Ironjustic
Thu, Mar-13-08, 17:16
"six months life expectancy"
"just three months 24 to 50 percent increase in their hearts'
ability to pump blood"
Clinical Trial Shows Ubiquinol Has Significant Effect On
Patients With Congestive Heart Failure Main Category:
Cardiovascular / Cardiology Also Included In: Clinical Trials
/ Drug Trials Article Date: 13 Mar 2008 - 2:00 PDT
Patients suffering from advanced congestive heart failure
exhibited significantly improved heart function after
supplementing with ubiquinol, according to a recent clinical
trial. Ubiquinol, only available in supplement form since late
2006, is the active antioxidant form of Coenzyme Q10 (CoQ10).
CoQ10, a vitamin-like substance found in every cell in the
body, plays a vital role in cellular energy production and
protects cells from free radical damage.
In the first clinical trial evaluating ubiquinol effects on
late-stage congestive heart failure, cardiologist Peter
Langsjoen found that critically ill patients who supplemented
with ubiquinol for just three months experienced a 24 to 50
percent increase in their hearts' ability to pump blood. In
some cases, patients' plasma levels of CoQ10, which are key to
overall heart health, more than tripled. At the start of the
study, each of the patients evaluated had a life expectancy of
less than six months. However, all demonstrated significantly
improved heart function by the trial's end, and survived past
initial expectations.
"The effects of ubiquinol on late-stage heart failure patients
resulted in striking improvements beyond anything I've seen in
25 years of cardiology practice," said Dr. Langsjoen, who
conducted the research in Tyler, Texas. "It is my strong
feeling that this ubiquinol product is a major breakthrough."
Scientists at Kaneka Corporation, the world's largest
manufacturer of CoQ10, developed the method to produce
ubiquinol, commercially available as KanekaQH(tm), for
supplemental use. Because the reduced ubiquinol reverts back
to CoQ10 when exposed to air and light, the process of
stabilizing the nutrient outside of the body took more than a
decade to test and perfect before it was launched a little
more than a year ago.
"Over the last several years, our team of scientists have
documented that KanekaQH can be several times more absorbable
than CoQ10, but to see that higher bioavailability translate
into such staggering improvements in these patients' lives is
particularly gratifying," said Dr. Robert Barry of Kaneka
Nutrients, L.P., who recently released a book entitled The
Power of KanekaQH(tm) (Ubiquinol): The Key to Energy, Vitality
and a Healthy Heart in which he documents some of the most
intriguing research to date on CoQ10 and ubiquinol in regards
to aging and heart health.
The oxidized form of CoQ10, ubiquinone, was first used as a
dietary supplement for cardiac patients in Japan 40 years ago.
It has since gained popularity worldwide for the many health
and condition-specific benefits identified in the thousands of
studies conducted since its discovery in 1957.
Two forms of CoQ10: Ubiquinone and Ubiquinol
Both ubiquinone and ubiquinol are essential to generating
cellular energy and sustaining life; however, the reduced
form, ubiquinol, is responsible for the powerful antioxidant
benefits associated with CoQ10. More than 90 percent of the
CoQ10 found in a healthy person's plasma is in its reduced
ubiquinol form.
For the past 40 years, only ubiquinone was available as a
supplement. KanekaQH(tm), the world's only supplemental
ubiquinol, has only been available for the past year. The
ingredient, manufactured exclusively by Kaneka, is currently
available in more than 30 consumer supplements and is the
subject of a number of new trials expected to begin in 2008.
"Cardiovascular patients, those fighting age-related diseases
and even healthy people over the age of 40 have a critical
need to optimize plasma CoQ10 levels within their bodies,"
explained Dr. Barry. "Because it's so much better absorbed by
the body, KanekaQH(tm) can raise CoQ10 levels more effectively
and, as we're seeing from Dr. Langsjoen's study, can have
tremendous health impact on those suffering from debilitating
diseases."
An abstract of Dr. Langsjoen's supplemental ubiquinol study is
available at http://www.kanekaqh.com/clinicaltrials. Full
results of the study are expected to be published in a major
scientific journal in 2008.
