half life of about 2-3 hours and, as a result, are taken 2-3 times a day. TCAs and SSRIs have half lives of about 15-24 hours. Most antidepressants do not have active metabolites (McKim, 2007). The exception is Prozac, whose metabolite blocks the enzyme responsible for the drugs destruction. The active metabolite of Prozac has a half-life of 16 days. Switching medications before the active metabolite of Prozac has been excreted can lead to a condition called Serotonin syndrome, which is discussed below.

Neurophysiology: How Do Antidepressants Work?

Antidepressants are believed to treat depression by increasing the activity of one or more of the monamine systems-serotonin (5-HT), dopamine (DA), and norepinephrine (NA)-in the brain (Duman, Heninger, & Nestler, 2000). Specific regions of the limbic system-such as the amygdala and hippocampus-and the medial forebrain bundle-including the NE fibres of locus coeruleus, serotonergic fibres in the raphe system, and dopaminergic fibres of the mesolimbic system-have been implicated in depression (Hercher, Turecki, & Mechawar, 2009). The three main classes of antidepressants differ depending on which monamine system(s) they target.

MAOIs work by blocking the activity of the monamine oxidase enzyme, which metabolizes the monamine neurotransmitters (MAs) 5-HT, DA, and NA. When this enzyme is blocked or inhibited, there is a build-up of neurotransmitters in the synaptic cleft, which leads to increased binding of MAs to the postsynaptic neuron. First generation MAOIs, such as Iproniazid, had an irreversible effect on the monamineoxidase enzyme, that is, they permanently destroyed it. This posed a serious problem as this enzyme metabolizes several other important chemical substances in the body aside from neurotransmitters, such as tyramine. Newer MAOIs are less "messy" or indiscriminate, that is, they generally alter the levels of only certain neurotransmitters, such as 5-HT and NE, and have irreversible effects.

SSRIs and TCAs work in similar ways. After neurotransmitters are released into the synaptic cleft, most are reabsorbed by the presynaptic neuron and recycled for subsequent use. SSRIs and TCAs increase MA neurotransmission, and supposedly alleviate depressive symptoms, by preventing the re-uptake receptors on the presynaptic neuron from reabsorbing MAs, causing an increased level of MAs in the synaptic cleft. SSRIs, as their name implies, specifically alter serotonin levels, whereas TCAs are less discriminate in their physiological effects. Newer drugs, such as Reboxetine, block the re-uptake of NE.

Harmful Effects

TCAs are the third most common cause of drug related deaths, next to only alcohol and heroine. SSRIs, although often advertised as the safest antidepressant, can also have potentially lethal effects on the body through a condition called serotonin syndrome, which occurs when 5-HT1A receptors are over stimulated (Birmes, Coppin, Schmitt, & Lauque, 2003). Serotonin syndrome can lead to unpleasant physical symptoms such as fever, shivering, and diarrhoea and cognitive symptoms such as disorientation and agitation. Serotonin syndrome often develops when antidepressants are co-prescribed with other medications or taken with psychostimulants such as amphetamines (Frank, 2008).

Soon after Fluoxetine was released in the late 1980's there were several claims that it induced intense, violent suicidal ideation in depressed patients (Teicher, Glod, & Cole, 1998). This possible link between antidepressants and suicide sparked much research and heated debate among experts in the field, and was the topic of many news reports and television talk shows. Although the preponderance of research supporting this link came in the form of case studies, the U.S. Food and Drug Administration (FDA) demanded that all drug manufacturers include warning labels about the potential dangerous effects of antidepressants. This official recognition by the FDA of the suicidal effects of antidepressants coupled with increased research attention led to many high-profile court cases in which antidepressants, Fluoxetine in particular, were blamed for violent crimes. Eric Harris, who is infamously known as one of the school shooters in the tragic Columbine massacre, had been taking antidepressants for about a year before the incident, and several news reports attempted to draw a link between Eric's violent behaviour and the suicidal effects of antidepressants (Cullen, 2009). Despite over two decades of research on the possible link between suicide and antidepressants, the issue is far from being settled. This is in part due to the fact that it is extremely difficult for researchers to investigate the topic. Suicidal ideation and attempts are, unfortunately, relatively common among people who are depressed anyway, so it is not clear whether the reported increase in suicidal ideation after taking antidepressants reflects a drug-induced effect or just a lack of response to the drug.

Nevertheless, attempts have been made to explicate the reported relationship between antidepressants and suicide. One such theory attributes the link not to a direct drug-induced effect or to even a lack of response to the drug but rather to a mismatch in symptom improvement (Machado-Vieira et al., 2008). One of the symptoms of depression (see appendix A for the full diagnostic criteria for Major Depressive Disorder) is lethargy, or lack of energy. People who are clinically depressed often report feeling extremely tired and lethargic, insofar as it is exhausting for them just to get out of bed in the morning and get dressed. According to this theory, such people are not at risk for completing suicide. Although they may be preoccupied with the idea of committing suicide, they lack the energy necessary to actually complete the suicide attempt. However, if they start taking an antidepressant, which generally improves physical energy before mood, they may have enough energy to finally carry out a suicide attempt. Although this theory makes intuitive sense, it is entirely speculative and currently lacking empirical support.

Some researchers have gone to the root of the issue and questioned the very assumption that antidepressants increase suicide. Contrary to this assumption, they argue, antidepressants prevent, rather than cause, suicide (Simon, Savarino, Operskalski, Wang, 2006). Large scale ecological studies have shown that the recent increase in the prescription of antidepressants, particularly SSRIs, has been associated with an overall decrease in the number of suicide rates (Gibbons et al., 2008; Milane, Suchard, Wong, & Licinio, 2006; Morgan, Griffiths, & Majeed, 2004). Such studies, however, due to the ecological nature of their design, do not permit cause and effect inferences. Individual level data gathered from drug trials do confirm a decrease in the incidence of suicides among patients taking antidepressants (Castelpietra et al., 2008; Isacsson, Osby, & Ahlner, 2009), suggesting that antidepressants may play a preventative role in suicide. These findings are relatively robust and have been well documented (Bramness & Walby, 2009). It's also possible, however, that other factors, such as general improvement in mental health care, are responsible for the overall decline in suicide rates (Kapusta et al., 2009).

