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"Science" behind copper peptides

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Josee
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Wed Apr 21, 2010 10:19 am      Reply with quote
Kassy_A wrote:

The study found, that after one month, copper-peptides had the most significant effect on collagen production. [b]Significant increases in collagen production were found in 70% of the persons treated with copper-peptide creams, 50% of the persons treated with the vitamin C cream, and 40% of the persons treated with retinoic acid."


And this SB link contains info on "all published studies"; (I knew I remembered reading that "70%" somewhere also.) Anyway, interesting reading for anyone who might have missed it;

http://www.skinbiology.com/copperpeptideregeneration.html#cosmetic


Yes I had read it , it's just that the abstract did not mention that the increase in collagen was significant and whether it was collagen I or collagen III. So that's why I wanted to read the full article.

In the article it does not say that it's significant (and at least the picture does not hint to that) and the increase was only on collagen I which I also wanted to know.

I think we should carry out an RCT study with all the EDS members ... it would surely make for an interesting publication! Smile

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Wed Apr 21, 2010 3:06 pm      Reply with quote
Josee, thanks for finding the complete study. I am curious what your thinking is on the 1st gen CP's now, and will you be trying the gen1 CP's?
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Wed Apr 21, 2010 5:15 pm      Reply with quote
thanks for bringing up this issue, bethany. i've often wondered the same thing.
also, maybe people who have success with cps also have acid-loving skin as well. my skin just hates acids, its the only thing that makes me sensitive and even pre-rosacea. retinoids work well for me, but acids just give me lots of broken capillaries. at any rate, i did not use a lot of acids while using cps, and had bad results.

--avalange

bethany wrote:


So that brings up an interesting question....are the CPs causing the improvement, or the acids? Because there are LOTS of studies showing improvement from acids.

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Wed Apr 21, 2010 6:38 pm      Reply with quote
rileygirl wrote:
Josee, thanks for finding the complete study. I am curious what your thinking is on the 1st gen CP's now, and will you be trying the gen1 CP's?


Mmm... I think that I'm a little more disappointed because I had a little bit of hope that this study showed a significant difference. If they don't say that it was significant, it means it wasn't (if you have a positive result, you don't forget to mention it!).

I think for me the main issue is that there are no studies that show that FGCP does anything for uninjured skin (i.e. improve wrinkles, collagen, etc, etc).

The only in vivo studies are on injured skin which is quite different from regular skin, and even then large FDA human trial failed. There are some things that happen during wound healing that I wouldn't want to happen to my skin in a continuous way.

Even though a cell culture study showed that CPs activate TIMPs, the fact that CPs activate metalloproteinases (MMPs) is quite concerning to me because I would like to stay away from things that have the potential to degrade collagen.

Also, the fact that GHK-Cu is rather unstable is also of concern to me because I don't want free copper running around my skin or my system giving it the opportunity to engage in some free-radical producing reaction.

I am also a special case because I do have a family history of Alzheimer's and so given the potential role of GHK-Cu on Abeta agreggation and free radical generation with the subsequent neuronal death... obviously concerns me.

There are a lot of people who had fantastic results with GHK-Cu which for me would be the best motivator to try them. However, there are people who had horrible effects and have quite dramatically claimed that the treatment ruined their skin and that it took over a year to go back to normal, even though they started with very diluted CPs.

So... given the fact that I'm not 100% sure on the safety or efficacy + people that have had severe adverse reactions... at least personally for me, it's not worth the risk.

If anything, I'd be more willing to try the GHK alone, without the copper, since it has also shown to increase collagen in fibroblast, does not have MMP activity, does not have any link to Alzheimer's, etc.

Again, I do know that some people have had positive life changing results with these CPs; in this case I'm just not willing to take the plunge.

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Wed Apr 21, 2010 7:43 pm      Reply with quote
Thank you, Josee. I agree with you, and I find myself thinking along those same lines at this time.
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Wed Apr 21, 2010 9:24 pm      Reply with quote
Josee wrote:
Even though a cell culture study showed that CPs activate TIMPs, the fact that CPs activate metalloproteinases (MMPs) is quite concerning to me because I would like to stay away from things that have the potential to degrade collagen.


Dr. Yarosh specifically mentioned MMPs in his book as not selective enough at this point, and that products that activate MMPs should be avoided. (however, this was not specifically in reference to CPs)

He also poo poo'd CPs in general due to the lack of science. I'll have to dredge out the book when I get back in town and see what he said.

However, things do work for some and not others, whether there is sufficient science behind them or not. I think people just have to go with what they are comfortable with.

Editing to add:
Josee, based on what you know now, what do you think is the BEST way for people to use CPs if they choose to do so? I saw some improvement on my pigmentation, so I know there can be some benefits, but the question is how to mitigate any risk.

Maybe use them a couple of days a week for limited periods of time?

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Fri Apr 23, 2010 2:02 pm      Reply with quote
bethany wrote:

Editing to add:
Josee, based on what you know now, what do you think is the BEST way for people to use CPs if they choose to do so? I saw some improvement on my pigmentation, so I know there can be some benefits, but the question is how to mitigate any risk.


I think if someone's curious enough, one should maybe try to do a split face trial. So in one half of the face the only difference would be just putting copper peptides (just the copper peptides, not the copper peptide creams that also have retinol, etc.).

Now I'm sure lots of people don't have the patience for that so what I would do is...

a. Use first generation
b. Start slow. Although people who have started slow have had bad reactions as well, the manufacturer recommends starting slow so I would just do it
c. I would use it for as little as possible
d. I would use it separate from any acid. In fact, I would try using a slightly neutral toner (to up the natural acid Ph of the skin) because it's better for absorption of the complex (but I would make sure I don't start getting any bad reactions like pimples from upping the Ph).
e. I would be VERY vigilant on any "uglies" episode. I think people use the "there are uglies which is damage coming up" as a metaphor to help people understand because in reality that does not happen biologically.

