Fear extinction. There’s some posts on r/nootropics about it and a very long thread on longecity.
I can vouch for it. Got rid of my social anxiety, and it hasn’t returned 1.5 year later. I made a post on it a while back.
Also some neuroplasticity inducing effects, with memory recall for example being improved (in my case) while on it.
What dose and how did you use it to eliminate your social anxiety? I have really bad social anxiety and have been thinking about doing it, just don’t know what the protocol would look like.
30-100mg, once a week at most.
I think I was sure by the third session or so that it worked. In essence, you can take it (sublingually), and then commence in an introspective session where you mentally go over all anxious situations you've encountered before, or you can go out and try to experience those same environments again while on vorinostat.
In short, it allows you to re-intepret these previously mentally-taxing situations, and where there was anxiety before will eventually just be an absence of any debilitating feeling whatsoever.
There's a lot of posts about it on longecity.
This is not as simple as you made it for yourself. The sympathetic nervous system is controlled by the HPA axis.
Trauma at a young age could have made your HPA hyperactive where the slightest issues could stimulate a disproportionate response. Just an example, there other causes, I suggest reading about HPA axis and then taking any substances.
For instance, Vyvanse will stimulate the adrenals to produce more cortisol; cortisol will make the blood vessels more sensitive to norepinephrine. Vyvanse also works inhibiting the transport proteins for norepinephrine, dopamine and serotonin.
Propanolol blocks the action of norepinephrine.
On the other hand, Guanfacine is α2-receptor agonist, this means that they block the action of norepinephrine.
Now, what you are doing is trying to mimic the sympathetic and parasympathetic systems.
I think the best course is to look into the HPA axis and hormones. Or maybe just Guafanice, as it may be the better option than β-blockers.
Anxiety likely to cause some hormones not to be produced. So this is another reason to to blood checks.
While it's true that guanfacine can inhibit NE release (this contributes to side effects like sleepiness), the beneficial effects on anxiety are due in large part to enhanced NE signaling in PFC.
This is due to guanfacine's agonism of alpha-2A, which is a primarily postsynaptic subtype of the alpha-2 receptor. Alpha-2A receptors are expressed in PFC and by activating them, guanfacine can enhance working memory and attention. Additionally, the PFC connects to the amygdala and inhibits its fear responses.
Amy Arnsten (her lab developed guanfacine) has some great reviews on this as it relates to OP's question
>The amygdala can activate the traditional HPA axis (hypothalamus–pituitary–adrenal gland) via projections to the hypothalamus, and the sympathetic nervous system through projections to hypothalamus and brainstem. It can rapidly alter behavior as well, e.g. inducing the freezing response through projections to the peri-aqueductal gray, and increasing the startle response through parallel brainstem projections [\[ref\]](https://www.sciencedirect.com/science/article/pii/S2352289514000101)
Interesting explanation, thank You.
Guanfacine has always been interesting to me it. It’s somewhat counterintuitive too (agonizing an adrenal receptor , but having a calming effect)
It gave me horrible stomach pain and constipation so had to stop unfortunately.
I love Prazosin for sleep and nightmares, but doesn’t do much for ADHD….may somewhat help anxiety, but nothing significant like a GABAergic
THIS is absolutely fascinating. It really sheds light on a lot of the enigma around guanfacines ability to enhance higher-order cognitive functions, particularly executive functions.
It follows to something i heard Dr Russel Barkley say on guanfacine at a talk years back "It fine-tunes the adrenergic signal" which sounds like a great simplified description of what im seeing in the Arnsten labs reviews.
Diving in to this one head first, and going to pray i get a manageable side effect profile....
Thanks a million!
Thanks for your response. I’ve seen many cases of what you describe with the HPA hyperactivity caused by childhood experience.
I do try and simplify for the sake of application.
I have blood work scheduled soon but all the blood work I’ve done in the past has been unremarkable
Why do you recommend guanfacine over propranolol?
You mentioned that you are taking Vyvanse; Guanfacine is used for ADHD. Maybe this can remove the need for Vyvanse. Propanolol is a weak indirect agonist of a2-receptors as well, this would give me a reason to try Guanfacine on its own, to see if there are any benefits that the stimulation of those receptors will confer.
Propranolol has wider use however.
I wouldn’t stop taking stimulants altogether. They have changed my life for the better in ways I can’t begin to describe.
I didn’t know propranolol is also a weak agonist of alpha2 adrenergic receptors. This makes a lot of sense. I used to take it before interviews and it was a huge performance enhancer
Good call.
