r/DrWillPowers

I recently started calcium d glucarate for pfs. I was in trt and quit after learning about theory and the same week of last injection I started CdG. By the end of that week I was getting insane night and morning wood as well as some decent libido. Then something weird happened. I had sex with girlfriend and the orgasm felt much better than previous expiriences. The next day I woke up and my penis was irritated and red. Now me and my girlfriend do not have stds and we retested after this expirience to rule it out. She was not affected only me. My pebis was shedding skin like crazy, and not on the shaft on the head, aswell as the surrounding foreskin was super red too. While that was happening I recovered full sensation in my penis I could feel hot and cold and touch but it wasnt the most pleasant since it was still irritated. After those 2 days the shedding significantly decreased althiugh it still did and I kept taking CdG. It been about a total of 3 weeks on cdg and I finished the bottled, but this week I started expiriencing crazy panic attack episodes, none were super string or lasted much until yesterday, I got a bad one to the point I thought I was dying and went to the ER. Ekg showed fine no signs of glucose related issues. They gave me some vistoril which calmed me down and knocked me out cold. This could be due to the fact my test levels might be plummeting as my hpta tries ti comeback on but im depleting its supply with CdG. Will keep updated since now its a matter of waiting for my test levels to comeback up, and see if I recover my previous baseline which was much better (daily nocturnal and morning wood). Ever since pfs ive had arousal which means my body initially tries to feel horny but it doesn't sustain, and I noticed last time I saw my gf that ny arousal was much stronger but still doesn't sustain and sadly my penis is numb again, although the foreskin retained its sensitivity. I'll have to wait and see what happens and hopefully these episodes stop and I bounce back. Would love if Dr.Powers sees this anecdote so please treat this post well im just reporting what ive been expiriencing. One more thing I would like to add is that the shed was very similar to when I first got pfs, I also had a shed but instead my oenis became cold and shirveled after.

Did any one else get brain zaps (like on ssri), muscle spasm(like benzo withdrawal) and insomnia(gaba-a) when crashed/crashing? My muscle spasms were extreme when crashed on anastrazole(which lowers gaba-a) they were so strong I could not straight out my legs. Maybe GABA-A and glutamate crashed and the system upregulated so much it’s now too much for it to handle? Or maybe it’s still too low?
I’m not sure , just wondering. Let me know your thoughts.

I’m sorry if this has been asked before I am a cis male 25 experiencing minor crown thinning I’m aware of Pfs so I wouldn’t touch a dht blocker. I’m just wondering if minoxdil on its own is okay

And to those with Pfs I am sorry

Any idea what may be causing it and has anything helped with this symptom? It fluctuates but it bothers me a lot and has been pretty constant for 27 months.

Hey, I just wanted to share the interesting variants I get when inputting all of the genes into gene.iobio.

I took 1/8 of a 5 mg pill of fin in May 2025. Stopped because I started noticing some minor penile burning later the same day. Three days later I crashed.

I’ve grouped the VCF variants separately from the BAM variants. The variants are in the same order that gene.iobio prioritized them in the UI.

I ran the patched WAR_POWERS script from u/Excellent-Push2833 to find gene deletions, but no hits were found (deletion_hits.tsv was empty).

VCF variants:

Gene: DGAT2
Consequence: Missense
Variant: c.1034C>T
Protein: p.Pro345Leu
rsID: rs138423103
Zygosity: Het
Ref Allele: C
Alt Allele: T
Freq: 0.0184% rare (popmax 0.0294%)
REVEL: 0.446
Source coordinates: chr11:75800375-75800376
ClinVar: uncertain significance

Gene: TET1
Consequence: Missense
Variant: c.5422G>A
Protein: p.Val1808Met
rsID: rs150708897
Zygosity: Het
Ref Allele: G
Alt Allele: A
Freq: 0.0893% rare (popmax 0.207%)
REVEL: 0.028
Source coordinates: chr10:68690825-68690826
ClinVar: likely benign

Gene: TPH1
Consequence: Missense
Variant: c.529G>A
Protein: p.Val177Ile
rsID: rs147638867
Zygosity: Het
Ref Allele: C
Alt Allele: T
Freq: 0.236% uncommon (popmax 0.406%)
REVEL: 0.419
Source coordinates: chr11:18029303-18029304
ClinVar: likely benign

Gene: UGT2B15
Consequence: Missense
Variant: c.1408C>T
Protein: p.Arg470Cys
rsID: rs147164238
Zygosity: Het
Ref Allele: G
Alt Allele: A
Freq: 0.324% uncommon (popmax 0.579%)
REVEL: 0.505
Source coordinates: chr4:68647289-68647290
ClinVar: likely benign

Gene: CUBN
Consequence: Missense
Variant: c.6469A>G
Protein: p.Asn2157Asp
rsID: rs144360241
Zygosity: Het
Ref Allele: T
Alt Allele: C
Freq: 0.526% uncommon (popmax 0.647%)
REVEL: 0.322
Source coordinates: chr10:16925418-16925419
ClinVar: benign/likely benign

