Cognitive reactivity (i.e., activation of a single schema or several associated schemas by a triggering event or events) results in maladaptive adjustments in cognition, increasingly drastic distortions, and elevated negative affective states, all of which proceed presentations of depression symptomology and influence the severity of behavioral reactions. 

Depression is Serious

In 2014, an estimated 15.7 million American adults age 18 and up and an estimated 2.8 million American youth ages 12-17 reported having one or more depressive episodes within the last year (Center for Behavioral Health Statistics and Quality, 2015; National Institute of Health, 2015). 

Depression is a debilitating mood disorder that affects an individual’s ability to do simple, daily tasks. 

Symptoms include, dramatic drops in energy, difficulty concentrating, trouble maintaining normal sleep patterns and a host of other symptoms that may last for more than two weeks. (American Psychiatric Association, [DSM-5], 2013).

Depression and depressive disorders affect a global estimate of 350 million people, affecting women, more so than men, and are responsible for 90% of all youth suicides (World Health Organization, 2016).

Is It Depression or Just a “Bad Mood”?

For someone examining the list of depressive symptoms and wondering if it is time to seek the help of a physician; it may be difficult to tell.  

It is not unusual to experience moments of feeling down.  Some people cancel plans with friends in favor of staying home alone on a Friday night. 

Others let the dishes and the laundry pile up because they ‘don’t feel like it’. Still others seek comfort from the indulgent combination of yoga pants, rocky road ice cream, and a Through the Wormhole marathon narrated by the soothing intonations of Morgan Freeman.  

Are these examples of people coping with depression?        

The impact that depressive symptoms have on a person’s daily functioning ability for extended periods is what differentiates depression from a bad mood.   A person with depression is unable to function mentally, emotionally, and physically, the way that he or she did before experiencing symptoms (National Institute of Mental Health, 2015).

This harrowing detail alone is enough to cause feelings of despair, for the individuals as well as for all who care for them, but people diagnosed with disorders of depression also face the somber realization that relying on their own determination and efforts to recuperate and restore the satisfaction that they once experienced in their lives may be a challenge.

Depression is a life-stealing illness that affects millions around the globe (WHO, 2016; NIMH, 2015).

Biological and Psychological Origins of Depression

Typically, theories of depression are grouped together under one of two categories: Biological or Psychological. This article is not inclusive of all theories of depression causation or all factors of vulnerability to depression.  

Some examples of biological causes of depression include genetic, biochemical, anatomical, and physiological aspects associated with depressive illnesses.

Some examples of psychological causes include cognitive-behavioral, emotional, sociological, and environmental aspects associated with depressive illnesses.

Depression is not a single diagnosis, but a cluster of disorders with numerous diagnostic specifiers, or labels, that may be applied depending on symptoms.

Even though two people may share the same diagnosis of a depressive illness, it is likely that their symptoms will vary and require different specifiers and subsequent treatments (Diagnostic and Statistical Manual of Mental Disorders, 5th   ed., APA, 2013). Researchers determined that depression has a heritability rate of 30-40% (Elder &Mosack, 2011).

Many agree with the biological theory, particularly that of genetics, and regard depression as a disorder of heredity.   An individual’s chances of developing depression can be up to three times more likely if he or she has an immediate family member that has been diagnosed with depression (NIMH, 2015). 

It might be logical to presume that physicians will soon be able to examine genetic information and predict who will develop depression and other diseases and who will not. 

A family history of depression might increase the vulnerability to depression, but what, specifically, encourages genes to mutate and what causes the alterations of alleles so that their expressions affect specialized processes, such as neurochemical transport, in only some patients; but not all, is as much of a mystery today as it was two decades ago (Medina et al., 2016; Munafo, 2012). 

It may be that the answers we seek are elusive with the outcomes of genetic epidemiology studies being confounded by variables that range from “cellular to biographical” which tend to make predictions of who will and who will not develop disease virtually unattainable (Munafo, 2012, pp. 915).

This fact challenges the assumptions of particular doctrines that subscribe to and promote essentialism using an “essence-prior-to-existence” philosophy (Haslem, 2011, pp. 819) and the implication of presenting data in this way suggests that if an individual’s genetic information reveals his or her vulnerability to developing depression or depressive disorders, there is little hope for improvement.

This misperception presupposes that the quality of health, therefore the quality of life, is at the mercy of personal biochemistry which encourages patients to expect the worst.  

Presenting genetic theory as causal and immutable, versus emphasizing the pliability of some aspects of depressive disorders, contributes to prognostic pessimism in patients regarding disease prognoses (Lebowitz, Ahn, & Nolen-Hoeksema, 2013).