Like with any other drug, there are certain risks associated with taking antidepressants. It's no secret that antidepressants have many unwanted side effects; in fact, there are about as many side effects for each drug as there is total number of drugs. Depending on the type of antidepressant, common side effects can include sexual dysfunction, dry mouth, constipation, irregular heartbeat, ringing in the ears, weight gain, and headaches, among others. Despite steadfast claims by the media that antidepressants induce suicidal ideation and aggression, however, extant research has failed to support this causal relationship. In fact, most of the literature suggests that antidepressants decrease, rather than increase, suicide.

The Monamine Hypothesis

The discovery of the therapeutic benefits of the first generation antidepressants Iproniazid and Imipramine, and the physiological mechanisms by which these drugs operated, gave rise to the formulation of the monamine theory of depression, which held that the disorder was caused by decreased activity of the monaminergic systems in the brain. Although this theory has received wide spread acceptance for many years, as evidenced by the steadily increasing rates of antidepressant prescriptions, there is a plethora of research calling for a complete revamp of the theory on the basis that it is oversimplified (Hindmarch, 2001; Pacher & Kecskemeti, 2004; Tang, 1999). Inspiring this recent surge in criticisms has been empirical findings that have questioned the overall efficacy of antidepressants in treating Major Depressive Disorder (see below for a review). Belmaker (2008) identified four main limitations of the monamine hypothesis: 1) The mechanism of action of several antidepressants are non-specific; 2) Monamine neurotransmitters are involved in multiple behaviours, not just ones governed by mood and emotion; 3) The placebo-drug difference in controlled studies indicates that monamine levels are causally involved in only 50% of depressed patients; and 4) Since neurotransmitter levels in the brain cannot be directly measured, the monamine theory is not falsifiable.

The effectiveness of antidepressants: Fact or fiction?

Recent research has called into question the effectiveness of antidepressants in treating people with depressive disorders (Ioannidis, 2008; Lacasse & Leo, 2005). Much of this criticism has been inspired by recent claims in the literature that antidepressants are often no more effective than placebos. For example, in a meta-analysis of 96 trials drug trials, involving 9566 people, Rief et al. (2009) concluded that as much as 68% of the improvement in people taking antidepressants can be attributed to the placebo effect. Kirsh et al. (2008) found that antidepressant efficacy increased as the level of baseline severity increased, but that this was not due to an increased responsiveness to the antidepressant, but rather to a decreased responsiveness to the placebo. Other researchers have pointed out that, due to the selective publication of antidepressant trials, the current literature overestimates the efficacy of antidepressants. For example, Turner et al. (2008) reviewed 74 drug trials submitted to the FDA and found that of the 37 studies with positive results all but one were published, whereas only 3 of the 36 studies with negative results were published.

No one is denying the potential therapeutic effects of antidepressants. About 50% of people taking antidepressants do experience some type of improvement in their depressive symptoms (Nierenberg et al., 2008), but an equal amount of patients don't respond at all to antidepressants, which suggests that the monamine theory alone cannot explain the pathophysiology of depression. It could be that those who do respond well to antidepressants represent a distinct sub-group of depressed patients, perhaps those who are more biologically predisposed to depression. Further research is needed to identify the genetic markers of depression, but available research has implicated several other neurobiological factors in the development of depression. Among these are an over-activity of hypothalamic-pituitary-adrenal axis (Dinan, 2001; Hindmarch, 2001; Leonard, 2001; Rot, Mathew, & Charney, 2009); hippocampal neural plasticity in response to stress (Hindmarch, 2001; McEwen & Magarinos, 2001; Roee et al., 2009); inflammatory response to stress (Maes, 2001; Miller, Rohleder, Stetler, & Kirschbaum, 2005); and levels of the brain-derived neurotrophic factor (BDNF) (Rot, Mathew, & Charney, 2009; Sandler, 2001). Taken together, this research highlights the need for novel approaches to treating depression (Rot, Mathew, & Charney, 2009).

As mentioned previously, research has failed to provide an adequate explanation for the frequently observed, and relatively robust, placebo effect. If all a person has to do to alleviate his/her depressive symptoms is to be told that a pill, which in reality is nothing more than sugar water, will treat his/her symptoms, and telling them does just that, then perhaps depression has more to do with personal attitudes and beliefs than genetics and molecular biology. Psychotherapy, then, which involves changing one's perceptions and attitudes, would seem to be a better approach to treating depression than antidepressants. Of course, a keen reductionist will be quick to point out that even psychological concepts, such as beliefs and attitudes, can be explained by neurological activity. After all, thoughts and emotions are just chemical reactions in the brain, right? True, but therapy does not have an inordinate amount of unpleasant and potentially lethal side effects-drugs do. Moreover, the continued use of antidepressants is based on the assumption that depression is caused by depleted MAs levels-an assumption of which many researchers have become increasingly sceptical, and rightly so.

The monamine theory of depression was developed over 50 years ago; every other theory in psychology that has been in existence for that long has either been abandoned or radically reconstructed. That physicians and psychiatrists have continued to prescribe antidepressants in exponential numbers despite the steady accumulation of research underscoring its limited effectiveness is an indication that they are either ignorant to the research or motivated to prescribe for other reasons.

References

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Writing Feedback / Compulsive buying disorder (CBD): Conceptualization and classification [6]

Abstract
Although not officially recognized as a mental disorder, compulsive buying is a serious and chronic problem that causes significant impairments in social, occupational, and interpersonal areas of functioning. In anticipation of the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-V), many researchers have argued for the acknowledgement of this condition as a mental disorder. In addition to reviewing the extant research on compulsive buying and the evidence supporting its validity as a mental illness, this paper explores the possible classifications of the disorder in the context of proposed revisions to the DSM-V. Although more research is needed to elucidate the nature of the disorder, it is concluded that CBD should be classified as an impulse control disorder, rather than an addiction or obsessive-compulsive disorder.

