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jpl26
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This combination was portruded to increase levels of NE by 1600%, which is a rather huge increase. Before trying it of course, I had to research what the combination would do to a bodybuilder.
(This is going to be a long thread, because the interactions are complex)
Article 1:
1: Res Exp Med (Berl). 1978 Jan 30;172(1):97-108. Related Articles, Links
[The effect of mainly alpha-adrenergic drugs, indirect sympathomimetrics and dopamine on exocrine pancreatic function. Studies in the isolated cat pancreas (author's transl)]
[Article in German]
Heidbreder E, Sieber P, Heidland A.
The influence of mainly alpha-adrenergic drugs (noradrenaline, adrenaline, phenylephrine), indirect sympathomimetics (ephedrine, tyramin) and dopamine on the exocrine pancreatic function of the isolated perfused organ of cats was studied. The injection of noradrenaline and adrenaline induced simultaneously a rapid depression of flow rate and an increase of perfusion pressure. Phenylephrine, indirect sympathomimetic drugs and dopamine did not change the perfusion pressure and the hydrelatic function (flow rate, secretion of chloride and total calcium). The protein and enzyme secretion was enhanced both in normal animals and cats pretreated by reserpine or 6-hydroxydopamine. The pancreatic protein secretion was inhibited by alpha-adrenolytic as well as beta-adrenolytic substances, tetracain and atropine. It is concluded, that mainly alpha-adrenergic drugs stimulate the pancreatic enzyme secretion in a cholinergic manner.
PMID: 25465 [PubMed - indexed for MEDLINE]
Purpose of the article:
- When taking any for of alpha-adrenergic drug....like an A-2 blocker like Yoh HCL, the pancreas will be stimulated so that more insulin is released in relation to a response to a meal. Therefore, if you ever do run Yoh HCL, you have to eat low glycemic meals, or the insulin shifts (up and down) caused by the food intake and the stimulated pancreas will make you feel quite tired.
Now, what is tyramine, and what exactly does it do?
This article should help clear up some doubts.
1: Drug News Perspect. 2001 Nov;14(9):539-43. Related Articles, Links
Epinephrine analogues.
Sneader W.
Department of Pharmaceutical Sciences, University of Strathclyde, Glasgow, Scotland.
Tyramine was the first epinephrine analogue to be introduced into medicine, in the early 1900s. It was followed by ephedrine and pseudoephedrine in the 1920s and by the amfetamines a decade later. The popularity of the amfetamines grew throughout the 1930s and 1940s; after that, there was a slowly dawning realization that they were being widely abused. Isoprenaline, introduced in the 1950s, was soon recognized as superior to epinephrine when used as an inhaler by asthmatics, and it remained the drug of choice for the relief of bronchospasm until around 1970. Orciprenaline, which featured an orcinol system, had a long duration of action and was active by mouth; Boehringer marketed it both as an inhaler and as a syrup for the prophylaxis of bronchospasm. The greatly superior bronchodilators salbutamol and terbutaline, launched in 1968 and 1970, respectively, incorporate further variation on the molecular theme that had led to the development of orciprenaline. (c) 2001 Prous Science. All rights reserved.
PMID: 12806441 [PubMed]
So, there you have it. Tyramine is simply an epinephrine analogue...like ephedrine, but obviously weaker. Still, it still has a direct impact in the Beta-adrenoreceptors like ephedrine does, just less. How much? That information I still haven't found.
Can Tyramine + Yohimbe HCL cause a rise in BP that is dangerous? Well...not really.
This article explains it in a bit more detail:
1: Neurochem Int. 2003 Nov;43(6):573-80. Related Articles, Links
In vivo monitoring of norepinephrine and its metabolites in skeletal muscle.
Tokunaga N, Yamazaki T, Akiyama T, Sano S, Mori H.
