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All 11 posts | Subject: Help a ditz with her Kava | Please login to post | Down | |
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Marcilla (Stranger) 07-31-03 05:50 No 450820 |
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Help a ditz with her Kava | ||||||
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Ok, I don't know if I'm having a blonde moment or what. I U'dTFSE, I Googled, I searched the vaults of Erowid, and I still don't get it. I've used Kava and been less than impressed with the results. It seems people are looking for about 500-1000mg kavalactones. Throat suggests adding a shot of alcohol to potentiate. So far, I'm following. So I calculate what I've been doing wrong. I had been using 2 TBS Kava root powder from either Kava King or Kava Kaui Awa blend mixed with 1 tsp granular lecithin to emulsify and potentiate. I would cover in Gatorade or OJ and shake vigorously then drink the whole mixture. My effects were very mild with a crashing effect shortly afterward and I would start puking if I redosed too many times. But my calculations, 2TBS equals about 55000mgs! Now neither Kava Kauai nor Kava King lists the percent of active Kava lactones, but I'm sure it's much more than 3.6% (which would equal 1000mg KL assuming 50% bioavailability from shaking method). I feel that I must be doing many times the recommended dosage, and yet still only getting mild effects? What am I missing? I'm not expecting to be tripping my tits off, but some people have made very positive posts. Do I just need to add alcohol? Is there some other substance that should be used to potentiate? Do I need to switch to Vanatua strain? Am I doing too *much*? Do my sources just suck? I mean, am I possibly getting less than 3.6% KL? Is my math off somewhere? Someone suggested http://www.ethnobotanicals.com/Kava-kava.html where they have an 84% available paste would that work better? 2 TBS of this stuff would quickly kill my bank account! What about the liquid extracts? I would seriously love to be able to take a little bottle to work and "Kava up" with a few drops. I don't have space at work or at home to keep a blender full of Kava smoothie in the fridge. Help me out someone who knows. Am I doing something wrong, or is Kava just not for me? Thanks!! XXOO, G Wiz This post is rated: total bimbo! |
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abolt (Hive Addict) 08-01-03 03:02 No 450979 
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Marcilla | ||||||
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If you are referring to the stuff known as Kava Kava that is the powdered root of a tree that is soaked in water and drunk, then yes I have tried it. After about 4 cupfulls, the only sensation I had was a numbing of the mouth. No other effects. Based on my experience, the stuff is crap. The Samoans I drank it with prefer regular booze Just my 1.2913 cents worth (adjusted for U.S. dollars) |
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RacerX (Hive Bee) 08-02-03 15:24 No 451250 |
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Liver toxic... | ||||||
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Just keep in mind that Kava is stressful to the liver. Don't indulge too often, and if you do use milk thistle and Ala. "Put the pedal to the metal" |
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Vitus_Verdegast (Hive Bee) 08-02-03 20:03 No 451296 
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yup, but evidence is still inconclusive... (Rated as: excellent) |
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...if the kava is taken in normal doses. From 82 reported cases only a handfull could only be related to kava alone, but excessive dosages were taken : Taken from: Is kava really hepatotoxic? An analysis of the known data on adverse effects of kava preparations on the liver By Mathias Schmidt, Harsewinkel http://www.uni-muenster.de/Chemie/PB/Kava/pdf/Review.pdf This is a fine monograph on kava toxicity! Check that reference list, contains 748 entries!  