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it was also an impromptu cover up too but i’m so happy with it

what i CAN do, however, is make my own post and hope to fuck that people see it, because i think it's important to understand how medications like ozempic work if you want to correctly fight back against people who think "everyone should take it." i'm not gonna put this under a readmore, because i've seen folks say they don't work well with some screen readers, and i want it to be as accessible as possible. but it is pretty dang long, just as a heads up - there's a lot of information that felt important to include. so, without further ado-

what is ozempic, exactly?

ozempic is a brand name of semaglutide, which is a GLP-1 agonist (not a GLP-1, nor a GLP-1 inhibitor). wegovy and rybelsus are other current brand names for semaglutide - ozempic and rybelsus are primarily marketed for managing type 2 diabetes, and wegovy is primarily marketed for weight loss, but they are all the same drug.

GLP-1 is short for glucagon-like-peptide-1, and is an endogenous peptide hormone - which, in simpler terms, means it's a protein (peptide) produced by your body (endogenous) to relay a signal to one or more organs (hormone). GLP-1 specifically is released when you eat food, and does a few different things. GLP-1 agonists are molecules that bind to the GLP-1 receptors, and produce the same effects. you can't just take GLP-1 itself the way you can just take (for example) insulin, because GLP-1 doesn't last very long - it gets broken down by a specific enzyme within a matter of minutes. so, GLP-1 agonists are molecules that do activate the receptors, but aren't broken down by the enzyme, and thus have longer-lasting effects.

okay, so what does GLP-1 do?

GLP-1, like i said, does a few different things, and GLP-1 receptors are found in a lot of different places! like... literally all over your body, and we're still finding out new things that it does. there's actually been some very cool studies that have found that its presence in the brain may help protect against things like parkinson's, alzheimer's, and TBIs. but that's all very new stuff and also not what we're here for - there's three main things it does that are relevant to this conversation.

first, because it is easiest to explain: it makes you feel full! when you eat food, and you're not hungry anymore? that's GLP-1, babey! (that's an oversimplification and there are a lot of factors that go into when you feel hungry and when you don't. they've actually done a lot of studies on the different satiety values of different foods, and it's really interesting stuff! if you constantly feel hungry even after eating, you might need to change up what you're eating and get in more foods with a high satiety value). but, this is the primary reason it causes weight loss - if you feel full, you're not gonna eat. this is also one of the obvious reasons you shouldn't give it to "everyone." tons of people already don't eat enough! and i don't think "well if they wouldn't eat anyway, isn't taking away their hunger better than making them suffer through it" is a good solution to issues like eating disorders and food scarcity (yes, i have seen that suggested).

the second thing it does is inhibit acid secretion in the stomach, stomach motility, and gastric emptying (i.e. food moving from your stomach into your intestine). this also contributed to a feeling of fullness, and in a generally healthy person who is not taking a GLP-1 agonist, this effect doesn't last long (because, as you may recall, GLP-1 is broken down pretty quickly). if you are taking a GLP-1 agonist, though, it can last a lot longer, which is the main reason some people get nausea and other gastrointestinal side effects. but! this is really dependent on both your dosage, and your own body, and not everyone is going to have these side effects - lots of people don't notice much of a difference. there are also people who naturally have too much gut motility, which can cause major problems like not absorbing enough nutrients from your food or not processing oral medication correctly. for those people, GLP-1 agonists would actually be really helpful for digestion!

please note that "decreased stomach motility" is not the same thing as "partial gut paralysis." gut paralysis is a wholly separate medical condition, whereas this is literally just a normal thing your body does, but made to last longer than it usually would.

before i get into the third thing it does, i wanna make sure we all understand The Very Basics Of Diabetes (since this is, after all, a diabetes medication). when you digest food, sugar is moved from your digestive tract into your bloodstream. in someone without diabetes, that increase in blood sugar triggers the secretion of insulin from specific cells in your pancreas, called beta-cells. insulin starts off a chain reaction that gets the sugar from your bloodstream to your various organs, which is important, because at a biomolecular level sugar is just energy (and your organs need it to do things).

