Cover model: Emmanuel Chan Photographed by Parandis Kazemi
Table of
Contents 3 6
Beyond Our Beloved Rats and Mice: Novel Animal Models Used in the Field of Addiction Science
Fentanyl: The Silent Killer Sawayra Owais
Farah Qaiser
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Sugar Addiction: Does it Mirror Drug Addiction? Luciana Escobar Saade
Narcissism Yashvi Asher
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Pornography and Addiction
No Help in Sight for Bees: Neonicotinoid Addiction and Colony Collapse Victoria A. Sajtovich
Addiction: In our minds, In our genes Eileen Liu
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Terese Pierre
Addiction Resources
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Addiction: Beyond the Inevitability of Our Biology" Ariana Tang
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Naloxone: The solution for an addicted nation? Denitsa Vasileva
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Can You Get Addicted to Video Games?
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2016-17 Executive Team
Rogges Anandarajah
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Get Involved
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ah j a Dear Readers, ar d n a n The Interneuron welcomes you back for another neuroscience-filled year! s A sher ar e g b We are proud to present you our first issue on addiction. og vi A Esco R We explore issues ranging from “Fentanyl: The Silent Killer” to video sh na s a i Y ia a iu w game addictions. This year, we have also added a debate format to our Luc en L a O e magazine where our contributors have an opportunity to explore Eile wayr Pierr r h opposing views on a controversial topic. In this issue, we tackle the age Sa ese aise tovic old nature vs. nurture debate in the context of susceptibility to addiction. Ter rah Q Saj y Fa toria Tang ileva b Additionally, the Interneuron is hoping to bring back Student Spotlights to provide a platform y ic na as h V for students to share their research experience and stories from the lab. We would also like to ap ia sa V r r g A nit to i showcase the work students have been involved with by hosting a competition later in the year. o e h D em P z Planning has already begun for this event but we’re also open to suggestions. What kind of nd s Ka a i t prizes would you like to win? What kind of food would you like to eat? Let us know what you’d Ar rand like to see and we’ll do our best to make it happen. Pa As always, thank you for taking the time to support the Interneuron. Our magazine would not be possible without our incredible editorial board, amazing contributors, or loyal readers. If you think you would like to contribute to our next issue, get involved by attending one of our next General Meetings. Join our mailing list by sending us an email at interneuron.utoronto@gmail.com to stay up to date with the latest neuroscience news. Happy reading! Priscilla and Ann Editors-in-Chief
Interneuron
Volume 4. Issue 1. October 2016
Beyond Our Beloved Rats and Mice: Novel Animal Models Used in the Field of Addiction Science Farah Qaiser
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our beloved rodents and primates have various limitations when it comes to modelling addiction
”
! When it comes to the field of addiction science, animal models have been proven, repeatedly, to be an immensely valuable tool in understanding the processes that lead to drug addiction and developing prevention and treatment strategies.
! It is important to develop further animal models in order to study more complex aspects of human physiology and support the development of innovative therapy. Luckily, there are various alternatives that the scientific community can turn to.
! Traditionally, the scientific community has carried out addiction research with rats and mice. These rodents have been deemed as favourites as they have an enhanced lifespan, reproduce quickly and can be inbred easily to produce identical strains. Speaking of genetics, it is interesting to note that the mouse genome has approximately 30,000 genes, where 99% have direct human homologs1.
! The model organism zebrafish (Danio rerio) is small and transparent during embryogenesis4. A key feature of this organism is its relatively simple nervous system, which is similar to that of human beings and can be surveyed easily with Magnetic Resonance Imaging/Histology4. In particular, zebrafish show great promise as a model given that genetic analyses, such as transgenesis and genome mutagenesis, can be easily carried out on them.
! In terms of vertebrates, primates are used as models in addiction research as they share several characteristics with humans and also display impulsive behaviour2. For example, a monkey’s lifespan is around 40 years, which means that repeated studies can be carried out mimicking long-term human drug abuse patterns. By the same token, it also allows for the development of effective treatments3. ! However, our beloved rodents and primates have various limitations when it comes to modelling addiction. For example, treatments which reduce drug abuse in rodents do not have the same level of success in humans.3 !
! Other notable mentions include the roundworm (Caenorhabditis elegans), where around 83% of the proteome has human homologous genes and the fruit fly (Drosophila melanogaster), whose strengths include low costs and highly conserved diseased pathways5 6. Interestingly, approximately 75% of human diseases have a corresponding pathway in D. melanogaster6. ! In terms of addiction science, what does the future hold for animal models? With innovative techniques such as CRISPR/Cas9 and optogenetics, it is now possible to perform gene therapy experiments with ease, and even target multiple genes at once – a feat that will be vital as the field of addiction science continues to progress7. It is also likely that we will see a shift towards using animal models that can realistically mimic human conditions.
References 1. Mouse Genome Sequencing Consortium (2002). Initial sequencing and comparative analysis of the mouse genome. Nature. 420, 520-562. doi:10.1038/nature01262 2. Winstanley, C., Olausson, P., Taylor, J., & Jentsch, J. (2010). Insight Into the Relationship Between Impulsivity and Substance Abuse From Studies Using Animal Models. Alcoholism: Clinical And Experimental Research, no-no. doi:10.1111/j.1530-0277.2010.01215.x 3. Carroll, M. & Lynch, W. (2016). How to study sex differences in addiction using animal models. Addiction Biology, 21(5), 1007-1029. doi:10.1111/adb.12400 4. Mathur, P. & Guo, S. (2010). Use of zebrafish as a model to understand mechanisms of addiction and complex neurobehavioral phenotypes. Neurobiology Of Disease, 40(1), 66-72. doi:10.1016/j.nbd.2010.05.016 5. Lai, C., Chou, C., Ch’ang, L., Liu, C. & Lin, W. (2000). Identification of Novel Human Genes Evolutionarily Conserved in Caenorhabditis elegans by Comparative Proteomics. Genome Research, 10(5), 703-713. doi:10.1101/gr.10.5.703 6. Pandey, U. & Nichols, C. (2011). Human Disease Models in Drosophila melanogaster and the Role of the Fly in Therapeutic Drug Discovery. Pharmacological Reviews, 63(2), 411-436. doi:10.1124/pr.110.003293 7. Crabbe, J. (2016). Progress With Nonhuman Animal Models of Addiction. Journal Of Studies On Alcohol And Drugs, 77(5), 696-699. doi:10.15288/jsad.2016.77.696
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Cover model: Emmanuel Chan Photographed by Parandis Kazemi
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Interneuron Volume 4. Issue 1. October 2016
Fentanyl: The Silent Killer Sawayra Owais
! !