Biologically you have the epidermis that renews constantly. So the only thing that can "come out" is just epidermal things basically which are sunspots but that's pretty much it. The "dryness" that people see while using Retin-A for example, is due to the keratolytic activity of the Retin-A. Because of the keratolysis, the stratum corneum starts peeling and thus we see the appearance of the skin as "dry" and... well you know the rest. But then with more use keratinocytes start reproducing faster, we develop tolerance to having a thinner epidermis, etc, etc. and our skin looks better. Also because of the keratolysis is that some people see the "purging".

But that is about it. All the damage of the collage from wrinkles, scars, etc. is on the dermis so it is biologically impossible for that to "come out". If there's any collagen remodeling it occurs within the dermis, it's reabsorbed within the dermis and that's it.

So if I started seeing anything more than some drying, I would stop the use immediately.

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Fri Apr 23, 2010 2:12 pm      Reply with quote
ScienceDaily (Oct. 4, 2005) —

As one of the services for patients with Alzheimer's disease, the Department of Psychiatry at the Saarland University Medical Center offers participation in a clinical phase II trial. This clinical trial aims to elucidate a potential beneficial effect of copper orotate (an organic copper salt), which is given together with a standard cholinesterase inhibitor. A diagnosis of mild to moderate dementia of the Alzheimer type is a prerequisite. Besides clinical investigations, laboratory investigations of blood and cerebrospinal fluid, and magnet resonance imaging of the brain will be carried out. The study is being conducted by Professor Dr. Thomas Bayer, the Head of the Division of Neurobiology, and Dr. Frank Pajonk, a Psychiatrist, at the Department of Psychiatry, Saarland University Medical Center.

Treatment starts after all prerequisites to participate have been met. Half of the patients receive 8 mg copper orotate per day, the other half a placebo. Both patients and psychiatrists are blinded. During the 12-month long double-blind phase, there will be extensive laboratory, clinical and neuropsychological tests. After the double-blind phase, we offer an open-label phase for all patients. At present, 15 patients have finished the double-blind phase. The copper medication is well tolerated.

Alzheimer is characterized by the presence of amyloid plaques, which are composed primarily of Aß peptide. Aß is produced within neurons and is liberated from the larger amyloid ß protein precursor (AßPP). Lower levels of copper have been reported in the brain of AßPP transgenic mice and post-mortem in AD patients. This concept has been found to be true also in vitro by Professor Dr. Gerd Multhaup (FU Berlin) in 1999. Two recent papers, which have been published in PNAS in 2003 have proven a beneficial effect of elevated copper in transgenic AßPP mice. In the present study, the teams led by Bayer and Multhaup have found that low copper level in blood correlates with advanced memory deficits, as tested by the well established ADAS-cog neuropsychological test battery. Patients with higher blood copper levels make fewer mistakes in this memory test. This result supports the notion of a mild copper deficiency in AD patients. An increased uptake of dietary copper may therefore be therapeutically relevant.

The study has been published in the September 2005 issue of the Journal of Alzheimer's Disease, Volume 8, Issue 1 published by IOS Press: "Cognitive decline correlates with low plasma concentrations of copper in patients with mild to moderate Alzheimer's disease" (JAD, Vol. 8, Issue 1).
...............................

Proc Natl Acad Sci U S A. 2003 Nov 25;100(24):14187-92. Epub 2003 Nov 14.
Dietary Cu stabilizes brain superoxide dismutase 1 activity and reduces amyloid Abeta production in APP23 transgenic mice.

Bayer TA, Schäfer S, Simons A, Kemmling A, Kamer T, Tepest R, Eckert A, Schüssel K, Eikenberg O, Sturchler-Pierrat C, Abramowski D, Staufenbiel M, Multhaup G.

Department of Psychiatry, Division of Neurobiology, University of the Saarland Medical Center, D-66421 Homburg, Germany. thomas.bayer@uniklinik-saarland.de

The Cu-binding beta-amyloid precursor protein (APP), and the amyloid Abeta peptide have been proposed to play a role in physiological metal regulation. There is accumulating evidence of an unbalanced Cu homeostasis with a causative or diagnostic link to Alzheimer's disease. Whereas elevated Cu levels are observed in APP knockout mice, APP overexpression results in reduced Cu in transgenic mouse brain. Moreover, Cu induces a decrease in Abeta levels in APP-transfected cells in vitro. To investigate the influence of bioavailable Cu, transgenic APP23 mice received an oral treatment with Cu-supplemented sucrose-sweetened drinking water (1). Chronic APP overexpression per se reduced superoxide dismutase 1 activity in transgenic mouse brain, which could be restored to normal levels after Cu treatment (2). A significant increase of brain Cu indicated its bioavailability on Cu treatment in APP23 mice, whereas Cu levels remained unaffected in littermate controls (3). Cu treatment lowered endogenous CNS Abeta before a detectable reduction of amyloid plaques. Thus, APP23 mice reveal APP-induced alterations linked to Cu homeostasis, which can be reversed by addition of dietary Cu.

.......................

Proc Natl Acad Sci U S A. 2003 Nov 25;100(24):14193-8. Epub 2003 Nov 14.
In vivo reduction of amyloid-beta by a mutant copper transporter.

Phinney AL, Drisaldi B, Schmidt SD, Lugowski S, Coronado V, Liang Y, Horne P, Yang J, Sekoulidis J, Coomaraswamy J, Chishti MA, Cox DW, Mathews PM, Nixon RA, Carlson GA, St George-Hyslop P, Westaway D.

Center for Research in Neurodegenerative Diseases, University of Toronto, Toronto, ON, Canada M5S 3H2.

Cu ions have been suggested to enhance the assembly and pathogenic potential of the Alzheimer's disease amyloid-beta (Abeta) peptide. To explore this relationship in vivo, toxic-milk (txJ) mice with a mutant ATPase7b transporter favoring elevated Cu levels were analyzed in combination with the transgenic (Tg) CRND8 amyloid precursor protein mice exhibiting robust Abeta deposition. Unexpectedly, TgCRND8 mice homozygous for the recessive txJ mutation examined at 6 months of age exhibited a reduced number of amyloid plaques and diminished plasma Abeta levels. In addition, homozygosity for txJ increased survival of young TgCRND8 mice and lowered endogenous CNS Abeta at times before detectable increases in Cu in the CNS. These data suggest that the beneficial effect of the txJ mutation on CNS Abeta burden may proceed by a previously undescribed mechanism, likely involving increased clearance of peripheral pools of Abeta peptide.



