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Herbal amphetamine alternative


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#1 Shulginstestsubject

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Posted 13 November 2010 - 01:01 AM


I can't stop reading about this herb called Salvia miltiorrhiza. There are some studies that indicate that it has the same dopamine releasing effects as amphetamine. Here is one of them from NCBI.

Salviae miltiorrhizae Radix (SMR), an eminent herb in the treatment of cardiovascular disorder (called blood stasis in traditional Chinese medicine), is widely used in China, Japan, Taiwan and Korea. SMR is also herbal medicines used in the treatment of drug addiction without scientific support for their mechanism of action. We evaluated the effect of SMR on superoxide production by rat microglias using a 2-methyl-6-(p-methoxyphenyl)-3,7-dihydroimidazo[1,2-a]pyrazin-3-one-dependent chemiluminescence assay. SMR dose-dependently inhibited superoxide production by microglias stimulated with phorbol myristate acetate or opsonized zymosan, while it had no effect on superoxide production by a hypoxanthinexanthine oxidase system. These results indicate that SMR does not have a scavenging effect, but has an inhibitory effect on superoxide generation by microglias. Although SMR is commonly used for treating chronic cerebral infarction, it may also have a protective effect on progression of Parkinson's disease or Alzheimer's disease. On the other hand, the present study investigated the effect of the medicinal plant on dopaminergic neurotransmission in comparison with amphetamine. The effect of crude water extracts (0.1 g/ml) of SMR on K+ (20 mM)-stimulated dopamine release from rat striatal slices was compared with amphetamine (10(-4) M) using high-performance liquid chromatography with electrochemical detection to measure endogenous dopamine. Amphetamine and SMR significantly increased K+-stimulated dopamine release (P<0.001) from rat striatal slices when compared with K+-stimulated alone. SMR potentiated the effect of amphetamine on K+-stimulated dopamine release (P<0.001) when compared with amphetamine alone. The results indicate that SMR may stimulate dopamine release in the same manner as amphetamine. It remains to be determined whether the effect of this extract on dopamine function is important in its therapeutic use in the treatment of drug addiction.

You'd think that this herb would have a stimulant effect comparable to that of amphetamine. But apparently there are many other mechanisms as play because I've read, on other forums, personal accounts of people trying this herb and receiving a sedative effect from it(mainly because it has an alkaloid that binds to benzodiazepine receptors). Is there anybody who knows a lot about this herb and can explain it's mechanism to me? I really would like to know if you can feel it's dopaminergic effects, like if it exhibits "rewarding" effects. For those who take it for it's psychoactive effects, do you feel like it's worth taking? Does it have any motivating, rewarding, antidepressant, etc effects? Thank you!

#2 NR2(x)

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Posted 13 November 2010 - 03:58 AM

Increased Metabolism, Increased Plasticity, but acutely its a sedative, similar to alcohol, therefore lower dosing. I have no experience with this substance.




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Edited by NR2(x), 13 November 2010 - 04:01 AM.

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#3 NR2(x)

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Posted 14 November 2010 - 05:53 AM

I understand the intent of the members of this site is to examine compounds that show neuroprotective and improved general cognitive function eg better learning(this is the definition of a nootropic). Searching for drugs that enhance reward should be conducted else where. I really dont believe that this substance would be rewarding. That being said I only have a lay person knowledge and only have a limited capacity to fit disperate material together.
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#4 Animal

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Posted 14 November 2010 - 02:39 PM

I understand the intent of the members of this site is to examine compounds that show neuroprotective and improved general cognitive function eg better learning(this is the definition of a nootropic). Searching for drugs that enhance reward should be conducted else where. I really dont believe that this substance would be rewarding. That being said I only have a lay person knowledge and only have a limited capacity to fit disperate material together.