Compulsive buying disorder (CBD): Conceptualization and classification

The DSM task force is busy preparing for the publication of its 5th edition of the Diagnostic and Statistical Manual of Mental Disorders, which is set to be released sometime in May, 2013 (American Psychiatric Association, 2010). In anticipation of its release, there has been a surge in research evaluating the current organization and classification of mental disorders in the DSM-IV-TR and several recommendations have been made for the 5th edition. Perhaps the most notable, and indeed the most controversial, revision being considered for the DSM-V is the introduction of several new disorders. One of the disorders being considered for inclusion is Compulsive Buying Disorder (CBD) . Below is a review of the extant research on CBD, including its symptomology, epidemiology, comorbidity, and possible classifications if and when it is included into the DSM.

Compulsive Buying Disorder (CBD): Definition, clinical symptoms, epidemiology, and comorbidity
Although it is not included in the DSM-IV-TR (American Psychiatric Association, 2000), Compulsive Buying Disorder (CBD) has received considerable attention in the literature since the 1990's, when clinical case studies first started to appear (McElroy, Keck, Pope et al., 1994; Schlosser, Black, Repertinger, & Freet, 1994). Currently, people presenting symptoms consistent with CBD are diagnosed with "Impulse Control Disorder Not Otherwise Specified". However, the classification of the disorder has been a topic of much debate. Notwithstanding this disagreement over the nosology of CBD, there is a general consensus within the literature that it is a serious condition (Hartson & Horan, 2002) characterized by excessively or poorly controlled preoccupations, urges, or behaviours with regard to shopping or buying (Black, 2001), which can lead to negative consequences such as remorse, excessive debt, marital and family conflict and even suicide attempts (O'Guinn & Faber, 1989; McElroy et al., 1997; Koran, Faber, Aboujaoude, Large, & Serpe, 2006).

The diagnostic criteria for CBD proposed by McElroy et al. (1994) has received widespread acceptance among researchers and has been used in several studies as a threshold for the disorder (see Appendix A for McElroy et al. (1994) diagnostic criteria for CBD). The core elements of the criteria include: (1) Frequent preoccupation with shopping or intrusive, irresistible, 'senseless' buying impulses; (2) clearly buying more than is needed or can be afforded; (3) distress related to buying behaviour; and (4) significant interference with work or social functioning.

The estimated prevalence of CBD in the adult U.S. population is about 5.8% (Koran et al., 2006), although prevalence rates as low 1.8% (Faber & O'Guinn, 1989) and as high as 8% (Magee, 1991) have been reported in the literature. Caution must be exercised, however, when interpreting such prevalence rates because, other than McElroy et al. (1994) proposed criteria which was based on 20 reported cases, CBD currently lacks a definitive criteria.

The age of onset for CBD appears to be in the late teens to early 20's (Black, 2001). The preponderance of people identified as compulsive buyers are female, constituting, on average, 80-95% of clinical samples (Schlosser et al., 1994; McElroy et al., 1994). However, a recent study (Koran et al., 2006) using a large general population sample found that the prevalence rates of CBD between men and women were only marginally different. The disparity between gender rates of CBD in clinical and community samples may be explained by female's greater willingness than men to seek therapy for their compulsive shopping.

Comorbidity rates among people with CBD are exceedingly high (McElroy et al., 1994; Schlosser et al., 1994). Among the Axis I disorders commonly associated with CBD are mood, anxiety, substance use and eating disorders. In Schlosser et al. (1994) clinical sample of 46 people with CBD, 60% met the criteria for at least one personality disorder, most commonly obsessive compulsive (22%). Furthermore, first-degree relatives (FDRs) of individuals with CBD are more likely to have psychiatric disorders such as alcohol or substance abuse, major depression, and anxiety disorders than FDRs of people without CBD (McElroy et al., 1994; Black et al., 1998).

Four distinct phases of CBD have been identified (Black, 2007): 1) anticipation; 2) preparation; 3) shopping; and 4) spending. In the first phase, the person has thoughts or preoccupations with having a certain item or shopping in general. The second phase involves preparing for shopping which may include deciding at which store to shop, what clothes to wear, and even which credit card to use. The third phase involves the actual act of shopping. Many people with CBD have reported that they feel exhilarated when shopping and in some this may lead to sexual feelings (Schlosser et al., 1994). Finally, the last phase involves the purchasing of the item, after which the person may be overwhelmed with feelings of shame and embarrassment (Hartston & Koran, 2002). Clothes, shoes, jewellery, and makeup are among the most common items purchased by women, whereas men are more likely to purchase electronic, hardware, and automotive products (Black, 2001; Black, 2007).

In a study exploring the antecedents and consequences of compulsive buying, Miltenberger et al. (2003) found that negative emotions such as depression, anxiety, boredom, and self-critical thoughts were common antecedents to compulsive buying, whereas euphoria and relief of negative emotions were often consequences. Thus, in individuals with CBD, shopping appears to be a primary response to stress (O'Guinn & Faber, 1989) and used as a means of mood elevation (Clark & Calleja, 2008). The pleasurable feelings associated with shopping in people with CBD are positively reinforcing and the alleviation of anxiety and depressed mood is negatively reinforcing, both of which serve to perpetuate the behaviour.

Research has consistently found that people who buy compulsively display higher rates of the compulsive personality trait, have lower self-esteems, depressed moods, more compromised self-perceptions and perfectionistic expectations, more decision making difficulties, and are more prone to fantasy than people with more normal buying behaviour (O'Guinn & Faber, 1989; Kyrios, Frost, & Steketee, 2004). Rose (2007) reported a positive correlation between narcissism, materialism, and compulsive buying, and a negative association between impulse control and each of these variables in people with CBD.

Criticism of CBD
Although many researchers have argued for the inclusion of CBD into the DSM, some feel that it is not a bona fide mental illness (Shirley & Avis, 2004). Compulsive shopping, they argue, and other similar controversial disorders such as "internet" and "sex addictions" are moral, rather than medical, problems. They also criticize the medical and scientific community's eagerness to "medicalize" deviant behaviour, which they perceive as attempts to create more conditions to treat with pharmaceutical drugs. Similar criticisms have been made towards attention deficit hyperactivity disorder (ADHD) and social anxiety disorder, which some argue are just normal traits that have been ascribed medical labels and treated with drugs (Hollander, 2006). However, creating a new diagnosis is a complex process, and much of the attack directed at the validity of certain mental disorders has come from armchair critics.

