Memory

Memory

She approached the filing cabinet, which seemed to be the only piece of furniture in the room and dragged a door open. The edges were sleek black and metallic. The handle of the drawer looked untouched. She knew this was not the case. The cabinet used to be filed with care. Each past experience in her memory was quantified in significance and filed according to feelings and significance in a diligent manner. Before everything became jumbled up, she could access a file whenever she wanted, pulling out a manila folder containing the appropriate context: place, time, scent and who was there. The room with the cabinet was an icy cold. In the Jumble it had absorbed a certain emptiness and with that emptiness came a bitter cold. The drawer felt cold in her hand as she pulled it open even.

While metal tends to adjust itself to the temperature of the hand touching it, this handle was entrenched in frigidity and showed no sign of moving. There was no one in the room with her who could witness what she saw when she opened the drawer. Everything that had once been organized was now a mess, many of her memories were torn into bits, illegible little notions of who had been where, or how she had felt. Everything inside her little memory cabinet was in pieces and there was no one to help her figure out how to put the bits back together or to make some complete picture of "the past". After all, it was her memory. Who else could come here? Who else would understand the system?

"I'm here for something specific," she said out loud, knowing that perhaps people could hear her, but there was no way they could tell where she was or what she was doing. Perhaps she would seem crazy to them. They didn't understand because their memory had not been vandalized like this. Their little cabinets -- or perhaps some of them had less old-fashioned filing systems -- were all perfectly in tact. Other people lived in the outside world, interacting with objects and others but she felt as if she mostly resided inside her head and her escape from all of that had been her memories which were now destroyed.

He had not taken enough of her when he left. It had not been sufficient for him to destroy the rest of the place. Outside of this room where the cabinet was kept, she'd had a beautiful arrangement of ceramic trinkets that seemed impenetrable to her, but in reality were merely ceramic objects that could easily be smashed upon the ground. And of course, when they were smashed they did so in little bits. With ease they embedded themselves in the soles of her feet and in other parts of her skin, drawing blood at first and later causing a dull throb more like a reminder of pain than pain itself. He had shattered every last one of her little trinkets and not being satisfied with destruction he set out to annhialite the contents of her cabinet.

She wept.

For a time she wondered how she would piece everything back together. Of course the past could no longer be reflected upon in the same way. Everything had to be re-transcribed for the cabinet's insides to be even close to normal. It would take work, which she had begun. She was always diligent and even it matters of restructuring the past she applied this same diligence. Through tears, through pain, through dull throbs, she had diligence at least.

Besides her efforts to piece scraps of paper together, jotting down what memory she could from them she was making new attempts to restore the contents of the cabinet so she could function. First there was the section of the cabinet dedicated to her "identity". It was probably best to scrap most of what had been destroyed anyways. It was not a pretty picture and now she felt more comfortable in her body, in her self. Her hair had grown longer. Her body had trimmed itself of excess fat. Her skin had been restored to a golden brown. Her smile seemed bigger and her notion of self was in general, more positive. What had been destroyed was all bad. Without memory, she could construct a new identity based off of her own feeling and not off of a projection on  a page written by a heavy hand.

She was also working on new memories that would effortlessly write themselves in and she could file them away, filling up the drawers of the cabinet with new material. One day at a time she worked on new memories that had nothing to do with him and his destruction. Then, there was a time when the memories seemed to be filling up the cabinet faster and faster.

She had made friends with someone else who could understand her system. His memories were destroyed too, but his "cabinet" (she was not certain it was a cabinet really) was in far greater disrepair. The hurricane that destroyed it was always on his lips, even after weeks and weeks had passed. She was afraid of him and his memories of her because she could smell the toxicity on his breath when he said her name. She was afraid because she did not want to brush too closely with his poison and disintegrate her new memories just when she'd built up a good thick set again. He was lovable and dangerous and they shared the same consciousness, the same skin, the same disrepair.

They never spoke of their damage but they communicated it all the same. She could sense the reflexive way he fell into things and could sense that she was a placeholder so he could perform the same habits of a lover he had grown accustomed to. He was a placeholder in a way, except the habits her performed were totally new to her. She had never been graced with this kind of affection before. This was the sign. Before every storm, there are signs of course. In the tropics, the birds are too quiet. The beetles pour into the house from every crack. He had just been an invasive beetle, pouring into her home, looking for a place to rest before the storm came. But he was the storm too... The storm. The beetle. The man. They were all the same - all black and twisted with satanic desire to defile what was once pure. (Heart, mind, home.)

They didn't speak of their damage but she could taste it on his mouth, like red wine, like marijuana. She could feel that sometimes he wanted to hurt her just to lash out at women. She could feel that she wanted to hurt him by falling in love with him and making their friendship some "big thing" to cause him guilt and grief. But their desire to hurt each other was tempered by their own pain, their own emptiness and instead of destroying each other their friendship became a blank notebook and they wrote in new memories to replace what they had lost. They guided each others' shaking hands and made promises they knew they could keep.

The future did not exist because they were so busy trying to replace the past with the present and when the future did come, they knew it would not matter what they were or what they had been because they had been nothing to each other but perfect and convenient. It did not matter therefore it did not exist. For a while they were able to write rich memories. Each second they spent together was a precursor to a romance they would never allow to begin. They lived in a world created by magic. God himself had a direct hand in placing him with her and her with him just for a time.

