Article Review: Bullying, Depression, and Suicide Risk in a Pediatric Primary Care Sample (Kodish, Herres, Shearer, et al, 2016)

Kodish, Herres, and Shearer, et al’s Bullying, Depression, and Suicide Risk in a Pediatric Primary Care Sample seeks to explore what, if any, causal relationship there may be between bullying and the prevalence of suicide among youth aged 14 to 24 years.  Uniquely, their study seeks to identify not only the relationship between bullying and suicide among youth, but also to distinguish between the different types of bullying and their associated effects on suicidal ideation, as well as to explore what role depression may have as a moderating factor between bullying and suicide risk.  Kodish, et al, derived their cohort for study from ten primary care practices located in rural and semi-urban Northeastern Pennsylvania,and used the Behavioral Health Screen (BHS) to arrive at a sample of 5,429 participants.

 

By using the DSM in conjunction with the BHS, the surveyors were able to assess risk for bullying by type (verbal, physical, and/or cyber) as well as the presence of depressive symptoms (using five factors gauged over a two week period), and also included a four item mean from the lifetime suicide scale that included questions to determine if the participant had felt life to be not worth living; had considered suicide; planned to commit suicide; or had attempted suicide.  Controlling for depression and demographics, the collected data was then analyzed to determine what relationship, if any, existed between the types of bullying and suicidal risk levels, as well as testing the interactions between each bullying type and incidences of depression (Kodish, et al, 2016).  It was determined that there is a statistically significant relationship between risk of suicide and all three types of bullying, with a cumulative bullying experience also associated with a heightened risk of suicide.  It should also be noted that significance was recognized between all four bullying factors (verbal, physical, cyber, cumulative) and incidences of depression, with a stronger link between bullying occurrences and suicide severity among patients with depressive symptoms.  While the effects of physical, cyber, and cumulative bullying experiences were found not to be statistically significant with regard to suicide attempts, patients who experienced verbal bullying were shown to be 1.5 times more likely to report a suicide attempt (Kodish, et al, 2016).

 

Overall, it was discovered that all three forms of bullying were linked to suicide risk severity, with the effect being acutely heightened when symptoms of depression were present.  Of the three forms of bullying assessed, it was discovered that verbal bullying had, by far, the most impact, which may be due to it being the most common type reported (25% of the sample cohort reported verbal abuse in bullying situations).  This may be due to the fact that it is usually delivered publicly and in person.  By contrast, physical bullying, which may be painful and socially humiliating, may have a lesser psychological impact than other forms of bullying.  This could be due to any number of factors (“David v Goliath”-type situation, physical confrontation being motivated by racism, etc).  In regards to cyber bullying, the fact that it is usually done anonymously as well as the fact that the Internet is impersonal in nature may have a curtailing effect on the impact of this particular type of bullying.  Depression has been shown in this particular study to definitely be a moderator between bullying and suicide risk, but further study is warranted to determine the overall extent to which this relationship exists, as well as determining the extent of moderation for each type of bullying.

 

Looking at the relationship between bullying, suicidal ideation and the relevance of associated depression provides insight into developing appropriate and effective treatment protocols for those who are most at-risk.  By establishing a solid connection between bullying, suicidal ideation, and depression, the authors have furthered insight into a serious issue facing our youth, and it should be noted that not only does this research benefit those who are bullied, but also those who do the bullying; youth who bully others have been found to be at significantly increased risk for suicide and depression as well.

 

Delving further into these issues will help to improve not only the understanding necessary for addressing the victims of bullying but also to understand what it is that causes a bully to victimize others, thus allowing earlier interventions for prevention of escalation, and ultimately the reversal of those trends that lead to bullying, depression, and suicidal ideation.  The authors note that assessing for these issues during primary care visits is warranted.  Going forward, improving the assessment for these issues through clinical interviews should be a priority for those not only in healthcare occupations, but also those who are likely to have the most social non-parental contact with children (teachers, clergy, etc).

