Book Review: Tar Beach from a Multicultural Perspective

Tar Beach by Faith Ringold. (1991) Tar Beach. Dragonfly Books, NY. ISBN: 978-0-517-88544-4.
by JenL’Insalata

Tar Beach is an illustrated children’s book set in Harlem in 1939. The story follows an eight-year-old African-American Immigrant by the name of eight-year-old Cassie Louise Lightfoot adjusting to her new home. She imagines herself flying over her apartment building where her family is playing a traditional card game, and her brother is asleep on a rooftop mattress (Ringgold, 1991).

The story uses colorful images that mirror artwork from her home as a metaphor. She imagines herself being the master of her new city with her prize possession being the George Washington Bridge. She flies over the rooftops and experiences the wonder of New York lights and sounds. She finds them exciting and new as she imagines herself being part of her new environment. Throughout the story she finds herself being both connected to her family and reminiscing about home, while intrigued by her new environment(Ringgold, 1991).

Multicultural Aspects

The book addressed the mixed emotions many immigrant children feel when moving to a new country. Immigrant children often struggle to adapt to their new culture and values surrounding creativity and individualism. Many struggle to learn the new language and orientating to the new environment (Ozer, 2015).

In the book, Littlefoot is surrounded by patterns bordering each page that reflect African artwork. The metaphor connects her to her traditional home. Throughout the narrative, she mentions viewing the sky and the lights with wonder, indicating a child-like excitement and possibly some apprehension. Floating over her family on the rooftop suggests that she might be reflecting on traditional gender roles of her native culture (Ringgold, 1991). Often, females and considered nurturers and caretakers. In the story, Littlefoot takes watch over her family and her new city in a loving and gentle manner.

The story does not show Littlefoot interacting with anyone outside of her family (Ringgold, 1991). This might suggest the social isolation she experiences due to a language barrier and differing cultural values. The constant sense of excitement and wonder suggests that she wants to acculturate and own her new environment as she mentions feeling rich and owning all she can see (Ringgold, 1991).

Personal Reflection

Tar Beach creates a safe and colorful word for readers to experience an immigrant child’s point of view. Rather than addressing the discrimination that is often associated with the immigrant experience, it utilizes a universal sense of childhood wonder and imagination. As with illustration, color, symbolism, and metaphor are used to further enhance the story and connect a deep emotional meaning.

Children experiencing the book might look on the main character as themselves or a playmate on an adventure in the sky. By creating a universal connectives, readers are able to internalize and relate to Littlefoot’s experience. Children might not recognize distinct cultural differences, and gravitate to the colorful, and textural illustrations. This allows Tar Beach to emphasize universal emotions and connect children of various cultures through a story about flying over a Harlem skyscape.



Ringgold, Faith. (1991). Tar Beach. Dragonfly Books, NY. ISBN: 978-0-517-88544-4.

Ozer, S. (2015). Predictors of international students’ psychological and sociocultural adjustment to the context of reception while studying at Aarhus University, Denmark. Scandinavian Journal Of Psychology, 56(6), 717-725.

Drug Reactivity: The Cannabis Debate


by Jen L’Insalata

From the earliest of records human have utilized substances in nature such as seeds, leaves, roots, and animal products for their medicinal qualities. Many of these substances were discovered to promote healing, prevent infection, reduce pain, and promote sleep. Some of the same substances which hold medicinal properties were also discovered to hold recreational properties educing euphoria, relaxation, and psychotropic qualities.

Cannabis is such a substance that in recent years has entered the public spotlight. Typically considered a recreational substance, the primary active ingredient Tetrahydrocannabinol or THC acts directly on the endogenous cannabinoid receptor CB1 located throughout the basal ganglia, limbic system, and hippocampus. Agonistic qualities of THC increases dopamine levels while blocking the CB1 receptors responsible for decreasing the reinforcement effect of dopamine (Pacher, Bátkai, & Kunos, 2006).

From a recreational standpoint, users seek out the various relaxation and psychoactive effects achieved most frequently by smoking. Effects are felt quickly and reinforced thorough he dopomergenic system. It is recognized that approximately 1/3 of individuals self-administer cannabis to cope with pain, anxiety, depression, and other stress and mood related disorders (Buckner, Heimberg, Matthews, & Silgado, 2012).

Cannabidiol or CBD; another active compound found in cannabis has shown to have a wider medicinal use with marked antiemetic properties, pain reduction properties, and anti-aggression and anti-anxiety properties. Current studies are exploring the use of CBD in treatment for PTSD, multiple sclerosis-, and other neurodegenerative disorders despite the rise in concern for cannabis dependency. In many cases studies show a marginal increase (0.997) cannabis use disorders among individuals utilizing it for medical purposes (Kevorkian, Bonn-Miller, Belendiuk, Carney, Roberson-Nay, & Berenz, 2015).

In many states cannabis has become legalized or decriminalized for recreational use and a growing number of recreational users seek a variety of THC and CBD effects. As with most substances cannabis users develop a tolerance to its effects and in turn may utilize the substance more frequently or in higher quantities to achieve the desired effect. The relationship between dose and effect is difficult to measure in that the dose being administered relies not only on the potency level of THC but also the individual’s inhalation strength. The size and strength of the inhalation combined with the extended length of time the smoke is held within the user’s lungs increased the dose administered.