This perspective is prevalent in patients diagnosed with disorders, as well as the general public, with 80% of Americans endorsing a vague explanation of “a chemical imbalance in the brain” as a cause of depression, and 64% of Americans endorsing the explanation of “a genetic or inherited problem” as a cause of depression (Pescosolido et al., 2010, pp. 518).

It is apparent that the majority views depression as a diagnosis of which recovery or remission are not possible, should causation be considered as purely biological. 

The acceptance of half-truths could be due, at least in part, to the aggressive promotion of negative aspects of psychiatric disorder diagnoses (e.g., depression) which add to patients’ perception of hopelessness.

This is a disservice to patients and does not align with psychologists’ responsibilities of preventing harm and further suffering to patients as specified in the Ethical Principles of Psychologists and Code of Conduct (American Psychological Association, 2014).

An approach that accentuates the positive possibilities, as well as informs of the negative realities, would include patient education regarding aspects of depressive disorders that could be transformable.

  A comprehensive view would better facilitate patients’ understanding, beliefs (i.e., expectations) and optimism regarding disease prognosis and could also alleviate patient stress (Pescosolido et al., 2010).

I am not disputing this abundance of evidence confirming the multitude of biological changes that are known to occur in patients diagnosed with depression and depressive disorders.

I am suggesting these biological changes to be part and parcel to an increase in vulnerability to depression; not to the causation of depression.  

Dr. Munafo (2012) states that the impossibility of predicting depressive diseases using genetics alone is due to confounding variables that occur on many levels and stem from a broad range of origins.  

One of the variables he mentions is the “occurrences of stressful life events” (pp. 916), implying that exposure to stressful events is associated with depression. 

This implication possibly connotes a psychological underpinning regarding depression and depressive disorder causation.                              

Exposure to Stress and Depression

Evidence shows that stress is associated with overwhelming amounts of perceived fear, pessimistic attitudes towards daily life, and a nagging sense of defeat and personal responsibility for failure, all of which contribute to the pathogenesis of physical and psychological disease (Selye, 1950, Weider & Selye,1953). 

Life is full of major stressful events (e.g., unpredictable

circumstances, uncontrollable losses) and events that may seem minor, but are chronic as well as

toxic (i.e., highly emotionally charged irritants that are experienced daily) both of which hinder biological mechanisms (Fossati, Radtchenko, & Boyer, 2004; Krishnan & Nestler, 2010; Medina et al., 2016), thought processes (Hankin et al., 2009; McIntyre & Cha, 2016; Patten, 2103) and emotional regulation (Beck & Alford, 2009; Lau, Segal, & Williams, 2004; Scher, Ingram & Segal, 2005) which contribute to destructive behavior (Abela & Hankin, 2008; Beck & Alford, 2009; Butler, Chapman, Forman & Beck, 2006), and to the development of disease (Cohen, Janicki-Deverts, & Miller, 2007; Hammen, 2005; Selye, 1950).

Chronic stress exposure (e.g., consistent financial insecurity, recurring marital conflict, coping with chronic illness) has been associated with a change in responses that are longer in duration or even permanent, compared to acute stress exposure (e.g., a sudden layoff from employment) that may cause negative emotions that are greater in intensity, but lasting for shorter periods (Cohen et al., 2007; Hammen, 2005;Ingram et al., 1998; Monroe & Simons, 1991; Patten, 2013). 

These changes in responses are the body’s adaptations to stress (Beck & Bredmeier, 2016; Selye, 1950; Weider & Selye, 1953).

Stress can be placed on the body and can also occur within the body and this, of course, includes the mind.        

Using an example of resistance training: the stress of curling dumb bells causes microscopic tears in the muscle fibers of the bicep.  

The body adapts to this stress by generating newer and stronger muscle fibers during periods of recovery in order to repair those tears, resulting in the bicep’s future potential to withstand heavier loads (LaStayo et al., 2003).

The stress caused by the resistance training of a muscle creates adaptations which, ultimately, benefit the overall health of the individual, whereas negative affective states associated with stress, particularly those caused by chronic exposure, elicit adaptations that jeopardize the overall health of the individual (Cohen, et al., 2007; Hammen, 2005; Selye, 1950, Weider & Selye, 1953;).

Weider & Selye (1953) re-classify these responses as “mal-adaptations” since the alterations that take place do not benefit the individual, but expose him or her to excessive amounts of risk for psychiatric and physical diseases (pp. 203).  

Some, but not all, maladaptive responses to stress that take place within the mind are the development of diathesis, schema, and cognitive distortions (for a brief review see Beck, 1967, 1979; Beck & Alford, 2009; Zuckerman, 1999).

Would Less Stress Equate to Less Depression?

Many people agree that stress and depression go hand-in-hand.  