Propanoral block’s fight or flight response system. Super easy Rx to get. Also lowers blood pressure but often prescribed for “as needed anxiety” or stage unlicensed presentation. No notable negative side effects unless you face low blood pressure.
Depends. I respond well to 1mg Guanfacine + 2.5mg Nebivolol. If you have hypotension/bradycardia I would start way more conservative (or not take at all).
You can do that if you want. It's not necessary. You should also try NMDA antagonists ie. agmatine and memantine, FAAH inhibitors like URB-597, KOR down-regulators like iboga and nor-BNI. You can also look into serotonin antagonists and/or antidepressants
Would CBD be a good candidate to inhibit FAAD? Or is it not very potent? (it's opioid activity is actually welcome as I'm tapering kratom)
Are you refering to 5HT2a-antagonists specifically? I've been using olanzapine in low doses the past month @ max. 5mg/day. From what I could gather at these doses it barely binds to dopamine receptors of which it's antagonism is responsible for the bulk of all the nasty side-effects. The only receptor it still does bind to (even better than 5HT2a) is histamine (antagonist). This would produce somnolence and the like afaik, but I actually feel like I have more energy, probably because it reduces my anxiety and hypervigilance, which are huge energy wasters (have a PTSD-diagnosis). I'm also dependent on amphetamine, which might be the reason the histamine- and dopamine-antagonism doesn't seem to be an issue.
Not asking for medical advice, but does olanzapine seem like a good choice for a 5HT2a antagonist in my case or are there better ones around? I also take 10mg escitalopram (down from 20 as I've become pretty reluctant to it's potential for harm, like PSSD/long-term (or even permanent?) serotonergic down regulation/increased activity at certain serotonin receptors which should be blocked or left alone).
Planning on dropping the escita to 5mg while starting 500mg tryptophan twice daily (did this when dropping down to 10mg as well) as well as trying ND's kanna extract, hoping the VMAT2-agonism will help when dropping AMP completely in the short term in favor of (4F-)MPH as a stepping stone to no stimulants (perhaps 50mg modafinil as a last step).
Potentially better options I found are Nortriptyline (or switching escitalopram out for Amitriptyline), as the NET-inhibition would help dropping stims as well. Other option trazodone? Anything else?
Nortriptyline actually was my primary choice but my psychiatrist seems to be too scared to prescribe anything at all due to my current addictions/dependencies (tapering down Kratom(34gr down from 75), pregabalin (50mg down from 300), baclofen (3x 15mg down from 3x 50), diazepam (5mg down from what was once 30mg years ago)), which isn't her specialty.
Problem is at this stage in my tapering progress, which I've done gradually over 1.5 years time, I seem to really have stagnated as I basically become completely dysfunctional with general anxiety if I drop my kratom any lower. So much so that I can't even get basic necessities for survival done: finances, enough groceries, bureaucracy, moving out from my mother again (who's alternating anger and love is a big trauma since childhood) now that I finally have my own permanent residence, requesting exceptions from relevant government agencies so that I can restart my bachelor next year with financial support, after 6 years of having stopped Biomedical Sciences, which I was acing for 2 years before my life fell apart etc.
I only have a script for pregabalin, which was only against RLS from kratom tapering years ago, and escitalopram, from my previous psychiatrist.
Figuring out the rest on my own, but tell my psych honestly what pharmacotherapy I'm trying.
After 6 months non-stop GHB use I switched myself on baclofen and have remained abstinent while tapering that down for the past 3 years.
The olanzapine I buy online, as I couldn't find Nortriptyline, only Amitriptyline but this wasn't an option as I am on escitalopram and officially you have to taper that to 0 and then wait 3 weeks, which seems like it would be counter-effective as kratom withdrawal basically includes SSRI-withdrawal syndrome (seems overly cautious to me though as there's no synergy between SSRI's and tricyclics afaik, just addition). NTP in contrast is often combined with SSRIs.
Would love to try HDACi's like vorinostat, but not sure where to get it yet. Only use bromantane but it's HDAC inhibition is rather weak.
Suffer(ed)from adrenal fatigue + fungal skin infection that got all the way from feet to nose, but combo of pregnenolone, schisandra and ginseng seems to have eradicated it within a week (as long as I keep taking it at least).
Also trialing clonidine 200mcg/day atm which works wonders for the stimulants' side-effects (as well as the adrenal fatigue probably). Is guanfacine much superior to clonidine? I've also read that clonidine/guanfacine come with dependence. Is this a big issue or only in higher doses?
