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.
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.
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.
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....
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).
I fully agree with this, have had the same happen although have noticed my stress has gone up in recent times and my drinking has followed up as well even though I'd totally given it up a year prior and restarted due to stress as well, whereas pre HRT I was drinking due to my hormone imbalance (the want for alcohol, pot or tobacco hasn't come back since starting hrt but it seems that stress does trigger my use of things, do have a vape but don't buy tobacco any more and not constantly tied to it either),
If an old man has high LH, that's a sign that his testosterone level is not enough for him (because his testicles cannot produce enough testosterone). Or rather not enough (for him) estradiol produced by aromatase from testosterone.
"Generally, a negative feedback relationship exists between testosterone and LH. However, this relationship may not be accurate in aging men. Several studies, including this study, consistently show LH increasing as a function of age in elderly men. Furthermore, increasing evidence indicates that LH may not be correlated with testosterone in aging men, which is consistent with our findings."
I think that this article authors' interpretation of their statistics is stupid. If you give (inject) those old men enough testosterone, LH will not be high. Different men have different sensitivity to testosterone, different thresholds of testosterone level when pituitary produces LH trying to increase testosterone production by testicles. When testosterone level and as a consequence level of estradiol produced by aromatase from testosterone is not enough high for hypothalamus and pituitary, likely these levels are not enough for the rest of the brain too, resulting in cognitive impairment / dementia.
"Few"... so there are differences, it's just semantics. Eliot didn't disprove anything, just doesn't like the idea that women might be biologically different - "inferior" - than men. What about she eats a cookie with a lethal dose of poison in it? It wouldn't matter, it's practically all just a cookie, what can be the contribution of the poison...
A chemical signal in human female tears lowers aggression in males
"Mammals use various bodily media to convey social chemical signals. For example, human social chemosignaling research has focused on sweat [1], and rodent research has focused on urine [2]. Social chemosignaling, however, also extends to media such as feces [3], milk [4], and tears [5–12]. Rodent tear signaling has been studied in 2 contexts: reproduction and aggression. In reproduction, a male-specific peptide secreted from the extraorbital lacrimal gland, named exocrine gland-secreting peptide 1 (ESP1), is transduced by female V2Rp5-expressing vomeronasal sensory neurons [5]. This triggers signals from the accessory olfactory bulb to hypothalamic and amygdaloid nuclei, which enhance female sexual receptive behavior [6]. The tear-bound signal ESP1 is also the primary signal in the Bruce effect, where a pregnant mouse will miscarry upon perceiving an ESP1 signal from a male who did not father the pregnancy [7]. These tear-bound signals function not only within species but also across species: Like ESP1 in mice, rat cystatin-related protein 1 (ratCRP1) is released from male rat tears and alters behavior in female rats. This same rat signal, however, also triggers predator avoidance in mice [9]. Beyond reproductive signaling, a primary domain for rodent tear signaling is aggression. The above noted tear signal ESP1 that promotes sexual behavior in females also increases aggressive behavior in males smelling their own ESP1 secretions [8]. However, most aggression-related tear signaling appears to block rather than promote aggression. This was first identified in blind mole rats, where subordinate males cover themselves in tears to reduce dominant male aggression toward them [10]. Similarly, mice pups emit in their tears exocrine gland-secreting peptide 22, which through a vomeronasal accessory olfactory pathway, reduces male sexual aggression toward them [11]. Finally, female mouse tear liquid contains signals that abolish intermale aggression by modulation of activity in aggression brain networks [12]. In contrast to this extensive body of research into rodent tear chemosignaling, there is only limited evidence for human tear chemosignaling. Human female tears contain a perceptually odorless chemical signal that when sniffed, lowers testosterone in human males [13,14], but the behavioral significance of this effect remains poorly understood. More specifically, one study found that sniffing tears drove a small but significant reduction in ratings of sexual arousal attributed to pictures [13], and the second study observed that despite significantly lowering testosterone, sniffing tears did not affect appetite [14]. Given that reduced male testosterone is associated with reduced male aggression [15], here, we set out to test the hypothesis that like in rodents, human tears contain a chemical signal that blocks aggression. Notably, there are indeed several instances of chemical signals altering hormonal-dependent behavior in humans [16]. Examples include maternal behavior [17,18], ingestive behavior [19,20], social behavior in general [21,22], and sociosexual behavior in particular [23–25]. In other words, that a chemical signal can alter human behavior is not unusual. Moreover, particularly emotional behaviors are a prime candidate for modulation by chemical signals [26], possibly a reflection of their shared neural substrates in the amygdaloid complex [27,28] and an extensive associated brain network spanning ventral temporal cortex, frontal cortex, anterior cingulate cortex, and insula striatum [29]. Given this neural link, and that human aggression can be measured behaviorally using various standardized tasks [30], we set out to measure the aggressive behavioral and brain response following sniffing emotional tears."
