I feel my estrogen "crashing" when I am due for my injection (EV). I get anxiety, depression, sadness, etc. after I inject, I feel better.
Since going high estrogen and lowering testosterone (not eliminating it), I have lost my taste for alcohol. While I only drank at certain social functions such as wine at a holiday meal with family, sangria at a summer pool party, etc. (at most once a month), and I would also sometimes (at most once a month) enjoy a shot of bourbon, a sweet liquor, or sweet mixed drink. Only one rock glass (not full), and after dinner/before bed. That is all basically gone.
Since the beginning of 2020, my stress and anxiety has been through the roof. The pandemic killed a business I have built from scratch and I have had to start over in new businesses twice, someone really close to me passed away from fentanyl, and coming out to my parents (whom my businesses are tied to theirs) was not the best. I concluded that since cortisol (the stress hormone) is involved with estrogen and testosterone production, the added stress affects my hormones or my hormones affects my stress and anxiety.
I have said before that progesterone, estrogen, and testosterone together are more than the sum of their parts. I believe that (oral) progesterone is magical as it has the best parts of estrogen and testosterone without the negatives (at least for me).
On Thu, May 12, 2022 at 12:45 PM Jessica Creel via groups.io <stuffedpinkowl@...> wrote:
i.e. the female represented by your gene structure has to be smarter than the male represented by your gene structure in order for your gene structure to represent a coherent survival strategy, otherwise the male, being larger, would simply eat the female.
better joke: God gave men a brain and a penis, but only enough blood to run one at a time....
Summary Estradiol decline can result in depressive disorders in females; nevertheless, the causes of this decline are unclear. In this study, we isolated estradiol-degrading Klebsiella aerogenes from the feces of premenopausal females with depression. In mice, gavaging with this strain led to estradiol decline and depression-like behaviors. The gene encoding the estradiol-degrading enzyme in K. aerogenes was identified as 3β-hydroxysteroid dehydrogenase (3β-HSD). Heterologously expressing 3β-HSD resulted in Escherichia coli obtaining the ability to degrade estradiol. Gavaging mice with 3β-HSD-expressing E. coli decreased their serum estradiol levels, causing depression-like behaviors. The prevalence of K. aerogene and 3β-HSD was higher in premenopausal women with depression than in those without depression. These results suggest that the estradiol-degrading bacteria and 3β-HSD enzymes are potential intervention targets for depression treatment in premenopausal women.
here are 12 studies regarding the "transgender brain"
A female-sized BSTc was found in male-to-female transsexuals. The size of the BSTc was not influenced by sex hormones in adulthood and was independent of sexual orientation. Our study is the first to show a female brain structure in genetically male transsexuals and supports the hypothesis that gender identity develops as a result of an interaction between the developing brain and sex hormones
We showed for the first time that INAH3 volume and number of neurons of male-to-female transsexual people is similar to that of control females. The female-to-male transsexual subject had an INAH3 volume and number of neurons within the male control range, even though the treatment with testosterone had been stopped three years before death.
The absence of serotonin transporter asymmetry in the midcingulate in MtF transsexuals may be attributed to an absence of brain masculinization in this region.
FtMs showed evidence of subcortical gray matter masculinization, while MtFs showed evidence of CTh feminization. In both types of transsexuals, the differences with respect to their biological sex are located in the right hemisphere.
We found that the sex difference in responsiveness to androstadienone was already present in pre-pubertal control children and thus likely developed during early perinatal development instead of during sexual maturation. Adolescent girls and boys with GD both responded remarkably like their experienced gender, thus sex-atypical.
Results revealed thicker cortices in MTF transsexuals, both within regions of the left hemisphere (i.e., frontal and orbito-frontal cortex, central sulcus, perisylvian regions, paracentral gyrus) and right hemisphere (i.e., pre-/post-central gyrus, parietal cortex, temporal cortex, precuneus, fusiform, lingual, and orbito-frontal gyrus). These findings provide further evidence that brain anatomy is associated with gender identity, where measures in MTF transsexuals appear to be shifted away from gender-congruent men.
