Letter(s) to D, as instructed by my therapist.

So as instructed by my counselor, I need to write D a letter about his inaction and how I feel about it.

31 January 2015

Dear D,

I’ve no idea what went wrong. I knew you will never keep your promises but is it so much to ask for you to call me back? I don’t know how you did it. You just left like that. Like nothing really matter to you anymore. How little I’m matter to you. I never heard from you anymore. We never talk anymore. How selfish you’re. You used to told me that you knew plenty of people in university but I’m a friend that you truly made. But what is happening now? Tell me. What went wrong? Did I do something wrong that you want to punish me by ignoring me?

—–

The things that I couldn’t tell you.

You were always the coping mechanism. Losing you is like losing a limb. I felt handicapped.

I am left with emotions that no one to share with. The joys, the tears, the pain. No one is telling me I will be okay.

Because everyday I wake up in the morning and I feeling terrible and misery and yet there is no one I can tell.

The nights where I feel tight chest and anxious and insomnia, I have no idea what to do with myself but to cry myself to sleep, hoping that will make the anxiety away.

I want you to know that I am in pain but I can never tell you that. I always blatantly saying I am fine.

I don’t want to put the burden on you. Somehow I always want to put up a happy face in front of you although I know I am not fine.

I am not fine. 

____

8 February 2015, 11.59pm

I give you too much power. That day when you mentioned about you tend to be passive aggressive to people. No doubt I agree with you. If I could, I would have dig you out repetitively on your face. By then I will be a nosy annoying nagging bitch. I don’t want to go there. I don’t want to pick a fight that I know I will lose. In the end, I feel bad about myself because of what you didn’t do. I blame myself for nothing. I can’t believe how much hell you’ve put me through. Or the hell I put myself through. Forgive is what I do. But when forgive consumes me, I don’t know what to do with myself. In turn, I want to be passive aggressive too. But what is the point? You never care and you never change anyway.

Discuss the role of genes and environment in the aetiology of schizophrenia.

Discuss the role of genes and environment in the aetiology of schizophrenia

Introduction

At the present moment, the aetiology of schizophrenia still remains elusive and replete scientists with more intriguing questions. This severe psychiatric disorder is found to affects around one percent of the human population. Meanwhile, the disorder manifests itself in a wide range of symptoms and peculiar behaviors, such as delusion, cognitive dysfunctions, paranoia, social withdrawal, hallucination and etc. (Pedersen, 2014). Nonetheless, schizophrenia can be characterized in terms of positive and negative symptoms. Positive symptoms can be managed with medication treatment whereas negative symptoms are harder to treat (Sims, 2002). Although researchers are equipped with an amazing array of sophisticated technology, researchers are still in a dearth of definitive answers as schizophrenia does not have a clear cut causes. On the other words, schizophrenia is a highly heterogeneous disease. Nonetheless, scientists are looking into plausible risk factors that could significantly attribute to the development of schizophrenia. Some significant findings have shown the contributions of gene and environment in the aetiology of schizophrenia. Meanwhile, latest studies suggested on the synergistic interplay between genotype and environment in the causality of schizophrenia.

Genetic liability

Based on a genome-wide association study (Purcell et al., 2009), a substantial polygenic variation (involvement of multiple alleles with very small effects) is found to attributes to the risk of schizophrenia. This can occur due to disruptive mutation across many genes, particularly on gene sets that involves the activity-regulated cytoskeleton-associated scaffold protein (ARC) (Purcell et al., 2014). According to Weickert et al. (2004), some schizophrenic patients have significantly reduced expression of dysbindin mRNA as compared to normal population, placing dysbindin as one of the aetiology factors in schizophrenia. It is also found that genetic variation in Neuregulin NRG1 increases individual’s susceptibility to schizophrenia, with elevated type I NRG1 mRNA in schizophrenia (Harrison,& Law, 2006). Meanwhile, other newer study has found the association between NOS1AP gene and schizophrenia, where its gene expression causes excessive protein production in brain (Carrel, 2014). The overabundance of protein affects the development of dendrites and causing abnormalities in brain structure. Nonetheless, according to van Os, Rutten, & Poulton (2008), genes are more likely to affect disorder indirectly through physiological pathways; influences the susceptibility of developing a psychological disorder.

