When I released Binary two years ago, the goal was to explain how sex is universally defined across species and debunk common sex spectrum arguments. It became a #1 bestseller in Biology. Now my latest book, The Sex Development Handbook, maps how sex develops in humans--from typical development to more than 25 DSDs--with each spread featuring a color-coded diagram and engaging commentary. Recommended as an essential read for high schools, colleges, and graduate schools, the handbook shows each human, even those with rare disorders, develops as a male or female, integrating real-world clinical practice into an accessible guide for a wide audience! Order here! theparadoxinstitute.org/prin…

Since 2020, the Paradox Institute has published 4 books reaching #1 in their categories. 1. The Sex Development Handbook, charting typical male and female development and 30+ DSDs. 2. Binary, debunking the sex spectrum myth. 3. It All Begins With Two, a beautifully illustrated children's book on male and female. 4. Please Don't Feed the Fears, an illustrated children's story on how to understand fear. Check out our book collection on our new website! 🔗 theparadoxinstitute.org/book…

Congratulations on the launch, and thank you for the years of careful, rigorous work that made this possible. The new Paradox Institute site is exactly what people need: a clear, sourced library of animations, articles, and books on the biology of sex, plus interactive sex development charts.

Hi everyone, I'm excited to announce the launch of our new website for Paradox Institute! It includes a beautiful library of all our work, and first-of-its-kind Interactive Sex Development Charts with more features to come, along with 30+ DSDs very soon. theparadoxinstitute.org

I think I’ve got a draft outline on the structure for the book I’m planning on sex differences in the human brain. The aim isn’t to catalogue hundreds of male–female differences, or argue from the outset that male & female brains are either “fundamentally different” or “basically the same”. I’m much more interested in what the evidence *actually* allows us to conclude. Current chapters: 1. Are Male and Female Brains Different? What does a sex difference actually mean? Means, overlap, variability, development, interactions and why apparently conflicting results can both be true. 2. How Does a Human Brain Become Sexually Differentiated? Chromosomes, hormones, development, puberty, plasticity and environment, including what animal experiments can, and importantly cannot, tell us about human sex differences. 3. If a Brain Becomes Less Male, Has It Become More Female? Masculinisation, feminisation, de-masculinisation and de-feminisation, and why a statistical shift towards the opposite sex (for whatever reason) doesn’t necessarily tell us the biological mechanism. 4. Men Have Larger Brains. Now What? Brain size and the surprisingly complicated question of how we should account for it. Ratios, ICV adjustment, matching and allometry can give different answers because they ask different questions. 5. Where in the Human Brain Are the Sexes Different? What the human evidence actually shows across brain structure, connectivity, development and variability, focusing on magnitude, overlap and replication rather than lists of significant regions. 6. Is There Such a Thing as a Male or Female Brain? Bringing together the mosaic debate, individual sex-typicality and sex classification. How can brains be mosaics while algorithms can still predict sex surprisingly well? 7. From Brains to Behaviour Does finding a brain difference actually explain a behavioural difference? Correlation, causation, mediation, plasticity and the limits of what neuroimaging can tell us. 8. So How Different Are Male and Female Brains? Returning to the original question with, hopefully, a much more nuanced answer. Importantly, I don’t want this to read like a statistics or research-methods textbook. The idea is to introduce these concepts gradually through actual neuroscience questions, experiments and controversies. USP: I’ll also develop and create a very large fictional Human Brain Variation Study that follows the reader throughout the book and chapters. I’ll code the population myself, meaning I’ll know its true underlying structure, and repeatedly analyse the same data in different ways to show how changing the question, sample, statistical model or correction methods can change the result. By the end, I’d like someone with no statistical training to have almost accidentally acquired the tools to understand why claims about male and female brains are often much more complicated than the headline suggests. Not because they’ve sat through a statistics lesson, but because they’ve spent the book learning how to ask better questions of the evidence. Thoughts so far?

'Breheny’s simple, honest approach to sex education stands in stark contrast to the way public schools teach about sex, the purpose of which, she said, is “just … to obfuscate and confuse.”' Thanks so much to @IWF and @SarahHopeWilder for the feature!

🦄 EXCLUSIVE: Inside the organization providing sex education material to combat ‘the gender unicorn’ Learn more from @SarahHopeWilder via @iwfeatures on @PdxInstitute: iwfeatures.com/profile/insid…: iwfeatures.com/profile/insid…

Doctors are still completely baffled over hormonal disorders like PMDD, endometriosis, and PCOS But they'll happily induce disorders in the name of "gender" Why? Because it's far more easy and lucrative to break something for them than it is to fix it Let me explain 🧵

One of my favorite case studies in the biology of sex is 47:XXY (SRY Negative), a combination of two genetic disorders into one that then cancel each other out, creating a fertile XXY female. 47:XXY is the most common sex chromosome disorder, causing Klinefelter Syndrome in the male embryos it affects. However, a much rarer form of 47:XXY exists, where a person is conceived without the essential chromosome material on the short arm of the Y chromosome, known as the p arm. The p arm holds the SRY gene, the switch for male development that encodes testes. Without this male-making material, the precarious genetic balance of the undifferentiated gonad begins to tilt towards the female genetic network. Now the WNT4, FOXL2, and RSPO1 network upregulates and suppresses the male system, resulting in the initial development of ovaries. In embryos with XY who are also missing SRY, this is where ovarian development stops. The young ovarian tissue degenerates and forms fibrous tissue called streak gonads, resulting in sterility. Something remarkable happens, however, in the XXY SRY negative (SRY-) embryo. Unlike XY embryos who only have one X chromosome, XXY has two. Essential genes for ovarian maintenance can now express themselves in double copy, providing proteins for development of the follicles and the Granulosa cells that support them. This in turn maintains the health of the ovaries and stops them from degenerating. From here, sex development continues to proceed as normal. For an in-depth analysis of 25 DSDs and many case studies, we published a first of its kind visual handbook on human sex development and DSDs, featuring beautiful development diagrams and accessible commentary. #1 in Embryology at release. Find out more and order your copy at: sexdevelopmenthandbook.com

Kier Starmer resigns, to be replaced by Kier Starmer the 2nd.