In laboratory studies, dosage is monitored by computerized mechanism and have observed effects on THC content ranging from 0.2% to 4.0%. The subjective effects have been measured and vary depending on the individual. Individuals are asked to use a visual analog scale consisting of 44 descriptors to describe the dosage effect on medicinal aspects including stomachache, headache and pain, mood, aspects such as anxiety levels, depression, and feeling of content (Ramesh, Haney, & Cooper, 2013).

Regulating dosage effects becomes difficult in social situation in that social stimuli may alter the individuals intended dosage. As dosage and frequency increases individuals may build up a tolerance to both the impairitive and the desired effects. As dependence is brought about by the reinforcement through the dopomergenic system, individual susceptibility relies heavily on multiple aspects from both biological and environmental components. In many cases the individual must experience a positive effect and be willing to smoke again in order to develop necessary reinforcement.

The perception that cannabis is relatively easy to find and attain has also increased its social acceptance. Examining behavioral economic reinforcement surrounding the cost of cannabis must also be considered. Use as an economic reinforcement follows similar patterns to other substances and individuals are willing to continue to purchase cannabis until a breaking point. Examining the average cost of a cannabis joint being between $7 to $9, the breaking point appears to be approximately $38 per joint. Regular users are estimated to consume approximate 20 joints per week to attain a moderate high. Regular users express comfort in spending between $100 and $200 a month on cannabis and would be willing to pay slightly more for what is perceived as higher quality (Collins, Vincent, Yu, Liu, & Epstein, 2014).  Legislation can be established using tax to increase the price of cannabis and in turn decrease its use in legal states in a similar manor to what is done with tobacco.




Buckner, J. D., Heimberg, R. G., Matthews, R. A., & Silgado, J. (2012). Marijuana-related problems and social anxiety: The role of marijuana behaviors in social situations. Psychology Of Addictive Behaviors, 26(1),

Collins, R. L., Vincent, P. C., Yu, J., Liu, L., & Epstein, L. H. (2014). A behavioral economic approach to assessing demand for marijuana. Experimental And Clinical Psychopharmacology, 22(3), 211-221. doi:10.1037/a0035318

Kevorkian, S., Bonn-Miller, M. O., Belendiuk, K., Carney, D. M., Roberson-Nay, R., & Berenz, E. C. (2015). Associations among trauma, posttraumatic stress disorder, cannabis use, and cannabis use disorder in a nationally representative epidemiologic sample. Psychology Of Addictive Behaviors, 29(3), 633-638. doi:10.1037/adb0000110

Pacher, P., Bátkai, S, & Kunos, G. (2006). “The Endocannabinoid System as an Emerging Target of Pharmacotherapy”. Pharmacological Reviews 58 (3): 389–462. doi:10.1124/pr.58.3.2PMC 2241751.PMID 16968947.

Ramesh, D., Haney, M., & Cooper, Z. D. (2013). Marijuana’s dose-dependent effects in daily marijuana smokers. Experimental And Clinical Psychopharmacology, 21(4), 287-293. doi:10.1037/a0033661

A Historical Perspective of Schizophrenia

schizophrenia1by Jen L’Insalata

Schizophrenia cannot be explained in its entirety by one particular theoretical model and the underlying neurobiological foundation for the disease is still relatively unknown.  Rather it is the descriptions and observations of the primary psychotic symptoms that have allowed several theories surrounding schizophrenia to evolve (Mishara, & Schwartz, 2013). Historically, schizophrenia was considered to be constructive in which anomalous experiences provide the construct of one self. Early clinical observations emphasized subjective self-experiences and altered self-awareness. The concept of self-experience is still referenced in modern work with schizophrenia. (Parnas, & Henriksen, 2014).

The earliest depictions of schizophrenia were recorded in France during the 12th century but were not linked to any particular disorder. Writing described individuals who deviated from what was considered to be normal self-perception; anomalous self-experiences. In many cases writing illustrate a disunity of consciousness in which a person’s thinking, perception, movement, and vision were disjointed and incongruent with presented stimuli (Parnas, & Henriksen, 2014).

The modern understanding of schizophrenia rose form the work of Emil Krapelin, an influential German psychiatrist working in the late 19th and early 20th century. Krapelin research surrounding the combination of symptoms and psychiatric illness from a biological origin highlighted two forms of psychosis; manic depression and dementia praecox (Ebert, & Bär, 2010). The disturbance known as Krapelin’s dementia praecox consisted of the phenomenon currently recognized as schizophrenia. During his research, Krapelin described the deterioration of what he believed to be perception and attention in combination with muscular tension (Mishara, & Schwartz, 2013).

Throughout the late 1800’s and early 1900’s core symptoms were studied by individuals from a psychodynamic perspective such as Carl Jung, Josef Berze, and Hans Walter Gruhle. Many of these theorists called attention to various cognitive and affective characteristics of the disorder. Jung in particular was fascinated by patients displaying confused speech which he described as a state of sleep-drunken-ness and confusion. Their theories critiqued by many other early psychotheorists and the phenomenon later was renamed schizophrenia in 1908 by Eugen Bleuler (Mishara, & Schwartz, 2013).

