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Following is an article published on our initial research that has lead to the development of NEUROTONEN. The active ingredients that are responsible for producing a reduction in craving have been identified and purified from the root of the kava plant. The isolated and purified ingredients are the active ingredients in NEUROTONEN.  Research is continuing as we continue to develop a greater understanding of addiction. We are continuing our research and invite you to participate in our studies involving various addictive substances. If you are interested in participating please contact us at staff@steinerlabs.com.

PUBLISHED IN THE PACIFIC HEALTH DIALOG

Kava as an Anticraving Agent: Preliminary Studies


ABSTRACT

Drug and alcohol abuse is one of our most expensive and damaging health risks. The financial and social costs of addiction have lead to a significant investment in prevention and treatment in an effort to reduce the incidence of drug abuse. One important area of research is the chemistry of craving. It is assumed that if the neurological process of craving can be interrupted then addiction can be successfully treated. The active ingredients found in kava, known as kavapyrones, have been found to bind to many sites in the brain that are associated with addiction and craving. In an effort to determine if kava can effect the craving associated with substances of abuse a craving survey and a craving pilot study was completed for alcohol, tobacco, cocaine and heroin. The preliminary findings indicate that kava may reduce the craving associated with addiction. In one investigation the participants reported a reduction in their desire for their drug of choice. In another investigation a standardized dose of kavapyrones lead to a statistically significant difference in abstinence between the experimental and placebo group for alcohol. The studies presented are considered preliminary.

INTRODUCTION

It is estimated that drug and alcohol abuse costs the nation an estimated $257 billion each year. In 1996, 940,000 persons in the United States received treatment for drug or alcohol abuse in one of 10,641 treatment facilities nationwide. One of the reasons for these remarkable statistics in that not enough is known about addictions and their health consequences. There are many types of treatment available, yet even those most respected have shown only limited success.

Biochemical investigation of addiction has focused on the loci of action of the substance of abuse in the brain. A great deal is known about the receptor sites for the substances of abuse. Many drugs have been designed to react with these receptor sites in an effort to find an effective treatment for addiction. Considerable knowledge has developed regarding the chemicals produced in the synaptic cleft associated with substances of abuse. To date a variety of drugs have been developed which have some ability to control the craving of addiction. It is assumed that if the craving for the substance of abuse is removed the addiction can then be successfully treated.

Drug craving is defined as "the desire to experience the effects of a previously experienced psychoactive substance". While there is considerable debate on exactly what constitutes craving there is significant correlation of tension, anxiety and restlessness with craving.1 Kavapyrones are commonly used to treat tension, anxiety and restlessness.2

Kava (Piper methysticum) is a plant indigenous to the Pacific Islands. All major Pacific Islands developed kava as a beverage and it is commonly consumed much like alcohol in western culture. Kava is traditionally prepared from the root of the plant that is worked in water to extract the active ingredients. The active ingredients have been identified to be a group of compounds known as kavapyrones.

Known as awa in the Hawaiian language kava has experienced a renewed interest as the residents of the Hawaiian Islands experience a continued resurgence of Hawaiian culture. kava has been cultivated since ancient times and it seems likely that the people who developed kava were much more aware of kava’s properties than we are today. When the actions of kava are considered against it’s lack of unwanted side effects is seems likely that the ancient Polynesians purposely developed the properties of kava to eliminate the undesirable properties of kava while accentuating kava’s positive properties. It is likely we have yet to discover all of the ways kava was used by the ancient Polynesians.

The commonly accepted actions of kava that are referenced in the literature are as an anti-anxiety agent3, antidepressant4, euphoriant5, muscle relaxant6, analgesic7, anticonvulsant8, and a treatment for hair loss.9 Kava consumption has been shown to have an inverse correlation to cancer incidence rates.10

Kava has become popular in the west as an anti-anxiety agent. No side effects have been identified when used on a daily basis in moderate amounts.11 Long-term heavy use has been found to cause a dermatological scaling that is reversed when the drug is discontinued.12 No irreversible side effects have been noted. Under normal usage mental and motor skills are not affected. When a moderate amount of kava and alcohol are consumed there are no synergistic effects. Kava is commonly consumed to achieve a relaxed state with a positive mood and a mild euphoria. kava is nonaddicting and does not cause craving or tolerance/dependence consequently intoxication is rare.13

