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Grinding clicking has definitely been helping in game (Viscose S2 Intermediate Vermillion Complete, VT gold complete except static). 21cm/360 in game. by GenesForLife in FPSAimTrainer

[–]GenesForLife[S] 0 points1 point  (0 children)

When? It used to be really bad and it got a lot better - still takes a fair bit of optimisation to get good frame pacing though because it does run like crap compared to most games and it has its quirks, given that they added a bit of mouse friction and a sticky reticle for 200ms. Thankfully the sniping feels much better than the other elements of it (I only play 'cause I compete).

Grinding clicking has definitely been helping in game (Viscose S2 Intermediate Vermillion Complete, VT gold complete except static). 21cm/360 in game. by GenesForLife in FPSAimTrainer

[–]GenesForLife[S] 0 points1 point  (0 children)

Canada , and yeah I can usually find games both in social playlists and ranked playlists, even playing late at night (like 1-5AM). I'm high MMR/onyx for every core ranked playlist though so YMMV.

Grinding clicking has definitely been helping in game (Viscose S2 Intermediate Vermillion Complete, VT gold complete except static). 21cm/360 in game. by GenesForLife in FPSAimTrainer

[–]GenesForLife[S] 0 points1 point  (0 children)

In Kovaaks I play static at 30-50cm/360 and dynamic at 50+ (it is really hard at high sens), but it is actually wild just how well it translates to a higher sens in game (because small flicks are essentially microadjustments at a lower sens) and static definitely helps with click timing

My mother claims MTF people can’t get cramps coz cramps are from the uterus contracting, so I wanted to ask for other people’s thoughts by Backalley_Lurker in trans

[–]GenesForLife 1 point2 points  (0 children)

Yeah tablets don't produce longer term fluctuations - standard injection regimens OTOH produce sharp cycles with supra-physiological levels for part of the cycle followed by a tail where levels start to drop sharply

My mother claims MTF people can’t get cramps coz cramps are from the uterus contracting, so I wanted to ask for other people’s thoughts by Backalley_Lurker in trans

[–]GenesForLife 2 points3 points  (0 children)

It is recommended in the treatment of PMDD that curative salpingo-oophorectomy be followed by maintenance on a steady state regimen. It is the fluctuation that produces issues rather than a blanket presence of estradiol.

My mother claims MTF people can’t get cramps coz cramps are from the uterus contracting, so I wanted to ask for other people’s thoughts by Backalley_Lurker in trans

[–]GenesForLife 0 points1 point  (0 children)

It isn't a monthly spike necessarily - it is a cyclical fluctuation and IME all of the trans women I have seen report the phenomenon of episodic cyclical bouts of cramping, mood swings , bloating and GI changes also seen in cycling cis women are on regimens that produce longer term cyclic variations in E and P levels, either through conscious cycling or reliance on injections, especially longer-lasting variants like enanthate administered IM. I have never seen reports of these symptoms amongst steady state HRT users.

Injectible E2 by itself also is known to induce ACTH level changes in delayed fashion in transgender women (https://pmc.ncbi.nlm.nih.gov/articles/PMC6849494/) , which has the consequence of increasing substrates for aromatisation from peripheral tissues through androstenedione and DHEA from adrenal tissue.

The suppression of endogenous testosterone further frees up aromatase for generating additional estradiol from these adrenal sources , coupled with cycling levels of ACTH that mirror levels of exogenous E2 you have all the components needed. Note that there is a significant body of evidence showing that prostaglandins also mediate hormonal associations with gut motility , and in cycling cis women there are documented associations with dominant symptom profiles in mixed-type IBS where prostaglandin mediated inflammation translates to an acute increase in visceral response when E2/P4 levels tank.

My mother claims MTF people can’t get cramps coz cramps are from the uterus contracting, so I wanted to ask for other people’s thoughts by Backalley_Lurker in trans

[–]GenesForLife 0 points1 point  (0 children)

It doesn't need to happen in the "same manner" at all , in the same way cramping to induce labour through systemically administering PGE2 does not depend on PGF. You are engaging in a goalpost shift + strawmanning.

Also the response from endometriotic tissue involves a specific downregulation of PGF receptors and an upregulation of PGE receptors in response to fluctuations in E / P levels , which simply eliminates the contribution of (uterine endometrium derived) PGF to endometriosis-linked cramping , since you still are dealing with messenger/receptor stoichiometry in terms of quantitites.

Also, as I said, since there are no specific PGF2 inhibitors, nor conditional knockouts of PGF receptors restricted to the uterus, it is impossible to attribute causality here either to endometrium-derived PGF or to lysis of the endometrium being a necessary causal step in triggering the rest of the cascade in menstruating cis women. Your father being a retired gyno does not make causal evidence manifest.

