SPOILERS Review: The Last Jedi

I think it’s difficult to assign a grade to The Last Jedi, because the quality of various plot threads differs dramatically. For me, The Force Awakens was a joy to watch (even if it was a carbon copy of A New Hope). The Last Jedi had so many glaring problems that it was difficult to sit back and simply enjoy the ride.

I’d like to focus on three categories; the weakest parts of the film, what was missing, and what I found to be excellent.

The opening sequence which sets the stage for the rest of the film is quite weak.  First, the stakes are rather low. The Empire is chasing a rebel ship (First Order, Resistance, whatever) which we’ve seen a thousand times, but we have no reason to really be worried, or even interested– only lame characters are getting killed, and this is basically the status quo of the Star Wars universe. Second, the idea of an extended, relatively slow, linear chase between starships is absurd, because the Empire has such an immense fleet that it would be trivial for them to coordinate with other craft and have them make lightspeed jumps into the path of the escaping rebel vessel.  So the core driving force of the plot arc is ridiculous within the Star Wars universe, and  limps out of the gate.

The Rose-Finn story arc is the most glaring mistake. It eats up considerable screen time, yet does not forward plot or character development, and has the shit-ass comic vibe of the prequels.  Rose is a poorly developed character (What skills does she have? What is her personality?).  Finn, who was an insecure, goodhearted, and just-brave-enough guy in Awakens, is now a bumbling idiot who relies on oversized rabbits to get him from one plot point to the next. Benicio Del Toro’s considerable acting talent is completely wasted on a character who’s a minor part of a pointless digression.

There are so many gags in the casino environment; the true hacker is a parody Frenchman, BB-8 shoots coins at enemies, they make a loud, obvious landing on a “pivotal” mission to save their friends. Contrast this with the realistic, lived-in world of Rogue One, when the protagonists meet the blind force-adept character. Notice how the frames of Rogue are not overloaded with shitty CGI, slapstick humor, and forgettable characters.

The duel between Finn and Phasma falls totally flat.  No one cares about Phasma– she’s not a part of this film’s plotline in any way. She is only thrown in because she is an action figure. Contrast her death with that of Boba Fett. His death was quick and minor, in accordance to his importance to the main plot arc. But he still matters more to the audience because he is fucking awesome, not a “chrome dome”.

Del Toro’s betrayal of Finn and Rose is similarly meaningless. Why would they expect a hacker-for-higher, who they met in a prison cell, to exhibit loyalty? Contrast this to Lando’s betrayal of Han Solo in Empire. We care about Han; he and Lando have a history together. The betrayal affects the plot and all of the main characters.

This betrayal occurs between Rose and Del Toro, two characters we don’t give a shit about, and it literally affects nothing because Pink Hair has a plan that takes care of the rebels regardless of Finn and Rose’s actions. Nobody cares–not the audience, not the other characters.

I could go on for pages, but let me just mention a few more awful things: Leia floats through space when she is dead; BB-8 can do anything now; Poe is one-dimensional, Luke plotting to murder his nephew is completely out of character, as is brushing off his shoulder to taunt Kylo; Maz Cantina flying around killing people while face-timing.

I also felt there were some major elements missing from this episode. There is no romance between Finn and Rey, or Kylo and Rey.  In my mind this seemed to be a big part of The Force Awakens, especially near the ending.  I was also disappointed that we didn’t learn more about the Knights of Ren/Snoke’s background (instead we had to follow Rose and Finn through an Episode One detour).  I was also a little disappointed that they didn’t recut the film to feature Leia’s on-screen death.  Now her death will just be part of the opening crawl in the next film, or mentioned as an off-camera event. If only there had been an appropriate time for character to die, like when she was floating lifeless through cold vacuum of space…

There were some truly amazing elements. I loved the communication between Kylo and Rey via the force.  Their relationship, and the relationship between the dark and light side of the force, is at the heart of this trilogy. What a fun way to illustrate that balance, between characters we actually care about.

I also love how Luke and Kylo both felt that the Jedi and the Sith had run their course and needed to be replaced with some new paradigm. Kylo, Rey, and Luke are all searching for meaning, and balance, and a way forward, and are looking to forge unsteady alliances. It’s compelling. Kylo and Rey’s performances are excellent, and Luke’s performance is good, especially given some of the bullshit he had to do.  He somehow kept the character slightly dignified.

