@Starcrossed
Doesnt necessarily suggest hypothyroidism, but with other stuff mentioned i guess u might be mildly hypothyroid (you have good high pulse, oral temp range, t4 and t3 not obviously skewed maybe slightly depends, tsh only a bit elevated, but blood loss adrenaline cold if u still are etc -
so maybe but not obviously hypo)
More salt can be helpful for the fight or flight thing as if you do have some level of hypothyroidism , sodium gets wasted more easily so isnt countering adrenaline well without replenishing often, (taking thyroid can increase adrenaline sensitivity too so more need for salt, but also lowers cortisol).
some people move up doses every 2 weeks until desired effect or hit a total of 25mcg - 50mcg t3 in multiple doses depending on severity
Theres some positive studies using vit A or vit D for abnormal menstrual bleeding. and vitamin b1
vit b1 https://pubmed.ncbi.nlm.nih.gov/24738933/
vit d https://www.jcdronline.org/admin/Uploads/Files/6564af6091d0d1.39699188.pdf
vit a (if fixing low levels) (these are extreme doses i wouldnt take but looks very helpful in potential, high doses get toxic so i would like to keep it under 5000iu, as even 10,000iu has some inflammatory / toxic potential) https://journals.co.za/doi/pdf/10.10520/AJA20785135_24314
Might be worth eating beef or sheep liver (in balance) if you dont, which gives Vit A, and copper, and a little iron.
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And if those 3 arent enough 2 targets may be 1. things that help mature blood vessels / stop leakiness. and 2. things that lower eNOS & nitric oxide , shown here to relate to the endometrial breakdown https://pubmed.ncbi.nlm.nih.gov/9915994/ and mentioned lower in this post too (need vasoconstriction in a specific place to stop bleeds which nitric oxide counters)
Some idea of mechanism (failure of vessels to mature so theyre more permable?) (or failure of spiral arterioles to constrict because of too much nitric oxide?)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10320491/
This review supports existing evidence that increased proangiogenic and decreased antiangiogenic factors cause impaired vessel maturation, resulting in more fragile and permeable vessels.
Conceivably, the genesis of AUB in patients with AUB-E and AUB-I is caused by a different combination of abnormalities in angiogenic factors. In general, VEGF expression increased and Ang-I decreased in patients with objectively defined AUB-E: this could suggest decreased vessel maturation in these patients. In patients with AUB-I, angiogenic factors were increased after short-term exposure and unchanged after long-term exposure to exogenous hormones. This could be in agreement with the fact that spotting complaints with exogenous hormone use gradually disappear over time (Hillard, 2014) and, hypothetically, angiogenesis in the endometrium will normalize. However, these findings should be interpreted with caution and do not imply causation.
Vasoconstriction of spiral arterioles is essential to limit menstrual blood flow, as a small increase in diameter will lead to an extensive increase in blood flow. For instance, if the diameter is increased 2-fold this will lead to a 16-fold decrease in flow resistance (Jain et al., 2022). Blumenthal et al. (2002) found an increase in eNOS in both the secretory and proliferative phase in patients with AUB-E (Blumenthal et al., 2002). As eNOS produces NO and NO increases vasodilatation, HMB could hypothetically be caused by an increase in spiral arteriole diameter under the influence of increased NO levels (Jeremy et al., 1999; Valdes et al., 2008). This could indicate that, apart from angiogenesis, several other mechanisms are involved in AUB.
. It is likely that in patients with AUB-E and AUB-I, a combination of different angiogenic mechanisms may play a role. This could be one of the explanations for why increased angiogenesis is not always associated with a change in MVD but could lead to vessels of insufficient quality or unstable vessels with an impaired function.
Cessation of menses requires (i) vasoconstriction of specialised endometrial spiral arterioles, (ii) an effective haemostatic response, including repair of damaged vasculature and (iii) timely reepithelialisation of the remaining denuded basal endometrium. This unique, scarless repair process is essential to maintain fertility and limit menstrual blood loss