Table of Contents (hide)
- 1. What is SSRI & SNRI Poop-Out / Tachyphylaxis
- 2. Will it Happen to Me?
- 3. What Causes SSRI & SNRI Poop-Out / Tachyphylaxis
- 4. What Can You Do About It
- 5. SSRI & SNRI Dosage Equivalents
Serotonin-Selective Reuptake Inhibitor Antidepressant Tachyphylaxis, in fancy doctor-speak, better known as SSRI poop-out, is when an SSRI that has been working for you, suddenly stops working and still doesn’t work no matter how much more you take. While this can happen to any medication, crazy or not, reuptake inhibitors in general and serotonin-selective reuptake inhibitors in particular, as a class are more susceptible to it; although individual drugs like Remeron or Gabitril might be failing as frequently as, if not more often than SSRIs.1 It also happens with Serotonin & Norepinephrine Reuptake Inhibitors (SNRIs), but nowhere near as often. I’ve included them here because SNRIs are often a good substitute for SSRIs, especially if SSRIs work well for someone but keep pooping out.
That depends. Let’s look at some numbers:
RESULTS: For the 103 subjects, there were 171 maintenance treatment intervals in which a subject received maintenance pharmacotherapy after having recovered from an episode of major depressive disorder. The median duration of maintenance treatment was 20 weeks. Tachyphylaxis occurred during 43 (25%) of these 171 maintenance treatment intervals. The subtype of melancholic (endogenous) major depressive disorder significantly elevated the risk of tachyphylaxis during the subsequent maintenance treatment interval. CONCLUSIONS: Despite the use of maintenance pharmacotherapy, major depression recurs in a considerable number of patients. Improved prophylaxis for these patients requires other treatment strategies based upon a greater understanding of recurrence. --Tachyphylaxis in unipolar major depressive disorder
That doesn’t mean that 25% of the people had it, it just happened 25% of the time.
The numbers from the literature are all over the map. Stahl estimated it at 20–30%. Based on everything I’ve read and all the anecdotal evidence I’ve found there is, at most, a ten percent chance of an SSRI/SNRI suddenly failing for no apparent reason for everyone, but 20–30% seems about right as soon as you’ve tried your second med no matter why the first one didn’t work for you.
And it’s not just people with unipolar depression:
OBJECTIVE: Tachyphylaxis often refers to the loss of antidepressant efficacy during long-term treatment. However, it may also refer to the gradual loss of efficacy after repeated antidepressant exposures over time. The aim of this study was to examine the phenomenon of tachyphylaxis in patients with Bipolar II major depression treated with either venlafaxine or lithium. --Does tachyphylaxis occur after repeated antidepressant exposure in patients with Bipolar II major depressive episode?
Now that most doctors admit poop-out exists, the researchers think it has more to do with the person than the med. I’m not sure which is the more likely cause, but I’m leaning towards the person, in that SSRI tachyphylaxis effect is usually due to a combination of genetics and behavior. This study pretty much nails it. They found that poop-out is usually due to one or more of a bunch of things, including genetics, non-compliance and trying to find a perfect drug in an imperfect world:
Residual symptoms are common among patients treated for MDD who do not achieve full remission. Incomplete remission is associated with increased risk of relapse, suicide, functional impairment, and higher use of health care resources. Several factors, including “downstream” neurochemical mechanisms and clinical factors such as lack of adherence, contribute to the high prevalence of residual symptoms. Various clinical strategies, including switching and substitution antidepressant therapies, are used to address unresolved depressive symptoms. Individual differences in therapeutic response contribute to inadequate treatment and are linked to numerous clinical and neurobiological factors, including noncompliance, underdosing, intolerance, disturbances in neural circuitry, and genetic variability in neurotransmitters. --Clinical Evidence and Potential Neurobiological Underpinnings of Unresolved Symptoms of Depression
We’ve written over and over that frequently switching meds for no good reason can lead to being treatment-resistant when one wouldn’t have been otherwise. Tachyphylaxis after Repeated Antidepressant Drug Exposure in Patients with Recurrent Major Depressive Disorder backs us up on that one. Lots of people are going to be treatment-resistant no matter what, and poop-out could be considered a form of treatment-resistance.
We hypothesized that a greater number of prior antidepressant exposures would result in a reduced response to venlafaxine, but not lithium, therapy.