Time runs out and within weeks she was going on her way and neither of them wanted to feel sad but they both did. When he said "I miss you" she did not want to believe it because no one had ever missed her before even if they claimed to love her. Her absence had never been felt and for someone like him to claim to feel her absence felt like a grave dishonesty. In order to counteract this injustice she clung to the words "I miss you" and never spoke them herself out of fear that he was lying and she would fall into a cruel cosmic trap.

He seemed to really fall in love with someone else once she was gone and although she wanted it to hurt her she felt nothing for him, not even jealousy. They spoke to each other every day for more than a month and then time paired with their separation and began to chip away at their contact. Speaking to each other became less frequent. They could not help each other write anymore and trying to write new memories on their own became difficult. There was nothing between them but those truncated memories they had written before. Time had cut them off, God had left them to deal with their destruction on their own.

That is the only way she could fix the mess in the cabinet, to clean it up all by herself. The work would take a while. Piecing together fragments of her past under dim lamp light would be no easy feat. Her helper would not be there to remind her that others felt pain and that her presence was significant enough to be missed. She was afraid to tell him how much she missed him too, and how much he had helped her those hot summer nights. His laughter and the ease with which he provoked hers had profound importance, energizing her to keep up the work of reorganizing her memory. Sometimes she wanted to tell him this. "You are important to me" is only five words after all and they had spoken so much to each other that the impact of five words (one of which wasn't even love) could not be so great as to cause her this much distress. Whenever she saw his face and heard his voice, she could not bear to tell him because she feared it would change.

She became more and more alone as they were apart. In the world she had traveled to people did not understand laughter. They did not understand ways to heal from pain, only feel it. These people did not understand what she had been through. They did not understand why she felt the way she did. They did not understand that all her memories were destroyed. She had tried to explain to a few of them that everything in her mind had been destroyed. I am turning over a new leaf. I am trying new things. Her explanations were not understood. Sometimes she wondered what it would be like if someone could inhabit this near empty room with her and see the mess. How can you expect me to heal from this? How can you expect me to fix all of this so quickly? I have to rewrite everything.

Of course no one could come see the cabinet and the only person who had understood was hardly real anymore.

Time was passing again and writing was becoming difficult. She was bogged down with her life and with writing even when things did not deserve to be written. She was desperate for memories. Since she had flown away from him the face of her destruction was appearing ever so often to remind her that she was incomplete. There was a constant reminder that he had smashed everything in her head to bits on purpose and had ripped her memories to shreds. It seemed that when she saw him he would take a few of her rewritten pages and undo her work. She tried her hardest to forgive but she could not forget as easily what he had done to her. Escape was impossible because he seemed to always seek her out. Just by existing in the same physical environment he taunted her, looking wistfully at her as she tried to ignore him and pretend he was dead. How dare he look at her like he missed her when he had never said the words and when he had left her with such an awful mess.

Her summer was gone. Her memories were being ripped up at a faster rate than she could write them. Her mind was becoming poisoned because she had no memories to saturate its space and toxins were seeping in. She felt death calling to her as he had long before and this time to end everything seemed like bliss compared to this perpetual attention to fixing memories that perhaps could not be fixed. She could not even express affection how she used to and she noted that with the way she held onto her "I miss you"'s.

Distraught she decided perhaps it was time to die. She closed the drawer to the cabinet that contained her memories. It no longer mattered whether some memories were good or some were bad. Organization did not matter and it did not matter if she created new memories or not. She looked at the room which was now void of shrapnel although her body was not. She looked at the clean walls and the metallic box that held her memories. She ran her hand across all the surfaces in the room cleaning off a layer of dust with her fingertips. She closed her eyes and began to accept that she would be in this room forever. She slipped into unconsciousness as she willed it. Death was a comfort. A little too much of this or a little too much of that and everything was over. She would never be alone again and she could work on writing. No one could touch her or her memories again.

The room could remain sterile and pristine with no invasion. Perpetual purity was attractive to her. She pulled out a black pen and began to write her last words into the walls. She wanted to create a memory that would last forever, a complete story that would never need to be revised or rewritten. Without consciousness to add and change and reformat, she could work with peace that she'd never had when her mind was being destroyed. This was her magnum opus. The white walls of the room seemed to grow brighter with her acceptance of life's finality.

unusual compat

Summertime makes me sick with how sweet it is. I hope I will still be able to taste the sea breeze and remember warmth and soft kisses in a month. I hope I will be able to smell the dope in months to come and remember breaking it up in manageable pieces as he lies next to me. The beach is relatively quiet, the vague cacophony of Vybz Kartel is the only noise, a subtle reminder of what our culture is reduced to for tourism. “Our culture” that will never really be mine and may not even be his. But here we are, in sweet summertime, St. Lucians in our own right. I used to fail at finding comfort in the uniqueness of my relationship to my culture but now it feels so much better knowing that I am not alone in my cultural confusion. Mixed. Black. White. American. Canadian. St. Lucian. Preppy. Poor. Rich. Nerdy. Reformed Catholic.  Similarity in this amalgamation of identities has drawn us together in a casual yet significant manner.

“I left Saint Lucia and never looked back.”

But here we are.

The breeze whips my hair out of my face as I stand on the porch, ancient cordless phone glued to my good ear. The porch is covered with egg containers, each filled with grotesque dried seeds for my mother’s garden. Our pink hammock swings in the breeze and a giant lizard shiftily crawls across the ceiling enjoying a feast of moths and other insects my porch light has drawn to its strategic position.

