Diclofenac Is Bad, Heres Proof, Debate Please...

proscar2

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https://www.ncbi.nlm.nih.gov/pubmed/10342040




RESULTS:
At a concentration of 3 micrograms/ml, nimesulide did not affect the PG production by chondrocytes. This concentration was superior to the highest level of nimesulide found in the synovial fluid of patients with rheumatoid arthritis 3 hours after the last oral administration of nimesulide (100 mg twice daily for 7 days). At 6 micrograms/ml a significant reduction in the PG content was obtained in the cellular phase in 5 out of the 8 cultures investigated. No similar effect was observed in the culture supernatants. Above this concentration nimesulide inhibited PG production in a dose-dependent manner. At concentrations ranging from 0.005 to 1 microgram/ml diclofenac did not significantly alter PG production. At therapeutic concentrations PGE2 production was totally inhibited by nimesulide, thus suggesting that PG inhibition is not linked to PGE2 production. Nimesulide inhibited PGE2 production by unstimulated (IC50 = 6 ng/ml) and IL-1 beta-stimulated (IC50 = 6.9 ng/ml) chondrocytes. At these concentrations, PGE2 production was fully inhibited by diclofenac. Furthermore, both nimesulide and diclofenac at therapeutic concentrations significantly decreased spontaneous and IL-1 beta-stimulated IL-6 production by human chondrocytes, but did not modify IL-8 production.

CONCLUSION:
From the results of this study we conclude that nimesulide and diclofenac at therapeutic concentrations are potent inhibitors of PGE2 and IL-6 production while they do not modify proteoglycan or IL-8 production.
 

Giiizmo

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Why and how is diclofenac bad? Related to what? The prostaglandin hypothesis? So it inhibits production of PGE2 but what about PGD2? So what?

You can't just barge in here, cut 'n crap some quoted portions of a study then ask for a discussion without first providing some input or at least putting things into context.

Here, I'll do the same. Then we can have a jolly round of pointless quote-fest that brings nothing of substance to the table.


Preparation and evaluation of a multimodal minoxidil microemulsion versus minoxidil alone in the treatment of androgenic alopecia of mixed etiology: a pilot study

Results:
[... The effect of microemulsions A, B, and C on mean hair count is shown in Table 3, indicating that, as the treatment period increased from baseline to 32 weeks, the hair count increased progressively in the group treated with the multimodal emulsion and to a greater extent than in the group treated with the microemulsion containing minoxidil alone, while the placebo group showed a marked decrease in hair count. The last column in Table 3 shows that the effect of the multimodal emulsion on hair count is highly significant compared with that of the minoxidil and placebo formulations (P = 0.009 and P < 0.001, respectively). [...

Conclusion:
All evaluations showed highly significant improvements using the multimodal minoxidil microemulsion in comparison with the minoxidil only formulation which, in turn, was significantly more effective than placebo. The pronounced effects of the multimodal minoxidil formulation compared with minoxidil alone could be attributed to the anti-inflammatory effect of diclofenac in reducing scalp and follicular microinflammation and the tea tree oil in resolving any existing microbial or fungal colonization of the hair follicles. These results indicate that androgenic alopecia is multifactorial and perhaps polygenic in nature. Hence, an effective multimodal microemulsion comprising minoxidil, an anti-inflammatory agent, and an anti-infective agent is recommended as being more promising than minoxidil alone. Diclofenac was used in the multimodal formulation instead of a cortisone derivative to reduce the risk of side effects, and tea tree oil was used on the basis that it is a highly effective natural anti-infective agent.15,16 Further study is planned in a larger patient population for an extended period to monitor the long-term effects in individuals with androgenic alopecia accompanied by hair follicle infection and/or microinflammation.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3686323/
 

proscar2

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is this enough in context enough for you?


I can post how i like! if you dont like it dont read it! do you own this forum? are you a mod? no well.............go do one!

1 diflofenac is bad related to........... pge2.......... can you read read? it says in the post.

2 i cant just barge in here? what is this your forum? are you a mod? do you own this site? NO? well I can post how i like! you dont like it tough!

3 in terms of context... considering i highlighted regarding pge2 and I'm assuming most people are enlightened about this then i have put it in context. and for the people that dont understand it then its not important to you and so...........................TOUGH. I'm not your teacher.......RESEARCH!

4 if you cant understand my posts...too bad, as i like to be brief. i haven't got time to waste to hold peoples hands, if you get it you get it , and your on my wavelength GREAT. If you dont understand and it doesn't make sense, it's no odds to me!!!! DON'T READ MY POSTS. do more research and get MORE KNOWLEDGE! this post will help inform those who

6 actually this was aimed at hair-cook, regarding a debate earlier, but i forgot to mention his name....


7 YOU GOT TOO MUCH TIME ON YOUR HANDS- ! gotta go... I've wasted ten min's responding to this rubbish










 

arnoldd

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Pgd2 and pge both are pro inflammatory, diclofenac is an antiinflammatory so its obvious why it inhibits pge2 too.
But you know alopecia is an inflammatory process, thats why it helps and some guys noticed some regrowth or better quality of hairs
 

whatevr

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What do you think about dimetindene? H1 receptor antagonist like cetirizine.
 

Giiizmo

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Arnoldd gets it.

@proscar2 : If you had bothered to read the excerpt I quoted, the study mentions that a microemulsion of minoxidil, tea tree oil and diclofenac provided superior regrowth in their test subjects compared to just minoxidil and tea tree oil. Now if diclofenac is "bad", why is that?

I see the mantra about increasing PGE2 and reducing PGD2 posted everywhere on this forum. Unfortunately, people still forget that there's little to no evidence backing that theory up. It's a sound theory and it possibly has a decisive impact on Androgenetic Alopecia as Cotsarelis thinks, but we still don't know if it's real or not and what's the role of prostaglandins in the grand scheme of things.

Just labeling something "bad" based on conjecture isn't rational.

And yes, I think that simply quoting a study without putting it in context fosters poor discussion and ends up clogging this subsection. I'm not a mod and it's ultimately none of my business but I'm sure I'm not alone when I say I'm tired of seeing new threads pop up that either provide no value or get abandoned because the OP didn't take a few extra minutes to try and bring people to pay enough attention to the topic.

/hugs and kisses
 
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