Early last year, I was scrolling through a news website and the word ‘fentanyl’ grabbed my attention. We had just learned about this powerful opioid, 100 times more powerful than morphine, in my pharmacology class. However, after quickly skimming the article, my delightful smile turned into a harrowed expression. The article described a young, middleclass couple who had died due to a fentanyl over-dose, leaving behind a 2 year old son. Little did I, and Canada, know that this was a precursor of the fentanyl tsunami that would throw tides across our nation. ! ! Fentanyl is an opioid, meaning it has pain-relieving effects. Before the synthesis of fentanyl, morphine and mepridine were the most readily available analgesics (1). However, Dr. Paul Janssen, a Belgian physician-scientist wanted a drug that produced faster pain relief and had fewer side effects as compared to the aforementioned products (1). After a few variations, fentanyl was created in 1960 and had the fastest onset of action (within 2 minutes, if administered intravenously) and safety margin for a potent opioid (1). ! ! Initially, fentanyl was used as an intraoperative analgesic, due to its fast onset of action. Further, it was discovered that large doses of fentayl could induce anesthesia without altering cardiovascular dynamics and preventing the release of stress hormones, a hidden gem for surgeons at the time (1). ! ! Unfortunately, in the early 1970s, the first reports of deaths related to fentanyl overdoses came trickling in. Fentanyl had begun to leave the fore as a surgical tool and entered as a potent, easily abused, painkiller. ! ! The timeline of fentanyl prescription and the recent influx of deaths caused by fentanyl overdoses may leave some scratching their heads. If fentanyl has been around for over half a century, why are we seeing such high rates of fentanyl overdoses now, especially in Canada? ! ! While a single cause cannot be pointed, it is largely due to the increase in clinician-prescribed opioids (2). Specifically, the introduction of OxyContin, another powerful (though less so than fentanyl) opened the floodgates for the abuse of prescription drugs (2). Physicians began prescribing this drug for a whole range of chronic pain ailments, and it easily found its way onto the street. In back alleys and clandestine laboratories, OxyContin is crushed, and laced
with several other street drugs, including fentanyl (2). When people take street OxyContin, they are unaware that it is laced with such high doses of fentanyl which can cause rapid respiratory depression leading to death (3). ! ! Evidently, the chicken and egg theory presents a problem here as we don’t know if physicians are providing pill-popping prescriptions at an alarming rate or if the increases in chronic pain disease have triggered these prescriptions. However, the astronomical increase in fentanylrelated deaths is a desperate call for action, enough to issue a public health emergency in British Columbia. However, there are two main barriers that serve as an obstacle in reducing these numbers. ! ! Clandestine laboratories in China are the main supplier of fentanyl to Canadians. Shipments arrive disguised in household objects like hole punchers or silica packets; virtually any object that weighs less than the critical amount of 30 grams as Canadian border guards cannot open these packages without the recipient’s consent (2). Indeed, it only takes a few hundred micrograms of fentanyl to cause death in a healthy adult (2). ! ! Another hurdle that Canadians previously faced was the strict dismissal of harm-reduction centres, like safe injection sites, by the Conservative government (3). These harm-reduction sites provide a safe and clean environment for individuals to consume drugs. ! ! What Canada needs is a shift in thinking that drug abuse affects certain kinds of people and needs to focus more on harm-reduction measures rather than declaring a war on drugs. Otherwise, the fentanyl crisis will only escalate and it will be called the silent killer no more.
References 1 Stanley, T. H. (2014). The Fentanyl Story. The Journal of Pain, 15(12), 1215–1226. https://doi.org/ 10.1016/j.jpain.2014.08.010 2 Howlett, K., Givannetti, J., Vanderklippe, N., & Perreaux, L. (2016, August 24). A Killer High: How Canada got addicted to fentanyl. Retrieved October 5, 2016, from http://www.theglobeandmail.com/ news/investigations/a-killer-high-how-canada-got-addicted-tofentanyl/article29570025/ 3 Sagan, A. (2016, August 10). Fentanyl deaths are a Canada-wide disaster. Retrieved October 5, 2016, from http://www.cbc.ca/news/world/fentanyl-deaths-are-a-canada-wide-disaster-1.3181725
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Sugar Addiction: Does it Mirror Drug Addiction? Luciana Escobar Saade
The Sugar Craze: ! Sugar used to be a luxury. In the 1700s, humans only consumed around 4 pounds of refined sugar a year1. Now, StatsCanada states that the average Canadian consumes around 88 pounds of sugar a year1! Questions have certainly been raised about our obsession with sugar. Can sugar become addictive? If it can, would it act the same way as a drug would? Let us explore where science stands in the field of sugar addiction as a model that mirrors drug addiction. What is the neurobiology of drug addiction? ! Drug addiction relies on the release of dopamine in the mesolimbic system, which associates the consumption of the drug with euphoria and increases motivation to continue consumption2. Dopamine release also occurs in the nucleus accumbens shell3. However, after continuous consumption of the substance, the dopaminergic release in the nucleus accumbens changes. Dopamine release weakens but does not show signs of habituation3. It is then released in anticipation of drug consumption within the dorsal striatum4. This region, along with the basolateral amygdala, is associated with increased motivation to consume drugs4. Impulsivity and a lack of control are a result of these structures, and the prefrontal, dorsolateral and inferior cortices becoming disabled5. What is the neurobiology of sugar addiction? ! In sugar-addicted rats, the dorsal striatum is involved in sugar-seeking behaviours, and dopaminergic release in the mesolimbic system enhances motivation for sugar consumption4. The major difference between the models for drug and sugar addiction is the specific neural pathways occurring in the nucleus accumbens. Conditioning results in an increase in dopamine within the nucleus accumbens for both sugar and drugs. However, for drugs this increase occurs in the shell whilst in sugar it occurs in the core6. This difference explains why habituation occurs for sugar but not drug consumption. For example, dopaminergic levels surge when sucrose is consumed but quickly return to baseline, whereas for cocaine and heroin,7 dopaminergic levels do not return to baseline8. What do these differences and similarities mean? ! Similarities between the two models show that it is in fact possible to become addicted to sugar. However, the
minor differences in mechanisms show that there are significant differences in the way the addiction occurs. Avena’s study9 demonstrated that rats gain dependency on sugar after an intermittent feeding schedule, after which the rats show signs of sugar-bingeing and withdrawal symptoms. In fact, the withdrawal symptoms paralleled that of opioids, including anxiety and teeth chattering9. A major criticism of this study was that dependency only occurred when the rats were under a strict schedule of intermittent consumption9. When rats were allowed to eat as much sugar as they wished, they did not develop this dependency4. Therefore, it may be understood that outside of rigorous experimental settings, sugar addiction does not happen. In addition, it is interesting to note that sugar itself is used in many drug addiction studies as the control to show how natural, nonpathological reward systems should function in the brain4. What can we conclude from all these studies? ! Sugar addiction is beginning to gain momentum in the scientific community, but is still far from becoming a scientific fact. Whilst animal models have been useful in determining whether or not sugar addiction parallels drug addiction, sugar addiction studies in humans are scarce4. Furthermore, these studies have always been laced with controversy. In fact, in the 1960s, the sugar industry paid a research group at Harvard to write an article that made sugar appear to have great health benefits with insignificant downsides10. Even now, 50 years later, scientific literature remains split on the topic. With rising levels of obesity, diabetes, and poor nutrition in our society, it is time to form a consensus about the addictive nature of sugar.