The number of neurons in the BSTc of male-to-female transsexuals was similar to that of the females (P = 0.83). In contrast, the neuron number of a female-to-male transsexual was found to be in the male range. Hormone treatment or sex hormone level variations in adulthood did not seem to have influenced BSTc neuron numbers. The present findings of somatostatin neuronal sex differences in the BSTc and its sex reversal in the transsexual brain clearly support the paradigm that in transsexuals sexual differentiation of the brain and genitals may go into opposite directions and point to a neurobiological basis of gender identity disorder.
These data suggest a pattern of activation away from the biological sex, occupying an intermediate position with predominantly female-like features. Because our MFTRs were nonhomosexual, the results are unlikely to be an effect of sexual practice. Instead, the data implicate that transsexuality may be associated with sex-atypical physiological responses in specific hypothalamic circuits, possibly as a consequence of a variant neuronal differentiation.
MTF transsexuals show a significantly larger volume of regional gray matter in the right putamen compared to men. These findings provide new evidence that transsexualism is associated with distinct cerebral pattern, which supports the assumption that brain anatomy plays a role in gender identity.
When comparing MTF transsexuals with male volunteers, activation patterns similar to female volunteers being compared with male volunteers were revealed We revealed a cerebral activation pattern in MTF transsexuals compared with male controls similar to female controls compared with male controls during viewing of erotic stimuli, indicating a tendency of female-like cerebral processing in transsexualism.
Our results show that the white matter microstructure pattern in untreated MtF transsexuals falls halfway between the pattern of male and female controls. The nature of these differences suggests that some fasciculi do not complete the masculinization process in MtF transsexuals during brain development.
All the genetic, postmortem, and in vivo scanning observations support the neurobiological theory about the origin of gender dysphoria, i.e., it is the sizes of brain structures, the neuron numbers, the molecular composition, functions, and connectivity of brain structures that determine our gender identity or sexual orientation. There is no evidence that one's postnatal social environment plays a crucial role in the development of gender identity or sexual orientation.
The third trimester of pregnancy also is associated with alot higher progesterone levels than any other time during pregnancy.
Have you added progesterone to your criteria?
Fascinating info for me
D
On Fri, 16 Dec 2022, 04:57 Trixie, <becker.darm@...> wrote:
I understand its important for the relationship between child and mother...but what goes on in a Transgender women mind??? What are the advantages for us??? I dont wanna much more feel like a pregnant women...Im feeling enough pregnant with E2 of 590...I wanna be so near it goes to be a cis women...thats my target. Can this help me? And if you say yes, why?
Am Fr., 2. Dez. 2022 um 19:28 Uhr schrieb noface 🇺🇦 <ns.nanika@...
Mapping the effects of pregnancy on resting state brain activity, white matter microstructure, neural metabolite concentrations and grey matter architecture
Abstract While animal studies have demonstrated a unique reproduction-related neuroplasticity, little is known on the effects of pregnancy on the human brain. Here we investigated whether pregnancy is associated with changes
to
resting state brain activity, white matter microstructure, neural metabolite concentrations and grey matter architecture using a comprehensive pre-conception cohort study. We show that pregnancy leads
to
selective and robust changes in neural architecture and neural network organization, which are most pronounced in the Default Mode Network.
These
neural changes correlated with pregnancy hormones, primarily third-trimester estradiol, while no associations were found with other factors such as osmotic effects, stress and sleep. Furthermore, the
changes
related to measures of maternal-fetal bonding, nesting behavior and the physiological responsiveness to infant cues, and predicted measures of mother-infant bonding and bonding impairments. These findings suggest
there
are selective pregnancy-related modifications in brain structure and function that may facilitate peripartum maternal processes of key
relevance
to the mother-infant dyad.
---
The weight map associated with the regression model for estradiol—reflecting the relative contribution of the voxels across the brain—indicates that the regions of strongest neural changes also
strongly
contribute to this regression (Supplementary Fig. 10). In fact, the
weight
map shows a remarkable similarity to the map of observed brain changes across pregnancy, suggesting that the levels of estradiol a woman is exposed to during gestation may exert effects across the brain and are likely to contribute to the overall pattern of observed neural changes.
Supplementary analyses involving the different sampling points of estradiol measurements across pregnancy were then performed to examine
the
timing of these effects. These analyses indicated associations with estradiol levels sampled in week 12 as well as a trend for an association with week 24 estradiol levels. Furthermore, associations or trends were observed for estradiol levels extracted from every sampled week of the third trimester (Supplementary Table 51), indicating that especially third-trimester estradiol levels are associated with the observed brain changes.