More information on supplemental ubiquinol is available at
http://www.kaneka= qh.com.
For more information on the numerous clinical research
conducted on CoQ10 over the past 50 years, visit
http://www.kanekaq10.com/clinicaltrials.=
About Kaneka Nutrients
Kaneka Nutrients L.P. is a wholly-owned subsidiary of Kaneka
Corporation (http://www.kaneka.co.jp/kaneka-e/), headquartered
in Japan. The company, based in Pasadena, Texas, manufactures
an array of unique nutritional ingredients for the supplement
and food & beverage industries. Kaneka is the largest
manufacturer of CoQ10 in the world, and the only company that
manufactures CoQ10 in the U.S.
Kaneka Nutrients
----------------------------------
Free Radic Biol Med. 1995 Dec ;19 (6):749-57 8582647 (P,S,E,B)
Endogenous ubiquinol prevents protein modification
accompanying lipid peroxidation in beef heart submitochondrial
particles.
[My paper] P Forsmark-Andr=E9e, G Dallner, L Ernster Division
for Medical Cell Biology, Clinical Research Centre at NOVUM,
Karolinska Institute, Huddinge, Sweden. This article is a
study of the relationship between lipid peroxidation and
protein modification in beef heart submitochondrial particles,
and the protective effect of endogenous ubiquinol (reduced
coenzyme Q) against these effects. ADP-Fe3+ and ascorbate were
used to initiate lipid peroxidation and protein modification,
which were monitored by measuring TBARS and protein
carbonylation, respectively. Endogenous ubiquinone was reduced
by the addition of succinate and antimycin. The parameters
investigated included extraction and reincorporation of
ubiquinone, and comparison of the effect of ubiquinol with
those of various antioxidant compounds and enzymes, as well as
the iron chelator EDTA. Under all conditions employed there
was a close correlation between lipid peroxidation and protein
carbonylation, and the inhibition of these effects by
endogenous ubiquinol. SDS-PAGE analysis revealed a
differential effect on individual protein components and its
prevention by ubiquinol. Conceivable mechanisms behind the
observed oxidative modifications of membrane phospholipids and
proteins and of the role of ubiquinol in preventing these
effects are considered.
---------------------------------------------
--------------------------------------------------------------
---------------=
----
http://atvb.ahajournals.org/cgi/content/full/15/6/740
(Arteriosclerosis, Thrombosis, and Vascular Biology.
1995;15:740-747.)
(c) 1995 American Heart Association, Inc.
Articles
Inhibition of the Oxidative Modification of LDL by Nitecapone
Markku O. Pentik=E4inen; Ken A. Lindstedt; Petri T. Kovanen
=46rom the Wihuri Research Institute, Helsinki, Finland.
Correspondence to Petri T. Kovanen, Wihuri Research Institute,
Kalliolinnantie 4, SF-00140 Helsinki, Finland.
Abstract We studied in vitro the ability of nitecapone,
3-[(3,4-dihydroxy-5- nitrophenyl)methylene]-2,4-pentanedione,
a novel water-soluble compound with antioxidative properties,
to inhibit the LDL oxidation promoted by copper ions, the
aqueous free radical generator 2,2'- azobis(2-amidinopropane)
hydrochloride (AAPH), and mouse peritoneal macrophages. In
these three oxidation systems, the extent of LDL oxidation was
determined by measuring the formation of conjugated dienes,
the formation of thiobarbituric acid-reactive substances, the
change in the electrophoretic mobility of LDL, and the uptake
of LDL by macrophages. When LDL oxidation was promoted by
copper ions, the reaction was found to be inhibited by
nitecapone added in a three- to five-molar excess of the
concentration of copper ions. The mechanism by which
nitecapone exerted its antioxidative effect in copper-mediated
LDL oxidation depended on binding and redox inactivation of
the copper ions. Moreover, nitecapone released LDL-bound
copper ions and so rendered the LDL particles more resistant
to oxidation. In contrast to a water-soluble -tocopherol
analogue that was rapidly consumed during the oxidative
process, nitecapone retained its inhibitory effect for at
least 2 days. Using immobilized metal ion affinity
chromatography, we showed that nitecapone binds both copper
and iron ions, whereas its affinity for zinc ions is low.
