Here, queer, pain is moderate to severe

The poem frames "him" as subordinate in several ways, not just to the narrator ("i fuck him on the floor": not that getting fucked is inherently subordinating, but the narrator has all the agency in the phrase, "he" doesn't decide what happens or where) but also to "his wife". She has filled the house with chintz, meaning it wasn't his decision or his actions. "Filled" is also a choice of words that suggests that there is no space for him in the home: the only place left for him, not already filled, is the floor. To me this framing invokes the trope of the henpecked husband, whose wife has taken dominion over the home and who has ceded its control to her because it, as the domestic space, is "supposed" to be hers.

This trope, of course, is misogynist in its normative rendition: it reinforces gender essentialism, it erases the significant material benefits such "henpecked" men derive from the domestic labor of their spouses, and it dismisses women's expressions of suffering and attempts at negotiating terms for their relationships as "nagging." In the narrator's dismissal of the wife's possessions as "chintz" (frivolous, feminine, contrasted with what is "real") we can see this same misogyny at play.

The narrator's misogyny, and the central fact of the poem which is that the husband is getting fucked by someone other than the wife, quite possibly flip the power dynamics of the poem on their heads. The wife is now subordinated: both by her social marginalization based on gender (a marginalization which drives her into the home and confines her there, like OP so cogently points out! As "he" has run out of room in the home and can only get fucked on the floor, so has she run out of room socially; the only place she can control and make decisions like filling it with chintz is the home), and by the narrator who is fucking her husband in her home.

There's an additional dynamic in reading the narrator as male, which most readers seem to have done: it invokes the particular, bitter misogyny that men-loving-men sometimes direct at women expressing femininity. There's an envy to it, of course--straight and straight-passing women get to (are forced to) express desire for men, have sex with men, marry men, love and be loved by men. His wife gets to be his wife: the narrator gets to fuck him, in their home. Straight and straight-passing women also get to (are forced to) perform femininity: they can buy chintz and decorate with it, without being devastatingly punished for it like people presumed to be men are from the time they're babies. The envy mixes with misogyny to produce disdain, disgust, dismissal. We can read the narrator fucking him on the floor of their home as an expression of power and dominance (again, not that the fucking has to mean the narrator is topping, or that topping is inherently dominant, but the phrasing is stark: "i fuck him", the narrator acts upon him as an object/recipient), not just over him but over the wife in absentia as well.

Noting that "to keep it real" is AAVE, we can also introduce race as a potential lens; is the narrator, despite their dominant language, subordinated based on race in this dynamic? Is the narrator not just claiming a dominant role, but perhaps also stereotyped and limited into it as a Black person? Is the disdain of the chintz also an expression of class difference, of a rejection of the display of white wealth on the part of the wife? This is pretty speculative, of course: the use of AAVE could also be appropriative, which would suggest another tactic by the narrator to lay claim to masculinity and toughness, since non-Black people often use AAVE to try to invoke racist stereotypes of strength, violence and resilience.

I think one of the things that makes the poem so compelling for being so short is the struggle at the heart of it, this complicated jostling for power between three people and their actions over time (the wife "has filled" the house, in the past: the narrator fucks him in the present, perhaps in the habitual). Who controls the house? Who controls "him"?

Sliding in with this at the tail end of Mermay...

You usually see octopus mermaids with the torso the other way, but a friend pointed out that octopi have their beaks amid the tentacles, and I thought it'd be fun to play with. Imagine being welcomed into an embrace by all those limbs.

Prints available on Inprnt!

I was originally planning on holding off sharing this until June, but then decided to hell with that; why wait?

FURTHER RESOURCES:

Intersections: Indigenous and 2SLGBTQQIA+ Identities – this booklet from the Native Women’s Association of Canada is more intended towards 2S folks, but is still a great read for anyone.

Two Spirits, One Voice – This video from Egale is a great, no more comments needed.

A Two-Spirit Journey: The Autobiography of a Lesbian Ojibwa-Cree Elder – This book by Ma-Nee Chacaby can be a difficult and emotional read, but very much worth it.

Becoming Two-spirit: Gay Identity and Social Acceptance in Indian Country – I have yet to read this book by Brian Joseph Gilley myself, but heard positive things about it.

