I can say that I have searched this forum for all the recommendations for lowering adrenaline and have tried most of them. Salt, sugar, Inosine, theanine, glycine, taurine niacinamide, other gaba agonists. They definitely help but adrenaline would still easily spike in a stressful situation. Supplementing with vitamin D makes me more resilient to adrenaline spikes than all the mentioned supplements.
There are numerous studies showing that light and vitamin D are effective for lowering blood pressure which I think is closely linked to adrenaline.
I always thought t3 lowers stress hormones. whats your reasoning behind t3 increasing?
Too much t3 and you can get loose stools and body rushes that are distinctive of adrenaline. Some people might not get this because of good glycogen stores and insulin sensitivity but I'm not completely sure why. Someone once said here that Ray says you should get some t4 because it's involved in adrenaline metabolism somehow. Maybe you can find it with a search.
I've tried many things for adrenaline and 1/4 grain of NDT twice a day is the best by far.
do you think its safe to take every day and for how long have you been taking it. also would be good to find out what brand you use. thanks
Clonidine = sexual dysfunction is a known side. I agree it makes one feel 'weird'.
GABA = reports of effect must be placebo effect? It doesn't cross the BBB. Whether there is some effect in the rest of the body that feels 'anxiolytic', I don't know. I've never felt a thing from it.
Urapidil- sympatholytic antihypertensive. an α1-adrenoceptor antagonist and 5-HT1A agonist. Studies suggest it crosses the BBB, has a central effect
Prazosin- α1-adrenoceptor antagonist known to cross the BBB and give significant central effect. Already used off-label for many years for anxiety/ptsd/etc.
Doxazosin- similar to prazosin but less central effect, greater body effect (e.g. in relaxing prostate, bladder-neck, etc. in BPH)
Pregabalin- decreases activation of amygdala and left insula in response to emotional images. Long term use is possibly bad juju...possible seizures etc.
Xanax- works fukin great. But NOT a solution for every day use. If one has the character, i.e. self-discipline, to NEVER take it two days in a row, one can avoid tolerance. Best is never more than twice a week. Never use more than half a 2mg bar. Best is a quarter-bar sublingual, as the speed of effect makes it feel more powerful/relieving, like half a bar, while the smaller dose minimizes bad juju.
Note that BZDs seem to -interfere- with fear-memory extinction, possibly via reduced arousal and decreased release of neurochemicals (e.g. noradrenaline) and stress hormones (e.g. glucocorticoids) that support extinction.
GABAergic system contributes to the anxiolytic-like effect of Lemongrass essential oil - Cymbopogon citratus
"Silexan is Lavender essential oil from Lavandula angustifolia flowers with proven clinical efficacy for anxiety disorders. In contrast to diazepam, it was devoid of any significant effect on locomotor activity and muscle-grip performance. All three doses of Silexan showed significant and dose-dependent anxiolytic activity- (3, 10, and 30 mg/kg, IP)
Is not recognized as benzodiazepine-like in rats trained to discriminate a diazepam cue.
Worked on subsyndromal anxiety and comparable to lorazepam in patients with GAD.
Had beneficial effects on typical co-morbidity of anxiety- disturbed sleep, somatic complaints, or decreased quality of life. Except for mild gastrointestinal symptoms, the drug was devoid of adverse effects, no withdrawal."
HPA axis dysregulation involving hypercortisolemia is a feature of stress-related disorders. Evidence suggests that chronic stress may lead to endocrine disruption and hypercortisolemia. Blockade of 5-HT7 receptors normalized increased acute stress-induced corticosterone secretion in chronically stressed animals. 5-HT7 receptor antagonists have been demonstrated to produce fast antidepressant-like efects.
vasodilatory properties of carvedilol and labetalol mediated by α-adrenergic blockade; but nebivolol's dilation effect is via eNOS via b3 agonism
Carvedilol, a vasodilating beta-blocker, which inhibits alpha1 as well as beta1 and beta2 adrenergic receptors.
2013 russians say- bisoprolol, carvedilol, and nebivolol was associated with significant elevation of parasympathetic part of vegetative nervous system tone, improvement of systolic blood flow in cavernous and dorsal arteries. Analysis of data obtained by Vasilchenko questionnaire demonstrated improvement of psychic and erectile components of sexual function. Thus bisoprolol, carvedilol, and nebivolol did not worsen sexual function of men with AH, improved spectral parameters of HRV and vascular blood flow in arteries of cavernous bodies
2001 Italians say- During the first month, sexual activity (intercourse per month) declined with both drugs; carvedilol 8.2 to 4.4, valsartan 8.3 to 6.6. Ongoing with the treatment the sexual activity further worsened with carvedilol (3.7/month) while fully recovered and also improved with valsartan 10.2 per month. The results were confirmed by the cross-over. Erectile dysfunction was a complaint of 15 patients with carvedilol (13.5%), one patient with valsartan (0.9%), and one patient in the placebo group.
Nebivolol- this is the best BB I've found. No sexual dysfunction. Possibly even a slight gain. It's the other 'vasodilating' BB (carvedilol is the only other BB that vasodilates).
Probably the religious fanatics will freak, since Neb. dilates via activating eNOS to produce NO. sinful
However, it activates eNOS by agonizing b3 adrenorecptors, and this b3-agonism is what produces..."Anxiolytic effects of beta3 adrenoceptor activation via GABAergic synapses in the basolateral amygdala."
Also, Nebivolol mediated lipolysis through β3AR in human adipocytes. Interestingly, in human adipocytes, nebivolol activated UCP1, PPARγ coactivator-1α (PGC-1α) and cytochrome c (CYCS) gene expression in a p38 MAPK-dependent manner. Also, nebivolol significantly reduced the diameter of lipid droplets in cultured adipocytes. Nebivolol, through β3AR, is able to induce lipolysis and promote thermogenic and mitochondrial biogenesis genes. See? It's Peaty after all! so there.
Nebivolol-induced relaxation of aorta results from both inhibition of alpha1-ARs and activation of beta3-ARs; so it has therapeutic potential for conditions of elevated sympathetic tone.
β3-adrenoceptor agonists in clinical development for overactive bladder syndrome. nebivolol?
Nebivolol enantiomers act on different targets.
D-nebivolol induced vasorelaxation by activating beta(2)- and beta(3)-adrenoceptors and antagonizing alpha(1)-adrenoceptors.
L-nebivolol induced vasorelaxation by activating only beta(3)-adrenoceptors in our model.
Our results emphasize that nebivolol is a beta(1)-adrenoceptor antagonist with several important pharmacological differences from other beta(1)-adrenoceptor antagonists
Nebivolol- highly β1-selective at ≤10 mg/day, 320-fold greater affinity for β1 than β2 in myocardium
Nebivolol- significant reductions in DBP with 5 to 40 mg dail,y and reductions in SBP at higher daily doses (10–20 mg)
β3 agonism stimulates eNOS
Both carvedilol and nebivolol may improve platelet function and prothrombotic state
"nicergoline induced an increase of slow activities (like alpha), the profile close to central depressants." By which they likely meant opiates or alcohol. I tried it for a month, can't say I ever felt any effect; although it was a pretty chaotic month.
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