Gene: CUBN
Consequence: Missense
Variant: c.3604G>T
Protein: p.Ala1202Ser
rsID: rs141740096
Zygosity: Het
Ref Allele: C
Alt Allele: A
Freq: 0.0368% rare (popmax 0.104%)
REVEL: 0.053
Source coordinates: chr10:17045075-17045076
ClinVar: conflicting classifications of pathogenicity

Gene: CHD7
Consequence: Missense
Variant: c.307T>A
Protein: p.Ser103Thr
rsID: rs41272435
Zygosity: Het
Ref Allele: T
Alt Allele: A
Freq: 1.303% common (popmax 1.909%)
REVEL: 0.063
Source coordinates: chr8:60741739-60741740
ClinVar: benign/likely benign

Gene: TBP
Consequence: Inframe deletion
Variant: c.279_281del
Protein: p.Gln95del
rsID: rs752404282
Zygosity: Het
Ref Allele: ACAG
Alt Allele: A
Freq: 0.403% uncommon (popmax 0.513%)
REVEL: not shown
Source coordinates: chr6:170561958-170561961
ClinVar: benign

Gene: TBP
Consequence: Inframe deletion
Variant: c.273_281del
Protein: p.Gln93_Gln95del
rsID: rs752404282
Zygosity: Het
Ref Allele: ACAGCAGCAG
Alt Allele: A
Freq: 0.0411% rare (popmax 0.203%)
REVEL: not shown
Source coordinates: chr6:170561958-170561967
ClinVar: benign

Gene: CYP1A1
Consequence: Missense
Variant: c.1390C>A
Protein: p.Arg464Ser
rsID: rs41279188
Zygosity: Het
Ref Allele: G
Alt Allele: T
Freq: 0.453% uncommon (popmax 0.813%)
REVEL: 0.518
Source coordinates: chr15:74720638-74720639
ClinVar: benign

Gene: SLC16A9
Consequence: Missense
Variant: c.1501T>G
Protein: p.Phe501Val
rsID: rs138607526
Zygosity: Het
Ref Allele: A
Alt Allele: C
Freq: 0.785% uncommon (popmax 1.388%)
REVEL: 0.111
Source coordinates: chr10:59652801-59652802
ClinVar: benign

Gene: NCOR1
Consequence: Missense
Variant: c.4218A>C
Protein: p.Leu1406Phe
rsID: rs61753150
Zygosity: Het
Ref Allele: T
Alt Allele: G
Freq: 0.968% uncommon (popmax 1.508%)
REVEL: 0.160
Source coordinates: chr17:16070460-16070461
ClinVar: benign

Gene: MTHFR
Consequence: Missense
Variant: c.1958C>T
Protein: p.Thr653Met
rsID: rs35737219
Zygosity: Het
Ref Allele: G
Alt Allele: A
Freq: 1.41% common (popmax 2.2%)
REVEL: 0.139
Source coordinates: chr1:11790693-11790694
ClinVar: benign

Gene: MC4R
Consequence: Missense
Variant: c.307G>A
Protein: p.Val103Ile
rsID: rs2229616
Zygosity: Het
Ref Allele: C
Alt Allele: T
Freq: 1.543% common (popmax 2.43%)
REVEL: 0.050
Source coordinates: chr18:60372043-60372044
ClinVar: benign

Gene: MT-ATP6
Consequence: Missense
Variant: c.334A>G
Protein: p.Thr112Ala
rsID: rs2001031
Zygosity: Hom
Ref Allele: A
Alt Allele: G
Freq: not shown
REVEL: not shown
Source coordinates: chrMT:8860-8861
ClinVar: benign

Gene: MT-ATP6
Consequence: Missense
Variant: c.529G>A
Protein: p.Ala177Thr
rsID: rs193303045
Zygosity: Hom
Ref Allele: G
Alt Allele: A
Freq: not shown
REVEL: not shown
Source coordinates: chrMT:9055-9056
ClinVar: benign

Gene: MT-CYB
Consequence: Missense
Variant: c.580A>G
Protein: p.Thr194Ala
rsID: rs2853508
Zygosity: Hom
Ref Allele: A
Alt Allele: G
Freq: not shown
REVEL: not shown
Source coordinates: chrMT:15326-15327
ClinVar: benign

Gene: EHMT1
Consequence: Splice acceptor in non-canonical transcripts
Variant: c.843A>T
Protein: p.Leu281Phe
rsID: rs1485591700
Zygosity: Het
Ref Allele: A
Alt Allele: T
Freq: 0.00156% very rare (popmax 0.00329%)
REVEL: 0.074
Source coordinates: chr9:137743390-137743391
ClinVar: not shown

Gene: EP400
Consequence: Inframe insertion
Variant: c.8189_8190insACAGCAGCAGCA
Protein: p.Gln2745_Gln2748dup
rsID: rs1555223311
Zygosity: Het
Ref Allele: A
Alt Allele: ACAGCAGCAACAG
Freq: 0.0142% rare (popmax 0.0194%)
REVEL: not shown
Source coordinates: chr12:132062548-132062560
ClinVar: not shown

