Has anyone been prescribed this med? If so what was your experience?
Probably more then you want to know
I trialled these Alpha-2 adrenergic agonist for for about a year, I experimented with clonidine for about 9 months at various low doses before swaping to guanfacine for maybe another 3 or so months at a dose closer to starting reference range. I had a specifc interest in these medication to enhance focus. There were little to no user reports for adults as this medication is mainly used in adhd children. Having used both guanfacine and clonidine I feel the effects are similar and my commentary/user report applies to both. These are similar class medications so I would assume it is in the vein of talking about something like ssris as whole although having tried various ssris I feel clonidine and guanfacine are more similar then that. The main reason I swapped and preferred guanfacine was that it is more selective and less sedating which is a major draw back of this medication.
Attention is covertly controlled by the brain. As a user experience when you are less distracted, you are better able to focus. Thus, in this way guanfacine regulates inhibitory control of attention.
Although these same general principles apply to the mechanism of actions behind stimulants. How both medications feel (ritalin vs alpha-2 adrenergic agonist) is completely different. Guanfacine seems to block out the distractibility noise before it appears. Stimulants seem to make the task at hand so enjoyable that they keep you on track despite the distractibility noise.
I think FDA preapproval and cross-marketing says something about the efficacy of this drug. I’m not sure pharmaceutical companies would invest in and push a drug like this for its indication in adhd from scratch/phase I trials. I’m not saying it doesn’t work, just really my personal experience makes me question the effect sizes in clinical practice.
I have read many polarised anecdotal reports that read; this makes me sedated I quit, or this medication is magic it saved my life. However, I’ve not heard one user state that it gives them a 'laser like focus.
Mechanistically, it modulates action in the prefrontal cortex and is primarily useful for hyperactivity and or emotional dysregulation. It does not affect inattention in the way stimulants can.
If you listen to Russell Barkley’s model of ADHD, you can see that emotional dysregulation is a major defining component of ADHD. Yet, emotional dysregulation is not part of the DSM-5 ADHD criteria. I think conceptually how this medication is marketed, tested and eventually prescribed is skewed towards it having efficacy in treating the hyperactivity component of the DSM-5 criteria. It however also treats the emotional aspect of adhd which is not currently in the DSM-5. It is therefore useful for affecting external behaviour. As a user experience, I conceptualise that fixing emotional dysregulation and reactivity also aids in reducing hyperactivity. In my personal experience, this medication has use cases and can be somewhat effective.
As you develop experience into ADHD medications, the ideas around what composites focus, attention and engagement are all intertwined, but within the framework of subjective experience, they can each be conceptually different. This drug is at least somewhat more nuanced than most. My take is that in the testing of these ADHD in children, the metrics are often measured by questionnaire responses from parents, teachers and clinicians. As an adult user of this medication, the subjective user experience and self-reporting of efficacy then become different. Irritability and emotional dysregulation are markers of ADHD in adults. As people with ADHD come into adulthood their hyperactivity symptoms tend to decline. This along with the difference in brain development between the paediatric and adult populations creates clinically different outcomes.
This is my experience, it is clear to me that this medication will do a few things:
Mildy reduces distraction without per se improving focus. Stimulants are different they give you drive. They make you enjoy what you are doing, this is not that. On a2a agonists you can choose what you want to do and the flow of it is that things just don’t seem to get in your way. Stuff does not distract you on this medication. You can do something but do you enjoy it? The subjective experience is not necessarily an enjoyable ride. On high doses of stimulants, you find yourself naturally engaged and enjoying things. On lower doses, you can squirrel away the hours and look at your watch to be like, “Oh where did all the time go?” This is not that experience on alpha-2 adrenergic agonists. I still feel like I could quit if I wanted to.
It dampens reflexive emotion, allowing greater opportunity for reflection and composition of thought in response to stimuli. I have found this helpful in improving my filter in conversation. It is especially useful in close and long-term relationships where the emotional valence is high. I am less annoyed by things and less reflexive. Because my reflection on emotion is better it facilitates greater emotional regulation and composition. I often inhibit my natural response, which is partly in composition a hyperactivity response. The end effect is that I am telling people less of what I think and they are less annoyed by me. I am less swayed by the emotional valence of content. I get along better and people seem to like me more. You might think this is great and it is, increasingly I show a lot more tact in navigating conversation. But I am also somewhat numbed. If I self-regulate the way I communicate, it becomes a form of co-regulation. The upside of this is that it makes me better in relationships, but ultimately the sedation and decreased motivation makes me feel I have less energy to engage with people. This medication provides a subtle but noticeable increase in my EQ.