 

Kodish, T., Herres, J., Shearer, A., Atte, T., Fein, J., & Diamond, G. (2016). Bullying, Depression, and Suicide Risk in a Pediatric Primary Care Sample. Crisis, 37(3), 241-246. doi:10.1027/0227-5910/a000378

 

 

Teresa King
PMHC Doctoral Intern

 

Friday Factoids: The Dangers of Synthetic Marijuana

 

 

While many states have decriminalized the possession, use, and cultivation of natural Cannabis for either medicinal or recreational purposes, a majority of states continue to follow Federal guidelines with their approach to natural Cannabis and the law.  This seems to be driving the popularity of synthetic marijuana in those states where natural Cannabis is still treated as a controlled substance.  Synthetic marijuana goes by many names such as Spice, K-2, “fake weed”, etc., and the biggest issue seems to be that although it binds to the same CB1 receptor in the brain, it acts as a full agonist, rather than just a partial agonist as in the case of THC. (NIDA, 2015; Walton, 2014)  Binding with a much greater efficiency seems to make it much more difficult for the body to process and metabolize the acting ingredient that gives the high the user is looking for, with the result that the effect is many times more powerful than that produced by THC.

 

While the active ingredients in synthetic marijuana are called “cannabinoids” due to their chemical resemblance to cannabinoids that are found in natural Cannabis, they are much more potent, and unpredictable, in their effects on the user.  Even though they are marketed as a safe and legal alternative, their effects can be so much more powerful that they can become life-threatening. (NIDA, 2015)  The fact that CB1 receptors are in every structure of the brain is a key part of what makes the issue so serious, as are the symptoms experienced during an overdose event.  CB1 receptors in the hippocampus (memory affect), temporal cortex (seizure initiation), prefrontal cortex (psychosis), and brain stem (cardiac, respiratory, and gastrointestinal affect) all contribute to the myriad of symptoms that occur during an overdose on synthetic marijuana having a lasting effect, while the effects of an “overdose” from THC in natural Cannabis tend to dissipate fairly quickly.   “Clinically, they just don’t look like people who smoke marijuana,” says Lewis Nelson, MD, at NYU’s Department of Emergency Medicine, Division of Medical Toxicology. “Pot users are usually interactive, mellow, funny. Everyone once in a while we see a bad trip with natural marijuana. But it goes away quickly. With people using synthetic, they look like people who are using amphetamines: they’re angry, sweaty, agitated.” (Walton, 2014)

 

Newly available and unregulated psychoactive compounds, including synthetic marijuana, belong to a drug group called “new psychoactive substances”, or NPS.  NPS are problematic in that as soon as a compound is added to the group for regulation, another is quickly made available, and the cycle continues.  Fundamental changes in drug policy, drug law, public perception/attitudes, and approaches to treatment will be necessary before the depth of the problem can be ascertained, and a suitable method for treatment and recovery developed and implemented.

 

References

NIDA (2015). Synthetic Cannabinoids. Retrieved November 24, 2016, from          https://www.drugabuse.gov/publications/drugfacts/synthetic-cannabinoids

 

Walton, A. G. (2014, August 28). Why synthetic marijuana is more toxic to the brain than pot. Forbes. Retrieved November 24, 2016, from http://www.forbes.com/sites/alicegwalton/2014/08/28/6-reasons-synthetic-marijuana-spice-k2-is-so-toxic-to-the-brain/#5e615f9249eb

 

Teresa King
Pennyroyal Doctoral Intern

 

 

 

Article Review: Early Identification of and Treatment for Borderline Personality Disorder

 

Sharp and Fonagy (2015) offer a review of the phenomenology, prevalence, etiology, clinical problems, and interventions for adolescents with BPD. Borderline personality disorder (BPD) is said to capture the core of personality pathology (Sharp & Fonagy, 2015).  The symptoms of BPD usually manifest in adolescence (Chanen & Kaess, 2012, as cited in Sharp & Fogay, 2015); yet many clinicians are hesitant to diagnose personality pathology in children due to the presumed normal emotional liability during this developmental period.  Interesting though, this period of turmoil has received only limited support in the research (Cicchetti & Rogosch, 2002, as cited in Sharp & Fonagy, 2015).  Furthermore, a poor prognosis is often associated with individuals that have problems throughout adolescence, and as cited by Paris (2015), pathological symptoms greater than one year should not be dismissed and may likely be associated with BPD.   Regardless, the symptoms of BPD compared to typical adolescence are often more severe, pervasive, long-standing, and reflected in both internalizing and externalizing disorders.