pages 96 - 100 : 7.1 Literature case: Strahl et al. (1998) (11)/Russmann et al. 2001 (12;13) Acute necrotic hepatitis The case described by Strahl et al. (1998) (11) was the first relatively well-documented case of a serious hepatic adverse event related to kava. The evaluation of the incidence was complicated by the fact that the kava preparation could not be identified with certainty. Based on the information by the authors, an ethanol extract with 60 mg kavalactones per unit was used. Communication with the German producers revealed that none of the companies had received any information about this case. Obviously, the authors did not file the obligatory report to the authorities. However, doubts regarding the intake of a kava product were, in this case, unfounded. With further details of the same case provided by third parties, a causal relationship to kava intake is probable (12;13). Additional sources: MCA identifier no. 10; EMEA identifier no. 4 Patient: female, 39 years Date of entry: Unknown Reported adverse effects: Acute necrotic hepatitis Preparation: Unknown, 60 mg kavalactones/day over 6 months Co-medication: • Paroxetine, 20 mg/day • Occasional use of St. John‘s wort. • Contraceptive (0.15 mg desogestrel + 0.02 mg ethinylestradiol) for 6 years. The patient was admitted to the hospital in order to investigate the elevated transaminases, bilirubin and lactatedehydrogenase. The hepatitis serology was negative; the sonography results were inconspicous. The histological image was consistent with a diffuse and necrotizing hepatitis, suggesting a viral or toxic genesis. After discontinuation of the medications, the liver values continued to rise for a week and then returned to normal. Six months later, a new increase of transaminases could be observed. A renewed kava intake was stated, this time without further co-medication. The clinical image hinted to a drug induced toxic hepatitis. Serology allowed the exclusion of hepatitis A, B and C, CMV, EBV, toxoplasmosis and leptospirosis. The sonographic image revealed a former hepatitis episode. The histopathological findings were consistent with an acute, necrotizing hepatitis. An autoimmune hepatits could not be excluded with certainty. After four weeks, the liver values improved, reaching normal levels after four months. Based on the positive rechallenge to kava, a lymphocyte transformation test was not considered as necessary. The shortened latency period, however, points towards an immunological sensitization on initial intake. Assessment of the co-medication: Whereas St. John’s wort does not have any known adverse liver effects, for paroxetin, transient elevations of liver enzymes are labeled. In the literature, severe cases of liver toxicity reportedly caused by paroxetine can be found (565-567). Liver function impairment by contraceptive treatment is discussed in section 9.2. Based on the positive rechallenge and the negative virus serology, one can assume that this case has indeed a causal relationship to kava. Russmann et al. (2001) (12) suspect a relationship to a cytochrome P450-2D6 deficiency: they investigated the metabolic pattern of the patient and found a congenital deficiency for this enzyme system. The reported incidence could, therefore, have been caused by an immunological event based on the hypersensitation to a reactive kava metabolite. This explanation is supported by a positive rechallenge and the shortened latency period in the second incidence. Allergic reactions to plant derived drugs or isolated ingredients can never be excluded. Most drugs state corresponding hints in the package leaflets. Even though rare cases of allergies to kava were described as dermatological events, the nature of immunologic reactions does not allow the exclusion of a participation of other organs in an allergic reaction. The case report was classified as “probable” by the MCA and the EMEA. 8. Causal relationship probable with overdosage of kava extract In addition to the above mentioned case report related to monograph conform dosage (Strahl et al. (11), there are two cases with a possible causal connection to kava, associated with non-recommended dosages. In one case, an immunological reaction and a concurrent cytochrom-P450-2D6 deficiency could be detected (IKS-case 2000-0014). 8.1 IKS-Case number 2000-0014 Cholestatic hepatitis with kava overdosing Case data in Stoller 2000 (14) and Russmann et al. (2001) (12;13) Additional sources: medicinal literature (12-14); MCA identifier no. 16; EMEA identifier no. 7 Patient: female, 33 years Date of entry: March 21, 2000 Adverse effects reported: Jaundice, cholestatic hepatitis Preparation: Laitan (70 mg kavalactones, acetone extract), 210 mg/day orally for 2-3 months. Co-medication: • Pain relief: 125 mg propyphenazone + 0.5 mg dihydroergotamine-mesylate+ 40 mg caffeine (Tonopan), taken once due to alcohol intake the evening before (see below). • Pain relief: 250 mg paracetamol (acetaminophen) + 150 mg propyphenazone + 50 mg caffeine (Saridon), taken to fight the hang-over from the day before (see below). • Homeopathic combination product (Exepta): Acidum silicicum D12 + Arnica montana D6 + Carbo vegetabilis D12 + Echinacea angustifolia D3 + Graphites D6 + Myristica sebifera D6 + Sulfuris iodidum D6, start of intake: February 5, 2000, last date of intake: February 20, 2000. Except for acetaminophen, the co-medication is inconspicious concerning hepatoxicity. Acetaminophen probably did not contribute