Nitecapone also inhibited LDL oxidation in the free
radical-mediated oxidation system (AAPH). In this system,
nitecapone showed synergistic antioxidative action with
ascorbic acid. Finally, nitecapone inhibited
macrophage-mediated LDL oxidation. Accordingly, nitecapone
appears to have a unique antioxidative profile in that it both
selectively chelates pro-oxidative transition metals and
scavenges free radicals. Moreover, nitecapone has the
potential of protecting LDL from oxidation in more complex
biological in vitro systems in which multiple modes of
oxidative stress act simultaneously, suggesting that this new
compound, already tested in humans for its ability to inhibit
catechol-O-methyltransferase activity, could potentially be
used as an antioxidant drug.
Key Words: nitecapone * LDL * lipid peroxidation *
atherosclerosis * macrophages --------------------------------
---------------------------------------------=
----
http://tinyurl.com/3yklcu
METHODS FOR IN VIVO REDUCTION OF IRON LEVELS AND COMPOSITIONS
USEFUL THEREFOR ----------------------------------------------
-------------------------------=
----
http://www.bentham.org/cmciema/sample/cmciema1-1/vaya/v-
aya-ms.htm
Metal Chelation The ability of antioxidants to chelate
transition metal ions can be followed spectroscopically High
molecular weight proteins bind directly or indirectly to redox
active metals and thus inhibit the production of
metal-catalyzed free radicals. Some low molecular weight
compounds, such as polyphenols, in addition to their ability
to donate hydrogen atom and thus to act as chain- breaking
antioxidants, can also chelate transition metal ions and hence
inhibit free radical formation.
Who loves ya. Tom
Jesus Was A Vegetarian! http://jesuswasavegetarian.7h.com
Man Is A Herbivore! http://tinyurl.com/a3cc3
DEAD PEOPLE WALKING http://tinyurl.com/zk9fk
"just three months 24 to 50 percent increase in their hearts'
ability to pump blood"
Clinical Trial Shows Ubiquinol Has Significant Effect On
Patients With Congestive Heart Failure Main Category:
Cardiovascular / Cardiology Also Included In: Clinical Trials
/ Drug Trials Article Date: 13 Mar 2008 - 2:00 PDT
Patients suffering from advanced congestive heart failure
exhibited significantly improved heart function after
supplementing with ubiquinol, according to a recent clinical
trial. Ubiquinol, only available in supplement form since late
2006, is the active antioxidant form of Coenzyme Q10 (CoQ10).
CoQ10, a vitamin-like substance found in every cell in the
body, plays a vital role in cellular energy production and
protects cells from free radical damage.
In the first clinical trial evaluating ubiquinol effects on
late-stage congestive heart failure, cardiologist Peter
Langsjoen found that critically ill patients who supplemented
with ubiquinol for just three months experienced a 24 to 50
percent increase in their hearts' ability to pump blood. In
some cases, patients' plasma levels of CoQ10, which are key to
overall heart health, more than tripled. At the start of the
study, each of the patients evaluated had a life expectancy of
less than six months. However, all demonstrated significantly
improved heart function by the trial's end, and survived past
initial expectations.
"The effects of ubiquinol on late-stage heart failure patients
resulted in striking improvements beyond anything I've seen in
25 years of cardiology practice," said Dr. Langsjoen, who
conducted the research in Tyler, Texas. "It is my strong
feeling that this ubiquinol product is a major breakthrough."
Scientists at Kaneka Corporation, the world's largest
manufacturer of CoQ10, developed the method to produce
ubiquinol, commercially available as KanekaQH(tm), for
supplemental use. Because the reduced ubiquinol reverts back
to CoQ10 when exposed to air and light, the process of
stabilizing the nutrient outside of the body took more than a
decade to test and perfect before it was launched a little
more than a year ago.
