Hello people, I've been rehabbing hypermobility for a while with great results but on forearm extension work my innermost extensor (of the digitorum or indicis) always pops on both hands, it very rarely causes pain and if it does it never lasts but I was wondering if anyone had any experience with this kind of popping and how they got around it
Anyone know why this happens and how to fix it?
I redownloaded the BAM several times
While I was taking Decapeptyl I started manifesting Gilbert Syndrome (later confirmed in my genome), due to some family drama I couldn't take HRT and did not take an initial AA to suppress the LH/FSH surge that GnRH agonists cause at the start, but despite that I instantly got ED, does anyone have a clue why that could be?
Could you check your called varients, on whether or not you have a 0.0 Alelle Frequency mutation at UGT2B7?
Our PFS and PSSD friends noticed they have it and I want to call more attention to it, to see whether or not it's a glitch
Please post your results as a reply to Powers's post
Let's hope some good comes out of it
I was always Hypermobile, mainly in my fingers and hips, but never had any pain, and don't pass the Beighton scale
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6 months on E and suddenly both my hands are wrecked, ECU subluxations, DRUJ instability, but I'm unsure whether to attribute it to laxity or not as I would expect pains to be well... In places I already was flexible in
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I'm a pianist and a gamer, but these are not necessarily pianist or gamer injuries, and they came so suddenly, does anyone have any experiences or support mechanisms?
Finally got my sequencing done, what would an average gene.iobio database look like? Am I expecting super high revel scores? High impact scores? ClinVar Pathogenicity reports? So far I don't feel like anything pops out, it probably shouldn't, but where exactly should I tune my attention?
SNPeek screams many reports at me, same with Genetic Genie, with here it's way more subtle, so also supposedly more nuanced
Sometimes it feels like I'm looking at someone else's Genome, the mutations on Gene.iobio look different than what I see elsewhere
Reading up on SHBG yields mixed results, some papers correspond to the powers method where only the bioavailable hormones yield an effect and knocking out the carrier proteins only removes the buffer while others suggest an endocytosis pathway is more important through Cublin/Megalin
How does Powers address this? It seems like the Free Hormone Hypothesis is just widely accepted here but I never saw it talked about, everybody seem to just look at SHBG as the end all be all, would really appreciate reading materials
Pathway viewer (https://pathway-viewer.toolforge.org/embed/WP697) is great, but it doesn't show the average levels, so it's hard to know how relevant each metabolite is.
Is 4 hydroxyestrone 3 glucoronide actually a relevant ending of a pathway or does it only represent 0.1% of estrone being metabolized? How water soluble is Estradiol Glucuronide compared to 4 Methoxyestradiol 2 Glucuronide? I could use intuition but I'd really prefer having something concrete
I'm self teaching so I'm not sure if this is the correct way to try and look at it so if anybody could steer me and set me off in the right direction, it would be greatly appreciated! :3
What does powers first recommend to combat SHBG?
Allowing T to rise or supplementing 20 mg of Boron?
9 months HRT
I take a 2 mg pill at morning and 2 2 mg pills at night as well as 6.25mg CPA every two days
My E is at 154 pg/ml and T (free and total), LH, FSH basically zero
SHBG was 124 nmol/l
Progress more or less stalled for 5 months until I reduced the CPA dosage to every two days instead of every day
Planning on switching to patches due to first pass effect plus more consistent levels (If anyone knows whether Sandoz or Estradot is better I appreciate any experiences)
Will also try Boron and letting my T increase a little somehow, afaik CPA halflife is around 40 hours so I am not sure about once every 3 days, I also cannot cut it into more than 4 pieces
I thought I more or less understood SHBG until I read this quote from the DHT backdoor Wiki page:
"Sex hormone-binding globulin (SHBH) transports the majority of circulating T to the cells of androgen target tissues, where it is then 5α-reduced to DHT."
Why does T not get transported in Albumin for example? I know the SHBG - Testosterone affinity is high but that should also technically make it a worse carrier for it as it's harder to diffuse into the cell
I understand that for us we are following more direct gene associations relating to our transition, as opposed to the techbro longevity BS most people look for, but with the amount of false positives/negatives I've been hearing about, how useful is it really?
Happened to me for the first 4 months of HRT or so, then just went away
I would just go about my day when suddenly I would notice I'm really yellow, or someone would point out I look like a ghost, only lasted for a couple minutes at a time tho
You're telling me this has a Korean in it??!?
Made with a friend