It is proposed that the anti-craving effects of kava are mediated through the dopaminergic neurons of the nucleus accumbens in the mesocorticolimbic dopamine reward system. Kava’s primary binding sites have been reported to be the hippocampus, amygdala and medulla oblongata.15 When kava is administered in vivo by microdialysis into the nucleus accumbens, increasing doses of kava produces increased levels of dopamine.5 The kavapyrone desmethoxyyangonin produces an increase in dopamine while the kavapyrone yangonin decreases dopamine to undetectable levels.5

ava is known to influence the function of GABAA receptors.15 It is through the influence on the GABAA receptor that kava likely produces anxiolytic effects similar to alcohol, benzodiazepines and barbiturates.14 However, alcohol, benzodiazepines and barbiturates are known antagonists of NMDA while kava is not.16 This finding supports the fact that kava produces either a mildly stimulating or a mildly sedating effect depending on the preparation and dose. It is also this difference that explains why kava produces little effects on mental and motor function.

Antidepressants affect the synaptic levels of norepinephrine and/or serotonin. Likewise kava has been shown to increase levels of norepinepherine, which may explain the antidepressant properties of kava.6 There are conflicting reports on kava's effect on serotonin.

The analgesia produced by kava appears to work via non-opiate pathways. A dose of 120 mg/kg of either dihydromethysticin or dihydrokavain was equivalent to 2.5mg/kg morphine.17

In a number of studies kava extracts have compared favorably to prescription medications such as the benzodiazepines and tricyclic antidepressants and without the side effects commonly seen with these drugs.3,18 Not only does kava appear to not impair reaction time, it appears to improve concentration. In two separate studies, oxazepam was found to slow reaction time, while kava enhanced performance.19,20

STUDY 1: PRELIMINARY CRAVING SURVEY

PARTICIPANTS

In an effort to determine if kava warranted investigation as an anticraving agent a survey was undertaken with the patrons of the local homeless shelter. kava was given to volunteer addicts and their response was noted. After dinner the clinic director asked for volunteers to help test a drink. Only subjects who were currently sober and desiring their drug were accepted into the test group.

METHODS

The kava was prepared as a tea. One cup of ground kava was added to one gallon of boiling water and allowed to cool for 1 hour. The tea was then filtered producing a clear brown beverage. The kava tea was served chilled. If the subject was sober and craving their drug they were allowed to drink as much kava as desired.

Approximately one hour after consumption the subjects were asked to give their opinion regarding how they felt about their desire for their substance of abuse.

Each subject was asked the following questions:

What is your first name and age?

What drugs do you take and how long have you taken these drugs on a daily basis?

When was the last time you have taken these drugs?

How much of the drink did you have tonight?

Did the drink have any effect on you and if so how would you describe what you feel?

Has there been a change in your desire for the drugs you take?

No placebo was used. No objective measures of craving was utilized. The determination of craving/no craving was subjective and based on the participant’s opinion. The subject’s names were changed. However names were chosen to reflect the subject’s ethnicity.

RESULTS

Table 1 kava consumption and its effect on craving

 
Name Age Sex Amount kava
consumed
Perception of effects Alcohol Tobacco Cocaine Heroin
Jose 52 M 24 oz relaxed X X X  
Gordon 57 M 24 oz no stress X X    
John 28 M 32oz NA X X X  
Lance 33 M 24 oz relaxed X X    
Mark 44 M 36oz relaxed O X    
Martin 28 M 24 oz peaceful X X    
Steve 31 M 38oz calm X X X  
Fred 49 M 38oz relaxed X X X  
Koa 37 M 48oz happy X X X  
Francis 42 M 48oz relaxed O X X  
 
X relieved craving, O no effect on craving

The results of this survey supported the hypothesis that kava has anticraving properties. It was decided to subject kava to a more formal test to determine if it has the potential to curb an addict’s craving sufficiently to attain abstinence.
 
STUDY 2: PILOT STUDY ON CRAVING AND ABSTINENCE

PARTICIPANTS

The subjects were homeless addicts who used the services of the local homeless mission. Signs were posted announcing the study at the mission and all patrons who felt they had a problem with drug addiction were invited to participate. The subjects were informed that there were two different formulas. If they felt that the medication was not effective they could switch to the other formula. They were not told what they were taking but were told that it was a plant extract and proven safe. The subjects were informed that if they joined the study they could quit at any time.

