Du tager dog endnu en gang fejl. Synes efterhånden ofte du lægger en bitter og rasmusmodsat tonalitet an her på boardet og det synes jeg er ærgerligt. Har siddet i lange diskussioner med dig før og har aldrig set dig anerkende at "my bad vidste jeg ikke/sorry jeg tog fejl" du hopper bare videre til næste tråd hvor du kan forsøge at ødelægge troværdigheden, ved at kaste om dig med videnskabelig lingo som de færreste kan eller har tid til at opponere imod. Nu får du et sidste skud her og så vil jeg komme tilbage til mit arbejde, anbefaler at du kaster dig over homeopati eller kakaoceremonier hvis du vil pille noget ned som evidensen sejler for..
Skrev ikke at det kurerer alt kræft men at man havde set op imod 99 forbyggelse af tumorigenesis ved lungekræft hvilket er godkendt reproduceret og man er i fuld gang med at se på det da det ikke kun er ved lunge kræft men også brystkræft,
https://pubmed.ncbi.nlm.nih.gov/25834398/ mund og svælgkræft,
https://www.nature.com/articles/s41598-020-73058-4 blærekræft
https://pubmed.ncbi.nlm.nih.gov/15833884/ at det har indvirkning på at forebygge hvorfor man også ser at øer der drikker meget kava har minimale tilfælde af disse. Det er så simpelt intet fusk og humbuk her men du er godt nok ude med riven skal jeg love for.
Og nej der er ikke evidens for at det kun var noble kava som har forårsager de leversvigt du taler om da man i senere opfølgning på mange af de studier fandt ud af at mange folk også drak heftigt ved siden selvom de fik fortalt at de ikke måtte samtidigt med kava men ikke turde indrømme det. Er det virkelig så svært at forestille sig når du ser på hvor meget ansvarsfralæggelse vi ser bare i dag? Hvis kava forårsagede leverskader som du påstår ville store dele af befolkningen på stillehavsøerne hvor de fleste mænd drikker store mængder daglig have stor prævalens af leversvigt hvilket de ikke har fordi de ikke blander det med medicin og alkohol. Du har læst det første du så på google om advarsler mht. kava og fundet få studier som allerede er outdatede og antastede for fejlagtige tolkninger og betvivler medicinalindustriens rolle i misinformation af naturmedicin? Det er bare direkte naivt. - Også fordi de tilfælde kom i 90'erne hvor der var en kava-goldrush og de brugte acetoneekstrakter af dårlig, halvmuggen plantemateriale og kavaarter man ikke engang må eksportere i dag så nej der er ikke risiko for leversvigt medmindre man er en så dårlig holdspiller at man ikke anerkender at man har drukket sprit ved siden af eller indrømmer man tager fejl og ødelægger det for alle de andre..
Two drug monitoring studies, including a total of 7078 patients taking 120-150mg kava extract per day, had not found a single case of liver damage [1].
In 2002 a systematic review of the safety of kava extract was undertaken. They reviewed the studies of many different clinical trials. They also included the results of two drug monitoring studies. Adults were taking 120-150mg kava extract for 6 weeks. While there were instances of negative interactions, they were limited to gastrointestinal upset, allergy, headache and dizziness. Two drug monitoring studies found no instances of liver injury out of the groups [2]. This study is applicable to those consuming kavas medicinally using extracts. This study doesn’t necessarily speak to those of us who consume kava traditionally in larger amounts, however it does lend evidence that the daily consumption of kavalactones does not directly lead to liver damage in healthy individuals. These studies also review theories of liver injury that occurred during the 1998-2002 time period.
[1] Ernst, E. “A re-evaluation of kava (Piper methysticum).” British journal of clinical pharmacology vol. 64,4 (2007): 415-7. doi:10.1111/j.1365-2125.2007.02932.x
(
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2048557/)
[2] Stevinson C, Huntley A, Ernst E. A systematic review of the safety of kava extract in the treatment of anxiety. Drug Saf. 2002;25(4):251-61. doi: 10.2165/00002018-200225040-00003. PMID: 11994028.
(
https://pubmed.ncbi.nlm.nih.gov/11994028/)
GGT is short for gamma-glutamyltransferase. This is a liver enzyme that is tested for in a good majority of metabolism tests. GGT is present in the cell membranes of tissues including liver, kidneys, bile ducts, pancreas, heart, and brain. It is involved in the metabolism of glutathione and the detoxification of pharmaceutical compounds among hundreds of different functions. Introduced over 40 years ago, tests for quantification of this enzyme are commonly measured as a sensitive but not very specific liver function test (Whitfield 2001).