If you wanna support an Indigenous LGBTQ+ artist who is very much relying on any and all shop orders and freelance art opportunities to pay their bills, consider checking out my online shop!!! I'm running a 20% off sale on everything!! Just click the link below and/or use the code "GAY" at checkout!!

a world without trans people has never existed and never will

a world without trans people has never existed and never will

Image 1: response by Doll Face (@ Smoke_nd_pearlz) "In 2012 i was diagnosed with a deadly blood disorder known as TTP. I was in the hospital for a month. A white nurse almost killed me because she thought i was drug seeking. I kept telling her my central line in my groin was hurting& she wouldn't give me any morphine just Tylenol.

I went septic later on that night because of the central line. I went into SVT and had to go to cardiac ICU for a week. I was 18. My TTP flared up again in 2016 and i went to the ER. I told the (white) doctor that i had TTP and that i needed to be admitted. He had my records right in front of him. I was just there 4 years earlier, the same hospital diagnosed me.

He told me that i didn't have TTP...i had ITP. He sent me home with steroids and pain meds. I cried and cried and sat at home all weekend until i could get to my hematologist. I called them and they had me come in immediately. Got labs drawn...my hemoglobin and platelets were VERY low. They did a direct admit: I had to get 14 bags of platelets and 3 bags of blood. My hematologist and his NP told me if i would've waited any longer i would've died.

More recently in 2022 i went to a freestanding ED because i thought i had the flu. I was in pain, my blood pressure was elevated, i had a fever. I told the black NP that i have TTP and asked them to do a cbc and ADAMTS13 level if they could. I got pain meds, waited for the (white) doc to come and see me. He told me ny labs were "fine" and that i just had a stomach virus. I didn't believe that so i asked him what my platelet count was. He told me 30k (normal platelet count in non chemo patients are 150k-400k) i almost lost my shit on him.

He went back and further with me for 10 minutes about how i wasn't having a TTP flare up and i told him to call the fucking hospital that I'm usually treated at and find me a bed. He begrudgingly did it. He came back not even 10 minutes later and said that the hospital i usually go to was full (it was around Christmas time) but after the on call hematologist at the level 1 trauma center downtown saw my blood work they wanted me to come in IMMEDIATELY. Hematologist told me if i would've waited any longer i would've been dead before Christmas.

Every time that I've almost died it was either at the hands of a white nurse or doctor. They don't take our pain or complaints seriously! They think we are drug addicts. I literally became a nurse because of this. We need black doctors. That lawsuit is just a bunch of fucking racists who are mad. Fuck them."

Image 2: response by Emmanuel Felton (@ emmanuelfelton), "A peer-reviewed study found Black patients matched with Black doctors were 27% less likely to die in the hospital. A separate study found Black residents live longer in counties with more Black primary care physicians. "Find A Black Doctor" exists because the disparities are real"

There's a lot of confusion about different "poxes" in this post (which wasn't my intention, and now I feel bad), so here's a general overview (also, obligatory apology for messiness, this was written at like 1 AM):

Smallpox:

Smallpox, caused by variola virus, was a massive problem historically. It existed in the Western hemisphere for thousands of years (genetic evidence of smallpox has been found in Egyptian mummies from ≈1500 BCE, but it was probably around long before then), and it was introduced to the New World during the Columbian exchange, which had devastating consequences for indigenous populations (which were already suffering from colonialist violence, which made epidemics much worse than they already would've been). Historically, smallpox had a case fatality rate between 30-50%, and survivors were often left disfigured or permanently disabled (you've probably seen pictures of smallpox scars, but smallpox can also cause blindness and other complications). Importantly, smallpox only affects humans—it has no animal hosts—which is why it's one of the few infectious diseases to have been completely eradicated. As of May 8, 1980, it officially no longer exists outside of certain designated American and Russian laboratories. (There are, however, concerns that it could be used as a bioweapon, which is why the government still stockpiles smallpox vaccines and antivirals. I wrote my bioethics term paper on this exact issue, and incidentally, it's one of the major reasons why I believe that STEM majors should take ethics courses!)

