Mike Arnold
Board Sponsor
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If anyone is interested in logging Vicaine PP, please let me know in the thread below. We will only be choosing a very limited number of loggers because we have a relatively small amount of inventory of this particular product.
I have posted some information on the product below...
Guys, Vicaine Om is now available! I will be providing a write-up on the product shortly, which will go in-depth on what it is and how it works.
In the meantime I will leave you with this...
"Vicaine PM is a opioid-based complex containing additional opioid potentiating, anti-tolerance and anti-inflammatory agents. There are no stimulants within Vicaine PM, making it an excellent alternative for anyone who wants to take the product at night (it won't interfere with sleep) or for those who desire a more pure opioid effect. Vicaine PM also contains 40% more tianeptine. In combination with its opioid potentiating and anti-inflammatory compounds, Vicaine PM supplies an extraordinarily potent opioid effect that is 50-75% stronger than the original Vicaine. Vicaine PM is an EXTREMELY powerful product. There is truly NOTHING else like it anywhere on the market."
Below I have posted several studies demonstrating the opioid potentiating, anti-tolerance, and anti-inflammatory effects of the secondary compounds in the new Vicaine PM.
A new and novel treatment of opioid dependence: Nigella sativa 500 mg.
Sangi S1, Ahmed SP, Channa MA, Ashfaq M, Mastoi SM.
Author information
Abstract
BACKGROUND: Opioid dependence is one of the major social and psychiatric problem of society. Unfortunately there is no non opiate treatment available. For centuries man has used plants for their healing proprieties. These plants play a fundamental part in all treatment modalities, both ancient and modern.
METHODS: This study was conducted to find non opiate treatment for opiate withdrawal. Total 35 known addicts of opiates were included in the study. This study was based on DSM IV criteria for opioid dependence.
RESULT: This study demonstrates that non opioid treatment for opioid addiction decreases the withdrawal effects significantly. It further demonstrates that there are no changes in physiological parameters of subjects during treatment (BP, Pulse rate etc.). There is increased appetite but no significant weight gain in the subjects.
CONCLUSION: Non opioid drug Nigella sativa is effective in long-term treatment of opioid dependence. It not merely cures the opioid dependence but also cures the infections and weakness from which majority of addicts suffer.
PMID: 19385474
Link: https://www.ncbi.nlm.nih.gov/pubmed/19385474#
Black Cumin (Nigella sativa) and Its Active Constituent, Thymoquinone: An Overview on the Analgesic and Anti-inflammatory Effects.
Amin B1, Hosseinzadeh H2.
Author information
Abstract
For many centuries, seeds of Nigella sativa (black cumin), a dicotyledon of the Ranunculaceae family, have been used as a seasoning spice and food additive in the Middle East and Mediterranean areas. Traditionally, the plant is used for asthma, hypertension, diabetes, inflammation, cough, bronchitis, headache, eczema, fever, dizziness, and gastrointestinal disturbances. The literature regarding the biological activities of seeds of this plant is extensive, citing bronchodilative, anti-inflammatory, antinociceptive, antibacterial, hypotensive, hypolipidemic, cytotoxic, antidiabetic, and hepatoprotective effects. The active ingredients of N. sativa are mainly concentrated in the fixed or essential oil of seeds, which are responsible for most health benefits. This review will provide all updated reported activities of this plant with an emphasis on the antinociceptive and anti-inflammatory effects. Results of various studies have demonstrated that the oil, extracts, and their active ingredients, in particular, thymoquinone, possess antinociceptive and anti-inflammatory effects, supporting the common folk perception of N. Sativa as a potent analgesic and anti-inflammatory agent. Many protective properties are attributed to reproducible radical scavenging activity as well as an interaction with numerous molecular targets involved in inflammation, including proinflammatory enzymes and cytokines. However, there is a need for further investigations to find out the precise mechanisms responsible for the antinociceptive and anti-inflammatory effects of this plant and its active constituents.
Georg Thieme Verlag KG Stuttgart · New York.
PMID: 26366755 DOI: 10.1055/s-0035-1557838
Link: https://www.ncbi.nlm.nih.gov/pubmed/26366755#
Effect of agmatine on the development of morphine dependence in rats: potential role of cAMP system
Feyza Aricioglu,a,b Andrea Means,b and Soundar Regunathanb,*
Author information ► Copyright and License information ►
The publisher's final edited version of this article is available at Eur J Pharmacol
See other articles in PMC that cite the published article.