to the hepatic event, as it was taken on the first day of the onset of symptoms. The patient stated a massive alcohol intake on February 12, 2000, with otherwise little alcohol consumption. The complaints started on February 13, firstly interpreted as a hang-over from alcohol, which led to the use of the pain medications listed above. Following the hangover, the patient suffered increasingly from inappetence, fatigue, epigastric pressure and severe weight loss. On February 20, she noticed a dark coloration of the urine, had orthostatic complaints and dyspnea when active. Laitan was discontinued. The patient was hospitalized on February 26, 2000. The virus serology for hepatitis A-C was negative, and there was only a weakly positive EBV-reaction which could indicate a reactivation of a previous infection. Obstruction of the bile ducts and autoimmune disease could be excluded. The transaminases were extremely elevated. The liver biopsy pointed towards a drug-induced, toxic hepatitis, and, despite the massive alcohol intake on February 12, an ethanolic genesis could be excluded. The patient had fully recovered by May 4, 2000. After recovery, a lymphocyte-transformation test was performed, which turned out positive for Laitan but negative for the homeopathic combination product. Subsequently, a cytochrome P450-2D6 deficiency could be detected in the patient. Considering the positive outcome of the lymphocyte transformation test, Russmann et al. (2001) (12;13) point towards an idiosyncratic-immunologic hepatitis, as in the case published by Strahl et al. (1998) (11). The Swiss IKS evaluated this case as „probable“, and with the conclusive documentation this evaluation should be accepted. The MCA and the EMEA, too, classified the case as “probable”. 8.2 IKS-Case number 2000-3502 Liver transplant after subfulminant hepatitis with kava overdosing. Case data in Stoller 2000 (14); Escher 2001 (15); Russmann et al. 2001 (13) The case was reported by a hospital. Additional sources: medicinal literature (13-15); MCA identifier no. 18; EMEA identifier no. 9 Patient: male, 50 years Date of entry: Unknown Reported adverse effects: Acute subfulminant hepatitis with liver transplant Preparation: Laitan (70 mg kavalactones, acetone extract), 210-280 mg kavalactones for 1.5 months Co-medication: • Paracetamol (acetaminophen) 500-1000 mg, shortly before transplant (not related to the evolution of this case; see below). • Occasional intake of evening primrose oil, but not in October and November 1999. • Yeast preparation. No hepatotoxic effects are known for evening primrose oil and yeast preparations. Kava was taken from the end of October to December 7, 1999. End of November, the patient noticed a dark coloration of the skin, similar to a sun tan. On December 5, an icteric condition developed. The liver values, determined on December 7, were extremely elevated. Subsequently, the kava preparation was discontinued. The virus serology for hepatitis A,B,C and E was negative, as well as HIV and CMV. The serology indicated signs of a previous EBV infection. The clinical symptoms, however, were not consistent with a EBV reactivation. An obstruction of the bile ducts could be excluded based on the sonographic examination. Escher et al. (2001) excluded an ethanolic genesis in this case (15). In the course of the hepatitis, an ascites and clinical symptoms of hepatic encephalopathy occured; the patient was intubated on December 13, 1999. A liver transplant was considered. Even before the liver transplant was made, the patient developed fever, a skin rash and serious symptoms of liver failure. The patient received 500–1000 mg paracetamol (acetaminophen) for fever reduction. The liver transplant was performed on December 16, 1999. The biopsy results showed distinct signs of toxic-necrotic hepatitis. After surgery, the subsequent toxicological blood tests indicated residual levels of paracetamol (acetaminophen) corresponding to the last dosage, as well as traces of lidocain, caffeine, atracurium and metoclopramide in the urine. The detection of caffeine is possibly related to the hospital breakfast and the detection of lidocaine (local anesthetic) and atracurium (muscle relaxant used for intubations) is most likely a result of the medication related to the intubation procedure. Presumably, this is also the case with metoclopramide, a motility-lowering drug. The IKS evaluated a causal relationship to kava as „probable“, as well as the MCA and the EMEA. The Swiss evaluation was based on an erroneous information. It refers, in addition to the Strahl publication (11), to six kava side effect cases supposedly listed by the WHO, which led to the impression of a regularly occurring adverse event. In reality, there were only three cases at the time of