It isn’t pleasant sedation like drinking a beer… obviously. It is not like benzodiazepines. It’s not heavy like APs. It is a natural tiredness. Unlike clonidine, which seems to wear off on me the reach (half-life) on guanfacine is huge. Before adjusting to the sedation of guanfacine, I just wanted to pass out at 3pm every day. In studies both mice and humans built a tolerance to the sedation, I did to the clonidine and I also have to the guanfacine. This also seems to be backed up by anecdotal user reports and dr observations. That said, sedation is the number one side effect of this drug and the most grappling and unpleasant. It is why most people quit this drug.
It reduces aggression. This has been shown in scientific studies of prisoners. In the gym, this medication definitely reduces my aggression. I’m into health and wellness and do powerlifting type stuff with a strength coach. I’m surprised I haven’t read an adult discuss this before. However, your focus and drive in the gym are noticeably absent and really lacklustre. Basically, in the gym it would appear that alpha-2 agonism affects your drive in a way that is anti-erogenic. In a roundabout way, I’ve experienced it marginally improves my focus, routine and consistency in getting to the gym, so it’s not all bad. Maybe I experienced less hyper energy, motivation and drive and more of a ‘just execute a plan’ type of motivation. Although your muscular strength is fine, this is the side effect I like the least. Reduced aggression is personally a problem I have with this medication as a person who is naturally passive and has a good handle on my aggression. Being extra chilled out isn’t really helpful. The simulants can counteract the sedation, but you are definitely still chilled out. For me, my hyper-ness and aggression is something that I harness in a positive way and are directly linked to my motivation and drive to complete a task. I definitely like to go out and attack the day if that makes sense.
I discovered somewhat unsurprising it is deployed in prison populations and autism, where behavioural aggression is an issue. The totality of the effects of this medication is that it kills your drive. It puts the dampener on.
You need a certain amount of brain development and metacognitive skills to understand aggression within yourself. It isn’t all bad and it is basically impossible to be assertive without any aggression. No one wants to be completely docile.
A child might not necessarily want to take this. It is very different taking this medication as an adult since it is a choice. The point could be made that the dampening and sedative effects of this medication can entail restrictive practice.
After realising how this medication affects my drive and seeing no one opening up the discussion about this, it prompted me to write about my experience. There is an inverted U curve in the response you get to this medication. If your baseline hyperactivity is too high, then it is possible this could lower the tone of that stimulation, yes. The effect being that it improves concentration. This is what this medication is marketed to do, but is that really what it does? The subjective experience is I think not and I can explain why.
The science says two important but not immediately self-evident things. It lowers systematic norepinephrine and strengthens connections in the prefrontal cortex. The a2a receptors on which guanfacine acts are preferentially distributed in the PFC. This means that guanfacine enhances PFC connectivity. In relation to the functions of the PFC, I have experienced the most pronounced effects in personality expression, moderating social behaviour and response planning before speaking. The lowering of systematic norepinephrine kills motivation, drive and lowers aggression. I am more thoughtful and like I said feel like I have higher EQ but ultimately this comes at the cost of motivation and drive. This medication is more of a systematic norepinephrine lower and PFC booster than anything else. Yes, it affects attention in that you have better self-regulation. However, it doesn’t affect focus in that it doesn’t give your ‘tunnel vision’ or increase engagement or enjoyment in a task. While there are subtle and nuanced effects in the PFC this medication is really a hyperactivity and behaviour regulator. Now, this is ultimately where the adult and child experience diverges. Children have an underdeveloped PFC hence why they struggle a lot with self-regulation, inhibition, and control, especially of anger. My ADHD is primarily inattentive. In alignment with the statements made by other anecdotal reports of users, this largely does not work for the inattentive type. However, where I diverge is that this is a simplification. If you view increased EQ as procognitive, then you can see how a medication that is a behavioural regulator can make you socially smarter and a better human. Social engagement and the environment have a massive flow on effect. Especially at an early age as the effects of improved social functioning compound over time and as you grow. As children with ADHD come of age, their hyperactivity symptoms naturally diminish. As a result, ADHD adults skew more towards their residual inattentive symptoms. Therefore, I bet this medication will work on kids better than it will work on adults. I imagine the drug companies know this hence why they have not yet funded studies or sought approval for ADHD in adults.
