Antioxidant supplements

[info225522]

E-Newcells - provider of the best Antioxidant suuplement in
the world. Exctracted from the Licorice roots, this
antioxidant vitamin with help in high cholesterol prevention
and to prevent heart attacks and heart disease. their website
is: http://www.e-newcells.com

[Mark Thors]

info225522@gmail.com wrote:
>
> E-Newcells - provider of the best Antioxidant suuplement in
> the world. Exctracted from the Licorice roots, this
> antioxidant vitamin with help in high cholesterol prevention
> and to prevent heart attacks and heart disease.

It's not a vitamin. Deficiency of a vitamin causes a
vitamin-deficiency disease like scurvy (lack of vitamin C) or
beri-beri (thiamine deficiency). There is no deficiency
disease associated with lack of any of the claimed components
of this licorice root extract.

Also note that 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.