2019 STUDY: results of 10 year finasteride usage

FMondego

C'est de quoi j'ai le plus de peur que la peur
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We evaluated the long-term (10-year) efficacy and safety of AGA treatment with 1 mg/day finasteride in a large study population (532 patients), as the first study of this kind in Japan, to our knowledge. A high objective efficacy was demonstrated by the MGPA, which revealed improvement and prevention of disease progression in 99.1% of the 532 Japanese men with AGA treated with 1 mg/day finasteride for 10 years. Furthermore, the outcome was similar to or better than that reported by other studies in Japan [8-10,13,17]. Differences have been known to occur in the progression of AGA symptoms between Japanese and Caucasian men [8,18]. This efficacy of the investigated treatment in Japanese men exceeded that reported in other studies in Caucasians. The superior response of Japanese men with AGA was reported to likely be attributable to their hair characteristics (greater diameter, black color, and lower density), which facilitated the detection of slight changes [10,19-23]. A novel finding observed in this study was the significant difference in the improvement of AGA following finasteride treatment between the N-H: I/II/III and N-H: IV/V/VI/VII groups at the first visit. The ROC analysis revealed a similar difference, that was performed to classify patients with improvement (MGPA≥5) and deteriorating (MGPA<5) condition at year 10 of treatment; the cut-off point was N-H: III (AUC: 0.746). Furthermore, the MGPA of the total study population and the N-H: I/II/III group at the first visit significantly improved from treatment year 5 to 10 (P<0.001). This efficacy was different from that of a 5-year study in Japanese men, which reported that the efficacy began to plateau after 4 years of treatment [10]. Several studies have reported that AGA progresses in N-H classification with age, [7,11,12,18] and that younger patients show more improvement than that of older patients with AGA treatment [24,25]. In this study, AGA patients at the early stage of N-H classification showed more improvement than patients at the later stage did.




Results
Patient Characteristics
The characteristics of all patients evaluated for AGA treatment efficacy were as follows: age at first visit, 37.8 ± 10.0 years; age range, 20–69 years; and values of each N-H at the first visit: I/II/III/IV/V/VI/VII, 6/116/204/124/61/18/3, respectively.

Efficacy Evaluation in 10 years treatment
Objective efficacy - Scalp photographs

The proportions of patients with improvement (MGPA ≥ 5) or prevention of disease progression (MGPA ≥ 4) at treatment year 10 were 91.5% (487/532) and 99.1% (527/532), respectively
. The efficacy evaluation showed that the MGPA improved significantly from year 1 through to year 10 of treatment compared with the baseline (MGPA = 4). The MGPA of each N-H group was linear according to the N-H number; the total was between N-H:III and N-H:IV (Figure 4 and Table 1). Receiver operating characteristic curve (ROC) analysis was performed to classify patients with improvement (MGPA ≥ 5) and deteriorating (MGPA<5) condition at year 10 of treatment; the cut-off point was N-H: III. (the area under the curve [AUC], which indicates the predictive value, was 0.746.). Furthermore, the MGPA of the total study population and the N-H:I/II/III group at the first visit improved from year 5 through to year 10, with statistically significant differences (P<0.001). The early stage AGA group (N-H: I/II/III at first visit) showed more improvement with long-term AGA treatment (10-year) with finasteride than the other groups did in the objective evaluation. The N-H classification of AGA patients improved by approximately 1 grade over the 10-year treatment with finasteride; significant differences were observed from pre-treatment (3.35 ± 1.11) to post-treatment (2.55 ± 1.30, P<0.001) in comparison of digitized classification.


Figure 4. Changes in modified global photographic assessment scores (MGPA) from before treatment through year 10 of treatment on each Norwood-Hamilton scale (N-H) group at first visit.


Safety Evaluation
During the study period for 10 years, no serious adverse reaction was recognized. Mild and temporary adverse reactions were recorded in 6.8% (36⁄532) of the entire study population by questionnaire. The adverse reactions were decreased libido (5.6%, n=30) and erectile dysfunction (3.0%, n=16). All adverse reactions were mild and all patients continued treatment for 10 years.