METHODS

The experimental agent was a standardized kava extract with each capsule containing 30 mg kavapyrones. The placebo was a similar looking vitamin capsule. A research assistant packaged 60 capsules of the standardized kava and 60 capsules of the placebo into randomly numbered identical closed containers. Each subject was identified by first name. The medication was distributed by another research assistance that was unaware of which packages contained the experimental medication or the placebo. A basic information sheet was keep for each participant that described the participant by first name and age. The patents drug history was taken and any relevant medical conditions were noted. When the medications were distributed a package was randomly selected and distributed to the subject and the code on the package was noted on the subjects information sheet. These information sheets were given to the first research assistant who read the code and prepared additional medication for the subject when needed.

The subjects were instructed to take one or two capsules every 3 to 4 hours as needed to control their cravings. One third of the test subjects received a placebo. The subjects were required to take the medication for one week to be included in the study. The data was collected weekly. The amount of substance abuse was based solely on the patient’s reports and the clinical appearance of the subject. There was no objective measure of craving. The study was designed to evaluate the subject’s ability to reach abstinence. The assumption was made that if abstinence is achieved in a long-term addict that the carving or desire for the substance of abuse is reduced.

The majority of test subjects entered the data pool in the first two weeks. At five weeks the trends were obvious and the study was concluded. Each subject was then identified as in the placebo or test group. At five weeks anyone who was not abstinent was recorded a failure irrespective of their level of drug use.

RESULTS

Alcohol

Four of the five individuals in the experimental group reached a minimum of two weeks of abstinence. None of the three subjects in the control group reached sobriety. The Pearson chi-square (1) = 3.7, p = .05.

Cocaine -all forms

Four cocaine subjects participated in the study. Two subjects began the study with the placebo but switched in the first week. Two of the subjects achieved abstinence. All subjects reported the medication was effective in reducing their cravings. The results were not statistically significant.

Heroin

The six heroin addicts who began the study were all dropped for non- compliance. None appeared to take the medication for more than a few days.

Tobacco

All individuals in the tobacco study group were also addicted to alcohol, cocaine or heroin. Data was collected on these individuals for their level of intake of their primary addiction and also the amount of tobacco consumed.

Most of the subjects entered the study to stop using cocaine, alcohol or heroin. Very few of the subjects were compelled to quit smoking as they recognized the insignificance of their smoking habit as it relates to their other more serious addiction. Most of the subjects experienced a gradual reduction in smoking as the study progressed.

Of the 10 subjects in the tobacco group three were given a placebo and all switched to kava. Three of the 10 reached two weeks of abstinence during the study. The results were not significant. In the future, in order to draw any valid conclusions, the test group for tobacco will be comprised of individuals only addicted to tobacco and interested in quitting.

The participants of the placebo study groups quickly recognized that they were receiving no benefit from their medication and universally requested to switch to the experimental group. No subjects requested to be switched from the experimental group to the placebo group. At the conclusion of the test all subjects were taking kava.

DISCUSSION

The two studies listed in this article are not intended to be scientifically valid. The purpose of the two investigations was to determine if further study is warranted. In spite of the very small sample size the results for the alcohol group was the most promising and produced a P=.05. The cocaine patients gave positive reports of the effectiveness of kava to reduce their carving however due to the sample size no conclusions can be drawn.

The amount of kava supplied in the second study would be considered a subclinical dose. It is likely the participants did feel a mild relaxation from 60 mg of kavapyrones as it was prescribed. However, this feeling would be nearly imperceptible when compared to one bowl of kava prepared in a traditional manner, which contains approximately 400 mg of kavapyrones. In spite of the low dose all participants recognized that they were getting some benefit from the experimental medication and all patients on the placebo soon requested to switch to kava. No participants requested to be switched form kava to the placebo.

Addiction is a significant health risk for the Hawaiian people and most other Pacific cultures. The population utilized for the preliminary studies were subjects who have repeatedly failed to recover from their addiction in spite of numerous attempts at rehabilitation. The subjects were comprised of the complete spectrum of ethnic and economic backgrounds. The only seemingly common trait amongst the subjects was that they all have lost everything as a result of their addiction.

Many ancient cultures developed addictive substances. These substances ranged from seemingly innocuous substances such as caffeine to devastating substances such as heroin. However, the ancient cultures of Hawaii and the Pacific Islands appear to have avoided addictive substances until they were introduced from the outside. The ancient Polynesians traveled extensively and it is likely they came into contact with substances such as betel nut and other addictive substances. There can be many reasons for this lack of addictive substances in many of the ancient Pacific cultures. One possible explanation would be that no addictive substances were available in the environment or that the Polynesians were never exposed to addictive substances from nearby cultures. Another possible explanation is that the Polynesians had developed a successful antidote for addiction in kava.

