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ArticleMedical Study on Testosterone effects to the female immune system
I came across this medical study. They studied the effects of testosterone on the immune systems of trans-id'd women. It was a small study, around 20, but this part was interesting.
The most dramatic differences after a year of testosterone-based GAHT were observed in the interferon and tumor necrosis factor (TNF) pathways, which have implications for both autoimmunity and fighting acute infections. The type 1 interferon pathway, which is usually upregulated in cisgender women compared to cisgender men, was downregulated in this cohort. Meanwhile, the TNF pathway, an inflammatory pathway, was upregulated in this cohort.
“So basically, we’re seeing that testosterone plays a key role in this [immune system overactivation] as well. Testosterone is downregulating the interferon response but upregulating this inflammatory response,” he says.
It continues saying Lupus and other autoimmune diseases is overactivation of interferon. I wonder how this plays into how many TIFs are sick.
The actual article is locked to academic access, but scientific american also wrote about the findings.
While this is just one study, the results may have implications for the health of transgender men taking masculinizing hormone therapy. “We can’t say that these individuals are now more susceptible to any infection, and so on, but what we can say is that their immune profiles do alter or change in a way that is more similar to [cisgender] men,” says study co-author Petter Brodin, a professor of pediatric immunology at the Karolinska Institute in Stockholm.
Anyway, i'm just trying to understand it. I bet the "more similar" to men bit is doing a lot of heavy lifting. What do you think?
The older TIFs I’ve seen on youtube all look like they’re in chronic inflammatory response. They’re overweight, swollen, red, and probably have high blood pressure. You never see old TIFs probably because they all die due to stress on the heart and kidneys.
Maybe we can convince lefties that TIPs don't care about climate change, since they won't live long enough to see it!
Just like TiMs, you will see a few old ones here and there. And some of them look decent, as in, not like they're about to fall apart if you cough in their general vicinity. But those are usually the ones with a balanced diet, who do sports and who generally look out for their health - and also didn't enter with a cocktail of EXTREME mental illnesses.
Buck Angel looks good- but keep in mind, she almost DIED. It's possible to be very good looking, athletic build, etc, and still be a mess. And she's still beating the odds in a way most won't. She's a former model and loves working out.
Absolutely correct. All I'm saying is that there's only a small pool of long term TiPs and the only ones that at least >look< functional are the ones who break a leg trying to stay functional. But you are indeed entirely correct about superficial looks not necessarily being key to tell a persons health.
I assume the older ones who look decent transitioned later in their lives.
ABC News also published a summary: https://abcnews.go.com/GMA/Wellness/women-turn-testosterone-hormone-health-risks/story?id=115906820
Some hot quotes: "Despite its growing interest among women, testosterone is not currently approved by the U.S. Food and Drug Administration for women."
"The American College of Obstetricians and Gynecologists has also expressed concern about the safety of testosterone in women, noting that in most cases, the hormone should not be prescribed for women under 40."
"In addition to the lack of research showing the benefits of testosterone for women, taking the hormone can also come with side effects, including unwanted hair growth, acne, liver damage, hair loss and birth defects."
Kinda transphobic, dontcha think?
yes. I also noticed a lot of brackets in the researcher's quotes in the Scientific American write up. I think they were to make the study less "transphobic" or something. Obviously, i think it'd be unethical to give women T for a study, but you'd think they would have done the simple tests of adding T to blood that they mentioned before every giving actual humans cross-sexed hormones.
"Now I have so much more energy and like motivation, even like feeling good, it makes me feel like I can do more,"
yeah, so will amphetamines and some SSRIs, etc. It's sad how hedonistic of a society we live in. You don't have to be happy & energetic all the time to be healthy, imho.
we can say is that their immune profiles do alter or change in a way that is more similar to [cisgender] men,
Ba ha ha ha the journalist had to insert [cisgender] because the professor just said "men."
"Dear Diary,
I have a heckin' MAN COLD! Omg I'm like, so validated right now! Going on T so that my ability to fight off infection is fucked up was the best decision I ever made. I'm gonna snuggle up with my cat and write Yaoi fiction. Here are some stickers I bought on Etsy."
I cannot believe we are putting young women on this. Underage girls. Hell, even older women.
I bet the "more similar" to men bit is doing a lot of heavy lifting. What do you think?
