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Response to HuckleB (Original post)

Sat Dec 17, 2011, 10:51 AM

5. I welcome the new FDA regulations that allow a percentage of rat feces in my peanut butter.

 

On the other hand, I think I'll stick with my protocol, keep my liver and kidneys, take my chances.

http://www.politicolnews.com/fda-needs-major-overhaul/
Safety comes first for any government to protect its citizens from fraudulent claims and known corruption in government. For the last 20 years the FDA has been run by ex -executives of drug companies. This alliance has made the FDA not only corrupt but has cost the government billions of dollars in health care costs. Why? Since the FDA approves drugs that are unsafe and unleashes this poisonous drugs on the American public they become ill from the side effects which are not disclosed. The bill for healthcare for the victims of these drugs are the taxpayer.

Read more: http://www.politicolnews.com/fda-needs-major-overhaul/#ixzz1gnuBmPAI



>>People don’t buy St. John’s wort (SJW) to correct a deficiency of SJW in their diet or in their bloodstream; they don’t buy it to “support” brain function; they buy it to treat depression. People don’t buy glucosamine to “support joint health” but to treat their arthritis pain. People don’t buy saw palmetto to “support prostate health” or correct a saw palmetto deficiency, but to relieve symptoms of benign prostatic hyperplasia or to prevent prostate cancer. The FDA’s “Quack Miranda warnings” are routinely ignored even by those few who actually read the fine print.<<

http://www.ncbi.nlm.nih.gov/pubmed/21914616
Psychiatrike. 2010 Oct-Dec;21(4):332-8.
History and therapeutic properties of Hypericum Perforatum from antiquity until today.
Istikoglou CI, Mavreas V, Geroulanos G.
Source

Department of Psychiatry, "Konstantopouleion" General Hospital, Nea Ionia, Athens.
Abstract

The St. John's wort has been recently one of the most popular therapeutic means that may be easily found in health food stores in various forms, such as capsules, liquid extracts, oils,ointments and others. The St. John's wort is not, however, a new pharmaceutical aid. The herb has a long and particular background as an antidepressant, anti-septic, anti-inflammatory,expectorant and tonic for the immune system, used for its alleviating properties. In fact, some of the previous reports on the herb's use originate from the Greek herbalist of the 1st AD century,Pedanios Dioskourides, as well as from his contemporary physicians, respectively Greek and Roman, Galinos and Plenius. In the treatise, Paracelsus (1493-1541 AD), the famous Swiss alchemist and physician,has been also mentioned to be using the St. John's wort. The historians consider that the name of the St. John's wort was given to it by the first Christians, who noticed that the plant blossomson about the 24th of June, the Saint John's-the Baptist's birthday, who was decapitated.

In our times, and mainly in the USA, the UK and Germany, the St. John's wort has been extensively usedfor the treatment of mild and moderate depression. According to researchers, the St. John's wort has an action equivalent to amitryptilline, fluoxetine and maprotiline, and is clearly more activethan placebo. Experimental protocols have been also in progress on the St. John's wort therapeutic action against diseases of our times, such as cancer, AIDS and hepatitis. According to what iswidely supported, the St. John's wort is considered as bridge between the conventional and the alternative medicine.

The St. John's wort pharmacodynamics as well as pharmacokinetics have beenalso extensively studied. The probable mechanism of the St. John's wort action is the suspension of monoaminoxidase (MAO) and the suspended reuptake of serotonine. Using the St. John's wort weopen the wide sphere of natural therapies. Such an extended approach may lead us to an increasing evaluation of our natural sources. Preserving what we have and renewing what we have destroyedis our only hope for the future of humanity, our planet and all the living organisms.

PMID:
21914616
[PubMed - in process]

http://www.ncbi.nlm.nih.gov/pubmed/21969849
Ther Adv Urol. 2011 Aug;3(4):193-8.
Serenoa repens extract in the treatment of benign prostatic hyperplasia.
Geavlete P, Multescu R, Geavlete B.
Source

Department of Urology, 'Saint John' Emergency Clinical Hospital, Vitan Barzesti 13, 042122 Bucharest, Romania.
Abstract

We are experiencing a revival of interest in phytotherapeutic agents, both in Europe and North America, especially as a consequence of patients' dissatisfaction with the adverse effects of the medical alternatives. One of the most frequently prescribed and studied such agents is Serenoa repens extract, derived from the berry of the dwarf palm tree. We aimed to review the most important published data regarding this type of treatment for benign prostatic hyperplasia. A review of the existing articles regarding the use of Serenoa repens extracts for benign prostatic hyperplasia was performed. The articles were analysed with regard to their relevance, scientific value and the size of the evaluated series.