Granted, the line between "excessive" and "compulsive" or "disordered" buying is arbitrary at best, but this is true of most, if not all, mental disorders in the DSM. Moreover, the clinical emphasis of CBD is not on the amount of the behaviour-many people in our culture of consumerism shop "excessively" or purchase items that they don't need-but rather the consequences of the behaviour. Asserting that conditions such as CBD, ADHD, and social phobia are "trivial" disorders, not worthy of diagnosis and treatment undermines the serious social, occupational, and interpersonal disruptions that these disorders often cause when untreated. Others have pointed out that including a disorder into the DSM, even if it is seemingly "trivial" or controversial, is very important for augmenting knowledge about that particular condition because it provides researchers with a specific set of criteria to use in their research (Hollander, 2006), which can then be used to refine and improve the disorder's criteria.

Compulsive Buying Disorder: Classification
Though it may not seem that important, the nosology of a mental disorder has profound implications. As mentioned previously, CBD is not currently recognized by the DSM-IV-TR as a mental disorder and, as such, the classification of CBD, upon inclusion into the DSM, has been a topic of much debate among researchers investigating the disorder. Three possible classifications for CBD have been proposed.

Option 1: CBD as an Addictive Disorder
The rationale behind classifying some impulse control disorders, such as compulsive shopping and pathological gambling (PB), as behavioural addictions is that they share many important features-clinical symptoms, comorbidity, family history, brain circuitry, and treatment responses to SSRI's-with substance addictions (Bernardo et al., 2008; Hollander, 2009).

Currently, the nomenclature of the DSM-IV-TR lacks the term "addiction". However, one of the proposed revisions being considered for the DSM-V is the removal of the "substance use disorder" (SUD) section and the adoption of an "addiction and related disorders" category. Many researchers have advocated for the complete abolishment of the terms "substance" and "dependence", as research has shown that these terms are misleading and problematic. For example, tolerance and withdrawal are generally considered to be the trademark symptoms of substance dependence, but people can become tolerant to and experience withdrawal symptoms from a drug without necessarily being addicted to it.

Thus, it is believed that changing the terminology will shift the focal point of the disorder from chronic use, tolerance, and withdrawal to the detrimental effects of the disorder to the person, their family, and occupation (Potenza, 2006). In addition to supporting this change in nomenclature, some researchers have argued that the scope of addictions should be extended beyond SUD's to include behavioural addictions, such as pathological gambling and sexual, internet, and shopping addictions (Goodman, 2001; Martin & Petry, 2005).

This increased pressure for the conceptualization of behaviours as potentially addictive is heavily supported by research highlighting the neurobiological similarities between impulse control disorders and substance addictions (Holden, 2001). There is a growing body of literature suggesting that the brain circuitry implicated in substance addictions-namely, the ventromedial prefrontal cortex and the dopaminergic mesolimbic pathway linking the ventral tegmental area to the nucleus accumbens, or as it is commonly referred to as, the "reward system"-is involved in impulse control disorders such as PG (Potenza, 2006). For example, in one study, a decreased activation of the ventral striatal and ventromedial prefrontal cortex was observed in people with PG during the presentation of gambling-related cues (Reuter, Raedler, Rose, Hand, Gläsche, & Büchel, 2005), a neurological finding that is consistent with research on people with SUD's.

Using Shaffer's (1999) definition of addiction ((1) craving state prior to behavioural engagement, or a compulsive engagement; (2) impaired control over behavioural engagement; and (3) continued behavioural engagement despite repeated adverse consequences) it could be argued that most, if not all, of the people identified in clinical samples as presenting symptoms consistent with CBD meet the criteria for an addiction. For example, they have preoccupations with buying items (1); irresistible urges and impulses to buy which can only be alleviated following a purchase (2); and a continuation of excessive spending despite personal, familial, occupational, and financial problems that are caused by, or at least in some way related to, the behaviour (3) (Black, 2001; Black, 2007; Dell'Osso, Allen, Altamura, Buoli, & Hollander, 2008).

Option 2: CBD as an Obsessive-Compulsive Disorder
Another categorical change being considered for the DSM-V is the creation of an obsessive-compulsive spectrum disorder (OCSP) category. This proposed revision reflects the recent shift in the literature from a categorical to a dimensional conceptualization of psychopathology. In light of this proposed change, some have argued that CBD should be placed along the obsessive-compulsive spectrum, with compulsive disorders, such as OCD, at one end and impulsive disorders, such as PG and CBD, at the other. The rationale for this is that people with CBD, like OCD, are preoccupied with persistent and intrusive thoughts about buying items, which causes anxiety and motivates the person to shop in order to alleviate the anxiety (Ridgway, Kukar-Kinney, & Monroe, 2008).

While obsessive-compulsive tendencies have been associated with CBD, people with this condition also score high on the personality traits impulsivity and sensation seeking and low on the trait conscientiousness (Rodriguez-Villarino et al., 2006). These personal variables are uncharacteristic of most individuals with OCD. Furthermore, there are several other significant differences between impulsive and compulsive disorders that are worth noting. For example, in compulsive disorders the thoughts tend to be egodystonic and the disorder is characterized by overestimation of harm, harm avoidance, risk aversion, and anticipatory anxiety (Dell'Osso et al., 2006). Conversely, in impulsive disorders the thoughts tend to be egosyntonic and the disorder is characterized by underestimation of harm and risk seeking. Moreover, the behaviours in impulse control disorders produce pleasurable and gratifying feelings, whereas the compulsive behaviours common in OCD are not pleasurable; in fact, they are often embarrassing, distressing, painful (i.e., excessive hand washing), and the primary motivation is to alleviate anxiety caused by obsessive and intrusive thoughts. The DSM-IV-TR (American Psychiatric Association, 2000) clearly defines compulsions as:

repetitive behaviours (e.g., hand washing, ordering, checking) or mental acts (e.g., praying, counting, repeating words silently) the goal of which is to prevent or reduce anxiety or distress, not to provide pleasure or gratification [italics added]. In mostcases, the person feels driven to perform the compulsion to reduce the distress that accompanies an obsession or to prevent some dreaded event or situation (p. 457).