He could be trying to address anhedonia, or a similar lack of hedonic tone, this is something that is frequently discussed on this site. Treating these kinds of psychological impairment can indirectly have a significantly enhancing effect cognitively. We all know the detrimental effects depressive states can have on a individuals intellectual capacity.
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#5 NR2(x)

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Posted 15 November 2010 - 04:36 AM

wow anti-cancer anti-addiction anti-hiv anti-diabetes and strongly neuroprotective, why wouldnt scientist be crawling all over this?

#6 Guacamolium

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Posted 17 November 2010 - 08:03 AM

I would just say "sida cordifolia" and call it a day. That's just me I guess... ;)
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#7 KimberCT

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Posted 17 November 2010 - 03:07 PM

It's also a pretty potent ACE-inhibitor judging from its effect on blood pressure and the nasty dry cough I developed.

#8 longevitynow

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Posted 17 November 2010 - 06:39 PM

Salvia Milt is famous in Chinese Medicine for blood circulation, I'm skeptical about it as an amphetamine substitute, even if it might act on some of the same receptors. Great for blood circulation, and I am curious about anyone having an actual experience with it as a stimulant. I've tried "Geranamine", aka "Methylhexaneamine (Forthan, Forthane, Floradrene, Geranamine), or dimethylamylamine (DMAA)" or 1,3 Dimethylamylamine; originally a decongestant. It is somewhat similar to ephedrine. I like ephedra and ephedrine in low doses. I feel more focused and less wired (again low doses, not with a bunch of other stimulants). As they are off the market/illegal/hard to get someone suggested Geranamine (which is contained in geranium). In a low dose it made me sharp for 4-5 hours and I didn't feel wiped afterwards as I would with caffeine or most other chemical stimulants.

#9 Shulginstestsubject

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Posted 17 November 2010 - 07:35 PM

Well I just feel that amphetamines WOULD be thee ideal drug for cognitive enhancement, motivation (more like initiative, motivation is more of a virtue), treatment for social anxiety, etc.. if it wasn't highly neurotoxic. My motivation behind the search for an herbal alternative is to find a compound that closely mimics it's action with none, or at least less, of the neurotoxicity. Also, I've come upon another compound called Thunbergia laurifolia.

Thunbergia laurifolia Linn. (TH) and Simplocos racemosa Roxb. (SY) are herbal medicines used in the treatment of drug addiction without scientific support for their mechanism of action. The present study investigated the effects of these medicinal plants on dopaminergic neurotransmission in comparison with amphetamine. The effect of crude water extracts (0.1 g/ml) of TH and SY on K+ (20 mM)-stimulated dopamine release from rat striatal slices were compared with amphetamine (10−4 M) using high-performance liquid chromatography with electrochemical detection to measure endogenous dopamine. Amphetamine and TH, but not SY, significantly increased K+-stimulated dopamine release (P<0.001) from rat striatal slices when compared with K+-stimulated alone. TH potentiated the effect of amphetamine on K+-stimulated dopamine release (P<0.001) when compared with amphetamine alone. The results indicate that TH may stimulate dopamine release in the same manner as amphetamine. It remains to be determined whether the effect of these extracts on dopamine function is important in their therapeutic use in the treatment of drug addiction.

Thoughts?

Also I do realize that botanical compounds DO have neurotoxic potential. I'm just sort of assuming that plants carry less addictive and neurotoxic properties. Correct me if I'm wrong to assume this.

Edited by Shulginstestsubject, 17 November 2010 - 07:37 PM.


#10 NR2(x)

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Posted 18 November 2010 - 04:23 AM

Salvia miltiorrhiza will increase GDNF, therefore i include info on how GDNF effects cognitive function, wow, Type of stuff, you take before bed and wake up feeling alive, might take a few weeks to become noticable,

Effect of GDNF on differentiation of cultured ventral mesencephalic dopaminergic and non-dopaminergic calretinin-expressing neurons.
Schaller B, Andres RH, Huber AW, Meyer M, Pérez-Bouza A, Ducray AD, Seiler RW, Widmer HR.

Department of Neurosurgery, University of Bern, CH-3010 Bern, Switzerland.