Abstract
Agmatine is an endogenous amine derived from arginine that potentiates morphine analgesia and blocks symptoms of naloxone-precipitated morphine withdrawal in rats. In this study, we sought to determine whether treatment with agmatine during the development of morphine dependence inhibits the withdrawal symptoms and that the effect is mediated by cAMP system. Exposure of rats to morphine for 7 days resulted in marked naloxone-induced withdrawal symptoms and agmatine treatment along with morphine significantly decreasing the withdrawal symptoms. The levels of cAMP were markedly increased in morphine-treated rat brain slices when incubated with naloxone and this increase was significantly reduced in rats treated with morphine and agmatine. The induction of tyrosine hydroxylase after morphine exposure was also reduced in locus coeruleus when agmatine was administered along with morphine. We conclude that agmatine reduces the development of dependence to morphine and that this effect is probably mediated by the inhibition of cAMP signaling pathway during chronic morphine exposure.
he most fascinating aspect of agmatine, an endogenous molecule, is its ability to potentiate the analgesic effect of morphine and at the same time to reduce the morphine dependence and withdrawal. The findings from this and previous reports suggest that increasing endogenous agmatine could offer novel therapeutic advantage in morphine analgesia and dependence. For example, combining agmatine with morphine during pain management, while reducing the effective dose of morphine, will also prevent the development of dependence to morphine.
Link: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2923207/
Effects of agmatine on tolerance to and substance dependence on morphine in mice.
Li J1, Li X, Pei G, Qin BY.
Author information
Abstract
AIM:
To study the effects of agmatine on tolerance to and dependence on morphine.
METHODS: Inhibitory effects of agmatine on tolerance to and substance dependence on morphine were observed in mouse tolerant models and in mouse jumping test, respectively.
RESULTS: Agmatine 0.125-2.5 mg.kg-1 prevented the development of tolerant to morphine in a dose-dependent manner. Pretreatment of mice with morphine induced an over 3-fold increase in analgesic ED50 (20.1, 14.4-28.0 mg.kg-1) than those with normal saline (6.3, 5.1-7.8 mg.kg-1). Pretreatment of mice with both of agmatine and morphine made morphine loss the ability to induce tolerance. Withdrawal jumps and loss in body weight induced by naloxone in morphine-dependent mice were prevented by agmatine (2.5-10 mg.kg-1) in a dose-dependent manner. ED50 of naloxone (21.4, 18.4-24 mg.kg-1) required to precipitate withdrawal jumps in mice pretreated with both agmatine and morphine was 8 times higher than that with morphine alone (2.5, 2.1-2.8 mg.kg-1). These effects of agmatine were blocked by idazoxan.
CONCLUSION: Agmatine prevented tolerance to and substance dependence on morphine in mice by activation of imidazoline receptors.
PMID: 10452098
Link: https://www.ncbi.nlm.nih.gov/pubmed/10452098
Agmatine potentiates the analgesic effect of morphine by an alpha(2)-adrenoceptor-mediated mechanism in mice.
Yeşilyurt O1, Uzbay IT.
Author information
Abstract
The effects of agmatine, which is an endogenous polyamine metabolite formed by decarboxylation of L-arginine, and a combination of agmatine and morphine on tail-flick test have been investigated in mice. Adult male Swiss-Webster mice were used in the study. Agmatine (10, 20 and 40 mg/kg), clonidine (0.15 mg/kg), yohimbine (0.625 and 1.25 mg/kg), or saline were injected into mice intraperitoneally. Morphine (1 and 2 mg/kg) was given subcutaneously. Agmatine alone did not produce any significant change on radiant tail-flick latencies, but it potentiated significantly and dose-dependently morphine-induced (1 mg/kg) analgesia. The potentiating effect of agmatine (40 mg/kg) on morphine-induced analgesia was blocked completely by yohimbine (0.625 mg/kg), a selective alpha(2)-adrenoceptor antagonist, pretreatment. Clonidine (0.15 mg/kg), an alpha(2-)adrenergic receptor agonist, caused a significant increase of the tail-flick latencies of the mice. Yohimbine (0.625 mg/kg) also blocked clonidine-induced analgesia. In addition, yohimbine (0.625 mg/kg) was ineffective on the tail-flick test and did not produce any significant change on the morphine-induced analgesia. Our results indicate that cotreatment of agmatine with morphine produces antinociceptive enhancement via an alpha(2-)adrenergic receptor-mediated mechanism and agmatine-morphine combination may be an effective therapeutic strategy for medical treatment of pain.
PMID: 11377923 DOI: 10.1016/S0893-133X(00)00245-1
Link: https://www.ncbi.nlm.nih.gov/pubmed/11377923
I have posted some information on the product below...