INTRODUCTION Premenopausal bilateral oophorectomy (PBO) is associated with later-life cognition, but the underlying brain changes remain unclear. We assessed the impact of PBO and PBO age on white matter integrity.
METHODS Female participants with regional diffusion tensor imaging (DTI) metrics of fractional anisotropy (FA) and mean diffusivity (MD) were included (22 with PBO < 40 years; 43 with PBO 40-45 years; 39 with PBO 46-49 years; 907 referents without PBO < 50 years). Linear regression models adjusted for age and apolipoprotein E (APOE) genotype.
RESULTS Females with PBO < 40 years, compared to referents, had lower FA and higher MD in the anterior corona radiata, genu of the corpus collosum, inferior fronto-occipital fasciculus, superior occipital, and superior temporal white matter. Females who underwent PBO between 45 and 49 also had some changes in white matter integrity.
DISCUSSION Females who underwent PBO < 40 years had reduced white matter integrity across multiple regions in later-life. These results are important for females considering PBO for noncancerous conditions.
Highlights Females with premenopausal bilateral oophorectomy (PBO) < 40 years had lower FA versus referents. Females with PBO < 40 years had higher MD in many regions versus referents. Adjusting for estrogen replacement therapy use did not attenuate results. Females with PBO 45-49 years also had some white matter changes versus referents.
---
My takeaway key point here is:
"...Further, more than 80% of females who underwent PBO at all ages used ERT; adjusting for ERT use did not affect the associations. Notably, the females in the current cohort would have been prescribed conjugated equine estrogens based on the years of PBO and transition through menopause for referents. It is not known whether other hormone regimens such as transdermal 17β-estradiol would have affected white matter integrity differently..."
"...Further, more than 80% of females who underwent PBO at all ages used ERT; adjusting for ERT use did not affect the associations. Notably, the females in the current cohort would have been prescribed conjugated equine estrogens based on the years of PBO and transition through menopause for referents. It is not known whether other hormone regimens such as transdermal 17?-estradiol would have affected white matter integrity differently..."
Besides differences between Premarin and estradol, doctors' gospels preach about ERT: "dosage the less the better, stop as soon as possible".
Sufficiently advanced incompetence is indistinguishable from malice.
Yes. This paper further supports that not E2's, and in small doses, are useless for the brain. At least here the evidence is for preparing, which is E1 and E1S primarily, and so you do get E2 out of that, but in very small quantities. I'm still curious about the effect of small dose "female normal" levels of testosterone on the brain. The theory of course is that estradiol is the primary brain sex hormone, and T is just a link in the chain. But there still is no conclusive study on the subject. If it makes a difference, and for who. The brain does have AR receptors, and they do do something. I'd be curious to know what.
"Estradiol is the most potent and ubiquitous member of a class of steroid hormones called estrogens. Fetuses and newborns are exposed to estradiol derived from their mother, their own gonads, and synthesized locally in their brains. Receptors for estradiol are nuclear transcription factors that regulate gene expression but also have actions at the membrane, including activation of signal transduction pathways. The developing brain expresses high levels of receptors for estradiol. The actions of estradiol on developing brain are generally permanent and range from establishment of sex differences to pervasive trophic and neuroprotective effects. Cellular end points mediated by estradiol include the following: 1) apoptosis, with estradiol preventing it in some regions but promoting it in others; 2) synaptogenesis, again estradiol promotes in some regions and inhibits in others; and 3) morphometry of neurons and astrocytes. Estradiol also impacts cellular physiology by modulating calcium handling, immediate-early-gene expression, and kinase activity. The specific mechanisms of estradiol action permanently impacting the brain are regionally specific and often involve neuronal/glial cross-talk. The introduction of endocrine disrupting compounds into the environment that mimic or alter the actions of estradiol has generated considerable concern, and the developing brain is a particularly sensitive target. Prostaglandins, glutamate, GABA, granulin, and focal adhesion kinase are among the signaling molecules co-opted by estradiol to differentiate male from female brains, but much remains to be learned. Only by understanding completely the mechanisms and impact of estradiol action on the developing brain can we also understand when these processes go awry."
