Change your network name. When the TV prompts you to connect, join the renamed network. Then, rename it back so everything else can connect again and the TV can't. I can think of a few potential problems with this, but, it might work?
Or blacklist the TV's MAC address in your router settings. Didn't think of that first for some reason.
Simple: A version specifier, or feature specifiers. Backward compatibility concerns vanish when I can opt-in to a newer spec. Old code keeps working, and new code doesn't suffer for legacy nonsense.
Sadly, the closest I've personally seen to this sort of thing in widespread use is `"use strict";` in JavaScript, which is only a single binary switch. You can't, say, turn on a new keyword, disable a keyword, switch to a different incompatible version of some browser API, etc.
I encourage all language designers to include a feature mechanism in a forward-compatible way. Don't overthink the difficulty: It doesn't need to do anything at first, it just needs to not be a parsing error. Treat it like a comment. FYI, this is the same as having a version number or header size in a binary file format's header, which all sane formats have (there are a lot of insane formats out there...).
Backwards compatibility is overrated. It should be future compatibility, so older browsers get to load a shim to implement new features. That way the onus of incompatibility falls on the older browsers, they get slower over time. Newer browsers get leaner. That's what you want.
Consider that not even a hard-line Christian puritan would agree with you in-principle. If publishers were forbidden from selling literature depicting incest, rape or genocide then the Old Testament would be removed from shelves. Clearly society has a tolerance for some of it.
As I recall, the term "rosebud" can refer to an intentional anal prolapse. I'm not sure if what porn actresses do is the same as the medical definition of an anal prolapse, though.
I think in the context of Citizen Kane and Orson Welles holding a snowglobe, it's referring to Marion Davies's clitoris (via the name of the sled, of course), which totally pissed off William Randolph Hearst.
>In the opening scene of the 1941 mystery Citizen Kane, the eponymous protagonist, played by Orson Welles, clenches a snow globe in his hand as he utters his last word: “rosebud.” The glass-encased spherical diorama of a snowy scene was a mere novelty at the time, but the film, in part, gave rise to its popularity.
Here's a snarky response from Gore Vidal to a letter from a ambulance chasing lawyer to the editor of the New York Review, questioning his veracity as the source of the rumor:
[From Gore Vidal's perspective, the claim that "Rosebud" was William Randolph Hearst's private term for Marion Davies's clitoris is plausible but unverifiable. Vidal acknowledges that he did not receive this information directly from Hearst or Davies but suggests that such details could easily have emerged within the intimate, alcohol-fueled circles of Hearst's entourage, including figures like Herman Mankiewicz, who co-wrote Citizen Kane. Vidal argues that Hearst's intense fury at the film might be partly explained by the personal significance of "Rosebud," even if Orson Welles himself was unaware of its connotations. While he admits the story is speculative, Vidal finds it intriguing and consistent with the gossipy, complex dynamics of Hearst's world.]
Here's Orson Welles mentioning "rosebud" on the set of a Paul Masson Commercial: ;)
What you REALLY don't want to know is what Orson Welles meant by "frozen peas", "in July", "and I'll go down on you", "fish fingers", "crumb crisp coating", and "beef burgers":
To me, unboxing videos are documentation, not entertainment. When I need to know exactly what's in a box and how it's packaged, an unboxing video is the only source of that information.
It's unfortunate that I had to scroll to the bottom of the page to see any mention of ADHD or executive dysfunction, when the linked post describes what is clearly a form of executive dysfunction! Instant temporary treatment is a stimulant such as caffeine (which has annoying side-effects) or amphetamine salts (commonly known as adderall). Long-term treatment is exercize, which can be as simple as balancing on one leg for ten minutes every day or using an elliptical machine. Running outside is a decent option, but take care to avoid damaging the knees, which will happen by running on hard surfaces.
Dr. Russell Barkley has good explanations of what different prescription ADHD drugs do, which I find gives insight into what's going wrong when you have an executive dysfunction: https://www.youtube.com/watch?v=LnS0PfNyj4U
In particular, the emotional blunting effect of stimulants erases the thought that what you do might not be good enough. You no longer care about what others think, so you can just do what you want to do. I personally find this also makes me a callous asshole if I'm not careful, which I believe is related to the modern epidemic of coffee zombies.
How is exercise a substitute for stimulant drugs? I've never seen this proven before; I've only seen correlations between people who are able to consistently exercise and people who have less severe ADHD, but that doesn't teach us anything we didn't already know (namely that consistent exercise is made more difficult by ADHD).
You... what? You can't be serious. Simply putting "exercise and adhd" into Google® got me multiple studies which say that exercise helps, along with many other websites (some reputable and others possibly not) all saying essentially the same thing. You can easily find licensed physicians giving this same advice to their patients, and they observe that it works. And, off the top of my head, exercising elevates dopamine and some other neurotransmitters, which are well-known to be deficient in people with ADHD. That's one of the reasons the drugs work: stimulants raise the levels of those neurotransmitters. Personally speaking, I've found that any activity or action that raises my dopamine level has the same effect on my executive function as a stimulant drug, although this can be a very short-lived improvement (worst case, it comes and goes entirely within ~5 minutes).
