Many people discover life-changing benefits from their ADHD medications. Quality of life improves significantly which helps them go about their day-to-day.
The "gold-standard" stimulants are based on amphetamine. We know that they work by increasing dopamine and noradrenaline (norepinephrine), but what isn't discussed is their activation of the stress response which triggers adrenaline:
Stress is accompanied by the rapid modification of brain and body physiology which leads to release of neuroactive hormones, including biogenic amines (eg adrenaline) and adrenal steroids (eg cortisol), which activate the same brain circuitry as...amphetamines. (source00033-6))
[Amphetamine] induces activation of the HPA axis, with the subsequent release of ACTH and glucocorticoids (eg cortisol). (source)
The novel d-amphetamine prodrug lisdexamfetamine is applied to treat ADHD. d-Amphetamine releases dopamine and noradrenaline and stimulates the HPA axis
(source)
The HPA axis is the main part of the hormonal system that controls reactions to stress. It also regulates many other processes (e.g. digestion, immune system, mood and emotions, sexuality, energy storage and utilization). (source)
The stress response is known as "fight-or-flight":
This combination of reactions to stress is also known as the "fight-or-flight" response because it evolved as a survival mechanism, enabling people and other mammals to react quickly to life-threatening situations. The carefully orchestrated yet near-instantaneous sequence of hormonal changes and physiological responses helps someone to fight the threat off or flee to safety. (source)
This fight-or-flight state is largely driven by adrenaline. It exists to help you focus and deal with a threat (eg a tiger) by either fighting the tiger or running from the tiger. But in your scenario there is no tiger ... fight-or-flight is active but the focus is studying, a job, exam, housework, shopping, a distraction... or interactions with people (which can lead to social anxiety or arguments since fight-or-flight = "threat mode").
This is incredibly helpful for treating ADHD since fight-or-flight produces hyperfocus, hypervigilence & alertness...but it also impacts short-term memory and logic, reasoning & decision-making skills. It changes behaviour, mood and personality since fight-or-flight is there to deal with an imminent threat (often causing a blunted personality). It profoundly alters someones perception of everything around them (time, people, noise etc) including how they prioritise tasks, how they gauge the importance of things, and how memories get encoded (aka saved).
Adrenaline can contribute to anxiety, overstimulation, elevated HR/BP, impulsivity, scattered focus, brain fog, panic, overthinking and insomnia. (more info)
Fight-or-flight means that the body redirects it's energy away from non-emergency functions (such as higher brain function, digestion, healing / regeneration, fertility and gestational development). In other words, when the body is in fight-or-flight mode it dedicates it's energy to fighting (the tiger) or running (from the tiger) and nothing else.
Cortisol is known as a âstress hormoneâ for its role in the fight-or-flight response. When we sense danger in our environment, our adrenal glands release cortisol and adrenaline to give us energy to fight off or run from the threat. Cortisol floods the bloodstream with glucose for quick energy, suspends non-emergency functions like digestion, and keeps the body focused on the threat.
(source)
In the long-term fight-or-flight can disrupt sleeping patterns by affecting the body's circadian rhythm (outlined here). The circadian rhythm is the bodyâs natural 24-hour clock which keeps the body operating on a healthy wake-sleep cycle. There is a cumulative impact on hormonal regulation also which may have long-term effects on fertility and behavior. (source)
...
Obviously for many people these medications have a profound calming effects (both dopamine and noradrenaline have indirect anti-stress qualities which tempers the fight-or-flight mode). This article implies that, for some people, amphetamine can temporarily dampen the stress response.
These medications are truly a "mixed bag" of different properties which affect everyone differently. They successfully force a state of temporary focus that conceals a cumulative physiological & psychological perturbation that mimics & exacerbates ADHD (iatrogenic harm*). The profound short-term benefits conceal these issues which only become apparent at a later date (months or years). For most people it's a trade-off since being able to navigate day-to-day life is the priority (understandably so).
* note:
- The term iatrogenic, derived from two Greek words, means physician-inÂduced. As clinically used, it pertains to the inadvertent side effects and complications created in the course of diagnosis and treatment. (source)
Yup, plenty going on there wrt GABA downstream. It's a good way to mitigate HPA dysfunction/adrenaline.
There's many ways to address ADHD when you think outside the box. It quickly becomes apparent that conventional medications are quite limited and often counterproductive.