Bleuler theorized individuals with schizophrenia experienced a general loose association with a fissure personality which was highly influenced by Jung’s work. Bleuler believed that such loose associations allowed aspects of the unconscious to invade the consciousness and lead to an ego disorder. The unconscious invasion would erode the functioning of the ego to the level in which it exists in dreams. Gruhle added to Bleuler’s work and theorized that the primary symptoms of schizophrenia operated independently and observed a dysfunction between the cognitive and the affective components of the disorder (Mishara, & Schwartz, 2013).

Josef Berze criticized Jung’s work and theories believing that the symptoms were due to a reduction in mental activity rather than attention. He theorized that mental activity is more closely related to consciousness than affect and highlighted the concept of a disruption in self as the essences of schizophrenia. Berze also noted diminished mental activity in goal setting, linguistic coherence, and the ability to access the autobiographical self. Much of his work was inspired by emerging neurobiological research. He theorized that schizophrenia symptoms originated at a subcortical area, specifically the thalamus which gave rise primitive drives and motivations (Mishara, & Schwartz, 2013).

Jaspers integrated and critiqued his predecessors work in his book General Psychopathology published in 1913. (Mishara, & Schwartz, 2013). Highly influenced by the philosopher Descartes, he solidified the concept of self-experience pertaining to schizophrenia. Jaspers recognized that an individual may have and recognize experiences that are invalid and referred to positive symptoms as first person symptoms (Parnas, & Henriksen, 2014).

During the 1940s Freud’s psychoanalytic work continued to influence much of the theories surrounding schizophrenia and emphasized an etiological root stemming from early relationships. Psychoanalytic writers produces detailed descriptions of the schizophrenic experience including disruptions in interpersonal relationships and the self-experience due to the psychosis (Hamm, & Lysaker, 2016).

Writers such a Freud and Searles illustrate individuals that were detached from the world and redirected psychic energies inward during psychosis. Such writings provide the concept of an altered self-experience from which the schizophrenic individual is unable to integrate life experiences. Psychodynamic approaches took a pessimistic view of schizophrenia treatment which failed to produce empirically supported and measurable treatment modalities. Eventually, such treatment modalities fell out of favor and were replaced by psychosocial and cognitive behavioral perspectives (Hamm, & Lysaker, 2016).

With the publication of the ICD 8 and 9, Schizophrenia was recognized as a disturbance of personality and involved disorder concepts of individual uniqueness and self-direction. During that time the term personality referred to a subjective self rather than the personality descriptions used in contemporary psychology. Research surrounding a subjective self could be measured using systematic approached however lacked reliability in its methods. This notion soon fell out of favor and was replaced with an operational model following the publication of the DSM-III in 1980 (Parnas, & Henriksen, 2014).

The DSM-III emphasized behavioristic components of schizophrenia which stress observable features over the subjectivity and inference of previous theories. Biological concepts such as genetics in the etiology of schizophrenia were highlighted and lead to the emergence of a spectrum of observable features and predictors. Among the most noted were deficits in emotion, eccentricity, and thought disorder which caused interpersonal difficulties in social and occupational function. The inclusion of the diathesis stress model illustrated how core vulnerability combined with environmental stressors and produce cognitive changes observed in schizophrenia (Parnas, & Henriksen, 2014).



Asenjo Lobos, C., Komossa, K., Rummel-Kluge, C., Hunger, H., Schmid, F., Schwarz, S., & Leucht, S. (2010). Clozapine versus other atypical antipsychotics for schizophrenia. The Cochrane Database of Systematic Reviews, (11), CD006633. Advance online publication.

Ebert, A., & Bär, K.-J. (2010). Emil Kraepelin: A pioneer of scientific understanding of psychiatry and psychopharmacology. Indian Journal of Psychiatry, 52(2), 191–192.

Hamm, J. A., & Lysaker, P. H. (2016). Psychoanalytic phenomenology of schizophrenia: Synthetic metacognition as a construct for guiding investigation. Psychoanalytic Psychology, 33(1), 147-160. doi:10.1037/a0038949

Mishara, A. L., & Schwartz, M. A. (2013). Jaspers’ critique of essentialist theories of schizophrenia and the phenomenological response. Psychopathology, 46(5), 309-19. doi:

Parnas, J., & Henriksen, M. G. (2014). Disordered Self in the Schizophrenia Spectrum: A Clinical and Research Perspective. Harvard Review of Psychiatry, 22(5), 251–265.

Spencer, E. K., & Campbell, M. (1994). Children with schizophrenia: Diagnosis, phenomenology, and pharmacotherapy. Schizophrenia Bulletin, 20(4), 713-725.

Psychotropic Medications and Children

childrenpills-e1463156827980by Jen L’Insalata

Historically children’s psychiatric treatment was comparable to those of adult populations. Diagnostic features were assumed to take on the same aspects of adult psychiatric features and therefore treatment was approached in the same manner. Contemporary views observe that emotional stress experienced by children and adolescents is due largely to situational experience. In these cases non-medication based treatment and psychotherapeutic interventions produce the best outcomes. However, research does take into consideration that many adult psychological and psychiatric disorders have their onset during childhood and can result in progressive neurobiological impairment. In the case of Bipolar disorder, Schizophrenia, and attention deficit/hyperactivity disorder (ADHD), pharmaceutical intervention is necessary to prevent neurological degradation (Preston, O’Neal, & Talaga, 2013).