Some researchers posit that stress is causal to depression since maladaptive responses are elicited when individuals encounter stressful experiences (Hammen, 2005; Selye, 1950; Weider & Selye, 1953; Zuckerman, 1999). 

Some individuals are more susceptible (i.e., vulnerable) to negative affect states associated with stress than others. 

These vulnerabilities, or diathesis, include many factors (e.g., biological, psychological and situational) and are thought to exist in latent states before stress exposure and before symptoms of disorders (e.g., depression) appear (Beck, 1967, 1979; Beck & Alford, 2009, Hankin et al., 2009; Ingram, et al., 1998; Zuckerman, 1999).

With the cumulative effects of additivity or chronic attrition, the presence of stress interacting with diatheses largely contributes to increased cognitive reactivity to stressful situations which in turn, induces escalating negative affective states (Cohen et al., 2007; Hankin et al., 2009; Ingram et al., 1998; Lau et al., 2004; Monroe & Simons, 1991).

Stress can occur on and affect many levels (e.g., biological, psychological, behavioral, social) and elicit maladaptive responses which increase the likelihood of psychological and psychiatric disorders (e.g., depression) as well as many other diseases (Cohen et al., 2007; Hammen, 2005; Patten, 2013; Selye, 1950; Weider & Selye, 1953).  

Does this imply, hypothetically, that if the growing multitudes of life stressors that are common to many people living in today’s post-industrial world were to be completely removed – the prevalence ofdepression would decrease; even vanish?

Dr. Kevin Strauss’s recent article Genomics for the People (Scientific American, 2015) describes the work of a clinic in the North American plains which conducts high-tech genetics research in the serene communities of isolated Amish and Mennonite settlements.  

I have only a basic knowledge of this peaceful group of people who settled here while seeking religious asylum in the 1600’s, but I know that they have seceded from the modernized majority in an effort to preserve their culture, faith, and social cohesion.  

The article contained several photos of the Amish and Mennonite people with content facial expressions and their bare feet in tall green grass.

Surprisingly, the technologically-advanced research clinic was raised and is supported by the Amish and Mennonite people with the hope of preventing disease in their future generations with the use of genomic-wide association studies.  

The clinic is the first occurrence of preventative mental health care in the community of the Old-Order Amish and Mennonite families of Pennsylvania (pp. 68). 

After several years of testing, Dr. Krauss and his team discovered the pathogenic missense variant, KCNH7, a psychiatric allele with pleiotropic effects, which researchers believe to have a significant role in the diagnoses of bipolar spectrum disorders, schizophrenia, schizoaffective disorder, and major depressive disorder that were found to be highly-penetrant in the quiet, slow-paced community of Amish and Mennonite families (Strauss et al., 2014). 

Dr. Krauss (2015) also mentions in his article that the environment of the community and the involvement of its members, who are concerned with the preservation of unity and peace, “serves to mediate positive psychological and behavioral changes in those afflicted with major affective disorders” (pp. 73).

The findings of Dr. Krauss (2014) and his team argue the assumption that there may be less prevalence of depressive disorders in environments that are considered to have lesser amounts of stressful life events that would potentially trigger symptoms of affective disorders (e.g., depression).

Negative Constructs of Cognition & Distortions

Genetic researchers concede that biological factors (e.g., genetics) influence the expression of depressive and psychiatric disorders, but the way that an individual responds to stress triggers is what determines whether or not he or she will experience depressive symptoms (Elder & Mosack, 2011; Sullivan et al., 2000).

Cognition encompasses the variables of perceiving (i.e., becoming aware), recognizing, which is identifying after encountering previously, conceiving, which is the process of formulating associations, judging, which is the process of drawing conclusions based on associations, and reasoning, which is considering various possibilities according to strict principals of validity and logic.  

When the cognitive variables of depression-vulnerable individuals are re-structured as a maladaptive response to negative life events (e.g., stress), constructs known as schemas are formed.  (Abela & Hankin, 2008; Beck & Alford, 2009; Dozois & Beck; 2008 Ingram et al., 1998;).

Schemas are internal configurations of informational processing patterns that are either conscious (i.e., having an immediate awareness as thought patterns are occurring) or subconscious (i.e., existing and transpiring within the mind without having an immediate awareness as thought patterns are occurring). 

If an individual happens to be aware of his or her thought patterns in the present moment, he or she may experience schemas as subtle reminders that contain words or events that depict scenes (Beck & Alford, 2009).  

Schemas are thought to exist in dormant states until triggered and activated by a familiar aspect of the situation that occurred when the schema was first formed (Dozois & Beck, 2008; Kovacs & Beck, 1978; Monroe & Simons, 1991). 