References 1. Sugar consumption among Canadians of all ages. (n.d.). Retrieved October 19, 2016, from http://www.statcan.gc.ca/pub/82-003-x/2011003/article/11540-eng.htm 2.Everitt BJ, Belin D. Economidou D et al (2008) Review. Neural mechanisms underlying the vulnerability to develop compulsive drug-seeking habits and addiction. Philos Trans R Soci Lond B Biol Scie 363:3125-3135 3. Di Chiara G (2005) Dopamine in disturbances of food and drug motivated behavior: a case of homology? Physiol Behav 86:9-10 4. Westwater, M.L., Fletcher, P.C. & Ziauddeen, H. (2016). Sugar addiction: the state of science. Eur J Nutr doi:10.1007/s00394-016-1229-6 5. Koob GF, Volkow ND (2010) Neurocircuitry of addiction. Neurophysiopharmacology 35:217-238 6. Pontieri FE, Tanda G, Di Chiara G (1995) Intravenous cocaine, morphine, and amphetamine preferentially increase extracellular dopamine in the “shell” as compared with the “core” of the rat nucleus accumbens. Proc Natl Acad Sci 92:12304-12308. 7. Rada P, Avena NM, Hoebel BG (2005) Daily bingeing on sugar repeated releases dopamine in the accumbens shell. Neuroscience 134:737-744 8. Avena NM, Long KA, Hoebel BG (2005) Sugar-dependent rats show enhanced responding for sugar after abstinence: evidence of a sugar deprivation effect. Physiol Behav 84:359-362 9. Avena NM, Rada P, Hoabel BG (2005) Evidence for sugar addiction: behavioural and neurochemical effects of intermittent, excessive sugar intake Neurosci Biobehav Rev 32:20-39 10. Harvard's Sugar Industry Scandal Is Just The Tip Of The ... (n.d.). Retrieved October 19, 2016, from http://www.huffingtonpost.com/entry/sugar-harvard-scandal-nutrition-study_us_57d8088ee 4b0aa4b722c6417
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Interneuron Volume 4. Issue 1. October 2016
Naloxone: The solution for an addicted nation? Denitsa Vasileva
! A recent video depicting a couple passed out from heroin overdose while their young son watches on has caused outrage in the United States. The video was released by the police in order to draw attention to the opioid addiction epidemic in the United States. Opioids include potent illegal drugs like heroin as well as powerful prescription pain killers such as morphine and fentanyl1. According to the National Institute of Drug Abuse (NIDA), deaths related to opioid overdoses have quadrupled in the United States between 2002 and 20131. The Center for Disease Control and Prevention (CDC) reported that more people died from drug overdoses in 2014 than in any other year recorded. The factors behind this epidemic are varied and complex, and are not exclusive to the United States. Canada is currently grappling with its own opioid epidemic, largely attributed to the rise of a synthetic opioid known as fentanyl. Fentanyl is a powerful and highly addictive pain medication usually prescribed to patients with severe chronic pain3. However, in recent years, it has become more accessible without a prescription, often through distributions from China3. The number of fatal fentanyl-related overdoses in British Columbia and Alberta alone skyrocketed from 42 in 2012 to 418 in 20153. A variety of measures are being considered in order to stem this epidemic. One of the most recent and most controversial method is to expand access to Naloxone – a medication that counteracts the effects of opioids, thus preventing overdose-related deaths4,5. ! Naloxone, also known as Narcan, is an opioid antagonist4. It works by binding to the opioid receptors in the body, reducing the effect of opioids on the central nervous system4. Naloxone is particularly effective during overdoses as it allows the patient to breathe normally and has no effect on people who have not taken opioids4. This medication comes in two forms: a nasal spray and a pocket-sized injection that provides the user with instructions on how to use it4,5. Like any medication, Naloxone has side effects, including profuse sweating and chest pains in severe cases4,5. In July 2016, the Ontario government classified Naloxone as an over-the-counter medication to be given for free to anyone “at risk of overdose.” The
decision sparked a great deal of controversy5. Numerous medical organization including Public Health Canada have claimed that expanding Naloxone availability will reduce the number of fatal overdoses and save lives5. Detractors say that easy accessibility to Naloxone will lead to an increase in opioid addiction – a claim that has not been substantiated by scientific evidence6. ! More justified is the concern that due to the availability of the antidote, opioid users would be less likely to call emergency personnel in the case of an overdose6. Naloxone is only effective for up to an hour after an overdose, after which symptoms such as difficulty breathing may return. This means that the patient would still need to see a paramedic to counteract the long-term effects of overdose6. These concerns show that, while access to Naloxone can save lives in the short run, a comprehensive strategy addressing the core social, economic and medical factors behind the opioid epidemic needs to be implemented.
