There isn’t a proper category for this product, as it’s not a supplement. However, I felt compelled to provide a review of it.
It’s a litlte strange how Listerine Zero got such high reviews and ratings on the Canadian Listerine site (http://www.listerine.ca/products/classic-clean/classic-clean-zero), but not anywhere close on the .com site (https://www.listerine.com/mouthwash/alcohol-free/listerine-zero-mouthwash), where it garnered 1 out of 5 stars for 41 of the 126 reviews. One wonders why…
I started searching the reviews after I had been given a free sample and started using it, and getting some nasty effects that I could liken to another product I had used years earlier. That product was Miracle Mineral Solution (MMS for short), which I reviewed here: http://www.supplementarium.com/supplements/817-miracle-mineral-solution-mms/reviews.
MMS is basically sodium chlorite, an industrial cleaning agent. I found that it caused the tissues in my mouth to slough off, and I could literally feel them coming off on my tongue as I ran my tongue along the sides of my mouth. A similar thing happened with Listerine Zero. If you look at the ingredients, it has sodium lauryl sulfate (SLS) listed as an “inactive ingredient”. Supposedly, the “4 essential signature oils” comprise the active ingredients, and are responsible for keeping one’s breath fresh. I would argue that it’s the sodium lauryl sulfate that is doing most of the work, killing the bacteria - and, unfortunately, destroying other good tissue in the process.
Even the top positive review on Amazon (https://www.amazon.com/product-reviews/B003QH1P6W/ref=cm_cr_arp_d_hist_1?pageNumber=1&filterByStar=one_star) mentions "possible mouth peeling", and there are plenty of negative reviews there that describe the skin peeling effects.
Another reviewer on the Listerine.com site identified SLS as the cause of huge chunks of cheek and gum tissue to be coming off; it was also confirmed by this reviewer’s dentist. SLS is an industrial detergent and known irritant, which you can read more about here: http://slsfree.net (and many other sites, if you search around).
All that Johnson and Johnson, the company behind this product, would respond to these negative reviews was how they want to gather additional information from and speak with the reviewers directly. However, that was over a year ago, and the product is still on our supermarket shelves, being bought and used by the unsuspecting public. I find it utterly disgraceful that such a dangerous product is allowed to be sold.
There isn’t a proper category for this product, as it’s not a supplement. However, I felt compelled to provide a review of it.
It’s a litlte strange how Listerine Zero got such high reviews and ratings on the Canadian Listerine site (http://www.listerine.ca/products/classic-clean/classic-clean-zero), but not anywhere close on the .com site (https://www.listerine.com/mouthwash/alcohol-free/listerine-zero-mouthwash), where it garnered 1 out of 5 stars for 41 of the 126 reviews. One wonders why…
I started searching the reviews after I had been given a free sample and started using it, and getting some nasty effects that I could liken to another product I had used years earlier. That product was Miracle Mineral Solution (MMS for short), which I reviewed here: http://www.supplementarium.com/supplements/817-miracle-mineral-solution-mms/reviews.
MMS is basically sodium chlorite, an industrial cleaning agent. I found that it caused the tissues in my mouth to slough off, and I could literally feel them coming off on my tongue as I ran my tongue along the sides of my mouth. A similar thing happened with Listerine Zero. If you look at the ingredients, it has sodium lauryl sulfate (SLS) listed as an “inactive ingredient”. Supposedly, the “4 essential signature oils” comprise the active ingredients, and are responsible for keeping one’s breath fresh. I would argue that it’s the sodium lauryl sulfate that is doing most of the work, killing the bacteria - and, unfortunately, destroying other good tissue in the process.
Even the top positive review on Amazon (https://www.amazon.com/product-reviews/B003QH1P6W/ref=cm_cr_arp_d_hist_1?pageNumber=1&filterByStar=one_star) mentions "possible mouth peeling", and there are plenty of negative reviews there that describe the skin peeling effects.
Another reviewer on the Listerine.com site identified SLS as the cause of huge chunks of cheek and gum tissue to be coming off; it was also confirmed by this reviewer’s dentist. SLS is an industrial detergent and known irritant, which you can read more about here: http://slsfree.net (and many other sites, if you search around).
All that Johnson and Johnson, the company behind this product, would respond to these negative reviews was how they want to gather additional information from and speak with the reviewers directly. However, that was over a year ago, and the product is still on our supermarket shelves, being bought and used by the unsuspecting public. I find it utterly disgraceful that such a dangerous product is allowed to be sold.
I think that Datbtrue has done enough for plenty of people to merit a bit of trust and good faith. If he says he's closing for serious health problems i think we should believe him.
As for archiving the site, this is being done by his moderators and they intend to get forum members onto another forum.
I have no reason to doubt good faith of Datbtrue.
We don't know yet though, whether admin rights were given to the moderators so that they can retrieve the content. Some people have said that this wasn't done, hence the topic of this thread.
I should have stated more clearly that the topic is more about why the content wasn't allowed to continue, as in, to be moved to another site. We all know that the original site was being shut down.
Unfortunately I don't believe that anybody was able to archive the site. He closed it down yesterday - one day earlier than originally planned - quite possibly to prevent anybody from doing this.