Each schema is linked to another based on similarity of content and multiple schemas form matrices of content-related themes that each contain a self-rehearsed narrative consisting of stored negative attributions (i.e., suspected internal or external sources of causation), beliefs (e.g., personal philosophies, expectations) and dysfunctional attitudes (e.g., mental, emotional and behavioral reactions) that were formed in response to previously experienced situations (Beck, 1967; Kovacs & Beck, 1978), particularly, negative interactions that occurred in early-life development (Beck, 2002; Lumely & Harkness, 2009).  

A triggered and fully-activated schema can spread activation potential (i.e., energy impulses) that triggers associated schemas (Hollon, 2010; Lau et al., 2004).   

Each fully-activated schema filters and sorts incoming information according to its maladaptive structure of negative biases (Beck, 2002; Piaget, 1926) which deludes healthy cognitive processing which distorts the individual’s

perception and interpretation of information leading to inaccurate presuppositions and errors in judgment (McIntyre & Cha, 2016).  In other words, cognitive reactivity (i.e., activation of a single schema or several associated schemas by a triggering event or events) results in maladaptive adjustments in cognition, increasingly drastic distortions, and elevated negative

affective states, all of which proceed presentations of depression symptomology and influence the severity of behavioral reactions. 

Evidence suggests that higher levels of cognitive reactivity and associated negative affective states are more likely to present in individuals whose predominant thinking habits contain preconceived and irrational inclinations toward negatively biased appraisals, associations and attributions, since the nature of an individual’s emotional reactions and subsequent behavioral responses matches the nature of his or her thought content (Beck, 1967, 1979, 2002; Beck & Alford, 2009; Dozois & Beck, 2008; Hankin et al., 2009; Hollon, 2010; Ingram et al., 1998; Kovacs & Beck, 1978; McItyre & Cha, 2016; Piaget, 1926;

Rubenstein et al., 2016; Scher et al., 2005; Seeds et al., 2010).

Beck, (1979) dubbed a three-fold combination of negatively inclined perceptions of the “self, the world, and the future” as the “negative cognitive triad” which he suggests is not only related to depression symptoms, but what he posits is the primary cause of depression, as well as many other mood disorders (Beck & Alford, 2009).

A therapeutic approach that teaches patients how to track, evaluate, and then reframe the dysfunctional views that drive cognitive distortions (e.g., schemas) equips them with tools to overcome problems and cope with situations which they perceived as hopeless.

The individual’s improvement in functioning is accomplished by re- evaluating and correcting his or her thinking (Beck, 1991, Butler et al., 2006; Morrison, 2014).

This approach has encouraged the spawning of several cognitive therapy modalities that, today, treat major depression and numerous other affective disorders, causing cognitive therapy to be recognized repeatedly for its efficacy (Beck, 1979; 1991; Beck & Alford, 2009; Butler et al., 2006; Hollon, 2010; McIntyre & Cha, 2016; Teasdale, 1995).

Certain mental activities, such as rumination and prospection have been shown to exacerbate negative affective states produced by negatively biased thinking patterns and cognitive distortions (Levens et al., 2009; Michl et al., 2013; Roepke & Seligman, 2015).

“Men are disturbed not by things, but by the view which they take of them.”

These words were of Greek philosopher Epictetus (135 C.E.) and may have been prophetic pertaining to the habitual and destructive thinking patterns of re-experiencing the past (e.g., rumination) and pre-experiencing the future (e.g., prospection) and the epidemiology of depression.

Rumination is the persistent, passive, and often subtle mental habits of attributing events to negative causes, re-experiencing scenarios of the negative consequences, and focusing intently on the presence of uncomfortable negative emotional states; without engaging in active problem-solving that could potentially lift depressed mood (Levens et al., 2009; Michl et al., 2013). Michl et al. (2013) found that self-reported events that were perceived as stressful predicted higher levels of rumination that lasted for prolonged periods of time that carry over to several different aspects of a person’s life.

Although the findings are of interest to the field, the results may be questionable since the sample population for this study consisted of adult and adolescent participants who were all from a lower socio-economic status community (e.g., per capita income of $18,404) in urban Connecticut.

The authors may have assumed that this sample would be more inclined to test positive for greater prevalence and severity of depressive symptoms and therefore be able to provide substantial amounts of rumination data, which would present a sampling bias. Also, the Ethical Principles of Psychologists and Code of Conduct (APA, 2016) emphasizes the eradication of biases in research that could be based on factors such as race, income, and social status and this may not have been addressed.

According to Michl et al., (2013), the sample of adolescents “(N=1065); 57.3% Hispanic/Latino” were from schools that were essentially chosen because of certain demographic characteristics and agreeableness to participate (pp. 341).

Testing a sample that is mainly composed of participants who are of minority racial and ethnic backgrounds and a lower socio-economic status, with over a quarter of the adolescent participants living in single-parent households, cannot provide information that can be generalized and ethically applied to the entire population.