There were two strains of variola virus: variola major and variola minor. Variola major was much more dangerous, with a much higher mortality rate; variola minor typically didn't cause severe disease. Fortunately, infection with one strain conferred immunity against the other. Both strains are now eradicated. (People sometimes confuse variola minor with other viruses like cowpox and horsepox, but they're different things.)

There were four clinical forms of smallpox: ordinary (classic smallpox, associated with the rash you usually see in pictures), modified (less severe, often occurred in vaccinated people who got infected anyway), malignant (caused a flat rash instead of the usual pustules, associated with immune dysfunction, almost always fatal), and hemorrhagic (caused severe bleeding, and also near-universally fatal.) All of the non-ordinary forms could be difficult to diagnose because they looked so different from typical smallpox. The less serious "modified" form was often confused with chickenpox, and the hemorrhagic form was sometimes assumed to be a completely different disease. Occasionally, historical sources will refer to hemorrhagic smallpox as "black pox," with or without an understanding that it's caused by the same virus as ordinary smallpox.

Other relevant viruses:

Cowpox, caused by cowpox virus (an orthopoxvirus similar to smallpox) causes mild disease in cows, humans, and several other animals. Infection with cowpox virus confers immunity to variola—Edward Jenner noticed this relationship and used material from cowpox lesions to inoculate people against smallpox.

Vaccinia virus, another orthopoxvirus, is the source of the modern smallpox vaccine. It's closely related to both cowpox and horsepox (weirdly, it's actually closer to horsepox), but it's distinct enough to be its own species. Infection usually causes mild symptoms, and, of course, confers immunity to smallpox.

Chickenpox is an entirely different thing. It's caused by the varicella-zoster virus, which is a herpesvirus, not a poxvirus at all! Infection with varicella-zoster does not confer immunity to smallpox or any other poxvirus—chickenpox is from a totally different family.

So why are the names so weird and confusing? Why is everything about all of this so weird and confusing?

There are multiple reasons for this, so bear with me.

Historically, a "pox" was any disease that caused a bumpy rash of pustles/blisters. Chickenpox, smallpox, and the other "poxes" all cause superficially similar rashes—thus the similar names. (Even though we know now that chickenpox comes from a completely different family, this wouldn't have been apparent before the dawn of modern medicine.)

Smallpox was given that name to differentiate it from syphilis, which was known as the "great pox" when it first appeared in Europe. (Fun[?] microbiology fact: There are debates about the origins of syphilis, but the most common theory holds that it originated in the New World, and Christopher Columbus brought it back to Spain. In that way, it's kind of the inverse of smallpox.) Historically, smallpox was also known by a variety of other names in different European, Asian, and African cultures. Again, this gets murky, because historical physicians sometimes struggled to distinguish between similar-looking-but-different diseases.

Other poxviruses are often named after the animals in which they were first identified. This is not a hard-and-fast rule, though, and it can sometimes be misleading (for example, monkeypox virus was first discovered in laboratory monkeys, but it more often affects rodents and other small mammals. The disease formerly known as "monkeypox" was recently renamed "mpox" because the name wasn't accurate.) Also, some poxviruses aren't named after animals at all! It's a weird and inconsistent system (but a lot of virus names are kinda weird and inconsistent).

Related to the above: We don't even know where the name "chickenpox" comes from. I mean, we know it was called a "pox" because it causes a pox-y rash, but we don't know where the "chicken" part originated. There are multiple theories about this, none of which are definitive. The disease itself has nothing to do with chickens.

Basically, a lot of the weirdness is a result of historical naming practices—people identified and named these diseases before modern virology existed, and those names stuck, so now we have similar names for superficially-similar-but-ultimately-different viruses, and names whose origins have been completely lost to time. Later, virologists muddied the waters further by naming newly-discovered poxviruses after the animals in which they were first seen, even when these animals aren't natural hosts or reservoirs of those viruses. It's a mess! And, again, all of this is complicated by the fact that some of these diseases were very hard to diagnose (or distinguish from one another) before modern medicine existed. Now, we can sequence viral DNA and figure out what's actually going on—which viruses caused which symptoms, whether those viruses were closely related, and whether being infected with one disease conferred immunity to another—but historical doctors and scientists didn't have those tools, so they were doing they best they could with very limited information, and that led to a lot of weirdness in terms of how these viruses were named and classified. Our current system inherited some of that weirdness, so here we are.