Department of Cardiac Physiology, National Cardiovascular Center Research Institute, 5-7-1 Fujishiro-dai, Suita, 565-8565, Osaka, Japan.
Quote:
Basal dialysate MHPG levels were not affected by pargyline, reserpine, or desipramine. Addition of tyramine (sympathomimetic amine, 600 microM), KCl (100 mM), and ouabain (Na(+)-K(+) ATPase blocker, 100 microM) caused brisk increases in dialysate NE levels (200.9+/-14.2, 90.6+/-25.7, 285.3+/-46.8 pg/ml, respectively). Furthermore, increases in basal dialysate NE levels were correlated with locally administered desipramine (10, 100 microM). Thus, dialysate NE and its metabolite were affected by local administration of pharmacological agents that modified sympathetic nerve endings function in the skeletal muscle. Skeletal muscle microdialysis with local administration of a pharmacological agent provides information about NE release, uptake, vesicle uptake and degradation at skeletal muscle sympathetic nerve endings.
Therefore, as you can see, tyramine does increase NE levels, but it also does it like ephedrine, through the Beta-1 cardiac receptor.
1: Naunyn Schmiedebergs Arch Pharmacol. 1997 Feb;355(2):239-49. Related Articles, Links
Influence of adrenoceptor and muscarinic receptor blockade on the cardiovascular effects of exogenous noradrenaline and of endogenous noradrenaline released by infused tyramine.
Schafers RF, Poller U, Ponicke K, Geissler M, Daul AE, Michel MC, Brodde OE.
Department of Nephrology and Hypertension, University of Essen, Germany.
This study aimed firstly to compare the in vivo cardiovascular effects of exogenously administered and of endogenously released noradrenaline; secondly to characterize the adrenoceptors mediating these responses; thirdly to assess the influence of parasympathetic tone on the cardiovascular effects of noradrenaline. In two randomised placebo-controlled studies, healthy, young, male volunteers received intravenous (i.v.) infusions of noradrenaline at six incremental doses of 10-160 ng/kg/min and-in order to release endogenous noradrenaline-tyramine at four incremental doses of 5-20 micrograms/kg/min.
Quote:
Noradrenaline and tyramine were administered in the absence and presence of alpha 1-adrenoceptor blockade with doxazosin (2 mg p.o.), alpha 2-adrenoceptor blockade with yohimbine (15 mg p.o.), selective beta 1-adrenoceptor blockade with bisoprolol (15 mg p.o.) and muscarinic receptor blockade with atropine (1.5 micrograms/kg i.v. loading dose followed by 0.15 microgram/kg/min by i.v. infusion). Vasoconstrictor effects were assessed by measurement of diastolic blood pressure (Pdiast) and myocardial effects by measurement of systolic time intervals, namely the duration of electromechanical systole corrected for heart rate (QS2c). I.v. noradrenaline increased Pdiast (delta max 17 mmHg) and this was nearly completely suppressed by doxazosin but only slightly blunted by yohimbine. Noradrenaline also slightly shortened QS2c (delta max -22 ms), and this was potentiated by both doxazosin and yohimbine and completely blocked by biosprolol. I.v. tyramine reduced Pdiast (delta max -7 mmHg), which was not affected by alpha 1-adrenoceptor blockade, and profoundly shortened QS2c (delta max -104 ms) which was significantly correlated with a marked increase in systolic blood pressure (Psyst) (delta max 57 mmHg). The shortening of QS2c and the rise in Psyst were not influenced by alpha-adrenoceptor blockade but were antagonized by bisoprolol. Atropine potentiated the blood pressure rise and the shortening of QS2c induced by i.v. noradrenaline and converted the fall in Pdiast induced by i.v. tyramine into an increase. Thus the cardiovascular effects of exogenous noradrenaline are mainly characterized by alpha 1-adrenoceptor-mediated vasoconstriction and the actions of endogenous noradrenaline (released by i.v. tyramine) by beta 1-adrenoceptor-mediated positive inotropic effects. The rise in Psyst with i.v. tyramine most likely reflects positive inotropism and not a vascular "pressor' response.
