Kava-kava Warning


I'm adding this write-up by John Kender, to make sure people do not only hear the good things of kava-kava, but also have some warning.   Please read through it, and make an informed decision.  Thanks - Amanda


I've done a bit of research on kava kava. I found three interesting things
about it, which I report here, even though they leave me feeling troubled.

The first is that some of the active ingredients in the herb are known to be
anti-fungals. The second is that prolonged and heavy use causes a
particular
type of a scaly skin condition called icthyosis (literally, "fish
inflammation"). The third is that one guess as to the cause of the skin
problem is that somehow the active ingredients disturb the cholesterol
content
of the skin.

What troubles me is that all three of these fit the yeast hypothesis. If it
is antifungal, and alters skin sterol content, and eventually affects the
normal environment of the skin, then it may be doing three things that would
attack yeasts along the way. This also fits with anecdotal reports that say
there is a lag of several days to a week for kava to have its full effect on
pulling; this lag means that its effect on pulling is not just due to its
sedative powers. So I am forced to conclude that there not only may be
something to reports of kava working, but also that it may work in ways that
I
ordinarily should like.

Nevertheless, I don't like it at all. Even if kava were a perfect skin
yeast
killer, there would still be no way to separate its skin effects from its
mind
effects. There's still not much known on the herb, but some of this is
worrisome, especially when it comes to its potentially bad interactions with
other chemicals.

I just can't endorse it. I'm even troubled to think that reporting the
potential relationships to skin yeasts above may cause people to do some
rash
things. I trust that anyone thinking of trying the herb will, instead,
check
with their physician first, learn its effects and side effects, and act
responsibly.

Authors
Miller LG.
Title
Herbal medicinals: selected clinical considerations focusing on known or
potential drug-herb interactions. [Review] [171 refs]
Source
Archives of Internal Medicine. 158(20):2200-11, 1998 Nov 9.
Abstract
Herbal medicinals are being used by an increasing number of patients who
typically do not advise their clinicians of concomitant use. Known or
potential drug-herb interactions exist and should be screened for. If used
beyond 8 weeks, Echinacea could cause hepatotoxicity and therefore should
not be used with other known hepatoxic drugs, such as anabolic steroids,
amiodarone, methotrexate, and ketoconazole. However, Echinacea lacks the
1,2 saturated necrine ring associated with hepatoxicity of pyrrolizidine
alkaloids. Nonsteroidal anti-inflammatory drugs may negate the usefulness
of feverfew in the treatment of migraine headaches. Feverfew, garlic,
Ginkgo, ginger, and ginseng may alter bleeding time and should not be used
concomitantly with warfarin sodium. Additionally, ginseng may cause
headache, tremulousness, and manic episodes in patients treated with
phenelzine sulfate. Ginseng should also not be used with estrogens or
corticosteroids because of possible additive effects. Since the mechanism
of action of St John wort is uncertain, concomitant use with monoamine
oxidase inhibitors and selective serotonin reuptake inhibitors is ill
advised. Valerian should not be used concomitantly with barbiturates
because excessive sedation may occur. Kyushin, licorice, plantain, uzara
root, hawthorn, and ginseng may interfere with either digoxin
pharmacodynamically or with digoxin monitoring. Evening primrose oil and
borage should not be used with anticonvulsants because they may lower the
seizure threshold. Shankapulshpi, an Ayurvedic preparation, may decrease
phenytoin levels as well as diminish drug efficacy. Kava when used with
alprazolam has resulted in coma. Immunostimulants (eg, Echinacea and zinc)
should not be given with immunosuppressants (eg, corticosteroids and
cyclosporine). Tannic acids present in some herbs (eg, St John wort and
saw palmetto) may inhibit the absorption of iron. Kelp as a source of
iodine may interfere with thyroid replacement therapies. Licorice can
offset the pharmacological effect of spironolactone. Numerous herbs (eg,
karela and ginseng) may affect blood glucose levels and should not be used
in patients with diabetes mellitus. [References: 171]

Authors
Heiligenstein E. Guenther G.
Title
Over-the-counter psychotropics: a review of melatonin, St John's wort,
valerian, and kava-kava.
Source
Journal of American College Health. 46(6):271-6, 1998 May.
Abstract
Use and availability of alternative healthcare products have revived in
the last few years. The prevalence of supplement use in the United States
is largely unknown but is thought to be widespread. In this article, four
of the common substances used to treat emotional problems are reviewed.
The plant or substance description, clinical indications, evidence of
therapeutic efficacy, mechanisms of therapeutic actions, dosages and
regimens, different commercially available preparations, and adverse
effects and toxicities are described for melatonin, St John's wort,
valerian, and kava-kava. That a product is "natural" does not mean that it
is either safe or effective. Many supplements are potent drugs that lack
sufficient data on safety, dose-response relationships, drug interactions,
and purity.

Authors
Suss R. Lehmann P.
Title
[Hematogenous contact eczema cause by phytogenic drugs exemplified by kava
root extract]. [German]
Source
Hautarzt. 47(6):459-61, 1996 Jun.
Abstract
The increasing promotion of herbal drugs may lead to allergic problems. A
case of systemic contact-type dermatitis after oral administration of kava
extract illustrates this special problem. The kava plant is a member of
the black pepper family; an intoxicant beverage prepared from the roots of
this plant is used ceremonially by many traditional societies of the
Southern Pacific. The beverage induces relaxation, enhances a sense of
sociability and promotes sleep. These effects are utilized in herbal drugs
containing kava, which are sold for insomnia, nervousness and depression.
The ichthyosiform kava dermopathy is a well-known side effect of excessive
use of kava; in this case report we describe an acute allergic side-effect
of kava extract.