..............................

J Neural Transm. 2008 Aug;115(Cool:1181-7. Epub 2008 Jun 28.
Intake of copper has no effect on cognition in patients with mild Alzheimer's disease: a pilot phase 2 clinical trial.

Kessler H, Bayer TA, Bach D, Schneider-Axmann T, Supprian T, Herrmann W, Haber M, Multhaup G, Falkai P, Pajonk FG.

Department of Psychiatry and Psychotherapy, Saarland University Hospital, Homburg/Saar, Germany.

Disturbed copper (Cu) homeostasis may be associated with the pathological processes in Alzheimer's disease (AD). In the present report, we evaluated the efficacy of oral Cu supplementation in the treatment of AD in a prospective, randomized, double-blind, placebo-controlled phase 2 clinical trial in patients with mild AD for 12 months. Sixty-eight subjects were randomized. The treatment was well-tolerated. There were however no significant differences in primary outcome measures (Alzheimer's Disease Assessment Scale, Cognitive subscale, Mini Mental Status Examination) between the verum [Cu-(II)-orotate-dihydrate; 8 mg Cu daily] and the placebo group. Despite a number of findings supporting the hypothesis of environmental Cu modulating AD, our results demonstrate that oral Cu intake has neither a detrimental nor a promoting effect on the progression of AD.




...............................
J Neural Transm. 2008 Dec;115(12):1651-9. Epub 2008 Oct 30.
Effect of copper intake on CSF parameters in patients with mild Alzheimer's disease: a pilot phase 2 clinical trial.

Kessler H, Pajonk FG, Bach D, Schneider-Axmann T, Falkai P, Herrmann W, Multhaup G, Wiltfang J, Schäfer S, Wirths O, Bayer TA.

Department of Psychiatry and Psychotherapy, Saarland University Hospital, Homburg/Saar, Germany.

A plethora of reports suggest that copper (Cu) homeostasis is disturbed in Alzheimer's disease (AD). In the present report we evaluated the efficacy of oral Cu supplementation on CSF biomarkers for AD. In a prospective, randomized, double-blind, placebo-controlled phase 2 clinical trial (12 months long) patients with mild AD received either Cu-(II)-orotate-dihydrate (verum group; 8 mg Cu daily) or placebo (placebo group). The primary outcome measures in CSF were Abeta42, Tau and Phospho-Tau. The clinical trial demonstrates that long-term oral intake of 8 mg Cu can be excluded as a risk factor for AD based on CSF biomarker analysis. Cu intake had no effect on the progression of Tau and Phospho-Tau levels in CSF. While Abeta42 levels declined by 30% in the placebo group (P = 0.001), they decreased only by 10% (P = 0.04) in the verum group. Since decreased CSF Abeta42 is a diagnostic marker for AD, this observation may indicate that Cu treatment had a positive effect on a relevant AD biomarker. Using mini-mental state examination (MMSE) and Alzheimer disease assessment scale-cognitive subscale (ADAS-cog) we have previously demonstrated that there are no Cu treatment effects on cognitive performance, however. Finally, CSF Abeta42 levels declined significantly in both groups within 12 months supporting the notion that CSF Abeta42 may be valid not only for diagnostic but also for prognostic purposes in AD.

........................

Protective Role For Copper In Alzheimer’s Disease

ScienceDaily (Oct. 13, 2009) — Two articles in a forthcoming issue of the Journal of Alzheimer’s Disease -- by Dr Chris Exley, Reader in Bioinorganic Chemistry in the Research Institute for the Environment, Physical Sciences and Applied Mathematics at Keele University, UK, and Dr Zhao-Feng Jiang, of Beijing Union University, Beijing, China -- have confirmed a potentially protective role for copper in Alzheimer’s disease.

Previous research has shown that copper is one component of the amyloid beta plaques which are found in the brains of people of Alzheimer’s disease.

A central tenet of the Amyloid Cascade Hypothesis of Alzheimer’s disease is the aberrant deposition in the brain of A?42 in ?-sheets in neuritic or senile plaques. The Keele team have shown in previous research in JAD that copper (Cu(II)) prevents the deposition of A?42 in ?-sheets while in the current research they show that Cu(II) abolishes the ?-sheet structure of preformed amyloid fibrils of A?42. A similar finding was made by the group of Jiang for the other form of beta amyloid, A?40, and together these observations strongly suggest that copper prevents both the formation and the accumulation of plaques in the brain.

Coincident with the copper-catalysed dissolution of ?-sheets of A?42, Exley’s group made the first observation of the in vitro formation of spherulites of this peptide. These spherical globules of amyloid have only previously been observed in vitro for the other amyloid-forming proteins insulin and ?-lactoglobulin. Copper appeared to have a role in the formation of spherulites of A?42 and this will be investigated in future research. The role of metals in the formation, deposition and metabolism of A? in Alzheimer’s disease is much debated and these new findings highlight a potential protective role for copper in Alzheimer’s disease.
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Fri Apr 23, 2010 3:01 pm      Reply with quote
Thank you for your contribution Alexes.

The studies you quoted, while useful,are unfortunately not enough to dispell the association between GHK-Cu or free Cu2+ and Alzheimer's

Study 1: does not measure free Cu2+ or GHK-Cu which is what has been possibly linked to Alzheimer's. In fact chelated copper (i.e. copper associated with a compound, has not generally being linked with Alzheimer's, except for a few complexes (GHK-Cu being one))


Study 2: was done in genetically mutated mice that have particular copper transport processes so it really has nothing to do with regular human beings and their copper homeostasis are already at least 5 years old and do not talk about free Cu2+ or GHK-Cu, which are the 2 compounds possibly linked to Alzheimer's.

Study 3: The follow-up was done for only one year and even though the patients were supplemented with copper, they did not have an increase in serum copper concentration

Study 4: Same thing as study 3 (it's the same sample)

Study 5&6: Both are in vitro studies where the authors themselves write that the significance of their results invivo is unknown.

