How allergies and vaccines may be contributing to the disproportionate increase in female transgender rates
There is a startling finding in the Cass Report that gender dysphoria is disproportionately affecting females. Below are two figures from the report:
Most female to male transgenders are lesbians, among whom a good portion are butch lesbians with masculinized sexual behavior and appearance. Trangenders have anectodally noted that being a butch lesbian is not a trend anymore having been replaced by the trend of female to male transgenders.
In butch lesbians, due to exposure to high testosterone levels (and probably other factors discussed herein), the balance in sexual arousal between the clitoris and the vagina is shifted to the clitoris. They find little pleasure in vaginal stimulation (hence intercourse), prefer masturbation and when exposed to even higher testosterone levels (like during hormone replacement therapy) their clitoris enlarges (called bottom growth), becomes more sensitive and is used as a small penis. This, together with masculinized appearance and behavior feeds into their gender disphoria.
One of the most important brain areas responsible for the regulation of sexual behavior, especially the thrusting reflex (and the corresponding urge), is the medial preoptic area (mPOA) in the hypothalamus.
The mPOA is 2.2 times larger in males than in females. In some studies it is smaller in homosexual males and a decrease in its size has been associated with same-sex preference in males.
According to Hofman and Swaab, the MPOA of 2- to 4-year-old children has 4 times more cells than the MPOA of newborns. It achieves a peak in number of cells around this age and thereafter the cell number gradually decreases through the years in both sexes, but faster in females.
Later research of Ahmed et al. has shown that the mPOA is enlarged with new cells during puberty in male rats.
At around age 6 begins the adrenarche when the adrenal glands start producing sexual hormones. The different trajectories in the graph of the male and female MPOA in respect to cell number may be due to the adrenarche.
This trajectory is supported by other research, like Kurth et al. (2021) who examined brains of people aged +5 and found that “between the ages 6 and 17, the differentiation between male and female brains increased over time, with maximum acceleration occurring around age 11” (when the gonads begin to release sexual hormones).
The male mPOA has much higher density of dendritic spine synapses, significantly more microglia than the female POA.
Experiments show that mast cells under the effect of sexual hormones start the masculinization of synaptic connectivity in the mPOA by releasing histamine, which activates neighboring microglia to release the spinogenic factor, PGE2 to increase the dendritic spine density of the POA.
Kathryn Lenz et al., in “Prenatal Allergen Exposure Perturbs Sexual Differentiation and Programs Lifelong Changes in Adult Social and Sexual Behavior” have shown that in rats when the fetus is exposed to allergies in utero the mast cells and the microglia become overactive. As a result, the dendritic spine density in the mPOA of females is increased, their sexual behavior is masculinized, while the spine density in themPOA of males is decreased and their sexual behavior is feminized.
But the allergies have a different effect on the female mPOA as compared to male mPOA:
According to Lenz et al.:
“The masculinization of dendritic spine density observed in neonatal females endured into adulthood, but the decrease observed in neonatal males was no longer evident in adulthood, with males gestated in allergic-challenged dams being indistinguishable from control males”
Allergen exposed females had higher mount rate, shorter mount latency and increased preference for female odours, while allergen exposed males had higher number of mounts (more masculine in this regard), but longer latency to mount, lower preference for female odors (less masculine).
Research shows that female mast cells are more reactive to stress than male mast cells and that early life stress increases mast cell sensitivity and mast cell-hyperactivation related diseases to a greater extent in females than males. See “Early life adversity drives sex-specific anhedonia and meningeal immune gene expression through mast cell activation”, “Perinatal androgens organize sex differences in mast cells and attenuate anaphylaxis severity into adulthood”, “Sexual dimorphism in the mast cell transcriptome and the pathophysiological responses to immunological and psychological stresses.
Microglia shape and sexually differentiate other brain areas involved in sexual behavior as well, like the nucleus accumbens, prefrontal cortex etc. into adolescence.
According to Cong Hu et al., microglia are important also in the etiology of autism. LGBT rates, allergies are much higher in people with autism. Hu et al. note that microglia with enhanced activation may be left in the brains of offspring due to early life inflammatory events, therefore predisposing the individual to lifelong dysfunctions.
Since mPOA in humans is in dynamic change postnatally, overactive mast cells and/or microglia could continue to exert a negative effect in its (and other brain areas) sexual differentiation until adolescence.
According to the Hygiene Hypothesis there is a skewing of inflammation toward allergic reactions (and mast cell activation) in children due to lack of exposure to bacteria and helminths.
High pollution burden also increases mast cell activation, while melatonin, which is decreased by exposure to artificial light, inhibits mast cell activation. These environmental factors are chronic exposures, hence may cause chronic overactivation of mast cells.
During the first year of life an important source of inflammation are vaccines. More than half of pregnant women in USA are vaccinated. Infants are repeatedly vaccinated at birth, and every two months during the first year of life, with an ever increasing amount of vaccines.
Childhood vaccines have inactivated pathogens or pathogen toxins, and the adjuvant aluminum hydroxide, which skews the immune response to Th2 mediated, typically involved in allergic reactions. In addition, while live pathogens enter the body through the skin, the airways, the mouth, the inoculated pathogens enter the body through puncture. Mast cells and basophils, immune cells that produce IgE, are typically involved in immune reactions to proteins and toxins entering through disrupted skin (like venom, insect bites, helminths).
So, while vaccines are not chronic exposures, like pollution and lack of bacteria/helminths, they are given in close succession during the first year of life, a period of fast brain and immune system development, when they can prime mast cells and microglia to be overactive to later life stresses, disrupting sexual differentiation of the brain, more so in the females due to their mast cells being more sensitive.
I appreciate the work that you’re doing to try to make scientific sense of the rise in transgender identification. I do want to offer a perspective. It’s been known for some time that transgender identification has risen astronomically in natal females over the past 10 years. The book “Irreversible Damage” by Abigail Shrier covers this extensively. I’ve often seen it stated that many or even the majority of these females are same-sex attracted and are gender non-conforming, but I haven’t seen much evidence to back this up. What are you basing this statement on?
In my personal, limited experience with my daughter and others I’m aware of, this is actually not the case. Until declaring a transgender identity at age 14 she was a very feminine girl, and it’s become clear as she’s gotten older that she is primarily or solely attracted to males.
I think this is important because it raises the question of whether there is a biological basis for transgenderism, or whether it is strictly a psychological and social phenomenon. Transgender activism is based on the assumption that it is a biologically determined, inborn trait that is not changeable. If this were true, then the position of activists would make sense - of course we should try to identify people with this trait as young as possible and treat them medically to relieve their suffering. Of course parents should accept and encourage this medical treatment, and those who do not are unfit parents and children should be removed from their care. Of course society should bend over backward to accommodate people with this medical condition, and insurance should pay for treatment. But as soon as you question the assumption that it is an inborn trait, the whole house of cards falls down.
I tend to believe it is a socially influenced psychological condition. It seems like you have the view that it does have a medical cause, but that cause is not inborn or permanent and can potentially be treated in other ways. It would be interesting to see what evidence exists, and how high the quality of that evidence is, that there are biological differences in trans-identifying people even prior to medical transition.