Gene: DRD4
Consequence: Missense
Variant: c.812G>C
Protein: p.Arg271Pro
rsID: rs767239460
Zygosity: Het
Ref Allele: G
Alt Allele: C
Freq: 0.0685% rare (popmax 0.0924%)
REVEL: 0.054
Source coordinates: chr11:640061-640062
ClinVar: not shown

Gene: DRD4
Consequence: Missense
Variant: c.850A>C
Protein: p.Ser284Arg
rsID: rs34662058
Zygosity: Het
Ref Allele: A
Alt Allele: C
Freq: 0.0572% rare (popmax 0.439%)
REVEL: 0.043
Source coordinates: chr11:640099-640100
ClinVar: not shown

Gene: NDUFS2
Consequence: Missense
Variant: c.968G>A
Protein: p.Arg323Gln
rsID: rs35086265
Zygosity: Het
Ref Allele: G
Alt Allele: A
Freq: 0.463% uncommon (popmax 0.943%)
REVEL: 0.525
Source coordinates: chr1:161210692-161210693
ClinVar: conflicting classifications of pathogenicity

Gene: EHMT2
Consequence: Missense
Variant: c.173C>T
Protein: p.Ser58Phe
rsID: rs115884658
Zygosity: Het
Ref Allele: G
Alt Allele: A
Freq: 1.205% common (popmax 1.948%)
REVEL: 0.085
Source coordinates: chr6:31896761-31896762
ClinVar: not shown

BAM variants:

Gene: KDM6A
Consequence: Splice donor variant
Variant: c.3300+1G>A
Protein: not shown
rsID: rs1602928572
Zygosity: Het
Ref Allele: G
Alt Allele: A
Freq: not shown
REVEL: not shown
Quality: Poor evidence of alternate allele
Read support: 2 ALT / 19 REF (depth 21; BAM depth 16)
Source coordinates: chrX:45079352-45079353
ClinVar: likely pathogenic

Gene: CHD3
Consequence: Missense in non-canonical transcripts
Variant: not shown
Protein: not shown
rsID: not shown
Zygosity: Het
Ref Allele: G
Alt Allele: T
Freq: not shown
REVEL: not shown
Quality: Sufficient depth and allele counts
Read support: 4 ALT / 16 REF (depth 20; BAM depth 14)
Source coordinates: chr17:7884933-7884934
ClinVar: uncertain significance

Gene: ARID1B
Consequence: Inframe deletion
Variant: c.534_536del
Protein: p.His179del
rsID: rs754114025
Zygosity: Het
Ref Allele: CCCA
Alt Allele: C
Freq: 0.09465% rare (popmax 0.3077%)
REVEL: not shown
Quality: Sufficient depth and allele counts
Read support: 2 ALT / 16 REF (depth 18; BAM depth 27)
Source coordinates: chr6:156778198-156778201
ClinVar: benign/likely benign

Gene: KDM6B
Consequence: Splice acceptor variant
Variant: c.457-2A>C
Protein: not shown
rsID: rs1271434435
Zygosity: Het
Ref Allele: A
Alt Allele: C
Freq: 0.6599% uncommon (popmax 0.7769%)
REVEL: not shown
Quality: Sufficient depth and allele counts
Read support: 8 ALT / 33 REF (depth 41; BAM depth 34)
Source coordinates: chr17:7846398-7846399
ClinVar: not shown

Gene: SMARCA2
Consequence: Splice acceptor variant
Variant: c.3079-2A>C
Protein: not shown
rsID: not shown
Zygosity: Het
Ref Allele: A
Alt Allele: C
Freq: not shown
REVEL: not shown
Quality: Poor evidence of alternate allele
Read support: 2 ALT / 21 REF (depth 23; BAM depth 23)
Source coordinates: chr9:2101568-2101569
ClinVar: not shown

Gene: SETD2
Consequence: Stop gained
Variant: c.325C>T
Protein: p.Gln109Ter
rsID: not shown
Zygosity: Het
Ref Allele: G
Alt Allele: A
Freq: not shown
REVEL: not shown
Quality: Poor evidence of alternate allele
Read support: 2 ALT / 22 REF (depth 24; BAM depth 21)
Source coordinates: chr3:47124311-47124312
ClinVar: not shown

Gene: MED23
Consequence: Frameshift variant
Variant: c.2276dup
Protein: p.Asn759LysfsTer7
rsID: rs765921048
Zygosity: Het
Ref Allele: A
Alt Allele: AT
Freq: not shown
REVEL: not shown
Quality: Poor evidence of alternate allele
Read support: 3 ALT / 31 REF (depth 34; BAM depth 30)
Source coordinates: chr6:131598705-131598706
ClinVar: not shown

Gene: KDM5D
Consequence: Stop gained
Variant: c.1102C>T
Protein: p.Gln368Ter
rsID: not shown
Zygosity: Het
Ref Allele: G
Alt Allele: A
Freq: not shown
REVEL: not shown
Quality: Poor evidence of alternate allele
Read support: 2 ALT / 20 REF (depth 22; BAM depth 21)
Source coordinates: chrY:19732156-19732157
ClinVar: not shown