Research surrounding the efficiency of two or more psychotropic medications is still limited and often time children are prescribed a combination of pharmaceutical agents to medicate disorders. The most common polypharmacy regimens include an antidepressant and a stimulant in combination with an antipsychotic and relate to the co-occurrence of a mood disorder and ADHD (Comer, Olfson, & Mojtabai, 2010).

Controversial Aspects

When medicating children there is no true informed consent and it is often the parents who facilitate the decision for medication treatment. In such instances, it becomes easier for parents to view the disorder as a chemical imbalance and ignore environmental components such as family dysfunction. Parents may rule out the need for psychological treatment in exchange for an easy chemical solution (Preston, O’Neal, & Talaga, 2013).

Many psychotropic medications have adverse side effects including addiction, which at an early age can lead to lifelong struggles with prescription abuse.  Stimulants such as Ritalin used to treat ADHD and benzodiazepines such as Xanax used to treat anxiety (Preston, O’Neal,  & Talaga, 2013) are among the most commonly abused prescription drugs among children and adolescents.

Pre-pubescent children have a higher hepatic rate then children who have entered puberty. Medication dosages prior to puberty are often metabolized faster and require a higher dose. Once a child enters puberty the dosage must continue to be monitored closely for toleration and side effects (Preston, O’Neal, & Talaga, 2013).

Parents often ignore the child’s beliefs and views surrounding medication and may have private consultations regarding treatment with doctors. When working with children it is important to address the child’s concerns surrounding psychotropic medication and mental health stigma (Preston, O’Neal, & Talaga, 2013). Doing so no only ensures that the child will comply with medication treatment, but also provide education and awareness to the outcome of their disorder.

Integrated treatment

The use of psychotropic medication in children is on the rise and in conjunction, doctors are moving toward a polypharmaceutical regime to manage childhood psychological distress. This is largely due to an emphasis of symptom reduction and the increasing number of psychiatrists specializing in pharmacotherapy. Emphasis and access to psychosocial interventions is sometimes limited, expensive (Comer, Olfson, & Mojtabai, 2010), and time consuming.

The Affordable Care Act of 2010 established the health home program for children with emotional disorders aimed at helping children meet both health and developmental goals. Aspects focus on behavioral health, education, child-welfare, and juvenile justice to create a continuum of care that care child and family focused. Policies aim at prevention and continued care while also controlling the cost of child psychiatric care. Aspects emphasize substance abuse and mental health issues that are common among children and adolescents and aim to prevent complications leading to behavioral health problems as adults (de Voursney, & Huang, 2016).

It is estimated that childhood mental health problems cost aproxamiatly 12.2 billion dollars annually and are some of the most prevalent concerns surrounding health, productivity, and crime. Conditions such as oppositional defiant and conduct disorder, substance abuse, post-traumatic stress disorder, anxiety and depression, and bipolar disorder (de Voursney, & Huang, 2016) lead to involvement in criminal and illegal activity, as well as social and societal dysfunction.

Stigmas surrounding the diagnosis of childhood mental health concerns inhibit the identification of children who may be at higher risk and the improper or inadequate treatment. The goal of the Affordable Care Act is to ensure continuity between a child’s home and school life to ensure therapeutic intervention as well as medical intervention (de Voursney, & Huang, 2016).



Comer, J. S., Olfson, M., & Mojtabai, R. (2010). National Trends in Child and Adolescent Psychotropic Polypharmacy in Office-Based Practice, 1996–2007.Journal of the American Academy of Child and Adolescent Psychiatry, 49(10), 1001–1010.

de Voursney, D., & Huang, L. N. (2016). Meeting the mental health needs of children and youth through integrated care: A systems and policy perspective. Psychological Services, 13(1), 77-91. doi:10.1037/ser0000045

Preston, J. D., O’Neal, J. H., & Talaga, M. C. (2013). Handbook of clinical psychopharmacology for therapists (7th ed.). Oakland, CA: New Harbinger. ISBN: 9781608826643.

Benzodiazepines and Anxiety

overmedicated-pharmaby Jen L’Insalata

Benzodiazepines, sometimes referred to as anti-anxiety medications, are intended for the use in treating severe rehabilitating panic attacks and panic disorder. However all too often, benzodiazepines are prescribed for generalized anxiety disorder. From a biological etiology, anxiety is the result of stimuli triggers that activate a series on neurochemical and hormonal responses that prepare the body and mind for immediate activation. This sequence is commonly referred to as the fight or flight response and the limbic system and amygdala become activated. The excitatory hormones cortisol, adrenaline, and norepinephrine are released and the locus coeruleus or gated chloride ion channels are excited (Preston, O’Neal, & Talaga, 2013).

Generalized anxiety disorder is the low level chronic stress experienced throughout an individual’s life. This differs from panic attack in that there is a persisting anticipation of stressful or dangerous events. The limbic system is kept on a lower level of alert but does not cross the threshold into full activation of the fight or flight response.

Panic disorder is characterized by a series of reoccurring panic attack which may appear to be unprovoked. There is strong evidence suggesting the biological etiology of panic attacks stem from hypersensitive neurons within the limbic system, specifically when concerning GABA (Preston, O’Neal, & Talaga, 2013).  This causes individuals to experience dizziness, nausea, chest palpitations, shortness of breath, and profuse sweating that accompany and intense fear.