It's sad that such a vast body of knowledge contributed by Dat - as well as many others - could very well be lost.
Losing not only this knowledge, but the person behind it all, is a terrible blow to all of humanity.
Someone posted a good comment there on why he might have shut it down so suddenly. It could be that he didn't have much faith in all the research he had done, his illness still progressed to the point it's at now. Who knows, he may have thought that his use of the IGF-1 LR3 hastened the illness?
So he could have pulled the plug with the notion that other people don't get misinformed on the benefits of IGF-1, etc.
This thread is about the controversy surrounding Datbtrue's site - datbtrue.co.uk - why do you think he didn't give the credentials to a mod or two to either allow it to continue, or to have the content from it archived or passed onto another site?
No doubt some people will say it's because of legal issues. Let's hear your thoughts!
To examine its biological activity in vivo, rMuFGF-18 was injected into normal mice and ectopically overexpressed in transgenic mice by using a liver-specific promoter. Injection of rMuFGF-18 induced proliferation in a wide variety of tissues, including tissues of both epithelial and mesenchymal origin. The two tissues which appeared to be the primary targets of FGF-18 were the liver and small intestine, both of which exhibited histologic evidence of proliferation and showed significant gains in organ weight following 7 (sometimes 3) days of FGF-18 treatment. Transgenic mice that overexpressed FGF-18 in the liver also exhibited an increase in liver weight and hepatocellular proliferation. These results suggest that FGF-18 is a pleiotropic growth factor that stimulates proliferation in a number of tissues, most notably the liver and small intestine.
This had me a little worried until I read the full text:
Treatments consisted of intraperitoneal injections with either 5 mg of rMuFGF-18 or vehicle per kg.
So we're talking about injection into an area that will likely cause a more systemic reaction, and a dose that is orders of magnitude higher than what is used to regenerate cartilage in knees, for instance (where it is injected IA).
The subject invention additionally provides a method of promoting cartilage repair in a patient which comprises administering an oxandrolone to the patient.
EXAMPLE 1: The effect of oxandrolone on inflammation
The rat model of carrageenan-induced paw edema is used to assay the anti-inflammatory activity of oxandrolone. In this model, rats are given a sub-plantar injection of carrageenan into the left hind paw. The paw volume is measured by a Hg-displacement volumeter before and at hourly intervals after paw injection. Rats are divided into three groups. One group receives a subcutaneous injection of oxandrolone long before carrageenan administration. A second group receives a subcutaneous injection of oxandrolone closer to carrageenan administration. The other group does not receive any pretreatment and serves as a control.
The swelling response is reduced indicating efficacy of oxandrolone as an anti-inflammatory agent.
EXAMPLE 2 : The effect of oxandrolone on Synovial Inflammation
As a model for synovial inflammation and the ability of oxandrolone to inhibit such inflammation, the knee-joint (synovial) inflammation model in rats is utilized. (Ginsburg et al . , in "Bayer-Symposium VI: Experimental Models of Chronic Inflammatory Diseases", 256-299, 1977, Springer-Verlag) .
In this model, inflammation is induced by intraarticular injection of bacterial lipopolysaccharide endotoxin (LPS) . The degree of inflammation is reflected by the swelling of the synovial tissue and is measured as the increase in weight postadministration. The LPS toxin and oxandrolone are co-administered.
The LPS-induced synovial inflammation is inhibited which indicates efficacy of oxandrolone as an inhibitor of synovial inflammation.
EXAMPLE 3: The effect of Oxandrolone on Adjuvant-Induced Arthritis
The induction of joint inflammation in rats by administration of Freund's adjuvant is considered to be the model of choice for experimental rheumatoid arthritis (Newbould (1963), Brit. J. Pharmacol. 21: 127). An injection of the adjuvant (Freund's adjuvant with killed Mycobacterium Tuberculosis) into the foot pad results in an initial swelling of the paw, reaching a plateau after 3 days, followed after 14 days by a second increase in,paw and joint swelling, which persists for another 7-10 days. The second phase is regarded as the phase of immunologically- induced chronic arthritis. To examine the efficacy of oxandrolone as an anti-arthritic drug, oxandrolone is given subcutaneously (in doses expressed as mg per kg body weight) to adjuvant-treated rats during 14-21 days after adjuvant administration. Oxandrolone is given daily or on alternating days. As a negative control, saline is given subcutaneously to a second group of adjuvant-treated rats.
Joint inflammation is reduced which indicates efficacy of oxandrolone as an inhibitor of arthritis.
And if we wish to delve into the mechanisms of its action, there is the following:
Androgens have been shown to inhibit IL-6 production by stromal and osteoblastic cells as well as stimulation of osteoclastogenesis by marrow osteoclast precursors [125, 126].
CONCLUSION: This followup study showed that individuals were more likely to be diagnosed as having RKOA if they had a higher BMI and increased circulating levels of IL-6. These results should stimulate more work on IL-6 as a potential therapeutic target.