Abstract
Glial cell line-derived neurotrophic factor (GDNF) is a potent survival factor for ventral mesencephalic (VM) dopaminergic neurons. Subpopulations of dopaminergic and non-dopaminergic VM neurons express the calcium-binding proteins calbindin (CB) and calretinin (CR). Characterization of the actions of GDNF on distinct subpopulations of VM cells is of great importance for its potential use as a therapeutic molecule and for understanding its role in neuronal development. The present study investigated the effects of GDNF on the survival and morphological differentiation of dopaminergic and non-dopaminergic neurons in primary cultures of embryonic day (E) 18 rat VM. As expected from our results obtained using E14 VM cells, GDNF significantly increased the morphological complexity of E18 CB-immunoreractive (CB-ir), tyrosine hydroxylase (TH)-ir, and CR-ir neurons and also the densities of CB-ir and TH-ir neurons. Interestingly, densities of E18 CR-ir neurons, contrarily to our previous observations on E14 CR-ir neurons, were significantly higher after GDNF treatment (by 1.5-fold). Colocalization analyses demonstrated that GDNF increased the densitiy of dopaminergic neurons expressing CR (TH+/CR+/CB-), while no significant effects were observed for TH-/CR+/CB- cell densities. In contrast, we found that GDNF significantly increased the total fiber length (2-fold), number of primary neurites (1.4-fold), number of branching points (2.5-fold), and the size of neurite field per neuron (1.8-fold) of the non-dopaminergic CR-expressing neurons (TH-/CR+/CB-). These cells were identified as GABA-expressing neurons. In conclusion, our findings recognize GDNF as a potent differentiation factor for the development of VM dopaminergic and non-dopaminergic CR-expressing neurons

Edited by NR2(x), 18 November 2010 - 04:28 AM.


#11 normalizing

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Posted 29 March 2016 - 10:52 PM

please continue with this thread, any updates developments reports!



#12 jaross

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Posted 30 March 2016 - 04:31 PM

Chinese Ephedra / Ma Huang.  My understanding is that its only bad for you in large doses or combined with caffeine.  I am no expert though I have tried a few stems (less then a grams worth) in tea form before.  Pleasant taste, and certainly has stimulating effects.

 

Also coca leaves / coca tea.  You can buy it on amazon, shipped to the USA.  I even had a package inspected by customs still get to me!  Yes, in large quantities and heavily refined/processed this is the stuff they make cocaine out of.. but the tea is much different/more mellow/less addicting/possibly even good for you.  


Edited by jaross, 30 March 2016 - 04:37 PM.


#13 normalizing

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Posted 30 March 2016 - 08:12 PM

jaross, novoandinastore offers full alkoloid coca leaves and powders im pretty sure its better than anything amazon will allow being sold on their website


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#14 sativa

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Posted 02 April 2016 - 07:14 PM

Yohimbe is a potent stimulant too. Combined with a bit of caffeine (green tea, coffee, guarana seed etc) you would be very very energised and stimulated.

#15 sativa

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Posted 28 July 2016 - 04:25 PM

Salvia miltiorrhiza (aka 'Dan shen') contains a sedative which acts as an MAGL inhibitor. MAGL degrades the endocannabinoid 2-AG, which acts upon CB1 (CNS) and CB2 (periphery) receptors.

Tanshinone IIA has been identified as a natural monoacylglycerol lipase (MAGL) inhibitor with an IC50 value of 48 nM.


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#16 gamesguru

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Posted 28 July 2016 - 04:47 PM

Pharmacological effects of Salvia miltiorrhiza (Danshen) on cerebral infarction
Tsai-Hui Lin and Ching-Liang HsiehEmail author (2010)

Danshen, the dried root of Salvia miltiorrhiza, is a Chinese medicine used to promote blood flow and treat vascular disease. The present article reviews the pharmacological effects of Danshen on cerebral infarction and possible interactions between Danshen and Western drugs. Danshen may reduce or prolong the development of atherosclerosis and may have anti-hypertensive and anti-platelet aggregation effects, which prevent cerebral infarction. Danshen may enhance endogenous anti-oxidative enzyme activities such as the expression of endothelial nitric oxide synthase and may scavenge oxygen free radicals. Prevention and treatment of cerebral infarction by Danshen involves multiple pathways, including anti-atherosclerosis, anti-hypertension, anti-platelet aggregation, anti-inflammatory and anti-oxidative effects.