RESULTS: The mean number of prior antidepressant and mood stabilizer exposures was significantly higher in venlafaxine non-responders versus responders (p=0.02). There was no significant association between response to lithium response and the number of prior antidepressant and mood stabilizer exposures (p=0.38). The odds of responding to venlafaxine or lithium therapy decreased with an increasing number of prior antidepressant exposures (p=0.04). --Does tachyphylaxis occur after repeated antidepressant exposure in patients with Bipolar II major depressive episode?
So if you have taken too many meds you might be stuck with lithium, or something else that doesn’t work as well as it should. Assuming you haven’t failed it because of real intolerable side effects and not just vanity weight gain, hair thinning and the like.
You know all of those articles and studies on how antidepressants don’t fare that much better than placebos in the clinical trials. Articles like Symptom Reduction and Suicide Risk in Patients Treated With Placebo in Antidepressant Clinical Trials, Efficacy of antidepressants in adults, and Selective Publication of Antidepressant Trials and Its Influence on Apparent Efficacy. So if a lot of people were merely responding to the placebo effect, then it makes sense, in a way, that SSRI poop-out is a spontaneous failure of an over-priced placebo. In How often do SSRIs and other new-generation antidepressants lose their effect during continuation treatment? Evidence suggesting the rate of true tachyphylaxis during continuation treatment is low Dr. Zimmerman et al. found that 24% of people who responded to the placebo experienced poop-out while ‘only’ 7% of those for whom the SSRIs actually worked had the meds fail on them. Why a placebo would poop-out on someone is still a mystery.
Medication-induced monoamine neurotransmitter (serotonin, norepinephrine, dopamine, and other less common ones) depletion is a controversial hypothesis in the world of psychopharmacology. The idea behind it is fairly straightforward: if a drug interferes with part of the process that literally recycles serotonin (the “reuptake” of “reuptake inhibitor” is the brain juice equivalent of putting something in the recycling bin), it follows that you could wind up with less serotonin to work with; just like soil that was normally flooded by the local river once every few years loses its productivity - despite all the fertilizers pumped into it - after the river is ‘tamed’ and doesn’t flood nearly as often.
Different meds will often work because they working on different receptors (e.g. 5HT1A) and/or in different parts of your brain, where your brain was still recycling serotonin like it was supposed to.
The problem is too many quacks and the antipsychiatry movement have latched onto the idea as proof that SSRIs (and therefore all crazy meds) will permanently prevent you from ever producing another drop of serotonin (or whichever neurotransmitters your meds are working with) ever again. Which is total bullshit. Especially since reuptake inhibitors don’t stop your brain from recycling monoamines, they merely slow down the rate at which your brain juice is recycled.
Based on my own experiences and the anecdotal evidence I’ve collected, my money is on medication-induced neurotransmitter depletion being a real phenomenon. And once you stop taking the meds that depleted the neurotransmitters involved your body will start producing them again. When is going to depend on a lot of stuff, but it is not going to be permanent.2
And if you think about it medication-induced neurotransmitter depletion is relatively easy to fix.
Another theory is the different receptors the meds work on in various parts of your brain develop a tolerance (become sensitized) to the extra serotonin and/or the way drug causes it to hang around. Thus switching meds works because you shift the effect around.
The first, and easiest3 thing to try when an SSRI poops-out on you is to get a prescription for pharmaceutical-grade 5-HTP, or find a brand of 5-HTP, or l-Tryptophan (which gets converted to 5-HTP), that you know is pure and consistent in dosage. Then you and your doctor figure out how much you need to take each day. 5-HTP supplements do convert to serotonin and can affect psychiatric disorders. That’s old news. If all you need is a few 5-HTP capsules a day, along with things exercise, fresh air and a better job, you aren’t depressed/anxious/whatever enough to be reading this site in the first place.
What? You want to know how much 5-HTP to take? Because of all those warnings about mixing l-tryptophan/5-HTP and serotonin syndrome, right?
That’s the problem. There is no right answer. The vast majority of studies about the effect of changing dietary tryptophan on serotonin in people with brain cooties are about depletion. Everyone is happy to prove taking serotonin away makes depression worse. Or it doesn’t. But they still have to cover the most obscure situations. I mean really obscure. There are very few out there where people are given l-tryptophan or 5-HTP while taking an SSRI. I’ve found all of two. In L-5-Hydroxytryptophan augments the neuroendocrine response to a SSRI researchers gave 50–200mgs of 5-HTP to people taking 20–40mg of Celexa for…nothing. They were professional guinea pigs and the researchers were testing their prolactin and cortisol levels, so it was all about measuring side effects. In the other, Use of nutritional supplements to increase the efficacy of fluoxetine in the treatment of anorexia nervosa it probably doesn’t matter that the abstract doesn’t state who took how much of what because it failed to make a difference. So for now you and your doctor are on your own.
