'Awa (or kava as it is popular known) is a root grown in the Pacific Islands where it has been used centuries for spiritual, medicinal and religious purposes. Taste our unique kava for a natural way for social relaxation, reduce anxiety and to help you get a good night’s rest.
"E hanai ‘awa a ikaika ka makani"
Feed with ‘awa so that the spirit may gain strength.
One offers ‘awa and prayers to the dead so that their spirits may grow strong and be a source of help to the family.
|
|
ʻAwa has become prominent in alternative medicine for its ability to relieve anxiety, depression, pain, insomnia, urinary problems without being addictive or impairing the user's judgment. So what are you waiting for! Mix it, Serve it, Gulp it! |
DID U know that?- It is considered food for the Gods!- Refusing kava offered to you is disrespectful!- No formal ceremony or gathering is complete without ʻawa! |
|
Kava me Up!
|
"I didnʻt know kava could taste this smooth! This is the best tasting kava Iʻve ever had and surely top-quality! Hit Them Up!"
- Cathy C. |
"Iʻve been drinking beer because Iʻve never had access to quality ʻawa and now I do! Its about time I drink the roots of my ancestors!"
-Kai K. |
"I canʻt say it enough, the quality easily surpasses every other kava Iʻve had. Trust me, I ʻve been mixing ʻawa for years! You wont be disappointed!"
- Sharron S. |
Kava drink and itʻs Effects
The following text is copied from The Kava Society, New Zealand https://kavasociety.nz.
Please visit them to learn more about how they are preserving kava traditions in the South Pacific!
Please visit them to learn more about how they are preserving kava traditions in the South Pacific!
As noted by V. Lebot and J. Lèvesque:
The remarkable medicinal properties and soothing effects of kava have been part of the wisdom of Pacific islanders for centuries. Melanesians, Polynesians and Micronesian people alike grind the fresh or dry roots of this plant to prepare their traditional beverage, which is the centerpiece for much solemn ritual as well as being the daily social drink for many appreciative Oceanians.
The specific effects of kava depend on the cultivar, plant's potency and method of consumption. But generally speaking, kava is known as a relaxing drink with potential to promote a sense of sociability, as well as feelings of peace and harmony without diminishing mental awareness or clarity. For many users, kava is a pleasant, refreshing and mentally uplifting drink that relieves fatigue, relaxes the body after hard work or effort, clears the mind and brings a sense of well-being.
Robert J. Gregory, a Massey University professor of psychology, offered the following description of kava's effects:
Kava makes you quiet and able to think and listen to your thoughts. Your mind opens to what has been and should be done. The subjective feeling after kava is to be slowed down, for it almost forces one to become quiet. Sometimes it is like entering a light relaxed dream. (...) The altered state of consciousness is subtle and mild. Noise, interference with thought processes, bright lights, movement, all hinder the effect, the mildly altered stream of thought. The subtle effect is maintained only if there is peace and quiet.
Even though kava has been an important component of the traditional Pacific Islands medicine (with its potential anti-anxiety, stress relieving properties are under current scientific research), most people consume it today as a traditional, relaxing and refreshing beverage and not a remedy for any health problems. This is also how we see, consume and promote kava.
One way to look at kava is to compare it to drinking coffee. Both kava and coffee are used as benign social drinks. While the latter can give a mild buzz and "kick" of energy, the former is known as a gently relaxing tonic.
The remarkable medicinal properties and soothing effects of kava have been part of the wisdom of Pacific islanders for centuries. Melanesians, Polynesians and Micronesian people alike grind the fresh or dry roots of this plant to prepare their traditional beverage, which is the centerpiece for much solemn ritual as well as being the daily social drink for many appreciative Oceanians.
The specific effects of kava depend on the cultivar, plant's potency and method of consumption. But generally speaking, kava is known as a relaxing drink with potential to promote a sense of sociability, as well as feelings of peace and harmony without diminishing mental awareness or clarity. For many users, kava is a pleasant, refreshing and mentally uplifting drink that relieves fatigue, relaxes the body after hard work or effort, clears the mind and brings a sense of well-being.