The scene in Snoke’s throne room is one of my favorite sequences in the entire saga. It was unpredictable, well acted, pivotal to the plot, and visually stunning. I feel that it surpassed any action sequence in another other Star Wars film.

Overall, the sequences surrounding the Sith and the Jedi range from good to fantastic. The other components of the film, range—to quote Norm McDonald—from shit to fucking shit.

Nevertheless, I want to see the film again. I hope JJ Abrams is able to salvage this trilogy in the next film.

Diabetes and Me

Introduction

There is a strong genetic component to Type One Diabetes (T1D), as evidenced by twin and familial studies. In monozygotic twins (identical twins, with the same genome), if one twin gets T1D, there is more than a 65 % chance that the other twin will get it by the age of 60 (1). If you are a sibling of a T1D patient, you are at higher risk for developing T1D than members of the general population; there is a 6% probability for siblings, compared to 0.4% among the white US population (2).

Importantly, the presence of T1D is not completely genetically determined; rather, your genetic makeup increases your susceptibility. This is obvious upon examining the monozygotic twin studies mentioned above; if T1D was fully genetic then you would expect 100% of monozygotic twins to be (or not be) diabetic, but this is not the case. Therefore, environmental factors must also play a role. Additionally, cases of T1D in western societies have doubled in the past 20 years, a rate of change presumably too quick to be caused by genetics alone.

Type One Diabetes is a polygenetic disease, meaning that many different genes affect the probability of contracting the condition. This contrasts with diseases such as cystic fibrosis, which manifest from mutations in a single gene and inheritance of the disease follows Mendelian genetics. Genes that increase one’s risk of developing T1D are called susceptibility genes. Researchers have identified over 40 different susceptibility genes for T1D, with a range of risk (3). Susceptibility genes that confer the highest risk are found on chromosome six, and are part of the major histocompatibility complex II (MHC II a.k.a. human leukocyte antigen II (HLA-II)). An estimated 50% of the genetic risk for T1D can be attributed to HLA locus (4).

The MHC II is involved in the immune response against bacteria and viruses. It is a protein complex embedded within the cellular membrane of specific cell types and is involved in displaying antigens (peptides derived from proteins inside the cell). Antigens that are derived from invading bacterial or viral proteins are displayed on MHC II complexes. This allows the immune system to target infected cells for destruction. MHC II also displays self-antigens (peptides derived from its own genome). This acts as a quality control so that the immune system doesn’t destroy your own cells. In autoimmune diseases, self-antigens, MHC complexes, and/or some other aspect of the immune system does not function properly, so the immune system destroys normal, healthy body tissues.  In T1D, immune cells destroy the pancreatic β cells. The immune response that is elicited against β cells is a complex topic which I plan to address in a future write-up. The MHC II genotype that confers the highest risk for T1D is DR3/4-DQ8 (DRB1*0301-DQA1*0501-DQB1*0201/DRB1*04-DQA1*0301-DQB1*0302). Given the importance of this genotype in T1D susceptibility, the rest of this article will be dedicated to trying to understand it.

 

What is DR3/4-DQ8?

The DR3/4-DQ8 genotype refers to specific types of MHC II complexes[1] displayed on specific cell surfaces. There are five types of MHC II complexes that can be displayed: DO, DM, DR, DQ, and DP. These complexes differ in their amino acid sequence (mainly at the peptide (antigen) binding site), and have been classified by serotyping. MHC II complexes are composed of two polypeptides (alpha (α) and beta (β)) that combine to form a heterodimer (two different polypeptides that come together to form a complex).

Therefore, the genotype of an MHC II complex depends on two genes, the α and β, which come together to form DO, DM, DR, DQ, and DP complexes. Given that there are five different types of MHC II complexes—each containing an alpha and beta peptide—and humans are diploid (contain two copies of each gene), the variation in MHC II complexes comes from twenty different genes. The DNA sequence varies among individuals for these genes, leading to different alleles for the MHC II complexes. These alleles are indicated by the number following the letter designation (i.e. DR3, DQ8). There can be thousands of different alleles within the HLA encoding region of chromosome six. Indeed, the HLA region is the most diverse region observed in the human genome, with over  six thousand alleles (5).

