Why not hormone replacement therapy for elderly patients?

With your history of TIAs, hormones seem very risky, regardless of your age. Have u tried other, nonhorminal medications?

Fezolinetant, an med designed for hot flashes, is the most effective nonhormonal medicine in population studies to stop hot flashes and increase sleep. Studies of populations doesn’t mean it’s necessarily the correct medication for any specific individual. You may need to experiment with your doctor and try a variety of meds, either alone or in combination, but I can tell you that in my practice I never had a patient with your story whose symptoms I couldn’t improve. In most I could resolve the symptoms entirely.

Gabapentin reduces flashes by half generally. It is also sedating and aids sleep. Sometimes it can be combined with doxepin, another sleeping aid, at low doses.

SSRIs/SNRIs (antidepressants ) like venlafaxine or paroxetine offer relief, though milder than hormones.

If a patient was only partially controlled, sometimes I would add clonidine, though this is a blood pressure lowering medication so if your BP runs in the low side, I would avoid it.

This is all to say thee are many alternatives to hormones. They might not work quite as easily as hormones. But they do work.

@laura1970
1. Risky how?
2. What is your field, that you have patients?
3. I had great experience 11 years on loestrin and would rather stay with a tried and true drug then play with unknowns.

First, loestrin is generally considered a birth control pill which generally have more estrogen than typical hormone replacement therapy for post menopausal women. tIAs are a “pre-stroke” as it were. Those with a history of TIAs have a markedly increased risk of stroke. Tias and strokes are thrombotic events, thrombus essentially means clot.

Combined oral contraceptives (as well as typical HRTs) like Loestrin elevate stroke and myocardial infarction risks, with relative risks doubling in certain users. Loestrin is contraindicated in women with a history of cerebrovascular disease, such as TIAs, due to heightened arterial and venous thrombotic risks. there are warnings in the papers that come in the box against use in those over 35 with risk factors like smoking or hypertension. Women using combined oral contraceptives face a 1.6- to 2-fold increased risk of ischemic stroke and myocardial infarction compared to non-users, with greater elevation in older age groups or those with prior vascular events, such as TIAs. TIAs signal underlying prothrombotic tendencies exacerbated by hormonal contraceptives, raising recurrence odds without discontinuation. For women over 65, estrogen-progestin combinations amplify thromboembolism risks beyond typical contraceptive populations.

There are many very large large well done studies to confirm these risks. Please discuss with an internist, gynecologist, cardiologist, or neurologist.

I am not telling you to change your medication, but please discuss with your doctor.

I am a disabled internist, I did a lot of hospital work and also had a private practice. My hospital work was at a large cardio thoracic surgery hospital, but I don’t practice now and I’m not dispensing medical advice, just recommending that you discuss this with your doctor. The sooner the better.

Have you considered that adderall is a stimulant and may cause or worsen hot flashes?

@laura1970 Loestrin is known as a low- or ultra-low-dose pill, meaning it has a lower amount of estrogen than regular birth control pills.
"Those with a history of TIAs have a markedly increased risk of stroke."
This is untrue.
"I’m not dispensing medical advice"
Except you are.

@jlam1950

I did not interpret the info given as medical advice. I am grateful for any relevant shred of info so that can be a better advocate and question asker when I am seeing my doctors.

I'd like to offer a gentle reminder of the community guidelines, particularly number 4. (https://connect.mayoclinic.org/blog/about-connect/tab/community-guidelines/)
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@laura1970
If you're going to say there are many studies I think you should cite your sources. That's not the research I'm coming across. Except in very old studies not recent. Plus I'm trying to balance out sleeping well without hot flashes without brain fog to make a differential diagnosis whether I've even had Tia's. I am not interested in only one person's reactions I would like a variety of people to respond

@jlam1950
https://link.springer.com/article/10.1186/s12905-023-02788-0
Meta analysis 2024
“ Compared with placebo (or no treatment), MHT was significantly associated with the risk of stroke in the overall population of postmenopausal women”
https://www.ahajournals.org/doi/full/10.1161/CIRCULATIONAHA.122.061559
2023. This article has is an excellent source for the history of the various large studies that guided treatment use. I have enclosed a few quotes. Please also note in the image, which is from this study, recognizes TIA as high risk for HRT

“ It is appropriate that no medical societies currently recommend HT for the primary or secondary prevention of cardiovascular disease (CVD”

“ Two decades later, in 1998, the HERS trial, the first randomized trial of EPT versus placebo for the secondary prevention of coronary heart disease (CHD) events among postmenopausal women with established CHD, found no overall cardiovascular benefit and a pattern of an early increase in CHD events with HT use, arguing against the initiation of HT for secondary prevention of CHD.5 The HERS data led to a slight reduction in HT-prescribing rates after its publication, but the early termination of the landmark Women’s Health Initiative (WHI) EPT trial in 2002, a primary prevention trial,6,7 led to a dramatic decline in the use of HT worldwide”
“ The WHI randomized trial enrolled women without CVD between 50 and 79 years of age and represents the largest randomized placebo-controlled trial of systemic HT designed to evaluate the risks and benefits for the primary prevention of chronic diseases, including CVD.6,7 Women with a uterus were randomly assigned to continuous combined oral CEE with medroxyprogesterone acetate (MPA; CEE+MPA) or placebo, and women without a uterus were randomly assigned to CEE alone or placebo. The initial publications that detailed WHI findings in 2002 (CEE+MPA) and 2004 (CEE alone), with a median age of 63.2 and 63.6 years at the time of enrollment, respectively, aggregated participants of all ages, and reported that compared with placebo, risks of CHD, stroke, and venous thromboembolism (VTE), including pulmonary embolism, were increased with HT”