Why aren't women who identify as men usually centered in this debate? Two major reasons: 1.) Behavioral averages Men are more disagreeable on average. They will often challenge a norm to establish or remove a boundary that stands between them and an objective. Women are more agreeable on average. They won't often challenge a norm, or enforce boundaries (usually because of fear or social ostracization) 2.) Force Men can also physically back up anything they want or don't want with force Women can't counter that force defensively to keep men out or offensively to try and get in And before someone comes along to argue for outliers, that's why I wrote "on average" for behavior, and used entire groups for force. On average, men have maintained sex segregated spaces by saying maintaining a boundary and female spaces were eroded because of males disagreeing with the boundary. On average, fewer women maintain the boundary, even if they disagree - this is evidenced by gyms, bathrooms, sports, orgs, etc where most women don't seem to challenge these men out of fear or other factors. As for force, collectively, *and* on average, women can't physically stop or force men. Some people will still probably disagree with this. They're free to do that. It doesn't change the evidence.

Help us make reality-based biology education accessible to everyone! Your donation supports the creation of books, animated videos, and educational resources that bring essential scientific truths to a wide audience. 🔗 theparadoxinstitute.org/dona…

"There's a reason you separate military and the police. One fights the enemies of the state, the other serves and protects the people. When the military becomes both, then the enemies of the state tend to become the people." - Commander William Adama, Battlestar Galactica

I have covered OT-DSD in my books and videos, but here’s an explanation of its biology. Many gender activists claim that Ovotesticular Disorder makes one “both male and female.” This is a scientifically false and harmful belief. OT-DSD results in gonadal tissue of both types (testicular and ovarian) in a single human. It affects both sexes. And it *does not* result in fully developed reproductive systems of both sexes. Instead, it results in one dominant system with vestigial tissue from the other. It begins when the male or female fetus is developing their gonads, and aberrant signals from genetic mutations tell one or both gonads to also develop tissue from the opposite sex. This can result in, as the example shows in the chart, a female with an ovary on one side and an ovotestis on the other, or a male with a testis and an ovotestis. There are more OT-DSD gonadal configurations than that, but that’s the idea. One sex development path is prominent, which is then disrupted partially by another path trying to activate at the same time. In the example charted below, the partial testis hormones AMH and T cause disruption of Müllerian duct development in the female fetus, resulting in slightly underdeveloped Müllerian ducts and slightly masculinized genitalia (growth of the clitoris, partial labial fusion). Treatment for OT-DSD depends on the individual’s development path and their unique sex-specific needs. It may involve hormone replacement therapy, elective surgery, necessary surgery if one of the gonads has a high risk for malignancy, and other potential treatments. Many gender activists do not care when they lie about serious conditions such as OT-DSD, because if they stopped lying, they could not use these conditions as tools to deconstruct sex and validate their own delusional beliefs.

To the best man I know, the amazing father of our children, the man who has taught so many and inspires others I know I'm not the only one grateful for everything he brings to the world Happy Father's Day @zaelefty 💕

A trans activist asked me, “Why is it so hard for you to accept that not everything fits into neat boxes?” Here is my response.

The typical paths of sex development for males vs females, charted. Males: - SRY gene -> SOX9 feedback loop - Gonads differentiate into testes - Testes produce AMH, disintegrating Mullerian duct - Testes produce T, differentiating the Wollfian duct - Some T into DHT, forming male external genitalia Females: - No SRY -> WNT4 and FOXL2 suppress SOX9 - Gonads differentiate into ovaries - Ovaries produce little AMH, unimpeded gene networks build the Mullerian duct - Ovaries produce little T -> COUP-TFII transcription factor helps disintegrate Wolffian duct - Low T -> Low DHT, forming female external genitalia

Great question! First, with the X chromosome, it’s evolved to undergo X-inactivation when there is more than one present, and only around 20% of genes on the inactivated X remain active. So with something like Trisomy X, the extra X chromosomes are inactivated, and a small portion of their genes remain active. This does cause minor issues with gene dosage, but it is far less damaging than other trisomies because of this much lower level of functional gene duplication. Second, with extra Y chromosomes, even though they do not undergo any inactivation, they have the least amount of genes out of any other chromosome, and none of its genes are essential to individual survival, so extra copies don’t cause any life threatening issues. Third, losing a chromosome is usually deadly. All monosomies of the autosomes, where you only have 1 autosome instead of a pair, almost always result in death of the embryo. The monosomy that has the best chance of survival is Monosomy X (Turner Syndrome). This is once again due to the concept of X-inactivation. Losing a second X chromosome means you are functionally losing far less genes than you would if you lost a second autosome. Monosomy X is not without severe and life threatening issues, but it’s far more survivable than the autosome monosomies.