---------------------

There is a wealth of studies linking free Cu2+ with Alzheimer's and there's a wealth of studies exploring copper (and other metal) chelates as a treatment for AD.
The homeostasis of copper in the body is quite complex and I am pretty sure that the issue will not be totally figured out for some years. To complicate things even more, the effect of copper changes depending on what it is complexed with. So sometimes copper can have even antagonistic effects depending on what it is bound to.

However, for me, a person who has a family history of Alzheimer's, given the hundreds of papers who have linked free Cu2+ to Alzheimer's, plus a recent paper that linked specifically GHK-Cu to Alzheimer's, taking some copper compound that generates free Cu2+ upon dissolution is not worth the risk, esp. when there's no good evidence that it actually does anything for uninjured skin.

Other people might take the risk and have great results. I just don't think it's worth it.

BTW I don't do this only with copper. I also stopped using aluminum to cook (I do still use aluminum in my deodorant since absorption is minimal compared to other sources of aluminum).

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Fri Apr 23, 2010 3:57 pm      Reply with quote
Thank you for your contribution Josee.
It was my intention to point out that while you claim there could possibly be a link between GHK and Alzheimer's, other studies are being conducted that prove a link between copper and Alzheimer's that is beneficial.
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Fri Apr 23, 2010 3:59 pm      Reply with quote
Thanks so much Josee and everyone else for their input. I just recently purchased FlexEffect program and copper is mentioned. Reading this post has helped me to make a decision not to go for it since anyway some time ago I had a bit high level of uric acid (nothing serious) and the word "copper" frightens me.
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Fri Apr 23, 2010 5:37 pm      Reply with quote
I’ve been following this discussion with a great deal of interest. I haven’t contributed too much because I have scientific dyslexia. However, I do have a few comments I’d like to make.

With regard to scientific studies on cosmetics: Wouldn’t it be wonderful if there was actual proof that the cosmetic creams that we spend our hard earned money on were actually going to deliver the over-the-top promises they make? Realistically though, cosmetic products are not subject to the rigorous testing and control that pharmaceutical products undergo. Even cosmeceuticals (which are supposed to contain a higher percentage of actives and usually have a doctor’s name attached to them) also fall into the category of “cosmetic”. This means that they don’t actually make any biological changes to the body. If the actives are at a high enough percentage to actually make biological changes, then they would be classified as a pharmaceutical and be subject to medical testing. This is something that cosmetic companies want to avoid as claims like “a visible difference to wrinkles in 30 days” would have to be substantiated.

So I would ask, are there any scientific studies for Valmont and other high-end products? How do they justify charging $600 for a jar of face cream? At least Dr Pickart is prepared to stand behind his research and products and sell them at a reasonable price point. I’m afraid I have a very cynical view of the skin care industry and view most lines as very expensive snake-oil. And what annoys me about scientific studies is that you can find one for whatever stance you wish to take (a bit like quotes out of the Bible!) But I would like to see some anti-aging products controlled in the same manner as pharmaceuticals - then, perhaps, they would be worth the money - instead of just paying for marketing and packaging.

With regard to it being biologically impossible for hidden damage to be brought to the surface of the skin, there are a few members on this thread that are currently trialling The Wonderbar (an incredibly expensive bar of soap that also purports to do this. Users are expected to endure something called “the healing crisis“ before their skin improves). At present, people are experiencing mixed results - and, of course, there are no scientific studies to support the Wonderbar’s claims and no explanation for its exorbitant cost.

On a personal level, I’m also somewhat sceptical of “The Uglies”. I have never had a real problem with CPs but I have stopped and started using them several times because I’ve convinced myself that The Uglies have set in. Realistically however, I appear to get The Uglies at about 3 pm every day (regardless of what product I’m using). I’m of the opinion that we spend way too much time gazing into magnifying mirrors searching for flaws that weren’t there yesterday. I wouldn’t be surprised if most uglies are brought about by doing way too much to our skin and drying it out excessively.

Lastly, I’d like to make a comment on the “mean girls” attitude and Dr Pickart bashing. As I’ve pointed out, I do use CPs, but I have no problem whatsoever with people such as Josee asking perfectly acceptable questions and putting forward her opinions on the subject. I’m always interested to hear anyone else’s viewpoint and she has raised some interesting issues. There has been a trend on the Forum lately to chastise and vilify people for asking questions and drawing attention to what they see as errors or misinformation. Personally, I have no issue with people expressing their opinions as long as they do so in a polite manner - it all makes for interesting discussion.

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Fri Apr 23, 2010 7:39 pm      Reply with quote
Keliu wrote:

With regard to it being biologically impossible for hidden damage to be brought to the surface of the skin, there are a few members on this thread that are currently trialling The Wonderbar (an incredibly expensive bar of soap that also purports to do this. Users are expected to endure something called “the healing crisis“ before their skin improves).


I have to believe that people that are creating these terms do it in a metaphorical way to help others understand.

Biologically, the dermis and the epidermis are separated by a membrane and dermal elements do not go up the epidermis. That is just basic histology and you will not find one single paper, article or book that claims otherwise.

This would be the same as saying... "I'm putting this cream on my face and it's making my face greasy because it brings the subcutaneous fat up" Rolling Eyes That just does not exist.

Melasma, hyperpigmentation, age spots are in the epidermis so sometimes, as the skin renews the layers that have those spot do go up (since that's how the skin naturally renews, the bottom layers divide and push other layers up) and so when those cells dehydrate and die it can make the sun spots a little more pronounced. That is also what happens when, for e.g. you do IPL. IPL targets the cells with melanine, kills them, they get dehydrated and for a little they seem "darker". Also if you have a keratolytic effect, your skin will look drier. But that's about it... not much else is going on in the epidermis. All the rest of the things, the sagging, the collagen, etc... are on the dermis and the dermis CANNOT come out to the epidermis.

Now you got me curious about this "healing crisis" so I asked in the other thread... will see!

