I was diagnosed 4+ years ago. I am 23 and have been putting off hormone therapy for a while with the help of Yaz. It bought be 3 years between my last surgery and the way I felt during my last period.

My doctor is a wonderful Endo Specialist and it took me a while to get to him, so I know I have picked the right one to trust with continuing my care. He has now told me that due to my recent symptoms, I should definitely consider one of the two options. I do not want to go back into surgery, but I also am scared of the hormones.

The side effects are so horrendous that I don't even think there's a 'lesser evil' of the two. I thought maybe you guys would help, not by deciding for me (obviously) but telling me about your experiences with one or the other so that my final decision will be based on a real experiences (other than reading and research). Please tell me your stories. Much love and respect.

TL;DR Tell me your experience with both drugs, do I want progesterone or the other fake menopause hormone?

Hi all

This isn't necessarily related to being trans, but it could be, and many of us here have ended up veritable experts on endocrinology over years of HRT, so hoping one of you may be able to shed light on what's causing my dodgy hormone levels!

In a nutshell I've got:

Prolactin - Very high (for over 6 months) FSH - Low LH - High T - Normal E - Normal SHBG/Thyroid hormones - Normal

It's confusing on a few levels. Firstly high prolactin (especially at my levels and for over 6 months) should be suppressing T and FSH/LH but it isn't?

Secondly FSH/LH levels should be the same as each other. They should either both be high or both be low, not one of each!

I have suspected klinefelters so hoping to have a karyotype test soon, but I don't know if that could cause this. Doc also wonders if I have a pituitary tumour, but that doesn't explain the FSH/LH.

Thanks!

P.S. I've been on finasteride for a couple weeks, not started E yet.

http://psycnet.apa.org/psycinfo/2005-01705-011

I understand that since Annovera lasts for a full year (compared to Nuvaring that only lasts a month) it would have more restrictions, but 2 hours vs 48 hours is a very drastic difference.

Annovera does release slightly less estrogen than Nuvaring (13mcg vs 15mcg), but it also releases more progestin (150mcg vs 120mcg), so I don’t feel like those slight variances would make that much of a difference.

Is Annovera just being overly conservative with the adherence guidelines since it’s new? Or is there really that much of a difference between the two of them, and if so, why?

EDIT:

First, when I say “can be removed for x hours/month,” I meant during the 21 day period you are supposed to have it in. I am aware you are supposed to remove it during the break week, but I am not talking about that.

Second, Many of you pointed out that on the Nuvaring website it states it cannot be removed for >3 hours, however, both Planned Parenthood and UC Berkeley state that it is still effective for up to 48 hours. So a follow-up question would be why do both Berkeley and Planned Parenthood (both reputable sources) state 48 hours as the limit?

EDIT 2: Okay I’m tired of people saying “are you sure you interpreted Planned Parenthood/Berkeley correctly?” So here is a direct quote from the Berkeley source listed above:

>> [for] delayed insertion of a new ring or delayed reinsertion of a current ring for <48 hours since a ring should have been inserted • Insert ring as soon as possible. • Keep the ring in until the scheduled ring removal day • No additional contraceptive protection is needed

And a quote from Planned Parenthood:

>> ...sometimes the NuvaRing might slip out of your vagina. If the ring has been out of your vagina for less than 2 days, rinse it in cool water and put it back in right away. If you put it back in within 48 hours, you’ll still be protected from pregnancy.

EDIT 3: CDC and WHO (see page 52) also recommend the <48hr rule

I noticed there are no discussions regarding GHRP and cardiovascular health.

GHRP has profound effects that people with heart failure may potentially benefit from.

I don't want to cite all the studies. Just Google "ghrp heart" and you will see some promising information.

I figured I'd bring some awareness to some.

Hi all, I am hoping to gather feedback on a theory I have regarding cortisol. The literature informs us that secretion of adrenocorticotropic hormone (ACTH) stimulates secretion of cortisol by the adrenal glands - this action is mediated by the hypothalamic-pituitary-adrenal (HPA) axis.

https://pubmed.ncbi.nlm.nih.gov/27104844/

The HPA axis is influenced by; the hypthalamus, the pituitary gland and the adrenal glands.

https://www.sciencedirect.com/topics/neuroscience/hypothalamic-pituitary-adrenal-axis

My hypothesis is that you aim to dampen the potential of hpa-axis hyperactivity and attenuate HPA dysregulaton - this accomplished by controlling ACTH release using a corticotropin releasing hormone antagonist or a drug which operates akin to a CRH. What are the opinions and thoughts on this approach?

thanks in advance