DISCUSSION
This study demonstrates the increased presence of IL-6 in the synovial fluid of patients with symptomatic cartilage lesions and OA donors when compared to healthy donors. Furthermore, we demonstrated for the first time that chondrocytes produce high concentrations of IL-6 during regeneration, especially osteoarthritic chondrocytes. However, IL-6 does not seem to play a direct role in cartilage matrix turnover. Furthermore, only in OA chondrocytes, IL-6 does seem to play a role in proliferation, although the effect was
different in explants in the presence of synovial fluid compared to 3D differentiation by expanded chondrocytes.
SIGNIFICANCE
Soluble mediators, including IL-6, in the synovial fluid of knees with symptomatic cartilage defects are thought to cause progression to osteoarthritis and also hamper cartilage regeneration after cartilage surgeries such as autologous chondrocyte implantation. Identifying and targeting those soluble mediators will increase the success of cartilage
repair surgery and prevent the progression to early osteoarthritis.
The major action of TD-198946 is distinct from the actions of the above strategies: it strongly induces chondrogenic differentiation of progenitors, as evidenced by a marked increase in the chondrogenic markers type II collagen and aggrecan, and it does this without promoting hypertrophy, which is often and undesirably observed with conventional chondrogenic agents including BMPs,21 TGF-β,13 insulin21 and insulin-like growth factor-1.22
Ember hasn't published anything yet it seems nor mentioned anything about adverse events, so I'm very curious if they came across any of this. Read More...
CONCLUSION: These results demonstrate a significant age-related decline in the chondrocyte response to IGF-1. The finding that increasing OA score was associated with a reduced response to intact IGF-1 but not des(1-3) IGF-1 suggests a role of increased production of inhibitory IGFBP in OA. Since the cells from older animals had a reduced response to both forms of IGF-1, the mechanism of the reduced response with age cannot be attributed to changes in IGFBP. Age-related changes in IGF receptors or, more likely, age-related alterations in intracellular signal transduction may also be involved.
I'm trying to get my head around the meaning of this:
RESULTS: ... There was a significantly reduced response to des(1-3) IGF-1 with increasing age, but no effect of OA score on response to des(1-3) IGF-1.
Fibroblast growth factor-18 (FGF18) has been reported to have significant anabolic effects on cartilage. We therefore examined its effects on repair of cartilage damage in a rat meniscal tear model of OA.
RESULTS: FGF18-induced dose-dependent increases in cartilage thickness of the tibial plateau, due to new cartilage formation at the articular surface and the joint periphery. The generation of new cartilage resulted in significant reductions in cartilage degeneration scores. The highest dose of FGF18 also induced an increase in chondrophyte size and increased remodeling of the subchondral bone.
CONCLUSIONS: The results of this study demonstrate that FGF18 can stimulate repair of damaged cartilage in a setting of rapidly progressive OA in rats.
These quotes are from the full text:
In addition, FGF18 produced dose-dependent increases in medial tibial cartilage thickness, from 243 21 to 319 77 µm (mean SD, p<0.05) in rats treated with vehicle or 5.0 µg of FGF18, respectively. The morphology of the repair tissue ranged from fibrous with proteoglycan deposition to fibrocartilage. Repair tissue appeared to originate from the marginal zone areas and extended across the degraded and sometimes intact surfaces. In nearly all areas, repair tissue appeared to integrate well with the margins of the remaining normal cartilage. Although the morphology of the repair tissue was different from hyaline cartilage, it appeared to effectively fill the defect and there were virtually no degenerative changes. In contrast to the FGF18-treated animals, rats treated with vehicle alone showed no signs of cartilage repair except in rare cases where erosion of the subchondral bone permitted influx of bone marrow stem cells.
One important point (highlighted) was mentioned in the study:
These data demonstrate that local delivery of FGF18 in a hyaluronan carrier can increase cartilage formation and can reduce cartilage degeneration scores in a rat model of osteoarthritis.
From the discussion:
Since osteophyte development appears to be a sequential process39, it is possible that the chondrophytes would undergo endochondral ossification with more time. However, little or no vessel invasion or bone formation was observed within the cartilaginous outgrowths over the time course of the present study. Additional long-term studies will clearly be required to resolve this issue.
CONCLUSION:
Sprifermin not only increases cartilage thickness, but also reduces cartilage loss. Subject-specific, location-independent analysis of both cartilage thinning and thickening represents a sensitive and informative approach for studying the effects of disease-modifying OA drugs.
Intraarticular sprifermin (recombinant human fibroblast growth factor 18) in knee osteoarthritis: a randomized, double-blind, placebo-controlled trial Read More...
Deca, equipoise, anavar, and Primobolan will ALL increase skeletal muscle while at the same time dramatically increase collagen syn and bone mass and density, leaving you with a substantially reduced chance of becoming injured than if you choose to use AAS like sus, cyp, or enth.
While testosterone will increase bone mass and density, even at supra-physiological levels, the result is weaker tendons due to inhibition of collagen syn.
*****
Testosterone thus opposes the benefits of Anavar for collagen synthesis, so I wouldn't use it even at low doses. Read More...
This was an earlier phase 1 study from 2010, which importantly showed that there was no ectopic bone formation using a single 1 mg dosage (the highest dosage group). Read More...