I’m leaning over the banister trying to measure the length of my hair against one of our house’s pillars and I’m listening to his voice, reflecting my experiences. Another person has gone through what I’ve gone through. I am not alone. Relating to someone about boarding school is one thing, but relating to a St. Lucian is another thing entirely, and it’s too rare for our meeting to just be hap and stance. We speak for perhaps an hour as I stand on the porch trying to see the full moon through the thick clouds that paint the sky a deep gray. Our experiences in the United States and our relationship to our almae matres are so closely aligned. It begins with culture shock and a complete lack of preparedness to work. Catholic School killed our thirst for knowledge and our love of learning. Readers, dreamers and creators quickly became stifled by rules and our unbearable lightness a problem which is far deeper than being a tragic mulatto of sorts. Children were not meant to be beaten into submission, to have their creativity massacred in favor of conforming to God’s rule.

Then of course, there’s the guilt. Who else understands the guilt that I’ve always felt? It starts like this: I don’t deserve to be the only person to have had this opportunity. He tells me about his cousin: his potential, his wealth and how he could have fit into a boarding school environment if given the chance. But the value system of his cousin’s family is different. And that’s what it comes down to for “people like us”. Our value systems are polarized to the general population of our country. We become drifting anomalies who will never quite belong because we value education over possessions and knowledge over attainable signifiers of wealth. We would have never been comfortable in a Ministry Job or at UWI. So we fled and in doing so we felt guilty.

“There are so many kids I went to school with who were a lot smarter than me and where are they now?” It’s like I’m speaking to myself or listening to a recording of every previous thought I’ve had. I think about their salaries that amount to less than 20,000 USD a year and their 90,000 dollar car loans and their meager houses and the fact that they are trapped here forever. They are trapped by this system because they did not get a chance to experience the world that we did. Our exposure to the evils of liberal American culture frighten them the way the thought of being like them frightens us. We become bonded by our guilt and our fear, perhaps not in a romantic way or even in a permanent way but it’s significant for us to get all this off our chests and push it out into the humid night because we have had these experiences alone for so long and all we crave is understanding.

The night is beautiful. I’m thrown back to my childhood feelings of loneliness and finding the sort of comfort you find when you figure out your emotions are not “crazy” and not every thought you have is a representation of how isolated you are from everyone else. The landline is pressed to my ear as if cellphones don’t exist, as if I’m so far into the past I’m making the decision to go to Groton again and again. Was it a mistake? If I could go back would I do it all over again?

“It was one of the best decisions I’ve ever made to this day,” I say, and as the words leave my mouth, I am certain this time it isn’t a lie. Finally I’m speaking about Groton without feeling totally tainted by either resentment or nostalgia — opposite sides of the same coin if you get to thinking about it. In hearing him talk about the person he has become and seeing that he is a few years further along than I am in his personal development, I feel renewed faith that everything I struggled with had a greater significance.

Our conversation reaches a natural conclusion early into the night. How do I feel? Alive. It would be cliched if I hadn’t spent so long simply feeling like I was surviving. I’ve survived Groton, Middlebury, summer in St. Lucia, but talking to him I feel more like I’ve been living. The dichotomy between simply surviving and living has been exaggerated by my feelings of isolation. For once I don’t feel an emotional ticking time bomb like I need to act fast or feel fast or think fast about anything. There is simply connection at the most basic level; it’s the ability to truly empathize and understand someone due to a shared experience. I press the little red button and remain on the porch staring at what I imagine to be Castor and Pollux for a minute or two before returning inside.

Emotional momentum from the deep satisfaction I felt about relating to someone about my high school experience has the odd effect of slowing me down. There is no need to rush into friendship or into love or into fretting about every emotion that pops into my head. I am comfortable with the breeze whipping around my brown legs and with the end of a phone call and with the end of my past relationship and in a sense with all my endings.

How do we fit in here? We never looked back when we left yet something seems to be compelling a return to a home where we may not be able to fit in ever again. Was it worth it? The response could only be an emphatic yes. Looking back into the past has never lacked loneliness like this. Before I return to the sticky indoor heat I wonder if I’m really looking at Castor and Pollux, twin stars, connected.

Going Gluten-Free

Over the summer, a friend of mine recommended that I read the book "Wheat Belly" by William Davis MD. I lean towards skepticism when presented with literature that suggests dietary change, especially given the American penchant for obsessions with fad-diets and obsessive attention to eating that leans upon a lot of unfounded research and media fueled paranoia regarding weight and appearance. The book was a gift so I figured that nothing bad could come of it, perhaps a few wasted hours but nothing more. I was determined to tear it apart; a need to criticize scientific research seems to have been drilled into me throughout my college career. I received the book, and over the course of a week or two I finally got through it. The writing was clearly not targeted at the scientific community and a lot of it sounded cheesy and tacky. After reading it, I decided to experiment with eliminating gluten from my diet; I admit I was seduced by the potential for reducing the intensity of my depressive episodes and feeling better about my body. The challenge appealed to me, so I set out with the idea that removing gluten from my life would be a difficult, but temporary challenge.