Vicaine PM
"Prohedonic Opioid Anti-inflammatory Complex"
Available Now!!!
20% OFF: arnold20
"Prohedonic Opioid Anti-inflammatory Complex"
Available Now!!!
20% OFF: arnold20
Guys, Vicaine Om is now available! I will be providing a write-up on the product shortly, which will go in-depth on what it is and how it works.
In the meantime I will leave you with this...
"Vicaine PM is a opioid-based complex containing additional opioid potentiating, anti-tolerance and anti-inflammatory agents. There are no stimulants within Vicaine PM, making it an excellent alternative for anyone who wants to take the product at night (it won't interfere with sleep) or for those who desire a more pure opioid effect. Vicaine PM also contains 40% more tianeptine. In combination with its opioid potentiating and anti-inflammatory compounds, Vicaine PM supplies an extraordinarily potent opioid effect that is 50-75% stronger than the original Vicaine. Vicaine PM is an EXTREMELY powerful product. There is truly NOTHING else like it anywhere on the market."
Below I have posted several studies demonstrating the opioid potentiating, anti-tolerance, and anti-inflammatory effects of the secondary compounds in the new Vicaine PM.
A new and novel treatment of opioid dependence: Nigella sativa 500 mg.
Sangi S1, Ahmed SP, Channa MA, Ashfaq M, Mastoi SM.
Author information
Abstract
BACKGROUND: Opioid dependence is one of the major social and psychiatric problem of society. Unfortunately there is no non opiate treatment available. For centuries man has used plants for their healing proprieties. These plants play a fundamental part in all treatment modalities, both ancient and modern.
METHODS: This study was conducted to find non opiate treatment for opiate withdrawal. Total 35 known addicts of opiates were included in the study. This study was based on DSM IV criteria for opioid dependence.
RESULT: This study demonstrates that non opioid treatment for opioid addiction decreases the withdrawal effects significantly. It further demonstrates that there are no changes in physiological parameters of subjects during treatment (BP, Pulse rate etc.). There is increased appetite but no significant weight gain in the subjects.
CONCLUSION: Non opioid drug Nigella sativa is effective in long-term treatment of opioid dependence. It not merely cures the opioid dependence but also cures the infections and weakness from which majority of addicts suffer.
PMID: 19385474
Link: https://www.ncbi.nlm.nih.gov/pubmed/19385474#
Black Cumin (Nigella sativa) and Its Active Constituent, Thymoquinone: An Overview on the Analgesic and Anti-inflammatory Effects.
Amin B1, Hosseinzadeh H2.
Author information
Abstract
For many centuries, seeds of Nigella sativa (black cumin), a dicotyledon of the Ranunculaceae family, have been used as a seasoning spice and food additive in the Middle East and Mediterranean areas. Traditionally, the plant is used for asthma, hypertension, diabetes, inflammation, cough, bronchitis, headache, eczema, fever, dizziness, and gastrointestinal disturbances. The literature regarding the biological activities of seeds of this plant is extensive, citing bronchodilative, anti-inflammatory, antinociceptive, antibacterial, hypotensive, hypolipidemic, cytotoxic, antidiabetic, and hepatoprotective effects. The active ingredients of N. sativa are mainly concentrated in the fixed or essential oil of seeds, which are responsible for most health benefits. This review will provide all updated reported activities of this plant with an emphasis on the antinociceptive and anti-inflammatory effects. Results of various studies have demonstrated that the oil, extracts, and their active ingredients, in particular, thymoquinone, possess antinociceptive and anti-inflammatory effects, supporting the common folk perception of N. Sativa as a potent analgesic and anti-inflammatory agent. Many protective properties are attributed to reproducible radical scavenging activity as well as an interaction with numerous molecular targets involved in inflammation, including proinflammatory enzymes and cytokines. However, there is a need for further investigations to find out the precise mechanisms responsible for the antinociceptive and anti-inflammatory effects of this plant and its active constituents.
Georg Thieme Verlag KG Stuttgart · New York.
PMID: 26366755 DOI: 10.1055/s-0035-1557838
Link: https://www.ncbi.nlm.nih.gov/pubmed/26366755#
Effect of agmatine on the development of morphine dependence in rats: potential role of cAMP system
Feyza Aricioglu,a,b Andrea Means,b and Soundar Regunathanb,*
Author information ► Copyright and License information ►
The publisher's final edited version of this article is available at Eur J Pharmacol
See other articles in PMC that cite the published article.