"Over the last several years, our team of scientists have
documented that KanekaQH can be several times more absorbable
than CoQ10, but to see that higher bioavailability translate
into such staggering improvements in these patients' lives is
particularly gratifying," said Dr. Robert Barry of Kaneka
Nutrients, L.P., who recently released a book entitled The
Power of KanekaQH(tm) (Ubiquinol): The Key to Energy, Vitality
and a Healthy Heart in which he documents some of the most
intriguing research to date on CoQ10 and ubiquinol in regards
to aging and heart health.
The oxidized form of CoQ10, ubiquinone, was first used as a
dietary supplement for cardiac patients in Japan 40 years ago.
It has since gained popularity worldwide for the many health
and condition-specific benefits identified in the thousands of
studies conducted since its discovery in 1957.
Two forms of CoQ10: Ubiquinone and Ubiquinol
Both ubiquinone and ubiquinol are essential to generating
cellular energy and sustaining life; however, the reduced
form, ubiquinol, is responsible for the powerful antioxidant
benefits associated with CoQ10. More than 90 percent of the
CoQ10 found in a healthy person's plasma is in its reduced
ubiquinol form.
For the past 40 years, only ubiquinone was available as a
supplement. KanekaQH(tm), the world's only supplemental
ubiquinol, has only been available for the past year. The
ingredient, manufactured exclusively by Kaneka, is currently
available in more than 30 consumer supplements and is the
subject of a number of new trials expected to begin in 2008.
"Cardiovascular patients, those fighting age-related diseases
and even healthy people over the age of 40 have a critical
need to optimize plasma CoQ10 levels within their bodies,"
explained Dr. Barry. "Because it's so much better absorbed by
the body, KanekaQH(tm) can raise CoQ10 levels more effectively
and, as we're seeing from Dr. Langsjoen's study, can have
tremendous health impact on those suffering from debilitating
diseases."
An abstract of Dr. Langsjoen's supplemental ubiquinol study is
available at http://www.kanekaqh.com/clinicaltrials. Full
results of the study are expected to be published in a major
scientific journal in 2008.
More information on supplemental ubiquinol is available at
http://www.kaneka= qh.com.
For more information on the numerous clinical research
conducted on CoQ10 over the past 50 years, visit
http://www.kanekaq10.com/clinicaltrials.=
About Kaneka Nutrients
Kaneka Nutrients L.P. is a wholly-owned subsidiary of Kaneka
Corporation (http://www.kaneka.co.jp/kaneka-e/), headquartered
in Japan. The company, based in Pasadena, Texas, manufactures
an array of unique nutritional ingredients for the supplement
and food & beverage industries. Kaneka is the largest
manufacturer of CoQ10 in the world, and the only company that
manufactures CoQ10 in the U.S.
Kaneka Nutrients
----------------------------------
Free Radic Biol Med. 1995 Dec ;19 (6):749-57 8582647 (P,S,E,B)
Endogenous ubiquinol prevents protein modification
accompanying lipid peroxidation in beef heart submitochondrial
particles.
[My paper] P Forsmark-Andr=E9e, G Dallner, L Ernster Division
for Medical Cell Biology, Clinical Research Centre at NOVUM,
Karolinska Institute, Huddinge, Sweden. This article is a
study of the relationship between lipid peroxidation and
protein modification in beef heart submitochondrial particles,
and the protective effect of endogenous ubiquinol (reduced
coenzyme Q) against these effects. ADP-Fe3+ and ascorbate were
used to initiate lipid peroxidation and protein modification,
which were monitored by measuring TBARS and protein
carbonylation, respectively. Endogenous ubiquinone was reduced
by the addition of succinate and antimycin. The parameters
investigated included extraction and reincorporation of
ubiquinone, and comparison of the effect of ubiquinol with
those of various antioxidant compounds and enzymes, as well as
the iron chelator EDTA. Under all conditions employed there
was a close correlation between lipid peroxidation and protein
carbonylation, and the inhibition of these effects by
endogenous ubiquinol. SDS-PAGE analysis revealed a
differential effect on individual protein components and its
prevention by ubiquinol. Conceivable mechanisms behind the
observed oxidative modifications of membrane phospholipids and
proteins and of the role of ubiquinol in preventing these
effects are considered.