Given the demographic characteristics, the participants of this sample are most likely exposed to an increased number of stressors of significant quality and intensity, compared to those individuals of demographic characteristics which are not represented in this study.

It would be interesting to analyze data collected from a similar study that is conducted with a sample that is broadly inclusive of all U.S. population demographic characteristics and therefore, a suitable sample representation of the population, as a whole.

Researchers conclude that negative rumination (i.e., a negative and destructive form of meditation) uses energy resources inefficiently, exacerbates depressive symptoms, exaggerates time ‘lost’ in a depressive episode, and increases vulnerability to future episodes (Levens et al., 2009; Michl et al., 2013).

Prospection is the mental and emotional simulation of possible futures (Roepke & Seligman, 2016). The automatic activity of healthy prospection assists in problem-solving, decision-making, and self-regulation.

While engaging in prospection, individuals rehearse potential future outcomes and pre-experience the corresponding emotions (e.g., anxiety, joy, hopelessness, excitement) that match the content of their visualizations.

When prospection activity is dysfunctional, individuals focus intently on representations of negative content with unfavorable future outcomes and experience tumultuous emotional correspondents, which exacerbates negative affect and depressive symptoms and feeds a vicious cycle (Roepke and Seligman, 2016).  

Similar to Beck’s “negative cognitive triad” (1979, pp. 259), researchers specify three equally dysfunctional styles of prospection that interact to fuel depressive symptoms.

These include the conjuring of images that portray catastrophic futures, the pessimistic analyzation of the details of these harmful future events, and negative inclinations toward having unhelpful attitudes regarding the future that are based on irrational beliefs and expectations (Roepke & Seligman, 2016).

The habitual construction of negative future scenarios encourages mental and emotional preparedness for events that have not yet occurred, which precipitates a much broader scope of negative future expectations and increases the level of negative emotional states that are pre-experienced during simulations.

Being concerned, even frightened is not the issue here; it is the consistently negative content in the patterns of the future simulations which tyrannize the mind that leads to cognitive and emotional impairment (McIntyre & Cha, 2016).

I do agree that a certain amount of balanced realism is necessary for useful reflection, honest introspection, and adaptive functioning.

Individuals who are inclined toward negative future expectations predetermine worst-case scenarios and fabricate reasons as to why the worst is more likely to occur compared to alternative scenarios that are of positive content (Roepke & Seligman, 2016).

Faulty prospection differs in comparison to other cognitive vulnerabilities (e.g., negative attributional style) in that it is strictly future-oriented (Roepke & Seligman, 2016).

Summary and Conclusion

After reviewing the literature and considering my personal experience as an individual who continues to live with the lasting effects of severe trauma, of which depression is a known comorbidity (Morris, Compas, & Garber, 2012), my interpretation of this review is that genetic polymorphisms (i.e., mutations), alterations in neuroplasticity, anatomical deficiencies and functional impairments of brain region structures, disruption to biochemical and ion transport within glial cells and the impedance of neurochemical transmission along neuro- circuitry pathways, are the results of biological maladaptive reactions to stress.

The expressions of these stable, genetic traits contribute to greater degrees of vulnerability to depressive disorders and other psychiatric diseases and are transferred from generation to generation in the form of mutated alleles within the DNA coding.

I concur: Genetics and stress appear to increase an individual’s vulnerability to his or her development of depression and depressive disorders, but the cause of the development of depression seems to be, not the cognitions themselves, but within the intricacies of the cognitive processing of new information before the cognitions are formed.

Exposure to stressful life events triggers a system that exists before a response is given and this system is activated before the appearance of depressive symptoms (Beck & Alford, 2009; Lau et al., 2004; McIntyre & Cha, 2016; Monroe & Simons, 1991; Patten, 2013; Rubenstein et al., 2016; Scher et l., 2005; Seeds & Dozois, 2010).

It is in this small space, following the provocation of triggers and before symptoms present, that depression and a multitude of other affective disorders are treated effectively with various modalities built on the foundation of Beck’s cognitive therapy (Beck, 1991; Butler et al., 2006; Hollon, 2010; MacKenzie & Kocovski, 2016; Morrison, 2014; Teasdale, Segal & Williams, 1995).

Although depression and depressive disorders consist of and are driven by multiple factors (Beck & Bredemeir, 2016), many of which are not covered here (e.g., chronic pain, grief, substance abuse) there is a dearth of empirical evidence supporting cognitive-behavioral theories of depression causation (Beck & Bredemeir, 2016), in comparison to empirical evidence which supports biological theories of depression causation (Januar et al., 2015).