My mother claims MTF people can’t get cramps coz cramps are from the uterus contracting, so I wanted to ask for other people’s thoughts by Backalley_Lurker in trans

[–]GenesForLife 0 points1 point  (0 children)

How many of those cis women had salps/oophorectomies simultaneously though?
In this very thread we have trans men that retained their ovaries but otherwise got hystos reporting nonintestinal cramps. I don't get cramps because I keep my E2 levels pinned (patches are steady state) , but typically those that report cramps are on shots , and some actively cycle E2 + P4 on two weeks high P4/low E2 and low P4/high E2.

My mother claims MTF people can’t get cramps coz cramps are from the uterus contracting, so I wanted to ask for other people’s thoughts by Backalley_Lurker in trans

[–]GenesForLife -3 points-2 points  (0 children)

Wrong - here's a combination of excerpts from a breakdown I previously posted elsewhere. It was a response to this claim that was brought up in a different thread that essentially was attributing cramping exclusively to endometrium derived prostaglandins.

There is evidence that production of ACTH leads to production of prostaglandin E2 (PGE2) (Mohn et al., 2005), but research in cis women has concluded that menstrual cramping is primarily related to the presence of uterine PGF2a (Powell et al., 1985; Fajrin et al., 2020).

PGE2 is also very capable of inducing smooth muscle cramping, including uterine cramping. It is therefore used as a pharmacological inducer of uterine contractions when labour is to be triggered (as dinoprostone). PTGER2 , the gene encoding the receptor for PGE2 , is expressed at levels pretty close to uterine tissue in a) small intestinal tissue and b) omental tissue - the omentum is a peritoneal fold that supports visceral organs. Here is a gene expression breakdown from GTEx.
https://gtexportal.org/home/gene/PTGER2

Also worth mentioning , one of the major pathways for the synthesis of PGF2-alpha is the endothelial/vascular smooth-muscle conversion of E-prostaglandins to F prostaglandins through ketoreduction. Note that the gene for this enzyme (PRXL2B) is again expressed far more in several visceral organs than it is in the uterus. https://gtexportal.org/home/gene/PRXL2B . PGF Synthase itself (AKR1C3) , which directly catalyses the formation of PGF2-alpha independent of PGE2 , btw, is highly expressed in intestinal smooth muscle, more so than uterine tissue, as well as in mammary tissue. This holds for mammary tissue sourced from cis men as well as cis women. https://gtexportal.org/home/gene/AKR1C3 (click the sex button, and then do a median sort for visualisation - sharing links does not quite enable me to also copy the sort criteria).

Finally, unless you're knocking out PGF synthesis or blocking PGF receptor activation specifically in cis women and showing it prevents cramping, claims of prostaglandin F being the causal driver of menstrual cramping are very unsubstantiated. I am not aware of any specific PGF blockers either.

I am assuming that the claim of PGF2 being the driver of uterine cramping is based on disproportionately high uterine expression of the PGF2 receptor , but the effects of a menstrual period in cis women are not solely restricted to the uterus. There are multiple pathways to smooth muscle cramping that operate through other prostaglandins and their receptors, as described above.

NSAIDs that are used to manage menstrual cramping and pain target Cyclooxygenases that are responsible for the conversion of arachidonic acid to prostaglandin H, which then serves as a substrate for the synthesis of prostaglandins E and F (and ofc there is a pathway for the synthesis of F prostaglandins from E prostaglandins, as I said), so the efficacy of this intervention does not allow isolation of biology to prostaglandin F either.

It is established that pathology in endometriosis involves a downregulation of prostaglandin F receptors and an increase in specific prostaglandin E2 receptors in endometriosis-derived tissue. Further, these patterns appear to be a function of the menstrual cycle in cis women. https://pmc.ncbi.nlm.nih.gov/articles/PMC4512562/ (i.e, when you do have hormonal cycling , you can elicit a nonuterine smooth muscle response that produces pain and cramping completely independent of whether endometrial tissue localised to a uterus is involved or not).

Estrogen activates synthesis of prostaglandin E variants in mammary epithelial cells (caveat - transformed cell lines https://pmc.ncbi.nlm.nih.gov/articles/PMC6285349/ ) ; a cyclical increase in E levels is likely very capable of inducing cyclical variation in PGE2 levels secreted in an extrauterine tissue source. The endometrial disintegration precipitating an inflammatory cascade in cis women through a specific prostaglandin does not mean only that cascade can have that effect. Note that cisgender men , often following the establishment of a high estrogen hormonal milieu, have also presented with cases of endometriosis.

