Posted by Dr. Bob on November 16, 2003, at 6:17:34
In reply to Re: OPCs/Flavay for manic depression? » taylor18, posted by Larry Hoover on November 11, 2003, at 8:20:28
Re: OPCs/Flavay for manic depression?
Posted by taylor18 on November 11, 2003, at 14:06:51
In reply to Re: OPCs/Flavay for manic depression? » taylor18, posted by Larry Hoover on November 11, 2003, at 8:20:28
Thank you for proving my point and replying to the most irrelevant part of the last post.
And I really don't see what the etymology of critical has to do with how OPCs benefit MD's.
But, anyhow:
critic - 1583, from L. criticus, from Gk. kritikos "able to make judgments," from krinein "to separate, decide." The Eng. word always had overtones of "censurer, faultfinder." Critical in this sense is from 1590; meaning "of the nature of a crisis" is 1649 (see crisis).
Perhaps you thought I might be referring to the English word?
--
Re: OPCs/Flavay for manic depression? » taylor18
Posted by Larry Hoover on November 11, 2003, at 18:11:17
In reply to Re: OPCs/Flavay for manic depression?, posted by taylor18 on November 11, 2003, at 14:06:51
> Thank you for proving my point and replying to the most irrelevant part of the last post.
>
> And I really don't see what the etymology of critical has to do with how OPCs benefit MD's.Because critical thinking is the only way to determine the answer to your question.
> But, anyhow:
>
> critic - 1583, from L. criticus, from Gk. kritikos "able to make judgments," from krinein "to separate, decide." The Eng. word always had overtones of "censurer, faultfinder." Critical in this sense is from 1590; meaning "of the nature of a crisis" is 1649 (see crisis).
>
> Perhaps you thought I might be referring to the English word?Read again what I said. I first used the word in this discourse. I told you what I meant by it. And I told you why I used it. Determining that there are other meanings does little but serve as an argument of distraction, non?
Apply your critical thinking to these, and tell me what you think.
Int J Clin Pharmacol Ther. 2002 Apr;40(4):158-68.
A review of the French maritime pine bark extract (Pycnogenol), a herbal medication with a diverse clinical pharmacology.
Rohdewald P.
Institute Pharmaceutical Chemistry, Westfalische Wilhelms-Universitat Munster, Germany. rohdewa@uni-muenster.de
OBJECTIVES: An increasing body of evidence indicates that Pycnogenol (PYC), a standardized extract of French maritime pine bark, has favorable pharmacological properties. This is a review of studies with both PYC and components of the preparation, that have helped to elucidate target sites and possible mechanisms for activity in men. METHODS: Studies appearing in peer reviewed literature, as well as results presented at international meetings not yet available as published papers, are included in this review. Additional data from published sources in German and French languages that are not widely available are also included. RESULTS: Chemical identification studies showed that PYC is primarily composed of procyanidins and phenolic acids. Procyanidins are biopolymers of catechin and epicatechin subunits which are recognized as important constituents in human nutrition. PYC contains a wide variety of procyanidins that range from the monomeric catechin and taxifolin to oligomers with 7 or more flavonoid subunits. The phenolic acids are derivatives of benzoic and cinnamic acids. The ferulic acid and taxifolin components are rapidly absorbed and excreted as glucuronides or sulphates in men, whereas procyanidins are absorbed slowly and metabolized to valerolactones which are excreted as glucuronides. PYC has low acute and chronic toxicity with mild unwanted effects occurring in a small percentage of patients following oral administration. Clinical studies indicate that PYC is effective in the treatment of chronic venous insufficiency and retinal micro-hemorrhages. PYC protects against oxidative stress in several cell systems by doubling the intracellular synthesis of anti-oxidative enzymes and by acting as a potent scavenger of free radicals. Other anti-oxidant effects involve a role in the regeneration and protection of vitamin C and E. Anti-inflammatory activity has been demonstrated in vitro and in vivo in animals. Protection against UV-radiation-induced erythema was found in a clinical study following oral intake of PYC. In asthma patients symptom scores and circulating leukotrienes are reduced and lung function is improved. Immunomodulation has been observed in both animal models as well as in patients with Lupus erythematosus. PYC antagonizes the vasoconstriction caused by epinephrine and norepinephrine by increasing the activity of endothelial nitric oxide synthase. Dilation of the small blood vessels has been observed in patients with cardiovascular disease, whereas in smokers, PYC prevents smoking-induced platelet aggregation and reduces the concentration of thromboxane. The ability to inhibit angiotensin-converting enzyme is associated with a mild antihypertensive effect. PYC relieves premenstrual symptoms, including abdominal pain and this action may be associated with the spasmolytic action of some phenolic acids. An improvement in cognitive function has been observed in controlled animal experiments and these findings support anecdotal reports of improvement in ADHD patients taking PYC supplements. CONCLUSIONS: There is much evidence showing that PYC has beneficial effects on physiological functions. Results from ongoing clinical research are required to confirm and extend previous observations.
J Atten Disord. 2002 Sep;6(2):49-60.
An experimental comparison of Pycnogenol and methylphenidate in adults with Attention-Deficit/Hyperactivity Disorder (ADHD).
Tenenbaum S, Paull JC, Sparrow EP, Dodd DK, Green L.
The Attention Deficit Center in St. Louis 63141, MO.