Benzodiazepines bind to chloride ion channels enhancing the flow of negative chloride ions. This inward flow of negatively charged chloride ions decreases neuron excitation and produces a calming effect on the brain. Benzodiazepines work by interacting with benzodiazepine receptors during presynaptic inhibition. By binding with the receptor sites, the calming effects of the influx of negative chloride ions as well as the effects of GABA are enhanced (Preston, O’Neal, & Talaga, 2013).

The first Benzodiazepine, chloriazepoxide was developed in 1957 for anxiety and insomnia. Since then several other forms of the drug have been developed with varying degrees of anti-anxiety and hypnotic properties. Benzodiazepine gained popularity in pharmisudical anxiety treatment due to its rapid effectiveness. Therapeutic effects can be experienced in as little as 30 minutes. Additionally, benzodiazepines are well tolerated by most individuals (Preston, O’Neal, & Talaga, 2013).

Although considered relatively non-addictive, I have seen numerous cases of benzodiazepine abuse while working with addictions. Many individuals utilizes benzodiazepine to escape unwanted generalized anxiety symptoms and do not have adequate coping skills. Such coping skills can be developed through psychotherapeutic means.

I have observed the use of benzodiazepines to alleviate anxiety cause by other drugs, withdrawal, and the lack of healthy coping skills. Many individuals use benzodiazepines as an intermediary drug or for relaxation purposes. I often observe the illicit use of benzodiazepine coupled with various forms of opiates, a combination that can often be fatal.

For this reason, I question and caution the frequent and over use of benzodiazepines as a primary pharmaceutical treatment for anxiety. As they are effective to reduce dehabilitating anxiety quickly, this medication should be reserved for panic attacks and panic disorder. If prescribed, the duration should be limited and quantity should begin at a low dosage.



Preston, J. D., O’Neal, J. H., & Talaga, M. C. (2013). Handbook of clinical psychopharmacology for therapists (7th ed.). Oakland, CA: New Harbinger. ISBN: 9781608826643.

Medicating Mood Disorders

adderallby Jen L’Insalata

 Mood disorders are a broad category with symptoms ranging from mild dysphoria and grief to chronic and intense clinical depression. Symptoms include both psychological and physical components and can emerge as a reaction to stimuli or spontaneously. Psychological symptoms include diminished self-esteem, sadness, and diminished self-worth; while physical symptoms include alterations in sleep, appetite, and fatigue (Preston, O’Neal, & Talaga, 2013).

Psychological based depression is often reactive, stemming from a stressor either known or unknown to the individual. Biologically based depression does not develop as a response to a stimuli, rather a number of neurobiological conditions are altered which effect neurotransmission within the limbic system. While prolonged reactive depression can lead to biological changes, often individuals show predisposed vulnerability and biological markers (Preston, O’Neal, & Talaga, 2013).

Psycho therapeutic intervention is a primary treatment for reactive depression through which the individuals learns coping skills and is able to address the underlying factors.  Vegetative and neurovegitatve conditions observed in the physical manifestations such as diminished concentration, psychomotor agitation, and changes to sleep and appetite alert practitioners to biological depression (Preston, O’Neal, & Talaga, 2013).  Treatment for biological components of depression includes medication to help stabilize symptoms.

Biological Etiology

Depression symptoms are brought about by the malfunction of norepinephrine, serotonin and dopamine transmission thought out the neurons of the limbic system and hypothalamus. It is believed that a depletion of these neurotransmitters leads to symptom manifestation. The monoamine hypothesis suggests that neurotransmitter depletion can occur in several ways (Preston, O’Neal, & Talaga, 2013).

Excessive reuptake can deplete levels of norepinephrine, serotonin, and dopamine. In this instance, significant amounts of the neurotransmitter are released by the presynaptic neuron into the synapse. The neurotransmitters are rapidly reabsorbed by the presynaptic neuron resulting in a diminished quantity of neurotransmitters reaching and binding with receptors on the opposing postsynaptic nerve (Preston, O’Neal, & Talaga, 2013).

Another instance suggests that there is a decrease number of neurotransmitters released into the synapse. This is possibly due to the reduction of neurons being synthesized, the inability of the vesicle to adequately store or migrate neurons across the membrane of the presynaptic neuron (Preston, O’Neal, & Talaga, 2013). Still a final instance of neurotransmitter abnormalities can occur when the naturally occurring levels of monoamine oxidase become too active. This shouts down and degrades the neurotransmitters themselves (Preston, O’Neal, & Talaga, 2013) resulting in depression symptoms.


Antidepressants are used to treat the biological aspect of depression. When combined with psychotherapy, the pharmisudical treatment of depression is highly effective. There are many medications used to treat depression but the most commonly prescribed fall into three categories; Selective Serotonin Reuptake Inhibitors (SSRIs), Serotonin and Norepinephrine Reuptake Inhibitors (SNRIs), and Tricyclic Antidepressants (TCAs).

Tricyclic Antidepressants (TCAs)

Tricyclic Antidepressants were first developed as an antipsychotic for the treatment of schizophrenia. The original TSA imipramine did not produce the desired antipsychotic effects but produced marked improvement with depressive symptoms. TSAs have a diverse philological profile and are considered a superior form of medicinal depression treatment. Action occurs at the two receptor transporters and three receptor proteins. This inhibits presynaptic reuptake of norepinephrine, serotonin, and blocks post synaptic adrenergic, muscarinic, and histamine H receptors (Hillhouse, & Porter, 2015).