We should also address two other common terms seen when viewing a liver metabolic test and those are AST and ALT. Both are highly concentrated in the liver, however ALT is a more specific indicator of liver injury. Normal ranges of ALT are from 3-30 U/L. Liver damage with ALT will begin to indicate when levels reach 3 times the normal upper range. GGT can help confirm the origin of other elevated enzymes, or can help support the suspicion of alcohol use in patients (Fancher, Kamboj, and Onate 2017).
In 2007 a study was performed on predominantly Tongan individuals in Hawaii. 62 subjects were tested. Subjects were screened for compromising liver conditions prior to the tests such as hepatitis, and co-administration of drugs which may affect the liver. Participants which were regular kava drinkers were found 5 times more likely to have increased levels of GGT on metabolism tests. This number closely correlates to BMI in kava drinkers linearly. Increased BMI → Increased GGT. This study found no association between kava drinking and elevated AST and ALT values which classically indicate liver issues/damage. Aqueous kava was, in this study, considered a possible contributing factor to increased levels of GGT. This study goes on to say that GGT elevation in these kava drinkers may be an artifact of GGT induction, rather than a sign of liver toxicity (Brown et al. 2007).
Brown, Amy C., Janet Onopa, Peter Holck, Pakieli Kaufusi, Derek Kabasawa, Winston J. Craig, Klaus Dragull, Arieh M. Levine, and Jonathan D. Baker. 2007. “Traditional Kava Beverage Consumption and Liver Function Tests in a Predominantly Tongan Population in Hawaii.” Clinical Toxicology 45 (5): 549–56.
Fancher, Tonya, Amit Kamboj, and John Onate. 2017. “Interpreting Liver Function Tests.” Current Psychiatry 6 (5): 61–68.
Whitfield, J. B. 2001. “Gamma Glutamyl Transferase.” Critical Reviews in Clinical Laboratory Sciences 38 (4): 263–355.
Here’s a sample of some claims of harm from the website betterhealth.vic.gov.au [1] which looks to be an official outlet for information, given the .gov address. The following is what they claim are side effects from continued kava consumption coupled with my response to that claim:
breathing difficulties NO
The source being used to make this claim refers to this NOT being correlated with kava usage [2].
visual changes, including sensitivity to light (photophobia) YES
This is likely true, and has been shown in a study dated 1985 [3].
slight alterations to blood cells, including white and red blood cells, and platelets PARTLY TRUE
When they say “slight” here they really mean it. A study was ran on rats and kavalactone extracts. They found slight changes to rats given an outrageous dose of 2000mg/kg. This would be similar to a human somehow managing to consume 158 grams of kavalactones per day. A few hematological numbers were off balance in this study, however platelets were not significantly altered even at this staggering amount per kg [2].
liver damage NO
This is referring to increased GGT/ALP numbers and these do not indicate liver damage. Liver damage is indicated by a doubling of AST/ALT number, and GGT/ALP are only used as indicators when the AST/ALT numbers are off.[4]
compromised immune function NO
The nearest I can find in research regarding this effect is on lymphocytes, and this was from one paper where an individual received liver damage by taking 210-280mg of Laitain in the year 2001 [5], which was likely part of the contaminated batch that caused the liver issues during that time.
kidney damage NO
“The present results support the previous findings indicating the safety of kava to the liver (Sorrentino et al., 2006; Lim et al., 2007). The increase in serum urea level, in the present results, was expected due to the increase in total protein level. Creatinine is a chemical waste molecule that is generated from muscle metabolism. It is transported through the bloodstream to the kidneys, where they filter most of the Creatinine and dispose it in the urine. As the kidneys become impaired, the Creatinine level in the blood will rise. Thus the measurement of serum Creatinine level has been found to be a fairly reliable indicator of kidney function. Therefore, the concomitant highly significant decrease in Creatinine level, in the present data, suggests that there may be no adverse effect on kidney function.” [6]
contact dermatitis – causing scaly, flaky rash on the skin YES
This is one effect that is well known among long term kava drinkers.