My conclusion is that several of these factors (i.e., vulnerabilities) may be present before depression symptoms appear and that symptoms are subsequent to the presence of cognitive impairments, which I believe is the root of depression symptom causation that can be treated effectively using one of many forms of cognitive therapy or cognitive-behavior therapy , which emphasizes the necessity to learn efficient coping strategies (Beck & Breidemeir, 2016; Elder & Mosack, 2011; Fossati et al., 2004; Krishnan & Nestler, 2010; Medina et al., 2016; Munafo, 2010; Selye, H., 1950; Weider & Selye, 1953; Zuckermann, M., 1999).

                                             References                                                                 1.

Abela, J. R., & Hankin, B. L. (Eds.). (2008). Handbook of depression in children and adolescents. pp. 35-78. Guilford Press. New York, NY; US. Retrieved from psychopatholgyperspective.pdf

American Psychiatric Association. (2013). Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, (DSM-5). APA, Washington, DC; USA. ISBN-10: 0890425558 Retrieved from

American Psychological Association. (2014). Ethical principles of psychologists and code of conduct. pp. 2. Retrieved from

Beck, A. T. (1967). Depression: clinical, experimental, and theoretical aspects. University of Pennsylvania Press. pp. 283. ISBN- 0812210328

Beck, A. T. (Ed.). (1979). Cognitive theory of depression, Guilford Press. pp. 13; pp. 259 ISBN- 9780898620009

Beck, A. T. (1991). Cognitive therapy: A 30-year retrospective. American Psychologist, 46(4), pp. 368-375. doi:10.1037/0003-066X.46.4.368 PMID: 2048795 Retrieved from

Beck, A. T. (2002). Cognitive models of depression. Chapter 2. In, Leahy, Robert L. (Ed); Dowd, E. Thomas (Ed). (2002). Clinical advances in cognitive psychotherapy: Theory and Application pp. 29-6. ISBN- 0-8261-2306-6 New York, NY, US: Springer Publishing Co, xiv, 446 pp.

Beck, A. T., & Alford, B. A. (2009). Depression: Causes and treatment, 2nd ed. University of Pennsylvania Press. ISBN:978-0-8122-1964-7

Beck, A. T., & Bredemeier, K. (2016). A unified model of depression integrating clinical, cognitive, biological, and evolutionary perspectives. Clinical Psychological Science, pp. 1-24. 2167702616628523 Retrieved from

Butler, A., Chapman, J., Forman, E., and Beck, A. (2006). The empirical status of cognitive- behavioral therapy: A review of meta-analyses. Clinical Psychology Review, 26, pp. 17- 31. doi:10.1016/j.cpr.2005.07.003 Retrieved from

Center for Behavioral Health Statistics and Quality. (2015). Behavioral health trends in the united states: Results from the 2014 national survey on drug use and health. HHS Publication No. SMA 15-4927, NSDUH Series H-50). Retrieved from

Cohen, S., Janicki-Deverts, D., & Miller, G. E. (2007). Psychological stress and disease. Journal of American Medical Association, 298(14), pp. 1685-1687. doi:10.1001/jama.298.14.1685 Retrieved from

Dar-Nimrod, I., & Heine, S. J. (2011). Genetic essentialism: on the deceptive determinism of DNA. Psychological bulletin, 137(5), pp. 800. doi:10.1037/a0021860 Retrieved from

Dozois, D. J., & Beck, A. T. (2008). Cognitive schemas, beliefs and assumptions. Risk factors in depression, 1, pp. 121-143. doi:10.1016/B9780-08-045078-0.00006-X Retrieved from

Elder, B. L., & Mosack, V. (2011). Genetics of depression: An overview of the current science. Issues in Mental Health Nursing, 32(4), 192-202. doi:10.3109/01612840.2010.541588 Retrieved from journalCode=imhn20

Epictetus., & Higginson, T. W. (1955). The Enchiridion. New York: Liberal Arts Press.

Fossati, P., Radtchenko, A., & Boyer, P. (2004). Neuroplasticity: from MRI to depressive symptoms. European Neuropsychopharmacology, 14, S503-S510. doi:10.1016/j.euroneuro.2004.09.001 Retrieved from 2004.09.001#!/search?ho=t&l=en&q=doi:10.1016%2Fj.euroneuro.2004.09.001

Hammen, C. (2005). Stress and depression. Annual Review of Clinical Psychology, 1(1), pp. 293 -319. doi:10.1146/annurev.clinpsy.1.102803.143938 Retrieved from

Hankin, B. L., Oppenheimer, C., Jenness, J., Barrocas, A., Shapero, B. G., & Goldband, J. (2009). Developmental origins of cognitive vulnerabilities to depression: Review of processes contributing to stability and change across time. Journal of Clinical Psychology, 65(12), 1327. doi:10.1002/jclp.20625 Retrieved from