For this reason, the medications prove effective and target many receptors on both end of the synapse. However there are many adverse side effects including unpleasant dry mouth and skin, blurred vison, bladder issues and even death. Additional symptoms involve a quick drop in blood pressure and light headedness. TCAs are considered toxic and can be lethal if the dosage is not accurate (Preston, O’Neal, & Talaga, 2013).

Selective Serotonin Reuptake Inhibitors (SSRIs)

Selective Serotonin Reuptake Inhibitors were developed in the 1960s with the aim of increasing the concentration in the synapse by the inhibition of the reuptake mechanisms of the presynaptic neuron. SSRIs bind the the reuptake receptors on the presynaptic neuron allowing adequate serotonin to bind with receptors on the post synaptic neuron (Hillhouse, & Porter, 2015).

SSRIs targets the serotonin receptor s and have very little effects on other receptors. This allows them to be as effective as TCAs with significantly fewer side effects. Most of the side effects observed have to do with the increase of serotonin and include mild nausea, insomnia, sedation, and restlessness. Over time, patients may experience a recurrence of symptoms that are similar to the initial depression they are being treated for. Patients may experience loss of energy, passivity, and decreased pleasure. Additional medication may be needed to augment some of the unwanted effects (Preston, O’Neal, & Talaga, 2013).

Serotonin and Norepinephrine Reuptake Inhibitors (SNRIs)

Serotonin and Norepinephrine Reuptake Inhibitors (SNRIs) were developed and introduced in the early 1990s and are considered duel action antidepressants. As the name suggests, SNRIs target and inhibit the reuptake of both serotonin and norepinephrine. For this reason it is possible that SNRIs may be more effective then SSRIs in the treatment of depression but studies how there are significantly more unwanted side effects (Preston, O’Neal, & Talaga, 2013, & Hillhouse, & Porter, 2015).



Hillhouse, T. M., & Porter, J. H. (2015). A brief history of the development of antidepressant drugs: From monoamines to glutamate. Experimental And Clinical Psychopharmacology, 23(1), 1-21. doi:10.1037/a0038550

Preston, J. D., O’Neal, J. H., & Talaga, M. C. (2013). Handbook of clinical psychopharmacology for therapists (7th ed.). Oakland, CA: New Harbinger. ISBN: 9781608826643.

CBT: Cognitive Behavioral Therapy

woodbrainby Jen L’Insalata

In most psychotherapeutic environments the term CBT is tossed around all the time. CBT in research; my insurance providers prefer CBT; CBT; CBT; CBT. So what is this CBT stuff? CBT is short for cognitive behavioral therapy and essentially addresses both thoughts and the underlying emotions that influence behavior. This is achieved by bringing together components of both cognitive therapy and behavioral therapy is a direct and effective manner.

Behavior Therapy

Behavior therapy is centered on the concept that human behavior serves a function and results from stimuli within the individual’s environment. Behaviors result in response to environmental stimuli and behavioral patterns result from the reinforcement or punishment received from the interaction between the individual and their particular environment. The psychosociocultural viewpoint encompasses a wide range of therapeutic strategies that aim to change the environmental factors that stimulate maladaptive behaviors (Wedding, & Corsini, 2014).

Cognitive Therapy

Cognitive theory is a theory of personality in which individuals respond to life events cognitively, motivationally, and behaviorally. An individual perceives, interoperates, and assigns meaning to particular life events. Maladaptive behaviors and affects are caused due to the misinterpretation of stimuli, situations, and events. Cognitive therapy aims to adjust the way the individual processes incoming information by examining the individual’s belief about their self, the world, and others (Wedding, & Corsini, 2014).

Five Concepts That Add Dimension

Both behavior and cognitive therapy recognize that personality is consistent and an individual’s response to environmental stimuli can be predicted. Behavior therapy acknowledges five core domains from which personality can be assessed. Behavior therapy teaches flexibility within an individual’s personality domains and introduces healthy coping mechanisms and responses for environmental stimuli (Wedding, & Corsini, 2014).

Cognitive therapy recognizes schemas to explain and predict responses to environmental stimuli and situational cues.  A network of affective, motivational, and behavioral schemas known as modes asses and interoperate situations. Some modes are rooted in instinct and are referred to as primal modes. Primal modes are often ridged, automatic, and absolute. Primal thinking leads to maladaptive behavior. Cognitive therapy teaches a client to consciously override primal modes through means of deliberate thinking and problem solving (Wedding, & Corsini, 2014).

Behavior therapy focuses on the behaviors and actions that are conditioned responses to external stimuli. Cognitive therapy focuses on the affect and mental interpretation of a particular stimuli (Zaretsky, Segal, & Fefergrad, 2007). Due to similarities, behavior therapy and cognitive therapy are often combined in a treatment known as cognitive behavioral therapy. CBT targets the bias mental interpretations acknowledged in cognitive therapy and teaches the client to regulate emotions causing maladaptive behaviors (Harvey, Bélanger, Talbot, Eidelman, Beaulieu-Bonneau, Fortier-Brochu, & … Morin, 2014).

CBT is often used as a primary treatment for depression and mood disorders.  By leveraging a client’s awareness of the changes in their cognition, (Zaretsky, Segal, & Fefergrad, 2007) treatment techniques encompassing mindfulness, relaxation, meditation, exposure, (Wedding, & Corsini, 2014) and modeling teach the client ways to regulate their affect and reduce symptoms (Zaretsky, Segal, & Fefergrad, 2007).