References 1. National Institute on Drug Abuse. (2014). What are opioids?. Retrieved October 13, 2016, from https://www.drugabuse.gov/publications/research-reports/prescription-drugs/opioids/what-a re-opioids 2. Center for Disease Control. (2015). Drug overdose deaths hit record numbers in 2014. Retrieved October 13, 2016, from http://www.cdc.gov/media/releases/2015/p1218-drug-overdose.html 3. The Globe and Mail. (2016). A Killer High: How Canada got addicted to fentanyl. Retrieved October 13, 2016, from http://www.theglobeandmail.com/news/investigations/a-killer-high-how-canada-got-addicte d-tofentanyl/article29570025/ 4. Harm Reduction Coalition. (n.d.). Understanding Naloxone. Retrieved October 13, 2016, from http://harmreduction.org/issues/overdose-prevention/overview/overdose-basics/understand ing-naloxone/ 5. Canadian Broadcasting Company. (2016). Ontario makes anti-opioid drug Naloxone available without prescription. Retrieved October 13, 2016, from http://www.cbc.ca/news/canada/toronto/ontario-makes-anti-opioid-drug-naloxone-availablewithout-prescription-1.3659176 6. Basrianelli, K. (2014). Nonprescription Naloxone: Pros and Cons. Pharmacy Practice Faculty Publications. University of Rhode Island. Retrieved October 13, 2016, from http://digitalcommons.uri.edu/cgi/viewcontent.cgi?article=1033&context=php_facpubs
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Narcissism Yashvi Asher ! Imagine a country, let’s call it Narcipolis, where all the citizens are obsessed with status, power and their appearance. You would see people hoisting not the flag of Narcipolis, but rather one broadcasting their poster faces. Unfortunately, they would also be more comfortable manipulating others for personal gain and show less empathy but more aggression when their self-inflated bubble pops. This is the world of the narcissists.1 ! A Narcissistic Personality Inventory (NPI) is the most commonly used measure of narcissism. It is comprehensive and assesses both normal and pathological forms. An example of the normal form of narcissism is a pep talk you give yourself before giving a speech in front of a large audience. It enhances your dispositional and subjective well-being and is based on real achievements. Pathological narcissism, on the other hand, exists as a duality of extreme vulnerability shrouded with grandiosity. These two forms – narcissistic vulnerability and narcissistic grandiosity have different manifestations unique to the individual and their environment. This is where the discrepancies in evaluating the neurological features of pathological narcissism arise. The grandiosity factor is often displayed as a distorted overconfidence of oneself to cover up deep feelings of low self-esteem that is easily bruised by the slightest criticism. Vulnerability in narcissism, on the other hand, is defined by feelings of shame and tolerance of treats to oneself.2 ! A recent study indicated that a higher Pathological Narcissistic Inventory score was associated with decreased cortical volume in key regions of the social brain network: the left medial pre-frontal cortex and post-central gyrus. There was also marked decrease in cortical thickness in the inferior frontal cortex. These brain regions function in the recognition of the desires and feelings of others, and would explain, to some extent, the impaired social facet of pathological narcissism.3 Another
study showed a higher incidence of narcissism in the United States than in Asian or Middle-Eastern countries, suggesting a cultural influence of this disorder.4This adds another layer of complexity since results found in one country are not comparable with those in others. It also incites further research to determine which factors in Western cultures promote narcissistic behaviours. ! Is there hope for a treatment? The mechanistic pathways are still not well understood and there are no specific drugs for treating pathological narcissism. However, psychotherapies that promote self-reflection have been shown to mitigate pathological symptoms. Because the dangers of narcissism often impair social relationships and are subject specific, behavioural therapies such as group or family therapy have been tested to promote modesty, empathy and mindfulness. This is similar to Heinz Kohut’s self-psychological approach where the goal of the therapist is to adopt an empathetic procedure to reduce the patient’s inflated, distorted sense of self. This can also help repair defective moods in the long run. A highly active, work intensive Cognitive Behavioural Therapy has also been implicated to show long term positive effects.5 All of these methods have the potential for improvement and yield promising results. Nonetheless, more biochemical and neurological assays need to be established for a more biological therapeutic approach. References: 1. Dingfelder, F Sadie. (2011). Reflecting on Narcissism. American Psychological Association. Vol 42.2, 64. 2. Barnett, M. & Womack, P. (2015). Fearing, not loving, the reflection: Narcissism, self-esteem, and self-discrepancy theory. Personality And Individual Differences, 74, 280-284. 3. Mao, Y., Sang, N., Wang, Y., Hou, X., Huang, H., & Wei, D. et al. (2016). Reduced frontal cortex thickness and cortical volume associated with pathological narcissism. Neuroscience, 328, 50-57. 4. Foster JD, Campbell WK, Twenge JM (2003) Individual differences in narcissism: inflated self-views across the lifespan and around the world. J Res Pers 37(6): 469-486 5. Ambardar, Sheenie. (2016) Narcissistic Personality Disorder Treatment & Management: Approach Considerations, Psychotherapy, Pharmacologic Therapy. Emedicine.medscape.com.
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Interneuron Volume 4. Issue 1. October 2016
Pornography and Addiction Terese Pierre
In modern North American society, sex and sexualisation dominate the music, film, advertising and fashion industry. However, pornography—photos or videos depicting sexual activity is still widely considered a tabooed topic due mainly to moral or religious reasons. Those who watch pornography are forced—either by society or their partners—to do it in secret. It’s an open secret, in a way, yet still heavily attached to a sense of shame. !