---------------------------------------------
--------------------------------------------------------------
---------------=
----
http://atvb.ahajournals.org/cgi/content/full/15/6/740
(Arteriosclerosis, Thrombosis, and Vascular Biology.
1995;15:740-747.)
(c) 1995 American Heart Association, Inc.
Articles
Inhibition of the Oxidative Modification of LDL by Nitecapone
Markku O. Pentik=E4inen; Ken A. Lindstedt; Petri T. Kovanen
=46rom the Wihuri Research Institute, Helsinki, Finland.
Correspondence to Petri T. Kovanen, Wihuri Research Institute,
Kalliolinnantie 4, SF-00140 Helsinki, Finland.
Abstract We studied in vitro the ability of nitecapone,
3-[(3,4-dihydroxy-5- nitrophenyl)methylene]-2,4-pentanedione,
a novel water-soluble compound with antioxidative properties,
to inhibit the LDL oxidation promoted by copper ions, the
aqueous free radical generator 2,2'- azobis(2-amidinopropane)
hydrochloride (AAPH), and mouse peritoneal macrophages. In
these three oxidation systems, the extent of LDL oxidation was
determined by measuring the formation of conjugated dienes,
the formation of thiobarbituric acid-reactive substances, the
change in the electrophoretic mobility of LDL, and the uptake
of LDL by macrophages. When LDL oxidation was promoted by
copper ions, the reaction was found to be inhibited by
nitecapone added in a three- to five-molar excess of the
concentration of copper ions. The mechanism by which
nitecapone exerted its antioxidative effect in copper-mediated
LDL oxidation depended on binding and redox inactivation of
the copper ions. Moreover, nitecapone released LDL-bound
copper ions and so rendered the LDL particles more resistant
to oxidation. In contrast to a water-soluble -tocopherol
analogue that was rapidly consumed during the oxidative
process, nitecapone retained its inhibitory effect for at
least 2 days. Using immobilized metal ion affinity
chromatography, we showed that nitecapone binds both copper
and iron ions, whereas its affinity for zinc ions is low.
Nitecapone also inhibited LDL oxidation in the free
radical-mediated oxidation system (AAPH). In this system,
nitecapone showed synergistic antioxidative action with
ascorbic acid. Finally, nitecapone inhibited
macrophage-mediated LDL oxidation. Accordingly, nitecapone
appears to have a unique antioxidative profile in that it both
selectively chelates pro-oxidative transition metals and
scavenges free radicals. Moreover, nitecapone has the
potential of protecting LDL from oxidation in more complex
biological in vitro systems in which multiple modes of
oxidative stress act simultaneously, suggesting that this new
compound, already tested in humans for its ability to inhibit
catechol-O-methyltransferase activity, could potentially be
used as an antioxidant drug.
Key Words: nitecapone * LDL * lipid peroxidation *
atherosclerosis * macrophages --------------------------------
---------------------------------------------=
----
http://tinyurl.com/3yklcu
METHODS FOR IN VIVO REDUCTION OF IRON LEVELS AND COMPOSITIONS
USEFUL THEREFOR ----------------------------------------------
-------------------------------=
----
http://www.bentham.org/cmciema/sample/cmciema1-1/vaya/v-
aya-ms.htm
Metal Chelation The ability of antioxidants to chelate
transition metal ions can be followed spectroscopically High
molecular weight proteins bind directly or indirectly to redox
active metals and thus inhibit the production of
metal-catalyzed free radicals. Some low molecular weight
compounds, such as polyphenols, in addition to their ability
to donate hydrogen atom and thus to act as chain- breaking
antioxidants, can also chelate transition metal ions and hence
inhibit free radical formation.
Who loves ya. Tom
Jesus Was A Vegetarian! http://jesuswasavegetarian.7h.com
Man Is A Herbivore! http://tinyurl.com/a3cc3
DEAD PEOPLE WALKING http://tinyurl.com/zk9fk