When addressing depression, cognitive therapy addresses the client’s negative views of one’s self, their experiences, and future. A client’s interpretation of their environment is often bleak and the client maintains a pessimistic bias toward themselves and their future. Motivational symptoms appear such as a lack of energy and sometimes paralysis that inhibits the completion of everyday life tasks. Increasing activity and social exposure combined with combating negative interpretations of situations are used to alleviate the cognitive components of depression (Wedding, & Corsini, 2014).

Behavior therapy addresses the conditioned response to stimuli. Behaviors increase due to reinforcement (Wedding, & Corsini, 2014). Maladaptive coping strategies and behaviors continue to reinforce depressive behaviors. Treatments focused on positive social exposure and activity work to reinforce positive experiences for the depressed individual and reduce exposure to negative experiences such as isolation. Exposure to positive stimuli aids in reinforcing non-depressive behaviors (Ryba, Lejuez, & Hopko, 2014).

Modeling behaviors occurs when an individual observers others in a sociocultural environment. Anxiety or phobias are maladaptive behaviors that can be learned through modeling abuse (Wedding, & Corsini, 2014). If an individual observes a social fear or anxiety about a particular situation, it is likely to be interoperated as a truth. An individual may model the anxious or phobic behavior learned from observation.

Behavior therapy addresses the hyperarousal brought on by anxiety and phobia by combining exposure and relaxation training. Practicing relaxation techniques while exposed to environmental stimuli helps alleviate the physical stress and tension associated with phobia and anxiety. Cognitive therapy teaches an individual to reevaluate the particular stimuli and interoperate it as less threatening (Wedding, & Corsini, 2014).

Substance abuse is often coupled with depression and anxiety. The recognition of psychosocial factors maintain the maladaptive belief and subsequent behaviors are addressed by combining cognitive and behavioral therapies (Harvey, Bélanger, Talbot, Eidelman, Beaulieu-Bonneau, Fortier-Brochu, & … Morin, 2014). Substance abuse may begin as a molded socioenvironmental behavior and become reinforced through positive social experiences. Reinforcement of addictive behaviors may be reinforced when a client engages in self-medication to alleviate depression and anxiety symptoms.

Stimulus control is a behavioral technique that can be used to help individuals with substance abuse issues and addiction. Principles of classical conditioning state that conditioned cues illicit behavioral responses.  Stimulus control aims to correct the problems associated with a particular stimuli (Wedding, & Corsini, 2014). For example, a client may associate a place or event with the acquisition and consumption of substances. Clients are encouraged to avoid places and situations which are cues for their addiction.



Wedding, D., & Corsini, R. J. (Eds.). (2014). Current psychotherapies (10th ed.). Belmont, CA: Brooks/Cole. ISBN: 9781285083711.

Zaretsky, A., Segal, Z., & Fefergrad, M. (2007). New developments in cognitive-behavioural therapy for mood disorders.Canadian Journal of Psychiatry, 52(1), 3-4. Retrieved from

Harvey, A. G., Bélanger, L., Talbot, L., Eidelman, P., Beaulieu-Bonneau, S., Fortier-Brochu, É., & … Morin, C. M. (2014). Comparative efficacy of behavior therapy, cognitive therapy, and cognitive behavior therapy for chronic insomnia: A randomized controlled trial. Journal Of Consulting And Clinical Psychology, 82(4), 670-683. doi:10.1037/a0036606

Ryba, M. M., Lejuez, C. W., & Hopko, D. R. (2014). Behavioral activation for depressed breast cancer patients: The impact of therapeutic compliance and quantity of activities completed on symptom reduction. Journal Of Consulting And Clinical Psychology, 82(2), 325-335. doi:10.1037/a0035363


Artwork by Toby Allen

By Jen L’Insalata

Stress has been cited for many adverse physical and mental health conditions and is linked to the proliferation of non-communicable disease epidemics in recent years. During the 1800’s most deaths were related to poor sanitary and hygienic conditions. Most deaths were attributed to outbreaks of cholera, Influenza, typhoid, and tuberculosis spread through unsanitary drinking water (Shern, Blanch, & Steverman, 2016).

In the 21st century, public health is still at risk. The US ranked 36th out of 194 for life expectancy in 2012 with the vast majority of deaths related to obesity, coronary heart disease, lung disease, and substance abuse. Most contemporary chronic illness has its roots in stress and it is estimated that nearly half of Americans will develop resulting mental health and addiction issues at some point during their lifetime (Shern, Blanch, & Steverman, 2016).

It is widely understood that a combination of genetic predisposition coupled with environmental influence shape over all human development. Many alterations in genetic material correlate with environmental stressors. In other words, genetic mutation and expression is strongly influenced by the environments which people are exposed to.

While manageable stress is considered important for healthy human development, toxic stress is not. Frequent, intense, and prolonged exposure to adversity including but not limited to physical and emotional abuse or violence, neglect, and economic hardship account for the source of much toxic stress. Acute or chronic exposure to traumatic events including death and sexual abuse also fall into the toxic stress category as does the persistence of less sever stressors including family instability and income insecurity (Shern, Blanch, & Steverman, 2016).