I started over the summer by seeing if I could go an entire day gluten free. My family's dynamic is such that a random drastic dietary change would not go over very well, so I decided to play it safe. I felt hungry, grouchy, starved and peeved afterwards. My only solace was that I could eat as much fruit as I want, but I was left out of much of the family meals and snacking events. I realized how hard becoming gluten free would be, especially at school where the meal plan is included in tuition so impossible to opt out of if you live on campus. My job wouldn't supply me with enough money to support myself independently from the meal plan. Despite the initial terror of realizing that I may be in over my head, I decided to proceed as I originally intended.

My first week on campus was a week before all other students arrived; dining halls were opening and serving far better food than they do usually so there wasn't too much of a struggle to find food to eat. The first week and a half felt like a detox. I was perpetually hungry, I wanted to buy out Dunkin' Donuts and wallow in pounds and pounds of wheat products. My determination to control my cravings and my sheer sense of will power prevented me from caving and I managed to make it through the first few weeks with no purposeful infractions and perhaps one accidental wheat ingestion. The list of things a gluten-free diet precludes is extensive and something I imagine most college students would find impossible. You must say no to: (most) Chinese food, soy sauce, pizza, ramen, bread, cakes, cookies, crackers, cereals, hot dogs, many salad dressings, granola, (some) ice cream, home fried potatoes and many other foods.

At the beginning of the semester, around three weeks after eliminating gluten from my diet I found that I never experienced bloating after eating or the feeling of hating myself after eating a huge meal. I didn't feel cravings for different foods as much as I did before. If I ate enough at each meal I lacked the sense of perpetual hunger I previously had. More likely a sign that I was recovering from depression than a dietary change, I found myself better able to be motivated to do things and was less overtired for no particular reason. (Now my over tiredness is a result of an odd sleeping schedule and perpetually being woken up by my roommate in the middle of the night.) I spent money on some gluten free snacks to stave off the perpetual hunger I felt during the first week or two of changing my diet. I bought yogurt, cheese, gluten free ginger snaps, gluten-free Ben and Jerry's ice-cream, and strawberries to keep in my fridge (which is actually only mine for the semester). I found the changes in how I felt to be compelling enough for me to continue being gluten-free. I'd gotten used to most of the challenges and I felt like I could keep it up as long as I felt like it.

This was a good idea, but the dining halls seemed to have other plans for me. If serving "nutritional yeast sauce" wasn't bad enough all other foods served were contaminated with gluten most nights except for plain white rice. As much as rice stripped of all nutritional value holds great appeal to me, I quickly found myself frustrated with my "rice, beans and carrots" meals or "spinach, tomatoes and italian dressing" meals. I had occasionally given myself one or two "off days" and eaten foods with small amounts of gluten in them and I figured that everything would be okay if I simply stopped being gluten free and went back to continuous wheat consumption. I ate a huge sandwich at a local café filled with all kinds of yummy wheat-y ingredients convinced that I was done for good. It was just too difficult to find a consistent source of gluten-free food and I was spending what I felt was too much money on other foods.

That night and all of the next day, I knew the sandwich was a mistake. I felt ill all night and my stomach felt like I had been poisoned. I lay in my bed feeling the light tinge of a headache coming on, put my stomach pain out of my head and fell asleep. All of the next day I felt perpetually nauseous. I felt sick to the point of vomiting and couldn't focus or eat the next day. I tried sipping water and slowly drinking soup thinking my problem was related to stress or dehydration. I hadn't slept much the night before and got a migraine around halfway through the day that knocked me off my feet until the day after. Due to that experience, I don't think I will ever return again to eating foods with wheat in them 100% of the time. If I'm  a guest or in a desperate situation, I'm sure I will have no choice, but I honestly feel as if there is something incompatible with human digestion in modern wheat. I am not the type to hop onto fad diets, to claim that coffee causes cancer one week and prevents heart disease the next. I am a skeptic, a critic, broke and hungry, yet in my experience I can't deny the positive effects I've seen after removing gluten from my life. I can't deny that every time I've slipped up I have become at the very least moderately ill. I'm not trying to change people's minds or convert them into giving up every delicious food on the planet, merely sharing my experience with becoming gluten free this semester.

24.

So recently I've found that I haven't written in a while and it's not because my mind is void of thoughts, rather I am finding difficulty organizing many of these thoughts into something coherent. Feedback is something that I am willing to accept when it comes to my writing, but I want feedback to not be in the form of something that is a mistake I could have easily avoided.

Now I'm going to just use this space and this time before class to come up with a list of topics I think I'd be interested in writing in over the next few months. I don't think I'll be able to undertake a writing project as big as the one I undertook over the summer (that yielded vastly underwhelming feedback which I think was largely due to the controversial nature of critiquing religion). No matter what, I'd like to get my brain thinking like a writer a little bit more than I currently do. I have been thinking a lot like a scientist and although this is valuable, sometimes it's helpful to expand the ways in which I collect and organize my thoughts.

1. Negotiating the emotional aspects of long distance relationships
2. The Significance of "Brotherhood" - Expectations v. Reality
3. Self-care techniques for College Students (who don't have money)
4. Summary of Gluten-Free Adventures During the Fall
5. "Serious" Relationships
6. Positive Female Friendships 

Thoughts on Sex

Why are some people so obsessed with changing who they are because of sex? People feel the need to pretend that they are either okay with casual sex because they feel the need to fit in with college hook up culture or they feel the need to act like all sex is life changing because they worry about being judged by the people around them. It's hard to imagine a world where all my female friends and acquaintances are honest about their sexual selves. 