Although anxiety may, and often does, precede an impulsive act, such as excessive shopping, the pleasurable feelings associated with the act also contribute significantly to its motivation, which precludes the behaviour from being classified as an OCD.

Other support for the designation of CBD as an OCSD has come from the high comorbidity rates (about 35%) of OCD in impulse control disorders (Fontenelle, Mendlowicz, & Versiani, 2005). However, this is tenuous evidence, not suffice to warrant the inclusion of impulse control disorders into the OCSD category. The comorbidity rates of anxiety in depression, eating disorders, and SUD's are high as well; does this mean that these disorders should be merged into one dimensional category?

Option 3: CBD an Impulse Control Disorder
The DSM-IV-TR includes the following description of impulse control disorders:
The essential feature of Impulse-Control Disorders is the failure to resist an impulse, drive, or temptation to perform an act that is harmful to the person or to others. For most of the disorders in this section, the individual feels an increasing sense of tension or arousal before committing the act and then experiences pleasure, gratification, or relief at the time of committing the act (APA, 2000, p. 663).

The DSM's description of an impulse control disorder seems to accurately characterize the core features of CBD. People with this disorder report an irresistible impulse or urge to shop. Moreover, after engaging in the act of buying something they report feeling a sense of gratification or relief.

One could argue, however, that substance dependence, barring the withdrawal and tolerance criteria, could be classified as an impulse control disorder. Goodman (2001) has made the argument that, "If substance dependence, which is readily acknowledged to be an addictive disorder, is also an impulse control disorder, then a condition that meets the diagnostic criteria for impulse-control disorder is not thereby precluded from also being identified as an addictive disorder" (p. 194). Granted, there are marked similarities between the concepts "addiction" and "impulse control". However, according to this viewpoint, any behaviour, such as eating, exercise, watching TV, setting fires, and stealing could be "technically" classified as an "addiction", which would trivialize the entire concept of the disorder. One has to question whether this is a path that psychology, a scientific discipline, should be heading down. Goodman's (2001) opinions, as anchored in research as they may be, reflect scientist's tendency to "pathologize" any deviant behaviour. Indeed, this is one of the criticisms of employing the term addiction and why the DSM task force has been so reluctant to include the term into its nomenclature.

Conclusions
Compulsive buying is indisputably a debilitating behaviour with severe consequences for the person and their family. People with CBD clearly exhibit the "three D's" of psychopathology: their behaviour is distressing, dysfunctional, and deviant. It appears that shopping in people with CBD is as a way of improving, if only temporarily, their negative moods. The abnormally high comorbidity rates in CBD suggest that people afflicted with this disorder have other underlying psychological and emotional problems that need to be addressed with therapy and/or medication. It is therefore concluded that CBD should be acknowledged by the DSM as a mental disorder and classified as an impulse control disorder (ICD) not otherwise specified (NOS). This will ensure that people experiencing these problems can be referred to therapy where they can receive a diagnosis and treatment. The DSM-V should list CBD as an example of an ICD-NOS so that therapists specifically, and the public generally, are aware of the fact that it is recognized as a mental disorder.

Although there are many clinical and neurobiological similarities between impulse control disorders and SUD's, labelling CBD as an addiction is problematic. CBD appears to be a manifestation of other recognized psychological problems rather than its own individual mental disorder. The excessive shopping in CBD is not so much the problem as is the high levels of depression, anxiety, and SUD's, and the person's poor stress-coping mechanisms, all of which contribute to the person's behaviour.

OCD is a heterogeneous disorder and, as such, its symptomology may be better understood if it is conceptualized as a dimensional, rather than a categorical, disorder (Castle & Phillips, 2006). However, there is simply not enough evidence to warrant the inclusion of CBD into the obsessive-compulsive spectrum. Furthermore, the research that is available suggests that compulsive behaviours, albeit similar in some respects to impulsive behaviours, are primarily engaged in to alleviate anxiety, not to produce pleasure. As such, the two disorders should be classified as separate psychiatric conditions.

To the average layperson, the classification of a mental disorder, such as CBD, may seem unimportant. After all, what's in a word? But the nosology of a mental disorder has profound and far-reaching implications for patients, researchers, therapists, and society as a whole.

From the perspective of the person with the disorder, if their excessive buying is deemed an addiction, which has a strong disease-like connotation, they may feel as though they are absolved from any legal or financial responsibility for their behaviour. From the perspective of treatment, it's more likely that the patient's symptoms will improve if they believe that their behaviour is as an impulse control disorder rather than an addiction. For example, if CBD is diagnosed as an addiction and treated as such, how is one to go about abstaining, which is the universally accepted and recommended treatment for addictions, from shopping or buying? The nosology of CBD even has implications at the societal level. For example, if CBD is labelled as an impulse control disorder rather than an addiction, the public may feel that punishment is a more appropriate response to the behaviour than treatment (Goodman, 2001).

Clearly, then, the classification of a mental disorder is not just a matter of terminology. Words are important and the ones that should be employed by the DSM to refer to CBD are "Impulse control disorder not otherwise specified".

Writing Feedback / Biological perspective on Sexual Orientation - "nature or nurture" approaches [14]

Many perspectives on the nature of sexual orientation exist, each one asserting its point of view as vehemently as the next. Contemporary explanatory models of sexuality have been based more on cultural and religious norms and social stereotypes than on actual objective, scientific facts. Over the last 20 years or so, however, a growing body of research on the biology of sexual orientation has been accumulating. Researchers have explored the relationships between sexual orientation and factors such as hormones, prenatal stress, cerebral asymmetry, neuroanatomy, otoacoustic emissions, anthropometrics, genetics, fraternal birth order, and developmental instability (Mustanski, Chivers, & Bailey, 2002). Although results have been mixed, a number of interesting findings have emerged.