 

bajskorven

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why do even you care about that? you are not even balding.
 
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i think another really important aspect of this study is the fact that it's not a Merck commissioned trial yet it finds the same results as the previous high quality Merck commissioned trials. just goes to show that the "b-but big pharma is lying to you bro!" argument against fin is retarded
 

FMondego

C'est de quoi j'ai le plus de peur que la peur
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finasterid is poison

9 months of finasteride use and I haven't turned into a tranny yet, is this shit even working tbh....


Some details before I share the pictures:


- I started taking finasteride at 19, 20 now
- I started balding at 15/16. It really started picking up at 18, basically went from nw1 to nw2.5 in 1 year
- I take 1mg daily

- Sourced from AllDayChemist
- Supplements I take/have used that may aid in hair growth and that I recommend are, Zinc, D3, Magnesium, viagra.






My hairline at the beginning:



At 6 months:



And now at 9 months:



sideeffects:

- more hair
- less cortisol (no worrying about hairline recession)
- more dopamin (no worrying about hairline recession)
- better sleep (no worrying about hairline recession)
- cure of depression (no worrying about hairline recession)
- more sex (baldcels dont even need a penis so why do they worry about finasterid killing their dick?)
 
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what about bloating? i don't mind if fin kills my penis but i don't want even a single ml of water weight added to my face
 

FMondego

C'est de quoi j'ai le plus de peur que la peur
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regarding penis shrinkage (jhas nothing to do with the study in op)


Quote:

I have read for years concerns from finasteride/dutasteride users that reducing their DHT may deprive their penises of androgen stimulation and lead to penile shrinkage over time. I have seen the animal studies showing this does in fact happen in rats. I have also read some claims from long term finasteride/dutasteride users that their penises have noticeably shrunken over the years.

This is especially pertinent to me now as I am on darolutamide, which is the most powerful androgen receptor antagonist (and completely experimental), so I looked to see what I could find. I found this study, showing that yes, in fact, androgen deprivation can definitely lead to penile shrinkage over time:

"The effects of long-term androgen deprivation therapy on penile length in patients with prostate cancer: a single-center, prospective, open-label, observational study."

Before therapy, the mean stretched penile length was 10.76 cm. After 24 months of ADT, mean penile length had decreased to 8.05 cm. However, these changes plateaued after 15 months.


https://www.ncbi.nlm.nih.gov/pubmed/21699669

So, in other words, with very aggressive androgen deprivation (much more aggressive than anyone here is considering), considerable penis shrinkage did occur. It was a fair amount. Penises shrunk from 10.76 cm stretched to 8.05 cm stretched after 24 months of treatment.

Fortunately, the effect plateaued over time, leveling off after 15 months, which suggests that no matter what, your dick won't shrivel away indefinitely until there's nothing left at all. But the amount of penis atrophy was considerable and should probably be taken seriously.

Is this relevant?
Before we go any further, it must be clarified that things like finasteride/dutasteride/RU do not block or reduce androgens to nearly even a fraction of the extent as the agents used in the study quoted above. So probably this is not even something to worry about for standard med users.

But I do think it is important to be aware of, given that we all have different androgen sensitivities throughout our bodies, and most of us are aiming to treat our hair loss for 40-50+ years, over which time even subtle effects could become more obvious.

Solutions
The first solution to avoiding this problem over time (besides just not worrying about it) would then obviously be to limit your anti-androgens (finasteride/dutasteride/RU/whatever) to the lowest dose possible.

The second solution, which I am debating employing for myself, would be to add a bit of topical androgen back to your penis, in the form of testosterone or DHT gel applied directly to the penis. DHT gel (Adractim) is commonly used in the penis enlargement community to help maximize androgen stimulation of the penis. Testosterone gel should work similarly.

The first trouble with this approach is DHT/test gels/creams fall under "anabolic steroids" and may be highly illegal depending on where you live. (Don't blame me if you get arrested trying to procure some.)