Authors
Norton SA. Ruze P.
Title
Kava dermopathy.
Source
Journal of the American Academy of Dermatology. 31(1):89-97, 1994 Jul.
Abstract
Kava is a psychoactive beverage used ceremonially for thousands of years
by Pacific Islanders. Kava is made from the root of the pepper plant,
Piper methysticum, found in Polynesia, Melanesia, and Micronesia. The
beverage is a nonfermented depressant with complex neuropharmacologic
properties that causes a tranquil state of intoxication. Kava also affects
the skin, causing a peculiar scaly eruption. The cutaneous effects were
first reported by members of Captain James Cook's Pacific expeditions, but
they have never been described in dermatologic literature. Heavy kava
drinkers acquire a reversible ichthyosiform eruption, kava dermopathy. The
cause is unknown but may relate to interference with cholesterol
metabolism. Today kava is used across the Pacific in both traditional
ceremonies and informal social events. In Western nations, kava is sold as
a relaxant by health food stores. This article explores the history of
kava dermopathy from Cook's early reports to its presence today.

Authors
Ruze P.
Title
Kava-induced dermopathy: a niacin deficiency?.
Source
Lancet. 335(8703):1442-5, 1990 Jun 16.
Abstract
Heavy chronic consumption of kava (Piper methysticum) is associated with a
pellagroid dermopathy that has been attributed to niacin deficiency. Over
200 male kava drinkers in the Tonga Islands were interviewed and examined
regarding the characteristic skin changes. A scaly rash suggestive of
ichthyosis and eye irritation were present in some heavy kava drinkers. 29
kava drinkers with prominent skin changes were randomised to receive
either 100 mg oral nicotinamide or placebo daily for three weeks. Skin
examinations and photographs showed clinical improvement in 5/15 of the
nicotinamide group and 5/14 of the placebo group. These data, along with
history and physical examination findings, suggest that niacin deficiency
is not responsible for the rash, which is more characteristic of an
acquired ichthyosis.

Authors
Mathews JD. Riley MD. Fejo L. Munoz E. Milns NR. Gardner ID. Powers
JR. Ganygulpa E. Gununuwawuy BJ.
Title
Effects of the heavy usage of kava on physical health: summary of a pilot
survey in an aboriginal community.
Source
Medical Journal of Australia. 148(11):548-55, 1988 Jun 6.
Abstract
Health status was assessed in 39 kava users and 34 non-users in a coastal
Aboriginal community in Arnhem Land. Twenty (27%) respondents were very
heavy (mean consumption, 440 g/week) users of kava; 15 (21%) respondents
were heavy (310 g/week) users of kava and four (5%) respondents were
occasional (100 g/week) users of kava. Kava users were more likely to
complain of poor health and a "puffy" face, and were more likely to have a
typical scaly rash, and slightly-increased patellar reflexes. Very heavy
users of kava were 20% underweight and their levels of gamma-glutamyl
transferase were increased greatly. Albumin, plasma protein, urea and
bilirubin levels were decreased in kava users, and high-density
lipoprotein cholesterol levels were increased. Kava users were more likely
to show haematuria, and to have urine which was poorly acidified and of
low specific gravity. The use of kava was also associated with an
increased red-cell volume, with a decreased platelet volume and with a
decreased lymphocyte count. Shortness of breath in kava users was
associated with tall P waves on a resting electrocardiogram, which
provided suggestive evidence of pulmonary hypertension. In common with
other Aboriginal communities, there was evidence of decreased lung
volumes, a high carriage rate of hepatitis B surface antigen, and of other
morbidity that was unrelated to the use of kava. On the basis of these
findings, there is a strong rationale for urgent social action to improve
health in Aboriginal communities and, in particular, to reduce the
consumption of kava and to improve the nutritional status of kava users.

Authors
Garner LF. Klinger JD.
Title
Some visual effects caused by the beverage kava.
Source
Journal of Ethnopharmacology. 13(3):307-11, 1985 Jul.
Abstract
Kava is a drink produced from the plant Piper methysticum and used as a
social and ceremonial beverage on many South Pacific islands. Visual
functions were measured in one subject following the taking of this drink.
A reduced near point of accommodation and convergence, an increase in
pupil diameter and disturbance to the oculomotor balance were noted. No
changes were recorded in visual or stereoacuity or in ocular refractive
error.

Authors
Singh YN.
Title
Effects of kava on neuromuscular transmission and muscle contractility.
Source
Journal of Ethnopharmacology. 7(3):267-76, 1983 May.
Abstract
The effects of kava, a native drink from Oceania, on neuromuscular
transmission and muscle contractility have been examined in mouse phrenic
nerve-hemidiaphragm and frog sartorius muscle preparations using twitch
tension and intracellular recording techniques. The extent of muscle
paralysis induced by kava was similar in both directly and indirectly
stimulated mouse hemidiaphragms. The neuromuscular blockade produced was
poorly reversed by calcium and by neostigmine. Intracellular recordings
from frog sartorius muscles showed that kava depressed the amplitude of
both miniature end-plate potentials (mepps) and end-plate potentials
(epps) but had no effect on the frequency of mepps. Kava greatly prolonged
the duration of mepps and epps and also slowed and depressed directly
elicited muscle action potentials. It is concluded that kava causes
paralysis by mechanisms similar to local anaesthetics.

Authors
Hansel R. Weiss D. Schmidt B.
Title
[Kawa-lactones: chain length and fungistatic effect. 17. Report on
contents from the Piper species]. [German]
Source
Archiv der Pharmazie und Berichte der Deutschen Pharmazeutischen
Gesellschaft. 301(5):369-73, 1968 May.