Therefore, the BP rise caused by the tyramine is not a bad "pressor" response, like indicated, but a natural positive one.
How to use this combination?
1. Take 0.2mg/Kg of bodyweight of Yohimbe HCL in the morning.
(This can be too highly stimulatory for some people, so you can start at 3-4mg, and work your way up over the course of a week)
2. Take approx. 1000mg Tyramine at the same time.
(Again, like mentioned above, this can stimulate people too much, so work your way up from 300mg to 1000mg over the course of a week.)
3. Caffeine 200mg: Not completely necessary, but it will increase the length of time the Yohimbe HCL is in your bloodstream and it's metabolites, Specially 11-hydroxylyohimbine.....which has a half-life of 9-11 hrs.
Yohimbe HCL on the other hand has a short half-life.....< 1.5hrs It deteriorates into it's metaboliotes very quickly.
4. If you're off caffeine. (A lot of people are forgoing it). You can add Green tea to this stack with positive effects. Get a total of about 900mg ECGC's per day. Just take the Green tea 2X/day.
So, what is the main purpose of this stack?
It's a stack you can use when you come of an extended ephedrine run, and your beta-receptors are shot, your T3 levels are low etc.... This will help with the recovery process(Give you the much needed energy that is often not seen after extended ephedrine cycles), not enhance(In some people maybe), but keep your adrenaline levels normal, therefore keeping thermogenesis stable, and therfore foregoing any bad fat deposition due to your shot Beta-adrenoreceptors, and low T3 levels.
Safety Rating: 8/10 Note: I gave it an 8/0 rating because there is one contra-indication: It cannot be used if you're on any MAO inhibitors, or alpha-blockers for high BP. So, if you're on these, sorry but this combination is not for you.
Efficiency rating: 9/10 (It works very well)
Price rating: 8/10 (It's not expensive at all. Look around supplement sites, and pick the brands you like most.
(This is going to be a long thread, because the interactions are complex)
Article 1:
1: Res Exp Med (Berl). 1978 Jan 30;172(1):97-108. Related Articles, Links
[The effect of mainly alpha-adrenergic drugs, indirect sympathomimetrics and dopamine on exocrine pancreatic function. Studies in the isolated cat pancreas (author's transl)]
[Article in German]
Heidbreder E, Sieber P, Heidland A.
The influence of mainly alpha-adrenergic drugs (noradrenaline, adrenaline, phenylephrine), indirect sympathomimetics (ephedrine, tyramin) and dopamine on the exocrine pancreatic function of the isolated perfused organ of cats was studied. The injection of noradrenaline and adrenaline induced simultaneously a rapid depression of flow rate and an increase of perfusion pressure. Phenylephrine, indirect sympathomimetic drugs and dopamine did not change the perfusion pressure and the hydrelatic function (flow rate, secretion of chloride and total calcium). The protein and enzyme secretion was enhanced both in normal animals and cats pretreated by reserpine or 6-hydroxydopamine. The pancreatic protein secretion was inhibited by alpha-adrenolytic as well as beta-adrenolytic substances, tetracain and atropine. It is concluded, that mainly alpha-adrenergic drugs stimulate the pancreatic enzyme secretion in a cholinergic manner.
PMID: 25465 [PubMed - indexed for MEDLINE]
Purpose of the article:
- When taking any for of alpha-adrenergic drug....like an A-2 blocker like Yoh HCL, the pancreas will be stimulated so that more insulin is released in relation to a response to a meal. Therefore, if you ever do run Yoh HCL, you have to eat low glycemic meals, or the insulin shifts (up and down) caused by the food intake and the stimulated pancreas will make you feel quite tired.
Now, what is tyramine, and what exactly does it do?
This article should help clear up some doubts.