As an adult, the conclusion to draw is that this medication is only useful as an adjunctive to stimulants. You basically need a stimulant to counteract the sedation to be able to effectively operate on this stuff. I had to use Ritalin a few times just to get me through the day. Stimulants raise your blood pressure and make you prone to insomnia this can help with BP and sleep. For me, it has social procognitive effects and a mild increase in attention is apparent. I’m sure this works equally well to take the edge off and control the jitters on amphetamines and high doses of stimulants. To me, this is not an effective sole agent but remains a useful adjunctive. I think because the benefits of this medication are subtle but multifactorial, it can still be useful. Pragmatically, I think appropriate dosing can be used to ameliorate BP, sleep or heart rate changes from stimulant usage. It can take months for the sedation tolerance to fully build and to see the full effects. I have found a low dose of guanfacine/clonidine means little in the way of sedation. I find this dose may help with cognition but my feeling is that dosing so low the effects on attention become a bit elusive. To appreciate the effects on attention, I think you have to dose to the upper end of your tolerance. The selectivity of guanfacine is appreciable and in my opinion produced a pronounced effect but only in comparison to clonidine.
Situationally low doses of these medications would be really quite beneficial because of rebound hypertension and sedation tolerance, they can’t really be used in this way. Especially because sedation isn’t a useful property when you need to go back to back with high-pressure days.
Surprisingly useful if you have anxiety, in my experience sedation aside fewer side effects and mood changes than antidepressants. Could be useful if friends or significant others thought you were too high energy or couldn’t control yourself, but as an adult, you are afforded the luxury of choosing the people who you surround yourself with. Incredibly nuanced and subtle medication. Useful when paired with stimulants and unique effects on social cognition. Prepare to spend time tuning the dosage and adjusting to this medication. On balance, increased medication load may not warrant the effectiveness of these drugs in long term usage. It does so many things really well. Just to me it is a prefrontal cortex booster more than an ADHD medication. I definitely wish I had discovered this back when I still had ptsd and anexity. 10/10 for those indications I would think.
This is easily one of the most interesting medications I’ve taken.
Yeah look my personal experience with medication is that new mediation can introduce a hyper-awareness around its effects. It is an exciting time and it is good to feel these things out, to see if it works for you. That said how much anyone fretts over initial effects is probably over pronounced. These things tend to play themselves out and in the end ultimately it either does or doesn’t work.
I was prescribed clonidine for ADHD and off-label sleep. The noradrenergic system plays a big role in the flight-fight-freeze response. A surprising effect was that clonidine helped hypervigilance a lot. The problem with clonidine is that it is quite sedating. How it is used in adhd is that it is commonly used as an adjunctive with a stimulant which is not appropriate in scz. I have read many case reports on this medication, and at an effective dose, clonidine is really just too sedating. It is mainly used for emotional regulation in adhd not so much attention and focus. I think the way it boosts signal strength in the PFC and the brain regions that noradrenergic α2 are preferentially distributed makes it work this way. It makes sense that it prescribed for children with adhd as a large part of there issues growing up is also social cohesion and being able to sit still and assimilate in a classroom. A sedative that helps boost social cognition will do wonders there. It also depends on what your baseline level of stimulation is if you are overly alert, jumpy, distracted or jittery and skew towards anexity/adhd it will help more.
I did a deep dive into this medication. Another issue is that it would be situationally useful but as the rebound hypertention you get on discontinuation isn’t good then yeah you have to take it continually and so sedation sucks. Not great to stack with sedating APs.
From the papers, guanfacine is a better agent and is less sedating also. You uncommonly hear of people getting depression when taking this long-term and I personally experienced this. Then again this is an uncommonly used medication in the adult population.
I can understand why researchers would think this right work in scz as an adjuctive but this 100% the case where they are testing something without understanding the subjective feeling, then additionally this medication combined with an antipsychotic. No researcher in their sane mind is going to do that to themselves for any extended period of time because they simply won’t function as well as they would have otherwise.
It is going to improve your EQ and resolve hypervigilance type symptoms at the cost of making you more sedated and less able to function well in life imo for the majority of people. This medication is very nuanced in it’s use in scz and has applications where overactivation is an issue namely during psychotic episodes and in hypervigilance.
I would highly recommend this medication to people who need sedation and anxiolytic effect (people taking benzos) but really if you are having issues with sedation then in scz I would just recommend a high dose of AP or the addition of OLZ or quetiapine. So again use case is limited in scz. Could potentially pair with Cariprazine, Aripiprazole/Brexpiprazole since they are ‘stimulating’ and are known to produce anxiety.
You might have improved test scores on this medication but in full review I would give it a skip unless you are already on benzos and it can act as a substitute for that. I’d personally much prefer to take this then benzos mainly because you can’t take benzos long term but this at least on paper seems a decent medication to take long term.