in diabetics, something in that process doesn't work right. the current understanding of type 1 diabetes is that it's an autoimmune condition in which your own body destroys a bunch of its beta-cells (typically around 70-80%, and it varies from person to person, which is why different people experience symptoms at different ages). since there aren't enough beta-cells producing insulin, your body needs added insulin to kick off that chain reaction. the current understanding of type 2 diabetes, on the other hand, is a metabolic syndrome primarily caused by genetics. your pancreas is working fine, and producing all the insulin you need, but the insulin receptors on some of your organs stop working (this is called insulin resistance), so they still aren't getting the sugar they need. your pancreas, in turn, ramps up insulin production, because your blood sugar is still high. after a while, your pancreas will start to sustain damage from being overworked, with up to a 50% decrease in function. (in theory, this is what "prediabetes" screening is supposed to prevent, but uh. it doesn't really correlate as well as we would like). the main reason that type 2 diabetes is associated with Being Old And Fat is because it can go for a long time undetected, so it's more likely to be diagnosed in older people, and because there's a high correlation between being fat and insulin resistance (last i looked into it, causation between the two is unclear), and higher insulin resistance means your symptoms become severe (and diagnosable) faster. let me make one thing very clear here. TYPE 2 DIABETES IS NOT DIRECTLY CAUSED BY BEING FAT. there are thin people who have it, and fat people who don't - unexplained weight loss is even one of the main symptoms to watch out for, because if your body can't process sugar, it starts burning fat (this is the basis of the keto diet. i'm not getting into that though, or i'd be here all day).

there's also gestational diabetes, and diabetes secondary to other conditions (like pancreatitis), but that is beyond the scope of this tumblr post. the main point here is Diabetes Is When Your Insulin-Blood Sugar Process Is Borked. which brings us to the third main thing GLP-1 does:

it triggers the secretion of insulin! in non-diabetics, you eat food, your body makes GLP-1, and while you're digesting that food, the GLP-1 is cozying up to the pancreas and getting it to release insulin for all that sugar that's entering your bloodstream. but! it also, very cool, prevents beta-cell exhaustion and increases beta-cell mass! since both main forms of diabetes involved beta-cells dying off, you can see where having a GLP-1 agonist to increase this effect would help with that. (it also does some other things that help with diabetes, but i will fully admit here that i don't understand those ones as well. i could probably figure it out with a deeper dive, but this is a basic overview post, not How To Become An Expert On Ozempic).

so, GLP-1 makes you feel full, slows down your digestive process, and helps with insulin production, and GLP-1 agonists do the same things but for longer. there's also other effects we're still studying, some of which seem really beneficial! but since we're still studying all the effects, there may be drawbacks we don't yet know about, and there are documented side effects that some people experience on semaglutide. there are also clear contraindications - anyone who struggles to eat enough as-is, anyone who already has low gut motility, and anyone who overproduces insulin (plus other, less obvious contraindications - ideally, a doctor familiar with your current health would be able to help you with that. ideally.) so no, not everyone should take ozempic.

but it's not an evil poison, either! it's a medication, and if it can help you address a problem, you should take it. sometimes that does mean weight loss, too - i know someone who gained a lot of weight after an injury that caused them to be unable to exercise (or even walk much) for two years. now, they've reached a point where they need to be able to exercise to strengthen their joints, but the extra weight adds so much strain that most exercise damages their joints instead. this person also has hypermobility, which is absolutely exacerbating the issue, but there's not really a fix for that right now. the point here, though, is that being fat is not inherently unhealthy, but there are genuine medical reasons why someone might need to lose weight.

wait, what does this have to do with gila monsters?

ah, yeah. that. someone on the post that inspired this all claimed that ozempic "partially paralyzes your internal organs," and someone else said that's because semaglutide is synthesized from gila monster venom, and that "black market ozempic" could contain actual venom, leading to the partial paralysis. which seems to be the result of a convoluted game of telephone, very nearly based in reality.

so, in the 1980s, a researcher named jean-pierre raufman was doing research on how animal venoms affect human physiology, and was especially interested in gila monsters. turns out there are a lot of bioactive molecules in a gila monster's venom, including one called exendin-4, which is very similar to GLP-1 but has a much longer half-life. that's the first GLP-1 agonist discovered, and was marketed under the brand name byetta (with the generic "exenatide," because there are regulations on how medications are named). GLP-1 agonists have actually been on the market for both diabetes and weight loss for a while at this point - victoza (liraglutide) was approved by the FDA for obesity in 2014. there's a ton of GLP-1 agonists either on the market or in trials right now, all of which have different half-lives and slightly different side effects (similar to how there's a lot of different SSRIs, even though they all affect the same pathway).

semaglutide, however, is not and has never been synthesized from gila monster venom. "black market ozempic" isn't going to have fucking gila monster venom in it. here is an article that describes the current primary method of synthesizing semaglutide, and a potential new option - neither involve gila monster venom, at any step. and, what's more, gila monster venom isn't even a paralytic! it causes edema, a rapid drop in blood pressure, weakness, and (most famously) excruciating pain. it usually isn't deadly, it just sucks ass. but it definitely isn't a paralytic in any way, and would not contribute to "partial gut paralysis" even if that's what was happening.