A study by Hirvonen et al. (2005) on genetic vulnerability has found alteration in dopamine system, where the increased in dopamine synaptic availability with increased susceptibility to schizophrenia. An association is found between the higher bindings of D2 receptor in caudate with poorer cognitive tasks performance (involving corticostriatal pathway) that related to schizophrenia risks. For which, this explains the use of dopamine D2 receptor blocking drugs in treating schizophrenic patients. Similarly, findings (Huttunen et al., 2008) have shown high heritability of schizophrenia to first degree relative (FDR). FDR of schizophrenic individuals have statistically higher level of striatal dopamine synthesis as compared to general population.

Nonetheless, despite high heritability and 80% of genetic liability for the illness, no single genetic variation is found to have significant contribution to the development of schizophrenia in individuals (Tandon, Matcheri,& Nasrallah, 2008). Meanwhile, according to Stepniak et al., (2014), their extensive polygenic genome-wide risk association study on schizophrenia has found to be lack of predictive capability when compared to environmental risk factors.

Environmental risks

Cannabis

A recent extensive study of 750 male schizophrenic patients (Stepniak et al., 2014) found that environmental factors are better and more significant predictor of schizophrenia than genetic risk factors. They found that the susceptibility of schizophrenia is proportionate with the increase in number, frequency and intensity of environmental factors. One of which, they identified the avoidable environmental risk such as cannabis use is highly associated with early onset of schizophrenia. Drug abusers who used high potency cannabis on the daily basis are on average having 6 years earlier onset of schizophrenia than non-cannabis users (Di Forti et al., 2014). Meanwhile, researchers found that certain type of cannabis which contains high level of Delta-9-Tetrahydrocannabinol (THC) and no Cannabidiol (CBD), i.e. skunk, has accounted for 32% of schizophrenia cases.

Prenatal environment and early childhood

Research has found obstetric complications (entailing intrauterine hypoxia) as one of the strongest predictor of schizophrenia risk (Walder, Faraone, Glatt, Tsuang,& Seidman, 2014). Similarly, it is found that the maternal exposure to considerable stress (like death of a relative) during the first trimester will increases the susceptibility of the offspring from having schizophrenia in their later life (Khashan et al., 2008).

According to Spauwen, Krabbendam, Lieb, Wittchen and van Os, (2006), the prolonged early childhood traumatic exposure may leads to increase in susceptibility to schizophrenia in adulthood by affecting the functioning of dopamine. It is said that highly stressful traumatic experience causes dopamine hyperactivity in mesocorticolimbic system. Meanwhile, the prolonged exposure to severe stressful trauma promotes the sensitization of dopaminergic system (Tidey,& Miczek, 1996), whereby elevated level of dopamine metabolism is found in sexually abused females (De Bellis et al., 1994). Thus, findings have shown the impact of prenatal and early childhood on neurodevelopment, subsequently attributes to the susceptibility to schizophrenia.

Meanwhile, numerous studies have shown that infection and immune responses are responsible in the aetiology of schizophrenia. Findings reported that children who are exposed to high levels of traffic-caused air pollution (ultrafine concentrated ambient particles- CAPs) during the first year of their life were more likely to develop neurodevelopmental disorders (Allen et al., 2014). Although the study is carried out on mice, the evidence found is promising; as after exposure of the air pollution, elevated levels of glutamate transmitter is observed in mice. Such heightened level of glutamate also observed in schizophrenic patients. The mice which exposed to CAPs had shown significantly larger lateral ventricle when compared to air-exposed mice (Figure 1). Thus, such evidence might explain the causation for the higher reported cases of schizophrenia in the urbanized environment.

Figure 1. The lateral ventricle is larger in the mice exposed to CAPS (right) as compared to air-exposed mice (left) (Allen et al., 2014).

On the other hand, a Danish study has found 45% of individuals who developed schizophrenia had a hospital contact with infection during childhood or adolescence prior to the diagnosis of schizophrenia (Blomström et al., 2014). Although the study could not isolate the types of infections involved, more recent findings by Smith (2014) has found one specific parasite (Toxoplasma gondii) that might have attributed to one-fifth of schizophrenia cases. Such parasite is transmittable through undercooked meat, cat feces and soil.