appetite loss, leading to malnutrition and weight loss YES, but Indirect
This is an indirect effect of kava due to meal planning and reduction of meal sizes, not to mention a belly full of liquid would cause you to eat less. Be that as it may, long term heavy kava users average a 19-21 BMI, so while this effect does happen, it’s indirect, as the kava isn’t making you lose weight.
loss of drive and motivation NO - Political
This is purely political. Video games can cause loss of drive and motivation as well as any other activity which draws time away from obligations. It’s a disappointment that this phrase is even used at all. To me, the phrase itself is lazy. Could there be other factors involved with a community of kava drinkers, disenfranchised from opportunities in the modern world due to being termed “savages?”. So many variables exist that could accompany this that pinning it on kava is simply irresponsible.
worsened symptoms of pre-existing mental illnesses such as schizophrenia. NO
No, this is purely misinformation, in fact kava has been shown to decrease instances of mental illness due to its regulatory effects on several important neurotransmitters [7]. This has been physically observed by researchers over the years watching kava drinkers in Arnem Land [8].
So, kava lovers, as you can see kava health claims aren’t all they’re stacked up to be. It’s about time we started addressing this plant for the reality in which it resides. It’s painfully obvious that these attempts to demonize kava were born from those with little understanding of kava.
[1] “Kava.” n.d. Accessed May 5, 2021.
https://www.betterhealth.vic.gov.au/hea ... iving/kava.
[2] Mathews, J. D., M. D. Riley, L. Fejo, E. Munoz, N. R. Milns, I. D. Gardner, J. R. Powers, E. Ganygulpa, and B. J. Gununuwawuy. 1988. “Effects of the Heavy Usage of Kava on Physical Health: Summary of a Pilot Survey in an Aboriginal Community.” The Medical Journal of Australia 148 (11): 548–55.
https://doi.org/10.5694/j.1326-5377.1988.tb93809.x.
[3] Garner, L. F., and J. D. Klinger. 1985. “Some Visual Effects Caused by the Beverage Kava.” Ethnopharmacol. 13 (3): 307–11.
https://doi.org/10.1016/0378-8741(85)90076-5.
[4] Clough, Alan R., Ross S. Bailie, and Bart Currie. 2003. “Liver Function Test Abnormalities in Users of Aqueous Kava Extracts.” Journal of Toxicology. Clinical Toxicology 41 (6): 821–29.
https://doi.org/10.1081/clt-120025347.
[5] Escher, M., J. Desmeules, E. Giostra, and G. Mentha. 2001. “Hepatitis Associated with Kava, a Herbal Remedy for Anxiety.” BMJ 322 (7279): 139.
https://doi.org/10.1136/bmj.322.7279.139.
[6] Noor, Neveen A. 2010. “Anxiolytic Action and Safety of Kava: Effect on Rat Brain Acetylcholinesterase Activity and Some Serum Biochemical Parameters.” African Journal of Pharmacy and Pharmacology 4 (11): 823–28.
http://dx.doi.org/.
[7] Krum, Bárbara Nunes, Catiuscia Molz de Freitas, Ana Paula Chiapinotto Ceretta, Caroline Pilecco Barbosa, Elizete de Moraes Reis, Rahisa Scussel, Emily da Silva Córneo, Ricardo Andrez Machado-de-Ávila, Aline Augusti Boligon, and Roselei Fachinetto. 2021. “Kava Decreases the Stereotyped Behavior Induced by Amphetamine in Mice.” Journal of Ethnopharmacology 265 (January): 113293.
https://doi.org/10.1016/j.jep.2020.113293.
[8] Cawte, John. 1986. “Parameters of Kava Used as a Challenge to Alcohol.” The Australian and New Zealand Journal of Psychiatry 20 (1): 70–76.
https://doi.org/10.3109/00048678609158867.
Germany, Palisi, and the Kava Act of 2002
Kava extract preparations have a history of over 130 years of medicinal use in europe. An estimated 450 million doses were consumed between 1991-2001. Prior to the year 2000, there was no known risk of any clinical significance, and kava was considered exceptionally safe [1]. In June 2002 BfArM (German Drug Regulatory Board) issued direction to completely remove all kava-containing, and kavain-containing drugs from the market. This direction cited “Undesirable effects on the liver” including acute toxic hepatitis, liver failure, and cases of transplantation [2]. Mold, pesticides and other contaminants were thought to have contributed to this situation [3], however at the time a swap had been made in kava variety. A change was made from beverage grade kavas, to non-beverage grade, also known as “Palisi”. These strains were used due to their high kavalactone contents and higher biomass as well as faster maturation times. The first harvests of this variety of kava for extraction by European drug companies coincides with the beginning occurrence of liver injury case reports in 1999-2000 in Switzerland [4].