Stress alters development   over the course of a lifetime. Prenatal exposure to stress impacts developing structures of the fetus leading to adverse effects on memory and cognition. Early childhood stress often results in diminished behavioral, emotional, and impulse control. Individuals exposed to toxic stress during late adolescence and early adulthood develop a heightened fear response and are hyper responsive to stress stimuli (Shern, Blanch, & Steverman, 2016). Additionally, stress amplifies the aging process on both the brain and the body as a whole.

Stress causes structural remodeling of the brain and weakens neuro-connections within in the brain. Exposure to stress activates stress hormones and raises cortisol levels. Persistent elevation of cortisol levels increases the adverse effects on the connective structures within the amygdala; a structure commonly linked to cognitive and emotional regulation (Shern, Blanch, & Steverman, 2016 & Pagliaccio, Luby, & … Barch, 2015).

Genetic mutations occur throughout the short alleles of the serotonin transport promoter and produced heightened monoamine oxidise A activity. Heightened activity along the Hypothalamic-Pituitary-Adrenal Axis greatly effects the monoamine/serotonin structures and leads to additional cortisol release. It is the relationship between cortisol and amygdala connectivity that is believed to be a foundational component of internalizing pathology (Pagliaccio, Luby, & … Barch, 2015).

Internalizing pathology such and depression and anxiety contribute additional stress to an individual’s life. Symptoms of both disorders have dehabilitating effects on one’s ability to function in a socioeconomic capacity and produce feeling of dependency on unhealthy relationships and substances. Thus the cycle of stress, cell malfunction, and disorder is perpetuated.



Pagliaccio, D., Luby, J. L., Bogdan, R., Agrawal, A., Gaffrey, M. S., Belden, A. C., & … Barch, D. M. (2015). Amygdala functional connectivity, HPA axis genetic variation, and life stress in children and relations to anxiety and emotion regulation. Journal Of Abnormal Psychology, 124(4), 817-833. doi:10.1037/abn0000094

Shern, D. L., Blanch, A. K., & Steverman, S. M. (2016). Toxic stress, behavioral health, and the next major era in public health. American Journal Of Orthopsychiatry, 86(2), 109-123. doi:10.1037/ort0000120


A Brief Overview of Neurons and Neurotransmission

neuronsJen L’Insalata

Preston, O’Neal, & Talaga (2013), presented the comparison of neural transmission to a telephone switchboard. In many ways, that analogy is accurate since neurotransmitters are essentially messages being sent from one nerve to another. Neurons utilize electrical and chemical stimulation to communicate and ultimately control human behavior.

To understand how transmissions are passed between neural pathways, one must first understand the basic structure of a nerve cell. The main body of the nerve cell or neuron is known as the soma. Its shape differs depending on its specific function but is contains the structures universal to all cells such as the nucleus, mitochondria, and cytoplasm. The axon is a slender tube like structure that emanates from the soma. It is often covered by a myelin sheath which aids in the conduction of information from one neuron to another; known as an action potential. Terminal buttons are the end points of axons which secrete hormones known as neurotransmitters. To do this an action potential must travel down the axon and reach the terminal buttons. The neurotransmitter either excites or inhibits the action potential allowing it to continue or cease its communication with the neighboring neuron. The dendrites of the neighboring neuron receive the transmission from the terminal button across a fluid filled gap called a synapse. The dendrite resembles the branches of a tree and allow the transmission to continue along the neural pathway (Carlson, 2014. & Saladin, 2012).


Neural transmission and action potentials are governed by the balance of positively and negatively charged ions such as sodium, potassium, and chloride. Polarization of the intracellular fluid by salutatory conduction and diffusions allows the transmission of the action potential down the length of the axon until it reaches the terminal buttons. If the action potential is strong enough at the terminal button, synaptic vesicles containing neurotransmitters are able to bind with the presynaptic membrane of the terminal button. This membrane essentially separates the end of the terminal button from the synaptic cleft. The synaptic vesicle is then able to release the neurotransmitter across the intracellular fluid which fills the gap, or synapse, between the terminal button and the opposing dendrite (Carlson, 2014. & Saladin, 2012).


Neurotransmitters are transported from the cell body to the terminal button by sac-like structures called vesicles. The vesicles bind to the membrane of the terminal button ans create tiny opening from which the neurotransmitter is released from the presynaptic neuron. Neurotransmitters are then ale to cross they synapse and bind with receptors on the dendrites of the postsynaptic neuron facilitating communication. While some neurotransmitters bind with the receptor sites on the post synaptic neuron, others are destroyed, or reabsorbed by the terminal button of the presynaptic neuron (Reed, Carlson, Quale, 2016).




Carlson, N. R. (2014). Foundations of behavioral neuroscience (9th ed.). Boston, MA: Pearson. ISBN: 9780205940240.

Preston, J. D., O’Neal, J. H., & Talaga, M. C. (2013). Handbook of clinical psychopharmacology for therapists (7th ed.). Oakland, CA: New Harbinger. ISBN: 9781608826643.

Reed, L., Carlson, L, Quale, S. (2016). Capella University Neurotransmission Retrieved from media/PSY7330/animation/transcript.htm1

Saladin. K.S. (2012). Anatomy and Physiology: The Unity of Form and Function. 6th ed. Mcgraw-Hill. New York, NY. ISBN978-0-07-337825-1.