Something as simple as emotional honesty is totally ignored by most young people pursuing sexual relationships for the first time. Too much importance is attached to "virginity" and it's presence or absence when in reality the most important part of any sexual relationship is honesty. Many men are concerned that having sex with a virgin will make her attached to them to a point that they are not ready for. While this may be true for some women, it isn't true for all and virginity has nothing to do with levels of attachment after a sexual encounter. Many women are not honest with themselves about what they want from a "relationship" and this creates problems for them in the future. 

You cannot fuck a guy into loving you, you cannot fuck your emotional problems away and relationships are not a cure to your psychological ills. How can I pound this into the heads of the people I'm surrounded by?

I hate when people look to me and my relationship as an example of a "perfect" situation where someone you start off just sleeping with turns into a relationship. It's such an incomplete picture of what happened between Andrew and me. It's an attempt to turn an exception and a strange occurrence into a standardized experience in an effort to make this chance event something that could happen to anyone and likely will. 

How do I advise people without inserting my own experiences into my advice? This is difficult for me because many people I interact with tend not to comprehend the extent to which I am honest with myself and with others. It's not something "comfortable" or "easy" but it's necessary. Recently, I've been trying to just stay away from giving other's sexual advice. It seems to overwhelm many people when I suggest that you can be interested in both casual sex and emotional sex and having one type of sex doesn't mean you are giving up on the other for life. 

Endocrinology Paper

Something I wrote for a biology class I took last semester, Endocrinology. It's long and has a lot of jargon but I hope at least someone reads it.

Eriche S------

Endocrinology – Spritzer

Spring 2013

Neural-Diathesis Stress Model and Applications to Schizophrenia Vulnerability, Onset, Progression, and Treatment

Schizophrenia has piqued the interest of researchers for years. Recently, discovering more information about the mechanisms that cause schizophrenia as well as finding effective treatments has moved to the forefront of neuroscience research. Schizophrenia has been linked to an excess of dopamine or oversensitivity of dopamine receptors that result in positive symptoms of the disease (Birtwistle, 1998). Antipsychotics that reduce the effects of dopamine have effects on positive schizophrenia symptoms, demonstrating a correlation between schizophrenia symptoms and dopamine activation. In recent research, another axis is being explored, where cortisol release in conjunction with dopamine is highly correlated to schizophrenia onset. The neural-diathesis stress model combines the effects of stress and dopamine on schizophrenia onset, progression and treatment, and provides a more complete picture of the neuronal pathways involved, opening up avenues for more effective treatments.

Cortisol may increase susceptibility to schizophrenia acting via the hypothalamo-pituitary axis (HPA) (Walker, 1997). Anti-psychotics decreasing HPA activation demonstrate the possibility that the HPA axis and dopamine are connected in schizophrenia’s positive symptoms. HPA activation increases transmission of dopamine as well as releasing cortisol. This suggests a link between stress response and dopamine release. A dopaminergic response to stress provides evidence for a connection between dopamine and cortisol, suggesting that they do not act independently on schizophrenia’s onset and positive symptoms (Mizrahi, 2012). Stress also increases a schizophrenic patient’s susceptibility to psychotic experiences, which further suggests an interaction between stressors and a biological response.

The biological connection between stress response and dopamine on schizophrenia’s positive symptoms is neurochemical sensitization of the mesolimbic system (Mizrahi, 2012). The mechanism through which cortisol and dopamine interact is through the prefrontal cortical D₁ dopamine receptors and their regulation of D₂ dopamine receptors, connected to cortisol release. The secondary effects on D₂ are the effects that may stimulate positive schizophrenia symptomology (Scornaiencki, 2009). Scornaiencki (2009) used Sprague Dawley rats injected with D­₁ or D₂ dopamine receptor agonists forced to perform stressful swim tests in order to measure the interactions between stress and dopamine. Dopamine reactivity was greatly increased in rats after the stressful swim tests. Since D₁ receptor agonists decreased dopamine reactivity significantly in injected rats but D₂receptor agonists did not have the same effects. D₁ receptors in the prefrontal cortex regulated D₂ stress response, this pathway may be the one that is affected in schizophrenia patients and is one probable connection between the HPA and dopamine release.

Other researchers used different methodology to determine a connection between dopamine and stress response. Dexamethasone suppression tests were used to measure HPA activity in patients with schizophrenia (Hori, 2012). In this study, levels of cortisol after dexamethasone treatment were measured in controls and schizophrenic patients. Cortisol/DHEAS ratios demonstrated abnormal HPA axis function. Compared to healthy patients, schizophrenia patients showed higher cortisol levels after treatment with dexamethasone, which should have suppressed cortisol due to negative feedback. Patients were simultaneously undergoing anti-psychotic treatment, which may have confounded results, however increased cortisol activation was clear in patients with schizophrenia.

The neurological development of the prefrontal cortex is another viable connection between the HPA axis and dopamine on schizophrenia. Schizophrenia’s symptoms have often been related to prefrontal cortex dysfunction in the dopamine hypothesis as well as the neural-diathesis stress model. Dysfunction of the prefrontal cortex causes cognitive deficits, thought disorders, hallucinations and delusions in patients (Arnsten, 2011). Within the pre-frontal cortex, cell network connections are marked and altered via dynamic network connectivity. Networks between neurons are strengthened by cAMP-HCN inhibition and formed by D₁-cAMP-HCN channel weakening.