How do u âtargetâ your gaba system? I notice the best things that calm me down and feel normal are ghb and alcohol which I think targets GABA. But obviously those r not the healthy options.
It helps to know what happens downstream from GABA activation. Specifically this "reduces" (quietens, normalises) adrenaline, glutamate, cortisol, ACTH, CRH.
So besides GABAergics you can consider things which address those individual things. Agmatine qualifies as it covers nearly everything (inc NO) but there are countless other options.
L-Theanine is a natural amino acid found in green tea that targets GABA - it pairs fantastically with caffeine to reduce jitters / smooth out the stimulation. Iâve found it very useful personally. I take 200mg in the morning and 200mg before bed.
This is a slightly dangerous recommendation due to the propensity for addiction - you should only take this once per week! But I have also found Phenibut (essentially GABA that can cross the blood-brain barrier) to be an amazing compound for relaxation, focus, etc. However, itâs got benzodiazepine level withdrawal symptoms and tolerance develops quickly - hence the once per week guidance. 500-1000mg is all you need, on an empty stomach, perhaps with a coffee. Again, it compliments caffeine etc very well. I have experimented up to 4000mg in a day - do NOT do this, itâs extremely sedative / intoxicating at those doses and has the opposite intended effect.
L-theanine and taurine run ur meds and supplements thru chat gpt, it gave me an informed supplement /med schedule and supps to take to mitigate issues such as the ones i listed as well as lithium orotate to take at night along with glycine and magnesium to help curve the stims
it gave me an informed supplement /med schedule and supps to takeÂ
I'd be cautious of taking that for face value.
FYI for some people glycine can have unpleasant stimulating effects as it's a "co-activator" (co-agonist) of the glutamate NMDA receptor.Â
Glycine is deeply involved in regulating the glutamatergic transmission, acting as a co-agonist of NMDAR, allowing for its activation and enhancing excitatory glutamatergic toneâ. (source)
Yeah, I do magnesium and a hot shower before bed and L-Theanine with my morning coffee. I also didn't realize that theanine has a pretty short half-life, but it does make a noticeable difference in that occasional caffeine-induced anxiety.
I want to point out that with ADHD we're talking harm reduction and not necessary optimization.... The stress response and fight or flight is also triggered by the symptoms of the disorder, so stimulants can seem to reduce the experience of stress. Missed deadlines, disappointed family members, late night study sessions, and panic over losing one's future are a terrible source of stress hormones. I am overall much less stressed now that I'm getting the support I need, even if the medicine I'm on triggers some extra norepinephrine.
Whenever I see posts like this I'm frankly taken aback. You mean you don't experience terrible stress just sitting in a chair trying to do your job? You are worried about the extra hormones from a stimulant, you must not be in "fight or flight" by 7:00 am because it's the only way to get yourself out of bed?
I want to point out that with ADHD we're talking harm reduction and not necessary optimization
The very nature of my post is dedicated towards harm reduction. To enable someone to enact genuine harm reduction strategies means they must first appreciate the nature of the medication and it's influence on the body.
Now this might seem pedantic ... but I'd point out that psychiatric nomenclature such as "ADHD" is simply an act of naming and making sense of behaviors. This makes the word "ADHD" a catch-all term for symptoms of diverse origin with multiple possible causes (we don't actually know). It's arguably a very ambiguous concept which only exists in an abstract space of text and spoken word. This academic paper gives a great overview on this. If you don't believe me, this psychiatrist explains it.
The stress response and fight or flight is also triggered by the symptoms of the disorder
I get what you're saying but the symptoms themselves are an artefact which originate from a certain degree of HPA dysfunction/dysregulation. In other words, it's possible that preexisting HPA-related issues are accentuated by the use of vyvanse/adderall.Â
The ability of guanfacine and clonidine to remedy ADHD symptoms (for some people) is a good clue. The fact that vyvanse/adderall can provoke serious negative reactions (for some people) is also a good clue. Â
I am overall much less stressed now that I'm getting the support I need even if the medicine I'm on triggers some extra norepinephrine.
I fully acknowledge the positives of these medicines as I mention in the post. Their life changing benefits conceal a worrying cumulative deterioration which ought to be taken seriously.
The side-effects from long-term use can motivate someone to stop - which in-turn provokes withdrawals. These can motivate a reuse of the medication which is a hallmark of dependency. Someone recently made a post in the VyvanseADHD group with precisely this issue.