Hold on a minute, does that mean kava is unsafe?
No, first of all because this pertains to kava extracts, and second because Vanuatu took action about the issue by creating and enacting the “Kava Act of 2002”. This document set rules that prevents the causal export of non-noble or non-beverage grade kavas [5]. This, combined with the German ban itself, put the proverbial breaks on the sale and export of these kavas to be extracted with solvents that were not suitable for daily drinking. Due to these and other efforts, in 2014 a German court ruled that banning kava was inappropriate, and the harms were best attributed to lack of product quality control, not inherent harm associated with appropriately sourced and manufactured products. Currently, in Germany, the law stands that kava can only be used under a prescriber’s direction, and not for self-care or recreational use, however it is not explicitly banned [6].
It’s obvious something happened which caused these severe reactions in the late 90s early 2000s, however it seems that the actions taken have reduced or eliminated the mass instances of acute liver injury, as evidenced by the lack of reports pertaining to it. The industry has matured and the knowledge of proper kava varieties and product quality has been disseminated from regulators and exporters all the way to the consumer level.
Update from Dr. Schmidt
After speaking to Dr. Mathias Schmidt in regards to the legality of kava in Germany at present, it seems BfArM, through a number of new decisions are now attacking kava again at different regulatory angles. One approach was to simply use the same arguments as the ban in 2002. It's been contested in court, and they are currently waiting for the courts to convene because they've been out for Covid.
Currently kava is not available as a prescription or otherwise. (M. Schmidt, personal communication, May 27, 2021)
[1] Kuchta, Kenny, Marie Hladikova, Michael Thomsen, Adolf Nahrstedt, and Mathias Schmidt. 2021. “Kava (Piper Methysticum) Extract for the Treatment of Nervous Anxiety, Tension and Restlessness.” Drug Research 71 (2): 83–93.
(
https://doi.org/10.1055/a-1268-7135.)
[2] BfArM. 2002. “Kava Removal.”
http://lrd.spc.int/ahp-publications/doc ... va-removal.)
[3] Teschke, Rolf, Samuel X. Qiu, and Vincent Lebot. 2011. “Herbal Hepatotoxicity by Kava: Update on Pipermethystine, Flavokavain B, and Mould Hepatotoxins as Primarily Assumed Culprits.” Digestive and Liver Disease: Official Journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver 43 (9): 676–81.
(
https://doi.org/10.1016/j.dld.2011.01.018.)
[4] Thomsen, Michael, and Mathias Schmidt. 2021. “Health Policy versus Kava (Piper Methysticum): Anxiolytic Efficacy May Be Instrumental in Restoring the Reputation of a Major South Pacific Crop.” Journal of Ethnopharmacology 268 (March): 113582.
(
https://doi.org/10.1016/j.jep.2020.113582.)
[5] Vanuatu. 2002. “Kava Act 2002.” 7. Republic Of Vanuatu.
(
https://biosecurity.gov.vu/images/Expor ... t-2002.pdf.)
[6] White, C. Michael. 2018. “The Pharmacology, Pharmacokinetics, Efficacy, and Adverse Events Associated With Kava.” Journal of Clinical Pharmacology 58 (11): 1396–1405.
(
https://doi.org/10.1002/jcph.1263.)
Today’s fact of the day will highlight an interesting disparity between how different regulatory bodies interpreted data related to the liver injury reports from the early 2000s. BfArM in Germany is the “Federal Institute for Drugs and Medical Devices”. This is the regulatory agency responsible for the kava ban which swept the world as other countries looked to Germany for direction. We’re going to take a look at one paper which focuses on four of these instances and how different each regulatory body saw the data as it was presented.
We’ll be addressing the following four specific instances;
(CD = Coadministered Drugs)
Case # 98004297
Ethanolic kava extract (120 mg/d, 10 m) for anxiety and restlessness. Prolonged kava treatment. Hydrochlorothiazide and Crataegus extract as CD. No ultrasound results. No exclusion of hepatitis A and C, CMV, EBV, HSV, and VZV, but LKM positive. Recurrent ALT increase despite kava cessation, suggesting kava independent cause. No further ALT follow up due to early death. Chronic pancreatitis at autopsy. Lethal outcome. Causality excluded for kava and excluded for CD. Diagnosis: LKM positive AIH and pancreatitis [1].