Exposure to chronic stress causes degradation of cAMP-HCN, collapsing the networks ability to fire signals appropriately (Arnsten, 2011). Chronic stress results in cortisol release as well as an increase in PKC signaling due to degradation of prefrontal cortex neuronal networks. In schizophrenia, patients have shown a lack of molecules that would normally reverse stress response as well as strengthen prefrontal cortex activity, suggesting that developing and strengthening these neuronal pathways is important. Exposure to stress ceases regulation of prefrontal cortex pathways that contain vulnerable circuitry; this is linked to the initial descent into illness – the first psychotic episode. Alterations in prefrontal cortex pathways show definitive links to positive schizophrenia symptomology.

Prefrontal cortex damage as a result of prenatal stress increases risk of schizophrenia development later in life; this model of prefrontal cortex damage integrates the HPA and dopaminergic systems as well (Martinez-Tellez, 2009). During the formation of the prefrontal cortex networks described above, some alterations take place that may directly impact the likelihood of patients developing schizophrenia. This could be important in development of prevention methods; decreasing prenatal stress levels may be easier than treating the disease directly. Inadequate stimulation of D₁ receptors that results in bad prefrontal cortex connections and loose associations between neurons is one effect of stress on prenatal prefrontal cortex damage. There is also the problem of too much D₁ stimulation which suppresses neuronal firing under mild stress conditions which increases dopamine release due to malfunctioning negative feedback loops (Arnsten, 2011).

This prenatal stress is often times due to bacterial infection; other researchers have used rat models to outline when this occurs prenatally and the role this may play in schizophrenia risk (Lin, 2012). Using lipopolysaccharide exposure, Lin (2012), examined the role of maternal bacterial infections on fetal brain development. Mothers who experienced bacterial infections produced offspring with reduced dopamine in the hippocampus and prefrontal cortex. There was a critical period for when prenatal stress would begin to have an effect on neuronal development. Martinez-Tellez (2009) determined that this critical period was around the middle of pregnancies. Infection and other prenatal stressors cause impairments in the HPA axis as well as in hippocampal dendrite morphology. These prenatal changes were shown to have post-natal effects in rat pups that were seen to have increased stress responses (Lin, 2012).  Given the link between stress and disease onset in humans, results from this study are applicable to human models.

Early exposures to stressors post-natally have also been connected to schizophrenia onset later in life. Benes (2004) suggests that mistakes in dopamine inputs to GABA pathways pre and post-natally may be responsible for schizophrenia onset in vulnerable patients. If pre-natally exposed to stressors, there are a number of post-natal factors that increase risk of schizophrenia development. Environmental triggers such as poverty, social marginalization and immigrant status have been stressors linked to increased risk in schizophrenia onset (Jones, 2006). Predispositions to schizophrenia are not the sole cause; cortisol release as a result of exposure to various environmental stressors must happen in conjunction with this predisposition (Benes, 2004). In the Benes (2004) study, rats injected with cortisol post-natally were also examined for dopaminergic responses. These rats possessed greater clusters of dopamine cells, signifying the connection between dopamine and stress within schizophrenia onset, as it relates to early stress.

One of the most highly correlated early traumas linked to schizophrenia is child abuse. A large percentage of schizophrenia patients have been abused throughout early childhood. At risk schizophrenia adolescents – who show schizotypal behaviors or schizotypal personality disorders - have higher baseline salivary cortisol levels than controls (Stilo, 2011). Consistently showing these higher cortisol levels is partially attributed to aging, but may also be attributed to early childhood trauma, described within the traumagenic neurodevelopmental model of schizophrenia (Read, 2001). Within this model, biological, psychological and social factors are combined to find more answers regarding schizophrenia onset. High levels of cortisol acting with dopamine may increase risk of disease onset, but the stressors of early childhood are very highly correlated to this excessive cortisol in the first place.

In adoption studies meant to assess the effects of child abuse on schizophrenia development, at risk children who lived with “healthy” adoptive families were compared to at risk children who lived with more abusive adoptive families. 3% of the children with health families developed schizophrenia, while 34% of at-risk patients raised by the abusive families developed schizophrenia later on (Read, 2011). Child abuse causes sensitization of stress axes to stressors, leading to minor threats being perceived as terrors, something that has relevance to schizophrenia’s positive symptoms like paranoia. Stress responses developed in childhood are long lasting; early childhood stress sensitization as the result of abuse may likely lead to baseline cortisol levels being higher throughout puberty and post-puberty during the ages where psychotic episode risk increases.

Another connection between dopamine and stress in the neural-diathesis stress model lies in the age of onset. Schizophrenia’s age of onset is roughly 19 years old, more generally described as “late adolescence” (Gogtay, 2011). Brain processes involved in puberty may play a role in schizophrenia onset due to positive feedback systems triggered by stress, which leads to a rapid increase in positive symptoms’ appearance (Thompson, 2004). In schizophrenia patients who had experienced positive symptoms triggered by an adolescent stress response, there were a higher number of dopamine (D2) receptors. Psychosocial stress worsens positive symptoms and triggers relapse (Walker, 1997).

Adolescence is a time when people are exposed to a large variety of psychosocial stressors, especially in high-pressure school systems that demand a lot academically and socially; this relationship to disease onset is not improbable. Sensitivity to these psychosocial stressors as well as a pre-existing vulnerability may trigger these initial pathways and activate positive symptoms. Since dopaminergic response to stress has been higher in patients vulnerable to schizophrenia, increased psychosocial stressors in adolescence specifically may act to trigger initial positive symptomology. However, the connection between cortisol and dopamine is not only found in early onset of the disease; there is something more than the stresses of adolescence at play in the development of schizophrenia’s symptomology.