Interactions between genetics and environment in aetiology of schizophrenia

More exciting findings have motivated researchers to look into the synergistic co-participation between genotype and environment (G x E) in the causality of schizophrenia. Such argued that the effect of one factor dependent on another (van Os, Rutten, & Poulton, 2008). Whereby, environmental factors in schizophrenia might induce DNA methylations that cause the changes in gene expression of neural system (EU-GEI, 2008).  According to Abdolmaleky et al. (2008), they have found potential heritable methylated cytosine residues that could influence the gene expression (of dopaminergic system) that could subsequently affect genetic susceptibility of individuals to certain disorders. Whereas, the hyper- and hypo-DNA methylation could alter the functionality of genes in major psychiatric disorders like schizophrenia. Therefore, the investigation on differential epigenetic alterations which induced by the environmental factors should be made, allowing a more comprehensive understanding towards the aetiology of schizophrenia (EU-GEI, 2008). Meanwhile, Meyer-Lindenberg et al. (2005) has found that catecholamine-O-methyltransferase (COMT) genotype which function as an enzyme that regulate prefrontal dopamine turnover. Presence of such allele can predict on increased of risk for schizophrenia, as it increases dopamine production in the midbrain. The absence of association between cannabis uses with heterozygous COMT valine with methionine alleles and homozygous COMT methionine is found, whereas adolescents with homozygous COMT valine158 allele are more likely to develop schizophrenia if they are exposed to cannabis (Arseneault et al., 2002).

A genome-wide interaction study has found some convincing evidence which shown interaction between single nucleotide polymorphisms and maternal cytomegalovirus that linked to higher risks of developing schizophrenia (Børglum et al., 2014). Whereby, that specific gene was not found to implicate schizophrenia previously, it shown a significant environment-gene interaction. Another 2014 study shown that prenatal health issues and family environmental disruption are significantly greater in genetic high-risk group, thus the evidence supports on the newly proposed ‘polygenic neurodevelopmental diathesis-stress model’ (Walder, Faraone, Glatt, Tsuang,& Seidman, 2014).  Therefore, schizophrenia susceptibility entails both independent and synergistic cofounding biological and environmental factors across development.

 

Conclusion

Recent findings have shed the light on the genetic architecture of schizophrenia, showing the unavoidable heterogeneity of common and rare variants, and de novo mutation in the aetiology of schizophrenia. Therefore, prevalence of schizophrenia can be reduced with evidence-based preventive measures such as reduce or avoid the environmental risk factors. Meanwhile, the discovery of early (genetic) markers for diagnosis of schizophrenia will definitely contributes to the earlier or within the crucial window of opportunity of therapeutic intervention for schizophrenia.

Reference

Allen, J. L., Liu, X., Pelkowski, S., Palmer, B., Conrad, K., Oberdörster, G., … Cory-Slechta, D. A. (2014). Early Postnatal Exposure to Ultrafine Particulate Matter Air Pollution:                             Persistent Ventriculomegaly, Neurochemical Disruption, and Glial Activation                               Preferentially in Male Mice. Environmental Health Perspectives122(9), 939–945.                       oi:10.1289/ehp.1307984

Abdolmaleky, H.M., Smith, C.L., Zhou, J.R., Thiagalingam, S. (2008). Epigenetic

alterations of the dopaminergic system in major psychiatric disorders. Methods of                           Molecular Biology, 448, 187–212.

Arseneault L, Cannon M, Poulton R, Murray R, Caspi A,& Moffitt TE. Cannabis use in                            adolescence and risk for adult psychosis: longitudinal prospective study. British Medical               Journal, 325(7374):1212–1213.

Blomström, A., Karlsson, H., Svensson, A., Frisell, T., Lee, B.K., Dal, H., …., Dalman, C.                        (2014). Hospital Admission with infection during Childhood and Risk for Psychotic                      Illness—A Population-based Cohort Study. Schizophrenia Bulletin, 40(6): 1518-1525                    doi:10.1093/schbul/sbt195

Børglum, A.D., Demontis, D., Grove, J., Pallesen, J., Hollegaard, M.V., Pedersen, C.B.,                           …,Mors, O. (2014). Genome-wide study of association and interaction with maternal                       cytomegalovirus infection suggests new schizophrenia loci. Molecular Psychiatry.                    19(3):325-33. doi: 10.1038/mp.2013.2.

Carrel, D., Hernandez, K., Kwon, M., Mau, C., Trivedi, M. P., Brzustowicz, L. M.,& Firestein,                B.L. (2014).NOS1AP, a protein implicated in schizophrenia, controls radial migration of                       cortical neurons. Biological Psychiatry. DOI: 10.1016/j.biopsych.2014.10.016)

De Bellis, M.D., Chrousos, G.P., Dorn, L.D., Burke, L., Helmers, K., Kling, M.A., Trickett,                     P.K.,&  Putnam, F.W.(1994). Hypothalamic-pituitary-adrenal axis dysregulation in             sexually abused girls. The Journal of Clinical Endocrinology and Metabolism,                          78(2):249-55.