Robert J. Gregory, a Massey University professor of psychology, offered the following description of kava's effects:
Kava makes you quiet and able to think and listen to your thoughts. Your mind opens to what has been and should be done. The subjective feeling after kava is to be slowed down, for it almost forces one to become quiet. Sometimes it is like entering a light relaxed dream. (...) The altered state of consciousness is subtle and mild. Noise, interference with thought processes, bright lights, movement, all hinder the effect, the mildly altered stream of thought. The subtle effect is maintained only if there is peace and quiet.
Even though kava has been an important component of the traditional Pacific Islands medicine (with its potential anti-anxiety, stress relieving properties are under current scientific research), most people consume it today as a traditional, relaxing and refreshing beverage and not a remedy for any health problems. This is also how we see, consume and promote kava.
One way to look at kava is to compare it to drinking coffee. Both kava and coffee are used as benign social drinks. While the latter can give a mild buzz and "kick" of energy, the former is known as a gently relaxing tonic.
World first clinical trial supports use of Kava to treat anxiety!
Kava Myths
Myth #1: Kava is alcohol
The ‘kava is alcohol’ myth is believed to have started when Johann Forster (1754-1794), a naturalist aboard Captain James Cook's Endeavour, gave kava its botanical name Piper methysticum. Methysticum is a Greek word meaning ‘intoxicating’, or according to Forster, ‘intoxicating pepper’ – Piper methysticum (Singh and Blumenthal, 1997; Steinmetz, 1960).
Added to this myth, was a report that masticating kava during preparation, ‘transformed the starch of the root into sugar, and that this by fermentation turned into alcohol’ (Lewin, 1998: 185).
Further, after drawing on an early 1800s report from Fiji, Thurn and Warton (1925) were adamant kava was ‘liquor … [with] its effects being similar to that of laudanum’ (102). Norton and Ruze (1994: 93) suggest that early European accounts of kava drinking not only associated kava with alcohol, but also opium, which further maligned kava's reputation.
Churchill (2010) suggests that from the outset, kava's botanical name suggested kava had an ‘intoxicating quality’, and that this made ‘it more difficult to correct the error’ (57).
Comments such as kava drinkers remaining clear-headed, and not interfering with reasoning, demonstrate that kava's effects on the brain are quite different to that of alcohol.
If a comparison was to be made between alcohol and kava, it would be described as a slightly drunk feeling in the body after consuming high volumes (Aronson, 2008). Cairney et al. (2003) who studied kava and mental clarity, found: ‘no impairment in cognitive or saccade function in individuals who were currently heavy kava users, nor was there any impairment in individuals who had been heavy kava users in the past but had abstained for longer than six months’ (389).
Thomson (2008) adds that ‘most people who drink kava for the first time … expend too much effort analysing its effects on them and can be heard muttering that they don't feel a thing’ (72).
Kava is not alcoholic; it is ‘nonfermented, non-alcoholic, nonopioid, [and] nonhallucinogenic’ (Norton and Ruze, 1994: 93), producing ‘a pleasant, warm, and cheerful, but lazy feeling, [making people] sociable, though not hilarious or loquacious; the reason is not obscured’ (Hocart, 1929: 59). Aronson (2008) removes ambiguity when he stated, ‘Reason and consciousness remain unaffected’ (183).
Professor Peter D’Abbs (1995), from the Darwin School of Medicine, verifies that kava use will ‘not lead to violent behavior’ often associated with alcohol use, does not ‘befuddle the mind and can be used to stimulate clear-headed discussion’ (169).
Where alcohol has the ability for some drinkers to: ‘release aggressive impulses; if anything kava inhibits or disassociates them. You cannot hate with kava in you’, argues Lemert (1967: 333).