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Salviae miltiorrhizae radix increases dopamine release of rat and pheochromocytoma PC12 cells.
Kim CH1, Koo BS, Kim KO, Kim JK, Chang YC, Lee IS. (2006)

The Radix of Salvia miltiorrhiza Bunge (Labiatae) (SMR), an eminent herb, is often included as an ingredient in various herbal remedies recommended for vascular circulation therapies. The present study investigated the effect of SMR on dopaminergic neurotransmission. Various extracts prepared from the stems of SMR were tested for cytotoxic activity on pheochromocytoma PC12 cells using the XTT assay method. The ethanol extract (IC50 > 100 microg/mL), water extract (IC50 > 100 microg/mL) and chloroform (IC50 = 90 microg/mL) fraction exhibited weak cytotoxic activity. However, the butanol (IC50 = 80 microg/mL) and ethyl acetate (EtOAc; IC50 = 70 microg/mL) fractions exhibited strong cytotoxic activity. Also, the extracts and fractions were investigated for dopamine release effects. The EtOAc fraction showed a stronger stimulatory effect on dopamine release activity than the other fractions. The effect of the crude EtOAc fraction (50 microg/mL) of SMR on K+ (20 mm)-stimulated dopamine (DA) release from rat striatal slices was compared with amphetamine (10(-4) m) using high-performance liquid chromatography with electrochemical detection to measure endogenous DA. The EtOAc fraction significantly increased K+ -stimulated DA release (p < 0.001) from rat striatal slices when compared with K+ -stimulated alone. The EtOAc fraction potentiated the effect of amphetamine on K+ -stimulated DA release (p < 0.001) when compared with amphetamine alone. To examine whether in vitro the EtOAc fraction treatment induces DA release in PC12 cells, the role of protein kinases was investigated in the induction of the EtOAc fraction-mediated events by using inhibitors of protein kinase C (PKC), mitogen activated protein kinase (MAP kinase) or protein kinase A (PKA). The PKC inhibitors chelerythrine (50 nm and 100 nm) and Ro31-8220 (100 nm) and the MAP kinase kinase inhibitor, PD98059 (20 microm), inhibited the ability of the EtOAc fraction of SMR to elicit the EtOAc fraction-stimulated DA release. The PKC activator, 12-O-tetradecanoyl phorbol 13-acetate (TPA, 100 nm) mimicked the ability of the EtOAc fraction of SMR to elicit DA release. In contrast, a selective PKA inhibitor, 50 microm Rp-8-Br-cAMP, blocked the development of EtOAc fraction-stimulated DA release. It was demonstrated that the EtOAc fraction of SMR stimulated DA release. Therefore the mechanism by which the EtOAc fraction of SMR induced the enhancement in EtOAc fraction-stimulated DA release is apparent.

 

