57 karma · joined March 23, 2025
Also medicine is an evidence-based practice because fundamentally our knowledge is woefully incomplete. Doctors are basically applied statisticians, the chemistry and biochemistry people are the researchers.
But the reaction to changes in areas like research and education isn't realized for years if not decades. So Trump doesn't feel the consequences. For non-economic spheres, the only real immediate reaction to these changes is the social reaction, which comes from people Trump is actively aligned against and entrenches his position.
I would be very suspect of a Medication Overuse Headache (MOH) due what appears to be acute/abortive use of painkiller medication as compared to a prophylactic usage of other drugs. I'll do this exercise mostly ignoring the #1 concern because presumably your doctors would be hyperaware of that.
# Pathways
0. Excedrin is combination of aspirin, acetaminophen, & caffeine.
1. Aspirin --> COX-1 (/2) inhibition --> Reduces Prostacyclin/Prostaglandin/Thromboxane Synthesis --> Decreased inflammation, nociceptor sensitization, pain signaling
2. Acetaminophen --> Central COX Inhibition, possible COX-3 inhibition (splice variant of COX-1) --> Reduces Prostacyclin/Prostaglandin/Thromboxane Synthesis --> Decreased inflammation, nociceptor sensitization, pain signaling
3.a. Acetaminophen --> Metabolized to N-Arachidonoylphenolamine (AM404) --> Inhibition of reuptake of Anadamide (endogenous cannabinoid) --> Increased activation of CB1 receptors
3.b. Acetaminophen --> Metabolized to N-Arachidonoylphenolamine (AM404) --> Transient Receptor Potential Vanilloid (TRPV1) agonist --> active? at periaqueductal (central) gray --> opioid receptors that send descending axons to modulate pain at the level of the dorsal horn of the spinal cord
4. Acetaminophen --> Enhancement of serotonergic descending inhibition (5-HT pathways)
5. Caffeine --> Adenosine anatagonist (nonselective A1, A2A, A2B) --> Inhibition of vasodilation --> Cerebral vasoconstriction
6. Caffeine --> Analgesic Adjuvant --> Enhances availability of aspirin and acetaminophen.
# Thoughts
1. Selective: -COX, +CB1, +TRPV1, +Opioid, -Serotenergic, -Adenosine, -Inflammation, +Vasoconstriction/-Vasodilation
2. Aspirin doesn't work in isolation.
3. Tylenol-3 (acetaminophen) doesn't work in isolation (surprising!!!).
4. Headaches probably not -COX mechanisms
5. Caffeine is likely needed for -adenosine, vasculature effect implicating cerebral vasodilation
6. Densensitization strongly implicates +CB1/+TRPV1 as well as -adenosine, +Sero, +Opioid.
# Concluding Thoughts
0. Need to address MOH, this should be a conversatio with your real doctor.
1. Then for the headache, normal first-line would probably be a TCA prophylaxis such as amitriptyline with bonus target +sero/+opioid. Assuming you've tried this.
2. The failure of your other drugs means you should probably try CGRP Inhibitors to target vascular and pain-signaling effects. Maybe even gepants (acute)
3. Botox could be a consideration in a complex CDH case.
4. Zebras: Ditan/Lasmiditan. I assumed +vasoconstriction, but could be -vasoconstriction which is why non-combination drugs failed. Target 5-HT1F and avoid vasoconstriction for symptomatic relief, but doesn't treat underlying. Probably avoid due to MOH.
# Clarifying questions for your doctor, not me
1. Is your headache pulsatile/throbbing (migrane) or dull, tight, & persistent (tension-type)?
2. Onset characterized by stress (tension-type)?
3. Is it unilateral (migrane) or bilateral (tension-type)?
# What I would do next
1. Make an appointment with a neurologist
2. Before the appointment, make a detailed headache diary (when your headaches start/end, intensity of the pain, location and quality of the pain, associated symptoms (nausea, light senstivity), any potential triggers, what you did to try to relieve the headache and if it worked)
All cards start suspended by default, and you unsuspend cards usually by tag. For example, lets say you watched a a popular third-party exam prep video from Boards & Beyond on Insulin. You would find the corresponding video has its own tag "tag:#AK\_Step1\_v12::#B&B::08\_Endocrinology::03\_Pancreas::03\_Insulin" which you would unsuspend all the cards for. That's the basic flow, but everyone does things a little differently.
Some people don't watch videos just do review questions from UWorld which are also tagged. Some people manage cards using a mix of tags and decks. Some people search and manually unsuspend cards individually. Some schools cross-tag cards with their lecture. Personally, I use an AI search to unsuspend cards by cross-referencing against a PDF of lecture for the day.
Custom tags can be protected when syncing from upstream: https://community.ankihub.net/t/protecting-fields-and-tags/1...
I made the mistake of just jumping in and I would say I spent the first 6 months using Anki “wrong” in the sense I would make bad cards, try to make mc questions, not enabling or optimizing FSRS, capping reviews, doing Anki before I knew the material, etc.
I’m someone who loves to learn from scratch/figure it out myself. I would never recommend watching a YouTube tutorial or following a guide for something you can figure out yourself, but I have to make an exception for Anki. Anki is one of those rare things where it’s simply just better to just copy what someone else is doing and figure out adjustments for your own workflow over time.
I’m in medical school which has basically mastered Anki. The AnKing deck, used by over a million medical students, has over 35,000 cards, cross-tagged by numerous study resources that exists on a single “deck” which receives regular updates. I regularly run basically instant queries on over 40,000+ cards.
Medical school Anki has basically mastered this workflow and the original commenters complaints are completely wrong/come from a misunderstanding of Anki’s data model.
To be put simply, ignoring subdecks, filtered decks, cards vs notes, etc.: cards can only belong to one deck, but can have multiple tags. What exactly do you want to see differently in the data model?
> I don't think that closed networks substantially improve security and I don't like the push to require them.
You know what, you're right this is a philosophical stance, as dumb as a stance I might think it to be. My actual issue with his "philosophy" is that he makes a broad generalization when the statement really just applies to his unique use case. I didn't consider it to be a philosophical stance because I didn't think he seriously meant it as a systematic approach for the entire world but honestly re-reading what he wrote I think he does actually.
Honestly I take bigger issue with what he believes is a stance against opiniated technology but all technology is inherently opiniated his opinions are just different.
If your claiming your philosophical stance is setting passwords doesn’t provide security, by your own reasoning in your case that’s just a matter of practicality. There is no philosophical argument.
> More generally, I don't think that closed networks substantially improve security and I don't like the push to require them.
I mean that’s just your opinion, not a philosophical stance, and it happens to be a empirically demonstrably false one.
> I don't like technology that tries to enforce its own opinion about social norms.
This statement is so vague it’s practically useless. It can just be selectively applied against anything you don’t like. All technology is opinionated. From the layout of your keyboard to this site, everything is shaped by and shapes social norms. It would also be an opinionated technology if it decided not to ask you to set a password by default. You might as well have said I don’t like WiFi passwords because I don’t like WiFi passwords and it would’ve carried the exact same message.