There are changes that happen at 3-4mo, which some of us reach by levels. And further changes that most of us won't reach. Pregnancy brain changes do not make women more woman. Plus it's not just just E involved in that. I'm just posting interesting articles on the subject of hormones and brain.
So what....???? Realy??? Oh Girl...10 mg blast my head to space and I cant thinking oin one direction...Im so confused if I do it.
Am Do., 15. Dez. 2022 um 19:01 Uhr schrieb Lena <Lena@...>:
I understand its important for the relationship between child and mother...but what goes on in a Transgender women mind??? What are the advantages for us??? I dont wanna much more feel like a pregnant
women...Im
feeling enough pregnant with E2 of 590...
neural changes correlated with pregnancy hormones, primarily third-trimester estradiol
Normal range for third-trimester estradiol is 10,000-40,000 pg/ml = 37000-147000 pmol/l.
I understand its important for the relationship between child and mother...but what goes on in a Transgender women mind??? What are the advantages for us??? I dont wanna much more feel like a pregnant women...Im feeling enough pregnant with E2 of 590...
neural changes correlated with pregnancy hormones, primarily third-trimester estradiol
Normal range for third-trimester estradiol is 10,000-40,000 pg/ml = 37000-147000 pmol/l.
I understand its important for the relationship between child and mother...but what goes on in a Transgender women mind??? What are the advantages for us??? I dont wanna much more feel like a pregnant women...Im feeling enough pregnant with E2 of 590...I wanna be so near it goes to be a cis women...thats my target. Can this help me? And if you say yes, why?
Am Fr., 2. Dez. 2022 um 19:28 Uhr schrieb noface 🇺🇦 <ns.nanika@...>:
Mapping the effects of pregnancy on resting state brain activity, white matter microstructure, neural metabolite concentrations and grey matter architecture
Abstract While animal studies have demonstrated a unique reproduction-related neuroplasticity, little is known on the effects of pregnancy on the human brain. Here we investigated whether pregnancy is associated with changes to resting state brain activity, white matter microstructure, neural metabolite concentrations and grey matter architecture using a comprehensive pre-conception cohort study. We show that pregnancy leads to selective and robust changes in neural architecture and neural network organization, which are most pronounced in the Default Mode Network. These neural changes correlated with pregnancy hormones, primarily third-trimester estradiol, while no associations were found with other factors such as osmotic effects, stress and sleep. Furthermore, the changes related to measures of maternal-fetal bonding, nesting behavior and the physiological responsiveness to infant cues, and predicted measures of mother-infant bonding and bonding impairments. These findings suggest there are selective pregnancy-related modifications in brain structure and function that may facilitate peripartum maternal processes of key relevance to the mother-infant dyad.
---
The weight map associated with the regression model for estradiol—reflecting the relative contribution of the voxels across the brain—indicates that the regions of strongest neural changes also strongly contribute to this regression (Supplementary Fig. 10). In fact, the weight map shows a remarkable similarity to the map of observed brain changes across pregnancy, suggesting that the levels of estradiol a woman is exposed to during gestation may exert effects across the brain and are likely to contribute to the overall pattern of observed neural changes.
Supplementary analyses involving the different sampling points of estradiol measurements across pregnancy were then performed to examine the timing of these effects. These analyses indicated associations with estradiol levels sampled in week 12 as well as a trend for an association with week 24 estradiol levels. Furthermore, associations or trends were observed for estradiol levels extracted from every sampled week of the third trimester (Supplementary Table 51), indicating that especially third-trimester estradiol levels are associated with the observed brain changes.
Mapping the effects of pregnancy on resting state brain activity, white matter microstructure, neural metabolite concentrations and grey matter architecture
Abstract While animal studies have demonstrated a unique reproduction-related neuroplasticity, little is known on the effects of pregnancy on the human brain. Here we investigated whether pregnancy is associated with changes to resting state brain activity, white matter microstructure, neural metabolite concentrations and grey matter architecture using a comprehensive pre-conception cohort study. We show that pregnancy leads to selective and robust changes in neural architecture and neural network organization, which are most pronounced in the Default Mode Network. These neural changes correlated with pregnancy hormones, primarily third-trimester estradiol, while no associations were found with other factors such as osmotic effects, stress and sleep. Furthermore, the changes related to measures of maternal-fetal bonding, nesting behavior and the physiological responsiveness to infant cues, and predicted measures of mother-infant bonding and bonding impairments. These findings suggest there are selective pregnancy-related modifications in brain structure and function that may facilitate peripartum maternal processes of key relevance to the mother-infant dyad.