Di Forti, M., Sallis, H., Allegri, F., Trotta, A., Ferraro, L., Stilo, S. A., …., Murray, R. M.                                           (2014). Daily Use, Especially of High-Potency Cannabis, Drives the Earlier Onset of                                    Ps         Psychosis in Cannabis Users. Schizophrenia Bulletin, 40 (6), 1509-1517.

Harrison, P.J. ,& Law, A.J. (2006). Neuregulin 1 and Schizophrenia: Genetics, Gene Expression,              and Neurobiology. Biological Psychiatry, 60,132–140.                                                                doi:10.1016/j.biopsych.2005.11.002

Hirvonen, J., van Erp, T.G., Huttunen, J., et al., 2005. Increased caudate dopamine D2 receptor                availability as a genetic marker for schizophrenia. Archives of General Psychiatry, 62,               371–378.

Huttunen, J., Heinimaa, M., Svirskis, T., et al., 2008. Striatal dopamine synthesis in first-degree                relatives of patients with schizophrenia. Biological Psychiatry, 63, 114–117.

Jirtle, R.L., Skinner, M.K.  (2007). Environmental epigenomics and disease susceptibility.             Nature Reviews Genetics 8, 253–262.

Khashan, A.S., Abel, K.M., McNamee, R., Pedersen, M.G., Webb, R.T., Baker,                                        P.N.,…., Mortensen, P.B. (2008). Higher risk of offspring schizophrenia following                        antenatal maternal exposure to severe adverse life events. Archives of General                          Psychiatry, 65, 146–152.

Pedersen, T. (2014). New Hope for Patients with Treatment-Resistant Schizophrenia. Psych                     Central. Retrieved on December 3, 2014, from                                                                                   http://psychcentral.com/news/2014/11/08/new-hope-for-patients-with-treatment-                            resistant-schizophrenia/77113.html

Purcell, S. M., Moran, J. L., Fromer, M., Ruderfer, D., Solovieff, N., Roussos, P., … Sklar, P. (2014). A polygenic burden of rare disruptive mutations in schizophrenia. Nature506(7487), 185–190. doi:10.1038/nature12975

Meyer-Lindenberg, A., Kohn, P.D., Kolachana, B., Kippenhan, S., McInerney-Leo, A.,                            Nussbaum, R., …., Berman, K.F. (2005). Midbrain dopamine and prefrontal function in                      humans: interaction and modulation by COMT genotype. National Neuroscience, 8,             594–596.

Smith, G. (2014). Estimating the population attributable fraction for schizophrenia when                           Toxoplasma gondii is assumed absent in human populations. Preventive Veterinary                        Medicine. DOI: 10.1016/j.prevetmed.2014.10.009

Sims A (2002). Symptoms in the mind: an introduction to descriptive psychopathology. Philadelphia: W. B. Saunders. ISBN 0-7020-2627-1.

 

Spauwen, J., Krabbendam, L., Lieb, R., Wittchen, H.U.,& van Os, J. (2006). Impact of                             psychological trauma on the development of psychotic symptoms: relationship with                       psychosis proneness. British Journal of Psychiatry, 188,527-33.

Stepniak, B., Papiol, S., Hammer, C.,  Ramin, A., Everts, S.,  Hennig, L., Begemann, M., &                       Ehrenreich, H. (2014). Accumulated environmental risk determining age at                         schizophrenia onset: a deep phenotyping-based study. The Lancet Psychiatry, 1(6), 444     -453. DOI: 10.1016/S2215-0366(14)70379-7PSYC2022

Tandon, R., Keshavan, M.S.,& Nasrallah, H.A.(2008). Schizophrenia, “just the facts” what we                 know in 2008. 2. Epidemiology and etiology. Schizophrenia Research, 102(1-3):1-18.         doi: 10.1016/j.schres.2008.04.011.

The European Network of Schizophrenia Networks for the Study of Gene-Environment                           Interactions(EU-GEI). (2008). Schizophrenia aetiology: Do gene-environment                               interactions hold the key? Schizophrenia Research, 102, 21–26.

Tidey, J.W., Miczek, K.A. (1996). Social defeat stress selectively alters mesocorticolimbic                        dopamine release: an in vivo microdialysis study. Brain Research. 721(1-2):140-9.