Excitotoxicity effects of glutamate on human neuroblastoma SH-SY5Y cells via oxidative damage.
Sun ZW1, Zhang L, Zhu SJ, Chen WC, Mei B. (2010)
OBJECTIVE:
To investigate the mechanisms of excitotoxic effects of glutamate on human neuroblastoma SH-SY5Y cells.
METHODS:
SH-SY5Y cell viability was measured by MTT assay. Other damaged profile was detected by lactate dehydrogenase (LDH) release and by 4', 6-diamidino-2-phenylindole (DAPI) staining. The cytosolic calcium concentration was tested by calcium influx assay. The glutamate-induced oxidative stress was analyzed by cytosolic glutathione assay, superoxide dismutase (SOD) assay and extracellular malondialdehyde (MDA) assay.
RESULTS:
Glutamate treatment caused damage in SH-SY5Y cells, including the decrease of cell viability, the increase of LDH release and the alterations of morphological structures. Furthermore, the concentration of cytoplasmic calcium in SH-SY5Y cells was not changed within 20 min following glutamate treatment, while cytosolic calcium concentration significantly increased within 24 h after glutamate treatment, which could not be inhibited by MK801, an antagonist of NMDA receptors, or by LY341495, an antagonist of metabotropic glutamate receptors. On the other hand, oxidative damage was observed in SH-SY5Y cells treated with glutamate, including decreases in glutathione content and SOD activity, and elevation of MDA level, all of which could be alleviated by an antioxidant Tanshinone IIA (Tan IIA, a major active ingredient from a Chinese plant Salvia Miltiorrhiza Bge).
CONCLUSION:
Glutamate exerts toxicity in human neuroblastoma SH-SY5Y cells possibly through oxidative damage, not through calcium homeostasis destruction mediated by NMDA receptors.

Methylation and its role in the disposition of tanshinol, a cardiovascular carboxylic catechol from Salvia miltiorrhiza roots (Danshen).
Tian DD1, Jia WW2, Liu XW2, Wang DD3, Liu JH2, Dong JJ2 (2015)
AIM:
Tanshinol is an important catechol in the antianginal herb Salvia miltiorrhiza roots (Danshen). This study aimed to characterize tanshinol methylation.
METHODS:
Metabolites of tanshinol were analyzed by liquid chromatography/mass spectrometry. Metabolism was assessed in vitro with rat and human enzymes. The major metabolites were synthesized for studying their interactions with drug metabolizing enzymes and transporters and their vasodilatory properties. Dose-related tanshinol methylation and its influences on tanshinol pharmacokinetics were also studied in rats.
RESULTS:
Methylation, preferentially in the 3-hydroxyl group, was the major metabolic pathway of tanshinol. In rats, tanshinol also underwent considerable 3-O-sulfation, which appeared to be poor in human liver. These metabolites were mainly eliminated via renal excretion, which involved tubular secretion mainly by organic anion transporter (OAT) 1. The methylated metabolites had no vasodilatory activity. Entacapone-impaired methylation did not considerably increase systemic exposure to tanshinol in rats. The saturation of tanshinol methylation in rat liver could be predicted from the Michaelis constant of tanshinol for catechol-O-methyltransferase (COMT). Tanshinol had low affinity for human COMT and OATs; its methylated metabolites also had low affinity for the transporters. Tanshinol and its major human metabolite (3-O-methyltanshinol) exhibited negligible inhibitory activities against human cytochrome P450 enzymes, organic anion transporting polypeptides 1B1/1B3, multidrug resistance protein 1, multidrug resistance-associated protein 2, and breast cancer resistance protein.
CONCLUSION:
Tanshinol is mainly metabolized via methylation. Tanshinol and its major human metabolite have low potential for pharmacokinetic interactions with synthetic antianginal agents. This study will help define the risk of hyperhomocysteinemia related to tanshinol methylation.

 

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Upregulation of Collagen Expression via PPARβ/δ Activation in Aged Skin by Magnesium Lithospermate B from Salvia miltiorrhiza.
Jung YR1, Lee EK1, Kim DH1, Park CH1,2, Park MH1, Jeong HO1 (2015)

This study investigated the agonistic activity of magnesium lithospermate B (1), isolated from Salvia miltiorrhiza, on peroxisome proliferator-activated receptor (PPARβ/δ) and the expressions of collagen genes (COL1A1 and COL3A1) and transforming growth factor-β1 (TGF-β1) in models of skin aging. The action of compound 1 as a PPARβ/δ agonist was determined by reporter gene assay, immunostaining, and Western blotting. To determine the antiaging effects of compound 1 on skin, aged Sprague-Dawley rat skin and ultraviolet B (UVB)-irradiated human skin fibroblasts were used. The results show that 1 presented a marked enhancement of both nuclear protein levels and activity of PPARβ/δ in fibroblasts. In addition, 1 prevented downregulation of PPARβ/δ activity in aged rat skin and UVB-induced fibroblasts. Furthermore, 1 increased the expressions of COL1A1, COL3A1, and TGF-β1 in vivo and in a cell culture system. Therefore, the present study shows that compound 1 prevents collagen degradation in aged rat skin and UVB-exposed fibroblasts through PPARβ/δ activation. The therapeutic and cosmetic applications of compound 1 need further investigation.