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Sat Apr 24, 2010 4:16 am      Reply with quote
Quote:
With regard to it being biologically impossible for hidden damage to be brought to the surface of the skin, there are a few members on this thread that are currently trialling The Wonderbar (an incredibly expensive bar of soap that also purports to do this. Users are expected to endure something called “the healing crisis“ before their skin improves). At present, people are experiencing mixed results - and, of course, there are no scientific studies to support the Wonderbar’s claims and no explanation for its exorbitant cost.


Whether it's a healing crisis or just your skin adjusting to the product, all strong products (retin-a, CPs, Wonderbar, etc.) have that effect on some skin to some degree. I personally am very results-oriented and could care less about the science of the products. But I'm happy for those who want to talk the science to do so. What I don't like is how personal these discussions become over time. There seem to be a number of reasons - people feel insulted if they use and like the products, they feel insulted if someone says something negative to one of their cronies, someone finds an article that contradicts an article someone else finds, someone doesn't accept the advice handed out by someone who thinks they're an authoritative source - and the list goes on.
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Sat Apr 24, 2010 4:17 am      Reply with quote
Josee wrote:

Melasma, hyperpigmentation, age spots are in the epidermis so sometimes, as the skin renews the layers that have those spot do go up (since that's how the skin naturally renews, the bottom layers divide and push other layers up) and so when those cells dehydrate and die it can make the sun spots a little more pronounced. That is also what happens when, for e.g. you do IPL. IPL targets the cells with melanine, kills them, they get dehydrated and for a little they seem "darker". Also if you have a keratolytic effect, your skin will look drier. But that's about it... not much else is going on in the epidermis. All the rest of the things, the sagging, the collagen, etc... are on the dermis and the dermis CANNOT come out to the epidermis.


dear josee,
is this not what dr. pickart is referring to, then, when sb claims that cps bring damage to the surface so it can be eradicated?

or, given the fact that what you state in your post is basic histology, on what basis can dr. p make such a claim?

also, keliu: the reason why i'm concerned about the science behind cps, and i think i speak for an entire community of people, is because cps might or might not be dangerous. this is like the nanoparticle debate in many ways--several consumers are holding out until further information is released about its effectivity and its safeness to use on the skin. when i buy a cream from valmont, the worst that happens if it doesn't work is that i waste $600. when i used cps, i had no idea i might have been causing longterm, irreversible damage to my skin. it wasn't just the "uglies," it was a major, distinctive loss of elasticity and a very noticeable change in texture. i'd honestly rather have made a bad monetary choice than undergo the year-long crisis my skin went through after $50 spent on cps and a few months of usage.

--avalange

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Sat Apr 24, 2010 5:43 am      Reply with quote
I have definitely seen the claims that CPs have damaged some people's skin - along with Retin-A, chemical peels, OCM. But this is the first time I've seen CPs labelled as dangerous.

Is anyone else of this opinion? And if this is the case, why haven't these dangers been discussed more widely? Or have I missed something?

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Sat Apr 24, 2010 8:02 am      Reply with quote
margarett wrote:
Thanks so much Josee and everyone else for their input. I just recently purchased FlexEffect program and copper is mentioned. Reading this post has helped me to make a decision not to go for it since anyway some time ago I had a bit high level of uric acid (nothing serious) and the word "copper" frightens me.


Hi margarett Smile ,

Before being frightened by the word "copper" from what has been posed in this thread, you may want to take a look at the latest scientific research that suggests the exact opposite of what was once thought:

Copper may protect against Alzehiemer's dsease.
Excessive copper has been blamed for many diseases - heart disease, cancer, etc. The problem is that most of this comes from data on blood plasma copper and diseases. But usually, high blood plasma copper is associated with low tissue copper. Most plasma copper - 95% - is in ceruloplasmin - an acute phase reactant that rises with stress and disease. Available copper in the plasma is 5% of the plasma copper and on albumin.

In every case so far, when all the data came in on a disease, it was found that higher tissue copper reduced the disease or condition.

For years, a German physician was preaching that copper caused Alzheimer's. Then a lab said rabbits fed cholesterol and copper developed brain plaques. This led to some very good studies in the best Alzheimer's research labs in Germany, Canada, and the USA and these labs came to the opposite conclusion; that more copper reduced brain plaques.

But the best study was one that gave supplemental copper to Alzheimer's patients. Those given more copper, had less mental decay. 8 mgs of supplemental copper daily is safe in the Alzheimer's patients.

See below.

Newer studies have found that more copper 2+ blocks the formation of plaques. See below.


1. Science News
Protective Role For Copper In Alzheimer’s Disease

ScienceDaily (Oct. 13, 2009) — Two articles in a forthcoming issue of the Journal of Alzheimer’s Disease -- by Dr Chris Exley, Reader in Bioinorganic Chemistry in the Research Institute for the Environment, Physical Sciences and Applied Mathematics at Keele University, UK, and Dr Zhao-Feng Jiang, of Beijing Union University, Beijing, China -- have confirmed a potentially protective role for copper in Alzheimer’s disease.

Previous research has shown that copper is one component of the amyloid beta plaques which are found in the brains of people of Alzheimer’s disease.

A central tenet of the Amyloid Cascade Hypothesis of Alzheimer’s disease is the aberrant deposition in the brain of Aβ42 in β-sheets in neuritic or senile plaques. The Keele team have shown in previous research in JAD that copper (Cu(II)) prevents the deposition of Aβ42 in β-sheets while in the current research they show that Cu(II) abolishes the β-sheet structure of preformed amyloid fibrils of Aβ42. A similar finding was made by the group of Jiang for the other form of beta amyloid, Aβ40, and together these observations strongly suggest that copper prevents both the formation and the accumulation of plaques in the brain.

Coincident with the copper-catalysed dissolution of β-sheets of Aβ42, Exley’s group made the first observation of the in vitro formation of spherulites of this peptide. These spherical globules of amyloid have only previously been observed in vitro for the other amyloid-forming proteins insulin and β-lactoglobulin. Copper appeared to have a role in the formation of spherulites of Aβ42 and this will be investigated in future research. The role of metals in the formation, deposition and metabolism of Aβ in Alzheimer’s disease is much debated and these new findings highlight a potential protective role for copper in Alzheimer’s disease.