 

Sharp and Fonagy (2015) report that studies for early detection of BPD in adolescence have shown that “chronic feelings of emptiness and inappropriate, intense anger” are considered the “most stable symptoms,” whereas identity disturbance, affective instability, and intense anger have the “greatest predictive power for development of BPD” (p. 1268). These characteristics are said to be consistent across age groups.  Additionally, for boys, paranoid ideation, and in girls, identity disturbance, have shown to be discriminating symptoms of BPD in adolescents.  Persistent self-harm behaviors are known to distinguish BPD from other disorders. Similar to adults with BPD, risk factors in adolescents with BPD are general impulsivity, risky behaviors, difficulty dealing with stress, and negative affect.  Impairment in social and academic functioning is also common.

 

As cited in Sharp and Fonagy (2015), Chanen & Kaess (2012) describe BPD as a developmental disorder. Research has indicated a mean age of onset at 18, with a standard deviation of 5- 6 years. Adolescence is said to be a critical period for the development of BPD due to the social demands (e.g., establishing stable friends, remaining close to family).  Furthermore, the social and emotional development in adolescence is associated with functional and structural brain changes.  While, BPD symptoms appear in adolescence, they are known to peak in early adulthood, with a decline in impulsive symptoms over time. Affective symptoms are more likely to persist.  Sharp and Fonagy (2015) have shown evidence for heterotypic developmental course, meaning that there is “coherence in the underlying organization or meaning of behaviors over time” (p. 1271).

 

Regarding comorbidity, BPD in adolescence is highly associated with internalizing and externalizing disorders. Sharp and Fonagy (2015) cite that around 70% of adolescents with BPD have comorbid mood disorders, 67% have anxiety disorders, and 60% have externalizing disorders.  Thus, the authors argue that BPD is a confluence of both externalizing and internalizing disorders, and is not a female expression of antisocial personality disorder.  Additionally, there is evidence that constitutional factors (i.e., temperament) and environmental factors have a role in BPD etiology.

 

Yet, it is also difficult to distinguish BPD from other clinical disorders. For identification of BPD, several measures have shown clinical utility (See Sharp & Fonagy, 2015, for a more comprehensive review).  Clinical assessment along with an objective measures is thought to be best clinical practice for precision in diagnosis. Regarding intervention, there is not a wealth of information available.  Programs such as Helping Young People Early (HYPE) and Dutch Emotion Regulation Training (ERT) are early intervention efforts for BPD.  They are based on cognitive analytic therapy and cognitive-behavioral elements and skills training, respectively. Cognitive-analytic therapy integrates psychoanalytic object relations theory and cognitive psychology and has demonstrated effectiveness and rapid recovery.  Mentalization-based treatment for adolescents has similar components to cognitive analytic therapy and has shown effectiveness by “improved mentalizing and reduced attachment avoidance” (p. 1281).  Dialectical behavior therapy (DBT) has also been adapted for treatment of BPD in adolescents. DBT targets emotional dysregulation, distress tolerance, and interpersonal difficulties.  Transference-focused psychotherapy is grounded in object relations theory and has been adapted for adolescents, but has not underwent RCT to assess its effectiveness.

 

Sharp and Fonagy (2015) conclude that successful interventions should contain extensive efforts to maintain engagement in treatment, have an evidence-based model of developmental pathology, and have an active therapist role, with a focus on validation and modeling of empathy, as well as the development of a strong attachment. Additionally, there should be a facilitation of trust and belief that something can be learned in therapy.  Treatment should focus on emotional processing and the connection between action and feelings, have structure to promote activity, proactivity, and self-agency, as well as be manualized, with supervision for deviations from the manual.   There should be a commitment to the approach in treatment between both the therapist and client.

 

Evidence-based treatments for BPD have common treatment characteristics (Bateman, Gunderson, & Mulder, 2015). They are structured (manual directed) and they encourage clients to control themselves (agency). Therapists help connect feelings and actions and are active, responsive, and validating. They also discuss cases with others (i.e., supervision and/or consultation).