Is It Addictive? ! Regarding pornography use—whether or not it is rampant, and especially in light of public stigmatization—the question of possible addiction is bound to come up. Is pornography use addictive? Is addiction a real phenomenon? What are the effects of pornography on the brain? ! The latest version of the DSM (Diagnostic and Statistical Manual of Mental Disorders) lists compulsive and problematic pornography viewing under the diagnosis of Hypersexual Syndrome.1 However, the DSM has been problematic with regards to mental disorders, specifically because it emphasizes behaviors rather than neurobiology. Addiction is no longer defined by behavior. ! Dr. Eric Nestler’s landmark 2005 paper classified all addiction as a dysfunction of the mesolimbic reward centers of the brain2. Addiction occurs when pleasure/reward pathways are hijacked by external drugs such as cocaine, or by natural processes relating to survival such as food and sex.2 This process both enables and increases neuronal learning through micro- and macro-neuroplastic change.3 ! Based on Nestler’s research, supraphysiologic levels of transcription factor DeltaFosB appear to be a marker for hyperconsumptive states of natural addiction. Not only is it a marker, but DeltaFosB is a facilitator of hyperconsumptive behavior.4 Overexpressing DeltaFosB in mice results in addictive hyperconsumptive behavior involving food5, wheel running6 and sexual activity.7 ! DeltaFosB is also critical for dendritic plasticity through its effect on the mesolimbic reward system in relation to both sexual behaviour and drug reward.8Thus, ‘Hypersexual syndrome’, as in the DSM, while descriptive behaviorally, does not accurately describe ‘sexual addiction’ in light of the current understanding of CSBs, as it ignores research about how learning changes the brain both micro- and macroscopically.9
9
! A 2016 German study compared internet pornography addiction (IPA) with internet gaming disorder as it relates to the “cognitive processes and emotional responses to specific internet-related cues” that are “considered crucial in the development and maintenance of addictive behavior.” Functional neuroimaging findings suggest that neuroadaptation in IPA is comparable to those found in people with other behavioral addictions, such as substance dependence. The ventral striatum, the region associated with reward anticipation, actively responds when confronted with pornographic material in people with IPA.10 Is it Harmful? ! If pornography addiction were viewed objectively, evidence indicates that it does indeed cause harm in humans. Not only is there a correlation between viewing child pornography and participating in actual sexual relations with children11, recent meta-analyses provide strong support for pornography-induced violence against women.12,13 ! In the past, there have been many pioneers— particularly of the feminist variety—that have spoken out against pornography, claiming that it poses a deep harm to women, who, they also claim, already exist as ‘second-class citizens,’ and whose existence is largely viewed, however subconscious, to satisfy the needs of men.. One such feminist critics is Catharine MacKinnon, who views pornography as oppression of women, as acting against women both in its production and consumption, and she ultimately implores for some form of legal action against this transgression.14 This discourse around pornography is often intensely intertwined with issues of free speech, but that is a topic for another magazine, perhaps.
! Some might say that not all pornography is about the objectification of women. There may be some companies that are actively working towards safer and more benevolent pornography that emphasizes healthy sexual boundaries. Judith Hill, another feminist writer, specifies what she calls ‘victim pornography,’ which she defines as “the graphic depiction of situations in which women are degraded,” 15 and which she, too, says is highly harmful and disrespectful to women. She thinks all pornography, no matter how avant-garde, is degrading, especially if the woman is in a subordinate position. ! The literature is also illuminating. There have been several studies done, all the way back to the 1970s, on a possible link between pornography and sexual violence against women. Survey research has consistently exhibited a relationship between pornography and a self-reported likelihood of committing rape. Moreover, exposure of male participants to pornography—especially violent pornography—has both increased their aggression and their acceptance of rape myths, such as, “Women make false rape claims after consenting,” and “Rape is a woman’s fault if she’s dressed provocatively.”16 ! In conclusion, not only is pornography addiction a behavior, it has neurobiological origins. While I do not have an issue with the watching of pornography by others, I understand why it is distressing for some.
References 1. Hilton, D., & Watts, C. (2011, December). Pornography addiction: A neuroscience perspective. Surgical Neurology International,2(1). 2. Nestler, E. J. (2005). Is there a common molecular pathway for addiction? Nature Neuroscience, 9(11) 3. Hilton, D. (2013, July 19). Pornography addiction a supranormal stimulus considered in the context of neuroplasticity. Brain and Addiction, 3. 4. Nestler, E. J. (2008). Transcriptional mechanisms of addiction: Role of DFosB. Philosophical Transactions of the Royal Society, 363 5. Olausson, P., Jentsch, J. D., Tonrson, N., Neve, R. L., Nestler, E. J., & Tayor, J. R. (2006). DeltaFosB in the nucleus accumbens regulates food reinforced instrumental behavior and motivation. Journal of Neuroscience, 26(36) 6. Werme, M., Messer, C., Olson, L., Gilden, L., Thoren, P., Nestler, E. J., et al. (2002). DeltaFosB regulates wheel running. Journal of Neuroscience, 22(18) 7. Wallace, D. L., Vialou, V., Rios, L., Carle-Florence, T. L., Chakravarty, S., Arvind Kumar, A., et al. (2008). The influence of DeltaFosB in the nucleus accumbens on natural reward-related behavior. Journal of Neuroscience, 28(4) 8. Pitchers, K. K., Vialou, V., Nestler, E. J., Laviolette, S. R., Lehman, M. N., & Coolen, L. M. (2013). Natural and drug rewards act on common neural plasticity mechanisms with DeltaFosB as a key mediator. Journal of Neuroscience, 33(8) 9. Georgiadis, J. R. (2006). Regional cerebral blood flow changes associated with clitorally induced orgasm in healthy women. European Journal of Neuroscience, 24(11) 10. Brand, M. (2016). PL-01: Internet pornography addiction: Theoretical models, behavioral data, and neuroimaging findings. Journal of Behavioral Addictions 5.S1: 1. 11. Bourke M, Hernandez A. (2009). The 'Butner Study' redux: A report of the incidence of hands-on child victimization by child pornography offenders. J Fam Violence, 24 12. Hald GM, Malamuth NM, Yuen C. (2010). Pornography and attitudes supporting violence against women: Revisiting the relationship in nonexperimental studies. Aggress Behav 2010;36 13. Hiltoin 2011 14. MacKinnon, Catharine A. (1985). Pornography, civil rights, and speech. Harvard Civil Rights-Civil Liberties Law Review. Harvard Law School. 20 (1): 10–68. 15. Hill, J. (1987). Pornography and Degradation. Hypatia, 2(2), 44. 16. Bergen, R., & Bogle, K. (2000). Exploring the Connection Between Pornography and Sexual Violence. Violence and Victims, 15(3), 228-229.