You may also consider this from an evolutionary angle. Mammals such as us are not meant to sit inside at a desk all day (whether that's school or any other menial work), so it's no surprize that doing that alters and impairs development versus the conditions we evolved to live in. It's really easy to encounter the biological equivalent of undefined behaviors and invalid state in modernity. If you don't know what I mean, here's an easier to see example: It's well-known in recent years that myopia (shortsightedness) is predominantly caused by insufficient exposure to sunlight as a child. As an aside, I find it very interesting that the reason sunlight exposure matters is it elevates dopamine in the retinas, and eyes with dopamine deficiency don't develop correctly.
Another angle is mental exercize: It's more difficult to physically exercize with ADHD, but it's possible, so mentally pushing past the difficulty (or, more likely, having someone encourage you and help you) can train you to do that with other things and teach you how to self-manage your symptoms with mental decisions / willpower. This is a pretty poor solution on its own, but it's a great force multiplier when combined with other strategies.
> And, off the top of my head, exercising elevates dopamine and some other neurotransmitters, which are well-known to be deficient in people with ADHD.
As far as I know, stimulant medications for ADHD treatment act as a reuptake inhibitor for those neurotransmitters. The end result is still somewhat the same (levels become higher on stimulants, and it absolutely can help with ADHD), but I've never really seen it stated that people with ADHD have a deficiency in dopamine, just that their brain needs more of it in order to catch their interest. Presumably because dopamine disappears way too quickly even if it's a perfectly fine amount of dopamine.
As someone with ADHD, I'm constantly multitasking because one task is often not enough to keep my interest. If I do many things at once though, it's much easier for me to stay focused. To my knowledge, this is also why music helps me focus while I work.
So I believe it's not necessarily anhedonia that leads to ADHD. Sure, depression-induced anhedonia can result in executive dysfunction, but depression's not what ADHD is (even though ADHD can easily cause depression). Things can keep my interest if they are rewarding enough to overpower my brain's natural "dopamine floor", I guess. I don't mean to imply that everyone with ADHD is the same, or that this can't be a source of symptoms for others, just that I don't see how a lack of exercise would be to blame for it.
> It's well-known in recent years that myopia (shortsightedness) is predominantly caused by insufficient exposure to sunlight as a child.
I think it can also be caused by staring at nearby objects too much of the time, like computer screens. IIRC your eyeballs use the sharpness of your peripheral vision to know whether to stop growing, and if you're always staring at nearby objects, then the persistent lack of sharpness in your peripheral vision will cause your eyeball to elongate too much, resulting in myopia. I am sure sunlight also affects it, but being in sunlight also often has the side effect of being outside where there are often faraway objects to focus on, which if done regularly will also signal to your eyes that they are done growing.
> mentally pushing past the difficulty [...] can train you to do that with other things and teach you how to self-manage your symptoms with mental decisions / willpower
So far I haven't seen evidence for myself that trying harder helps. Sometimes things happen (things like trauma) that manage to keep me motivated and functional for a while, but I haven't found a working strategy to manufacture this motivation at will yet.
Great convo, love all the details on both sides! There's shockingly little long-term study of executive dysfunction because it's so new, so I understand your dubiousness. I never read that before about neurotransmitter reuptake, but it seems plausible -- it's really hard to say. My fave AD(H)D site (low bar...) quotes a doctor saying (in 2024);
ADHD was the first disorder found to be the result of a deficiency of a specific neurotransmitter — in this case, norepinephrine — and the first disorder found to respond to medications to correct this underlying deficiency.
But then a basic search on the actual lit paints a much murkier picture:
We found no significant differences in NET availability or regional distribution between patients with ADHD and healthy controls in all investigated brain regions (F1,41 < 0.01; P = .96). Furthermore, we identified no significant association between ADHD symptom severity and regional NET availability.
Which is a synechdoche of the broader dynamics around the disease IMO; lots of confident people with degrees saying stuff, often while trying to sell you services or medications, but the lit is still mostly vague. The only solid finding I know about ADHD is that it lowers life expectancy... TL;DR: I wouldn't personally be so confident it's about reuptake rather than production.
To give my hot science take, I think this is a somewhat inevitable result of our differential-diagnosis-based psychiatry system. ADHD is, objectively speaking, a set of symptoms. Common sense tells us that there's some common causes in the population, sure, but treating it as a causal condition rather than a opaque descriptor leads to a lot of confusion and heartache, IMHO. Such as;
Sure, depression-induced anhedonia can result in executive dysfunction, but depression's not what ADHD is (even though ADHD can easily cause depression).