1: Drug News Perspect. 2001 Nov;14(9):539-43. Related Articles, Links
Epinephrine analogues.
Sneader W.
Department of Pharmaceutical Sciences, University of Strathclyde, Glasgow, Scotland.
Tyramine was the first epinephrine analogue to be introduced into medicine, in the early 1900s. It was followed by ephedrine and pseudoephedrine in the 1920s and by the amfetamines a decade later. The popularity of the amfetamines grew throughout the 1930s and 1940s; after that, there was a slowly dawning realization that they were being widely abused. Isoprenaline, introduced in the 1950s, was soon recognized as superior to epinephrine when used as an inhaler by asthmatics, and it remained the drug of choice for the relief of bronchospasm until around 1970. Orciprenaline, which featured an orcinol system, had a long duration of action and was active by mouth; Boehringer marketed it both as an inhaler and as a syrup for the prophylaxis of bronchospasm. The greatly superior bronchodilators salbutamol and terbutaline, launched in 1968 and 1970, respectively, incorporate further variation on the molecular theme that had led to the development of orciprenaline. (c) 2001 Prous Science. All rights reserved.
PMID: 12806441 [PubMed]
So, there you have it. Tyramine is simply an epinephrine analogue...like ephedrine, but obviously weaker. Still, it still has a direct impact in the Beta-adrenoreceptors like ephedrine does, just less. How much? That information I still haven't found.
Can Tyramine + Yohimbe HCL cause a rise in BP that is dangerous? Well...not really.
This article explains it in a bit more detail:
1: Neurochem Int. 2003 Nov;43(6):573-80. Related Articles, Links
In vivo monitoring of norepinephrine and its metabolites in skeletal muscle.
Tokunaga N, Yamazaki T, Akiyama T, Sano S, Mori H.
Department of Cardiac Physiology, National Cardiovascular Center Research Institute, 5-7-1 Fujishiro-dai, Suita, 565-8565, Osaka, Japan.
Quote:
Basal dialysate MHPG levels were not affected by pargyline, reserpine, or desipramine. Addition of tyramine (sympathomimetic amine, 600 microM), KCl (100 mM), and ouabain (Na(+)-K(+) ATPase blocker, 100 microM) caused brisk increases in dialysate NE levels (200.9+/-14.2, 90.6+/-25.7, 285.3+/-46.8 pg/ml, respectively). Furthermore, increases in basal dialysate NE levels were correlated with locally administered desipramine (10, 100 microM). Thus, dialysate NE and its metabolite were affected by local administration of pharmacological agents that modified sympathetic nerve endings function in the skeletal muscle. Skeletal muscle microdialysis with local administration of a pharmacological agent provides information about NE release, uptake, vesicle uptake and degradation at skeletal muscle sympathetic nerve endings.
Therefore, as you can see, tyramine does increase NE levels, but it also does it like ephedrine, through the Beta-1 cardiac receptor.
1: Naunyn Schmiedebergs Arch Pharmacol. 1997 Feb;355(2):239-49. Related Articles, Links
Influence of adrenoceptor and muscarinic receptor blockade on the cardiovascular effects of exogenous noradrenaline and of endogenous noradrenaline released by infused tyramine.
Schafers RF, Poller U, Ponicke K, Geissler M, Daul AE, Michel MC, Brodde OE.
Department of Nephrology and Hypertension, University of Essen, Germany.
This study aimed firstly to compare the in vivo cardiovascular effects of exogenously administered and of endogenously released noradrenaline; secondly to characterize the adrenoceptors mediating these responses; thirdly to assess the influence of parasympathetic tone on the cardiovascular effects of noradrenaline. In two randomised placebo-controlled studies, healthy, young, male volunteers received intravenous (i.v.) infusions of noradrenaline at six incremental doses of 10-160 ng/kg/min and-in order to release endogenous noradrenaline-tyramine at four incremental doses of 5-20 micrograms/kg/min.