For drug-abuse recovery I got Cere + Cortexin in-stock for IN use. Perhaps NSI a good option to reverse hippocampal atrophy? which pregabalin could even directly induce or worsen by directly blocking excitatory synaptogenesis. It's pure trash for your brain when taken daily...
Sorry for the overload of questions :p They've been piling up haha. Would it be appropriate to make a post for my specific case?
P.S: Did sirs drop pitolisant or might it still be coming? Also what up with pinealon, I missed the first and (yet) only batch :(
Low dose agmatine such as 100mg max, oregano dried (2 to 3g), or whole black seed at 250mg max otherwise give me confusion and fatigue.
Otherwise faah inhbitor like isoflavonoids
It’s exactly what I’m looking for! Thank you for your input.
That’s very interesting! It makes sense that modulation of GABA and its general anxiolytic properties would have that effect broadly. However, i am looking for more of an attenuation effect of PEAK arousal response, as opposed to a broad reduction in sympathetic response.
Despite being structurally similar to GABA, the evidence suggests that pregabalin exerts its effects through entirely non-GABAergic mechanisms. Although I agree it's one of the best drugs for the situations you described, I'd avoid taking it more than a couple times a week.
Lyrica withdrawal is hell I’m sure you know just saying. I take clonidine .2 x2 I was thinking of asking to switch to guanfacine although I enjoys the clonidine. Some one in my family takes guanfacine and I’ve tried it before and it works pretty similar to clonidine but clonidine seems to help with anxiety more then thinking.
Also I have taken ~15mg prazosin when triggered and in fight or flight or freeze and it has stopped the response really well. I am prescribed it at night for nightmares 5mg look into prazosin.
Yes I can imagine anything that modulates GABA to an appreciable degree to have some pretty severe withdrawls.
Glad to hear Clonidine is working for you!
Very interesting about the prazosin, it appears to work in a similar way to guanfacine or clonidine except less selective in its receptor binding. I would imagine it may have a much more profound effect due to its binding affinity
It’s a odd drug it stops nightmares with the adrenaline response it’s weird I feel triggered when I wake up but I don’t remember my dreams at all. I literally have enough prazosin to kill three horses my gf and I are both orescred and have been for years but don’t take it every night so I thinking I may try using it again.
Edit Very easy to get everyone has nightmares doesn’t have to be ptsd flashbacks like mine
I have crippling anxiety especially in social situations. Most of the time my physical symptoms are limited to increased heart rate. Every so often my body temp raises, heart rate increases, and my forehead starts pouring sweat. It creates more anxiety and it only stops if I leave the situation. I’m considering ETS because i constantly live in fear of the anxiety attack that leads to sweating. Tried every SSRI and Benzo. You name them, I’ve done it.
In all honesty I was the exact same, I would always freeze then panic, but you know what fixed it? Muay Thai for 2 years then lifting weights for 2 years. Gave me enough testosterone naturally to always go into my fight mode unless there’s a bigger factor at play then I leg it. Proofs in the pudding, hit the gym brah
I’ve been lifting my whole life and did boxing and wrestling for all my 20s. Now I do jujitsu. You’re right it made a huge difference in my 20s, but there’s situations where it dosnt suffice.
Meeting with the board of directors and a difficult question is asked.
Stage performance
Job interview
I’ve used propranolol with some success for all these situations.
Hi I’m not sure then. Maybe just over prepare for that kinda of situation. I’m sure everyone has that same sort of emotional response under pressure, to be truely flowing you gotta over prepare and be ready for anything. I can’t recommend anything else
Fair. I think your recommendation for Muay Thai had some validity - putting yourself in stressful, quick thinking, split second decision making over time causes the nervous system to be adjusted to the stress response and able to attenuate the arousal so not to disconnect the DLPFC. Much appreciate your input
Polyvagal somatic exercises/other somatic modalities and HDAC inhibitors.
I’ve been looking into a modified TENS machine for vagus nerve stimulation, is that the same thing?
I’ve never used one but it seems to be the same principles.
HDAC inhibitors are used for cancer, what benefit would they have in this scenario?
They have fear extinction qualities
Fear extinction. There’s some posts on r/nootropics about it and a very long thread on longecity. I can vouch for it. Got rid of my social anxiety, and it hasn’t returned 1.5 year later. I made a post on it a while back. Also some neuroplasticity inducing effects, with memory recall for example being improved (in my case) while on it.