Added to this myth, was a report that masticating kava during preparation, ‘transformed the starch of the root into sugar, and that this by fermentation turned into alcohol’ (Lewin, 1998: 185).
Further, after drawing on an early 1800s report from Fiji, Thurn and Warton (1925) were adamant kava was ‘liquor … [with] its effects being similar to that of laudanum’ (102). Norton and Ruze (1994: 93) suggest that early European accounts of kava drinking not only associated kava with alcohol, but also opium, which further maligned kava's reputation.
Churchill (2010) suggests that from the outset, kava's botanical name suggested kava had an ‘intoxicating quality’, and that this made ‘it more difficult to correct the error’ (57).
Comments such as kava drinkers remaining clear-headed, and not interfering with reasoning, demonstrate that kava's effects on the brain are quite different to that of alcohol.
If a comparison was to be made between alcohol and kava, it would be described as a slightly drunk feeling in the body after consuming high volumes (Aronson, 2008). Cairney et al. (2003) who studied kava and mental clarity, found: ‘no impairment in cognitive or saccade function in individuals who were currently heavy kava users, nor was there any impairment in individuals who had been heavy kava users in the past but had abstained for longer than six months’ (389).
Thomson (2008) adds that ‘most people who drink kava for the first time … expend too much effort analysing its effects on them and can be heard muttering that they don't feel a thing’ (72).
Kava is not alcoholic; it is ‘nonfermented, non-alcoholic, nonopioid, [and] nonhallucinogenic’ (Norton and Ruze, 1994: 93), producing ‘a pleasant, warm, and cheerful, but lazy feeling, [making people] sociable, though not hilarious or loquacious; the reason is not obscured’ (Hocart, 1929: 59). Aronson (2008) removes ambiguity when he stated, ‘Reason and consciousness remain unaffected’ (183).
Professor Peter D’Abbs (1995), from the Darwin School of Medicine, verifies that kava use will ‘not lead to violent behavior’ often associated with alcohol use, does not ‘befuddle the mind and can be used to stimulate clear-headed discussion’ (169).
Where alcohol has the ability for some drinkers to: ‘release aggressive impulses; if anything kava inhibits or disassociates them. You cannot hate with kava in you’, argues Lemert (1967: 333).
Of interest is kava's use in several drug-addiction therapy programmes, encapsulated in the title of Steiner's (2001) article, ‘Kava as an anti-craving agent’, which reports the preliminary results of kava to mitigate alcohol, tobacco and/or cocaine craving.
Braun and Cohen (2010) also discuss the value of kava to benzodiazepine withdrawal. They report that kava ‘may have an anxiolytic effect beyond the benzodiazepines’ (281), and that ‘withdrawal symptoms following discontinuation of benzodiazepines occurred somewhat less frequently under treatment with WS®1490 [kava extract], and even if they did occur, the anxiolytic effect remained’ (282).
Further, kava has been used as part of two District Health Board (New Zealand (NZ)) addiction rehabilitation programmes; one in the Bay of Plenty aimed at alcohol which is now in its seventh year (Crowley, 2015, personal communication) and the other in Marlborough, a NZ smoking cessation programme entitled ‘Kava-cation’ which boasts a 90% success rate (Daunauda, 2016). Moreover, Marotta (2018, personal communication) reports the use of kava and talk therapy, modelled on traditional Pacific kava use systems as extremely valuable in his work with heroin addicts in Thailand and Massachusetts, USA.
Leading kava expert, Dr Vincent Lebot (1991) adds weight to this discussion when stating: ‘by pharmacological standards, kava is not classified as a drug, as its consumption never leads to addiction or dependence. It has psychoactive properties but is neither an hallucinogenic nor a stupefacient’ (169).
Braun and Cohen (2010) also discuss the value of kava to benzodiazepine withdrawal. They report that kava ‘may have an anxiolytic effect beyond the benzodiazepines’ (281), and that ‘withdrawal symptoms following discontinuation of benzodiazepines occurred somewhat less frequently under treatment with WS®1490 [kava extract], and even if they did occur, the anxiolytic effect remained’ (282).