evaluation, but the searched keywords „hepatitis“, „cholestatic hepatitis“, „liver cell damage“ and „jaundice“ resulted in six hits from the database, which is easily explained by overlapping symptom reports in the three corresponding cases. The relevant WHO-cases correspond to the BfArM cases 93015209, 94006568 and 94901308. While for case no. 94006568 the causality to kava is very questionable, in the other two case reports a causal relationship to co-medication (diazepam and terfenadine, respectively) is an alternative explantion of the event. Thus, at the time of the evaluation only the publication by Strahl et al. (1998) (11) would have supported the evaluation. However, the causality to kava in this case is possible, keeping in mind that the dosage exceeded the recommended range. References: (11) Strahl S, Ehret V, Dahm HH, Maier KP. Nekrotisierende Hepatitis nach Einnahme pflanzlicher Heilmittel. Dtsch med Wschr 1998; 123(47):1410-1414. (12) Russmann S, Lauterburg BH, Helbling A. Kava hepatotoxicity. Ann Int Med 2001; 135(1):68-69. (13) Russmann S, Escher M, Stoller R, Lauterburg BH. Hepatotoxicity of Kava Kava (Piper methysticum) containing herbal drugs. Recent cases in Switzerland and investigations regarding the mechanism. J Exp Klin Pharmakol Toxicol 2001; 363(4):S40. (14) Stoller R. Leberschädigungen unter Kava-Extrakten. Schweiz Ärzteztg 2000; 81(24):1335-1336. (15) Escher M, Desmeules J. Hepatitis associated with Kava, a herbal remedy for anxiety. Br Med J 2001; 322(20.01.01):139. (565) Cadranel JF, Di M, V, Cazier A, Pras V, Bachmeyer C, Olympio P et al. Atrium and paroxetine-related severe hepatitis. J Clin Gastroenterol 1999; 28(1):52-55. (566) de Man RA. Ernstige hepatitis toegeschreven aan paroxetine (Seroxat). Ned Tijdschr Geneeskd 1997; 141(11):540-542. (567) Odeh M, Misselevech I, Boss JH, Oliven A. Severe hepatotoxicity with jaundice associated with paroxetine. Am J Gastroenterol 2001; 96(8):2494-2496. A Dream Within A Dream (http://www.poedecoder.com/Qrisse/works/dreamw.html) |
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tpower9s2003 (Newbee) 08-04-03 18:33 No 451645 
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"Now neither Kava Kauai nor Kava King... | ||||||
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"Now neither Kava Kauai nor Kava King lists the percent of active Kava lactones" This usually implies that it was not standardized. Does it even mention that the potency was verified? Many "dietary supplements" lie on their contents or actives content (which in this case ISN'T EVEN NOTED...) and there is no law saying they can't, as they are merely supplements according to the FDA. Don't expect much from kava...it will not replace good old pot, or compliment it. It might allow larger doses of amphetamines without as much periphial effect, therefore you just got more high.... "True love" is a thrill Add a methyl group or two Get it in a pill! |
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Rhodium (Chief Bee) 09-04-04 12:10 No 529542 
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Kava-kava Enhances both Cognition and Mood (Rated as: excellent) |
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Enhanced cognitive performance and cheerful mood by standardized extracts of Piper methysticum (Kava-kava) Richard Thompson, Willibald Ruch, Rüdiger U. Hasenöhrl Hum Psychopharmacol Clin Exp, 19(4), 243-250 (2004) (https://www.rhodium.ws/pdf/kava.improves.cognition.and.mood.pdf) Abstract The acute effects of the herbal anxiolytic Kava-kava (Piper methysticum G. Forster) on emotional reactivity and cognitive performance were investigated in a double-blind randomized placebo-controlled trial involving healthy volunteers. Subjects' reports of mood change were assessed with the state-trait-cheerfulness-inventory, which measures the three concepts of cheerfulness, seriousness and bad mood as both traits and states. Cognitive performance was examined with the Sperling partial report and the Sternberg item recognition task, which were used as an index for visual attention and short-term memory processing. The intake of a single dose of Kava extract (300 mg; p.o.) led to an increase in state cheerfulness, while the phytopharmacon did not influence state seriousness and bad mood. The mood-elevating effects of Kava were most prominent in trait cheerful subjects, indicating that trait cheerfulness moderated the drug-induced increase in cheerful mood. Furthermore, Kava improved the accuracy and the speed of performing the partial report and the item recognition task, indicative of a beneficial effect of the phytopharmacon on visual attention and short-term memory retrieval, respectively. Thus, unlike conventional benzodiazepine-type anxiolytics, which tend to impair cognitive performance and to increase the occurrence of negative affective states, Kava is a potent anxiolytic agent, which, additionally, can facilitate cognitive functioning and can increase positive affectivity related to exhilaration. The Hive - Clandestine Chemists Without Borders |