Figure 1. MHC class II complexes are embedded in the membranes of antigen presenting cells. They are composed of two proteins (alpha and beta) that form an antigen binding site. Each polypeptide (corresponding to a single gene) has intracellular and transmembrane domains, as well as two extracellular domains. The B1 and A1 extracellular domains form the site where processed antigens are presented (the peptide binding site).

 

So let’s take a closer look at the DR3/4-DQ8 genotype: DRB1*0301-DQA1*0501-DQB1*0201/DRB1*04-DQA1*0301-DQB1*0302.

MHC II complexes are identified by the first two letters (DR and DQ for the above genotype).

Because each complex is composed of an alpha and beta there should be a B or A designation after the two-letter code. Above we see that DR does not have an alpha (A) gene described—this is because the DRA1 is non-variant (no alleles), so people don’t bother writing it.

The “/” designates the second set of alleles (from the other chromosome—remember, humans are diploid).

Some will refer to DRB1*0301-DQA1*0501-DQB1*0201 as DR3-DQA1*0501-DQB1*0201 or just DR3 or DQB1*0201.

Similarly, DRB1*04-DQA1*0301-DQB1*0302 can be called DR4-DQA1*0301-DQB1*0302 or DR4 or DQB1*0302 or DQ8.

Presumably, some abbreviate these genotypes to just DR3 or DR4 (or DQ8). Often the DR3/4-DQ8 genotype is referred to as “heterozygous”. This is because the individual has two different alleles for DR (i.e. DR3 and DR4, where homozygous would be DR3/DR3 or DR4/DR4).

The DQB1*0302 allele is often referred to as DQ8 and is linked to DR4.  Presumably, if you are DR4 than you are automatically DQ8 (as I have suggested above).

 

Figure 2. Chromosome 6 pair representing the gene organization for a DR3/4-DQ8 individual. The genes are transcribed and translated to form the protein complexes below (Figure 3).

Figure 3. Representation of the complexes expressed in a DR3/4-DQ8 cell. Alleles specific to the DR and DQ MHC II complexes increase susceptibility to T1D. These susceptibility alleles are often referred to as DR3 and DR4 (or DQ8). Some hypothesize that the heterozygous individuals can form chimera DQ complexes that have atypical antigen specificity.

 

DR3/4-DQ8—What’s the risk?

Of people who have T1D, approximately 40% have the DR3/4-DQ8 genotype, as compared to 2.4% of the general population (2). If a child is DR3/4-DQ8, the risk of developing diabetes is between 1 in 15 and 1 in 25, as compared to 1 in 300 for the general population (though by which age of diagnosis this risk is calculated at is unclear to me)(6). Patients with this genotype typically present disease phenotypes at an early age (within childhood). It’s likely that if you were diagnosed with T1D after childhood you probably do not have this genotype. However, having part of this genotype can increase susceptibility—95% of patients have DR3 or DR4 alleles, compared to ~40% of the U.S. white population (7).

Being recently diagnosed with T1D and having genotyping data from 23andme, I wanted to know if I could learn anything about my own genetic susceptibility. It looks like 23andme used to provide information on T1D susceptibility but probably got rid of it after issues with the FDA.

However, 23andMe genotypes many positions which are not included in susceptibly reports. This data can be accessed through the “browse raw data” tab, downloaded, and fed into other programs like Promethease to get more info. The quickest way to determine if an individual is DR3/4-DQ8 is to genotype two positions of the MHC-II locus: rs7454108 and rs2040410 (8). Presumably, this is because alleles are linked, so if you know the genotype at one position you can be reasonably confident of the sequence at neighboring positions (haplotypes). If rs7454108 is C/T then you are DR4 (8). 23andme doesn’t genotype rs2040410 but you can use a proxy SNP: rs2187668 (9). If rs2187668 is A/G or A/A you are DR3 (8). If you have both (DR3 and DR4) then you are DR3/4-DQ8 (8). These statements are summarized in an algorithm represented in Figure 4.  Disclaimer: this algorithm may not be correct, please consult the corresponding references for further information, and please let me know if I missed something.

The Barker et al. paper that describes these two SNPs (8) has no discussion on using these SNPs for identifying if an individual is homozygous for DR3 or DR4. However, I propose that these SNPs can be used to predict homozygosity for two reasons.

First, of 1,191 DR3/4-DQ8-positive individuals in the T1DGC, 94% were AG/CT (rs2040410/rs7454108) and 4.6% were AA/CT.