 

van Os, J., Rutten, B. P. F., & Poulton, R. (2008). Gene-Environment Interactions in                                 Schizophrenia: Review of Epidemiological Findings and Future Directions.                                    Schizophrenia Bulletin, 34(6), 1066–1082. doi:10.1093/schbul/sbn117

Walder, D.J., Faraone, S.V., Glatt, S.J., Tsuang, M.T.,& Seidman, L.J. (2014). Genetic liability,                prenatal health, stress and family environment: risk factors in the Harvard Adolescent                     Family High Risk for schizophrenia study. Schizophrenia Research, 157(1-3):142-8. doi:              10.1016/j.schres.2014.04.015.

Weickert, C.S., Straub, R.E., McClintock, B.W., Matsumoto, M., Hashimoto, R., Hyde, T.M.,      Kleinman, J.E. (2004). Human dysbindin (DTNBP1) gene expression in normal brain and              in schizophrenic prefrontal cortex and midbrain. Archives of General Psychiatry.                                  61(6):544-55.

Therapy Talk #4

So I went to see my university counselor for the 4th time. I was slightly jittery before meeting her. I even came out with a list of stuffs I wanted to talk to her. imageSilly, isn’t it? Because I don’t want to waste my biweekly meeting with her. 50 minutes simply do no justice to my predicaments.  I need to get them out of my system ASAP.

Today is pretty productive. We started off discussing about my mood last week and weeks back then. Before we even start, she automatically took out the waste bin. “I know you will need it later.”  She gets me. I guess I am the emotional, cry baby type. “Yeah I know.”  It’s almost ritualistic but I feel better after I cry, and there is no way I can talk straight out those sensitive topics without touching my emotional side.

I spent adequate amount of time complaining to her about D and how his inaction makes me feel. We did a little role play. But I couldn’t make myself scolding D, roleplayed by my therapist, no matter how upset I am. That’s not how D and I work. Then later I mentioned that I want to send birthday gift to D, while I am split between the prank glitter boom or a t-shirt. We did have a good laugh about the idea of prank glitter, but because of my tendency of self-blaming, self-hatred and guilt-ridden person, she warned me to think thrice before making a decision and think of the possible (bad or good) consequences.

One thing she mentioned that the possible reason that he is ignoring me is that he is homesick that, any communication with the past will make him miss home. That’s why he is so inaction. She might be right and I nodded.

She also dug around, wonder if I am seeing anyone. I brushed off because I know I have attachment issues. I am not lovable blah blah blah. I also blatantly mentioned about how I feel about queer guys. I told her that I have the tendency of liking gay guys. She is slightly curious about it and decided that we can work on that too, work on my personal identity. Towards the end, we decided to work on two topics: my emotional attachment/fuck up relationship with D and my personal identity for this semester. She also gave me a homework. Write a letter to D, about the things I want to confront him, his inaction. Of course, she repetitively warned me never send it to him but bring it to next session. I nodded. I know what to do. And as my problem with D is more imminent, we decide to work on that first. We’ll see.

A self-reflective journey.

Disclaimers: I wrote this for one of my counseling course. I figured that I want to share it to the world, anonymously of course. But as usual, please have the common courtesy, don’t try to plagiarize.

Autobiography

When I was young, my friends always envied me. My mother is a doctor, my dad was a manager and I have two elder brothers. In the eyes of others, I had this perfect model family that everyone might have dreamed of. Nonetheless, they are just the surface level. I grew up playing with boy toys and boyish haircut for most part of my childhood. I was raised in an unconventional family where gender roles did not apply to my parents, as my father took care of us as a housefather as sickness forced him to retire early, leaving my mother to bear the burden of sole breadwinner to our family. Life is decent as my mother could still provide a living for us with her occupation as a doctor. My extroverted mother always preoccupied with her busy social life, while my father is rather introverted, prefer to stay at home and read. Therefore, for half of my childhood, my father took care of me. Meanwhile, my parents give me the autonomy and freedom to do what I want as I am the “good girl” type that they trusted me that I will not do things out of ordinary.

Changes and Impermanence in Life

But soon, my siblings outgrown, one by one moved out of house to further their study in college. As time passes, each of us has grown up a little more. Each of us is more engaged with our own personal agendas. Later, I moved out of house soon after my high school to pursue my A-level. I can feel the family being more disengaged with the distance and occasional quarrels between family members or my parents. There was once in a private conversation, my mother blurted to me about the story of her good friend’s marital problem, later proceed to talking about her relationship with my father, “you know if anything ever happens (divorce), it has nothing to do with you.” At that time, I did feel the tension in the family but I did not pay much attention as I was never around to notice the changes. Nonetheless, in deep down I might have tried to avoid confrontations as much as possible by being absence.