The second trouble is that adding extra androgens to your system may undo any benefits you are getting from your hair loss treatment. The hope would be that the test/DHT gel/cream would stay "local" to the penis, but the penis is so incredibly vascular, this is almost certainly completely unrealistic.

In my case as I am using daro topically to my scalp, I would not be worried about a little extra DHT/test circulating from penile application. It would never overwhelm my topical daro. But if you are on a more conventional/safe regimen, then the extra DHT/test could be problematic. You'd probably have to monitor carefully if you were trying anything like this.
 

lltvyr

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regarding penis shrinkage (jhas nothing to do with the study in op)


Quote:

I have read for years concerns from finasteride/dutasteride users that reducing their DHT may deprive their penises of androgen stimulation and lead to penile shrinkage over time. I have seen the animal studies showing this does in fact happen in rats. I have also read some claims from long term finasteride/dutasteride users that their penises have noticeably shrunken over the years.

This is especially pertinent to me now as I am on darolutamide, which is the most powerful androgen receptor antagonist (and completely experimental), so I looked to see what I could find. I found this study, showing that yes, in fact, androgen deprivation can definitely lead to penile shrinkage over time:

"The effects of long-term androgen deprivation therapy on penile length in patients with prostate cancer: a single-center, prospective, open-label, observational study."

Before therapy, the mean stretched penile length was 10.76 cm. After 24 months of ADT, mean penile length had decreased to 8.05 cm. However, these changes plateaued after 15 months.


https://www.ncbi.nlm.nih.gov/pubmed/21699669

So, in other words, with very aggressive androgen deprivation (much more aggressive than anyone here is considering), considerable penis shrinkage did occur. It was a fair amount. Penises shrunk from 10.76 cm stretched to 8.05 cm stretched after 24 months of treatment.

Fortunately, the effect plateaued over time, leveling off after 15 months, which suggests that no matter what, your dick won't shrivel away indefinitely until there's nothing left at all. But the amount of penis atrophy was considerable and should probably be taken seriously.

Is this relevant?
Before we go any further, it must be clarified that things like finasteride/dutasteride/RU do not block or reduce androgens to nearly even a fraction of the extent as the agents used in the study quoted above. So probably this is not even something to worry about for standard med users.

But I do think it is important to be aware of, given that we all have different androgen sensitivities throughout our bodies, and most of us are aiming to treat our hair loss for 40-50+ years, over which time even subtle effects could become more obvious.

Solutions
The first solution to avoiding this problem over time (besides just not worrying about it) would then obviously be to limit your anti-androgens (finasteride/dutasteride/RU/whatever) to the lowest dose possible.

The second solution, which I am debating employing for myself, would be to add a bit of topical androgen back to your penis, in the form of testosterone or DHT gel applied directly to the penis. DHT gel (Adractim) is commonly used in the penis enlargement community to help maximize androgen stimulation of the penis. Testosterone gel should work similarly.

The first trouble with this approach is DHT/test gels/creams fall under "anabolic steroids" and may be highly illegal depending on where you live. (Don't blame me if you get arrested trying to procure some.)

The second trouble is that adding extra androgens to your system may undo any benefits you are getting from your hair loss treatment. The hope would be that the test/DHT gel/cream would stay "local" to the penis, but the penis is so incredibly vascular, this is almost certainly completely unrealistic.

In my case as I am using daro topically to my scalp, I would not be worried about a little extra DHT/test circulating from penile application. It would never overwhelm my topical daro. But if you are on a more conventional/safe regimen, then the extra DHT/test could be problematic. You'd probably have to monitor carefully if you were trying anything like this.
These are the exact studies I've been showing people like 10 years already. Luckily I just yesterday found out the human penis doesn't have androgen receptors which probably isn't the case for rats. We should stop worrying about this efect based on rat studies. The shrinkage isn't a direct efect of androgen depletion, but less nerve firing and less bloodflow. It's the use-it-or-lose-it-principle which everyone long knows about the penis. If you're castrated, you stop having nocturnal spontanous erections and stop having sex. The penis shrinks because of inactivity. Nothing else.