Further, kava has been used as part of two District Health Board (New Zealand (NZ)) addiction rehabilitation programmes; one in the Bay of Plenty aimed at alcohol which is now in its seventh year (Crowley, 2015, personal communication) and the other in Marlborough, a NZ smoking cessation programme entitled ‘Kava-cation’ which boasts a 90% success rate (Daunauda, 2016). Moreover, Marotta (2018, personal communication) reports the use of kava and talk therapy, modelled on traditional Pacific kava use systems as extremely valuable in his work with heroin addicts in Thailand and Massachusetts, USA.
Leading kava expert, Dr Vincent Lebot (1991) adds weight to this discussion when stating: ‘by pharmacological standards, kava is not classified as a drug, as its consumption never leads to addiction or dependence. It has psychoactive properties but is neither an hallucinogenic nor a stupefacient’ (169).
Myth #2: Kava causes Liver Damage
The suggestion that kava damages the liver, first surfaced in early 2000 following reports in Western Europe that 83 patients taking kava tablets died (Schmidt et al., 2005). This led to what is commonly known as the European Kava Ban. At the time of the ban, European doctors were estimated to have been prescribing 70 million (tablet) doses of kava daily, with most of this supplied for alleviating anxiety symptoms (Schmidt et al., 2005: 186).
The withdrawal of kava from the European markets led to a 12-year court battle which was not resolved until 2014 by the Federal Court of Germany. The final ruling by the Court was that it was unlikely kava had caused the reported deaths, and that liver damage from kava was so rare it was negligible. The Court rejected claims of liver damage caused by kava, and specified that these assertions were a gross misrepresentation of the possible effects (Kuchta et al., 2015; Schmidt, 2014).
Kava and liver damage – The medical evidence Showman et al. (2015) provide a valuable review of the kava hepatotoxicity claim and counter claim literature (60–61) which includes potential ‘Mechanisms of toxicity’ (61–63). They summarize that although there is evidence of a link between ‘kava and liver toxicity demonstrated in vivo and in vitro, in the history of Western kava use, toxicity is still considered relatively rare. Only a fraction of the handful of cases reviewed for liver toxicity could be, with any certainty, linked to kava consumption and most of those involved the co-ingestion of other medications/supplements. That means that the incident rate of liver toxicity due to kava is one in 60–125 million patients’ (65).
Singh (2014) discusses additional potential mechanisms of toxicity; adulterants added to kava to artificially boost weight to increase sale profit. This can include ‘sawdust, flour, and the dregs from the extraction of sugarcane’ (42). As Aporosa warned in a recent radio interview, exporters who engage in this type of unethical practice are playing a risky game, one that could have widespread implications should the adulterant contain bacteria, ‘salmonella for instance, and if someone gets sick … this could threaten kava importation’ as it will be ‘kava’ that will be cited as the health threat and not the adulterant (Kumar et al., 2018, interview: 45 seconds).3 To assist in safeguarding kava quality, the World Health Organization (WHO) and UN have developed a Kava Codex Alimentarius Quality Standard which should be in place by 2020. Commenting on this Codex, Vanuatu kava expert Dr Vincent Lebot stated Tonga, Fiji, Samoa and Vanuatu were also seeking to register the word ‘kava’ as a traditional beverage associated with...
