Alcoholic Depressed Schizoid Thomas Harper, the Cynical Philosopher hypoxic anoxic injury

I haven’t often talked about myself on this blog. That is, when I bother to post anything at all. Maybe this is strange, since that is what personal blogs are meant for, aren’t they? I’m just not one to talk about myself. That’s probably why I don’t post often and why I have an even harder time “marketing” myself – my blog, my novel nanoxia deep silence 2, etc. I just never found myself to be all that interesting of a topic, unless I could talk about myself in some conceptual or theoretical sense – like when I got really into personality theory a little over a decade ago (I’m an INTP by the way, for people who care about such things.

I am a thirty-three (almost thirty-four) year old heterosexual white male.

I live in michigan (hence the polar vortex thing). According to my 23andme results, I am 55.6% dutch and german (mostly dutch), 30.7% british isles (I have scottish ancestry on my father’s side) and 13.7% danish. My maternal haplogroup is h5a1 and my paternal haplogroup is R-S660.

I have suffered all of my adult life with alcoholism. Compared to other alcoholics I know, I actually became actively addicted quite late. I started (over)drinking when I was 19 years old. Things ramped up quickly. I was in active addiction until early 2018, going in and out of rehabs and hospitals since early 2017 when things came to a head.

I was in my second year of graduate school and had my oral exam scheduled for late may, the passing of which would make me a phd candidate. I spent all of april and may in my apartment ‘studying’ (which is why I didn’t have to go to the lab and work) for this exam. What I was really doing was keeping myself in a drunken stupor 24/7 for two months while watching and then re-watching buffy the vampire slayer and angel. When the day of my oral exam was fast approaching, I called my school’s recovery center. They got me into diffuse anoxic brain injury an in-patient rehab.

Less than a week after I got out I was drinking again. And so I went to an outpatient treatment (I.O.P. – intensive outpatient) that lasted three months. During that time I also did my ‘ninety-in-ninety’ (ninety meetings in ninety days) at alcoholics anonymous. I really hated AA – both because I hate being around other people (more on that later) and I’m an atheist, so the whole “higher power” thing just rubbed me the wrong way. On the very last day of my I.O.P. I went through their little graduation ceremony, walked out the building, and went straight to the liquor store.

The I.O.P. Ended in october of 2017. I spent from october 2017 until late january of 2018 going through a series of sober periods and relapses (each lasting approximately a week). I ended up in the hospital a couple times from withdrawal. In late january (almost one year ago at the time of writing this post) I finally ended up having to drop out of graduate school and move back home to live with my parents. I had one very short relapse over the last year back in september of 2018, but otherwise have been sober. But I am still living at my parent’s house working as a dish washer at a restaurant.

I display all the hallmarks of MDD – feelings of hopelessness, low self-esteem, suicidal ideation, periods where I can barely get out of bed, lack of interest in anything, and lack of motivation. I would say it is the latter two that end up bothering me the most. They stop me from doing the things I want to do with my life. They prevent me from being the person I imagine myself being in my own mind. And, to make it more concrete, they are the reason my posting on this blog is so sporadic. Currently, I am taking 450 mg of wellbutrin (bupropion), 150 mg of effexor (venlafaxine), and 600 mg of neurontin (gabapentin) for my depression and anxiety.

But, more recently, I was officially diagnosed (by an actual expert, not myself) as having schizoid personality disorder (SPD). Basically, SPD is like shyness on steroids. In hindsight, I’ve most likely had this since at least middle school as well. The following are symptoms from the hypoxic brain injury following cardiac arrest DSM V; I have bolded symptoms that sort of apply to me and bolded+highlighted in red the symptoms that strongly apply to me:

All the therapists and experts told me that alcoholics and addicts had a tendency to isolate and I thought “yeah that sounds exactly like me.” but all the alcoholics and addicts I met in rehab or AA talked about all the nutty things they did while drunk. I never had any adventures while drunk. The experts told us that part of getting sober and healthy was cutting off anoxic encephalopathy pathophysiology our actively using friends, but my drinking was only ever just me, alone, sitting in my room in my underwear, never talking to anyone, no matter how drunk I was (it didn’t act as a social lubricant for me). I never had alcoholic or addict friends.