If it helps, I take 1000mg of l-tyrosine every day to augment the norepinephrine reuptake of the TCA I take, as I had Strattera-induced norepinephrine depletion. I can feel the difference if I take too little, or too much.
If the amino acid l-tryptophan/5-HTP doesn’t work the next step is to take a serotonin agonist like BuSpar, with or without the l-tryptophan.
If one SSRI fails on you, and augmenting it with amino acids and/or BuSpar doesn’t work, do you have a future with other SSRIs? Unfortunately the answer is: maybe. If switching meds is the only thing that seems to work, then it gets really crazy.
- Changing meds all the time is a potential cause of tachyphylaxis.
- But if a med up and quits on you, and prescription-strength, pharmaceutical grade l-tryptophan/5-HTP, or an add-on serotonin agonist like BuSpar doesn’t work what choice do you have?
- So you try another SSRI, and as long as that works you’re OK.
- Until that one stops working.
- Lather, rinse, repeat.
- Until you’ve been through every SSRI available.
- And every SNRI as well.
- Which could be evidence it’s been the placebo effect all along.
- If you eventually make your way back around to the first med you tried and it works again, that’s more evidence it was probably the placebo effect.
- Especially if the first med was Paxil, or you try Paxil again and it works for a few weeks (or how ever long these drugs are working for you), because Paxil often doesn’t work the second time around.
- Although, if you were hit with SSRI discontinuation syndrome right away, that would indicate some kind of failure in how the medication was absorbed, or that you’re dealing with serotonin depletion. In which case augmenting the SSRI with l-tryptophan/5-HTP or BuSpar should work.
- Unless the discontinuation syndrome is “all in your head,” as it were.
- Still, you could have a really messed-up brain and/or liver and/or endocrine system and/or something else they haven’t figured out is involved that causes SSRIs & SNRIs to work for only a limited amount of time.
- So unless you get into a double-blind clinical trial for a new SSRI or SNRI, get the placebo, and respond positively to it, you’ll never know for sure if this mess has been due to a variant on the placebo effect (and you shouldn’t be taking meds and reading this site) or if you’re an outlier (and one of the people this site was created for).
- Because if you were born to quickly burnout on SSRIs, it’s possible that starting with a TCA or an SNRI (see below), or going to one of them as drug #3 instead of another SSRI, could have avoided this hassle.
- But you’re probably hosed now, because after failing six or seven meds, nothing is going to work as well as it could have. Not an SSRI, not an SNRI, not Lamictal, not Abilify, not lithium, nothing.
- Or maybe you’d be treatment-resistant no matter what you did because of genetics and/or your lifestyle prior to seeking real treatment for psychiatric problems.
- I’m sorry if you’re not going to sleep for the next year or two because you’ll be ruminating over this night after night after night. Welcome to my world.
Not so much two meds - because taking one med is usually way better than taking two - but meds that work on two neurotransmitters are much less likely to poop-out than those that work on just one.
Dual Reuptake Inhibitors Incur Lower Rates of Tachyphylaxis Than Selective Serotonin Reuptake Inhibitors: A Retrospective Study and Beyond Remission, Rationale, and Design of the Prevention of Recurrent Episodes of Depression with Venlafaxine for Two Years (PREVENT) Study, a large, two-year long trial sponsored by Wyeth, found that SNRIs and TCAs were less likely to poop-out than SSRIs. As Wyeth makes two SNRIs (Effexor and Pristiq) that part of that result isn’t surprising, that cheap-as-dirt4 TCAs were also proved to be unlikely to poop-out was refreshing to read.
If two SSRIs fail on you, either due to poop-out or they just didn’t work all that well, try a med from another class. That’s just common sense.
Trying to nail down equivalent dosages for SSRIs is a lot harder than you may think. Even though they are all supposed to be serotonin-selective reuptake inhibitors, only Lexapro is truly selective. All the others mess with more than serotonin, although there is no agreement as to any of that being clinically relevant. In a way it is almost like antipsychotics, in that there is one property they all do - D2 antagonism for antipsychotics5 - and that’s good enough to use in order to figure out which is equivalent to which in case you need to switch in an emergency situation.