Research has provided evidence that prenatal factors may be involved in sexual orientation. The neurohormonal theory attempts to explain sexual orientation in terms of prenatal testosterone levels which are involved in differentiating physiological, neural, and anatomical structures of both sexes. Swaab and Hofman (1990) found clear differences in the superchiasmatic nucleus (SCN) of the hypothalamus between homosexual and heterosexual men (as cited in Alexander, 2000). Adam et al. (2007) compared neural activation to preferred sexual stimuli and nonpreferred sexual stimuli in heterosexual and homosexual men and discovered that within the amygdala the latter had greater activity for preferred sexual stimuli than the former, suggesting the possibility that male homosexual brains may be characterized by atypical patterns of neural activity. Whether this result was a cause or consequence of the participant's homosexuality, however, is debatable. Other research has postulated that developmental instability in utero may be related to homosexuality. For example, Miller, Hoffmann, and Mustanksi (2008) found that overall index of bodily fluctuating asymmetry (FA) was positively correlated with homosexuality in men. Research by Martin, Puts, & Breedlove (2008), however, failed to confirm the results of the latter. In fact, the researchers reported that FA was lower in homosexual men than heterosexual men.

The most favourable finding to have emerged from the neurohormonal research is the fraternal birth order effect, which was first documented by Blanchard and Bogaert (1996) (as cited in Bogaert, 2006). The researchers found that there was a significant correlation between homosexuality in males and the number of biological older brothers in a Canadian sample. Since then several other studies have confirmed these results in samples from across the world. For example, Blanchard and Lippa (2007) reported that results from an online BBC survey involving 159,779 respondents revealed that older brothers increased the odds of homosexuality in men. Another study (Rahman, Clarke, & Morera, 2009) found evidence of the fraternal birth order effect in a sample of 100 heterosexual and 100 homosexual men. It appears that the fraternal birth order effect has no bearing on female sexuality (Bogaert, 1997). Bogaert (2006) demonstrated that only the number of biological older brothers, and not any other siblings, such as non-biological brothers, significantly predicted homosexuality in men. Moreover, rearing time with older siblings, whether biological or nonbiological, had no effect on sexual orientation, suggesting a prenatal origin to the fraternal birth order effect. Recent studies have indicated that the fraternal birth order effect is evident in right-handed males but not in non-right-handed males (Blanchard & Lippa, 2007; Blanchard, 2008).

The maternal immune system hypothesis was developed to explain these results and posits that the fraternal birth order effect reflects progressive immunization of some mothers to male-antigens with each successive male foetus (Bogaert, 2002). With respect to the interaction of handedness and the fraternal birth order effect, two explanations have been proposed (Blanchard, 2008): It could be that non-right handed foetuses are insensitive to the presence of maternal male-antigens or that mothers of non-right handed foetuses do not produce anti-male antibodies. Although many researchers agree that this explanation, on the surface, seems plausible, it is lacking concrete, empirical support (James, 2004).

Research has also attempted to indentify genetic factors that influence sexual orientation. Concordance rates of homosexuality tend to be higher in monozygotic twins (who share 100% of the same genes) than dizygotic twins (who share 50% of the same genes) (Kendler at al., 2000; Kirk et al., 2000). Ellis et al. (2008) looked at blood type and Rh factor in both heterosexual and homosexual participants and discovered that male and female homosexuals were significantly more likely to be Rh negative than heterosexuals. The researchers also found that female homosexuals exhibited higher incidences of blood A type than male homosexuals, compared to heterosexual male and females who exhibited identical frequencies of the blood type A. Thus, chromosomes 9 and 1, which are responsible for blood type and Rh factor, may be involved in sexual orientation.

The extant research on sexual orientation has not gone without its fair share of criticism. Because the prevalence of homosexuals is relatively low within a given population, random sampling is not a viable option in experiments. Instead, researchers often have to place ads in homosexual magazines, recruit participants from recognized gay areas, or rely on word of mouth, all of which increase the chances of sampling biases. Another problem is researchers tendency to define sexuality in "either or" terms; that is, participants are classified as either gay or straight. Sexual orientation, like gender, is not a fixated entity for which criteria can easily be defined. For example, it is not uncommon for male prisoners to have sex with other males yet still consider themselves "straight". Also, although some individuals do not engage in sexual relations with the same sex, they do frequently fantasize about it. Thus, it is more fruitful for researchers to place sexual orientation along a continuum, with homosexuality and heterosexuality at the extreme ends and bisexuality in the middle. Furthermore, Alexander (2000) comments that research on human sexuality should employ the "double confirmation method", whereby sexual dimorphism is established before sexual orientation differences. In other words, a firm understanding of the biological differences between the sexes is necessary before researchers can even consider the possible prenatal factors involved in sexual orientation. It's also been noted that studies exploring the etiology of female homosexuality are lacking (Mustanski, Chivers, & Bailey, 2002). The most profound limitation of the literature on sexual orientation is its predominant usage of correlational studies, which make casual attributions next to impossible.

Despite the considerable amount of research that has been generated over the last two decades on the biology of sexual orientation, psychology's understanding of the topic is far from complete. This is not surprising, though, when one takes into consideration the complexity of the issue at hand and the fact that in the not so distant past homosexuality was classified in the DSM-III as a mental disorder. Researchers studying human sexuality are faced with two daunting tasks. Not only do they have to find consistent, biological differences between people of different sexual orientations, but they have to clearly demonstrate that these biological differences (i.e., number of biological older brothers, blood type), and not other confounding variables (i.e., social upbringing, sexual experiences), account for sexual orientation. For example, neurological differences between homosexuals and heterosexuals could be caused by prenatal factors, but it's also just as likely that postnatal sexual experiences may have caused the differences in brain structures (Alexander, 2000).

Although it's not likely that future research will be able to identify the exact etiological pathway from which sexual preferences in human beings develops, the articles summarized above should make it clear that biology influences a person's sexual orientation to some extent. Future research should take a scientific interactionist approach to studying sexual orientation, which acknowledges the importance of both biology and the environment. Such an approach is likely to produce more cogent findings than the current "nature or nurture" approaches.

Writing Feedback / Personality: A Trait Interactionist Perspective [10]

The nature of human personality has long been an interest of philosophers, psychologists, and intellectuals alike who have been, and still continue to be today, puzzled by the wide range of traits and behaviours that characterize human beings. Indeed, if there is one consistent finding that has emerged from the extant research on personality with which every personologist agrees, it is that personality is as diverse and complex as the day is long. That being said, in my exploration of the different personality theories postulated over the years I have encountered some that seem to be, at least in my opinion, better adept at sufficiently explaining human behaviour. I have integrated these different perspectives into my own multi-faceted theory of personality, which I have labelled trait-interactionism.