Abstract
Agmatine is an endogenous amine derived from arginine that potentiates morphine analgesia and blocks symptoms of naloxone-precipitated morphine withdrawal in rats. In this study, we sought to determine whether treatment with agmatine during the development of morphine dependence inhibits the withdrawal symptoms and that the effect is mediated by cAMP system. Exposure of rats to morphine for 7 days resulted in marked naloxone-induced withdrawal symptoms and agmatine treatment along with morphine significantly decreasing the withdrawal symptoms. The levels of cAMP were markedly increased in morphine-treated rat brain slices when incubated with naloxone and this increase was significantly reduced in rats treated with morphine and agmatine. The induction of tyrosine hydroxylase after morphine exposure was also reduced in locus coeruleus when agmatine was administered along with morphine. We conclude that agmatine reduces the development of dependence to morphine and that this effect is probably mediated by the inhibition of cAMP signaling pathway during chronic morphine exposure.
he most fascinating aspect of agmatine, an endogenous molecule, is its ability to potentiate the analgesic effect of morphine and at the same time to reduce the morphine dependence and withdrawal. The findings from this and previous reports suggest that increasing endogenous agmatine could offer novel therapeutic advantage in morphine analgesia and dependence. For example, combining agmatine with morphine during pain management, while reducing the effective dose of morphine, will also prevent the development of dependence to morphine.
Link: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2923207/
Effects of agmatine on tolerance to and substance dependence on morphine in mice.
Li J1, Li X, Pei G, Qin BY.
Author information
Abstract
AIM:
To study the effects of agmatine on tolerance to and dependence on morphine.
METHODS: Inhibitory effects of agmatine on tolerance to and substance dependence on morphine were observed in mouse tolerant models and in mouse jumping test, respectively.
RESULTS: Agmatine 0.125-2.5 mg.kg-1 prevented the development of tolerant to morphine in a dose-dependent manner. Pretreatment of mice with morphine induced an over 3-fold increase in analgesic ED50 (20.1, 14.4-28.0 mg.kg-1) than those with normal saline (6.3, 5.1-7.8 mg.kg-1). Pretreatment of mice with both of agmatine and morphine made morphine loss the ability to induce tolerance. Withdrawal jumps and loss in body weight induced by naloxone in morphine-dependent mice were prevented by agmatine (2.5-10 mg.kg-1) in a dose-dependent manner. ED50 of naloxone (21.4, 18.4-24 mg.kg-1) required to precipitate withdrawal jumps in mice pretreated with both agmatine and morphine was 8 times higher than that with morphine alone (2.5, 2.1-2.8 mg.kg-1). These effects of agmatine were blocked by idazoxan.
CONCLUSION: Agmatine prevented tolerance to and substance dependence on morphine in mice by activation of imidazoline receptors.
PMID: 10452098
Link: https://www.ncbi.nlm.nih.gov/pubmed/10452098
Agmatine potentiates the analgesic effect of morphine by an alpha(2)-adrenoceptor-mediated mechanism in mice.
Yeşilyurt O1, Uzbay IT.
Author information
Abstract
The effects of agmatine, which is an endogenous polyamine metabolite formed by decarboxylation of L-arginine, and a combination of agmatine and morphine on tail-flick test have been investigated in mice. Adult male Swiss-Webster mice were used in the study. Agmatine (10, 20 and 40 mg/kg), clonidine (0.15 mg/kg), yohimbine (0.625 and 1.25 mg/kg), or saline were injected into mice intraperitoneally. Morphine (1 and 2 mg/kg) was given subcutaneously. Agmatine alone did not produce any significant change on radiant tail-flick latencies, but it potentiated significantly and dose-dependently morphine-induced (1 mg/kg) analgesia. The potentiating effect of agmatine (40 mg/kg) on morphine-induced analgesia was blocked completely by yohimbine (0.625 mg/kg), a selective alpha(2)-adrenoceptor antagonist, pretreatment. Clonidine (0.15 mg/kg), an alpha(2-)adrenergic receptor agonist, caused a significant increase of the tail-flick latencies of the mice. Yohimbine (0.625 mg/kg) also blocked clonidine-induced analgesia. In addition, yohimbine (0.625 mg/kg) was ineffective on the tail-flick test and did not produce any significant change on the morphine-induced analgesia. Our results indicate that cotreatment of agmatine with morphine produces antinociceptive enhancement via an alpha(2-)adrenergic receptor-mediated mechanism and agmatine-morphine combination may be an effective therapeutic strategy for medical treatment of pain.
PMID: 11377923 DOI: 10.1016/S0893-133X(00)00245-1
Link: https://www.ncbi.nlm.nih.gov/pubmed/11377923