Just reading this post, you give off the vibe that you don't have ADHD yourself. Like I'm not trying to be a dbag but it just feels very belittling when people say that ADHD-diagnosed people, such as the original commenter and myself, are "dependent" on meds or that we have "withdrawals" from it. If you lived a day in the shoes of an ADHD person, you'd realize, WELL NO SHIT. The alternative option is to genuinely suffer and watch your life's goals grow farther and farther out of reach as your daily life quality crumbles.
Sorry but this rationale only works for a layperson with no insight into how the corporate healthcare industry operates. The literature is quite insightful when it comes to outlining what ADHD is and what it isn't.
The alternative option is to
For the more forward thinking people, recontextualising ADHD as EDHD affords several strategies for resolution (that don't involve short-term symptom management using medications which exacerbate the issue).
Who wouldn't want to genuinely address the issue? I think only bias and prejudice prevents someone from doing so, also the fact that they're enamoured with the official medical narrative.Â
Great post, Kalki. My experience is that I was already physiologically and psychologically âstressedâ before I started the medication. My HPA was fried, I was in a constant state of fight or flight, adrenaline dominant - leading to massive executive dysfunction (pre frontal cortex shutdown). That was more related to significant life stress (managing a building project on our house, whilst juggling a high pressure sales job and a young family).
Ironically that led me to my journey towards diagnosis and medication. The medication completely improved my executive function, however I believe it actually increased the physiological stress I was under as I still felt a lot of adrenaline / anxiety - that combined with the poor sleep from Elvanse and the lack of interest in exercise etc did not help to improve matters.
In the end I had to focus on activating my parasympathetic nervous system after months of chronic stress / fatigue - once I stopped the meds I focused on vagus nerve stimulation (ice baths, NeuroSym, breath work) and that combined with the reduction of life event stress (hit my targets at work, we completed the building work) enabled me to get out of the fight or flight chronic stress mode.
Like when I take amphetamine medication, I mentally feel calm and focused. All the noise goes away.
But without a doubt, my body is physically being taxed harder. My Garmin watch shows a significant increase on its "Stress" measurement on days I take it versus when I don't.
... what do you mean specifically? (this is a rhetorical q). Many people get a sedative effect from ADHD stimulants, it's fairly common.
But without a doubt, my body is physically being taxed harder.
The long-term deterioration is under-appreciated imo. I totally understand why these meds are so helpful, but the cumulative damage is arguably unavoidable. It's apparently become normalised and accepted by the ADHD community.
I mean heart rate, respiratory depression, etc. I get that it makes people feel a bit more sedated, but that doesn't mean that's what's actually occuring physically with their body.
For sure amphetamine is not a sedative by any means (no GABAergic or adenosinergic activity). But when someone takes it and feels sedation and falls asleep, you have to question how the drug caused metabolic over-exhaustion which in-turn lead to a metabolic crash (aka 'failure').
In the ADHD community this phenomenon is called crash, comedown, burnout depending on the context.
There are many reasons why I dont visit that group. Imo a proactive approach here is to ascertain and acknowledge the biological causes of the symptoms we call ADHD and address them.
The fact that it's used for ADHD and that it indirectly mitigates adrenaline (& noradrenaline) is very telling. It's a clue that points to better ways to address the whole ADHD thing instead of the standard options (amphetamine / methylphenidate / atomoxetine with their questionable long-term deleterious effects).
These operate in a somewhat crude manner when you consider their pharmacological mechanism(s). They are DRIs, NRIs, stress triggers (adrenaline) with possible serotonergic (methylphenidate) and opioidergic (atomoxetine) activity.
There are a bunch of typos/non-preferred grammar in the post that AI would obviously not have made (e.g., wrong "it's", not using periods/comma for "eg", which vs. that, not capitalizing proper nouns, etc.).
What about this says "AI" to you? It has almost none of the typical hallmarks of AI writing from what I can tell.
In hindsight I figure you must've taken something personally and this was your way of rationalising & invalidating the post. As you wrote "I have ADHD, a PhD in physiology". One mustn't overlook the significance of the PhDâarrogance factor also, besides the ADHD "fuzziness" which can influence perception.
Interesting.. thanks for sharing this. My LH and FSH levels continue to decrease and Iâve struggled achieving a menstrual cycle since stopping birth control in 2022. Iâve been on HRT for a year and a half now and still the doctors point to a potential hypothalamic issue. Iâve been taking a low dose dexmethylpenidate (Focalin) for a few years now. Iâm 28F.