For the following years, I pursue my study in Hong Kong. The family warm soon replaced by new profound friendships. Nonetheless, I did not feel homesick as most of the time I am preoccupied with study and contented with my new life. I found the distance with my family could not be reconciled with more conversations through Skype. Nonetheless, each year I devote some time to visit my parents and spend time with my family; to patch things up and make up for my absentee. However, I found that my parents have aged more each time I visit them, each time I find myself sadden to see and frustrated with what I have missed during my absence. I started to think that death might just be around the corner. Subsequently the fear creeps in, fearing that it will take away everything; the constancy of life.

The incident

Early this year I received a surprise call from my elder brother, he nervously broke the news that he is engaged to his current fiancé and a baby is coming really soon. I remembered I nonchalantly ended the conversation because I was too shocked to give him a reaction.

Later, it started with an emotional breakdown on a random bus ride. I remembered vividly I was dreaded in the sudden burst of emotion as I recalled a short conversation I had with my elder brother, learning that he will be getting engaged and have a baby boy soon enough. To me, my unexpected public outburst seemed to be out of place, absurd and somewhat silly because I do believe the additions to my core family will definitely add joy into my family; given my parents love children very much. At that moment, I dismissed that incident as tears of joy.

Incongruence in self

Everything was fine on the surface, but I felt differ since then; something has changed. I found myself getting emotional every time I think about my family; even there is nothing upset about it. Even the slightest thought the word “family” was suffice to trigger the emotion. For some time, I find myself having emotional distress, soon become insufferable and almost dysfunctional to my everyday life. I could not understand how and why I felt this way. Oblivious to what I have felt previously, I found myself being incongruent and felt the deep-seated anxiety. The episode became the fulcrum for the review of my life, undergone “organismic valuing process”.

Reflection on experience

Coincidentally, I took a few counseling and art therapy classes that encouraged me to contemplate and reflect on my feelings and life. I realized, with the unprecedented birth of my nephew and new sister-in-law, my core family has changed and extended. Unknowing to me previously, now I realized that I am no longer the youngest in my family, and I missed being loved and cared for. I enjoyed the “permanence” of my core family, protection and eternal love from my family. However, I have been taking it for granted. All these time, my core family has given me the sense of constant and stability in these 21 years of my life.  I recalled the phase quoted by Viktor Frankl in his book Man’s Search for Meaning, “the angels are lost in the contemplation of infinite glory” (Frankl, 2006, p.64). Perhaps, I had this frivolous notion of an “eternal glory”, where my family would remain unchanged and intact. When the illusion of (spiritual and psychological) security breaks, I realized I have been trapped in the struggle between consciousness and progression of life, and yearning for permanence yet the knowing the fact of flux. For times, I felt lonely as I could not be present with my new family members given the physical distance. On the other hand, I felt the deepest anxiety and fear with the thought of knowing that too soon my other family members will face the transitoriness of life; whether having extended family of their owns, illness or even death. “Only true absolute is that there are no absolute,” (Yalom, 1980, p. 423). I reached the epiphany where there is nothing absolutely right, true or static.

Besides, I am aware of the fact that I am truly alone. So to speak, what I have experienced, Erich Fromm will call it as existential loneliness. For which, I find my university experience has been overwhelming, while try to fit in the environment has make it worst after many failed attempts. Although I am in Hong Kong, with the densest population in the world, I had the epiphany that I am aware of being existentially alone. Without the presence of my beloved family and friends, I found my life almost suffocating if not difficult enough. I longed for love and attention from others. For some time, I found myself lost in this ever-changing life.

At one point, I pondered, “What is the meaning of life?”

I yearned for the answer and knowledge. While, I am fortunate to stumble upon a few great writings that could relieve my predicament. One of which is the book by Viktor Frankl’s Man’s Search for Meaning. His writing has given me the courage to see my life differently. His arduous experience as Nazi prisoner made aware that the difficulty of my life is rather trivial, and his impeccable endurance is the most admirable quality that I hope I can have. He pointed out that we must see that life is meaningful, and meaningful under all circumstances including the most difficult one. I find his writing to be particular inspiring and gave me some insights about life.