In addition to being approximates, the equivalences given aren’t something where you can easily double the dosage on one and expect the dosage on the corresponding one to also be twice as much. How they affect those receptors in your in brain - and anywhere else you have receptors they affect - as well as the pharmacokinetics aren’t linear for all of them. This leads to odd things, like Lexapro often being more effective at a lower dosage while Celexa - the drug from which it is derived - is usually more effective at a higher dosage. And how Paxil’s efficacy essentially tops out at 20mg a day, as any dosage above 20mg either won’t make a difference because of diminishing returns, or works due to Paxil’s effect as a norepinephrine reuptake inhibitor, a sigma-1 agonist, and/or as a CYP2D6 inhibitor.
Potency, while important in calculating equivalence, isn’t everything.
There is a frequent misconception that potency refers to the dose of a drug needed to produce an effect. That is wrong. Instead, it refers to the concentration of a drug needed to produce an effect. Two drugs may be able to produce exactly the same effect, but the concentration needed of each drug may be quite different. The drug that requires a lower concentration to achieve the same magnitude of effect is the more potent drug regardless of the dose needed to achieve that concentration. --Dr. Sheldon Preskorn
This is yet another example of the importance of a drug’s pharmacokinetics. Effect is a factor of potency and various bioavailability aspects. Pure, or free base6 paroxetine is 14 times as potent as free base fluoxetine, but because of its screwy pharmacokinetics and the way the salts are absorbed, 10mg of Paxil (paroxetine hydrochloride) is the equivalent of 20mg of Prozac (fluoxetine hydrochloride).7
And effect is not the same as efficacy. Just because two meds are relatively equivalent at how much more serotonin they’re letting your brain soak in, that doesn’t necessarily mean they’ll work the same way for you.
This guide isn’t concerned with efficacy. It’s only purpose is to give you some rough numbers in case you must switch SSRIs immediately, due to a severe allergic reaction, some other equally bad side effect, or sudden tachyphylaxis (poop-out) that has resulted in SSRI discontinuation syndrome, or some other worst-case scenario.8
20mg Celexa (citalopram HBr) = 10mg Lexapro (escitalopram oxalate) = 50mg Luvox (fluvoxamine maleate) = 10mg Paxil (paroxetine HCl)9 = 20mg Prozac (fluoxetine HCl) = 50mg Zoloft (sertraline HCl) = 75mg Effexor (venlafaxine HCl)10 = 50mg Pristiq (desvenlafaxine succinate)11 = 20mg of Cymbalta (duloxetine HCl)
To give you an idea of the effect of non-linear pharmacokinetics, and because it might be useful in some situations.
5mg Celexa (citalopram HBr) = 2.5mg Lexapro (escitalopram oxalate) = 25mg Luvox (fluvoxamine maleate) = 5mg Paxil (paroxetine HCl) = 5mg Prozac (fluoxetine HCl)12 = 10mg Zoloft (sertraline HCl)13 = 6.25mg Effexor (venlafaxine HCl)14 = you can’t get that small with Pristiq and Cymbalta.
Here are the averages of the above meds’ Ki values from the NIMH Psychoactive Drug Screening Program’s database. The lower the number, the greater the strength.
Once again: binding potency of the base substance at the serotonin transport (reuptake) sites is just one factor in determining the overall strength (not efficacy) of a drug. It just happens to be the simplest and is usually close enough. Once again I need to stress an important difference: I’m not using the generic names in this table, but the base chemicals that you’re not going to get at a regular pharmacy15. While many drugs, such as most AEDs, are in their base form, for whatever reasons most antidepressants are not. As such I used the active ingredient in the dosage equivalents, which is why the math does not add up.
SERT: Serotonin transport, the mechanism that is being inhibited by a reuptake inhibitor.
|Ingredient free base||Ki at SERT|
For more data like the above, see the page on TCAs
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2 Unless, of course, you're that one person in 100,000 who lost the genetic lottery. Fortunately taking an agonist for whichever neurotransmitters involved will correct that. You may have to deal with side effects you really don't like, but that would suck a lot less than no serotonin, norepinephrine, dopamine, whatever action at all.
3 In theory.
4 Except for protriptyline - the one I take - which costs over $300 a month. Probably because only 99 other people in North America take it.
5 Although some third-generation APs, like Abilify, don't even do that. They're partial D2 agonists and D3 antagonists.
6 Really, that's the term for it. Sometimes the term "freebase tar" is used. Anyone who came across this page trying to find information of illicit drugs will probably have better luck on Wikipedia.
7 Now you might understand why I'm so anal about using the complete chemical name instead of just the base active ingredient in some places, even though I don't know the difference between a hydrochloride and hydrobromide salt.