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7is (Hive Bee) 09-05-04 06:51 No 529652 
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Differences between kava extracts (Rated as: excellent) |
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Kava lactones and the kava-kava controversy. Whitton PA, Lau A, Salisbury A, Whitehouse J, Evans CS. Phytochemistry. 2003 Oct;64(3):673-9. Kava-kava is a traditional beverage of the South Pacific islanders and has had centuries of use without major side effects. Standardised extracts of kava-kava produced in Europe have led to many serious health problems and even to death. The extraction process (aqueous vs. acetone in the two types of preparations) is responsible for the difference in toxicity as extraction of glutathione in addition to the kava lactones is important to provide protection against hepatotoxicity. The Michael reaction between glutathione and kava lactones, resulting in opening of the lactone ring, reduces the side effects of the kava kava extracts. This protective activity was demonstrated using Acanthamoebae castellanii in which 100% cell death occurred with 100 mg ml(-1) kava lactones alone, and 40% cell death with a mixture of 100 mg ml (-1)glutathione and 100 mg ml (-1) kava lactones. A comparison of kava lactone toxicity with other pharmaceutical products is discussed and recommendations made for safe usage of kava-kava products http://leb.net/gibran/works/sand/sand.html |
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blunts (Newbee) 09-05-04 22:02 No 529748 |
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Kava is weak | ||||||
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When swim used to work in a drug store with a wide variety of Kava Kava prodcuts, he would occasionally consume between 20-40 capsules to provide a nice buzz. As others have said, it wont replace alcohol or pot, but it will produce a slight buzz, an easy going feeling and a sort of floating feeling for a little while. swim would usually take Natures Resource brand, which had a standardized kavalactone concentration, but other standardized brands also worked too. |
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honey_badger (Hive Bee) 09-06-04 01:40 No 529791 
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kava culture | ||||||
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i grew up in three different cultures , two of them have kava in their culture. now the most potent kava comes from vanuartu, and some time is slightly green, papa new guinee has some which is almost as strong, but fiji kava is the weakest. swim suspect that the imported one is the same as the fiji weaker ones you can get in western culture. this is ture wether the vanuartu peole pick it differntly at different times, or have another type of stran, the vanuartu kava is the most potent,and is the one you should look out for, i would suggest you travel there and try it with the natives, perhaps you could start an import business that use the most potent karva in the world,  
epistemologicide- http://217.159.169.126/~creator/public/ZPE/files/consolidated_knowledge.pdf |
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ChemoSabe (Hive Addict) 09-06-04 01:57 No 529796 
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Kava Kava Kickdown | ||||||
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Hey EpistoJemmaHoenyBadger, Didn't you say that you used to give out a joke Kava Kava kickdown to the Island guests at some resort you worked because you knew it would make their boners fizzle? Does kava kava really have boner deflating properties? united black NASCAR drivers of America |
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honey_badger (Hive Bee) 09-06-04 02:03 No 529798
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karva makes you impotent | ||||||
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i must warn you that too much karva will make your dick limp, thanx chemo for giving me up , yes i did used to take honey mooners to the staff village at the end of the night, and said come back and experience the real fiji, and culture with the natives in a special ceremony,just so the man would be impotent for the night, and i could see the look on the future wife to bs face in the morning, it would bee all like , he doesent love me!![i]
epistemologicide- http://217.159.169.126/~creator/public/ZPE/files/consolidated_knowledge.pdf |
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