---
The weight map associated with the regression model for estradiol—reflecting the relative contribution of the voxels across the brain—indicates that the regions of strongest neural changes also strongly contribute to this regression (Supplementary Fig. 10). In fact, the weight map shows a remarkable similarity to the map of observed brain changes across pregnancy, suggesting that the levels of estradiol a woman is exposed to during gestation may exert effects across the brain and are likely to contribute to the overall pattern of observed neural changes.
Supplementary analyses involving the different sampling points of estradiol measurements across pregnancy were then performed to examine the timing of these effects. These analyses indicated associations with estradiol levels sampled in week 12 as well as a trend for an association with week 24 estradiol levels. Furthermore, associations or trends were observed for estradiol levels extracted from every sampled week of the third trimester (Supplementary Table 51), indicating that especially third-trimester estradiol levels are associated with the observed brain changes.
Spironolactone begins blocking testosterone in minutes, and has a half-life of 1.4 hours. For me it was a great way to check whether feeling "head in a vise" angry was due to too much T, or feeling tired and unmotivated was due to already having too little T. Even a single 25 mg tablet made a sudden dramatic difference, and 100 mg at once would pretty much wipe out all my energy - for an hour or two. And then it was gone... (Apparently some people consider 200 mg per day appropriate, so maybe I'm hypersensitive, but the timing of the effects should be similar for everyone.)
Bica and some other antiandrogens build up over days and persist for weeks, so their effect is not useful for this kind of experiment. But much more comfortable if you decide you need less T.
"Dont know hell where this brain issues starts to kick in. As if dysphoria was not enough :("
Started GAHT on Aug 13 @ 11mg. Skin softened, smoothed and oiliness went away. At third dose during week 3 my skin returned to being oily and leathery. No notice of emotional change.
September 3, dropped dose to 9mg. Skin became soft, smooth and oiliness went away again. Nipples began to hurt. No notice of emotional change.
September 12, dropped dose to 7mg. Skin still soft, smooth and no oiliness. Nipples still hurt and something is getting bigger behind the nipples. Sperm is now almost non existent, slight white and clear. Testicles size has decreased some. No noticeable emotional change.
September 19, 7mg. Continuation of September 12.
Began Finasteride September 6, .25mg daily.
I wouldn't be too scared about adjusting your dose up and down a bit. At least you're Diy and you're taking responsibility for your own actions. If it was a jacket wearer they'd be screwing with your hormones and you'd be at their mercy experiencing whatever they wanted you to endure.
You've got people here that's been there done that for years and decades to consult with for suggestions and help.
Last time I was advised to down the dosage, but am hesitating to. My fogetting habit is still here, do u people think i should really down my dose.
Nobody can "advise you" properly, because you are you, everybody's a bit different, and only you know how the different levels feel for you. Take Lena for example. She injects 11mg/wk EEn and feels great. Some people get the same result, some people get a different result. You won't find out how that works for you until you try it.
About hesitation - same. Try, and you'll find out, no harm done in the process. Cis women have lousy levels for a part of a month, and mediocre at best for the rest of the month.
Endogenous cis E2 production is somewhere around 0.1-0.3mg/day, depending on that time of the month. Works out to about 0.5-2mg/wk, different every week, and it works fine for most of them. This is from Yen & Jaffe's Reproductive Endocrinology, pg.89 btw.
I gotta say, I felt more emotionally unstable, and more depressed when I felt depressed, on higher dosages, and it takes a bit of time to adjust to a dosage change, but EEn helps vs EV, and with stuff like EV more frequent dosage helps too when your overall dosage is less. Even when you use EEn, 5mg twice a week will have more effect than 11mg once a week. YMMV of course.
But basically, if you feel like something's off and you need a change, make a change and see if it went in the right direction. It's pretty simple. Hundreds of millions of women (menopause) live for decades without E. It's sad obviously. But, compared to that, underdosing DIY E by one of us for a week or two, having the means to correct that, essentially immediately, is sooo non-issue. The only barrier is overexpression of paranoia. Which, yes, we are very prone to.
