X-Message-Number: 28019
Date: Fri, 9 Jun 2006 12:18:55 -0700 (PDT)
From: Doug Skrecky <>
Subject: astaxanthin: the carotenoid of choice

[Astaxanthin is a red-orange carotenoid pigment which (unlike
beta-carotene) offers powerful protection against atherosclerosis, and
cancer. It had also been successfully used  to treat male infertility, and
diabetic neuropathy.]

Biol Pharm Bull. 2006 Apr;29(4):684-8.
Antihypertensive potential and mechanism of action of
astaxanthin: III. Antioxidant and histopathological effects in
spontaneously hypertensive rats.
  We investigated the effects of a dietary astaxanthin (ASX-O) on
oxidative parameters in spontaneously hypertensive rats (SHR), by
determination of the level of nitric oxide (NO) end products
nitrite/nitrate (NO2-/NO3-) and lipid peroxidation in ASX-O-treated
SHR. Oral administration of the ASX-O significantly reduced the plasma
level of NO2-/NO3- compared to the control vehicle (p<0.05). The lipid
peroxidation level, however, was reduced in both ASX-O- and olive
oil-treated groups. We also analyzed the post-treatment effects of ASX-O
on the vascular tissues by examining the changes in the aorta and coronary
arteries and arterioles. The dietary ASX-O showed significant reduction
in the elastin bands in the rat aorta (p<0.05). It also significantly
decreased the [wall : lumen] aerial ratio of the coronary arteries. These
results suggest that ASX-O can modulate the oxidative condition
and may improve vascular elastin and arterial wall thickness in
hypertension.

[A mere 16 mg/day boosted pregnancy rates from 10.5% to 54.5%.]

Asian J Androl. 2005 Sep;7(3):257-62.
Combined conventional/antioxidant "Astaxanthin" treatment for male
infertility: a double blind, randomized trial.
  AIM: To evaluate the treatment of male infertility with a strong
natural antioxidant, in addition to conventional treatment. METHODS: Using
a double blind, randomized trial design, 30 men with infertility of > or
=2 months and female partners with no demonstrable cause of infertility
received conventional treatment according to the guidelines of the World
Health Organization (WHO), and either a strong antioxidant Astaxanthin 16
mg/day (AstaCarox, AstaReal AB, Gustavsberg, Sweden) or placebo for 3
months. The effects of treatment on semen parameters, reactive oxygen
species (ROS), zona-free hamster oocyte test, serum hormones including
testosterone, luteinizing hormone (LH), follicle stimulating hormone
(FSH) and Inhibin B, and spontaneous or intrauterine insemination
(IUI)-induced pregnancies were evaluated. RESULTS: ROS and Inhibin B
decreased significantly and sperm linear velocity increased in the
Astaxanthin group (n = 11), but not in the placebo group (n = 19). The
results of the zona-free hamster oocyte test tended to improve in the
Astaxanthin group in contrast with the placebo group, though not reaching
statistical significance. The total and per cycle pregnancy rates among
the placebo cases (10.5 % and 3.6 %) were lower compared with 54.5 % and
23.1 % respectively in the Astaxanthin group (P = 0.028; P =
0.036). CONCLUSION: Although the present study suggests a positive effect
of Astaxanthin on sperm parameters and fertility, the results need to be
confirmed in a larger trial before recommending Astaxanthin for the
complementary treatment of infertile men.

[Here policosanol reduced lipid inflitration of the aorta by a mere 12%,
and red yeast rice extract (lovastatin) by 20%. The combination of
policosanol and red yeast rice extract reduced this by 33%. The addition
just 1.2 mg/kilogram/day of a haematococcus pluvialis algae extract to
this combination dramatically boosted this inhibition to 92%! The
equivalent dosage for a 70 kilogram (154 lb) human would be mere 84 mg of
this extract, which was standardized to 2.5% astaxanthin, or 2 mg
astaxanthin equivalents. So forget policosanol, and forget red yeast rice
(or lovastatin). By comparison, this astaxanthin containing yeast extract
offers a far more powerful inhibition of atherosclerosis. It should be
noted that it does this without lowering either cholesterol or
triglycerides. This all points back to the unfortunate obsession of much
of the medical community with lipids, when the real main driver of
atherosclerosis has been repeatedly been proven to lie elsewhere.]