Multiple mechanisms of action have been attributed to this extract, including antiandrogenic action, an anti-inflammatory/anti-oedematous effect, prolactin signal modulation, and an antiproliferative effect exerted through the inhibition of growth factors. Regarding efficacy, European Association of Urology guidelines state that Serenoa repens extracts significantly reduce nocturia in comparison with placebo. However, the guideline committee is unable to make specific recommendations about phytotherapy of male lower urinary tract symptoms owing to the heterogeneity of the products and the methodological problems associated with meta-analyses.

Most of the published trials regarding Serenoa repens phytotherapy demonstrate a significant improvement of urinary status and a favourable safety profile. Also, some authors have credited it with giving a significant improvement in erectile function and decreasing complications following transurethral resection of the prostate, especially bleeding. The results of phytotherapy with Serenoa repens extracts are very promising. More high-quality, randomized, placebo-controlled studies are required in order to demonstrate without doubt the true therapeutic value of these products. Particular attention must be focused on differentiating between registered preparations, which are regulated as drugs, and those considered to be food supplements.

PMID:
21969849
[PubMed]
PMCID: PMC3175703

Free PMC Article

http://www.ncbi.nlm.nih.gov/pubmed/22089456
J Rheumatol. 2011 Nov 15. [Epub ahead of print]
Glucosamine Sulfate Reduces Prostaglandin E2 Production in Osteoarthritic Chondrocytes Through Inhibition of Microsomal PGE Synthase-1.
Kapoor M, Mineau F, Fahmi H, Pelletier JP, Martel-Pelletier J.
Source

From the Osteoarthritis Research Unit, University of Montreal Hospital Research Centre (CRCHUM), Notre-Dame Hospital, Montreal, Quebec, Canada.
Abstract
OBJECTIVE:

Glucosamine sulfate (GS) has been inferred to have a potential antiinflammatory effect on osteoarthritis (OA). We investigated its effect on prostaglandin E(2) (PGE(2)) in human OA chondrocytes, and the level in the PGE(2) pathway at which its effect takes place.
METHODS:

We investigated the effect of GS treatment (0.05, 0.2, 1.0, and 2.0 mM) in OA chondrocytes in the absence or presence of interleukin 1ß (IL-1ß; 100 pg/ml). We determined the expression levels and protein production/activity of PGE(2), cyclooxygenase-1 (COX-1), COX-2, microsomal PGE synthase-1 (mPGES-1), glutathione, and peroxisome proliferator-activated receptor-&#947; (PPAR&#947, using specific primers, antibodies, and assays.
RESULTS:

GS treatment at 1 and 2 mM significantly inhibited (p &#8804; 0.03) production of endogenous and IL-1ß-induced PGE(2). GS in both the absence and presence of IL-1ß did not significantly modulate COX-1 protein production, but GS at 1 and 2 mM demonstrated a decrease in COX-2 glycosylation in that it reduced the molecular mass of COX-2 synthesis. Under IL-1ß stimulation, GS significantly inhibited mPGES-1 messenger RNA expression and synthesis at 1 and 2 mM (p &#8804; 0.02) as well as the activity of glutathione (p &#8804; 0.05) at 2 mM. Finally, in both the absence and presence of IL-1ß, PPAR&#947; was significantly induced by GS at 1 and 2 mM (p &#8804; 0.03).
CONCLUSION:

Our data document the potential mode of action of GS in reducing the catabolism of OA cartilage. GS inhibits PGE(2) synthesis through reduction in the activity of COX-2 and the production and activity of mPGES-1. These findings may, in part, explain the mechanisms by which this drug exerts its positive effect on OA pathophysiology.

PMID:
22089456
[PubMed - as supplied by publisher]

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HuckleB Dec 2011 OP
laconicsax Dec 2011 #1
BuddhaGirl Dec 2011 #2
HuckleB Dec 2011 #3
laconicsax Dec 2011 #4
HuckleB Dec 2011 #40
LineReply I welcome the new FDA regulations that allow a percentage of rat feces in my peanut butter.
HysteryDiagnosis Dec 2011 #5
HuckleB Dec 2011 #6
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HuckleB Dec 2011 #9
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BuddhaGirl Dec 2011 #7
dixiegrrrrl Dec 2011 #15
HuckleB Dec 2011 #22
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