Twenty-four adults (24 to 53 years old) with Attention-Deficit/Hyperactivity Disorder (ADHD), Combined Type, were studied in a double-blind, placebo-controlled, crossover study of Pycnogenol and methylphenidate. Pycnogenol is an antioxidant derived from the bark of the French maritime pine tree. Methylphenidate is a standard pharmaceutical intervention for ADHD. Anecdotal reports suggest that Pycnogenol improves concentration in adults with ADHD without adverse side effects. Participants received Pycnogenol, methylphenidate, and placebo, each for three weeks, in a randomized and counterbalanced order. Although ADHD symptoms improved during treatment, neither methylphenidate nor Pycnogenol outperformed the placebo control, as measured by self-report rating scales, rating scales completed by the individual's significant other, and a computerized continuous performance test. The conservative dosage levels and relatively brief length of treatment may have contributed to the absence of significant differences among treatment conditions. Implications for future research are noted.
Ann N Y Acad Sci. 2002 May;957:260-70.
Cellular protection with proanthocyanidins derived from grape seeds.
Bagchi D, Bagchi M, Stohs S, Ray SD, Sen CK, Preuss HG.
Department of Pharmacy Services, Creighton University School of Pharmacy & Allied Health Professions, Omaha, Nebraska 68178, USA. debsis@creighton.edu
Grape seed proanthocyanidins have been reported to possess a broad spectrum of pharmacological and medicinal properties against oxidative stress. We have demonstrated that IH636 proanthocyanidin extract (GSPE) provides excellent protection against free radicals in both in vitro and in vivo models. GSPE had significantly better free radical scavenging ability than vitamins C, E and beta-carotene and demonstrated significant cytotoxicity towards human breast, lung and gastric adenocarcinoma cells, while enhancing the growth and viability of normal cells. GSPE protected against tobacco-induced apoptotic cell death in human oral keratinocytes and provided protection against cancer chemotherapeutic drug-induced cytotoxicity in human liver cells by modulating cell cycle/apoptosis regulatory genes such as bcl2, p53 and c-myc. Recently, the bioavailability and mechanistic pathways of cytoprotection by GSPE were examined on acetaminophen-induced hepatotoxicity and nephrotoxicity, amiodarone-induced pulmonary toxicity, doxorubicin-induced cardiotoxicity, DMN-induced immunotoxicity and MOCAP-induced neurotoxicity in mice. Serum chemistry changes, integrity of genomic DNA and histopathology were assessed. GSPE pre-exposure provided near complete protection in terms of serum chemistry changes and DNA damage, as well as abolished apoptotic and necrotic cell death in all tissues. Histopathological examination reconfirmed these findings. GSPE demonstrated concentration-/dose-dependent inhibitory effects on the drug metabolizing enzyme cytochrome P450 2E1, and this may be a major pathway for the anti-toxic potential exerted by GSPE. Furthermore, GSPE treatment significantly decreased TNFalpha-induced adherence of T-cells to HUVEC by inhibiting VCAM-1 expression. These results demonstrate that GSPE is highly bioavailable and may serve as a potential therapeutic tool in protecting multiple target organs from structurally diverse drug- and chemical-induced toxicity.
Nitric Oxide. 2001 Apr;5(2):137-49.
Protection of primary glial cells by grape seed proanthocyanidin extract against nitrosative/oxidative stress.
Roychowdhury S, Wolf G, Keilhoff G, Bagchi D, Horn T.
Otto-von-Guericke University, Institute for Medical Neurobiology, Leipziger Strasse 44, Magdeburg, D-39120, Germany.
Previous studies showed that proanthocyanidins provide potent protection against oxidative stress. Here we investigate the effects of grape seed proanthocyanidin extract (GSPE) as a novel natural antioxidant on the generation and fate of nitric oxide (NO) in rat primary glial cell cultures. GSPE treatment (50 mg/L) increased NO production (measured by NO(2-) assay) by stimulation of the inducible isoform of NOS. However, GSPE failed to affect the LPS/IFN-gamma-induced NO production or iNOS expression. Similar responses were found in the murine macrophage cell line RAW264.7. GSPE did not show any effect on dihydrodichlorofluorescein fluorescence (ROS marker with high sensitivity toward peroxynitrite) either in control or in LPS/IFN-gamma-induced glial cultures even in the presence of a superoxide generator (PMA). GSPE treatment alone had no effect on the basal glutathione (GSH) status in glial cultures. Whereas the microglial GSH level declined sharply after LPS/IFN-gamma treatment, the endogenous GSH pool was protected when such cultures were treated additionally with GSPE, although NO levels did not change. Glial cultures pretreated with GSPE showed higher tolerance toward application of hydrogen peroxide (H(2)O(2)) and tert-butylhydroperoxide. Furthermore, GSPE-pretreated glial cultures showed improved viability after H(2)O(2)-induced oxidative stress demonstrated by reduction in lactate dehydrogenase release or propidium iodide staining. We showed that, in addition to its antioxidative property, GSPE enhances low-level production of intracellular NO in primary rat astroglial cultures. Furthermore, GSPE pretreatment protects the microglial GSH pool during high output NO production and results in an elevation of the H(2)O(2) tolerance in astroglial cells. Copyright 2001 Academic Press.
poster:Dr. Bob
thread:280213
URL: http://www.dr-bob.org/babble/social/20031113/msgs/280213.html