Gene: KDM5D
Consequence: Missense variant splice region variant
Variant: c.1090G>A
Protein: p.Ala364Thr
rsID: not shown
Zygosity: Het
Ref Allele: C
Alt Allele: T
Freq: not shown
REVEL: not shown
Quality: Sufficient depth and allele counts
Read support: 2 ALT / 16 REF (depth 18; BAM depth 15)
Source coordinates: chrY:19732586-19732587
ClinVar: not shown

Gene: KAT6A
Consequence: Missense variant
Variant: c.5090A>C
Protein: p.Gln1697Pro
rsID: rs750469825
Zygosity: Het
Ref Allele: T
Alt Allele: G
Freq: 0.02331% rare (popmax 0.0504%)
REVEL: 0.129
Quality: Sufficient depth and allele counts
Read support: 5 ALT / 26 REF (depth 31; BAM depth 24)
Source coordinates: chr8:41933130-41933131
ClinVar: not shown

Gene: TBP
Consequence: Protein altering variant
Variant: c.228_231delinsA
Protein: p.Gln95del
rsID: not shown
Zygosity: Het
Ref Allele: GCAG
Alt Allele: A
Freq: not shown
REVEL: not shown
Quality: Poor sequence depth
Read support: 4 ALT / 0 REF (depth 4; BAM depth 20)
Source coordinates: chr6:170561964-170561967
ClinVar: not shown

Gene: UGT2B7
Consequence: Missense variant
Variant: c.801_802delinsTC
Protein: p.Tyr268His
rsID: rs386675647
Zygosity: Hom
Ref Allele: AT
Alt Allele: TC
Freq: not shown
REVEL: not shown
Quality: Sufficient depth and allele counts
Read support: 29 ALT / 0 REF (depth 29; BAM depth 28)
Source coordinates: chr4:69098619-69098621
ClinVar: not shown

Gene: SETD1B
Consequence: Inframe deletion
Variant: c.3150_3191del
Protein: p.Ser1052_Ser1065del
rsID: not shown
Zygosity: Het
Ref Allele: TCATCATCCTCGGGGTCCTCAACCACCTCACCCTCGTCCTCGG
Alt Allele: T
Freq: not shown
REVEL: not shown
Quality: Sufficient depth and allele counts
Read support: 2 ALT / 18 REF (depth 20; BAM depth 31)
Source coordinates: chr12:121817540-121817582
ClinVar: not shown

Gene: NSD2
Consequence: Missense variant
Variant: c.63G>A
Protein: p.Met21Ile
rsID: not shown
Zygosity: Het
Ref Allele: G
Alt Allele: A
Freq: not shown
REVEL: 0.441
Quality: Poor evidence of alternate allele
Read support: 4 ALT / 42 REF (depth 46; BAM depth 40)
Source coordinates: chr4:1900717-1900718
ClinVar: not shown

Gene: NCOA3
Consequence: Missense variant
Variant: c.1709C>T
Protein: p.Pro570Leu
rsID: not shown
Zygosity: Het
Ref Allele: C
Alt Allele: T
Freq: not shown
REVEL: 0.211
Quality: Poor evidence of alternate allele
Read support: 2 ALT / 23 REF (depth 25; BAM depth 24)
Source coordinates: chr20:47636095-47636096
ClinVar: not shown

Gene: MYC
Consequence: Missense variant
Variant: c.454G>A
Protein: p.Gly152Ser
rsID: rs1248173307
Zygosity: Het
Ref Allele: G
Alt Allele: A
Freq: not shown
REVEL: 0.283
Quality: Poor evidence of alternate allele
Read support: 2 ALT / 22 REF (depth 24; BAM depth 19)
Source coordinates: chr8:127738671-127738672
ClinVar: not shown

Gene: MBD2
Consequence: Missense variant
Variant: c.374A>G
Protein: p.Glu125Gly
rsID: not shown
Zygosity: Het
Ref Allele: T
Alt Allele: C
Freq: not shown
REVEL: 0.394
Quality: Sufficient depth and allele counts
Read support: 5 ALT / 21 REF (depth 26; BAM depth 21)
Source coordinates: chr18:54224186-54224187
ClinVar: not shown

Gene: KCNQ4
Consequence: Missense variant
Variant: c.50A>G
Protein: p.Asp17Gly
rsID: not shown
Zygosity: Het
Ref Allele: A
Alt Allele: G
Freq: not shown
REVEL: 0.424
Quality: Sufficient depth and allele counts
Read support: 6 ALT / 29 REF (depth 35; BAM depth 29)
Source coordinates: chr1:40784143-40784144
ClinVar: not shown

Gene: KDM6A
Consequence: Missense variant
Variant: c.731C>T
Protein: p.Thr244Ile
rsID: not shown
Zygosity: Het
Ref Allele: C
Alt Allele: T
Freq: not shown
REVEL: 0.234
Quality: Poor evidence of alternate allele
Read support: 2 ALT / 20 REF (depth 22; BAM depth 17)
Source coordinates: chrX:45051785-45051786
ClinVar: not shown