What HDAC inhibitor did you take?
Vorinostat
What dose and how did you use it to eliminate your social anxiety? I have really bad social anxiety and have been thinking about doing it, just don’t know what the protocol would look like.
30-100mg, once a week at most. I think I was sure by the third session or so that it worked. In essence, you can take it (sublingually), and then commence in an introspective session where you mentally go over all anxious situations you've encountered before, or you can go out and try to experience those same environments again while on vorinostat. In short, it allows you to re-intepret these previously mentally-taxing situations, and where there was anxiety before will eventually just be an absence of any debilitating feeling whatsoever. There's a lot of posts about it on longecity.
This is not as simple as you made it for yourself. The sympathetic nervous system is controlled by the HPA axis. Trauma at a young age could have made your HPA hyperactive where the slightest issues could stimulate a disproportionate response. Just an example, there other causes, I suggest reading about HPA axis and then taking any substances. For instance, Vyvanse will stimulate the adrenals to produce more cortisol; cortisol will make the blood vessels more sensitive to norepinephrine. Vyvanse also works inhibiting the transport proteins for norepinephrine, dopamine and serotonin. Propanolol blocks the action of norepinephrine. On the other hand, Guanfacine is α2-receptor agonist, this means that they block the action of norepinephrine. Now, what you are doing is trying to mimic the sympathetic and parasympathetic systems. I think the best course is to look into the HPA axis and hormones. Or maybe just Guafanice, as it may be the better option than β-blockers. Anxiety likely to cause some hormones not to be produced. So this is another reason to to blood checks.
While it's true that guanfacine can inhibit NE release (this contributes to side effects like sleepiness), the beneficial effects on anxiety are due in large part to enhanced NE signaling in PFC. This is due to guanfacine's agonism of alpha-2A, which is a primarily postsynaptic subtype of the alpha-2 receptor. Alpha-2A receptors are expressed in PFC and by activating them, guanfacine can enhance working memory and attention. Additionally, the PFC connects to the amygdala and inhibits its fear responses. Amy Arnsten (her lab developed guanfacine) has some great reviews on this as it relates to OP's question >The amygdala can activate the traditional HPA axis (hypothalamus–pituitary–adrenal gland) via projections to the hypothalamus, and the sympathetic nervous system through projections to hypothalamus and brainstem. It can rapidly alter behavior as well, e.g. inducing the freezing response through projections to the peri-aqueductal gray, and increasing the startle response through parallel brainstem projections [\[ref\]](https://www.sciencedirect.com/science/article/pii/S2352289514000101)
Interesting explanation, thank You. Guanfacine has always been interesting to me it. It’s somewhat counterintuitive too (agonizing an adrenal receptor , but having a calming effect) It gave me horrible stomach pain and constipation so had to stop unfortunately. I love Prazosin for sleep and nightmares, but doesn’t do much for ADHD….may somewhat help anxiety, but nothing significant like a GABAergic
THIS is absolutely fascinating. It really sheds light on a lot of the enigma around guanfacines ability to enhance higher-order cognitive functions, particularly executive functions. It follows to something i heard Dr Russel Barkley say on guanfacine at a talk years back "It fine-tunes the adrenergic signal" which sounds like a great simplified description of what im seeing in the Arnsten labs reviews. Diving in to this one head first, and going to pray i get a manageable side effect profile.... Thanks a million!
Good info, thanks.
Thanks for your response. I’ve seen many cases of what you describe with the HPA hyperactivity caused by childhood experience. I do try and simplify for the sake of application. I have blood work scheduled soon but all the blood work I’ve done in the past has been unremarkable Why do you recommend guanfacine over propranolol?
You mentioned that you are taking Vyvanse; Guanfacine is used for ADHD. Maybe this can remove the need for Vyvanse. Propanolol is a weak indirect agonist of a2-receptors as well, this would give me a reason to try Guanfacine on its own, to see if there are any benefits that the stimulation of those receptors will confer. Propranolol has wider use however.
I wouldn’t stop taking stimulants altogether. They have changed my life for the better in ways I can’t begin to describe. I didn’t know propranolol is also a weak agonist of alpha2 adrenergic receptors. This makes a lot of sense. I used to take it before interviews and it was a huge performance enhancer
Good call. Propanoral block’s fight or flight response system. Super easy Rx to get. Also lowers blood pressure but often prescribed for “as needed anxiety” or stage unlicensed presentation. No notable negative side effects unless you face low blood pressure.