Second, DR3/4-DQ8-positive individuals in the British cohort were 87.4% AG/CT and 10% AA/CT, and in the DAISY all positive individuals were AG/CT.

In these cohorts, the CT genotype was always present for DR4 individuals, but the DR3 genotype was either AG or AA. An AA genotype at rs2040410 would predict homozygosity, but this is not the case in some of these cohorts (i.e. 10% DR3/4-DQ8 positive individuals were AA/CT in the British cohort).

Therefore, rs2040410 is not that great for predicting DR3 homozygosity. But the provided algorithm uses a proxy SNP (rs2187668) which seems to be better for predicting homozygosity (10).

Figure 4. A. Algorithm for determining DR3/4-DQ8 genotype from 23andme data. This chart is largely based off (8). The authors demonstrated that these two SNPs can be used to identify DR3/4-DQ8 individuals. However, they use rs2040410 for DR3, whereas this algorithm uses rs2187668. This is because 23andme doesn’t genotype rs2040410, but rs2187668 is a proxy SNP for rs2040410 (9). The percentage of individuals with this genotype is reported below (SNPedia, European ancestry). SNPedia uses the compliment for rs2187668 (i.e. if 23andme reports C/C than use G/G (as used here)). The heterozygous genotype is CT/AG (rs7454108/rs2187668). If the genotype is A/G for rs2187668 but not C/T for rs7454108 then the individual is DR3/X (~20%), and if rs7454108 is C/T but not A/G for rs2187668 then the individual is DR4/X (~25%), where X is some other DR allele (not DR3 or DR4). B. SNP sequence and corresponding alleles. Percentage of population taken from SNPedia. DRX is some other DR allele.

 

Interpreting the risk of individual alleles is complicated because HLA-II alleles seem to play a protective role. There are at least three alleles that seem to play a protective role against T1D: DQB1*0602, DRB1*0403, and DRB1*1401 (11). However, 23andMe does not genotype these positions and/or there is no information regarding these SNPs on SNPedia. Consequently, this leaves any protective role of SNPs out of the above algorithm.

After about ten months on the wait list, I finally met with a genetics counselor to discuss the genetics of T1D and the chance of my potential off-spring being DR3/4-DQ8. I learned, from a clinical perspective, the genetics of T1D is still very far in the research realm and therefore little can be said about the risk of the disease for my potential off-spring.

In her 20 years of being a genetics counselor, at a well-known university hospital, she has not once seen a T1D patient to discuss the genetics behind the disease. I told her about the SNPs from GWAS studies and she seemed unimpressed. She informed me that GWAS studies have not provided anything to genetic councilors yet, and she seemed suspect about the prospect.

Indeed, since one of the first publications on GWAS in 2007, I cannot find a clear example of it being applied in the clinic. However, this is still a very young field in scientific terms, and I imagine the results of GWAS will start to materialize within the years to come (if not in the clinic at least in the lab).

Nonetheless, I learned from my 23andme data that I am DR3/DRX, and that I inherited my DR3 allele from my father (he is also DR3/DRX, whereas my mother is DRX/DRX). My wife is DR4/DRX. If I understand correctly, this would mean that the probability of our off-spring being DR3/DR4 is 25%. This seems quite high.

 