I guess rats penises have AR and are dependent on the constant stimulation of maximum androgens. Rats penises also have a bone.

What would be interesting to know is if these castrated men can regrow their penises once they stop their castration. Unfortunately these are all old end-stage cancer patients who don't have much time left to live anymore. We probably cannot stop their treatment for a long enough time to see this efect. After the cancer becomes castration-resistant chemotherapy begins which hits the body bad with its sideeffects and a luxury function such as sexual function gets shut down first anyway.
 

FMondego

C'est de quoi j'ai le plus de peur que la peur
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A literature review of adverse side effects associated with 5αRIs shows that persistent sexual side effects were only documented in low-quality studies with strong bias selection as participants were part of an Internet blog. The only high-quality study documenting persistent sexual side effects showed that these were more frequent in the placebo than in the treatment group, implying that the effects were not necessarily related to the treatment. A significant placebo/nocebo effect has been documented among patients informed about possible side effects of finasteride and this may explain the high prevalence of reported sexual dysfunction including persistent dysfunction in subjects participating in Internet groups and blogs. Psychiatric side effects were only documented in moderate- or low-quality studies including studies performed on patients with sexual side effects, which could influence patient's mood. Most of these studies recruited patients through the same Internet patient website.

 
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A literature review of adverse side effects associated with 5αRIs shows that persistent sexual side effects were only documented in low-quality studies with strong bias selection as participants were part of an Internet blog. The only high-quality study documenting persistent sexual side effects showed that these were more frequent in the placebo than in the treatment group, implying that the effects were not necessarily related to the treatment. A significant placebo/nocebo effect has been documented among patients informed about possible side effects of finasteride and this may explain the high prevalence of reported sexual dysfunction including persistent dysfunction in subjects participating in Internet groups and blogs. Psychiatric side effects were only documented in moderate- or low-quality studies including studies performed on patients with sexual side effects, which could influence patient's mood. Most of these studies recruited patients through the same Internet patient website.

almost all the anti finasteride propoganda is rooted in anecdotes from people online, poorly conducted observational studies or mechanistic data. outcome data from high quality RCTs is what you want and those results shine a very positive light on fin
 

FMondego

C'est de quoi j'ai le plus de peur que la peur
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literally all the anti finasteride propoganda is rooted in anecdotes from people online, poorly conducted observational studies or mechanistic data. outcome data from high quality RCTs is what you want and those results shine a very positive light on fin
well yeah obviously

however im not saying side effects dont exist at all. side effects exists. but it just doesnt affect the majority of people taking it. the truth is most people who stop taking finasterid dont do it because they experience side effects. they do it because they dont see a positive effect regarding hairloss or they just get lazy, accepting their hairloss like most men (something which many people here cant even imagine. could be one reason for higher reports of side effects on the internet if i think about it: people who seriously consider suicide because of hairloss are not in the best psychological condition before fin and obviously could be more likely to experience nocebo effects then mentally well adjusted guys).

if i experience more serious side effects of fin one day i will just stop taking it. simple as that. but i wont project my situation to everybody else and claim just because i got side effects everybody else will get them too.
 

Adrian_B

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Where is this source from? Someone should doublecheck to make sure the study wasn't paid for by some company trying to make a profit from selling Finasteride. Doublechecking to see who published the study, and where, can also help identifying if a company may have paid some shitty journal to publish the results.
 

FMondego

C'est de quoi j'ai le plus de peur que la peur
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Where is this source from? Someone should doublecheck to make sure the study wasn't paid for by some company trying to make a profit from selling Finasteride. Doublechecking to see who published the study, and where, can also help identifying if a company may have paid some shitty journal to publish the results.
the link is ar the bottom.


do you also apply the same standards to fin horror stories or do you believe everything without any second questions in that regard?