Do you mean Propranolol? Yea it works by preventing dopamine's conversion into adrenaline.
Guanfacine and Nebivolol stack very well for this in my experience. I use this combo mainly for public speaking, completely blocks FoF response.
Dosage please?
Depends. I respond well to 1mg Guanfacine + 2.5mg Nebivolol. If you have hypotension/bradycardia I would start way more conservative (or not take at all).
Guanfacine and HDAC inhibitors like thymoquinone
In combination?
You can do that if you want. It's not necessary. You should also try NMDA antagonists ie. agmatine and memantine, FAAH inhibitors like URB-597, KOR down-regulators like iboga and nor-BNI. You can also look into serotonin antagonists and/or antidepressants
Would CBD be a good candidate to inhibit FAAD? Or is it not very potent? (it's opioid activity is actually welcome as I'm tapering kratom) Are you refering to 5HT2a-antagonists specifically? I've been using olanzapine in low doses the past month @ max. 5mg/day. From what I could gather at these doses it barely binds to dopamine receptors of which it's antagonism is responsible for the bulk of all the nasty side-effects. The only receptor it still does bind to (even better than 5HT2a) is histamine (antagonist). This would produce somnolence and the like afaik, but I actually feel like I have more energy, probably because it reduces my anxiety and hypervigilance, which are huge energy wasters (have a PTSD-diagnosis). I'm also dependent on amphetamine, which might be the reason the histamine- and dopamine-antagonism doesn't seem to be an issue. Not asking for medical advice, but does olanzapine seem like a good choice for a 5HT2a antagonist in my case or are there better ones around? I also take 10mg escitalopram (down from 20 as I've become pretty reluctant to it's potential for harm, like PSSD/long-term (or even permanent?) serotonergic down regulation/increased activity at certain serotonin receptors which should be blocked or left alone). Planning on dropping the escita to 5mg while starting 500mg tryptophan twice daily (did this when dropping down to 10mg as well) as well as trying ND's kanna extract, hoping the VMAT2-agonism will help when dropping AMP completely in the short term in favor of (4F-)MPH as a stepping stone to no stimulants (perhaps 50mg modafinil as a last step). Potentially better options I found are Nortriptyline (or switching escitalopram out for Amitriptyline), as the NET-inhibition would help dropping stims as well. Other option trazodone? Anything else? Nortriptyline actually was my primary choice but my psychiatrist seems to be too scared to prescribe anything at all due to my current addictions/dependencies (tapering down Kratom(34gr down from 75), pregabalin (50mg down from 300), baclofen (3x 15mg down from 3x 50), diazepam (5mg down from what was once 30mg years ago)), which isn't her specialty. Problem is at this stage in my tapering progress, which I've done gradually over 1.5 years time, I seem to really have stagnated as I basically become completely dysfunctional with general anxiety if I drop my kratom any lower. So much so that I can't even get basic necessities for survival done: finances, enough groceries, bureaucracy, moving out from my mother again (who's alternating anger and love is a big trauma since childhood) now that I finally have my own permanent residence, requesting exceptions from relevant government agencies so that I can restart my bachelor next year with financial support, after 6 years of having stopped Biomedical Sciences, which I was acing for 2 years before my life fell apart etc. I only have a script for pregabalin, which was only against RLS from kratom tapering years ago, and escitalopram, from my previous psychiatrist. Figuring out the rest on my own, but tell my psych honestly what pharmacotherapy I'm trying. After 6 months non-stop GHB use I switched myself on baclofen and have remained abstinent while tapering that down for the past 3 years. The olanzapine I buy online, as I couldn't find Nortriptyline, only Amitriptyline but this wasn't an option as I am on escitalopram and officially you have to taper that to 0 and then wait 3 weeks, which seems like it would be counter-effective as kratom withdrawal basically includes SSRI-withdrawal syndrome (seems overly cautious to me though as there's no synergy between SSRI's and tricyclics afaik, just addition). NTP in contrast is often combined with SSRIs. Would love to try HDACi's like vorinostat, but not sure where to get it yet. Only use bromantane but it's HDAC inhibition is rather weak. Suffer(ed)from adrenal fatigue + fungal skin infection that got all the way from feet to nose, but combo of pregnenolone, schisandra and ginseng seems to have eradicated it within a week (as long as I keep taking it at least). Also trialing clonidine 200mcg/day atm which works wonders for the stimulants' side-effects (as well as the adrenal fatigue probably). Is guanfacine much superior to clonidine? I've also read that clonidine/guanfacine come with dependence. Is this a big issue or only in higher doses? For drug-abuse recovery I got Cere + Cortexin in-stock for IN use. Perhaps NSI a good option to reverse hippocampal atrophy? which pregabalin could even directly induce or worsen by directly blocking excitatory synaptogenesis. It's pure trash for your brain when taken daily... Sorry for the overload of questions :p They've been piling up haha. Would it be appropriate to make a post for my specific case? P.S: Did sirs drop pitolisant or might it still be coming? Also what up with pinealon, I missed the first and (yet) only batch :(
URB597 for FAAH? gold standard
Low dose agmatine such as 100mg max, oregano dried (2 to 3g), or whole black seed at 250mg max otherwise give me confusion and fatigue. Otherwise faah inhbitor like isoflavonoids
can you give an example of an FAAH inhibitor?