I don't have an issue with any of these specifics per-se, and I'm sure you're accurately describing your life (and mine, tbh!), but I don't believe this level of ontological separation is helpful in the longterm. Some people with depression and ADHD might have a completely different cause than people with one of either, or even than other people with both. This is why I like the 'software debugging' metaphor; it's easier to iteratively try improvements to an opaque system than it is to find the "true" cause or "real" solution. E.g.:
So far I haven't seen evidence for myself that trying harder helps. Sometimes things happen (things like trauma) that manage to keep me motivated and functional for a while, but I haven't found a working strategy to manufacture this motivation at will yet.
You're not broken for being imperfect, you're just human - I would encourage you not to let this dissuade you from pushing yourself! I consider failure-to-motivate as a cognitive event in a system with a million inputs, not a subconscious choice you made because you're broken/sinful/lazy.
In those terms, I agree with your interlocutor; regular moderate exercise can really only help, in 99% of cases. It doesn't have to fix to help :)
> lots of confident people with degrees saying stuff
This seems to be the case for so many diagnoses, ugh. I often feel like I have more paws-on experience with certain things than a lot of professionals out there, but I don't know if I'll ever really get to be an authority on any of this stuff, which is kind of a shame, in my opinion. I wish I could contribute what I know.
Some disorders are particularly often misunderstood which always feels a bit sad to me. Would one normally write a book in this situation?
> I wouldn't personally be so confident it's about reuptake rather than production.
I'm not necessarily as confident that it's definitely about reuptake as I am just not exactly convinced that it's definitely about production, if that makes any sense. Mostly because I personally have a case that I suspect of being about reuptake, even though I don't really have a way to verify that for sure. (I may never.)
If inhibiting reuptake has the same or a similar enough effect as increasing production, how is one to tell the difference? Many stimulants (like the amphetamines) act as releasing agents at the same time anyway; I happen to best like (and currently use) dexedrine, which happens to also be a dopamine releasing agent and not just a reuptake inhibitor. This fun fact naturally leads to "Hmm how exactly am I supposed to know for sure which mechanism of action is actually the one helping me the most". Or of course the possibility of "both is good, I could use both".
Thing is, we just really don't know right now and I'm not sure of any way to become any more certain about this myself. I definitely think this deserves to be an active area of research (there are many things I'd love to be active areas of research), but I don't know of anything ongoing at the moment. You never know though exactly what research may be ongoing, a paper could appear at any moment about this exact topic, but I'm not aware of any right now.
I will say though that in my opinion, I think the ongoing research into psilocybin could potentially turn out to be quite insightful and possibly relevant, because in my experience, serotonergic psychedelics temporarily disappear my ADHD, and they're also sorta almost a kind of stimulant (or at least LSD certainly is), so... close enough? Maybe not exactly close enough, but it's certainly some of the most exciting drug/brain research that I've seen in years. Here is which paper grabbed my attention and got me so excited about this: https://pmc.ncbi.nlm.nih.gov/articles/PMC11291293/
> I don't believe this level of ontological separation is helpful in the longterm. Some people with depression and ADHD might have a completely different cause than people with one of either, or even than other people with both.
Yes, of course. I don't mean to suggest that these diagnoses do a perfect (or even good enough in many cases) job of identifying root causes, because all they really are is those sets of symptoms that satisfy certain diagnostic criteria. So I therefore also don't mean to suggest that everybody with ADHD has the exact same root cause that I do, because it's currently impossible to test for that. (It's even hard to test for equivalence between two people, because we don't even know the objective difference between a lower level of dopamine in an otherwise normal brain and a higher level of dopamine reuptake in an otherwise normal brain, so we wouldn't know what to test equivalence with.)
It's hard enough just for me to find someone who's autistic in the same exact way that I am, let alone someone who also happens to match up with any of my other differences. (I think so far I've only found two other such people in total.) I just mean to say that I've never seen ADHD be caused by anhedonia, but I have seen and heard of many other things that could be confused for something like that. (It's really easy to confuse these things, which is probably why you say this level of separation isn't helpful.)
> you're just human
I get what you mean (that nobody's perfect), but I am otherkin, so please don't specifically call me human! (I should probably add this to my HN profile to be honest - not that people usually read profiles before they comment, but still)
> I would encourage you not to let this dissuade you from pushing yourself!
It doesn't entirely. I just can't always count on the push working because of how frequently it just doesn't. I can't recall how many times that I've fully, definitely decided to do something, turned to get up, and then just frozen in place. I had literally already fully decided to do the thing and was fully committed and my brain just suddenly said No. I literally freeze until I give up. The body simply refuses to move for that purpose in particular.
I have a hypothesis that this ability for the body to "disagree" with me could have been a contributing factor to my huge separation between mind and body, but I also have Dissociative Identity Disorder... so dissociation in all things, even between thoughts, is pretty normal for me at this point.
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