Probably
https://med.stanford.edu/news/all-news/2024/02/women-autoimmune.html
I do wonder if females with autoimmune disorders are more likely to TIF out
To a certain point, it’s likely. Depression and other mental health issues are often comorbid with trans. Autoimmune disorders are often comorbid or linked to mental health issues, as well, because of how they create a disconnect of the feeling of the body and health and the mental state. Trans is literally defined as just feeling “born in the wrong body”… so it’s a pretty good assumption to make for TIFs, since women often have a lot more thought behind themselves and their social appearance. Add on the fact that women are more likely to have autoimmune issues than men… perfect recipe.
Another explanation for the connection between depression and autoimmune disorders - and immune disorders such as the primary immune deficiency diseases and AIDS - is "the cytokine theory of depression," which holds that inflammation caused by an excess of cytokines is at the root of many cases of depression in both physically well and physically ill people.
This theory also holds that impaired immune function and high levels of inflammation play a big role in determining patients' response - and lack of response - to the SSRI drugs that have become the mainstay treatment for depression since the introduction of Prozac 35 years ago. The cytokine theory of depression is one of the plausible explanations put forward for why SSRI drugs don't work for a large chunk of the depressed people who take them, especially those with major depressive disorder that's severe, moderate-to-severe and recurrent.
The cytokine theory of depression was first proposed in the 1980s, but it didn't gain much traction or get much investigation initially because the man who originally came up with the theory died unexpectedly before his work was completed and ready for publication. Moreover, once the SSRI antidepressant Prozac was introduced in 1988 followed by a slew of other SSRIs under different brand names like Zoloft, the medical establishment and mainstream media sided with Big Pharma by adopting, promoting and championing the single-minded view that the serotonin theory of depression is the only theory of depression that has any merit and thus the only theory that should be taken seriously. This happened despite the fact that to this day, the evidence base for the serontonin theory of depression that the SSRI drug industry is built on remains extremely weak to non-existent.
Mounting evidence indicates that inflammatory cytokines contribute to the development of depression in both medically ill and medically healthy individuals. Cytokines are important for development and normal brain function, and have the ability to influence neurocircuitry and neurotransmitter systems to produce behavioral alterations. Acutely, inflammatory cytokine administration or activation of the innate immune system produces adaptive behavioral responses that promote conservation of energy to combat infection or recovery from injury. However, chronic exposure to elevated inflammatory cytokines and persistent alterations in neurotransmitter systems can lead to neuropsychiatric disorders and depression.
Mechanisms of cytokine behavioral effects involve activation of inflammatory signaling pathways in the brain that results in changes in monoamine, glutamate, and neuropeptide systems, and decreases in growth factors, e.g. brain derived neurotrophic factor. Furthermore, inflammatory cytokines may serve as mediators of both environmental (e.g. childhood trauma, obesity, stress, and poor sleep) and genetic (functional gene polymorphisms) factors that contribute to depression’s development.
https://pmc.ncbi.nlm.nih.gov/articles/PMC3741070/
Major depressive disorder (MDD) is a leading cause of disability throughout the world with a global prevalence of 2.6–5.9% [1]. The total estimated number of people living with depression worldwide increased by 49.86% from 1990 [when SSRI antidepressants first became the mainstay treatment] to 2017 [2]. According to worldwide projections, MDD will be the single major cause of burden of all health conditions by 2030 [3].
Despite available pharmacotherapeutic options, 30–60% of patients with MDD are not responsive to available treatments [5] and the rate of remission of the disease is often < 50% [6], while recurrence rates are more than 85% within 10 years of a depressive episode, and average about ≥ 50% within 6 months of assumed clinical remission [4].
Indeed, there exists no compelling evidence that current treatments are capable of disease modification in MDD patients. Thus, therapeutic deficiency in treatment outcomes reflects the demand for revitalizing psychiatric therapeutics with novel pharmacotherapeutic options that engage non-monoaminergic molecular targets.
https://jneuroinflammation.biomedcentral.com/articles/10.1186/s12974-021-02100-7
In this report, we aimed to explore the association between cytokines and later severity of depression or suicidal ideation and behavior, which may be potential treatable targets of depression.
Depression patients with suicidal attempts have high levels of blood pro-inflammatory cytokines such as TGF-β, CRP, and decreased levels of anti-inflammatory cytokines such as IL-4 [24, 25]. They also exhibit increased in IL-1β, IL-6, TNF-α levels and decreased IL-10, IL-1 receptor antagonists levels in the prefrontal cortex [18].
High levels of interleukin-1β and tumor necrosis factor-α were predictive of middle-term severe depressive symptoms and suicidal ideation and behavior respectively.
Plasma IL-1β levels are significantly associated with depression and depressive severity [29], and also related to treatment-refractory depression [5].