healthy and safe raw materials used to prepare the beverage … kava is banned in the EU and banned in Australia and we believe this is due to a major misunderstanding regarding what kava is … We want to promote kava for what it is, a very healthy traditional beverage … If some companies elsewhere want to extract the active ingredients and prepare some capsules or whatever, this is not called kava any more. Like if you put caffeine in a capsule, you cannot call it coffee; if you put in dry raisin peel, you cannot call it wine, and same for tea. Kava is kava; it is the traditional beverage prepared by cold water extraction of the ground organs of the plant Piper Methysticum, and nothing else. We want to protect the geographical origins and the healthy quality kava plants we use here on an original basis. (Blades, 2018; also see Procyk and Lebot, 2013)
Linked to concerns of kava hepatotoxicity is an increase in gamma-glutamyl transpeptidase (GGT) levels in the blood following kava use. In their article, Moulds and Malani (2003) first addressed this matter in 2003 when they asked rhetorically: ‘How relevant is the finding that some … heavy kava drinkers have raised serum GGT levels?’, responding: ‘raised GGT levels do not necessarily imply “subclinical” liver toxicity’ (452).
When questioned by the author in 2009 about their subclinical liver toxicity comment, former Dean of Fiji School of Medicine, Professor Robert Moulds, commented that the abnormalities can be a concern among doctors who may not be conversant with liver function tests of kava drinkers, pointing to his colleagues article: ‘while elevated GGT and white blood cells [lymphocytes] were abnormal [to those unfamiliar with kava's effects on the liver], this does not mean that this abnormality is of concern’ (Malani, 2002: 7).
Mantesso (2016) also confirms that, kava ‘may throw out the liver function a little bit, altering liver enzymes. Now that's not necessarily saying it's causing liver damage.’ Moreover, Evans (2009) explains that ‘nonsteroidal anti-inflammatory drugs, lipid-lowering drugs, antibiotics, histamine blockers (used to treat excess stomach acid production), antifungal agents, seizure medication, antidepressants, and hormones such as testosterone’, can elevate GGT levels, although these continue to be routinely prescribed (24).
In making the case for kava, it is worth extrapolating the rarity of kava hepatotoxicity (liver damage as mentioned above) against the risk level posed by other commonly prescribed drugs. A comparison with Diazepam, a widely prescribed benzodiazepine that has similar effects to kava, is useful at this point.
Schmidt et al. (2005), who investigated 83 kava toxicity reports that had been influential to initiating the Kava Ban in Europe, pointed out that: ‘only three cases could be attributed to kava with high probability’. Of these cases it was suspected that other factors were responsible for the negative reaction (Schmidt et al., 2005: 182). The study reported 12 ‘probable’ cases of liver failure would account for a kava toxicity rate ‘of 0.23 cases per 1 million daily doses’ (187). Schmidt and colleagues note that at the time of the European Kava Ban, diazepam toxicity rates accounted for 2.12 cases of per million daily doses (187).
In another study, kava hepatotoxicity rates were compared with that of Paracetamol/Panadol. In that study, Rasmussen (2005) reported that these commonly prescribed over-the-counter pain medications accounted for ‘an estimated 458 deaths due to acute liver failure in the U.S. each year’, and summarized that kava was ‘dramatically’ safer than the popular readily available analgesic's (7).
In an article which considers rates of kava hepatotoxicity, Baker (2011) argues that attempting to calculate risk between kava and commonly prescribed pharmaceutical drugs is ambiguous. For instance, he explains that simply trying to estimate ‘the number of people taking a specific medication’ is a challenge in and of itself, whereas ‘counting cases of adverse reaction’ is even more difficult (374).
Regardless that the risk determination of well-controlled pharmaceuticals is ambiguous and problematic, these continue to be widely prescribed. Conversely, while ‘the frequency of toxicity from any kava-containing substance is exceedingly low; low enough that it can be difficult to ever observe it in the relatively small populations in which kava is traditionally consumed’, kava tends to draw a higher level of criticism than a number of well controlled and regularly prescribed pharmaceuticals known to be associated with hepatotoxicity (Baker, 2011: 379–380) such as Diazepam and Paracetamol/Panadol as explained above.
The withdrawal of kava from the European markets led to a 12-year court battle which was not resolved until 2014 by the Federal Court of Germany. The final ruling by the Court was that it was unlikely kava had caused the reported deaths, and that liver damage from kava was so rare it was negligible. The Court rejected claims of liver damage caused by kava, and specified that these assertions were a gross misrepresentation of the possible effects (Kuchta et al., 2015; Schmidt, 2014).