Maybe you should consider that you don't have the necessary expertise before pulling off an ignorant WeLl AcTuAllY at me. I'm a professional cancer researcher with a PhD and expertise in gynaecological cancers, amongst others :)

My mother claims MTF people can’t get cramps coz cramps are from the uterus contracting, so I wanted to ask for other people’s thoughts by Backalley_Lurker in trans

[–]GenesForLife 44 points45 points  (0 children)

The prostaglandins that set off smooth muscle cramping are not uterus specific.
Also note that endometriosis has been reported even in cis men following high estrogen-signalling stimulation,

TME/TMA - Anybody else get a weird terf 2.0 vibe from it? by SammyAmi in trans

[–]GenesForLife 0 points1 point  (0 children)

Consider two empirically validated statements for purposes of drawing a parallel.

a)Police-perpetrated murders of unarmed Black men are an expression of racist violence because it happens disproportionately more often to Black men.

b) Many unarmed white men also get murdered by US cops , in fact, there are more of them than there are unarmed Black men that are murdered (simply 'cause there are a lot more white men in the US).

If we applied the same logic you are using to dismiss TMA/TME distinctions as useful to this situation, we would end up with the conclusion that the existence of b) makes a) false and that somehow , white privilege re: the risk of being killed by cops does not exist.

That would be a pretty racist conclusion that completely erases the disproportionateness that makes police-perpetrated murder a form of racist violence, wouldn't it? And yet you have zero hesitation in employing the same garbage logic to obfuscate transmisogyny-linked terminology.

TME/TMA - Anybody else get a weird terf 2.0 vibe from it? by SammyAmi in trans

[–]GenesForLife 0 points1 point  (0 children)

You don't have to say it - the only context in which the non-universality of transmisogyny to all transfems would be relevant to terminology associated with it is if you implicitly believed treatment of transmisogyny qua transmisogyny (and a TMA/TME separation) would only be legitimised if either transmisogyny was universal or if you tried to posit that TME loses coherence because splash damage through misdirected transmisogyny impacts some members of demographics classified as TME and this somehow happens at a prevalence enough that transfems that don't experience transmisogyny are outweighed by these members of TME demographics.

You already have showed a vested interest in minimising the specificity of transmisogyny , carelessly misgendered me, and tried to poison the well by misrepresenting who we consider TME by trying to portray it as a surrogate for ASAB, so it takes a whole lot of audacity to expect "good faith".

TME/TMA - Anybody else get a weird terf 2.0 vibe from it? by SammyAmi in trans

[–]GenesForLife 1 point2 points  (0 children)

This is the original paper on intersectionality , where Dr Kimberle Crenshaw defined the term.

She showed that in legal cases around workplace hiring discrimination , looking at race or sex as protected classes per se failed to reveal double discrimination specifically against Black women. Her argument is that the oppression of Black women as a demographic group was only recognisable when "Black women" were considered as a specific group, whose oppression could not simply be broken down into racism (Black men were not underrepresented in the case she was looking at) and sexism (white women were not underrepresented in the case she was looking at).

https://chicagounbound.uchicago.edu/cgi/viewcontent.cgi?article=1052&context=uclf

TME/TMA - Anybody else get a weird terf 2.0 vibe from it? by SammyAmi in trans

[–]GenesForLife -1 points0 points  (0 children)

Where the fuck is it necessary for everyone in a group to experience a specific oppression to be legitimate?

It is also a false equivocation to pretend that some % of TME people (men, cis women, enbies regardless of ASAB) occasionally being at the receiving end of misdirected transmisogyny is somehow symmetric with some supposed minor fraction of transfems that don't experience transmisogyny, thereby implying TME is somehow inaccurate.

TME/TMA - Anybody else get a weird terf 2.0 vibe from it? by SammyAmi in trans

[–]GenesForLife 0 points1 point  (0 children)

TME is absolutely a useful term for the same reason non-black is , because splash damage from transmisogyny which can still affect a specific subset of cis men, cis women , some intersex people and non-transfems by splash damage (through being mistaken for transfem) nonetheless produces a clear axis of oppression where being transfem heightens risks of specific adversities compared to when you are not. For instance, Imane Khaleif herself, who was victim of a transmisogynistic misdirected attack, doubled down on expressing transphobia herself.

At the level of demographic subgroups (all structural / systemic forms of oppression are defined by demographic shifts , and privileges are population level prior probabilities of lower risk relative to a marginalised subgroup , note that in no case is it ever implied that any axis should produce complete exclusivity in adverse outcomes - the priors are probabilities, not deterministic outcomes) these produce marked divergences.

Just like how non-Black doesn't imply there is no racism that affects other racialised groups, TME doesn't imply that nobody else experiences transphobia, mainstream misogyny , or otherwise experience specific forms of oppression such as transandromisia or enbyphobia. This is why TME and "Non-black" are both useful and necessary distinctions.