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Interneuron Volume 4. Issue 1. October 2016
No Help in Sight for Bees: Neonicotinoid Addiction and Colony Collapse Victoria A. Sajtovich
! There is increasing concern in both academic and political circles over the global demise of bee populations, given their essential role in agricultural crop pollination.1,2,3 Lack of nutrition, pathogens, and physiological stress have all been attributed to the rapidity of their decline, but a particular class of pesticides, neonicotinoids, is becoming a bewilderingly apparent cause of colony collapse.2,3,4,5 Neonicotinoids, or “neonics” for short, have an effect on bees that is analogous to nicotine on the human brain.4 Like cigarettes, neonicotinoids antagonize the acetylcholine receptor following consumption.4 This stimulates the reward pathway in the bee brain.4 Over time, repetitive stimulation of this receptor results in addictive behaviours that eventually lead to aberrant foraging, poor reproduction, cytotoxicity, and death.3,4 In a two-choice feeding assay, leading scientists of Newcastle University demonstrated that two different species of bees actually prefer nectar containing neonicotinoid pesticides: both species consumed far more sucrose laced with the neonicotinoids imidacloprid and thiamethoxam than sucrose solution alone.5 ! The attraction is undeniably pharmacological rather than gustatory; the same research group demonstrated that bees cannot taste the neonicotinoids in their food by analysing excitatory and inhibitory responses from gustatory and sucrose-sensitive neurons.5 Upregulation of nicotinic acetylcholine receptor α 1 and α 2 subunits has also been identified in a transcriptional regulation study out of Zürich, further supporting the neonicotinoid addiction model.6 The same study found creb and pka to be downregulated; genes implicated in long term memory.6 In an agricultural landscape dominated by conventional farming methods, these findings are particularly alarming.2,3,4 Continual neonicotinoid use is perpetuating the vicious cycle of bee addiction, colony collapse, lower crop yields, and higher pesticide usage.1,2,3 Clearly, more research and public education is needed on issue of bee addiction to save these fragile populations from self-extinction. After all, bees don’t have the luxury of Narcotics Anonymous.
References: [1] Liberal Party of Canada. (2014). The “Bees and Farming” Resolution: Moratorium on Neonicotinoids in Canada. (Policy Resolution 2). Montreal, QC: Liberal Party of Canada. Retrieved from: http://www.liberal.ca/policy-resolutions/2-bees-farming-resolution-moratorium-neonicotinoids-canada-2/ [2] Castillo, C., Veiga P. W., Martin J. L., et al. (2015). Canadian National Honey Bee Health Survey. National Bee Diagnostic Centre. Retrieved from: https://www.thenbdc.ca/sites/default/files/2015_national_honey_bee_health_survey_online_0.pdf [3] Whitehorn, P. R., O’Connor S., Wackers F. L., and Goulson D. (2012). Neonicotinoid Pesticide Reduces Bumble Bee Colony Growth and Queen Production. Science, 336(6079), 351-352. doi: 10.1126/science.1215025 [4] Christen V., Mittner F., and Fent K. (2016). Molecular Effects of Neonicotinoids on Honey Bees (Apis mellifera). Environmental Science and Technology, 50(7), 4071-4081. doi: 10.1021/acs.est.6b00678 [5] Kessler S. C., Tiedeken E. J., et al. (2015). Bees prefer food containing neonicotinoid pesticides. Nature, 521(74), 74– 76. doi:10.1038/nature14414 [6] Rundlӧf M., et al. (2015). Seed coating with a neonicotinoid coating negatively affects wild bees. Nature, 521(7), 77-80. doi: 10.1038/nature14420
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reinforcement, which increases the likelihood of certain behaviour. Variable ratio reinforcement is very effective at promoting a behaviour because it provides rewards on a more unpredictable scale; a common example is slot machines. Another factor is the sunk cost fallacy. Someone who’s poured hundreds of hours into a game is probably not going to consider dropping it lightly.
Can You Get Addicted to Video Games? Rogges Anandarajah
! When discussing addiction, the first image that often comes to mind is some kind of drug; video games and the Internet are generally not discussed in terms of addiction. However, an addiction refers to an out of control behaviour that the addicted pursue at almost any cost, and, by that definition, it is quite possible to see video game and internet usage as the subject of an addiction. In fact, the DSM V (Diagnostics and Statistical Manual of Mental Disorders) now features a section on internet gaming addiction. ! So, what gives video games the potential to be addictive? One of the biggest draws is instant gratification. When was the last time it took players weeks to make progress, gain a new item, or get a new power in a game? The answer is usually never— most video games are designed in a way to allow most players to progress regularly. The ability to progress much more quickly in video games than in real life creates a considerable amount of reinforcement. Reinforcement is anything that increases the likelihood of a behaviour, in the case of video games, it refers to properties of the video games that encourage continued playing. Video games also provide variable ratio
! Despite the viability of video game addictions, the odds are that most people who play a lot of video games are not addicted. In the prototypical case of addiction (drugs), there is evidence of such behaviour hijacking the person’s neural circuits. Such studies do not exist for people who play an inordinate amount of video games. At the current state of research, it can’t be determined if there are similar biological incidents in people addicted to video games. Most studies addressing the prevalence of video game addiction estimate this rate to be between 0.5%-3%. Given such a low rate of video game addiction, a lot of research is directed towards validating the tests and methods used to diagnose. One old diagnostic method used to be how much time was spent in total on video games, but given the ubiquity of video games and the Internet, that’s no longer viable. Imagine a game developer or game tester who spends several hours a day working on a game and playing through to see how it runs. Would these people qualify as having an addiction? The biggest issue with the field of research into video game addiction is the lack of it. The amount of behavioural and neuroimaging studies that exist for drug and food addiction simply do not exist for video games and the internet. While the studies that do exist provide valuable information, there remains much more research to be done. ! Video game addiction is a serious problem and is often comorbid with higher rates of depression, anxiety, and impulsiveness. Fortunately, as current assessment methods would describe it, you’re unlikely to have it. So if you’re hours into the latest AAA title or years into an old RPG, you’re probably just having fun— not addicted.