Meanwhile, I am fortunate enough to learn more about Buddhism philosophy in one of my lecture class “Life and Buddhism”. Although I do not identify myself as a religious person, I found a few philosophy taught by Buddha on life are particularly appealing to me as they resonate my predicament. It is said that life is impermanence, where our existence are conditioned in which we are subjected to constant state of flux without exception. Therefore, the attachment towards these conditioned phenomena will become the cause of human suffering (Mahāthera, 1994). Knowing the fact, at least it gave me some solace.

As such, I began to understand my assumptions that responsible for my life predicaments. I am aware that my anxiety has arisen from my reluctance of accepting the true nature of reality. With the new profound understanding, I had a heightened awareness of my fabricated and constructed reality. Thus, I began to embrace my fear and anxiety towards impermanence of life. I learned to be mindful and more attentive to my own feelings, especially fear and anxiety. I realized that those feelings are mine, escape is impossible and irrational resistance only makes it worst. Alan Watts once said, “To remain stable is to refrain from trying to separate yourself from a pain because you know that you cannot. Running away from fear is fear, fighting pain is pain” (Watts, 1951, p. 97). By simply being aware of the present moment, I acknowledge and learned to accept my feelings, yearnings and my humanity. As what Satir believed, to be congruent is to be harmony with one’s self (Lee, 2002). Acceptance is a beginning. It affects how I see the past, whilst affecting my future.

I learned to be vulnerable does not mean I am weak, whereby I have sought help from counseling service in the university. I found my experience as a client is particularly empowering as I see it as my desire, courage and commitment to change for a better. Meanwhile, it has further strengthened my determination to pursue a counseling profession in near future. I believed my past struggles allowed me to understand the pain and difficulties of others with a sense of humility, as a wounded healer.  “When I am in touch with myself, my feelings, my thoughts, with what I see and hear, I am growing toward becoming a more integrated self. I am more congruent, I am more “whole,” and I am able to make greater contact with the other person” (Satir, 1987, p. 23). By learning myself, I believed it helps to develop on my wisdom of helping others. Nonetheless, being self-aware is insufficient. I must act upon it, with my freedom of choice. I need to bear the responsibility, put effort into initiation and springs into action. Therefore, I strive to be my authentic self, to be the master of self.

References

Frankl, Viktor E. (2006). Man’s search for meaning. Boston, MA: Beacon Press.

Fromm, E. (1956). The Art of Loving. Harper & Row

Mahāthera, N. (1994). Fundamentals of Buddhism: Four Lectures. Sri Lanka: Buddhist

Publication Society.

Lee, Bonnie K.. (2002). Congruence in Satir’s Model: Its Spiritual and Religious Significance.

Contemporary Family Therapy, 24(1), 57-78.

Schon, D. (1983). The Reflective Practitioner. London: Temple Smith.

Satir, V. (1987). The Therapist Story.  Journal of Psychotherapy & The Family, 3(1) 17-25.

Watts, A. (1951). The Wisdom of Insecurity. Pantheon Books.

Yalom, I (1980). Existential psychotherapy. New York: Basic Books.

A fantasy conversation.

Forgive me. Things have been in impasse and if you have read about Irvin Yalom’s book Every Day Gets a Little Closer, I’ll be the Ginny. But this time I’ll be having a fantasy conversation with my therapist, as below.

Me: Why D is not making the initiative to call me back? I’ve been very very patient with him and he’s really burning at the back of my head. It’s really taking a toll on me. He’s….non-doing is killing me.

Therapist: When did you last contacted him?

Me: Almost 10 days ago. I messaged him, He said he was still busy with projects. Which is a lie. I’ve messaged him twice, but rejected twice. I was hoping that he’ll call me back soon but I kept waiting, hoping but that didn’t happen. I just wait and wait like a fool. I haven’t been talking to him for more than 2 months. And there is nothing I can do about it.

Therapist: It appears to me something is gong on. I can sense a lot of anger, resentment, and maybe frustrations. What do you want to talk to him about?

Me: You know, everything. We used to talk about everything and now he just shut me out completely and I’m not too sure what to do with myself.

Therapist: Do you see yourself dependent on him? Emotionally?

Me: Maybe…. Yes.

Therapist: How do you deal with your feelings all these time? I meant during his absentee. How did you manage to compose yourself?

Me: No. I’m not doing well. I felt more emotional. I felt isolated and alone and nobody cared about me. I just ended up crying for the wrong reasons….. or no good reasons.