 

Overall, there is a delicate balance in assessing BPD in adolescents compared to recognizing the potential for emotional liability during this developmental period. Yet, understanding the clinical picture, as well as the distinguishing pervasive features of BPD, will help differentiate it from either normal turmoil and/or other disorders.  Finally understanding treatment options can help clinicians gain confidence in identifying and providing subsequent treatment for adolescents with BPD.

 

 

References
Bateman, A. W., Gunderson, J., & Mulder, R. (2015). Treatment of personality disorder. The Lancet, 385, 735-743.

 

Sharp, C., & Fonagy, P. (2015). Practitioner review: Borderline personality disorder in adolescence – recent conceptualization, intervention and implications for clinical practice. The Journal of Child Psychology and Psychiatry, 56(12), 1266-1288.

 

Dannie S. Harris, MA
WKPIC Doctoral Intern

Friday Factoids Catch-Up: Memory, the Real McCoy?

Memories develop starting at birth and continue to develop throughout the life cycle as we age. The brain remembers by association, strengthening neural connections through repetition (“use it or lose it principle”) (Willingham, 2007).  Research has shown that, although memory is often considered to be a singular ability in and of its self, it is actually a process of at least three inter-related functions: encoding, storage, and retrieval.  The first step to creating a memory is encoding, a crucial step involving the conversion of the perceived item of interest into a construct that can be stored, and then later recalled through retrieval processes, from either short- or long-term memory at some point in the future.  The process of storage occurs between encoding and retrieval, when the memory exists only as a possibility for remembrance. (Arbuthnott, et al., 2001)  Memories are, in a sense, us; they chart our life details.  There are several types of memory processes that deal with differing aspects of how memories are formed.  Short- and long-term memory are the two most common forms people tend to recognize, but there are others, such as associative, elaborative, and autobiographical, that come into play.

 

The study of memory in early childhood is centered around development as it relates to the cognitive self, and a particularly important aspect of early memory centers on childhood amnesia, specifically the fading ability to recall events that occur during early childhood.  Although children may remember events prior to ages 3-4, those memories also tend to fade with time as we age. (Goleman, 1993; Willingham, 2007)  Most adults remember very little prior to age 3 or 4, since this is the age at which our cognitive memory first begins to truly function.  Prior to that age, the cognitive and language skills that are necessary for the processing of external events are not yet developed fully enough to allow this processing to occur, which is essential to the storing of events as memories. (Kihlstrom, 1994)   As aging occurs and cognitive and language skills improve, new knowledge is also being acquired, as well as the establishment of a sense of self.  During the aging process in children, major developments occur in the expansion of memory, perhaps with less processing being required to enable long-term storage.  According to a study published by the New York Times, memories that are autobiographical in nature begin when children learn about themselves and their early years through their parents. (Goleman, 1993)  Over time, as we navigate through the aging process, some memories fade, some are lost, and others are distorted as a natural result of the progression of time and aging.

 

Traditionally, faulty memory has often been associated with either the elderly or those who have suffered a traumatic brain injury, but the ongoing research that has occurred over the last couple of decades tells a different story.  There are certainly instances where people’s memories are obviously faulty, and often this is due to such factors as dementia, Alzheimer’s, concussion, or some other such factor exerting an influence on the brain’s ability to manifest an effective and accurate recall of prior events.  However, the distortion of memories, from the changing of details to the outright planting of false memories, has become an area of real interest and research due to the fact that the accuracy of memories can have much greater implications than just those that directly affect the individual in their quest for resolution of a particular psychological issue.  The likelihood of false memories, in conjunction with the fact that there is still much about the mind that we do not yet understand, make it a dangerous prospect for the therapist to suggest too much.  The evidence exists that people can be led to believe that they have experienced events in their lives that are patently untrue, or at the least, highly unlikely to ever have occurred. (Loftus, 2004)  One particular study showed that even a brief exposure to a false memory of a childhood event serves to boost their confidence that the event actually occurred. (Sharman, Powell, 2012; Garry, et al., 1996; Sharman, et al., 2005)  This was attributed to a phenomenon called imagination inflation.  The study participants were asked to rate their confidence levels on a range of childhood events that occurred prior to 10 years of age.  They were then asked two weeks later to imagine events that they indicated did not occur, and rate their confidence of the event occurrences a second time.  The confidence ratings of the events that did not happen were rated higher in confidence of their occurrence the second time around than the events that actually occurred, which were used as control events.