8 That usually involves no money and plenty of leftovers. Visit Needy Meds* for information on getting free meds from the drug companies. You really, really, really don't want to get in that situation, nor do you want to depend on this site for anything more than a rough idea of how long you can last as you do something to get some meds from a county / free clinic. Bring your leftovers to trade, as that might even get you more of what you need.
9 The dosage should be the same for Pexeva and other brands of paroxetine mesylate. The dosages and titration schedules in the Pexeva PI sheet are identical to Paxil's.
10 I know, Effexor isn't an SSRI, but at these dosages it doesn't do enough norepinephrine reuptake inhibition to make a difference.
11 Pristiq is even less of an SSRI than Effexor, and 25mg would be at lot closer than 50mg, but this is the lowest dosage you can get.
12 You can get this dosage only with the oral solution.
13 You can try splitting a tablet, but using the oral concentrate would be so much easier.
14 You can get this dosage only with the immediate-release form. And good luck quartering a 25mg tablet.
15 I'm not even sure if a compounding pharmacy can make you a pill with pure, unadulterated paroxetine. Although I'm fairly certain I've seen the base ingredient for some SSRI or other antidepressant available outside of the US, so it may be possible to get something made. You need to ask someone else as to why anyone would want to do because I have no clue if it is a good idea or not.
SSRI & SNRI Poop-Out/Tachyphylaxis & Dosage Equivalents by Jerod Poore is copyright © 2010 Jerod Poore
Date created: Date created: 27 November 2010 Last edited by: JerodPoore on: February 23, 2014, at 04:22 PM
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1 While there are plenty of books to help you with hypochondria, for some reason there’s not much in the way of websites. Then again, staying off of the Internet is a large part of curing/managing the disorder.
2 Remember kids, Microsloth operating systems are like TOS Star Trek movies with in that every other one sucks way, way more. With TOS Star Trek movies you don’t want to bother watching the odd-numbered ones. With Microsloth OS you don’t want to buy and install the even-numbered ones. Anyone who remembers ME and Vista knows what I mean.
3 Have I mentioned how open source operating systems for commercial applications is one of the dumbest ideas in the history of dumb ideas?
[begin rant] I rent a dedicated server for Crazymeds. It’s sitting on a rack somewhere in Southern California along with a bunch of other servers that other people have rented. The hardware is identical, but no two machines have exactly the same operating systems. I don’t even need to see what is on any of the others to know this. If somebody got their server at the exact same time, with the exact same features as I did, I’m confident that there would be noticeable differences in some aspects of the operating systems. So what does this mean? For one thing it means that no two computers in the same office of a single company have the same operating system, and the techs can spend hours figuring out what the fuck the problem could be based on that alone. It also means that application software like IP board that runs the forum here has to have so many fucking user-configurable bells and whistles that even when I read the manual I can’t find every setting, or every location that every flag needs to be set in order for a feature to run the way I want it to run. And in the real world it means you can get an MBA not only with an emphasis on resource planning, but with an emphasis on using SAP - a piece of software so complex there are now college programs on how to use it. You might think, “But don’t people learn how to use Photoshop or Adobe Illustrator in college?” Sure, in order to create stuff. And in a way you’re creating stuff with SAP. But do you get a Bachelor of Fine Arts degree with an emphasis on Photoshop?
Back in the Big Iron Age the operating systems were proprietary, and every computer that took up an entire room with a raised floor and HVAC system, and had less storage and processing power than an iPhone, had the same operating system as every other one, give or take a release level. But when a company bought application software like SAP, they also got the source code, which was usually documented and written in a way to make it easy to modify the hell out of it. Why? Because accounting principles may be the same the world over, and tax laws the same across each country and state, but no two companies have the same format for their reports, invoices, purchase orders and so forth. Standards existed and were universally ignored. If something went wrong it went wrong the same way for everyone, and was easy to track down. People didn’t need to take a college course to learn how to use a piece of software.
I’m not against the open source concept entirely. Back then all the programmers read the same magazines, so we all had the same homebrew utilities. We even had a forerunner of QR Code to scan the longer source code. Software vendors and computer manufacturers sponsored conventions so we could, among other things, swap recipes for such add-ons and utilities. While those things would make our lives easier, they had nothing to do with critical functions of the operating system. Unless badly implemented they would rarely cause key application software to crash and burn. Whereas today, with open source everything, who the hell knows what could be responsible some part of a system failing. [/end rant]
Author: Jerod Poore Date Modified: 2014–03–09 Date Published: 2010–11–27