TL;DR: Poxvirus names are messy. Smallpox is caused by variola virus, which has two strains: variola major (the more severe one) and variola minor (less severe). Cowpox and vaccinia are different viruses in the same family, and being infected with one of them confers immunity to smallpox. Chickenpox isn't a poxvirus at all, but a herpesvirus—it just happens to cause a pockmark-y rash that looks superficially similar to smallpox pustules (and mild forms of smallpox were historically confused with chickenpox).

(P.S. none of this is super relevant to the average person, so don't feel bad if you didn't know any of it. Unless you are a history major inventing new conspiracies about smallpox, in which case you definitely should feel bad.)

Sources & further reading under the cut!

Here it is:

Imagine, if you will, a queue of people who have lost children, parents, siblings and friends to smallpox. People who don't really understand how the vaccine will save them but don't care, because it'll mean they never have to grieve another smallpox death again.

Upstairs in Jenner's house there is a framed certificate from the World Health Assembly that declares the total eradication of smallpox. When was this momentous event, you ask? 1980.

these are all really good and important things to be aware of and I recommend gathering that info for any new meds. i don't say this to like, blame people who were not given this info by their doctors and who took meds without being given this information, but rather to give people resources for being more in control of their own medical treatment going forward 💜

CYP450 is a family of enzymes in humans. enzymes are chemicals that speed up chemical reactions; in this case, in our bodies, CYP450 enzymes process the vast majority of currently available medications. because of that, they're responsible for most drug interactions.

different substances - including medications, supplements, and even foods - can affect the CYP enzymes in different ways.

a CYP inhibitor blocks the CYP enzymes from working to process the medication. that means you can end up with more of the medication in your body than you expect. that can cause mild, moderate, or severe side effects. good examples of CYP inhibitors are St. John's wort, grapefruit, and isoniazid (a tuberculosis medication).

a CYP inducer encourages the CYP enzymes to work faster. that means you can end up with less of the medication in your body than you expect. that medication may not work as well. this can be especially dangerous in cases where, for example, you're suppressing a dangerous effect (like autoimmunity or transplant rejection). some examples of CYP inducers are insulin, tobacco, prednisone, and in some cases, St. John's wort again.

a CYP substrate is just a substance/medication that is affected by an inhibitor or inducer. birth control is a very common substrate, and its effectiveness is affected by many medications.

each substrate is related to a different family of CYP enzymes, like CYP3A4 or CYP2D6. each one responds to different inhibitors and inducers.

you can see why they often don't tell patients this stuff: It is complicated. this is pharmacokinetics! it's difficult stuff. but i really, really believe it's important. knowing how your medications affect each other can save your life. doctors and pharmacists often do not check medication interactions. sometimes it really is up to us to understand what we're putting in our bodies.

at the very least, i urge you to check drug interactions with the drugs.com interaction checker. this checker automates some of the work of cross-referencing CYP relationships. if you have an account, you can save your drug list and cross-check all of your meds at the same time. keep in mind that not all "severe" interactions will necessarily apply to you; i recommend reading the "for professionals" version of the warning to make informed decisions about whether or not you want to be concerned. (this is also something you can discuss with a good doctor if you have the good fortune to have one.)

but, if you have the capacity, at a certain number of medications (i am taking 20+) it really is worth getting to know how they interact with CYP enzymes, what effects you might need to be watching out for (more intense effects from a higher concentration of medication? less intense effects as the medication can't attain high enough concentrations to work as it normally does?), and what meds might be the culprits of new problems as you add more medications.

to cross-check CYP relationships directly, i recommend the flockhart table. search for a medication (ctrl+f helps) and you can see all its documented CYP relationships. (they also have a mobile friendly version, but i find it slightly harder to interpret.)

here's how i do it.

start with a medication or substance. let's say i'm about to start celecoxib (Celebrex), a non-steroidal anti-inflammatory drug (NSAID). on the flockhart table, it's listed as an inhibitor of CYP2D6. (ctrl+f is helpful here.)