Environmental triggers of stress response and stress sensitization in adolescents are similar to ones experienced in children; abuse seems to be more highly correlated in children. Use of cannabis and psychostimulants have been connected to increasing risk of schizophrenia; this is likely via dopamine pathway stimulation (Di Forti, 2011). These drugs have been linked to first episodes of psychosis. Adolescence is typically a time when experimentation with these drugs may come about; in conjunction with higher cortisol levels, over-activity of the two pathways may occur leading to onset of first psychotic symptoms.

Urban residence and migration have also been highly correlated to schizophrenia onset likely because of the intensity of these two stressors. Urban settings may, somewhat counterintuitively, increase feelings of social isolation; threats to the social self are seen as forming the sort of stress response that increases the risk of schizophrenia development (Jones, 2007). Di Forti (2011) shows that in urban areas with the least amounts of social cohesion, schizophrenia rates are the highest. Migrant and ethnic minority groups may also experience higher amounts of stress leading to psychotic episodes as a result of poverty, racial discrimination, unemployment and isolation from family members. Migrant and ethnic minorities are also more likely to reside in urban areas. Environmental stressors that control the release of cortisol should be avoided in high risk patients, however, in some of the cases above like migration or urban residence, this is not a realistic option; exposure to stressors and schizophrenia risk are increased among these groups.

If early childhood abuse and prenatal stressors have such a large effect on schizophrenia onset, there must be an explanation for why the average age of onset is not much earlier than “late adolescence”. Although these early responses show strong correlations to schizophrenia onset, the trigger for most psychotic episodes is thought to lie in post-pubertal maturation of neuronal pathways (Stilo, 2011). In longitudinal studies of healthy controls, age increases were positively correlated to increases in cortisol levels. Schizotypal “at-risk” patients presented with significantly higher baseline cortisol levels than controls; higher baseline cortisol levels combined with a natural increase in cortisol with age increase likelihood of psychotic episodes. Childhood, adolescent and prenatal stressors in typical schizophrenia cases may not be enough to solely cause psychotic episodes. Neuromaturation triggering latent vulnerability may explain why cortisol levels have effects on expression of schizotypal symptomology when they do. Schizotypal symptoms typically appear in adolescence with full-blown psychotic episodes as a result of increases in HPA axis activation occurring towards the end of adolescent neuromaturational processes. Cortisol effects are not only found in disease onset, but also in disease progression.

Schizophrenic patients have higher baseline cortisol levels than controls before the onset of psychotic episodes (Jones, 2007). Treatments for schizophrenia that concurrently raise cortisol levels cause positive symptoms of schizophrenia to worsen. Throughout schizophrenia’s development, continued exposure to stressors plays a role in symptom’s worsening. Hippocampal damage has been found in cohorts of schizophrenia patients; this directly affects the HPA axis and release of cortisol, leading to excess cortisol production and increases of positive symptomology, not just at the onset of schizophrenia. Sensitivity to dopamine stress responses has implications in relapse or conversion to psychosis, showing that stress response is connected to schizophrenia throughout disease progression (Mizrahi, 2012).

Raison (2003) found that the HPA axis released less cortisol over time in stress-disorders that began with high levels of cortisol; this is not in contradiction with Jones (2007), rather demonstrates the likely progression of HPA axis and hypothalamic degradation in schizophrenic patients. Prolonged stress, from continuously high levels of cortisol may eventually damage the HPA structures responsible for producing cortisol, down-regulating cortisol in the long run by either stopping the production of upstream hormones like CRH and ACTH or by alterations in enzymes that metabolize glucocorticoids.

Brenner (2009) focused longitudinal research specifically on schizophrenic patients stress response. After first psychotic episodes, patients were found to have less reactive stress responses to psychosocial stressors, which supported the Raison (2003) finding. Stress and coping mechanisms correlate to schizophrenia patients’ quality of life; high quality of life is significant to management of positive symptoms (Brenner, 2009). Schizophrenics typically report lower quality of life than healthy controls. Use of less effective coping strategies may be connected to cortisol reactivity. Emotionally focused coping and the blunted cortisol response are maladaptive for schizophrenia patients. HPA dysregulation that causes a weaker cortisol response could lead to neurological changes that debilitate cognition and lead to misjudgment of coping technique effectiveness in patients with low cortisol responses to psychosocial stress. Drug treatments are often not enough for disease management; using the neural-diathesis stress model may provide new insight in how stress responses can be used to determine more effective coping strategies for patients and improve quality of life.

Typical drug treatments for schizophrenia are dopamine partial agonists (Miyamoto, 2005). Drugs that target dopaminergic systems frequently come with a host of side effects – researchers seek out different treatments that do not act upon dopaminergic pathways. Cortisol response in different drug treatments is an area of interest for drug developers as well as researchers who seek to better understand schizophrenia causation and progression. Ritsner (2005) looked at changes in cortisol / DHEA ratios in schizophrenic patients treated with different antipsychotic drugs of the same class like haloperidol, clothiapine and risperidone in conjunction with anti-Parkinson’s drugs to control for side effects that mimic Parkinson’s disease symptoms. Higher baseline cortisol/DHEA ratios predicted that a patient would be more likely to respond to treatment.