References Diagnostic and statistical manual of mental disorders: DSM-5. (2013). Washington, D.C.: American Psychiatric Association. Van Rooij, A. J., Schoenmakers, T. M., Van den Eijnden, R., Vermulst, A. A., & Van de Mheen, D. (2012, September 13). Video Game Addiction Test: Validity and Psychometric Characteristics. Cyberpsychology, Behavior, and Social Networking, 15(9), 507-511. Retrieved October 10, 2016. Black, D. W., & Shaw, M. (2008, May). Internet addiction: Definition, assessment, epidemiology and clinical management. CNS Drugs, 22(5), 353-365. Retrieved October 10, 2016. @. (n.d.). Are Video Games Addictive? Retrieved October 10, 2016, from https://www.psychologytoday.com/blog/media-spotlight/201308/are-video-games-addictive Dallas, M. E. (n.d.). Internet Addiction May Be Red Flag for Other Mental Health Issues: Study: MedlinePlus Health News. Retrieved October 10, 2016, from https://medlineplus.gov/news/fullstory_161028.html Chamary, J. V. (n.d.). Science Explains Why You're Addicted To Pokémon GO. Retrieved October 10, 2016, from http://www.forbes.com/sites/jvchamary/2016/07/12/science-collecting-pokemon/#286055c86d2e Photo: http://cdn.makeuseof.com/wp-content/uploads/2013/10/video-game-addiction-what.jpg
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Interneuron Volume 4. Issue 1. October 2016
Addiction: In our minds, In our genes Eileen Liu
! What makes smokers feel the urge to smoke numerous cigarettes a day? And how do alcoholics build the tolerance to take shots after shots? Is addiction explained by nature or nurture, biological or environmental factors? The environment may play a significant role in addiction; however, the nature aspect should not be overlooked. The mechanism of neurotransmission, the brain reward pathway, andgenetic inheritance all contribute to the nature view in understanding addictive behaviours. ! Neurons communicate via neurotransmitters, which are chemical messengers that carry neural signals between one neuron to the next. Once released, neurotransmitters dock onto receptors on the neighbouring neuron to cause a systemic effect in our bodies. The use of substances such as alcohol, tobacco, cocaine and heroin can affect neurotransmission in our brains, particularly in the reward center by influencing levels of dopamine—the neurotransmitter responsible for feelings of reward and pleasure. In addition, studies have discovered that genetic inheritance may contribute to addiction. What are these underlying mechanisms that occur in the brains of addicts? And what are the genes responsible for these addictive temptations? ! When we obtain pleasurable rewards such as food, sex, or drugs, dopamine neurons in the ventral tegmental area (VTA) are activated and subsequently cause the nucleus accumbens (NAcc) to release large amounts of dopamine.4 Many drugs follow this same mechanism, known as the reward pathway. For instance, nicotine, an addictive stimulant found in cigarettes and tobacco, acts by directly binding to nicotinic receptors in the VTA and increasing dopamine release in the NAcc.1 Overall effects on the body include increased heart rate and blood pressure, reduced appetite, and increased alertness.5 ! With an understanding of the reward pathway, we can begin to understand the driving forces for developing addictive behaviours. Using position emission tomography (PET) imaging, research has shown that the brains of alcoholics have decreased number of dopamine D2 receptors compared to those of nonalcoholics.6 Once the VTA is activated by the reward stimulus (ie., alcohol), there is an increase of dopamine release in the NAcc. D2 receptors located in the NAcc modulate dopamine activity. With continuous strong activation of the VTA, dopamine activity rises above baseline, and over time, the D2 receptors receiving dopamine become desensitized and down-regulated. The individual will no longer feel the same rewarding feeling as with the initial dopamine increase, hence becomes desensitized. In other words, the baseline of “normal” dopamine activity increases, thus requiring even more addictive stimuli to satisfy the individual. This is the underlying mechanism of addiction. Think about how alcoholics have such high tolerance compared to
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non-alcoholics. Non-alcoholics will probably feel the effects of alcohol quickly after a couple drinks, whereas alcoholics need a lot of drinks before the effects kick in. ! One might ask, is there a specific gene regulating addictive behaviours? Recent research by Newcastle University discovered that a mutation in gene Gabrb1 caused excessive drinking of alcohol.2 In this study, mice were given a choice between drinking diluted alcohol and water. Results showed that, while normal mice displayed no preference to alcohol, mice with the gene Gabrb1 mutation preferred to drink the diluted alcohol up to almost 85% of their fluid consumption. The gene Gabrb1 codes for an important subunit of the GABAA receptor, which is activated by the brain’s main inhibitory neurotransmitter—GABA. Mutation in the gene Gabrb1 is associated with the GABAA receptor activating even in the absence of GABA. Subsequent neurotransmission to the NAcc stimulates the mice’s desire for more alcohol. In other words, the mice’s alcohol addiction is produced by a mutation in the specific gene Gabrb1 causing abnormal activation of GABAA receptor that would otherwise be triggered by GABA to inhibit addictive behaviour. ! In addition, twin studies illustrate that genes play a role in addiction. Research concluded greater resemblance of substance use between monozygotic twins compared to dizygotic twins.3 Although environmental factors were found to play a minor role in some drugs, only genetic factors played a role in sedative, stimulant, cocaine and opiates use. Therefore, twin resemblance in substance use has shown some heritable factors in addiction. ! Perhaps there are more than just environmental factors influencing our addictive behaviours. We must not underestimate the strong biological evidence for addiction. The processes in our brain’s reward centre, neurotransmitter dysregulation, as well as genetic inheritance all play important roles in understanding the nature aspect of these craving temptations.
References 1. Tomkins D., Sellers E. (2001). Addiction and the brain: the role of neurotransmitters in the cause and treatment of drug dependence. CMAJ. 164(6), 817-821. 2. Newcastle University. (2013, November 26). Gene mutation for excessive alcohol drinking found. ScienceDaily. Retrieved October 19, 2016 from www.sciencedaily.com/releases/2013/11/131126123931.htm 3. Kendler K. S., Aggen S. H., Tambs K., & Kjennerud, T. R. (2006). Illicit psychoactive substance use, abuse and dependence in a population-based sample of Norwegian twins. Psychological Medicine, 36(7), 955–962. http://doi.org/10.1017/S0033291706007720 4. National Institute on Drug Abuse. (January 2007). The reward pathway. Retrieved October 20, 2016 from https://www.drugabuse.gov/publications/teaching-packets/neurobiology-drug-addiction/sect ion-ii-reward-pathway-addiction/3-reward-pathway 5. National Institute on Drug Abuse. (June 2007). Legal Doesn’t Mean Harmless. Retrieved October 20, 2016 from https://www.drugabuse.gov/publications/brain-power/grades-6-9/legal-doesn't-mean-harml ess-module-2/background. 6. Volkow, N. D., Wang, G.-J., Fowler, J. S., Logan, J., Hitzemann, R., Ding, Y.-S., Pappas, N., Shea, C. and Piscani, K. (1996), Decreases in Dopamine Receptors but not in Dopamine Transporters in Alcoholics. Alcoholism: Clinical and Experimental Research, 20: 1594–1598. doi:10.1111/j.1530-0277.1996.tb05936.x
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NURTURE
Addiction: Beyond the Inevitability of Our Biology
! Addiction – is it a completely uncontrollable phenomenon, at the mercy of receptors, genetics, and neurotransmitters? Or is it more like a piece of clay – molded into its shape by the hands of the environment? I believe that the environment has a greater influence.