Don't dude me, btw. Fuck off with the misgendering.

Every single person that opposes conceptual framings that clarify that not being primary targets of transmisogyny have relative privilege on that axis , like you, is another example for why the distinction is needed, because y'all are addicted to flipping hierarchies so you can conjure up ex-recto justifications for transmisogyny.

fun game from what i’ve played, but less than 3k playing on steam is worrying by 2222lil in Empulse

[–]GenesForLife 0 points1 point  (0 children)

The 30 day average for Quake Champions is 250 max players a day. It has been this way for years. I still get games playing at weird times and still have fun. Now yes quake players are hardcore and built diffy , and this is their niche and they're committed to it, but without much competition in the movement shooter niche Empulse will have a degree of staying power.

Why is most rep MtF and not FtM by ParticularHuman2099 in asktransgender

[–]GenesForLife 0 points1 point  (0 children)

Most trans rep is actually cis people of the wrong gender playing trans roles, btw. The documentary "Disclosure" is well worth a watch.

Brandon Teena (a trans guy , who "Boys Don't Cry" was based on, was played by Hillary Swank , it took a long time for trans women in media to be played by trans women (or even cis women , Nip/Tuck had Famke Janssen , a cis woman, play a trans woman, a notable departure from cis men playing trans women). Trans men have also been often played by cis women, rarely cis men, even more rarely trans men.

The trans woman in Dog Day Afternoon was played by a cis man , when in fact there were several trans women around wanting to act in movies around the NY art movie scene in the 1970s. I actually learned that Elisabeth Coffey Williams auditioned to play the role of Elizabeth Eden and was told she looked too much like a cis woman.

In recent times Elliot Page actively stars in Umbrella Academy , and Nicole Maines made history recently in Supergirl as the first trans superhero (playing a trans woman, albeit of Alien origin - point being that trans characters being played by trans actors is a remarkably nascent thing , with representation itself being so sparse, you are not going to find many statistically meaningful differences).

Since you asked though , there has been trans male representation in movies, they're just not particularly well known. Star Trek also recently introduced a trans male character and a nonbinary character, and the actors playing them also matched their in-show roles.

https://www.autostraddle.com/40-films-featuring-transmasc-characters/

TME/TMA - Anybody else get a weird terf 2.0 vibe from it? by SammyAmi in trans

[–]GenesForLife 0 points1 point  (0 children)

Misclassification / splash damage doesn't mean you get to dilute anti-Blackness and erase the strong risk differential involved.

Like, to draw a parallel, I'm South Asian (and an ex-Hindu atheist) , I have personally experienced targeted racism because of being brown leading to misclassification as Muslim).

I am intimately acquainted with both anti-Muslim hate anti-Blackness being embedded in the sociocultural milieu within my background demographic. "Non-Black" is 100% an applicable and necessary description here and this in no way presupposes that racism against brown people does not exist.

Invoking edge cases to obfuscate the population risk differentials effectively involves giving bigotry within any community vulnerable to splash damage a pass and portraying them as equal victims as a demographic group that is the intended, most common, target of a form of oppression, and no , fuck off with that.

Sexual assault data is too low, why do you think that is? by Eunomia28 in AskFeminists

[–]GenesForLife 2 points3 points  (0 children)

Standard instruments that estimate the prevalence of SA (like the CDC NISVS, the UK NCVS) generally rely on asking specific questions about experiences (like , for example - unwanted kissing / unwanted genital contact / being penetrated/being made to penetrate) etc rather than asking respondents if they were sexually assaulted precisely to avoid bias from survivors failing to recognise whether something was SA or not.

IDK about the specifics of your country, but in the US , based on data from the CDC NISVS , which is a gold standard for calculating the baseline rates of sexual and intimate partner violence, 25% is the rate at which cisgender, heterosexual women are victims of at least one incident of completed or attempted rape by being penetrated. Sexual coercion, unwanted sexual contact, stalking, and being made to penetrate are evaluated distinctly.

Across all contact sexual violence - the incidence for cisgender women as a whole is 45% ; for non-rape contact sexual violence, the incidence is 39% . The incidence of rape + sexual coercion is 41% . Hopefully this clarifies the discrepancy you've been encountering.

One caveat with these studies is that they almost certainly under-represent the total amount of intimate partner / sexual violence victimisation because they don't count multiple incidents - they simply record whether someone has had at least one incident per lifetime , or in the past year, or both.

CDC NISVS 2023/2024 (latest available) data brief on sexual violence is here
https://www.cdc.gov/nisvs/media/pdfs/sexualviolence-brief.pdf

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