Gene: HDAC8
Consequence: Missense variant
Variant: c.478C>A
Protein: p.Leu160Met
rsID: not shown
Zygosity: Het
Ref Allele: G
Alt Allele: T
Freq: not shown
REVEL: 0.642
Quality: Poor evidence of alternate allele
Read support: 2 ALT / 20 REF (depth 22; BAM depth 19)
Source coordinates: chrX:72495228-72495229
ClinVar: not shown

Gene: CYP2C19
Consequence: Missense variant
Variant: c.990_991inv
Protein: p.Ile331Val
rsID: rs1554854489
Zygosity: Het
Ref Allele: CA
Alt Allele: TG
Freq: not shown
REVEL: not shown
Quality: Sufficient depth and allele counts
Read support: 14 ALT / 0 REF (depth 14; BAM depth 24)
Source coordinates: chr10:94842865-94842867
ClinVar: not shown

Gene: AGO2
Consequence: Missense variant
Variant: c.10_11delinsAA
Protein: p.Gly4Lys
rsID: not shown
Zygosity: Het
Ref Allele: CC
Alt Allele: TT
Freq: not shown
REVEL: not shown
Quality: Sufficient depth and allele counts
Read support: 2 ALT / 11 REF (depth 13; BAM depth 11)
Source coordinates: chr8:140635496-140635498
ClinVar: not shown

Gene: AGO1
Consequence: Missense variant
Variant: c.163T>A
Protein: p.Tyr55Asn
rsID: not shown
Zygosity: Het
Ref Allele: T
Alt Allele: A
Freq: not shown
REVEL: 0.581
Quality: Poor evidence of alternate allele
Read support: 2 ALT / 23 REF (depth 25; BAM depth 24)
Source coordinates: chr1:35888564-35888565
ClinVar: not shown

Gene: COMT
Consequence: Missense variant
Variant: c.259G>A
Protein: p.Glu87Lys
rsID: not shown
Zygosity: Het
Ref Allele: G
Alt Allele: A
Freq: not shown
REVEL: 0.451
Quality: Poor evidence of alternate allele
Read support: 2 ALT / 23 REF (depth 25; BAM depth 20)
Source coordinates: chr22:19962785-19962786
ClinVar: not shown

Gene: AR
Consequence: Missense variant
Variant: c.452C>T
Protein: p.Ala151Val
rsID: not shown
Zygosity: Het
Ref Allele: C
Alt Allele: T
Freq: not shown
REVEL: 0.372
Quality: Sufficient depth and allele counts
Read support: 2 ALT / 16 REF (depth 18; BAM depth 16)
Source coordinates: chrX:67545598-67545599
ClinVar: not shown

Gene: ABCC4
Consequence: Missense variant
Variant: c.542T>C
Protein: p.Leu181Pro
rsID: not shown
Zygosity: Het
Ref Allele: A
Alt Allele: G
Freq: not shown
REVEL: 0.942
Quality: Sufficient depth and allele counts
Read support: 5 ALT / 26 REF (depth 31; BAM depth 26)
Source coordinates: chr13:95210771-95210772
ClinVar: not shown

Gene: ABCB7
Consequence: Missense variant
Variant: c.1845_1851delinsGAGAATT
Protein: p.Val617Ile
rsID: not shown
Zygosity: Het
Ref Allele: TACTCTT
Alt Allele: AATTCTC
Freq: not shown
REVEL: not shown
Quality: Sufficient depth and allele counts
Read support: 3 ALT / 20 REF (depth 23; BAM depth 19)
Source coordinates: chrX:75062412-75062419
ClinVar: not shown

Gene: ABCB7
Consequence: Missense variant splice region variant
Variant: c.247G>A
Protein: p.Ala83Thr
rsID: not shown
Zygosity: Het
Ref Allele: C
Alt Allele: T
Freq: not shown
REVEL: 0.196
Quality: Sufficient depth and allele counts
Read support: 2 ALT / 10 REF (depth 12; BAM depth 11)
Source coordinates: chrX:75112972-75112973
ClinVar: not shown

Gene: TAF9
Consequence: Splice donor in non-canonical transcripts
Variant: c.-111+236dup
Protein: not shown
rsID: rs200123392
Zygosity: Het
Ref Allele: A
Alt Allele: AC
Freq: 0.8541% uncommon (popmax 1.64%)
REVEL: not shown
Quality: Sufficient depth and allele counts
Read support: 3 ALT / 24 REF (depth 27; BAM depth 37)
Source coordinates: chr5:69369226-69369227
ClinVar: not shown

Gene: HDAC9
Consequence: Missense in non-canonical transcripts
Variant: c.1467+6128_1467+6129delinsTC
Protein: not shown
rsID: rs386710892
Zygosity: Het
Ref Allele: CA
Alt Allele: TC
Freq: not shown
REVEL: not shown
Quality: Sufficient depth and allele counts
Read support: 19 ALT / 26 REF (depth 45; BAM depth 34)
Source coordinates: chr7:18654811-18654813
ClinVar: not shown