 

There are several techniques that have been used to attempt to determine the validity of false memories through “planting” of events that were false and never actually occurred, including hypnosis, guided imagery/imagination, dream interpretation, and picture cuing, and all proved successful at inducing false memories in research study participants in statistically significant numbers.  One of the earliest studies that specifically attempted to plant false memories for an entire event used a technique that came to be called the “lost in the mall” technique, which utilized stories about events that happened to participants as related by their parents, and included one wholly false story that was verified as having never occurred, usually lost in a mall, or, alternatively, spilling punch on a bride’s parents at a wedding or having a serious accident.  Based on the results of a series of interviews that utilized memory recovery techniques, 20%-25% of the study participants confirmed a memory of these false events even though they never actually occurred. It was also determined that these false memories exhibited high levels of detail and emotional responses in those that developed them. (Laney, Loftus, 2013)

 

Scoboria et al. (2004) posited a model for autobiographical beliefs and memories that, based on their research, indicated the memories, thoughts, and beliefs concerning plausibility of an event are of a “nested” format.  For a person to remember an event, they necessarily have to believe that it occurred, meaning that the memory itself is nested within confidence.  It also needs to be personally plausible, so confidence is nested within personal plausibility.  The event has to be plausible generally, so personal plausibility is nested within general plausibility. While the research shows that false beliefs and memories will increase due to repeated exposures, brief exposure to false events does not increase confidence or implant false memories. (Sharman, Powell, 2012)

 

The research on false memory has firmly established that people can be led to believe that they have experienced events that have never actually occurred.  Not only can these false memories be wrapped in exquisite detail and sensory associations of recollection, conveying all the characteristics of being the genuine article, but they can be extremely far-fetched in their subject matter such that they are extremely unlikely to be true, yet people will still insist on having experienced them.  The consequences of false memories can have far-reaching, and often unintended, consequences.  There are documented cases of people having spent decades of their lives in prison based on testimony that relied on what turned out to be an instance of false memory, and were only exonerated because of DNA evidence.  While this is an extreme example of the consequences of reliance on memory to be infallible, it clearly illustrates that memory is fluid, malleable, and completely vulnerable to improper influence and subsequent dubious recall.  As a Clinical Psychology student, I previously held to the belief that a memory which is uncovered during therapy is more than likely to be true.  After all, why would a profession devoted to helping people end up doing harm by implanting false memories?  In my opinion, it is not intentional harm on the part of the therapist but, rather, a misuse of techniques which can, and sometimes does, lead to disastrous consequences.  Knowing that memories can become twisted and confused should be reason enough to become skeptical of any method of regression treatment or therapy.

 

References
Arbuthnott, K. D., Arbuthnott, D. W., Rossiter, L. (2001). “Guided imagery and memory: implications for Psychotherapists”. Journal of Counseling Psychology Vol. 48, No. 2, 123-132. Retrieved from Ebscohost, November 17, 2016.

 

Durbin, P. G., Ph.D. Beware false memories in regression hypnotherapy. Retrieved November 16, 2016, from http://alchemyinstitute.com/false-memory.html

 

Goleman, D. (1993, April 6). Studying the secrets of childhood memory. The New York Times. Retrieved from http://www.nytimes.com

 

Kihlstrom, J. E. (1994). “Hypnosis, delayed recall and the principles of memory”. The International Journal of Clinical & Experimental Hypnosis. 1994, Vol. XLII, No. 4, 337-344. Retrieved from Ebscohost, November 15, 2016.

 

Laney, C., Loftus, E. F. (2013). “Recent advances in false memory research”. South African Journal of Psychology 43(2) 137-146. Retrieved from Ebscohost, November 17, 2016.

 

Loftus, Elizabeth F. (2004). ”Memories of things unseen”. Current Directions in Psychological Science. 2004. Vol. 13, No. 4, 145-147. Retrieved from Ebscohost, November 15, 2016.