Ariana Tang
! Take, for example, parent-child relationships. The “Still-Face Experiment” by Dr. Edward Tronick is tough to watch. In the experiment, a mother, while interacting with her child, abruptly ceases interaction and any facial expression. The sudden lack of facial expression mimics the absence of emotional connection between a mother and child, and as soon as it ceases, the child becomes incredibly distressed. This experiment is often used to demonstrate the emotional impact that neglect has upon a child. ! So how does this tie in with addiction? A study in 20083 examined the correlation between depressive symptoms, addiction, hormonal regulation, and childhood experiences. The data collected from the experiment concluded that neglect led to changes in hormone levels that made these individuals more neurobiologically vulnerable to addiction. ! In addition, another study8 showed that Internet-addicted teenagers were more likely to perceive their parents as, on one end of the spectrum, more unfavorably judgmental and more overly involved, and on the other hand, less emotionally warm and responsive. ! In another study, researchers found that both authoritarian and neglectful parenting led to an increased likelihood of substance use, whereas the parenting styles in-between led to better outcomes; thus concluding that extremes at either end of the parenting spectrum were detrimental1. However, parenting is complex, and it would be reductionist to solely throw the blame on parents. The environment itself, too, has a large influence on addiction. ! Back in 1972, almost 15% of the soldiers set to return to the US from the Vietnam War had developed heroin dependence. For a country which had just launched their “war on drugs”, it was definitely a concern. What happened in the next few months, though, was astonishing. Of the soldiers who developed dependence, only 5% relapsed in the following year, and 12% relapsed at least once in three years4. The National Institute on Drug Abuse reports that the relapse rate of drug addiction is 40 to 60%9. Evidently, these numbers are significantly lower! ! What happened here? Their environment changed. Dr. Sanjay Gupta likens it to ice cream and television: “Perhaps, like me, watching television cues you to eat a bowl of popcorn or ice cream. I don't need the ice cream by
any means, and didn't even think about it a few minutes earlier, but the combination of environmental factors led me to the freezer.” 4. ! In one experimental study7, half of a group of morphine-addicted rats stayed in their original environment where they developed morphine addiction, while the other half were relocated to a new environment. Rats that remained in their original environment showed a higher preference for morphine and relapsed at a quicker rate compared to the ones which were relocated7. ! Although addiction is a complex problem, one approach for recovery that has shown promise is environmental enrichment, which is complex environmental stimulation that aims to enhance brain activity. After environmental enrichment, addiction-associated brain regions in rats displayed decreased responsiveness to cocaine6. Furthermore, rats raised alongside other rats and exposed to novel toys showed lower concentrations of dopamine in the striatum, as well as higher densities of dopamine receptors in the nucleus accumbens5. The use of cocaine blocks the reuptake of dopamine, leading to higher levels of dopamine in the synapse, and the decrease of dopamine receptors is known as receptor downregulation – a response to drug use. ! In 2015, Johann Hari presented a highly popular Ted Talk titled “Everything you think you know about addiction is wrong.” He argues that addiction develops as a result of a lack of human connection. He said: “It’s not your morality, it’s not your brain, it’s your cage. Addiction is an adaptation to your environment”2. Because addiction is so highly influenced by the environment, it is not final, and there is hope.
References 1. Calafat, A., García, F., Juan, M., Becoña, E., & Fernández-Hermida, J. (2014). Which parenting style is more protective against adolescent substance use? Evidence within the European context. Drug And Alcohol Dependence, 138, 185-192. http://dx.doi.org/10.1016/j.drugalcdep.2014.02.705 2. Flanders, L. (2016). ‘Addiction Is an Adaptation to Your Environment’: An Interview With Johann Hari.The Nation. Retrieved 13 October 2016, from https://www.thenation.com/article/addiction-is-an-adaptation-to-your-environment-an-interview-with-johann-hari/ 3. Gerra, G., Leonardi, C., Cortese, E., Zaimovic, A., Dell'Agnello, G., & Manfredini, M. et al. (2008). Adrenocorticotropic hormone and cortisol plasma levels directly correlate with childhood neglect and depression measures in addicted patients. Addiction Biology, 13(1), 95-104. http://dx.doi.org/10.1111/j.1369-1600.2007.00086.x 4. Gupta, S. (2015). Vietnam, heroin and the lesson of disrupting addiction. CNN. Retrieved 5 October 2016, from http://www.cnn.com/2015/12/21/health/vietnam-heroin-disrupting-addiction 5. Nader, MA, & Czoty, PW. (2005). PET Imaging of Dopamine D2 Receptors in Monkey Models of Cocaine Abuse: Genetic Predisposition Versus Environmental Modulation | American Journal of Psychiatry. (2005). American Journal Of Psychiatry, 162(8), 1473-1482. http://dx.doi.org/10.1176/appi.ajp.162.8.1473 6. Solinas, M., Chauvet, C., Thiriet, N., El Rawas, R., & Jaber, M. (2008). Reversal of cocaine addiction by environmental enrichment. Proceedings Of The National Academy Of Sciences, 105(44), 17145-17150. http://dx.doi.org/10.1073/pnas.0806889105 7. Thompson, T. & Ostlund, Jrr., W. (1965). Susceptibility to readdiction as a function of the addiction and withdrawal environments. Journal Of Comparative And Physiological Psychology, 60(3), 388-392. http://dx.doi.org/10.1037/h0022588 8. Xiuqin, H., Mengchen, L., Jinan, W., Ying, Z., Ran, T., & Huimin, Z. (2010). Mental health, personality, and parental rearing styles of adolescents with Internet addiction disorder. - PubMed - NCBI. Ncbi.nlm.nih.gov. Retrieved 14 October 2016, from https://www.ncbi.nlm.nih.gov/pubmed/20712498 9. How effective is drug addiction treatment?. National Institute on Drug Addiction. Retrieved ! 20 October 2016, from https://www.drugabuse.gov/publications/principles-drug-! addiction-treatment-research-based-guide-third-edition/frequently-asked-questions/how-! effective-drug-addiction-treatment
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Interneuron
Volume 4. Issue 1. October 2016
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