References

1. Redondo, M.J., Jeffrey, J., Fain, P.R., Eisenbarth, G.S. and Orban, T. (2008) Concordance for islet autoimmunity among monozygotic twins. N Engl J Med, 359, 2849-2850.
2. Steck, A.K. and Rewers, M.J. (2011) Genetics of type 1 diabetes. Clin Chem, 57, 176-185.
3. Barrett, J.C., Clayton, D.G., Concannon, P., Akolkar, B., Cooper, J.D., Erlich, H.A., Julier, C., Morahan, G., Nerup, J., Nierras, C. et al. (2009) Genome-wide association study and meta-analysis find that over 40 loci affect risk of type 1 diabetes. Nat Genet, 41, 703-707.
4. Mehers, K.L. and Gillespie, K.M. (2008) The genetic basis for type 1 diabetes. Br Med Bull, 88, 115-129.
5. Noble, J.A. and Erlich, H.A. (2012) Genetics of type 1 diabetes. Cold Spring Harb Perspect Med, 2, a007732.
6. Rewers, M., Bugawan, T.L., Norris, J.M., Blair, A., Beaty, B., Hoffman, M., McDuffie, R.S., Jr., Hamman, R.F., Klingensmith, G., Eisenbarth, G.S. et al. (1996) Newborn screening for HLA markers associated with IDDM: diabetes autoimmunity study in the young (DAISY). Diabetologia, 39, 807-812.
7. Steck, A.K., Armstrong, T.K., Babu, S.R., Eisenbarth, G.S. and Type 1 Diabetes Genetics, C. (2011) Stepwise or linear decrease in penetrance of type 1 diabetes with lower-risk HLA genotypes over the past 40 years. Diabetes, 60, 1045-1049.
8. Barker, J.M., Triolo, T.M., Aly, T.A., Baschal, E.E., Babu, S.R., Kretowski, A., Rewers, M.J. and Eisenbarth, G.S. (2008) Two single nucleotide polymorphisms identify the highest-risk diabetes HLA genotype: potential for rapid screening. Diabetes, 57, 3152-3155.
9. Romanos, J. and Wijmenga, C. (2009) Comment on: Barker et al. (2008) Two single nucleotide polymorphisms identify the highest-risk diabetes HLA genotype: Diabetes 57:3152-3155, 2008. Diabetes, 58, e1; author reply e2.
10. Monsuur, A.J., de Bakker, P.I., Zhernakova, A., Pinto, D., Verduijn, W., Romanos, J., Auricchio, R., Lopez, A., van Heel, D.A., Crusius, J.B. et al. (2008) Effective detection of human leukocyte antigen risk alleles in celiac disease using tag single nucleotide polymorphisms. PLoS One, 3, e2270.
11. Baker, P.R., 2nd and Steck, A.K. (2011) The past, present, and future of genetic associations in type 1 diabetes. Curr Diab Rep, 11, 445-453.

 

[1] Writing “MHC II complexes” is redundant, as the C in MHC stands for complex, but I want to emphasize the fact that there is more than one MHC II and it’s not clear to me how to pluralize MHC II. Also using the phrase “MHC II molecules” can be confusing as a MHC II complex is composed of two protein molecules that come together to form a MHC complex.

Diabetes Diagnosis

For at least three months I had an insatiable thirst and dry mouth. Despite the gallons of water I was drinking on a daily basis, my thirst could not be quenched. Even with its five-star review on Amazon, Biotene mouthwash proved futile in alleviating my dry mouth.  Other maladies included: frequent urination, losing about 20lbs, flushed face, overall weakness, and tiredness. I attributed all of this to me just acclimating to North Carolina, as I had just moved from Michigan a few months prior.

A quick google search of these symptoms returns a diagnosis of diabetes. My fiancé had done this and suggested that I might have diabetes. I laughed it off because I tend to associate online self-diagnosis with hypochondriacs- people who, after searching for an explanation for their headache on WebMD, are suddenly dying of cancer.  Plus, diabetes seemed an unlikely explanation considering I exercise, eat well, and have no family history of the disease.  But my symptoms matched, which lead me to the ultimate test—measuring my blood glucose concentration. This can be done by purchasing a glucometer at a pharmacy. So I went to a Rite Aid after dinner one night and purchased a glucometer. I figured the box would contain everything I needed, but it lacked the glucose test strips (which cost ~1.30$ each). It was already late (~11:30pm) so I went to sleep and planned to try again tomorrow. On my way to work the following morning, I stopped at a CVS to buy some glucose test strips. You have to buy strips specifically made for your glucometer. In the glucometer aisle I could not find any test strips, but did find the glucometer I had purchased the night before with 10 “free” test strips included. So I repurchased the meter just so I could get the test strips. Little did I know at the time that the test strips are sold behind the counter in the pharmacy. I went to my car and tested my blood glucose. The glucometer read 420 mg/dL (milligrams per deciliter) so I googled the normal range (80-120 mg/dL). Also I picked up ketone test strips while at CVS. When your cells can’t absorb glucose because you have no/low insulin, the cells start to metabolize fats and proteins, the products of which are ketones. Thus, the presence of ketones in the urine can be measure of a diabetic state. A high blood ketone level is dangerous. Ketones are a weak acid (pK_a ~4) and lower the pH of your blood leading to changes in protein structure and hence function. This is called diabetic ketoacidosis (DKA). The symptoms include nausea, vomiting, fatigue, confusion, difficulty breathing, and can escalate into a diabetic coma. The internet said if high blood glucose and high urine ketone levels I should go to the emergency room (see figure). I called my sister, who is a nurse, to confirm this course of action. She indeed did, and I drove to the nearest ED (emergency department) (what they call it now-a-days).