 

Sharman, S. J., Powell, M. B. (2012). “Do cognitive interview instructions contribute to false beliefs and       memories?”. Journal of Investigative Psychology and Offender Profiling. 10: 114-124 (2013).

 

Willingham, D. T. (2007). Cognition: The thinking animal (3rd ed.). Upper Saddle River, New Jersey: Pearson.

 

Teresa King
Pennyroyal Doctoral Intern

 

Friday Factoids Catch-Up: Heroin and Fentanyl–A Match Made in Hell

 

Heroin use has always been a serious issue where drug abuse is concerned, but in the last few years it has become even more deadly due to fentanyl being added to give it more “kick”.  Dealers have begun including fentanyl to improve the potency of their product; however, the equipment they use to measure out amounts for trafficking don’t usually measure at levels fine enough to ensure that the amount of fentanyl that has been added stays below overdose levels.  To add to the danger, fentanyl sold at the street level is usually manufactured in “underground” labs which produce a far less pure product than pharmaceutical-grade labs, which can cause unpredictable effects on the body (Bond, 2016).

 

Heroin is classified by the DEA (Drug Enforcement Agency) as a Schedule I drug, while fentanyl is classified as a Schedule II drug.  Both are opioid derivatives; however, while heroin is synthesized directly from morphine, fentanyl is a synthetic opioid analgesic, with a potency of 50x to 100x that of morphine (NIDA, 1969, 2011, 2014).  While both have a high potential for abuse, there is a wide gulf between the two drugs with regard to the amount required to induce an overdose.  An average sized adult male would take around 30g of heroin to produce an overdose situation, roughly an amount similar to 7 packets of sugar.  By contrast, it would only take around 3g of fentanyl (little more than a ½ packet) to produce an overdose (Bond, 2016).

 

Fentanyl-laced heroin quickly reached crisis levels as it began to gain popularity among users.  In March of 2015, the (DEA) issued a nationwide alert in response to a surge in overdose deaths from heroin laced with fentanyl (19 March 2015).  While heroin has been recognized as having a high potential for abuse since the mid-1900s, fentanyl wasn’t added as a Schedule II substance until 2015, after recognizing that a variant, acetyl fentanyl, was being manufactured by Mexican cartels and smuggled stateside for distribution (10 September 2015).  The problem has surged so much that “the National Forensic Laboratory Information System, which collects data from state and local police labs, reported 3,344 fentanyl submissions in 2014, up from 942 in 2013” (Leger, 2015).

 

Due to the resurgence in popularity of heroin among IV drug users in recent years, it would seem that fentanyl-laced heroin and the associated use risks and health issues with regard to overdosing are going to be an issue for some time to come.

 

References
Bond, A. (2016, September 29). Why fentanyl is deadlier than heroin, in a single photo. Retrieved November 10, 2016, from https://www.statnews.com/2016/09/29/fentanyl-heroin-photo-fatal-doses/

 

DEA Issues Alert on Fentanyl-Laced Heroin as Overdose Deaths Surge Nationwide – Partnership for Drug-Free Kids. (2015, March 19). Retrieved November 10, 2016, from http://www.drugfree.org/news-service/dea-issues-alert-fentanyl-laced-heroin-overdose-deaths-surge-nationwide/

 

Fentanyl-Laced Heroin Worsening Overdose Crisis, Officials Say – Partnership for Drug-Free Kids. (2015, September 10). Retrieved November 10, 2016, from http://www.drugfree.org/news-service/fentanyl-laced-heroin-worsening-overdose-crisis-officials-say/

 

Leger, D. L. (2015, March 18). DEA: Deaths from fentanyl-laced heroin surging. Retrieved November 10, 2016, from http://www.usatoday.com/story/news/2015/03/18/surge-in-overdose-deaths-from-fentanyl/24957967/

 

NIDA (2011). Fentanyl. Retrieved November 10, 2016, from https://www.drugabuse.gov/drugs-abuse/fentanyl

 

NIDA (1969, rev. October 2014). Heroin. Retrieved November 10, 2016, from https://www.drugabuse.gov/publications/drugfacts/heroin

 

Teresa King
Pennyroyal Doctoral Intern