Kava and liver damage – The medical evidence Showman et al. (2015) provide a valuable review of the kava hepatotoxicity claim and counter claim literature (60–61) which includes potential ‘Mechanisms of toxicity’ (61–63). They summarize that although there is evidence of a link between ‘kava and liver toxicity demonstrated in vivo and in vitro, in the history of Western kava use, toxicity is still considered relatively rare. Only a fraction of the handful of cases reviewed for liver toxicity could be, with any certainty, linked to kava consumption and most of those involved the co-ingestion of other medications/supplements. That means that the incident rate of liver toxicity due to kava is one in 60–125 million patients’ (65).
Singh (2014) discusses additional potential mechanisms of toxicity; adulterants added to kava to artificially boost weight to increase sale profit. This can include ‘sawdust, flour, and the dregs from the extraction of sugarcane’ (42). As Aporosa warned in a recent radio interview, exporters who engage in this type of unethical practice are playing a risky game, one that could have widespread implications should the adulterant contain bacteria, ‘salmonella for instance, and if someone gets sick … this could threaten kava importation’ as it will be ‘kava’ that will be cited as the health threat and not the adulterant (Kumar et al., 2018, interview: 45 seconds).3 To assist in safeguarding kava quality, the World Health Organization (WHO) and UN have developed a Kava Codex Alimentarius Quality Standard which should be in place by 2020. Commenting on this Codex, Vanuatu kava expert Dr Vincent Lebot stated Tonga, Fiji, Samoa and Vanuatu were also seeking to register the word ‘kava’ as a traditional beverage associated with...
healthy and safe raw materials used to prepare the beverage … kava is banned in the EU and banned in Australia and we believe this is due to a major misunderstanding regarding what kava is … We want to promote kava for what it is, a very healthy traditional beverage … If some companies elsewhere want to extract the active ingredients and prepare some capsules or whatever, this is not called kava any more. Like if you put caffeine in a capsule, you cannot call it coffee; if you put in dry raisin peel, you cannot call it wine, and same for tea. Kava is kava; it is the traditional beverage prepared by cold water extraction of the ground organs of the plant Piper Methysticum, and nothing else. We want to protect the geographical origins and the healthy quality kava plants we use here on an original basis. (Blades, 2018; also see Procyk and Lebot, 2013)
Linked to concerns of kava hepatotoxicity is an increase in gamma-glutamyl transpeptidase (GGT) levels in the blood following kava use. In their article, Moulds and Malani (2003) first addressed this matter in 2003 when they asked rhetorically: ‘How relevant is the finding that some … heavy kava drinkers have raised serum GGT levels?’, responding: ‘raised GGT levels do not necessarily imply “subclinical” liver toxicity’ (452).
When questioned by the author in 2009 about their subclinical liver toxicity comment, former Dean of Fiji School of Medicine, Professor Robert Moulds, commented that the abnormalities can be a concern among doctors who may not be conversant with liver function tests of kava drinkers, pointing to his colleagues article: ‘while elevated GGT and white blood cells [lymphocytes] were abnormal [to those unfamiliar with kava's effects on the liver], this does not mean that this abnormality is of concern’ (Malani, 2002: 7).
Mantesso (2016) also confirms that, kava ‘may throw out the liver function a little bit, altering liver enzymes. Now that's not necessarily saying it's causing liver damage.’ Moreover, Evans (2009) explains that ‘nonsteroidal anti-inflammatory drugs, lipid-lowering drugs, antibiotics, histamine blockers (used to treat excess stomach acid production), antifungal agents, seizure medication, antidepressants, and hormones such as testosterone’, can elevate GGT levels, although these continue to be routinely prescribed (24).