I went to WakeMed Emergency services on April 5^th 2016. Upon admittance to the ED, point of care blood glucose taken and measured to be 377 mg/dL. I was then hooked up to an IV for hydration. Blood was also drawn for labs. A test of ketones within the urine would reveal a measure of 4+ (no units, but apparently this is the highest number on their scale). The lab results were never shown or discussed with me, even after asking the nurse if I could see them he told me in his shitty little southern accent they would be online in “my chart” (two days later the results would appear online).

Katherine was the PA seeing me and after some reflection on my visit I think she needs training in the diabetes field. She is a nice and personable women but the way she handed my situation is alarming. Furthermore, her ability to communicate medical-related information is poor. For instance, when asked what was in the IV drip bag she responded “Fluid”. I responded with confusion: “Fluid?” hoping to get a little bit more information but all I got in response was “Yes, fluid”. This is of course an absurd response, it’s like saying the bag is filled with liquid. Even more her descriptions of Type I and II diabetes seemed opposite of what I had just read while waiting (ketones in the urine is more common in type 1 diabetes-ADA). Which leads me to her diagnosis: she suggested I had Type II diabetes and that I should take metformin (oral pill). What evidence she used to come to this conclusion is a mystery. She also told me that if any doctor tries to give me insulin that I should go to a different doctor because that is the last thing I should do. This statement is the complete opposite of what I needed at that time. She was dangerously wrong.

Apparently confident in her diagnosis, she allowed for my discharge with a blood glucose level of 283 mg/dL and 4+ ketones (see image for ketone level accessed in bathroom after being discharged). Katherine’s incompetence should have been caught by the MD in charge. I did not talk to a MD while in the ED but according to” MyChart” (online records) the doctors who share responsible for this dangerous misdiagnosis are Toni and Eduardo. Their lack of oversight cannot be explained away by being too busy as the ED was almost vacant during my stay.

The following day I met with my primary care doctor, not an MD but a nurse practitioner (NP). My fasting blood glucose was in the 300s mg/dL and I still had ketones in my urine. They also drew blood for labs and he informed me that I did have diabetes and that the symptoms are more consistent with type 1. But he said I need to see an endocrinologist so they can diagnose me. So he gave me a referral to an endocrinologist. I met with the lady who does the referrals and the quickest one she could get me was 34 days away. However, I had to take a diabetes class and she could get me in the next day.

In conclusion, my NP thought that I didn’t have type II, but still kept me on a prescription specifically for type II diabetes, in fact he increased my prescription two-fold. Metformin does nothing for a person with type 1 and in fact can have side effects. Additionally, he had evidence that my blood glucose concentration was high for at least 2 months because my A1C level was off the charts. I remember this specifically because he told me that my A1C was at least 14. I asked 14 what? He said that’s a good question let me look. It’s percent. This means at least 14% of my hemoglobin was glycosylated. He also knew that my ketones levels in my piss were still high too. So what did he do, pass me off to the referral lady to make an appointment 34 days away. If he cared for my health he would have tried everything he could to get me in as soon as possible to the endo and/or told me to go the emergency room. There is one other option, he is incompetent.

The diabetes class was at the endocrinologist and I figured it would be filled with 20 people and include vague statements about diabetes. However, it was a one-on-one meeting with a RN, and when I arrived she informed me that she told the doctors that I need to be seen immediately. She had reviewed my labs and decided I needed medical attention immediately. They also took my blood glucose (~300 mg/dL). Two doctors came in and told me to go to the emergency room immediately and that they will admit me for monitoring because I was in DKA. They also informed me that I did indeed have type I diabetes and that I need insulin. So they gave me a shot of ten units of Humolog (fast-acting insulin). For some reason doctors and nurses like to call the insulin by the trade/brand name, which just confuses new patients because there are multiple companies. The doctors told me to go to Duke University hospital and that I cannot drive myself. One endocrinologist told me she called ahead to the endo team there and told them the story and that I would meet with some of them. This would turn out not to be true. Luckily I had a friend visiting who could drive me. The doctors seemed pretty concerned that in my previous visits with health professionals they did not take the correct course of action.