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#17 normalizing

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Posted 28 July 2016 - 09:40 PM

Salvia miltiorrhiza (aka 'Dan shen') contains a sedative which acts as an MAGL inhibitor. MAGL degrades the endocannabinoid 2-AG, which acts upon CB1 (CNS) and CB2 (periphery) receptors.
 

Tanshinone IIA has been identified as a natural monoacylglycerol lipase (MAGL) inhibitor with an IC50 value of 48 nM.

 

 

 

interesting you posted a sedative action of a herb in a thread about amphetamine herbal replacements. well done
 


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#18 Reformed-Redan

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Posted 28 July 2016 - 11:42 PM

In case you guys and gals are interested I found a natural flavonoid derivative of Oroxylin A that's actually more potent than methylphenidate at dopamine reuptake.

 

Best thing I found thus far and synthesis is pretty cheap. 

 

See here:

 

http://www.longecity...amine-reuptake/



#19 sativa

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Posted 29 July 2016 - 01:46 AM

Salvia miltiorrhiza (aka 'Dan shen') contains a sedative which acts as an MAGL inhibitor. MAGL degrades the endocannabinoid 2-AG, which acts upon CB1 (CNS) and CB2 (periphery) receptors.

Tanshinone IIA has been identified as a natural monoacylglycerol lipase (MAGL) inhibitor with an IC50 value of 48 nM.


interesting you posted a sedative action of a herb in a thread about amphetamine herbal replacements. well done
Yes, it would be relevant for someone intending to use Salviae Miltiorrhizae as a herbal amphetamine alternative to know that it has sedative action. Also, the traditional use is relevant and indicative that perhaps this plant is not a valid amphetamine replacement:

Actions: relieve restlessness and induce tranquilization.


In my experience, catuaba would be a good amphetamine mimicker. Add some adrenaline stimulation from cinnamaldhyde and perhaps Orexin release (and MAOB inhibition?) from olive leaf extract...this might be quite powerful.

Edited by sativa, 29 July 2016 - 02:04 AM.


#20 normalizing

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Posted 29 July 2016 - 01:50 AM

^ you propose suma and now catuaba but ive done both of those with no results. olive leaf extract did not do anything either but i wasnt expecting anything anyway. just kind of disappointing with the various recommendations of catuaba and suma and not a single reliable report by anyone using those except you. NCBI has just one study better than suma on catuaba claiming antidepressant effect in rats, but it seems the exact source is not revealed and also it seems the methanolic extract works only and as we know, methanol is not a good idea for a solvent



#21 playground

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Posted 29 July 2016 - 01:52 AM

Dan shen (aka red sage, chinese sage or tan shen)

Is one of two ingredients in danhong.

 

What's interesting about danhong ?

It cures neuropathy.

And it does so better than NGF.

(which, when you think about it, is an incredible observation)

 

Interested readers can read the specially pre-prepared thread:

http://www.longecity...anhong-and-ngf/

 

 



#22 normalizing

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Posted 29 July 2016 - 01:54 AM

^ it cures neuropathy? oh wow. strong words here. if that thing "cures" neuropathy, so many will be cured of it and it will be in the primetime news but instead its on the infomercials late late nights when fat lazy slobs with no jobs observe whats the latest fad to get on and "cure" their ointments. anyway good try


Edited by normalizing, 29 July 2016 - 01:55 AM.