2. JOURNAL OF ALZHEIMER'S DISEASE
Volume 18, Number 4, December 2009
Pages 811-817
Emily House, Matthew Mold, Joanna Collingwood, Alex Baldwin, Steven Goodwin, Christopher Exley
Copper Abolishes the β-Sheet Secondary Structure of Preformed Amyloid Fibrils of Amyloid-β42
Abstract: The observation of the co-deposition of metals and amyloid-β42 (Aβ42) in brain tissue in Alzheimer’s disease prompted a myriad of investigations into the role played by metals in the precipitation of this peptide. Copper is bound by monomeric Aβ42 and upon precipitation of the copper-peptide complex thereby prevents Aβ42 from adopting a β-sheet secondary structure. Copper is also bound by β-sheet conformers of Aβ42, and herein we have investigated how this interaction affects the conformation of the precipitated peptide. Copper significantly reduced the thioflavin T fluorescence of aged, fibrillar Aβ42 with, for example, a 20-fold excess of the metal resulting in a ca 90% reduction in thioflavin T fluorescence. Transmission electron microscopy showed that copper significantly reduced the quantities of amyloid fibrils while Congo red staining and polarized light demonstrated a copper-induced abolition of apple-green birefringence. Microscopy under cross-polarized light also revealed the first observation of spherulites of Aβ42. The size and appearance of these amyloid structures were found to be very similar to spherulites identified in Alzheimer’s disease tissue. The combined results of these complementary methods strongly suggested that copper abolished the β-sheet secondary structure of pre-formed, aged amyloid fibrils of Aβ42. Copper may protect against the presence of β-sheets of Aβ42 in vivo, and its binding by fibrillar Aβ42 could have implications for Alzheimer’s disease therapy.


3. Increased dietary copper have a slightly positive effect on Alzheimer's patients

J Neural Transm. 2008 Dec;115(12):1651-9. Epub 2008 Oct 30.
Effect of copper intake on CSF parameters in patients with mild Alzheimer's disease: a pilot phase 2 clinical trial.

Kessler H, Pajonk FG, Bach D, Schneider-Axmann T, Falkai P, Herrmann W, Multhaup G, Wiltfang J, Schäfer S, Wirths O, Bayer TA.

Department of Psychiatry and Psychotherapy, Saarland University Hospital, Homburg/Saar, Germany.

A plethora of reports suggest that copper (Cu) homeostasis is disturbed in Alzheimer's disease (AD). In the present report we evaluated the efficacy of oral Cu supplementation on CSF biomarkers for AD. In a prospective, randomized, double-blind, placebo-controlled phase 2 clinical trial (12 months long) patients with mild AD received either Cu-(II)-orotate-dihydrate (verum group; 8 mg Cu daily) or placebo (placebo group). The primary outcome measures in CSF were Abeta42, Tau and Phospho-Tau. The clinical trial demonstrates that long-term oral intake of 8 mg Cu can be excluded as a risk factor for AD based on CSF biomarker analysis. Cu intake had no effect on the progression of Tau and Phospho-Tau levels in CSF. While Abeta42 levels declined by 30% in the placebo group (P = 0.001), they decreased only by 10% (P = 0.04) in the verum group. Since decreased CSF Abeta42 is a diagnostic marker for AD, this observation may indicate that Cu treatment had a positive effect on a relevant AD biomarker. Using mini-mental state examination (MMSE) and Alzheimer disease assessment scale-cognitive subscale (ADAS-cog) we have previously demonstrated that there are no Cu treatment effects on cognitive performance, however. Finally, CSF Abeta42 levels declined significantly in both groups within 12 months supporting the notion that CSF Abeta42 may be valid not only for diagnostic but also for prognostic purposes in AD.

4. Science News

Intake Of Dietary Copper Helps Alzheimer's Patients

ScienceDaily (Oct. 4, 2005) —

As one of the services for patients with Alzheimer's disease, the Department of Psychiatry at the Saarland University Medical Center offers participation in a clinical phase II trial. This clinical trial aims to elucidate a potential beneficial effect of copper orotate (an organic copper salt), which is given together with a standard cholinesterase inhibitor. A diagnosis of mild to moderate dementia of the Alzheimer type is a prerequisite. Besides clinical investigations, laboratory investigations of blood and cerebrospinal fluid, and magnet resonance imaging of the brain will be carried out. The study is being conducted by Professor Dr. Thomas Bayer, the Head of the Division of Neurobiology, and Dr. Frank Pajonk, a Psychiatrist, at the Department of Psychiatry, Saarland University Medical Center.

Treatment starts after all prerequisites to participate have been met. Half of the patients receive 8 mg copper orotate per day, the other half a placebo. Both patients and psychiatrists are blinded. During the 12-month long double-blind phase, there will be extensive laboratory, clinical and neuropsychological tests. After the double-blind phase, we offer an open-label phase for all patients. At present, 15 patients have finished the double-blind phase. The copper medication is well tolerated.

Alzheimer is characterized by the presence of amyloid plaques, which are composed primarily of Aß peptide. Aß is produced within neurons and is liberated from the larger amyloid ß protein precursor (AßPP). Lower levels of copper have been reported in the brain of AßPP transgenic mice and post-mortem in AD patients. This concept has been found to be true also in vitro by Professor Dr. Gerd Multhaup (FU Berlin) in 1999. Two recent papers, which have been published in PNAS in 2003 have proven a beneficial effect of elevated copper in transgenic AßPP mice. In the present study, the teams led by Bayer and Multhaup have found that low copper level in blood correlates with advanced memory deficits, as tested by the well established ADAS-cog neuropsychological test battery. Patients with higher blood copper levels make fewer mistakes in this memory test. This result supports the notion of a mild copper deficiency in AD patients. An increased uptake of dietary copper may therefore be therapeutically relevant.

The study has been published in the September 2005 issue of the Journal of Alzheimer's Disease, Volume 8, Issue 1 published by IOS Press: "Cognitive decline correlates with low plasma concentrations of copper in patients with mild to moderate Alzheimer's disease" (JAD, Vol. 8, Issue 1).