Gene: HDAC9
Consequence: Splice donor in non-canonical transcripts
Variant: c.1468-8170_1468-8169delinsTA
Protein: not shown
rsID: rs386710893
Zygosity: Het
Ref Allele: GT
Alt Allele: TA
Freq: not shown
REVEL: not shown
Quality: Sufficient depth and allele counts
Read support: 28 ALT / 12 REF (depth 40; BAM depth 37)
Source coordinates: chr7:18658043-18658045
ClinVar: not shown

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ANYONE WHO IS CHARGING ANYTHING IN THERE IS NOT ENDORSED BY ME TO DO SO

​For a while now, discussions around the gut’s role in these conditions focused heavily on glucuronidation. While that is absolutely a vital piece of the puzzle, treating it as the whole story misses the bigger picture. Over the last two decades, medical science has realized that the gut microbiome is not just a tube for digesting food. It communicates directly with our most vital systems through the gut-brain axis, the gut-liver axis, and the gut-heart axis.

​When we look at PFS and PSSD through this lens, it becomes clear that the gut microbiome might actually be the engine driving and sustaining these relentless symptoms. Through a chaotic mix of immune, hormonal, and epigenetic mechanisms, the gut can keep the body trapped in a state of dysfunction. We are seeing these exact same mechanisms being brought to light by researchers studying Chronic Fatigue Syndrome (CFS) and Long Covid.

​1. The Disappearing Shield and the Rise of Dysbiosis

​Finasteride does not just lower hair loss hormones. It crashes critical neurosteroids like allopregnanolone and DHT. Think of these specific compounds as the protective armor for your gut lining and its local immune system. When Finasteride drops that shield, the gut environment changes drastically. The friendly, supportive bacteria die off, and opportunistic, unhelpful strains take over, creating a state of dysbiosis. It is highly likely that the medication worsens an existing gut imbalance. In fact, having a fragile, imbalanced microbiome to begin with might actually be the hidden risk factor that tips someone into full-blown PFS in the first place.

​2. The Missing Biological Keys

​A healthy gut microbiome produces short-chain fatty acids, with butyrate being one of the most important. Butyrate acts as the body's natural mechanic. It is an HDAC inhibitor, which is a scientific way of saying it is a biological key that unlocks and turns on genes that have been silenced. In a depleted PFS microbiome, you lose this crucial molecule. Without butyrate to flip the switch, the genes responsible for producing and utilizing androgens stay locked in the "off" position, keeping the body trapped in a suppressed, silenced epigenetic state.

​3. The Second Brain's Panic Mode

​The gut is often called our second brain, and it actually manufactures its own neurosteroids and calming chemicals, specifically those that bind to our soothing GABA receptors. When dysbiosis sets in, this localized chemical factory breaks down. The gastrointestinal tract stops producing these calming signals. This robs the body of its natural brakes, leaving the nervous system locked in a state of high alert. This localized starvation of calming neurosteroids drives the relentless anxiety, panic, and neuroendocrine dysfunction that so many people experience daily.

​4. The Recycling Plant Gone Rogue

​We also have the issue of hormone recycling, driven by a specific community of gut bacteria known as the estrobolome. When certain dysbiotic bacteria overgrow, they overproduce an enzyme called beta-glucuronidase. This enzyme essentially unpacks hormones and toxins that your liver has already boxed up for the dumpster. Instead of leaving the body as waste, these active hormones are reabsorbed straight back into the bloodstream, creating a toxic, endless loop of hormonal imbalance.

​5. The Leaky Roof and Brain Fire

​Perhaps the most devastating impact of all is the "leaky gut" phenomenon. When the intestinal barrier becomes weak and compromised, bacterial toxins called lipopolysaccharides (LPS) escape the gut and spill directly into the bloodstream. Your immune system reacts violently to this invasion, triggering massive systemic inflammation.

​This inflammation travels up to the brain, breaches the blood-brain barrier, and activates microglial cells. You can think of microglia as the brain's immune system alarm bells. Once they start ringing, the fallout is staggering:

​Dopamine Dysregulation: The inflammation scrambles reward pathways, creating profound anhedonia, emotional numbness, and a total loss of libido.

​BDNF Drops: Brain-Derived Neurotrophic Factor is essentially miracle-Gro for your brain. When inflammation tanks your BDNF levels, your brain loses its plasticity, leading to the heavy, suffocating brain fog characteristic of PFS.

​Sympathetic Overdrive: The nervous system is forced into a permanent fight-or-flight state. This chronic tension directly fuels physical symptoms like erectile dysfunction, pelvic floor tightness, and premature ejaculation.

​Why the Whole Ecosystem Matters:

​This interconnected web perfectly explains why CDG does not work for everyone. CDG is a great tool for targeting the beta-glucuronidase recycling problem, but taking it is like using a bucket to bail out a flooding river while the dam is still broken.

​On the other hand, Fecal Microbiota Transplants (FMT) have shown real promise for some sufferers because they do not just patch a single leak. FMT introduces an entirely new, functioning ecosystem to replace the damaged soil of the gut.