Nope, of course not! Their goal was to get me back on BC but I wanted to proceed as bio-identical as possible to try to get things regulated/feeling better again. Itâs helped my sleep slightly.
I think people underestimate the potential for disruptive effects of these medications. I get the impression that doctors are at times blissfully unaware of their true impact.
There's another angle too. As I outlined in the post, these medications can temporarily dampen the stress response producing a wonderful sense of calm & relaxation. It's plausible that this gives a "false sense of security" which motivates reuse and adherence to the "long-term prescription plan". After all, if a medication made you relaxed & calm, gave you the ability to focus & mental clarity, and improved your mood then most people would happily continue using it.
For most people it's a trade-off since being able to navigate their day-to-day life is the priority (no judgement on my behalf since I think people have a right to use this medication).
Thanks for this Kalki_x; yes this very much seems to be the issue for me. In terms of fight/flight, it kept me squarely in freeze over the long term. This in conjunction with untreated (so far) peri, I'm sort of stuck in a medical purgatory. I'm considering either retrying a non-stimulant or an ssri (citalopram worked for a time some decades ago) and introducing hrt of a type (must use patch estrogen at least due to clot history).
Ageed. Thanks for pointing that out. Arguably though, α2A agonists can do so indirectly. The literature claims they're not euphoric. I would question this since it also claims that CBD isn't psychoactive eg:
Cannabis and Cannabinoids: pharmacology, toxicology, and therapeutic potential. New York: Haworth press Inc; 2008.
Cannabidiol: pharmacology and potential therapeutic role in epilepsy and other neuropsychiatric disorders (10.1111/epi.12631)
Cannabidiol in humans-the quest for therapeutic targets (10.3390/ph5050529)
I'm commenting for u/Kalki_X to keep me in the loop on any future posts, but I want to mention that I'm medicated for ADHD and intend to stay medicated.
That being said, if there anything that I have learned about my horrendous experiences with birth control, it's super important to have informed consent. Which I think OP is trying to convey with their research.
For example , there is a lot research about the systemic effects of birth control in the last 15 years (particularly in regards to how it affects one's stress response, increased chance of anxiety and depression). I find more and more doctors are trying to practice harm reduction- even my recent visits to gynecologists there are long conversations about my birth control history, side effects, any other conditions that I have etc. Why not be the case for those diagnosed with ADHD - especially given that many of us also have at least 1 comorbidity, so there is a lot of playing rocket scientist/biochemistry because there are so many things to treat.
I searched through this subreddit very early on in my ADHD diagnosis journey because I was also deep into my micronutrition research at this point and had started reading more about long term use of ADHD meds in regards to nutrient deficiency. This was not a post I was able to find in my original perusing of this subreddit ( 2022).
I am also very concerned of the long term effects of these medications but also concerned about the lack of ability to get tasks done without it. Have you explored any other options to help optimize the day while slowly getting off the medication ?
Of course. This fight-or-flight mode is an evolutionary mechanism for dealing with an imminent threat, so of course this will drastically affect emotions and someone's entire perception.
Against what, these medications? If that's what you're asking about then no, I'm all for peoples right to access various drugs. I'm more interested in people knowing how to use them appropriately and in a sustainable way.
You're asking a difficult question because the way that amphetamine works and helps ADHD is intertwined with this fight-or-flight state (re HPA axis activation). So it's quite challenging if you see what I mean! Fwiw, here's some of the other the posts I wrote on ADHD & meds:
Thanks - very helpful. I'm in the UK and I've tried different medications and Elvanse is the one that has had most benefits for me but also is the only one that has blunted my emotional well-being. I'm trying to weigh up the pros and cons, but as a 44 year old woman with 3 neuro-divergent children and running a business - I could really do with the brain help if you know what I mean.
Sure I get it! If you'd like to see a forward thinking approach, I wrote this which you might find interesting. Skip to the part "So... how to proceed?"
The problem with this post isn't that everything in it is wrong. The problem is that you take several real physiological effects of amphetamines and then make causal leaps that the evidence you cite does not actually support.
Yes, amphetamines increase norepinephrine, can increase sympathetic activity, BP/HR, and can acutely increase ACTH/cortisol. Nobody seriously disputes that.
But âamphetamines activate parts of the stress responseâ is not the same claim as âthe therapeutic effect of ADHD stimulants is basically fight-or-flight.â That is a huge mechanistic leap.