think through what the words mean. it's an inhibitor, so it makes the enzymes not work as well. it might increase blood levels of medications that are processed by CYP2D6.

what medications are processed with that enzyme? the flockhart table lists them if you click on the name of the medication you're curious about. CYP2D6 substrates include amitriptyline (Elavil), aripiprazole (Abilify), atomoxetine (Strattera), duloxetine (Cymbalta), oxycodone (Oxycontin), and propranolol, among others.

what effects do i need to be watching for based on the affected medications? for an inhibitor, we're looking for stronger effects; for an inducer, we're looking for weaker effects. let's say i take oxycodone daily. i want to keep an eye on the way i feel when i take oxycodone. am i feeling "higher" than usual? am i feeling dazed or dizzy or numb? or let's say i take propranolol. am i feeling dizzier or more lightheaded? am i having nightmares that i wasn't before?

here's another example. what if i want to check for a substance that might not be listed on the flockhart table? grapefruit is a good example.

wikipedia is actually a great source for this (though in some cases i recommend just searching "[substance] CYP" and seeing what pops up).

head to the list of CYP450 modulators on wikipedia. ctrl+f finds three instances of grapefruit: naringenin (a CYP1A1 inhibitor), generic 'flavonoids' (inhibiting CYP2A6), and bergamottin (a powerful CYP3A4 inhibitor).

think through what the words mean. any substrate medications processed by 1A1, 2A6, or 3A4 enzymes might be dangerously increased in my bloodstream if i consume grapefruit (or anything containing those substances; earl grey tea actually contains bergamottin, too!)

what medications are processed with those enzymes? this i can check on the flockhart table, or i can stay on wikipedia. atorvastatin - a cholesterol medication - is a substrate of 3A4. so is diazepam (Valium). valproic acid, an anti-seizure medication, is a substrate of 2A6. i'm having more trouble finding substrates of 1A1. it's not listed on the flockhart table. there is a paper published that mentions theophylline (an asthma medication) and difloxacine (a fluoroquinolone antibiotic).

what effects do i need to be watching for based on the affected medications? at a glance here, i'd be worried about having too much valium or valproic acid in my system (if i took those meds) - those could have pretty serious effects on my central nervous system. likewise, having too much of that fluoroquinolone antibiotic (if i took it - and i wouldn't, because if you have hEDS you should not take fluoroquinolones unless it's a matter of life or death!) could increase my risk for serious musculoskeletal side effects like tendon rupture. it could also disrupt my bacterial microbiome.

the physician who created the flockhart table, the late dr. david flockhart, was an exemplary physician who truly, truly cared about patients - a rare treasure. everyone's CYP-related genes are different, and it affects the way we respond to medication. we know that, just as we know that CYP relationships can cause serious and harmful drug interactions. but we don't put it into clinical practice. dr. flockhart wanted to change that, and he did pave the way towards that future. we're not there yet. but i do recommend his table.

i hate that this is not something that is widely taught and widely understood. i hate that we have this knowledge about how people metabolize drugs and how drugs work with each other and we often just do not talk about it at all. i hate that i was not instructed on the risks of taking clonazepam (a benzodiazepine, in the same class as Valium) and hydrocodone (Vicodin, an opioid) simultaneously. i experienced central nervous system depression - difficulty breathing, dizziness, confusion, fatigue - multiple times as a teenager before i figured out that i shouldn't take them close together. needless to say, mixing those two drug classes can be extremely dangerous. i got lucky and just felt awful. but at certain doses or under certain circumstances, taking those two simultaneously could kill someone. Does kill people, in fact!

a responsible doctor - one of my favorite doctors! - prescribed me those medications. he just wasn't thinking. it happens all the time.

we should not have to be doing all this work. but often doctors and pharmacists simply do not think about it. and the literature they hand out with medications, while helpful, is not going to cover all possible interactions, especially for polypharmacy patients or people on unusual medications.

likewise, you should know what medications interact with your conditions - like i mentioned fluoroquinolones and hEDS earlier. or how morphine tends to activate mast cells. that's something i can't cover here, though.