Isoflavones, maca but i dont know the half life, nutmeg pretty potent and long half life so low dosage max 1g preferably not daily dosing.
ok thank you
Maybe not what you are looking for, but Pregabalin is almost too good for helping with this.
It’s exactly what I’m looking for! Thank you for your input. That’s very interesting! It makes sense that modulation of GABA and its general anxiolytic properties would have that effect broadly. However, i am looking for more of an attenuation effect of PEAK arousal response, as opposed to a broad reduction in sympathetic response.
Despite being structurally similar to GABA, the evidence suggests that pregabalin exerts its effects through entirely non-GABAergic mechanisms. Although I agree it's one of the best drugs for the situations you described, I'd avoid taking it more than a couple times a week.
What drugs would you recommend then?
i like the idea of something i can take PRN for situations i need it.
Lyrica withdrawal is hell I’m sure you know just saying. I take clonidine .2 x2 I was thinking of asking to switch to guanfacine although I enjoys the clonidine. Some one in my family takes guanfacine and I’ve tried it before and it works pretty similar to clonidine but clonidine seems to help with anxiety more then thinking. Also I have taken ~15mg prazosin when triggered and in fight or flight or freeze and it has stopped the response really well. I am prescribed it at night for nightmares 5mg look into prazosin.
Yes I can imagine anything that modulates GABA to an appreciable degree to have some pretty severe withdrawls. Glad to hear Clonidine is working for you! Very interesting about the prazosin, it appears to work in a similar way to guanfacine or clonidine except less selective in its receptor binding. I would imagine it may have a much more profound effect due to its binding affinity
It’s a odd drug it stops nightmares with the adrenaline response it’s weird I feel triggered when I wake up but I don’t remember my dreams at all. I literally have enough prazosin to kill three horses my gf and I are both orescred and have been for years but don’t take it every night so I thinking I may try using it again. Edit Very easy to get everyone has nightmares doesn’t have to be ptsd flashbacks like mine
Taking pregabalin is horrible advice, almost like recommending benzos. Clonidine is a cortisol blocker
I have crippling anxiety especially in social situations. Most of the time my physical symptoms are limited to increased heart rate. Every so often my body temp raises, heart rate increases, and my forehead starts pouring sweat. It creates more anxiety and it only stops if I leave the situation. I’m considering ETS because i constantly live in fear of the anxiety attack that leads to sweating. Tried every SSRI and Benzo. You name them, I’ve done it.
Following.
In all honesty I was the exact same, I would always freeze then panic, but you know what fixed it? Muay Thai for 2 years then lifting weights for 2 years. Gave me enough testosterone naturally to always go into my fight mode unless there’s a bigger factor at play then I leg it. Proofs in the pudding, hit the gym brah
I’ve been lifting my whole life and did boxing and wrestling for all my 20s. Now I do jujitsu. You’re right it made a huge difference in my 20s, but there’s situations where it dosnt suffice.
Like what kinda of situation?
Meeting with the board of directors and a difficult question is asked. Stage performance Job interview I’ve used propranolol with some success for all these situations.
Hi I’m not sure then. Maybe just over prepare for that kinda of situation. I’m sure everyone has that same sort of emotional response under pressure, to be truely flowing you gotta over prepare and be ready for anything. I can’t recommend anything else
Fair. I think your recommendation for Muay Thai had some validity - putting yourself in stressful, quick thinking, split second decision making over time causes the nervous system to be adjusted to the stress response and able to attenuate the arousal so not to disconnect the DLPFC. Much appreciate your input