Hi Tc,
Apologies for the extremely long post. Yesterday I took the liberty to read your initial posts to get a better picture of your situation. I'm so sorry you've been struggling for a whole year after your oophorectomy.
These are just random thoughts, but maybe one of them can shed a light on your ongoing issues.
FSH has a very complex and yet to be fully understood molecular regulation. Have a quick look at this article, it's very techy, but it's good to give you the general idea.
https://jme.bioscientifica.com/view/journals/jme/60/3/JME-17-0308.xmlRegarding Gilbert's Syndrome (I prefer that term), considering it a ‘benign' condition doesn't really help. Not that it's a ‘malignant' condition. It's a genetic variation and it should be taken into consideration and be properly investigated. This link shows how common it is and yet it's generally disregarded by patients and medical staff. It might not cause any trouble UNTIL another condition comes into play.
https://rachelarthur.com.au/a-hat-trick-week-for-gilberts-syndrome-guys-and-gals/Gilbert's importance regarding drug metabolism.
https://www.gpnotebook.co.uk/simplepage.cfm?ID=-1596981241‘Although Gilbert's syndrome does not lead to progressive liver damage it has attracted attention regarding the pharmacogenetics of drug metabolism.
Apart from being the only physiological UGT capable of bilirubin glucuronidation, UGT1A1 also catalyzes the glucuronidation of
2-hydroxy-estrone and estradiol, and a number of therapeutic drugs such as ethinylestradiol, gemfibrozil, metabolites of irinotecan, simvastatin and buprenorphine'
You have mentioned an eating disorder on one of your previous posts. I don't know if you really had/have an eating disorder, but this article's description of endocrine manifestations of eating disorders is strikingly similar to your current blood tests results and symptoms.
https://academic.oup.com/jcem/article/96/2/333/2709494Endocrine Manifestations of Eating Disorders
The important bits:
'Anorexia Nervosa
The gonadal axis
The primary changes in this axis are described under hormonal changes. Secretion of androgens including in particular testosterone is deficient in this syndrome, suggesting that gonadal sources are compromised. Although smaller longitudinal studies suggest compromise with improvement in recovery, adrenal precursors appear to be normal in large cross-sectional studies. Low estradiol levels are also seen in anorexia due to a lack of ovarian stimulation. However, estrogen metabolism is also altered. Estradiol, which normally undergoes 16α-hydroxylation, is channeled to 2-hydroxylation and the formation of a
catechol estrogen (2-hydroxyestrone) in the undernourished state. This compound has no intrinsic biological activity and acts as an antiestrogen. Thus, the very low estrogen levels seen in anorexia are compounded by an endogenously produced antiestrogen. The lack of adipose tissue may also contribute to the hypoestrogenic state by limiting the extraovarian sources of estrogen because fat converts androstenedione to estrone and testosterone to estradiol.
Bone
Considerable confusion in the pathogenesis of bone loss in anorexia nervosa has led to the widespread belief that estrogen replacement will prevent bone loss. Multiple randomized studies have shown, however, that neither estrogen replacement nor oral contraceptive therapy is effective and, in fact, bone loss and fractures may continue in treated women.
These observations would suggest that estrogen deficiency alone cannot explain the skeletal findings in anorexia nervosa. In the pure hypoestrogenic model, both formation and resorption of bone increase. In contrast, anorexia has been associated with an uncoupling of markers of bone turnover and with a suppression of bone formation that reverses with refeeding. This appears to be the dominant mechanism. Bone resorption on the other hand is increased and does not normalize until menses return, associated with endogenous estrogen secretion. However, it is possible that the restoration of menses is associated with improvement in the secretion of
other important neuropeptides that may positively affect bone mass.
Androgens, which also have an anabolic effect on bone, are also known to be depressed in anorexia nervosa. However, a 1-yr randomized study of oral dehydroepiandrosterone did not demonstrate significant effect of treatment. A 3-wk study with testosterone administration also did not have consistent effects on bone, but
mood was improved .
This link is old but it shows how liver issues can affect oestrogen and FSH blood levels.
https://aasldpubs.onlinelibrary.wiley.com/doi/pdf/10.1002/lt.20160Increase in oestrogen and FSH after liver transplant:
‘In addition, FSH increased after OLT (orthopedic liver transplantation) in both postmenopausal and premenopausal women, suggesting central suppression of the hypothalamic–pituitary function in female patients with advanced liver disease, a mechanism for which there is also some evidence in male patients with chronic liver disease.'
According to this NHS presentation, a prolactin test is recommended
https://heeoe.hee.nhs.uk/sites/default/files/clark_anna_womens_health_02.03.2017.pdfGilbert's is such an interesting condition, it has been associated with protection against some diseases.
http://www.medsci.org/v16p0135.pdfMaybe you need lower oestrogen doses, it may seem counterintuitive, but hormone regulation is extremely fine-tuned. This article is about transgender, but I have decided to post it because while looking for ‘low FSH and low oestrogen' on the internet, I was astonished by the number of transgender forums and articles hits.
http://www.scielo.br/scielo.php'script=sci_arttext&pid=S1807-59322018000100221Finally, I congratulate you for reading this post
BeaR.
Author
Topic: What the heck is my body doing (Read 10349 times)