info225522{at}gmail.com wrote:
> 
> A friend of mine sent me to this website to check out their product.
> Their antioxidant vitamins are produced from licorice root and are
> made to assist in many health problems.

Licorice root is hazardous.
It causes high blood pressure and reduces
potassium below the safe level.  How do we
know whether your licorice root extract
will do the same thing?


Food Chem Toxicol. 1993 Apr;31(4):303-12.
Glycyrrhizic acid in liquorice--evaluation of
health hazard.
St0rmer FC, Reistad R, Alexander J.
National Institute of Public Health, Oslo, Norway.

Literature on case reports, clinical studies and
biochemical mechanisms of the sweet-tasting compound
glycyrrhizic acid in liquorice was critically reviewed
to provide a safety assessment of its presence in
liquorice sweets. A high intake of liquorice can cause
hypermineralocorticoidism with sodium retention and
potassium loss, oedema, increased blood pressure and
depression of the renin-angiotensin-aldosterone system.
As a consequence, a number of other clinical symptoms
have also been observed. Glycyrrhizic acid is
hydrolysed in the intestine to the pharmacologically
active compound glycyrrhetic acid, which inhibits the
enzyme 11 beta-hydroxysteroid dehydrogenase (in the
direction of cortisol to cortisone) as well as some
other enzymes involved in the metabolism of
corticosteroids. Inhibition of 11 beta-hydroxysteroid
dehydrogenase leads to increased cortisol levels in
the kidneys and in other mineralocorticoid-selective
tissues. Since cortisol, which occurs in much larger
amounts than aldosterone, binds with the same affinity
as aldosterone to the mineralocorticoid receptor, the
result is a hypermineralocorticoid effect of cortisol.
The inhibitory effect on 11 beta-hydroxysteroid
dehydrogenase is reversible; however, the compensatory
physiological mechanisms following
hypermineralocorticoidism (e.g. depression of the
renin-angiotensin system) may last several months.
It is not possible, on the basis of existing data,
to determine precisely the minimum level of
glycyrrhizic acid required to produce the described
symptoms. There is apparently a great individual
variation in the susceptibility to glycyrrhizic acid.
In the most sensitive individuals a regular daily
intake of no more than about 100 mg glycyrrhizic acid,
which corresponds to 50 g liquorice sweets (assuming
a content of 0.2% glycyrrhizic acid), seems to be
enough to produce adverse effects. Most individuals
who consume 400 mg glycyrrhizic acid daily experience
adverse effects. Considering that a regular intake of
100 mg glycyrrhizic acid/day is the lowest-observed-
adverse-effect level and using a safety factor of 10,
a daily intake of 10 mg glycyrrhizic acid would
represent a safe dose for most healthy adults. A
daily intake of 1-10 mg glycyrrhizic acid/person has
been estimated for several countries. However, an
uneven consumption pattern suggests that a
considerable number of individuals who consume large
amounts of liquorice sweets are exposed to the risk
of developing adverse effects.


Am J Med Sci. 2003 Mar;325(3):153-6.
An unusual cause of hypokalemic paralysis: chronic
licorice ingestion.
Lin SH, Yang SS, Chau T, Halperin ML.
Division of Nephrology, Department of Medicine,
Tri-Service General Hospital, Nationa Defense
Medical Center, Taipei, Taiwan.

Long-term licorice ingestion is a well-known cause
of secondary hypertension and hypokalemia.
Nevertheless, its initial presentation with a very
severe degree of hypokalemia and paralysis is
exceedingly rare. We report an elderly Asian man
who presented to the emergency department with
marked muscle weakness that progressed to paralysis.
His blood pressure was 160/96 mm Hg. The major
biochemical abnormalities were hypokalemia
(plasma K+ concentration, 1.8 mmol/L) and metabolic
alkalosis (HCO - 3 , 36 mmol/L). His renal
potassium excretion was higher (transtubular
potassium gradient of 9). Plasma renin activity and
aldosterone concentration were suppressed and
cortisol concentration was normal. A detailed
history revealed that he had ingested tea flavored
with 100 g of natural licorice root containing 2.3%
glycyrrhizic acid daily for 3 years. Note that renal
potassium wasting and hypertension persisted for
2 weeks after discontinuing licorice consumption
along with KCl supplement and spironolactone.
Long-term licorice ingestion should be kept in mind
as a cause of paralysis with an extreme degree of
hypokalemia to avoid missing this recognizable and
curable medical disorder.


J Hum Hypertens. 1995 May;9(5):345-8.
Is blood pressure commonly raised by moderate
consumption of liquorice?
Sigurjonsdottir HA, Ragnarsson J, Franzson L,
Sigurdsson G.
Department of Medicine and Chemical Pathology,
Reykjavik City Hospital, University of Iceland.

It is well known that excessive liquorice intake
can induce sodium and fluid retention,
hypokalaemia, hypertension and inhibition of the
renin-angiotensin system. We tested whether
regular moderate liquorice consumption (50 g and
100 g daily) raises blood pressure (BP) in a
normotensive population. Ingestion of 100 g of
liquorice daily (n = 30) caused a significant
rise in systolic blood pressure (SBP) by a mean
of 6.5 mm Hg (P < 0.001) and a fall in plasma
potassium by 0.24 mmol/l (P < 0.001); the highest
rise in SBP observed was 19 mm Hg. In a subgroup
of 13 women the consumption of 50 g of liquorice
daily also caused a significant rise in SBP of
5.6 mm Hg (P < 0.001) and DBP of 3.4 mm Hg
(P = 0.002). A significant change in the
cortisol/cortisone ratio in urine was observed
during 100 g liquorice consumption indicating
inhibition of 11 beta-hydroxysteroid dehydrogenase
in kidneys. The results indicate that
liquorice-induced hypertension might be more
common than has been appreciated and it important
for medical doctors to be on the alert for this
effect in both the prevention and treatment of
hypertension.
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