Therapist: Does it helps? The crying? Other than that what did you do?

Me: Nothing. There is nothing I can do. I just get emo the whole day. I’m still amazed that how much he can do to me, well. his not doing doing to me.

Therapist: So have you thought of what are you going to do about this?

Me: Kill myself? I felt like nothing. I’m nothing to him anyway. To anyone.

Therapist:  We had our agreement, remember?

Me: Yes. And I’m not dead and sitting right in front of you.

……

I don’t know how to keep the conversation gong and now I’m too pissed and upset about everything.

Petrified.

I got moody all day again.

Petrified.

That constant heart pounding feeling.

Thub. Thub. Thub. Thub…..

All I can feel, all day is my heart pounding with the speed of train. I can feel it on my chest and my veins.

Nothing really calms me down.

Breathe. 

Nothing calms me down. My hands are shaking. My knees are weak.

Breathe.

I need to be calm.

Breathe. 

I went outdoor for some sun. It has been a sunny day. I sat down in the park in my university compound just to sun myself a little, in hoping that will ease my anxiety; calms my nerves down. It helped me.

It was a roller coaster day. I’m in my first week of university (senior year) and the add-drop period has been a great tension and stress to me. But things finally settled. I finally got my credit bearing internship and working in lab will be a new thing to me. I am nervous. I don’t really like to work in tight space. It gives me jittery feelings. I just got my last semester’s results too. There are surprises but it was fine. I got my CGPA improved but still not good enough to get first honor. It just not good enough.

I am my worst enemy.

I always put my academics as my top priority. I woke up feeling tired from yesterday’s restless night, force myself go to school. After all, if I don’t have my study, I have nothing else with me. That is all I got and at least it is something that could get my mind off a bit, force me to leave my house. I started my semester with 6 hours back-to-back lectures. I’m just tired, moody but I tried to put up a face to people, because that is what others expect from me.

Smile. 

But my mind is wallowing about how pathetic I am. Semester after semester, I am still sitting alone in class.

Pathetic.

I am my worst enemy.

Bad day.

So, I missed my appointment with my counselor today. Not a good way to start the day. Don’t get me wrong, I didn’t miss my appointment on purpose. It just that I wasn’t sleeping so well yesterday, and my rescheduled appointment (out of sudden, through phone call a few weeks earlier) was 10 in the morning (I was forced to choose this slot, it was the earliest time that I can meet her 😦 ) and I’m never good with morning appointment. I ended up waking up 10.30am, shocked then freaked out. I immediately called the office to reschedule, but the earliest time I could meet her is February, which is ridiculous because I need to see her before my school starts. I couldn’t just start my school with a mess. So I proceed to call my counselor and talked a little, just to let off some steam and I think my cracky morning voice made me sounds terrible as if I just cried or something and she let me to see her next Tuesday.

At the mean time, I just feel bad. I just wanna cry for no good reason.

I’m the little fox.

If everything needs explanation or reason, I should figure out my life with explanations and reasons too.

I need D. The only reason I keep going back to him or throwing myself at him is that he makes me feel good every time I got into a bad place. Because I have nowhere/no one else to go to. Because when my life got miserable, he was there. When I reached rock bottom, he was there. And now, he is so far away that I have to deal with myself all alone. That is painful to me. He has the leash on me that when he left, I lost my sense of direction.

I’m the little fox in the story of Le Petit Prince and he is the little prince. He tamed me and when he left, I’m the lost cause. And now, with him not calling me back after more than a week, and I asked him again yesterday (a blow at my self-respect) and he said he is still busy. Confused, feeling fucked up because it just reflected me as the problematic, psychotic or a crazy bitch. Maybe I am. But I need him like a drug to soothes my mind and heart. I just need him.

Nevertheless, he is so out of reach and I need to settle things on my own. I’m not used to that and I need to work on this with my counselor.

I miss my friends.

Another outdated news from my friend. I just came back from the long journey and it appears to me that the act of me walking away from my routine life makes me realize that, I miss out so much and others seemed like, living their lives without me; so far away from me. Fat bitch just got laid for her first time. Someone just confessed to slim bitch. And D? I’ve no idea how he’s doing.

Yes, I’m here still complaining and whining in the middle of night. Look at there, it’s 2.13am. I can’t deny I’m just a whiny little bitch who just can’t stop and be content with her life and move on.

Maybe I just need my friends.

I miss my friends.