Another symptom not listed above that people with SPD seem to experience is what is called maladaptive daydreaming (MD). Why it’s not listed above is because the DSM doesn’t identify MD as a psychological disorder. But it definitely describes me. I think it is why I (at least attempt to) write novels. I have tons of ideas for novels, all of which are born of the fantasy worlds I frequently visit while daydreaming. It’s also why I really don’t mind having a repetitive job like washing dishes – I simply put in my earbuds, turn up the music, and retire to my fantasy worlds throughout the entire shift. The characters in my head are much better company for me than the vast majority of people I know in real life.

The C(-1019)G rs6295 SNP has been investigated for association with suicide attempts, and psychiatric disorders. One study found an association of the variant with schizophrenia. Some studies associate homozygous C(-1019)G genotype with depression. The polymorphism has also been investigated for links anoxic brain injury nursing care plan to personality traits. Persons with the G-allele of the polymorphism may have higher personality score for the NEO PI-R neuroticism (more likely to experience such feelings as anxiety, worry, fear, anger, frustration, envy, jealousy, guilt, depressed mood, and loneliness) and TPQ harm avoidance (excessive worrying, pessimism, shyness, and being fearful, doubtful, and easily fatigued) traits. One study found higher score on temperament and character inventory self-transcendence scale for G-allele subjects among mood disorder patients (self-transcendence is the capacity to expand self-boundaries intrapersonally (toward greater awareness of one’s philosophy, values, and dreams), interpersonally (to relate to others and one’s environment), temporally (to integrate one’s past and future in a way that has meaning for the present), and transpersonally (to connect with dimensions beyond the typically discernible world)).

DRD2/ANKK1 taq1a polymorphism (rs1800497, glu713lys) is located ~10 kb downstream from the DRD2 gene (placing it in the 3`-UTR of the DRD2 gene) in the ankyrin repeat and kinase domain containing 1 (ANKK1) gene. The A1 allele of rs1800497 has consistently been implicated in addiction disorders (noble, 2000; smith et al., 2008; chen et al., 2011) and has also been reported to be a risk factor for depression. In a longitudinal study of 2347 adult males, the A1 allele was associated with an increased risk of developing depressive symptoms at follow-up (odds ratio 2.55; roetker et al., 2012). The taq1a polymorphism or a variant in linkage disequilibrium with taq1a appears to affect D 2 receptor binding, perhaps explaining the reported associations between taq1a and psychiatric and addiction disorders. Relative to the A2 allele, the A1 allele has been associated with reduced striatal glucose metabolism (noble et al., 1997) and reduced binding of the D2/3 receptor antagonist, [11C]raclopride, in studies of healthy subjects (thompson et al., 1997; pohjalainen et al., 1998; jonsson et al., 1999).

The minor “A” allele in rs1076560 causes altered splicing of DRD2 protein, which decreases the ratio of D2S and D2L and subsequently increases anoxic brain damage after cardiac arrest dopamine signaling. The D2 long isoform (D2L) is mainly postsynaptic and is a target for haloperidol, and the D2 short (D2S) isoform is mainly presynaptic and serves as an autoreceptor regulating (inhibiting) dopamine synthesis and release. The minor “A” allele has been associated with lower working memory and schizophrenia. The minor “A” allele is also found to increase risk for psychiatric disorders such as schizophrenia and also the risk for developing substance dependence.

Heterozygosity CA in rs2283265 causes a slight decrease in the number of D2S receptors. The minor “A” allele is associated with increased risk of schizophrenia, decreased performance of working memory and attentional control tasks (AA and AC), increased susceptibility of cocaine and heroin addiction (AA and AC), and a tendency to make negative (poor) life decisions.

The COMT gene codes for the COMT enzyme, which breaks down dopamine in the brain’s prefrontal cortex. The anoxie cérébrale conséquences wild-type allele is a (G), coding for a valine amino acid (val158); the (A) substitution polymorphism changes the amino acid to a methionine (val158met). This alters the structure of the resultant enzyme such that its activity is only 25% of the wild type. As a result, A allele carriers have more dopamine in their prefrontal cortex, which may be responsible for many of the neuropsychological associations listed below.