Case # 94901308
Acetonic kava extract (210 mg/d, 1.5 m) for unknown indication. Daily kava overdose. Furosemide, Atenolol, and Terfenadine as CD. Known Terfenadine overdose with up to 300 mg daily (allowed maximal 120 mg). ALT 950 U/L, AST 1045 U/L, and ALP 315 U/L. ALT normalisation not documented after 2 months. Kava unrelated cause due to recurrent increase of ALT. Complete exclusion diagnostic work-up, but HSV-IgM positive. Cessation of initial steroid treatment at time when HSV hepatitis was diagnosed. Favourable outcome. Causality excluded for kava and excluded for CD. Diagnosis: HSV-hepatitis [1].
Case # 01003950
No data available. Undeclared indication. Unassessable case. Unclear case, not suitable as index case for a possible subsequent re-administration (see case 10, identical patient). ALT, AST, and ALP not recorded. Favourable outcome. Causality excluded for kava and not assessable for CD. Diagnosis: Questionable liver disease of unknown etiology [1].
Case # 02002090
Ethanolic kava extract (50 mg/d, 0.25 m) for stress. Sulfasalazine, Diclofenac, Progesterone, Omeprazole, Butylscopolaminium-bromide as CD. ALT 572 U/L, AST 220 U/L, and ALP 163 U/L. ALT course poorly documented. Exclusion of hepatitis A, B, C, CMV, and EBV mentioned but specific data not documented AMA, SLA/LP, and LKM with negative results, but ANA not reported. Known Bechterew’s disease and adipositas as co-morbidity. Favourable outcome. Causality possible for kava and unlikely for CD. Diagnosis: Liver disease of unknown etiology, possibly related to kava [1].
These cases were seen rather differently by each agency [2]. Table 2 shows the differing conclusions between countries and their scientific regulatory bodies. Where BfArM found probable and certain links to kava, other agencies found little to no evidence of kava being the key factor in these injury reports. This is only a small snapshot of the indiscrepancies in interpretation, and highlights the non-agreement between scientific bodies in regards to harm caused by kava. This brings even more questionability in the decision to ban kava products in Germany, which continues to harm the South Pacific to this day.
[1] Teschke, Rolf. 2010. “Kava Hepatotoxicity--a Clinical Review.” Annals of Hepatology 9 (3): 251–65.
https://doi.org/10.1016/S1665-2681(19)31634-5.
[2] Gruenwald, Joerg, and Juergen Skrabal. 2003. “Kava Ban Highly Questionable: A Brief Summary of the Main Scientific Findings Presented in the ‘in Depth Investigation on EU Member States Market Restrictions on Kava Products.’” Seminars in Integrative Medicine 1 (4): 199–210.
https://doi.org/10.1016/j.sigm.2004.01.001.
The longer one sticks around the various pages and forums on the internet, the more likely they are to run across user concerns related to liver toxicity. Generally, this is a concern of new users just beginning to venture into the kava world. These concerns are thought to stem entirely from the 2001-2002 FDA safety alert issued for kava. Interestingly, the pages from the national institute of mental health currently led to error pages when researching and following links for this information [1].
Between the late 1990s and early 2000s just over 100 hepatoxic cases were reported to be associated with kava consumption, with the majority of users consuming them as an anxiolytic agent. We’ll go ahead and point out here how it is questionable that these issues only spring from a specific period in time. Since then, scientists have been attempting to discover what the cause of this issue has been. They’ve looked at several possible causes. These causes include pipermethystine, flavokavain B, yangonin, methysticin, kavain, ethanol, co-medicated drugs, and mold hepatotoxins. Currently substantiated evidence is lacking for all of these [3]. Currently, research has liver injury from kava separated into two types.
Unpredictable, idiosyncratic types, and predictable intrinsic types [2].
Idiosyncrasy:
A characteristic, habit, mannerism, or the like, that is peculiar to an individual.
The physical constitution peculiar to an individual.
A peculiarity of the physical or the mental constitution, especially susceptibility toward drugs, food, etc.