Quote:
Noradrenaline and tyramine were administered in the absence and presence of alpha 1-adrenoceptor blockade with doxazosin (2 mg p.o.), alpha 2-adrenoceptor blockade with yohimbine (15 mg p.o.), selective beta 1-adrenoceptor blockade with bisoprolol (15 mg p.o.) and muscarinic receptor blockade with atropine (1.5 micrograms/kg i.v. loading dose followed by 0.15 microgram/kg/min by i.v. infusion). Vasoconstrictor effects were assessed by measurement of diastolic blood pressure (Pdiast) and myocardial effects by measurement of systolic time intervals, namely the duration of electromechanical systole corrected for heart rate (QS2c). I.v. noradrenaline increased Pdiast (delta max 17 mmHg) and this was nearly completely suppressed by doxazosin but only slightly blunted by yohimbine. Noradrenaline also slightly shortened QS2c (delta max -22 ms), and this was potentiated by both doxazosin and yohimbine and completely blocked by biosprolol. I.v. tyramine reduced Pdiast (delta max -7 mmHg), which was not affected by alpha 1-adrenoceptor blockade, and profoundly shortened QS2c (delta max -104 ms) which was significantly correlated with a marked increase in systolic blood pressure (Psyst) (delta max 57 mmHg). The shortening of QS2c and the rise in Psyst were not influenced by alpha-adrenoceptor blockade but were antagonized by bisoprolol. Atropine potentiated the blood pressure rise and the shortening of QS2c induced by i.v. noradrenaline and converted the fall in Pdiast induced by i.v. tyramine into an increase. Thus the cardiovascular effects of exogenous noradrenaline are mainly characterized by alpha 1-adrenoceptor-mediated vasoconstriction and the actions of endogenous noradrenaline (released by i.v. tyramine) by beta 1-adrenoceptor-mediated positive inotropic effects. The rise in Psyst with i.v. tyramine most likely reflects positive inotropism and not a vascular "pressor' response.
Therefore, the BP rise caused by the tyramine is not a bad "pressor" response, like indicated, but a natural positive one.
How to use this combination?
1. Take 0.2mg/Kg of bodyweight of Yohimbe HCL in the morning.
(This can be too highly stimulatory for some people, so you can start at 3-4mg, and work your way up over the course of a week)
2. Take approx. 1000mg Tyramine at the same time.
(Again, like mentioned above, this can stimulate people too much, so work your way up from 300mg to 1000mg over the course of a week.)
3. Caffeine 200mg: Not completely necessary, but it will increase the length of time the Yohimbe HCL is in your bloodstream and it's metabolites, Specially 11-hydroxylyohimbine.....which has a half-life of 9-11 hrs.
Yohimbe HCL on the other hand has a short half-life.....< 1.5hrs It deteriorates into it's metaboliotes very quickly.
4. If you're off caffeine. (A lot of people are forgoing it). You can add Green tea to this stack with positive effects. Get a total of about 900mg ECGC's per day. Just take the Green tea 2X/day.
So, what is the main purpose of this stack?
It's a stack you can use when you come of an extended ephedrine run, and your beta-receptors are shot, your T3 levels are low etc.... This will help with the recovery process(Give you the much needed energy that is often not seen after extended ephedrine cycles), not enhance(In some people maybe), but keep your adrenaline levels normal, therefore keeping thermogenesis stable, and therfore foregoing any bad fat deposition due to your shot Beta-adrenoreceptors, and low T3 levels.
Safety Rating: 8/10 Note: I gave it an 8/0 rating because there is one contra-indication: It cannot be used if you're on any MAO inhibitors, or alpha-blockers for high BP. So, if you're on these, sorry but this combination is not for you.
Efficiency rating: 9/10 (It works very well)
Price rating: 8/10 (It's not expensive at all. Look around supplement sites, and pick the brands you like most.