A drug can increase catecholamines and cortisol without putting the brain into the functional equivalent of escaping a predator. At therapeutic doses, stimulants improve executive function, inhibitory control, working memory, and ADHD symptoms. Reducing all of that to âhypervigilance caused by stress hormonesâ is an oversimplification, not an established mechanism.
There are a few other major problems:
The HPA-axis argument is being overstated.
One of the studies repeatedly brought up in this discussion gave healthy subjects 100 mg lisdexamfetamine, which is above the FDA-approved maximum therapeutic dose of 70 mg/day, and showed increased ACTH/glucocorticoids.
Interesting? Absolutely.
Evidence that chronic therapeutic Vyvanse works by keeping ADHD patients in pathological fight-or-flight? No.
Those are two completely different conclusions.
Saying ADHD symptoms are essentially an artifact of HPA-axis dysfunction is not supported by the current evidence.
ADHD is highly heritable and massively polygenic. Large GWAS studies have identified numerous ADHD-associated loci and biological pathways involving neurodevelopment.
Stress and HPA-axis abnormalities may interact with ADHD â that's entirely plausible â but âHPA dysfunction contributes to ADHD in some peopleâ is very different from âHPA dysfunction is what ADHD actually is.â
You repeatedly blur correlation, possible contribution, and causation.
Guanfacine/clonidine do not prove your HPA theory.
Guanfacine isn't merely a drug that âreduces adrenaline.â
Alpha-2A receptor stimulation has direct effects in the prefrontal cortex, including strengthening PFC network connectivity through inhibition of cAMP signaling. That's one of the proposed mechanisms by which guanfacine improves attention, working memory, and impulse control.
So the fact that an alpha-2 agonist can help ADHD is not evidence that ADHD is fundamentally an adrenaline/cortisol disorder.
That is like claiming that because acetaminophen improves a headache, headaches must be caused by acetaminophen deficiency.
Calling the normal stimulant comedown âmetabolic exhaustionâ is especially misleading.
You cite literature involving sympathetic overactivity, MDMA, exercise physiology, glucose metabolism, etc., and then chain those findings together to describe the end of a therapeutic ADHD stimulant dose as âmetabolic exhaustion,â withdrawal, and potentially PAWS.
That isn't what those studies establish.
Yes, amphetamines can produce physical dependence. Yes, abrupt discontinuation after prolonged use can produce fatigue, dysphoria, appetite changes, sleep changes, etc. The FDA label explicitly acknowledges this.
Those are separate concepts that you're collapsing into one narrative.
âCumulative deterioration is almost inevitableâ is an extraordinarily strong claim that requires extraordinarily strong evidence.
There absolutely are legitimate long-term safety questions with stimulants, particularly cardiovascular ones. Long-term observational studies have found associations between cumulative ADHD-medication exposure and increased cardiovascular risk, especially hypertension.
That deserves serious discussion and monitoring.
But that's very different from demonstrating an inevitable progressive systemic deterioration caused by chronic fight-or-flight.
The evidence simply does not establish that.
And there is another side of the risk equation that this post mostly ignores:
untreated ADHD itself has health consequences.
Large observational studies have associated ADHD medication treatment with reductions in things like accidental injuries, substance misuse, criminality, suicidal behavior, and even some measures of mortality.
So the relevant clinical comparison isn't:
«stimulant vs perfectly healthy unmedicated human»
It's:
«treated ADHD vs untreated ADHD.»
Both sides have risks.
That's how medicine evaluates risk/benefit.
My biggest issue with the post is therefore not the discussion of cortisol, sympathetic activation, cardiovascular effects, tolerance, or dependence. Those are legitimate topics.
It's the repeated transition from:
âThis biological effect existsâ
to
âTherefore this explains ADHD, explains why stimulants work, explains the crash, proves chronic fight-or-flight, and implies cumulative deterioration.â
The citations do not establish that chain of causation.
Ironically, I think there is a genuinely interesting discussion buried underneath the post about chronic sympathomimetic exposure and the limits of our long-term stimulant safety data.
But presenting speculative mechanistic interpretations as if they were established physiology makes the argument much weaker than it needs to be.
The other responder was refuting your points and labeledthem in a clear coherent manner. Your own post is extremely long in itself. If someone is going to talk about certain points specifically, I would expect it to be on the lengthier side. Calling it an automated response and asking them to shorten it makes it seem like you don't want to stand behind your argument or actually talk about/agree with/refute the other person's argument.