5.
Proc Natl Acad Sci U S A. 2003 Nov 25;100(24):14187-92. Epub 2003 Nov 14.
Dietary Cu stabilizes brain superoxide dismutase 1 activity and reduces amyloid Abeta production in APP23 transgenic mice.

Bayer TA, Schäfer S, Simons A, Kemmling A, Kamer T, Tepest R, Eckert A, Schüssel K, Eikenberg O, Sturchler-Pierrat C, Abramowski D, Staufenbiel M, Multhaup G.

Department of Psychiatry, Division of Neurobiology, University of the Saarland Medical Center, D-66421 Homburg, Germany. thomas.bayer@uniklinik-saarland.de

The Cu-binding beta-amyloid precursor protein (APP), and the amyloid Abeta peptide have been proposed to play a role in physiological metal regulation. There is accumulating evidence of an unbalanced Cu homeostasis with a causative or diagnostic link to Alzheimer's disease. Whereas elevated Cu levels are observed in APP knockout mice, APP overexpression results in reduced Cu in transgenic mouse brain. Moreover, Cu induces a decrease in Abeta levels in APP-transfected cells in vitro. To investigate the influence of bioavailable Cu, transgenic APP23 mice received an oral treatment with Cu-supplemented sucrose-sweetened drinking water (1). Chronic APP overexpression per se reduced superoxide dismutase 1 activity in transgenic mouse brain, which could be restored to normal levels after Cu treatment (2). A significant increase of brain Cu indicated its bioavailability on Cu treatment in APP23 mice, whereas Cu levels remained unaffected in littermate controls (3). Cu treatment lowered endogenous CNS Abeta before a detectable reduction of amyloid plaques. Thus, APP23 mice reveal APP-induced alterations linked to Cu homeostasis, which can be reversed by addition of dietary Cu.


6. Proc Natl Acad Sci U S A. 2003 Nov 25;100(24):14193-8. Epub 2003 Nov 14.
In vivo reduction of amyloid-beta by a mutant copper transporter.

Phinney AL, Drisaldi B, Schmidt SD, Lugowski S, Coronado V, Liang Y, Horne P, Yang J, Sekoulidis J, Coomaraswamy J, Chishti MA, Cox DW, Mathews PM, Nixon RA, Carlson GA, St George-Hyslop P, Westaway D.

Center for Research in Neurodegenerative Diseases, University of Toronto, Toronto, ON, Canada M5S 3H2.

Cu ions have been suggested to enhance the assembly and pathogenic potential of the Alzheimer's disease amyloid-beta (Abeta) peptide. To explore this relationship in vivo, toxic-milk (txJ) mice with a mutant ATPase7b transporter favoring elevated Cu levels were analyzed in combination with the transgenic (Tg) CRND8 amyloid precursor protein mice exhibiting robust Abeta deposition. Unexpectedly, TgCRND8 mice homozygous for the recessive txJ mutation examined at 6 months of age exhibited a reduced number of amyloid plaques and diminished plasma Abeta levels. In addition, homozygosity for txJ increased survival of young TgCRND8 mice and lowered endogenous CNS Abeta at times before detectable increases in Cu in the CNS. These data suggest that the beneficial effect of the txJ mutation on CNS Abeta burden may proceed by a previously undescribed mechanism, likely involving increased clearance of peripheral pools of Abeta peptide.
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Sat Apr 24, 2010 8:23 am      Reply with quote
At the risk of ruffling any feathers here, I have some interesting information I feel I should share on this subject. I do sometimes still use the GHK-Cu serum from PSF (mainly after peels or when my skin acts up in reaction to trying a new product or changes in the weather or my hormones). I emailed PSF the other day asking their view on first generation copper peptide versus second generation copper peptides & why there are not more studies available (or being done) on CP use on healthy (not wounded) but aging skin. Basically they said that they are currently doing a study on GHK-Cu on intact, aging skin & that their scientists believe that the second generation CP's are not even real peptides.

I'm not trying to start an argument here, but what they replied to me is interesting & really makes me think. I just wanted to share it with the other members that are trying to figure out this copper peptide mystery as well. Here's their reply:

"Dear Heather,
Thank you for your email. I can understand your frustration & confusion in
regard to copper peptides. Due to patent restrictions, open research on
this ingredient until recently has been somewhat restricted. We use the
GHK-Cu (Gly-His-Lys+Cu2) in our Bio-Copper Serum due to the fact that this
is the only copper peptide complex that has published research to support
its safety & efficacy. To be frank, it is the belief of our chief
scientist that the so called “second generation” copper peptides or copper
chloride+hydrolyzed soy protein is not a real copper peptide, but a copper
and protein complex. Unlike GHK-Cu, this copper complex is not naturally
found in the body. Skin cells have no receptors to accept this molecule.
Therefore, it is broken down into free copper ions and protein fragments
which apparently have little to no benefit for skin.

Until more research is done on the copper/soy digest complex, I would not
recommend its use to any of our customers. This would be the case even if
we did not produce a GHK-Cu product. Copper is a trace metal that can
trigger edema, contact dermatitis, pro-oxidation by hydroxyl radicals &
DNA damage if not bound to a particular peptide in a specific, controlled
sequence. Copper complexes other than those naturally found in the body
(such as GHK-Cu) have been found to promote double-strand DNA damage,
dependent on their geometric structures and types of ligands. This is why
we have concerns with the copper chloride/hydrolyzed soy protein material.
Please note that the INCI ingredient name for this material denotes that
it is not an actual peptide, but a combination of two different
ingredients (copper and protein). This view is also shared by the Procyte
Corporation, which for years held the patent to GHK-Cu and sponsored &
published many of the studies on the use & safety of GHK-Cu on skin.