In developing a theory of personality one must address a number of concomitant topics, namely, motivation, the unconscious, consistency of behaviour, and the ubiquitous debate of nature or nurture. Throughout the essay I will be touching upon these important topics when appropriate.

According to Gordon Allport, personality is not an abstraction or a fictional phenomena but rather an entity that exists within an individual and lies behind specific acts and behaviours. Thus, Allport disagreed with B. F. Skinner's claim that personality was simply a collection of learned environmental responses. Instead, he theorized that traits, which are biological in nature, are the fundamental building blocks of personality and it is the specific pattern of these traits that determines how a person will behave in a situation. That each person confronts and responds to an environmental experience differently is best captured by Allport's statement that, "The same fire that melts the butter hardens the egg" (in Hergenhahn, Olson, & Cramer, 2003, p. 159). Allport's famous definition of personality as, "the dynamic organization within the individual of those psychophysical systems that determines his characteristic behaviour and thought", illustrates four important aspects of his theory as well as mine (in Hergenhahn, Olson, & Cramer, 2003, p. 156).

Personality is dynamic. It is constantly changing and adapting but always in ways that are consistent with the overall personality structure. By this Allport meant that a person is not quite the same person as they were before an experience. In fact, many would argue that a rigid, inflexible personality is maladaptive and leads to neurosis. In many ways I am a different person today than I was in the past. Attending university has revolutionized the way I perceive and think about the world, but the basic, fundamental personality traits that characterize me as an individual- namely, introversion, preference for sameness/familiarity, and self-consciousness- have remained stable.

The term "psychophysical" highlights the interaction of both biological and cognitive factors in the expression of personality. This concept is integral to my theory as I believe that personality involves not only behaviour but thoughts (i.e., perceptions, interpretations, expectations) and emotions. Albert Bandura disapproved of taking a reductionist approach to studying personality as he argued that it would eventually lead to psychology being, "reduced to biology, biology to chemistry, and chemistry to physics, with the final stop in atomic particles"( in Hergenhahn, Olson, & Cramer, 2003, p. 299).

By stating that traits determine one's behaviour, Allport is suggesting that personality is generated from within rather than controlled by external factors, as Skinner would argue. Though it is influenced by the environment to some extent, behaviour is driven by the internal personality structure. Perhaps the most dominant theme running through all of Adler's work is his emphasis on the individual and his/her characteristic behaviour and thought (Hergenhahn, Olson, & Cramer, 2003). According to Allport, no two human beings are alike.

A temperament is the innate, biological aspect of one's personality that determines how he/she perceives and responds to the world. That some infants come out of the womb more reactive than others is evidence that we are not born as blank slates of human nature. Hans Eysenck, a temperament personologist, developed three personality traits, called superfactors, which he believed had clear biological origins and which composed a person's temperament. They were neuroticism (contrasted with emotional stability), extroversion, (contrasted with introversion), and psychoticism. Research has demonstrated that these three traits are highly heritable, exhibited by nonhuman animals, widespread across many cultures, and relatively consistent across the lifespan (Hergenhahn, Olson, & Cramer, 2003). Eysenck took his research a step further by attempting to establish the biological basis of personality.

The ascending reticular activating system (ARAS) in the brain is responsible for excitatory and inhibitory patterns in the cerebral cortex. Eysenck argued that an introvert is characterized by higher levels of cortical excitation or arousal, controlled by the ARAS, than an extrovert. In other words, introverts' threshold for cortical excitation or arousal is lower than that of an extrovert such that the same intensity of environmental stimulation (i.e., music) is experienced stronger by an introvert than an extrovert. Thus, introverts are said to be "stimulus shy" while extroverts are "stimulus weak" or "hungry". The latter is supported by the fact that, on average, extroverts tend to listen to louder music and prefer to be around more people than introverts; facts to which I, an introvert, can attest.

The limbic system, or as Eysenck referred to it as, the visceral brain, regulates emotional expression and controls autonomic responses such as heart beat and blood pressure. Neurotics, Eysenck postulated, are characterized by higher levels of autonomic activity, controlled by the limbic system, than emotionally stable people. The Seinfeld character George Costanza is the epitome of a neurotic. He is anxious, insecure, self-conscious, and self-loathing, and overreacts to even the slightest inconvenience. The English idioms "Don't make a mountain out of a molehill" and "Don't cry over spilled milk" are clearly statements by which neurotics do not live.

Eysenck had difficulty explaining the biological underpinnings of the trait psychotisicm. However, because it was included to make distinctions between abnormal people, psychoticism did not play a major role in Eysenck's research on the personality structure of normal, healthy people. Thus in my theory, temperament, which is the core of our personality and remains relatively stable throughout our lives, consists of extroversion/introversion and neuroticism/emotional stability.

Eysenck's superfactors are what Raymond Cattell would classify as constitutional source traits, which are genetically determined and differ from environmentally moulded traits, which develop from experience. Eysenck believed that the former were not influenced by early experience and did not arise from learning, a point with which I take issue. Like Cattell, I believe that early experiences can exert a strong effect on personality traits, including those that are largely biological. The environment can serve to reinforce or weaken certain personality traits through the principles of operant conditioning and observational learning. For example, aggression, which I believe has a strong biological basis, can be influenced by one's environment. Let's suppose, for arguments sake, you have two boys who are both equally predisposed to aggression but who grow up in completely different environments. The one boy, who lives in a poorer neighbourhood in which violence is quite prevalent, is more likely to consistently behave aggressively than the other boy who lives in a peaceful, middle-class neighbourhood. Although both boys have a tendency to respond to provocation with aggression, the environment in which the first boy grew up reinforced or strengthened that tendency such that it manifests into aggression more in him than in the other boy. Cattell estimated that one third of personality is biological and the remaining two thirds is environmental (Hergenhahn, Olson, & Cramer, 2003); others have claimed that as much as 75% of personality is hereditary. Such estimates have proven to be difficult to scientifically validate, however. Clearly, though, both biology and the environment contribute to the development of personality.