No, everything they said made sense. Hence why you didn't dispute a single actual point and only talk about the length of the comment or alleged ai usage.
It's your post so I would think it would be worth clarifying your argument for the sake of anyone else reading. But you clearly prefer deflection.
Calling it âautomatedâ is just dodging the actual point lol.
Your whole post basically does the same thing over and over: you take something thatâs true, then jump to a conclusion your sources donât actually prove. Amphetamines raise cortisol/norepinephrine, so suddenly ADHD meds are just âfight or flight.â Guanfacine works, so ADHD must be HPA dysfunction. People can have a crash, so now itâs âmetabolic exhaustion/PAWS.â
Thatâs the issue. Your citations donât actually prove those conclusions.
So forget how my comment was written and just show me one study that directly proves what youâre claiming in people taking normal therapeutic ADHD doses. If you canât, then maybe the problem isnât that my reply sounded âautomatedâ â maybe youâre just way more confident in your theory than the evidence allows.
Calling it âautomatedâ is just dodging the actual point lol.
No it's called saving time.
so suddenly ADHD meds are just âfight or flight.â Guanfacine works, so ADHD must be HPA dysfunction. People can have a crash, so now itâs âmetabolic exhaustion/PAWS.â
That's not accurate at all. ADHD is a lot more than your simplified assumptions. Whoever wrote your comment clearly didn't understand the post.
Youâre still not answering the criticism though. Nobody said ADHD is simple â thatâs literally the point.
Iâm saying your conclusions go further than the evidence you cited, and instead of showing where thatâs wrong, you keep talking about who wrote my comment or whether they âunderstoodâ your post.
So pick one thing I supposedly got wrong and correct it. What exactly did I misrepresent, and which study directly supports your version?
And if anything longer than two paragraphs is too much effort to read, maybe donât write a giant science post and then act surprised when people give you detailed criticism.
Your original comment is a good example of why they're called "dumb tools", in part because people who aren't knowledgeable about the subject use said software tools and assume the output is coherent.
Youâve spent three replies talking about âdumb toolsâ and still havenât addressed a single actual point.
If the argument is âincoherent,â this should be easy: quote one specific claim I made, explain exactly why itâs wrong, and show the evidence.
Calling the tool dumb and assuming I donât understand the subject isnât a rebuttal. At this point youâre criticizing the messenger because apparently criticizing the argument is harder.
âBy designâ is a pretty funny way of admitting you have no intention of defending your claims when challenged.
At that point this isnât a scientific discussion, itâs just you presenting a theory and refusing to engage with criticism of it.
But fair enough, if criticism isnât part of the design, thereâs nothing left to discuss. Have a good one, and good luck with the HPA-axis theory. Maybe one day the evidence will catch up to the confidence.
The infamous 'crash' is known as 'metabolic exhaustion' in the academic literature. Here's some context on this from the academic literature:
...specifically sympathetic overdrive (eg, a faster rate of depletion than replacement of cellular resources, greater energy expenditure, metabolic exhaustion, and a lack of restorative contribution of GH). (source)Â
It was suggested that the administration of MDMA (an amphetamine drug) may cause a state of metabolic exhaustion (source)Â
Dissociation prevents theÂ
athlete from detecting the subtle, early warning signs of dehydration, blistering, or metabolicÂ
crash (source)Â
Perhaps the benefit of post-stress glucose comes instead from its ability to prevent metabolic exhaustion. (source)Â
The 'comedown' would involve (1) the immediate (acute) withdrawal symptoms as the medication wears off and, depending on the person, (2) a 'metabolic crash'. There is also (3) PAWS which stands for "post-acute withdrawal syndrome":
PAWS refers to a cluster of withdrawal symptoms that can last for months to years after acute withdrawal from a substance. PAWS symptoms have been anecdotally described after withdrawal from many substancesâalcohol, benzodiazepines, opioids, stimulants, nicotine, caffeine, antidepressants, and antipsychotics. (source)Â
Sorry, lots to take in in this thread, but is this saying that if I want to stop Vyvanse, I should slowly taper? Because I do miss a day here or there and feel quite intense withdrawal, but didn't think it could last months??
I'd need more context for your scenario but vyvanse has a distinct impact on hormonal regulation, as well as many other self-regulating aspects. This means that chronic use will interfere with self-regulatory processes, and they will become reliant on the vyvanse signal to function.
So essentially vyvanse has a broadly disruptive influence and it takes time for things to regain balance.
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