Haslam, N. (2011). Genetic essentialism, neuro-essentialism, and stigma: Commentary on Dar- Nimrod and Heine (2011). Psychological Bulletin, 137(5), pp. 819-824. doi:10.1037/a0022386 Retrieved from

Hollon, S. D. (2010). Aaron T. Beck: The cognitive revolution in theory and therapy, bringing psychotherapy research to life, pp. 63-74. doi:10.1037/12137-006 Retrieved from 22816-006

Ingram, R. E., Miranda, J., & Segal, Z. V. (1998). Cognitive vulnerability to depression. Guilford Press. ISBN: 1572303042

Kovacs, M., & Beck, A. T. (1978). Maladaptive cognitive structures in depression. American Journal of psychiatry, 135(5), 525-533. doi:10.1176/ajp.135.5.525
Retrieved from

Krishnan, V., & Nestler, E. J. (2010). Linking molecules to mood: new insight into the biology of depression. American Journal of Psychiatry, 167(11), pp. 1305-1320. doi:10.1176/appi.ajp.2009.10030434 Retrieved from

Lau, M. A., Segal, Z. V., & Williams, J. M. G. (2004). Teasdale’s differential activation hypothesis: Implications for mechanisms of depressive relapse and suicidal behaviour. Behaviour Research and Therapy, 42(9), 1001. doi:10.1016/j.brat.2004.03.003 Retrieved from


LaStayo, P., Woolf, J., Lewek, M., Snyder-Mackler, L., Reich, T., Lundstedt, S. 2003. Eccentric muscle contractions: Their contribution to injury, prevention, rehabilitation, and
sport. Journal of Orthopaedic & Sports Physical Therapy, 33(10), pp. 557-571. PMID:14620785 doi:10.2519/jospt.2003.33.10.557 Retrieved from

Lebowitz, M. S., Ahn, W. K., & Nolen-Hoeksema, S. (2013). Fixable or fate? Perceptions of the biology of depression. Journal of consulting and clinical psychology, 81(3), pp. 518. doi:10.1037/a0031730 Retrieved from

Levens, S., Muhtadie, L; & Gotlib, I. (2009). Rumination and impaired resource allocation in depression. Journal of Abnormal Psychology, 118 (4), pp. 757-766. doi:10.1037/a0017206 Retrieved from 20626-007

Lumley, M. N., & Harkness, K. L. (2009). Childhood maltreatment and depressotypic cognitive organization. Cognitive Therapy and Research, 33(5), 511-522. doi:10.1007/s10608-009- 9257-7 Retrieved from!/sear ch?ho=t&l=en&q=10.1007%2FBF01173414

MacKenzie, M., and Kocovski, N. (2016). Mindfulness-based cognitive therapy for depression: Trends and developments. Psychology Research and Behavior Management, 9, pp. 125- 132. doi:10.2147/PRBM.S63949 Retrieved from

McIntyre, R. S., (Eds.); & Cha, D. S. (2016). Cognitive Impairment in Major Depressive Disorder: Clinical Relevance, Biological Substrates, and Treatment Opportunities. Cambridge University Press. ISBN: 9781107024632

Medina, A., Watson, S. J., Bunney Jr., W., Myers, R. M., Schatzberg, A., Barchas, J., Akila, H., Thompson, R. C. (2016). Evidence for alterations of the glial syncytial function in major depressive disorder. Journal of Psychiatric Research, 72, pp. 15-21. doi:10.1016/j.jpsychires.2015.10.010 Retrieved from X

Michl, L., McLaughlin, A., Shepherd, K., Nolen-Hoeksema, S. (2013). Rumination as a mechanism linking stressful life events to symptoms of depression and
anxiety: Longitudinal evidence in early adolescents and adults. Journal of Abnormal Psychology, 122(2), pp. 339-352. doi:10.1037/a0031994 Retrieved from 17531-002

Monroe, S. M., & Simons, A. D. (1991). Diathesis-stress theories in the context of life stress research: Implications for the depressive disorders. Psychological Bulletin, 110(3), pp. 406-425. doi:10.1037/0033-2909.110.3.406 Retrieved from 05606-001

Morris, M. C., Compas, B. E., & Garber, J. (2012). Relations among posttraumatic stress disorder, comorbid major depression, and HPA function: A systematic review and meta- analysis. Clinical Psychology Review, 32(4), pp. 301-315. doi:10.1016/j.cpr.2012.02.002 Retrieved from main.pdf?_tid=9c3075f2-58e4-11e6-a425- 00000aacb35e&acdnat=1470165137_7b877155207f5955527dd01ab947fa1c

Morrison, A.P. (2014). A casebook of cognitive therapy for psychosis. pp. 20, Routledge. ISBN-10: 1583912061