Other personality traits, such as the Big Five's conscientiousness, openness to experience, and agreeableness, as well as many of Cattell's factors such as superego strength and self-sufficiency fall within the category of environmentally moulded traits. The list of personality describing terms is infinite, as Allport discovered when he reviewed a dictionary and found 18,000 of them. Based on research using factory analysis, Cattell and Eysenck proposed that traits that were highly correlated with each other were likely influenced by an underlying general factor or source trait; the exact number of which was open to interpretation. Cattell's theory included 16 factors which he believed accounted for the diversity of human personality. Eysenck proposed that the personality structure consisted of three superfactors which formed a hierarchal structure in which higher order traits are correlated with a cluster of subordinate traits. For example, traits such as sociable, lively, active, and sensation-seeking are highly correlated with the general factor extroversion. In my theory, an individual's personality structure consists of a temperament and five to ten personality traits. The nature of the latter traits depends heavily on learning and experience.

Is personality consistent? In the strictest literal sense of the word, no. If personality was consistent across every situation than one could, given the appropriate personal and environmental factors, predict human behaviour, which we know is next to impossible. I think that it is more fruitful to view personality as a predisposition or a tendency to interpret and respond to the environment in a certain way. Allport and Eysenck stressed the fact that traits, though biological, are not deterministic; they merely provide a range of possible behaviours. The environment determines the extent to which a particular trait is expressed. This is where the social cognitive theory comes in to play, to which we now turn.

Proposed by Albert Bandura, the theory of reciprocal determinism posits that behaviour is the outcome of the ongoing interaction between personal factors, such as traits, perceptions, and expectations, and situational factors, such as social settings, people, and rewards and punishments. According to social-cognitive theory, learning plays an important role in personality, specifically observational or vicarious learning. Mischel and Bandura criticized traditional personality theories for overemphasizing the importance of personal variables while deemphasizing the importance of situational variables. Neither theorist studied traditional personal variables such as traits or unconscious wishes and desires. Instead, they focused on internal, cognitive processes, such as perceptions of the self and the world and expectations, and their effects on behaviour. In my opinion, the unconscious is simply that which we cannot understand, a position similarly held by Adler and Kelly who believed that only experiences compatible with one's personality can be experienced consciously (Hergenhahn, Olson, & Cramer, 2003). I disagree, however, with Mischel and Bandura's contention that only cognitive, and not biological, variables interact with the environment to produce behaviour. Personality traits predispose people to interpret and construe the world in a certain way which influences their behaviour. I like to think my theory is a compromise between the two perspectives- trait and social-cognitive- in that I have emphasized the importance of both cognitive and biological variables in determining behaviour.

Allow me to use a personal example to illustrate reciprocal determinism. A friend of mine, whom we'll call Allan, is what most would consider an introvert. He is shy, quiet, reserved, and generally prefers solitary activities such as reading. There are certain situations, however, in which Allan is more apt to be outgoing, sociable, and even somewhat boisterous. When Allan is around his close friends and has had a few drinks he seems to "open" up. The interaction of personal factors, such as Allan's expectation that alcohol "loosens" him up, and environmental factors, such as Allan's friends around whom he feels comfortable being and who cheer him on (positive reinforcement), results in Allan behaving more gregariously than he normally does. However, if Allan were to find himself in novel social situation in which he knew very few people, such as a classroom on the first day of school, his introverted tendency would likely result in him being more shy and conservative.

Now that I have established the foundation of the personality structure, I must address an important topic relating to human behaviour. That is, what motivates us to behave the way we do?

I share an opinion similar to that of Allport's on this matter in that I believe that, although humans are essentially animals and as such driven by the same biological instincts as our evolutionary ancestors, there is more to human motivation than the satisfaction of primitive, bodily needs. Because survival for humans today is much easier than it was in the past, we have an abundance of "free" energy that can be diverted to socially productive behaviours, such as relationships, occupations, education, and art. Allport referred to this as the "Principle of organizing energy level", whereby energy no longer needed for basic adaptation can be used instead for setting and attaining long-term personal goals (Hergenhahn, Olson, & Cramer, 2003). Abraham Maslow's Hierarchy of Needs supports this position, as an individual who has failed to satisfy their most basic survival needs cannot move on to more important personal and social needs such as belongingness, love, and esteem. I also believe that within each individual is a drive for self-enhancement or improvement and a yearning to maximize one's potential as a human being. Alfred Adler called it social interest, an innate need to develop a perfect society. Allport called it propriate striving whereby people create long term goals that give meaning to life and Carl Rogers described it as actualization, a tendency to seek experiences that will enhance the quality of life (Hergenhahn, Olson, & Cramer, 2003).

Whether this need to grow and develop as a human being is innate or acquired is open for debate. The only conceivable way of determining the answer to such a question is to completely remove humans from society and observe how they behave without societal restrictions and regulations. Freud would predict that humans would act on their innate, animalistic impulses and behave sexually promiscuous and aggressive. For Maslow, giving complete freedom, humans would create a peaceful, loving, and functional society conducive to individual growth and development (Hergenhahn, Olson, & Cramer, 2003). I find myself on the fence on this matter. While I acknowledge that survival is a strong instinct that has been genetically endowed to us by our evolutionary ancestors, for whom it served an important purpose, history shows us that some human beings have engaged in acts of pure selfless, and in some cases even dangerous, altruism. How can evolutionary and psychoanalytical theories explain the motives behind these actions?

My concept of human personality incorporates many different perspectives into one, integrative theory, which I have termed Trait-Interactionisim. The label emphasizes the importance of two prominent theories of personality: trait and social-cognitive theories. In its most rudimentary form, I like to think my personality theory is based on the work of Gordon Allport, who believed that personality is guided by traits which are psychophysical structures that exist within an individual. I then expanded on this notion that personality is embedded within the central nervous system by including the work of Hans Eysenck, who attempted to pinpoint the exact neurological structures in the brain that were responsible for personality. I then combined the trait theories with the social-cognitive theory, which emphasizes the importance of internal perceptions and expectations about the world that influence our behaviour. The most significant theory to have emerged from this perspective is reciprocal determinism, which purports that aspects of the individual interact with aspects of the environment to create behaviour. In a nut shell, my theory conceptualizes human personality as the interaction of biological, cognitive, and environmental variables at any given time.