Roughly speaking, the predominant wisdom (known colloquially as the warrior/worrier hypothesis; summary at [ PMID 17008817]) posits that people with val alleles have increased COMT activity and lower prefrontal extracellular dopamine compared with those with the met substitution. Val158 alleles may be associated with an advantage in the processing of aversive stimuli (warrior strategy), while met158 alleles may be associated with an advantage in memory and attention tasks (worrier strategy). Under conditions of increased dopamine release (eg, stress), individuals with val158 alleles may have improved dopaminergic transmission and better performance, while individuals with met158 alleles may have less efficient neurotransmission and worse performance. Some evidence suggests that val158 alleles are associated with schizophrenia, while met158 alleles are associated with anxiety.

Burst firing of ventral tegmental area (VTA) neurons causes synaptic dopamine release into pyramidal cells of the prefrontal cortex (PFC). Because these cells contain little dopamine transporter (DAT), the dopamine diffuses out of the synapse to bind extrasynaptic D1 receptors where it is inactivated by COMT. The higher activity val158 COMT allele breaks down the dopamine before it diffuses out of the synapse, which decreases D1 receptor activation, shifting the balance to favor intrasynaptic D2 receptor activation. Cognitive performance may be critically dependent on the D1/D2 binding ratio, with a relative lack of D1-signaling causing impulsivity, distractibility and poor working memory performance with schizophrenia at the extreme end (winterer & weinberger 2004). A relative lack of D2-signaling, on the other hand, may fail to signal the presence of reward information, a signal that is required to engage the PFC in updating its working memory system (weinberger et al. 2001 anoxic event). The rs1800497 taq1a allele of the D2 receptor decreases the expression level of the D2 receptor, which would allow dopamine to diffuse out of the synapse and activate the D1 receptors. The met 158/val 158 heterozygotes increased the benefit to working memory by more slowly digesting dopamine, allowing even more of the neurotransmitter to diffuse out of the synapse and activate D1 receptors.

M2 muscarinic receptors act via a G i-protein coupled receptor, which causes a decrease in camp in the cell, generally leading to inhibitory-type effects. They appear to serve as autoreceptors – a type of receptor located in the membranes of presynaptic nerve cells. It serves as part of a negative feedback loop in signal transduction. It is only sensitive to the neurotransmitters or hormones released by the neuron on which the autoreceptor sits. Similarly, a heteroreceptor is sensitive to neurotransmitters and hormones that are not released by the cell on which it sits. A given receptor can act as either an autoreceptor or a heteroreceptor, depending upon the type of transmitter released by the cell on which it is embedded. Studies show an association between T/T homozygosity in the rs324650 and G/G homozygosity in the rs324640 of the CHRM2 gene and intelligence. In one study of ~300 caucasians, the T/T and G/G homozygous anoxic brain damage recovery stories genotypes appeared to typically have a 4-point higher IQ than the A/T or A/G heterozygous genotypes, which had a 4-point higher IQ (on average) than the A/A homozygous genotypes of either SNP. Earlier work had observed that the T/T rs324650 SNP increased chances of alcohol dependence.

The synaptosomal associated protein of 25 kd (SNAP25) gene plays an integral role in synaptic transmission, and is differentially expressed in the mammalian brain in the neocortex, hippocampus, anterior thalamic nuclei, substantia nigra, and cerebellar granular cells. SNAP25 is a component of the SNARE complex, which is central to synaptic vesicle exocytosis, and, by directly interacting with different calcium channel subunits, it negatively modulates neuronal voltage-gated calcium channels, thus regulating intracellular calcium dynamics. SNAP25 may also regulate postsynaptic receptor trafficking, spine morphogenesis, and plasticity. Studies have suggested a possible involvement of SNAP25 in learning and memory, both of which are key components of human intelligence. In addition, the SNAP25 gene lies in a linkage area implicated previously in human intelligence.