Inflammatory system plays a complicated role in depression. Plasma cytokines, a family of polypeptides, include interleukin (IL), interferon (IFN), tumor necrosis factor (TNF), tumor transforming growth factor (TGF), etc. Cytokines are generally divided into pro-inflammatory (IL-1β, IL-2, IL-6, IL-12, IL-15, TNF-α, IFN-γ, etc.) and anti-inflammatory cytokines (IL-4, IL-5, IL-10, IL-13, etc.) [5]. Some pro-inflammatory cytokines are upregulated in depression people [6], and also positively correlated with the severity of depressive symptoms [7].
Cytokines imbalance causing dysregulation of hypothalamic-pituitary-adrenal (HPA) axis and neurogenesis is considered to be a key factor in the development and treatment of depression [8]. Plasma cytokines can penetrate the blood brain barrier (BBB) to affect brain function directly or activate microglia in the central nervous system (CNS), and also communicate with the neuroendocrine system by transmitting signals to the hypothalamus and stimulates the release of corticotropin releasing hormone (CRH), adrenocorticotropic hormone (ACTH) and glucocorticoids ultimately [9, 10]. Glucocorticoids lead to neuronal atrophy in the depression related prefrontal cortex and hippocampus [11].
Cytokines are involved in glutamatergic and monoamine neurotransmission in the CNS. They reduce the level of glutamate transporters and increases the level of glutamate [12]. Glutamatergic synapses are associated with depression related cerebral regions, including prefrontal cortex and hippocampus [11]. Pro-inflammatory cytokines regulate 5-hydroxytryptamine (5-HT) turnover in brain and decrease levels of 5-HT in the synaptic cleft, which may influence neuroplasticity and finally result in depression [13, 14]. They also inhibit neurogenesis by activating nuclear factor κB [15].
Within brain tissue, microglia expresses the P2X7 ion channel, and releases IL-1β through NLRP3 inflammasome complex. The P2X7-NLRP3-IL-1β pathway is associated with depression [34]
The treatment response of depression is associated with specific genetic variants and methylation status of the gene IL-1β [30]. Higher level of IL-1β mRNA molecules predicts poor antidepressant response [31]. And IL-1β decreases after one month antidepressant treatment [32]. IL-1β, produced by macrophages, endothelial cells and astrocytes, can cross the blood brain barrier and alter the HPA-axis [33].
The improvement of depressive symptoms after treatment [with] antidepressants is related to the reduction of cytokines including IL-1β and IL-6 [22].
Targeting inflammation may be a potential strategy to treat depression.
https://bmcpsychiatry.biomedcentral.com/articles/10.1186/s12888-024-05639-w
That's very interesting. I had not heard of cytokine. Thanks and keep talking about the failure of SSRIs and the debunked serotonin chemical imbalance theory.
Super interesting! Also SSRIs have only a 2-3% effective rate above placebo. It worked for me (panic disorder) to reset my body but I’m not sure if it’s needed in all or many cases of true depression (not situational depression)
It is very easy to get depressed when your autoimmune disease makes you tired all the time. When you are always exhausted, you realize you don't have enough energy to do a lot of things you want and need to do.
In this society, people who do not "work hard" (whatever-in-the-hell-that-means) are thought to be "lazy" and often chastised as if it's a moral failing (Thank you %$@#%! Puritan Work Ethic) to need to sleep for 12 hours a day. Feeling like a failure from that one thing alone, because of how widespread the idea is a very simple cause of depression right there.
Females are more prone to non-lethal immune disorders in general
A TIF at my work is very, very underweight and identifies as having fibromyalgia. I wonder if it's actually from this?
Possibly. I have read somewhere (if someone knows where I'd appreciate the link to save it to my sources!) that T can/will put women into perimenopausal or menopausal conditions which include a reduction of bone density aka Osteoporosis. If she is also underweight then her body is likely already depraved of nutrients. So it's not much of a stretch to consider that she is in chronic pain from a mix of those two issues.
Plus, as far as I know - and again, please correct me if I'm wrong - Fibromyalgia is oftentimes just a way for Drs to be able to provide you with medications legally, often for lack of a Diagnosis. At least that's what two acquaintances with Fibromyalgia told me.
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I mean, if - and only if - I remember correctly, T puts women into (Peri-)Menopausal states and that lowers bone density. I just definitely know it thickens the blood. Upon a google search, OLDER women may profit from higher blood serum Testosterone. So again, if someone has the TiF study in that on hand I'd appreciate it. Hysto dot net says it increases risks of Osteoporosis.
afaik, drs don't really know what causes fibromyalgia. I've had people suggest i have it... that was back in the late 2000s though. It's become a lot more ... publicized since then i think.