The presentation of this preliminary information will hopefully encourage further research into the use of kava for the treatment of addictions. The studies presented in this report have limited scientific value and do not allow for any meaningful conclusions in regard to kava’s usefulness in the treatment of addictions.

REFERENCES

1. Gossop M, Powell J, Grey S, Hajek P. What do opiate addicts and cigarette smokers mean by "craving"? A pilot study. Drug and Alcohol Dependence, 1990; 26(1): 85-7.

2. Uebelhack R, Franke L, Schewe HJ. Inhibition of platelet MAO-B by kava pyrone-enriched extract from Piper methysticum Forster (kava-kava). Pharmacopsychiatry, 1998; 31(5): 187-92.

3. Volz HP, Kieser M. Kava-kava extract WS 1490 versus placebo in anxiety disorders in a randomized placebo-controlled 25-week outpatient trial. Pharmacopsychiatry, 1997; 30: 1-5.

4.  Warnecke G. Psychosomatic dysfunctions in the female climacteric. Clinical effectiveness and tolerance of Kava Extract WS 1490. Fortschritte Der Medizin, 1991; 109(4): 119-122.

5. Baum SS, Hill R, Rommelspacher. Effect of kava extract and individual kavapyrones on neurotransmitter levels in the nucleus accumbens of rats. Progress in Neuropsychopharmacology and Biological Psychiatry, 1998; 22(7): 1105-1120.

6. Seitz U, Schule A, Gleitz J. [3H]-monoamine uptake inhibition properties of kava pyrones. Planta Medica, 1997; 63: 548-549.

7. Jamieson DD, Duffield PH. The antinociceptive actions of kava components in mice. Clinical and Experimental Pharmacology and Physiology, 1990; 17(7): 495-507.

8. Kretzschmar R, Meyer HJ. Comparative studies on the anticonvulsant activity of the pyrone compounds of Piper methysticum Forst. Archives of International Pharmacodynamics, 1969; 177: 261-267.

9. United States Patent #5585386. Rosedbaum,G. Alpha-pyrone compositions for inducing/stimulating hair growth and/or retarding hair loss. Paris, France.1996

10. Steiner GG. The correlation between cancer incidence and kava consumption. Hawaii Medical Journal, 2000; 59(11): 420-422.

11. Mark Blumenthal, Senior Editor. The complete German Commission E monographs, Therapeutic guide to herbal medicines. American Botanical Council, Boston, Mass.; 1998.

12. Norton SA, Ruze P. Kava dermopathy. Journal of the American Academy of Dermatology, 1994; 31(1): 89-97.

13. Lebot V, Merlin M, Linstrom L. Kava the Pacific Drug. Yale University Press ,New Haven, Connecticut; 1992: 10.

14. Jussofie A, Schmiz A, Hiemke C. Kavapyrone enriched extract from Piper methysticum as modulator of the GABA binding site in different regions of rat brain. Psychopharmacology, 1994; 116(4): 469-474.

15. Boonen G, Haberlein H. Influence of genuine kavapyrone enantiomers on the GABA-A binding site. Planta Medica, 1998; 64(6): 504-506.

16. Walden J, von Wegerer J, Winter U, et al. Effects of kawain and dihydromethysticin on field potential changes in the hippocampus. Progress in Neuro-psychopharmacology and Biological Psychiatry, 1997; 21(4): 697-706.

17. Bruggemann F, Meyer HJ. Die analgetische wirkung der kawa-inhaltsstoffe dihydrokawain und dihydromethistizin. Arzneimittelforschung, 1963; 13: 407-409.

18. Woelk H et al., 1993, Volz HP et al., 1997. Woelk H, Kapoula S, Lehrl S, et al. Treatment of patients suffering from anxiety in a double-blind study: Kava special extract versus benzodiazepines. Ztschr Allegemeinmed, 1993; 69: 271-277.

19. Heinze HJ, Munthe TF, Steitz J, et al. Pharmacopsychological effects of oxazepam and kava-extract in a visual search paradigm assessed with event-related potentials. Pharmacopsychiatry, 1994; 27: 224-230.

20. Munte TF, Heinze HJ, Matzke M, et al. Effects of oxazepam and an extract of kava roots (Piper methysticum) on event-related potentials in a word recognition task. Neuropsychobiology, 1993; 27: 46-53.

 
     
 
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