Other research has been done looking at only plasma cortisol levels as opposed to cortisol/DHEA ratios (Meltzer, 2000 and Cohrs, 2006). Cohrs (2006) sought to clarify antipsychotic effects on schizophrenics, but rather than looking at cortisol/DHEA ratios, he looked at the upstream glucocorticoid hormone, ACTH, as well as cortisol levels in schizophrenic patients being treated with olanzapine, quetiapine and haloperidol. Olanzapine and quetiapine are atypical antipsychotics that have been shown to reduce positive symptoms as well as negative symptoms. These drugs have also been effective in treating comorbid disorders like PTSD. This study tests the hypothesis, mentioned briefly earlier, that antipsychotics will act on cortisol levels. Atypical antipsychotics are more likely to show changes, since they have been connected to reducing symptoms of comorbid depression, which is characterized by over-activation of HPA axis. Olanzapine and quetiapine decreased plasma cortisol levels as well as ACTH levels from the baseline, whereas haloperidol did not have the same effect (Cohrs, 2006). These atypical antipsychotics act both on dopaminergic systems as well as cortisol, which may make them more effective treatments than current typical dopaminergic antipsychotics.

Meltzer (2000) looked at the antipsychotic drug apomorphine and it’s effects on plasma cortisol levels in treated schizophrenic patients; unlike the Cohrs study (2006) Meltzer (2000) also looked at the effects on psychopathology to ensure effectiveness of the drug and to possibly find a correlation between drug effectiveness and plasma cortisol levels. Plasma cortisol response was significantly blunted in schizophrenic patients as opposed to controls. Patients who had previously responded to other antipsychotics showed more reactive cortisol response to apomorphine. Ritsner (2005) showed that higher levels of baseline cortisol/DHEA ratios predicted drug responsiveness; this finding could be related to Meltzer’s (2000) findings in that responders did not have higher cortisol levels as a result of previous treatment, but their higher cortisol levels allowed them to be more responsive to drugs in the first place. Cortisol response to apomorphine may also predict whether or not a patient will respond to future antipsychotic drugs.

Studies of different clinical drugs are inconclusive regarding cortisol’s role in antipsychotic drug treatment. Cortisol levels seem to result in different coping mechanisms and responsiveness to treatments; cortisol levels also change based on different treatments regimens. A lack of conclusive evidence on cortisol’s role in schizophrenia treatment means more research needs to be done to fully understand how the neural-diathesis stress model can be employed in developing schizophrenia treatments. Baseline cortisol is a good predictor for coping methods outside of antipsychotic treatment (Brenner, 2011). Cortisol response as well as cortisol levels seem to be related to antipsychotic drug treatment, but this appears to be dependent on the drug and whether or not baseline cortisol levels or cortisol/DHEA ratios will allow a patient to respond to drugs.

The neural-diathesis stress model provides some conclusive results with regards to the connection between cortisol and dopaminergic pathways. The HPA axis that regulates cortisol production is directly connected to dopaminergic pathways. These two pathways interact in schizophrenia patients; this has been demonstrated by showing that common antipsychotic drugs dull the cortisol response in patients treated. Stress via cortisol response has effects on schizophrenia risk and onset at different stages of development. Increased pre-natal stress can increase schizophrenia risk, as well as early childhood traumas like abuse. In adolescence, the cortisol increases associated with post-pubescence increase the risk of a first psychotic episode. Decreased cortisol response reduces the ability to cope well with symptoms and have a higher quality of life. Decreased cortisol response is also linked to being a non-responder with many anti-psychotic drugs.

A link is clearly present between stress and schizophrenia; the link between dopamine pathways and stress response is in the neurological development of the prefrontal cortex as well as the neurochemical sensitization of the mesolimbic system. The prefrontal cortex connection between stress and dopamine is found within the dopamine receptors; D₁ receptors in the prefrontal cortex regulate the D₂stress response. A cortisol-dopamine connection is demonstrated through cAMP-HCN, which strengthens prefrontal cortex neuronal networks; these neuronal networks are formed through D₁-cAMP-HCN channel weakening. Chronic stress damages cAMP-HCN, which in turn damages neuronal networks.

Future research should focus on solidifying the connection between cortisol and dopaminergic pathways in order to find more definitive results about the connections between the two in schizophrenic patients. Longitudinal studies looking at cortisol levels periodically throughout a schizophrenic’s life – before the first psychotic episode –throughout disease progression may provide data on when exactly cortisol levels are blunted and why this may occur. Understanding the connections between dopamine and cortisol more thoroughly could provide better information for drug developers looking to improve antipsychotics that act solely on dopamine pathways. Currently, conflicting information about cortisol response either being blunted or heightened makes this difficult.  Although more complex, large scale longitudinal research would provide the best data with regards to cortisol levels and dopamine activity’s connection throughout the progression of the disease, beginning with patients who are at risk – patients with schizotypal personalities for example – and following up with research on patients who eventually develop schizophrenia. Perhaps then we can develop better treatments of schizophrenia that manage symptoms more effectively with fewer side effects.

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I feel a lot of things today but I don't feel much like going into details until I have a conversation with my boyfriend. I am making plans to start my four week gluten-free life and I'm not sure if I should post about it here or make a side blog. I think I will feel better if I can just post some things on here and remember to post daily even if I have a lot to do. I go back to school to start work on the third and I'll begin chronicling my new dietary changes then.