:niro:

my favorite stories on propeciahelp is when guys who started finasterid in their 30s for a couple of years claim finasterid made them age and caused wrinkles in that time

:banderas:

or when people say they got permanent side effects for years after taking 1 (!) pill

:banderas:
 

foreheadman

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tl'dr


FIn side effects is from low free test from high shbg and high estrogen. High free test normal estrogen guys don't get sides
 

lltvyr

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A literature review of adverse side effects associated with 5αRIs shows that persistent sexual side effects were only documented in low-quality studies with strong bias selection as participants were part of an Internet blog. The only high-quality study documenting persistent sexual side effects showed that these were more frequent in the placebo than in the treatment group, implying that the effects were not necessarily related to the treatment. A significant placebo/nocebo effect has been documented among patients informed about possible side effects of finasteride and this may explain the high prevalence of reported sexual dysfunction including persistent dysfunction in subjects participating in Internet groups and blogs. Psychiatric side effects were only documented in moderate- or low-quality studies including studies performed on patients with sexual side effects, which could influence patient's mood. Most of these studies recruited patients through the same Internet patient website.

Lmao. More possible to get post finasteride syndrome from placebo than finasterid :D:D.

That's what I've been telling. PFS is just post finasteride stress.
 

lltvyr

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almost all the anti finasteride propoganda is rooted in anecdotes from people online, poorly conducted observational studies or mechanistic data. outcome data from high quality RCTs is what you want and those results shine a very positive light on fin
I can't belive they are even allowed to do internet forum based scientific studies. It's usually called bro science. But when it gets publicity like this people doing good on fin may start to have baseless anxiety as well.

And the whole thing about only getting it months after being off the drug... wtf... Against any logic.

Good medical practice: exclude anxiety disorder, exclude low T, only then prescribe finasteride. Good specialists are already doing this.
 

lltvyr

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Where is this source from? Someone should doublecheck to make sure the study wasn't paid for by some company trying to make a profit from selling Finasteride. Doublechecking to see who published the study, and where, can also help identifying if a company may have paid some shitty journal to publish the results.
Disclosure Statement
Dr. Tosti received honoraria as a consultant, advisory board participant, speaker or book author from the following companies: Aclaris, Incyte (Consultant and PI), Kythera, P&G, DS Laboratories, Merck (Consultant and Speaker over 3 years ago), Taylor & Francis (Author), Springer-Verlag (Author), and National Alopecia Areata Foundation (Scientific Board Member).

Dr. Shapiro reports the following: Replicel Life Sciences Inc. (Cofounder and Stockholder), Johnson and Johnson (Consultant), Aclaris (Consultant), Samumed (Consultant), Incyte (Consultant), L'Oreal Paris (Consultant), Merck (Consultant and Speaker over 3 years ago), Bayer (Consultant), Kythera (Consultant), Up to Date (Author), National Alopecia Areata Foundation (Scientific Board Member), Cicatricial Alopecia Research Foundation Board of Directors. All consultancies are present except for Merck.

Dr. Bergfeld reports the following: P&G (Consultant and research), Bayer Health (Consultant), Samumed, Incyte, Aclaris, Cassiopea, Allergan, and Merck investigator for finasteride (in the past, over 20 years ago, no relationship now).

Raymond Fertig has no conflicts of interest to report.


Let this feed all the conspiracies and thinking that all doctors are sellouts and have no professional honor and honesty.
 

lltvyr

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Lmao. More possible to get post finasteride syndrome from placebo than finasterid :D:D.