The metabolic idiosyncratic type of hepatotoxicity seems to be related to an individual’s inability to process certain chemicals through enzymatic metabolism. In this respect the person in question’s genes may not have expressed in a way that allows them to process kavalactones at all. This type of reaction is extremely rare. If all cases related to liver injury were indeed from kava, the estimated risk would still be less than .3 cases per 1 million doses daily [4]. This reaction would represent even far less than this.
Intrinsic:
belonging to a thing by its very nature
The predictable, intrinsic type of hepatotoxicity are toxicities that essentially can be preventable through appropriate measures. Here we get into the realm of poor-quality kava products and mold hepatotoxins, flavokavain B, kava varieties, and past liver injury or issues. Something to keep in mind is that during this time, a few batches of poor-quality kava extracts may have been sufficient to cause a limited number of individuals dose dependent hepatotoxic reactions of this predictable intrinsic type (Teschke 2011). In other words, just a small amount of contaminated product could have fired off the whole issue of liver toxicity.
The reality is we may actually never know what caused these liver issues back in the early 2000s. Researchers missed the chance to analyze the kava products taken by the patients with toxic liver disease reportedly connected to or had a high probability of being caused by kava. As such, we can only speculate as to the culprits during this time. With this in mind we should also keep in context the recent studies on individual constituents of kava. It’s interesting in that kava research has identified many compounds as possibly toxic in the kava plant, however they require doses far greater than any taken by kava consumers to reach this level. Many of these studies were run in vitro and compounds were added directly to cells or cell cultures. These conditions are not necessarily relevant to whole kava extracts commonly used in humans, and virtually any chemical compound used at untherapeutic amounts may produce cytotoxicity in a dose-dependent way [3].
In conclusion we’re closer, but we’re still far from understanding what happened 20 years ago, however we can say that through these attempts at finding it, we’ve discovered traditional kava presents an impressive safety profile tracing back thousands of years. As long as noble “beverage” grade kavas are selected for daily consumption, only below ground parts of the plant are used, and the rhizomes and roots are peeled, issues are extremely rare, being limited only to idiosyncratic reactions in healthy individuals.
[1] Kava. (n.d.). Retrieved January 26, 2021, from
https://ods.od.nih.gov/HealthInformation/kava.aspx[2] Teschke R, Qiu SX, Lebot V. Herbal hepatotoxicity by kava: update on pipermethystine, flavokavain B, and mould hepatotoxins as primarily assumed culprits. Dig Liver Dis. 2011 Sep;43(9):676-81. doi: 10.1016/j.dld.2011.01.018. Epub 2011 Mar 4. PMID: 21377431.
pubmed.ncbi.nlm.nih.gov
Herbal hepatotoxicity by kava: update on pipermethystine, flavokavain B, and mould hepatotoxins as primarily assumed culprits - PubMed
Herbal hepatotoxicity by the anxiolytic kava (Piper methysticum Forst. f.) emerged unexpectedly and was observed in a few patients worldwide. Liver injury occurred after the use of traditional aqueous kava extracts in the South Pacific region and of acetonic and ethanolic extracts in Western...
pubmed.ncbi.nlm.nih.gov pubmed.ncbi.nlm.nih.gov
[3] Teschke R, Sarris J, Lebot V. Contaminant hepatotoxins as culprits for kava hepatotoxicity--fact or fiction? Phytother Res. 2013 Mar;27(3):472-4. doi: 10.1002/ptr.4729. Epub 2012 May 14. PMID: 22585547.
pubmed.ncbi.nlm.nih.gov
Contaminant hepatotoxins as culprits for kava hepatotoxicity--fact or fiction? - PubMed
The culprit of kava hepatotoxicity will continue to remain a mystery in humans, if the underlying reaction is of idiosyncratic, unpredictable, and dose-independent nature due potentially to some metabolic aberration in a few individuals emerging from kava use. In addition, kava hepatotoxicity is...
pubmed.ncbi.nlm.nih.gov pubmed.ncbi.nlm.nih.gov
[4] Bian T, Corral P, Wang Y, Botello J, Kingston R, Daniels T, Salloum RG, Johnston E, Huo Z, Lu J, Liu AC, Xing C. Kava as a Clinical Nutrient: Promises and Challenges. Nutrients. 2020 Oct 5;12(10):3044. doi: 10.3390/nu12103044. PMID: 33027883; PMCID: PMC7600512.