At the ED I was set up in a room and hooked up to an IV. My friend stayed with me, so despite waiting about three hours for a doctor to see us I had company. We saw one doctor doing her residency, the emergency room doctor, and then two doctors from internal medicine. After nearly five hours and four doctors using their stethoscopes to listen to my heart and lungs, I was admitted into the hospital. The time was probably around 8pm, and I had not eaten since about 11am. Combined with 10 units of fast acting insulin my blood glucose dropped to 74 mg/dL. I asked the nurse if I could eat and she said yes. So my buddy got us veggie foot-longs from subway, which was in the hospital. Before eating I told the nurse that I would be needing an insulin shot. About an hour later my blood glucose was taken and was still high so an additional two units was administered via syringe injection into my subcutaneous fat layer. Blood glucose measurements would be taken every hour throughout the night until 5am, when it stabilized.  This is important to assess my response to insulin, as too much insulin can lead to hypoglycemic state and passing out. At 6am I awoke to Dr. Blood’s cold beady eyes. He wanted a listen.

The next day in the hospital came with a new nurse. She apparently was the diabetes specialist among the nurses, as told to me later by one of her colleagues. This was a surprise to me as I had to call her three times: to take my blood glucose before my meal, to take insulin before my meal, and to take my blood glucose two hours after my meal. She did not tell me to do any of this I had just read it in the book they gave me. Which suggests a less competent person would have done none of the above and continued with chronic high blood glucose in a hospital setting-what a joke. Sure my nurse may have been really busy and forgot to relay this info to me, but given that she told me the most banal anecdote about her friend who was low (hypoglycemic state) and ran a stop sign on a bike in front of a cop, so that he could get to his glucose tablets quicker, suggests otherwise (not to mention her telling me about the little kid movie Frozen).

After meeting with another diabetes teacher and eating lunch I was able to leave. I headed to a Walgreens pharmacy to pick up my prescriptions, which included long-acting insulin (Tujeo)) to be taken every night before I go to sleep, fast-acting insulin (Novolog) to be taken before every meal, emergency glucagon to be administered by someone who finds me passed out, needles, alcoholic wipes, lancets, and glucose test strips. A two-month supply of insulin costs me $40, however without insurance it would have cost $900.

With my prescriptions in hand, I started my new life of at least four injections a day and constant blood glucose monitoring. This may sound depressing but I feel much better compared to how I was feeling the previous three months before insulin treatment.  My energy and thirst returned back to normal. I was seriously addicted to water; the first drink was always so pleasurable. It reminded me of what this comedian once said, and I’m paraphrasing: I feel bad for people who aren’t addicts because they will never know the joy of getting something you crave over and over again. Additionally, reducing life to small pragmatic problems, like how much insulin to inject before each meal, gives me a weird sense of purpose, no matter how trivial.

Although it may seem like I’m just putting people down throughout this piece, probably to make myself feel better, I like to think holding medical professionals to high standards is a good way to select for the best. If you suck at being a medical professional just stop because people’s lives are at stake. The best way to know if you suck is if people tell you. I don’t expect anyone to adhere to this advice but it just feels good to write.  I have sent an email compliant to Wake Med describing my experience and calling out the PA and doctors, but all I have received are emails and phone calls asking me to pay my bill (notice not contacting me to see how I am doing). In contrast, Duke has sent me multiple feedback surveys.  Since this was my first real interaction with medical professionals I was naive and hesitant to speak up, one reason being out of fear of embarrassing them (i.e. asking a question they didn’t the answer to). After going through this experience I will be more respectfully forthright and I call on you to do the same.

 

Some interesting facts about Type 1:

-Type 1 diabetes is an autoimmune disease. My immune system is killing my insulin-producing Beta cells, housed within the islet of the pancreas.

-50% of people diagnosed with type 1 are diagnosed after 18. (JDRF)

-80% of people diagnosed with type 1 have no family history. (JDRF)

-Identical twins have identical genes. Yet when one twin has type 1 diabetes, the other     gets the disease at most only half the time. (ADA)

-You inherit a predisposition to the disease then something in your environment triggers it. (ADA)

-The environmental trigger(s) is(are) unknown but some hypothesize viruses. (ADA)

-Type 1 diabetes develops more often in winter than summer and is more common in places with cold climates. (ADA)