​Huge credit to u/bturner534 for laying the groundwork on these concepts. We are finally starting to view this condition not just as a localized issue, but as a system-wide crisis centered right in the gut.

I’m curious how people here think about the risk-benefit calculation around SSRIs now that PSSD is receiving more recognition.

I have fairly severe OCD, specifically a sensorimotor/metacognitive presentation. I’ve tried therapy, lifestyle changes, NAC, and I’ve been taking 30 mg of buspirone for months without any meaningful improvement. At this point, an SSRI is the obvious conventional next step, but the possibility of persistent sexual dysfunction is the main thing stopping me.

I understand that nobody can give me a reliable personal percentage of developing PSSD, and I’m not asking Dr. Powers or anyone here for individualized medical advice. I’m more interested in the general decision-making framework.

Currently, I suffer immense amounts of pain due to my OCD, which causes (or is caused by?) my anxiety and situational depression. I have been told by many people including my Psychiatrist that I should try an SSRI. Should I? What is the smartest move to make?

Hi Dr P, this write up is from Discord user @jungledude2004 (he doesn’t have Reddit anymore as doesn’t want to ruminate, so I am posting on his behalf).
He believes these findings will be helpful.

(He wanted me to note that he didn’t use AI. He originally wanted to format it with AI, but ExcellentPush said you would rather him write it up naturally and leave it as is).

As always, appreciate the work and focus you give to our community. You have given so many of us hope.

“Dearest William,

I found this fuckass condition on the internet and it’s really similar to what PFS/PSSD people deal with.

One of the most harrowing symptoms of post-drug syndromes is the sheer mental torture many individuals face, such as: anhedonia, low motivation, and a lack of thrill, to name just a few. While these symptoms can cause huge changes to someone's lifestyle, they need not be permanent.

An interesting aspect of PFS/PSSD is how much it shares in common with another condition: Hepatic Encephalopathy (HE). HE is characterized by the liver's inability to get rid excess of neurotoxic substances accumulating in the brain, with symptoms including mood disturbances, anhedonia, and tremors.¹ This overlaps closely with what's reported in PFS/PSSD. Excess GABA-A activity has been linked to the cognitive impairment and sedation seen in HE patients.²

Neurosteroid changes appear to drive this effect. In one study, brain levels of pregnenolone, allopregnanolone, and THDOC were elevated 2.6-fold, 1.7-fold, and 4.7-fold, respectively, in a rat model of HE — concentrations high enough to meaningfully enhance GABA-A receptor activity.³ Similarly, allopregnanolone and THDOC levels in mice with toxic liver injury induced HE produced sedation and elevated allopregnanolone has also been found in autopsied brain tissue of cirrhotic HE patients. THis has lead researchers to propose that the increased GABAergic tone seen in HE stems from these elevated neurosteroid levels.²

One of the key boogeymen in Dr Powers Theory is THDOC. Potential treatments for this kind of neurosteroid buildup include NSAIDs such as indomethacin.³⁻⁵

References
Mayo Clinic Staff. "Hepatic Encephalopathy." Mayo Clinic, 31 May 2025, mayoclinic.org/diseases-conditions/hepatic-encephalopathy/symptoms-causes/syc-20583828. Accessed 18 Aug. 2026.
Ahboucha, Samir, Gilles Pomier-Layrargues, and Roger F. Butterworth. "Increased Brain Concentrations of Endogenous (Non-Benzodiazepine) GABA-A Receptor Ligands in Human Hepatic Encephalopathy." Metabolic Brain Disease, vol. 19, nos. 3–4, 2004, pp. 241–251.
Ahboucha, Samir, et al. "Increased Brain Levels of Endogenous Neurosteroids in a Rat Model of Hepatic Encephalopathy." Neurochemistry International, vol. 52, no. 4–5, 2008, pp. 605–612. PubMed.
Butterworth, Roger F. "Neurosteroids in Hepatic Encephalopathy: Novel Insights and New Therapeutic Opportunities." The Journal of Steroid Biochemistry and Molecular Biology, vol. 160, 2016, pp. 94–97. https://doi.org/10.1016/j.jsbmb.2015.11.006.
Ahboucha, Samir, et al. "Neurosteroids and Hepatic Encephalopathy: An Update on Possible Pathophysiologic Mechanisms." Current Molecular Pharmacology, vol. 1, no. 2, 2008, pp. 127–135.”

I have mild-ish PSSD. Hypothesia, pleasureless orgasm, low libido (however extreme emotional numbing).

For 3 months now I have these days where my brain kinda has a light switch turned off and I get really bad PSSD symptoms as mentioned above. I literally feel it happen and it's like i've been drugged. I cant feel anything at all and I feel "heavy".

Then I start getting these panic attacks when I come out of it every single time. I have panic attacks often since Ive been off but propranolol usually helps. In these panic attacks, they DONT. It only helps the heartrate.

The panic attack symptoms: sounds feel like daggers, like extremely irritable and scary to me. Racing thoughts, walking around feeling wired. Breathing becomes harder. This weird magnet feeling on my head. And it lasts for like an hour. DPDR goes up too. Tingly feelings around my body. Way worse orthostatic hypotension.