Munafò, M. R. (2012). The serotonin transporter gene and depression. Depression and anxiety, 29(11), pp. 915-917. doi:10.1002/da.22009 Retrieved from

National Institute of Health. (2015). Prevalence of depression in adults and adolescents in the united states. The Depression Booklet. Retrieved from adults.shtml and among-adolescents.shtml

National Institute of Mental Health. (2015). Depression: What you need to know. National Institute of Mental Health. Retrieved from

Patten, S. B. (2013). Major depression epidemiology from a diathesis-stress conceptualization. BMC Psychiatry, 13, pp. 19. doi:10.1186/1471-244X-13-19. Retrieved from

Pescosolido, B. A., Martin, J. K., Long, J. S., Medina, T. R., Phelan, J. C., & Link, B. G. (2010). “A disease like any other”? A decade of change in public reactions to schizophrenia, depression, and alcohol dependence. American Journal of Psychiatry, 167(11), pp. 1321- 1330. doi:10.1176/appi.ajp.2010.09121743 Retrieved from

Piaget, J., & The Hegeler Institute. (1926). Psychology: Translated from the french by marthe sturm. Monist, 36(3), 430-455. doi:10.5840/monist192636333 Retrieved from 2636333#!/search?ho=f&l=en&q=DOI:%2010.5840%2Fmonist192636333

Roepke, A. M., & Seligman, M. E. (2016). Depression and prospection. British Journal of Clinical Psychology, 55(1), pp. 23-48. doi:10.1111/bjc.12087 Retrieved from

Rubenstein, L., Freed, R., Shapero, B., Fauber, R., Alloy, L. (2016). Cognitive attributions in depression: Bridging the gap between research and clinical practice. Journal of Psychotherapy Integration, 26(2), pp. 103-115. doi:10.1037/int0000030 Retrieved from!/sea rch?ho=t&l=en&q=10.1037%2Fint0000030%20%20

Scher, C. D., Ingram, R. E., & Segal, Z. V. (2005). Cognitive reactivity and vulnerability: Empirical evaluation of construct activation and cognitive diatheses in unipolar depression. Clinical psychology review, 25(4), pp. 487-510. doi:10.1016/j.cpr.2005.01.005 Retrieved from

Seeds, P. M., & Dozois, D. J. (2010). Prospective evaluation of a cognitive vulnerability-stress model for depression: The interaction of schema self-structures and negative life
events. Journal of Clinical Psychology, 66(12), pp. 1307-1323. doi:10.1002/jclp.20723 Retrieved from #!/search?ho=t&l=en&q=doi:10.1002%2Fjclp.20723%20

Selye, H. (1950). The physiology and pathology of exposure to stress. Oxford, England: ACTA, Inc., pp. 203. PsycINFO Database Record. 2012. APA. Retrieved from

Strauss, K. A., Markx, S., Georgi, B., Paul, S. M., Jinks, R. N., Hoshi, T., McDonald, A., First, M., Liu, W., Benkert, A., Heaps, A., Tian, Y., Chakravarti, A., Bucan, M., and Puffenberger, E. (2014). A population-based study of KCNH7 and bipolar spectrum disorders. Human Molecular Genetics, 23(23), pp. 6395-6406. doi:10.1093/hmg/ddu335 Retrieved from

Strauss, K., M.D., (2015). Genomics for the People. Scientific American, 313(6), pp. 67-73. Sullivan, P. F., Neale, M. C., & Kendler, K. S. (2000). Genetic epidemiology of major

depression: review and meta-analysis. American Journal of Psychiatry, 157(10), pp. 1552-1562. Retrieved from

Teasdale, J. D., Segal, Z., & Williams, J. M. G. (1995). How does cognitive therapy prevent depressive relapse and why should attentional control (mindfulness) training
help? Behaviour Research and Therapy, 33(1), 25-39. doi: 10.1016/0005- 7967(94)E0011-7 Retrieved from 7967(94)E0011-7

Weider, Arthur (Ed.)., & Selye, H. (1953). The general-adaptation-syndrome in its relationships to neurology, psychology, and psychopathology. Contributions Toward Medical Psychology: Theory and Psycho-Diagnostic Methods, 1, pp. 234-274. New York, NY, US: Ronald Press Company, xxv, 455 pp. doi:10.1037/11419-011 Retrieved from

World Health Organization. (2016). Global statistics: Depression. Depression Fact Sheet. World Health Organization, Geneva, Switzerland. Retrieved from

Zuckerman, M. (1999). Diathesis-stress models. American Psychological Association, pp. 3-23. Washington, DC; US. doi:10.1037/10316-001 Retrieved from

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Mia Vivone - Professional Consultant and Life Coach Specializing in Trauma