Arzneimittelforschung. 2005;55(6):312-7.
Antiatherosclerotic efficacy of policosanol, red yeast rice extract and
astaxanthin in the rabbit.
  The effects of policosanol (P), of extract of red yeast rice (rice
fermented with Monascus purpureus) (RYE) and of astaxanthin
(A) (constituents of Armolipid) were investigated in a model of
experimental atherosclerosis provoked in the rabbit by atherogenic
cholesterol-enriched feed (ACEF). P and RYE and their combination were
able to lower the increase of serum total cholesterol and of LDL
cholesterol elicited by 3-month feeding with ACEF. They also were able to
reduce the increase of blood malondialdehyde (MDA), a tracer of lipid
peroxidation by the free radicals released by ACEF. When combined, the
substances developed either additive or potentiated effects, supporting
the rationale of their combination. Remarkable was the protective effect
on lipid infiltration in the aortic wall provoked by ACEF, which was
reduced by P and by RYE and almost completely prevented by the addition
of A to the P-RYE combination. The results support the rationale of a
combination of P, RYE and A as a useful food supplement in hyperlipemic
patients.

Biofactors. 2004;20(1):49-59.
Prevention of diabetic nephropathy by treatment with astaxanthin in
diabetic db/db mice.
  Oxidative stress is implicated as an important mechanism by which
diabetes causes nephropathy. Astaxanthin, which is found as a common
pigment in algae, fish, and birds, is a carotenoid with significant
potential for antioxidative activity. In this study, we examined whether
chronic administration of astaxanthin could prevent the progression of
diabetic nephropathy induced by oxidative stress in mice. We used female
db/db mice, a rodent model of type 2 diabetes, and their non-diabetic
db/m littermates. The mice were divided into three groups as
follows: non-diabetic db/m, diabetic db/db, and diabetic db/db treated
with astaxanthin. Blood glucose level, body weight, urinary albumin, and
urinary 8-hydroxydeoxyguanosine (8-OHdG) were measured during the
experiments. Histological and 8-OHdG immunohistochemical studies were
performed for 12 weeks from the beginning of treatment. After 12
weeks of treatment, the astaxanthin-treated group showed a lower level of
blood glucose compared with the non-treated db/db group; however, both
groups had a significantly high level compared with the db/m mice. The
relative mesangial area calculated by the mesangial area/total glomerular
area ratio was significantly ameliorated in the astaxanthin-treated group
compared with the non-treated db/db group. The increases in urinary
albumin and 8-OHdG at 12 weeks of treatment were significantly inhibited
by chronic treatment with astaxanthin. The 8-OHdG immunoreactive cells in
glomeruli of non-treated db/db mice were more numerous than in the
astaxanthin-treated db/db mice. In this study, treatment with astaxanthin
ameliorated the progression and acceleration of diabetic nephropathy in
the rodent model of type 2 diabetes. The results suggested that the
antioxidative activity of astaxanthin reduced the oxidative stress on the
kidneys and prevented renal cell damage. In conclusion, administration of
astaxanthin might be a novel approach for the prevention of diabetes
nephropathy.

[Astaxanthin is superior to beta-carotene and canthaxanthin in inhibiting
cancer.]

Anticancer Res. 1999 May-Jun;19(3A):1849-53.
A comparison of the anticancer activities of dietary beta-carotene,
canthaxanthin and astaxanthin in mice in vivo.
  The anticancer activities of beta-carotene, astaxanthin and
canthaxanthin against the growth of mammary tumors were studied in female
eight-wk-old BALB/c mice. The mice were fed a synthetic diet containing
0, 0.1 or 0.4% beta-carotene, astaxanthin or canthaxanthin. After 3
weeks, all mice were inoculated with 1 x 10(6) WAZ-2T tumor cells into the
mammary fat pad. All animals were killed on 45 d after inoculation with
the tumor cells. No carotenoids were detectable in the plasma or tumor
tissues of unsupplemented mice. Concentrations of plasma astaxanthin (20
to 28 mumol/L) were greater (P < 0.05) than that of beta-carotene (0.1 to
0.2 mumol/L) and canthaxanthin (3 to 6 mmol/L). However, in tumor
tissues, the concentration of canthaxanthin (4.9 to 6.0 nmol/g) was
higher than that of beta-carotene (0.2 to 0.5 nmol/g) and astaxanthin
(1.2 to 2.7 nmol/g). In general, all three carotenoids decreased mammary
tumor volume. Mammary tumor growth inhibition by astaxanthin was
dose-dependent and was higher than that of canthaxanthin and
beta-carotene. Mice fed 0.4% beta-carotene or canthaxanthin did not show
further increases in tumor growth inhibition compared to those fed 0.1%
of each carotenoid. Lipid peroxidation activity in tumors was lower (P <
0.05) in mice fed 0.4% astaxanthin, but not in those fed beta-carotene
and canthaxanthin. Therefore, beta-carotene, canthaxanthin and especially
astaxanthin inhibit the growth of mammary tumors in mice; their
anti-tumor activity is also influenced by the supplemental dose.

Rate This Message: http://www.cryonet.org/cgi-bin/rate.cgi?msg=28019