That's what I've been telling. PFS is just post finasteride stress.
Also what's common about anxiety disorders: random unrelated unexplainable sudden symptoms all over the place. These guys always tell they just one day woke up feeling like that. Like overnight. Typical anxiety. An actual physical erectile dysfunction develops slowly and smoothly. If one day you are rock hard and the next moment not it is anxiety.
 

lester

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dr tosti and dr shapiro



came across Dra. Bruna Rezende while researching about them




:dre:
 

3/10CurryCel

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We evaluated the long-term (10-year) efficacy and safety of AGA treatment with 1 mg/day finasteride in a large study population (532 patients), as the first study of this kind in Japan, to our knowledge. A high objective efficacy was demonstrated by the MGPA, which revealed improvement and prevention of disease progression in 99.1% of the 532 Japanese men with AGA treated with 1 mg/day finasteride for 10 years. Furthermore, the outcome was similar to or better than that reported by other studies in Japan [8-10,13,17]. Differences have been known to occur in the progression of AGA symptoms between Japanese and Caucasian men [8,18]. This efficacy of the investigated treatment in Japanese men exceeded that reported in other studies in Caucasians. The superior response of Japanese men with AGA was reported to likely be attributable to their hair characteristics (greater diameter, black color, and lower density), which facilitated the detection of slight changes [10,19-23]. A novel finding observed in this study was the significant difference in the improvement of AGA following finasteride treatment between the N-H: I/II/III and N-H: IV/V/VI/VII groups at the first visit. The ROC analysis revealed a similar difference, that was performed to classify patients with improvement (MGPA≥5) and deteriorating (MGPA<5) condition at year 10 of treatment; the cut-off point was N-H: III (AUC: 0.746). Furthermore, the MGPA of the total study population and the N-H: I/II/III group at the first visit significantly improved from treatment year 5 to 10 (P<0.001). This efficacy was different from that of a 5-year study in Japanese men, which reported that the efficacy began to plateau after 4 years of treatment [10]. Several studies have reported that AGA progresses in N-H classification with age, [7,11,12,18] and that younger patients show more improvement than that of older patients with AGA treatment [24,25]. In this study, AGA patients at the early stage of N-H classification showed more improvement than patients at the later stage did.




Results
Patient Characteristics
The characteristics of all patients evaluated for AGA treatment efficacy were as follows: age at first visit, 37.8 ± 10.0 years; age range, 20–69 years; and values of each N-H at the first visit: I/II/III/IV/V/VI/VII, 6/116/204/124/61/18/3, respectively.

Efficacy Evaluation in 10 years treatment
Objective efficacy - Scalp photographs

The proportions of patients with improvement (MGPA ≥ 5) or prevention of disease progression (MGPA ≥ 4) at treatment year 10 were 91.5% (487/532) and 99.1% (527/532), respectively
. The efficacy evaluation showed that the MGPA improved significantly from year 1 through to year 10 of treatment compared with the baseline (MGPA = 4). The MGPA of each N-H group was linear according to the N-H number; the total was between N-H:III and N-H:IV (Figure 4 and Table 1). Receiver operating characteristic curve (ROC) analysis was performed to classify patients with improvement (MGPA ≥ 5) and deteriorating (MGPA<5) condition at year 10 of treatment; the cut-off point was N-H: III. (the area under the curve [AUC], which indicates the predictive value, was 0.746.). Furthermore, the MGPA of the total study population and the N-H:I/II/III group at the first visit improved from year 5 through to year 10, with statistically significant differences (P<0.001). The early stage AGA group (N-H: I/II/III at first visit) showed more improvement with long-term AGA treatment (10-year) with finasteride than the other groups did in the objective evaluation. The N-H classification of AGA patients improved by approximately 1 grade over the 10-year treatment with finasteride; significant differences were observed from pre-treatment (3.35 ± 1.11) to post-treatment (2.55 ± 1.30, P<0.001) in comparison of digitized classification.


Figure 4. Changes in modified global photographic assessment scores (MGPA) from before treatment through year 10 of treatment on each Norwood-Hamilton scale (N-H) group at first visit.


Safety Evaluation
During the study period for 10 years, no serious adverse reaction was recognized. Mild and temporary adverse reactions were recorded in 6.8% (36⁄532) of the entire study population by questionnaire. The adverse reactions were decreased libido (5.6%, n=30) and erectile dysfunction (3.0%, n=16). All adverse reactions were mild and all patients continued treatment for 10 years.



Didn’t read faggot.


Give a 4 line summary or don’t bother posting
 
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