pubmed.ncbi.nlm.nih.gov
Kava as a Clinical Nutrient: Promises and Challenges - PubMed
Kava beverages are typically prepared from the root of Piper methysticum. They have been consumed among Pacific Islanders for centuries. Kava extract preparations were once used as herbal drugs to treat anxiety in Europe. Kava is also marketed as a dietary supplement in the U.S. and is gaining...
pubmed.ncbi.nlm.nih.gov pubmed.ncbi.nlm.nih.gov
In this study 21 smoking but otherwise healthy (normal blood counts, electrolytes, and liver function) individuals took part in a 7-day clinical trial. Individuals were screened for diseases or impairments prior to study. Alcohol dependent individuals and pregnant/breastfeeding women were excluded. This trial sought to measure levels of carcinogens (cancer causing substances) related to smoking tobacco products and their rate of elimination when combined with kava. This trial focuses on NNK specifically. NNK is a nicotine-derived nitrosamine ketone. It’s what occurs in tobaccos that have been fire cured, and occurs during the physical burning process. NNK or 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone is an indisputable carcinogen. Once NNK is activated it initiates a cascade of signaling pathways, resulting in uncontrolled cellular proliferation and tumorigenesis (cancer)[1]. The primary objective of this study was to compare urinary totals of the metabolites of NNK before and after kava consumption. This would give the researchers an idea of how well kava helps in removing the NNK from the body. This study used Gaia Herbs kava caps at 3 capsules per day. Fasting except for water was required 1 hour prior to and after each dose. The participants in this study were not looking to quit smoking.
Kava was given to participants to measure the effect it had on cortisol (the stress hormone). Out of the 21 people, 15 showed reduced levels of plasma cortisol. In this part of the study they found kava resulted in a 59% reduction in urinary TCE (Total cortisol equivalent) in the zero to six-hour study period, indicating kava’s stress reliving abilities. Interestingly cortisol reduction was more pronounced in smokers with higher baseline cortisol levels.
The results of this study show that NNAL (a metabolite of NNK) significantly increased in the urine with kava exposure. The study shows the number doubled. This is good. You want NNK and its metabolites to be gone as quickly as possible. This may lead to mitigating some of the harmful effects of tobacco and reduce the satisfaction from smoking. The data generated by this pilot trial support pursuit of further preclinical and clinical studies to confirm kava’s benefits. In short, it’s excellent news, but not necessarily something I would consider a “cure” for lung cancer at this point. I do wish the study was longer than 7 days, as I believe more interesting results would have been discovered. Don’t smoke, but if you do, this study may lend some credence to kava’s chemoprotective properties. The figure below shows levels of NNAL and cortisone during the study.
figure3.jpg
Akopyan, Gohar; Bonavida, Benjamin (2006). "Understanding tobacco smoke carcinogen NNK and lung tumorigenesis". International Journal of Oncology. 29 (4): 745–52. doi:10.3892/ijo.29.4.745. PMID 16964372.
Wang Y, Narayanapillai SC, Tessier KM, Strayer LG, Upadhyaya P, Hu Q, Kingston R, Salloum RG, Lu J, Hecht SS, Hatsukami DK, Fujioka N, Xing C. The Impact of One-week Dietary Supplementation with Kava on Biomarkers of Tobacco Use and Nitrosamine-based Carcinogenesis Risk among Active Smokers. Cancer Prev Res (Phila). 2020 May;13(5):483-492. doi: 10.1158/1940-6207.CAPR-19-0501. Epub 2020 Feb 26. PMID: 32102948; PMCID: PMC7461349.
According to the book, Kava, an Ethnobotanical Review of a Treasured Plant, there are five deaths associated with kava extract, extract meaning the Kava may or may not be noble and is extracted using acetone, alcohol, or chloroform. Also, extracts may pull alkaloids out of the root. In four of the five cases, other drugs such as mood drugs and blood pressure drugs were also being used at the time of death. The fatality point was either liver failure or heart failure in all cases, suggesting an underlying liver or heart condition, dangerous combination of substances, or impure kava extract, as the book notes there are not any known cases of death from Kava in traditional preparation.
Her er en masterlist af kava-studier jeg anbefaler at du læser igennem for gider ikke diskuttere med dig. Det er langt fra første gang at du forsøger at discredit og trækker i land på den måde, i stedet for bare at anerkende at der måske var noget du ikke vidste.
https://kavaforums.com/forum/threads/ma ... ost-192895