As for studies, there are published studies on GHK-Cu and wound healing,
collagen synthesis & inhibition of scar tissue formation. We are currently
doing a pilot study investigating the use of GHK-Cu on intact, aging skin.
We do not how far this study will go – if the pilot study stirs up enough
interest that a third party wishes to undertake more research on this
topic, then we will be thrilled. The problem that we face as a
manufacturer is that any independent studies that we carry out, even if
published & peer reviewed, will be criticized and doubted, since we are
also selling this material. For credible research to ensue on this
subject, a third party would have to find this topic deserving enough to
take over the research on their own, devise & carry out a study & report
their findings. With cures for diseases such as cancer and AIDS still
evading the scientific & medical community, I do not know that a
researcher would find the use of copper peptides on wrinkles a worthy
endeavor, and would spend the time acquiring funding for such a study that
would provide no long term benefit in their eyes. And if we were to
sponsor the study, as has been done in the past by other cosmetic
manufacturers, then the findings again would be constantly questioned &
dismissed as purchased research.

I understand your desire to compare GHK-Cu with the “second generation”
copper/soy protein complex, however we believe that such a comparison is
impossible for a few reasons. Firstly, the two materials are completely
different – maybe not apples & oranges, but…let’s say oranges &
grapefruits. One material is a true copper peptide, and the other is a
combination of copper and soy protein. Secondly, there is no publically
available research on the copper/soy protein material. The firm that holds
the patent on this material cites only research done on GHK-Cu and will
not release any studies (if they exist) on the copper/soy complex for
comparison. This makes it impossible for me to answer your question. I’m
not trying to be evasive, but I only deal with facts, and I do not have
enough information on the copper/soy material to make an informed argument
other than to again state that it is the belief of our scientists that
random mixtures of copper and proteins should be avoided and that the only
safe & effective copper protein complex that can or should be applied to
skin is GHK-Cu (Gly-His-Lys+Cu2).

I hope that I was able to answer some of your questions. Thank you again
for contacting Pure Skin Formulations."

So...what do you all think? Question
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Sat Apr 24, 2010 8:40 am      Reply with quote
doodlebug wrote:
......Skin cells have no receptors to accept this molecule. Therefore, it is broken down into free copper ions and protein fragments which apparently have little to no benefit for skin. ......Copper is a trace metal that can trigger edema, contact dermatitis, pro-oxidation by hydroxyl radicals & DNA damage if not bound to a particular peptide in a specific, controlled sequence. Copper complexes other than those naturally found in the body (such as GHK-Cu) have been found to promote double-strand DNA damage, dependent on their geometric structures and types of ligands. ......So...what do you all think? Question


It scares me.....I have not started using the 2nd generation Copper Peptides yet......
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Sat Apr 24, 2010 8:52 am      Reply with quote
Doodlebug, thanks for the info. It occurs to me that these folks have something of a conflict of interest since they only sell first gen.

Comments like "apparently have little to no benefit for skin" are red flags, given that we have anecdotal evidence from many who have observed benefit from second gen. However, this sentence: "Copper complexes other than those naturally found in the body (such as GHK-Cu) have been found to promote double-strand DNA damage,dependent on their geometric structures and types of ligands." is worrisome. I wonder if they can cite the research that demonstrates the damage?

Most of us use products every day that have more anecdotal than scientific support. As long as we aren't harming ourselves, that isn't a problem (for me, anyway!) So far, I'd have to say that I haven't seen any scientific proof that second gens work or that they cause harm.
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Sat Apr 24, 2010 9:44 am      Reply with quote
doodlebug wrote:
The firm that holds
the patent on this material cites only research done on GHK-Cu and will
not release any studies (if they exist) on the copper/soy complex for
comparison. This makes it impossible for me to answer your question. I’m
not trying to be evasive, but I only deal with facts, and I do not have
enough information on the copper/soy material to make an informed argument....


This is similar to the views that Josee had expressed about this matter.
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Sat Apr 24, 2010 9:50 am      Reply with quote
Hermosa,
No, I thought of that too, I realize that they only sell the first generation peptides, but I was just trying to get another point of view from different researchers in the cosmetic industry. Also, I agree with you that most products have anectdotal proof rather than scientific proof - I do think it's a bit ridiculous to expect studies to be done on every cosmetic ingredient out there. But on ingredients that can actually alter your DNA - umm...I'd like some more info on that! No, they didn't cite any studies - what I copied & pasted was their entire reply. Maybe Josee has some info on this? This is all way above my head! Laughing

Hermosa wrote:
Doodlebug, thanks for the info. It occurs to me that these folks have something of a conflict of interest since they only sell first gen.

Comments like "apparently have little to no benefit for skin" are red flags, given that we have anecdotal evidence from many who have observed benefit from second gen. However, this sentence: "Copper complexes other than those naturally found in the body (such as GHK-Cu) have been found to promote double-strand DNA damage,dependent on their geometric structures and types of ligands." is worrisome. I wonder if they can cite the research that demonstrates the damage?

Most of us use products every day that have more anecdotal than scientific support. As long as we aren't harming ourselves, that isn't a problem (for me, anyway!) So far, I'd have to say that I haven't seen any scientific proof that second gens work or that they cause harm.
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Sat Apr 24, 2010 10:00 am      Reply with quote
doodlebug wrote:
But on ingredients that can actually alter your DNA - umm...I'd like some more info on that!


I agree wholeheartedly. Thanks for copying the info you got from PSF, doodlebug.
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Sat Apr 24, 2010 10:12 am      Reply with quote
Star Model wrote:
margarett wrote:
Thanks so much Josee and everyone else for their input. I just recently purchased FlexEffect program and copper is mentioned. Reading this post has helped me to make a decision not to go for it since anyway some time ago I had a bit high level of uric acid (nothing serious) and the word "copper" frightens me.


Hi margarett Smile ,

Before being frightened by the word "copper" from what has been posed in this thread, you may want to take a look at the latest scientific research that suggests the exact opposite of what was once thought:


Well, if you read what I wrote, I never mentioned "ALzheimer"; that did not cross my mind. I know that copper can be a cause to raise uric acid. Yes, I am frightened by the word copper, you bet! Very Happy I don't want to end up with gout!
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Sat Apr 24, 2010 11:00 am      Reply with quote
I am very glad we have this thread and as one who has been on the fence and continues to stay there I appreciate all input. I have to admit that I although happy for those using these products who are very pleased with them, I myself find much of the information available or not in some cases to be quite a concern.

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