In making the case for kava, it is worth extrapolating the rarity of kava hepatotoxicity (liver damage as mentioned above) against the risk level posed by other commonly prescribed drugs. A comparison with Diazepam, a widely prescribed benzodiazepine that has similar effects to kava, is useful at this point.
Schmidt et al. (2005), who investigated 83 kava toxicity reports that had been influential to initiating the Kava Ban in Europe, pointed out that: ‘only three cases could be attributed to kava with high probability’. Of these cases it was suspected that other factors were responsible for the negative reaction (Schmidt et al., 2005: 182). The study reported 12 ‘probable’ cases of liver failure would account for a kava toxicity rate ‘of 0.23 cases per 1 million daily doses’ (187). Schmidt and colleagues note that at the time of the European Kava Ban, diazepam toxicity rates accounted for 2.12 cases of per million daily doses (187).
In another study, kava hepatotoxicity rates were compared with that of Paracetamol/Panadol. In that study, Rasmussen (2005) reported that these commonly prescribed over-the-counter pain medications accounted for ‘an estimated 458 deaths due to acute liver failure in the U.S. each year’, and summarized that kava was ‘dramatically’ safer than the popular readily available analgesic's (7).
In an article which considers rates of kava hepatotoxicity, Baker (2011) argues that attempting to calculate risk between kava and commonly prescribed pharmaceutical drugs is ambiguous. For instance, he explains that simply trying to estimate ‘the number of people taking a specific medication’ is a challenge in and of itself, whereas ‘counting cases of adverse reaction’ is even more difficult (374).
Regardless that the risk determination of well-controlled pharmaceuticals is ambiguous and problematic, these continue to be widely prescribed. Conversely, while ‘the frequency of toxicity from any kava-containing substance is exceedingly low; low enough that it can be difficult to ever observe it in the relatively small populations in which kava is traditionally consumed’, kava tends to draw a higher level of criticism than a number of well controlled and regularly prescribed pharmaceuticals known to be associated with hepatotoxicity (Baker, 2011: 379–380) such as Diazepam and Paracetamol/Panadol as explained above.
Disclaimer
The information provided herein and content related to this website is for educational information only. Please do not use advice, suggestions, or counsel from any text or content on the site or related sites to diagnose, treat or with the hope to cure any illness or health condition. If any healthy or safety concerns arise from the use of our products, please consult a physician or medical professional. Unda Kava 808 and its owners, operators, employees, agents or staff cannot be held responsible for, and will not be liable for the inaccuracy or application of information provided on the website nor with regards to use of the products sold on the site. None of our statements have been evaluated by the FDA. Furthermore, we are required by law to inform our customers that we are not doctors and cannot offer any medical advice. Kava is not intended to diagnose, treat or cure any disease. We are not health care professionals and cannot provide answers or give advice as it relates to the use of Kava and the effects it may have on your health or well-being. If we are asked for hypotheticals or any other variations of a hypothetical situation, we will have to decline a response. Please direct all questions you may have regarding Kava to your doctor should you choose to use or consume our products.
The information provided herein and content related to this website is for educational information only. Please do not use advice, suggestions, or counsel from any text or content on the site or related sites to diagnose, treat or with the hope to cure any illness or health condition. If any healthy or safety concerns arise from the use of our products, please consult a physician or medical professional. Unda Kava 808 and its owners, operators, employees, agents or staff cannot be held responsible for, and will not be liable for the inaccuracy or application of information provided on the website nor with regards to use of the products sold on the site. None of our statements have been evaluated by the FDA. Furthermore, we are required by law to inform our customers that we are not doctors and cannot offer any medical advice. Kava is not intended to diagnose, treat or cure any disease. We are not health care professionals and cannot provide answers or give advice as it relates to the use of Kava and the effects it may have on your health or well-being. If we are asked for hypotheticals or any other variations of a hypothetical situation, we will have to decline a response. Please direct all questions you may have regarding Kava to your doctor should you choose to use or consume our products.