But thing is afterwards my PSSD symptoms are alleviated more. I get actual orgasms, my libido is slightly better, the emotional numbing is a bit better, and my head doesn't feel heavy. Happens every single time I get these kinds of panic attacks.

My idea is that glutamate becomes higher in these moments from GABA going down (because recovery; its bound to change the chemicals) and that GABA being alleviated helps my symptoms as it might be the source of my PSSD?

I wasn’t sure where else to ask about this. I’ve been wondering a few things about bicalutamide.

So to my understanding, bicalutamide does not work by lowering overall T, but instead by blocking androgen receptors.

I would assume this leaves testosterone to be bound to SHBG, which also increases free estradiol percentage.

Is that assumption correct?

Would this result in more bioavailable E2 than monotherapy?

Hey im a pfs patient and I was on trt for about 6 weeks and quit because Dr.Powers said it could be bad. I then proceeded to also start using calcium d glucarate daily, today was my last dose. For context I stopped trt around 3 weeks ago which means the trt is mostly out of the system by now meaning my test levels are probably very low. My testicle do feel alot fuller so im assuming my natural production is kicking in. However this past week ive had 3 episodes of what I can only describe as fasting hypoglocemia. If I go more than 4 plus hours sometimes 5 or 6 my heart will begin slowly beating fast, then I'll feel like I gotta breathe deeply, slowly it transitions into shakiness and ultimately anxiety. It always stops once i eat if it gets that bad I'll have a sugary drink to get me out of it so I know it has something to do with glucose. Will CdG and quitting trt cause this? Im a fairly healthy guy (despite pfs) and ive fasted before whole days and donde 0 carb diets and never expirienved any of this. Im very concerned. Today ive had snack throughout the day to feel fine and havent felt anything, but im still very worried. Id Dr.Powrers or anyone can let me know it'll be much help.

How about castration trials. I have seen only one testimony until now. Did I miss other testimonies, still ongoing or didn’t it work after all?

Anyone else share this? I took finasteride 7 years ago and feel like i'm slowly getting worse. I measured my night time erections and barely got any, I am on cialis too.

Hey Everyone,

I built a search tool with the recovery database I made a while back. I cleaned up a lot of false entries (I used programming to extract stories— didn't have a 100% success rate) and tidied things up, so it should be good to go. There are over 800 recovery stories. You can sort by diagnosis, treatment, and recovery level.

Check it out here: https://www.postexposurefoundation.com/recovery-database

Also, I am a one man band and I can make mistakes. If you see anything that looks off or a duplicate— just DM me or contact me via the website :) I hope you find this helpful!

PFS is so weird. The body still seems to work yet no libido. Also no morning erections despite daily nocturnal ones...

what test should I consider before considering a protocol. I’m a severe long hauler w PFS/PSSD. Thenk you i am looking forward to more information coming out from the patients going through Castration protocol.

It’s been a while since I’ve last been on this sub, so I just wanted to give an update about how I’m doing ever since I saw results with pimavanserin.

For those who haven’t read it, basically: SSRI induced anhedonia; took pimavanserin; (practically) fully treated

If I mention some things which conflict with my previous post without mentioning it, I apologise as my recall is terrible - just take this post as authoritative.

Non-sexual-anhedonia wise, I’d say I’m about 95% of the way there to being fully normal. I don’t think I’ll get that last 5% but I’m so okay with that, given how I was 0% six months ago. I’ve picked up hobbies I dropped years ago, I WANT to do so many things now (as opposed to out of habit or necessity) and overall I’m just happier. I’m to the point where a good song will have me dancing in the mirror, or if I’m really enjoying an activity I’ll start humming or singing. Cheesy but accurate.

Sexually, the case is interesting. Libido wise and Mechanistically, I’m normal - but the actual act (eg sex, masturbation) isn’t pleasurable. This is something I’m working on fixing independently. Pimavanserin hasn’t fully treated this specific symptom, although in terms of desire it has significantly restored the “wanting” sexual aspect. This somewhat makes sense, given how Pimavanserin works pharmacologically.

I don’t take Pimavanserin anymore and I’ve noticed no worsening of symptoms.

I want to clarify that my response is probably at least partially idiosyncratic. I had no depression (never had and still don’t) and my anhedonia was purely induced by an SSRI. Please don’t assume it’s a blanket fix for all anhedonic phenotypes, especially ones with depression (Pimavanserin failed its stage 3 clinical trials as an adjunct for depression). Also, I never lost my consummatory pleasure, at least not in the same way my anticipatory pleasure took a massive blow. Even at my worst, food still tasted good and music was nice to listen to, even if I physically could not get out of bed. I wouldn’t expect Pimavanserin to restore consummatory pleasure as much as it would desire and wanting - for example it made me want sex more but the act is still blunted.

Please ask any questions you might have.

The worst part of PSSD for me is the emotional numbing and lack of connection to loved ones. Is this being looked into? Or just the sexual side effects? Because i think everyone with severe PSSD would agree that they would take numb genitals and the full sexual symptom package over not feeling human due to lack of emotions, empathy and all of that.