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#23 sativa

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Posted 29 July 2016 - 01:56 AM

^ you propose suma and now catuaba but ive done both of those with no results. olive leaf extract did not do anything either but i wasnt expecting anything anyway. just kind of disappointing with the various recommendations of catuaba and suma and not a single reliable report by anyone using those except you. NCBI has just one study better than suma on catuaba claiming antidepressant effect in rats, but it seems the exact source is not revealed and also it seems the methanolic extract works only and as we know, methanol is not a good idea for a solvent


I made a basic catuaba water extract and have used this many tines, both orally (as a tea) and intranasally (as the dried water extract) - effects include increased stamina, alertness and energy.

It sounds like all of your self experimentations are not a valid representation of the common person.

Perhaps you have a unique brain/body chemistry that causes you to have poor results.

Olive leaf is very stimulating to me, it increases my alertness.

Edited by sativa, 29 July 2016 - 01:57 AM.

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#24 normalizing

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Posted 29 July 2016 - 01:58 AM

^ kind of contradictory to use olive leaf which gives you energy, alertness and then catuaba which does the same. im not sure if you really know for sure which does what since you admitted combining, using many pills herbs at once.


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#25 sativa

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Posted 29 July 2016 - 02:01 AM

^ kind of contradictory to use olive leaf which gives you energy, alertness and then catuaba which does the same. im not sure if you really know for sure which does what since you admitted combining, using many pills herbs at once.

I've used each separately. Despite having never combined them, I'm familiar with the pharmacology of both catuaba and olive leaf and theorize they would combine well.

Perhaps don't assume so much...

Edited by sativa, 29 July 2016 - 02:01 AM.

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#26 playground

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Posted 29 July 2016 - 05:58 PM

This suggestion that Danshen is herbal amphetamine .... is just such bullshit.

 

I have taken danshen many times. 

It does not have amphetamine-like, stimulatory, effects.

Danshen is a medicinal plant, it thins the blood, in China they give

it to patients with neuropathy, with circulatory disorders, with heart disease,

and with stroke, etc. 

 

Someone is either trolling this thread,  or they're trying to off load danshen.

 



#27 normalizing

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Posted 29 July 2016 - 08:35 PM

thats good playground but you have been on this thread for quite a while and just now you are like WAIT, DANSHEN IS NOT STIMULATING all meanwhile just adding to the trolling


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#28 limerence

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Posted 02 August 2016 - 12:29 PM

I like Coca Tea and Jarrows Green Tea supplements (Jarrows has by far the best of the 6 or so brands ive tried). I take 3-6 "40mg caffeine" tabs/day. Terrefic energy and the high amounts of theanine are great as well. Coca Tea probably has the dopamine properties youre looking for though. Coca Tea makes me kinda dumb in a certain way, while it does greatly increase dopamine/other levels without frying you. I really like the green tea caps though, only stimulant I need these days. Too bad good quality coke is so rare these days, heh. SAM-e is pretty stimulating too, 800mg, again not the same stim as amph.



#29 sativa

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Posted 02 August 2016 - 07:56 PM

thats good playground but you have been on this thread for quite a while and just now you are like WAIT, DANSHEN IS NOT STIMULATING all meanwhile just adding to the trolling


Ignore this playground, some of normalizing's reasoning and posts are quite distorted and troll like in nature, respectively.

Back on topic, I think a limited and incomplete insight into dan shens pharmacology, traditional use and properties gives a distorted picture of its effects. So, no trolling for this thread just incomplete data.
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#30 playground

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Posted 04 August 2016 - 05:34 AM

There's an interesting article about Danshen on NaturalNews.org.

 

http://www.naturalne...hen_herbal.html

 

Seriously, we should all make a mental note of this herb.

In this article, one doctor says that as many as 80% of the

heart complications/surgeries could be avoided with the

use of Danshen.   There's lots of evidence, scientific and

clinical that this herb really does 'cure' circulatory conditions,

heart disease, neuropathy etc. 

 

Knowing about Danshen might come in very useful the day

your grandparents, parents,  aunts, uncles...etc..  become ill.

And of-course, there's also the day that YOU become ill.

 

 


  • Ill informed x 1




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