“ Expert opinion suggests that it is reasonable to lower the dose of HT or discontinue HT after several years of use”

“ The WHI clinical trials found that women with metabolic syndrome randomly assigned to CEE+MPA and CEE alone compared with placebo, had a 2-fold increased CVD risk”
https://www.frontiersin.org/journals/rehabilitation-sciences/articles/10.3389/fresc.2022.825147/full
A review article 2022
“ late post-menopausal women (i.e., >10 years since menopause onset), there was no change in CVD risk and mortality with HT, though there was an increased risk of stroke and venous thromboembolism “
https://www.ahajournals.org/doi/full/10.1161/STROKEAHA.121.038659
2022
“women exposed to HRT had a significant higher rate of ischemic stroke (HR, 1.12 [95% CI, 1.01–1.24]”

“ The increased hazard rate remained significant only for any stroke during remaining years of exposure (HR, 1.18 [95% CI, 1.05–1.32]; Table S8; Figure 2B). After discontinuation, women who had been exposed to HRT continued to have a higher hazard rate of any stroke (HR, 1.16 [95% CI, 1.02–1.32]). These results were similar when including blood pressure in the model”

“ We have shown that both OC use and oral HRT is associated with an increased risk of any stroke,”

“ We found an ≈20% increased event rate of any stroke among women who had ever initiated HRT. This estimate is slightly lower than those reported from the WHI (Women’s Health Initiative) trials,17,32,33 and observational studies18 (30%–40%). However, the WHI trial only covered a selected population of postmenopausal women within a specific age range (50–79 years),34 as compared with our participants’ age range at recruitment (37–73 years). Our study included a longer follow-up time and a longer duration of average use, and our estimates are therefore weighted toward a long-term effect as compared with the WHI. When we analyzed stroke subtypes, an increased risk of stroke was observed also for subarachnoid hemorrhage. This adds to previous knowledge, where the risk of subarachnoid hemorrhage in previous studies has not been possible to evaluate due to limited power.17,18 This has not only clinical significance but also gives new insights on a possible additional mechanism of exogenous hormones, given the important differences in the pathogenesis of stroke subtypes, especially ischemic and hemorrhage.”

“ In our study, we observed an increased risk among previous HRT users compared with nonusers. This could be a result of sudden estrogen withdrawal, which may cause vasoconstriction and potentially trigger stroke events in women at high risk of stroke, as the vasodilatory effects of estrogen abruptly drop.38,39 However, it is also possible that atherosclerotic lesions are built up during treatment as a result of various processes, including elevated C-reactive protein levels during HRT use,40 and that these lesions remain and result in higher stroke risk persisting also after discontinuation”

“ Our findings indicate that HRT is associated with an increased risk of stroke, regardless of the timing of initiation or duration.”

Of note this is just from the first page of studies, of which there were very many

@jlam1950 yes loestrin was probably given this name to convey “low estrogen “
There are several forms of loestrin. Loestrin 1/20, loestrin 1.5/20 and loestrin 24 Fe.

Loestrin contains ethinyl estrodiol 10-30 mcg per pill depending on the type. 15 mcg of ethinyl estradiol is roughly equivalent to 1.5 mg of oral micronized estradiol in a young woman (as liver ages this equivalency changes). As an aside the average dose of oral estradiol for post menopausal women is 0.5-2 mg, This is a synthetic estrogen. it more potent (about 100 x more potent than natural estrogen), thus allowing a lower dose. They were manufactured for better absorption and stability, and are broken down less easily by the liver. This leads to differences in metabolism, receptor binding, and side effects. They have increased bioavailability which means more drug ends up in the bloodstream. Because they are broken down in the liver, as one ages and the liver’s ability to ‘detoxify’ or break down molecules decreases, the amount of synthetic estrodiol in the body increases.

Also, synthetic estrogens elevate hepatic (liver) protein synthesis more, leading to more blood clot, stroke and cholesterol risk, especially when taken orally. Btw, The lowest risk for clots, stroke (thrombotic) risk is with transdermal (skin patch) natural estrogen. Transdermal natural estradiol can be given at doses of 25- 100 mcg per day because it bypasses the first pass effect (the metabolism and inactivation of orally administered drugs, food too, in the GI tract, mostly liver, before they reach the general blood circulation, reducing bioavailability- meaning only a fraction of pill becomes active in the bloodstream) with direct bloodstream delivery. I probably could write this more succinctly. If questions, I am happy to try to better explain.

Synthetic estrogen was also has increased receptor activation which also makes them stronger than natural estrogen. They bind up to 2x better (affinity) than natural estradiol.